Path Heart

Path Heart

A 17-year-old boy complains of pain in his legs when he runs more than 400 meters. Physical examination shows +1 dorsalis pedis pulses and +4 radial pulses. Blood pressure is 160/96 mm Hg in the upper extremity and 130 mm Hg in the lower extremity. A high-pitched, blowing early diastolic murmur is heard in the right second intercostal space, and it does not increase in intensity with deep, held inspiration. An arterial blood gas shows a normal Pao2 and oxygen saturation. Which of the following lesions is most likely present?

A. Aortic dissection

B. Aortic valve stenosis

C. Patent ductus arteriosus

D. Postductal coarctation of the aorta

E. Takayasu’s arteritis

QID: 108249

Option D (Postductal coarctation of the aorta) is correct. Strong pulses in the upper extremities and diminished pulses in the lower extremities associated with pain in the legs with running (claudication) are indicative of postductal coarctation of the aorta. Proximally there may be dilation of the aorta leading to aortic regurgitation (early diastolic murmur). The blood pressure and pulse amplitude is increased in the upper extremities from increased blood flow into the upper extremity vessels. There is at least a 10 mm Hg drop in blood pressure in the lower extremities. Systemic hypertension is due to reduced renal blood flow leading to activation of the renin-angiotensin-aldosterone system. Aldosterone causes renal retention of sodium, and angiotensin II constricts the peripheral resistance arterioles. There is no shunting of blood between chambers of the heart and arterial blood gases are normal. Collateral vessels develop between the anterior and posterior intercostal arteries and between the superior epigastric artery and inferior epigastric arteries to bypass the area of constriction in aorta. The collateral circulation between the anterior and posterior intercostal arteries leads to rib notching, which is visible on chest radiographs (see Fig. 10-12F in Rapid Review Pathology, 3rd edition).

Option A (Aortic dissection) is incorrect. Aortic dissection occurs in elderly men with hypertension or in young individuals with defects in collagen (e.g., Ehlers-Danlos syndrome) or elastic tissue (Marfan syndrome). Blood enters an intimal tear and dissects proximally and/or distally through the weakened media of the aorta. Aortic dissections produce pain that radiates to the back and are often associated with absent (not increased) upper extremity pulses.

Option B (Aortic valve stenosis) is incorrect. Aortic valve stenosis causes a systolic ejection murmur (not diastolic murmur). The pulse amplitude in the upper extremities is the same as that in the lower extremities.

Option C (Patent ductus arteriosus) is incorrect. Patent ductus arteriosus causes a continuous machinery-like murmur. The pulse amplitude in the upper extremities is the same as that in the lower extremities.

Option E (Takayasu’s arteritis) is incorrect. Takayasu’s arteritis is an elastic artery vasculitis that occurs in young Asian women. Pulses in the upper extremities are absent (not increased).

2. A 65-year-old man on the 5th day of hospitalization for an acute anterior myocardial infarction has recurrence of chest pain and an increase in both creatine kinase (CK)-MB and troponin I and T. Examination of the heart and lungs is normal. Which of the following is most likely responsible for the laboratory test abnormalities?

A. Myocardial rupture

B. Papillary muscle dysfunction

C. Reinfarction

D. Right ventricular infarction

E. Ventricular aneurysm

QID: 108387

Option C (Reinfarction) is correct. CK-MB isoenzymes, a marker for acute myocardial infarction, are usually gone by 3 days. Therefore, reappearance of CK-MB after 3 days indicates reinfarction or further extension of an existing myocardial infarction. Troponins I and T are the gold standard for diagnosing an acute myocardial infarction. However, troponin I remains increased for a week, while troponin T remains increased for 10 to 14 days; therefore, they cannot be used to diagnose a reinfarction.

Option A (Myocardial rupture) is incorrect. Rupture of the myocardium either produces a murmur (e.g., mitral regurgitation from posteromedial papillary muscle infarction) or cardiac tamponade with muffling of the heart sounds and jugular neck vein distention and muffled heart sounds. Neither of these findings are present in the patient.

Option B (Papillary muscle dysfunction) is incorrect. The posteromedial papillary muscle is supplied by the right coronary artery. Dysfunction or infarction due to thrombosis of the artery should produce the pansystolic murmur of mitral valve regurgitation. Cardiac examination is normal in the patient.

Option D (Right ventricular infarction) is incorrect. The right coronary artery supplies the right ventricle. Infarction of the right ventricle produces signs of right-sided heart failure, which include neck vein distention and the murmur of tricuspid valve regurgitation. These findings are not present in the patient.

Option E (Ventricular aneurysm) is incorrect. Ventricular aneurysms are a late finding in an acute myocardial infarction. They produce a precordial bulge with systole due to blood entering the aneurysm and expanding it out. They do not produce reappearance of CK-MB.

3. The figure shows a transverse section of the left and right ventricle from the enlarged heart of a 55-year-old man. Which of the following clinical disorders is most likely responsible for the changes in the left ventricle?

From Kumar V, Fausto N, Abbas A: Robbins and Cotran’s Pathologic Basis of Disease, 7th ed. Philadelphia, WB Saunders, 2004, pp 561, Fig. 12-3A.

A. Acute myocardial infarction (MI)

B. Aortic valve regurgitation

C. Dilated cardiomyopathy

D. Essential hypertension

E. I Mitral stenosis

QID: 107612

Option D (Essential hypertension) is correct. Cardiac muscle undergoes hypertrophy (increase in size) as an adaptation to an increase in workload. This occurs when muscle contracts against an increase in afterload (resistance the heart must overcome to pump blood out of the heart) or preload (increased volume of blood that the ventricle must eject). Sustained pressure in the ventricles increases wall stress, which produces changes in gene expression. Changes in gene expression result in duplication of sarcomeres, which are the contractile elements of muscle. Changes in gene expression related to an increase in afterload result in concentric thickening of the ventricular wall, which is present in this patient. Muscle thickening is due to sarcomere duplication parallel to the long axes of the cells. Essential hypertension is the most common cause of concentric hypertrophy. The increase in afterload is in the peripheral resistance arterioles, which are vasoconstricted in hypertension.

Option A (Acute myocardial infarction (MI)) is incorrect. The gross manifestation of an acute MI is a pale infarction of cardiac muscle, which is not present in this heart.

Option B (Aortic valve regurgitation) is incorrect. Improper closing of the aortic valve leads to volume overload in the left ventricle as blood drips back into the left ventricle in diastole. This increases preload in the left ventricle, which causes dilation and hypertrophy of the left ventricle. Changes in gene expression related to an increase in preload result in lengthening of the muscle due to sarcomeres replicating in series.

Option C (Dilated cardiomyopathy) is incorrect. Dilated cardiomyopathy is characterized by generalized enlargement of the heart with dilation of atria and ventricles, which are not evident in this heart.

Option E (I Mitral stenosis) is incorrect. Stenosis of the mitral valve leads to problems in opening the valve. Because less blood enters the left ventricle, the workload on the ventricle is reduced; hence, there is no stimulus for left ventricular hypertrophy.

4. A 62-year-old man complains of fatigue. Physical examination shows a harsh systolic ejection murmur, grade 4/6, that radiates into the carotid arteries. Laboratory studies show a mild microcytic anemia. A urine dipstick test is positive for blood. The photograph shows a representative section of the peripheral blood smear. Which of the following laboratory studies would most likely identify the cause of the microcytic anemia?

From Goldman L, Ausiello, D: Cecil's Medicine, 23rd ed, Saunders Elsevier, 2008, p 1174, Fig. 161-10.

A. Direct Coombs’ test

B. Enzyme assay for pyruvate kinase

C. Hemoglobin electrophoresis

D. Osmotic fragility test

E. Serum ferritin test

QID: 108047

Option E (Serum ferritin test) is correct. The systolic ejection murmur indicates aortic stenosis, and the fragmented RBCs (schistocytes) in the peripheral blood indicate the presence of a microangiopathic hemolytic anemia due to intravascular destruction of the RBCs as they hit the stenotic and dystrophically calcified valve. The damaged cells release hemoglobin directly into the blood. Haptoglobin, a protein synthesized in the liver, combines with the free hemoglobin to form complexes that are phagocytosed by macrophages in the spleen and completely degraded causing very low to absent serum haptoglobin levels. The excess hemoglobin in the plasma is then filtered into the urine producing a red color and a positive dipstick for blood. Chronic hemoglobinuria eventually causes iron deficiency and a microcytic anemia. Serum ferritin is the best screening test for iron deficiency. Since ferritin is a soluble iron-binding protein, some ferritin leaks out of bone marrow macrophages and directly reflects the ferritin stores in the bone marrow. In iron deficiency, ferritin stores are decreased; therefore, serum ferritin is also decreased. Aortic stenosis is the most common cause of a hemolytic anemia associated with schistocytes.

Option A (Direct Coombs’ test) is incorrect. The direct Coombs’ test detects the presence of IgG and/or C3b on the surface of RBCs. It is useful when autoimmune hemolytic anemia is suspected. Autoimmune hemolytic anemia is usually normocytic; however, it would not explain

the presence of schistocytes in the peripheral blood and aortic stenosis.

Option B (Enzyme assay for pyruvate kinase) is incorrect. When anemia is caused by pyruvate kinase deficiency, the peripheral blood smear shows dehydrated RBCs with thorny projections, unlike the cells shown in the photograph. In addition, pyruvate kinase deficiency produces a normocytic (not microcytic) anemia.

Option C (Hemoglobin electrophoresis) is incorrect. Hemoglobin electrophoresis detects changes in the concentration of normal and abnormal forms of hemoglobin, such as hemoglobin S in sickle cell disease.

