Neuroblastoma: Opsoclonus-myoclonus 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
Dystonia: is a syndrome of prolonged repetitive muscle contractions. This condition may be the result
of impaired function of the basal ganglia. Cervical dystonia (spasmodic torticollis), blepharospasm, and
writers cramp are the most common types of focal dystonia.
P 53 gene: High levels of dietary aflatoxin exposure is associated with a G:C T:A transversion in
codon 249 of the p53 gene a mutation thought to greatly increase the risk of developing hepatocellular
carcinoma. (Although the p 53 mutation is associated with lung cancer (about 60% of p 53 cancers);
it is associated with lung cancer that is due to or associated with smoking. High frequency of
transversions - hot spot at codons 157 and 158 in lung cancer). Aflatoxins: The mold that produces
aflatoxin may be found in the following foods: Peanuts and peanut butter,Tree nuts such as pecans,
Corn, Wheat, and Oil seeds such as cottonseed (moldy grains) High levels of dietary aflatoxin intake
have been strongly associated with hepatocellular. These aflatoxins are categorized as A1, B2, G1,
and G2, with aflatoxin B1 the most common and most toxic. Transcription factor for p21, blocks G1 to
S phase in the cell cycle.

Kawasaki disease: is a vasculitis of medium-sized arteries that presents with fever, bilateral
conjunctivitis, cervical lymphadenopathy and mucocutaneous involvement. Formation of coronary
artery aneurysms is the most serious complication of Kawasaki disease. 1. Fever , 2. Bilateral
conjunctivitis, 3. Lymphadenopathy, 4. Cutaneous involvement:
1. Oropharyngeal: Erythema of the palatine mucosa, fissured erythematous lips, strawberry tongue
2. Peripheral extremities: Edema of hands and feet, erythema of palms and soles, desquamation of
the fingertips (periungual) 3. Generalized rash: Polymorphous (usually urticarial) erythematous rash
beginning on the extremities and moving to the trunk (centri petal spread) Red tongue: Kawasaki
disease and scarlet fever (strep inf)
Dissecting aneurysms: of the aorta are associated with longstanding hypertension and Marfan
syndrome.
Membranoproliferative glomerulonephritis: Type I is associated with upper respiratory tract
infections and causes a nephrotic sediment. Type II causes nephritic sediment. Both are caused by
immune complex deposition in the glomerular basement membrane. Subendothelial Humps may been
seen on Electron microscopy
Mononeuritis multiplex: is a peripheral neuropathy of multiple individual nerves. It is associated
with a variety of diseases including Wegener granulomatosis and polyarteritis nodosa.
Pulmonary cavities: occur following resolution of pulmonary tuberculosis, histoplasmosis or
sarcoidosis
Ewing sarcoma: is a malignant bone tumor. It occurs in older children and teenagers predominantly
in the long bones. Clinically, Ewing sarcoma may resemble acute osteomyelitis. X-ray: onio skin layering
(periosteal elevation), also sunburst patterns is seen here. Genetic: translocation 11:22, produces EWS-FLI1 fusion protein
Wilms tumor (nephroblastoma): occurs in children 2-4 years old. It presents with a palpable flank
mass. Parents may discover this mass when bathing the child. On light microscopy Wilms tumor
resembles primitive metanephric tissue.
Medulloblastoma is the second most common brain tumor in children. It arises in the cerebellum
and causes gait and limb ataxia. It does not cause opsoclonus-myoclonus syndrome.
Gastric adeocarcinoma: There are two morphological variants of gastric adenocarcinoma. Intestinal
type forms a solid mass that projects into the stomach lumen and is composed of glandular-forming
cuboidal or columnar cells. Diffuse carcinoma (linitis plastica) infiltrates the stomach wall and displays
a signet-ring pattern on light microscopy. Signet-ring carcinomas consist of cells that do not form
glands. Cells often contain abundant mucin droplets that push the nucleus to one side and lead to the

characteristic appearance of a signet ring in profile. On gross examination, signet-ring carcinomas

