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Cardiology

Lupus-like syndrome = SE of Procainamide (Type IA antiarrhythmic) (It inhibits Na and K


channels, prolongs QRS complex and QT interval, prolongs effective refractory period (ERP)).
The most common cause of secondary hypertension are renal artery stenosis and primary
hyperaldosteronism.
Beta blockers lower BP in part by reducing renin secretion from the kidneys (beta-1).
Beta blockers decrease AV conduction and therefore should be used cautiously in pts. with first-
degree heart block.
In addition to their negative inotropic effect, the more cardioselective (non-dihydropyridine)
calcium channel blockers (verapamil, diltiazem) can also reduce HR by slowing impulse
transmission through the AV node.
ACE inhibitors are first-line therapy for HTN in Diabetics because of their nephroprotective
actions. SE = cough (due to bradykinin accumulation).
Beta blockers are contraindicated in Diabetics because of hypoglycemic masking.
Thiazide diuretics can exacerbate glycemic control in diabetics, because it causes hypokalemia
and stimulate sympathetic nervous system via intravascular volume depletion.
An imbalance between myocardial oxygen supply and demand underlies the pathophysiology of
angina.
Nitroglycerins primary mechanism of action is dilated peripheral veins, which reduces preload
and therefore myocardial oxygen demand. It also has direct effects on the coronary arteries, so
it can be useful for all three forms of angina.
Digitalis (cardiac glycoside) for CHF works by increasing inotropic effect, decreasing chronotropic
effect, increasing ejection fraction. Its side effects include cholinergic effects (e.g. diarrhea,
vomiting, increased PR interval), arrhythmias, and blurry yellow vision. Digitalis/digoxin toxicity
is treated by stopping the medication and administering potassium, magnesium, and anti-
digoxin Fab fragments. Lidocaine is given for digoxin-induced arrhythmias.
Heart failure is classified by two general types: systolic (pump) and diastolic (filling) dysfunction,
with considerable overlap. The initial adaptive physiologic responses (increased sympathetic
activity, fluid retention, and myocardial hypertrophy) become maladaptive when prolonged,
leading to progressive deterioration of cardiac function and eventual death.
When thinking about heart failure, categorize the findings according to whether they suggest
left-sided versus rt-sided heart failure, preserved versus reduced ejection fraction, and
compensated versus decompensated cardiac output.
Aortic stenosis most commonly presents as crescendo-decrescendo systolic murmur heart
loudest at the upper right sternal border and radiating to both carotid arteries. A delayed
carotid upstroke and narrowed pulse pressure are associated findings. Decreased cardiac output
(in decompensated states) and increased myocardial oxygen demand are important
consequences of aortic stenosis. It follows that natural history of this condition leads to angina,
syncope, heart failure, and premature death.
Defects in LDL receptor or internalization of LDL receptor cause Familial Hypercholesterolemia.
The metabolic syndrome is characterized by abdominal obesity, dyslipidemia, insulin resistance,
and HTN. It is a marker for increased cardiovascular risk. TX of the metabolic syndrome consists
of treating each of its components with lifestyle modifications, and pharmacologic agents to
control weight, improved lipid profiles, heighten insulin sensitivity, and lower BP. Cholesterol-
lowering medications include statins (most potent for lowering LDL-C), niacin (most potent for
increasing HDL-C), fibrates, and bile-sequestering resins.
In general, there is NO direct parasympathetic innervation of the vasculature. However,
vasodilation of arterioles can be caused by exogenous cholines. These drugs act on
uninnervated M3-receptors on endothelial cells and stimulate release of nitric oxide. Nitric oxide
diffuses to the adjacent smooth muscle, resulting in vasodilation and decreased peripheral
resistance.
When blood pressure drops, arterial baroreceptors located with carotid sinus (afferent limb
mediated by glossopharyngeal nerve) sense decreased vessel stretch and fire less frequently.
This response increases efferent sympathetic outflow and inhibits parasympathetic outflow,
which helps restore the BP by increasing HR and stimulating peripheral vasoconstriction.
