NSG 6020 3P EXAM 2026/2027 | Newest Questions and
Verified Answers | Attempt Score 94.67% | South
University | Pass Guaranteed - A+ Graded
Section 1: Pathophysiology (Questions 1-40)
Subsection 1A: Cellular Function, Inflammation & Immunity (Questions 1-10)
Q1: A patient with severe hyperkalemia (K+ 7.2 mEq/L) presents with peaked T waves on ECG.
The underlying pathophysiology of this cardiac membrane instability is primarily due to:
A. Influx of calcium ions causing prolonged depolarization.
B. Altered resting membrane potential leading to increased excitability and slowed
repolarization. [CORRECT]
C. Inhibition of the sodium-potassium ATPase pump causing rapid depolarization.
D. Increased permeability of the myocardial cell membrane to sodium.
Correct Answer: B
Rationale: Hyperkalemia decreases the concentration gradient for potassium, raising the resting
membrane potential (making it more positive/closer to threshold), which initially increases
excitability but slows repolarization (peaked T waves) and can lead to fatal arrhythmias (Bates'
Guide, 2026; McCance & Huether).
Q2: A 65-year-old patient presents with confusion, lethargy, and a serum sodium level of 115
mEq/L. The pathophysiologic mechanism most likely responsible for these neurologic symptoms
is:
A. Rapid intracellular movement of sodium causing neuronal hyperexcitability.
B. Cerebral edema due to water shifting from the extracellular to the intracellular compartment.
[CORRECT]
C. Increased renal retention of potassium causing neuronal toxicity.
D. Depletion of cerebrospinal fluid leading to brain shrinkage.
Correct Answer: B
Rationale: Hyponatremia creates a hypoosmolar ECF, causing water to move into the
intracellular compartment, including the brain, resulting in cerebral edema, increased ICP, and
neurologic symptoms like confusion (McCance & Huether, 2026).
,Q3: A patient with a prolonged seizure presents with an arterial blood gas (ABG) showing: pH
7.20, PaCO2 25 mmHg, HCO3- 10 mEq/L. Interpret the acid-base balance and the expected
compensatory mechanism.
A. Uncompensated respiratory acidosis.
B. Partially compensated metabolic acidosis. [CORRECT]
C. Fully compensated respiratory alkalosis.
D. Partially compensated respiratory acidosis.
Correct Answer: B
Rationale: The low pH and low HCO3- indicate metabolic acidosis. The low PaCO2 indicates
the lungs are compensating by blowing off CO2 (hyperventilation), but the pH is not yet normal,
making it partial compensation (Bates' Guide, 2026).
Q4: A patient with a bee sting develops acute respiratory distress, urticaria, and hypotension
within minutes. This reaction is mediated by:
A. IgG antibodies causing complement activation and cell lysis.
B. IgE antibodies cross-linking mast cells, causing massive degranulation of histamine and
leukotrienes. [CORRECT]
C. T-cell mediated cytotoxicity destroying vascular endothelium.
D. Immune complex deposition activating the complement cascade.
Correct Answer: B
Rationale: Type I hypersensitivity (anaphylaxis) is an immediate reaction mediated by IgE bound
to mast cells and basophils; antigen cross-linking causes degranulation of vasoactive amines
(histamine) (McCance & Huether, 2026).
Q5: A patient with systemic lupus erythematosus (SLE) has a positive ANA and anti-dsDNA
antibody. The pathophysiologic mechanism of tissue damage in SLE is primarily:
A. Type II hypersensitivity causing direct cell lysis of erythrocytes.
B. Type III hypersensitivity causing tissue damage from immune complex deposition in vessels
and organs. [CORRECT]
C. Type IV hypersensitivity with T-cell-mediated granuloma formation in the lungs.
D. Type I hypersensitivity causing chronic bronchoconstriction.
Correct Answer: B
Correct Answer: B
Rationale: SLE is a classic prototype of Type III hypersensitivity, where autoantibodies
(anti-dsDNA) form immune complexes that deposit in tissues (kidneys, skin, joints), activating
complement and causing inflammation (McCance & Huether, 2026).
