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A 59-year-old woman with a 10-year history of type 2 diabetes mellitus is noted by her physician to have bilateral pitting edema of the ankles and feet. No erythema is noted. On questioning, the patient also reports shortness of breath on exertion and states that she has been using 3 pillows at night in order to sleep comfortably. Question 1 of 6 This patient's symptoms are most suggestive of which of the following? / A. Cellulitis / B. Congestive heart failure / C. Gynecologic cancer / D. Lipedema / E. Thrombophlebitis Explanation - Q: 1.1 Close The correct answer is B. The combination of leg edema and pulmonary edema (as indicated by shortness of breath and sleeping on multiple pillows) strongly suggests that the patient has congestive heart failure involving both ventricles. Heart failure is a pathologic state in which an abnormality of cardiac function leads to failure of the heart to pump blood throughout the body at a rate sufficient to meet the body's requirements. Some of the adaptive mechanisms that compensate for the failing heart include increasing preload (through the Frank-Starling mechanism), myocardial hypertrophy (to restore elevated ventricular wall stress to within normal limits), redistribution of cardiac output from non-vital organs to vital organs, and neurohumoral adjustments. Congestion develops behind the failing ventricle, with left ventricular failure causing signs and symptoms of pulmonary congestion, and right ventricular failure causing signs and symptoms of systemic congestion. Cellulitis (choice A) is usually markedly erythematous. Gynecologic cancer (choice C) and thrombophlebitis (choice E) are causes of unilateral leg edema. Lipedema (choice D) is not a true edema (and would not show pitting), but is instead the deposition of fatty tissues around the ankles of obese individuals. *** Any comments? E-mail to [email protected] *** Question 2 of 6 A chest x-ray film demonstrates pulmonary venous congestion and interstitial edema indicative of pulmonary edema. Which of the following physiologic mechanisms is most likely the immediate cause of the pulmonary edema? / A. Damage to endothelial cells / B. Damage to the epithelial lining of the alveoli / C. EIevated pulmonary capillary pressure / D. Low serum albumin / E. Poor lymphatic drainage of fluid Explanation - Q: 1.2 Close The correct answer is C. The cause of pulmonary edema in congestive heart failure is an increase in the hydrostatic pressure at the level of the capillaries of the lung. This increased pressure serves to drive fluid out of the capillaries and into the alveoli. The other reasons cited in the choices can also cause pulmonary edema, but occur in other clinical settings. Damage to endothelial cells (choice A) can occur in vasculitis. Damage to the epithelial lining of the alveoli (choice B) can occur in pneumonia and respiratory distress syndrome. Low serum albumin (choice D) can be seen in liver and kidney disease. Poor lymphatic drainage (choice E) can be seen in lungs with chronic damage due to severe emphysema or fibrosis. *** Microsoft beyond the screen, Kleptomania above the screen *** Question 3 of 6 A chest x-ray film additionally demonstrates a markedly enlarged cardiac shadow with dilation of both the right and left ventricles. Echocardiography shows dilated, hypokinetic ventricles. The physician prescribes several medications, including captopriI. Which of the following best characterizes captopriI? / A. ACE inhibitor / B. AIpha blocker / C. Beta blocker / D. Diuretic / E. Positive inotrope Explanation - Q: 1.3 Close The correct answer is A. ACE inhibitors, including captopril, enalapril, and lisinopril, are becoming mainstays in the treatment of congestive heart failure, more formally known as dilated congestive cardiomyopathy. These agents inhibit the conversion of angiotensin I to angiotensin II, thereby interrupting the renin-angiotensin-aldosterone loop. The functional result is vasodilation, with a reduction in both cardiac afterload and cardiac preload. Furthermore, the ACE inhibitors, such as captopril and enalapril, are proven to delay the progression of this condition by protecting the ventricles from deleterious remodeling. Alpha-blockers (choice B) are not commonly used in CHF, although carvedilol has some alpha-blocking activity. Carvedilol is a non-cardioselective alpha- and beta-blocker (choice C) approved by the FDA for the treatment of both ischemic and non-ischemic heart failure; its alpha blocking effects confer vasodilatory activity. Catecholamine production is enhanced in the early development of CHF to compensate for decreasing cardiac output. Beta-blockers are beneficial in heart failure, since they diminish the chronic sympathetic nervous system stimulation; they may also be beneficial through the following mechanisms: improving cardiac output, increasing diastolic filling time, and decreasing arrhythmias. Loop