are often characterized by diffuse involvement of the stomach wall. They have a plaque-like
appearance and are ill-defined. Often they infiltrate large areas of the stomach wall causing a leatherbottle stomach (Linitis plastica).
Rugal thickening: with acid hypersecretion is a characteristic finding in the stomach of a patient
with Zollinger- Ellison syndrome.
Rapid intraluminal expansion: Intestinal-type gastric adenocarcinomas may reach a large size
and expand within the gastric lumen.
Progressive mucosal atrophy: Chronic gastritis is most commonly associated with H. pylon. Longstanding inflammation of the gastric mucosa can lead to diffuse gland atrophy and intestinal
metaplasia. Chronic atrophic gastritis increases risk of gastric carcinomas
Von Willebrand disease (vWF deficiency): causes impairments of platelet function and
coagulation pathway abnormalities. It is associated with prolonged bleeding time, prolonged PH
(platelet adhesion) and decreased platelet aggregation in response to ristocetin. It binds GP Ib-IX
receptors on the platelet membrane and mediates platelet aggregation and adhesion to subendothelial
collagen. Von Willebrand factor also serves as a carrier for factor VIII. Deficiency of vWF causes both
impaired platelet function and coagulation pathway abnormalities. platelets aggregate normally in
response to ADP. . vWF serves as a carrier for factor VIII and prolongs its half-life. The half-life of factor
VIII bound to vWF is 12 hours while the half-life of free factor VIII is 2 hours. Decreased levels of vWF,
therefore lead to functional deficiency of factor VIII (also called antihemophilic factor). This causes
prolonged bleeding after tooth extraction and other minor surgeries, as well as prolonged PH.
The definitive diagnosis of von Willebrand disease is made by measuring the levels of different
fractions of vWF factor. Treatment includes desmopressin (DDAVP)I which stimulates vWF release from
endothelium. Blood products containing vWF are used in severe forms of von Willebrand disease. von
Willebrand (vWF) disease is an inherited bleeding disorder and would not delay presentation until the
sixth decade of life. In von Willebrand disease, only PH is elevated, which is due to a factor VIII
deficiency, as vWF carries factor VII
Glanxmann thrombasthenia: Hereditary deficiency of GP lIb-Illa receptors occurs in Glanzmann
thrombasthenia. It manifests with mucocutaneous bleeding and increased bleeding time. Platelet
aggregation in response to ristocetin is normal, but is decreased with addition of ADP.
Deficiency of thromboxane A2 : is associated with aspirin treatment, due to irreversible
inactivation of COX in platelets. The result is decreased platelet adhesion and aggregation. The
ristocetin aggregation test is normal.
Kartageners Syndrome: Primary ciliary dyskinesia, caused by an autosomal recessive mutation in
the microtubule-associated protein dynein, can cause Kartageners syndrome in about 50% of patients
(variable penetrance). Kartageners syndrome is characterized by male infertility, situs inversus,
recurrent sinusitis, and bronchiectasis.
Cleft lip: is the result of failure of the maxillary and medial nasal processes to fuse during
development. Cleft lip is not known to be related to defects in ciliary structure or function.
Burkitt lymphoma: has a starry sky appearance due to the presence of macrophages and
apoptotic bodies in a sea of medium-sized lymphocytes. The rates of mitosis and apoptosis in the
cancerous tissue are high. Almost all cases of Burkitt lymphoma are associated with translocations
of the C-MYC gene on chromosome 8, usually onto the Ig heavy chain region of chromosome 14
[t(8:14)]. Almost all cases of endemic Burkitt lymphoma are associated with EBV infection. EBV has
been implicated in the immortalization of lymphoma cells.
Follicular lymphoma: there is overexpression of the antiapoptotic BCL-2 as a result of that (14:18)
translocation. Follicular lymphoma causes generalized lymphadenopathy and tends to affect the
elderly. Jaw involvement would be very unusual.
N-MYC oncogene: is usually seen in neuroblastoma and small cell carcinoma of the lung.

The BCR-ABL rearrangement: is found in chronic myelogenous leukemia (CML) and some forms of
acute lymphoblastic leukemia (ALL). The translocation causes increased tyrosine kinase activity.
Holoprosencephaly: results from failure of forebrain cleavage into cerebral hemispheres. It is an
example of a congenital malformation, a primary abnormality in a development process. Incomplete
division of the forebrain into two hemispheres is called holoprosencephaly. Holoprosencephaly is an
example of a malformation. The term malformation describes a primary defect in the cells or tissues
that form an organ (an intrinsic developmental abnormality). Normally the division of the
prosencephalon happens during the 5th week of embryonic development. Thus holoprosencephaly is a
malformation that originates very early in fetal life. Holoprosencephaly is associated with trisomy 13
(Patau syndrome) and trisomy 18 (Edwards syndrome). It may also occur as a consequence of fetal
alcohol syndrome. Other examples of malformation include: congenital heart disease anencephaly,
polydactyly and syndactyly.
Amniotic band syndrome: is an example of a disruption (secondary destruction of a previously
well-formed tissue or organ).
Congenital hip dislocation, clubbed feet and flat facies (Potter syndrome) are examples of
deformations (secondary to extrinsic compression).

