Solutions | Advanced Pathophysiology,
Pharmacotherapeutics & Physical Assessment | NP
Prep | Pass Guaranteed - A+ Graded
Advanced Pathophysiology
Q1: A 58-year-old male with a 40-pack-year smoking history presents with hemoptysis
and weight loss. Chest CT reveals a spiculated mass in the right upper lobe. Biopsy
confirms adenocarcinoma. Which genetic mutation would most likely be targeted with a
tyrosine kinase inhibitor in this patient?
A. KRAS mutation
B. EGFR mutation [CORRECT]
C. TP53 mutation
D. RB1 mutation
Correct Answer: B
Rationale: EGFR mutations are common in non-smokers with lung adenocarcinoma but
can occur in smokers and are targetable with EGFR tyrosine kinase inhibitors (erlotinib,
gefitinib, osimertinib). Option A (KRAS) is common in smokers but currently has limited
,targeted therapy options. Option C (TP53) is a tumor suppressor mutation seen in many
cancers but isn't targetable with TKIs. Option D (RB1) is a cell cycle regulator; mutations
are seen in small cell lung cancer, not typically targetable.
Q2: A patient with chronic alcohol use disorder presents with confusion, ataxia, and
ophthalmoplegia. MRI shows mammillary body atrophy. Which vitamin deficiency
explains this pathophysiology?
A. Vitamin B12
B. Thiamine (Vitamin B1) [CORRECT]
C. Folate
D. Niacin
Correct Answer: B
Rationale: Wernicke encephalopathy (confusion, ataxia, ophthalmoplegia) and
subsequent Korsakoff syndrome result from thiamine deficiency, which impairs glucose
metabolism and leads to lactic acidosis and cellular energy failure. Mammillary body
atrophy is characteristic. Option A causes subacute combined degeneration. Option C
causes megaloblastic anemia without neurological deficits. Option D causes pellagra
(dermatitis, dementia, diarrhea).
,Q3: In the pathophysiology of acute respiratory distress syndrome (ARDS), which
cellular event is primarily responsible for the non-cardiogenic pulmonary edema?
A. Left ventricular failure
B. Increased pulmonary capillary permeability due to neutrophil-mediated endothelial
injury [CORRECT]
C. Lymphatic obstruction
D. Decreased oncotic pressure from hypoalbuminemia
Correct Answer: B
Rationale: ARDS involves diffuse alveolar damage from inflammatory mediators (IL-6,
IL-8, TNF-α) causing neutrophil activation and endothelial injury, leading to protein-rich
fluid leakage. Option A describes cardiogenic pulmonary edema. Option C causes
chylothorax, not ARDS. Option D contributes to peripheral edema but isn't the primary
mechanism in ARDS.
Q4: A patient with systemic lupus erythematosus develops glomerulonephritis. Renal
biopsy shows "wire loop" lesions and subendothelial immune complex deposits. Which
hypersensitivity reaction type is responsible?
A. Type I hypersensitivity
, B. Type II hypersensitivity
C. Type III hypersensitivity [CORRECT]
D. Type IV hypersensitivity
Correct Answer: C
Rationale: SLE glomerulonephritis involves immune complex deposition (DNA-anti-DNA
complexes) activating complement, characteristic of Type III hypersensitivity. Wire loop
lesions result from subendothelial deposits. Option A involves IgE and mast cells
(anaphylaxis). Option B involves antibody-mediated cytotoxicity (Goodpasture's). Option
D is T-cell mediated (contact dermatitis, granuloma formation).
Q5: A 45-year-old woman presents with fatigue, weight gain, cold intolerance, and a
goiter. TSH is elevated, free T4 is low, and anti-TPO antibodies are positive. Which
pathophysiological process is occurring?
A. TSH receptor stimulating antibodies activating thyroid hormone production
B. Autoimmune destruction of thyroid follicular cells leading to hypothyroidism
[CORRECT]
C. Iodine deficiency causing impaired thyroid hormone synthesis
D. Pituitary adenoma secreting excess TSH