diuretics (choice D), such as bumetanide and furosemide, are also considered to be first-line agents in the treatment of heart failure. These agents are indicated for the treatment of edema associated with CHF, hepatic cirrhosis, and renal disease, as well as treatment of hypertension (furosemide and torsemide). Digoxin (choice E) causes a positive inotropic effect by inhibiting the Na+/K+ ATPase in cardiac cell membranes. This inhibition leads to increased intracellular sodium, which alters the driving force for the Na+/Ca2+ exchange mechanism, leading to a decrease of calcium removal from the cell. This results in increased calcium storage in the sarcoplasmic reticulum, which when released, increases contractile force. Digitalis also modifies autonomic outflow. Question 4 of 6 An increase in which of the following is the most likely explanation for the edema in her legs? / A. Interstitial colloid osmotic pressure / B. Lymph flow / / / C. PIasma colloid osmotic pressure D. Right atrial pressure E. Stroke volume Explanation - Q: 1.4 Close The correct answer is D. Right atrial pressure rises in congestive heart failure, which elevates venous pressure throughout the body. This increase in venous pressure can cause excessive fluid loss from the microcirculation and the development of peripheral edema. Fluid loss from the capillaries washes protein molecules from the interstitial compartment and thereby decreases interstitial colloid osmotic pressure (choice A). Increased lymph flow (choice B) is a consequence rather than a cause of the edema. Increased plasma colloid osmotic pressure (choice C) would tend to decrease the development of edema. Stroke volume (choice E) has no effect on the formation of peripheral edema. Question 5 of 6 As this patient's condition progresses, she is started on digoxin. Her most recent digoxin blood level was 2.0 ng/mL. She will be at the highest risk for developing digoxin toxicity if she has which of the following conditions? / A. Hypokalemia / B. Hyponatremia / C. Hypophosphatemia / D. Vitamin B12 deficiency / E. Vitamin K deficiency Explanation - Q: 1.5 Close The correct answer is A. Digoxin is a cardiac glycoside indicated for the treatment of congestive heart failure, atrial fibrillation, and atrial flutter. The therapeutic drug serum levels for digoxin are 0.5 to 2.2 ng/mL. Toxicity typically occurs when digoxin levels are > 2.5 ng/mL, unless the patient is hypokalemic, then toxicity can occur at any therapeutic concentration. Hypokalemia sensitizes the myocardium to digoxin and may reduce the positive inotropic effects of the medication. Other signs and symptoms of digoxin toxicity include nausea, vomiting, anorexia, and appearance of yellow-green halos in the visual field, as well as the development of cardiac arrhythmias. Although hyponatremia (choice B) and hypophosphatemia (choice C) can result in the development of other pathological disturbances, they do not potentiate digoxin toxicity. Vitamin B12 deficiency (choice D) is associated with the development of pernicious anemia. Vitamin K deficiency (choice E) is associated with the development of clotting disorders. Furthermore, vitamin K deficiency is known to potentiate warfarin toxicity. *** Help your best friend to know Kleptomania, send trial *** Question 6 of 6 This patient's condition is associated with which of the following 5-year mortality rates? / A. 5% / B. 30% / C. 50% / D. 70% / E. 95% Explanation - Q: 1.6 Close The correct answer is D. In temperate zones, dilated congestive cardiomyopathy is most commonly the result of diffuse coronary artery disease with diffuse ischemic myopathy, which produces chronic myocardial fibrosis with diffuse loss of myocytes. Other causes are very diverse and can include a wide variety of infections, granulomatous disease, metabolic disorders, drugs and toxins, cancers, connective tissue disorders, familial neuromuscular disorders, and pregnancy. The dilated chambers usually function poorly, leading to a low ejection fraction. Tachycardia and increased end-diastolic volume initially maintain cardiac output, but often eventually fail with disease progression to adequately supply the tissues with oxygenated blood. Overall, dilated congestive cardiomyopathy is more often fatal than many cancers, with a 5-year mortality rate of 70%. A 55-year-old woman consults a physician because of edema involving her lower legs. While both of her ankles are swollen, the left one is much more swollen than the right. Physical examination additionally demonstrates a swollen, tender, bluish, cord-Iike structure immediately below the skin on her left lower leg extending from her ankle to near her knee. Edema at sites other than the ankles is not apparent on physical examination. The patient has not been having any other symptoms. The woman works as a nurse and had a long airplane trip during the previous week. Question 1 of 5 The tender cord-Iike structure is most likely which of the