Potter syndrome is also an example of a sequence: In Potter syndrome, the primary problem is kidney failure.
The kidneys fail to develop properly as the baby is growing in the womb. The kidneys normally produce the amniotic fluid (as
urine). Potter phenotype refers to a typical facial appearance that occurs in a newborn when there is no amniotic fluid. The lack
of amniotic fluid is called oligohydramnios. Without amniotic fluid, the infant is not cushioned from the walls of the uterus. The
pressure of the uterine wall leads to an unusual facial appearance, including widely separated eyes.
2 morphological variants of gastric adenocarcinoma: Intestinal type forms a solid mass that
projects into the stomach lumen and is composed of glandular-forming cuboidal or columnar cells.
Diffuse carcinoma (linitis plastica) infiltrates the stomach wall and displays a signet-ring pattern on
light microscopy.
Burkitt lymphoma: has a starry sky appearance due to the presence of macrophages and
apoptotic bodies in a sea of medium-sized lymphocytes. The rates of mitosis and apoptosis in the
cancerous tissue are high. Almost all cases of Burkitt lymphoma are associated with translocations of
the C-MYC gene on chromosome 8, usually onto the Ig heavy chain region of chromosome 14 [t(8:14)].
(African type) Burkitt lymphoma: jaw involvement is a characteristic feature.
BCR-ABL rearrangement: is found in chronic myelogenous leukemia (CML) and some forms of acute
lymphoblastic leukemia (ALL). The translocation causes increased tyrosine kinase activity.
follicular lymphoma: there is over expression of the antiapoptotic BCL-2 as a result of that (14:18)
translocation. Follicular lymphoma causes generalized lymphadenopathy and tends to affect the
elderly.
BCR-ABL rearrangement: is found in chronic myelogenous leukemia (CML) and some forms of acute
lymphoblastic leukemia (ALL). The translocation causes increased tyrosine kinase activity.
Polycystic Kidney Disease (ARPKD): {Autosomal recessvie} manifests in infants. Most of these
patients die shortly after birth or during the first years of their lives. Mnemonic: remember in life
ADULTS are DOMINANT, and BABIES are NOT dominant.
Autosomal Dominant (adult) Polycystic Kidney Disease (ADPKD: It is the most frequent
genetic cause of renal failure in adults, accounting for 10% of patients on dialysis in the United States.
Its mode of inheritance is autosomal dominant. Although the patients are born with multiple cysts of
both kidneys, they remain asymptomatic until their fourth or fifth decade of life. The cysts enlarge
progressively as patients age. When the cysts become large enough to cause renal dysfunction, the

symptoms develop though the true mechanism for renal dysfunction in this disease has yet to be
determined with absolute certainty. Pain and abdominal discomfort (due to dilatation of the cysts and
stretching of the renal capsule) is one of the most common initial symptoms. Others include
hematuria, proteinuria (usually less than 2 gm/day) polyuria, and hypertension.
Trinucleotide repeat mutations: Occur when a three-nucleotide sequence is abnormally repeated.
Such mutations cause fragile X syndrome, myotonic dystrophy, and Huntington disease.
Autosomal recessivediseases: Albinism, ARPKD (formerly known as infantile polycystic kidney disease), cystic
fibrosis, glycogen storage diseases, hemochromatosis, Kartagener syndrome, mucopolysaccharidoses (except Hunter syndrome),
phenylketonuria, sickle cell anemia, sphingolipidoses (except Fabry disease), thalassemias, Wilson disease.
Thromboangiitis obliterans (Buergers disease): Is usually seen among heavy cigarette smokers
with onset before age 35, and is associated with hypersensitivity to intradermal injections of tobacco
extracts. This segmental thrombosing vasculitis often extends into contiguous veins and nerves,
encasing them in fibrous tissue.
Temporal arteritis: Predominantly involves medium to smaller branches of the carotid artery,
especially the temporal arteries. Granulomatous inflammation of the media characterizes temporal
(giant cell) arteritis the most common form of systemic vasculitis in adults.
Malignant hypertension: ) Onion-like concentric thickening of arteriolar walls as a result of
laminated SMC and reduplicated basement membranes. (diastolic pressures >1201 30 mm Hg).
Polyarteritis nodosa: Transmural inflammation of the arterial wall with fibrinoid necrosis.
Atherosclerosis:

Lipid-filled intimal plaques that bulge into the arterial lumen.

