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Notes
Study the apolipoproteins
The ductus arteriosus is derived from the sixth embryonic aortic arch. A patent ductus arteriosus
can cause a thrill and a continuous murmur on physical exam.
Patent ductus arteriosus is an embryonic structure that allows fetal blood to pass directly from the
pulmonary artery to the systemic circulation thereby bypassing the pulmonary circulation. During
embryonic development, the head, neck and upper thorax region develop from a set of arches
know as pharyngeal arches. Each arch is associated with a cranial nerve and an aortic arch. The
sixth aortic arch gives rise to the pulmonary arteries and the ductus arteriosus.
-Imprinting: is produced by DNA methylation, which is an epigenetic process in which genes can
be silenced by the attachment of methyl groups to cytosine residues in the DNA molecule.
-Aneuploidy: is result of nondisjunction during mitosis or meiosis.
Genomic imprinting refers to the phenomenon in which an offspring's genes are expressed in a
parent-specific manner. Genomic imprinting is produced by DNA methylation, which is an
epigenetic process in which genes can be silenced by the attachment of methyl groups to cytocine
residues in the DNA molecule.
Genomic imprinting refers to the phenomenon in which an offspring's genes are expressed in a
parent specific manner. Genomic imprinting is produced by DNA methylation, which is an
epigenetic process in which genes can be silence by the attachment of methyl groups to cytosine
residues in the DNA molecule.
Aspirin irreversibly inhibits COX-1 and COX-2. COX-2 is an inducible enzyme that is normally
undetectable in most tissues except in the case of inflammation. COX-2 is an enzyme with a
molecular weight of 72 kD.
The most common pathogens causing nosocomial bloodstream infections -Coagulase-negative
staphylococci -Staphylococcus aureus -Enterococci -Candida species
Homogeneous deposition of eosinophilic hyaline material in the intima and media of small arteries
and arterioles characterizes hyaline arteriolosclerosis, which is typically produced by long-standing
nonmalignant hypertension and/or diabetes.
Among the arteritides, the transmural inflammation with fibrinoid necrosis is most characteristic of
PAN. fever, malaise, weight loss, abdominal pain, and melena are frequent symptoms of PAN.
PAN is associated with hepatitis B infection in 10-30% of cases.
Among the arteritides, transmural inflammatio with fibrinoid necrosis is most characteristic of PAN,
Fever, malaise, weight loss, abdominal pain, and melena are melena are frequent symptom of
PAN. PAM is associated with hepatitis B infection in 10-30% of cases.
Henoch-Schonlein purpura is an small vessel leukocytoclastic angiitis, is asociated with IgA and
C3 deposition in children 3 - 11 years old.
Polyarteritis nodosa Is a segmental transmural necrotizing inflamation of medium-to small-sized
arteries. Renal artery involvement is often prominent. Vessels of the kidneys, heart, liver, and
gastrointestinal tract are most commonly involved in resulting ischemia, infarction or hemorrhage.
Cutaneous manifestations occur in up to one-third of patients, and include palpable purpura. The
lung is very rarely involved.
PAN is segmental, transmural, necrotizing inflammation of medium to small sized arteries. Renal
artery involvement is often prominent. Vessels of the kidney, heart, liver and GI tranct are most
commonly involved in resulting ischemia, infarction or hemorrhage. Cutaneous manifestations
occur in up to on third of pctes and include palpable purpura. The lung is very rarely involved.
Ingestion of beta-aminopropionitrile, a chemical found in certain kinds of sweet peas, causes
"angiolathyrism" a change in the elasticity of the aorta that mimics the myxomatous degeneration
seen in patients with Marfan syndrome. This coompound inhibits lysyl oxidase, and enzyme
responsible for cross- linking elastin fibers and collagen fibers. Normal fx of this enzyme is
responsible for maintaining the elastic lamina and ensuring the integrity of the aorta.
The major cause of AAA is atherosclerosis. Atherosclerotic atheromas can sufficiently progress to
weaken the underlying media of the aortic wall.
Aortic aneurysm are often caused by artherosclerosis, atherosclerotic atheromas can sufficiently
progess enough to weaken the underlying media of the aortic wall. Intimal (fatty) streaks the
earliest lesion of atherosclerosis, are composed of intimal lipid-filled foam cells. which are derived
from macrophages and smooth muscle cells that have engulfed lipoproteins, predominantly LDL.
These complexes then insudate into the intima through an injured, leaky endothelium.
The cause of abdominal aortic aneurysm is atherosclerosis. The atheromas can sufficiently
progress enough to weaken the underlying media of the aortic wall. Intimal streaks, the earliest
lesion of atherosclerosis, are composed of intimal lipid filled foam cells, which are derived from
macrophages and smooth muscle cells that have engulfed lipoproteins, predominantly LDL. These
complexes then insudate into the intima through an injured, leaky endothelium.
Cutaneous, strawberry-type capillary hemangiomas are common, beningn, congenital tumors,
which are composed of unencapsulated aggregates of closely packed, thin-walled capillaries.
Initially strawberry hemangiomas grow in proportion to the growth of the child, before eventually
regressing. In 75-95% of cases, the vascular tumor regress completely by age 7.
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A benign glomus tumor (glomangioma) can produce a very tender, small (a few millimeters in
diameter), red-blue lesion under the nail bed. This type of tumor originates from the modified
smooth muscle cells that control the thermoregulatory functions of dermal glomus bodies.
Osler-Weber-Rendu syndrome It is a hereditary hemorrhagic telangiectasia. AD with presence of
telangiectasia in the skin as well as the mucous membranes of the lips, oropharynx, respiratory
tract, GI tract, and urinary tract, brain, liver, spleen as well.
Persistent lymphedema (with chronic dilatation of the lymphatics channels) predisposes to the
development of lymphangiosarcoma, a rare malignant neoplasm of the endothelial lining of
lymphatic channels. This cancer may arise approximately 10 years after radical mastectomy with
axilary node dissection for breast.
Hepatic angiosarcoma is associated with exposure to carcinogens such as arsenic, thorotrast, asn
polyvinyl chloride. Tumor cell express DC31, an endothelial cell marker.
Hepatic angiosarcoma is associated with exposure to carcinogens such as arsenic, thorotrast, and
polyvinyl chloride. Tumor cells express CD 31, an endothelial cell marker.
A paraneoplastic syndrome of hypercoagulability may be seen in some patietnts with cancer,
specially adenocarcinomas of the pancreas, colon, or lung. Superficial venous thromboses may
thus appear in one site and then resulve, only to recur in another site, producing "Trousseau's
syndrome," or migratory superficial thrombophlebitis-an indication of visceral cancer.
Chirg-straus syndrome is an idiopathic systemic vasculatis associated with adult-onset asthma,
eosinophilia, and p-ANCA. Additional clinical criteria for this diagnosis include a history of allergy,
mono-or polyneuropathy, migratory/transient pulmonary infiltrates, and paranasal sinus
abnormalities.
Atherosclerosis is initiated by repetitive endothelial cell injury, which leads to a chronic
inflammatory state in the underlying intima of large elastic arteries as well as large and mediumsize muscular arteries.
Injured endothelial cells can release growth fcts that promote SMC migration and proliferation,
such as platelet-derived growth fct. They also express surface vascular cell-adhesion olecules that
allows adherence of monocytes and lymphocytes as well has diapedesis into intima, such as
VCAM-1. The can release citokines, and growth fcts to promote SMC migration and prolif in the
intima, then fibrogenesis.
The vascular reaction to endothelial and intimal injury is intimal hyperplasia and fibrosis,
predominantly mediated by reactive smooth muscle cells that migrate from the media to the
intima.
Inflammatory macrophages in the intima may reduce plaque stability by secreting
metalloproteinases, which degrade collagen.
Right heart failure increases central venouse pressure (CVP) - Increased capillary hydrostatic
pressure - Incresed net plasma filtration - Incresed interstitial fluid pressure
Aldosterone excess will cause hypertension, hypokalemia, metabolic alkalosis and depressed
renin. Alternatively, hypoaldosteronism is the cause of the type IV renal tubular acidosis.
Aldosterone antagonists such as spironolactone or eplerenone can be used as medical therapy for
Conn's syndrome.
Aldosterone excess will cause hypertension, hypokalemia, metabolic alkalosis and depressed
renin. Alternatively hypoaldosteronism is the cause of type IV renal tubular acidosis. Aldosterone
antagonists such as spironolactone or splerenone can be used as medical therapy for Conn's
syndrome.
Thiazide diuretics and dihydropyridine calcium antagonists are presently first line drugs to treat
isolated systolic hypertension in nondiabetic pctes (where an ACE-I or ARB would be utilized first).
Amlodipine can cause bilateral ankle swelling and flushing.
Amlodipine is a calcium channel blocker used in hypertension that can lead to flushing and
peripheral edema.
Isolated systolic HTA is a common form of HTA, especially in the elderly (only systolic pressure is
elevated). There is discrepancy as to where the cutoff for elevated systolic HTA; it ranges
anywhere from over 140/160mmHg. Thiazide diuretics and dihydropyridine calcium antagonists
are presently first line drugs to treat isolated systolic HTA in non diabetis pctes (where an ACE-I or
ARB whould be utilized first). RAM of Ca channel blocker: flushing and peripheral edema.
The cutaneous flushing associated with niacin is mediated by prostaglandins and can be
prevented with aspirin pre tto. Capsaicin reduces pain by decreasing the level of substance P in
the peripheral nervous system.
The cutaneous flushing associated with niacin is mediated by prostaglandins and can be
prevented with aspirin pre treatment(because this effect is mediated by prostaglandins, so give
aspirin before 30-60 minutes before give nicotinic acid administration). Capsaicin reduces pain by
decreasing the level of substance P in the peripheral nervous system.
Most stains are metabolized by cytochrome P-450 3A4, with the exception of pravastatin.
Concomitant administration of drugs that inhibit statin metabolism (e.g. macrolides) is associated
with increased incidence of statin-induced myopathy and rhabdomyolysis. Acute renal failure is a
possible sequela of rhabdomyolusis.
Most statins are metabolized by cytochrome P-450 3A4, with the exeption of pravastatin.
Concomitant administration of drugs that inhibit statin metabolism (e.g. macrolides) is associated
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with increased incidence of statin-induced myopathy and rhabdomyolysis. Acute renal failure is a
possible sequela of rhabdomyolysis.
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Niacin can potentiate the effects of some anti-hypertensive medications because of its
vasodilatory effects. Dose adjustment may be required. Niacin also causes insulin resistence and
oftentimes necessitates an increase in diabetes medications.
Niacin can potentiate the effects of some anti-hypertensive medications because of its
vasodilatory effects. Dose adjustment may be required. Niacin also causes insulin resistance and
oftentimes necessitates an increase in diabetes medications.
Bile acid-binding resins are unique among hypolipidemic agents in that they increase blood
triglyceride levels. Fibric acid derivatives are the first line treatment for hypertriglyceridemia.
Bile acid-binding resins (cholestyramine, colestipol and colesevelam) are unique among
hpolipidemic agents in that they increase blood triglyceride levels. Fibric acid derivatives are the
first line tto for hypertriglyceridemia.
Simvastatin decreases and cholestiramine increases hepatic cholesterol production
independently. Combination therapy results in a net decrease in hepatic cholesterol synthesis and
plasma LDL level. Agents that increase hepatic cholesteril synthesis (e.g. fibrates and bile acidbinding agents) are associated with an increased risk of gallstones.
Fenoldopam is a newer parenteral agent that is classified as a selective dopamine-1 receptor
agonist. It causes arteriolar dilation and natriuresis leading to decreased systemic vascular
resistance and blood pressure reduction. Since fenoldopam is the only intravenous agent that
improves renal perfusion, it may be exceptionally beneficial in hypertensive patients with
concomitant renal insufficiency.
Losartan has as Mx of Action: - Increased: Renin, Angiotensin I, Angiotensin II - Decreased:
Aldosterone - No change: Bradykinin
ARBs work by blocking AT-1 receptors and inhibiting the effects of angiotensin II. This results in
arterial vasodilation and decreased aldosterone secretion. Since ARBs work at the level of AT-1
receptors and do not affect ACE activity, they do not interfere with bradykinin degradation or
levels. By blocking AT-1 receptors, ARBs also interfere with negative feedback mechanisms
resulting in increased renin, angiotensin I, and angiotensin II levels.
One major pathway that regulates the RAAS involves the beta adrenergic receptor pathway. Beta
1 receptors located on juxtaglomerular cells. Beta adrenergic blockers like propranolol inhibit renin
release by blocking beta 1 receptor mediated pathway. Also reducee angiotensin I, angiotensin II,
and aldosterone levels. Since beta blockers do not affect ACE activity, they do not affect
bradykinin levels.
ACE inhibitors can cause an acute rise in the serum creatinine by blocking angiotensin mediated
efferent arteriole vasoconstriction. This leads to a reduction in renal filtration fraction. For pctes
dependent on efferent arteriole constriction to maintain renal perfusion (those with renal artery
stenosis), ACE inhibitors can be deprimental by precipitating acute renal failure.
The HOPE trial demostrates the potential benefits of ACE inhibitors in pctes with significant
cardiovascular and peripheral vascular disease (decrease BP, decrease risk of MI, stroke, death).
Although ACE inhibitor therapy should be considered in most pctes, the development of ARF
(actue renal failure) may preclude the use of these agents in pctes with extensive athersclerotic
disease and concomitant bilateral artery stenosis.
Tto with statins causes hypatocytes to increase their LDL receptor density as a means of
increasing their uptake of circulating LDL.
The combination of statins plus fibrates increases the risk of myopathy in pctes being treated for
hyperlipidemia. Statin use is also associated with hepatotoxicity. The combination of fibric
derivatives and bile acid-binding resins increases the risk for cholesterol gallstones. This reflects
an increased cholesterol concentration in bile.
Pctes with familial hypoalphaproteins(low HDL) are at increased risk of developing premature
coronary artery disease. Niacin (vitamin B3) is the best agent currently available to increased HDL
cholesterol levels.
Estudia todo esto buaaa
Streptokinase is a thrombolytic agent that acts by converting plasminogen into plasmin, which
subsequently degrades fibrin. It most common side effect is hemorrhage. Streptokinase is a
foreign protein derived from Streptococci and can induce hypersensitivity reactions.
Fatty oxidation inhibitors are newer agents that inhibits fatty acid oxidation and shift energy
production to glucosa oxidation, thus promoting oxygen efficiency. This not only decreases the
amount of oxygen needed to support cardiac funtion, but also decreases potencially toxic fatty
acid metabolite production.
Fatty oxidation inhibitors are newer agents that inhibit fatty acid oxidation and shift energy
production to glucose axidation, thus promoting oxygen efficiency. This not only decreases the
amount of oxygen needed to support cardiac function, but also decreases potentially toxic fatty
acid metabolite production.
Cilostazol is a phosphodiesterase inhibitor used in patients with intermitent claudication. In
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addition to inhibition of platelet aggregation, cilostazol is also a direct arterial vasodilator.

Cilostazol has been shown to be superior to aspirin in the treatment of peripheral arterial disease.
Blanching of a vein into which norepinephrine (NE) is being infused together with induration and
pallor of the tissues surrounding the IV site are signs of the NE extravasation and resulting
vasoconstriction. Tissue necrosis is best prevented by local injection of an alpha1 blocking drug,
such as phentolamine.
Blanching of a vein into which NE is being infused together with induration and pallor of the
tissues surrounding the IV site are signs of NE extravasation and resulting vasocontriction. Tissue
necrosis is best prevented by local injection of alpha 1 blocking drug, such as phentolamine.
Blanching of a vein into which norepinephrine (NE) is being infused together with induration and
pallor of the tissues surrounding the IV site are signs of NE extravasation and resulting
vasoconstriction. Tissue necrosis is best prevented by local injection of an alpha 1 blocking drug,
such as phentolamine.
Nitroprusside treat hypertensive emergency. It has a quick onset of action and short duration of
action. Nitroprusside is initially metabolized to cyanide, with subsequent conversion to thiocyanate
by liver rhodanase. Thus, one major disadvantage of its use involves the risk for developing
cyanide toxicity. Sodium thosulfate is used to treat cyanide toxicity and works by donating sulfur to
liver rhodanase to enhance conversion of cyanide to thiocyanate.
alpha-1 adrenergic agonnists increase both systolic and diastolic blood pressure via stimulation of
alpha-1 adrenoreceptors in the vascular walls. Elevated systemic blood pressure is associated
with a reflex increase in vagal influence on the heart. This results in decreased heart rate,
contractility, and conductance.
Epinephrine increases systolic blood pressure (alpha1 + Beta1), increases heart rate (beta1), and
either increases or decreases diastolic blood pressure depending on the dose (either alpha1 or
beta2 predominates), Pretreatment with propranolol eliminates the beta effects of epinephrine
(vasodilatation and tachycardia), leaving only the alpha effect(vasoconstriction).
Norepinephrine stimulation cardiac beta-1 adrenoreceptors, which utilize the cAMP signal
transduction pathway. Stimulation of these receptors by norepinephrine causes increases in cAMP
concentration within cardiac myocytes.
Norepinephrine stimulates cardiac beta-1 adrenoreceptors, which utilize the cAMP signal
transduction pathway. Stimulation of these receptors by norepinephrine causes increases in cAMP
concentration within cardiac myocytes.
Vd=amount of drug given(mg)/plasma concentration of drug(mg/dL) Characteristics of a drug such
as high molecular weight, high plasma protein binding, high charge, and hydrophilicity tend to trap
the drug in the plsma compartment resulting in a low Vd (3-5L).
Phenoxybenzamine is a nonselective, irreversible alpha-1 and alpha-2 adrenergic antagonist that
effectively reduces the number of receptors available for norepinephrine binding. Because
phenoxybenzamine is an irreversible antagonist, even very high concentrations of norepinephrine
cannot overcome its inhibitory effects.
Phenoxybenzamine is a nonselective, irreversible alpha-1 and alpha-2 adrenergic antagonist that
effectively reduces the number of receptors available for norepinephrine binding. Because
Phenoxybenzamine is a nonselective, irreversible alpha-1, alpha-2 adrenergic antagonist that
effectively reduces the number of receptores available for norepinephrine binding. Because
d
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The tto of choice for diabetic ketoacidosis is intravenous hydration with normal saline and insulin.
These therapies will result indecreases in the serum glucose, osmolarity, and potassium, as well
as increases in serum bicarbonate and sodium.
Biventricular pacemakers requires 2 or 3 leads: 1) Right Atrial 2) Right Ventricular 3) Atrio
Ventricular groove on the posterior aspect of the heart course through the coronary sinus.
Left ventricular leads in biventricular pacemakers course through the coronary sinus, which
resides in the atrioventricular groove on the posterior aspect of the heart.
Cysteine becomes an essential amino acid in patients with homocystinuria, as the defective
enzyme cystathionine synthetase producess the substrate used by cystathionase for endogenous
production of cysteine.
Cysteine becomes an essential aa in pctes with homocystinuria, as the defective enzyme
cystathionine synthetase produces the substrate used by cystathionase for the endogenous
production of cysteine.
estudia esto
The chi-square test for independence is used to test the association between 2 categorical
variables. In the case of an exposure status and a binominal outcome, patients are divided into 2
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groups based on exposure, and the number of patients that experience each outcome is recorded
in a 2x2 table.
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A reliable test is reproducible in that it gives similar results on repeat measurements. Realiability is
maximal when random error is minimal.
The two sample t test is a statistical method commonly employed to compare the means of 2
groups of subjects.
Tetralogy of Fallot, transposition of the great vessels, and truncus arteriosus are three major
cyanotic heart diseases that can be caused by abnormal migration of neural crest cells through
the primitive truncus arteriosus and bulbus cordis.
Turner syndrome: Elevated levels of LH and FSH.
Evolution of MI Final stage of healing process begins 2 weeks after MI (Type I collagen). Fibrosis
continues until about 2 months after infaarction, forming dense collagenous scar (type I collagen).
Acute cardiac transplant rejection occurs weeks following transplantation and is primarily a cellmediated process. On histopathologic analysis of an endomysial biopsy, a dense mononuclear
lymphocytic infiltrate w/cardiac myocyte damage will be visualized. Tto: immunosuppressive
drugs.
Tto of a coagulase-negative staphylococcal infection involves initial empiric tto w/ Vancomycin with
or without rifampin or gentamicin due to the widespread antibiotic resistance of S. epidermidis,
especially in nosocomial infections.
Th treatment of a coagulase-negative staphylococcal infection involves initial empiric treatment
with vancomycin with or without rifampin or gentamicin due to widespread antibiotic resistance of
S. epidermidis, especially in nosocomial infections.
Viridans streptococci are normal inhabitants of the oral cavity and are a cause of transient
bacteremia after dental procedures in healthy and diseased individuals. In order to cause
subacute bacterial endocarditis they require preexisting valve damage leading to the local
deposition of fibrin required for them to adhere.
Fixed atherosclerotic plaques obstructing > 75% of the lumen of a coronary artery are associated
with stable angina.
The carcinoid syndrome can cause predominantly right-sided endocardial fibrosis which may
progress to pulmonic stenosis and/or restrictive cardiomyopathy. The severity of carcinoid heart
disease correlates with plasma levels of serotonin and urinary excretion of serotonin metabolite, 5hydroxyindoleacetic acid.
The carcinoid syndrome can cause predominantly right-sided endocardial fibrosis which may
progress to pulmonic stenosis and/or restrictive cardiomyopathy. The severity of carcinoid heart
disease correlates with plasma levels of serotonin and urinary excretion of the serotonin
metabolite, 5-hydroxyinoleacetic acid.
Causes of dilated cardiomyopathy Viral myocarditis (Coxsackie B) Peripartum cardiomyopathy
Alcohol abuse Chronic supraventricular tachycardias Cardiotoxic drugs (eg, doxorubicin) Thiamine
deficiency (wet beriberi)
Causes of Hypertrophy cardio myopathy are single point missense mutations in the genes for beta
myosin heavy chain (35-50%), myosin binding protein C (15-25%), cardiac troponin T (15-20%), or
tropomyosin (<5%)
Unprovoked syncope is a previously asymptomatic young person may result from a congenital QT
prolongation syndrome. The two most important congenital syndromes w/ QT prolongation Romano-Ward syndroem and Jervell and Lange-Nielsen syndrome- are thought to result from
mutations in a K channel protein that contributes to the delayed rectifier current (Ik) of the cardiac
action potential.
Hypertrophic cardiomyopathy (HCM) is characterized by asymetric ventricular septal hypertrophy
and variable dynamic left ventricular outflow tract obstruction which may produce a systolic
ejection murmur. Decreases in the LV end diastolic volume increase the obstruction, causing the
murmur of HCM to b enhanced. Actions like standing suddenly from the supine position and the
Valsalva maneuver decrease venous return and thus accentuate the murmur.
Decreased outward K current during the repolarization phase of cardiac action potential results in
QT prolongation. is an incresed risk of episodic polymorphic ventricular tachycardia, including
torsades de points.
Jervell and Lange-Nielsen syndrome(AR): MC congenital long-QT syndromes. It is accompanied
by congenital neurosensory deafness.
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Constrictive pericarditis is a chronic condition in which the normal pericardial space is replaced by
a thick, fibrous shell that restricts ventricular filling leads to increased jugular pressure and often
results in a positive Kusssmaul sign. There may also be a pericardial knock, which occurs earlier
in diastole than the S3 heart sound.
- Right coronary artery: inferior wall of left ventricle and possible sinus disfux. ST elevations (II, III,
aVF). - Proximal Left Anterior Descending: ateroseptal wall. ST elev: V1-V4. - Circunflex: Lateral
left ventricle wall. ST elev (V5, V6, aVL)
- RCA Oclussion: inferior wall of the left ventricle (ST elevation in II, III, aVF, possible Sinus node) -
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LAD Oclussion: anteroseptal transmural ischemia, ST elevations in lead V1-V4. - LCX Oclussion:
transmural ischemia lateral wall of the left ventricle, ST elevations V5 and V6 and possibly I and
aVL.
Aging in the heart Decresed in left ventricular chamber size, particular in the apex to base
dimension. This chamber lenghth decrease causes the basal ventricular septum to bulge into the
left ventricular outflow tract (sigmoid septum). Atrophy cause deposition of amyloidthen
progressive acumulation of cytoplasmic granules cointaining brownish lipofuscin pigment
The normal morphological changes in the aging heart include a decrease in left ventricular
chamber apex-to-base dimensions, development of a sigmoid-shaped ventricular septum,
myocyte atrophy with interstitial fibrosis, and accumulation of cytoplasmic lipofuscin pigment.
Hypertensive heart disease is associated with concentric hypertrophy of the left ventricle.
Golden yellow or brownish cytoplasmic granules may be either lipofuscin or hemosiderin. The
prussian blue stain, which detects intracellular iron, can differentiate the two. In the Prussian blue
histochemical reaction, colorless potassium ferrocyanide is converted by iron to blue- black ferric
ferrocyanide.
Extended consumption (for longer than three months) of appetite suppressants such as
fenfluramine or phentamine is associated with an incidence of pulmonary hypertension.
Pulmonary hypertension classically manifests with dyspnea on exertion, and can progress to cor
pulmonale with right ventricular hypertrophy, potentially leading to suden cardiac death.
The foramen ovale is patent in 20-30% of the normal adults. Although it ussually remains
functionally closed, any abnormality increasing right atrial pressure above left atrial pressure can
produce a right to left shunt across a patent foramen ovale.
The most likely cause of fatigue and new onset cardiac murmur is a young adult is bacterial
endocarditis. Acute, diffuse, proliferative glomerulonephritis secondary to circulating immune
complexes may complicate bacterial endocarditis and can result in acute renal insufficiency.
The patogenesis of nonbacterial thrombotic endocarditis (NBTE) often involves hypercoagulable
state. When the hypercoagulability is the result of the procoagulant effects of circulating products
of cancers, the resulting cardiac valve vegetations may also be called marantic endocaditis. The
pathophysiology of NBTE is similar to that of Trousseau's syndrome (migratory thrombophebitis)
which may also be induced by disseminated cancers.
Almost all cases of mitral stenosis are caused by chronic rheumatic heart Ds. Infective
endocarditis of the mitral valve tends to cause destruction and regurgitation. Congenital heart
defects may produce mitral regurgitation, but are generally not associated with stenosis. Mitral
valvular calcinosis generally does not impair valve function. Rheumatoid arthritis and tertiary
syphilis only rarely affect cardiac valves.
In the rare cases of lethal acute rheumatic fever, the cause of death is heart failure due to severe
myocarditis. Mitral stenosis after acute rheumatic fever requires years or decades to develop.
Interstitial myocardial granulomas, or Aschoff bodies, are typically found in acute rheumatic
carditis. Aschoff bodies contain plump macrophages with abundant cytoplasm and central, round
to ovoid nuclei with central, slender ribbons of chromatin (Anitschkow cells).
Interstitial myocardial granulomas, or Aschoff bodies, are typically found in acute rheumatic
carditis. Aschoff bodies contain plump macrophages with abundant cytoplasm and central, roundto-ovoid nuclei central, slender ribbons of chromatin (Anitschkow cells).
Sydenham chorea is the most common acquired chorea of childhood and is the sole neurologic
manifestation of acute rehumatic fever. A patient with this disorder whould be at increased risk for
chronic rheumatic heart disease, including mitral and aortic involvement.
The process of calcifications is defined by 2 stages: initiation (mitochondria: dead or dying cells)
and propagation (can perforate the cell memb). On hematoxilin and eosin staining, these deposits
typically appear as dark purple, sharp-edged aggregates. If the deposit develops lamellated outer
layers, it is described as a psammoma body.
An insoluble pigment composed of lipid polymers and protein complexed phospholipids, lipofuscin
is considered a sign of wear and tear or aging. This yellow brown, finely granular perinuclear
pigment is the product of free radical injury and lipid peroxidation. It is commonly seen in the heart
and liver of aging or cachectic, malnourished pctes.
Lipofuscin is the product of lipid peroxidation, accumulating in aging cells (especially in pctes with
malnutrition and cachexia).
Patent ductus arteriosus (PDA) is associated with prematurity and congenital rubella infection.
Therapy with indomethacin successfully closes this defect in the majority of pctes.
Prostacyclin (Prostaglandin I2) is produced from prostaglandin H2 by prostacyclin synthase in
vascular endothelial cells. When secreted it vasodilates, inhibits platelet aggregation, and
increases vascular permeability. The function of prostacyclin oppose those of thromboxane A2.
These substances work in concept to ensure vascular homeostasis. Synthetic prostacyclin is used
in tto of pulmonary hypertension, peripheral vascular Ds and Raynaud Sx.
vascular endothelial cells. When secreted, it vasodilates, inhibits plateet aggregation, and
increases vascular permeability. The functions of prostacyclin oppose those of thromboxane A2.
These substances work in concert to ensure vascular homeostasis.
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vascular endothelial cells. When secreted, it vasodilates, inhibits platelet aggregatio, and
increases vascular permeability. The functions of prostacyclin oppose those of thromboxane A2.
These substances work in concert to ensure vascular homeostasis.
A diamond-shaped (crescendo-decrescendo) systolic murmur is characteristic for aortic stenosis.
The most common cause of this vavular heart disease is degenerative (senile) calcinosis of the
aortic leaflets.
A mid-systolic click followed by a murmur during the remainder of systole is relatively specific for
mitral valve prolapse(MVP). MVP is most often caused by defects in mitral valve connective tissue
proteins that predispose to myxomatous degeneration. This results in streching and eloongation of
the valve leaflets and chordae tendineae by chronic hemodynamic stress.
Estudiar murmurs con bedside maneuvers.
Pulsus paradoxus is an important clue to cardiac tamponade. It is defined as a decrease in the
systolic pressure of 10 mmHg or more during inspiration as compared with the pressure during
exhalation.
Pulsus paradoxus: is an important clue to cardiac tamponade. It is defined as a decrease in the
systolic pressure of 10 mmHg or more during inspiration as compared with the pressure during
exhalation.
The incresed in size of a mycyte after and isquemia is due to incresed Ca and Na intracellular
which will drive water to come inside the cell and swell the cell and mitochondria.
Repetitive low flow causes myocardial hibernation that can be reversed by reperfusion. Myocardial
stunning is a less severe form of ischemia-induced reversible loss of contractile funtion.
-Restrictive cardiomyopathy (dyastolic dysfuntion) may be idiopathic or due to amyloidosis,
sarcoidosis, metastatic cancer, or products of inborn metabolic errors. - Dilated cardiomyopathy
(systolic dysfuntion) may be caused by infectious myocarditis and cardiotoxic agents including
alcohol and doxorubicin.
Diastolic heart failure is characterized by a decrease in ventricular diastolic compliance but normal
ventrcular contractile performance. As a result , LVEDP must be increased in order to achieve a
normal LVEDV and stroke volume. Systolic heart failure results from a decrease iin both LVEDP
and LVEDV to improve stroke volume.
- Diastolic heart failure: decrease in ventricular diastolic compliance but normal ventricular
contractile performance, increased LVEDP, normal LVEDV and normal stroke volume. - Systolic
heart failure: decrease ventricular contractile performance (decreased ejection fraction) and
increase in both LVEDP and LVEDV to improve the stroke volume.
Auscultatory findings in an ASD include a wide and fixed splitting of S2. Additional associations
btwn auscultatory findings and cardiac lesions are as follows. 1. Systolic ejection murmur
accentuated by standing: hypertrophic obstructive cardiomyopathy. 2. Early diastolic decrescendo
murmur decreased by amyl nitrite: Ao regurgitation. 3. Late diastolic murmur eliminated by atrial
fibrilation: mitral (and/or tricuspid) stenosis.
-Ausculatatory findings in an ASD include and fixed splitting of S2. -Systolic ejection murmur
accentuated by standing: hypertrophic obstructive cardiomyopathy. -Early diastolic decrescendo
murmur decreased by amyl nitrite: aortic regurgitation. -Late diastolic murmur eliminated by atrial
fibrilation: mitral (and/or tricuspid) stenosis.
Wide, fixed splitting of the second heart sound is a characteristic auscultatory finding in patients
with ASD. A hemodynamically significant ASD can produce chronic pulmonary HTA as a result of
left to right intracardiac shunting. Eisenmenger Sx is the late onset reversal of a L to R shunt due
to pulmonary vascular sclerosis resulting from chronic pulmonary HTA. Closure of the ASD may be
required to prevent irrev pulmonary vascular sclerosis and a permanent Eisenmenger Sx.
In pctes with TOF, squatting increases SVR and decreases right to left shunting, thereby
increasing pulmonary blood flow. Squatting thus counteracts arterial desaturation during
hypoxemic spells.
Estudiar murmurs y ocn que maniobras incrementan o disminuyen su intensidad
The best, more reliable and most continuous auscultatory indicator of the severity of mitral
stenosis is the A2-OS interval. The shorter this interval, the more severe the stenosis.
Aortic stenosis may cause exertional syncope. The murmur of Aortic stenosis is a systolic ejectiontype, crescendo-decrescendo murmur that starts after the first heart sound and typically ends
before the A2 component of the second heart sound. The intensity of the Aortic stenosis murmur is
proportional to the magnitude of the left ventricle to aorta pressure gradient during systole.
AA presystolic sound on cardiac auscultation that immediately precedes S1 is most often an S4
gallop. An S4 requires normal atrial contraction and results from rapid emptying of atrial blood into
a ventricle with reduced compliance (stiff ventricle)
A presystolic sound on cardiac auscultation that immediately precedes S1 is most often an S4
gallop. An S4 requires normal atrial contraction and results from rapid emptying of atrial blood into
a ventricle with reduced compliance (stiff ventricle).
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An abnormally prominent, unsloping left atrial "v wave" during cardiac catheterization is a major
hemodynamic finding of mitral regurgitation.
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Mitral regurgitation results in a blowing, holosystolic murmur heard best over the cardiac apex with
radiation to the axila. Rheumatic heart disease is a very common cause of mitral regurgitation in
underdeveloped countries.
Pulsus paradoxus is defined by a decrease in systolic blood pressure of greater than 10mmHg
with inspiration, and occurs in the setting of acute cardiac tamponade, contrictive pericarditis,
severe obstructive lung disease, and restrictive cardiomyopathy.
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Pulsus paradoxus can occur in the setting of severe obstructive pulmonary disease such as
asthma. Beta-adrenergic agonists control acute asthma exacerbations by causing bronchial
smooth muscle relaxation cia increased intracellular cAMP.
Aortic regurgitation is characterized by early diastolic murmur and is most commonly caused by
aortic dilatation or a bicuspid aortic valve in developed countries.
The third heart sound (S3) is a low-frequency sound ocurring just after S2 that is commonly
associated with increased left ventricular end-systolic volume, which occurs in the setting of left
ventricular systolic failure.
S3 is a low frequency sound occuring just after S2 that is commonly associated with increased left
ventricular end systolic volume, which occurs in the setting of the left ventricular systolic failure.
S3 heart sound occurs early in diastole and is thought to be created by a suden deceleration of
the entering blood column as the ventricle reaches its elastic limit. This produces a reverberation
of blood between the ventricular walls, which is heard as a low-frequency sound.The S3 heart
sound develops when there is an imbalance btwn the force with which blood is pushed into the
ventricle and the ability of the ventricle to accomodate this blood flow.
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Collateral microvessels form adjacent pathways for flow to areas distal to an occluded vessel.
Adenosine and dipyridamole are selective vasodilators of coronary vessels that can cause
coronary steal, a phenomenon in which blood in ischemic areas is reduced due to arteriolar
vasodilation in nonischemic areas. Coronary steal can lead to hypoperfusion and worsening of
existing ischemia.
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Nitrate drugs mimic the action of endothelial derived relaxing fact (nitric oxide, NO). They are
transformed to NO at the vascular smooth muscle cell membrane wich lead to increased cGMP,
decreased intracellular calcium and myosin dephosphorylation. Increase cGMP will decreased
intracellular calcium concentration, decreased activity of myosin light chain kinase and finally
myosin light chain dephosphorylation and smooth muscle relaxation.
Nitrate drugs mimic the action of endothelial derived relaxing factor (nitric oxide, NO). They are
transformed to NO at the vascular smooth muscle cell membrane which leads to increased cGMP,
decreased intracellular calcium and myosin dephosphorylation.
Nitroglycerine is primarily venodilator. it decreases preload which decreases myocardial oxygen
demand and thereby treats angina pectoris.
Sublingual or aerosolized nitroglycerin is a rapidly acting agent taken by pctes with stable angina
pectoralis as needed to rapidly relieve their symptoms. Nitrates act primarily as venodilators
causing a decrease in cardiac work by decreasing left ventricular filling volume or preload.
Nitrates act primarily as venodilators causing a decrease in cardiac work by decreasing left
centricular filling colume or preload.
Nitroglycerine and Isosorbide dinitrate undergo considerable first-pass metabolism in the liver
when taken by the oral route. Interestingly, isosorbide mononitrate is nearly 100% bioavailable
when taken by the oral route.
Nitroglycerine and Isosorbide dinitrate undergo considerable first-pass metabolism in the liver
when taken by the oral route. Interestingly, isosorbide mononitrate is nearly 100% bioavailable
when taken by oral route.
All nitrates, both long and short acting, are most commonly associated with the side effects of
headache and facial flushing. These reactions occur because of the vasodilatory properties of
nitrates in the meninges and skin.
Nitrates can lead to a reflex tachycardia by causing a relative hypotension that the body responds
to with catecholamine release. This adverse effect can be prevented by administering betaadrenergic blockers with nitrates.
Using nitrates with phosphodiesterase (PDE) inhibitors used for erectile dysfunction and
pulmonary hypertension causes a profound systemic hypotension because they both increase
intracellular cGMP which causes vascular smooth muscle relaxation. Their use together is
absolutle contraindicated.
Nifedipine is effective as an antihypertensive agent and has a minimal effect on AV conduction
unlike each of the other drugs listed. Nifedipine causes peripheral vasodilation (vasculature
specific) shich may result in reflex tachycardia. Therefore this antihypertensive drug is useful for
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patients with bradycardia.

