NURS 611 Advanced Pathophysiology: Infectious Diseases and Sepsis
2026 |Maryville
1. According to the Sepsis-3 guidelines, which clinical tool is used to identify
patients outside the ICU who are at high risk of poor outcomes?
A. SIRS Criteria
B. MODS Score
C. APACHE II Score
D. qSOFA Score
Answer: D
Rationale: The qSOFA (quick Sequential Organ Failure Assessment) score is a simplified
version of the SOFA score used to identify patients outside the ICU with suspected infection
who are likely to have poor outcomes, focusing on respiratory rate, altered mentation, and
systolic blood pressure.
2. Which molecular mechanism is primarily responsible for the massive
vasodilation observed during septic shock?
A. Inhibition of the renin-angiotensin system
B. Inducible nitric oxide synthase (iNOS) activation and NO production
C. Decreased production of prostacyclins
D. Upregulation of alpha-1 adrenergic receptors
Answer: B
Rationale: In sepsis, inflammatory cytokines trigger the expression of iNOS in vascular
smooth muscle cells, leading to excessive production of nitric oxide (NO), which causes
profound vasodilation and hyporesponsiveness to vasopressors.
,3. Which component of the Gram-negative bacterial cell wall binds to the
TLR4/MD-2 complex to initiate a pro-inflammatory cascade?
A. Lipopolysaccharide (LPS)
B. Teichoic acid
C. Peptidoglycan
D. Flagellin
Answer: A
Rationale: LPS (endotoxin) is the primary PAMP of Gram-negative bacteria that binds to
Toll-like receptor 4 (TLR4), triggering the NF-κB pathway and the release of pro-
inflammatory cytokines.
4. During the early stages of sepsis, the ‘cytokine storm’ is characterized by high
levels of which primary mediators?
A. IL-10 and TGF-beta
B. Interferon-gamma and IL-4
C. IgE and Histamine
D. TNF-alpha, IL-1, and IL-6
Answer: D
Rationale: TNF-alpha, IL-1, and IL-6 are the classic pro-inflammatory cytokines released
by macrophages and monocytes that drive the systemic inflammatory response in sepsis.
5. What is the pathophysiological significance of the endothelial glycocalyx
degradation in sepsis?
A. It increases systemic vascular resistance.
B. It leads to vascular leakage, edema, and microvascular thrombosis.
C. It prevents leukocyte adhesion to the vessel wall.
D. It enhances the production of endogenous anticoagulants.
Answer: B
, Rationale: The glycocalyx is a protective layer on the endothelium. Its degradation in
sepsis increases vascular permeability, promotes fluid shift into the interstitium, and
exposes adhesion molecules, leading to thrombosis and inflammation.
6. Which condition is defined by the Sepsis-3 criteria as sepsis plus the need for
vasopressors to maintain MAP ≥ 65 mmHg and a serum lactate level > 2
mmol/L?
A. Severe Sepsis
B. Septic Shock
C. Refractory Sepsis
D. Multiple Organ Dysfunction Syndrome
Answer: B
Rationale: Septic shock is a subset of sepsis in which underlying circulatory and
cellular/metabolic abnormalities are profound enough to substantially increase mortality,
specifically requiring vasopressors and having elevated lactate.
7. In the context of sepsis-induced coagulopathy, what role does Tissue Factor
(TF) play?
A. It inhibits the extrinsic pathway of coagulation.
B. It initiates the coagulation cascade by binding to Factor VIIa.
C. It acts as a potent fibrinolytic agent.
D. It degrades thrombin to prevent clot formation.
Answer: B
Rationale: In sepsis, inflammatory cytokines induce the expression of Tissue Factor on
monocytes and endothelial cells, which activates the extrinsic pathway, leading to
widespread thrombin generation and potentially DIC.
2026 |Maryville
1. According to the Sepsis-3 guidelines, which clinical tool is used to identify
patients outside the ICU who are at high risk of poor outcomes?
A. SIRS Criteria
B. MODS Score
C. APACHE II Score
D. qSOFA Score
Answer: D
Rationale: The qSOFA (quick Sequential Organ Failure Assessment) score is a simplified
version of the SOFA score used to identify patients outside the ICU with suspected infection
who are likely to have poor outcomes, focusing on respiratory rate, altered mentation, and
systolic blood pressure.
2. Which molecular mechanism is primarily responsible for the massive
vasodilation observed during septic shock?
A. Inhibition of the renin-angiotensin system
B. Inducible nitric oxide synthase (iNOS) activation and NO production
C. Decreased production of prostacyclins
D. Upregulation of alpha-1 adrenergic receptors
Answer: B
Rationale: In sepsis, inflammatory cytokines trigger the expression of iNOS in vascular
smooth muscle cells, leading to excessive production of nitric oxide (NO), which causes
profound vasodilation and hyporesponsiveness to vasopressors.
,3. Which component of the Gram-negative bacterial cell wall binds to the
TLR4/MD-2 complex to initiate a pro-inflammatory cascade?
A. Lipopolysaccharide (LPS)
B. Teichoic acid
C. Peptidoglycan
D. Flagellin
Answer: A
Rationale: LPS (endotoxin) is the primary PAMP of Gram-negative bacteria that binds to
Toll-like receptor 4 (TLR4), triggering the NF-κB pathway and the release of pro-
inflammatory cytokines.
4. During the early stages of sepsis, the ‘cytokine storm’ is characterized by high
levels of which primary mediators?
A. IL-10 and TGF-beta
B. Interferon-gamma and IL-4
C. IgE and Histamine
D. TNF-alpha, IL-1, and IL-6
Answer: D
Rationale: TNF-alpha, IL-1, and IL-6 are the classic pro-inflammatory cytokines released
by macrophages and monocytes that drive the systemic inflammatory response in sepsis.
5. What is the pathophysiological significance of the endothelial glycocalyx
degradation in sepsis?
A. It increases systemic vascular resistance.
B. It leads to vascular leakage, edema, and microvascular thrombosis.
C. It prevents leukocyte adhesion to the vessel wall.
D. It enhances the production of endogenous anticoagulants.
Answer: B
, Rationale: The glycocalyx is a protective layer on the endothelium. Its degradation in
sepsis increases vascular permeability, promotes fluid shift into the interstitium, and
exposes adhesion molecules, leading to thrombosis and inflammation.
6. Which condition is defined by the Sepsis-3 criteria as sepsis plus the need for
vasopressors to maintain MAP ≥ 65 mmHg and a serum lactate level > 2
mmol/L?
A. Severe Sepsis
B. Septic Shock
C. Refractory Sepsis
D. Multiple Organ Dysfunction Syndrome
Answer: B
Rationale: Septic shock is a subset of sepsis in which underlying circulatory and
cellular/metabolic abnormalities are profound enough to substantially increase mortality,
specifically requiring vasopressors and having elevated lactate.
7. In the context of sepsis-induced coagulopathy, what role does Tissue Factor
(TF) play?
A. It inhibits the extrinsic pathway of coagulation.
B. It initiates the coagulation cascade by binding to Factor VIIa.
C. It acts as a potent fibrinolytic agent.
D. It degrades thrombin to prevent clot formation.
Answer: B
Rationale: In sepsis, inflammatory cytokines induce the expression of Tissue Factor on
monocytes and endothelial cells, which activates the extrinsic pathway, leading to
widespread thrombin generation and potentially DIC.
