A 35-year-old man presents to the physician with concerns that a “bad flu” he has had for the past 10 days is getting worse and causing sleeplessness. On presentation today, his sore throat has improved; however, fever and chest and body aches persist despite the use of ibuprofen. He reports sharp, intermittent chest pain that worsens with exertion. He has not traveled outside the United States recently and does not have a history of substance abuse or alcohol use. Physical examination shows the temperature is 38.3°C (100.9°F), the heart rate is 110/min, the blood pressure is 120/60 mm Hg, and the oxygen saturation is 98% on room air. There is bilateral pedal edema at the level of the ankle. Auscultation reveals normal S1 and S2 and a third early diastolic heart sound. Jugular vein distention is observed. An ECG shows sinus tachycardia and diffuse ST-segment elevation throughout the precordial leads with 1.0-mm PR-segment depression in leads I and II.
Laboratory results
WBC 14,000/mm3
Lymphocyte count 70%
Hematocrit 45%
CRP 56 mg/dL
Troponin T 1.15 ng/mL
Troponin I 0.2 ng/mL
Ck-MB 22 ng/mL
Coxsackie type b viral antibody positive
A chest x-ray shows clear lung fields bilaterally and a mildly enlarged cardiac silhouette. Transthoracic ultrasound reveals a left ventricular ejection fraction of 30%. Which of the following is the cause of difficulty sleeping for this patient?
Q62
A 33-year-old woman schedules an appointment at an outpatient clinic for the first time after moving to the US from Peru a few months ago. She complains of easy fatigability and shortness of breath with minimal exertion for the past 6 months. She further adds that her breathlessness is worse when she goes to bed at night. She is also concerned about swelling in her legs. As a child, she says she always had sore throats. She does not smoke or drink alcohol. Medical records are unavailable, but the patient says that she has always been healthy apart from her sore throats. The blood pressure is 114/90 mm Hg, the pulse is 109/min, the respiratory rate is 26/min, and the temperature is 36.7°C (98°F). On examination, she is icteric with distended jugular veins. Bilateral basal crepitations are audible on auscultation of the lungs. Also, a high-pitched apical holosystolic murmur is audible that radiates to the left axilla. A transthoracic echocardiogram reveals mitral regurgitation with an ejection fraction of 25%. Treatment should focus on which of the following?
Q63
A 62-year-old woman is hospitalized after a recent viral illness complicated by congestive heart failure. She has a past medical history of obesity and hypertension controlled on lisinopril but was otherwise healthy until she developed fatigue and edema after a recent viral illness. In the hospital, she is started on furosemide to manage her fluid status. On day 5 of her admission, the patient’s temperature is 100.0°F (37.8°C), blood pressure is 136/88 mmHg, pulse is 90/min, and respirations are 14/min. The patient continues to have normal heart sounds, but with crackles bilaterally on lung auscultation. Edema is 3+ up to the bilateral knees. On labs, her leukocyte count is now 13,000/mm^3, up from 9,000/mm^3 the day before. Differential shows that this includes 1,000 eosinophils/mm^3. Creatinine is 1.7 mg/dL from 1.0 mg/dL the day before. Which of the following is most likely expected on urinary analysis?
Q64
A 58-year-old man is brought to the Emergency Department after 2 days of shortness of breath, orthopnea, and lower limb edema. His past medical history is significant for hypertension and a myocardial infarction 3 years ago that required a coronary arterial bypass graft. He has not been able to take prescribed medicine in several months due to recent unemployment and issues with insurance. On admission, his blood pressure is 155/92 mmHg, heart rate is 102/min, respiratory rate is 24/min, and temperature is 36.4°C (97.5°F). On physical examination there are fine rales in both lungs, regular and rhythmic cardiac sounds with an S3 gallop and a grade II/VI holosystolic murmur. Initial laboratory tests are shown below:
Na+ 140 mEq/L
K+ 4.2 mEq/L
Cl- 105 mEq/L
BUN 20 mg/dL
Creatinine 0.8 mg/dL
The patient is stabilized and admitted to the hospital. The next day his blood pressure is 110/60 mmHg, heart rate is 110/min, respiratory rate is 18/min, and temperature is 36.4°C (97.5°F). This morning's laboratory tests are shown below:
Na+ 135 mEq/L
K+ 3.2 mEq/L
Cl- 102 mEq/L
BUN 45 mg/dL
Creatinine 1.7 mg/dL
Which of the following best explains the changes seen in this patient?