Option D (Osmotic fragility test) is incorrect. The osmotic fragility test is used to confirm a diagnosis of hereditary spherocytosis, in which the osmotic fragility of RBCs is increased. Hereditary spherocytosis is a normocytic anemia and spherocytes are present in the peripheral blood not schistocytes.

5. A 28-year-old man with a history of intravenous drug abuse died of complications related to septicemia. He had a history of fever and a pansystolic murmur at the apex that did not increase in intensity on deep, held inspiration. The photograph shows a valvular lesion that was present at autopsy. Which of the following valvular disorders and pathogen is the most likely cause of death?

From Damjanov I, Linder J: Pathology: A Color Atlas. St. Louis, Mosby, 2000, p 11, Fig. 1-16.

A. Aortic regurgitation and Staphylococcus aureus

B. Mitral regurgitation and S. aureus

C. Mitral stenosis and Streptococcus viridans

D. Tricuspid regurgitation and S. aureus

E. Tricuspid regurgitation and Staphylococcus epidermidis

QID: 108027

Option B (Mitral regurgitation and S. aureus) is correct. The patient had acute bacterial endocarditis (ABE; fever, septicemia, heart murmur) involving the mitral valve. Mitral valve regurgitation produces a pansystolic murmur that does not increase in intensity with deep, held inspiration. The mitral valve in the photograph shows bulky vegetations (see arrow) located along the margin or line of closure of the valve. S. aureus is the most common pathogen in acute infective endocarditis associated with intravenous drug abuse. The tricuspid valve is the most common valve involved followed by the aortic and mitral valve.

Option A (Aortic regurgitation and Staphylococcus aureus) is incorrect. Aortic regurgitation is associated with a high-pitched diastolic blowing murmur that occurs immediately after S2. As with all left-sided valvular murmurs and abnormal heart sounds, it does not increase in intensity with deep, held inspiration.

Option C (Mitral stenosis and Streptococcus viridans) is incorrect. The heart sounds associated with mitral stenosis begin with an opening snap in early of mid diastole followed by a mid-diastolic rumbling murmur. Bacterial endocarditis that is not associated with intravenous drug abuse is most often due to S. viridans, which is a pathogen that can only seed a previously damaged valve.

Option D (Tricuspid regurgitation and S. aureus) is incorrect. Although the tricuspid valve is the most common valve involved in ABE due to intravenous drug abuse, the pansystolic murmur most often located along the left parasternal border increases on deep, held inspiration, which distinguishes it from mitral regurgitation.(The negative intrathoracic pressure increases on deep inspiration and draws blood into the right side of the heart causing all heart murmurs and abnormal heart sounds to increase in intensity.)

Option E (Tricuspid regurgitation and Staphylococcus epidermidis) is incorrect. S. epidermidis is the most common cause of ABE associated with prosthetic heart valves.

6. A mother notes in her 1-month-old baby girl clear fluid in the umbilicus. She brings this to the attention of her pediatrician, who not only verifies the presence of the fluid but also palpates a midline mass. At surgery a cystic mass is noted that connects to the urinary bladder. What is the most likely diagnosis?

A. A

B. B

C. C

D. D

E. E

F. F

QID: 108417

Option D is correct. In congestive heart failure, the cardiac output is decreased and the kidney reabsorbs a slightly hypotonic fluid producing hyponatremia (↓ serum Na+ = ↑TBNa+/↑↑TBW). An increase in total body sodium (TBNa+) is clinically manifested by weight gain, dependent pitting edema, and body effusions. Since POsm and serum Na+ parallel each other, hyponatremia produces a decreased POsm; therefore, the overall height of the interrupted squares is decreased. Since excess fluid is being added to the ECF compartment (primarily the interstitial space), the ECF compartment is expanded. Hyponatremia establishes an osmotic gradient causing water to shift from the ECF into the ICF compartment causing expansion of that compartment as well. This emphasizes the importance of restricting water and sodium in heart failure and using diuretics to eliminate excess sodium and water. Other edema states that can be associated with schematic D are cirrhosis and the nephrotic syndrome.

Option A is incorrect. A represents an isotonic loss of fluid (e.g., secretory diarrhea in cholera

and traveler’s diarrhea; loss of whole blood). Serum sodium remains normal (also POsm) when equal amounts of water and sodium are lost (↔serum Na+ = ↓TBNa+/↓TBW). Only the ECF compartment is contracted. A decrease in TBNa+ produces signs of volume depletion (hypotension, dry mucous membranes, tenting of the skin). There is no osmotic gradient; therefore, the ICF compartment is normal.

Option B is incorrect. Schematic B occurs when there is a hypertonic loss of fluid (e.g., diuretics, Addison’s disease, 21-hydroxylase deficiency). Loss of hypertonic fluid produces a hyponatremia (↓serum Na+ = ↓↓TBNa+/↓TBW). Since fluid is lost, the ECF compartment is contracted. Hyponatremia establishes an osmotic gradient; therefore, water shifts into the ICF compartment.

Option C is incorrect. Schematic C occurs when there is an isotonic gain of fluid (e.g., excessive infusion of normal (0.9&percnt;) saline. The serum sodium remains normal (↔serum Na+ = ↑TBNa+/↑TBW); therefore, the POsm is normal. Since fluid is being added to the ECF, it is expanded. There is no osmotic gradient; therefore, the ICF remains normal. The treatment is diuretics.

Option E is incorrect. Schematic E occurs when there is a hypotonic loss of sodium (e.g., sweating, osmotic diuresis, glucosuria). The serum sodium is increased (hypernatremia; ↑ serum Na+ = ↓TBNa+/↓↓TBW), causing an increase in POsm and an increase in the height of the interrupted squares. Since fluid is being lost, the ECF compartment is contracted. Hypernatremia establishes an osmotic shift; therefore, water moves out of the ICF compartment. F is incorrect. Schematic F occurs when there is a hypertonic gain of sodium (e.g., excessive infusion of sodium bicarbonate; infusion of a sodium containing antibiotic). The serum sodium is increased (hypernatremia; ↑ serum Na+ = ↑↑TBNa+/↑TBW), causing an increase in POsm and an increase in the height of the interrupted squares. Since fluid is being added, the ECF compartment is expanded (pitting edema; body effusions). Hypernatremia establishes an osmotic shift; therefore, water moves out of the ICF compartment.

7. A 48-year-old man is admitted to the hospital for an acute myocardial infarction (MI). Four days later, he suddenly becomes short of breath. Physical examination shows a pansystolic murmur at the apex that does not increase in intensity with deep, held inspiration. Bibasilar inspiratory crackles are heard in both lung bases. There is no neck vein distention. Laboratory studies show absence of serum creatine kinase MB (CK-MB) and increased serum troponin-I (cTnI) and troponin-T (cTnT). Which of the following complications has most likely occurred in this patient?

A. Anterior wall rupture

B. Interventricular septum rupture

C. Posterior wall rupture

D. Posteromedial papillary muscle rupture

E. Rupture of a ventricular aneurysm

QID: 108244

Option D (Posteromedial papillary muscle rupture) is correct. The posteromedial papillary muscle in the left ventricle is supplied by the right coronary artery (RCA) (see Fig. 10-5, Rapid Review Pathology, 3rd edition). Rupture of this muscle causes acute mitral regurgitation (pansystolic murmur at the apex that does not increase in intensity with deep, held inspiration), which leads to left-sided heart failure (pulmonary edema with bibasilar inspiratory crackles). Serum CK-MB peaks in 24 hours and returns to normal within 72 hours; therefore, it is not expected to be increased on day 4. Both cTnI and cTnT peak in 24 hours and return to normal within 7 to 10 days, which is an expected finding.

Option A (Anterior wall rupture) is incorrect. The entire anterior portion of the heart and the anterior two-thirds of the interventricular septum is supplied by the left anterior descending (LAD) coronary artery. Rupture of the anterior wall causes cardiac tamponade and rapid death. There are no murmurs with this type of rupture.

Option B (Interventricular septum rupture) is incorrect. The entire anterior portion of the heart and the anterior two-thirds of the interventricular septum are supplied by the LAD coronary artery. Rupture of the interventricular septum causes a systolic murmur with a left-to-right shunt, resulting in right-sided heart failure. Signs of right-sided heart failure are not present in this patient (e.g., neck vein distention, dependent pitting edema).

Option C (Posterior wall rupture) is incorrect. The entire posterior portion of the left ventricle, the posterior one-third of the interventricular septum, and the right ventricle are supplied by the RCA. Rupture of the posterior wall of the heart is uncommon and causes cardiac tamponade and rapid death. It is not associated with heart murmurs.

Option E (Rupture of a ventricular aneurysm) is incorrect. Ventricular aneurysms occur 4 to 8 weeks after a myocardial infarction. They produce a precordial bulge that correlates with systole (not present in this patient). The aneurysms rarely rupture because their walls are composed of scar tissue. Congestive heart failure is the most common complication.

8. The photograph is a histologic section of a pathologic finding in the left anterior descending coronary artery of a 56-year-old man. Which of the following drugs is most frequently used to prevent the pathologic finding in the coronary artery?


A. Abciximab

B. Alteplase

C. Aspirin

D. Ticlopidine

E. Warfarin

QID: 108035

Option C (Aspirin) is correct. The histologic section shows a thrombus (red-colored) occluding the lumen of the coronary artery. Directly underneath the thrombus is a fibrous cap (blue-colored lesion), the pathognomonic lesion of atherosclerosis. Directly beneath the blue fibrous cap is a core of necrotic material containing cholesterol (clear, needle-shaped spaces). There is a small fissure at the edge of the fibrous cap (disrupted plaque) that contains necrotic atheromatous debris. This debris was responsible for initiating the formation of a platelet thrombus in the lumen of the vessel. Aspirin is the most frequently used medication to prevent platelet aggregation. It does so by irreversibly inhibiting platelet cyclooxygenase activity. This prevents the production of prostaglandin H2 and its conversion to thromboxane A2 by the enzyme thromboxane synthase in the platelet. Thromboxane A2 is a potent vasoconstrictor and platelet aggregator.