The aortic arch and carotid sinuses also have chemoreceptors. Chemoreceptors work to
maintain P02, PCO2, and pH.
HTN, age, smoking, dyslipidemia, family history, and elevated C-reactive protein (CRP) and
homocysteinuria are risk factors for coronary artery disease.
Insulin stimulates lipoprotein lipase protein synthesis. If this enzyme is low as in Type 1 diabetes,
then TG accumulate in the circulation and can develop atherosclerosis.
Pulmonary:
Histamine (Gq-H1) = bronchoconstriction leading to respiratory symptoms.
The predominant mechanism of respiratory suppression of the barbiturates, benzos, opioids,
and general anesthetics is to make the medullary respiratory center less responsive to increase
in paCo2.
Asthma: Wheezing, cough (that is worse late at night or early morning), chest tightness, and
dyspnea. Symptoms are often triggered or worsened by exercise, cold air, or inhaled noxious
particles. A history of prolonged upper respiratory tract infections is also characteristic of
asthma. Pathology includes smooth muscle hypertrophy secondary to recurrent
bronchoconstriction and mucosal edema (with a relative eosinophilia) secondary to chronic
subacute inflammatory process. Curshmanns spirals and Charcot-Leyden crystals are found in
the mucus of asthmatics.
Diagnosis of Asthma: Disproportionate decrease in the FEV1/FVC ratio in response to
Methachoine.
Management of Asthma: Steroids, beta-2 agonists, mast cell stabilizers, anticholinergics,
leukotriene receptor antagonists, 5-lipoxygenase inhibitors, and theophylline.
Asthmatics who also suffer from rhinitis and nasal polyps may develop fatal bronchospasm from
ingesting aspirin, ibuprofen, and naproxen. Avoid them.
Hypersensitivity Pneumonitis: wheezing and dyspnea; often triggered or worsened by variety of
antigens (including occupational exposures). Diffuse infiltrates on chest x-ray. Biopsy may show
noncaseating granulomas or mononuclear cell infiltrates. Reversible if offending agent removed;
otherwise progresses to pulmonary fibrosis.
Allergic bronchopulmonary aspergillosis caused by aspergillus (and could be another fungi)
typically occurs in asthmatics and manifests with dyspnea, fever, eosinophilia, and infiltrates on
x-ray. TX are corticosteroids.
Progressive dyspnea and other overlapping symptoms are seen in emphysema and chronic
bronchitis (because they are both COPD).
Emphysema: Hyperresonance of the chest, decreased breath sounds bilaterally, prolonged
expiratory phase, PURSED LIP breathing, FEV1/FVC < 75%, increased anteroposterior diameter
(barrel chest), and flattening of the diaphragm. Pathology is that the lung parenchyma gets
destroyed from the pathologic activation of proteases. The destruction of alveolar elastin results
in permanent abnormal enlargement of the air spaces distal to the terminal bronchiole. This is
accompanies by destruction of the alveolar walls, but without obvious fibrosis. TX includes short
acting beta2-agonist such as albuterol for acute symptoms, ipratropium, and glucocorticoids for
long-term.
Chronic bronchitis: Productive cough, cyanosis, crackles, and wheezing. Productive cough for 3
months in at least 2 consecutive years. FEV1/FVC < 75%. Pts. are often hypoxemic and
hypocapnic. Pathology includes hypertrophy of submucosal glands and goblet cells, resulting in
mucus hypersecretion. TX is bronchodilators and corticosteroids.
Asbestosis: Exertional dyspnea; with advanced disease, dyspnea at rest, dry cough, chest pain,
and recurrent resp. tract infections. Look for history of exposure. Ferruginous bodies (or
asbestos bodies) which are fibers of asbestos lined by hemosiderin deposits. These are yellow to
brown rod-shaped bodies stain positively with Prussian blue.
Methemoglobinemia is another potential cause of cyanosis. In conditions such as pyruvate
kinase def. or G6PD def. or following exposure to oxidizing agent such as benzocaine, the
mechanisms that defend against oxidative stress with the RBCs are overwhelmed, and the
ferrous Fe2+ of the heme is oxidized to ferric Fe3+. This converts hemoglobin to
methemoglobin, which is unable to bind oxygen.
