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Cardiology Clinical Case / MCQS / Uworld for Usmle step 2 / case 4

 Cardiology Clinical Case  / MCQS / Uworld for Usmle step 2 / case 4 with answer and explanation and references and Educational objective

A 46-year-old man comes to the physician with exertional dyspnea and dry cough. He also has occasional episodes of suffocating nighttime cough that is only relieved by sitting up. Past medical history is significant for myocardial infarction 6 months ago and hypercholesterolemia. Current medications include metoprolol, aspirin, and rosuvastatin. The patient does not use tobacco or illicit drugs but drinks alcohol on social occasions. His father died of a stroke and his mother has type 2 diabetes mellitus. His blood pressure is 150/1 00 mm Hg and pulse is 60/min. Chest examination shows bibasilar crackles. The cardiac apex is palpated in the left sixth intercostal space.  Bilateral pitting leg edema is present. Which of the following is most likely to be associated with this patient's condition?

 

A.  Constriction of the efferent renal arterioles

B.  Decreased intraglomerular pressure

C.  Decreased renal venous pressure

D.  Decreased plasma colloid pressure

E.  High sodium delivery to the distal tubule

F.   Increased renal blood flow

 

Answer : A

Explanation :

 

This patient's presentation (exertional dyspnea, paroxysmal nocturnal dyspnea, pulmonary and peripheral edema) and history of myocardial infarction suggest decompensated systolic congestive heart failure (CHF). Decreased cardiac output in such patients leads to neurohumoral adaptations, including increased sympathetic nervous system tone, activation of the renin-angiotensin-aldosterone system (RAAS), and increased secretion of antidiuretic hormone. These compensatory mechanisms attempt to maintain cardiac output and systemic pressure by increasing myocardial contractility, peripheral vasoconstriction, and expansion of extracellular fluid  volume.

 

Decreased renal perfusion seen in CHF and subsequent RAAS activation lead to increased angiotensin II levels. Angiotensin II causes numerous effects including:

 

      Vasoconstriction of both the afferent and efferent glomerular arterioles, leading to an increase in renal vascular resistance and a net decrease in renal blood flow (Choice F).

      Preferential vasoconstrict ion of efferent renal arterioles, which increases intraglomerular pressure (Choice B) in an attempt to maintain adequate glomerular filtration rate (GFR).

       Direct stimulation of sodium resorption in the proximal tubules and increased secretion of aldosterone from the adrenal glands, which in turn promotes further sodium resorption in the cortical collecting tubule. These actions lead to decreased sodium delivery to the distal tubule (Choice E) and an increase in extracellular fluid volume.

 

(Choice C) Patients with systolic CHF and reduced cardiac output have an increase in renal vascular resistance and overall venous pressures due to activation of the sympathetic nervous system and RAAS.

 

(Choice D) Decreased plasma colloid pressure is the mechanism responsible for peripheral and/or generalized edema in patients with severe proteinuria and hypoalbuminemia.

 

Educational objective:

In patients with congestive heart failure, activation of the renin-angiotensin-aldosterone system (RAAS) and production of angiotensin II causes preferential vasoconstriction of efferent renal arterioles, which increases intraglomerular pressure in order to maintain adequate glomerular filtration rate (GFR).

 

 

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