Option A (Abciximab) is incorrect. Abciximab is a monoclonal antibody that is directed against

the glycoprotein (Gp) IIb/IIIa fibrinogen receptor on platelets. Fibrinogen, which is later converted into fibrin, is responsible for causing the platelet to aggregate to form a thrombus. Abciximab is very expensive and is most often used after angioplasty or stenting to prevent thrombus formation.

Option B (Alteplase) is incorrect. Alteplase is a recombinant tissue plasminogen activator that is used to lyse a preexisting platelet thrombus. Plasminogen activators cause the release of plasmin within the thrombus which leads to cleavage of the fibrin strands holding the thrombus together. It is not used to prevent a platelet thrombus.

Option D (Ticlopidine) is incorrect. Ticlopidine (or clopidogrel) inhibits ADP-induced expression of platelet GpIIb:IIIa receptors, which prevents fibrinogen binding and platelet aggregation. It is expensive and is most often used if patients are allergic to aspirin.

Option E (Warfarin) is incorrect. Warfarin is an anticoagulant that inhibits the formation of venous clots. Venous clots frequently develop in areas of stasis (e.g., deep veins of the lower leg) and are produced by localized activation of the coagulation system leading to the formation of fibrin strands that entrap the blood that is present in the vessel lumen. Hence, the thrombus is composed of RBCs, WBCs, and platelets held together by fibrin strands. Hence, an anticoagulant like warfarin or heparin prevents activation of the coagulation system and the formation of fibrin, which, in turn, prevents a venous clot from forming. Warfarin and heparin do not prevent platelet aggregation and the formation of a platelet thrombus.

9. A 22-year-old woman saw her physician because of a severe sore throat. Three weeks later, she complained of fever, pains in the knees, and a rash on the arms that consisted of a circular ring of erythema around normal skin. Other findings on physical examination included bibasilar inspiratory crackles, an S3 and S4 heart sound, and a pansystolic murmur at the apex that radiated into the axilla. Both murmur and S3 and S4 heart sounds did not increase in intensity on deep, held inspiration. Which of the following test results is most likely present in this patient?

A. Increased anti-streptokinase O (ASO) titer

B. Normal serum anti-DNAase B titers

C. Positive blood culture

D. Positive serum antinuclear antibody test

E. Positive throat culture for Staphylococcus aureus

QID: 108030

Option A (Increased anti-streptokinase O (ASO) titer) is correct. This patient developed acute rheumatic fever (ARF) several weeks after a group A streptococcal (Streptococcus pyogenes) pharyngitis. Clinical findings in ARF include sore throat, followed within several weeks by fever, joint pain, subcutaneous nodules, and skin changes (erythema marginatum, as in this case). The pansystolic murmur at the apex is caused by mitral regurgitation due to a sterile endocarditis (see Fig. 10-13 in Rapid Review Pathology, 3rd edition), and the bibasilar inspiratory crackles and S3 and S4 heart sounds are caused by left-sided heart failure due to myocarditis, which decreases the force of contraction leading to a systolic dysfunction type of heart failure. Valvular regurgitation and the myocarditis produce left ventricular volume overload, which is responsible for the abnormal heart sounds. The S3 heart sound is due to blood entering a volume overloaded chamber in early diastole, while the S4 heart sound is due to blood entering a noncompliant left ventricle in late diastole. Cardiac damage is caused by antibodies directed against the streptococcal M proteins (virulence factor), which cross-react with antigens in the heart and other tissues (i.e., type II hypersensitivity reaction). Type IV hypersensitivity has also been implicated in the disease. Blood cultures are negative, because rheumatic fever causes immunologic damage (fibrinoid necrosis) to the heart and tissues. The serum antistreptolysin O titers are increased and are useful in confirming the diagnosis.

Option B (Normal serum anti-DNAase B titers) is incorrect. In ARF, anti-DNAase B antibodies are increased, because DNAase B is an important inflammatory enzyme associated with Streptococcus pyogenes infections involving the skin and throat.

Option C (Positive blood culture) is incorrect. The blood culture is negative in ARF. It is not an example of infective endocarditis.

Option D (Positive serum antinuclear antibody test) is incorrect. In ARF, antibodies are directed against the M protein (virulence factor) of Streptococcus pyogenes and not against nuclear antigens (e.g., DNA, histones, acidic nuclear proteins, nucleolar antigens).

Option E (Positive throat culture for Staphylococcus aureus) is incorrect. In ARF, the throat culture is positive for Streptococcus pyogenes, a group A streptococcus.

10. A 62-year-old man was admitted to the hospital with severe retrosternal chest pain that radiated down the left arm. Three days later, he developed a ventricular arrhythmia and died. In the hours shortly after the patient first experienced chest pain, which of the following biochemical changes would have marked the beginning of irreversible damage to the cardiac muscle?

A. Decreased intracellular pH

B. Decreased Na+, K+-ATPase activity

C. Increased activity of phosphofructokinase

D. Increased concentration of cytosolic Ca2+

E. Increased conversion of pyruvate to lactate

QID: 107617

Option D (Increased concentration of cytosolic Ca2+) is correct. An increase in cytosolic Ca2+ concentration marks the beginning of irreversible damage to the cardiac muscle. Normally, a Ca2+ ATPase pump pumps Ca2+ out of the cytosol into the interstitial fluid. Calcium within the cytosol activates phospholipase in the cell membrane, proteases in the cytosol, and endonucleases in the nucleus, which produces irreversible injury and death of the cell.

Option A (Decreased intracellular pH) is incorrect. Decreased intracellular pH marks hypoxic change that is still reversible if O2 becomes available to hypoxic tissue, in this case, cardiac muscle. The nicotinamide adenine dinucleotide plus hydrogen (NADH) that is normally shuttled into the mitochondria for adenosine-5'-triphosphate (ATP) synthesis is used in anaerobic glycolysis to convert pyruvate to lactate, which reduces the intracellular pH.

Option B (Decreased Na+, K+-ATPase activity) is incorrect. Decreased Na+, K+-ATPase activity marks hypoxic change that is reversible if O2 becomes available to hypoxic tissue. During the early stages of an myocardial infarction (MI), lack of O2 in the muscle leads to reduced synthesis of ATP, which normally drives the ATPase pump. A dysfunctional Na+, K+ ATPase pump causes Na+ and H2O to move into cells, causing cellular swelling.

Option C (Increased activity of phosphofructokinase) is incorrect. Increased phosphofructokinase activity marks hypoxic changes that are reversible if O2 becomes available to hypoxic tissue. In the early stages of an MI, lack of O2 in cardiac muscle causes ATP synthesis to shift to anaerobic glycolysis in the cytosol. This triggers increased activity of phosphofructokinase, the rate-limiting reaction of glycolysis.

Option E (Increased conversion of pyruvate to lactate) is incorrect. Increased conversion of pyruvate to lactate occurs in anaerobic glycolysis, which is a reversible finding if O2 becomes available to the hypoxic tissue.

11. The photograph shows the heart of a 25-year-old woman who died in a car accident. Which of the following best describes the valvular lesion located in the left side of the heart?

From Kumar V, Fausto N, Abbas A: Robbins and Cotran’s Pathologic Basis of Disease, 7th ed. Philadelphia, WB Saunders, 2004, p 592, Fig. 12-23.

A. Diastolic blowing murmur after S2

B. Midsystolic click followed by a murmur

C. Opening snap followed by a mid-diastolic rumbling murmur

D. Pansystolic murmur located at the apex

E. Systolic ejection murmur located in the right second intercostal space

QID: 108028

Option B (Midsystolic click followed by a murmur) is correct. The photograph shows the posterior leaflet of the mitral valve being prolapsed (projected into) the left atrium. Mitral valve prolapse (MVP) is the most common valvular lesion in the United States. A systolic click occurs when the valve prolapses into the left atrium during systole and is suddenly restrained by the chordae tendineae. The murmur following the click is caused by mitral regurgitation as blood leaks underneath the valve cusps into the left atrium. Most patients with MVP are asymptomatic. Redundancy of the valve leaflet (which looks like a parachute) is due to an increase of dermatan sulfate in the valve causing myxomatous degeneration. The most serious complication of MVP is rupture of the chordae leading to acute mitral regurgitation and left-sided heart failure.

Option A (Diastolic blowing murmur after S2) is incorrect. A diastolic blowing murmur in the left side of the heart that occurs after S2 characterizes aortic regurgitation. Regurgitation murmurs are problems with closing of the valve; hence, blood dripping back into the left ventricle in early diastole is responsible for the murmur.

Option C (Opening snap followed by a mid-diastolic rumbling murmur) is incorrect. An opening snap followed by mid-diastolic rumbling murmur characterizes mitral stenosis. Recall that stenosis murmurs are problems with opening of the valve; hence, localizing the murmur of mitral stenosis in diastole. In mitral stenosis, the leaflets of the mitral valve are fibrotic and frequently calcified. It is most often caused by recurrent attacks of rheumatic fever over a period of time ranging from 2–10 years.

Option D (Pansystolic murmur located at the apex) is incorrect. A pansystolic murmur located at the apex characterizes mitral regurgitation. Since there is no obstruction to blood flow, the blood redirected into the left atrium produces a murmur throughout systole; hence the term pansystolic. Both the left atrium and left ventricle become volume overloaded. The mitral regurgitation in MVP follows a systolic click and does occur throughout systole unless there is rupture of the chordae.

Option E (Systolic ejection murmur located in the right second intercostal space) is incorrect. A systolic ejection murmur in the right second intercostal space characterizes aortic stenosis, in which the area of the valvular orifice is reduced. Ejection murmurs have a diamond-shaped appearance (crescendo-decrescendo) on a phonocardiogram. The aortic valve is normal in this heart.

