Cardiomegaly

A 45-year-old woman presents to her primary care physician complaining of fatigue, weight gain, and shortness of breath. She has alwaysbeen an active athlete, but in the past 2 weeks, has found it impossible to jog for more than a few minutes, after which she feels tired andwinded. She feels like her appetite is normal or has even declined, but she notices that she has gained 15 pounds and her pants and shoesno longer fit welI. She has very little energy, and is sleeping poorly, with occasional difficulty breathing at night. She denies any pain, fever, orchills. Review of her chart reveals an up-to-date health screening including a normal baseline mammogram, a normaI Pap smear in the lastyear, and total cholesterol of 165 mg/dL two years ago. On physical examination, she appears comfortable, has a temperature of 36.8 C(98.2. F), blood pressure of 135/68 mm Hg, pulse of 90/min, and respiratory rate of 24/min. She appears fatigued but not in acute distress,and her skin appears normaI. Expiratory wheezes are heard at the bases of both lungs. Her heart has a normaI-sounding S1 and S2, with aII/IV soft holosystolic murmur heard best at the apex of the heart. Her abdomen is modestly distended, and her ankles are edematous. Achest x-ray film reveals cardiomegaly as well as increased vascular markings in the lung beds and bilateral small pleural effusions.Laboratory studies show:Question 1 of 5Which of the following is the most likely diagnosis?/ A. Acute leukemia/ B. Cardiomyopathy/ C. Fibromyalgia/ D. Hypothyroidism/ E. Major depressive disorder*** Any other useful examples for our users? ***

Explanation - Q: 1.1 Close

The correct answer is B. This woman has many of the classic symptoms of heart failure, with symptoms of both poor forward cardiac output (fatigue, poor appetite) and of vascular congestion in both the right and left atria (edema, abdominal distension that may be ascites, cardiomegaly, pulmonary vascular congestion and effusions seen on chest x-ray, dyspnea with exertion, and paroxysmal nocturnal dyspnea.)

Acute leukemia (choice A) is a potential cause of fatigue, poor energy, and poor nutritional status (which can cause edema and pleural effusion). Usually some abnormality will be apparent, most commonly pancytopenia, due to replacement of bone marrow with leukemic cells; the leukocyte count may be elevated due to the presence of leukemic cells in the peripheral blood. They often present with bleeding or infectious complications of pancytopenia. Anemia could potentially cause a murmur due to elevated cardiac output, but an acute leukemia would not typically cause

cardiomegaly or pulmonary edema.

Fibromyalgia (choice C) is a potential cause of fatigue, poor energy, and poor sleep, especially in women ages 25-45: its principal sign, however, is diffuse musculoskeletal pain and stiffness, with characteristic tender trigger points. It is not consistent with this patient's chest x-ray abnormalities or cardiac and lung findings.

Based on examination, this patient could certainly have hypothyroidism (choice D). Symptoms are usually insidious in onset and include fatigue, poor appetite with weight gain, poor sleep and possibly, obstructive sleep apnea. Patients often complain of constipation, cold intolerance, stiffness and muscle cramping, as well as decreased intellectual activity. Severe hypothyroidism can result in cardiomegaly, pericardial effusion, and symptoms of cardiac failure. The skin often appears dry, rough, and doughy in texture. The normal TSH, however, makes hypothyroidism in this patient very unlikely: The TSH is nearly always elevated, as most hypothyroidism is primary, which means the pituitary is secreting maximal TSH in an attempt to stimulate a hypofunctional thyroid gland. Rarely, TSH may be normal or depressed (even undetectable) in pituitary or hypothalamic failure. To rule this out, one might test first for T4 and T3 levels. Normal levels of these, in conjunction with the normal TSH, would rule out hypothyroidism as a cause of this clinical presentation.

Major depression (choice E) should always be in the differential for a patient who presents with disturbances in sleep, appetite, and energy, and can also result in weight loss or gain. These "vegetative signs" of depression may be the presenting abnormality in a depressed patient who does not note a mood disturbance themselves. One should also ask about depressed mood, anhedonia (loss of interest in or inability to take pleasure in activities the person normally enjoys), an inability to concentrate and carry on usual intellectual activities, feelings of worthlessness or guilt, and suicidal ideation. Depression cannot, however, on its own, produce the physical findings this patient has, which taken together, are worrisome for some physiologic abnormality.

Question 2 of 5Which of the following is the most likely cause of the patient's murmur?/ A. Aortic insufficiency/ B. Aortic stenosis/ C. High-output flow murmur/ D. Mitral regurgitation/ E. Mitral stenosis/ F. Pulmonic insufficiency/ G. Pulmonic stenosis/ H. Tricuspid regurgitation

/ I. Tricuspid stenosis*** If your relatives ever use the Kleptomania... ***


The correct answer is D. Mitral regurgitation is characterized by a holosystolic murmur heard best at the apex, often with a blowing sound, which may radiate to the axilla.

