NR507 Advanced Pathophysiology
midterm exam Practice questions
with answers/ NR 507 Advanced
Pathophysiology Week 4 Practice
Test
Question 1
A 62-year-old patient with COPD and acute hypercapnic respiratory failure is being
evaluated for oxygen therapy. Which oxygen delivery method is most appropriate to
avoid suppression of hypoxic drive?
A. Venturi mask at 24% oxygen
B. Non-rebreather mask at 15 L/min
C. Nasal cannula at 6 L/min
D. Simple face mask at 10 L/min
Answer: A. Venturi mask at 24% oxygen
Rationale: In COPD patients with chronic hypercapnia, the hypoxic drive often becomes
the primary stimulus for breathing. A Venturi mask at 24% delivers precise low oxygen
concentration, minimizing the risk of suppressing hypoxic drive. High-flow devices
deliver higher FiO₂ concentrations that can worsen hypercapnia by reducing the
respiratory drive .
, Why wrong: Non-rebreather masks deliver high FiO₂, risking respiratory depression.
Nasal cannula at 6 L/min and simple face masks also deliver higher concentrations than
appropriate for this patient population.
Question 2
A patient with type 2 diabetes mellitus is started on metformin. Which cellular
mechanism best explains its primary glucose-lowering effect?
A. Stimulation of pancreatic beta-cell insulin secretion
B. Activation of AMP-activated protein kinase (AMPK) in hepatocytes
C. Inhibition of intestinal alpha-glucosidase enzymes
D. Potentiation of incretin hormones such as GLP-1
Answer: B. Activation of AMP-activated protein kinase (AMPK) in hepatocytes
Rationale: Metformin activates AMPK, which suppresses hepatic gluconeogenesis and
increases peripheral insulin sensitivity. It does not directly stimulate insulin secretion
(sulfonylureas do this). Alpha-glucosidase inhibitors block carbohydrate absorption, and
GLP-1 potentiation is the mechanism of DPP-4 inhibitors and GLP-1 receptor agonists .
Question 3
A 35-year-old female with SLE has a complement C3 level of 42 mg/dL (normal 90-180).
Which BEST explains the low complement in active SLE?
A. The liver is unable to synthesize complement in SLE patients
B. Immune complex deposition activates and consumes complement components
causing low C3 and C4 levels
C. SLE patients produce autoantibodies that directly neutralize complement proteins
D. Complement deficiency is a genetic predisposition to developing SLE
Answer: B. Immune complex deposition activates and consumes complement
components causing low C3 and C4 levels
,Rationale: In active SLE, anti-dsDNA antibodies form immune complexes that activate
the classical complement pathway, consuming C3 and C4. Low complement levels
(especially C3, C4) correlate with disease activity and lupus nephritis. Rising complement
levels indicate improving disease activity .
Question 4
A 52-year-old male with rheumatoid arthritis has elevated RF and anti-CCP antibodies.
Synovial biopsy reveals pannus formation. Which inflammatory mediator is MOST
responsible for joint destruction in RA?
A. IL-4 and IL-13
B. TNF-α and IL-6 driving synovial fibroblast activation and osteoclast-mediated
bone erosion
C. IL-10 and TGF-β
D. IL-17 and IL-23 exclusively
Answer: B. TNF-α and IL-6 driving synovial fibroblast activation and osteoclast-
mediated bone erosion
Rationale: TNF-α and IL-6 are primary pathogenic cytokines in RA. TNF-α activates
synovial fibroblasts (pannus formation) and osteoclasts (bone erosion). IL-6 drives the
acute phase response and joint inflammation. Biologic therapies targeting TNF-α
(etanercept, adalimumab) and IL-6 (tocilizumab) are highly effective .
Question 5
A 6-year-old child develops hemolytic uremic syndrome (HUS) following E. coli O157:H7
gastroenteritis. Lab work shows microangiopathic hemolytic anemia, thrombocytopenia,
and acute kidney injury. Which BEST describes the mechanism of renal injury?
A. IgE-mediated mast cell degranulation in glomeruli
B. Shiga toxin damages glomerular endothelial cells causing thrombotic
microangiopathy
, C. Immune complex deposition activating complement
D. T cell-mediated delayed hypersensitivity
Answer: B. Shiga toxin damages glomerular endothelial cells causing thrombotic
microangiopathy
Rationale: HUS pathophysiology: Shiga toxin → endothelial cell injury → platelet
activation and fibrin deposition → thrombotic microangiopathy → mechanical RBC
destruction (schistocytes) + thrombocytopenia + AKI. Classic triad: microangiopathic
hemolytic anemia, thrombocytopenia, AKI .
Question 6
A 38-year-old female with myasthenia gravis has autoantibodies against acetylcholine
receptors (AChR) at the neuromuscular junction. Her symptoms worsen with activity and
improve with rest. This BEST represents which type of hypersensitivity?
A. Type I IgE-mediated
B. Type II antibody-mediated (receptor blocking/destruction)
C. Type III immune complex-mediated
D. Type IV T cell-mediated
Answer: B. Type II antibody-mediated (receptor blocking/destruction)
Rationale: Myasthenia gravis is a Type II hypersensitivity disorder where autoantibodies
bind to and block/destroy acetylcholine receptors at the neuromuscular junction. This
prevents neuromuscular transmission, causing muscle weakness that worsens with
activity. Unlike most Type II reactions that cause cell destruction, some Type II
antibodies can stimulate receptors (as in Graves' disease) .