following? / A. Artery / B. Ligament / C. Lymphatic channel / D. Tendon / E. Vein Explanation - Q: 2.1 Close The correct answer is E. The structure is most likely an inflamed vein. Large superficial veins are common on the legs. The superficial arteries (choice A) of the legs are usually much less apparent and located deeper than are the veins. Ligaments (choice B) attach bone to bone, and can be palpated, but not usually seen, in the feet and at the knee. Lymphatic channels (choice C) are usually invisible on surface examination, unless they are markedly inflamed and accompanied by skin erythema. Then they appear as red lines. Tendons (choice D) also produce cord-like structures, but they are pale in color and do not appear blue through the skin. A 55-year-old woman consults a physician because of edema involving her lower legs. While both of her ankles are swollen, the left one is much more swollen than the right. Physical examination additionally demonstrates a swollen, tender, bluish, cord-Iike structure immediately below the skin on her left lower leg extending from her ankle to near her knee. Edema at sites other than the ankles is not apparent on physical examination. The patient has not been having any other symptoms. The woman works as a nurse and had a long airplane trip during the previous week. Question 2 of 5 Which of the following is the most likely cause of the increased edema in the patient's left lower leg? / A. Congestive heart failure / B. Lymphatic obstruction / C. Pulmonary failure / D. Renal failure / E. Venous obstruction Explanation - Q: 2.2 Close The correct answer is E. While on paper, leg edema can have a very large number of potential causes, an acute exacerbation of leg edema limited to one leg and accompanied by an obviously damaged vein should make you think of superficial thrombophlebitis. This condition occurs when thrombosis of a vein induces an accompanying inflammation of the vein (which essentially always happens). Superficial thrombophlebitis that occurs in previously healthy legs does not always induce ankle edema because the venous return via other routes is usually adequate. However, exacerbation of ankle edema can, as in this case, be the presenting complaint if a patient's legs are already damaged. In this case, the working history of being a nurse implies that the patient may have a history of long periods of walking and standing, which may lead to dependent edema in the ankles. Superimposed on this is a recent history of a long airline flight, which can act as a trigger for thrombophlebitis secondary to the prolonged immobilization experienced on the flight. Congestive heart failure (choice A) and renal failure (choice D) would produce bilateral ankle edema, and possibly edema visible in other sites. Lymphatic obstruction (choice B) can also produce localized edema, but this woman has an obviously inflamed vein, and that is the more likely cause. Pulmonary failure (choice C), unless due to pulmonary edema secondary to congestive heart failure, would be unlikely to be associated with ankle edema. Question 3 of 5 Which of the following is the most serious complication of this condition? / A. Focal arterial obstruction / B. Involvement of deep leg veins / C. Obstruction of a joint space / D. Rupture of an involved tendon / E. Secondary lymphangiosarcoma Explanation - Q: 2.3 Close The correct answer is B. Superficial thrombophlebitis often resolves spontaneously without sequelae, but should always be taken very seriously because the same patients who develop superficial thrombophlebitis may either have an extension of the clot into the deep veins (with increased risk of potentially fatal pulmonary embolism) or may develop a separate deep venous clot concurrently or at a later date. In hospitalized patients with superficial thrombophlebitis, it is thought that as many as 10% eventually develop pulmonary embolus (typically from an undiagnosed or later deep vein thrombosis), and of this subset of patients with pulmonary embolus, 20% die. The artery (choice A), joint space (choice C), and tendons (choice D) are not directly involved by this disease process. Lymphangiosarcoma (choice E) is a rare complication of chronic lymphatic obstruction. Question 4 of 5 Which of the following techniques is most useful for initial evaluation of the presence of this complication? / A. Computed tomography / B. D-dimer levels in serum / C. Duplex ultrasonography / D. Magnetic resonance imaging / E. Prothrombin time Explanation - Q: 2.4 Close The correct answer is C. The accurate diagnosis of deep vein thromboses is a problematic area of medicine, because no completely reliable diagnostic technique is easily available. Various techniques of physical diagnosis have been proposed, but can be misleading in most people's hands, and leave an erroneous impression that the patient does not have deep vein involvement when it is actually present. Both Duplex ultrasound (a combination