The murmur of aortic insufficiency (choice A) is a decrescendo diastolic murmur. Remember that the aortic valve is open during systole; a systolic murmur, then, cannot represent regurgitant aortic flow due to an improperly closed valve.

Aortic stenosis (choice B) does produce a systolic murmur caused by turbulent flow across a narrowed aortic valve during systole. This murmur is usually a crescendo-decrescendo murmur, often with a harsh quality, and is characteristically heard best at the base of the heart; it may radiate to the carotids as well.

High-output states (choice C) can cause a similar soft systolic murmur to that described here. However, this patient's history is most consistent with cardiac failure, which is a low-output state.

Mitral stenosis (choice E) causes a murmur due to turbulent low-velocity flow during diastolic filling of the left ventricle through a narrowed mitral orifice. This results in a soft diastolic murmur heard best at the apex. Remember that the mitral valve is closed during systole, therefore, an abnormal mitral sound in systole must be the sound of abnormal regurgitant flow through a closed valve.

The right-sided murmurs are less common, similar in quality, and usually less loud than the left-sided murmurs (given that pressures on the right are usually lower):

Pulmonic insufficiency (choice F), when audible, therefore causes a soft diastolic murmur at the right upper sternal border.

Pulmonic stenosis (choice G) causes a crescendo-decrescendo systolic murmur also heard at the base of the heart.

Tricuspid regurgitation (choice H) causes a holosystolic murmur at the left lower or right lower sternal border.

Tricuspid stenosis (choice I) when audible, is a diastolic murmur heard best at the same location

Question 3 of 5

BIood in the pulmonary veins is at the same pressure (during all phases of the cardiac cycle) as blood in which of the following?/ A. Aorta/ B. Left atrium/ C. Left ventricle/ D. Right atrium/ E. Right ventricle


The correct answer is B. The pressures in two chambers, which are not separated by a closed valve, will be equal. The pulmonary vein empties into the left atrium, and no valve separates the two chambers, therefore the pressures are equal in all phases of the cardiac cycle. This patient's pulmonary vascular congestion is likely due to elevated pulmonary venous pressure, which is, in turn, likely due to elevated left atrial pressures.

Pressures in the aorta (choice A) will be higher than pressures in the pulmonary veins during the cardiac cycle.

The left ventricle (choice C) is separated from the left atrium and the pulmonary veins by the mitral valve. The pulmonary veins and the left atrium are at the same pressure as the left ventricle during diastole, when the mitral valve is open. With complete mitral insufficiency, the pulmonary veins are completely exposed to left ventricular pressures during systole, resulting in severe pulmonary edema.

The right atrium (choice D) is not in communication with the pulmonary veins, being separated from them by, in sequence, the tricuspid valve, the right ventricle, the pulmonic valve, the pulmonary arterial system, and the pulmonary capillary bed.

The right ventricle (choice E), during systole, is at the same pressure as the pulmonary artery, not the pulmonary veins. During diastole, the pulmonary arterial pressure exceeds right ventricular pressure, and the valve is closed.

Question 4 of 5To improve her shortness of breath, the patient is given furosemide. What is the molecular mechanism and site of action of this drug?/ A. ADH antagonism of in the collecting ducts/ B. AIdosterone antagonism in the distal tubule/ C. BIockade of sodium reabsorption in the proximal tubule/ D. BIockade of sodium transport in the distal tubule/ E. Inhibition of carbonic anhydrase in the proximal tubule/ F. Inhibition of sodium-potassium-chloride cotransport in the loop of Henle


The correct answer is F. The Na-K-2Cl cotransporter in the loop of Henle operates via an ATP-dependent sodium-potassium exchange pump in the cell that creates a gradient for sodium diffusion from the urine space into the cell. This maintains the sodium concentration gradient of the renal medulla. Furosemide is the most commonly used loop diuretic; it acts by blocking the action of the cotransporter in the thick ascending limb of the loop of Henle.

ADH antagonism (choice A) is not an important diuretic drug mechanism, however, certain drugs, most notably lithium, inhibit ADH's action, resulting in nephrogenic diabetes insipidus.

Aldosterone promotes the reabsorption of sodium in the late distal tubule and collecting system and promotes the excretion of potassium. Aldosterone receptor antagonism (choice B) is the mechanism of action of potassium-sparing diuretics such as spironolactone.

Sodium reabsorption in the proximal tubule (choice C) is a largely passive process, which is coupled to the transport of organic solutes and anions and also to chloride transport, via both transcellular and paracellular mechanisms.

The thiazide diuretics work primarily by blocking sodium transport in the early portion of the distal tubule (choice D).

Acetazolamide inhibits carbonic anhydrase (choice E), preventing the luminal transformation of bicarbonate into CO2, which diffuses back into the cell. Inhibition of this enzyme increases both bicarbonate and sodium concentrations in the urine, resulting in high urine pH and metabolic acidosis.