Tumors at the apex of the lung are known as Pancoast tumors. They are MC seen with
squamous cell carcinoma of the lung. Ipsilateral ptosis, miosis, anhydrosis (Horners syndrome).
Note that in Lambert-Eaton syndrome, ptosis is Bilateral.
Another commonly seen complications of lung tumors is superior vena cava syndrome (often
associated with small cell carcinoma), in which the superior vena cava is compressed by the
growing tumor. This impairs venous drainage of the head and upper limbs, resulting in swelling
and purple discoloration of the arms and face.
Small Cell Cancer of the lung: Dyspnea, rapid unexplained wt loss, SIADH.
Elevated ACE are frequently associated with sarcoidosis. The hypercalcemia that develops in
sarcoidosis is due to increased production of 1,25-dihydroxyvitamin D3 by the macrophages in
granulomas. It is also associated with Bells palsy.
Sarcoidosis: lung, skin, anterior uveitis, polyarthritis, bilateral hilar lymphadenopathy,
noncaseating granulomas. TX is glucocorticoids.
A pneumothorax can cause a mixed resp and metabolic acidosis because of both impaired
ventilation, which increases CO2 levels; and increase anaerobic metabolism which increases
plasma levels of acids such as lactic acidosis.
Pneumothorax sudden onset of severe dyspnea with sharp pain in ones side. The trachea and
mediastinum WILL shift away from the side of the pneumothorax. Hyperresonance, absence of
breath sounds. Commonly associated with asthma, emphysema, Marfans, trauma.
Nephrology:
The causes of acute renal failure (ARF) are divided into 3 groups: prerenal, renal (intrinsic), and
postrenal (obstructive).
Common causes of postrenal failure include BPH or prostate cancer, bladder tumors, and
urinary retention (due to neurogenic bladder or anticholinergic, opiate, or sympathomimetic).
The diagnosis of obstructive renal failure is made, in part, by detection of hydronephrosis
(pelvicalicectasis) on renal ultrasound.
Acute tubular necrosis (ATN) is the MCC of intrinsic renal failure. ATN can be ischemic or toxic.
Toxins capable of ATN include cisplatin, aminoglycosides, vancomycin, amphotericin, IV contrast
agents, and myoglobin.
Ischemic ATN is distinguished from prerenal azotemia by the presence of muddy brown casts
in the urinary sediment and an FENa+ >2%. Prerenal azotemia, in contrast, show bland
sediment, by a FENa+ <1%.
NSAIDs-induced decrease GFR
NSAIDs can cause AIN, nephrotic syndrome, and most commonly Hemodynamic renal failure
from inhibition of vasodilatory prostaglandins. Pts. with advanced age, renal dysfunction, or CHF
are at the highest risk for NSAID-induced acute renal failure (ARF).
MC conditions that cause eosinophilia include helminthic infections, asthma, allergy, drug-
induced acute interstitial nephritis (AIN), Hodgkins lymphoma.
AIN is classically a triad of fever, rash, and peripheral eosinophilia in a setting of ARF after
introduction of a new drug. Agents are penicillins, cephalosporins, sulfonamides, NSAIDs, PPIs.
HTN is both major cause and a major complication of chronic renal failure (CRF).
CRF is characterized by normocytic anemia (due to loss of renal erythropoietin production),
hyperkalemia, hypocalcemia, hyperphosphatemia, and mixed anion gap/non-anion gap
metabolic acidosis.
Uremia is a clinical syndrome in renal failure that shows nausea, pruritis, malaise, seizures,
confusion, bleeding pericarditis, and fluid overload.
CRF results in secondary hyperparathyroidism. Increase PTH, in turn, can cause abnormal bone
formation (osteitis fibrosa cystica), whereas deficiency of activated vit d can (in adults) lead to
osteomalacia. The full spectrum of bony changes resulting from high PTH, low Ca2+, and chronic
acidosis is called renal osteodystrophy.
Berry aneurysm is associated with Autosomal dominant adult polycystic disease (ADPKD).