Nifedipine is effective as an antihypertensive agent and has a minimal effect on AV conduction
unlike each of the other drugs listed. Nifedipine causes peripheral vasodilation (vasculature
specific) which may result in reflex tachycardia. Therefore this antihypertensive drug is useful for
pctes with bradycardia.
Nifedipine causes peripheral vasodilation which may result in reflex tachycardia. Therefore this
antihypertensive drug is useful for pctes with bradycardia.
Digitalis (digoxin) leads to AV block and ventricular tachyarrythmias. Hyperkalemia is frequently
found in acute digoxin toxicity. However, please note - hypokalemia increase pcte susceptibility to
the toxic effect of digoxin.
Digitalis (digoxin) it leads to AV block and ventricular tachyarrhythmias. Hyperkalemia is frequently
found in acute digoxin toxicity. However, please note- hypokalemia increase pcte susceptibility to
the toxic effects of digoxin.
The mechanism of action of digitalis is the inhibition of the Na-K-ATPase in cardiac pacemaker
cells leading to AV nodal blockade (increased diastolic filling time for greater contraction by the
Frank-Starling mechanism) and increased contractility from increased intracellular calcium.
The Mx of action of digitalis is the inhibition of the Na-K-ATPase in cardiac pacemaker cells
leading to AV nodal blockade (increased diastolic filling for greater contraction by the FrankStarling mechanism) and increased contractility from increased intracellular calcium.
M of A of digitalis, it inhib of the Na-K-ATPase in cardiac pacemaker cells leading to AV nodal
blockade (increased diastolic filling time for greater contraction by the Frank-Starling mechanism)
and increased contractility from increased IC Ca. Ca gluconate should not be given to pctes for
hyperkalemia in the setting of digoxin toxicity. Digoxin and K compete with each other for Na-KATPase; thus digoxin toxicity results on hyperkalemmia. Hypokalemia worsens digoxin toxicity
Phosphodiesterase inhibitors lead to increased cardiac contractility via increased intracellular
cAMP concentration. cAMP promotes increased intracellular calcium in cardiac myocytes and is
normally metabolized by phosphodiesterases. In vascular smooth muscle, increases in cAMP
cause vasodilation, a well-known side effect of phosphodiesterase inhibitors which can
occasionally limit their use in hypotensive pctes.
cAMP concentrations. cAMP promotes increased intracellular calcium in cardiac myocytes and is
cause vasodilation, a well known side effect of phosphodiesterase inhibitors which can
occasionally limit their use in hypotensive pctes.
cAMP concentration. cAMP promotes increased intracellular calcium in cardiac myocytes and is
cause vasodilation, a well-known side effect of phosphodiesterase inhibitors which can
occasionally limit their use in hypotensive patients.
It is important to know the difference in the cardioselectivity and vascular selectivity of the 3
classes of calcium channel blockers. Verapamil: heart (but the RAM are constipation and gingival
hyperplasia, and bradycardia, first, second and third degree AV nodal block in 1-2% of patients
treated). Nifedipine: peripheral vasculature Diltiazen: heart and peripheral vasculature.
Digoxin will increase cardiac contractility by blocking the Na-K-ATPase in cardiac myocytes
leading to an increased intracellular calcium concentration, and it will decrease AV nodal
conduction by a mechanism of increased parsympathetic tone.
In this case, digoxin toxicity manifested as changes in color vision and anorexia. Digoxin toxicity
can also cause ventricular dysrhythmias, headache, fatigue and confusion.
In this c ase, digoxin toxicity manifested as changes in color vision and anorexia. Digoxin can also
cause ventricular dysrhythmias, headache, fatigue and confusion.
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RAM of Adenosine: chest burning (bronchospasm), flushing and high grade block as adverse
reactions (remember, this is the drug used for chemical stress tests!)
Amiodarone along with the class IA and the remainder of the class III antiarrhythmic agents will
cause a prolongation of the QT interval on the EKG. These drugs have this effect because they all
slow phase 3 repolarization in the ventricular myocardium. Amiodarone is unique n that it does not
predispose to torsade de points as the remainder of these agents do.
Amiodarone along with the class IA and the remainder of the class II antiarrythmic agents will
slow phase 3 repolarization in the ventricular myocardium. Amiodarone is unique in that it does not
predispone to torsade de pointes as the remaider of these agents do.
Amiodarone along with the class IA and the remainder of the class III antiarrythmic agents will
slow phase 3 repolarization in the ventricular myocardium. Amiodarone is unique in that it does not
predispose to torsade de points as the remainder of these agents do.
Amiodarone is a class III antiarrythmic drug that also exhibits properties of class I, II and IV
agents. It prolongs QT interval via its effect on potassium mediated repolarization (phase 3) of
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myocardial cells. But the amiodarone amigo does not cause torsade de pontes.
Class II antiarrythmics such as amiodarone, sotalol, ibutilide and dofetilide will slow K efflux from
the ventricular myocyte, prolong repolarization and prolong the refractory period.
Class III antiarrythmics such as amiodarone, sotalol, ibutilide and dofetilide will slow potassium
efflux from the ventricular myocyte, prolong repolarization and prolong the refractory period.
minoxidil hydralazine
Direct arteriolar vasodilation like hydralazine and minoxidil are effective antihypertensives.
Because they cause significant arteriolar vasodilation, they also cause reflex sympathetic
activation resulting in tachycardia and edema. To counteract these compensatory effects, these
agents are often given in combination with sympatholytics and diuretics.
Dobutamine is a relatively selective beta-1 adrenergic agonist that increases heart rate,
contractility, conduction velocity, and myocardial oxygen consumption.
Patients who have overdose on beta blockers should be treated with glucagon, which increases
heart rate and contractility independent of adrenergic receptors. Glucagon activates G proteincoupled receptors in cardiac myocytes, causing activation of adenylate cyclase and raising
intracellular cAMP. The results is calcium release from intracellular stores and increased sinoatrial
node firing.
Bipolar disorder is commonly treated with lithium, an anti-maniac medication. Lithium has been
linked to cases of Ebstein's anomaly in infants exposed in utero. Ebstein's anomaly is
characterized by apical displacement of the tricuspid valve leaflets, decreased right ventricular
volume, and atrialization of the right ventricle.
Bipolar disorder is commonly treated with lithium, and antimaniac medication. Lithium has been
linked to cases of Ebstein's anomaly in infants exposed in utero. Ebstein's anomaly is
characterized by apical displacement of the tricuspid valve leaflets, decreased right ventricular
volume, and atrialization of the right ventricle.
Sotalol has both beta adrenergic blocking properties and class 3 antiarrythmic (K channel
blocking) properties. It prolongs both the PR interval and the QT interval.
Sotalol has both beta-adrenergic blocking properties and class 3 antiarrythmic (K channel
blocking) properties. It prolongs both the PR interval and the QT interval.
In pctes with hypertension and chronic myocardial failure, ACE inhibitors are considered to be the
most effective long term tto option, as they inhibit myocardial remodeling and the associated
deterioration of ventricular contractile function, in addition to reducing blood pressure. A beta
blocker would also be beneficial for these pctes.
In pctes with HTA and chronic ischemic myocardial failure, ACE inhibitors are considered to be the
most effective long-term tto option, as they inhibit myocardial remodeling and the associated
deterioration of ventricular contractile function, in adition to reducing blood pressure. A beta
blocker would also be beneficial for these pctes.
Combined use of non-dihydropyridine calcium channel blockers (eg. verapamil, diltiazem) and
beta adrenergic blockers (eg, atenolol) can have additive chronotropic effects yielding severe
bradycardia and hypotension.
Combined use of non-dihydropyridine calcium channel blockers (verapamil, diltiazem) and betaadrenergic blockers (atenolol) can have additive negative chronotropic effects yielding severe
bradycardia and hypotension.
Isoproterenol is an agonist at both beta-1 and beta-2 adrenergic receptors and has little or no
alpha adrenergic agonist effects. It causes a dose dependent increase in myocardial contractility
and a dose dependent decrease in systemic vascular resistance.
Isoproterenol is an agonist at both beta1 and beta2 adrenergic receptors and has little or no alpha
adrenergic agonist effects. It causes a dose dependent increase in myocardial contractility and a
dose dependent decrease in systemic vascular resistence.
Metoprolol is a selective beta1 adrenergic antagonist. beta 1 are found in cardiac tissue and on
renal juxtaglomerular cells. In addition to the exerting cardiac effects, metoprolol also blocks
catecholamine-induced renin release by the kidney.
Thiazide diuretics cause elevations in the serum LDL, calcium, uric acid and glucose levels. They
lower serum potassium, serum sodium and blood pressure.
Thiazide diuretics cause elevations in the serum LDL, calcium, uric acid and glucose levels. The
lower serum potasium, serum sodium and blood pressure.
Beta-blockers, including esmolol, slow AV conduction. Delayed conduction through the AV node
causes PR interval prolongation.
Beat-blockers, including esmolol, slow AV conduction. Delayed conduction through the AV node
causes PR interval prolongation.
Torsades of pointes: can be caused by agents that prolong QT interval such as: antiarrhythmic
agents, quinidine, procainamide, disopyramide, ibutilide, dofetilide and sotalol have been
implicated.
Beta-1 receptors are found in cardiac tissue and on renal juxtaglomerular cells, but not on
vascular smooth muscle. Blockade of the beta-1 receptor leads to decreasing cAMP levels in
cardiac and renal tissue without affecting cAMP levels in vascular smooth muscle.
beta 1 receptors are found in cardiac tissue and on renal juxtaglomerular cells, but not on vascular
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smooth muscle. Blockade of the beta 1 receptor leads to decreasing cAMP levels in cardiac and
renal tissue without affecting cAMP levels in vascular smooth muscle.
Study antiarrythmics
Class 1C antiarrythmic are potent sodium channel blockers that exhibit strong use-dependence by
prolonging the QRS duration to greater extent at higher heart rates. Class III antiarrythmics block
the repolarizing potassium current and demostrate reverse use-dependence (the slower the heart
rate, the more the QTc interval is prolonged).
Only 10% of total perfusion through the myocardial capillaries of the LV occurs during systole,
while the majority of the left ventricular blood flow occurs during diastole. The systole reduction in
coronary blood flow is greatest in the subendocardial myocardium of the LV.
Intravenous fluid infusions increase the intravascular colume by varying degrees depending on the
composition of the solute. The resultant preload increase causes increased ventricular myocardial
sarcome length and thus increase stroke and cardiac output.
NO is the most important mediator of coronary vascular dilation in large arteries and pre-arteriolar
vessels. It is synthesized from arginine and oxygen by endothelial cells and causes vascular
smooth muscle relaxation by a guanylate cyclase-mediated cGMP second messenger system.
Adenosine, a product of ATP metabolism, acts as a vasodilatory element in the small coronary
arterioles.
Nitric oxide is the most important mediator of coronary vascular dilation in large arteries and prearteriolar vessels. It is synthesized arginine and oxygen by endothelial cells and causes vascular
smooth muscle relaxation by a guanylate cyclase-mediated cGMP second messenger system.
Adenosine, a product of ATP metabolism, act as a vasodilatory element in the small coronary
arterioles.
AV shunts can be congenital or acquired, acquiered forms can result from medical interventions or
penetrating injuries. AV shunts increase preload and decrease afterload by routing blood directly
from the arterial system to the venous system, bypassing the arterioles. High-volume AV shunts
can eventually result in high-output cardiac failure.
Arteriovenous (AV) shunts can be congenital or acquired; acquired forms can result can results
from medical interventions or penetrating injuries. AV shunts increase preload and decrease
afterload by routing blood directly from the arterial system to the venous system, bypassing the
arterioles. High volume AV shunts can eventually result inhigh-output cardiac failure.
The Fick principle can be used to calculate the cardiac output. It states that the cardiac output is
equal to the oxygen consumption by the tissues divided by the arteriovenous oxygen difference.
buaaaa
Nitroprusside is a short-acting balanced venous and arterial vasodilator that decreases both
preload and afterload. Since these changes are balanced, stroke volume is maintained
Calcium effluc prior to myocyte relaxation is accomplished through the use of Ca-ATP ase and
Na+/Ca2+ exchange mechanisms.
Calcium efflux prior to myocyte relaxation is accomplished through the use of Ca-ATPase and
Na/Ca exchange mechanisms.
The electrical impulsers are transmited through the conduction system to the ventricles which
depolirize from apex to base and from endocardium to epicardium.
Atrial fibrillation occurs due to irregular, chaotic electrical activity within the atria. While some of the
atrial impulses are transmitted to the ventricles, most are not due to the AV nodal refractory period.
Atrial natriuretic peptide is secreated by atrial cardiomyocytes and bind to the natriuretic peptide
receptor A (NPR-A) on cell membranes, activating guanylate cyclase and forming cGMP. ANP
lowers blood pressure through peripheral vasodilation, natriuresis, and diuresis.
Atrial Natriuretic Peptide - Kidney: ANP dilates afferent arterioles, Inc GFR and urinary expresion
of Sodium and water. Limits sodium reabsorption (in prox tubule and inner medullary collecting
duct) and inhibits renin secretion. - Adrenal gland: ANP restricts aldosterone secretion. Blood
Vessels: relax smooth vessels of arterioles and venules.
Precipitatin factors for isolated episodes of AF include binge alcohol consumption ("holiday heart
syndrome"), increased cardiac sympathetic tone, and pericarditis. On EKG, AF shows an irregular
series of QRS complexes and absent p waves. P waves are always absent in AF because
coordinated atrial contractions do not occur.
In pctes with heart failure, compensatory activation of the renin-angiotensin-aldosterone pathway
and sympathetic nervous system results in increase afterload (from excessive vasocontriccion),
excess fluid retention, and deleterious cardiac remodeling.
Deficit of Vit A Bitot's spots (abnormal squamous cell proliferation and keratinization of the
conjunctiva), cornela perforation, keratomalacia, nonspecific dermatologic abnormalities, and
humoral and cell mediated immune system inhibition via damage done to phagocytes and T cell
lynphocytes. Death can result if the condition is untreated. Vict A can be of benefit in the tto of
measles infection.
Telomerase is an enzyme that possesses reverse transcriptase (RNA-dependent DNA
polymerase) activity and is normally expressed in stem cells as well as cancer cells. However,
cancer cells are immortal because these cells continue to divide without aging and shortening of
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7
588
Biochemistr
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Immunolog
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Dermatolo
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113
2
Immunolog
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Dermatolo
gy
113
3
Immunolog
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207
8
207
8
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Immunolog
y
Dermatolo
gy
Dermatolo
gy
207
9
166
9
885
8
Immunolog
y
Microbiolog
y
Microbiolog
y
Dermatolo
gy
Dermatolo
gy
Dermatolo
gy
104
2
Pathology
Dermatolo
gy
111
0
111
4
Pathology
Dermatolo
gy
Dermatolo
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111
7
Pathology
Dermatolo
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186
7
Pathology
Dermatolo
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186
7
Pathology
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187
8
Pathology
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193
7
Pathology
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206
5
Pathology
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Pathology
their telomeres.
When mRNA is first trancribed from DNA it is an unprocessed form called pre-mRNA or
heterogeneous nuclear nuclar mRNA(hnRNA). Several processing steps are required before
finalized mRNA molecules can leave the nucleus, including 5'-capping, poly A tail addition, and
intron splicing. Cytoplasmic P bodies play an important role in mRNA translation regulation and
mRNA degradation.
When mRAN is firts transcribed from DNA, it is in an unprocessed called pre-mRNA or
heterogenous nuclear mRNA (hnRNA). Several processing steps are required before finalized
mRNA molecules can leave the nucleus, including 5-capping, poly A tail addition, and intron
splicing. Cytoplasmic P bodies play an important role in mRNA translation regulation and mRNA
degradation.
what?
Langerhans cells are dendritic cells found in the skin that act as professional antigen presenting
cells. These cells are derived from the myeloid cell line and they posses characteristic racquetshaped intracytoplasmic granules known as Birbeck granules.
Chediak-Higashi: Is a inmunodeficiency that results from a defect in neutrophil phagosome
lysosome fusion. This causes abnormal gigant lysosomal inclusions that are visible n light
microscopy of peripheral blood smear. Suffer of recurrent staphylococci and streptoococci
infections. Abnormal melanin storage in melanocytes causes partial oculocutaneous albinism.
Poison ivy dermatitis is one form of allergic contact dermatitis, which is a type IV hypersensitivity
Rx. Type IV hypersensitivity Rx are mediated primarily by T lymphocytes. The cutaneous lesions in
poison ivy dermatitis are typically linear eryhtematous papules, vesicles, or bullae that are pruritic.
Pctes with SCID present with recurrent infections caused by bacteria, viruses, fungi, and
oportunistic pathogens as well as failure to thrive and chronic diarrhea within the first year of life.
Pctes with Severe Combined Immunodeficiency present with recurrent infections caused by
bacteria, viruses, fungi, and opportunistic pathogens as well as failure to thrive and chronic
diarrhea within the first year of life.
The candida skin test gauges the activity of the cell-mediated immune response. The active cells
in the cell-mediated response are macrophages, CD4 and CD8 T lymphocytes and NK cells.
Rubeola (measles) Rubella (German measles)
Pseudomonna auruginosa is a major pathogen in burn pctes. Only a few specific penicillins
(ticarcillin, piperacilin) and cephalosporins(ceftazidime, cefepime) have activity against it. Certain
amioglycosides, fluoroquinolones ()ciprofloxacin, levofloxacin, and carbapenems (imipenem,
meropenem) are also effective.
Herpes zoster (shingles) develops due to reactivation of varicella-zoster virus in the dorsal root
ganglia (sensory neurons). It presents with a painful vesicular rash in a adermatomal distribution.
On light microscopy intracellular inclusions in keratinocytes and multinucleated gigant cells
(positive Tzanck smear) are seen. Skin biopsy: acantholysis (loss of intracellular conections) of
keratinocytes and intraepidermal vesicles.
Vitiligo is a relatively common dondition with partial or complete loss of epidermal melanocytes.
-Urticaria: superficial dermal edema and lymphatic channel dilation. -Psoriasis:
acanthosis(increase thickness of stratum spinosum). -Ezcematous dermatitis: spongiosis
(intracellular epidermal edema). -Eczematous dermatitis: acantholysis(loss of cohetion between
keratinocytes in the epidermis or in adnexal structures. Often asociated with spongiotic
dermatitis.). - Dyskeratosis: abnormal prepature keratinization of infividual keratinocytes(strongly
eosinophilic).
Psoriasis: Hyperkeratosis, acanthosis, rete ridge elongation, mitotic activity above the epidermal
basal cell layer, and a reduced or absent stratum granulosum. Neutrophils may form spongiotic
clusters in the superficial dermis and the parakeratotic stratum corneum (Munro microabscesses).
A yellowish eyelid papule or plaque containing lipid-laden macrophages is most likely
xanthelasma. Xanthelasma may occur in association with primary or secondary hyperlipidemia.
Cholestatic conditions such as primary biliary cirrhosis are a potential cause of
hypercholesterolemia leading to xanthelasma.
A yellowish eyelid papule or plaque containing lipid laden macrophages is most likely
xanthelasma. Xanthelasma may occur in association with primary or secondary hyperlipidemia.
Cholestatic conditions such as primary biliary cirrhosis are a potencial cause of
hypercholesterolemia leading to xanthelasma.
Red blood cell extravasation into the slin or subcutaneous tissue results in the formation of
petechiae (<5mm in diameter), purpura (5mm to 1 cm in diameter), or ecchymoses (>1cm in
diameter). These lesions do not completely blanch under pressure, unlike telangiectasias.
Axilary lymph node dissection is a risk factor for the development og chronic lymphedema
involving the ipsilateral arm. Chronic lymphedema predisposes to the development of
angiosarcoma (Stewart-Treves syndrome).
Penphigus vulgaris is an autoimmune bullous against desmosomal protein 3 and 1, painful, flaccid
bullae and erosions of the skin and mucosal membranes. Often, the bullae are sufficiently flaccid
856
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Pharmacol
ogy
Dermatolo
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602
Biochemistr
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Endocrinol
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Endocrinol
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Endocrinol
ogy
Biochemistr
y
Biochemistr
y
Endocrinol
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Endocrinol
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997
Biochemistr
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Endocrinol
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998
Biochemistr
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Endocrinol
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998
100
9
101
0
101
9
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Endocrinol
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101
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103
1
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138
3
141
7
147
3
212
0
212
1
212
1
212
1
120
1
771
Biochemistr
y
Biochemistr
y
Biochemistr
y
Biochemistr
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Biochemistr
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Biochemistr
y
Biochemistr
y
Biostatistics
Endocrinol
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Endocrinol
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Endocrinol
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Endocrinol
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Endocrinol
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Endocrinol
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Endocrinol
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Endocrinol
602
934
994
997
998
Embryology
that the patient has inadvertently ruptured them prior the presentation, with only erosions
remaining. The bullae spread laterally with pressure (Asboe-Hansen sign), and new bullae may
form with gentle traction (Nikolsky sign).
Tto of psoriasis ranges from tropical therapies to systemic tto with conventional and biological
drugs. Topical vitamin D analogs (calcipotrie, calcitriol, and tacalcitol) bind to the vit D receptor and
inhibit keratinocyte proliferation and stimulate keratinocyte differentiation.
Phenylethanolamine-N-methyltransferase (PNMT), which is responsible for the synthesis of
epinephrine, is under the control of cortisol.
Phenylethanolamine-N-methyltransferase (PNMT), which is responsible for the synthesis of
epinephrine, is under control of cortisol.
Aldose reductase converts glucosa into sorbitol, which is further metabolized into fructose by
sorbitol dehydrogenase. This pathway is most active in the seminal vesicles. The lens also
contains significant levels of sorbitol dehydrogenase, which become overwhelmed in the setting of
hyperglycemia. Other tissues, such as the retina, renal papilla, and Schwann cells, have much
less sorbitol dehydrogenase activity.
buaaaaaaaaa
After 12 to 18 hours of fasting, gluconeogenesis is the principal source of blood glucose.
Gluconeogenesis uses many of the bidirectional enzymes involved in the process of glycolysis,
but a few unidirectional enzymes need to be bypassed. The initial committed step of
gluconeogenesis involves the convertion of pyruvate to oxaloacetate, and oxaloacetate to
phosphoenolpyruvate.
After 12 to 18 hours of fasting, gluconeogenesis is the principal source of blood glucose.
Gluconeogenesis uses many bidirectional enzymes involved in the process of glycolysis, but a few
unidirectional enzymes need to be bypassed. The initial committed step of gluconeogenesis
involves the conversion of pyruvate to oxaloacetate, and oxaloacetate to phosphoenolpyruvate.
In Pyruvate dehydrogenase deficiency we can give with confidence Lysine and Leucine because
they are exclusively ketogenic and would not increase the blood lactate level in pctes suffering
from pyruvate dehydrogenase deficiency.
Lysine and leucine are exclusively ketogenic and would not increase the blood lactate level in
pctes suffering from pyruvate dehydrogenase deficiency.
buaaa cheka
what?
Glucokinase is a glucose sesor within pancreatic beta cells. Inactivating mutations of the enzyme
result in mild hyperglycemia that can be exacerbated by pregnancy.
Under anaerobic conditions, NADH transfers protons to pyruvate to fomr lactate and to regenerate
NAD. NAD is required to convert glyceraldehyde-3-phosphate to 1-3-biphosphoglycerate in
glycolysis. Inhibition of lactare dehydrogenase in strenuously exercising skeletal muscles would
eventually lead to an inhibition of glycolisis due to intracellular depletion of NAD
Under anaerobic conditions, NADH tranfers protons to pyruvate to form lactate and to regenerate
NAD. NAD is required to convert glyceraldehyde-3-phosphate to 1-3-biphosphoglycerate in
glycolysis.
buaaa
Fructose 2,6-biphosphate activates glycolysis by inducing phophofructokinase-1 and inhibits
gluconeogenesis by inhibiting fructose 1,6-biphosphatase. High concentrations of fructose 2,6bisphosphate also decreases the gluconeogenic conversion of alanine to glucose. Fructose 2,6biphosphate concentration is regulated by a bifunctional enzyme composed of
phosphofructokinase-2 and fructose 2,6-biphosphatase.
buaaaaaaaaaaaa
buaaa
estudia las organellas y sus fx
no se como es esto
hoooo
Amino acids with three titratable protons include histidine, arginine, lysine, aspartic acid, glutamic
acid, cysteine and tyrosine.
Aa with three titratable protons include histidine, arginine, lysine, aspartic acid, glutamic acid,
cysteine and tyrosine.
mmm
Genetic association of MEN 2A and 2B is a germ-line mutation of the RET proto-oncogen (origin in
ogy
343
Genetics
Endocrinol
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Endocrinol
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579
Genetics
582
Genetics
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757
Histology
842
4
Histology
Endocrinol
ogy
Endocrinol
ogy
220
Pathology
221
Pathology
225
Pathology
Endocrinol
ogy
585
Pathology
624
Pathology
768
Pathology
Endocrinol
ogy
Endocrinol
ogy
Endocrinol
ogy
768
Pathology
Endocrinol
ogy
769
Pathology
848
Pathology
Endocrinol
ogy
Endocrinol
ogy
925
Pathology
Endocrinol
ogy
929
Pathology
931
Pathology
Endocrinol
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Endocrinol
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931
Pathology
Endocrinol
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980
Pathology
980
Pathology
988
Pathology
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Endocrinol
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Endocrinol
Endocrinol
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Endocrinol
ogy
the neural crest cells). Both chromaffin cells of adrenal medulla and parafollicular cells (C-cells) of
the thyroid originate from neural crest. A common, germ-line mutation in neural crest cells can
cause tumors in both the adrenal medulla dna the thyroid; this phenomenon is seen in MEN types
2A and 2B
47 XXY is the most common karyotype producing Klinefelter syndrome. Pctes present with tall
stature, small firm testes, azoospermia and gynecomastia. Mild retardation may be present.
Kallman syndrome: absence of GnRH secretory neurons in the hypothalamus due to defective
migration from the olfactory placode. These patients have central hypogonadism and anosmia,
and often present with delayed puberty.
Klinefelter Syndrome: seminiferous tubules are progressively destroy and hyalinized, causing the
testes to be small and firm. Serum inhibin levels are decreased as a result of the damage to the
seminiferous tubules. The intestinal Leyding cells are damaged as well, resulting in low
testosterone levels and erectile dysfunction. Because of the low circulating levels of testosterone
and inhibin, LH and FSH are elevated (loss of feedback inhibition).
- Free Ribosomes: synthetize proteins that are used in the cytosol and cellular organelles. Ribosomes attached to RER: synthetize secretory, membrane bound, and lysosomal proteins.
All sympathetic preganglionic neurons release acetylcholine, which activates nicotinic
acetylcholine receptors on postganglionic neuron. Medullary chromaffin cells are modified
postganglionic sympathetic neurons that release catecholamines into the bloodstream. The
neurons that innervate sweat glnds are also different from most postganglionic sympathetic
neurons in that they release acetylcholine.
Sheehan syndrome causes panhypopituitarism alspo commonly have hypothyroidism and
hypocortisolism.
- The anterior pituitary is formed from an out-puching of the pharyngeal roof and is called Rathke's
pouch. The posterior pituitary gland arises from an extension of the hypothalamic neurons. Craniopharyngiomas are tumors arising from Rathke's puch remnants in the anterior pituitary.
They characteristically hav three components: solid, and calcified. They present during childhood,
usually, with mass effect and visual deficits.
Hemorrhage into a preexisting pituitary adenoma is called pituitary apoplexy. It presents with a
sudden severe headache and cranial nerve paralysis, with other more chronoc symptoms of
pituitary tumor. Since signs of meningial irritation can be seen, it is very important to evaluate the
visual fields for bitemporal hemianopsia. Cardiovascular collapse can occur due to adrenocortical
deficiency.
Glucagonomas: - Hyperglycemia - Stomatitis - Cheilosis - Abd pain - Necrolitis migratory
erythema, an elevated erythematous rash typically in the groin area.
hCG has a estructural similarity to TSH. In very high concentrations, which may be observed in
pctes with some testicular tumors, it can stimulate. TSH receptors and cause hyperthyroidism.
Granulomatous thyroiditis: - Features of thyrotoxicosis - Tenderness over the thyroid gland Incresed ESR, markedly-reduced radioactive iodine uptake. - Mixed, cellular infiltration with
ocassional multinucleate gigant cells.
Features of thyrotoxicosis, tenderness over the thyroid gland, increased ESR, and a markedlyreduced radioactive iodine uptake are diagnostic of granulomatous thyroiditis. Mixed, cellular
infiltration with occasional multinucleate gigant cells are characteristic histologic findings.
Mononuclear, parenchymal infiltration with well-developed germinal germinal centers is a
characteristic histological finding of Hashimoto's thyroiditis.
- Diabetes type I: A strong linkage with HLA class II gene makeup, pancreatic islet infiltration with
leukocytes (insulinitis), and antibodies against islet antigenes. - Diabetes II: Pancreatic islet
amyloid deposition.
Patients with anorexia nervosa often experience amenorrhea due to loss of pulsatile secretion of
gonadotropin-releasing hormone (GnRH) from the hypothalamus. It is important to remember that
the defect in anorexia-related amenorrhea begins in the hypothalamus, not the pituitary or ovaries.
Low estrogen levels over the long-term can result in osteoporosis if left untreated.
Hypertension with low plasma renin activity is suggestive of primary hyperaldosterolism, a
condition biochemically characterized by hypokalemia and metabolic alkalosis.
Waterhouse-Friderichsen: It is associated with Neisseria meningitidis septicemia with adrenal
hemorrhage. Caused shock, hyponatremia, hypokalemia, and hypoglycemia (adrenal crisis). In
addition to features of adrenal crisis, thsi pcte also has fever, vomiting, nuchal rigidity and
petechial rash, clinical signs strongly suffestive of meningococcal meningitis.
The presence of shock in combination with hyponatremia, hyperkalemia, and hypoglycemia is
strongly suggestive of adrenal crisis. In addition to features of adrenal crisis, this patient also has
fever, vomiting, nuchal rigidity and petechial rash, clinical signs strongly suggestive of
meningococcal meningitis. The association of Neisseria meningitidis septicemia with adrenal
hemorrage is called Waterhouse-Friderichsen syndrome.
Hydrochlorotiazide causes hypercalcemia by increasing the distal tubular reabsorption of filtered
calcium. The increased serum calcium levels usually suppress PTH.
Hydrochlorothiazide causes hypercalcemia by increasing the distal tubular reabsorption of filtered
calcium. The increased serum calcium levels usually supress PTH.
Multiple endocrine neoplasia type 2B consists of the medullary thyroid cancer,
ogy
165
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165
9
165
9
Pathology
166
0
Pathology
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166
0
Pathology
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208
0
208
1
208
1
853
1
Pathology
Endocrinol
ogy
Endocrinol
ogy
Endocrinol
ogy
Endocrinol
ogy
211
Pathophysi
ology
Pathophysi
ology
Endocrinol
ogy
Endocrinol
ogy
224
Pathophysi
ology
Endocrinol
ogy
226
Pathophysi
ology
Endocrinol
ogy
608
Pathophysi
ology
Pathophysi
ology
Endocrinol
ogy
Endocrinol
ogy
610
Pathophysi
ology
Endocrinol
ogy
612
Pathophysi
ology
Endocrinol
ogy
772
Pathophysi
ology
Endocrinol
ogy
772
Pathophysi
ology
Endocrinol
ogy
793
Pathophysi
ology
Pathophysi
ology
Endocrinol
ogy
Endocrinol
ogy
Pathophysi
Endocrinol
213
609
924
924
Pathology
Pathology
Pathology
Pathology
Pathology
Endocrinol
ogy
Endocrinol
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Endocrinol
ogy
pheochromocytomas, mucosal neuromas, and marfanoid habitus. Pheochromocytomas should be

excluded in all pctes with medullary thyroid cancer.
Psammoma bodies and ground glass, grooved nuclei are characteristic microscopic features of
papillary cancer of the thyroid gland.
Medullary carcinoma of the thyroid gld is characterized by extracellular deposits of myloid formed
by calcitonin secreted from neoplastic parafollicular C-cells.
-Familial medullary thyroid cancer have germ-line mutations of the RET proto-oncogene. The
microscopy: uniform polygonal or spindle-shaped cells with extracellular amyloid deposits. Amiloid
stains with Congo red. -Follicular hyperplasia with tall cells in a variant of papillary thyroid cancer
is typicall in older individuals. - Follicular adenoma: colloid-cointaining microfollicles.
Thyroid neoplasies - RET proto-oncogene=> Medullary thyroid cancer (spindle shape) - RAS
mutation => Follicular thyroid cancer and some Follicular adenomas. - Inactivating mutations of
p53 => Anaplastic thyroid cancer
Activating mutations of the RET proto-oncogen are strongly associated with medullary thyroid
cancer. RAS mutations are common in follicular thyroid cancer and some follicular adenomas.
Inactivating mutations of p53 are fairly common in anaplastic thyroid cancer.
buuuu
The tto of congenital adrenal hyperplasia involves low doses of exogeous corticosteroids to
suppress excessive ACTH secretion and reduce stimulation of the adrenal cortex.
Tto of congenital adrenal hyperplasia involves low dses of exogenous corticosteroids to suppress
excessive ACTH secretion and reduce stimulaion of the adrenal cortex.
Sulfonylurea or meglitinide abuse and insulinoma can cause increased insulin, c-peptide, and proinsulin levels. The only way to distinguish btwn insulinoma and sulfonylurea or meglitinide abuse is
by screening the urine or blood for hypoglycemic agents.
buaa
Anytime a patient has bitemporal hemianopsia, a pituitary tumor should be suspected. The most
common funtional pituitary tumor is a prolactinoma. Secreting prolactinomas inhibit the entire axis
of GnRH-LH/FSH-sex hormones, causing impotence in men and amenorrhea in women of
reproductive age (hypogonadotropic amenorrhea).
1. Growth hormone increaes linear growth by stimulating th production of IGF-1 from the liver. 2.
Defective growth hormone receptors will lead to decrease in linear growth and is called Laron
dwarfism. It is characterized by high serum levels of growth hormone in the presence of low IGF-1
levels.
The SIADH: -Low plasma sodium and osmolarity -Inappropriately concentrated urine -Incresed
urinary sodium -Normal body fluid volume An important cause of SIADH is a paraneoplastic effect
secondary to small cell carcinoma of the lung.
An ACTH surge with a resultant increase in steroid "half-product" excretion is a normal reaction to
metyrapone administration, because metyrapone blocks the last step of cortisol synthesis.
Depression of the entire hypothalamus-pituitary-adrenal axis by glucocorticoid therapy is the most
common cause of adrenal insufficiency. Adrenal crisis can be precipitated in these pctes under
stressful situations (infections or surgery) if their glucocorticoid dose is not appropiately increased.
17 alpha hydroxylase deficiency impairs the synthesis of androgens, estrogens, and cortisol but
does not inhibit mineralocorticoid production. Boys appear phenotypically female at birth, but girls
develop normal genitalia. Patients typically present with hypogonadism, hypertension, and
hypokalemia.
Cushing Syndrome secondary to adrenal adenoma/carcinoma will present with low ACTH levels.
In contrast, Cushing syndrome caused by pituitary adenoma will present with elevated ACTH
levels that are supressed by high-dose, but not low-dose, dexamethasone. Serum ACTH levels
are generally markedly elevated when there is ectopic ACTH production by malignant tumors;even
high-dose dexamethasone does not cause suppression.
Pctes with osteoporosis can be treated w/estrogen and progesterone. Estrogen causes increase
in total T4, but thyroid function remains normal (similar in pregnancy because is a hyperestrogenic
stage). 99% of circulating thyroid hormoones are bound to plasma proteins (Thyroid binding
globulin-TBG). TBG levels increase with estrogen use because the catabolism of TBG decreases
when estrogen is present.
Increase in levels of thyroid binding globulin lead increase in circulating total T4 and total T3.
However, the level of free thyroid hormone is normal. Increase in TBG is typically seen in
pregnancy, with the use of oral contraceptives, or with hormone replacement therapy.
endocrino pathways
Patients with Diabetes Mellitus type 1 are pro to develop other autoimmune
endocrinipathies(Hashimoto thyroiditis, Graves disease and Adisson's disease or
hypoadrenocorticism). Also are in risk to other autoinmune Ds including vitiligo and pernicious
anemia. - Primary Adrenal insufficiency: Hyponatremia, hyperkalemia, hypocloremia and
metabolic acidosis.
Pctes with type 1 Diabetes Mellitus are prone to develop other autoimmune endocrinopathies,
ology
ogy
930
Pathophysi
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979
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8
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8
209
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549
Pharmacol
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581
Pharmacol
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581
Pharmacol
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584
Pharmacol
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599
Pharmacol
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604
Pharmacol
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605
Pharmacol
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Pharmacol
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Pharmacol
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Endocrinol
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Endocrinol
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including Hashimoto thyroiditis, Graves disease, and Addison disease (hypoadrenocorticism).

