USMLE USMLE Certifications USMLE-STEP-1 Questions & Answers

• Question 151:

  Apatient calls 911 because of severe substernal crushing pain that has not responded to three nitroglycerin tablets taken sublingually. The paramedic team suspects that the patient has suffered an acute myocardial infarction. His blood pressure is 110/70 and his heart rate is 70, with occasional premature extra beats. After initial treatment in the hospital, the patient. is found to be suffering from more severe hypotension (his blood pressure is now 70/40) and reduction of cardiac function with reduced left ventricular ejection fraction. His urine output is low and he has mental clouding. Which of the following is the pharmacologic treatment of choice for this condition in this patient?

  A. atenolol

  B. digoxin

  C. dopamine

  D. norepinephrine

  E. procainamide

  Correct Answer: C

  Section: Pharmacology The description of the patient's reduced cardiac function and elevated left ventricular filling pressure, with reduced peripheral perfusion (clouded mentation, reduced urine output) indicates cardiogenic shock, decreased blood pressure due to decreased cardiac output. In cardiogenic shock, a drug is needed that increases myocardial contractility without increasing heart rate and peripheral resistance. In addition, renal artery dilation is desirable to prevent renal shutdown. Dopamine (choice C), an agonist at dopamine, beta-, and alphaadrenoceptors, increases myocardial contractility with little increase in peripheral resistance and lower renal arterial resistance. Atenolol (choice A), a beta-1-selective blocker, is inappropriate in the setting of reduced cardiac function, although it may be quite appropriate later when the patient's condition is stabilized. Digoxin (choice B), a cardiac glycoside, may increase cardiac contractility but has a slow onset of action and may exacerbate arrhythmias. Norepinephrine (choice D) increases myocardial contractility but also greatly increases peripheral resistance, a situation that must be avoided in cardiogenic shock. Procainamide (choice E), a group IA antiarrhythmic agent, is not indicated because the patient does not have an arrhythmia.

• Question 152:

  Apatient calls 911 because of severe substernal crushing pain that has not responded to three nitroglycerin tablets taken sublingually. The paramedic team suspects that the patient has suffered an acute myocardial infarction. His blood pressure is 110/70 and his heart rate is 70, with occasional premature extra beats. What drug should be administered immediately, even before the patient reaches the hospital?

  A. aspirin

  B. dobutamine

  C. lidocaine

  D. metoprolol

  E. streptokinase

  Correct Answer: A

  Section: Pharmacology Immediate administration of one aspirin tablet by mouth (choice A) has been shown to reduce morbidity and mortality from myocardial infarction. Because this dose is essentially free from adverse effects, this therapy is appropriate even before the diagnosis is confirmed by ECG or other means. Dobutamine (choice B) is a beta-1-selective agonist that has positive inotropic action. It is not appropriate at this time because there is no evidence of heart failure. Lidocaine (choice C), an antiarrhythmic, is not appropriate at this time because the patient is in sinus rhythm with only occasional arrhythmic beats. Metoprolol (choice D), a betablocking drug, is often used after the acute period of a myocardial infarction, but is inappropriate until the patient's condition is stabilized. Streptokinase (choice E), a thrombolytic agent, is inappropriate because coronary thrombosis has not been confirmed and this IV drug is given in the hospital setting.

• Question 153:

  The change in elimination rate after hour 12 when sodium bicarbonate was administered is expected if drug W is which of the following chemical types?

  A. nonelectrolyte

  B. strong acid

  C. strong base

  D. weak acid

  E. weak base

  Correct Answer: D

  Section: Pharmacology By inspection of the graph, it is observed that administration of sodium bicarbonate increases the rate of elimination of the drug (the slope of the line increases and the half-life is shortened). Sodium bicarbonate causes alkalinization of the urine. Alkalinization causes increased ionization of weak acids and accelerates their urinary excretion because the ionized (charged) forms cannot be easily reabsorbed through the tubular epithelium, whereas the uncharged forms of many weak acids are readily reabsorbed. Urinary alkalinization is a strategy sometimes used to hasten the excretion of weak acids, such as aspirin, in overdose situations. Excretion of a nonelectrolyte (choice A) is unaffected by changes in urinary pH because the polarity of nonelectrolytes is insensitive to pH. A strong acid (choice B) is fully ionized (unprotonated) at all attainable urinary pH values so that alteration of urinary pH has no effect on its excretion. A strong base (choice C) is similarly fully charged at all attainable urinary pH values so that alteration of urinary pH has no effect on its excretion. Excretion of a weak base (choice E) is slowed by alkalinization of urinary pH because the uncharged form of a base is readily reabsorbed from the tubular urine predominates.

• Question 154:

  Figure shows plasma concentrations of drug W in a patient following intravenous (IV) injection of a single dose of 10 mg of the drug, an agent eliminated from the body by renal excretion. At hour 12, the patient is treated with sodium bicarbonate (arrow).

  

  Use the data before hour 12 to calculate the half-life ( ) for drug W.

  

  A. 0.5 hour

  B. 1 hour

  C. 3 hours

  D. 7 hours

  E. 10 hours

  Correct Answer: C

• Question 155:

  Figure shows plasma concentrations of drug W in a patient following intravenous (IV) injection of a single dose of 10 mg of the drug, an agent eliminated from the body by renal excretion. At hour 12, the patient is treated with sodium bicarbonate (arrow).

  

  Use the data before hour 12 to calculate the volume of distribution (Vd) for drug W.

  A. 1 L

  B. 10 L

  C. 25 L

  D. 50 L

  E. 100 L

  Correct Answer: B

• Question 156:

  Additive and potentially dangerous sedative interactions may occur between sedativehypnotic drugs and which of the following herbal preparations?