12. A febrile 30-year-old woman with systemic lupus erythematosus (SLE) has a 4-day history of precordial chest pain that increased when she leaned back and decreased when she leans forward. She now complains of progressively worsening dyspnea. Physical examination shows muffled heart sounds and neck vein distention during inspiration. Blood pressure and pulse amplitude both decrease during inspiration. What is the most likely diagnosis?


B. Constrictive pericarditis

C. Dilated cardiomyopathy

D. Pericarditis with effusion

E. Restrictive cardiomyopathy

QID: 108242

Option D (Pericarditis with effusion) is correct. Pericarditis with effusion is the most common cardiac manifestation of SLE. Inflammation of serosal epithelium (e.g., pericardium, pleura) is a characteristic finding in SLE. Immunocomplexes directed against the pericardium cause increased vessel permeability and leakage of a fibrinous exudate onto the serosal surface, producing a friction rub heard over the precordium during filling and emptying of the heart (see Fig. 2-7 in Rapid Review Pathology, 3rd edition). Fluid accumulates in the pericardial sac producing a “water bottle” configuration on a chest x-ray (see Fig. 10-24 in Rapid Review Pathology, 3rd edition). This prevents filling of the right side of the heart during inspiration (neck vein distention), when venous blood is normally drawn into the right side of the heart by the increasing negative intrathoracic pressure. Decreased right-sided filling causes a decrease in cardiac output, resulting in decreased pulse amplitude and blood pressure during inspiration as well; this is called pulsus paradoxus. The pain caused by inflammation of the pericardium is aggravated by leaning back and is relieved by leaning forward. Fluid must be removed from the pericardial sac by paracentesis or death will occur.

Option A (Aortic dissection) is incorrect. Aortic dissection occurs in elderly men with hypertension or young individuals with defects in collagen (Ehlers-Danlos syndrome) or elastic tissue (Marfan syndrome). Blood enters an intimal tear and dissects proximally and/or distally through the weakened media of the aorta. Pain radiates into the back and is often associated with absent upper extremity pulses.

Option B (Constrictive pericarditis) is incorrect. Constrictive pericarditis is most often idiopathic or a complication of tuberculosis. Incomplete filling of the cardiac chambers is caused by thickening of the parietal pericardium. Constrictive pericarditis is not a complication of the pericarditis associated with SLE.

Option C (Dilated cardiomyopathy) is incorrect. Dilated cardiomyopathy is associated with an enlarged heart with dilation of atria and ventricles as well as biventricular congestive heart failure. Signs of right-sided heart failure (e.g., dependent pitting edema) or left-sided heart failure (e.g., pulmonary edema) are not present in this patient.

Option E (Restrictive cardiomyopathy) is incorrect. Restrictive cardiomyopathy is characterized by decreased ventricular compliance (decreased filling of the heart) caused by an infiltrative disease of the myocardium (e.g., amyloid). Pericardial effusions are not usually present.

13. A 28-year-old man has fever, fatigue, difficulty breathing, and substernal chest pain while walking or at rest. The patient has a history of alcohol abuse. Physical examination shows bibasilar inspiratory crackles, distention of the jugular neck veins, hepatomegaly, and

dependent pitting edema. Pansystolic murmurs along the left parasternal border and apex are present as well as S3 and S4 heart sounds. A chest radiograph shows generalized enlargement of all chambers and alveolar infiltrates in the lungs. The ejection fraction was 10&percnt; (normal ≥ 55&percnt;). Laboratory studies reveal an increase in cardiac-specific troponins and creatine kinase (CK)-MB. The photograph shows a histologic section of myocardial tissue from a subendocardial biopsy. Which of the following is the most likely cause of the heart disease?


A. Acute rheumatic fever

B. Coronary artery thrombosis

C. Ischemic heart disease

D. Toxin-induced myocarditis

E. Viral myocarditis

QID: 108026

Option E (Viral myocarditis) is correct. The histologic section shows an extensive lymphocytic infiltrate (round nuclei) and dissolution of myocardial fibers, which are characteristic of a viral-induced acute myocarditis. Clinical findings include left-sided heart failure (dyspnea, bibasilar inspiratory crackles, alveolar infiltrates); right-sided heart failure (neck vein distention, hepatomegaly, dependent pitting edema); tricuspid and mitral valve regurgitation (pansystolic murmur due to dilated valve rings) with S3 and S4 heart sounds related to volume increases in both ventricles; a decreased ejection fraction (systolic dysfunction due to decreased contractility); and myocardial damage (increased cardiac-specific troponin levels and CK-MB). Coxsackievirus is the most common viral cause of myocarditis. In this patient, the myocarditis has produced dilated (congestive) cardiomyopathy. This patient will likely require a cardiac transplantation.

Option A (Acute rheumatic fever) is incorrect. A patient with rheumatic fever would have a

history of group A streptococcal infection (usually pharyngitis) and other features of acute rheumatic fever including polyarthritis, subcutaneous nodules, and erythema marginatum.

Option B (Coronary artery thrombosis) is incorrect. Histologic features of thrombosis leading to a myocardial infarction include coagulation necrosis (loss of nuclei and cross-striations) and a neutrophilic infiltrate, neither of which are present in the histologic section.

Option C (Ischemic heart disease) is incorrect. Chronic ischemic heart disease is associated with patchy replacement of myocardial tissue by collagen.

Option D (Toxin-induced myocarditis) is incorrect. There is nothing in the history to suggest toxin exposure (e.g., diphtheria toxin, alcohol, drugs); hence, this is an unlikely cause of the dilated cardiomyopathy.

14. A 55-year-old woman with a history of chronic rheumatic heart disease suddenly developed weakness and sensory changes in the right side of the face and right upper extremity. On auscultation, an opening snap and mid-diastolic rumble located at the apex of the chest was heard. Pulse was irregular, and there was a loss of a wave in the jugular venous pulse. On day 3 of hospitalization, the patient had cardiorespiratory arrest and died. The photograph shows the gross appearance of the brain at autopsy. Which of the following underlying conditions best explains the cause of the lesion?

From Damjanov I, Linder J: Pathology: A Color Atlas. St. Louis, Mosby, 2000, p 408, Fig. 19-25B.

A. Cerebral atherosclerosis

B. Embolism from the heart

C. Metastatic carcinoma

D. Ruptured berry aneurysm

E. Systemic hypertension

QID: 108174

Option B (Embolism from the heart) is correct. The patient’s mitral stenosis (opening snap followed by a mid-diastolic rumble) with atrial fibrillation (irregularly irregular pulse) secondary to left atrial dilation. A thrombus most likely developed in the left atrium and embolized to the brain, causing an infarction in the left cerebral cortex in the distribution of the middle cerebral artery. The photograph shows a wedge-shaped hemorrhagic infarction that extends to the surface of the brain. It is hemorrhagic because the embolus was broken down by the fibrinolytic system, causing reperfusion of the infarcted area of the brain.

Option A (Cerebral atherosclerosis) is incorrect. The majority of cerebral infarctions are due to thrombosis overlying an atheromatous plaque located in the middle cerebral artery. This produces a pale (not hemorrhagic) infarction that extends up to the surface of the brain.

Option C (Metastatic carcinoma) is incorrect. Metastases to the brain usually are multiple, nonhemorrhagic, and peripherally located at the junction of the white and gray matter. The history does not suggest the presence of an underlying cancer in this patient.

Option D (Ruptured berry aneurysm) is incorrect. Most ruptured berry (saccular) aneurysms are located at the junction of the anterior cerebral artery and anterior communicating artery. Rupture usually is into the subarachnoid space rather than the brain parenchyma.

Option E (Systemic hypertension) is incorrect. Hypertension causes vascular changes in small vessels, causing rupture of a vessel into the brain parenchyma. Most intracerebral hemorrhages are located in the basal ganglia, particularly the putamen and external capsule rather than the periphery of the brain.

15. A 60-year-old man with angina pectoris and a 35-pack-year history of smoking cigarettes suddenly clutches his chest and dies. He had no previous history of a heart murmur. Which of the following findings is most likely present at autopsy?


B. Coronary artery thrombosis

C. Hypertrophic cardiomyopathy

D. Rupture of the anterior wall of the left ventricle

E. Severe coronary artery atherosclerosis

QID: 108246

Option E (Severe coronary artery atherosclerosis) is correct. Sudden cardiac death is defined as death within 1 hour after the onset of symptoms (e.g., chest pain). Severe coronary artery atherosclerosis, often involving multiple vessels, is present at autopsy. Coronary artery thrombosis is present in <20&percnt; of cases. Smoking is one of the most common environmental contributors to sudden cardiac death. It often precipitates ventricular arrhythmias.

Option A (Aortic dissection) is incorrect. Aortic dissections cause pain radiating into the back and are not a common cause of sudden death.

Option B (Coronary artery thrombosis) is incorrect. Severe coronary artery atherosclerosis, often involving multiple vessels, is present at autopsy in sudden cardiac death. Coronary artery thrombosis occurs in <20&percnt; of cases.

Option C (Hypertrophic cardiomyopathy) is incorrect. Hypertrophic cardiomyopathy is characterized by asymmetric hypertrophy of the interventricular septum. The conduction system in the septum is abnormal, which may precipitate fatal arrhythmias. Although there is a variant that occurs in the elderly, it would not be the most common cause of sudden cardiac death.

Option D (Rupture of the anterior wall of the left ventricle) is incorrect. Rupture of the anterior wall leading to cardiac tamponade and death usually occurs 3 to 7 days following an acute anterior myocardial infarction, not immediately after the onset of symptoms of chest pain.

