UTA NURS 5220 ADVANCED PATHOPHYSIOLOGY
COMPREHENSIVE ACTUAL FINAL EXAM PREP 2026
ALL QUESTIONS AND CORRECT DETAILED
ANSWERS WITH RATIONALES ALREADY A GRADED
WITH EXPERT FEEDBACK |NEW AND REVISED
1. A patient with chronic alcoholism develops portal hypertension and
ascites. Which pathophysiological mechanism is the primary contributor
to the development of ascites in this patient?
A. Increased plasma oncotic pressure due to hyperalbuminemia
B. Decreased plasma oncotic pressure due to hypoalbuminemia
from impaired hepatic synthesis
C. Increased hydrostatic pressure in the hepatic sinusoids only
D. Decreased antidiuretic hormone secretion
Rationale: In cirrhosis, hepatocyte damage reduces albumin synthesis,
leading to hypoalbuminemia and decreased plasma oncotic pressure.
This allows fluid to leak into the peritoneal space. Portal hypertension
(increased hydrostatic pressure) also plays a role, but the primary
mechanism for ascites formation is the decreased oncotic pressure.
Option B is correct.
2. A 62-year-old patient with heart failure is receiving furosemide.
Laboratory results show sodium 130 mEq/L, potassium 3.2 mEq/L, and
chloride 88 mEq/L. Which acid-base disturbance is most likely?
A. Metabolic acidosis
B. Metabolic alkalosis
C. Respiratory acidosis
D. Respiratory alkalosis
Rationale: Loop diuretics (furosemide) increase renal excretion of
chloride, sodium, and potassium, leading to contraction alkalosis.
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Hypochloremia and hypokalemia maintain the alkalosis. Option B is
correct.
3. A patient with type 1 diabetes mellitus presents with nausea,
vomiting, deep rapid breathing (Kussmaul respirations), and a fruity
odor on the breath. Arterial blood gas shows pH 7.25, pCO2 30 mmHg,
HCO3- 12 mEq/L. Which compensatory mechanism is occurring?
A. Increased alveolar ventilation to lower pCO2 (respiratory
compensation)
B. Renal retention of bicarbonate
C. Increased cardiac output to buffer acids
D. Hepatic production of ketone bodies
Rationale: In diabetic ketoacidosis, metabolic acidosis triggers
peripheral chemoreceptors, increasing the rate and depth of breathing
(Kussmaul) to exhale CO2, thereby lowering pCO2. This is respiratory
compensation. Renal compensation (B) takes hours to days. Hepatic
ketogenesis (D) causes the acidosis, not compensates. Option A is
correct.
4. A 58-year-old woman with a 30-pack-year smoking history presents
with a chronic cough, hemoptysis, and weight loss. A chest CT reveals a
central lung mass with ipsilateral hilar lymphadenopathy. Which genetic
abnormality is most commonly associated with this presentation (small
cell lung cancer)?
A. TP53 mutation and RB1 loss
B. KRAS mutation
C. EGFR mutation
D. ALK rearrangement
Rationale: Small cell lung cancer is strongly associated with TP53 and
RB1 mutations. KRAS, EGFR, and ALK are more common in
non-small cell lung cancer (especially adenocarcinoma). Option A is
correct.
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5. A patient with sickle cell disease develops acute chest pain, fever, and
hypoxemia. Chest X-ray shows a new pulmonary infiltrate. Which
pathophysiological process is the direct cause?
A. Pulmonary embolism from deep vein thrombosis
B. Vaso-occlusion of pulmonary microvasculature by sickled
erythrocytes
C. Fat embolism from bone marrow infarction
D. Bacterial pneumonia due to functional asplenia
Rationale: Acute chest syndrome in sickle cell disease results from in
situ sickling and vaso-occlusion in pulmonary vessels, leading to
infarction and inflammation. While infection (D) may occur,
vaso-occlusion is the primary mechanism. Option B is correct.
6. A 70-year-old woman with osteoporosis falls and sustains a hip
fracture. Which cellular process is primarily responsible for her
underlying bone fragility?
A. Increased osteoblast activity
B. Increased osteoclast activity relative to osteoblast activity
C. Decreased parathyroid hormone secretion
D. Excessive calcitonin release
Rationale: Osteoporosis results from bone resorption exceeding
formation. Increased osteoclast activity (or decreased osteoblast
activity) leads to net bone loss. Estrogen deficiency after menopause
increases osteoclast activity. Option B is correct.
7. A patient with rheumatoid arthritis develops ulnar deviation and
swan-neck deformities. Which pathological process directly causes these
deformities?
A. Synovial pannus formation eroding articular cartilage and
ligaments
B. Deposition of monosodium urate crystals
C. Degeneration of articular cartilage due to mechanical stress
D. Autoantibodies against acetylcholine receptors
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Rationale: Rheumatoid arthritis involves chronic synovitis with
pannus (granulation tissue) that invades and destroys cartilage, bone,
and ligaments, leading to deformities. Urate crystals (B) cause gout.
Mechanical degeneration (C) describes osteoarthritis. Antibodies
against acetylcholine receptors (D) cause myasthenia gravis. Option A
is correct.
8. A 45-year-old man presents with episodic severe headache,
palpitations, diaphoresis, and hypertension. Between episodes, blood
pressure is normal. Which tumor is most likely?
A. Pheochromocytoma
B. Adrenocortical adenoma
C. Carcinoid tumor
D. Medullary thyroid carcinoma
Rationale: Paroxysmal hypertension with headache, palpitations, and
diaphoresis is classic for pheochromocytoma (catecholamine-secreting
tumor). Option A is correct.
9. A patient with chronic kidney disease stage 4 has serum phosphate 6.2
mg/dL and calcium 7.8 mg/dL. Which compensatory response is
expected?
A. Increased parathyroid hormone secretion (secondary
hyperparathyroidism)
B. Decreased vitamin D activation
C. Increased fibroblast growth factor-23
D. Decreased calcium excretion
Rationale: Hyperphosphatemia and hypocalcemia stimulate PTH
secretion to increase phosphate excretion and calcium resorption.
Option A is correct.
10. A newborn is diagnosed with cystic fibrosis after presenting with
meconium ileus. Which cellular transport defect is the underlying cause?
A. CFTR gene mutation causing defective chloride and bicarbonate
transport