usmle step 1 notes

8/12/2019 USMLE Step 1 Notes

1/5

Cardiology

Lupus-like syndrome = SE of Procainamide (Type IA antiarrhythmic) (It inhibits Na and Kchannels, 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 impulsetransmission through the AV node.

ACE inhibitors are first-line therapy for HTN in Diabetics because of their nephroprotectiveactions. 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 dilate d peripheral veins, which reduces preload

and therefore myocardial oxygen demand. It also has direct effects on the coronary arteries, soit can be useful for all three forms of angina.

Digitalis (cardiac glycoside) for CHF works by increasing inotropic effect, decreasing chronotropiceffect, increasing ejection fraction. Its side effects include cholinergic effects (e.g. diarrhea,vomiting, increased PR interval), arrhythmias, and blurry yellow vision. Digitalis/digoxin toxicityis 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 sympatheticactivity, 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 suggestleft-sided versus rt-sided heart failure, preserved versus reduced ejection fraction, andcompensated versus decompensated cardiac output.

Aortic stenosis most commonly presents as crescendo-decrescendo systolic murmur heartloudest at the upper right sternal border and radiating to both carotid arteries. A delayedcarotid upstroke and narrowed pulse pressure are associated findings. Decreased cardiac output(in decompensated states) and increased myocardial oxygen demand are importantconsequences 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.


2/5

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 consistsof treating each of its components with lifestyle modifications, and pharmacologic agents tocontrol 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 onuninnervated M3-receptors on endothelial cells and stimulate release of nitric oxide. Nitric oxidediffuses to the adjacent smooth muscle, resulting in vasodilation and decreased peripheralresistance.

When blood pressure drops, arterial baroreceptors located with carotid sinus (afferent limbmediated 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 tomaintain P02, PCO2, and pH.

HTN, age, smoking, dyslipidemia, family history, and elevated C-reactive protein (CRP) andhomocysteinuria 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 increasein paCo2.

Asthma: Wheezing, cough (that is worse late at night or early morning), chest tightness, anddyspnea. Symptoms are often triggered or worsened by exercise, cold air, or inhaled noxiousparticles. A history of prolonged upper respiratory tract infections is also characteristic ofasthma. Pathology includes smooth muscle hypertrophy secondary to recurrentbronchoconstriction and mucosal edema (with a relative eosinophilia) secondary to chronicsubacute inflammatory process. Curshmanns spirals and Charcot -Leyden crystals are found inthe mucus of asthmatics.

Diagnosis of Asthma: Disproportionate decrease in the FEV1/FVC ratio in response toMethachoine.

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 fromingesting aspirin, ibuprofen, and naproxen. Avoid them.


3/5


4/5

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 impairedventilation, which increases CO2 levels; and increase anaerobic metabolism which increasesplasma levels of acids such as lactic acidosis.

Pneumothorax sudden onset of severe dyspnea with sharp pain in ones side. The trachea andmediastinum WILL shift away from the side of the pneumothorax. Hyperresonance, absence ofbreath sounds. Commonly associated with asthma, emphysema, Marfans, trauma.

Nephrology:

The causes of acute renal failure (ARF) are divided into 3 groups: prerenal, renal (intrinsic), andpostrenal (obstructive).

Common causes of postrenal failure include BPH or prostate cancer, bladder tumors, andurinary 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 contrastagents, and myoglobin.

Ischemic ATN is distinguished from prerenal azotemia by th e presence of muddy brown castsin the urinary sediment and an FENa+ >2%. Prerenal azotemia, in contrast, show blandsediment, by a FENa+


5/5

usmle step 1 notes

Documents