of realtime and Doppler ultrasound techniques) and plethysmography (using volume and pressure changes to look at venous filling) can be used to diagnose deep vein thromboses, and are often used in conjunction as they tend to miss and pick up slightly different cases. Computed tomography (choice A) and magnetic resonance venography (choice D) can also be used, but are very expensive and not warranted in most cases. Serum indicators of clotting problems, such as D-dimers (choice B) and prothrombin time (choice E) are too nonspecific to be helpful in diagnosing deep vein thrombosis. Question 5 of 5 Following the appropriate studies, which demonstrated the most serious complication of this condition, the decision is made to anticoagulate the patient. Which of the following is the most appropriate initial choice of medications? / A. Intravenous Coumadin / B. Intravenous heparin / C. Oral aspirin / D. OraI Coumadin / E. Oral heparin Explanation - Q: 2.5 Close The correct answer is B. A patient with a known deep venous thrombosis is usually initially anticoagulated with intravenous heparin, then switched over the next days to weeks to oral Coumadin (choice D). These patients may also be treated with fibrinolytic agents, particularly if the deep vein clot is extending or has recently developed. Heparin is not available orally (choice E), and Coumadin is not usually given intravenously (choice A). Aspirin (choice C) is not effective in preventing venous clots (which are triggered predominantly by stasis). A fifty-year-old alcoholic man presents to the emergency department complaining of shortness of breath and ankle swelling. He has a history of intravenous drug use and had a previous episode of upper GI bleeding. On examination, he is a malnourished man in mild distress. His sclera are icteric, and his abdomen is distended. He has moderate pretibial edema, and his mentation is slightly impaired. Laboratory studies show a conjugated hyperbilirubinemia. Question 1 of 5 Which of the following is the most likely diagnosis? / A. Choledocholithiasis / B. Congestive heart failure / C. Hemolytic anemia / D. Hepatic cirrhosis / E. Renal failure Explanation - Q: 3.1 Close The correct answer is D. This patient's constellation of symptoms and signs can be explained by cirrhosis of the liver with portal hypertension. His shortness of breath and distended abdomen are a product of ascites from portal hypertension and liver cirrhosis. As ascites fluid accumulates, intra- abdominal pressure increases. This can lead to decreased diaphragmatic excursion, atelectasis, and shortness of breath. His history of GI bleeding suggests varices, which are a result of portal hypertension. The jaundice results from decreased flow of bile out of the cirrhotic liver. His altered mentation is from the liver's decreased ability to detoxify nitrogenous metabolites. Choledocholithiasis (choice A), or stones in the common bile duct, can cause a conjugated hyperbilirubinemia, but it is typically accompanied by severe right upper quadrant pain and it does not cause ascites. Congestive heart failure (choice B) would cause edema and shortness of breath, but it would not cause jaundice. Severe heart failure (especially right heart failure) can cause hepatic congestion, and mild ascites, but given the patient's history and symptoms, the CHF diagnosis can be excluded. Hemolytic anemia (choice C) causes an unconjugated hyperbilirubinemia. Hemolysis liberates free heme, which is a precursor to bilirubin. The rate of production of bilirubin from this heme exceeds the liver's conjugating capacity and unconjugated hyperbilirubinemia with jaundice results. It does not produce ascites. The patient's edema could be the result of renal failure (choice E), but renal failure would fail to explain the rest of his symptoms. Renal failure does not cause jaundice or GI bleeding. Question 2 of 5 A serum analysis is performed and it is found that the patient is infected with Hepatitis C. Which of the following best describes the Hepatitis C virus? / A. FIavivirus / B. Picornavirus / C. Poxvirus / D. Reovirus / E. Rhinovirus Explanation - Q: 3.2 Close The correct answer is A. The hepatitis C virus is a Flavivirus-like organism. It is less likely than hepatitis B to cause a fulminant infection, but it is more likely to cause a chronic infection. 