MSN 612 FINAL EXAM (2026/2027 Academic Year)
Advanced Nursing Practice Review Material
Section I: Advanced Pathophysiology (Questions 1-20)
1. A 65-year-old male with a 40-year history of smoking presents with shortness of breath. ABG
shows: pH 7.32, PaCO2 68 mm Hg, HCO3- 32 mEq/L. What is the acid-base disturbance?
A. Acute Respiratory Acidosis
B. Partially Compensated Metabolic Alkalosis
C. Partially Compensated Respiratory Acidosis
D. Uncompensated Respiratory Alkalosis
Correct AnswerC. Partially Compensated Respiratory Acidosis
• Rationale for C: Low pH (acidemia) + High PaCO2 (Respiratory cause). HCO3- is elevated
(metabolic compensation) but not enough to normalize pH (7.35-7.45), indicating partial
compensation.
• Rationale for A: Acute would have normal HCO3- (24).
• Rationale for B: pH is acidic, not alkalotic.
• Rationale for D: PaCO2 is high, not low.
2. In Type 2 Diabetes Mellitus, which cellular mechanism is primarily responsible for insulin
resistance?
A. Autoimmune destruction of beta cells in the islets of Langerhans
B. Downregulation of GLUT-4 transporters in skeletal muscle and adipose tissue
C. Increased C-peptide secretion by the pancreas
D. Alpha cell hyperplasia leading to excess glucagon
Correct AnswerB. Downregulation of GLUT-4 transporters in skeletal muscle and adipose tissue
• Rationale for B: Insulin resistance is characterized by impaired translocation of GLUT-4 to the
cell membrane, preventing glucose entry.
• Rationale for A: This describes Type 1 DM.
• Rationale for C: C-peptide is low or normal in Type 2, not high.
• Rationale for D: Alpha cell dysfunction contributes but is not the primary cellular mechanism for
resistance.
,3. A patient with chronic heart failure is taking Furosemide and Digoxin. Which electrolyte imbalance
poses the highest risk for Digoxin toxicity?
A. Hypernatremia (Na+ 155 mEq/L)
B. Hypokalemia (K+ 3.2 mEq/L)
C. Hypercalcemia (Ca+ 11.5 mg/dL)
D. Hypermagnesemia (Mg+ 3.0 mEq/L)
Correct AnswerB. Hypokalemia (K+ 3.2 mEq/L)
• Rationale for B: Low serum potassium increases the binding of digoxin to cardiac sodium-
potassium ATPase pumps, leading to toxicity.
• Rationale for A: Sodium affects volume status, not digoxin binding directly.
• Rationale for C: Hypocalcemia potentiates digoxin, but hypercalcemia has less direct risk than
hypokalemia.
• Rationale for D: Hypermagnesemia is protective against arrhythmias.
4. Which lab finding is most consistent with a diagnosis of disseminated intravascular coagulation
(DIC) secondary to sepsis?
A. Elevated platelet count and elevated fibrinogen
B. Decreased PT/INR and decreased aPTT
C. Decreased fibrinogen and elevated D-dimer
D. Normal schistocytes on peripheral smear
Correct AnswerC. Decreased fibrinogen and elevated D-dimer
• Rationale for C: DIC consumes clotting factors (low fibrinogen) and activates fibrinolysis (high D-
dimer).
• Rationale for A: Platelets are low in DIC (thrombocytopenia).
• Rationale for B: PT/INR and aPTT are prolonged due to factor depletion.
• Rationale for D: Schistocytes (RBC fragments) are typically present in microangiopathic
hemolytic anemia (MAHA) seen in DIC.
5. A patient with end-stage renal disease (ESRD) presents with muscle twitching, confusion, and a
prolonged QT interval. EKG shows peaked T waves. What is the priority intervention?
A. Administer IV calcium gluconate
B. Administer IV insulin and dextrose
C. Administer IV normal saline bolus
D. Prepare for emergent hemodialysis
Correct AnswerA. Administer IV calcium gluconate
• Rationale for A: The patient has hyperkalemia (peaked T waves). IV calcium gluconate stabilizes
the cardiac membrane immediately, even before potassium is lowered.
, • Rationale for B: Insulin/dextrose shifts K+ into cells but takes 15-30 min; cardiac stabilization
comes first.