16. A 52-year-old woman had a 10-year history of chronic left-sided and right-sided heart failure and, most recently, pulmonary hypertension. As a child and young adult, she had numerous episodes of pharyngitis. At autopsy, the heart showed thickening of the mitral valve leaflets and fusion of the commissures. There was thickening of the right ventricular wall and atherosclerosis of the pulmonary artery. The pulmonary vessels prominently protruded from the cut surface of the lung parenchyma. Which of the following is the most likely cause of the valvular disease?

A. Ischemic heart disease

B. Libman-Sacks endocarditis

C. Mitral valve prolapse (MVP)

D. Recurrent bacterial endocarditis

E. Recurrent rheumatic fever

QID: 108038

Option E (Recurrent rheumatic fever) is correct. The patient had chronic recurrent rheumatic fever and developed mitral stenosis. Recall that in rheumatic fever antibodies directed against the M proteins of certain strains of group A streptococci cross-react with antigens present in cardiac valves (most commonly the mitral valve) and other tissues. Repeated valve inflammation leads to repair by fibrosis, dystrophic calcification, and eventual stenosis of the valve. This leads to atrial dilation and hypertrophy and an increase in pulmonary venous pressure resulting in pulmonary edema and pulmonary venous hypertension. Increased pulmonary vein pressure caused right ventricular hypertrophy and right-sided heart failure. The combination of pulmonary hypertension and right ventricular hypertrophy is called cor pulmonale. Gross signs of pulmonary hypertension are atherosclerosis of the pulmonary artery and prominent vessels on cut sections of the lungs.

Option A (Ischemic heart disease) is incorrect. Ischemic heart disease produces heart failure with dilation of the mitral and tricuspid valve rings leading to regurgitation murmurs; however, there is no damage to the valves leading to mitral or tricuspid stenosis.

Option B (Libman-Sacks endocarditis) is incorrect. Libman-Sacks endocarditis is the most common valvular disease in systemic lupus erythematosus. Sterile vegetations occur on the mitral valve and chordae leading to valve dysfunction characterized by mitral regurgitation rather than mitral stenosis.

Option C (Mitral valve prolapse (MVP)) is incorrect. MVP, where there is redundancy of the valve tissue due to myxomatous degeneration, is more likely to be associated with mitral regurgitation than mitral stenosis.

Option D (Recurrent bacterial endocarditis) is incorrect. Recurrent bacterial endocarditis is more likely to produce mitral regurgitation rather than mitral stenosis, because the bacteria destroy the valve leaflet and often cause rupture of the chordae tendineae.

17. A 55-year-old man with a lengthy history of chronic ischemic heart disease has difficulty breathing. Physical findings include bibasilar inspiratory crackles, distention of the neck veins, and tender hepatomegaly. The photograph shows the left ankle after finger pressure was applied to the skin. Which of the following chemical alterations is most likely operative in this patient?

From Forbes C, Jackson W: Color Atlas and Text of Clinical Medicine, 2nd ed. St. Louis, Mosby, 2003, Fig. 5-8.

A. Decreased plasma renin activity

B. Decreased serum concentration of antidiuretic hormone (ADH)

C. Decreased serum concentration of atrial natriuretic peptide (ANP)

D. Decreased total body sodium concentration

E. Increased serum concentration of aldosterone

QID: 108004

Option E (Increased serum concentration of aldosterone) is correct. Increased serum concentration of aldosterone (secondary aldosteronism) is partly responsible for retention of sodium in this patient and the presence of pitting edema (slide). Pitting edema is due to an alteration in Starling’s pressure (increased in plasma hydrostatic pressure and/or decrease in oncotic pressure). Sodium retention increases plasma hydrostatic pressure and decreases oncotic pressure (dilutes serum albumin due to an excess in plasma volume). The fluid that accumulates in the interstitial tissue is protein-poor and cell-poor (i.e., transudate). The patient

has signs and symptoms of both left-sided heart failure (dyspnea and bibasilar inspiratory crackles) and right-sided heart failure (distention of neck veins, hepatomegaly, and dependent pitting edema). Right-sided heart failure causes a backup of blood into the venous system, which increases the hydrostatic pressure and is the primary factor causing the pitting edema. In biventricular heart failure, decreased cardiac output decreases renal blood flow, which activates the renin-angiotensin-aldosterone (RAA) system, which leads to an increase in the serum concentration of aldosterone.

Option A (Decreased plasma renin activity) is incorrect. In biventricular heart failure, decreased cardiac output activates the RAA system and leads to an increase (not decrease) in plasma renin activity.

Option B (Decreased serum concentration of antidiuretic hormone (ADH)) is incorrect. In biventricular heart failure, a decrease in cardiac output automatically stimulates the release of ADH from the posterior pituitary gland, leading to an increase (not decrease) in serum concentration of the hormone. ADH increases renal reabsorption of free water (water without electrolytes) and produces hyponatremia, which would have been present in this patient.

Option C (Decreased serum concentration of atrial natriuretic peptide (ANP)) is incorrect. Biventricular failure causes volume overload in both atria. When either atrium is dilated with blood, ANP is released, with a subsequent increase (not decrease) in the serum concentration. ANP has a diuretic effect in the kidneys, which helps the kidneys eliminate sodium. Brain natriuretic peptide would also be increased because of distention of the ventricles.

Option D (Decreased total body sodium concentration) is incorrect. In biventricular heart failure, decreased cardiac output activates the RAA system. The increase in aldosterone is partly responsible for retention of sodium in this patient and contributes to an increase (not decrease) in total body sodium, which is invariably present in the pitting edema states (e.g., right-sided heart failure, cirrhosis, nephrotic syndrome). The primary source for the increase in total body sodium is increased renal reabsorption of sodium in the proximal tubules of the kidneys.

18. A 58-year-old man had a sudden onset of difficulty breathing and substernal chest pain with radiation down the inner aspects of both arms that lasted for a few hours. The patient subsequently died in a coronary care unit. The photograph shows a cross-section of the left and right ventricles. The anterior portion of the heart is at the top. Based on the gross appearance of the infarction and location, which of the following would most likely have been present on the day of his death?

From Damjanov I, Linder J: Pathology: A Color Atlas. St. Louis, Mosby, 2000, p 22, Fig 1-47.

A. Increased serum creatine kinase (CK)-MB

B. Increased serum troponins I and T

C. Q waves in leads I and aVL

D. Q waves in leads I, V4−V6, and aVL

E. Q waves in leads V1−V4

QID: 108029

Option B (Increased serum troponins I and T) is correct. The patient had an acute myocardial infarction (MI) involving the posterior wall of the left ventricle. Note the bright yellow area of infarction (coagulation necrosis) and the rim of dark red granulation tissue (blood vessels + collagen formation) surrounding the infarction (white arrow in photograph). These findings are present approximately 1 week after a transmural (Q-wave) infarction. The posterior wall of the left ventricle is supplied by the right coronary artery; therefore, a right coronary artery thrombosis is most likely responsible for the infarction. The serum concentration of troponins I and T begin to increase 3 to 12 hours after cardiac injury, peak within 24 hours, and return to normal within 7 to 10 days; hence, these would have been increased at the time of death.

Option A (Increased serum creatine kinase (CK)-MB) is incorrect. Levels of CK-MB begin to increase 4 to 8 hours after infarction, peak in 24 hours, and return to normal within 1.5 to 3 days. Therefore, CK-MB would not have been present at the time of death.

Option C (Q waves in leads I and aVL) is incorrect. Q waves in leads I and aVL are present in an infarction involving the lateral wall of the left ventricle, which is supplied by the left circumflex coronary artery.

Option D (Q waves in leads I, V4−V6, and aVL) is incorrect. Q waves in leads I, V4–V6, and aVL occur in an anterolateral wall infarction of the left ventricle due to thrombosis of the

midportion of the left anterior descending coronary artery or the circumflex coronary artery.

Option E (Q waves in leads V1−V4) is incorrect. Q waves in leads V1–V4 are present in an anterior wall infarction of the left ventricle and are most often due to thrombosis of the left anterior descending coronary artery.

19. The photograph shows the cut surface of the liver removed at autopsy from a 65-year-old woman with hepatomegaly. Which of the following is the most likely cause of this disorder?


A. Alcohol abuse

B. Biventricular heart failure

C. Metastatic disease

D. Portal vein thrombosis

E. Viral hepatitis

QID: 108101

Option B (Biventricular heart failure) is correct. The photograph shows a mottled, cut surface of the liver. The dark areas represent congested central veins. These findings are indicative of centrilobular necrosis (“nutmeg liver”), which is most often caused by left-sided heart failure (LHF) and right-sided heart failure (RHF). LHF decreases cardiac output causing hypoperfusion of the liver. This results in ischemic necrosis of hepatocytes located around the central vein. RHF causes a backup of systemic venous blood into the central veins and sinusoids, which produces congestion of central veins and sinusoids and necrosis of hepatocytes around the central vein. Clinical findings include painful hepatomegaly with or without jaundice. Increased transaminases are caused by ischemic necrosis. Left untreated, it may progress to cardiac cirrhosis with fibrosis around the central veins.

Option A (Alcohol abuse) is incorrect. Alcohol abuse most often causes a fatty liver, which has a fatty, yellow appearance (not a mottled, cut surface).

Option C (Metastatic disease) is incorrect. Liver metastasis is associated with nodular masses surrounded by a normal-appearing liver.

Option D (Portal vein thrombosis) is incorrect. Portal vein thrombosis does not cause liver congestion, because the portal vein normally empties blood into the liver. However, patients develop portal hypertension, ascites, and splenomegaly.

Option E (Viral hepatitis) is incorrect. Viral hepatitis causes generalized hepatomegaly; however, it is not associated with vessel congestion.