*** Time goes. Kleptomania is expiring. Order now at http://www.structurise.com/kleptomania/order.htm ***Question 5 of 5What important physiologic effect will starting this patient on an angiotensin-converting-enzyme inhibitor achieve?/ A. Decrease in arteriolar resistance, resulting in less resistance to forward cardiac output/ B. Decrease in cardiac filling pressures, resulting in less pulmonary congestion/ C. Increase in arteriolar resistance, resulting in improved blood pressure/ D. Increase in left-ventricular end-diastolic volume, improving stroke volume via Starling forces/ E. Increase in myocardial contractility, resulting in improved stroke volume/ F. Stabilization of myocardial membranes, resulting in reduced risk of arrhythmia


The correct answer is A. In cardiac failure, the juxtaglomerular apparatus releases renin in response to low blood pressure or low flow states. Renin cleaves angiotensinogen into angiotensin I, which is then cleaved by angiotensin-converting enzyme (ACE) into angiotensin II. Angiotensin II is a potent vasoconstrictor and increases blood pressure. This, however, increases the resistance against which the heart must pump, thereby reducing cardiac output. By reducing angiotensin II activity, systemic vascular resistance (normally high in cardiac failure, in an attempt to maintain blood pressure in the presence of low flow) is reduced, permitting the heart to eject more volume against a lower aortic pressure. This is often described as "afterload reduction" and is the mainstay of therapy in congestive heart failure. Paradoxically, blood pressure may not change: the reduced resistance, by permitting increased flow, may result in no net change in pressure. This is most easily understood as a physiologic manifestation of Ohm's law: V = IR. In electricity, this law means that voltage is equal to current times resistance. Blood pressure is analogous to voltage, cardiac output to current flow, and the resistance in this case is the resistance of the systemic vasculature.

Reduction of cardiac filling pressures (choice B) or "preload," is also an important aspect of the treatment of heart failure. In heart failure, the heart operates at high filling pressures and high left ventricular end-diastolic volume (LVEDV) because both aldosterone and ADH promote the retention of fluid in response to low forward flow and decreased effective circulating volume. The result is vascular congestion in the pulmonary veins due to the high LV diastolic pressure, resulting in symptomatic pulmonary edema. By reducing this preload, congestive symptoms can be relieved, and LVEDV can be reduced without significant loss of stroke volume. ACE inhibitors, however, do not reduce preload: drugs that do this are nitrates (which act as venodilators) and diuretics.

Increasing arteriolar resistance (choice C) in heart failure increases the "afterload" against which the heart must eject and does not improve cardiac output.

Increasing LVEDV (choice D) is usually helpful in hypovolemia or other states in which inadequate volume is available to the heart, thereby limiting cardiac output. This happens in the portion of the Starling curve at low LVEDV, where an increase in LVEDV results in a large increase in stroke volume. Patients in symptomatic heart failure like this patient operate at very high LVEDV and benefit from its reduction.

Increasing myocardial contractility (choice E) is beneficial in heart failure, and is the mechanism of action of inotropic drugs. This is not a mechanism of ACE inhibitors.

Prevention of arrhythmia (choice F) is also important in heart failure, as the dilated heart is vulnerable to both atrial and ventricular arrhythmias. This is not a direct action of ACE inhibitors, however.

*** We appreciate your suggestions at [email protected] ***A 23-year-old man presents to the urgent care clinic complaining of severe throat pain, fever, chills, and diffuse joint pains. He first developedsymptoms two weeks ago and was evaluated by another physician at the same clinic. A throat culture was done, and the patient was given aprescription for antibiotics that he did not filI. He now returns with a worsening of his symptoms. He has since developed severe joint pain andswelling, which first affected his right wrist, then spread to both knees, and now has also affected his left ankle. He also complains ofmoderate to severe chest discomfort and shortness of breath. His temperature is 38.7 C (101.6 F), blood pressure is 118/86 mm Hg, pulseis 104/min, and respirations are 20/min. There is an exudate on his oropharynx and bilateral anterior cervical lymphadenopathy. On lungexamination, there are bibasilar crackles, and the cardiac examination reveals tachycardia, but a normal rhythm and no murmurs or rubs.Examination of his joints reveals synovitis in his right wrist, Ieft ankle, and both knees. A c `.Í ... . ..Í. 1 .. Í . . ;.. 1 `....`.``-..--.....`..```..`-.-`.--.`Question 1 of 5 :

Which of the following is the most likely cause of this patient's cardiac findings?/ A. Acute myocardial infarction/ B. Aortic dissection/ C. Mitral regurgitation/ D. Myocarditis/ E. Wolff-Parkinson-White (WPW) syndrome


The correct answer is D. The patient has myocarditis, which is an inflammation of the cardiac muscle. It is most commonly the result of an infectious process. Signs and symptoms can range from an asymptomatic state to arrhythmias, heart failure, and death. The patient often has an antecedent infection, and in this case, he had an exudative pharyngitis.

Acute myocardial infarction (choice A) usually presents with severe squeezing left-sided chest pain that can radiate down the left arm. Patients are generally middle-aged, and can have risk factors for cardiac disease such as hypertension, diabetes, hypercholesterolemia, or a history of tobacco use. The electrocardiogram can vary from nonspecific T wave changes to ST segment elevation.

