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NR 507 Advanced Pathophysiology Final Exam | 2025/2026 Verified Correct Answers | Chamberlain

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NR 507 Advanced Pathophysiology Final Exam | 2025/2026 Verified Correct Answers | Chamberlain

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NR 507 Advanced
Pathophysiology Final Exam |
2025/2026 Verified Correct
Answers | Chamberlain
Question 1
In a patient with acute myocardial infarction, the primary mechanism leading to
cellular necrosis is?

A. Increased ATP production B. Prolonged ischemia causing ATP depletion and
membrane failure C. Enhanced antioxidant defenses D. Activation of apoptotic
pathways only

B. Prolonged ischemia causing ATP depletion and membrane failure

Rationale: Ischemia disrupts oxidative phosphorylation, depleting ATP and
leading to Na+/K+ ATPase failure, cellular edema, and calcium influx, culminating
in necrosis; this reflects the cascade from reversible to irreversible injury in cardiac
pathophysiology.

Question 2
In systemic lupus erythematosus (SLE), the pathophysiologic hallmark is?

A. Type I hypersensitivity B. Immune complex deposition causing type III
hypersensitivity C. Direct T-cell mediated cytotoxicity D. Autoantibody
production against nuclear antigens only

B. Immune complex deposition causing type III hypersensitivity

Rationale: SLE involves autoantibodies (e.g., anti-dsDNA) forming complexes
that deposit in tissues, activating complement and causing vasculitis/nephritis; this
multi-organ autoimmune process underlies flares and chronic damage.

,Question 3
A patient with chronic kidney disease (CKD) stage 4 develops metabolic acidosis
primarily from?

A. Increased renal bicarbonate reabsorption B. Decreased ammonia buffer
synthesis and H+ excretion C. Hyperventilation compensation D. Dietary acid
overload alone

B. Decreased ammonia buffer synthesis and H+ excretion

Rationale: CKD impairs proximal tubule ammoniagenesis and distal H+ secretion,
reducing net acid excretion and causing anion gap acidosis; this contributes to bone
buffering and muscle wasting if untreated.

Question 4
In Parkinson's disease, the loss of dopaminergic neurons in the substantia nigra
leads to?

A. Unopposed cholinergic activity causing rigidity B. GABA excess in basal
ganglia C. Dopamine hypersensitivity in striatum D. Serotonin depletion in cortex

A. Unopposed cholinergic activity causing rigidity

Rationale: Dopamine deficiency disrupts direct/indirect pathways, increasing
cholinergic tone and causing bradykinesia/rigidity; levodopa restores balance but
risks dyskinesia from pulsatile stimulation.

Question 5
The pathophysiologic basis for insulin resistance in type 2 diabetes mellitus
involves?

A. Impaired IRS-1/PI3K signaling in adipocytes and myocytes B. Beta-cell
hyperplasia C. Decreased glucagon secretion D. Increased incretin effect

A. Impaired IRS-1/PI3K signaling in adipocytes and myocytes

, Rationale: Chronic hyperinsulinemia desensitizes insulin receptors, reducing
GLUT4 translocation and glucose uptake; this peripheral defect exacerbates
hyperglycemia and lipotoxicity.

Question 6
In acute respiratory distress syndrome (ARDS), the exudative phase is
characterized by?

A. Protein-rich edema and hyaline membrane formation in alveoli B.
Fibroproliferative scarring C. Neutrophil predominance only D. Surfactant
overproduction

A. Protein-rich edema and hyaline membrane formation in alveoli

Rationale: Endothelial/alveolar injury increases permeability, leaking plasma
proteins and forming hyaline membranes; this impairs gas exchange, with Berlin
criteria defining severity by PaO2/FiO2 ratio.

Question 7
A patient with Addison's disease experiences hyperpigmentation due to?

A. Elevated ACTH stimulating melanocytes in the absence of cortisol feedback B.
Increased MSH from pituitary adenoma C. Adrenal hyperplasia D. Ectopic ACTH
from lung cancer

A. Elevated ACTH stimulating melanocytes in the absence of cortisol feedback

Rationale: Primary adrenal insufficiency removes cortisol suppression, raising
POMC-derived ACTH/MSH; this causes diffuse pigmentation, a diagnostic clue
alongside hyponatremia.

Question 8
In Alzheimer's disease, neurofibrillary tangles are primarily composed of?

A. Hyperphosphorylated tau protein forming paired helical filaments B. Beta -
amyloid plaques C. Alpha-synuclein Lewy bodies D. Ubiquitin inclusions

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