,Q6: Following a myocardial infarction, a patient's cardiac muscle cells swell, the nuclei become
pyknotic, and cellular contents are released into the interstitium. This process is characteristic
of:
A. Apoptosis
B. Coagulative necrosis [CORRECT]
C. Liquefactive necrosis
D. Caseous necrosis
Correct Answer: B
Rationale: Ischemic injury to myocytes causes coagulative necrosis, characterized by
coagulated proteins maintaining cell outlines (coagulative pattern) before being cleared by
macrophages (McCance & Huether, 2026).
Q7: A patient presents with a fever of 39°C, tachycardia, and an elevated white blood cell count.
The systemic inflammatory response is mediated by the release of which primary pyrogen?
A. Interleukin-2 (IL-2)
B. Tumor necrosis factor-alpha (TNF-α) and Interleukin-1 (IL-1) [CORRECT]
C. Interleukin-4 (IL-4)
D. Interferon-gamma (IFN-γ)
Correct Answer: B
Rationale: TNF-α and IL-1 are the primary endogenous pyrogens produced by macrophages
that act on the hypothalamus to increase the thermoregulatory set point, causing fever
(McCance & Huether, 2026).
Q8: A patient with a viral infection produces specific antibodies to destroy the virus. These
antibodies belong to which class of immunoglobulins, and what is the primary mechanism of
action?
A. IgM; neutralization of the virus to prevent host cell entry. [CORRECT]
B. IgG; opsonization of host cells for phagocytosis.
C. IgA; activation of the classical complement pathway.
D. IgE; release of histamine from mast cells.
Correct Answer: A
Rationale: The primary (first) immune response to a new virus produces IgM antibodies. A key
mechanism is neutralization, where the antibody binds to the viral surface antigen, preventing it
from attaching to host cells (McCance & Huether, 2026).
Q9: A patient with Grave's disease develops exophthalmos (proptosis). The pathophysiology of
this finding involves:
A. Deposition of autoantibodies in the extraocular muscles causing inflammation and edema.
, B. Overproduction of thyroid hormone causing increased metabolic rate of orbital fat.
C. Hypothyroidism leading to mucopolysaccharide deposition in the orbit.
D. Compression of the optic nerve by a benign thyroid nodule.
Correct Answer: A
Rationale: In Graves' disease, TSH receptor-stimulating antibodies cross-react with antigens in
the retro-orbital tissue, stimulating fibroblasts and causing glycosaminoglycan deposition,
inflammation, and edema of extraocular muscles (McCance & Huether, 2026).
Q10: A patient develops SIRS (Systemic Inflammatory Response Syndrome) secondary to a
severe infection. Which set of clinical criteria defines SIRS?
A. Heart rate >90, RR >20, Temp >38.3°C or <36°C, WBC >12,000 or <4,000. **[CORRECT]**
B. Heart rate >110, RR >24, Temp >40°C, WBC >20,000.
C. Systolic BP <90 mmHg, lactate >4 mmol/L, urine output <0.5 mL/kg/hr.
D. PaO2/FiO2 ratio <200, bilateral infiltrates, no CHF.
Correct Answer: A
Rationale: SIRS is a clinical syndrome characterized by a dysregulated host response to a
stressor, defined by two or more of the following: Temp >38 or <36, HR >90, RR >20, WBC
>12,000 or <4,000, or >10% bands (McCance & Huether, 2026).
Subsection 1B: Cardiovascular & Respiratory Pathophysiology (Questions 11-20)
Q11: A patient with left-sided heart failure (systolic dysfunction) develops dyspnea on exertion,
orthopnea, and bilateral crackles. The primary pathophysiologic mechanism for these
pulmonary symptoms is:
A. Increased pulmonary vascular resistance causing right-to-left shunting.
B. Backward transmission of elevated left atrial pressure causing pulmonary congestion and
edema. [CORRECT]
C. Decreased oncotic pressure from liver congestion.
D. Overexpansion of the lungs due to increased tidal volumes.
Correct Answer: B
Rationale: In systolic HF, decreased cardiac output leads to increased LV end-diastolic
pressure, which backs up into the left atrium and pulmonary vasculature, increasing hydrostatic
pressure and pushing fluid into the interstitium (pulmonary edema), manifesting as crackles and
dyspnea (McCance & Huether, 2026).
Q12: Atherosclerosis begins with endothelial injury, leading to lipid accumulation in the intima.
