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Examen

NUR 3123 Pathophysiology - Final Exam Review 2025(UF

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NUR 3123 Pathophysiology - Final Exam Review 2025(UFNUR 3123 Pathophysiology - Final Exam Review 2025(UFNUR 3123 Pathophysiology - Final Exam Review 2025(UF

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Subido en
23 de julio de 2025
Número de páginas
32
Escrito en
2024/2025
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NUR 3123

Pathophysiology

Final Exam Review

(Questions & Solutions)

2025




1

,1. A 58-year-old man with chronic hypertension presents with acute
pulmonary edema. His renin activity is elevated despite high blood
pressure. Which mechanism best explains this finding?
A. Baroreceptor‐mediated renin release from afferent arteriole
B. Increased sympathetic stimulation of the kidney
C. Direct angiotensin II feedback inhibition loss
D. Enhanced atrial natriuretic peptide secretion

Correct ANS: A
Rationale: Chronically elevated arterial pressure desensitizes renal
baroreceptors, so reduced afferent arteriole stretch paradoxically
stimulates renin release, worsening volume overload.

---

2. A patient develops acute respiratory distress syndrome (ARDS) after
sepsis. Which pathophysiologic change primarily causes refractory
hypoxemia?
A. Alveolar overdistension
B. Surfactant hypersecretion
C. Increased capillary permeability
D. Bronchoconstriction

Correct ANS: C
Rationale: Inflammatory mediators in ARDS increase pulmonary
capillary permeability, leading to protein‐rich fluid in alveoli, impaired gas
exchange, and hypoxemia unresponsive to oxygen.

---

3. A 45-year-old woman with long-standing type 1 diabetes shows
microalbuminuria. The earliest glomerular lesion in diabetic nephropathy
2

,is:
A. Mesangial expansion
B. Glomerular basement membrane thickening
C. Nodular sclerosis (Kimmelstiel-Wilson)
D. Podocyte foot process effacement

Correct ANS: B
Rationale: Hyperglycemia induces nonenzymatic glycosylation,
thickening the basement membrane, which precedes mesangial matrix
expansion and nodular sclerosis.

---

4. A cirrhotic patient develops tense ascites. Which factor most
contributes to fluid accumulation in the peritoneal cavity?
A. Increased plasma oncotic pressure
B. Splanchnic vasodilation
C. Decreased portal venous pressure
D. Reduced lymphatic drainage only

Correct ANS: B
Rationale: Portal hypertension and splanchnic arterial vasodilation
lower effective circulating volume, activating sodium retention and
causing transudation of fluid into the abdomen.

---

5. A patient with acute rheumatic fever presents with mitral stenosis
years later. What structural valve change underlies this stenosis?
A. Commissural fusion and leaflet thickening
B. Chordae tendineae elongation
C. Papillary muscle hypertrophy
D. Annular calcification

Correct ANS: A
3

, Rationale: Rheumatic inflammation leads to fusion of valve
commissures and thickening of leaflets, narrowing the orifice and
impeding flow.

---

6. In Alzheimer disease, accumulation of extracellular amyloid-β plaques
disrupts synaptic communication. This results primarily from:
A. Tau hyperphosphorylation
B. Increased α-secretase activity
C. Imbalance of β- and γ-secretase processing of APP
D. Microglial‐mediated demyelination

Correct ANS: C
Rationale: Aberrant β- and γ-secretase cleavage of amyloid precursor
protein generates insoluble amyloid-β fragments that aggregate and
impair neuron function.

---

7. A 30-year-old woman with multiple sclerosis reports worsening leg
weakness. Demyelination in the central nervous system slows nerve
conduction by:
A. Decreasing sodium channel density at nodes
B. Increasing capacitance of axonal membrane
C. Blocking neurotransmitter release
D. Enhancing potassium leak currents

Correct ANS: B
Rationale: Loss of myelin increases membrane capacitance and reduces
insulation, resulting in slower action potential propagation and
conduction block.

---


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