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NR507 ADVANCED PATHOPHYSIOLOGY FINAL COMPREHENSIVE EXAM QUESTIONS AND ANSWERS

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NR507 ADVANCED PATHOPHYSIOLOGY FINAL COMPREHENSIVE EXAM QUESTIONS AND ANSWERS

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NR507 ADVANCED
PATHOPHYSIOLOGY FINAL
COMPREHENSIVE EXAM QUESTIONS
AND ANSWERS



1. A patient presents with massive proteinuria, hypoalbuminemia, and generalized edema.

Which of the following is the most likely underlying pathophysiological mechanism?

A. Inflammatory damage to the basement membrane causing hematuria


B. Immune complex deposition leading to a decrease in GFR


C. Obstruction of the renal tubules by cast proteins


D. Increased glomerular permeability to plasma proteins due to podocyte injury


Answer: D


Conceptual Explanation: Nephrotic syndrome is characterized by massive proteinuria

due to increased glomerular permeability, often resulting from podocyte injury or

effacement, which allows proteins to leak into the filtrate.


2. In Myasthenia Gravis, the progressive muscle weakness is primarily caused by which

mechanism?

A. Demyelination of the peripheral motor nerves

,B. Reduced synthesis of dopamine in the substantia nigra


C. Autoantibody-mediated destruction of acetylcholine receptors at the neuromuscular

junction


D. Hyper-excitability of the motor cortex neurons


Answer: C


Conceptual Explanation: Myasthenia Gravis is an autoimmune disorder where antibodies

attack or block acetylcholine receptors at the neuromuscular junction, impairing signal

transmission to muscles.


3. Chronic activation of the renin-angiotensin-aldosterone system (RAAS) in heart failure

leads to which of the following deleterious effects?

A. Vasodilation and sodium excretion


B. Improved renal perfusion and decreased cardiac workload


C. Decreased secretion of B-type natriuretic peptide (BNP)


D. Myocardial remodeling and increased ventricular afterload


Answer: D


Conceptual Explanation: While RAAS initially maintains blood pressure, chronic

activation leads to persistent vasoconstriction (increased afterload), fluid retention, and

myocardial fibrosis/remodeling, worsening heart failure.

, 4. Which clinical finding is characteristic of the Syndrome of Inappropriate Antidiuretic

Hormone (SIADH)?

A. Hypernatremia and low urine specific gravity


B. Dehydration and polyuria


C. Hyponatremia and high urine osmolality


D. Increased serum osmolality and hyperkalemia


Answer: C


Conceptual Explanation: SIADH involves excessive ADH release, leading to water

retention, dilutional hyponatremia, and highly concentrated urine despite normal or

increased intravascular volume.


5. What is the primary pathophysiological defect in Sickle Cell Disease?

A. A deficiency in the production of alpha-globin chains


B. A single amino acid substitution in the beta-globin chain causing hemoglobin

polymerization


C. The absence of glucose-6-phosphate dehydrogenase


D. Defective iron absorption in the gastrointestinal tract


Answer: B

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