These pctes are at increased risk for other non-endocrine autoimmune disorders as well, including
vitiligo and pernicious anemia.
Pctes with classic, salt-wasting 21-hydroxylase deficiency have deficient cortisol and aldosterone
synthesis combined with adrenal androgen overproduction. Male infants have normal genitalia and
present 1-2 weeks after birth with vomiting, hypotension, hyponatremia, and hyperkalemia.
Females present at birth with ambiguous genitalia.
Secondary hyperparathyroidism is seen in pctes with chronic renal failure. These pctes have an
elevated serum PTH, acompanied by normal to low serum calcium levels, and high serum
phosphorous levels. Circulating 1,25 dihydroxy Vit D levels are low due to the deficiency of 1 alpha
hydroxylase, an enzyme that resides in the kidneys.
The diarrheal caused by celiac Ds can lead to Vit D deficiency through malabsorption. Pctes with
Vit D deficiency have decreased serum phosphorus, increased serum parathyroid hormone
(secondary hyperparathyroidism), and low serum calcium. They may also have symptoms such as
bone pain and muscle weakness.
Serine phosphorilation of the insulin receptor's beta subunit could be involved. This
phosphorylation of serine interferes with down-stream signaling because serine kinase, instead of
tyrosine kinase, becomes activated. Serine phosphorylation is a known Mx of insuline resistance
induced by TNF-alpha, glucagon and glucocorticoides. Free fatty acids also decrease insulin
secretion, which prevents the compensatory rise of insulin that is required to overcome insuline
resitance.
Free FA and serum TG are belived to increase insulin resistance in overweight individuals.
Leuprolide is a GnRH agonist that causes first a transient increase, then a decrease in both
testosterone and DHT levels. Finasteride causes a discordant decrease in DHT level.
Leuprolide is an GnRH agonist that causes first a transient increment, then a decrease in both
Leuprolide is a GnRH agonist that causes first a transient increase, then a decrease in both
The secretion of prolactin is controlled by the inhibitory effect of hypothalamic dopamine.
Hyperprolactinemia causes hypoganadism by inhibiting the release of gonadotrophin-releasing
hormone from the hypothalamus. Risperidone and other antipsycotics cause hyperprolactinemia
by their antidopaminergic action.
The acute effects of corticosteroids on the CBC include: increased neutrophil count, and
decreased lymphocyte, monocyte, b asophil, and eosinophil counts. The increase in neutrophil
count from demargination of neutrophils previously attached to the vessel wall.
Tamoxifen is used for the treatment of osteoporosis and breast cancer. However it is associated
with an increased incidence of endometrial cancer and thromboembolic disease.
Tamoxifen and raloxifene are called "selective estrogen receptor modulators (SERMs)" because of
their tissue-selective estrogen agonist and antagonist properties. Tamoxifen is useful for the tto of
osteoporosis and breast cancer. However, it is associated with an increased incidence of
ndometrial cancer and thromboembolic disease.
Tamoxifen and raloxifen are called "selective estrogen receptor modulators (SERMs)" because of
their tissue-selective estrogen agonist and antagonist properties. Tamoxifen is useful for the tto of
osteoporosis and breast cancer. however, it is associated with an increased incidence of
endometrial cancer and thromboembolic Ds.
Anastozole is a selective inhibitor of aromatase, the enzyne responsible for the conversion of
androgens to estrogens. ketoconazole is an antifungal agent that decreases androgen synthesis
by inhibiting multiple enzyme pathways involved in the synthesis of androgens. Inhibition of the
epidermal growth fct and HER2/neu pathways by trastuzumab leads to the apoptosis of breast
cancer cells. Activation of the HER2/neu receptor leads to activation of tirosine kinase.
Thiazolidinedione therapy: RAMs: Fluid retention with resultant gain and edema, is a common side
effect. This excess fluid can exacerbate underlying congestive heart failure.
1. Thiazolidinediones decrease insulin resistence by binding the peroxisome proliferator activated
receptor gamma (PPAR-gamma), which is a transcriptional regulator of the genes involved in
glucose and lipid metabolism(process called "transactivation"). 2. Adiponectin levels are low in
type 2 diabetes, and treatment with TZD increases the levels of adiponectin.
Troglitazone was withdrawn from the market due to hepatotoxicity, periodic liver function tests are
now recommended in all patients treated with thiazolidinediones. The other important side effect of
TZDs includes fluis retention, which can exacerbate congestive heart failure in patients with
underlying cardiac dysfunction.
Thiazolidinediones bind to peroxisome proliferator-activated receptor-gamma (PPAR-gamma), a
receptor that belongs to the steroid and thyroid superfamily of nuclear receptors.
Alpha-glucosidase inhibitors decrease the activity of disaccharidases on the intestinal brush
border (remember, disaccharidases are membrane-bound enzymes).
Thyroid function tests should be monitored in pctes receiving amiodarone therapy. Amiodarone is
associated with many side effects: thyroid dysfunction, corneal micro-deposits, blue-gray skin
discoloration, drug-related hepatitis, and pulmonary fibrosis.
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5
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Thionamides (methimazole and propylthiouracil) decresed the formation of thyroid hormones via
inhibition of the enz thyroid peroxidase. Propylthiouracil also decreases the periferal conversion of
T4 to T3.
Tto for hirsutism: spironolactone, flutamide (inhibits binding to testosterone receptors) and
finasteride (5-alpha-reductase inhibitor).
Flutamide is a non-steroid anti-androgen that competes with testosterone and DHT for
testosterone receptors. It is used for tto of prostate cancer in combination with GnRH.
1. Anion inhibitors (perchlorate, pertechnetate) block iodine absorption by the thyroid gld via
competitive inhibition. 2. Thionamides (methimazol and propylthiouracil) decrease the formation of
thyroid hormones by inhibiting thyroid peroxidase. 3. Iodine salts inhibit synthesis as well as
release of thyroid hormones.
Administration of K iodine may prevent thyroid absorption of radioactive iodine isotopes by
competitive inhibition.
buaaa
TZDs activate PPAR-gamma (peroxisome proliferator activated receptor gamma), which is the
nuclear receptor that alters the transcription of genes responsible for glucose and lipid
metabolism. Thiazolidinediones exert their glucose-lowering effect by decreasing insulin
resistance. RAM of TZD: fluid retention, weight gain, and the precipitation of congestive heart
failure from fluid retention.
Adrenal crisis: hypotension, tachycardic and hypoglycemic (vomiting, abdominal pain, weight loss,
and hyperpigmentation). Tto High doses of hydrocortisone.
Loss of consciousness brought by severe hypoglycemia is typically treated with intramuscular
glucagon in the nin-medical setting and intravenous dextrose in the medical setting.
Anovulation is a common cause of infertility. One way to treat anovulation is the administration of
drugs that act like FSH and LH. TTo with menotropin (human menopausal gonadotropin) acts like
FSH and leads to the formation of the dominant ovarian follicle. Ovulation is then induced by
administration of a large dose of hCG, which stimulates the LH surge.
FSH is elevated in patients with menopause. LH is not so much elevated. The most important test
if the FSH for menopause patients.
LH stimulants the release of testosterone from the Leyding cells of the testes; FSH stimulates the
release of inhibin B from the Sertoli cells in the seminiferous tubules. Testosterone and inhibin B
induce negative feedback in LH and FSH production, respectively.
Estudia la relacion que existe entre hypotalamo pituitary gonada pathway Incresed FSH, Normal
LH, will make the Inhibin B be impaired
Cortisol has several permissive effects. For Ejm, cortisol increases vascular and bronchial smooth
muscle reactivity to catecholamines.
Thyroid peroxidase catalyses iodine oxidation, the formation of mono- and diiodotyrosine, and the
coupling that forms T3 and T4.
Estudiar los receptores
It is related to the D glucose and the L glucose ? also carriers.
C peptide can be used as a marker of the total rate of endogenous beta cell insulin secretion
under steady state conditions. Sulfonylureas increase the rate of insulin secretion and C peptide
levels in patients with type 2 diabetes (glyburide)
C peptide can be used as a marker of the total rate of endogenous beta cell insulin secretion
under steady state conditions. Sulfonylureas increase the rate of insulin secretion and C peptide
levels in pctes with type 2 diabetes.
Neuromuscular hyperexcitability can become clinically apparent when serum calcium levels are <
or = 7.0mg/dL. A common cause of hypocalcemia is primary hypoparathyroidism, which is often
due to loss of parathyroid tissue during thyroidectomy.
Superior mesenteric artery occurs when the transverse portion of the duodenum is entrapped
between the SMA and Ao, causing symptoms of partial intestinal obstruction. This Sx occurs when
the Aortomesenteric angle critically decreases, secondary to diminished mesenteric fat, produced
lordosis or surgical correction of scoliosis.
The third part of the duodeum courses horizontally across the abdominal Ao and IVC at the level
of the 3rd lumbar vertebra. Here it is in close association with the uncinate process of the
pancreas and the superior mesenteric vessels.
Sleen is not a gut derivative; it forms from the mesodermal dorsal mesentery. The splenic artery,
however, is a branch of the celiac trunk (the primary blood supply of the foregut).
Lactose (galactosyl beta-1,4-glucose or milk sugar is a dissaccharide) present in milk.
adasd
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Embryology
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Embryology
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Pyridoxal phosphate is a necessary cofactor in the synthesis of delta-aminolevulinic acid (which is

elevated in cases of lead poisoning).
Trypsinogen is activated to trypsin by duodenal enteropeptidase. Trypsin is essential for protein
digestion and absorption in two ways. It degrades complex peptides to dipeptides and Aa, and it
activateds other proteases such as carboxypeptidase, elastase and chymotrypsin.
Correct order of enzymes that repair damage: Glycosylase, endonuclease, lyase, DNA
polymerase, ligase.
note buaa
Glucose induced decreased adenylate cyclase activity leads to low intracellular concentrations of
cAMP. Low cAMP levels, in turn, cause poor binding of catabolite activator protein (CAP) to the
CAP-DNA binding domain, leading to decreased expression of the structural genes of the lac
operon.
Bacterial mRNA can be polycistronic, meaning that one mRNA codes for several proteins. An
example of polycistronic mRNA is the bacterial operon, which codes for the proteins necessary for
lactose metabolism by E.coli, the transcription and
Amatoxins are found in a variety of poisonous mushrooms (Ejm. Amanita phalloides, known as
death cap) and are potent of RNA polymerase II (halting mRNA synthesis).
very important to study
Positive predictive value depends on the PREVALENCE of a specific disease in the population
being tested.
Intestinal atresia distal to the duodenum occurs due to vascular accidents in utero. If the superior
mesenteric artery is obstructed, so called "apple-peel" atressia occurs. This manifests as a blindending proximal jejunum with absence of a long length of small bowel and dorsal mesentery. The
terminal ileum distal to the atresia assumes a spiral configuration around an ileocolic vessel.
Imperforate anus is a result of abnormal development of anorectal structures. It manifest during
the first days of life by inability to pass meconium. Alternatively, meconium may discharge from the
urethra or vagina if a fistula is present. Pctes with an imperforate anus often have other congenital
malformations, with urogenital tract anomalies being the most common.
Meckel diverticulum is a remnant of the omphalomesenteric (vitelline) duct. It is connected to the
ileum and is located 2 feet proximal to the ileocecal valve. It often contains acid-secreting extopic
gastric tissue, which may cause ulceration of the adjacent mucosa and lower GI bleeding
(melena/hematochezia). Meckel's diverticulum is a true diverticulum and consists of all parts of the
intestinal wall.
99mmTc-pertechnetate scan: detects the presence of gastric mucosa so it Dx Meckel diverticulum.
Meckel diverticulum is a failure of obliteration of omphalomesenteric duct.
Meckel diverticulum: occur due to failure of obliteration of the omphalomesenteric duct. Lower GI
bleeding is the most common manifestation and occurs due to acid secretion by ectopic gastric
mucosa present in the diverticulum.
Lower GI bleeding is one of the common presentations of Meckel diverticulum. This diverticulum
often contains ectopic gastric mucosa which produces acid causing possible ulceration and
bleeding. 99mmTc-pertechnetate scan identifies ectopic gastric epithelium and helps to Dx Meckel
diverticulum.
Neural crest cells migrating to the intestinal wall very early during embryonic development
(submucosal-Meissner, myenteric-Auerbach). Theses parasympathetic ganglia are responsible for
intestinal peristalsis. Neural crest cells more caudally along the vagal nerve fibers. They are
present in the wall of proximal colon at 8yh week of gestation and in the rectum by 12th week.
I do not understand it Two allele loci are said to be more in linkage disequilibrium when a pair of
alleles are inherited together in the same gamete (haplotype) more of less often than whould be
expected given ramdom chance. It is important to understand that this can occur even if the genes
are in different chromosomes.
Two allele loci are said to be in linkage disequilibrium when a pair of alleles are inherited together
in the same gamete (haplotype) more or less often than would be expected given random chance.
It is important to understand that this can occur even if the genes are in different chromosomes.
Unique to the duodenum, the compound tubular Brunner's glands of the submucosa secrete
alkaline mucus into ducts that empty into the crypts of Lieberkuhn. Peyer's, in contrast, are
lymphoid aggregates specific to the ileum.
Local defense against Candida is performed by T cells, whereas systemic infection is prevented
by neutrophils. For this reason, localized candidiasis is common in HIV positive pctes, while
neutropenic individuals are more likely to have systemic disease.
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Ig A protease is produced by N.meningitidis and N. gonorrhoeae. This enzyme claves secretory

IgA at its hinge region rendering it ineffective. Secretory IgA exists on mucosal surfaces and in
secretions and acts to bind and inhibit the action of pili and fibriae as well as other cell surface
antigens that normally mediate mucosal adherence and penetration.
The second most common cause of severe combined immunodeficiency (SCID) is autosomal
recessive deficiency of adenosine deaminase, an enzyme necessary for the elimination of
elimination of excess adenosine within cells. Toxic levels of adenosine accumulate within
lymphocyte in this condition, leading to lymphocyte cell death and resultant cellular and humoral
immune deficiency. Tto is using vectors that infect the patient stem cells with the gene coding for
adenosine deaminase
Secretory form of IgA consists of two immunoglobulin monomers, J chain and secretory
component. This immunoglobulin is abundant in tears, saliva, mucus and colostrum. It is
particularly important to provide the infant with passive mucosal immunity. Most of the components
of IgA are produced by plasma cells, the secretory part is produced by the epithelial cells(helps for
the movements and prevents degradation in secretions).
Secretory form of IgA consist of two immunoglobulin monomers, J chain and secretory
component. This immunoglobulin is abundant in tears, saliva, mucus and colostrum. It is
particularly important as a component of the colostrum, or the first breast milk fed to an infant after
birth, where is Fx to provide the infant with passive mucosal immunity.
NK cells recognize and kill cells with decreased MHC class I antigen cell surface expression, such
as virus-infected cells and tumor cells. They are large lymphocytes that contain perforins and
granzymes in cytoplasmic granules. NK cells kills target cells by inducing apoptosis.
Severe IgA deficiency predisposes patients to chronic giardiasis.
Giardia lamblia causes injury to the duodenal and jejunal mucosa by adhering to the intestinal
brush border and relasing molecules that induce a mucosal inflammatory response. Secretory IgA,
which impairs adherence, is the major component of adaptive immunity against G. lamblia
infection. Severe IgA deficiency predisposes pctes to chronic giardiasis.
Of the cytokines released in the setting of tissue injury, TGF-beta and IL10 are thought to downregulate local cytokine production and inflammatory reactions contributing to the systemic acute
phase response. IL-1, IL4, IL-5, IL12 stimulate local immune reactions, and may therefore be
considered proinflammatoy. IL-1 also acts systemically to promote fever and other aspects of the
acute phase response.
Inheried defects involving INF-gamma pathway result in disseminated mycobacterial disease in
infancy or early childhood. Patients require lifelong treatment with antimycobacterial agents. IFN
gamma binds to its receptor, leading to receptor dimerization of Janus kinases 1 and 2. This
results in nuclear signaling via STAT1 and transcription of IFN gamma regulated genes, which
promote microbacterial killing by phagocytes.
nia
IL-8 is a chemokine produced by macrophages that induces chemotaxis and phagocytosis in
neutrophils. Other significant chemotactic agents include n-formylated peptides, leukotriene B4, 5HETE (the leukotriene precursor), and complement component C5a.
IL-8 is a chemokine produced by macrophages that induces chemotaxis and phagocytosis in
neutrophils. Other significant chemotactic agents include n-formylated peptides, Leucotrine B4, 5HETE (the leukotriene precursor), and complement component C5a.
Traveler's diarrhea is most frequently related to ETEC that produces heat labile (LT, choleragenlike) and heat stable (ST) enterotoxins. LT activates adenylate cyclase leading to increased
intracellular cAMP, and ST activates gualylate cyclase leading to increased intracellular cGMP.
Both cause water and electrolyte loss and watery diarrhea.
buaa
Shigella infection is due to mucosal invasion, is the most significant factor in causing disease.
Shigella gains access to the gut mucosal epithelium, specifically by entering M cells in Peyer's
patches. It then escapes the phagosome, spreds laterally to other epithelial cells, and releases
shiga toxin. The process of cellular invasion induces a robust inflammatory response in the host, it
is the response that is primarily responsible for the diarrhea seen in shigellosis.
Depending on the age and condition of host, as few as 10 cells of any Shigella species can cause
infection, although the infectious dose is ussually much higher. Other organisms that can cause
diarrhea with only a small inoculum include Campylobacter jejuni (500), Entamoeba histolytica (as
few as one organism), and Giardia lamblia (as few as one organism).
Thyfoid fever is caused by Salmonella typhi and paratyphi, and causes a clinical presentation of
scalating fever with initial diarrhea or constipation followed by hepatosplenomegaly, the formation
of "rose spots" on the abdomen, and possible hemorrhagic enteritis with bowel perforation.
C. difficile Toxin A attracts neutrophils causing mucosal inflamation, loss of water into the gut
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lumen and diarrhea, as well as mucosal death. Toxin B, the cytotoxin, causes actin
depolymerization, loss of cellular cytosqueleton integrity, cell death and mucosal necrosis.
C. difficile Toxin A attracts neutrophils causing mucosal inflammation, loss of water into the gut
lumen and diarrhea, as well as mucosal death. Toxin B, the cytotoxin, cuases actin
depolymerization, loss of cellular cytoskeleton integrity, cell death and mucosal necrosis.
C. difficile Toxin A attracts neutrophils causing mucosal inflammation, loss of water into the gut
lumen and diarrhea, as well as mucosal death. Toxi B, the cytotoxin, causes depolymerization,
loss of cellular cytoskeleton integrity, cell death and mucosal necrosis.
Campylobacter jejuni is curved Gram negative rod with a filament that allows it to move in a
characteristic "corkscrew" fashion. It is the most common cause of acute gastroenteritis in children
and adults in industrialized countries. Transmission is via fecal-oral route. The organism can be
acquiered from: 1. Domestic animals: cattle, sheep, and chickens. 2. Contaminated food,
undercooked poultry and unpasteurized milk.
Campylobacter infection is a common cause of inflammatory gastroenteritis and can be acquiered
from domestic animals (cattle, chickens, dogs) or from contaminated food. The diarrhea is
inflammatory and is accompanied by fever, abdominal pain and tenesmus. Campylobacter
infection is associated with Guillan Barre syndrome.
This iodine-stained stool smear shows Giardia lamblia cysts. Giardia is the most common enteric
parasite in the US and Canada, and is a common cause of diarrhea in campers/hikers.
Metronidazol is a treatment of choice.
Strongiloides stercoralis infection begings following skin penetration by filariform (infectious) larva
and can be diagnosed by finding rhabditiform (noninfectious) larvae in the stool. Rhabditiform
larvae can mature into filariform larva in the human GI tract, precipitating an autoinfection cycle
that occurs enterely within the affected individual.
-The small bowel mucosa of patients with lactase deficiency: normal. -Celiac disease: atrophy on
the intestinal vili. - Whipple Ds: Distended macrophages in the intestinal lamina propia. -Ulcerative
colitis: Collection of neutrophils within the crypt lumina. -Gastrointestinal lymphomas: Massive
infiltration of the intestinal lamina propia with atypical lymphocytes.
Crohn's disease is associated with increased activity of the NF-kB protein(because of the
activation of the NOD2 receptor), which is responsible for cytokine productions. When the
appropiate immune response to intracellular microbes is blunted, the microbes persist and induce
chronic inflammation with the gastrointestinal tract.
Crohn's Ds is associated with increased activity of the NF-kB protein, which is responsible for
cytokine production. When the appropiate immune response to IC microbes is blunted, the
microbes persist and induce chronic inflammation within the GI tract.
An anal fissure is a tear in the lining of the anal canal distal to the dentate line that occurs most
often on the posterior midline. Patients complain of severe tearing pain associated with the
passage of bowel movements. There may be a skin on physical examination. Anal fissures are
associated with low-fiber diets and constipation.
Colon cancer may be completely asymptomatic and is often found on screening colonoscopy. The
most common location for this malignancy is the rectosigmoid colon. The ascending colon is the
second most common location of colorectal carcinomas.
Barret esophagus is an intestinal metaplasia of esophageal epithelium. It occurs in GERD and is
the most important risk fct for development of esophageal adenocarcinoma. As the sequence of
GERD -> Barrett esophagus -> esophageal adenocarcinoma is well recognized, early diagnosis
and regular monitoring of patients with gastroesophageal reflux is important.
Calcinosis, Raynaud syndrome, Esophageal dysmotility, Sclerodactyly, and Telangiectasia
comprise CREST syndrome. It is systemic sclerosis variant that mostly involves skin of the face
and fingers. The pathogenesis of systemic sclerosis is unknown, although immunologic
hyperreactivity is suseccted. An unknown antigen is though to stimulate accumulation of CD4
lymphocytes in skin and other tissues. CD4 lymphocytes secrete biologically active substances
and stimulate fibroblasts
Acute erosive gastropathy can be caused by a number of factors, including nonsteroidal antiinflammatory drugs use, head trauma, severe burns, acute stress, and alcohol or tobacco use.
Erosions are defined as mucosal defects that do not fully extend the muscularis mucosa. Acute
erosive gastropathy can cause upper GI hemorrhage that leads to melena.
Abetapoproteinemia is an inherited inability to synthesize apolipoprotein B, an important
component of chylomycrons and very low-density lipoprotein. Lipids absorbed by the small
intestine cannot be transported into the blood and accumulate in the intestinal epithelium. Lipids
absorbed by the small intestine cannot be transported into the blood and accumulate in the
intestinal epithelium, resulting in enterocytes with clear or foamy cytoplasm.
Submucosal (Meissner) and myenteric (Auerbach) autonomic plexi are absent in the affect of the
bowel in Hirschsprung disease. The submucosa of the narrowed area is the most superficial layer
where the absence of ganglion cell can be seen.
Chrons disease: Increased activity of TH1 helper cells increases production of IL-2, interferon
gamma, and TNF, causing subsequent intestinal injury.
buaaa
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Gastrointe
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Gastrointe
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Gastrointe
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Gastrointe
Chron's disease is associated with oxalate kidney stones. Impaired bile acid absorption in the
terminal ileum leads to loss of bile acids in the feces with subsequent fat malabsorption. Lipids
then bind calcium ions, and the resulting soap complex is excreted. Free oxalate (which is
normally bound by calcium ions to form an unabsorbable complex) is absorbed and forms urinary
calculi.
Long-standing ulcerative colitis is associated with an increased risk of colorectal cancer. The
duration and extent of colitis are the most significant risk fcts. Unlike sporadic colorectal
carcinomas, colitis-associated carcinomas are more likely to arise from non-polypoid dysplastic
lesions, be multifocal in nature, develop early p53 mutations and late APC gene mutations, and be
of a higher histological grade.
Colitis-associated carcinoma is more likely to: 1. Affect younger pctes. 2. Progress from flat and
non polypoid dysplasia. 3. Histologically appear mucinous and/or have signet ring morphology 4.
Developed early p53 mutations and late APC gene mutations, opposite that of sporadic disease 5.
Be distributed within the proximal colon (especially with Chron's Ds or concurrent primary
sclerosing cholangitis) 6. Be multifocal in nature.
Pctes with Crohn's Ds affecting the terminal ileum are prone to the development of gallstones.
Decreased bile acid reabsorption and its loss via feces increases the lithogenicity of bile.
Cholesterol precipitates and forms gallstones.
The most typical location for intussusception is at ileocolic junction. Intussusception is most
common in children younger than 2 years old. In this age group, it often occurs without any
structural cause (sometimes associated with viral infection). In patients older than 2 years of age,
a lead point, such as Meckel diverticulum, foreign body, or intestinal tumor, should be sought.
-Progression from normal mucosa to a small polyp: due to mutation of the APC tumor suppressor
gene. -Increase in the size of the polyp: Mutation of K-ras protooncogene. -Malignant
transformation: of adenoma into carcinoma requires mutation of 2 genes (p53 and DCC).
Adenomatous polyps contain dysplastic mucosa and are premalignant. Regular screening with
timely excision of polyp is effective for the prevention of colon adenocarcinoma. Studies have
linked increased activity of COX-2 to some forms of colon adenocarcinoma and suggest that
aspirin use decreases adenomatous polyp formation.
Chronic alcohol abuse cause a number of systemic effects due to both the direct toxic actions of
ethanol and its metaolites and alcohlism-associated vitamin deficiencies. Macrocytosis (MCV
>100fL) is often seen in patients with chronic alcoholism. It may occur secondary to poor nutrition
(folate or vitamin B12 deficiency) but may also result from direct toxicity of alcohol on the marrow.
Oh abuse is 1 of the 2 MC causes of acute pancreatitis (gallstones are the other). Macrocytosis,
as AST:ALT ratio>2, and elevated gamma-glutamyltransferase (GGT) are indirect indicators of
chronic consumption. Macrocytosis can occur independently of folate or cobalamin deficiency.
Pancreatic pseudocyst is a common complication of acute pancreatitis. It is collection of fluid rich
in enzymes and inflammatory debris. Its walls consist of granulation tissue and fibrosis. Unlike true
custs, pseudocysts are not lined by epithelium.
-Pancreatic pseudocyst: common complication of acute pancreatitis. It is a collection of fluid rich in
enzymes and inflammatory debris. Its walls consists of granulation tissue and fibrosis. Npot lined
by epithelium. -True cysts: lined by epithelium. -Serous pancreatic neoplasm: glycogen-rich
cuboidal epithelium. -Mucinous neoplasm of the pancreas: columnar mucinous epithelium.
-Pancreatic adenocarcinoma: atypical cells forming papillary projections.
Smoking is the most important enviromental risk fct for pancreatic cancer. Age >50 years old,
chronic pancreatitis, DM, and genetic predisposition also increase the risk of this malignancy.
80% of acute pancreatitis are caused by gallstones and chronic alcoholism. Less common causes
account for the other 20%. Inherited or acquiered hypertriglyceridemia can cause acute
pancreatitis if the serum level of triglycerides exceeds 1000mg/dL
ggg
Shigella exhibits specificity for the M (microfold) cells that lie in the base of mucossal villi within a
Peyer's patch region of the ileum mucosa.
Diarrhea, weight loss, and epigastric region calcifications in a pcte with chronic alcoholism suggest
chronic pancreatitis with resulting pancreatic exocrine insufficiency and malabsorption.
Causes of nictalopia: 1. Toxic retinopathy due to phenothiazines or chloroquine 2. Vitamin A
deficiency 3. Congenital rubell, syphilis or other infections 4. Diabetic retinopathy
Vitamin A deficiency can cause night blindness. Vit A deficiency may result from any cause of fat
soluble Vit malabsorption, including chronic cholestasis from biliary obstruction.
-Type B chronic gastritis typically affects the gastric antrum and is ussually the result of H. pylory
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Pathology
133
Pathophysi
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Pathophysi
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433
Pathophysi
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190
7
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190
7
Pathophysi
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193
8
Pathophysi
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841
Pharmacol
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Gastrointe
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125
8
Pharmacol
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170
9
Pharmacol
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170
9
Pharmacol
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Gastrointe
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Gastrointe
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Gastrointe
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845
5
Pharmacol
ogy
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755
Physiology
154
6
Physiology
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168
0
180
4
Anatomy
180
4
Anatomy
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180
5
Anatomy
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832
6
832
6
Anatomy
Genitourin
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Anatomy
Anatomy
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infection of the gastric mucosa. This type of gastritis is associated with an increased risk of gastric
adenocarcinoma and MALT lymphoma.
Helicobacter pylori can cause duodenal ulcers and is typically found in greatest concentration in
the prepyloric are of the gastric antrum. As a result, biopsy of the prepyloric area would have the
greatest yield of the organism.
Lactase deficient indicidual hace increased stool osmotic gap, increased beath hydrogen content,
and decresed stool pH upon lactose challenge.
Nests of mast cells within the mucosa will cause gastric hypersecretion.
Trypsin can activate all of the proteolytic pancreatic enzymes, including its own zymogenic form.
Premature activation of trypsinogen before it reaches the duodenal lumen can result in
autodigestion of the pancreatic tissues. Multiple inhibitory Mxs exists to reeduce the premature
activation of trypsinogen, including cleavage inactivtion of trypsin by trypsin itself. Gene mutations
that render trypsin insensitive to cleavage inactivation cause hereditary pancreatitis.
D-xylose is a monosaccharide; thus, its absorption does not require pancreatic enzymes and is
not affected by pancreatic insufficiency. Oral administration of a fixed dose of D-xylose can be
used to differentiate between malabsorption of pancreatic versus gastrointestinal mucosal etiology.
D-xylose is a monosaccharide; thus, its absorption does not require pancreatic enzymes and is
not affected by pancreatic insufficincy. Oral administration of a fixed dose of D-xylose can be used
to differentiate between malabsorption of pancreatic versus gastrointestinal mucosal etiology.
VIPomas are non-beta pancreatic islet tumors that hypersecrete VIP. VIP increases intestinal
chloride loss into the stool, which causes excess losses of the accompanying water, Na and K as
well. VIP also inhibits gastric acid secretion. Somatostatin inhibits the secretion of VIP and is used
to treat the symptoms of VIPoma.
Dimercaprol is a chelating agent used in the tto of arsenic poisoning. It displaces arsenic ions from
sulfhydryl groups of enzymes and facilitates their excretion. Arsenic causes poisoning by
inactivating numerous enzymes involved in cellular metabolism. Symptoms of poisoning include
stomach pains, vomiting and delirium in addition to a garlic odor on the breath.
Meperidine has reported to cause less constriccion of the sphincter of Oddi
Bioavailability and curves (pharmacology)
Bioavailability refers to the fraction of administrated drus that reaches the systemic circulation in a
chemically unchanged form. Bioavailability for a drug administered by a non-intravenous route is
always less than 1. It can be determined by examining a graph of plasma concentration versus
time and then applying formula: F=(AUC oral x dose IV)/ (AUC IV x dose oral)
Tto of chronic hepatitis C involves the use of interferon alpha and ribavirin. Ribavirin's mechanism
of action is multifactorial and includes inducing lethal hypermutation, inhibing RNA polymerase
and inosine monophosphate dehydrogenase (depleting GTP), causing defective 5'-cap formation
on viral mRNA transcripts, and modulating a more effective immune response.
Metabolism yields: - 4 cal per gram of protein or CHO. - 9 cal per gram of Lipids. - 7 cal per gram
of ethanol.
Pancreatic exocrine secretions are the major source of HCO3 entering the duodenum. Secretin is
the hormone that stimulates the release of HCO3- rich secretions from the exocrine pancreas.
Secretin is produced by S enteroendocrine cells in the duodenal mucosa in response to
stimulation by intraluminal acidity. Hydrochloric acid is the most potent stimulus for secretin
release.
The proximal 1/3 of the ureter receives its blood from branches of the renal artery. For this reason,
this portion of the donor ureter is typically viable after renal transplantation.
The urethers cross over the common/external iliac vessels and under the gonadal vessels (and
ovarian vessels in the female). They pass lateral the internal iliac vessels and medial to the
gonadal vessels as they enter the true pelvis.
The ureters cross over the common/external iliac vessels and under the gonadal vessels (and
ovarian vessels in the female). The pass lateral to the iliac vessels and medial to the gonadal
vessels as they enter the true pelvis
The left gonadal (testicular or ovarian) vein drains into the left renal vein, coomonly leading to leftsided varicoceles in males with obstructions of the left renal vein. The right gonadal vein directly
into the inferior vena cava.
Due to its intra abdominal origin, lymphatic drainage of the testis is to the para-aortic lymph nodes.
In contrast, lymph drainage from the scrotum goes into the superficial inguinal nodes.
- Para-aortic nodes: receive lymph drainage from testis. - Superficial inguinal nodes: receive
lymph drainage from scrotum. - Deep inguinal nodes: received lymph drainage from glands penis
& superficial nodes.
866
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202
7
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7
202
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Anatomy
837
Embryology
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837
Embryology
183
1
312
Embryology
742
Immunolog
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Genitourin
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747
Immunolog
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747
Immunolog
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Genitourin
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750
Immunolog
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Genitourin
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676
Microbiolog
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723
Microbiolog
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114
1
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115
4
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8
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155
1
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193
2
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747
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caramba
Clues to point toward psychogenic impotence include sudden onset and the presence of morning
erections.
Single nucleotide deletions shift the reading frame, often creating a premature stop codon or
dramatically changing the protein structure.
bu
Releasing fctors recognize the stop codons (UAA, UAG and UGA) to terminate preoteins
synthesis. They facilitate release of the ppolypeptide chain from the ribose and dissolution of the
ribose mRNA complex.
In normal fetal development, the ureters are fully canalized before the metanephros begings to
produce urine (8-10th week of gestation). Inadequate recanalization of ureteropelvic junction, the
junction bwtn the kidney and the ureter, is the most common cause of fetal hydronephrosis.
isra
buaa
-Elevated AFP: multiple gestation, neural tube defect (including spine bifida, anencephaly), and
abdominal wall defects. -Low AFP: Down syndrome.
Glomerulonephritis and photosensitive skin rash and arthralgias in a young female are suggestive
of SLE.
The acute hemolytic transfusion reaction is an antibody-mediated (Tyoe II) hypersensitivity
reaction wherein host antibody binds antigen on transfused donor red blood cells, activating
complement. The complement membrane attack complex causes erythrocyte lysis, and
anaphylatoxines mediate vasodilation and symptoms of shock.
The acute hemolytic transfusion is and antobody mediated (Type II) hypersensitivity Rx wherein
host antibody binds antigen on tranfused donor red blood cells, activating complement. The
complement memb attack complex causes erythrocyte lysis, and anaphylatoxins mediate
vasodilation and symptoms of shock.
The acute hemolytic transfusion reaction is an antibody mediated (Type II) hypersensitivity
reaction wherein host antibody binds antigen on transfused donor red blood cells, activating
complement. The complement membrane attack complex causes erythrocyte lysis, and
anaphylatoxins mediate vasodilation and symptoms of shock.
Eosinophils play in host defense during parasitic infection. When stimulated by IgE bound to a
parasitic cell, they destroy the parasite via antibody-dependent cellular cytotoxicity (ADCC) with
enzymes from their cytoplasmic granules. Another function of eosinophils is regulation of type I
hypersensitivity reactions.
Enterotoxins, exfoliative toxins and TSST-1 are the toxins with superantigen activity.
Superantigens interact with major histocompatibility complex molecules on antigen presenting
cells and the variable region of the T lymphocyte receptor to cause nonspecific "widespread"
activation of T cells resulting in the release of interleukin-2 (IL-2) from te T cells and IL-1 and TNF
from macrophages. The immune cascade, in turn, is responsible for the effects of TSS.
Protein M is the major virulence fct for Streptococcus pyogenes. It inhibits phagocytosis and
complement activation, mediates bacterial adherence, and is the target of type-specific humoral
immunity to S. pyogenes.
Gram -negative sepsis is caused by release of LPS from bacterial cells during division or by
bacteriolysis; LPS is not actively secreated by bacteria. Lipid A is the toxic component of LPS; it
causes activation of macrophages leading to the widespread release of IL-1 and TNF-alpha, which
cause the signs and symptoms of septic shock: fever, hypotension, diarrhea, oliguria, vascular
compromise, and DIC.
Chlamidia trachomatis serotypes L1 through L3 cause lymphogranuloma venereum (LGV), a
sexually transmitted disease characterized by painless ulcers with later progression to painful
inguinal lymphadenopathy and ulceeration. Histologically, LGV is characterized by chlamydial
inclusion bodies in the cellular cytoplasm.
Urinary tract infection characterized by dysuria and hematuria is most likely hemorrhagic cystitis.
Acute hemorrhagic cystitis is children may caused by bacteria or viruses, though in a majority of
cases no infectious agent can be cultured from urine. The most common known virus in this case
is adenovirus (serotypes 11 and 21 bubgroup B)
A UTI w/ dysuria and hematuria (hemorrhagic cystitis). This in children may be caused by bacterial
or viruses, though in a majority of cases no infectios agent will be culture in the urine. The MC
known viral cause of hemorrhagic cystitis in children (males) is adenoviru; serotypes 11 and 21 of
adenovirus subgroup B have been particularly implicated in this illness.
Antiviral drugs currently recommended for the treatment of primary genital herpes include the
nucleoside analogs (acyclovir). These nucleoside analogs are incorporated into newly replicated
viral DNA and ultimately terminate viral DNA chain synthesis.
Pelvic inflammatory disease is most commonly caused by Neisseria gonorrhoeae or Chlamydia
trachomatis and is strongly associated with an increased incidence of ectopic pregnancy.
853
8
Microbiolog
y
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854
1
Microbiolog
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258
Pathology
Genitourin
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333
Pathology
580
Pathology
Genitourin
ary
Genitourin
ary
810
Pathology
Genitourin
ary
811
Pathology
Genitourin
ary
813
Pathology
Genitourin
ary
813
Pathology
Genitourin
ary
814
Pathology
Genitourin
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815
Pathology
Genitourin
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815
Pathology
Genitourin
ary
815
Pathology
Genitourin
ary
818
Pathology
Genitourin
ary
834
Pathology
Genitourin
ary
834
Pathology
835
Pathology
Genitourin
ary
Genitourin
ary
835
Pathology
Genitourin
Enterobius vermicularis infection occurs most frequently in school-age children and presents with
perianal pruritus. Diagnosis is made by the "Schotch tape" test. Albendazole or mebendazole is
the first like tto, with Pyrantel pamoate as an alternate agent preferred in pregnant patients.
The clinical manifestations of schistomiasis result from a Th2 mediated immune response directed
against the eggs. This results in granulomatous inflamation and fibrosis, which ultimately causes
ulceration and scarring of bowel or bladder/ureters. Eggs that settle into the presinusoidal radicals
of the portal vein cause periportal "pipestem" fibrosis (pathognomonic for hepatic
schistosomiasis), which will results in restriction of portal venous fow and portal Hypertension
Polycystic ovarian syndrome is associated with oligomenorrhea, obesity, hirsutism and polycystic
ovaries. These pctes are at increase risk for developing endometrial adenocarcinoma and type 2
diabetes mellitus. Hormonal dysregulation (progesterone deficiency, acyclic estrogen production,
and elevated LH level). The effects of abnormally high levels of unopposed estrogen on the
endometrium increase the long-term risk of endometrial hyperplasia and endometrial
adenocarcinoma.
Nodularity of the uterosacral ligaments and fixed retroversion of the uterus are commonly found in
pctes with endometriosis on vaginal examination.
In patients with cryptorchidism, the seminiferous tubules become atrophic and hyalinized as a
result of temperature-induced damage, resulting in a significantly depressed sperm count as well
as decreased inhibin levels. Hormonal function of Leyding cells is usually not impaired. Thus,
secondary sexual characteristics and sexual performance are normal.
A pcte with signs of renal failure and toe gangrene or livedo reticularis following an invasive
vascular procedure likely has atheroembolic renal disease. Light microscopy shows cholesterol
emboli obstructing renal arterioles.
Bening Prostate hyperplasia is characterized by a combination of epithelial and stromal
hyperplasia, predominantly in the periurethral and transition zones. On palpation, the prostate has
a rubbery consistency, in contrast to prostate cancer, where the glands is nodular and verm firm.
Urinary retention leads to increased pressure in the urinary tract, causing characteristic
morphological changes. The bladder wall hypertrophies, to increase its contractile force.
Idiopathic hypercalciuria is the most common cause of calcium kidney stone disease. This
condition is characterized by normal serum calcium levels with high levels of calcium excreted in
the urine. Other causes of calcium nephrolitiasis include hyperoxaluria, hyperuricosuria, low
urinary volume, and hypocitraturia.
Idiopathic hypercalciuria is the most common cause of calcium kidney stone disease. This
condition is characterized by normal serum levels with high levels of calcium excreted in the urine.
Other causes of calcium nephrolitiasis include hyperoxaluria, hyperuricosuria, low urinary volume,
and hypocitraturia.
Cystinuria results from a defect in the renal proximal tubules, which results in decreased
resorption of the aminoacid cystine. The clinical manifestation is recurrent stone formation from a
young age. Urinalysis shows pathognomonic hexagonal cystine crystals. The sodium cyanidenitroprusside test, which detects cystine's sulfhydryl groups, is diagnostic.
Cystinuria is an inborn defect pf the transporter of cystine, ornithine, arginine and lysine. It is
inherited in an autosomal recessive fashion. The only manifestation of this disorder is
nephrolitiasis that is classically presents as renal colic during the 2nd or 3rd decades of life.
Urinalysis shows pathognomonic hexagonal cystine crystals.
Cystinuria is an inborn defect of the transporter of cystine, ornithine, arginine and lysine. It is
inherited in an AR fashion. The only manifestation of this disorder is nephrolithiasis that classically
presents as renal colic during the 2nd and 3rd decade of life. Urinalysis shows hexagonal cystine
crystals.
Cystinuria is an inborn defect of the transporter of cystine, ornithine, arginine and lysine. It is
inherited in an autosomal recessive fashion. The only clinical manifestation of this disorder is
nephrolitiasis that classically presents as renal colic during the 2nd or 3rd decades of life.
Urianalysis shows pathognomonic hexagonal cystine crystals.
Clear cell carcinoma is the most common subtype of renal cell carcinoma and is composed of
large, rounded or polygonal cells with clear cytoplasm. The classic triad of hematuria, flank pain,
and palpable mass occurs in a minority of pctes. Non specific symptoms are paraneoplastic
syndromes are more common. These tumors are often detected incidentally at an advanced
stage, and the lung is the most common site for metastasis.
Papillary necrosis occurs in pctes with sickle cell disease or trait, diabetes mellitus, analgesic
nephropathy, or severe obstructive pyelonephritis. Acute colocky flank pain, gross hematuria and
the passage of tissue fragments in urine are characteristic.
Papillary necrosis -Sickle cell disease or traint -Analgesic nephropathy -Diabetes mellitus -Acute
pyelonephritis and urinary tract obstruction.
-Pathology of the renal papilla (papillary necrosis) is common in patients with sickle cell disease,
diabetes mellitus, analgesic nephropathy, and in severe acute pyelonephritis. -Interstitial nephritis:
fever, maculopapular rash and symptoms of acute renal failure one t three weeks after beginning
tto with beta lactam atb. Peripheral eosinophilia and eosinophiluria. Symptoms resolve completely
after cessation of the medication.
Fever, rash and oliguria one to three weeks after anitiation of beta lactam antibiotic, NSAID,
ary
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Pathology
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Pathology
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Genitourin
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817
Pathophysi
ology
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Genitourin
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Genitourin
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954
Pathophysi
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954
Pathophysi
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955
Pathophysi
ology
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955
Pathophysi
ology
Genitourin
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846
8
846
8
Pathophysi
ology
Pathophysi
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100
0
Pharmacol
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Genitourin
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100
0
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110
4
110
4
Pharmacol
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111
8
111
8
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195
0
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824
9
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sulfonamides, rifampin, diuretics can cause Acute Interstitial Nephritis. IgE mediated
hypersensitivity combined with cell mediated Rx. Peripheral eosinophilia, eosinophiluria (detected
by Hansel or Wright stain). Symptoms always resolve completely after cessation of the offending
medication.
Fever, maculopapular rash and symptoms of acute renal failure one to three weeks after
beginning tto with a beta lactam antibiotic or a number of the other drugs are highly suggestive of
acute interstitial nephritis. Peripheral eosinophilia and eosinophiluria are important clinical clues.
Symptoms resolve completely after cessation of the medication.
Straints of Papilloma virus that are carcinogenics: 16, 18, 31, 33
TNF alpha is one of the cytokines that induces the systemic inflammatory response. In high
concentrations, TNF-alpha causes symptoms of septic shock and cachexia. Other cytokines
responsible for inducing the systemic inflammatory response include IL-1 and IL-6
- Prevent Calculi formation: citrate and high fluid intake. - Promote salt crystalization: Increased
concentrations of calcium, phosphate, oxalate, and uric acid.
Renal calculi occur when there is an imbalance of the factors that facilitate and prevent stone
formation. Increased concentrations of calcium, phosphate, oxalate, and uric acid promote salt
crystallization, whereas increased potasium citrate and high fluid intake prevent calculi formation.
5 alpha reductase converts testosterone to dihydrotestosterone (DHT). DHT mediates
development of the external genitalia in the male fetus. Male neonates with 5alpha-reductase
deficiency are born with feminized external genitalia that typically masculinize at puberty. Small
phallus and hypospadias are commonly found.
5 alpha reductase converts testosterone to dihydrotestosterone (DHT). DHT mediates
development of the external genitalia in the male fetus. Male neonates with 5 alpha reductase
deficiency are born with feminized external genitalia that typically masculinize at puberty. Small
phallys and hypospadias are common found.
Aromatase converts androgens into estrogens in the ovaries, testes, placenta and other peripheral
tissues. Genetic def of this enzyme leads to an inability to synthesize estrogens. It presents with
maternal virilization during pregnancy and masculinization of the female fetus.
Aromatase converts androgens into estrogens in the ovaries, testes, placenta and other peripheral
tissues. Genetic deficiency of this enzyme leads to an inability to synthesize estrogens. It presents
with maternal virilization during pregnancy and masculinization of the female fetus.
After vasectomy, viable sperm remain in the portion of the vas deferens proximal to the ligation.
20% of pctes still have viable sperm in their ejaculate after 3 months and at least 20 ejaculations.
After vasectomy, viable sperm remain in the portion of the cas deferens proximal to the ligation.
Twenty percent of patients still have viable sperm in their ejaculate after 3 months and at least 20
ejaculations.
Enterococci produce aminoglycoside-modifying enzyme that transfer different chemical groups
(acetyl, adenyl or phosphate) to the aminoglycoside molecule and therefore impair antibiotic
binding to ribosomal subunits.
Enterococci produce aminoglycoside-midifying enzymes that trnasfer different chemical groups
(acetyl, adenyl or phosphate) to the aminoflycoside molecule and therefore impair antibiotic
binding to ribosomal subunits.
Trimethoprim, methotrexate and pyrymethamine all prevent the reduction of folic acid to
tetrahydrofolate by inhibiting dihydrofolate reductase.
Trimethoprim, methotrexate, and pyrimethamine all prevent the reduction of folic acid to
tetrahydrofolate by inhibiting dehydrofolate reductase. Trimethroprim restricts microbial groth
through this process, and works particularly well in conjunction with sulfonamide because
sulfonamide sulfonamide inhibits a diferent step in the production of folic acid.
Atrial natriuretic peptide, NO, sildenafil(prevent degradation of cGMP) all of them caused incresed
of cGMP
Sildenafil is a selective inhibitor of the cGMP phosphodiesterase, and use of this drug will prevent
degradation of cGMP leading to higher intracellular levels. NO and ANP act via a cGMP second
messenger system (NO being primarily responsible for causing erection), and binding of these
hormones to their receptors will also increase intracellular cGMP concentrations.
Clhamydia trachomatis lacks peptidoglycan within the cell wall, and Ureaplasma urealyticum lacks
a cell wall enterely. Therefore, they are not effectively treated by penicillins and cephalosporins.
Antiribosomal antibiotics, like macrolides and tetracyclines, are effective against these organisms.
Urge incontinence, or overactive bladder syndrome, is caused by unhibited bladder contractions
(detrusor inestability). It results in a sense of urgency accompanied by an involuntary loss of urine.
If behavioral therapy alone is unsuccessful, use antimuscarinic drug (targeting M3 receptor.
Caution with elderly, may cause confution and functional decline)
Fracture where the frontal, parietal, temporalm and sphenoid bones meet in the skull is important
because in this region the skull is thin and has the middle meningeal artery. The middle meningeal
artery is a branch of the maxilary artery, which itself is a branch of the external carotid artery.
Riboflavin (vitamin B2) is a precursor of the coenzymes FMN and FAD. FAD participates in
tricarboxylic acid cycle as a coenzyme of succinate dehydrogenase, whhich converts succinate
into fumarate. The Dx is established with performance of the erythrocyte glotathione reductase
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assay or evaluation of the urinary riboflavin excretion.

