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NSG 5140 Advanced Pathophysiology – 200 Q&As on Mechanisms of Disease (Cardiac, Renal, Endocrine, Neuro) 2026/2027 (THE ULTIMATE GUIDE)

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Graduate-level pathophysiology review covering cellular adaptation (hypertrophy vs. hyperplasia), ischemia/inflammation, heart failure (BNP, preload/afterload), acid-base disorders (metabolic alkalosis from vomiting, DKA anion gap), renal disorders (SIADH, nephrotic syndrome, AKI), endocrine (diabetes, thyroid, adrenal), neuro (stroke, ICP, Parkinson’s), and shock (septic, cardiogenic). Each answer includes a mechanism-focused rationale.

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NSG 5140 Advanced Pathophysiology
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NSG 5140 Advanced Pathophysiology

Voorbeeld van de inhoud

NSG 5140 ADVANCED PATHOPHYSIOLOGY

MIDTERM EXAM / ACTUAL EXAM QUESTIONS

AND VERIFIED ANSWERS WITH RATIONALES

GRADED A+ LATEST



1. A patient with chronic hypertension develops left ventricular wall
thickening. Which mechanism best explains this adaptation?
A. Increased myocyte number due to cell division
B. Increased myocyte size due to increased workload
C. Replacement of cardiac cells with fibrous tissue
D. Transformation of cardiac cells into smooth muscle
Correct Answer: B
Rationale: Cardiac myocytes are terminally differentiated and respond to
increased workload by hypertrophy (increased cell size), not hyperplasia.


2. During ischemic injury, loss of ATP most directly leads to:
A. Increased oxidative phosphorylation
B. Failure of the sodium–potassium pump
C. Increased protein synthesis
D. Mitochondrial membrane stabilization
Correct Answer: B
Rationale: ATP depletion causes failure of the Na⁺/K⁺ ATPase pump, leading to
cellular swelling and eventual cell death.

,3. Which mediator is primarily responsible for early vasodilation in acute
inflammation?
A. Leukotrienes
B. Histamine
C. Prostaglandins
D. Tumor necrosis factor-α
Correct Answer: B
Rationale: Histamine released from mast cells causes rapid vasodilation and
increased vascular permeability during acute inflammation.


4. Apoptosis differs from necrosis because apoptosis:
A. Causes inflammation
B. Is always pathologic
C. Requires ATP
D. Results in cell membrane rupture
Correct Answer: C
Rationale: Apoptosis is an energy-dependent, programmed process that does
not provoke inflammation.


5. Which immunoglobulin is produced first during a primary immune
response?
A. IgA
B. IgE
C. IgG
D. IgM
Correct Answer: D

,Rationale: IgM is the first antibody produced in an initial immune response and
is effective in complement activation.


6. Type II hypersensitivity reactions are characterized by:
A. Immune complex deposition
B. IgE-mediated mast cell activation
C. Antibody-mediated cell destruction
D. T-cell mediated cytotoxicity
Correct Answer: C
Rationale: Type II hypersensitivity involves IgG or IgM antibodies targeting
antigens on cell surfaces, leading to cell injury or lysis.


7. A patient with left-sided heart failure is most likely to develop:
A. Peripheral edema
B. Hepatomegaly
C. Pulmonary congestion
D. Ascites
Correct Answer: C
Rationale: Left ventricular failure increases pulmonary venous pressure, leading
to pulmonary edema and congestion.


8. The earliest pathophysiologic event in atherosclerosis is:
A. Plaque rupture
B. Foam cell formation
C. Endothelial dysfunction
D. Smooth muscle migration
Correct Answer: C

, Rationale: Endothelial injury increases vascular permeability to lipoproteins and
promotes inflammation, initiating atherosclerosis.




9. Which mechanism contributes most to essential hypertension?
A. Reduced cardiac output
B. Increased sympathetic nervous system activity
C. Aldosterone deficiency
D. Decreased systemic vascular resistance
Correct Answer: B
Rationale: Essential hypertension is strongly associated with increased SNS
activity and RAAS activation, increasing vascular resistance.


10. Elevated B-type natriuretic peptide (BNP) levels indicate:
A. Myocardial necrosis
B. Ventricular volume overload
C. Decreased preload
D. Acute coronary syndrome
Correct Answer: B
Rationale: BNP is released in response to increased ventricular stretch due to
volume overload.


11. Chronic hypoxia causes pulmonary hypertension primarily through:
A. Increased left ventricular preload
B. Pulmonary vasoconstriction
C. Increased alveolar ventilation
D. Decreased pulmonary capillary pressure

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NSG 5140 Advanced Pathophysiology
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