Aortic dissection (choice B) would present as sudden onset of severe chest pain, which often radiates to the back. Patients can have hypotension, depending on the severity of the dissection, or hypertension, which is often a predisposing factor. Patients can also have unequal pulses in their extremities, if the dissection affects one of the major arteries branching off the aortic arch.

Mitral regurgitation (choice C) is a result of mitral valve insufficiency, in which there is a regurgitant flow of blood across the mitral valve, from the left ventricle, into the left atrium, during systole. It is often due to rheumatic heart disease, but can also result from mitral valve prolapse, or papillary muscle rupture. Physical examination should reveal a holosystolic murmur, heard best at the apex.

Wolff-Parkinson-White (WPW) syndrome (choice E) is a ventricular preexcitation syndrome associated with an atrioventricular bypass track. Patients often have paroxysmal tachycardias, and an electrocardiogram will often reveal a shortened PR interval, a delta wave, and a wide QRS complex.

*** http://www.structurise.com/kleptomania - your source of klepting technologies ***Question 2 of 5What underlying condition can explain the patient's upper respiratory as well as cardiac and joint signs and symptoms?/ A. Acute rheumatic fever/ B. Budd-Chiari syndrome/ C. Ebstein's anomaly/ D. Sjögren syndrome/ E. Takayasu arteritis


The correct answer is A. Acute rheumatic fever is an inflammatory disorder that affects multiple systems. There are five major criteria for rheumatic fever: carditis, migratory polyarthritis, subcutaneous nodules, Sydenham chorea, and erythema marginatum. There are also minor criteria: fever, arthralgia, elevated acute phase reactants, and a prolonged PR interval.

Budd-Chiari syndrome (choice B) is an occlusion of the major hepatic veins, which leads to congestive liver disease. Patients often have abdominal pain, jaundice, and hepatomegaly.

Ebstein's anomaly (choice C) is due to an anomalous attachment of the tricuspid leaflets, and results in downward displacement of the tricuspid valve into the right ventricle. This results in tricuspid regurgitation. Symptoms

can vary from cyanosis to arrhythmias.

Sjögren syndrome (choice D) is an autoimmune disorder characterized by inflammatory changes in glands, producing dry eyes and dry mouth.

Takayasu arteritis (choice E) is a vasculitis syndrome that affects medium to large arteries, in particular, the aortic arch and its branches. It is also known as "pulseless disease" because patients have weak or absent pulses in their upper extremities. It primarily affects young Asian females.

Question 3 of 5Which of the following test results would help confirm the most likely diagnosis?/ A. EIevated antinuclear antibody/ B. Low anti-deoxyribonuclease B titer/ C. Low anti-hyaluronidase titer/ D. Low anti-streptolysin O titer/ E. Throat culture positive for group A streptococci


The correct answer is E. To meet criteria for the diagnosis of rheumatic fever, patients must have either two major, or 1 major and 2 minor criteria, plus evidence of an antecedent streptococcal infection. A throat culture positive for group A streptococci would fulfill the criteria in the presence of myocarditis and migratory polyarthritis.

Elevated antinuclear antibody (choice A) is not associated with rheumatic fever. In the appropriate clinical setting, it is helpful in the diagnosis of rheumatologic disorders such as systemic lupus erythematous.

Anti-streptolysin O (choice D), anti-deoxyribonuclease B (choice B), and anti-hyaluronidase (choice C) are all streptococcal antibody tests. In the setting of rheumatic fever associated with a recent group A streptococcal infection, the titers for these antibody tests would be elevated (in the absence of infection, they may actually be undetectable). A significant titer of any of these antibody tests would meet criteria for the documentation of an antecedent streptococcal infection.

*** $29.95 for endless klepting at http://www.structurise.com/kleptomania ***Question 4 of 5A biopsy of the affected cardiac tissue would most likely show which of the following?/ A. Angiosarcoma/ B. Aschoff body/ C. Atheromas/ D. Hyperplastic arteriolosclerosis

/ E. Libman-Sacks lesionsExplanation - Q: 2.4 Close

The correct answer is B. The Aschoff body is the classic lesion of rheumatic fever. It is an area of focal interstitial myocardial inflammation. It is characterized by large cells, known as Anitschkow myocytes, and Aschoff cells, which are multinucleated giant cells.

Angiosarcoma (choice A), a rare malignant tumor affecting the vascular tissue, can occur in the skin, breast, liver, or musculoskeletal system.

Atheromas (choice C) are fibrous plaques within the intima of arteries. They are a finding of atherosclerosis.

Hyperplastic arteriolosclerosis (choice D) is characterized by concentric, laminated thickening of arteriolar walls. It often occurs in the kidneys, and may lead to malignant nephrosclerosis.