Thrombotic thrombocytopenic purpura (HP) and hemocytic uremic syndrome (HUS): are two
points on a spectrum of disease that is characterized by the pentad of fever neurologic manifestations,
acute renal failure thrombocytopenia, and microangiopathic hemolytic anemia. Thrombotic
thrombocytopenic purpura is usually seen in adults with predominant central nervous system (CNS)
manifestations. HUS is usually seen in children with predominant renal failure and mild CNS
manifestations.
Disseminated intravascular coagulation: is a common complication associated with sepsis,
particularly in gram-negative bacterial sepsis. DIC generally occurs due to the introduction of factors
that initiate intravascular thrombosis, which is followed by the consumption of coagulation factors,
then coagulopathy, and bleeding.
You should suspect DIC in any sick patient who has both an elevated prothrombin time (PT) and
partial thromboplastin time (PH). Besides a rise in both PT and PH, platelets & fibrinogen levels
decrease, while fibrin degradation products, particularly D-dimer, are elevated (indicate lyses of crosslinked fibrin) in DIC. PTT=25 to 35 sec; PT normal =11.5 to 13 Seconds.

Prothrombin Time (PT): The prothrombin test specifically evaluates the presence of factors VII, V, and X, (5 7,10)
prothrombin, and fibrinogen. A prothrombin time within the 11 -15 second range (depends on the source of thromboplastin used)
indicates that the patient has normal amounts of the above clotting factors. A prolonged prothrombin time indicates a deficiency
in any of factors VII, X, V, prothrombin, or fibrinogen. It may mean that the patient has a vitamin K deficiency (vitamin K is a
co-factor in the synthesis of functional factors II (prothrombin), VII, IX and X) or a liver disease (the liver is the site of synthesis
of the plasma protein factors). The prothrombin time of patients receiving a vitamin K-competing coumarin drug such as warfarin
(anticoagulation therapy used in deep venous thrombophlebitis) will also be prolonged, usually in the range of one and one half
to two times the normal PT time.
(Activated) Partial Thromboplastin Time test: {PTT} The activated partial thromboplastin time (aPTT) is a test
performed to investigate bleeding disorders and to monitor patients taking an anticlotting drug such as heparin which
inhibits factors X and thrombin, while activating anti-thrombin. PTT measures the integrity of the intrinsic
system (Factors XII, XI, VIII, IX) (8,9,11,12)and common clotting pathways. Increased levels in a person
with a bleeding disorder indicate a clotting factor may be missing or defective. At this point, further investigation is

needed and warrants the use of sensitive assays for specific coagulation factors. Liver disease decreases production
of factors, increasing the PTT.
Elevated PTT an PT: 1. DIC; 2. Vitamin K deficiency;
Only Elevated PTT: Hemophilia A or B: Intrinsic pathway coagulation defect.
. A: deficiency of factor VIII = increased PTT.
. B: deficiency of factor IX = increased PTT.
Macrohemorrhage in hemophiliahemarthroses (bleeding into joints), easy bruising,
Increase in the PTT. Treatment: recombinant factor VIII (in hemophilia A).