Estudiar los tipos de interaccion Genome recombination between two defective viruses coinfecting the same host cell can yield a cytopathic wild-type genome. Recombination is gene
exchange that occurs through the crossing over of two double-stranded, non fragmented DNA
molecules. Reassortment describes the mixing of genome segments in two or more segmented
viruses that infect the same host cell.
Phenotypic mixing refers to co-infection of a host cell by two viral strain, resulting in progeny
virions that contain nucleocaspid proteins from one strain and the genome of the other strain.
Since there is no change in the underlying viral genomes (no genetic exchange), the next
generation of virions revert to their original, unmixed phenotypes.
Phenotypic mixing refers to co-infecttion of a host cell by two viral strains, resulting in progeny
virions that contain nucleocapsid proteins from one strain and the genome of the other strain.
Since there is no change in the underlying viral genomes (no genetic exchange), the next
generation of virions revert to their original, unmixed phenotypes.
Neonates with Edwards syndrome (47,XX,+18) have micrognathia, microphtalmia, malformed and
low-set ears. Note that rocker bottom feet are seenm as with Patau syndrome (trisomy 13. The
presence of clenched hands with overlapping fingers is considered one of the distinguishing
features of this syndrome)
IFN alpha and beta act on neighboring cells (paracrine signaling), stimulating them to synthesize
antiviral proteins that degrade intracellular mRNA and impair protein synthesis. IFN gamma is
produced mainly by NK and T cells and functions to promote Th1 differentiation, induce class II
MHC expression, and activate macrophages.
Interferons alpha and beta are produced by a wide variety of eukaryotic cells in response to viral
infections. These interferons act on neighboring cells (paracrine signaling), stimulating them to
synthesize antiviral protein that degrade intracellular mRNA and impair protein synthesis.
Interferon gamma is produced mainly by NK and T cells and Fx to promote Th1 differentiation,
induce class II MHC expression, and activate macrophages.
Major adaptative immune mechanisms that prevent reinfection with the influenza virus include
anti-hemagglutinin IgG antibodies in circulation and mucosal anti-hemagglutinin IgA antibodies in
the nasopharynx.
Thayer Martin medium makes grow N. gonorrhoeae Has Vancomycin (inh gram positive), colistin
or polimyxin (inh gram neg), nystatin (inh yeast), trimethoprin (inh Proteus).
Corynebacteria diphteriae will grow on cysteine-tellurite agar as a dark black, slightly iridescent
colonies. It also be cultured in Loffler's medium where it will develop cytoplasmic metachromatic
granules (visualizable after staining with an aniline dye such as methylene blue). More rapid
diagnostic mechanisms such as the immunochromatographic strip assay are being developed.
Otitis media in childhood: steptococcus pneumonia, Nontypable Haemophilus influenae. Acute
bronchitis: Influenza A & B, coronavirus, respiratory syncytial virus and human metapneumovirus
being the most commonly implicated. H influenza complications: meningitis, pneumonia, sepsis
and epiglottitis.
The Haemophilus influenza type B vaccibe is composed of cell wall polysaccharide conjugated
with protein toxoid from either diphteria or tetanus. This vaccination can be given as early as 2
months of age and has drastically reduced the incidence of clinical disease caused by H.
influenzae such as meningitis, pneumonia, sepsis and epiglotitis.
Diphteria infections is associated with a 5-10% mortality rate, especially in younger pctes or those
with myocarditis. Cardiomyopathy is the most common cause of death. Tto includes diphteria
antitoxin (passive immunization), antibiotics, and active immunization. Of these, passive
immunization with antitoxin is the most important and has the greatest effect on prognosis.
Children aged one to three years who develop gigngivomastitis characterized by ulcerative lesions
with intranuclear inclusions are likely experiencing primary infection with herpes simplex virus type
1 (HSV-1). HSV-1 and other herpesviruses are enveloped and possess double-stranded DNA
genomes.
Changes in host range are most commonly caused by mutation in the viral encoded surface
glycoprotein that mediates virion attachment to target host cell plasmalemma receptors. Mutations
in viral encoded capsid proteins, RNA polymerases, endonucleases, or proteases could
nonspecifically affect viral replication in the standard host cell but would be less likely to
significantly after the range of host cell types that an enveloped RNA virus could successfully
infect.
The viruses that involves reassortment of genomic segments of the human strain with genomic
segments of the animal are orthomyxoviruses and rotaviruses.
Viruses with segmented genomes (orthomyxoviruses and rotaviruses) are capable of genetic
shifts through reassortment. Reassortment involves exchange of entire genome segments, a far
more dramatic process than the point responsible for genetic drift.
Structural gene (gag, pol, and env) products include nucleocapsid proteins p24 and p7 (from the
gag gene) and envelope glycoproteins gp120 and gp41 (from the env gene). Important enzymes
are produced from transcription and translation of the pol gene. The regulatory tat and rev genes
are required for viral replication.
study
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102
0
Biochemistr
y
Biochemistr
y
Hematolo
gy
Hematolo
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103
5
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106
2
124
1
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3
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133
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Hematolo
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In the HIV replication cycle, polyprotein precursors are encoded for by the structural genes (gag,
pol, and env). Only the env gene polyprotein product is glycosilated to gp160 and proteolytically
cleaved within the endoplasmic reticulum and Golgi apparatus to form the envelope glycoproteins
gp120 and gp41.
Of all the antivirals agents that bind and inhibit DNA polymerase in herpesvirus and reverse
transcriptase in HIV, the pyrophosphate analog foscarnet is one of few that do not require
intracellular activation by viral or cellular kinases.
nn
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Monophosphorilation of acyclovir by a viral thymidine kinase is the first (and rate limiting) step in
the conversion of acyclovir to its active triphosphate form. Acyclovir and related drugs (famciclovir,
valaciclovir) are more effective against herpes simplex virus and varicella zoster virus than
cytomegalovirus and Epstein Barr Virus.
The most common cause of retinitis in HIV positive pctes is cytomegalovirus infection.
Cytomegalovirus retinitis most frequent affects AIDS pctes with a CD4 lymphocyte count <50
cells/uL. It is best treated with ganciclovir
Oseltamivir is a neuraminidase inhibitor useful in the tto and prevention of both influenza A and B
virus infections. This medication impairs the release of newly formed virions from infected host
cells and impairs viral penetration of mucous secretions that overlie the respiratory epithelium.
HIV-1 protease inhibitors and glucocorticoids are strongly associated with medication-induced
body fat redistribution syndrome, which is chararterized by the redistribution of body fat from the
extremieties to the abdominal viscera and the subcutaneous adipose tissues of the thorax,
posterior neck, and supraclavicular region.
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Fever, cutaneous flushing, dry oral mucosa, dilated poorly reactive pupils and confusion are all
signs of anticholinergic toxicity. TCA particularly amitriptyline, have antimuscarinic side effects that
may mimic atropine toxicity.
-HbF: alpha2 gamma2 (high affinity for oxygen and is produced during the final month of
gestation). -HbA: alpha2 beta2 (the switching occurs during the first 6 month of life).
Pyruvate kinase deficiency causes hemolytic anemia due to faiulure of glycolysis and resultant
failure to generate sufficient ATP to maintain erythrocyte structure. In this case, splenic
hypertrophy results from incresed work of the splinic parenchyma, wich must remove these
deformed erythrocytes from the circulation.
Transketolase and transaldolase carry nonoxidative reactions of HMP shunt. Some cells do not
use the oxidative phase reactions to produce cytosolic NADPH, but all cells can synthesize ribose
from fructose-6-phosphate using the nonoxidative reactions.
Vitamin K assistance of glutamate residue crboxylation is essential for some clotting factor
production.
HbS aggregate iin the deoxygenated state. HsS polymers form fibrous strands that reduce red
blood cell memb flexibility and promote sickling. Sickling occurs under all conditions associated
with anoxia including low pH and high 2,3-DPG. These inflexible erythrocytes predispose to
microvascular occlusion and microinfarction.
-HbS contains valine in place of glutamic acid in the 6th amino acid position of the beta sunit. This
promotes hydrophobic interaction among Hb molec and results in polymerization of HbS molec
and red blood cell distortion. -HbC: contains lysine in place of glutamic acid residue at the 6th
position. HbC has a very low electrophoretic mobility (compared to HbS and HbA). Pctes
w/homozygous HbC dS generally have mild hemolityc anemia but lack the sickling or
microinfaction
Cobalamin (Vit B12) deficiency results in homocystinemia due to impaired methionine resynthesis. Homocystinuria occurs in cobalamin (Vit B12) deficiency because homocysteine
methyltransferase, the enzyme that converts homocysteine and methyltetrahydrofolate to
methionine and tetrahydrofolate, requires B 12 as a cofactor.
Decreased heme concentration results in an increase in hepatic ALA synthase activity, which in
turn, leads to increased formation of gamma aminolevulinic acid and protoporfilinogen. Increased
formation of gamma aminolevulinic acid and porphobilinogen occurs because heme normally
serves to inhibit the synthesis of ALA synthase.
Decreased heme concentration results in an increase in hepatic ALA synthase activity, which in
turn, leads to increased formation of gamma aminolevulinic acid and porphobilinogen. Increased
formation of gamma aminolevulinic acid and porphobilinogen occurs because normally serves to
inhibit the synthesis of ALA synthase.
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In the lungs, the binding of oxygen drives the release of H and CO2 from hemoblobin (Haldane
effect). In the peripheral tissues, high concentrations of CO2 and H facilitate oxygen unloading
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5
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141
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145
6
147
0
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y
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y
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gy
Hematolo
gy
147
0
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gy
184
7
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194
0
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208
6
208
6
208
7
854
0
Biochemistr
y
Biochemistr
y
Biochemistr
y
Biochemistr
y
Hematolo
gy
Hematolo
gy
Hematolo
gy
Hematolo
gy
854
2
854
2
Biochemistr
y
Biochemistr
y
Hematolo
gy
Hematolo
gy
863
2
Biochemistr
y
Hematolo
gy
117
2
120
2
Biostatistics
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140
3
Genetics
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from Hb (Bohr effect).

Normally, 2,3-DPG forms ionic bonds with the two beta subunits of HbA in the tissues after
hemoglobin has been deoxygenated. Fetal hemoglobin binds oxygen with a higher affinity to
interact with 2,3-DPG. Ultimately, the fetal Hb must be able to extract O2 from maternal Hb in the
placenta.
The secondary and terciary structures of myoglobin and the hemoglobin beta subunits are almost
identical(the alpha subunits are also very similar to myoglobin). Because individual hemoglobin
subunits are structurally similar to myoglobin, their oxygen-binding behavior is also similar. That is
if a hemoglobin molecule is dissociated, the individual subunits will have a hyperbolic oxygendissociation curve.
Nitrites are oxidizing agents that are effective in the treatment of cyanide poisoning due to their
ability to cause methemoglobinemia. Methemogloobin contains ferric rather than ferrous iron.
Cyanide finds to ferric iron more avidity than to mitochondrial cytochrome enzymes, which saves
these mitochondrial enzymes from cyanide's toxic effect.
Nitrates are oxidizing agents that are effective in the treatment of cyanide poisoning due to their
hability to cause methemoglobinemia. Methemoglobin contains ferric rather than ferrous iron.
Cyanide binds to ferric iron more avidly than to mitochondrial cytochrome enzymes, which saves
these mitochondrial enzymes from cyanide's toxic effect.
Methemoglobinemia causes dusky discoloration to the skin (similar to cyanosis), and because
methemoglobin is unable to carry oxygen, a state of functional anemia is induced. The blood
partial pressure of O2, however will be unchanged in this condition because oxygen's partial
pressure is a measure of O2 dissolved in the plasma and is not related to Hb function.
Heme oxygenase converts heme to biliverdin, a pigment that causes the greenish color to develop
in bruises several days after an injury.
Hb C is caused by missense mutation that results in a glutamate residue being substituted by
lysine in the beta globin chain. This results in an overall decrease in negative charge for the Hb
molecule. The speed of Hb movement during gel electrophoresis is HbA>HbS>HbC
Hemoglobin C is caused by a missense mutation that results in a glutamate residue being
substituted by lysine in the beta globin chain. This result in an overall decrease in negative charge
for the hemoglobin molecule. The speed of hemoglobin movement during gel electrophoresis is
Hb A > Hb S > Hb C
Folate deficiency inhibits the formation of deoxythymidine monophosphate (dTMP), which limits
DNA synthesis and promotes megaloblastosis and erythroid precursor cell apoptosis. Because
thimidine suplementation can moderately increase dTMP levels, it can reduce erythroid precursor
cell apoptosis.
Beta-thalasemia is caused by mutations that result in defective transcription; processing, and
translation of beta-globin mRNA. Most commonly, these mutations cause aberrant splicing of
precursor mRNA or premature chain termination during mRNA translation.
The Kozal Sequence plays a role in the initiation of translation. A mutation three bases upstream
from the start codoon (AUG) in this sequence is associated with thalasemia intermedia.
The Kozak sequence plays a role in the initiation of translation. A mutation three bases upstream
from the start codon (AUG) in this sequence is associated with thalassemia intermedia.
Mutation of Kozak sequence of beta-globin gene is associated with thalasemia intermedia wich
results in hypochromic, microcytic anemia.
The chronic myeloproliferative disorders (polycitemia vera, essential thrombocytosis, and primary
myelofibrosis) often have a mutation (V617F) in the cytoplasmic tyrosine kinase, Janus kinae 2
(JAK2). This results in constitutive tyrosine kinase activity, and consequently, cytosineindependent activation of STAT transcription fcts.
Allopurinol or rasburricase: Prevention of tumor lysis syndrome after quimiotherapy often involves
hydration and the use of these 2 hypouricemic agents.
Tumor lysis syndrome can develop during chemotherapy for cancers with rapid cell turnover (eg,
poorly differentiated lymphomas and leukemias), substantial tumor burden, or high sensitivity to
chemotherapy. It is characterized by hyperphosphatemia, hypocalcemia, hyperkalemia, and
hyperuricemia. Prevention of tumor lysis syndrome often involves hydration and the use of
hypouricemic agents such as allopurinol or rasburicase.
The PI3K/Akt/mTOR pathway is an intracellular signaling patway important for anti-apoptosis,
cellular proliferation, and angiogenesis. Mutations in growth factor receptors, Akt, mTOR, or PTEN
that enhance the activity of this pathway contribute to cancer pathogenesis.
95% of all observations lie within two standard deviations of the mean.
Selection of control subjects in case-control studies is intended to provide an accurate estimation
of exposure frequency among the non-diseased general population. Cases and controls are often
matched in order to decrease confounding. However, matching must be carefully performed so as
to not introcude selection bias.
The cytogenic defect t(15;17) is associated with acute promyelocytic leukemia (AML type M3).
Translocation of the gene for the retinoic acid receptor alpha from chromosome 17 to chromosome
15 leads to formation of the fusion gene PML/RAR alpha. This abnormal fusion gene product
inhibits differentiation of myeloblasts and triggers the development of acute promyelocytic
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537
Immunolog
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558
Immunolog
y
Immunolog
y
Immunolog
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gy
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113
4
161
4
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Immunolog
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764
3
Immunolog
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848
0
Immunolog
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853
2
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109
7
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137
5
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149
5
149
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149
6
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559
leukemia.
Folicular lymphoma is a non Hodgkin lymphoma of follicular B lymphocytes. Pctes with follicular
lymphoma characteristically have a translocation btwn chromosomes 14 and 18 which causes Bcl2 overexpression. Bcl-2 is considered a protooncogen because it has anti-apoptotic effects.
Alternative splicing is a process where the exons of a gene are reconnected in multiple ways
during post-transcriptional processing. This creates different mRNA sequencess and
subsequently, different protein isforms. It is a normal phenomenon in eukaryotes that greatly
increases the biodiversity of proteins encoded by the genome.
The Wislott-Aldrich syndrome consists of the triad of eczema, thrombocytopenia and combined Blymphocyte and T-lymphocyte deficiency. Onset disease is early in life with thrombocytopenia
present at bith and eczema and repeated infections, particularly by encapsulated organisms,
following at 6-12 months of age.
The Wiskott-Aldrich syndrome consist of the triad of eczema, thrombocytopenia and combined Blymphocyte and T-lymphocyte. Onset of disease is early in life with thrombocytopenia present at
birth and eczema and repeated infections, particularly by encapsulated organisms, following at 6
to 12 months birth and eczema and repeated infection (encapsulated) following at 6 to 12 month
of age. Tto is with HLA-matched bone marrow transplantation.
T cell Maturation - Positive Selection: Cortex - Negative Selection: Medulla
Positive selection: occurs in the cortex of the thymus. Negative selection: occurs in the medula of
the thymus.
Immature T lymphocytes express both the CD4 and CD8 cell surface antigens in addition to a
complete TCR or a pro-TCR. These lymphocytes exists in the thymic cortex where they undergo
positive selection and in the thymic medulla where they undergo negative selection.
location
nnnn
The primary immune response to a new antigen initially results in plasma cells that only produce
IgM. Isotype switching later occurs in the germinal centers of lymph nodes and requires interaction
of the CD40 receptor on B cells with the CD40 ligand (CD154) expressed by activated T cells. IgG
is the main serum.
Atypical lynphocytes observed in the peripheral blood smeears of patients with infectious
mononucleosis represent activated CD8+ cytotoxic T-lynphocytes. These activated T-lynphocytes
function to destroy virally-infected B-llynphocytes.
1. Margination 2. Rolling: neutrophils roll on the endothelium via binding of sialylated carbohydrate
groups (Sialyl Lewis X or PSGL-1, to L-selectin on neutrofils or E-selectin/P-selectin on endothelial
cells). 3. Activation 4. Tight adhesion and crawling: neutrophils become firmly atached to endot via
CD18 beta 2 integrins (Mac-1 and LFA-1) to intercellular adhesion molecule-1 (ICAM-1)on endot
cells. 5. Transmigration: Neutrophils migrate out of vasculature (PECAM-1)
-DiGeorge syndrome causes an extreme deficiency in the number of mature T lynphocytes,
leading to poor development of the lymph node paracortex. -Agammaglobulinemia causes an
absence of B cells preventing primarily lymphoid follicles and germinal centersn from forming in
the lymph node cortex.
E. coli stranin 0157:H7 can cause hemolytic-uremic syndrome (HUS). HUS is a rare condition
affecting mostly children under the age of 10. This strain of E.coli most commonly contracted after
eating undercooked ground beef.
Host cell receptor-virion/virion protein binding specificities include: -CD4 w/ HIV gp120 -CD21 w/
EBV gp350 -erythrocyte(also in megakaryocytes, placenta, and fetal liver and heart, bone marrow)
P antigen w/ parvovirus B19. Epstein-Barr virus is the ubiquitous herpesvirus responsible for acute
infectious mononucleosis, nasopharyngeal carcinoma, lymphomas, and Burkitt's lymphoma.
Erythema Infectiosum (fifth Ds) The rash is rResult at least partly from local immune complex
deposition once serum level of virus specific IgM and IgG have attained high enough levels.
A febrile respiratory illness in a child followed by the sudden appareance of red, flushed cheeks
approximately 2-5 days later is characteristic of erythema infectiosum (parvovirus B19 infection).
This virus is highly tropic for erythroid precursor cells and replicated predominantly in the bone
marrow.
In pctes with sickle cell anemia and other hemolytic disorders, the most common viral cause of an
aplastic crisis is infection of erythroid progenitor cells with parvovirus B19, a non-enveloped,
single-stranded DNA virus.
In patients with Sickle cell anemia and other chronic hemolytic disorders, the most common viral
cause of an aplastic crisis is infection of erythroid progenitor cells with parvovirus B19, a nonenveloped, single-stranded DNA virus.
Epstein-Barr virus commonly affects B cells, stimulatinf them to enter the cell cycle and proliferate
continuously (a process termend "transformation" or "immortalization"). EBV is an oncogenic virus
that promotes polyclonal B cell proliferation and heterophil antibody production.
vW deficiency causes impairments of platelet function and coagulation pathway abnormalities. It is
associated with prolong bleeding time, prolong PTT and decreased platelet aggregation in
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872
Pathology
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889
Pathology
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890
Pathology
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gy
890
Pathology
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gy
890
Pathology
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894
Pathology
896
Pathology
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gy
Hematolo
gy
896
Pathology
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897
Pathology
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897
Pathology
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942
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response to ristocetin.
Inherited causes of hypercoagulability should be considered in patients younger than age 50 who
present with thrombosis and no obvious explanation for an acquired prothrombotic state. The
factor V Leiden mutation, which causes factor Va resistance to inactivation by activated protein C,
may account for approximately 20% of cases of atypical venous thrombosis.
Vitamin K is a fat-soluble vitamin that is necessary for the g-carboxylation of coagulation factors II,
VII, IX and X. In the body, vitamin K exists in two forms: K1 (phylloquinone), derived from geen
vegetables, and menaquinone, derived from gut flora.
Vitamin B12 and folic acid deficiency cause similar hematological pictures. However, neurological
dysfunction is only seen in patients with vitamin B12 deficiency. if megaloblastic anemia due to
vitamin B12 deficiency is mistakenly treated with folate alone, the neurologic dysfunction can
worsen. Vitamin B12 deficiency also causes axonal demyelination and degeneration(peripheral
nerves, spinal cord: posterior and lateral columns, and the cerebrum).
Schistocytes (helmet cells) are fragmented erythrocytes. they occur secondary to mechanical
trauma from microangiopathic hemolytic anemias or prosthetic cardiac valves. Intravascular
hemolytic anemias are characterized by: decreased serum haptoglobin levels as well as increased
Hb, LDH, and bilirrubin
AL amyloidosis is associated with multiple myeloma and other monoclonal plasma cell dyscrasias.
Amyloid protein is derived from monoclonal immunoglobulin light chains, and often forms deposits
in the kidneys, heart, tongue and nervous system.
Hereditary spherocytosis results from red cell cytoskeleton abnormalities, most commonly spectrin
and ankyrin abnormalities. Hemolytic anemia, jaundice, and splenomegaly are classic clinical
manifestations of this disease and diagnosis is made by peripheral smear and osmotic fragility
testing.
Hereditary spherocytosis are small RBC and have more intensely-staining cytoplasm. The most
helpful red cell index in making the Dx of hereditary spherocytosis is the MCHC. An elevated
MCHC indicates membrane loss nd red cell dehydration. Dx is best confirmed by osmotic fragility
testing. which is not offered as a choice here.
In hereditary spherocytosis, mean corpuscular hemoglobin concentration (MCHC) is increased
because of mild dehydratation of the red blood cell. Markers of hemolysis, such as elevated LDH,
reticulocytosis, and decreased haptoglobin are often evident.
In hereditary spherocytosis, mean corpuscular hemoglobin concentration (MCHC) is increased
because of mild dehydration of the red blood cell. Markers of hemolysis, such as elevated LDH,
reticulocytosis, and decreased haptoglobin are often evident.
- G6PD has an X-linked recessive inheritance. - Hereditary spherocytosis follows an autosomaldominant inheritance pattern.
Sicle cell pctes become functionally asplenic, and thus are at an especially increased risk for
infection by encapsulated organisms (Streptococcus pneumoniae and Hemophilus influenza).
Salmonella is the most common cause of osteomyelitis in children with sickle cell disease;
Staphylococcus aureus and E. coli are the next most common causes of osteomyelitis in these
pctes.
Sickle cell pctes become functionally asplenic, and thus are at an especially risk for infection by
encapsulated organisms (Streptococcus pneumoniae and Haemophilus influenza). Salmonella is
the most common cause of osteomyelitis in children with sickle cell Ds; Staphylococcus aureus
and Escherichia coli are the next most common causes of osteomyelitis in these pctes.
1. Suspect Paroxismal Nocturnal Hematuria (PNH) in pctes wih hemolytic anemia, a
hypercuagulable state, and pancytopenia. 2. PNH commonly causes thrombosis; since it is a stem
cell disorder, it is often associated with pancytopenia, as well. 3. The deficiency of CD55 and
CD59 proteins is diagnositic of PNH; this deficiency disallows the inactivation of complement.
1. Suspect PNH in patients with hemolytic anemmia, a hypercoagulable state, and pancytopenia.
2. PNH commonly causes thrombosis; since it is a stem cell disorder, it is often associated with
pancytopenia , as well. 3. The deficiency of CD 55 and CD 59 proteins is diagnostic of PNH; this
deficiency disallows the inactivativation of complement.
Low escretion od radiolabeled cobalamin after administration of intrinsic factor suffests another
cause of poor cobalamin absorption. Causes of intestinal malabsorption of B12 include: pancreatic
insufficiency, intestinal bacterial overgrowth or ileal disease.
Bleeding after tooth extraction and a history of hemarthrosis is suggestive of hemophilia.
decreased levels of factor VIII or IX lead to failure to convert prothrombin into thrombin and
deficient thrombus formation. Addition of thrombin to the blood of a patient with hemophilia results
in clotting.
Fct VIII is synthesized by the liver and stored in endothelial cells. Desmopressin acetate (DDAVP)
is a synthetic vasopressin analog that releases von Willebrand Fct and Fct VIII from the
endothelium. It is used for the tto of mild to moderate hemophilia A.
Vitamin K dependent coagulation factors (II, VII, IX, X) are initially produced by the liver in an
inactive form, and are the activated by a vitamin K dependent process.
DIC in pregnant patients: - Erly identification of the onset => fibrinogen and platelet count Prolong PTT nad PT -Thrombocytopenia and microangiopathic hemolitic anemia -Low fibrinogen
-Elevated fibrin split products (D-dimer) -Low fct V and VIII
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Auer rods are deformed azuphilic granules found in the cytoplasm of myeloblasts that stain
positively for myeloperoxidase. Auer rods are found in abundance in AML M3 (acute promyelocytic
leukemia).
Auer rods are found in AML. Auer rods are not found in ALL. In CML there are more mature cells
and fewer blasts.
The underlying biochemical feature of megaloblastosis is a defect in DNA synthesis. in chronic
alcoholics, megaloblastic anemia can result from a nutritional deficiency of folate, which impairs
synthesis of purine and pyrimidine bases.
The underlying biochemical feature of megaloblastosis is a defect in DNA synthesis. In chronic
alcoholics, megaloblastic anemia can result from a nutritional deficiency of folate, which impairs
synthesis of purine and pyrimidine bases.
Follicular lymphoma is characterized by aggregates of packed follicles that obscure the normal
lymph node architecture. 90% of patients with follicular lymphoma have the t(14;18) translocation,
wich causes overexpression of the antiapoptotic BCL2
Pure red aplasia is a rare form of marrow failure characterized by severe hypoplasia of marrow
erythroid elements in the setting of normal granulopoiesis and thrombopoiesis. Pure red cell
aplasia is associated with thymoma, lymphocytic leukemias, and prvovirus B19 infeccion.
Pure red cell aplasia is a rare form of marrow failure characterized by severe hypoplasia of
marrow erythroid elements in the setting of normal granulopoiesis and thrombopoiesis. Pure red
cell aplasia is associated with thymoma, lymphocytic leukemias, an parvovirus B19 infection.
Increased bone marrow erythropoiesis results in an accelerated release of immature red blood
cells (reticulocytes) into the bloodstream. Reticulocytes contain bluish cytoplasm and reticular
precipitates of residual ribosomal RNA.
The reticulocyte is an immature RBC that is slightly larger and bluer than a mature RBC. It lacks a
cell nucleus but retains a basophilic, reticular (mesh-like) network of residual ribosomal RNA. The
ribosomal RNA appears blue microscopically after the application of the Wright-Giemsa stain. After
spending a day or so in the bloodstream, the reticulocytes are transformed into mature red blood
cells that have a lifespan of approximately 120 days.
Acute lymphoblastic leukemia (ALL) is the most common malignancy of chilhood. B cell ALL is
responsible for aproximately 70-80% of all cases of ALL, whereas T-cell accounts for 15-17% of all
cases of ALL. T cell ALL often presents as a mediastinal mass that can cause respiratory
symptoms, dysphagia, or superior vena cava syndrome.
Acute lymphoblastic leukemia (ALL) is the most common malignancy of childhood. B-cell ALL is
responsible for approximately 70-80% of all cases of ALL, whereas T cell ALL accounts for 15-17%
of all cases of ALL. T-cell ALL often presents as a mediastinal mass that can cause respiratory
symptoms, dysphagia, or superior vena cava syndrome.
Hemolytic uremic syndrome affects young children and manifests with acute renal failure,
microangiopathic hemolytic anemia and thrombocytopenia. Characteristic laboratoriy
abnormalities include decresed RBC count, hematocrit and platelet count and incresed bleeding
time, LDH, BUN and creatinine
Coarse erythrocyte basophilic stippling and microcytic hypochromic anemia are common
peripheral blood smear findings in lead poisoning. High-risk groups include young children
ingesting paint chips and industrial workers inhaling particulate lead.
1-9% of Caucasians worldwide are heterozygote carriers of factors V Leiden(single aminoacid
substitution, glutamine for arginine, near the protein C cleavage site in her coagulation factor V
gene product), which is modified to resist activated protein C. The resulting hypercoagulable state
predisposes to deep vein thromboses, which are the source of most pulmonary emboli.
von Wilebran disease is the most common inherited bleeding disorder. It is functional factor VIII
and platelet defect that prolongs the bleeding time and PTT.
Autoimmune platelet destruction is a common cause of thrombocytopenia and should be
suspected in pctes with ecchymoses, petechiae, and mucosal bleeding without signs or symptoms
of TTP/HUS, pancytopenia, marrow failure, or splenomegaly.
AML can present with persistent infection and coagulopathy causing hemorrhagic signs and
symptoms. Bone marrow biopsy in APL classically revels promyelocytes with intracytoplasmic
Auer rods. APL is associated with a t(15;17) chromosomal translocation that causes fusion of the
alpha retinoic acid receptor gene and PML gene.
HbA2 is elevated in beta thalasemia minor (trait) and beta thalassemia intermedia because beta
globin chain underproduction causes decreased synthesis of HbA1
no entender buaa
Polycytemia vera is a clonal myeloproliferative Ds of pluripotent hematopoietic stem cells. Virtually
all pctes with polycitemia vera have a mutation in JAK2, a non-receptor tyrosine kinase associated
with the erythropoietin receptor (a type I cytokine receptor).
Aspirin produce irreversible COX inhibition. Other NSAIDs causes reversible COX inhibiton.
1. Hydroxyurea increases Fetal Hb synthesis by an unknown Mx. Hydroxyurea is reserved for
pctes w/ frequent pain crises. 2. Gardoos channel blockers hinder the efflux of K and water from
the cell, preventing dehydration of erythrocytes and reducing the polymerization of Hb S.
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HbS is the result is a result of a point mutation that substitutes a valine in the sixth position of beta
chain for glutamic acid. The abnormal beta chain of HbS causes it to polymerize when
deoxygenated or dehydrated, resulting in the characteristic sickling of red blood cells.
Hemolytic anemia is a possible side effect of dapsone, antimalarials, sulfonamide, TMP-SMX and
is most significant in patients deficient for glucose 6 phosphate dehydrogenase (G6PD). G6PD
deficiency anemia is characterized by episodes of hemolytic anemia precipitated by oxidative
stress (drugs, infections). Peripheral smear typically show bite cells and Heinz bodies (requires
special preparation).
Heparin: activates antithrombin III. Warfarin: inhibits vitamin K dependent -carboxylation of
glutamic acid residues of clotting factors II, VII, IX and X (vitamin K dependent clotting factors).
Abcifliximab is a blocker of GP IIb/IIIa is either deficient or defective in pctes with Glanzmann
thrombasthenia.
Neutropenia is seen in about 1 percent of patients on ticlopidine or clopidrogrel and typically
presents with fever and mouth ulcers. though this is rare, it is a serious complication and complete
blood count should be monitored biweekly for the first three months.
Neutropenia is seen in about 1% of pctes on ticlopidine and typically presents with fever and
mouth ulcers. Though this is rare, it is a serious complication and complete blood count should be
monitored biweekly for the first three months.
Antiplatelet drug work by one of three basic mechanisms: 1) blocking the formation of ligands
(aspirin, decreases thromboxane A2 formation), 2) blocking interaction of ligands with receptors on
platelets (clopidogrel and ticlopidine work as ADP antagonists), or 3) interfering with intracellular
signaling (cilostazol and dipyridamole increase cAMP by decreasing phosphodiesterase activity).
Protamine sulfate binds with heparin causing chemical inactivation. Vitamin K is used for reversal
of warfarin effect. Aminocaproic acid and tranexamic acid inhibit fibrinolysis.
Antithrombin III, protein C and protein S are natural anticoagulants that are present in the blood.
Warfarin inhibits protein C and S synthesis and thus can pose a risk of paradoxical thrombosis in
patients with congenital deficiency of protein C and S. This is usually seen in the first week of
therapy.
Rat poison (rodenticides) cointain brodifacoum, a long acting 4-hydroxycumarin derivative. If
patient has ingested a quantity of rodenticide sufficient to cause coagulopathy and abnormal
bleeding, immediate treatment with fresh plasma and vitamin K, is required.
Rituximab is a monoclonal antibody directed against the CD20 antigen. Its introduction has
improved the prognosis of some lymphomas.
Rituximab is a monoclonal antibody directed against the CD20 antigen. Its introduction has
improved the prognosis of some lymphomas.
Neutropenia is a significant adverse effect of ganciclovir therapy, and its incidence is increased
with coadministration of zidovudine. Both drugs can affect DNA synthesis in hematopoietic stem
cell lines, resulting in bone marrow suppression.
zlfks;ldf
NNRTI: nevirapine, efavirenz, delavirdine
Both unfractionated heparin and Low Molec Weight Heparin can bind to antithrombin to increase
its activity against Fct Xa. Only unfractionated heparin is able to bind to both antithrombin and
thrombin to allow antithrombin to inactivate thrombin.
Ranibizumab and pegaptanib Are drugs anti-VEGF therapy
Raltegavir is an integrase inhibitor that disrupts the ability of HIV to integrate its genome into the
host cell chromosomes, thus preventing host cellular machinery from being used to synthesize
HIV mRNA
Raltegravir is an integrase inhibitor that disrupts the ability of HIV to integrate its genome into the
host cell's chromosomes, thus preventing host cellular machinery from being used to synthesize
HIV mRNA
-Carbon monoxide (CO) binds to hemoglobin with much higher affinity than O2, thus preventing
oxygen binding to heoglobin. It also reduces oxygen unloading from hemoglobin in the tissues.
COpoisoning does not affect the PaO2 and does not precipitate methemoglobinemia.
-Methemoglobinemia: results from drugs (dapsone, nitrites) as well as enzyme deficiencies and
hemoglobinopathies.
alpha ketoglutarate dehydrogenase requires thiamine as a cofactor. Administration of glucose to
thiamine deficient pctes (ejm alcoholics) will result in Wernicke encephalopathy due to increased
thiamine demand. Wernike encephalopathy presents with acute confusion, ophthalmoplegia, and
ataxia.
Debranchin genzyme deficiency (Cori disease) leads to incomplete glycogen degradation. Alpha1,6-glucosidic branch points cannot be degraded, so small chain dextrin-like material accumulates
within the cytosol of hepatocytes. Patients with this illness present with the non-specific finsings of
hypoglycemia, hypertriglyceridemia, ketoacidosis and hepatomegaly.
Acetyl-CoA is an important allosteric activator of gluconeogenesis that acts by increasing the
activity of pyruvate carboxylase.
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I do not understand the concept of these