Libman-Sacks lesions (choice E) are small vegetations that occur on valvular heart tissue. They can occur on either side of the valve, and are associated with endocarditis in systemic lupus erythematous.

uest|on 0The patient continues to deteriorate, he develops worsening heart failure, and requires transfer to the intensive care unit for use of aninotropic agent to increase his cardiac output. Which of the following agents would most likely be used?/ A. Benazepril/ B. Diltiazem/ C. Dobutamine/ D. Metoprolol/ E. Phenylephrine*** $29.95 for endless klepting at http://www.structurise.com/kleptomania ***


The correct answer is C. Dobutamine is a positive inotropic agent used in severe cases of heart failure that require inotropic support.

Benazepril (choice A) is an angiotensin converting enzyme inhibitor. Medications in this class can be used in heart failure to decrease afterload, but they do not have any direct affect on cardiac tissue.

Diltiazem (choice B) and metoprolol (choice D) are both negative inotropic agents. When used in the setting of acute heart failure, the patient's course can worsen, although beta blockers such as metoprolol and carvedilol (mixed alpha and beta blocker) are sometimes cautiously used in some

patients with CHF.

Phenylephrine (choice E) is an alpha-receptor agonist. It causes vasoconstriction, and is used in severe cases of hypotension.

*** Request more tips by using Kleptomania ***A 78-year-old man had been previously active, but found that his health was declining. Over a four-month period, his ability to perform evenvery minimal exercise, such as walking around his yard, declined precipitously. The family took him from doctor to doctor, none of whom wereinitially able to figure out what was wrong with him. Because of the patient's age, most of the physicians that the family consulted wereunwilling to do much other than to listen to the family's story and then run a few screening tests. In some ways, he acted as if he were incongestive heart failure, but he initially had no evidence of fluid overload and his lungs were clear. The cardiac profile on chest X-ray wasslightly enlarged. His ECG studies were interpreted as within the normal range for his age. Angiography studies showed no evidence ofsignificant coronary artery occlusion. Pulmonary function studies were unrevealing.Question 1 of 6Following a Thanksgiving meaI, the patient's condition worsened markedly over the next few hours, and he was taken to an emergencydepartment. At that point, the patient was in obvious, severe, congestive heart failure with evidence of fluid overload and pulmonary edema.Intravenous furosemide was started, which over the next few hours markedly improved his clinical condition. Furosemide is classified aswhich of the following?/ A. Carbonic anhydrase inhibitor/ B. Loop diuretic/ C. Osmotic diuretic/ D. Potassium-sparing diuretic/ E. Thiazide diuretic


The correct answer is B. Large, salty, holiday meals are notorious for setting off (potentially fatal) exacerbations of what might have been previously mild congestive failure. There are a number of drugs with diuretic activity that can increase the amount of urine that is produced. Pharmacologists subclassify these drugs based on the mechanisms by which they act. Furosemide is a diuretic that is commonly used in the hospital setting in intravenous form to rapidly reduce the degree of fluid overload present in a patient in severe congestive heart failure. This diuretic acts by inhibiting the Na/K/2Cl cotransporter on the luminal membrane of the

thick ascending portion of the loop of Henle. It is consequently classified as a loop diuretic, as is ethacrynic acid, which has a similar mechanism of action.

Carbonic anhydrase inhibitors (choice A), such as acetazolamide and dorzolamide, act on the proximal convoluted tubule to reduce Na+ resorption secondary to an inhibition of CO2 formation with resulting decreased intracellular bicarbonate and H+ levels.

Osmotic diuretics (choice C), such as mannitol, inhibit water reabsorption throughout the nephron.

Potassium-sparing diuretics (choice D), such as spironolactone, amiloride, and triamterene, act at the level of the collecting tubules and ducts by acting as aldosterone receptor antagonists.

Thiazide diuretics (choice E), such as hydrochlorothiazide, indapamide, and metolazone, inhibit the Na/Cl cotransporter in the distal convoluted tubule.

Question 2 of 6The patient is seen the following morning by a cardiologist. The cardiologist does a very careful physical examination. He notes that the heartsounds appear distant. He then has the patient lie at an angle of 30 to 45 degrees, and does a careful examination of the right jugular pulse,which he finds very worrisome. The pulse is both very elevated and shows dramatic x and y descents. Further, he notes that the venousdistention paradoxically increases during inspiration. This last finding is sometimes called which of the following?/ A. Chvostek's sign/ B. Corrigan's sign/ C. Homans' sign/ D. KussmauI's sign/ E. Murphy's sign*** If your relatives ever use the Kleptomania... ***


