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Exam (elaborations)

NSG 3113 Pathophysiology Comprehensive Question Bank | Practice Questions with Verified Answers

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NSG 3113 Pathophysiology Comprehensive Question Bank | Practice Questions with Verified Answers

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NSG 3113 Pathophysiology Comprehensive Question
Bank | Practice Questions with Verified Answers

Question 1
A client experiences severe myocardial ischemia, leading to a sudden
depletion of intracellular ATP. Which of the following cellular
consequences occurs first as a result of this ATP deficit?
A. Influx of potassium and efflux of sodium
B. Failure of the Na+/K+-ATPase membrane pump, leading to
intracellular accumulation of sodium and water
C. Rupture of lysosomal membranes releasing proteolytic enzymes
D. Complete nuclear dissolution (karyolysis)
Correct Answer: B. Failure of the Na+/K+-ATPase membrane pump,
leading to intracellular accumulation of sodium and water
Detailed Rationale: ATP depletion impairs the energy-dependent
Na+/K+-ATPase pump. Sodium and water accumulate inside the cell,
causing acute cellular swelling and vacuolation before irreversible
membrane damage occurs.
Question 2
A client with severe diarrhea presents with lethargy, confusion, and
muscle twitching. Laboratory findings show a serum sodium level of 122
mEq/L. Which pathophysiological shift explains the neurological
symptoms?

,A. Hyperosmolar extracellular fluid drawing water out of brain cells,
causing shrinkage
B. Hypoosmolar extracellular fluid causing water to shift into brain cells
via osmosis, leading to cerebral edema
C. Direct autoimmune destruction of cortical neurons by circulating
antibodies
D. Depletion of intracellular potassium driving membrane
hyperpolarization
Correct Answer: B. Hypoosmolar extracellular fluid causing water to
shift into brain cells via osmosis, leading to cerebral edema
Detailed Rationale: Severe hyponatremia reduces the osmolality of the
extracellular fluid. Water moves down its osmotic gradient into brain
cells, causing cellular swelling (cerebral edema), increased intracranial
pressure, and neurological manifestations.
Question 3
A client experiencing a severe panic attack presents with
lightheadedness, numbness and tingling in the fingers, and rapid, deep
respirations (tachypnea). Which primary acid-base imbalance is
occurring?
A. Metabolic acidosis
B. Metabolic alkalosis
C. Respiratory acidosis
D. Respiratory alkalosis
Correct Answer: D. Respiratory alkalosis

,Detailed Rationale: Hyperventilation blows off excessive carbon dioxide
(PaCO2), decreasing carbonic acid in the blood and elevating pH,
resulting in acute respiratory alkalosis.
Question 4
What is the primary vascular response that occurs immediately
following acute tissue injury during the inflammatory phase?
A. Prolonged vasoconstriction followed by sustained vasodilation and
increased vascular permeability
B. Immediate permanent constriction of all local capillaries to prevent
bleeding
C. Proliferation of fibroblasts and collagen deposition within minutes
D. Complete shutdown of lymphatic drainage
Correct Answer: A. Prolonged vasoconstriction followed by sustained
vasodilation and increased vascular permeability
Detailed Rationale: Acute tissue injury triggers brief transient
vasoconstriction to minimize bleeding, rapidly followed by mast cell
degranulation releasing histamine and bradykinin, causing vasodilation
and increased vascular permeability (exudation).
Question 5
What is the basic genetic pattern and molecular defect in Sickle Cell
Anemia?
A. Autosomal dominant mutation resulting in excessive spectrin
production

, B. Autosomal recessive point mutation in the beta-globin chain gene,
substituting valine for glutamic acid and causing hemoglobin
polymerization under low oxygen
C. X-linked recessive deletion of the alpha-globin gene cluster
D. Trisomy of chromosome 11 affecting iron metabolism
Correct Answer: B. Autosomal recessive point mutation in the beta-
globin chain gene, substituting valine for glutamic acid and causing
hemoglobin polymerization under low oxygen
Detailed Rationale: Sickle cell anemia is an autosomal recessive
disorder caused by a single amino acid substitution (valine for glutamic
acid) in the hemoglobin beta chain. Under hypoxic conditions, mutant
hemoglobin molecules polymerize, distorting red blood cells into rigid
sickle shapes.
Question 6
What is the initial event in the pathogenesis of atherosclerosis?
A. Smooth muscle cell proliferation in the tunica media
B. Endothelial injury caused by risk factors such as hyperlipidemia,
hypertension, or toxins, leading to endothelial dysfunction
C. Calcification of the fibrous cap
D. Thrombotic occlusion of the entire lumen
Correct Answer: B. Endothelial injury caused by risk factors such as
hyperlipidemia, hypertension, or toxins, leading to endothelial
dysfunction

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