- Pantothenic acid (is a coenzyme A): essential cofactor for conversion of oxaloacetate to citrate
and then succinyl-CoA. Also is important dor the synthesis of Vitamin A, Vit D, cholesterol,
steroids, heme A, fatty acids, amino acids, and proteins.
The biologically active form of pantothenic acid is a coenzyme A, which binds w/ oxaloacetate in
the first step of the TCA (Krebs) cycle to form citrate and the succinyl-CoA.
The oxidative reactions of the HMP shunt are necessary for anabolic reactions that use NADPH as
an electron donor (including cholesterol and fatty acid synthesis). In addition, NADPH produced
via the HMP shunt is the only method of reducing glutathione (and thus oxidaytive damage)
available to red blood cells.
Biochemical Rx Cytoplasm: Reactions of the pentose phosphate pathway. Mitochondria: boxidation of fatty acids, ketogenesis, citric acid cycle, parts of the urea cycle (carbamoyl
phosphate synthetase 1 and ornithine transcarbamoylase) and pyruvate carboxylation.
Biochemical process for cellular metabolism occur in distinctic within cells. For example, beta
oxidation of fatty acids, ketogenesis, the citric acid cycle, parts of the urea cycle (carbamoyl
phosphate synthetase 1 and ornithine transcarbamoylase) and pyruvate carboxylation all occur
exclusively within the mitochondria. All the reactions of the pentose phosphate pathway occur in
the cytoplasm.
Hypoglycemia in the setting of a high intracellular ratio of NADH to NAD+ can occur when a
metabolic fuel other than glucose (ethanol) is present. Hepatic ethaanol catabolism produces
NADH and inhibits gluconeogenesis
-Skeletal muscle carnitine deficiency: Myoglobinemia, weakness following exercise, elevated
muscle triglycerides, hypoketonemia. -Medium chain acyl-CoA dehidrogenase (MCAD) deficiency:
hypoglycemia, hypoketonemia. -Carnitine deficiency impairs fatty acid transport into mitochondria,
restricting ketone body production.
The 16S rRNA is found in the prokariotic 30S ribosomal subunit and it contains a sequence
complementary to the Shine-Dakgarno sequence on mRNA
The prokaryotic 16S rRNA sequence is found in the 30S ribosomal subunit. The 16S rRNA
contains a sequence complementary to the Shine-Dalgarno sequence on mRNA. Binding of these
two complementary sequences is necessary for initiation of protein translation.
A homeobox is a highly conserved DNA sequence, usually about 180 nucleotides in length.
Homeobox genes typically code for DNA-binding transcription factors which alter the expression of
genes involved in morphogenesis.Morphogenesis is the proper formation and placement of
tissues, organs and structural elements of the body. Homeobox genes code for DNA-binding
transcription factors that play an important role iin morphogenesis.
Enhancers/repressors may be located anywhere upstream, downstream or even within the
transchibed gene. In contrast, promoter regions are typically located 25 or 70 bases from their
associated genes.
The TATA BOX is a promoter region that binds transcription factors and RNA polymerase II during
the initiation of transcription. It is located approximately 25 bases upstream from the beginning of
the coding region. The CAAt box is located 60-80 bases upstream of the begining (5' end) of the
coding region.
Examples of proteins that are able to bind DNA include transcription factorsm steroids, thyroid
proteinsm Vitamin D receptors, retinoic acid receptors, DNA trnascription and replication proteins.
Other choices are N-myc. The MYC proteins are mammalian transcription factors. C myc is the
protein that is overexpressed in Burkitt lynphoma.
c-Jun and c-Fos are nuclear transcription factors that directly bind DNA via leucine zipper motif.
The genes that code for c-Jun and c-Fos are proto-oncogenes, genes that can become
oncogenes following a mutation or with constitutive expression.
c-Jun is a DNA -binding protein. c-Jun and c-Fos are nuclear transcription fcts that directly bind
DNA via leucine zipper motif. The genes that code for c-Jun nd c-Fos are proto-oncogenes, genes
that can become oncogenes following a mutation or wih constitutive expression.
On average, autosomal recessive conditions affect 25% of offspring of assimptomatic
heterozygous carrier parents. Classic galactosemia is an autosomal recessive Ds.
Often referred to as delta agent or the hepatitis delta virus, hepatitis D virus is a replicationdefective RNA virus that is only capable of causing infection when encapsulated with HBsAg.
Therefore, HDV infection can arise either as an acute coinfection with hepatitis B virus (w/ the
HBV established first to provide the HBsAg for the HDV) or as a superinfection of a chronic HBV
carrier. In populations vaccinated w/ recombinant HBsAg, then Hepat D virus would not replicate.
virus
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Neonates born to HBsAg- and HBeAg-positives mothers are at high risk of chronic infection,
experience fast HBV replication, and demostrate mild hepatic injury histologically.
The HBsAg of hepatitis B virus must coat the HDAg of hepatitis D virus before it can infect
hepatocytes and multiply
Hepatitis E virus is an unenveloped, single-stranded RNA virus spread through the fecal-oral
route. The most concerning feature of hepatitis E infection is the high mortality rate observed in
infected pregnant women.
Hepatitis A virus can be inactivated with water chlorination, bleach (1:100 dilution), formalin,
ultraviolet irradiation, or boiling to 85 C for one minute.
Hepatitis A virus infection is most commonly silent or subclinical ("anicteric") in children but can
also present as an acute, self-limited illness characterized by jaundice, malaise, fatigue, anorexia,
nause, vomiting, right upper quadrant pain, or an aversion to smoking.
Replication of the hepatitis B genome occurs within a newly synthesized capsid through the action
of reverse transciptase on an RNA template. The mature capsid contains partially double-stranded
circular DNA and reverse transcriptase.
Vertical transmission of hepatitis B from pregnant females can occur in women with active
hepatitis B infection. The HBeAg (a marker of viral replication and increased infectivity) in the
mother greatly increases the risk of vertical transmission of the virus. Because of this concern, the
new borns of all mothers with active hepatitis B are passively immunized at birth with hepatitis B
immune globulin (HBIG), followed by active immunization with a recombinant HBV vaccine.
Vertical transmission of hepatitis B from pregnant females to the unborn child can occur in women
with active hepatitis B infection. The presence of HBeAg (a marker of viral replication and
increased infectivity) in the mother greatly increases the risk of vertical transm of the virus. Bcs of
this concern, the newborns of all mothers with active hepatitis B are passively immunized at birth
with hepatitis B immune globulin (HBIG), followed by active immunization with HBV vac.
If HBeAg persists for several months and host anti-HBeAg remain at low or undetectable levels,
suspect chronic hepatitis B infection with Hhigh infectivity.
Most enveloped nucleocaspid viruses acquire their lipid bilayer envelope by budding through the
plasma membrane of the host cell. Exceptions include the herpesviruses, which bud through and
acquire their envelope from the host cell nuclear membrane.
Chloroquine: tto of choice for uncomplicated malaria contracted in a chloroquine-sensitive
geografic region. It eliminates susceptible erythrocytic forms of all Plasmodia species. Primaquine
is added in the tto of infections with P. vivax and P. ovale in order to eradicate the intrahepatic
stages of these two malaria species (prevent disease relapse).
Chloroquine is the tto of choice for uncomplicated malaria contracted in a chloroquine-sensitive
geographic region. It eliminates susceptible erythrocytic forms of all Plasmodia species.
Primaquine is added in the tto of the infections w/ P. vivax and P. ovale in order to intrahepatic
stages of these two malarial species.
Cavernous hemangioma is the most common benign liver tumor. Microscopically, these tumors
consist of cavernous, blood-filled vascular spaces of variable size lined by a single epithelial layer.
The bipsy of a suspected hemangioma is not advisable. as the procedure has been known to
cause fatal hemorrhage and is low diagnostic yield.
Alpha fetoprotein is a useful marker in the evaluation of cirrhotic pctes who are at increased risk
for developing hepatocellular carcinoma. Regular monitoring of AFP in this pcte population is
recomended.
- Aflatoxins exposure is associated with a G:C -> T:A transversion in codon 249 of p53 gene, a
mutation thought increase the risk of developing hepatocellular carcinoma.
-Estrogen increase hepatic HMG-CoA reductase activity (increase biosynthesis of cholesterol). Supression of cholesterol 7 alpha hydroxylase activity(by fibrates) reduces the conversion of
cholesterol to bile acids, resulting in excess cholesterol secretion in bile. - Promote formation of
gallstones: fibrates, octreotide, or ceftriaxone.
Estrogenic influence facilitates the biosynthesis of cholesterol by increasing hepatic HMG-CoA
eductase activity. Suppression of cholesterol 7 alpha hydrolase activity (by medications such as
fibrates) reduces the conversion of cholesterol to bile acids, resulting in excess cholesterol
secretion in bile.
Estrogen -induced cholesterol hypersecretion and progesterone-induced gallbladder hypomotility.
Brown pigment stones typically arise secondary to infection of the biliary tract, which results in the
release of beta-glucuronidase by injured hepatocytes and bacteria. The presence of this enzyme
contibutes to the hydrolysis of bilirubin glucuronides and increases the amount of unconjugated
bilirubin in bile. Therefore biliary infections w/ E. coli, Ascaris lumbricoides, or the liver fluke
Opisthorchis sinensis elevates the risk of developing brown pigment stones.
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Brown pigment stones typically secondary to infection of the biliary tract, which results in the
release of beta-glucuronidase by injured hepatocytes and bacteria. The presence of this enzyme
contributes to the hydrolysis of bilirubin glucuronides and increases the amount of unconjugated
bilirubin bile.
Slow or incomplete gallbladder emptying in response of cholecystokinin stimulation, gallbladder
hypomotylity is a common occurrence in the Western world and cause formation of biliary
slundge(cholesterol monohydrate crystals, calcium bilirubinate, and mucus). Risk fcts for this
condition include pregnancy, rapid weight loss, prolong use of total parenteral nutrition or
octreotide, and high spinal cord injuries.
A positive HIDA scan confirms cystic duct obstruction, which is necessary for a definitive diagnosis
of acute calculous cholestasis. Nonobstructing biliary stones seen by ultrasaund are suggestive
but not diagnostic of the condition.
A positive HIDA scan confirms cystic duct obstruction, which is necessary for a definitive diagnosis
of acute calculous cholestasis. Noonobstructing biliary stones seen by ultrasound are suggestive
but not diagnostic of the condition.
Dubin-Johnson syndrome is charactrized by a defect in the hepatic excretion of bilirubin
glucoronides across the canalicular membrane. Grossly, the liver is strikingly black. Histological
features are normal, though a dense pigment composed of epinephrine metabolites within the
lysosomes can be seen.
Dubin Johnson Sx is characterized by a defect in the hepatic excretion of bilirubin glucuronides
across the canalicular membrane. Grossly, the liver is strikingly black. Histological features are
normal, though a dense pigment composed of epinephrine metabolites within lysosomes can be
seen.
Hepatitis B infection causes the hepatocellular cytoplasm to fill with the spheres and tubules of
HBsAg (the hepatitis B surface antigen) and take on the finely granular, eosinophilic appearance
commonly describe as "ground glass."
Cirrhosis is characterized by diffuse hepatic fibrosis with replacement of the normal lobular
architecture by fibrous-lined parenchymal nodules("nodular parenchymal regeneration"). C.
Micronodular: <3mm in diameter C. Macronodular: >3mm in diameter
Cirrhosis is microscopically characterized by diffuse hepatic fibrosis with replacement of the
normal lobular architecture b fibrous-lined parenchymal nodules.
Halothane anesthetics, such as halothane, can be associated with a lethal fulminant hepatitis that
cannot be histologically distinguished from acute viral hepatitis. Pctes present with significatly
elevated aminotransferase levels, a prolonged prothrombin time, and eosiniphilia.
The pathogenesis of alcohol-induced hepatic steatosis appears related primarily to a decrease in
free fatty acid oxidation secondary to excess NADH production by the 2 major alcohol metabolism
enzymes, alcohol dehydrogenase and aldehyde dehydrogenase.
Alcohol-induced hepatic steatosis The pathogenesis appears related primarily to a decrease in
free fatty acid oxidation secondary to excess NADH production by the 2 major alcohol metabolism
enzymes, alcohol dehydrogenase and aldehyde dehydrogenase.
Hepatitis B infection has 2 phases: - Proliferative phase:The hepatocyte has on its surface HBsAg,
and HBcAg, MHC class I (this activates CD8+ T linphocytes wich responds by destroying the
infected hepatocytes OjO note that the viral itself does not have a cytopathic effect) - Integrative
phase: The HBV DNA is incorporated into the host genome of those hepatocytes that survive the
inmune response. Infectivity ceases and liver dism when antibodies appear and replic stops.
Stable chronic hepatitis is te most likely outcome for a pcte acutely infected with hepatitis C virus,
followed closely by chronic hepatitis progressing to cirrhosis.
The Kayser-Fleisher ring is an ophthalmologic finding most strongly associated with Wilson's Ds. It
is seen most frequently in pctes with neuropsychiatric complications. Basal ganglia atrophy is
typically present in these pctes.
The Kayser-Fleicher ring is an ophtalmologic finding most strongly associated with Wilson's
Disease. It is seen most frequently in patients with neuropsyquiatric complications. Basal ganglia
atrophy is typically present in these patients.
The diagnosis of alpha 1 antittripsin deficiency should be suspected in all patients with premature
onset (<50 years) of chronic bronchitis, emphysema, as well as in nonsmokers suffering from
chronic obstructive pulmonary disease. A history of neonatal hepatitis with cholestasis should
heighten suspicion for A1AT deficiency.
Primary biliary cirrhosis is a chronic liver Ds characterized by Autoinmune destruction of the
intrahepatic bile ducts and cholestasis (elevated alkaline phosphatase). The condition is most
common in middle-aged women, with severe pruritus (especially at night). The condition is most
common in middle-aged women, with severe pruritus (especially at night) one of the first
symptoms reported.
Primary biliary cirrhosis and graft vs host disease have similar histologic findings, including
granulomatous bile duct destruction and a heavy lymphocyteporedominant portal tract infiltrate.
xantelasma is suggestive also of cholestasis
ary
system
Hepatobili
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Hepatobili
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Hepatobili
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403
Pathology
881
Pathology
170
1
Pathology
99
Pathophysi
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99
Pathophysi
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100
Pathophysi
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362
Pathophysi
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364
Pathophysi
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364
Pathophysi
ology
780
Pharmacol
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819
Pharmacol
ogy
857
Pharmacol
ogy
857
Pharmacol
ogy
116
7
Pharmacol
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171
4
Pharmacol
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171
6
Pharmacol
ogy
177
4
Pharmacol
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201
9
Pharmacol
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201
9
Pharmacol
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Hepatobili
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114
9
163
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Hepatobili
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Hepatobili
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system
Hepatobili
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Hepatobili
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The classic picture of primary biliary cirrhosis is a middle-aged Caucasian female with a long
history of pruritus and fatigue who now develops pale stool and xanthelasma (suggestive of
cholestasis).
Reye Sindrome Hepatic failure, hyperammonemia on the CNS leading to cerebral edema
- Budd-Chiari Sx: occlusion of the hepatic vein, which drains blood from the liver and portal
circulation into the circulation. Bx: centrilobular congestion and fibrosis. - Portal vein thrombosis:
causes portal hypertention, splenomegaly, and varicosities at portocaval anastomoses. Bx: No
change in hepatic parenchyma. Ascitis is uncommon as the obstruction is presinusoidal.
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A moderately elevated alkaline phosphatase (elevated in liver, bone, intestine, kidney, placenta,
leukocytes and some neoplasms) of unclear etiology should be followed up with gamma-glutamyl
transpeptidase(elevated in kidney, spleen, heart, lung, brain).
Cirrhotic patients have hyperestrinism secondary to the damaged liver's inability to metabolize
circulating estrogens (specifically androstenedione)
Gilbert Syndrome Dx in pctes with apparent liver disease who have mild unconjugated
hyperbilirubinemia that appears provoked by one of the classic triggers.
When prolonged reduction in the bile flow causes intestinal malabsorption and nutritional
deficiencies of the fat-soluable vitamins (A,D,E, and K) in particular. Therefore, condition
associated with fat soluable vitamin deficin=ency, such as osteomalacia, would most likely occur in
patients with prolonged cholestasis.
Digestive disorders such as cholestasis can cause malabsorption and nutritional deficiencies of
the fat-soluable vitamins. This may result in osteomalacia, which is frequently associated with
Vitamin D deficiency.
Treatment with many of the hypolipidemic drugs (especially statins) warrants monitoring of liver
function tests. Statins are known to cause myopathy and liver toxicity in some patients.
Protease inhibitors are nti HIV medications that inhibit cleavage if the polypeptide precursor into
mature viral proteins. Their side effects as a class include hyperglycemia, lipodystrophy, and drugdrug interactions due to inhibition of cytochrome p-450
sulfation and glucuronide conjugation
Acetaminophen toxicity can be effectively treated by sulfhydryl group supplementation. N-acetyl
cysteine providdes the sulfhydryl groups. NAC also acts as a glutathione substitute and binds to
the toxic metabolite.
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Chekar t1/2=(Vd x In2) / CL
In firs order kinetics, a constant fraction (or proportion) of drugs is metabolized per unit time based
on the serum concentration. In zero orden kinetics, a constant amount of drug is metabolized per
unit time, indeependent of concentration.
Isoniazid (INH) can be directly hepatotoxic, causing acute hepatic dyspunction in 10-20% of
patients. In a smaller percentage of cases, frank hepatitis may develop, causing fever, anorexia,
and nausea.
Zidovudine is a nucleoside reverse transcriptase inhibitor used to treat HIV infection. It
competitively binds to reverse transcriptase and is incorporated into the viral genome as a
thymiidine analog. Zidovudine does not have 3'-OH group, making 3'-5' phosphodiester bond
formation impossible.
Zidovudine (AZT) is a nucleoside reverse transcriptase inhibitor used to treat HIV infection. It
competitively binds to reverse transcriptase and is incorporated into the viral genome as a
thymidine analog. AZT does not have a 3'-OH group, making 3'-5' phosphodiesterase bond
formation impossible.
Common peroneal nerve injury as it traces the lateral aspect of the fibular neck is common. Bony
fracture and compression are the most common causes. Clinically this manifests as foot drop.
The musculocutaneo nerve inervates the flexor muscles of the upper arm and provides sensory
innervation to the lateral forearm. The musculocutaneous nerve is derived from the upper trunk of
the brachial plexus and can be injured by forceful injuries that cause separation of the neck and
163
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170
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Anatomy
181
1
181
1
Anatomy
195
6
196
9
762
1
Anatomy
762
1
Anatomy
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857
9
102
8
Anatomy
Biochemistr
y
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Musculosk
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124
4
Biochemistr
y
Musculosk
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124
4
124
6
209
0
Biochemistr
y
Biochemistr
y
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y
Musculosk
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Musculosk
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Musculosk
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880
2
Biochemistr
y
Musculosk
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880
2
127
1
168
4
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y
Biostatistics
Musculosk
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193
5
193
5
Genetics
538
Immunolog
y
Musculosk
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538
Immunolog
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Musculosk
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740
Immunolog
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Musculosk
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Anatomy
Anatomy
Anatomy
Anatomy
Anatomy
Embryology
Genetics
Musculosk
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Musculosk
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Musculosk
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Musculosk
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shoulder.
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Improperly fitted crutches can cause radial nerve injury, resulting in weakness of all forearm, wrist
and finger extensors ("wristdrop").
The deep brachial artery and radial nerve course along the posterior aaspect of the humerus.
Midshaft fractures of the humerus risk injury to these structures. Supracondylar fractures are
associated with injury to the brachial artery.
Winged scapula: produced by injury of the long thoracic nerve that results in the paralysis of the
serratus anterior.
Injury to the long thoracic nerve results in paralysis of the serratus anterior. This presents as a
winged scapula, which means that the medial border adn inferior angle sticks out posteriorly like a
bird's wing when the pcte presses anteriorly against a wall.
Medial femoral circunflex artery provides the majority of the blood supply to the femoral head and
neck; injury to this vessel can cause avascular necrosis of the femoral head.
buaa
Muscles used when sitting up from the supine position include the external abdominal obliques,
the resctus abdominis, and the hip flexors. The iliopsoas muscle is the most important of the hip
flexors and includes the psoas major, psoas minor, and iliacus. The rectus femoris, sartorius,
tensor fascia lata, and the medial compartment of the tight also contribute to hip flexion.
Muscles used whrn sitting up from the supine position include the external abdonmial obliques, the
resctus abdominis,and the hip flexors. The iliopsoas muscle is the most important of the hip flexors
and includes the psoas major, psoas minor, and iliacus. The rectus femoris, sartorious, tensor
fascia lata, and the medial compartment of the thigh also contribute to hip flexion.
The most common elbow injury in children is the radial head subluxation of the annular ligament
Glycogen degradation is coupled with skeletal muscle contraction due to calcium-mediated
myophosphorylase activation. Increased calcium in the cytosol allosterically activates
phosphorylase kinase which them phosphorylates (activates) muscle phosphorylase.
Ehlers-Danlos syndrome is a heritable connective tissue disease associated with abnormall
collagen formation. EDS ussually manifests clinically as over-flexible (hypermobible) joints, overelastic (hyperelastic) skin, and fragile tissue susceptible to bruising, wounding, and hemarthrosis.
- Marfan syndrome: fibrillin-1 gene defect. -Keratin 5 and 14 defect results in epidermolysis bullosa
simplex. - Collagen defect: Ehlers-Danlos syndrome.
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Gout can occur with increased frequency in pctes with activating mutations in 5-phosphoribosyl-1pyrophosphate (PRPP) synthetase duee to an increased production of purines, which results in
hyperuricemia.
Rheumatoid Arthritis: Dx is made by anti-cyclic citrulinated peptide antibodies (anti-CCP). Tissue
inflamation causes arginine residues in proteins such as vimentin to be enzymatically converted
into citrulline through a process called citrullination.
Antibodies to citrulinated peptides/proteins have a high specificity for rheumatoid athritis.
Positive Predictive and Negative Predictive Value are influence by Ds prevalence whereas
specificity and sensitivity are not.
Caudal regression syndrome is a condition characterized by sacral agenesis causing lower
extremity paralysis and urinary incontinence. This condition is commonly associated with poorly
controlled maternal diabetes.
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The presence of lactic acidosis and ragged red skeletal mucle fibers histologically suggest a
mitochondrial myopathy. There may be variable expression of mitochondrial DNA defects in
different affected family members due to heteroplasmy, which is the coexistence of both mutated
and wild type versions of mitochoondrial genomes in an individual cell.
Leukocyte adhesion deficiency results from the autosomal resessive genetic absence of CD18.
This leads to the inability to synthasize integrins. Integrins are necessaryfor leukocytes to exit the
bloodstream, and sequelae of this illness include recurrent skin infections WITHOUT pus
formation, delayed deatachment of the umbilical cord and poor wound healing.
Leukocyte adhesion deficiency results from the autosomal recessice genetic absence of CD18.
This leads to the inability to synthesize integrins. Integrins are necessary for leukocytes to exit the
bloodstream, and sequelae of this illness include recurrent skin infections WITHOUT pus
formation, delayed detachment of the umbilical cord and poor wound healing.
Myasthemia gravis results from an autoimmune type II, antibody mediated, hypersensitivity
reaction against skeletal myocyte surface acetylcholine receptors. Goodpasteure sybdrome
similarly involves autoantibodies against basement membrane collagen of glomerular and alveolar
epithelia (Type II hypersensitivity). A type III hypersensitivity mechanism applies to
748
Immunolog
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752
Immunolog
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754
Immunolog
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Immunolog
y
Immunolog
y
Immunolog
y
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760
Immunolog
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845
Microbiolog
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972
Microbiolog
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973
Microbiolog
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311
Pathology
Musculosk
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316
Pathology
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629
Pathology
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700
Pathology
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702
Pathology
984
Pathology
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145
1
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871
0
Pathology
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640
Pathophysi
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759
760
poststreptococcal glomerulonephritis, hypersensitivity pneumonitis, and possibly Churg-Strauss

syndrome.
Polymyositis presents with symetric proximal muscle weakness. Muscle biopsy revels
inflammation, necrosis and regeneration of muscle fibers. Preceding damage to myocytes with
subsequent over-expression of MHC class I proteins on the sarcolema leads to infiltration with
CD8 T lymphocytes and myocyte damage.
The seronegative spondyloarthropathies include ankylosing spondylitis, reactive arthritis, psoriatic
arthritis and arthritis associated with inflammatory bowel disease. Individuals expressing HLA B 27
are at increased risk for the reonegative spondylopathies.
estudia mas esto
bommmm
IL4 is produced by the TH2 subset of T helper cells. It facilitates grow of B cells and TH2
lymphocytes, and stimulates antibody isotype switching, particularly to IgE.
C. tetani produces the protein exotoxin tetanospasmin that blocks release of inhibitory
neurotransmittersb from inhibitory motor interneurons in the CNS. Tetanus is prevented by
immunization with toxoid that triggers the production of antitoxin antibodies (active immunity).
C tetani produces the protein exotoxin tetanospasmin that blocks release of inhibitory
neurotransmitters from inhibitory motor interneurons in the CNS. Tetanus is prevented by
immunization with toxoid that triggers the production of antitoxin antibodies (active immunity).
Erythema infectiosum (fifth disease) is caused by parvovirus B19 and is transmitted most
commonly via the respiratory route. Symptoms of this infection include a bright-red rash on the
cheeks ("slapped cheeks") and lacelike rash on the trunk and extremities.
1. Pulmonary anthrax also known as woolsorters disease, is caused by inhalation of spores MC
while working w/ goat hair or hides. Hemorrhagic mediastinitis evident as widened mediastinum on
chest-x ray is an important clue. 2. Microscopy: long chains ("serpentine" or "medusa head" on
appearance). 3. Bacillus anthracis produces antiphagocytic capsule that is required for
pathogenicity. The capsule is unique in that it contains D-glutamate instead of polysaccharide.
Ecthyma gandrenosum is a cutaneous necrotic disease w/ a strong assoc w/ Pseudomonas
aeruginosa bacteriana and septicemia. It occurs after P. auruginosa invades perivascularly and
releases tissue destructive exotoxins causing vascular destruction and resultant insufficiency of
blood flow to patches of skin which become edematous and subsequently necrose. Pseudomonas
infect are common in neutropenic pctes, hospitalized pctes, pctes with burns and chronic
indweling catheters.
Vitamin C is necessary for the hydroxylation of proline and lysine residues in pro-collagen. Pctes
with Vit C deficiency demostrate perifollicular hemorrhages, easy bruising and gum disease.
Additionally in children, bony deformities and subperiosteal hemorrhages are characteristic.
Avascular necrosis of the femoral head is strongly associated with the following conditions: 1.
Sickle cell disease: thrombotic occlusion of arteries. Embolic occlusion (fat emboli, air emboli) can
also cause avascular necrosis. 2. SLE: impaired blood supply to femoral head. High dose of
steroid therapy and alcoholism: unknown mechanism.
Osteoporosis (porous bones) represents loss of "total bone mass" that results in trabecular
thinning. Subperiosteal resorption with cystic degeneration is characteristic of
hyperparathyroidism. Vitamin D deficiency results in "excessive unmineralized osteoid", resulting
in low mineral density. Osteopetrosis is characterized by "the presistence of primary,
unmineralized spongia in the medullary canals."
The most common defect achondroplasia is an activation mutation of the fibroblast growth factor
receptor-3 at the epiphyseal growth plate which inhibits growth at the epiphyseal growth plate. The
results is shot, thick tubular long bones in the appendicular (limb)skeleton and normal axial (spine)
length. Short stature is growth hormone/IGF-1 deficiency is proportional; that is, the axial and
appendicular skeleton are proportionate.
In osteogenesis imperfecta there is an impairment of bone matrix formation.
Hypercalcemia in sarcoidosis is caused by increased extrarenal formation of 1,25-dihydroxy
vitamin D by activated macrophages. The hypercalcemia of sarcoidosis suppresses PTH
secretion.
The oresence of rhomboid shaped calcium pyrophosphate crystals is diagnostic of pseudogout.
These crystals are positively birefringent under polarized light. The knee joints is involved in more
than 50% of cases.
A psoas abscess can occur as the result of hematogenous or lymphatic seeding from a distant site
or by spread from an adjacent site. Patients can present with fever, back of flank pain, inguinal
mass, and difficulty walking. Inflammation of the psoas muscle pain when the hip is extended
(psoas sign).
Osteoclasts are derivative from the hematopoietic phagocytic cell lineage. The differentiation of
osteoclasts is mainly goberned by the RANK-ligand and the Monocyte colony-stimulating factor,
both of which are produced by osteoblasts. The overexpression of RANK receptors in
hypostrogenic states incresed bone resorption due to incresead osteoclastic activity. In short, low
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116
8
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2
121
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142
5
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177
5
832
3
Pharmacol
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848
1
Pharmacol
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852
3
Pharmacol
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638
Physiology
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824
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138
2
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155
8
166
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206
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Anatomy
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Physiology
Physiology
estrogen means a lower bone mass.