The initial visible lesion is:
Verified Answers | Attempt Score 94.67% | South
University | Pass Guaranteed - A+ Graded
Section 1: Pathophysiology (Questions 1-40)
Subsection 1A: Cellular Function, Inflammation & Immunity (Questions 1-10)
Q1: A patient with severe hyperkalemia (K+ 7.2 mEq/L) presents with peaked T waves on ECG.
The underlying pathophysiology of this cardiac membrane instability is primarily due to:
A. Influx of calcium ions causing prolonged depolarization.
B. Altered resting membrane potential leading to increased excitability and slowed
repolarization. [CORRECT]
C. Inhibition of the sodium-potassium ATPase pump causing rapid depolarization.
D. Increased permeability of the myocardial cell membrane to sodium.
Correct Answer: B
Rationale: Hyperkalemia decreases the concentration gradient for potassium, raising the resting
membrane potential (making it more positive/closer to threshold), which initially increases
excitability but slows repolarization (peaked T waves) and can lead to fatal arrhythmias (Bates'
Guide, 2026; McCance & Huether).
Q2: A 65-year-old patient presents with confusion, lethargy, and a serum sodium level of 115
mEq/L. The pathophysiologic mechanism most likely responsible for these neurologic symptoms
is:
A. Rapid intracellular movement of sodium causing neuronal hyperexcitability.
B. Cerebral edema due to water shifting from the extracellular to the intracellular compartment.
[CORRECT]
C. Increased renal retention of potassium causing neuronal toxicity.
D. Depletion of cerebrospinal fluid leading to brain shrinkage.
Correct Answer: B
Rationale: Hyponatremia creates a hypoosmolar ECF, causing water to move into the
intracellular compartment, including the brain, resulting in cerebral edema, increased ICP, and
neurologic symptoms like confusion (McCance & Huether, 2026).
,Q3: A patient with a prolonged seizure presents with an arterial blood gas (ABG) showing: pH
7.20, PaCO2 25 mmHg, HCO3- 10 mEq/L. Interpret the acid-base balance and the expected
compensatory mechanism.
A. Uncompensated respiratory acidosis.
B. Partially compensated metabolic acidosis. [CORRECT]
C. Fully compensated respiratory alkalosis.
D. Partially compensated respiratory acidosis.
Correct Answer: B
Rationale: The low pH and low HCO3- indicate metabolic acidosis. The low PaCO2 indicates
the lungs are compensating by blowing off CO2 (hyperventilation), but the pH is not yet normal,
making it partial compensation (Bates' Guide, 2026).
Q4: A patient with a bee sting develops acute respiratory distress, urticaria, and hypotension
within minutes. This reaction is mediated by:
A. IgG antibodies causing complement activation and cell lysis.
B. IgE antibodies cross-linking mast cells, causing massive degranulation of histamine and
leukotrienes. [CORRECT]
C. T-cell mediated cytotoxicity destroying vascular endothelium.
D. Immune complex deposition activating the complement cascade.
Correct Answer: B
Rationale: Type I hypersensitivity (anaphylaxis) is an immediate reaction mediated by IgE bound
to mast cells and basophils; antigen cross-linking causes degranulation of vasoactive amines
(histamine) (McCance & Huether, 2026).
Q5: A patient with systemic lupus erythematosus (SLE) has a positive ANA and anti-dsDNA
antibody. The pathophysiologic mechanism of tissue damage in SLE is primarily:
A. Type II hypersensitivity causing direct cell lysis of erythrocytes.
B. Type III hypersensitivity causing tissue damage from immune complex deposition in vessels
and organs. [CORRECT]
C. Type IV hypersensitivity with T-cell-mediated granuloma formation in the lungs.
D. Type I hypersensitivity causing chronic bronchoconstriction.
Correct Answer: B
Correct Answer: B
Rationale: SLE is a classic prototype of Type III hypersensitivity, where autoantibodies
(anti-dsDNA) form immune complexes that deposit in tissues (kidneys, skin, joints), activating
complement and causing inflammation (McCance & Huether, 2026).