The correct answer is D. The sign described is Kussmaul's sign. The act of inflating the lungs during inspiration lowers the pressure in the chest while increasing that in the abdomen, drawing blood from the abdomen into the chest (and increased abdominal pressure helps to directly drive blood toward the chest). If the right atrium cannot fill, then the jugular venous pressure rises paradoxically (not so much from blood flow from the head as from the abdomen, because the inferior vena cava and superior vena cava are functionally connected through the right atrium). Kussmaul's sign is seen in patients who have non-compliant right ventricles. It can also be seen in patients with severe ascites (which increases the intra-abdominal pressure). This case illustrates the importance of considering the jugular venous pulse

as well as the arterial pulse, since the cardiologist was able to find a number of significant findings pertaining to the jugular venous pulse, which other physicians had missed. The jugular venous pressure can be used at the bedside to estimate the right atrial filling pressure. The jugular venous pressure is estimated by measuring the height of the visible venous pulse above the sternal angle, and then adding 5 cm (corresponding to how far below the sternum the right atrium is located). The jugular venous waveform has an A wave, which is followed by an X descent, then a V wave, and finally a Y descent. The A wave (first rise in pressure) reflects the right atrial contraction, while the X-descent reflects right atrial diastole, and then early right ventricular systole. The V wave is the second major positive wave, and reflects continued venous inflow into the right atrium in opposition to a closed mitral valve. The following Y-descent is the negative deflection that occurs when the tricuspid valve opens in early diastole.

Chvostek's sign (choice A) is seen in tetany, and is a facial muscle spasm occurring when the facial nerve is tapped anterior to the external auditory meatus.

Corrigan's sign (choice B), which suggests aortic regurgitation, is a full, hard arterial pulse, which is followed by a sudden collapse.

Homans' sign (choice C) is pain at the back of the knee or calf when the ankle is dorsiflexed, and suggests venous thrombosis of the leg.

Murphy's sign (choice E) is pain on palpation of the right subcostal area during inspiration, and is frequently seen in acute cholecystitis.

Question 3 of 6This patient most likely has which of the following?/ A. Acute myocarditis/ B. Congestive cardiomyopathy/ C. OId left ventricle myocardial infarction/ D. Recent left ventricle myocardial infarction/ E. Restrictive cardiomyopathy


The correct answer is E. The "distant" heart sounds and jugular venous pulse findings both suggest that this patient has restrictive cardiomyopathy that is limiting the heart's ability to fill during diastole and is also impairing ventricular contraction. Other findings that may be encountered on physical examination in patients with restrictive cardiomyopathy include S3 and/or S4 heart sounds, occasional mitral or tricuspid regurgitation murmurs, and, if the patient is in secondary congestive failure, peripheral edema and pulmonary rales. Restrictive cardiomyopathy is relatively rare and the findings on physical examination are subtle, and consequently this patient's history of missed diagnosis is unfortunately not all that uncommon. Underlying causes

of restrictive cardiomyopathy include endomyocardial fibrosis, Loeffler eosinophilic endomyocardial disease, hemochromatosis, amyloidosis, sarcoidosis, scleroderma, carcinoid heart disease, and glycogen storage disease. Patients typically present at an advanced stage of the disease, and may have symptoms of angina, shortness of breath, peripheral edema, and ascites with abdominal discomfort (related to pooling of blood in the liver and other abdominal organs). Once the diagnosis is suspected, echocardiography typically demonstrates normal to symmetrically thickened heart chamber walls with rapid early-diastolic filling and slow late-diastolic filling (the cardiac chambers are acting more or less like poorly distensible plastic bags). Cardiac catheterization will more or less repeat the observations seen in the analysis of the jugular venous pulse, typically showing elevated ventricular end-diastolic pressure, normal to slightly decreased ejection fraction, and prominent x and y descents.

Acute myocarditis (choice A) can cause congestive cardiomyopathy (choice B), but the heart is usually larger and the constrictive findings seen in this case would not be present.

While recent and old myocardial infarctions affecting the right ventricle may produce similar jugular venous findings to those seen in this case, left ventricular infarction (choices C and D) would not impair right ventricular filling and contraction.

Question 4 of 6An endomyocardial biopsy is performed, which demonstrates eosinophilic acellular deposits within the myocardial biopsy. When recut,histological sections are stained with Congo red and viewed under polarized light, and the deposits appear bright green. These deposits aremost likely to be composed of which of the following?/ A. Amyloid/ B. Fibrin/ C. Hemosiderin/ D. Melanin/ E. Uric acid*** Copy file lists and folder trees from Explorer ***


The correct answer is A. Amyloid deposits are suspected when hematoxylin and eosin-stained histological sections show extracellular eosinophilic deposits. The presence of amyloidosis is confirmed when the characteristic "apple-green birefringence" on Congo red stain is demonstrated.

Fibrin deposits (choice B) are also red on hematoxylin and eosin stain, but

show no fluorescence with Congo red stain.

Hemosiderin (choice C) causes yellow brown deposits; melanin (choice D) causes brown-black deposits; and uric acid (choice E) causes yellow crystalline deposits.

*** Visit http://www.structurise.com/kleptomania for new versions ***Question 5 of 6Which of the following features of proteins is most likely responsible for the bright green appearance of the Congo red-stained materiaI?/ A. Beta pleated sheet configuration/ B. Calcium binding/ C. Iron containing heme moiety/ D. Multiple alpha helices/ E. Presence of multiple subunits


The correct answer A. It was originally assumed by biochemists that amyloid was always composed of the same material. It came as something of a shock when antibody techniques were developed that demonstrated that the antigenicity of amyloid in different clinical settings varied markedly. The common feature these proteins shared that accounted for both the affinity for Congo red and their characteristic regular fibrillar structure on electron microscopy turned out to be that the proteins all have a beta pleated sheet tertiary (secondary according to some biochemical purists) configuration, best demonstrated by X-ray diffraction.