20. A 50-year-old man had an acute anterior myocardial infarction (MI) 4 days ago, and he now complains of substernal chest pain with radiation into the left arm and jaw. Physical examination shows no cardiac or pulmonary abnormalities. Laboratory studies show increases in serum creatine kinase MB (CK-MB), serum troponin-I (cTnI), and serum troponin-T (cTnT). Which of the following is the most likely cause of the chest pain?

A. Angina pectoris

B. Pericarditis

C. Reinfarction

D. Right ventricular infarction

E. Rupture of the anterior wall

QID: 108240

Option C (Reinfarction) is correct. After an uncomplicated acute MI, serum CK-MB peaks in 24 hours and returns to normal within 72 hours. Therefore, the presence of CK-MB on day 4, after an MI, indicates reinfarction. Both cTnI and cTnT peak in 24 hours and return to normal within 7 to 10 days following an uncomplicated MI. The presence of cTnI and cTnT on day 4 is expected.

Option A (Angina pectoris) is incorrect. Angina pectoris causes myocardial ischemia without causing myocardial cell injury. Angina pectoris does not lead to an increase in CK-MB, troponin-I, and troponin-T.

Option B (Pericarditis) is incorrect. Pericarditis is inflammation of the surface lining of the heart, causing precordial chest pain and a pericardial friction rub. Pericarditis does not damage the myocardial tissue and lead to an increase in the cardiac enzymes.

Option C (Right ventricular infarction) is incorrect. Isolated right ventricular infarction is extremely rare, because the blood vessels perfusing the right ventricle are usually too small to develop occluding atheromas. Right ventricular infarction produces signs of right-sided heart failure (neck vein distention, dependent pitting edema), which are not present in the patient.

Option D (Rupture of the anterior wall) is incorrect. Rupture caused by necrosis of the myocardial wall usually occurs on days 3 to 7 following an MI. Rupture of the anterior wall produces cardiac tamponade with muffled heart sounds and neck vein distention followed by rapid death. The patient has a normal cardiac exam.

21. A 55-year-old man with chronic ischemic heart disease complains of muscle weakness. The photograph shows the ECG in the patient. Which of the following drugs is most likely to be responsible for these findings?

From Goldman L, Bennet JC: Cecil Textbook of Medicine, 21st ed. Philadelphia, WB Saunders, 1999, Fig 102-7.

A. Aldosterone blocker

B. β-Adrenergic blocker

C. Calcium channel blocker

D. Digitalis

E. Loop diuretic

QID: 108005

Option E (Loop diuretic) is correct. Loop diuretics are associated with hypokalemia (decreased serum K+ concentration), which can produce both muscle weakness and the characteristic ECG pattern of a prominent U wave (positive wave) following the T wave. Loop diuretics cause hypokalemia by blocking the Na+-K+-2 Cl− cotransport system in the thick ascending limb in the renal medulla. This causes increased exchange of Na+ for K+ in the late distal tubules and collecting tubules and increased urinary loss of K+ resulting in hypokalemia. Hypokalemia causes muscle weakness by interfering with the normal repolarization of muscle.

Option A (Aldosterone blocker) is incorrect. An aldosterone blocker (e.g., spironolactone) interferes with the normal exchange of Na+ for K+ in the late distal and collecting tubules, resulting in increased urinary loss of Na+ (diuretic effect) and retention of K+ (hyperkalemia). Hyperkalemia produces a peaked T wave on an ECG.

Option B (β-Adrenergic blocker) is incorrect. β-Adrenergic blockers inhibit the Na+, K+-ATPase pump, causing Na+ to move into cells and K+ out of cells (may produce hyperkalemia). Hyperkalemia produces peaked T waves.

Option C (Calcium channel blocker) is incorrect. Calcium channel blockers produce sinus bradycardia. They do not produce electrolyte abnormalities (e.g., hypokalemia).

Option D (Digitalis) is incorrect. Digitalis inhibits the Na+, K+-ATPase pump in cardiac muscle, which normally enhances the movement of Na+ into the muscle and the opening of calcium channels resulting in an increase in muscle contraction. Since K+ is pumped out of the cell, hyperkalemia may occur in digitalis toxicity.

22. The heart shown in the photograph is from a 22-year-old man, who died suddenly while playing softball. Physical examination prior to death revealed a systolic ejection type murmur that decreased in intensity when the patient was supine and increased in intensity when he stood up. What is the most likely cause diagnosis?

From Schoen FJ: Interventional and Surgical Cardiovascular Pathology: Correlations and Basic Principles, Saunders, 1989.

A. Aortic regurgitation

B. Aortic stenosis


D. Mitral stenosis

E. Mitral valve prolapse (MVP)

QID: 108229

Option C (Hypertrophic cardiomyopathy) is correct. The patient had hypertrophic cardiomyopathy, the most common cause of sudden cardiac death in young people. The familial form (most common) is autosomal dominant with nearly complete penetrance. Abnormal genes are mapped to chromosome 14, where there is usually a mutation in the myosin heavy chain gene. There is hypertrophy of the myocardium with disproportionately greater hypertrophy of the interventricular septum (IVS) than the free left ventricular wall, as evident in the photograph. IVS hypertrophy may obstruct blood flow through the outflow tract; however, most patients do not have severe obstruction of the outflow tract. As blood exits the left ventricle, the anterior leaflet of the mitral valve is drawn against the asymmetrically hypertrophied IVS causing the obstruction. Aberrant myofibers are present in the conduction system. Because the left ventricle is hypertrophied, it is noncompliant and restricts filling. A harsh systolic ejection murmur is best heard along the left sternal border and has a palpable double apical impulse. Murmur intensity increases (obstruction worsens) with decreased preload (e.g., standing up) and decreases (obstruction lessens) with increased preload (e.g., lying supine). Increasing preload opens the outflow track. Sudden death is due to ventricular tachycardia/fibrillation, most likely related to the aberrant myofibers in the conduction system.

β-Blockers are the mainstay of therapy, because they prolong diastole allowing for more blood to enter the left ventricle.

Option A (Aortic regurgitation) is incorrect. Aortic regurgitation is characterized by an early diastolic murmur directly after the second heart sound. The left ventricle would be dilated and hypertrophied.

Option B (Aortic stenosis) is incorrect. Aortic stenosis is characterized by a systolic ejection murmur due to a stenotic aortic valve (normal in this patient). Murmur intensity increases with an increase in preload (decreases in hypertrophic cardiomyopathy) and decreases in intensity with a decrease in preload (increases in hypertrophic cardiomyopathy). Aortic stenosis is associated with syncope but not sudden cardiac death.

Option D (Mitral stenosis) is incorrect. Mitral stenosis is characterized by the presence of an opening snap followed by a diastolic rumble. The mitral valve is normal in this patient.

Option E (Mitral valve prolapse (MVP)) is incorrect. MVP produces a midsystolic ejection click followed by a murmur. There is no redundancy of the mitral valve leaflets in the photograph. MVP does not cause sudden cardiac death except when associated with Marfan syndrome, where conduction defects are often present.

23. A 65-year-old man with a history of coronary artery disease complains of severe substernal chest pain for the past 24 hours. He states that the pain also radiates down the left arm. A blood sample is drawn for electrolytes and serum creatine kinase (CK) isoenzyme MB. Owing to technical difficulties in collecting the blood, the sample is visibly hemolyzed. The serum potassium and CK isoenzyme MB are both increased. An ECG shows a Q wave in the anterior leads; however, there are no T-wave abnormalities present. Which of the following correctly describes the test results?

Serum potassiumSerum CK-MBA.False negative True positiveB.False positive False positiveC.False positive True positiveD.True positive False positiveE. True positive True positive

A. false negative, true positive

B. false positive, false positive

C. false positive, true positive

D. true positive, false positive

E. true positive, true positive

QID: 108334

Option C (false positive, true positive) is correct. A true positive (TP) test result is a positive test result in a person with disease, while a false positive (FP) test result is a positive test result in a person without disease. The patient has chest pain for 12 hours with radiation of the pain down the arm and into the jaw and a Q wave in an ECG. These changes are consistent with an acute myocardial infarction (AMI). A hemolyzed blood sample falsely increases the serum potassium (pseudohyperkalemia), because potassium is the major intracellular cation. Further confirmation that it is a FP test result is that the ECG does not show peaked T waves, which is a sign of pathologic hyperkalemia. The CK-MB is a true positive test result, because it begins increasing approximately 6 to 8 hours after an AMI and peaks in 24 hours. It is not falsely increased by hemolysis.

Option A (false negative, true positive) is incorrect. A false negative (FN) test result is a negative test result in a person with disease. The serum potassium is a FP test result (not a FN) and the serum CK-MB is correctly classified as a TP test result.

Option B (false positive, false positive) is incorrect. The serum potassium is correctly classified as a FP test result; however, the serum CK-MB is a TP test result (not a FP).

Option D (true positive, false positive) is incorrect. The serum potassium is a FP test result (not a TP), and the serum CK-MB is a TP test result (not a FP).

Option E (true positive, true positive) is incorrect. The serum potassium is a FP test result (not a TP), and the serum CK-MB is correctly classified as a TP test result.

24. The photograph shows the superior view of an unopened aortic valve in a 55-year-old man. Which of the following complications commonly occurs with this type of aortic valve lesion?

From Silver MD, Gotlieb AI, Schoen FJ: Cardiovascular Pathology, 3rd edition, Churchill Livingstone, 2001, p. 424, Fig. 13.26B.