The RANK receptor/RANK-ligand interacttion is essential for the formation and differentiation of
osteoclasts. The over-expression of RANK receptors in hyperestrogenic states causes increased
bone resorption due to increased osteoclastic activity. In short, low estrogen means a lower bone
mass.
Sunlight exposure catalyses the first reaction in the chain of active vitamin D synthesis: 7dehydrocholesterol transforms to cholecalciferol (Vitamin D3). The, 25-hydroxylation occurs in the
liver and the kidney enzyme 1 alpha hydroxylase catalyses the final step in the synthesis of active
vitamin D.
Biphosphonates are structural analogs of pyrophosphate, an important component of
hydroxyapatite.
NSAIDs are the first-line therapy for treatment of acute fouty arthritis. Cochicine is considered as
second-line therapy due to its side effects of nausea and diarrhea. Glucocorticoids are indicated in
patients with contraindication to both NSAIDs and colchicine, such as patients with realn failure.
Uricosuric agents and allopurinol are contraindicated during acute attacks, however are used as
prophylactic treatment in certain patients.
Colchicine inhibits polymerization and microtubule formation in leukocytes, reducing neutrphil
chemotaxis and emigration to sites inflamed by uric acid crystal deposition in acute gouty arthritis.
Many pctes treated with cochicine also develop diarrhea as the gastrointestinal mucosa is
adversaly affected by colchicine.
Piperacillin-tazobactam is a combination of extended spectrum penicillin with beta lactamase
inhibitor. It is effective against most Gram (-) enteric rods, including Pseudomonas aeruginosa and
Bacteroides fragilis.
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The paralytic action of nondepolarizing neuromuscular junction (NMJ)blocking drugs can be
reversed by anticholinesterase agents such as neostigmine. Succinylcholine is a depolarizing NMJ
blocker that is augmented by neostigmine during phase I block but reversed by eostigmine during
phase II block. The duration of paralysis caused by succinylcholine depends largely on its
catabolism by plasma cholinesterase.
A decrease in the intravascular fluid volume stimulates aldosterone secretion and lead to
increased excretion of potassium and hydrogen ions in the urine. This results in hypokalemic
metabolic alkalosis, which is a common side effects of most diuretics other than the potassiumsparing class. Hypokalemia manifests with muscle weakness and cramping.
Tetracyclines are also contraindicated in children less than 8 years old of age because of possible
brone growth retardation and staining of permanent teeth.
Acute extrapyramidal symptoms (eg, dystonic reactions akatisia, and parkinsonism) are related to
an imbalance btwn Dopamine (D2) and Muscarinic (M1) activity in the nigrostriatal tract.
TRaditional-high potency antipsycotics (haloperidol, fluphenazine) strongly block D2 receptors and
are the most likely to cause extrapyramidal symptoms.
Adverse effects of Succinylcholine -Malignant hyperthermia (especially with halothane) in
genetically suceptible patients. -Severe hyperkalemia in patients with burns, myopathies, crush
injuries & denervation. -Bradycardia from parasympathetic stimulation or tachycardia from
sympathetic ganglionic effects.
The suffic of a biological agent indicates wheter a medication is a monoclonal antibodi (mab), a
receptor molecule (cept), or a kinase inhibitor (nib). Monoclonal antibodies also include in their
names the type of target (bacterial or immune system) abd their origen (human or mouse).
Osteoblast activity: is reflected by the serum level of bone-specific alkaline phosphatase.
Osteoclast activity: is reflected in: tartrate-resistant acid phosphatase, urinary hydroxyproline and
urinary deoxypyridinoline (deoxypyridinoline is the most reliable of the three).
T tubules are invagiations of the sarcolema that extend into each muscle fiber. They transmit
depolarization signals to the sarcoplasmic reticulum and trigger the release of Ca. The uniform
distribution of T tubules coordinated contraction of all myofibrils.
The resting membrane potential is the diference in the electrical changes across the cell
membrane under steady-state conditions. High potasium efflox and some sodium influx are
responsible for the value of the resting potential, which is typically about -70mV.
During skeletal muscle contraction, calcium is released from the sarcoplasmic reticulum and binds
troponin C thereby allowing the binding of actin to myosin.
buaaa
Myasthemia gravis is an autoimmune disease that results in a decrease in acetylcoline receptors
on the postsynaptic terminal of the muscle end plate. This results in decreased ability of
acetylcholine to bind and open postsynaptic nicotinic cation channels, thereby decreasing the end
plate potential.
The treatment of myasthemia gravis involves cholinesterase inhibitors, immunosuppressants and
possibly thymectomy. Cholinesterase inhibitors may cause adverse effects related to muscarinic
overstimulation, wich can be ameriorated by use of an antimuscarinic agent like scopolamine.
-Mesolimbic-mesocortical: Reculates behavior. Schizophrenia is the disease asoc. -Nigrostriatal:
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Coordination of voluntary movements. Parkinsonism is the disease asoc. -Tuberoinfundibular:

Controls prolactin secretion. Hyperprolactinemia is the disease asoc.
All sensory paathways except olfaction (smell) have relay nuclei in the thalamus. The VPL
receives impulses from spinothalamic and medial lemniscus pathways, the VPM from the
trigeminal and gustatory pathways, and the lateral and medial geniculate bodies are relay nuclei
from the visual and auditory pathways, respectively.
All sensory pathways except olfaction (smell) have relay nuclei in the thalamus. The VPL receives
impulses from spinothalamic and medial lemniscus pathways, the VPM from the trigeminal and
gustatory pathways, and the lateral and medial geniculate bodies are realy nuclei for the visual
and auditory pathways, respectively.
The stapedius muscle is innervated by stapedius nerve, a branch of facial nerve (CN VII).
Paralysis of the stapedius muscle allows wider oscillation of the stapes, and leads to increased
sensitivity to sound (Hyperacusis).
NF type I (von Recklinghausen's disease) is a comoon AD disorder resulting from a defect in NF-1
gene on chromosome 17. Cutaneous and subcutaneous neurofibromas are common in this
condition and are tumors of Schwann cells, which are embryologically derived from the neural
crest.
The tight junctions between endothelial cells in the capillary beds of the CNS form the blood-brain
barrier. Solutes and fluids cannot more freely across the capillary membrane in the CNS; material
can only move transcellulary by diffusing across the epithelial plasma membranes or by carriermediated transport.
Upper motor neuron lesions cause spasticity, hyperreflexia, and paresis. Corticospinal tract,
internal capsule (posterior limb), and primary motor cortex lesions can cause these symptoms.
The first arch can be poorly formed during embryonic development resulting in first arch
syndrome. Abnormalities include malformations of the mandibule, maxila, malleus, incus, zygoma,
vomer, palate, and temporal bone. The first arch is associated with the trigeminal nerve.
Sciatica is a painful condition characterized by shooting pain down the posterior thigh and leg that
typically results from impigment of one of the spinal nerves as it leaves the vertebra; column,
Compression of the S1 root results specifically in pain purely in the posterio thigh and leg as well
as diminution of the ankle jerk reflex.
Saddle anesthesia and loss of the anocutaneous reflex are symptoms of caudal equina syndrome,
which is associated with damage to the S2 through S4 nerve roots.
The anterior cerebral arteries supply the medial portions of the two hemispheres. oclussion
causes weakness of the contralateral legs and sensory deficits of the contralateral legs, trunks
and genitals. There may also be behavior and mood changes due to injury of the frontal lobe
structures.
The vagus nerve provides some cutaneous sensation to the posterior external auditory canal via
its small auricular branch. Sensation to the rest of the canal is from CNV3. A vasovagal syncopal
episode results from stimulation of the vagus nerve, leading to a decrease in blood pressure and
heart rate.
Ear cannal inervation X: posterior external auditory wall. IX: inner surface of the tympanic
membrane. V3: rest of the canal inervation.
Hydrocephalus in infants presents with irritability, poor feeding, increased head circunference and
enlarged ventricles on CT. Long-term sequelae of hydrocephalus include lower extremity spasticity
due to streching of the periventricular pyramidal tracts, visual disturbances, and learning
disabilities.
The combination of fixed segmental loss of upper extremity pain and temperature sensation,
upper extremity lower motor neuron signs, and/or lower extremity upper motor neuron signs in the
setting of scoliosis suggest a diagnosis of syringomyelia.
Trochlear nerve palsy is characterized by vertical diplopia.
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Troclear nerve palsi is characterized by vertical diplopia.
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The third branch of the trigeminal nerve (CN V3) exits the skull through the foramen ovale and
innervates the muscles of mastication, including the masseter, the medial and lateral pterygoids,
and the temporalis muscles.
The thalamic syndrome is characterized by total sensory loss on the contralateral side of the body.
Although there are no motor deficits, propioception is often profoundly affected and may lead to
difficulty ambulating and falls.
Lacunar infarctions are the result of small vessel lipohyalinosis and atherosclerosis involving the
penetrating vessels supplying the deep brain structures(basal ganglia, posterior limb of internal
capsule, pons, and cerebellum). Uncontrolled hypertension and diabetes mellitus are risk fcts for
this condition.
Lacunar infarctions are the result of small lipohyalinosis and atherosclerosis involving the
penetrating vessels supplying the deep brain structures, Uncontrolled hypertension and diabetes
mellitus are risk fct for this condition.
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The third cranial nerve (oculomotor) carrying general somatic efferent fiber and general visceral
efferent parasympathetic fiber exits the midbrain and courses between the posterior cerebral and
superior cerebellar arteries. An aneurysm arising from either artery can lead to a non pupil sparing
third nerve palsy, which clinically presents with unilateral headache, eye pain, diplopia, dilated
nonreactive pupil, and ptosis with the ipsilateral eye in a down and out position.
Intraventricular hemorrhage (IVH) is a common complication of prematurity. It is common in infant
born before 32 weeks gestation and/or with birth weight <1500g and almost always occurs within
the first 5 postnatal days. The IVH in preterm infants originates from the germinal matrix, a high
cellular and vascularized layer in the subventricular zone from which neurons and glial cells
migrate out during brain development.
Neonatal intraventricular hemorrhage ussually occurs in the fragile germinal matrix and increases
in frequency with decreasing age and birth weight(<32weeks gestation and/or birth weight<1500g
and almost always occurs within the first 5 postnatal days). It is a common complication of
prematurity that can lead to long-term neurodevelopmental impairment.
A lesion in the optic tract can produce contralateral homonymous hemianopia and a relative affect
pupillary defect (Marcus Gunn pupil) in the contralateral eye.
Among drugs of abuse, PCP(phencyclidine) is the most likely to induce violent behavior. Violence
and subsequent trauma are the most common causes of death with PCP intoxication. Other lethal
side effects commonly associated with drug abuse include myocardial infarction and stroke with
cocaine and respiratory depression with opioids.
Phencyclidine (PCP) is hallucinogen that workds primarily by antagonizing the NMDA receptor.
Modeerate amounts cause dissociative symptoms, including detachement and withdrawal. At
higher doses, PCP can induce agitation, hallucinations and violent behavior. A taxia, nystagmus
and memory loss are other distinguishing symptoms of PCP abuse.
Therapy for acute mania is a mood stabilizing agent (lithium, valproate, or carbamazepine) plus an
atypical antipsycotic (olanzapine).
Therapy for acute mania is a mood stabilizing agent (lithium, valproate or carbamazepine) plus
atypical antipsicotic (olanzapine).
Patients that need to be awake during the day but has a anxiety disorder and panic attacks and or
cannot sleep well ... please treat with a benzodiazepine of short duration of action such as
triazolam while you wait fot the initiation of action of the SSRI
Obstructive sleep apnea: most common causes are obesity, tonsillar hypertrophy, and
hypotiroidism. Obstructive sleep apnea may lead to pulmonary hypertension and right ventricular
failure.
Pctes with delusional disorder harbor non-bizarre delusions but do not meet the criteria for
schizophrenia and can function without significant impairment in day to day life.
Schiziaffective disorder is characterized by symptoms of schizophreniain the presence of
prominent mood symptoms. A periodof at least 2 weeks of psycotic symptoms in the absence of
mood symptoms is required for the diagnosis.
Schizoaffective disorder is characterized by symptoms of schizophrenia in the presence of
prominent mood symptoms (major depressive, maniac, or mixed). A period of at leat 2 weeks of
psycotic symptoms in the absence of mood symptoms is required for the diagnosis.
squizo what?
-Psycotic disorder: symptoms last less than one month. -Schizophrenoid Disorder: Symptoms last
1 to 6 months. -Schizophrenia: symptoms last more than 6 months.
Differentiation of delirium and dementia 1. Onset: Acute in delirium vs gradual in dementia 2.
Consciousness: Impaired in delirium vs intact in dementia. 3. Course: Fluctuating symptoms in
delirium vs progressive decline in dementia. 4. Prognosis: Reversible symptoms in delirium vs
irreversible symptoms in dementia. 5. Memory impairment: Global in delirium vs remote spared in
dementia.
Clinicians have ethical and moral obligations to report elder abuse, neglet, and exploitation. If
there is reason to suspect abuse or neglet, the pcte should be interviewed alone to avoid
intimidation by possible abusers. 3 questions you should ask: 1. Do you feel safe where you live?
2. Who prepares your meals? 3. Who handles your checkbook?
Hypocretin-1(orexin-A) and hypocretin-2 (orexin-B) are neuropeptides produced in the lateral
hypothalamus that Fx to promote wakefulness and inhibit REM sleep-related phenomena. Most
pctes who have narcolepsy with cataplaxy demostrate undetectable level of hypocretin-1 in their
cerebrospinal fluid.
Chronic thiamine (B1) deficiency leads to the dimished ability of cerebral cells to utiliza glucose.
The mechanism is decreased function of the enzymes that use B1 as a cofactor (pyruvate
dehydrogenase, alpha ketoglutate dehydrogenase, and transketolase). Thiamine deficiency can
be diagnosed by measuring erythrocyte transketolase activity.
Chronic B1 deficiency leads to the dimished ability of cerebral cells to utilize glucose. The
mechanism is decreased function of the enzymes that use vitamin B1 as a cofactor (pyruvate
dehydrogenase, alpha ketoglutarate dehydrogenase, and transketolase). Thiamine deficiency can
be diagnosed by measuring erythrocyte transketolase activity.
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Vitamin A overuse can result in intracraneal hypertension, skin changes and hepatosplenomegaly.
Vit A teratogenicity: microcephaly, cardiac anomalies, and fetal death (specially first trimester of
pregnancy).
estudia
Peroxisomal diseases: impairement of very long chain fatty acids with branch points at oddnumbered carbons can not undergo mitochondrial beta oxidation
Propionil CoA is derived from aminoacids (Val, Ile, Met, and Thr), odd-numbered fatty acids, and
cholesterol side chains. Congenital deficiency of propionyl CoA carboxylase, the enzyme
responsible for the conversion of propionyl CoA to methylmalonyl CoA, leads to the development
of propionic acidemia.
Methylmalonic acidemia (also known as methylmalonic aciduria) results from defect in the
isomerization reaction that transforms methylmalonyl CoA to succinyl CoA entering the TCA cycle.
Catabolism of isoleucine, valine, threonine, methionine, cholesterol, and odd-chain fatty acids
leads to formation of propionic acid, which is then converted to methylmalonic acid by biotindependent carboxylation. Isomerization of methylmalonyl CoA forms succinyl CoA, which
subsequently enters the TCA cycle. Defects in this isomerization reaction lead to the development
of methylmalonic acidemia.
Methylmalonic acidemia (also known as methylmalonic aciduria) results from a defect in the
isomerization reaction that transforms methylmalonyl CoA to succinyl CoA , prior to succinyl CoA
entering the TCA Cycle. Laboratory: metabolic acidosis w/large anion gap, ketosis and
hypoglycemia.
Alanine is the major amino acid responsible for tranferring nitrogen to the liver for disposal. During
the catabolism of protein, amino groups are tranferred to alpha ketoglutarate to form glutamate.
Glutamate is then processed in the liver to form urea, the primary disposal form of nitrogen in
humans. Free amonia is also excreted into the urine by the kidney for regulation of acid base
status.
Alanine is the major amino acid responsible for tranferring nitrogen to the liver for disposal. During
the catabolism of proteins, aminogroups are tranfered to alpha-ketoglutamate. Glutamate is then
processed in the liver to form urea, the primary disposal form of nitrogen in humans. Free amonia
is also excreted into the urine by the kidney for regulation of acid-base status.
Ornithine transcarbamoylase deficiency is the most common disorder of the urea cycle, resulting
in severe neurological abnormalities due to high blood and tissue ammonia levels.Increased urine
orotic acid excretion is typical.
Ornithine transcarbamoylase deficiency is the most common disorder of the urea cycle, resulting
in severe neurological abnormalities due to high blood and tissue ammonia levels. Increased urine
orotic acid excretion is typical.
Ornithine transport into mitochoondria is essential for urea formation, as ornithine is needed to
combine with carbamoyl phosphate within the mitochondria to form citrulline in the second step of
the urea cycle. Urea cycle defects cause neurological damage primarily due to the accumulation
of ammonia. Protein restriction would improve this condition.
Ornithine transport into mitochondria is essential for urea formation, as ornithine is needed to
combine with carbamoyl phosphate within mitochondria to form citruline in the second step of the
urea cycle. Urea cycle defects cuse neurological damage primarily due to the accumulation of
amonia. Protein restriction would improve this condition.
DNA polymerase I has 5' to 3' exonuclease activity in addition to its 5' to 3' polymerase and 3' to 5'
exonuclease activities. This 5' to 3' exonuclease activity is used to remove the RNA primer (which
initiates DNA polymerization) and to remove damaged DNA.
The zinc containing gamma aminolevulinate dehydratase and ferrochelatase are enzymes in the
heme biosynthetic pathway that are inactivated by lead. Thus in lead poisoning, gamma ALA and
protoporphyring IX accumulate, and the population of heme is decreased, leading to microcytic
anemia secondary to a la og hemoglobin.
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The nitrogen atoms in the urea molec are derived from NH3 and aspartate in the urea cycle.
Remember that carbamoyl phosphate synthetase I (CPS I) is a rate limiting enzyme in the urea
cycle reaction and is activated by N acetylglutamate.
The nitrogen atoms in the urea molecule are derived from NH3 and aspartate in the urea cycle.
Remember that carbamoyl phosphate synthetase I (CPS I) is the rate limiting enzyme in the urea
cycle reaction and is activated by N-acetylglutamate (NAG).
Transamination reactions typically occur between an amino acid and an alpha keto acid. The
amino group from the amino acid is transferred to the alpha keto acid, and the alpha keto acid tun
becomes an amino acid. Pyridoxal phosphate (vitamin B6) serves as a cofactor in amino acid
transamination and in decarboxylation reactions.
BH4 is a cofactor used by hydroxylase enzymes in the systhesis of tyrosine, dopa, and serotonin,
as well as NO. Serotonin is synthesized from tryptophan, and the initial step in this reaction is
catalyzed by an enzyme that uses BH4 as a cofactor. Enzyme dihydrobiopterin reductase
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deficiency causes defective regeneration of BH4, and is an uncommon cause of

phenylketonuria(PKU).
Homocystinuria is caused by syctathionine synthetase deficiency. Affected individuals manifest
with symptoms resembling those of Marfan syndrome, particularly ectopia lentis, and many
experience some form of developmental delay. They are also at high risk of developing
thromboembolism. About 50% of affected pctes respond to high doses of Vitamin B6(pyridoxine).
Homocystinuria is caused by cystathionine synthetase deficiency. Affected individuals manifest
with symptoms resembling those of Marfan syndrome, particularly ectopia lentis, and many
experience some form of developmental delay. They are also at high risk of developing
thromboembolism. About 50% of affected pctes respond to high doses of vitamin B6 (pyridoxine).
Homocystinuria is caused by cistathionine synthetase deficiency. Affected individuals manifest with
symptoms resembling those of Marfan syndrome, particularly ectopia lentis, and many experience
some form of developmental delay. They are also at high risk of developing thromboembolism.
About 50% of affected patients respond to high doses of vitamin B6 (pyridoxine).
Niemann Pick disease is an autosomal recessive disorder characterized by a deficiency of the
sphingomyelinase enzyme and resultant accumulation of shingomyelin. Patients present in infancy
with loss of motor skills, hepatosplenomegaly, hypotonia and a cherry red macular spot. Foamy
histiocytes are the classic finding on tissue histology. Death occurs before age 3.
In pctes with Alzheimer Ds, beta amyloid protein loses its alpha-helical configuration and forms
beta sheets, which are less soluble and therefore prone to aggregating. Agreggations of beta
sheets are the primary component of the extracellular senile (neuritic) plaques found in Alzheimer
pctes.
A protein's primary structure is the sequence of aminoacids linked by covalent peptide bonds.
Proteins may also assume a secondary structure, such as the alpha-helix or beta-sheet, due to
subsequent hydrogen bonding. In patients with Alzheimer disease, beta amyloid protein loses its
alpha-helical configuration and forms beta sheets, which are less soluble and therefore prone to
aggregationg.
A patient with orotic aciduria (impaired de novo pyrimidine synthesis) will present with
hypochromic megaloglastic anemia, neurologic abnormalities, growth retardation and excretion of
orotic acid in the urine. Uridine supplementation improves symtoms by inhibiting carbamoyl
phosphate synthetase II.
A pcte with orotic aciduria (impaired de novo pyrimidine synthesis) will present with hypochromic
megaloblastic anemia, neurologic abnormalities, growth retardation and excretion of orotic acid in
the urine. Uridine supplementation improves symptoms by inhibiting carbamoyl phosphate
synthetase II.
A pcte with orotic aciduria (impaired de novo pyrimidine synthesis) will present with hypochromic
megaloblastic anemia, neurologic abnormalities, growth retardation and excretion of orotic acid in
the urine. Uridine supplementation improves symptoms by inhibiting carbamoyl phosphate
synthetase II.
Lesch-Nyhan sindrome is an X linked recessive disorder caused by a defect in hypoxanthine
guanine phosphoribosyltransferase (HGPRT).This results in failure of the purine salvage pathway.
Because they are not recycled, increased amounts of the purine bases hypoxanthine and huanine
are degraded to uric acid. De novo purine synthesis must increase to replace the lost bases.
Lesch-Nyhan syndrone is an X-linked recessive disorder caused by a defect in hyopoxanthineguanine phosphoribosyltransferase (HGPRT). This results in failure of the purine salvage pathway.
Because they are nor recycled, increased amounts of the purine bases hypoxanthine and guanine
are degraded to uric acid. De novo purine synthesis must increase to replace the lost bases.
Ubiquitin is a protein that undergoes ATP-dependent attachment to other proteins, labeling them
for degradation. These modified proteins enter the proteosome and are degraded into small
peptides. Impairment of the ubiquitin-proteasome system can contribute to the development of
neurodegenerative disorders, including Parkinson and Alzheimer's diseases.
The concept of latent period can be applied to both disease pathogenesis and exposure to risk
modifiers. The initial steps in pathogenesis and/or exposure to a risk fct sometimes occur years
before clinical manifestations of a disease are evident. Additionally, exposure to risk modifiers may
need to be continuous over certainn period of time before influencing the outcome.
Remember that the confidence interval equation has to have the sample size written!!! Remember
sample size!! the raiz cuadrada del sample size.
Polyhydramnios refers to excessive accumulation of amniotic fluid, and is typically related to either
decreased fetal swallowing or increased fetal urination. Fetal anomalies associated with impaired
swallowing include gastrointestinal obstruction due to duodenal, esophageal, or intestinal atresia
and anencephaly.
-The risk of neural tube defects in valproate exposed neonates is reported to be from 1-3%, as
valproate inhibits intestinal folic acid absorption, resulting teratogenesis.
Craniopharyngiomas are calcified cystic tumors. They arise from the remnants of Rathke's pouch
(an embryonic precursor of the anterior pituitary). Craniopharingiomas commonly cause
headaches, growth failure, and bitemporal hemianopia.
Craniopharingiomas are calcified cystic tumors. They arise from the remmants of Rathke's pounch
(an embryonic precursor of the anterior pituitary). Craniopharingiomas commonly cause
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headaches, growth failure, and bitemporal hemianopia..

"Red ragged" muscle fibers are seen in mitochondrial diseases. Muscle fibers have this
appearance because abnormal mitochondria accumulate under the sarcolemma. Mitochondrial
diseases show maternal inheritance.
Alzheimer disease (onset <60 years old) 1. Amyloid precursor protein (APP) gene on chromosome
21. 2. Presenilin 1 gene on chromosome 14. Presenilin 2 gene on chromosome 1 Both APP and
persenilin gene mutations are thought to promote the production of A beta amyloid. Late-onset
familiar Alzheimer ds is assoc with the epsilon4 allele of Apolipoprotein E. The exact mechanism is
not known. It is thought that the ApoE4 protein may be involved in the formation of senile plaques.
Mitochondria diseases: 1. Leber hereditary optic neuropathy: leads to bilateral vision loss. 2.
Myoclonic epilepsy with ragged red fibers: myoclonic seizures and myopathy associated with
exercise. Skeletal muscle biopsy shows irregularly shaped muscle fibers (ragged red fibers). 3.
Mitochondrial encephalomyopathy with acidosis and stroke like episodes (MELAS): seizures,
stroke like episodes with residual neurologic deficit, muscle weakness, increase lactate acid seric.
Heteroplasmy: mixture of two types of genetic material that is responsible for the clinical variability
of mitochondria diseases.
Friederich ataxia is an autosomal recessive condition. The mutaded gene on chromosome 9 has
an increased number of trinucleotide repeats. Friederich ataxia is often associated with
hypertrophic cardiomyopathy, diabetes mellitus, kyphoscoliosis, and foot deformities.
Alteration of gene expression in Huntington disease is belived to occur due to hypermethylation of
histones. Hyper methylated histones bind DNA and prevent transcription of certain genes. This
leads to the disruption of synthesis of some neurotrophic proteins.
The fragile X mental retardation 1 gene is located on the long arm of the X chromosome. An
increased number of CGG trinucleotides repeats leads to hypermethylation of cytosine bases and
subsequent gene inactivation. This defect is the cause of fragile X sindrome, which manifests as
mental retardation, facial dysmorphism, and macroorchidism.
The fragile X mental retardation 1 gene is located on the long arm of the X chromosome. An
increased number of CGG trinucleotide repeats to hypermethylation of cytosine bases and
subsequent gene inactivation. This defects is the cause of fragile X syndrome, which manifests as
mental retardation, facial dysmorphism, and macroorchidism.
Tay-Sachs Ds is an AR disorder caused by a deficiency in beta hexosaminidase A, which results in
accumulation of GM2 ganglioside. It is characterized by progressive neurodegeneration and a
cherry red macula spot. In contrast to Niemann-Pick Ds there is no hepatosplenomegaly.
Kinesin is a microtubule-associated, ATP powered motor protein that facilitates the anterograde
transport of NT-cointaining secretory vesicles down axons to synaptic terminals.
Cerebellar ataxia, telangiectasias, and increased risk of sinopulmonary infections constitude a
characteristic triad of ataxia telangiectasia Thos illness exhibits autosomal recessive inheritance,
and the defect is in a gene that codes for the ATM gene which plays a role in DNA break repair.
The immune deficiency primarily manifests as an IgG deficiency and predisposes o infections of
the upper and lower ariways.
Ataxia telangiectasia is an AR disorder resulting from a defect in DNA repair genes. The DNA of
these pctes is hypersensitive to ionizing radiation. Manifesttions include cerebelar ataxia,
oculocutaneous telangiectasias repeated sinopulmonary infections, and an increased incidence of
malignancy.
Deficiency of the complemet factors that form the membrane attack complex (C5b-C9) results in
recurrent infections by Neisseria species.
Cryptococcus neoformans is present in soil and pigeon droppings(yest form single cells only). The
yeast is transmitted via the respiratory route, with the lungs as the primary site of entry. In
immunocomprmised pctes, lung infection may be followed by dissemination of C neoformans,
often the CNS.
Cryptococcus neoformans causes meningoencephalitis in HIV (+) pctes. The latex agglutination
test detects the polysaccharide capsule of Cryptococcus and is used for diagnosis. India ink
staining of the CSF shows round or oval budding yeast.
Neisseria meningitidis gains access to the CNS b first colonizing the nasopharynx and
subsequently invading the mucosal epithelium and gaining access to the bloodstream. Though the
blood, it spreads to choroid plexus, gains access to the CNS through the blood-brain barrier, and
initiates and inflammatory process.
Meningococcal lipooligosaccharide (LOS) is responsible for many of the toxic effects observed in
meningitis and meningococcemia (production of TNF alpha, IL 1 beta, IL-6, IL-8). Blood levels of
LOS correlate closely with morbility and mortality. Additionally LOS has been implicated to cause
cutaneous petechia and hemorrhagic bullae found in meningococcemia. It is also belived that
cause bilateral adrenal cortical hemorrhage characteristic of the Water-Friderichsen Sindrome.
Meningococcal lipiiligosaccharide (LOS) is responsible for many of the toxic effects observed in
meningitis and meningococcemia. Blood levels of LOS correlate closely with morbility and
mortality.
Congenital toxoplasmosis is transmitted transplacentally. The fetus is affected only if the mother is
infected w/toxoplasmois during the first six month of pregnancy.Its classic triad includes
hydrocephalus, intracraneal calcifications and chorioretinitis.
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E. coli is a frequent cause of neonetal meningitis, second only to Group B Streptococci. The
capsule synthesized by some E. coli (K-1 antigen) is a virulence factor that allows the bacteria to
survive hematogenous spread and to stablish meningeal infection. Most strains of E.colo causing
neonatal meningitis do possess this K-1 antigen.
Listeria monocytogenes is an opportunistic agent and a facultative intracellular parasite that grows
within macrophages in immunocompromised human hosts. It is able to multiply at 4C a unique
feature that laboratories exploit when culturing the organism, a process called cold enrichment.
Listeriosis is most commonly transmitted through food ingestion and causes sepsis and meningitis
in inmunocompromised adults. Listeria can also cause neonatal meningitis. Listeria grows well in
cold temperatures (cold enrichment) and thus can contaminate refigerated food. Listeria is a gram
positice rod with V or L formations resembling corynebacterium, but its tumbling motility is a
unique feature.
Clostridia are Gram positive spore-forming anaerobic rods. C. botulinum is the bacteria
responsible for botulism, a toxin-mediated disease. Local injections of botulism toxin into muscle
are used to treat focal dystonias, achalasia and spasms.
The clinical presentation of restlessness, agitation, and dysphagia progressing to coma 30 to 50
days following an exposure to cave bats is strongly suggestive of rabies encephalitis (rabies virus
travels retrograde via peripheral nerves to the dorsal root ganglia and then to the brain).
Prophylactic vaccination is approved rabies vaccine consists of various rhabdovirus strains grown
in tissue cell culture and then inactivated to produce killed virus vaccine.
Neisseria meningitidis Immunity against these bacteria is provided by antibodies against their
polysaccharide capsules.
Enterovirus infection is the most common cause of aseptic meningitis, accounting for up to 90% of
cases. The enteroviruses are a family of single-stranded RNA viruses that include the
coxackieviruses, echoviruses and polioviruses. Enteroviruses are so-named because of their
fecal-oral transmission and ability to replicate in the GI tract. They do not typically cause
gastroenteritis.
Enteroviruses are the most common cause of viral aseptic meningitis. The enterovirus group
incldudes the coxsackieviruses, echoviruses and polioviruses. Poliovirus can cause lower motor
neuron injury in addition to meningitis, especially in non immunized individuals from endemic
regions.
Subacute headache, fever, and neck stiffness in the presence of the lymphocytic CSF pleocytosis,
modestly elevated CSF protein level, and otherwise normal CSF parameters points to a diagnosis
of aseptic meningitis. Enteroriruses, including coxsackievirus and echovirus are the most common
causes of aseptic meningitis.
In AIDS pctes, the radiographic finding of ring-enhancing lesions in both cerebral hemispheres is
most often indicative of toxoplasmosis. First line tto of toxoplasmosis includes a combination of
pyrimethamine and sulfadiazine.
Primary CNS lymphoma is typically composed of B lymphocytes and most commonly occurs in
immunocompromised pctes (such as those with AIDS).
Primary CNS lymphoma is typically composed of B-lymphocytes and most commonly occurs in
immunocompromised patients (such as those woth AIDS).
Cortical atrophy is a common sequelae of advanced HIV infection.
Normal pressure hydrocephalus occurs in elderly pctes. it causes the triad of ataxic gait and
urinary incontinence, then dementia. These symptoms are explained by distortion of
periventricular white matter. Bladder control is influenced by descending cortical fibers that run in
the distended paraventricular area. Later, loss of cortical inhibition on the sacral micturition center
causes the development of urge incontinence.
Micturition reflex (urination) is regulated by: 1. Sacral micturition center: S2-S4 level, they contract
the bladder. Parasympathetic fibers travel from S2-S4 ventral white matter within pelvic nerves
and stimulate cholinergic receptors in the bladder wall. 2. Pontine micturition center: located in the
pontine reticular formation. It coordinate relaxation of external urethral sphincter with bladder
contraction during voiding. 3. Cerebral cortex: inh sacral micturition center.
The cells most susceptible to ischemia are the pyramidal cells of the hyppocampus and neocortex
and the Purkinje cells of the cerebellum. The hippocampus is the first area damaged during global
cerebral ischemia.
Hemiparesis with the arm affected more than the lg occurs due to occlusion of the middle cerebral
artery (MCA). If the occluded MCA is the dominant hemisphere (usually left), aphasia may also
occur.
Profound cerebral hypoperfusion may lead to global cerebral ischemia (also called ischemichypoxic encephalopathy). Watershed infarcts occur between the zones of perfusion of the anterior,
middle, and posterior cerebral arteries. These infarcts appear as bilateral wedge-shaped bands of
necrosis over the cerebral convexity, just lateral to the interhemispheric fissure.
Profound cerebral hypoperfusion may lead to global cerebral ischemia (also called ischemichypoxic encephalopathy). Watershed infacts occur betwen the zones of perfusion of the anterior,
middle, and posterior cerebral arteries. These infarcts appear as bilateral wedge-shaped bands of
necrosis over the cerebral convexity, just lateral to the interhemispheric fissure.
Anemia associated with neurologic abnormalities is fairly specific to vitamin B12 deficiency.
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Neurological damage associated with B12 deficiency includes subacute, combined degeneration
of the posterior and lateral spinal columns. Increased serum level of methylmalonic acid is Dx of
Vitamin B12 deficiency.
Anemia associated with neurologic abnormalities is fairly specific to vitamin B12 deficiency.
Neurological damage associated with Vit B12 deficiency includes subacute, combined
degeneration of the posterior and lateral spinal columns. Increased serum level of methylmalonic
acid is diagnostic of vitamin B12 deficiency.
Meniere disease is characterized by the triad: tinnitus, vertigo and sensorioneural hearing loss. Its
pathogenesis is related to an incresed volume and pressure of endolynph in the vestibular
apparatus.
important to know
A cerebellar hemagioblasoma is associated with congenital cysts of kidneys, liver, and/or
pancreas is highly suggestive of von Hippel-Lindau disease, a rare autosomal dominant condition.
The changes in the body of a neuron after the axon has been severed are calles axonal reaction.
This process reflects an increased protein synthesos that facilitates axon repair. Enlarged,
rounded cells with peripherally located nuclei are dispersed finely granular Nissl substance are
seen.
The changes in the body of a neuron after the axon has been severed are called axonal reaction.
This process reflects an increased protein synthesis that facilitates axon repair. Enlarged, rounded
cells with peripherally located nuclei and dispersed finely granular Nissl substance are seen.
Transtentorial (uncal) herniation is a complication of an ipsilateral mass lesion, such as a
hemorrhage or brain tumor. The first sign of uncal herniation is a fixed and dilated pupil on the side
of the lesion. Ipsilateral paralysis of oculomotor muscles, contralateral or ipsilateral hemiparesis,
and contralateral homonymous hemianopsia with macular sparing may be also occur.
-Charcot-Bouchard pseudoaneurysms: Cause by hypertension. Small arteries that profuse the
basal ganglia and internal capsule. Intracerebral hemorrhage in the areas of basal ganglia,
internal capsule, thalamus, pons. -Berry (saccular) aneurysms: Asoc ADPKD, Marfan, EhlersDanlos syndrome. Cicle of Willis, anterior and posterior comuunicating, middle cerebral.
Subarachnoid hemorrhage.
Cerebral amyloid angiopathy is a common cause of recurrent lobar hemorrhage, This type of
intracranial hemorrhage has a lower mortality rate and more benign clinical course than
hemorrhagic strokes associated with hypertension.
Subarachnoid hemorrage occurs due to rupture of saccular (berry) aneurysm or arteriovenous
malformation. Severe vasospasm 4-12 days after the initial insult is the major cause of morbility
and mortality in patients recovering from SAH. Nimodipine, a aselective calcium channel blocker,
is often prescribbed to provent this vaasospasm.
- Arnold Chiari type I: low-lying cerebellar tonsils que sale por el foramen magnum. It may be
asyntomatic in infants, but in adults manifests with headaches and cerebellar syntoms (such us
ataxia). Arnold Chiari II: causes syntoms of compression of the medulla such as difficulty
swallowing, dysphonia, stridor, and apnea. Lumbar myelomeningocele ussually leads to leg
paralysis. If untreated, hydrocephalus can cause mental impairment.
- Epidural hematoma: Middle meningeal artery. - Subdural hematoma: Bridging cortical veins. Subarachnoid hemorrage: Aneurysm or AV malformation of anterior and posterior communicating
arteries.
Epidural hematoma occurs due to tear of the middle meningeal artery. It wis often associated with
temporal bone fracture, and is located between the bone and dura mater. Clinical presentation is
characterized by a "lucid interval", followed by loss of conciousness.
Horner's syndrome clinically presents with partial ptosis, miosis, anhidrosis, and enophtalmos that
occurs due to interruption of the sympathetic innervation to the head. 1. Partial ptosis: sympathetic
denervation of Muller muscle of the upper eyelid. 2. Miosis: sympathetic denervation of fibers to
the dilator pupillae muscle. 4. Enophtalmos: eye being positionaded deeper in the orbit.
In pctes with Alzheimer Ds, there are decreased levels of acetylcholine in the nucleus basalis of
Meynert and hippocampus. Diminished activity of choline acetyltransfeerase in these cerebral
structures is the cause.
In patients with Alsheimer disease, there are decreased levels of acetylcholine in the nucleus
basalis of Meynert and hippocampus. Diminished activity of choline acetyltransferase in these
cerebral structures is the cause.
Alzheimer disease have a decresed acetylcholine levels in the hipocampus and nucleus basalis of
Meynert (this nucleus is located at the base of the forebrain and widely projects to the neocortex).
This occurs due to the deficiency of the choline acetyltransferase.
Neurologic paraneoplastic syndromes such as paraneoplastic cerebellar degeneration are
considered to be autoinmune.
Paraneoplastic cerebellar degeneration is a type of paraneoplastic syndrome most commonly
associated with cancers of the lung, breast, ovary, uterus, and lymphoma. The most common
antibodies seen are anti Yo (Breast, ovary), anti P/Q (lungs), anti Hu (lungs). These antibodies
react against tumor cells cross-react with neurons and cause degeneration of the cerebellum.
Patients present with limb and truncal ataxia, lack of coordination, dysarthria, and nystagmus.
Subthalamic nucleus is one of the components of the basal ganglpia. Damage to his nucleus
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(most often due to lacunar stroke) leads to hemibalism. The involuntary flinging movements of one
side of the body (arm and/or leg) that constitutes hemibalism are always contralateral to the
lesion.
Subthalamic nucleus is one of the components of the basal ganglia. Damage to this necleus (most
often due to lacunar stroke) leads to hemibalism. The involuntary flinging movements of one side
of the body (arm and le/or leg) that constitutes hemibalism are always contralateral to the lesion.
The phrenic nerve arises from the C3-C5 segments of the spinal cord and inervates the ipsilateral
hemidiaphragm. Intrathoracic spread of a lung cancer may irritate the phrenic nerve, causing
hiccups and diaphracmatic paralysis with dyspnea.
Severe vitamin E deficiency closely resembles the clinical presentation of Friedereich ataxia.
Vitamin E is a lipid-soluble vitamin that has antioxidantive properties. Degeneration of the
posterior columns and spinocerebellar tracts are seen in Vit E deficiency and Friedreich ataxia.
Friedreich ataxia: AR Ds mutation of a gene on chromosome 9. Degeneration of the
spinocerebellar tracts.
Amyoatrophic lateral sclerosis causes both upper and lower motor neuron lesions. Loss of
neurons of anterior horns (LMN): causes muscle weakness and atrophy. Demyelination of the
lateral corticospinal tract (UMN lesion): sppasticity and hyperreflexia.
The hippocampus is the area of the brain demostrating the greatest degree of atrophy in
Alzheimer's disease. Hippocampal atrophy on MRI is highly suggestive of the diagnosis.
In the brain: the lesion is liquefactive necrosis caused by lisosomal degradation of the cells.
Astrocytes proliferate around the necrotic area.
Liquefactive necrosis is characterized by complete digestion and removal of necrotic tissue with
formation of cystic cavity. Hypoxic CNS injury is often followed by liquefactive necrosis. Abscess
formation due to bacterial or fungal infection is another example of this type of necrosis.
- Synaptophysin stain: found in presynaptic vesicles of neurons, neuroendocrine and
neuroesctodermal cells. - Glial fibrillary acidic protein: found in astrocytomas including
glyoblasoma multiforme, oligodentrogliomas, ependymomas and peripheral neural sheath tumors.
Huntington: decreased GABA.
HSV-1 encephalitis has a predilection for the temporal lobe. This site-specific damage causes
restricted symtoms, including aphasia, olfatory hallucinaions(amygdala involvement), and
peronality changes (amygdala involvement). Macroscopic brain examination revels edema and
hemorrhagic necrosis of the temporal lobes.
Rapid response to acyclovir indicates that this patient has a viral infection, most likely caused by
herpes simplex. Thee atypical "viral pattern" of CSF includes lymphocytic pleocytosis, normal
glucose, and elevated protein. A few RBCs may alsoo be present in the CSF, due to hemorrhagic
destruction of the temporal lobes.
Central nervous system involvement insyphilis (neurisyphilis) may manifest as a number of
different syndromes. Tabes dorsalis occurs due to degeneration of the dorsal columns and dorsal
roots of the spinal cord. Loss of propioception and vibration senses, ataxia, and Argyll Robertson
pupils may be seen.
Positive VDRL of the spinal fluid indicates neurosyphilis (<10% of patients with terciary syphilis)
Subacute sclerosing encephalitis is a rare complication of measles infection. It occurs several
years after apparent recovery from initial infection. Oligoclonal bands of antibodies to the measles
virus found in the CSF of these pctes. Antibodies to the M component of the measles virus are
absent.
years after apparent recovery from initial infection. Oligoclonal bands of antibodies to the measles
virus are found in the CSF of these pctes. Antibodies to the M component of the measles virus are
absent.
years after apparent recovery from initial infection. Oligoclonal bands of antiobodies to the
measles virus are found in the CSF of these patients. Antibodies to the M component of the
measles virus are absent.
Creutzfeldt-Jakob disease causes rapidly progressive dementia and myoclonic jerks. On
microscopic examination, mmultiple vacuoles are seen in the gray matter of the brain (spongiform
encephalopathy). The pathogenesis of the disease is linked to an abnormal protein (prion).
Polymyalgia rheumatica occurs in more than half pctes with temporal arteritis. It is characterized
by neck, torso, shoulder, and pelvic girdle pain and morning stiffness. Fatigue, fever and weight
loss may also occur. Monocular vision loss is a common complication of temporal arteritis.
Multiple sclerosis manifests with carious self-limiting neurilogic symptoms, usually in pctes 20-30
years old. The most common initial symptom are optic neuritis, internuclear ophthalmoplegia and
sensory deficits. Symptoms usually worsen with heat expose.
Multiple sclerosis The common initial symptoms include: 1) Optic neuritis: visual disturbances,
particulartly central scotoma, accompanied by painful eye movements. 2) Internuclear
ophthalmoplegia: impaired eye adduction during the lateral gaze due to demyelination of the
medial longitudinal fasciculus. 3. Cerebellar disfuntion: includes tremor, ataxia and nystagmus. 4)
Sensory and motor symtoms: include bowel and bladder dysfunction.
Multiple sclerosis occurs most commonly as a relapsing-remitting central nervous system disorder
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characterized by recurrent episodes of demyelination and subsequent partial remyelination. There

