NUR 631 PHYSIOLOGY AND PATHOPHYSIOLOGY MIDTERM
ACTUAL EXAM 2026-2027 COMPLETE QUESTIONS AND
DETAILED ANSWERS (VERIFIED ANSWERS) 100%
GUARANTEED PASS
1. Which of the following best describes the primary mechanism of action of a medication that
acts as a competitive antagonist at a receptor site?
A. It binds to a different site on the receptor, altering its shape.
B. **It reversibly binds to the same receptor site as the agonist, blocking its effect.**
C. It irreversibly binds to the receptor and causes a maximal response.
D. It increases the number of receptors available for agonist binding.
Rationale:A competitive antagonist reversibly binds to the same orthosteric site as the agonist,
preventing agonist binding without activating the receptor. High agonist concentration can
overcome this block.
2.During hypovolemic shock, baroreceptor-mediated activation of the sympathetic nervous
system leads to which vascular change?
A. Vasodilation of renal arteries
B. **Vasoconstriction of arterioles in the splanchnic circulation**
C. Decreased total peripheral resistance
D. Preferential vasodilation of cerebral vessels
Rationale: Sympathetic activation causes α1-adrenergic–mediated vasoconstriction in
nonessential vascular beds (splanchnic, renal, cutaneous) to maintain perfusion to the heart and
brain.
,3. A patient with metabolic alkalosis is found to have a plasma bicarbonate of 38 mEq/L and a
PaCO₂ of 48 mm Hg. This compensatory response is best described as:
A. Metabolic compensation, appropriate but incomplete
B. **Respiratory compensation via hypoventilation**
C. Respiratory compensation via hyperventilation
D. Mixed metabolic and respiratory alkalosis
Rationale: In metabolic alkalosis, the respiratory system compensates by hypoventilation
(increased PaCO₂) to raise H₂CO₃, partially normalizing pH. The expected PaCO₂ ≈ 0.7 × HCO₃
+ 20.
4. Which statement correctly describes action potential propagation in a myelinated axon?
A. Depolarization occurs at every point along the axolemma.
B. **Saltatory conduction occurs at the nodes of Ranvier.**
C. Conduction velocity is slower than in unmyelinated axons of the same diameter.
D. Sodium channels are uniformly distributed along the myelin sheath.
Rationale:Myelination restricts voltage-gated Na⁺ channels to the nodes of Ranvier.
Depolarization jumps between nodes (saltatory conduction), increasing velocity and energy
efficiency.
5.In a patient with type 1 diabetes mellitus, the development of hyperglycemia and ketosis is
primarily due to which underlying deficiency?
A. Glucagon deficiency
B. **Absolute insulin deficiency**
C. Insulin receptor downregulation
D. Increased glucose transporters (GLUT4)
Rationale:Lack of insulin prevents glucose uptake in muscle/adipose (via GLUT4) and allows
unchecked lipolysis, producing free fatty acids converted to ketones in the liver.
6. Which finding on a complete blood count is most consistent with a diagnosis of pernicious
anemia?
A. Microcytic, hypochromic red blood cells
B. **Macrocytic red blood cells with hypersegmented neutrophils**
, C. Normocytic anemia with reticulocytosis
D. Thrombocytosis and leukoerythroblastosis
Rationale:Vitamin B₁₂ deficiency in pernicious anemia impairs DNA synthesis, causing
megaloblastic maturation: macrocytic RBCs and hypersegmented neutrophils (≥5 lobes).
7. The renin-angiotensin-aldosterone system (RAAS) is activated in response to which of the
following stimuli?
A. Increased atrial natriuretic peptide (ANP)
B. **Decreased renal perfusion pressure sensed by juxtaglomerular cells**
C. Hypernatremia at the macula densa
D. Increased mean arterial pressure above 120 mm Hg
Rationale:Reduced afferent arteriolar pressure or decreased NaCl delivery to the macula densa
stimulates renin release from JG cells, initiating angiotensin II and aldosterone production.
8.In asthma, the early-phase reaction (within minutes of allergen exposure) is primarily
mediated by:
A. Eosinophil infiltration and major basic protein release
B. **Mast cell degranulation with release of histamine and leukotrienes**
C. T-lymphocyte activation and interleukin-4 production
D. Neutrophil chemotaxis and protease activity
Rationale: Cross-linking of IgE on mast cells triggers degradation, releasing preformed
mediators (histamine) and newly synthesized leukotrienes, causing bronchospasm and mucus
secretion.
9. A patient with chronic heart failure develops hyponatremia despite total body sodium excess.
This is best explained by:
A. Excessive dietary water restriction
B. **Nonosmotic release of antidiuretic hormone (ADH)**
C. Primary adrenal insufficiency
D. Decreased thirst mechanism
Rationale: Low effective circulating volume in heart failure stimulates nonosmotic ADH
release, causing water retention disproportionate to sodium, leading to dilutional hyponatremia.