A. Acute myocardial infarction (MI)

B. Aortic dissection

C. Hemolytic anemia

D. Hypertension

E. Ischemic stroke

QID: 108034

Option C (Hemolytic anemia) is correct. The photograph shows a bicuspid aortic valve with severe aortic stenosis due to fibrocalcific involvement of the two valve cusps. A common complication of severe aortic stenosis is an intravascular hemolytic anemia with schistocytes (fragmented RBCs; microangiopathic hemolytic anemia), which may lead to chronic iron-deficiency anemia from loss of hemoglobin in the urine. Serum haptoglobin levels are often zero, because haptoglobin combines with free hemoglobin in the plasma and is removed from the circulation by splenic macrophages. Absent haptoglobin levels is a sign for cardiovascular surgeons to replace the valve.

Option A (Acute myocardial infarction (MI)) is incorrect. Aortic stenosis is the most common valvular lesion associated with angina with exercise due to concentric hypertrophy of the left ventricle. The thickened muscle wall does not receive sufficient blood flow during exercise resulting in angina from subendocardial ischemia. There is no increased risk for a myocardial infarction.

Option B (Aortic dissection) is incorrect. Aortic dissection is associated with hypertension and connective tissue disorders leading to cystic medial degeneration. It is not a complication of

aortic stenosis.

Option D (Hypertension) is incorrect. In aortic stenosis, the diminished area of the stenotic valve orifice eventually leads to a decrease in stroke volume and cardiac output, which reduces systolic pressure but has no effect on diastolic pressure. It is not a cause of hypertension.

Option E (Ischemic stroke) is incorrect. Aortic stenosis is the most common valvular lesion associated with syncope with exercise. However, it is not associated with an ischemic stroke, which is most often related to atherosclerosis or embolic disease to the middle cerebral artery.

25. A 59-year-old man had an acute anterior myocardial infarction (MI). Six weeks later, he saw his physician because of fever and precordial chest pain that was less severe when he leaned forward. On physical examination, a friction rub was heard over the precordium. Which of the following mechanisms is most likely involved in the pathogenesis of abnormality in the heart?

A. Alteration in Starling’s pressure

B. Immunologic reaction

C. Rupture of the anterior wall

D. Ventricular aneurysm

E. Viral infection

QID: 108031

Option B (Immunologic reaction) is correct. The patient has fibrinous pericarditis producing a pericardial friction rub (see Fig. 2-7 in Rapid Review Pathology, 3rd edition). Because of the MI 6 weeks earlier, an immunologic reaction is the likely cause. In Dressler’s syndrome (post–MI syndrome), the patient develops antibodies against the pericardial tissue, which is frequently damaged in a transmural (Q wave) infarction. Antibodies are directed against pericardial antigens (type II hypersensitivity reaction) leading to acute inflammation with a subsequent increase in vessel permeability and production of a fibrinous exudate that covers the surface of the heart. Clinical manifestations of Dressler’s syndrome include fever, precordial friction rub, and pain that increases on inspiration but lessens when the patient leans forward. Fibrinous pericarditis also may occur in the first week of an acute transmural infarction. However, the pericarditis in this time frame is due to increased vessel permeability not related to immunologic damage of the pericardium.

Option A (Alteration in Starling’s pressure) is incorrect. An alteration in Starling’s pressure

refers to increased hydrostatic pressure or decreased oncotic pressure within the vascular compartment. The transudate produced by this change is poor in proteins and cells, unlike the fibrinous exudate that is associated with a fibrinous pericarditis.

Option C (Rupture of the anterior wall) is incorrect. A rupture of the anterior wall occurs 3 to 7 days after an acute MI, causing cardiac tamponade and death.

Option D (Ventricular aneurysm) is incorrect. A ventricular aneurysm is clinically recognized within 4 to 8 weeks after a transmural infarction. It presents with a precordial bulge during systole as blood enters the aneurysm causing anterior chest wall movement. The most common complications are heart failure and embolization of clot material. There is no association with fibrinous pericarditis.

Option E (Viral infection) is incorrect. Coxsackievirus is the most common cause of pericarditis. This patient’s history of a previous MI indicates that an immunologic cause for the pericarditis is more likely than an infection.

26. The photograph shows a skin lesion on a mentally retarded 25-yr-old man who also has reddish-brown papules on his nose, cheeks, and chin. What additional findings may be present in this patient?

Courtesy of The Honickman Collection of Medical Images in memory of Elaine Garfinkel and The Jefferson Clinical Images Collection (through the generosity of JMB, AKR, LKB and DA)

A. Acoustic neuroma

B. Arteriovenous malformation in meninges

C. Meningioma

D. Renal cell carcinoma

E. Rhabdomyoma of the heart

QID: 108198

Option E (Rhabdomyoma of the heart) is correct. The patient has tuberous sclerosis, an autosomal-dominant neurocutaneous disorder. It is characterized by mental retardation, seizures beginning in infancy, adenoma sebaceum (red-brown papules on the face), hypopigmented skin lesions (“ash leaf” lesions; see photograph) and various hamartomatous lesions. Astrocyte proliferations occur in the subependyma and are the cause for seizure activity. Angiomyolipomas commonly occur in the kidneys, and rhabdomyomas may occur in the heart (almost 100&percnt; predictive of tuberous sclerosis).

Option A (Acoustic neuroma) is incorrect. Neurofibromatosis is also a neurocutaneous syndrome like tuberous sclerosis and the type 2 variant is associated with acoustic neuromas, often bilateral.

Option B (Arteriovenous malformation in meninges) is incorrect. Sturge Weber syndrome is a neurocutaneous syndrome with a vascular malformation of the face in a trigeminal nerve distribution and ipsilateral arteriovenous malformation in the meninges.

Option C (Meningioma) is incorrect. Neurofibromatosis has an increase in meningiomas in the brain. The lesions in the brain in tuberous sclerosis are astrocyte hamartomas.

Option D (Renal cell carcinoma) is incorrect. Angiomyolipomas of the kidney do occur in tuberous sclerosis; however, they are hamartomas and do not progress into a renal cell carcinoma.

27. A 55-year-old man has an anterior myocardial infarction. He is placed on aspirin, heparin, and warfarin. Which of the following sets of hemostasis studies is most likely to be present in this patient?

Platelet Count

Bleeding TimePT PTT

A.Normal · Normal·B.Normal Normal Normal·C. · · · ·D.Normal ↑ ↑ ↑E. Normal Normal ↑ ↑

PT, prothrombin time; PTT, partial thromboplastin time.

A. platelet count normal, bleeding time increased, PT normal, PTT increased

B. platelet count normal, bleeding time normal, PT normal, PTT increased

C. platelet count decreased, bleeding time increased, PT increased, PTT increased

D. platelet count normal, bleeding time increased, PT increased, PTT increased

E. platelet count normal, bleeding time normal, PT increased, PTT increased

QID: 108378

Option D (platelet count normal, bleeding time increased, PT increased, PTT increased) is correct. In an acute anterior myocardial infarction, aspirin is used to prevent thrombus formation either in the coronary arteries or the damaged endothelium in the left ventricle. Aspirin prevents platelet aggregation causing prolongation of the bleeding time without affecting the platelet count. Patients are frequently anticoagulated with heparin and warfarin. Heparin enhances antithrombin III activity leading to neutralization of many of the coagulation factors including thrombin and X in the final common pathway. This prolongs the PT and the PTT, although the latter test is a better test to follow heparin therapy. Warfarin inhibits further activation of the vitamin K–dependent coagulation factors (II, VII, IX, and X). Since factors II and X are in the final common pathway, the PT and PTT are both prolonged; however, the former test is a better test to follow warfarin therapy when it is converted into the international normalized ratio.

Option A (platelet count normal, bleeding time increased, PT normal, PTT increased) is incorrect. This set of studies is most often associated with classic von Willebrand disease. In this autosomal dominant disorder, there is a deficiency of von Willebrand factor (vWF), which is necessary for platelet adhesion to areas of endothelial injury. This prolongs the bleeding time without affecting the platelet count. In the circulation, vWF also complexes with factor VIII coagulant (VIII:C), which prevents degradation of VIII:C. Therefore, deficiency of vWF automatically leads to decreased factor VIII:C activity and prolongation of the PTT. The PT is normal because it does not evaluate VIII:C in the intrinsic pathway.

Option B (platelet count normal, bleeding time normal, PT normal, PTT increased) is incorrect. PT normal, PTT increased) is incorrect. This set of studies is consistent with a coagulation factor deficiency in the intrinsic coagulation pathway: XII, XI, IX, or VIII. Of the four choices, factor VIII would be the most common deficiency in a patient with hemophilia A.

Option C (platelet count decreased, bleeding time increased, PT increased, PTT increased) is incorrect. This set of data in which all the tests are abnormal is most often seen in disseminated intravascular coagulation (DIC). Tissue thromboplastin activates the extrinsic coagulation system causing the formation of fibrin thrombi within the microcirculation. Factors I, II, V, and VIII are consumed in the fibrin clots, which results in anticoagulation (PT and PTT are both

increased). Fibrin thrombi also trap platelets causing thrombocytopenia, which, in turn, is responsible for producing a prolonged bleeding time.

Option E (platelet count normal, bleeding time normal, PT increased, PTT increased) is incorrect. This set of data is most consistent with a patient that is taking warfarin and/or heparin. Rat poison contains warfarin, which blocks epoxide reductase rendering vitamin K inactive. This prevents further γ-carboxylation of the vitamin K–dependent coagulation factors: factors II (prothrombin), VII, IX, and X. Since factors X and II are in the final common pathway, both the PT and PTT are prolonged. The PT evaluates factors VII, X, V, II, and I (fibrinogen), while the PTT evaluates factors XII, XI, IX, VIII, X, V, II, and I. The platelet count and bleeding time are not affected by warfarin. Heparin enhances antithrombin III activity, which neutralizes activated serine proteases.

28. A 75-year-old man was admitted to the hospital with severe substernal chest pain that radiated into the left arm and jaw. On day 5 of hospitalization, he developed acute mitral valve regurgitation and died. The photograph shows a transverse section of the heart at autopsy with the anterior portion of the heart at the top. Which of the following coronary arteries was most likely responsible for the gross changes in the heart?