Question 7
A 42-year-old female with Graves' disease has thyroid-stimulating immunoglobulins
(TSI) that bind to TSH receptors on thyroid cells. Unlike most Type II hypersensitivity
midterm exam Practice questions
with answers/ NR 507 Advanced
Pathophysiology Week 4 Practice
Test
Question 1
A 62-year-old patient with COPD and acute hypercapnic respiratory failure is being
evaluated for oxygen therapy. Which oxygen delivery method is most appropriate to
avoid suppression of hypoxic drive?
A. Venturi mask at 24% oxygen
B. Non-rebreather mask at 15 L/min
C. Nasal cannula at 6 L/min
D. Simple face mask at 10 L/min
Answer: A. Venturi mask at 24% oxygen
Rationale: In COPD patients with chronic hypercapnia, the hypoxic drive often becomes
the primary stimulus for breathing. A Venturi mask at 24% delivers precise low oxygen
concentration, minimizing the risk of suppressing hypoxic drive. High-flow devices
deliver higher FiO₂ concentrations that can worsen hypercapnia by reducing the
respiratory drive .
, Why wrong: Non-rebreather masks deliver high FiO₂, risking respiratory depression.
Nasal cannula at 6 L/min and simple face masks also deliver higher concentrations than
appropriate for this patient population.
Question 2
A patient with type 2 diabetes mellitus is started on metformin. Which cellular
mechanism best explains its primary glucose-lowering effect?
A. Stimulation of pancreatic beta-cell insulin secretion
B. Activation of AMP-activated protein kinase (AMPK) in hepatocytes
C. Inhibition of intestinal alpha-glucosidase enzymes
D. Potentiation of incretin hormones such as GLP-1
Answer: B. Activation of AMP-activated protein kinase (AMPK) in hepatocytes
Rationale: Metformin activates AMPK, which suppresses hepatic gluconeogenesis and
increases peripheral insulin sensitivity. It does not directly stimulate insulin secretion
(sulfonylureas do this). Alpha-glucosidase inhibitors block carbohydrate absorption, and
GLP-1 potentiation is the mechanism of DPP-4 inhibitors and GLP-1 receptor agonists .
Question 3
A 35-year-old female with SLE has a complement C3 level of 42 mg/dL (normal 90-180).
Which BEST explains the low complement in active SLE?
A. The liver is unable to synthesize complement in SLE patients
B. Immune complex deposition activates and consumes complement components
causing low C3 and C4 levels
C. SLE patients produce autoantibodies that directly neutralize complement proteins
D. Complement deficiency is a genetic predisposition to developing SLE
Answer: B. Immune complex deposition activates and consumes complement
components causing low C3 and C4 levels
,Rationale: In active SLE, anti-dsDNA antibodies form immune complexes that activate
the classical complement pathway, consuming C3 and C4. Low complement levels
(especially C3, C4) correlate with disease activity and lupus nephritis. Rising complement
levels indicate improving disease activity .
Question 4
A 52-year-old male with rheumatoid arthritis has elevated RF and anti-CCP antibodies.
Synovial biopsy reveals pannus formation. Which inflammatory mediator is MOST
responsible for joint destruction in RA?
A. IL-4 and IL-13
B. TNF-α and IL-6 driving synovial fibroblast activation and osteoclast-mediated
bone erosion
C. IL-10 and TGF-β
D. IL-17 and IL-23 exclusively
Answer: B. TNF-α and IL-6 driving synovial fibroblast activation and osteoclast-
mediated bone erosion
Rationale: TNF-α and IL-6 are primary pathogenic cytokines in RA. TNF-α activates
synovial fibroblasts (pannus formation) and osteoclasts (bone erosion). IL-6 drives the
acute phase response and joint inflammation. Biologic therapies targeting TNF-α
(etanercept, adalimumab) and IL-6 (tocilizumab) are highly effective .
Question 5
A 6-year-old child develops hemolytic uremic syndrome (HUS) following E. coli O157:H7
gastroenteritis. Lab work shows microangiopathic hemolytic anemia, thrombocytopenia,
and acute kidney injury. Which BEST describes the mechanism of renal injury?
A. IgE-mediated mast cell degranulation in glomeruli
B. Shiga toxin damages glomerular endothelial cells causing thrombotic
microangiopathy
, C. Immune complex deposition activating complement
D. T cell-mediated delayed hypersensitivity
Answer: B. Shiga toxin damages glomerular endothelial cells causing thrombotic
microangiopathy
Rationale: HUS pathophysiology: Shiga toxin → endothelial cell injury → platelet
activation and fibrin deposition → thrombotic microangiopathy → mechanical RBC
destruction (schistocytes) + thrombocytopenia + AKI. Classic triad: microangiopathic
hemolytic anemia, thrombocytopenia, AKI .
Question 6
A 38-year-old female with myasthenia gravis has autoantibodies against acetylcholine
receptors (AChR) at the neuromuscular junction. Her symptoms worsen with activity and
improve with rest. This BEST represents which type of hypersensitivity?
A. Type I IgE-mediated
B. Type II antibody-mediated (receptor blocking/destruction)
C. Type III immune complex-mediated
D. Type IV T cell-mediated
Answer: B. Type II antibody-mediated (receptor blocking/destruction)
Rationale: Myasthenia gravis is a Type II hypersensitivity disorder where autoantibodies
bind to and block/destroy acetylcholine receptors at the neuromuscular junction. This
prevents neuromuscular transmission, causing muscle weakness that worsens with
activity. Unlike most Type II reactions that cause cell destruction, some Type II
antibodies can stimulate receptors (as in Graves' disease) .
Question 7
A 42-year-old female with Graves' disease has thyroid-stimulating immunoglobulins
(TSI) that bind to TSH receptors on thyroid cells. Unlike most Type II hypersensitivity