Q65
A 71-year-old woman comes to the physician because of progressive shortness of breath and swollen legs for 4 weeks. She has tried sleeping in a raised position using 2 pillows but still wakes up occasionally from a choking sensation. She returned from a safari tour in Tanzania 3 months ago. She has type 2 diabetes mellitus, arterial hypertension, and gastroesophageal reflux disease. Her sister has polymyalgia rheumatica. Her current medications include insulin, enalapril, and omeprazole. She has smoked one half-pack of cigarettes daily for 45 years. Her temperature is 37°C (98.6°F), pulse is 112/min, respirations are 22/min, and blood pressure is 119/76 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 90%. Examination shows pitting edema below the knees and jugular venous distention. Crackles are heard at both lung bases. A photograph of her tongue is shown. Her hemoglobin concentration is 10.0 g/dL, leukocyte count is 6,100/mm3, and erythrocyte sedimentation rate is 62 mm/h. ECG shows sinus rhythm and low-voltage QRS complexes. Echocardiography shows symmetrical left ventricular hypertrophy, reduced diastolic filling, and an ejection fraction of 55%. Which of the following is the most likely cause of this patient's symptoms?
Q66
Background and Methods:
Aldosterone is important in the pathophysiology of heart failure. In a double-blind study, we enrolled 1,663 patients who had NYHA class III or IV heart failure, a left ventricular ejection fraction of no more than 35%, and who were being treated with an angiotensin-converting-enzyme inhibitor, a loop diuretic, and in most cases digoxin. A total of 822 patients were randomly assigned to receive 25 mg of spironolactone daily and 841 to receive placebo. The primary endpoint was death from all causes.
Results:
The trial was discontinued early, after a mean follow-up period of 24 months, because an interim analysis determined that spironolactone was efficacious. There were 386 deaths in the placebo group (46%) and 284 in the spironolactone group (35%; relative risk of death, 0.70; 95% confidence interval, 0.60 to 0.82; P<0.001). This 30% reduction in the risk of death among patients in the spironolactone group was attributed to a lower risk of both death from progressive heart failure and sudden death from cardiac causes. The frequency of hospitalization for worsening heart failure was 35% lower in the spironolactone group than in the placebo group (relative risk of hospitalization, 0.65; 95% confidence interval, 0.54 to 0.77; P<0.001). In addition, patients who received spironolactone had a significant improvement in the symptoms of heart failure, as assessed on the basis of the New York Heart Association functional class (P<0.001). Gynecomastia or breast pain was reported in 10% of men who were treated with spironolactone, as compared with 1 percent of men in the placebo group (P<0.001). The incidence of serious hyperkalemia was minimal in both groups of patients.
To which of the following patients are the results of this clinical trial applicable?
Q67
A 52-year-old man presents to the emergency department with 1-month of progressive dyspnea, decreased exercise tolerance, and inability to sleep flat on his back. He says that he been getting increasingly short of breath over the past few years; however, he attributed these changes to getting older. He started becoming very concerned when he was unable to climb the stairs to his apartment about 3 weeks ago. Since then, he has been experiencing shortness of breath even during activities of daily living. His past medical history is significant for heroin and cocaine use as well as periods of homelessness. Physical exam reveals a gallop that occurs just after the end of systole. Which of the following could lead to the same pathology that is seen in this patient?
Q68
A 30-year-old woman visits her local walk-in clinic and reports more than one week of progressive shortness of breath, dyspnea on effort, fatigue, lightheadedness, and lower limb edema. She claims she has been healthy all year round except for last week when she had a low-grade fever, malaise, and myalgias. Upon examination, her blood pressure is 94/58 mm Hg, heart rate is 125/min, respiratory rate is 26/min, and body temperature is 36.4°C (97.5°F). Her other symptoms include fine rattles in the base of both lungs, a laterally displaced pulse of maximum intensity, and regular, rhythmic heart sounds with an S3 gallop. She is referred to the nearest hospital for stabilization and further support. Which of the following best explains this patient’s condition?
Q69
A 65-year-old man comes to the physician because of a 10-month history of progressive shortness of breath and a cough productive of a small amount of white phlegm. Bilateral end-expiratory wheezing is heard on auscultation of the chest. Pulmonary function tests show total lung capacity that is 108% of predicted, an FEV1 that is 56% of predicted, and an FEV1:FVC ratio of 62%. Which of the following interventions is most likely to slow the decline in FEV1 in this patient?
Q70
A 82-year-old man who is currently being managed by the internal medicine service agrees to be examined by medical students as part of their training in physical examination. He is visited by a small group of medical students under the instruction of a preceptor and allows the students to make observations. They find that he has bibasilar crackles that are most prominent during inspiration as well as some wheezing. Furthermore, he coughs up some sputum during the exam, and this sputum is found to have a rust color. He does not report any pain and no skin findings are seen. Which of the following conditions best explains this patient's physical exam findings?
Heart failure US Medical PG Practice Questions and MCQs
Question 61: A 35-year-old man presents to the physician with concerns that a “bad flu” he has had for the past 10 days is getting worse and causing sleeplessness. On presentation today, his sore throat has improved; however, fever and chest and body aches persist despite the use of ibuprofen. He reports sharp, intermittent chest pain that worsens with exertion. He has not traveled outside the United States recently and does not have a history of substance abuse or alcohol use. Physical examination shows the temperature is 38.3°C (100.9°F), the heart rate is 110/min, the blood pressure is 120/60 mm Hg, and the oxygen saturation is 98% on room air. There is bilateral pedal edema at the level of the ankle. Auscultation reveals normal S1 and S2 and a third early diastolic heart sound. Jugular vein distention is observed. An ECG shows sinus tachycardia and diffuse ST-segment elevation throughout the precordial leads with 1.0-mm PR-segment depression in leads I and II.