• Rationale for C: Saline is for prerenal azotemia, not acute cardiac protection in ESRD.
• Rationale for D: Dialysis is definitive but takes time to set up; calcium is immediate.
6. In asthma, which inflammatory mediator is primarily responsible for late-phase bronchospasm (4-8
hours after exposure)?
A. Histamine
B. Leukotrienes (LTD4, LTE4)
C. Epinephrine
D. Bradykinin
Correct AnswerB. Leukotrienes (LTD4, LTE4)
• Rationale for B: Leukotrienes are released from mast cells and eosinophils during the late phase,
causing sustained bronchoconstriction, mucus secretion, and airway remodeling.
• Rationale for A: Histamine causes the immediate reaction (10-15 min).
• Rationale for C: Epinephrine is a bronchodilator, not a mediator of inflammation.
• Rationale for D: Bradykinin causes pain and cough but not the primary late-phase constriction.
7. A patient with liver cirrhosis develops ascites and asterixis. What is the primary pathophysiological
mechanism of asterixis (liver flap)?
A. Accumulation of manganese in the basal ganglia
B. Failure of the liver to detoxify ammonia leading to impaired neurotransmission
C. Direct alcohol toxicity on the cerebellum
D. Hypoglycemia due to reduced gluconeogenesis
Correct AnswerB. Failure of the liver to detoxify ammonia leading to impaired neurotransmission
• Rationale for B: Ammonia crosses the blood-brain barrier, affects astrocyte function, and alters
glutamatergic and GABAergic neurotransmission, causing metabolic encephalopathy and
asterixis.
• Rationale for A: Manganese accumulation occurs in TIPS patients but is not the primary
mechanism.
• Rationale for C: Cerebellar atrophy is from chronic ETOH, but asterixis is metabolic.
• Rationale for D: Hypoglycemia causes tremor, but asterixis is specifically hepatic.
8. Which cytokine is the primary endogenous pyrogen responsible for fever in septic shock?
A. Interleukin-10 (IL-10)
B. Tumor Necrosis Factor-alpha (TNF-α)
C. Transforming Growth Factor-beta (TGF-β)
D. Interleukin-4 (IL-4)
Advanced Nursing Practice Review Material
Section I: Advanced Pathophysiology (Questions 1-20)
1. A 65-year-old male with a 40-year history of smoking presents with shortness of breath. ABG
shows: pH 7.32, PaCO2 68 mm Hg, HCO3- 32 mEq/L. What is the acid-base disturbance?
A. Acute Respiratory Acidosis
B. Partially Compensated Metabolic Alkalosis
C. Partially Compensated Respiratory Acidosis
D. Uncompensated Respiratory Alkalosis
Correct AnswerC. Partially Compensated Respiratory Acidosis
• Rationale for C: Low pH (acidemia) + High PaCO2 (Respiratory cause). HCO3- is elevated
(metabolic compensation) but not enough to normalize pH (7.35-7.45), indicating partial
compensation.
• Rationale for A: Acute would have normal HCO3- (24).
• Rationale for B: pH is acidic, not alkalotic.
• Rationale for D: PaCO2 is high, not low.
2. In Type 2 Diabetes Mellitus, which cellular mechanism is primarily responsible for insulin
resistance?
A. Autoimmune destruction of beta cells in the islets of Langerhans
B. Downregulation of GLUT-4 transporters in skeletal muscle and adipose tissue
C. Increased C-peptide secretion by the pancreas
D. Alpha cell hyperplasia leading to excess glucagon
Correct AnswerB. Downregulation of GLUT-4 transporters in skeletal muscle and adipose tissue
• Rationale for B: Insulin resistance is characterized by impaired translocation of GLUT-4 to the
cell membrane, preventing glucose entry.
• Rationale for A: This describes Type 1 DM.
• Rationale for C: C-peptide is low or normal in Type 2, not high.
• Rationale for D: Alpha cell dysfunction contributes but is not the primary cellular mechanism for
resistance.
,3. A patient with chronic heart failure is taking Furosemide and Digoxin. Which electrolyte imbalance
poses the highest risk for Digoxin toxicity?