  A. Echinacea

  B. gingko biloba

  C. ginseng

  D. kava

  E. St John's wort

  Correct Answer: D

  Section: Pharmacology Unregulated herbal preparations are in heavy use by the public and several have been documented to interact with regularly prescribed drugs. Kava (choice D) has sedative actions and interacts additively with sedativehypnotics and sedative-antihistaminics. Echinacea (choice A) has no reported drug interactions to date but many preparations contain alcohol, which may increase sedation with alcohol- containing beverages. Gingko biloba (choice B) has antiplatelet activity and should not be used with aspirin or other antiplatelet drugs. Ginseng (choice C) may cause CNS stimulation and should not be used by patients with epilepsy and those taking psychoactive drugs. St John's wort (choice E) may inhibit metabolism of certain drugs.

• Question 157:

  Which of the following descriptions best describes the molecular mechanism underlying the therapeutic actions of the statins such as atorvastatin?

  A. binding to peroxisome proliferatoractivated receptor-alpha (PPAR-alpha) resulting in stimulation of lipoprotein lipase activity

  B. increased fecal excretion of bile acid resulting in increased conversion of cholesterol to bile acid

  C. inhibition of hepatic cholesterol synthesis resulting in increased expression of LDL receptors

  D. inhibition of hepatic VLDL secretion resulting in reduced production of IDL and LDL

  E. inhibition of lecithin:cholesterol acyltransferase activity resulting in decreased conversion of IDL to LDL

  Correct Answer: C

  Section: Pharmacology Hepatic intracellular cholesterol levels are tightly controlled through regulation of endocytotic uptake of cholesterol within LDL particles, de novo synthesis of cholesterol, incorporation into VLDL particles, and loss due to conversion to bile acids. Inhibition of cholesterol biosynthesis through statin inhibition of the enzyme 3-hydroxymethylglutaryl- CoA reductase (HMG-CoA reductase) lowers intracellular cholesterol levels. This lowering results in increased expression of the genes for the LDL receptor and HMG-CoA reductase. Increased expression of LDL receptors leads to increased endocytic uptake of LDL particles from the blood and consequent reduction of circulating levels of LDL cholesterol. Choice D is incorrect because the statins do not affect hepatic VLDL secretion. Inhibition of VLDL secretion is probably the mechanism of action for nicotinic acid in lowering VLDL and LDL. Choice E is incorrect because the statins do not affect lecithin:cholesterol acyltransferase (LCAT) activity. Binding to PPAR-alpha and activation of lipoprotein lipase (choice A) appears to be the mechanism for lowering elevated VLDL levels by the fibric acids such as gemfibrozil. Bile acid- binding resins such as cholestyramine promote increased fecal excretion of bile acids (choice B) and ultimately lead to increased expression of hepatic LDL receptors.

• Question 158:

  A 73-year-old woman complains of difficulty sleeping, exercise fatigue, and shortness of breath. Examination reveals mental confusion, swollen ankles, pulmonary rales, and dyspnea while supine. Immediate treatment of the patient may be needed if signs and symptoms, especially those of pulmonary congestion, worsen rapidly. Which of the following would be most beneficial in treating acute, severe pulmonary edema?

  A. amiloride

  B. furosemide

  C. hydrochlorothiazide

  D. losartan

  E. metoprolol

  Correct Answer: B

  Section: Pharmacology Rapid worsening of pulmonary congestion is suggestive of life-threatening acute cardiac decompensation (acute heart failure). Furosemide, a loop diuretic, is one of the most effective agents available because it has powerful diuretic action and also reduces pulmonary vascular pressures. Amiloride (choice A) is a much less efficacious diuretic with primary action in the collecting tubule of the nephron and little or no effect on pulmonary vessels. Hydrochlorothiazide (choice C) is a diuretic of intermediate efficacy that acts in the distal convoluted tubule. Losartan (choice D) is an angiotensin receptor blocker and is not effective in acute reduction of congestive symptoms. Metoprolol (choice E) is a betaadrenoreceptor blocker that is valuable in the long-term, chronic therapy of HF, but not effective(and usually contraindicated) in acute decompensation.

• Question 159:

  Which of the following drugs blocks the action of angiotensin II at the AT1 receptor?

  A. bradykinin

  B. enalapril

  C. losartan

  D. ondansetron

  E. prazosin

  Correct Answer: C

• Question 160:

  A 73-year-old woman complains of difficulty sleeping, exercise fatigue, and shortness of breath. Examination reveals mental confusion, swollen ankles, pulmonary rales, and dyspnea while supine.

  46. Chronic treatment of this patient with an angiotensin-converting enzyme (ACE) inhibitor such as captopril may be beneficial because ACE inhibitors (in addition to other effects) are known to exert which of the following responses?

  A. decrease both ventricular preload and afterload

  B. increase coronary perfusion

  C. increase efficiency of oxygen extraction by cardiac and skeletal muscle

  D. produce a positive inotropic effect and negative chronotropic effect

  E. promote ventricular remodeling and compensatory enlargement

  Correct Answer: A

  Section: Pharmacology ACE inhibitors decrease ventricular preload and afterload through the inhibition of ACE and the consequent decrease in production of the pressor peptide angiotensin II, along with prolongation of the actions of the vasodilator peptide bradykinin (which is normally degraded by ACE). ACE inhibition also reduces angiotensin II-dependent augmentation of sympathetic nervous system activity. Choice B is incorrect in that ACE inhibitors exert no direct effects on coronary perfusion. Choice C is incorrect because efficiency of oxygen extraction by muscle is unaffected by ACE inhibitors. Choice D is incorrect because ACE inhibitors exert no direct effects on cardiac force or rate. Use of ACE inhibitors reduces ventricular remodeling and compensatory enlargement (choice E), a very valuable effect in heart failure.