Laboratory results
WBC 14,000/mm3
Lymphocyte count 70%
Hematocrit 45%
CRP 56 mg/dL
Troponin T 1.15 ng/mL
Troponin I 0.2 ng/mL
Ck-MB 22 ng/mL
Coxsackie type b viral antibody positive
A chest x-ray shows clear lung fields bilaterally and a mildly enlarged cardiac silhouette. Transthoracic ultrasound reveals a left ventricular ejection fraction of 30%. Which of the following is the cause of difficulty sleeping for this patient?
A. Impaired gaseous exchange caused by pulmonary edema
B. Progressive cardiac ischemia caused by a plaque event
C. Decreased cardiac contractility due to cardiac myocyte injury (Correct Answer)
D. Lobar consolidation due to Staphylococcus aureus
E. Diffuse alveolar damage and hyaline membrane formation
Explanation: ***Decreased cardiac contractility due to cardiac myocyte injury***
- The patient presents with **myocarditis** following a viral infection (positive Coxsackie B antibody), leading to inflammation and injury of cardiac myocytes. This results in **decreased cardiac contractility**, significantly reducing the **ejection fraction (30%)** and causing **heart failure** symptoms like pedal edema, jugular venous distension, and difficulty sleeping due to orthopnea and paroxysmal nocturnal dyspnea, which are common in heart failure.
- The **elevated troponins** and **CK-MB** confirm cardiac myocyte injury, and the ECG findings of diffuse ST-segment elevation and PR-segment depression are classic for **pericarditis**, which often coexists with or results from myocarditis, contributing to the chest pain and overall cardiac dysfunction.
*Impaired gaseous exchange caused by pulmonary edema*
- While **pulmonary edema** can impair gaseous exchange and cause difficulty sleeping, the chest X-ray in this case shows **clear lung fields**, suggesting that significant pulmonary edema is not the primary mechanism.
- The **oxygen saturation is 98%**, indicating adequate oxygenation despite the heart failure, so impaired gaseous exchange is not the direct cause of sleeplessness.
*Progressive cardiac ischemia caused by a plaque event*
- The patient's presentation with a preceding **viral illness**, diffuse ST-segment elevation, and **positive Coxsackie B antibodies** points towards **inflammatory conditions** like myocarditis and pericarditis, rather than an ischemic event due to a plaque rupture.
- There is no mention of **risk factors for coronary artery disease**, and the chest pain characteristics are more consistent with pericarditis (sharp, intermittent, worsening with exertion) than with typical angina from a plaque event.
*Lobar consolidation due to Staphylococcus aureus*
- **Lobar consolidation** due to *Staphylococcus aureus* would typically present with symptoms of **pneumonia**, such as productive cough, dyspnea, and focal lung findings on examination and chest X-ray, none of which are described.
- The chest X-ray shows **clear lung fields**, ruling out lobar consolidation as the cause of the patient's symptoms.
*Diffuse alveolar damage and hyaline membrane formation*
- **Diffuse alveolar damage** and **hyaline membrane formation** are characteristic features of **Acute Respiratory Distress Syndrome (ARDS)**, which would manifest as severe hypoxemia and diffuse bilateral infiltrates on chest X-ray.
- This patient has **clear lung fields** and **normal oxygen saturation**, making ARDS an unlikely diagnosis.
Question 62: A 33-year-old woman schedules an appointment at an outpatient clinic for the first time after moving to the US from Peru a few months ago. She complains of easy fatigability and shortness of breath with minimal exertion for the past 6 months. She further adds that her breathlessness is worse when she goes to bed at night. She is also concerned about swelling in her legs. As a child, she says she always had sore throats. She does not smoke or drink alcohol. Medical records are unavailable, but the patient says that she has always been healthy apart from her sore throats. The blood pressure is 114/90 mm Hg, the pulse is 109/min, the respiratory rate is 26/min, and the temperature is 36.7°C (98°F). On examination, she is icteric with distended jugular veins. Bilateral basal crepitations are audible on auscultation of the lungs. Also, a high-pitched apical holosystolic murmur is audible that radiates to the left axilla. A transthoracic echocardiogram reveals mitral regurgitation with an ejection fraction of 25%. Treatment should focus on which of the following?
A. Increase coronary blood flow
B. Increase inotropy of cardiac muscle
C. Increase left ventricular end diastolic pressure
D. Decrease total peripheral resistance (Correct Answer)
E. Increase the rate of SA node discharge
Explanation: ***Decrease total peripheral resistance***
- The patient presents with symptoms and signs consistent with **mitral regurgitation (MR)** and **heart failure (HF)**, likely secondary to **rheumatic heart disease** (history of recurrent sore throats). The low ejection fraction (25%) indicates **systolic dysfunction**.