Selective or non-selective binding to calcium (choice B) is common in proteins.

Heme moieties containing iron (choice C) are a part of myoglobin and hemoglobin.

Alpha helices (choice D) are a common secondary structure in proteins, but do not contribute to the protein forming amyloid.

The presence of multiple subunits (choice E) is also common in proteins, but does not contribute to a protein forming amyloid.

Question 6 of 6Which of the following would most likely be found in the Congo red-stained extracellular deposits with the bright green appearance underpolarized light?/ A. Amyloid AA/ B. Beta-2-microglobulin/ C. Beta protein precursor

/ D. Immunoglobulin light chains/ E. Transthyretin


The correct answer is D. Amyloidosis occurs in a large variety of forms. Primary amyloidosis is one of the more common forms of systemic amyloidosis, and can affect a variety of organs, including the heart, kidney, peripheral nerve, gastrointestinal tract, and respiratory tract. In primary amyloidosis, the amyloid is composed of immunoglobulin light chains, and the disease is now interpreted as a plasma cell disorder closely related to multiple myeloma. This interpretation is clinically significant, as it has led to modern treatments of primary amyloidosis (which formerly had a dismal prognosis) with the chemotherapies designed for multiple myeloma. The treatments are affective only if the disease is recognized and passed to the appropriate specialists as early as possible in the clinical course.

Amyloid AA (choice A) is seen in inflammation-associated amyloidosis and familial Mediterranean fever.

Beta-2-microglobulin (choice B) comprises the amyloid of dialysis-associated amyloidosis.

Beta protein precursor (choice C) comprises the amyloid seen in the brains of patients with Alzheimer's disease and Down syndrome.

Transthyretin (choice E) comprises the amyloid seen in familial amyloidosis and senile cardiac amyloidosis.

A 40-year-old man presents to the emergency department complaining of severe shortness of breath. The breathlessness has beenworsening over the past few years, and the patient reports growing tachypneic with mild exertion, and sometimes even at night. Onexamination, he has generalized edema, jugular venous distention, and hepatic distention. Cardiac examination shows a right ventricularheave, a right-sided S3, and S4 with a pulmonary ejection click. A chest x-ray film shows cardiomegaly and widening of the hilar vessels,including the pulmonary arteries. An electrocardiogram shows talI, peaked P waves in leads lI, III, and aVF, right axis deviation, and rightventricular hypertrophy.Question 1 of 5Which of the following is the most likely diagnosis?/ A. Cor pulmonale/ B. Hypertrophic cardiomyopathy/ C. Left ventricular failure/ D. Myocardial infarction

/ E. Pulmonary embolus (acute)Explanation - Q: 4.1 Close

The correct answer is A. This patient has cor pulmonale, which is defined as enlargement of the right ventricle secondary to diseases of the lung, thorax, or pulmonary circulation. In this case, it is chronic, given the duration of the patient's symptoms and the presence of many clinical sequelae of the condition: edema, jugular venous distention, hepatic distention, and right ventricular heave. The electrocardiogram also supports the diagnosis of enlargement of the right ventricle showing right axis deviation due to the increase in the mass of the right heart. Evidence of right atrial enlargement is also present, i.e., the tall peaked P waves in leads II, III, and aVF (P pulmonale).

Hypertrophic cardiomyopathy (choice B) is an anomaly in which the myocardium hypertrophies. The fibers are erratic and conduction abnormalities and outflow obstruction may result. Typically, this disorder presents in the second decade of life, and will manifest as dysrhythmia and/or shortness of breath. In addition, a right axis deviation would be inconsistent with this cardiomyopathy because the left ventricle hypertrophies, as well as the right. Thus, this diagnosis is unlikely.

Left ventricular failure (choice C) often accompanies right ventricular failure, but in this case, the right-sided symptoms, such as systemic edema, jugular venous distention, and hepatic congestion, are more pronounced. Left-sided failure shows engorgement of the entire pulmonary tree in conjunction with pulmonary edema.

Myocardial infarction (choice D) is unlikely. The ECG findings are not consistent with the pattern typically seen in MI. In addition, this patient does not suffer from the symptoms of myocardial infarction, such as chest pain, pressure, jaw numbness, and diaphoresis.

Pulmonary embolus (choice E) may cause acute right heart strain and failure, but this patient has a chronic condition. Chronic emboli may produce increased resistance in the pulmonary tree and a picture similar to this.