DIC
Patients bleed
Coagulation cascade is activated
PT and PTT are prolonged
Low fibrinogen and increased FDP

TTP-HUS
Usually do not bleed
Only platelets are activated
Normal PT and PTT
Normal fibrinogen

Thrombocytopenic purpura (ITP), thrombocytopenia: is a peripheral blood abnormality and

fever is absent. Some medical professionals call ITP immunopathic thrombocytopenic purpura
because the thrombocytopenia is due to antibody complex. Coagulation studies such as PT and PH will
be normal. Because the platelets are so sticky in ITPI spontaneous bleeding is very uncommon,
unless the platelet count is less than 10000 /cmm.
Autoimmune hemolytic anemia (AHA): is associated with either warm or cold antibodies that
cause hemolytic anemia. Coagulopathy is not a component of AHA.
Paroxysmal nocturnal hemoglobinuria (PNH): is a complement-activated hemolytic anemia that
is commonly associated with thrombocytopenia and leukopenia. Note that this patient has leukocytosis
secondary to sepsis.
Keloids: Excessive collagen formation during tissue repair results in keloids. Keloids usually extend
beyond the borders of the original wound, do not regress and recur after resection. Unlike keloids,
hypertrophic scars are limited to the area of the wound and may regress spontaneously though this is
uncommon. Keloids and hypertrophic scars consist of connective tissue rich in fibroblasts,
myofibroblasts and bundles of collagen fibers that lie in a disorganized fashion in hypertrophic scars
and in a parallel arrangement in keloids.
Hypertrophic scars:
this is uncommon

are limited to the area of the wound and may regress spontaneously though

Wound healing: Wound healing is generally believed to proceed in three phases:

1. The inflammatory phase consists of movement of neutrophils (within first 24 hours) and
macrophages (2-3 days) to the damaged area and phagocytosis of necrotic debris and bacterial
contaminants.

2. The proliferative phase begins 3-5 days after the injury. Fibroblasts and endothelial vascular cells
proliferate to form connective tissue and blood vessels (neovascularization) respectively. During this
phase, granulation tissue looks pink, friable and edematous.
3. The maturation phase is characterized by fibrosis (scar formation) and starts during the second
week after the injury. During this phase active fibroblasts synthesize collagen elastin and other
components of the connective tissue matrix. By 6-8 weeks initial scar formation is complete and the
wound reaches 30-40% of normal tensile strength during this time. Maturation of the scar continues for
the next several months with a slowly progressive increase in tensile strength occurring over that span
of time.
Subungual splinter hemorrhages: Microemboli from the valvular vegetations of bacterial
endocarditis are the most common cause of subungual splinter hemorrhages. The presence of these
lesions necessitates careful cardiac auscultation to detect a possible new-onset regurgitant murmur
Partial mole: will have a triploid karyotype (69xxx or 69xxy). Patients present with vaginal bleeding
and lower abdominal pain. Unlike complete moles, partial moles are associated with low risk of
invasive trophoblastic disease.

Choriocarcinoma: can develop after molar pregnancy abortion or normal pregnancy. It presents with
vaginal bleeding and symptoms of metastatic disease (e.g. cough with lung metastases).
Inappropriately elevated hCG levels suggest choriocarcinoma.
Abruptio placentae: (premature placental separation) can occur in the third trimester of pregnancy.
It manifests with vaginal bleeding hypertonic uterus, and intense painful contractions.
Ruptured tubal pregnancy: will present with vaginal bleeding, abdominal pain, and signs of
hemorrhagic shock. Curettage will reveal endometrial lining showing gestational changes. Fetus and
trophoblast are absent.
Malignant mesothelioma: is a rare neoplasm that arises from the pleura or peritoneum. It is
strongly associated with asbestos 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 ton of i laments. This tumor is extremely rare.
Asbestos exposure is the only significant risk factor. Individuals involved in asbestos mining and
industrial applications of asbestos (e.g. insulation, shipbuilding) are at risk for this neoplasm.
The symptoms of mesothelioma include dyspnea and chest pain. Hemorrhagic pleural effusions are
frequently present. Nodular or smooth pleural thickening is the main finding on radiographic studies
and macroscopic examination. The lung parenchyma is intact. Electron microscopy (EM) is the gold
standard for diagnosis. EM will show tumor cells with numerous, long, slender microvilli and abundant
tonofilaments.