- Decreasing **total peripheral resistance (TPR)** (afterload) reduces the resistance against which the left ventricle must pump, thereby increasing **forward flow** into the aorta and reducing the regurgitant volume into the left atrium through the incompetent mitral valve. This improves cardiac output and reduces symptoms of heart failure.
*Increase coronary blood flow*
- While increased coronary blood flow is always beneficial for cardiac function, the primary problem in this patient is **valvular heart disease** leading to volume overload and systolic dysfunction, not primarily **coronary artery disease**.
- Addressing coronary perfusion would not directly resolve the immediate hemodynamic burden imposed by severe mitral regurgitation and heart failure.
*Increase inotropy of cardiac muscle*
- **Positive inotropes** increase the force of myocardial contraction and might initially seem helpful given the low ejection fraction. However, in pure MR, increasing contractility can **worsen regurgitation** by increasing the pressure gradient across the incompetent valve.
- The goal in MR is to reduce **afterload** to promote forward flow, not necessarily to increase the force of contraction against a leaking valve.
*Increase left ventricular end diastolic pressure*
- An **increased left ventricular end-diastolic pressure (LVEDP)** is indicative of **volume overload** and **heart failure**, and it is a pathological finding, not a therapeutic goal.
- Therapeutic interventions aim to decrease LVEDP by reducing preload and/or improving cardiac output, thereby alleviating congestion.
*Increase the rate of SA node discharge*
- Increasing the **heart rate** (SA node discharge) in a patient with heart failure and MR would be detrimental as it **reduces diastolic filling time**, further decreasing cardiac output, and **increases myocardial oxygen demand**.
- Tachycardia would worsen symptoms and contribute to ventricular dysfunction rather than improving it.
Question 63: A 62-year-old woman is hospitalized after a recent viral illness complicated by congestive heart failure. She has a past medical history of obesity and hypertension controlled on lisinopril but was otherwise healthy until she developed fatigue and edema after a recent viral illness. In the hospital, she is started on furosemide to manage her fluid status. On day 5 of her admission, the patient’s temperature is 100.0°F (37.8°C), blood pressure is 136/88 mmHg, pulse is 90/min, and respirations are 14/min. The patient continues to have normal heart sounds, but with crackles bilaterally on lung auscultation. Edema is 3+ up to the bilateral knees. On labs, her leukocyte count is now 13,000/mm^3, up from 9,000/mm^3 the day before. Differential shows that this includes 1,000 eosinophils/mm^3. Creatinine is 1.7 mg/dL from 1.0 mg/dL the day before. Which of the following is most likely expected on urinary analysis?
A. Nitrites positive
B. Leukocyte esterase positive (Correct Answer)
C. Bacteria > 100 CFU/mL
D. Crystals
E. Red blood cell casts
Explanation: ***Leukocyte esterase positive***
- This patient is experiencing a possible **drug-induced interstitial nephritis**, likely due to **furosemide**, given the new onset **eosinophilia**, rising creatinine, and exposure to a new medication.
- **Leukocyte esterase** detects WBCs in the urine, which are characteristic of interstitial nephritis due to inflammation in the renal interstitium.
*Nitrites positive*
- **Nitrites** are typically positive in **bacterial urinary tract infections (UTIs)**, indicating the presence of nitrate-reducing bacteria.
- The clinical picture of **eosinophilia** and **acute kidney injury** makes a primary UTI less likely in this case.
*Bacteria > 100 CFU/mL*
- A high **bacterial colony count** is a hallmark of a **bacterial urinary tract infection**, but the patient's symptoms are more consistent with drug-induced kidney injury, not infection.
- The presence of **eosinophilia** and **elevated creatinine** further points away from a straightforward UTI as the primary issue.
*Crystals*
- **Crystals** in the urine can indicate conditions like **nephrolithiasis** (kidney stones) or certain metabolic disorders, but they do not explain the patient's acute kidney injury with eosinophilia.
- This finding would not align with the suspected diagnosis of **drug-induced interstitial nephritis**.
*Red blood cell casts*
- **Red blood cell casts** are highly indicative of **glomerulonephritis**, suggesting direct damage to the glomeruli.
- While acute kidney injury is present, the associated **eosinophilia** and recent medication change are more characteristic of acute interstitial nephritis, not glomerulonephritis.