ACTUAL EXAM 2026-2027 COMPLETE QUESTIONS AND
DETAILED ANSWERS (VERIFIED ANSWERS) 100%
GUARANTEED PASS
1. Which of the following best describes the primary mechanism of action of a medication that
acts as a competitive antagonist at a receptor site?
A. It binds to a different site on the receptor, altering its shape.
B. **It reversibly binds to the same receptor site as the agonist, blocking its effect.**
C. It irreversibly binds to the receptor and causes a maximal response.
D. It increases the number of receptors available for agonist binding.
Rationale:A competitive antagonist reversibly binds to the same orthosteric site as the agonist,
preventing agonist binding without activating the receptor. High agonist concentration can
overcome this block.
2.During hypovolemic shock, baroreceptor-mediated activation of the sympathetic nervous
system leads to which vascular change?
A. Vasodilation of renal arteries
B. **Vasoconstriction of arterioles in the splanchnic circulation**
C. Decreased total peripheral resistance
D. Preferential vasodilation of cerebral vessels
Rationale: Sympathetic activation causes α1-adrenergic–mediated vasoconstriction in
nonessential vascular beds (splanchnic, renal, cutaneous) to maintain perfusion to the heart and
brain.
,3. A patient with metabolic alkalosis is found to have a plasma bicarbonate of 38 mEq/L and a
PaCO₂ of 48 mm Hg. This compensatory response is best described as:
A. Metabolic compensation, appropriate but incomplete
B. **Respiratory compensation via hypoventilation**
C. Respiratory compensation via hyperventilation
D. Mixed metabolic and respiratory alkalosis
Rationale: In metabolic alkalosis, the respiratory system compensates by hypoventilation
(increased PaCO₂) to raise H₂CO₃, partially normalizing pH. The expected PaCO₂ ≈ 0.7 × HCO₃
+ 20.
4. Which statement correctly describes action potential propagation in a myelinated axon?
A. Depolarization occurs at every point along the axolemma.
B. **Saltatory conduction occurs at the nodes of Ranvier.**
C. Conduction velocity is slower than in unmyelinated axons of the same diameter.
D. Sodium channels are uniformly distributed along the myelin sheath.
Rationale:Myelination restricts voltage-gated Na⁺ channels to the nodes of Ranvier.
Depolarization jumps between nodes (saltatory conduction), increasing velocity and energy
efficiency.
5.In a patient with type 1 diabetes mellitus, the development of hyperglycemia and ketosis is
primarily due to which underlying deficiency?
A. Glucagon deficiency
B. **Absolute insulin deficiency**
C. Insulin receptor downregulation
D. Increased glucose transporters (GLUT4)
Rationale:Lack of insulin prevents glucose uptake in muscle/adipose (via GLUT4) and allows
unchecked lipolysis, producing free fatty acids converted to ketones in the liver.
6. Which finding on a complete blood count is most consistent with a diagnosis of pernicious
anemia?
A. Microcytic, hypochromic red blood cells
B. **Macrocytic red blood cells with hypersegmented neutrophils**
, C. Normocytic anemia with reticulocytosis
D. Thrombocytosis and leukoerythroblastosis
Rationale:Vitamin B₁₂ deficiency in pernicious anemia impairs DNA synthesis, causing
megaloblastic maturation: macrocytic RBCs and hypersegmented neutrophils (≥5 lobes).
7. The renin-angiotensin-aldosterone system (RAAS) is activated in response to which of the
following stimuli?
A. Increased atrial natriuretic peptide (ANP)
B. **Decreased renal perfusion pressure sensed by juxtaglomerular cells**
C. Hypernatremia at the macula densa
D. Increased mean arterial pressure above 120 mm Hg
Rationale:Reduced afferent arteriolar pressure or decreased NaCl delivery to the macula densa
stimulates renin release from JG cells, initiating angiotensin II and aldosterone production.
8.In asthma, the early-phase reaction (within minutes of allergen exposure) is primarily
mediated by:
A. Eosinophil infiltration and major basic protein release
B. **Mast cell degranulation with release of histamine and leukotrienes**
C. T-lymphocyte activation and interleukin-4 production
D. Neutrophil chemotaxis and protease activity
Rationale: Cross-linking of IgE on mast cells triggers degradation, releasing preformed
mediators (histamine) and newly synthesized leukotrienes, causing bronchospasm and mucus
secretion.
9. A patient with chronic heart failure develops hyponatremia despite total body sodium excess.
This is best explained by:
A. Excessive dietary water restriction
B. **Nonosmotic release of antidiuretic hormone (ADH)**
C. Primary adrenal insufficiency
D. Decreased thirst mechanism
Rationale: Low effective circulating volume in heart failure stimulates nonosmotic ADH
release, causing water retention disproportionate to sodium, leading to dilutional hyponatremia.