is relative preservation of axons in acute MS plaques, with axonal degeneration seen mostly in
chronic plaques. Internuclear ophthalmoplegia and optic neuritis are common symptoms of MS.
Decresed oligodendrocyte: - Multiple sclerosis - Progresive multifocal leukoencephalopathy
Guillan Barre syndrome is an acute demyelinating peripheral neuropathy. It affects young adults
and is usually preceded by febrile illness. Segmental demyelination of peripheral nerves and an
endoneural inflammatory infiltrate are seen on light microscopy.
Mex of the development of Diabetes neuropathy: 1. Non enzymatic glycosilation of proteins leads
to increased thickness hyalnization, and narrowing of walls of the arteries. 2. Intracellular
hyperglycemia occurs in peripheral nerves. Acumulating glucose is converted into sorbitol and
fructose by aldose reductase. Sorbitol increases cell osmolarity and facilitates water influx into the
cell. The result is osmotic damage to axons and Schwann cells.
Most important Mx of development of diabetic neuropathy: 1) Non-enzymatic glycosilation of
proteins leads to incresed thickness, hyalinization, and narrowing of the walls of the arteries. 2)
Intracellular hyperglycemia occurs in peripheral nerves. . Accumulating glucose is converted into
sorbitol and fructose by aldose reductase. Sorbitol increases cell osmolarity and facilitates water
influx into the cell. The result is osmotic damage to axons and Schwann cells.
Meningiomas arise from cells of the arachnoid villi. They are slow-growing and cause syntoms due
to compression of adjacent brain structures. Personality changes reflect compression of the frontal
lobe, as ocurred in this patient. A more classic presentation is the presence of the new onset
seizure in an adult.
Pilocytic astrocytoma: cyst tumor in the cerebellum of a child. Biopsy will show a well differentiated
neoplasm comprised of spindle cells with hair-like glial processes that are associated with
microcysts. These cells are mixed with Rosenthal fibers and granular eosinophilic bodies.
Pilocytic astrocytomas and medulloblastomas arise in the cerebellum, microscopic findings must
be relied in to determine which type of tumor this pcte has. Meduloblastoma: Sheets of primitive
cells (deeply basophilic nuclei and scant cytoplasm it measn small, round, blue cells) w/ many
mitotic figures.
The pineal region is the most comoon location of brain hgerminomas, Histollogically, germinomas
are similar to testicular seminomas. Classic symptoms of pineal germinomas are precocious
puberty (can occur in males and is caused by beta HCG), Parinaud syndrome (includes paralysis
of upward gaze and of convergence-these cymptoms occur due to compression of the tectal area
of midbrain), and obstructive hydrocephalus(aqueductal compression).
Opsoclonus-myoclonua is a paraneoplastic syndrome associated with neuroblastoma. This tumor,
associated with an increased number of copies of the N-myc gene, is the most common
extracranial neoplasm in children.
Carpal tunnel syndrome is caused by medial nerve compression. It is the most common example
of compression (entrapment) neuropathy and is associated with repetitive wrist movements.
Carpal tunnel syndrome is also associated with hypothyroidism, diabetes mellitus, rheumatoid
arthritis and dialysis-associated amyloidosis.
Dystrophin is a structural component of skeletal m. fibers. It links a component of the cytoskeleton
(actin) to transmembrane proteins (alpha and beta dystrophiglycans) that are connected tot he
extracellular matrix. Loss of dystrophin results in cellular injury (myonecrosis). On light microscopy,
variation of muscle fiber size and angulated fibers are seen. Some fibers have centrally located
(internalized) nuclei.
Duchenne muscle dystrophy manifest with proximal muscle weakness and atrophy. True
hypertrophy of the distal muscle is noted early in the disease as distal muscles compensate for
weak proximal ones. Later, muscles fibers of the distal extremities are replaced by fat and
connective tissue (pseudohypertrophy).
Myotonic dystrophy is and AD disorder. It is caused by an increased number of trinucleotide
repeats (CTG) on myotonia-protein kinase gene. Sustained muscle contraction (myotonia), along
with weakness and atrophy, is common. Cataracts are seen in almost all pctes. Frontal balding
and gonadal atrophy are other common features.
Myotomic dystrophy is an AD disorder. It is caused by an increased number of trinucleotide
repeats (CTG) on myotonia-protein kinase gene. Sustained muscle contraction (myotonia), along
with weakness and atrophy, is common. Cataracts are seen in almost all patients. Frontal balding
MYotonic dystrophy is an AD disorder. It is caused by an increased number of trinucleotide
reepeats (CTG) on myotonia-protein kinase gene. Sustained muscle contraction (myotonia), along
with weakness and atrophy, es common. Cataracts are seen in almost all pctes. Frontal balding
Vitamin E deficiency can occur in individuals suffering from fat malabsorption or
abetalipoproteinemia. Deficiency of this fat-soluble vitamin is associated with increased
susceptibility of the neuronal and erythrocyte membranes to oxidative stress.
Vitamin E deficiency can occur in individuals suffering from fat malabsorption or
abetalipoproteinemia. Deficiency of this fat-soluable vitamin is associated with increased
susceptibility of the neuronal and erythrocyte membranes to oxidative stress.
The exact Mx of tolerance of Morphine is unknown but may be involve increased phosphorylation
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of opioid receptors, increased adenylyl cyclase activity, or increased NO levels. Activation of

NMDA(N methyl D aspartato) receptor by glutamate is belived to enhance morphine tolerance by
increasing phosphorylation of opioid receptors and increasing NO oxide levels. NMDA receptor
blockers (ketamine), block actions of glutamate and decrease morphine tolerance.
Pufferfish poissoning is caused by tetrodotoxin, a neurotoxin produced by microorganisms
associated with the fish. Tetrodotoxin binds to voltage-gated sodium channels in nerve and cardiac
tissue, preventing sodium influx and depolarization.
Calcium channel blockers, specifically Nimodipine, can be used to assist in the prevention of
cerebral vascular spasm following SAH. This is an alternative use of calcium channel blockers.
Calcium channel bloquers, specifically Nimodipine can be used to assist in the prevention of
cerebral vascular spasm following SAH. This is an alternative use of calcium channel blockers.
The first generation antihistaminics. chlorpheniramine and diphenhydramine, have antimuscarinic,
anti-alpha adrenergic, and anti-serotoninergic properties that are responsable for the majority of
side effects.
Buspirone is a selective agonist of the 5HT 1A receptor and is a sfe effective tto for generalized
anxiety disorder. It has no muscle relaxant or anticonvulsivant properties. Buspirone has a minimal
to no hypnotic, sedative or euforic effects.
Primidone is metabolized to phenobarbital and phenylethylmalonamide (PEMA). All three
compounds are active anticonvulsants.
Primidone is an atiepileptic that is metabolized to phenobarbital and phenylethylmalonamide
(PEMA), also active anticonvulsivants. Primidone has its own antiseizure effects but less often
causes lethargy.
Selegiline is an inhibitor of MAO, type B and can prevent MPTP-induced damage of dopaminergic
neurons. Selegiline is used clinically to delay the progression of Parkinson Ds Combined for better
results with: selegiline, anticholinergics, amantadine. If there is not response then add
levodopa/carbidopa
- Vitamine B6 increases the peripheral metabolism of levodopa, wich decreases its
effectiveness.The more peripheral conversion of levodopa there is, the less levodopa enters the
central nervous system. - Cimetidine cause gynecomastia, inh cytochrome P450 and Incresed
levels of warfarin, phenytoin, propranolol, metoprolol, quinidine and theophylline.
Most over the counter vitamins B6. Vitamin B6 supplementation should not be taken by those on
levodopa therapy, however, because B6 increases the peripheral metabolism of levodopa and
decreases its effectiveness. The more peripheral conversion of levodopa there is, the less
levodopa enters the central nervous system.
Antimuscarinic agents are ussually preferred in pctes with medication induced Parkinsonism.
Levodopa is contraindicated for drug induced Parkinsonism because it can precipitte psycosis.
Levodopa cannot be used to treat drug induced Parkinsonism because it can precipitate psycosis.
Dopamine agonists cannot be used to either as they can exacerbate underlaying psicosis and can
reduce the effects of antipsycotic medication. So best tto are the anticholinergics such as
trihexyphenidyl and benzotropine.
buaaaaaaaa
Adding carbidopa can reduce most of the peripheral side effects of levodopa. However, behavioral
changes from levodopa can actually worsen with addition of carbidopa because more dopamine
becomes available to the brain.
Both DOPA decarboxylase and catechol-O-methyltransferase (COMT) blockers increase levodopa
availability to the brain. Entacapone and tolcapone are the currently available COMT inhibitors.
Benzodiazepines can cause daytime drowsiness (a "hangover") and can increase the risk of falls
in elderly. The severity of this side effects depends on the half life of the drug. Long acting
benzodiazepines cause more severe dorwsiness than short acting ones. On the other hand, long
acting bezodiazepines are far less likely to cause dependence (less addicting).
Benzodiazepines (lorazepam) are first agents in the management of status epilepticus. Phenytoin
(or fosphenytoin) is administered simultaneously to rpevent the recurrence of seizures. Phenytoin
inhibits neuronal high frequency firing by reducing the ability of sodium (Na) channels to recover
from inactivation.
- Tiagabine: inhibitor of GABA uptake. - Topiramate: Blocks Na channels and enhances the effect
of GABA. - Vigabatrin: inhibits GABA transaminase and increases GABA concentration.
Gabapentin: increases brain GABA concentration.
mmm
- Phenytoin, carbamazepine and valproic acid inhibits neuronal high frequency firing by reducing
the ability of Na channels to recover from inactivation. - Ethosuximide is belived to block T type
calcium channels in thalamis neurons causing hyperpolarization and is approved for the tto of
abscence seizures.
Tto for akatisia is decreasing the dose of the neuroleptic or adding antiparkinsonian agents.
Risperidone is the atypical antipsycotic least likely to cause EPS, while clozapine is the typical
antipsycotic least likely to cause EPS. Therefore, tardive diskinesia is best managed by
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decreasing the dose or discontinuing the offending antipsycotic and replacing it with clozapine.
Because clozapine is associated with agranulocytosis, it is typically considered to be a medication
of last resort.
- High potency antipsycotics: (Haloperidol, fluphenazine, pimozide) cause most likely
extrapyramidal symptoms and NOT anticholinergic and antihistamine side effects. - Low potency
agents: (chlorpromazine, thioridazine) most likely to cause anticholinergic and antihistamine
effects. - Second generation of antipsycotis, atypicals (clozapine, risperidone, olanzapine) improve
both positive and negtive symptoms of squizophrenia.
Traditional high potency agents are more likely to cause extrapyramidal symptoms and less likely
to cause anticholinergic and antihistamine side effects, while low potency antipsycotics are more
likely to cause anticholinergic and antihistamine side effects.
Clozapine acts on D4 receptors. Due to the risk of life-threatening agranulocytosis with clozapine,
the FDA requires periodic monitoring of the white blood cell count (WBC) for the duration of
treatment. The other important side effects of clozapine is seizure.
- Thioridazine: causes retinal deposits that resemble retinitis opigmentosa. - Chlorpromazine:
associated with corneal deposits.
Thioridazine causes retinal deposits that resemble retinitis pigmentosa. Chlorpromazine is
associated with Corneal deposits.
Imipramine is a TCA. Antidepressants when used in the depressice phase of bipolar disorder, are
like to cause a rapid switch to mania.Other drugs listed are mood stabilizers or related drugs.
Antidepressants, when used in the depressive phase of bipolar disorder without an antipsycotic or
mood stabilizer, can precipitate a mania.
Lead to Incresed proximal tubular absorption of sodium: - Renal injury - Drugs (NSAID, thiazide
diuretics, ACE inhibitors)
Lithium side effects: Lithium used in pregnancy is associated with fetal cardiac malformation,
especially Ebstein's anomaly of the tricuspid valce. Also in a normal person Lithium can cause
hypothyroidism and nephrogenic diabetis insipidus and can accumulate in patients with renal
inssuficiency. Serum thyroid stimulating hormone levels, lithium levels, and renal function (blood
urea nitrogen and creatinine) should be measured routinely.
MAO inhibitors are particularly useful in pctes with atypical depression and treatment-resistant
depresion. The remain characteristic of atypical depression distinguishes it from major depression
is mood reactivity.
The most common causes of death in pctes with TCA overdose are refractory hypotension and
cardiac arrythmias. Inhibition of fast sodium channels in cardiac myocytes (and His-Purkinje
system) is thought to be the major underlying cellular event. Fluid resuscitation with normal saline
and hypertonic sodium bicarbonate administration are crucial in these pctes.
cardiac arrhythmias. Inhibition of fast sodium channels in cardiac myocytes (and His-Punkinje
and hypertonic sodium bicarbonate are crucial in these pctes.
cardiac arrythmias. Inhibition of fast sodium channels in cardiac myocytes (and His-Purkinje
hypertonic sodium bicarbonate administration are crucial in these pctes.
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TCAs such as imipramine, doxepin, amitriptyline, and clomipramine have stronger anticholinergic
properties than heterocyclics or SSRIs and should be used with caution in pctes with benign
prostatic hyperplasia (BPH), as they may cause urinary retention.
Sertraline is a serotonin-specific reuptake inhibitor (SSRIs) that has a better side effect compared
to tricyclic antidepressants (TCAs). Sexual dysfunction is a relatively common side effect of the
SSRIs and limits their use for many pctes.
Sertraline is serotonin-specific reuptake inhibitor (CCRIs) that has a better side effect profile
compared to tricyclic antidepressants (TCAs). Sexual dysfunction is a relatively common side
effect of the SSRIs and limits their use for many patients.
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The onset of action of a gas anesthetic depends on its solubility in the blood (blood/gas partition
coeficient). Drugs with high blood/gas partition coeficients are more soluable in the blood,
demostrate slower equilibration with the brain, and have longer onset times.
Dopamine agonists have a chemical structural similar to the neurotransmitter dopamine and
directly stimulate dopamine receptors. There are two classes of dopamine agonists: 1. Ergot
compounds-bromocriptine and pergolide. 2. Nonergot compounds-pramipexole and ropinerole.
Medications that may cause seizures include bupropion (antidepressant), clozapine (antipsycotic
at high doses), isoniazid (anti-tuberculosis drug, if given without pyridoxine), ciprofloxacin
(antibiotic), and imipenem (antibiotic).
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Tricyclic nti-depressants (TCAs) can have quinidine-like effect on the cardiac conduction system,
potentially causing QRS and QT prolongation and cardiac dysrhythmias. These effects are due to
inhibition of fast sodium channels. In instances of cardiovascular toxicity due to TCA overdose, the
most effective intervension is hypertonic sodium bicarbonate (NaHCO3). NaHCO3 can correct
QRS prolongation, reverse hypotension, and treat ventricular dysrhythmias.
Tricyclic anti depressants can have quinidine like effect on the cardiac conduction system,
potentially causing QRS and QT prolongation and cardiac dysrrhythmias. These effects are due to
inhibition of fast sodium channels. In instances of cardiovascular toxicity due to TCA overdose, the
most effective intervention is hypertonic bicabonate (NaHCO3). NaHCO3 can correct QRS
prolongation, reverse hypotension, and treat ventricular dysrhythmias.
buaaaaaaaa
Co administration of an SSRI and MAO inhibitor can produce excessive serotonin levels
secondary to decreased reuptake and decreased metabolism. Excessive serotonin levels can lead
to the development of a potentially fatal condition known as serotonin syndrome. To avoid the risk
for serotonin syndrome, it is recommended to wait at least 14 days after MAO inhibitor
discontinuation before initiating SSRI therapy. This should allow sufficient time for regeneration of
MAO.
Co administration of an SSRI and MAO inhibitor can produce excessive serotonin levels
secondary to decresed reuptake and decreased metabolism. Excessive serotonin levels can lead
to the development of a potentially fatal condition known as serotonin sindrome. To avoid the risk
for serotonin syndrome, it is recommended to wait at least 14 days after MAO inhibitor
discontinuation before initiating SSRI therapy. This should allow sufficient time for regeneration of
MAO.
Pentazocine is an opioid narcotic specifically designed to produce analgesic effects with little to no
abuse potential. Pharmacologically, it works through partial agonist activity and weak antagonist
activity at mu receptors. Because of its weak antagonistic effects, it can cause withdrawal
symptoms in patients who are dependent or tolerant to morphine or other opioids.
The minimal alveolar concentration (MAC) is measure of potency of an inhaled anesthetic. It is the
concentration of the anethetic in the alveoli that renders 50% of pctes unresponsive to painful
stimuli (ED 50). Potency is inversely proportional to the MAC: the lower the MAC, the more potent
the anethetic.
Thiopental is a short-acting barbiturate used for induction of anesthesia. After equilibration with the
brain it rapidly redistributes into skeletal muscles and adipose tissue, which results in rapid
recovery from anethesia.
Thiopental -IV anestetic barbiturate, highly lipid soluble -GABA receptor (increase inhibitory effect)
-Equilibrates 1 min after adm and causes loss of consciousness. - Acumulation is in the brain
followed by rapid redistribution into skeletal muscles and adipose tj(5-10 min of adm).
Massive hepatic necrosis is a rare but severe complication of halothane exposure. It occurs due to
direct liver injury by halothane metabolites and formation of autoantibodies against liver proteins.
Light microscopy shows massive centrilobular hepatic necrosis.
Almost all volatile anesthesics increase cerebral blood flow. It is an undesirable effect as it results
in increased ICP. Other important effects of inhalation anesthetics are myocardial depression,
hypotension, respiratory depression and decreased renal function.
Malignant Hyperthermia occurs after administration of inhalation anesthetics and/or
succinylcholine to genetically succeptible individuals. It is treated with dantrolene that blocks
ryanodine recceptors and prevents release of Ca into the cytoplasm os skeletal muscle fibers.
Malignant hyperthermia occurs after administration of inhalation anesthetics and/or
succinylcholine to genetically susceptible individuals. It is treated with dantrolene that blocks
ryanodine receptors and prevents release of Ca into the cytoplasm of skeletal muscle fibers.
Thiopental has a rapid plasma decay becauseof the redistribution of the drug to other tissues
throught the body.
GABA A and GABA C receptors are ion channels, while the GABA B receptor is linked to a G
protein. Benzodiazepines, barbituirates, and alcohol all bind to different components of the GABA
A receptor and facilitates the inhibitory action of GABA in the central nervous system.
Lithium, valproic acid, and carbamazepine are mood stabilizing agents. Valproic acid and
carbamazepine also work as anticonvulsants. Valproic acid increases the inhibitory effect of GABA
in the CNS.
Phenytoin: Inhibits the voltage gated Na channels in neurons. Increased the expresion of plateletderived grow factor (PDGF) so when the macrophages are exposed to them ... they produce
gingival hyperplasia. Megaloblastic anemia, Induces the P450 cytocrome oxidase system.
Acute neonatal narcotic withdrawal presents with symptoms of pupillary dilation, rhinorrhea,
sneezing, nasal stuffiness, diarrhea, nausea, and vomiting. Chills, remors, and jittery movements
occur commonly as well, and can rarely lead to seizures. Opium solution given as diluted tincture
of opium is the treatment of choice and can be given orally. The dose is initially titrated to the
patient's symptoms and eventually tapered off.
Study the Opioid receptors
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Exacerbation of myastemia gravis is a pcte treated with cholinesterase inhibitors occurs due to
myasthemic or cholinergic crisis. The edrophonium (Tensilon) test helps to differentiate these two
conditions. Clinical or cholinergic crisis. The edrophonium administration indicates that the pcte is
un dertto (myasthenic crisis).
Myastemia gravis is treated with: cholinesterase inhibitors such as physostigmine, neostigmine
and pyridostigmine.
Atropine is indicated for the tto of bradycardia as it decreases vagal influence on the SA and AV
nodes. A common side effect if increased intraocular pressure. It may precipitate acute-angle
glaucoma in susceptible individuals.
Organophosphates stimulate both mscarinic and nicotinic cholinergic receptors. Atropine reverses
muscarinic effects but does not prevent the development of nicotinic effects such as muscle
paralysis. Pralidoxine is the only medication that reverses both muscarinic and nicotinic effects of
organophosphates by restoring cholinesterase from its bond with these substances.
- Alpha receptors: inhibits insulin secretion. - Beta receptors: stimulate insulin receptors. Phenoxybenzamine: long acting alpha blocker (tto for pheochromocytoma).
Alpha receptors inhibit insulin secretion and beta receptors stimulate insulin secretion.
Pretreatment with an alpha blocker would result in predominance of beta effects.
Alpha receptors inhibit insulin secretion and beta receptors stimulate insulin secretion.
Pretreatment with an alpha blocker would result in predominance of beta effects.
buaaa
1. The adrenal glands are directly innervated by preganglionic neurons using acetylcholine. 2.
Sweat glands are innervated by a two neuron efferent system where bot neurons use
acetylcholine.
The autonomic nervous system utilizes three types of signal pathways: cAMP, IP 3, and ion
channels. Nicotinic receptors are ligand gated ion channels that open after binding acetylcholine.
This results in an immediate influx of Na and Ca into the cell and an outflux of K from the cell.
Cholinergic agonists bind to muscarinic receptors on endothelial cells and promote release of NO
(also called Endothelium-derived relaxing factor). NO activates guanylate cyclase and diminishes
endothelium calcium concentration. This produces vasodilation.
Glaucoma, a disease due to increased intraocular pressure, develops due to decreased outflow or
increased production of aqueous humor. Timolol and other beta blockers decrease aqueous
humor production by the ciliary epithelium.
Ampicillin is the treatment of choice for Listeria. It is not sensitive to cephalosporins. Listeria
causes disease in neonates and immunocompromised adults
Memorize the CYP 450 inducers and inhibitors. Phenobarbital and other barbiturates can induce
hepatic microsomal enzymes, causing increased metabolism and clearance of warfarin.
Barbituirates may also increase hepatic synthesis of clotting factors.
Anticholinergic poisoning, botulism, and organophosphate toxicity effect nicotinic and muscarinic
acetylcholine receptors differently, and thus produce different symptomatologies. Muscarinic
antagonists inhibit the postsynaptic action of acetylcholine, botulinum neurotoxin blocks the
presynaptic exocytosis of acetylcholine vesicles and organophosphates prevent degradation of
acetylcholine within the synaptic cleft. Botulinic toxin is heat-labile, so heating food prior to eat.
Beta adrenergic receptor blockade reduces blood pressure and cardiac work, which is beneficial in
the acute tto of myocardial ischemia. However, when noncardioselective agents are used, adverse
effect like bronchoconstriction (dose-dependent)may be seen.
Serotonin syndrome is characterized by confusion, agitation, tremor, tachycardia, hypertension,
clonus, hyperreflexia, hyperthermia, and diaphoresis. Any drugs that increase serotonin levels,
including combinations of SSRIs and MAO and high doses of SSRIs, can precipitate this
syndrome. Tryptophan is a precursor for serotonin.
Serotonin syndrome is characterized by confusion, agitation, tremor, tachycardia, hypertension,
clonus, hyperreflexia, hyperthermia, and diaphoresis. Any drugs that increase serotonin levels,
including combinations of SSRIs and MAO inhibitors and high doses of SSRIs, can precipitate this
syndrome. Tryptophan is a precurson for serotonin.
Cyproheptadine is an antihistamine with anti-serotonergic properties that can be caused in the tto
of the serotonin syndrome.
Cyproheptadine is an antihistamine with anti-serotonergic properties that can be caused in the tto
of the serotonin syndrome.
transeptidase se ha unido con cefalosporins
Penicillins and cephalosporins function by irreversibly binding to penicillin-binding proteins such as
transpeptidases.
A change in the structure of penicillin-binding proteins that prevents cephalosporin binding is one
mechanism of bacterial resistence to cephalosporins.
The etiology of narcolepsy is belived to be due to low levels of the stimulatory neurotransmitter
orexin (hypocretin), which is involved in maintaining wakefulness and suppressing REM sleeprelated phenomena. -Modafinil is a non amphetamine stimulant, has become the first line agent
because it is effective, well tolerated and drug abuse is rare.
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Tto for narcolepsy includes shcedule daytime naps and psycostimulants (modafinil-non
amphetamine that engance dopaminergic signaling); others can be amphetamines (RAM: HTN,
arrythmia, psycosis), for daytime sleepiness. Narcolepsy is belived to be due to low levels of the
stimulating NT orexin (hypocretin), which is involved in maintaining wakefulness and suppressing
the REM sleep related phenomena.
Migrane headaches are unilateral, ave a pulsating or throbbing quality, and are associated with
photophobia, phonophobia, and nausea. Triptans are serotonin 5-HT 1B/ 5-HT 1D agonists used
as abortive therapy during an acute migraine. Beta-blockers, antidepressants (amitriptyline and
venlafaxine), and anticonvulsivants (valproate and topiramate) are commonly used for migrane
prophylaxis.
Beta-endorphin is one endogenous opioid that is derived from proopiomelanocortin (POMC).
POMC is a polypeptide precursor that goes though enzymatic cleavage and modification to
produce not only beta endorphins, but also ACTH and MSH. The fact that beta endorphin and
ACTH are derived from the same precursor suggest that there may be close psycological
relationship between the stress axis and the opioid system.
The length constant is a measure of how far along an axon an electrical impulse can propagate. A
low length constant reduces the distance an impulse can travel. Myelination increases the length
constant and decreases the time constant, both of which improve axonal conduction speed.
Demyelination thus impairs stimulus transmission.
Progressively weakening diaphragmatic contractions during maximal voluntary ventilation with
intact phrenic nerve stimulation indicate neeuromuscular junction pathology (Myasthemia gravis)
and/or abnormaly rapid diaphragmatic muscle fatigue (restrictive lung or chest wall disease).
buaa
847
6
Pharmacol
ogy
Neurology
775
Physiology
Neurology
131
8
Physiology
Neurology
165
7
Physiology
Neurology
165
7
200
7
Physiology
Neurology
Physiology
Neurology
857
3
Physiology
Neurology
857
3
Physiology
Neurology
147
7
Biochemistr
y
Oncology
117
6
123
1
172
4
Biostatistics
Oncology
The resting potential of the neuronal membrane is close to the equilibrium potential of potassium
because the resting membrane is most permeable to potassium. Changes in the membrane
potential occur in response to changes in neuronal membrane permeability to various cellular ions.
The more permeable the membrane becomes to a cellular ion, the more that ion's equilibrium
potential contributes to the total membrane potential.
Suprachiasmatic nucleus regulates circadian rhythm. It processes light information received from
the retina and relays it to other hypothalamic nuclei and the pineal gland to modulate body
temperature and the production of hormones such as cortisol and melatonin. Melatonin
supplementation is recommended for the tto of insomnia associated with jet lag.
Hypothalamic nuclei - Ventromedial: Mediates satiety; destruction leads to hyperphagia.
Stimulated by leptin. -Lateral: Mediates hunger; destruction leads to anorexia. Inhibited by leptin.
-Anterior: Mediates heat dissipation via parasympathetics; destruction leads to hyperthermia.
-Posterior: Mediates heat conservation via sympathetics; destruction leads to hypothermia.
-Arcuate: Secretion of dopamine (inhibits prolactin), growth hormone-releasing hormone &
gonadotropin.
After UV damage, pyrimidine dimers are formed in cellular DNA, which are recognized by specific
endonuclease which initiates the process of repair by nicking the strand at the thymine dimer. This
action signals the removal and replacement of this damaged DNA.
Relative Risk reduction(RRR)
Biostatistics
Oncology
number needed to harm
Microbiolog
y
Oncology
423
Pathology
Oncology
578
Pathology
Oncology
650
Pathology
Oncology
103
9
Pathology
Oncology
108
3
Pathology
Oncology
108
5
Pathology
Oncology
HIV positive patients often experience reactivation of latent EBV infections with a resulting
increased incidence of EBV-induced lymphoproliferative disorders, including the aggressive nonHodgkin's diffuse B-cell.
Prognosis of colorectal adenocarcinoma is directly related to the STAGE of the tumor (not to
grade!!!).
Oral contraceptives reduce the risk of non-hereditary ovarian and endometrial cancer. Multiparity
and breast-feeding also decrease the risk of ovarian cancer.
Small cell carcinoma of the lung is the most aggressive lung neoplasm. This tumor is thought to
have a neuroendocrine origin. Tumor cells express neuroendocrine markers (neuron specific
enolase, chromogranin, and synaptophysin) and contain neurosecretory granules in the
cytoplasm. Some small cell carcinomaas express neurofilaments.
TNF-alpha was shown to induce a wasting syndrome (cachexia) in experimental animals. It is
thought to mediate paraneoplastic cachexia in humans by suppressing appetite, inhibiting
lipoprotein lipase and increasing insulin resistance of peripheral tissues. In bacterial infections,
TNF alpha produces fever along with IL-1, mediates many of the symptoms of septic shock and
causes hepatic release of acute-phase reactants such as C reactive protein and fibrinogen.
Hereditary breast cancer associated with mutation of BRCA-1 and BRCA-2. These are tumor
suppressor genes that function in gene repair and regulation of the cell cycle(responsible for DNA
repair). Mutation of these genes increases the risk of breast and ovarian cancer.
Chronic myelogenous leukemia is a myeloproliferative disorder of adults. Blast crisis can occur
and crries a worse prognosis. Translocation 9;22 with formation of the bcr-abl fusion protein is
characteristic. This fusion protein has tirosine kinase activity that can be pharmacologically
108
6
171
8
Pathology
Oncology
Pathology
Oncology
175
4
Pathology
Oncology
175
5
Pathology
Oncology
176
0
179
7
Pathology
Oncology
Pathology
Oncology
189
0
Pharmacol
ogy
Oncology
189
1
189
2
Pharmacol
ogy
Pharmacol
ogy
Oncology
201
8
Pharmacol
ogy
Oncology
828
1
Pharmacol
ogy
Oncology
844
Anatomy
870
3
Anatomy
Pulmonolo
gy
Pulmonolo
gy
870
3
Anatomy
Pulmonolo
gy
148
8
203
9
203
9
204
3
118
3
123
3
482
Biochemistr
y
Biochemistr
y
Biochemistr
y
Biochemistr
y
Biostatistics
Pulmonolo
gy
Pulmonolo
gy
Pulmonolo
gy
Pulmonolo
gy
Pulmonolo
gy
Pulmonolo
gy
Pulmonolo
gy
183
3
802
Embryology
301
Immunolog
y
Immunolog
y
557
Biostatistics
Embryology
Genetics
Oncology
Pulmonolo
gy
Pulmonolo
gy
Pulmonolo
gy
Pulmonolo
gy
inhibited with Imatinib (Gleevec).