*** Send Kleptomania trial anywhere ***Question 2 of 5Pulmonary hypertension is suspected in the patient, and a Swan-Ganz catheter is placed. Which of the following denotes the correctanatomic sequence of vessels that would be traversed by the catheter if it was introduced into the left subclavian vein?/ A. Left subclavian vein, Ieft brachiocephalic vein, superior vena cava, right atrium, right ventricle, pulmonary artery

/ B. Left subclavian vein, Ieft common carotid, superior vena cava, right atrium, right ventricle, pulmonary artery/ C. Left subclavian vein, Ieft jugular vein, Ieft atrium, Ieft ventricle, aorta/ D. Left subclavian vein, Ieft jugular vein, superior vena cava, right atrium, right ventricle, pulmonary artery/ E. Left subclavian vein, superior vena cava, right atrium, right ventricle, pulmonary artery


The correct answer is A. The correct sequence for a catheter inserted into the left subclavian vein is as follows: left subclavian vein, left brachiocephalic vein, superior vena cava, right atrium, right ventricle, pulmonary artery. With this catheter in place, a variety of cardiac parameters can be measured, including pressures in the pulmonary artery. Thus, this catheter can aid in establishing the diagnosis of pulmonary hypertension.

Calcium channel blockers can be used in this setting to decrease pulmonary vascular resistance. Which of the following is the calciumchannel blocker that will have the most predominant effect on vascular smooth muscle?/ A. Diltiazem/ B. Hydrochlorothiazide/ C. Nifedipine/ D. Pseudoephedrine/ E. Verapamil


The correct answer is C. The calcium channel blockers vary in the propensity to affect vascular smooth muscle versus their effect on cardiac muscle. Thus, in this case, it is important to select an agent that has maximum ability to relax the smooth muscle in the pulmonary vessels. The effect on smooth muscle is as follows: nifedipine>diltiazem (choice A) >verapamil (choice E). The effect on cardiac muscle is as follows: verapamil>diltiazem>nifedipine. Thus nifedipine is the agent of choice.

Hydrochlorothiazide (choice B) is a diuretic, and thus would have no effect on the vascular smooth muscle.

Pseudoephedrine (choice D) is an alpha agonist, and therefore would cause vasoconstriction.

*** Your time worth $29.95 for infinite klepting at http://www.structurise.com/kleptomania ***Question 4 of 5Which of the following physiologic stimuli will result in decreased pulmonary vascular resistance?/ A. Decreased cardiac output/ B. Increased cardiac output/ C. Low O2 tension/ D. Lung volumes near residual volume (RV)/ E. Lung volumes near total lung capacity (TLC)


The correct answer is B. A unique feature of the pulmonary circulation is that it maintains itself as a low-pressure system. Many of the mechanisms that control pulmonary vasculature differ from those of the systemic circulation. One of these features is that pulmonary vasculature resistance is decreased in response to increased cardiac output. This is accomplished through distention of open capillaries and the recruitment of collapsed capillaries. Thus, the resistance in the pulmonary tree decreases in response to increased right ventricular output. In the pathologic state of pulmonary hypertension, in which the resistance is elevated and the ventricle fails, this decreased cardiac output (choice A) may compound the problem and trigger increased resistance in spite of the primary elevation.

Low O2 tension (choice C) in the pulmonary vessels initiates vasoconstriction. In the systemic circulation, low O2 tension initiates vasodilation.

Lung volume also affects pulmonary vascular resistance. The curve of lung volume versus pulmonary vascular resistance is U-shaped. This effect is due to the fact alveolar and extra-alveolar vessels act as resistors in series (additive), and these vessels have little intrinsic support. Thus, resistance in these vessels is affected by pleural pressures. At low lung volumes (choice D), the alveolar vessels are open, but extra-alveolar vessels are compressed. At high lung volumes (choice E), the alveolar vessels are compressed by distended alveoli, but the extra-alveolar vessels become distended due to the increase in transmural pressure. Thus a U-shaped curve describes this relationship.

Question 5 of 5Some of the examination findings indicate hepatic congestion. Which of the following terms is commonly used to identify the macroscopicpattern of red, depressed hepatic nodules with pale periphery that accompanies the chronic hepatic congestion seen in this condition?/ A. Centrilobular hemorrhage/ B. Cirrhosis

/ C. Fatty change/ D. Nutmeg liver/ E. Piecemeal necrosis


The correct answer is D. Chronic passive congestion of the liver leads to a macroscopic pattern known as nutmeg liver. This is due to the congestion of blood in the centrilobular region (dark) with hypoxia and fatty change in the more peripheral hepatocytes. When viewed macroscopically, this pattern resembles that seen in a cross section of a nutmeg, hence the name.

In this condition, centrilobular hemorrhage (choice A) usually only occurs in severe acute ischemia. This patient has a chronic condition, and thus most likely will have nutmeg liver instead.

Cirrhosis (choice B) of the liver may result from chronic damage caused by chronic congestion. It however produces a scarred, whitish, shrunken liver, and not the pattern seen here.

Fatty liver (choice C) would produce a large, smooth yellow liver and would not resemble the pattern seen here.

Piecemeal necrosis (choice E) is a microscopic finding of scattered hepatocellular necrosis. This diagnosis cannot be made macroscopically.

Cardiomegaly

Documents

Transcript of Cardiomegaly