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NR 507 WEEK 8 FINAL EXAM NR-507 ADV PATHOPHYSIOLOGY QUESTIONS AND CORRECT ANSWERS WITH RATIONALES GRADED A+ LATEST

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NR 507 WEEK 8 FINAL EXAM NR-507 ADV PATHOPHYSIOLOGY QUESTIONS AND CORRECT ANSWERS WITH RATIONALES GRADED A+ LATEST

Institution
NR507 Advanced Pathophysiology
Course
NR507 Advanced Pathophysiology

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NR 507 WEEK 8 FINAL EXAM NR-507 ADV
PATHOPHYSIOLOGY QUESTIONS AND
CORRECT ANSWERS WITH RATIONALES
GRADED A+ LATEST

1. A 58-year-old patient presents with fatigue, jaundice, and right upper quadrant
pain. Laboratory studies reveal elevated AST and ALT, hyperbilirubinemia, and
prolonged PT. Which is the most likely diagnosis?
A. Acute viral hepatitis
B. Chronic hepatitis C infection
C. Nonalcoholic fatty liver disease
D. Autoimmune hepatitis
Answer: A. Acute viral hepatitis
Rationale: Acute viral hepatitis often presents with jaundice, fatigue, and right
upper quadrant pain. Laboratory findings include markedly elevated AST and ALT
and prolonged PT due to impaired liver synthetic function. Chronic hepatitis C
usually has minimal symptoms early, and NAFLD often presents with mild ALT
elevations. Autoimmune hepatitis is less common and often associated with
positive autoantibodies.


2. A patient with long-standing hypertension presents with new-onset proteinuria
and a declining glomerular filtration rate (GFR). Which pathophysiologic process
is most likely contributing to renal injury?
A. Immune complex deposition
B. Glomerular hyperfiltration and hypertrophy
C. Tubular necrosis due to ischemia
D. Direct bacterial invasion
Answer: B. Glomerular hyperfiltration and hypertrophy

,Rationale: Chronic hypertension causes increased intraglomerular pressure,
leading to hyperfiltration and compensatory hypertrophy, eventually resulting in
glomerulosclerosis and proteinuria. Immune complex deposition is more typical of
glomerulonephritis. Tubular necrosis occurs in acute ischemic injury.


3. A 65-year-old male presents with sudden-onset dyspnea, pleuritic chest pain,
and hemoptysis. Vitals reveal tachycardia and hypoxemia. Which pathophysiologic
mechanism is primarily responsible for his hypoxemia?
A. Hypoventilation
B. V/Q mismatch due to pulmonary embolism
C. Right-to-left shunt
D. Diffusion limitation
Answer: B. V/Q mismatch due to pulmonary embolism
Rationale: Pulmonary embolism causes obstruction of pulmonary arteries, leading
to areas of the lung that are ventilated but not perfused (V/Q mismatch), resulting
in hypoxemia. Hypoventilation would cause hypercapnia, which is not the primary
feature here. Right-to-left shunt and diffusion limitation are less acute mechanisms
in this scenario.


4. Which cytokine is most directly responsible for the fever associated with
systemic inflammatory response syndrome (SIRS)?
A. Interleukin-1 (IL-1)
B. Interleukin-10 (IL-10)
C. Tumor necrosis factor-beta (TNF-β)
D. Transforming growth factor-alpha (TGF-α)
Answer: A. Interleukin-1 (IL-1)
Rationale: IL-1 acts on the hypothalamus to induce fever during systemic
inflammation. IL-10 is anti-inflammatory, TNF-β is less involved in fever, and
TGF-α primarily promotes cell growth rather than fever.

,5. A patient with type 2 diabetes mellitus presents with fatigue and hyperglycemia.
Laboratory results reveal ketonuria, metabolic acidosis, and hyperosmolar serum.
What is the most likely mechanism contributing to his hyperosmolar state?
A. Excess insulin leading to glycogen storage
B. Osmotic diuresis secondary to hyperglycemia
C. Increased ketone production in the liver
D. Autoimmune destruction of beta cells
Answer: B. Osmotic diuresis secondary to hyperglycemia
Rationale: In hyperosmolar hyperglycemic state (HHS), extreme hyperglycemia
leads to osmotic diuresis, dehydration, and hyperosmolar serum. Excess insulin
would lower glucose, ketone production predominates in DKA, and autoimmune
beta-cell destruction is typical of type 1 diabetes.


6. Which of the following best explains the progression from compensated to
decompensated heart failure in left ventricular systolic dysfunction?
A. Persistent sympathetic activation leading to remodeling
B. Reduced preload with venous pooling
C. Increased renal perfusion improving fluid balance
D. Enhanced myocardial contractility
Answer: A. Persistent sympathetic activation leading to remodeling
Rationale: Chronic sympathetic activation initially compensates for reduced
cardiac output but eventually contributes to myocardial remodeling, fibrosis, and
progression to decompensated heart failure. Reduced preload and enhanced
contractility would temporarily improve function, not worsen it.

, 7. A patient with chronic kidney disease develops anemia. Which factor is most
responsible for this condition?
A. Iron deficiency from dietary restrictions
B. Reduced erythropoietin production by the kidneys
C. Hemolysis due to uremia
D. Decreased platelet aggregation
Answer: B. Reduced erythropoietin production by the kidneys
Rationale: CKD leads to decreased renal production of erythropoietin, causing
normocytic, normochromic anemia. Iron deficiency may contribute but is not the
primary cause. Hemolysis is not a major factor, and platelet aggregation affects
bleeding, not anemia.


8. A 70-year-old female presents with sudden-onset confusion, headache, and a
blood pressure of 220/120 mmHg. CT scan shows intracerebral hemorrhage.
Which vascular pathophysiologic mechanism most likely contributed to this event?
A. Atherosclerotic plaque rupture
B. Chronic hypertension leading to small vessel rupture
C. Venous thrombosis
D. Embolic arterial occlusion
Answer: B. Chronic hypertension leading to small vessel rupture
Rationale: Long-standing hypertension causes lipohyalinosis and microaneurysm
formation in small cerebral arteries, increasing the risk of intracerebral
hemorrhage. Atherosclerotic plaque rupture and emboli typically cause ischemic
strokes.

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Institution
NR507 Advanced Pathophysiology
Course
NR507 Advanced Pathophysiology

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