Question 64: A 58-year-old man is brought to the Emergency Department after 2 days of shortness of breath, orthopnea, and lower limb edema. His past medical history is significant for hypertension and a myocardial infarction 3 years ago that required a coronary arterial bypass graft. He has not been able to take prescribed medicine in several months due to recent unemployment and issues with insurance. On admission, his blood pressure is 155/92 mmHg, heart rate is 102/min, respiratory rate is 24/min, and temperature is 36.4°C (97.5°F). On physical examination there are fine rales in both lungs, regular and rhythmic cardiac sounds with an S3 gallop and a grade II/VI holosystolic murmur. Initial laboratory tests are shown below:
Na+ 140 mEq/L
K+ 4.2 mEq/L
Cl- 105 mEq/L
BUN 20 mg/dL
Creatinine 0.8 mg/dL
The patient is stabilized and admitted to the hospital. The next day his blood pressure is 110/60 mmHg, heart rate is 110/min, respiratory rate is 18/min, and temperature is 36.4°C (97.5°F). This morning's laboratory tests are shown below:
Na+ 135 mEq/L
K+ 3.2 mEq/L
Cl- 102 mEq/L
BUN 45 mg/dL
Creatinine 1.7 mg/dL
Which of the following best explains the changes seen in this patient?
A. Urinary tract obstruction
B. Diuretic therapy (Correct Answer)
C. Chronic renal failure
D. Glomerular basement membrane damage
E. Cholesterol emboli
Explanation: ***Diuretic therapy***
- The patient's initial presentation is consistent with **acute decompensated heart failure**, characterized by shortness of breath, orthopnea, lower limb edema, rales, S3 gallop, and a holosystolic murmur (likely mitral regurgitation due to ventricle dilation). The initial normal kidney function (BUN 20, creatinine 0.8) and electrolyte values support acute heart failure.
- The subsequent drop in blood pressure (155/92 to 110/60 mmHg), increase in heart rate (102 to 110/min), and significant rises in BUN (20 to 45 mg/dL) and creatinine (0.8 to 1.7 mg/dL) with a decrease in potassium (4.2 to 3.2 mEq/L) strongly suggest **diuretic-induced volume depletion** leading to worsened renal function (prerenal azotemia) and hypokalemia.
*Urinary tract obstruction*
- This would typically present with symptoms like **dysuria**, frequency, or hesitancy, and acute kidney injury with a more prominent rise in creatinine relative to BUN, none of which are described.
- Obstruction would be less likely to cause a significant drop in blood pressure and hypokalemia, as seen in this patient.
*Chronic renal failure*
- While kidney function has worsened, the initial labs showed normal kidney function, ruling out **chronic disease** as the cause of the acute deterioration.
- Chronic renal failure would typically present with elevated BUN and creatinine for an extended period, which is not the case here.
*Glomerular basement membrane damage*
- Conditions involving **glomerular damage**, such as glomerulonephritis, typically present with proteinuria, hematuria, and often hypertension, which are not detailed in this scenario.
- The acute changes in electrolytes and BUN/creatinine are more indicative of a **hemodynamic issue** rather than a primary glomerular pathology.
*Cholesterol emboli*
- While a patient with a history of CABG is at risk for **cholesterol emboli**, this condition typically causes acute kidney injury, livedo reticularis, eosinophilia, and digital ischemia, which are not described.
- It would not explain the rapid electrolyte shifts and clear signs of volume depletion seen in this patient.
Question 65: A 71-year-old woman comes to the physician because of progressive shortness of breath and swollen legs for 4 weeks. She has tried sleeping in a raised position using 2 pillows but still wakes up occasionally from a choking sensation. She returned from a safari tour in Tanzania 3 months ago. She has type 2 diabetes mellitus, arterial hypertension, and gastroesophageal reflux disease. Her sister has polymyalgia rheumatica. Her current medications include insulin, enalapril, and omeprazole. She has smoked one half-pack of cigarettes daily for 45 years. Her temperature is 37°C (98.6°F), pulse is 112/min, respirations are 22/min, and blood pressure is 119/76 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 90%. Examination shows pitting edema below the knees and jugular venous distention. Crackles are heard at both lung bases. A photograph of her tongue is shown. Her hemoglobin concentration is 10.0 g/dL, leukocyte count is 6,100/mm3, and erythrocyte sedimentation rate is 62 mm/h. ECG shows sinus rhythm and low-voltage QRS complexes. Echocardiography shows symmetrical left ventricular hypertrophy, reduced diastolic filling, and an ejection fraction of 55%. Which of the following is the most likely cause of this patient's symptoms?
A. Tuberculosis
B. Rheumatoid arthritis
C. Endocardial fibroelastosis
D. Multiple myeloma (Correct Answer)
E. Systemic sclerosis
Explanation: ***Multiple myeloma***
- This patient presents with **heart failure with preserved ejection fraction (HFpEF), low-voltage QRS on ECG, an elevated ESR, anemia, and macroglossia**, which are classic clinical features of **amyloid cardiomyopathy** secondary to **light chain (AL) amyloidosis**.
- **AL amyloidosis** is most commonly associated with **multiple myeloma** or other monoclonal gammopathies, and the presence of these cardiac and systemic findings strongly points to this underlying etiology.
*Tuberculosis*
- While tuberculosis can cause **pulmonary symptoms** and **anemia**, it typically presents with **fever, night sweats, weight loss**, and often **apical lung involvement** or pleural effusions, which are not characteristic here.
- It does not explain the **symmetrical left ventricular hypertrophy, low-voltage QRS**, or **macroglossia** seen in this patient.