buaaa
Proliferation signals activate CDK4 (cyclin-dependent kinase-4), resulting in hyperphosphorylation
of the Rb protein. Because hyperphosphorylated Rb is inactive, cells are allowed to trnasition
unchecked from the G1 phase to the S phase in the cell cycle.
Benign lymph node enlargement in response to antigenic stimulation is associated with a
polyclonal proliferation of lymphocytes. A monoclonal lymphocytic proliferation is strong evidence
of malignancy.
- c-myc is a nuclear phosphoprotein that fx as a transcription actvator controlling proliferation,
diferentiation, and apoptosis. - Chromosome 18 has bcl-2 gene if we mutated this gene the
apoptosis inhibitor protein Bcl-2 is overexpressed. - Bcr-abl if it is mutated ... it will promote
mitogenesis and incresed tyrosine kinase activity. - cyclin D1 on chromosome 11. The anormality
incresed production of cyclin D1, promoter of G1 to S-phase transition during the cell cycle.
Proto oncogenes (tumor promoters) Anti-oncogenes (tumor supressors)
Pro-carcinogens are metabolized by cytochrome P450 monooxygenase, an enzyme system
present in hepatic microsomes and the endoplasmic reticula of varied other tissues. Cytochrome
P450 monooxygenase metabolizes steroid, alcohol, toxins,and other foreign substances by
rendering them soluble and easier to excrete.
6 mercaptopurine and 6 thioguanine are cytotoxic and inh de novo purine synthesis. Both drugs
are degraded by the liver by xanthine oxidase. So if y you give allopurinol (wich inhibits the
xanthine oxidase) with bot drugs then you will have an increased of toxicity of the 6 mercaptopurol
Cladribine is a purine analog that archives high intracellular concentrations because it is resistant
to degradation by adenosine deaminase. Cladribine is a drug of choice for hairy cell leukemia.
Methotrexate and 5-FU both effectively inhibit thymidylate formation. but the chemotherapeutic
effect of methotrexate is overcome by N5 formyl tetrahydrofolate (folinic acid, leucovorin)
suplementation.
Etoposide and podophylin inhibit topoisomerasa II's ability to seal the strand breaks it induces,
causing chromosomal breaks to accumulate and eventual cell death. The 2 major uses are for
testicular cancer and small cell lung cancer. Podophyllin is used topically to treat genital warts.
Some patients with non-small cell lung carcinoma (NSCLC)harbor a chromosomal rearragement
that creates a fusion gene between EML4 (echinoderm microtubule-associated protein-like 4) and
ALK (anaplastic lymphoma kinase). This results in a constitutive active tyrosine kinase that causes
malignancy.
bua
The internal laryngeal (branch of the superior laryngeal nerve of the vagus) nerve mediates the
affect limb of the cough reflex above the vocal cords. Foreign bodies (chicken or fish bones) can
become lodged in the piriform recess and may cause damage to the nerve, impairing the cough
reflex.
The internal laryngeal nerve mediates the afferent limb of the cough reflex above the vocal cords.
Foreign bodies (ejm chiken or fish bones) can become lodged in the piriform recess and may
cause damage to the nerve, impairing the cough reflex.
Streptomycin inhiits the initiation of proteins by binding to and distorting the structure of the
prokaryotic 30S ribosomal subunit.
The nucleolus is the site of ribosomal subunit maturation and assembly. RNA polymerase I
synthesizes the vast majority of rRNA from within the nucleolus.
The nucleolus is the site of ribosomal subunit maturation and assembly. RNA polymerase I
synthesizes the vast majority of rRNA from within the nucleolus.
buaaa horrible
An outlier is defined as an extreme and unusual observed in a dataset. The mean, standard
deviation, variance, and rance are sensitive to outliers. The mode is more resistannt to outliers.
Memorize the formulas of NPV, PPV, sensitivity, specificity.
Phospholipids, including dipalmitoyl phosphatidylcholine, are a major component of pulmonary
surfactant. The amniotic fluid lecithin (phosphatidilcholine) to sphingomyelin ratio (L/S ratio) is
measured in order to asses fetal lung maturity. The fetal lungs are considered mature when they
are producing adequate surfactant to yield an L/S ratio greater than 2.
The most highly oxygenated blood in the fetus is carried by the umbilical vein, wich empties
directly into the inferior vena cava via the ductus venosus.
buaaa
IFN gamma secreted by T lymphocytes contributes to granuloma formation.
Vhronic Granulomatous Ds is an X linked disoorder resulting in deficiency of NADPH oxidase, the
enzyme responsible for formation of reactive oxygen species in neutrophil phagolososomes.
797
Immunolog
y
Pulmonolo
gy
113
0
Immunolog
y
Pulmonolo
gy
122
0
176
3
Immunolog
y
Immunolog
y
Pulmonolo
gy
Pulmonolo
gy
176
4
199
5
Immunolog
y
Immunolog
y
Pulmonolo
gy
Pulmonolo
gy
212
8
266
Immunolog
y
Microbiolog
y
Pulmonolo
gy
Pulmonolo
gy
731
Microbiolog
y
Pulmonolo
gy
958
Microbiolog
y
Pulmonolo
gy
958
Microbiolog
y
Pulmonolo
gy
960
Microbiolog
y
Pulmonolo
gy
962
Microbiolog
y
Pulmonolo
gy
963
Microbiolog
y
Pulmonolo
gy
965
Microbiolog
y
Pulmonolo
gy
967
Microbiolog
y
Pulmonolo
gy
137
7
Microbiolog
y
Pulmonolo
gy
144
Microbiolog
Pulmonolo
Neutrophils affected by this disorder are unable to kill catalase-producing organisms

(Staphylocossus, Serratia, E.coli,etc) but they remain effective in killing non-catalase-producing
organisms.
-Granuuloma in Sarcoidosis is caused by TH1 type CD4+ helper T cells, particularly IL-2 and
Interferon gamma (IFN gamma). - TH2 type CD4 helper T cells predominantly drive humoral
immune responses. Their products include IL-4, which promotes IgE antibody production by B
cells, and IL-5, which promotes the production and activation of eosinophils and B-cell synthesis of
IgA.
Selective Ig A deficiency predisposes to recurrent sinopulmonary and GI tract infections due to the
absence of secretory Ig A. It is also associated with an anaphylactic response to transfused blood
products due to an immune response against transfused IgA which the patient's body recognizes
as foreign.
TBC Macropharges that form the Langerhans cells are activated by CD4+ Th1 lynphocytes
Primary agammaglobulinemia: X linked agammaglobulinemia is a B-cell immunodeficiency
disorder in wich Bruton tyrosine kinase funtion is necesary for the proper maturation of B-cells
(CD19, CD20, CD21)
The Haemophilus influenzae type b (Hib) vaccine contains capsular polsaccharide conjugated with
diphteria toxoid.
SCID is a disorder marked by combined T and B cell dysfunction. Some important features
include: frequent fungal, viral, and bacterial infections early in life; marked
hypogammaglobulinemia; thymic hypoplasia; persistent diarrhea; failure to thrive; severe
lymphopenia; and lack of clinically apparent involvement of any other organ systems.
Omalizumab is an effective and acceptable add-on therapy for pctes with severe allergic asthma.
It has been shown to be effective in reducing dependency on both oral and inhaled steroids.
Histoplasma capsulatum is a dimorphic fungus located intracellularly within macrophages. It
affects the lungs and reticuloendothelial system. It is present in bird and bat droppings, and is
endemic to the Mississippi and Ohio River basins. Because the fungus targets histiocytes and the
reticuloendothelial system, it may cause lynphadenopathy and hepatosplenomegaly.
S. pneumoniae are Gram-positive, alpha-hemolytic, optochin-sensitive, bile sensitive diplococci. S.
viridans is also palpha-hemolytic, but it is optochin-resistant. S. pyogenes ((Group A strep)
appears as Gram-positive cocci in chains and can be identified by its susceeptibility to bacitracin.
Ifection with Mycoplasma pneumoniae can result in the formation of cold agglutinins. Other
illnesses resulting in cold agglutinin formation include EBV infection and hematologic malignancy.
Cold agglutinins are antibodies specific for red blood cells that only cause agglutination, or
clumping, of red blood cells at low temperatures.
Infection with Mycoplasma pneumonia can result in the formation of cold agglutinins. Other
illnesses resulting in cold agglutinin formation include EBV infection and hematologic malignancy.
Cold agglutinins are antibodies specific for red blood cella that only cause agglutination, or
clumping, of red blood cells at low temperatures.
Legionella pneumophila causes Legionnaire's disease that is propensit to affect smokers and is
characterized by very high fever, diarrhea, headache, and confusio. Laboratory studies frequently
show hyponatremi. L. pneumophilia is a gram negative rod that is not often detected in Gram
stain.
The H influenzae type b (Hib) vaccine is composed of polyribosyl-ribitol-phosphate (PRP), a
component of the Hib capsule, CONJUGATE WITH DIPHTERIA OR TETANUS TOXOID. immune
activation with antibody production and memory B lymphocyte induction against PRP provides
lasting immunity against Hib in children as young as 2 months old. Epiglottitis is almost exclusively
caused by H influenzae type b.
H. influenza is a "blood loving" organism. Part of the laboratory identification process of H.
influenza is demostration of the requirement X (hematin) and V (NAD) factors for growth. This can
be accomplished by growing H. influenza in the presence of S. aureus and demostrating the
"satellite phenomenon" where H. influenza grow only near the beta-hemolytic S. aureus colonies
because they produce the needed X and V factors.
The Hib vaccine consists of PRP capsular polysaccaride conjugated with either tetanus or
diphtheria toxoid. Protein conjugation causes a T-cell mediated immune response leading to
immunoglobulin class switching and generation of memory B-lymphocytes. This response would
not occur with pure polysaccharide immunization.
Rapidly progressing fever, severe sore throat, drooling and progressive airway obstruction
potencially accompanied by stridor are the presenting symptoms of acute epiglottitis. This illness is
most commonly caused by H. influenzae type b, but the Bib vaccine has dropped the incidence of
this disease considerably. H. influenza type b can still cause disease in unimminized or improperly
immunized pctes as well as fully immunized pctes in some cases.
Ether and other organic solvents can inactivate the "enveloped" viruses, which by definition have
an outer lipid bilayer coat acquired from the host cell plasma or nuclear membranes. The solventinduced disruption or dissolution of the envelope lipid results in a loss of viral infectivity. Nonenveloped viruses are generally resistant to the action of the ether.
Chronic granulomatous disease (CGD)results from a genetic defect in NADPH oxidase(who
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participates in the killing of microbes within neutrophil phagolysosomes). Pctes with CGD develop
recurrent pulmonary, cutaneous, lymphatic, and hepatic infections, with a tendency toward
granuloma formation, usually beginning in childhood. These infections are predominantly caused
by: Staphylococcus aureus, Pseudomona cepacia (Burkholderia cepacia), Serratia
marcenscens,Nocadia, Aspergillus
HIV Treatment - Pregnancy: Nucleoside Analogos (Zidovudine-ZDV, AZT; a Retroviral reverse
transcriptase inhibitor. All of them reduce 2/3 perinatal transmission. - During labor: ZDV(ev) Infant for 6 weeks post partum: ZDV
All organisms in the Mycoplasma genus, including Ureaplasma, lack peptidoglycan cell walls and
are therefore resistant to agents thhat attack the peptidoglycan cell wall such as penicillinsm
cephalosporins, carbapenems and vancomycin, Mycoplasma infections can be treated with antiribosomal agents like tetracycline and erythromycin.
Tissure damage and resultant abscess formation primarily caused by lysosomal enzyme release
from neutrophils and macrophages.
Thickened bronchial walls, neutrophil infiltration, mucous gland enlargement, and patchy
squamous metaplasia of the brnchial mucosa are features of chronic bronchitis. Cigarette smoking
is the leading cause of chronic bronchitis.
Elevations of the Reid index above the normal value of 40% correlate well with the duration and
severity of chronic bronchitis.
- Hyperacute Rx(within minutes): Preformed antibodies against ABO or human leukocytes
antigens(HLA).Graft blood vessels spasm and DIC. - Acute Rx(1-2 weeks): It represents the
recipient Rx to HLA of the graft. Cell mediated immune response and CD8 T cells play a central
role. - Chronic Rx(month or years): Inflamation of the small bronchioles. Bronchiolotis obliterans.
Small cell carcinoma is strongly associated with smoking and ussually is centrally located. This
tumor arises from the primitive cells of the basal layer of the bronchial epithelium.
Immunihistochemical stains are frequently positive fro neuroendocrine markers, such as neuron
specific enolase, chromogramin and synaptophysin.
Malignant mesothelioma is a rare neoplasm that arises from the pleura or peritoneum. It is
strongly associated with asbestosis exposure. Hemorrhagic pleural effusions and pleural
thickening are characteristic. Electron microscopy is the gold standard for diagnosis, revealing
tumor cells with numerous, long, slender microvilli and abundant tonofilaments.
Insidious-onset progressive exertional dyspnea, pulmonary function tests showing profile, and
surgical biopsy showing extensive interstitial fibrosis together with paraseptal and subpleural
cystic airspace enlargement (honeybomb lung) are characteristic of idiopathic pulmonary fibrosis.
The incidental chest x-ray finding of fibrocalcific parietal pleural plaques in the posterolateral midlung zones and over the diaphragm are highly suggestive of asbestosis.Small pleural effusions
which are exudative and possibly blood stained may occasionally be noted.
Cystic fibrosis is a common cause of congenital bilateral absence of the vas deferens, resulting in
azoospermia. A diagnosis of CF can be made based on this urogenital anomaly with an abnormal
sweat chloride test or an abnormal nasal transepithelial potential difference.
Pulmonary hypertension develops in pctes with scleroderma as a result of damage to the
pulmonary arterioles. It manifests with an accentuated pulmonary component of the second heart
sound and signs of right-sided heart failure.
Patients with sarcoidosis or other granulomatous diseases are prone to developing hypercalcemia
secondary to high levels of active Vitamin D (calcitriol).
Pulmonary tuberculosis is a disease passed from person to person through the transmission of
aerosolized respiratory secretions that contain Mycobacterium tuberculosis organisms. The
smaaller droplets deposit organisms in the alveoli of lower lung fields. These organisms are
engulfed by alveolar macrophages that allow for intracellular bacterial proliferation.
Secondary reactivation tuberculosis occurs in patients who have been preciously infected with
tuberculosis. Primary tuberculosis causes the formation of Ghon foci in the lower lung fields.
Reactivation tuberculosos occurs in immunosuppressed patients, and is characterized by apical
cavitary lesions and hemoptisis.
Primary infection by M. tuberculosis occur after inhaling the organism in the aerosolized
respiratory secretions of an infected person. Initial M. tuberculosis infection is characterized by a
Ghon complex, which consists of a lowe lobe lung lesion (Ghon focus) and ipsilateral hilar
adenopathy.
The tissue destruction caused by M. tuberculosis infection is the direct result of host immune
activation and inflammation through a type IV delayed-type hypersensitivity reaction (This
hypersensitivity reaction stems from the TH1 lymphocyte stimulation of both macrophages and
CD8+ cytotoxic T lymphocytes).
The cytokines IL-1, IL-6, and TNF-alpha mediates systemic inflammatory response and stimulate
hepatic secretion of acute-phase proteins (eg, fibrinogen). High levels of circulating fibrinogen
increase the erythrocyte sedimentation rate (ESR), wich is a nonspecific marker of inflamation.
Prolonged, burning substernal pain and ST segment elevation in lead I and V3-V6 is suggestive of
anterolateral ventricle infarction. Common consequences of left ventricle infarction include left
ventricular failure, cardiogenic acute pulmonary edema, pulmonary venous hypertension
(congestion), and transudate of plasma into the lung interstitium and alveoli.
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The green discoloration of pus or sputum noted during bacterial infections is associated with the
release of myeloperoxidase (MPO) from neutrophil azurophilic granules. MPO is a hemecontaining pigmented molecule.
Smoker pcte with decreased breath sounds on the right and his chest x-ray show opacification of
the right hemitorax with deviation of the trachea toward the opacified side. The direction of the
trachea deviation is important because the trachea deviates toward the opacified lung with lung
volume loss (atelectasis) and away from the opacified lung with a large pleural effusion.
- Centriacinar emphysema: the pathogenesis of heavy smoking predominantly involves
intraalveolar release of proteases, especially elastase, from infiltrating neutrophils and from
alveolar macrophages. -Type I pneumocytes: 95% inner epithelial lining of alveoli. Type II: source
of pulmonary surfactant and the main cell type responsable for repair of alveolar epithelium.
In asthma, eosinophils are recruited and activated by IL-5 secreted by Th2 type helper T-cells.
Most common causes of Metabolic Alcalosis: 1. Loss of hydrogen ions from the body: Vomit and
nasogastric succion causes decrease serum chloride(<10mEq/L) which is calles salineresponsice. Tto: isotonic saline. 2. Thiazide and loop diuretics: increase loss of Na, followed by
loss Cl (Reabs of HCO3 for maintain cellular neutrality). Vol [] caused incres aldosterone (reabs
Na and H2O and waste H and K in urine). Urinary Cl is increased. Causing metabolic alkalosis
cloride rpta.
Asthma and alpha-1 antitrypsin deficiency emphysema have: Decresed of FEV1/FVC, Incresed of
TLV, but the Diffusing capacity is decresed in alpha 1 antitrypsin deficiency due to damage of the
alveolo while in asthma it is incresed do to incresed of the lung volumes.
Patients with cystic fibrosis: The cystic fibrosis transmembrane conductance regulator (CFTR)
protein is mutated in patients with cystic fibrosis. In normal indivicuals, the CFTR protein serves as
a chloride channel that regulates the flow of sodium, chloride and water across the epithelial
membranes of the airways, biliary tree, intestines, vas deferens, sweat ducts, and pacreatitis
ducts.
Cheyne-Stokes respiration is commonly seen in cardiac disease (advance congestive heart
failure) and neurologic Ds (stroke, brain tumors, traumatic injury). It frequently is a poor prognostic
sign in individuals with either neurological or cardiac disease.
Cheyne stokes respiration it is commonly seen in advanced congestive heart failure.
Corticosteroids have the strongest and most predictable effects on the inflammatory component of
asthma.
Study the mechanism of action of asthma drugs.
Seizures are the major cause of morbility and mortality from theophylline intoxication.
Tachyarrhythmias are the other major concern.
The main group of antifungal drugs are the polyenes, azoles, echinocandins and pyrimidines. The
polyene antifungals (anphoterici B and nystatin) act by binding ergosterol in the fungal cell
membrane
The main groups of antifungal drugs are the polyenes, azoles, echinocandins and pyrimidines.
The polyene antifungals (amphotericin B and nystatin) act by binding ergosterol in the fungal cell
membrane.
Anphotericin B causes: Incresed: BUN, Creatinine (mas aun si se utiliza con Aminoglycosides,
cyclosporine.. por eso no uses estos juntos) Decresed: Mg, K Anemia (supression if renal
erythropoietin)
Azoles inhibit the synthesis of ergosterol by the fungal cytochrome P450 enzymes. They also
supress the human P450 system, resulting in many drug-drug interactions.
Azoles inhibit the synthesis of ergosterol by the fungal cytochrome P450 enzymes. They also
suppress the human P450, reuslting in many drug-drug interactions.
Mycobacteria resistance to isoniazid can be accomplished through non-expression of the
catalase-peroxidase enzyme or through genetic modification of the isoniazid binding site on the
mycolic acid synthesis enzyme.
Isoniazid is chemically related to pyridoxine, also known as Vitamin B6. It inhibits mycolic acid
synthesis in mycobacterial cells and is specific to the mycobacteria. Mycolic acid is a ling
branches chain saturated fatty acid used in the mycobacterial cell wall and in the formation of the
virulence factors.
Isoniazid is chemically related to pyridoxine, also know as Vitamin B6. It inhibits mycolic acid
synthesis in mycobacterial cells and is specific to the mycobacteria. Mycolic acid is a long
branched chain saturated fatty acid used in the mycobacterial cell wall in the formation of virulence
fcts.
Resistance of Mycobacterium tuberculosis are due to: - Decrease in bacterial expression of the
catalase-peroxidase enzyme that is required for isoniazid activation once the drug enters the
bacterial cell. - Modification of the protein target binding site for isoniazid.
Rifampin is an antimycobacterial drug that blocks the action of the bacterial DNA-dependent RNA
polymerase, thereby inhibiting transcription. The subsequent absence of mRNA leads to a
deficiency of proteins necessary for bacterial survival. Rifampin resistence is acquired by
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modification of the rifampin binding site on the bacterial DNA-dependent RNA polymerase.
Rifampin is an antimycobacterial drug that blocks the action of the bacterial DNA-dependent RNA
polymerase, thereby inhibiting transcription. The subsequent absence of mRNA leads to a
deficiency of proteins necessary for bacterial survival. Rifampin resistance is acquired by
modification of the rifampin binding site on the bacterial DNA dependent RNA polymerase.
Isoniazid is chemically similar to pyridoxine (Vit B6). Because of this similarity, isoniazid can
complete with Vitamin B6 in the synthesis of multiple neurotransmitters (including GABA), resulting
in defective end products. Isoniazid also increases the urinary excretion of pyridoxine.
-The aminoglycoside streptomycin protein synthesis by inactivating the 30S (small) ribosomal
subunit. -Decreased activity of bacterial catalase-peroxidase is one mechanism of mycobacterial
resistance to isoniazid. -Structural alteration of enzymes involved in RNA synthesis (DNAdependent RNA polymerase) is the mechanism through which organisms become resistant to
rifampin.
Ethambutol is an antimycobacterial agent that inhibits carbohydrate polymerrization, thereby
preventing peptidoglycan cell wall synthesis. One unique adverse effect of ethambutol is optic
neuritis, which typically presents in conjunction with decreased visual acuity, central scotoma and
color blindness.
Mycobacterium avium is a common opportunistic pathogen that causes disseminated disease
(MAC) in HIV+ pctes. Weekly azytromycin is used as a prophylaxis in pctes at risk for MAC (HIV+
pctes w/ CD4 counts less than 50 cells/mL).
Mycobacterium avium is a common opportunistic pathogen that causes disseminated Ds (MAC) in
HIV+ pctes. Weekly azithromycin is used as prophylaxis in pctes at risk for MAC (ejm HIV+ pctes
with CD4 count less than 50 cells/mL).
N-acetylcysteine is a mucolytic agent used in the treatment of CF. N-acetylcysteine works by
cleaving the disulfide bonds within mucus glycoproteins, thus loosening thick sputum.
Varenicline is a partial agonist of nicotinic acetylcholine receptors. It can assist patients with
cessation of tobacco use by reducing withdrawal cravings and attenuating the rewarding effects of
nicotine.
-10-15 microm: upper respiratory tract. -2.5-10 microm: mucociliary transport (Trachea and
bronchi). -<2microm: phargocytized by macrophages (terminal bronchi, alveoli).
Hypercapnea produces cerebral vasodilatation via a decresed in cerebral vascular resistance.
HYpocapnea causes cerebral vasoconstriction and decresed cerebral blood flow.
Cystic fibrosis is a common autosomal recessive disease that usually results from a mutation in
the CFTR gene chromosome 7. The CFTR protein is a transmembrane ATP-gated chloride
channel.
Cystic fibrosis is a common autosomal recessice Ds that ussually results from a mutation in the
CFTR gene on chromosome 7. The CFTR protein is a transmembrane ATP-gated chloride
channel.
Determining the difference between the alveolar and arterial PO2 (A-a gradient) can help
determine the cause of hypoxemia. The arterial PO2 is mesuared with an arterial blood gas
analysis, and the alveolar PO2 is determined using the alveolar gas equation. The A- gradient
normally does not exceed 10-15 mmHg.
The blood flow per minute in systemic and pulmonary circulations in a young military recruit with
high-intensity physical excercise have to be the same.
Restrictive lung diseases are associated with decreased lung volumes, as well as increased
expiratory flow rates at the correzponding lung volumes. The expiratory flow rates are increased
due to decreased lung compliance (increase elastic recoil) and increased radial traction extended
on the conducting airways by the fibrotic lung.
buAA
Pulmonary embolism: Asociated with hypoxemia and respiratory alkalosis.
cheka conceptos
The horseshoe kidney, both kidneys are fused together at the poles in early embryonic life. The
isthmus of horseshoe kidney ussually lies anterior to the aorta and inferior vena cava and
posterior to the inferior mesenteric artery. This centrally located isthmus becomes trapped behind
the inferior mesenteric artery during the relative ascent of the kidney.
Fabry disease is an inherited deficiency of alpha-galactosidase A that causes accumulation of the
globoside ceramide trihexoside in tissues. The earliest manifestation of Fabry disease are
angiokeratomas, hypohidrosis and acroparesthesia. Without enzyme replacement, patients
typically develop progressice renal failure.
Fabry Ds is the inherited deficiency of alpha-galactosidase A that causes accumulation of the
globoside ceramide trihexoside in tissues. The earliest manifestation of Fabry Ds are
angiokeratomas, hypohidrosis and acroparesthesia and acroparesthesia. Without enzyme
replacement, pctes typically develop progressive renal failure.
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Primase is a DNA-dependent RNA polymerase that incorporates short RNA primers into
replicating DNA.
Primase is a DNA dependent RNA polymerase that incorporates short RNA primers into replicati
ng DNA.
- Ureteric bud: collecting system of the kidney (collecting tubules and ducts, major and minor
calyces, renal pelvis, and the ureters). - The metanephric mesoderm (blastema): glomeruli,
Bowman's space, proximal tubules, the loop of Henle, and distal convoluted.
Renal angiomyolipoma is a benign tumor composed of blood vessels, smooth muscle and fat.
Bilateral renal angiomyolipomas are associated with tuberus sclerosis, an autosomal dominant
condition.
Renal angiomyolipoma is a benign tumor composed of blood vessels, smooth muscle, and fat.
Bilateral renal angiomyolipomas are associated with tuberous sclerosis, an autosomal dominant
condition.
Pctes with both sporadic and hereditary (associated with Von Hippel-Lindau disease) renal cell
carcinmas are found to have deletions of the VHL gene on chromosome 3p
Acute cellular rejection of a transplanted organ the tto of active acute rejection is with systemic
corticosteroids in addition to continued use of calcineurin inhibitors.
Hyperacute rejection is a process that is mediated by preformed recipient antibodies against
antigens on the host organ (Type II hypersensitivity). Examples of such mistmaches include ABO
blood group antibodies and anti-HLA antibodies. This form of rejection occurs immediately upon
perfusion of the transplanted organ by recipient blood and is often diagnosed intraoperatively due
to immediate mottling of the organ.
ADPKD is one of the most common inherited disorders in humans. It is the most frequent genetic
cause of renal failure in adults, accounting for 10% of pctes on dialysis in the US. Its mode of
inheritance is Autosimal Dominant.
buaa
Glomerulonefritis post estreptococica has a microscopy that shows deposits of IgG, IgM, and C3
When IgA nephropathy is associated with extra-renal symptoms, it is considered a component of
Henoch-Schonlein disease. - Skin: purpuric lesions on extensor surfaces of arms, legs, and
buttocks. -GI syndrome: abodminal pain, vomiting, intestinal bleeding, and intussusception. Renal involvement: IgA nephropathy.
Painless hematuria 2-3 days following an upper respiratory traact infection is suggestive of IgA
nephropathy (Berger disease). Diagnosis is made via the detection of IgA deposits in the
mesangium of glomeruli on immunofluorescence microscopy. When IgA nephropaty is
accompanied by extrarenal symptoms (e.g. abdominal pain, purpuric skin lesions), the Dx is
Henoch-Schonlein purpura.
ANCA-associated RPGN is also called paauci immune GN due to the absence or scarcity of Ig
and C3 deposits. Patients present with renal failure, pulmonary symptoms (cough, dyspnea,
hemoptisis), and upper respiratory tract symptoms (epistaxis, mucosal ulceration, chronic
sinusitis). Crescents are found on light microscopy.
Poststreptococcal glomerulonephritis -Kids: 95% recovery completly, 1-2% develop chronic
glomerulonephritis and less than 1% progress to RPGN. -Adults: 60% resolve completely, 40%
develop chronic glomerulophritis ir RPGN.
Nephrotic syndrome: loss of anticoagulants factors specially antithrombin III and is responsible for
the thrombotic and thromboembolic complications.
Poststreptococcal glomerulonephritis: represent immune complexes composed of IgG, IgM and
C3.
Granulomatosis with polyangitis (Wegener's) is a cause of rapidly progressive (crescentic)
glomerulonephritis (RPGN)type 3 (pauci-immune). The symptoms of nephritis are accompanied by
signs of upper and lower respiratory tract involvement. Crescents on light microscopy, the absence
of deposits on immunofluorescence, and elevated serum c-ANCA are diagnostic.
Nephrotic Sx is a massive proteinuria (>3.5 gm/day), hypoalbuminemia, generalized edema,
hyperlipidemia, and lipiduria. Depending on the ratio of low-to high-molecular weight proteins in
the edema, hyperlipidemia, and lipiduria. Depending of the ratio of low to high molec weight
proteins in the urine with nephrotic Sx, proteinuria can be either highly or poorly selective. Minimal
change Ds is a highly selective proteinuria: low-molec weight proteins (albumin and tranferrin)
Nephrotic syndrome is characterized by massive proteinuria (>3.5 gm/day), hypoalbuminemia,
generalized edema, hyperlipidemia , and lipiduria. Depending on the ratio of low-to high molecular
weight proteins in the urine with nephrotic syndrome, proteinuria: mostly low-molecular weight
proteins, such as albumin and tranferrin, are excreted.
Diabetic nephropathy starts with glomerular hyperfiltration and lead to an increase in mesangial
matrix and thickening of GBM.Diabetes affects glomeruli and arterioles. The classic morphologic
features of thickening of diabetic nephropathy include nodular glomerulosclerosis (K-W nodules),
dissuse glomerulosclerosis , and hyaline arteriolosclerosis. ACE inhibitors and ARBs can prevent
the progression of diabetic nephropathy.
Ischemic changes in renal papillae - DM - Analgesic nephropathy - Sickle cell anemia
Ethylene glycol ingestion leads to acute renal failure due to the precipitation of calcium oxalate
crystals in renal tubules and subsequent damage to tubular epithelium. Typical clinical findings
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include anion gap metabolic acidosis, increased osmolar gap, and presence pf calcium oxalate
crystals in urine.
Most patients with ATN experience tubular re-epithelization and regain renal function. When ATN
is associated with multi-organ failure, renal function may be permanently impaired (foci of
interstitial scarring can be seen on light microscopy).
Henoch-Schonlein purpura generally affects young children and is classically preceded by an
upper respiratory infection. This IgA mediated hypersensitivity (leukocytoclastic) vasculitis
commonly causes abdominal pain, join pain, lower extremity palpable purpura and hematuria.
Microalbuminuria detection is the preferred method for diagnosing incipient diabetic nephropathy,
the leading cause of end stage renal disease in the United States.
Hysterectomy are specially risky because the ureters course just posterior to the uterine arteries,
which are ligated in this procedure.
Acute rejection of an allograft can be antibody-mediated or cell-mediated. The latter of the two is
asociated with linphocytic infiltration of the renal parenchyma
Anti-CD3 antibodies such as muromonab-CD3 (OKT3) inhibit T-lynphocytes wich is useful in the
treatment of acute rejection in pctes w/ kidney, heart, and liver transplants
Idiopathic membranous nephropathy is associated with circulating IgG4 antibodies to the
phospholipase A2 receptor, which might play role in the development of the Ds.
Idiopathic membranous nephropathy is associated with circulating IgG4 antibodies to the
phospholipase A2 receptor, which might play a role in the development of the disease.
TRnasitional cell carcinoma of the bladder typically presents as gross hematuria in an elderly man.
A history of smoking or occupational exposure to rubber, plastic, aromatic amine-containing dyes,
textilesm or leather increases the risk of developing transitional cell carcinoma.
Lysis of tumor cells due to chemotherapy causes intracellular ions (K, Phosphorous, uric acidmetabolite of tumor nucleic acid)Uric acid is soluble at physiologic pH, but can precipitate in
normally acid enviroment of distal tubules and collecting ducts. The prevention of tumor lysis
syndrome includes urine alkalinization and hydration, as high urine flow and high pH along the
nephron prevents crystallization and precipitation of uric acid.
The renal hypoperfusion characteristic of renal artery stenosis activates the renin-angiotensinaldosterone system. The hypertrophied smooth muscle cells of the afferent and efferent
glomerular arterioles synthesize renin, which increases angiotensin II - mediated vasoconstriction
and aldosterone-mediated sodium and water retention.
Amphotericin B is a polyene antifungal notorious for its renal toxicity. Severe hypokalemia and
hypomagnesemia are commonly seen during therapy, and often require daily supplementation.
Amphotericin B is a polyene antifungal notorious for its renal toxicity. Severe hypokalemia and
hypomagnesemia are commonly seen during therapy, and often require daily supplementation.
Mannitol increased plasma and fluid osmolarity causes extraction of water from the intestinal
space into the vascular space or tubular lumen, with subsequent diuresis. In the brain, water
redistribution from the tissues into the plasma helps reduce edema and intracranial pressure in the
setting of cerebral edema. One of the more severe toxicities of aggressive osmotic diuretics is
pulmonary edema.
Calcineurin is activated and desphosphorylates NFAT (nuclear factor of activated T cells), wich
allows it to enter the nucleus and binds to an interleukin-2 IL-2) promoter. The IL-2 stimulates the
growth and diferrentiation of T cells,a nd is therefore and important component of immune
response. Cyclosporine and tracolimus, two of the more commonly used immunosuppressants in
kidney transplants, inhibit calcineurin activation.
Acyclovir can cause crystalline nephropathy if adequate hydration is not also provided.
Foscarnet is an analog of pyrophosphate that can chelate calcium and promote nephrotoxic renal
magnesium wasting. These toxicities can result in symptomatic hypocalcemia and
hypomagnesemia.
Thiazide diuretics effectively increase calcium reabsorption from the nephron. They are indicated
in patients with nephrolitiasis secondary to hypercalciuria and contraindicated in hypercalcemia.
5 alpha reductase inhibitors (finasteride, dutasteride) catalyze conversion of testosterone to
dihydrotestosterone in the prostate. These drugs reduce prostate volume and work in the fixed
component bladder outlet obstruction.
Loop diuretics inhibit the NKCC2 and stimulate prostaglandin release. Prostaglandins have
vasodilatory effects (increased GFR and enhanced drug delivery). If we give NSAID drugs like
ibuprofen we will contrarest the action of the diuretics, we will decreased the diuretic response.
check the variation of GFR, RPF, FF in diferent patologic cases.
The ascending limb of the loop of Henle is impermeable to water regardless of serum vasopressin
levels. Reabsorption of electrolytes by the Na/K/2Cl cotransporter occurs in the thick ascending
limb and contributes to formation of the corticomedullary concentration gradient.
Regardless of the patient's hydration status, the majority of free water reabsorption in the nephron
occurs in the proximal tubule passively with the reabsorption of solutes.
Aldosterone is a component of the renin-angiotensin-aldosterone system that acts on the principal
and intercalated cells of the renal collecting tubules to cause resorption of sodium and water and
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loss of potassium and hydrogen ions.

Acute salicylate intoxication first causes an acute respiratory alkalosis. If high doses are ingested,
this phase is soon followed by superimposed metabolic acidosis due to organic acid accumulation.
There may also be a slight metabolic alkalosis resulting from volume contraction related to
vomiting.
Acute salicylate intoxication first causes an acute respiratory alkalosis. If high doses are ingested,
this phase is soon followed by a superimposed metabolic acidosis due to organic acid
accumulation. There may also be a slight metabolic alkalosis resulting from volume contraction
related to vomiting.
FF = GFR(or creatinine clearance)/ RPF(PAH clearance)
Physiology
Renal
buaa
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Check the tubular filtration substances
Physiology
Renal
Winter's formula (PaCO2=[1.5 x HCO3]+8 =/-2)
Physiology
Renal
estudia las ecuaciones
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Total Filtration Rate of Substance A (Inulin Clearance)(Plasma Concentration of Substance A) Net

Excretion Rate of Substance A (Inulin Clearance)(Plasma Concentration of Substance A)-(Tubular
Reabsorption of Substance A).
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Embryology
Vasopressin prduces a V2 receptor-mediated increase in permeability to water and urea at the

luminal membrane of the inner medullary collecting duct. The increase in urea reabsorption
corresponds to a decrease in the fractional excretion of urea and a decrease in renal clearance of
urea from plasma.
Elevated serum aldosterone levels can manifest with hypertension, hypokalemia, and muscle
weakness. Increased levels of both renin and aldosterone are indicative of secondary
hyperaldosteronism, wich can be caused by renovascular disease, malignant hypertension, and
renin secreting tumors.
buaaa
- Sertoli cells: Produce the Mullerian Inhibiting Factor (MIF) who produce the involution of
paramesonephric ducts. - Leyding cells: testosterone (internal genitalia develop), DHT (male
exteranl genitalia develop).
beta hCG produced by the human conceptus becomes detectable in maternal serum only after the
blastocyst successfully implants. Im plantation generally occurs on day 6 after ovulation. Generally
beta hCG is detectable in the maternal serum about 8 days after ovulation but can take up to 11
days.
A complete mole results from fertilization of an ovum that is devoid of genetic material and
subsequent reduplication of the paternal genetic complement giving a characteristic 46 XX
genotype.
Tretament of gonococcal genital tract infections must always include treatment for Chlamydia as
well; the usual treatment is a third-generation cephalosporin as well as azithromycin or
doxycycline.
Granulosa cell tumors are estrogen-secreting primary ovarian tumors. The hyperestrogenic state
that results can cause endometril hyperplasia and abnormal uterine bleeding. It also predisposes
to endometrial adenocarcinoma.
PCOS is clinically characterized by obesity, hyperandrogenism, oligomenorrhea, infertility, and
enlarged ovaries with multiple cysts. They have persistently elevated estrogen, androgen, and
luteinizing hormone (LH) levels, resulting in hyperandrogenism, chronic anovulation,
oligomenorrhea and multiple ovarian cysts.
Patients with policystic ovarian syndrome (PCOS) who desire fertility are treated with clomiphene,
which is an estrogen receptor modulator that decreases negative feedback inhibition on the
hypothalamus by circulating estrogen and thereby increases gonadotropin production.

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addition to inhibition of platelet aggregation, cilostazol is also a direct arterial vasodilator.

patients with bradycardia.

pheochromocytomas, mucosal neuromas, and marfanoid habitus. Pheochromocytomas should be

including Hashimoto thyroiditis, Graves disease, and Addison disease (hypoadrenocorticism).

Pyridoxal phosphate is a necessary cofactor in the synthesis of delta-aminolevulinic acid (which is

Ig A protease is produced by N.meningitidis and N. gonorrhoeae. This enzyme claves secretory

assay or evaluation of the urinary riboflavin excretion.

from Hb (Bohr effect).

I do not understand the concept of these

poststreptococcal glomerulonephritis, hypersensitivity pneumonitis, and possibly Churg-Strauss

estrogen means a lower bone mass.

Coordination of voluntary movements. Parkinsonism is the disease asoc. -Tuberoinfundibular:

Troclear nerve palsi is characterized by vertical diplopia.

deficiency causes defective regeneration of BH4, and is an uncommon cause of

headaches, growth failure, and bitemporal hemianopia..

characterized by recurrent episodes of demyelination and subsequent partial remyelination. There

of opioid receptors, increased adenylyl cyclase activity, or increased NO levels. Activation of

number needed to harm

inhibited with Imatinib (Gleevec).

Neutrophils affected by this disorder are unable to kill catalase-producing organisms

loss of potassium and hydrogen ions.

Check the tubular filtration substances

Winter's formula (PaCO2=[1.5 x HCO3]+8 =/-2)

estudia las ecuaciones

Total Filtration Rate of Substance A (Inulin Clearance)(Plasma Concentration of Substance A) Net

Vasopressin prduces a V2 receptor-mediated increase in permeability to water and urea at the

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