2026/2027 | Grade A Practice | Updated PA | Verified
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Section 1: Cellular Biology, Adaptation & Genetic Disorders
(Q1-10)
Q1. A nursing student is reviewing cellular adaptation concepts. Which cellular
change represents metaplasia rather than dysplasia?
A. Cervical epithelial cells showing loss of normal maturation with nuclear
hyperchromasia and increased mitotic figures
B. Bronchial epithelium transforming from pseudostratified ciliated columnar to
stratified squamous in a chronic smoker
C. Cardiac muscle cells enlarging in response to chronic hypertension
D. Endometrial glands proliferating during the secretory phase of the menstrual cycle
Correct Answer: B
Rationale: Metaplasia is the reversible replacement of one differentiated cell type
with another (squamous replacing columnar in response to chronic irritation). A
describes dysplasia (disordered growth with atypia), C describes hypertrophy
(increase in cell size), and D describes hyperplasia (increase in cell number).
Q2. A patient presents with acute myocardial infarction. The nurse understands that
the area of irreversible injury is characterized by which cellular change?
A. Cellular swelling with dispersed ribosomes and blebbing of the plasma membrane
B. Nuclear pyknosis, karyorrhexis, and karyolysis with loss of membrane integrity
C. Decreased ATP production with reversible mitochondrial swelling
,D. Accumulation of intracellular water and sodium with decreased extracellular
potassium
Correct Answer: B
Rationale: Irreversible cell injury is marked by nuclear changes (pyknosis =
condensation, karyorrhexis = fragmentation, karyolysis = dissolution) and plasma
membrane rupture, which are the defining features of necrosis. A, C, and D describe
reversible injury patterns where cellular architecture remains intact.
Q3. A nurse is caring for a patient with autoimmune destruction of pancreatic beta
cells. Which pathophysiological process is occurring?
A. Apoptosis triggered by intracellular signaling cascades without inflammation
B. Necrosis caused by severe ischemia with release of cellular contents
C. Programmed cell death mediated by cytotoxic T-lymphocytes and cytokines
D. Autophagy as a survival mechanism during nutrient deprivation
Correct Answer: C
Rationale: Type 1 diabetes involves autoimmune-mediated destruction of beta cells
through cytotoxic T-cell attack and inflammatory cytokines (IFN-γ, TNF-α), which is a
form of immune-mediated cell death. A describes physiological apoptosis, B
describes ischemic necrosis, and D describes autophagy, a survival pathway.
Q4. A patient with chronic kidney disease develops uremia. Which cellular adaptation
is most likely responsible for the patient's left ventricular hypertrophy?
A. Hyperplasia of cardiac myocytes
B. Hypertrophy of cardiac myocytes in response to increased afterload
C. Metaplasia of cardiac connective tissue
D. Dysplasia of coronary artery endothelium
Correct Answer: B
Rationale: In CKD, hypertension and volume overload increase cardiac afterload,
causing myocyte hypertrophy (increased cell size without division, as adult
, cardiomyocytes are terminally differentiated). A is incorrect (cardiomyocytes do not
hyperplasia in adults), C and D are irrelevant to pressure overload adaptation.
Q5. A newborn is diagnosed with Down syndrome (Trisomy 21). Which genetic
mechanism is responsible for this condition?
A. A single gene mutation on the X chromosome
B. Nondisjunction during meiosis resulting in three copies of chromosome 21
C. Deletion of a portion of chromosome 22
D. Expansion of trinucleotide repeats in the FMR1 gene
Correct Answer: B
Rationale: Down syndrome is caused by meiotic nondisjunction (failure of
chromosome 21 homologs to separate), resulting in trisomy 21 in 95% of cases. A
describes X-linked recessive disorders, C describes DiGeorge syndrome (22q11.2
deletion), and D describes Fragile X syndrome.
Q6. A patient with emphysema has decreased alpha-1 antitrypsin levels. Which
pathophysiological mechanism explains the development of panacinar emphysema
in this patient?
A. Uncontrolled protease activity destroying alveolar walls due to insufficient
antiprotease defense
B. Chronic bronchial inflammation causing mucus plugging and airway obstruction
C. Autoimmune destruction of type II pneumocytes
D. Excessive collagen deposition in the alveolar interstitium
Correct Answer: A
Rationale: Alpha-1 antitrypsin deficiency allows unchecked neutrophil elastase
activity, which destroys alveolar walls and elastic tissue, causing panacinar
emphysema. B describes chronic bronchitis, C is not a recognized mechanism, and D
describes restrictive lung disease (fibrosis).