*Rheumatoid arthritis*
- Rheumatoid arthritis is a **chronic inflammatory autoimmune disease** primarily affecting the **joints**, although it can have **extra-articular manifestations**.
- It does not typically cause **symmetrical left ventricular hypertrophy** with **low-voltage QRS** or **macroglossia**, and while it can cause an elevated ESR, it does not explain the complete clinical picture.
*Endocardial fibroelastosis*
- **Endocardial fibroelastosis** is a rare condition characterized by diffuse fibrous thickening of the **ventricular endocardium**, primarily seen in **infants and children**.
- It is an unlikely diagnosis in a **71-year-old adult** and does not typically present with the systemic features like **macroglossia** or progressive anemia and high ESR seen here.
*Systemic sclerosis*
- **Systemic sclerosis (scleroderma)** is a connective tissue disease that can affect multiple organs, including the **heart, lungs, and skin**.
- While it can cause **pulmonary hypertension** and **restrictive cardiomyopathy**, it usually presents with characteristic skin thickening, Raynaud's phenomenon, and telangiectasias, and does not typically cause **macroglossia** or the specific constellation of findings seen in AL amyloidosis.
Question 66: Background and Methods:
Aldosterone is important in the pathophysiology of heart failure. In a double-blind study, we enrolled 1,663 patients who had NYHA class III or IV heart failure, a left ventricular ejection fraction of no more than 35%, and who were being treated with an angiotensin-converting-enzyme inhibitor, a loop diuretic, and in most cases digoxin. A total of 822 patients were randomly assigned to receive 25 mg of spironolactone daily and 841 to receive placebo. The primary endpoint was death from all causes.
Results:
The trial was discontinued early, after a mean follow-up period of 24 months, because an interim analysis determined that spironolactone was efficacious. There were 386 deaths in the placebo group (46%) and 284 in the spironolactone group (35%; relative risk of death, 0.70; 95% confidence interval, 0.60 to 0.82; P<0.001). This 30% reduction in the risk of death among patients in the spironolactone group was attributed to a lower risk of both death from progressive heart failure and sudden death from cardiac causes. The frequency of hospitalization for worsening heart failure was 35% lower in the spironolactone group than in the placebo group (relative risk of hospitalization, 0.65; 95% confidence interval, 0.54 to 0.77; P<0.001). In addition, patients who received spironolactone had a significant improvement in the symptoms of heart failure, as assessed on the basis of the New York Heart Association functional class (P<0.001). Gynecomastia or breast pain was reported in 10% of men who were treated with spironolactone, as compared with 1 percent of men in the placebo group (P<0.001). The incidence of serious hyperkalemia was minimal in both groups of patients.
To which of the following patients are the results of this clinical trial applicable?
A. An 82-year-old female with NYHA class II heart failure with an LVEF of 22%, taking lisinopril, furosemide, and digoxin
B. An 86-year-old female recently found to have an LVEF of 34%, currently taking furosemide and carvedilol
C. A 78-year-old male with NYHA class II heart failure and LVEF 36%
D. A 65-year-old male with newly diagnosed NYHA class IV heart failure and a LVEF of 21%, about to begin medical therapy
E. A 56-year-old male with NYHA class III heart failure with an LVEF of 32%, currently taking lisinopril, furosemide, and digoxin (Correct Answer)
Explanation: **A 56-year-old male with NYHA class III heart failure with an LVEF of 32%, currently taking lisinopril, furosemide, and digoxin**
- This patient perfectly matches the **inclusion criteria** of the RALES trial: **NYHA class III or IV heart failure**, **LVEF ≤ 35%**, and current treatment with an **ACE inhibitor (lisinopril)**, a **loop diuretic (furosemide)**, and **digoxin**.
- The study's findings regarding spironolactone's benefits are directly applicable to such a patient, as they meet all the **demographic and clinical characteristics** of the study population.
*An 82-year-old female with NYHA class II heart failure with an LVEF of 22%, taking lisinopril, furosemide, and digoxin*
- This patient has **NYHA class II heart failure**, which is **less severe** than the inclusion criteria of **NYHA class III or IV** in the study.
- While other criteria (LVEF, medication regimen) are met, the **lower NYHA class** means the direct applicability of the study's findings might be limited, as the benefits might not be as pronounced in less severe heart failure.
*An 86-year-old female recently found to have an LVEF of 34%, currently taking furosemide and carvedilol*
- This patient is not taking an **ACE inhibitor** (like lisinopril), which was a required background medication for all participants in the RALES trial.
- While carvedilol (a beta-blocker) is also crucial in heart failure management, the study specifically investigated spironolactone as an add-on to an **ACE inhibitor-based regimen**.
*A 78-year-old male with NYHA class II heart failure and LVEF 36%*
- This patient has **NYHA class II heart failure**, which is **less severe** than the study's inclusion criteria of **NYHA class III or IV**.
- Additionally, his **LVEF of 36%** is above the study's threshold of **≤ 35%**, making him ineligible for direct application of these results.