60-90% of cases become chronic, and ultimately 40% progress to cirrhosis. The synergy of hepatitis C and alcohol is particularly damaging, and this certainly contributed to this patient's pathology. The picornavirus is a small RNA virus ( "pico" + RNA) (choice B). The most well known virus in this group causes polio. Poxviruses (choice C) do not cause hepatitis. They are known to cause molluscum contagiosum and smallpox. The reovirus (choice D) family consists of two distinct classes of virus; the rotavirus and the enteric calicivirus. Rotavirus can cause diarrheal illness, particularly in children. The enteric caliciviruses cause gastroenteritis in adults and children. Neither causes hepatitis C. Rhinoviruses (choice E) are a cause of " the common cold." Question 3 of 5 Which of the following best describes the pathophysiology underlying this patient's distended abdomen? / A. Decreased intra-abdominal pressure, decreased plasma oncotic pressure / B. Decreased portal hydrostatic pressure, decreased plasma oncotic pressure / C. Decreased portal hydrostatic pressure, increased plasma oncotic pressure / D. Increased portal hydrostatic pressure, decreased plasma oncotic pressure / E. Increased portal hydrostatic pressure, increased plasma oncotic pressure Explanation - Q: 3.3 Close The correct answer is D. Many things contribute to the accumulation of ascites fluid, but the exact mechanism is not completely understood. Known contributors include: increased portal hydrostatic pressure (from portal hypertension secondary to obstructed portal flow), decreased plasma oncotic pressure (from hypoalbuminemia secondary to failing hepatic synthesis), and a renal retention of sodium (secondary to a perceived hypovolemia from splanchnic sequestration of fluid). None of the other answer combinations occur in ascites. *** Kleptomania: click-click to browse any URL on the screen! *** Question 4 of 5 During the patient's hospitalization, his mental status deteriorates. He becomes unconscious and a flapping tremor is elicited at the wrist. Scant blood is passed per rectum. His vital signs remain stable, and his hemoglobin falls 1g/dL. EIectrolytes are normaI. Which of the following explains his altered mental state? / A. Encephalopathy secondary to gastrointestinal bleeding / B. Hypovolemia secondary to rapid accumulation of ascites fluid / C. Hypoxia secondary to gastrointestinal bleeding / D. Poor cerebral perfusion secondary to gastrointestinal bleeding. / E. Severe azotemia secondary to renal failure Explanation - Q: 3.4 Close The correct answer is A. This patient suffers from hepatic encephalopathy precipitated by gastrointestinal bleeding. In this patient, the gastrointestinal bleeding increased the amount of nitrogenous substrate available to colonic flora. These flora metabolize nitrogenous compounds into amines, which may act as neuromodulators. In patients with normal portal circulation, the liver would metabolize these compounds into nontoxic substances. In this patient, the portal hypertension causes shunting of blood into the systemic circulation without passing through the liver, producing hepatic encephalopathy. The asterixis, or flapping tremor, confirms this diagnosis. The fluid shifts in ascites are slow (compare with choice B), and would not cause altered mental status. The kidneys "sense" this fluid shift as hypovolemia and retain fluid accordingly. Hypoxia (choice C) is a common cause of altered mental status. It is unlikely that a drop in hemoglobin of only 1g/dL would cause hypoxia in the absence of any other catastrophic event. This patient has suffered a minor GI bleed. Given that the vitals are stable and the hemoglobin has fallen only slightly, it is unlikely that there is hemodynamic instability that would cause an altered level of consciousness (choice D). There is no evidence of renal failure in this scenario. The electrolytes are normal, and thus azotemia from renal failure (choice E) is an unlikely cause for this patient's altered mental status *** Kleptomania: click-click to write e-mail to any e-address on the screen! *** Question 5 of 5 Lactulose syrup is administered to this patient after he developed altered mental status. Which of the following best describes how lactulose will help restore mental function? / A. Lactulose acts as an osmotic diuretic to decrease intracranial pressure / B. Lactulose acts as an osmotic laxative to aid in evacuation of gastrointestinal blood / C. Lactulose is bactericidal to intestinal flora / D. Lactulose restores the integrity of the blood-brain barrier / E. Lactulose stabilizes axonal transmission of neural impulses Explanation - Q: 3.5 Close The correct answer is B. Lactulose is administered to patients with hepatic encephalopathy for several reasons. Following a GI bleed, removal of protein (and thus nitrogenous toxins) from the colonic lumen is paramount. Lactulose is a non-absorbable disaccharide that acts as an osmotic laxative to remove nitrogenous toxins (and their proteinaceous precursors) from the colon. In addition, bacterial metabolism of lactulose decreases the gut pH, which protonates the amines to the less absorbable ammonium form. Lactulose is not absorbed from the gut so it could not act as an osmotic diuretic (choice A). Mannitol is an osmotic diuretic used to decrease intracranial pressure. Lactulose is not bactericidal to intestinal flora (choice C). Lactulose is not absorbed from the gut and thus cannot act on the bloodbrain barrier (choice D). Lactulose is not absorbed from the gut and thus cannot affect axonal transmission (choice E).