NUR 3125 – Pathophysiology Across
the Lifespan, Final Exam 2025/2026 –
Verified Questions
MULTISYSTEM & SHOCK STATES (1–20)
1. The hallmark pathophysiologic feature common to ALL forms of shock is:
A. Vasodilation
B. Inadequate tissue perfusion and cellular hypoxia
C. Hypertension
D. Increased cardiac output
B. Inadequate tissue perfusion and cellular hypoxia
Rationale: Shock = impaired oxygen delivery (DO₂) or utilization → anaerobic metabolism →
lactic acidosis regardless of etiology.
2. In septic shock, the primary mechanism of hypotension is:
A. Massive cytokine-induced vasodilation + myocardial depression
B. Hypovolemia
C. Pump failure
D. Obstruction
A. Massive cytokine-induced vasodilation + myocardial depression
Rationale: TNF-α, IL-1, NO → iNOS upregulation → refractory vasodilation; IL-6 → troponin
leak → ↓contractility.
3. Systemic Inflammatory Response Syndrome (SIRS) is triggered by:
A. Danger-associated molecular patterns (DAMPs) or pathogen-associated molecular patterns
(PAMPs) activating TLRs
B. Direct myocardial injury
C. Hypovolemia alone
D. Adrenal insufficiency
A. Danger-associated molecular patterns (DAMPs) or pathogen-associated molecular
patterns (PAMPs) activating TLRs
Rationale: Leads to NF-κB activation → cytokine storm → multisystem organ dysfunction
(MODS).
4. The most common cause of death in MODS is:
A. Lung → ARDS → refractory hypoxemia
B. Kidney failure
, C. Liver failure
D. Coagulopathy
A. Lung → ARDS → refractory hypoxemia
Rationale: Pulmonary endothelial injury → permeability edema → P/F <100 → highest mortality
in sequential organ failure.
5. Disseminated intravascular coagulation (DIC) in sepsis is initiated by:
A. Tissue factor expression on monocytes/endothelium → extrinsic pathway activation
B. Platelet activation only
C. Fibrinolysis excess
D. Anticoagulant deficiency
A. Tissue factor expression on monocytes/endothelium → extrinsic pathway activation
Rationale: TF-factor VIIa → thrombin burst → microthrombi + consumption coagulopathy.
6. In anaphylactic shock, the primary mediator of bronchoconstriction and hypotension is:
A. Histamine via H1 receptors
B. Leukotrienes
C. PAF
D. Tryptase
A. Histamine via H1 receptors
Rationale: IgE cross-linking → mast cell degranulation → immediate vasodilation and increased
vascular permeability.
7. The pathophysiologic triad of fat embolism syndrome is:
A. Respiratory distress, petechiae, neurologic abnormalities
B. Hypotension, tachycardia, fever
C. Pulmonary edema, rash, renal failure
D. Coagulopathy, jaundice, shock
A. Respiratory distress, petechiae, neurologic abnormalities
Rationale: Fat globules → pulmonary capillaries → mechanical obstruction + free fatty acid
toxicity.
8. Acute respiratory distress syndrome (ARDS) is characterized by:
A. Non-cardiogenic pulmonary edema due to alveolar-capillary membrane injury
B. Cardiogenic edema
C. Chronic fibrosis
D. Airway obstruction
A. Non-cardiogenic pulmonary edema due to alveolar-capillary membrane injury
Rationale: Neutrophil activation → protease/elastase → type I pneumocyte destruction →
protein-rich exudate.
the Lifespan, Final Exam 2025/2026 –
Verified Questions
MULTISYSTEM & SHOCK STATES (1–20)
1. The hallmark pathophysiologic feature common to ALL forms of shock is:
A. Vasodilation
B. Inadequate tissue perfusion and cellular hypoxia
C. Hypertension
D. Increased cardiac output
B. Inadequate tissue perfusion and cellular hypoxia
Rationale: Shock = impaired oxygen delivery (DO₂) or utilization → anaerobic metabolism →
lactic acidosis regardless of etiology.
2. In septic shock, the primary mechanism of hypotension is:
A. Massive cytokine-induced vasodilation + myocardial depression
B. Hypovolemia
C. Pump failure
D. Obstruction
A. Massive cytokine-induced vasodilation + myocardial depression
Rationale: TNF-α, IL-1, NO → iNOS upregulation → refractory vasodilation; IL-6 → troponin
leak → ↓contractility.
3. Systemic Inflammatory Response Syndrome (SIRS) is triggered by:
A. Danger-associated molecular patterns (DAMPs) or pathogen-associated molecular patterns
(PAMPs) activating TLRs
B. Direct myocardial injury
C. Hypovolemia alone
D. Adrenal insufficiency
A. Danger-associated molecular patterns (DAMPs) or pathogen-associated molecular
patterns (PAMPs) activating TLRs
Rationale: Leads to NF-κB activation → cytokine storm → multisystem organ dysfunction
(MODS).
4. The most common cause of death in MODS is:
A. Lung → ARDS → refractory hypoxemia
B. Kidney failure
, C. Liver failure
D. Coagulopathy
A. Lung → ARDS → refractory hypoxemia
Rationale: Pulmonary endothelial injury → permeability edema → P/F <100 → highest mortality
in sequential organ failure.
5. Disseminated intravascular coagulation (DIC) in sepsis is initiated by:
A. Tissue factor expression on monocytes/endothelium → extrinsic pathway activation
B. Platelet activation only
C. Fibrinolysis excess
D. Anticoagulant deficiency
A. Tissue factor expression on monocytes/endothelium → extrinsic pathway activation
Rationale: TF-factor VIIa → thrombin burst → microthrombi + consumption coagulopathy.
6. In anaphylactic shock, the primary mediator of bronchoconstriction and hypotension is:
A. Histamine via H1 receptors
B. Leukotrienes
C. PAF
D. Tryptase
A. Histamine via H1 receptors
Rationale: IgE cross-linking → mast cell degranulation → immediate vasodilation and increased
vascular permeability.
7. The pathophysiologic triad of fat embolism syndrome is:
A. Respiratory distress, petechiae, neurologic abnormalities
B. Hypotension, tachycardia, fever
C. Pulmonary edema, rash, renal failure
D. Coagulopathy, jaundice, shock
A. Respiratory distress, petechiae, neurologic abnormalities
Rationale: Fat globules → pulmonary capillaries → mechanical obstruction + free fatty acid
toxicity.
8. Acute respiratory distress syndrome (ARDS) is characterized by:
A. Non-cardiogenic pulmonary edema due to alveolar-capillary membrane injury
B. Cardiogenic edema
C. Chronic fibrosis
D. Airway obstruction
A. Non-cardiogenic pulmonary edema due to alveolar-capillary membrane injury
Rationale: Neutrophil activation → protease/elastase → type I pneumocyte destruction →
protein-rich exudate.