*A 65-year-old male with newly diagnosed NYHA class IV heart failure and a LVEF of 21%, about to begin medical therapy*
- This patient has **newly diagnosed heart failure** and has not yet started the **background medical therapy** (ACE inhibitor, loop diuretic, digoxin) that all study participants were already receiving.
- The trial evaluated spironolactone as an **add-on therapy** to existing standard care, not as initial therapy for newly diagnosed heart failure patients.
Question 67: A 52-year-old man presents to the emergency department with 1-month of progressive dyspnea, decreased exercise tolerance, and inability to sleep flat on his back. He says that he been getting increasingly short of breath over the past few years; however, he attributed these changes to getting older. He started becoming very concerned when he was unable to climb the stairs to his apartment about 3 weeks ago. Since then, he has been experiencing shortness of breath even during activities of daily living. His past medical history is significant for heroin and cocaine use as well as periods of homelessness. Physical exam reveals a gallop that occurs just after the end of systole. Which of the following could lead to the same pathology that is seen in this patient?
A. Myosin mutation
B. Vitamin B1 deficiency (Correct Answer)
C. Turner syndrome
D. Amyloid production
E. Radiation therapy
Explanation: ***Vitamin B1 deficiency***
- The patient exhibits symptoms of **dilated cardiomyopathy (DCM)**, including progressive dyspnea, decreased exercise tolerance, orthopnea, and a gallop rhythm. **Vitamin B1 deficiency** (beriberi) is a known cause of **high-output cardiac failure**, which can lead to DCM.
- The patient's history of **heroin and cocaine use** and **homelessness** puts him at high risk for nutritional deficiencies, including thiamine (Vitamin B1).
*Myosin mutation*
- **Myosin mutations** are a common cause of **hypertrophic cardiomyopathy (HCM)**, not dilated cardiomyopathy.
- HCM is characterized by a **thickened ventricular wall** and impaired diastolic filling, not primarily ventricular dilation as suggested by the patient's symptoms.
*Turner syndrome*
- Turner syndrome is associated with **coarctation of the aorta** and **bicuspid aortic valve**, but not typically dilated cardiomyopathy.
- These conditions can lead to cardiovascular complications but present differently than the patient's symptoms.
*Amyloid production*
- **Amyloidosis** commonly causes **restrictive cardiomyopathy**, characterized by **stiffening of the ventricular walls** and impaired diastolic filling, leading to symptoms of heart failure.
- While amyloid can affect the heart, it typically presents with a non-dilated, stiff heart rather than the ventricular dilation seen in DCM.
*Radiation therapy*
- **Radiation therapy** to the chest can cause **restrictive cardiomyopathy**, **pericardial disease**, or **coronary artery disease**.
- It is not a common cause of dilated cardiomyopathy presenting with this specific clinical picture and risk factors.
Question 68: A 30-year-old woman visits her local walk-in clinic and reports more than one week of progressive shortness of breath, dyspnea on effort, fatigue, lightheadedness, and lower limb edema. She claims she has been healthy all year round except for last week when she had a low-grade fever, malaise, and myalgias. Upon examination, her blood pressure is 94/58 mm Hg, heart rate is 125/min, respiratory rate is 26/min, and body temperature is 36.4°C (97.5°F). Her other symptoms include fine rattles in the base of both lungs, a laterally displaced pulse of maximum intensity, and regular, rhythmic heart sounds with an S3 gallop. She is referred to the nearest hospital for stabilization and further support. Which of the following best explains this patient’s condition?
A. Lymphocytic infiltration (Correct Answer)
B. Eosinophilic infiltration
C. Giant cell infiltration
D. Granulomatous infiltration
E. Fibrosis and calcification
Explanation: ***Lymphocytic infiltration***
- The patient's presentation with **heart failure symptoms** (shortness of breath, edema, S3 gallop, displaced PMI) preceded by a **viral-like illness** (fever, malaise, myalgias) is highly suggestive of **acute myocarditis**.
- **Lymphocytic infiltration** is the hallmark histological finding in **viral myocarditis**, where **cytotoxic T-lymphocytes** attack virally infected cardiomyocytes.
*Eosinophilic infiltration*
- **Eosinophilic myocarditis** is a distinct form of myocarditis often associated with **hypersensitivity reactions** (e.g., drug-induced, parasitic infections, autoimmune conditions).
- While it can cause heart failure, the preceding viral-like illness is less characteristic, and eosinophils would be prominent histologically.
*Giant cell infiltration*
- **Giant cell myocarditis** is a rare, aggressive form of myocarditis characterized by **multinucleated giant cells** and **extensive necrosis**.
- It typically presents with rapid onset, severe heart failure, and often requires urgent transplantation, and is not typically preceded by a simple viral prodrome.
*Granulomatous infiltration*
- **Granulomatous inflammation** in the heart is seen in conditions like **sarcoidosis** or **tuberculosis**.