Bronchioloalveolar carcinoma is a variant of adenocarcinoma. It almost always arises at the

periphery of the lung and has a characteristic distribution along the alveolar septa without vascular
and lymphatic spread. On chest x-ray it appears as a peripheral mass or as an area of pneumonia-like
consolidation.
Small cell carcinoma: usually arises from the major bronchi. On chest imaging it is seen as a hilar
mass. Neuroendocrine markers such as chromogranin and synaptophysin are usually positive.
Squamous cell carcinoma: also arises from the major bronchi. Imaging will show a hilar mass.
Histologically, it is characterized by keratinization and intercellular bridges. This tumor can sometimes
present as a cavitary lung lesion
Bronchioloalveolar carcinoma: is a variant of adenocarcinoma. It almost always arises at the
periphery of the lung and has a characteristic distribution along the alveolar septa without vascular
and lymphatic spread. On chest x-ray it appears as a peripheral mass or as an area of pneumonia-like
consolidation
Factor V Leiden: One to nine percent of Caucasians worldwide are heterozygote carriers of factor V
Leiden, 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. The major clinical
manifestations of factor V Leiden include deep vein thrombosis (DVT) cerebral vein thrombosis, and
recurrent pregnancy loss. Because pulmonary thromboembolism occurs in approximately 5O% of all
individuals with untreated DVTs, the young woman presented here is at significant risk of developing a
pulmonary thromboembolism at some point in her lifetime.
Factor V Leiden is the most common cause of inherited thrombophilia, with the heterozygote
prevalence of this genetic mutation ranging from 1-9% in Caucasian populations worldwide
Recurrent hemarthroses: are suggestive of hemophilia (factor VIII or IX deficiency), not factor V
Leiden.
Major causes of splenic infarction: include sickle cell anemia, infectious endocarditis, and
myeloproliferative disorders. Moreover, the factor V Leiden mutation is associated with deep venous
(not arterial) thrombosis.
Pericardial tamponade: The triad of muffled heart sounds elevated jugular venous pressure and profound hypotension
indicates pericardial tamponade. Rupture of the ventricular free wall as a consequence of an acute transmural Ml can cause
tamponade. Rupture usually occurs 3 to 7 days after the onset of total ischemia, when coagulative necrosis, neutrophil infiltration,
and enzymatic lysis of connective tissue have sufficiently weakened the infarcted myocardium.
COPD: COPD encompasses chronic bronchitis and emphysema. Heavy smoking is the most common cause. Chronic bronchitis
and emphysema have similar effects on FEV1/FVC during pulmonary function testing (PFT). The hallmark of an obstructive
PFT profile is decreased FEV1/FVC (FEV1%) due to expiratory airflow obstruction. Chronic obstructive pulmonary disease
(COPD) in a heavy smoker may consist of both emphysema and chronic bronchitis and thus may present with both progressive
exertional dyspnea (characteristic of emphysema) and frequent respiratory infections (characteristic of chronic bronchitis). On
pulmonary function testing all COPD yields a decreased FEV1/FVC ratio. Emphysema also tends to increase TLC and RV. In
contrast, restrictive lung diseases can cause reduced lung volumes and increased FEV1/FVC.
Alveolar ventilation: Arterial PaCO2 is a direct indicator of the status of alveolar ventilation. Hypocapnia implies ongoing
alveolar hyperventilation. Upper airway obstruction, reduced ventilatory drive, respiratory muscle fatigue, and decreased chest
wall compliance are possible cause alveolar hypoventilation, which would cause hypercapnia. Ex: A 45-year-old male presents
to the ER with severe dyspnea of recent onset. He says he has never experienced symptoms like this before. Arterial blood gases
show a Pa02 of 54 mmHg and a PaCO2 of 26 mmHg
Cardiac catheterization: (choosing Aortic Regurgitation) The murmur of AR is a diastolic decrescendo
murmur heard loudest in early diastole when the pressure gradient between the aorta and the left
ventricle is maximal. {choice C}

(Choice A) This time point corresponds to the opening of the aortic valve during systole
(Choice B) This point corresponds to the closure of the aortic valve. The A2 heart sound is heard here. At this instant there is not
yet regurgitant flow from the aorta to the left ventricle, so no murmurs are audible.
(Choice C) The peak intensity of an AR murmur occurs after closure of the incompetent aortic valve, at the point when the
pressure gradient between the aorta and the left ventricle is at its maximum
(Choice D) Time point D occurs in mid-diastole
(Choice E) Time E marks the onset of left atrial contraction at the end of ventricular diastole
The principal site of uric acid precipitation: Uric acid (pKa = 5.4) is soluble at physiologic pH, but precipitates in an acidic
environment. The lowest pH along the nephron is found in the distal tubules and collecting ducts; so these are the segments of the
nephron that become obstructed by uric acid crystals. (Collecting ducts due to low urine pH)