From Damjanov I, Linder J: Anderson’s Pathology, 10th ed. St. Louis, Mosby, 1996, p 374, Fig. 17-13.

A. Left anterior descending coronary artery (LAD)

B. Left circumflex coronary artery

C. Left main stem coronary artery

D. Right coronary artery

QID: 107618

Option D (Right coronary artery) is correct. The patient had an acute myocardial infarction secondary to a coronary artery thrombosis. An infarct is the gross manifestation of coagulation

necrosis that is present in underlying tissue. The gross specimen shows an extensive pale yellow infarct in the left ventricle, which involves the posterior wall and posteromedial papillary muscle (the round structure projecting into the ventricular lumen) of the mitral valve. The posteromedial papillary muscle most likely ruptured producing the acute mitral valve regurgitation and death. This area of the left ventricle is in the distribution of the right coronary artery. The infarct is pale because of the increased density of myocardial tissue, which prevents the infiltration of blood into surrounding dead tissue from necrotic blood vessels.

Option A (Left anterior descending coronary artery (LAD)) is incorrect. The LAD supplies the anterior portion of the left ventricle and anterior two-thirds of the interventricular septum.

Option B (Left circumflex coronary artery) is incorrect. In general, the left coronary artery supplies the anterior portion of the heart, not the posterior portion of the heart.

Option C (Left main stem coronary artery) is incorrect. The left circumflex coronary artery supplies the lateral portion of the left ventricle.

29. A 48-year-old man complains of fever and several fainting spells over the past few months. He states that he faints when he stands up and not when he is lying down. He also complains of pain in the left upper quadrant that is aggravated by inspiration as well as pain in the right flank. Physical examination shows a normal blood pressure when lying down and sitting up. A late diastolic murmur is heard. The spleen is enlarged and tender, and a splenic friction rub is present. There is right flank pain on percussion. A urine dipstick is positive for blood, and RBCs are present in the urine sediment. What is the most likely diagnosis?

A. Calcific aortic stenosis

B. Hypertrophic cardiomyopathy

C. Left atrial myxoma

D. Mitral stenosis

E. Pericardial effusion

QID: 108247

Option C (Left atrial myxoma) is correct. Cardiac myxomas are the most common primary cardiac tumors in adults (see Fig. 10-28 in Rapid Review Pathology, 3rd edition). Symptoms include nonspecific complaints such as fever and malaise. The tumor has a ball-valve effect that

causes sudden blockage of blood flow through the mitral valve, resulting in episodic fainting spells. A diastolic murmur similar to that of mitral stenosis is also present. Peripheral embolization of tumor also occurs. Infarctions of the spleen cause pain in the left upper quadrant and friction rubs. Infarctions of the kidneys cause flank pain and hematuria.

Option A (Calcific aortic stenosis) is incorrect. Calcific aortic stenosis is associated with a systolic ejection murmur. Angina with exercise occurs because of ischemia of the subendocardium in the concentrically hypertrophied left ventricle. The decreased cardiac output through the stenotic valve causes syncope with exercise. Peripheral embolization does not occur.

Option B (Hypertrophic cardiomyopathy) is incorrect. Hypertrophic cardiomyopathy is characterized by asymmetric hypertrophy of the interventricular septum causing findings similar to those described for calcific aortic stenosis. Peripheral embolization does not occur.

Option D (Mitral stenosis) is incorrect. Mitral stenosis is a complication of chronic rheumatic fever. Left atrial dilation and thrombus formation with embolization is a common finding. The patient has no history of recurrent rheumatic fever and physical exam does not reveal an opening snap in early diastole in this patient.

Option E (Pericardial effusion) is incorrect. A pericardial effusion produces muffled heart sounds and is not associated with syncope or with peripheral embolization.

30. A 2-day-old newborn male infant with respiratory distress syndrome (RDS) has a continuous harsh murmur that is heard over the entire precordium. Which of the following sets of oxygen saturation (Sao2) values in the cardiac chambers and vessels is most likely present in this patient?

RARVPAPVLVA0Normal SaO2757575959

595

A 7575759595

95

B 7580809595

95

C 8080809595

95

D 7575859595

95

E 7575759580

80

RA, right atrium; RV, right ventricle; PA, pulmonary artery;PV, pulmonary vein; LV, left ventricle; Ao, aorta.

A. Aortic regurgitation

B. Aortic stenosis


D. step-up of SaO2 in pulmonary artery

E. Mitral valve prolapse (MVP)

QID: 108230

Option D (step-up of SaO2 in pulmonary artery) is correct. The patient has the classic machinery murmur (continuous murmur) of a patent ductus arteriosus (PDA). This neonate has hypoxemia (decreased arterial Po2) secondary to RDS; therefore, closure of the ductus is not stimulated. When oxygenated blood (Sao2 95&percnt;) is shunted into a chamber or vessel with venous blood (Sao2 75&percnt;), there is a step-up of Sao2 (approximately 80&percnt;) in the venous blood; this is called a left-to-right shunt. Similarly, when venous blood is shunted into a chamber or vessel with oxygenated blood, there is a step-down of the Sao2 (˜80&percnt;) leading to clinical cyanosis; this is called a right-to-left shunt. In PDA, there is a left-to-right shunt causing blood to flow from the aorta (where pressure is high) through the PDA to the pulmonary artery (where pressure is low), which causes a step-up of Sao2 in the pulmonary artery (85&percnt; versus normal of 75&percnt;).

Option A (Aortic regurgitation) is incorrect. The patient has a heart murmur consistent with a PDA; therefore, there should be a step-up of SaO2 in the pulmonary artery.

Option B (Aortic stenosis) is incorrect. A step-up of Sao2 in the right ventricle (80&percnt; versus 75&percnt;) and pulmonary artery (80&percnt; versus 75&percnt;) characterizes a ventricular septal defect (VSD), a left-to-right shunt. VSD is the most common type of congenital heart disease. If a VSD is not corrected, cyanosis, or Eisenmenger’s syndrome, may eventually occur. This is due to volume overload in the right side of the heart from the left-to-right shunt causing pulmonary hypertension and right ventricular hypertrophy. When pressure in the right heart is greater than the pressure in the left heart, the shunt reverses and becomes right-to-left, causing a step-down in SaO2 in the left ventricle and aorta leading to cyanosis if SaO2 < 80&percnt;.

Option C (Hypertrophic cardiomyopathy) is incorrect. A step-up of Sao2 in the right atrium (80&percnt;), right ventricle (80&percnt;), and pulmonary artery (80&percnt;) characterizes an

atrial septal defect (ASD, left-to-right shunt), which is most often the result of a patent foramen ovale. If an ASD is not corrected, cyanosis and Eisenmenger’s syndrome may eventually occur.

Option E (Mitral valve prolapse (MVP)) is incorrect. A step-down of Sao2 in the left ventricle (80&percnt;) and aorta (80&percnt;) characterizes tetralogy of Fallot (right-to-left shunt), which is the most common type of cyanotic congenital heart disease. It consists of an overriding aorta (least common defect), VSD, pulmonary stenosis, and right ventricular hypertrophy. The degree of pulmonic stenosis determines the severity of the right-to-left shunt. If the stenosis is not severe, then most of the venous blood enters the pulmonary artery and is oxygenated; hence, the patient is often acyanotic (SaO2 > 80&percnt;). However, when the stenosis is severe, most of the venous blood is shunted through the VSD into the left ventricle (right-to-left shunt), leading to cyanosis. Note that the pulmonary vein has normally oxygenated blood (95&percnt;), because once blood enters the lungs through the stenotic pulmonic valve it is oxygenated.

31. A 50-year-old man with ischemic heart disease has signs of both left- and right-sided heart failure. Which of the following is characteristic of both types of heart failure?

A. Bibasilar inspiratory crackles

B. Decreased cardiac output

C. Dependent pitting edema

D. Jugular neck vein distention

E. Paroxysmal nocturnal dyspnea

QID: 108241

Option B (Decreased cardiac output) is correct. The heart fails when it cannot pump blood delivered to it by the venous system. Therefore, cardiac output is decreased whether the heart failure is left-sided or right-sided.

Option A (Bibasilar inspiratory crackles) is incorrect. Bibasilar inspiratory crackles are a sign of left-sided heart failure, a “forward” heart failure causing a decreased cardiac output and backup of blood in the left ventricle, left atrium, and pulmonary capillaries. Increased pulmonary capillary hydrostatic pressure causes fluid (transudate) to enter the interstitium of the lung and eventually the alveoli (pulmonary edema). Air entering alveoli containing fluid produces inspiratory crackles that are best heard at the base of both lungs.

Option C (Dependent pitting edema) is incorrect. Dependent pitting edema is a sign of right-

sided heart failure, a “backward” heart failure causing systemic venous congestion. The increase in hydrostatic pressure in the venous system causes fluid (transudate) to leak into the interstitial space through the venules, leading to dependent pitting edema.

Option D (Jugular neck vein distention) is incorrect. Jugular neck vein distention is a sign of right-sided heart failure. In right-sided heart failure, blood builds up in the venous system causing distention of the jugular veins (see Fig. 10-3 in Rapid Review Pathology, 3rd edition).

Option E (Paroxysmal nocturnal dyspnea) is incorrect. Paroxysmal nocturnal dyspnea is a sign of left-sided heart failure, which occurs primarily at night when the patient is supine in bed. At this time, gravity does not impede blood flow to the right side of the heart, and fluid from the interstitial space enters the venous system. Excess blood enters the failed left ventricle and backs up into the lungs, causing pulmonary edema and dyspnea, which awakens the patient. Symptoms resolve when the patient stands up and gravity decreases venous return to the right side of the heart.

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