- While these can cause heart failure, the clinical picture here is not typical for **cardiac sarcoidosis** (which often presents with conduction abnormalities) or active tuberculosis.
*Fibrosis and calcification*
- **Fibrosis and calcification** represent chronic or healed myocardial injury rather than an acute inflammatory process.
- While these can lead to heart failure (e.g., in dilated cardiomyopathy), they are the end-stage consequences of disease, not the initial cellular infiltration explaining acute myocarditis.
Question 69: A 65-year-old man comes to the physician because of a 10-month history of progressive shortness of breath and a cough productive of a small amount of white phlegm. Bilateral end-expiratory wheezing is heard on auscultation of the chest. Pulmonary function tests show total lung capacity that is 108% of predicted, an FEV1 that is 56% of predicted, and an FEV1:FVC ratio of 62%. Which of the following interventions is most likely to slow the decline in FEV1 in this patient?
A. Salmeterol therapy
B. Fluticasone therapy
C. Smoking cessation (Correct Answer)
D. Alpha-1 antitrypsin therapy
E. Breathing exercises
Explanation: ***Smoking cessation***
- This patient's symptoms (progressive shortness of breath, cough, end-expiratory wheezing) and PFT results (reduced FEV1, reduced FEV1:FVC ratio, normal TLC) are highly suggestive of **COPD**, which is primarily caused by smoking.
- **Smoking cessation** is the only intervention clearly shown to slow the rate of FEV1 decline in patients with COPD, thereby improving long-term prognosis.
*Salmeterol therapy*
- **Salmeterol** is a long-acting beta-agonist (LABA) that provides bronchodilation and symptom relief in COPD.
- While it improves symptoms and quality of life, it does **not alter the natural history of the disease** or slow the decline in FEV1.
*Fluticasone therapy*
- **Fluticasone** is an inhaled corticosteroid (ICS) used in COPD, often in combination with LABAs, particularly for patients with frequent exacerbations.
- ICS therapy can reduce exacerbations but does **not slow the FEV1 decline** in COPD and may increase the risk of pneumonia.
*Alpha-1 antitrypsin therapy*
- **Alpha-1 antitrypsin deficiency** is a genetic cause of emphysema, typically presenting at a younger age or with a strong family history. This patient's history does not directly point to this diagnosis.
- While augmentation therapy with alpha-1 antitrypsin can slow lung function decline in genetically deficient individuals, it is **ineffective for typical smoking-induced COPD**.
*Breathing exercises*
- **Breathing exercises**, such as pursed-lip breathing, are components of pulmonary rehabilitation programs.
- They can improve symptoms, exercise tolerance, and quality of life but do **not impact the underlying disease progression** or FEV1 decline in COPD.
Question 70: A 82-year-old man who is currently being managed by the internal medicine service agrees to be examined by medical students as part of their training in physical examination. He is visited by a small group of medical students under the instruction of a preceptor and allows the students to make observations. They find that he has bibasilar crackles that are most prominent during inspiration as well as some wheezing. Furthermore, he coughs up some sputum during the exam, and this sputum is found to have a rust color. He does not report any pain and no skin findings are seen. Which of the following conditions best explains this patient's physical exam findings?
A. Tall, thin males
B. Protein C/S deficiency
C. Left heart failure (Correct Answer)
D. Long bone fractures
E. Smoking
Explanation: ***Left heart failure***
- **Bibasilar crackles** and **wheezing** ("cardiac asthma") in an elderly patient, combined with **rust-colored sputum**, are classic signs of **pulmonary edema** due to acute decompensated left heart failure.
- The rust color of the sputum can indicate the presence of **hemosiderin-laden macrophages** (heart failure cells), which result from chronic pulmonary congestion.
*Tall, thin males*
- This patient demographic is primarily associated with **spontaneous pneumothorax**, which presents as sudden onset chest pain and shortness of breath, not bibasilar crackles or rust-colored sputum.
- While spontaneous pneumothorax can cause respiratory distress, the other findings do not align with this condition.
*Protein C/S deficiency*
- Deficiencies in Protein C or S are inherited thrombophilias that increase the risk of **venous thromboembolism**, including **pulmonary embolism**.
- While a pulmonary embolism can cause respiratory symptoms, it is less likely to present with bibasilar crackles and rust-colored sputum in this manner without other signs of acute embolization.
*Long bone fractures*
- **Long bone fractures** are a significant risk factor for **fat embolism syndrome**, which can cause respiratory distress, neurological symptoms, and a petechial rash.
- However, the patient's presentation with bibasilar crackles, wheezing, and rust-colored sputum is not typical for fat embolism syndrome, and there is no history of trauma.
*Smoking*
- While smoking is a major risk factor for many respiratory diseases like **COPD** and **lung cancer**, it does not directly cause the acute presentation of bibasilar crackles, wheezing, and rust-colored sputum in the same way as left heart failure.
- COPD typically involves chronic cough, sputum production (often clear or white), and wheezing, but not typically rust-colored sputum indicative of acute pulmonary edema.