A. Hypernatremia (Na+ 155 mEq/L)
B. Hypokalemia (K+ 3.2 mEq/L)
C. Hypercalcemia (Ca+ 11.5 mg/dL)
D. Hypermagnesemia (Mg+ 3.0 mEq/L)
Correct AnswerB. Hypokalemia (K+ 3.2 mEq/L)
• Rationale for B: Low serum potassium increases the binding of digoxin to cardiac sodium-
potassium ATPase pumps, leading to toxicity.
• Rationale for A: Sodium affects volume status, not digoxin binding directly.
• Rationale for C: Hypocalcemia potentiates digoxin, but hypercalcemia has less direct risk than
hypokalemia.
• Rationale for D: Hypermagnesemia is protective against arrhythmias.
4. Which lab finding is most consistent with a diagnosis of disseminated intravascular coagulation
(DIC) secondary to sepsis?
A. Elevated platelet count and elevated fibrinogen
B. Decreased PT/INR and decreased aPTT
C. Decreased fibrinogen and elevated D-dimer
D. Normal schistocytes on peripheral smear
Correct AnswerC. Decreased fibrinogen and elevated D-dimer
• Rationale for C: DIC consumes clotting factors (low fibrinogen) and activates fibrinolysis (high D-
dimer).
• Rationale for A: Platelets are low in DIC (thrombocytopenia).
• Rationale for B: PT/INR and aPTT are prolonged due to factor depletion.
• Rationale for D: Schistocytes (RBC fragments) are typically present in microangiopathic
hemolytic anemia (MAHA) seen in DIC.
5. A patient with end-stage renal disease (ESRD) presents with muscle twitching, confusion, and a
prolonged QT interval. EKG shows peaked T waves. What is the priority intervention?
A. Administer IV calcium gluconate
B. Administer IV insulin and dextrose
C. Administer IV normal saline bolus
D. Prepare for emergent hemodialysis
Correct AnswerA. Administer IV calcium gluconate
• Rationale for A: The patient has hyperkalemia (peaked T waves). IV calcium gluconate stabilizes
the cardiac membrane immediately, even before potassium is lowered.
, • Rationale for B: Insulin/dextrose shifts K+ into cells but takes 15-30 min; cardiac stabilization
comes first.
• Rationale for C: Saline is for prerenal azotemia, not acute cardiac protection in ESRD.
• Rationale for D: Dialysis is definitive but takes time to set up; calcium is immediate.
6. In asthma, which inflammatory mediator is primarily responsible for late-phase bronchospasm (4-8
hours after exposure)?
A. Histamine
B. Leukotrienes (LTD4, LTE4)
C. Epinephrine
D. Bradykinin
Correct AnswerB. Leukotrienes (LTD4, LTE4)
• Rationale for B: Leukotrienes are released from mast cells and eosinophils during the late phase,
causing sustained bronchoconstriction, mucus secretion, and airway remodeling.
• Rationale for A: Histamine causes the immediate reaction (10-15 min).
• Rationale for C: Epinephrine is a bronchodilator, not a mediator of inflammation.
• Rationale for D: Bradykinin causes pain and cough but not the primary late-phase constriction.
7. A patient with liver cirrhosis develops ascites and asterixis. What is the primary pathophysiological
mechanism of asterixis (liver flap)?
A. Accumulation of manganese in the basal ganglia
B. Failure of the liver to detoxify ammonia leading to impaired neurotransmission
C. Direct alcohol toxicity on the cerebellum
D. Hypoglycemia due to reduced gluconeogenesis
Correct AnswerB. Failure of the liver to detoxify ammonia leading to impaired neurotransmission
• Rationale for B: Ammonia crosses the blood-brain barrier, affects astrocyte function, and alters
glutamatergic and GABAergic neurotransmission, causing metabolic encephalopathy and
asterixis.
• Rationale for A: Manganese accumulation occurs in TIPS patients but is not the primary
mechanism.
• Rationale for C: Cerebellar atrophy is from chronic ETOH, but asterixis is metabolic.
• Rationale for D: Hypoglycemia causes tremor, but asterixis is specifically hepatic.
8. Which cytokine is the primary endogenous pyrogen responsible for fever in septic shock?
A. Interleukin-10 (IL-10)
B. Tumor Necrosis Factor-alpha (TNF-α)
C. Transforming Growth Factor-beta (TGF-β)
D. Interleukin-4 (IL-4)