,Q6: Following a myocardial infarction, a patient's cardiac muscle cells swell, the nuclei become
pyknotic, and cellular contents are released into the interstitium. This process is characteristic
of:
A. Apoptosis
B. Coagulative necrosis [CORRECT]
C. Liquefactive necrosis
D. Caseous necrosis
Correct Answer: B
Rationale: Ischemic injury to myocytes causes coagulative necrosis, characterized by
coagulated proteins maintaining cell outlines (coagulative pattern) before being cleared by
macrophages (McCance & Huether, 2026).
Q7: A patient presents with a fever of 39°C, tachycardia, and an elevated white blood cell count.
The systemic inflammatory response is mediated by the release of which primary pyrogen?
A. Interleukin-2 (IL-2)
B. Tumor necrosis factor-alpha (TNF-α) and Interleukin-1 (IL-1) [CORRECT]
C. Interleukin-4 (IL-4)
D. Interferon-gamma (IFN-γ)
Correct Answer: B
Rationale: TNF-α and IL-1 are the primary endogenous pyrogens produced by macrophages
that act on the hypothalamus to increase the thermoregulatory set point, causing fever
(McCance & Huether, 2026).
Q8: A patient with a viral infection produces specific antibodies to destroy the virus. These
antibodies belong to which class of immunoglobulins, and what is the primary mechanism of
action?
A. IgM; neutralization of the virus to prevent host cell entry. [CORRECT]
B. IgG; opsonization of host cells for phagocytosis.
C. IgA; activation of the classical complement pathway.
D. IgE; release of histamine from mast cells.
Correct Answer: A
Rationale: The primary (first) immune response to a new virus produces IgM antibodies. A key
mechanism is neutralization, where the antibody binds to the viral surface antigen, preventing it
from attaching to host cells (McCance & Huether, 2026).
Q9: A patient with Grave's disease develops exophthalmos (proptosis). The pathophysiology of
this finding involves:
A. Deposition of autoantibodies in the extraocular muscles causing inflammation and edema.
, B. Overproduction of thyroid hormone causing increased metabolic rate of orbital fat.
C. Hypothyroidism leading to mucopolysaccharide deposition in the orbit.
D. Compression of the optic nerve by a benign thyroid nodule.
Correct Answer: A
Rationale: In Graves' disease, TSH receptor-stimulating antibodies cross-react with antigens in
the retro-orbital tissue, stimulating fibroblasts and causing glycosaminoglycan deposition,
inflammation, and edema of extraocular muscles (McCance & Huether, 2026).
Q10: A patient develops SIRS (Systemic Inflammatory Response Syndrome) secondary to a
severe infection. Which set of clinical criteria defines SIRS?
A. Heart rate >90, RR >20, Temp >38.3°C or <36°C, WBC >12,000 or <4,000. **[CORRECT]**
B. Heart rate >110, RR >24, Temp >40°C, WBC >20,000.
C. Systolic BP <90 mmHg, lactate >4 mmol/L, urine output <0.5 mL/kg/hr.
D. PaO2/FiO2 ratio <200, bilateral infiltrates, no CHF.
Correct Answer: A
Rationale: SIRS is a clinical syndrome characterized by a dysregulated host response to a
stressor, defined by two or more of the following: Temp >38 or <36, HR >90, RR >20, WBC
>12,000 or <4,000, or >10% bands (McCance & Huether, 2026).
Subsection 1B: Cardiovascular & Respiratory Pathophysiology (Questions 11-20)
Q11: A patient with left-sided heart failure (systolic dysfunction) develops dyspnea on exertion,
orthopnea, and bilateral crackles. The primary pathophysiologic mechanism for these
pulmonary symptoms is:
A. Increased pulmonary vascular resistance causing right-to-left shunting.
B. Backward transmission of elevated left atrial pressure causing pulmonary congestion and
edema. [CORRECT]
C. Decreased oncotic pressure from liver congestion.
D. Overexpansion of the lungs due to increased tidal volumes.
Correct Answer: B
Rationale: In systolic HF, decreased cardiac output leads to increased LV end-diastolic
pressure, which backs up into the left atrium and pulmonary vasculature, increasing hydrostatic
pressure and pushing fluid into the interstitium (pulmonary edema), manifesting as crackles and
dyspnea (McCance & Huether, 2026).
Q12: Atherosclerosis begins with endothelial injury, leading to lipid accumulation in the intima.
The initial visible lesion is:
