NR 507 / NR507 Advanced Pathophysiology
Midterm Exam | ACTUAL EXAM | Questions &
Verified Answers | Latest Update –
Chamberlain University
1
Which intracellular change is the earliest microscopic indicator of irreversible cell injury?
A.
Clumping of nuclear chromatin
B.
Detachment of ribosomes from rough endoplasmic reticulum
C.
Plasma-membrane blebbing
D.
Mitochondrial swelling with amorphous densities
Correct Answer: D
Rationale: Mitochondrial swelling followed by the appearance of amorphous, flocculent
densities is the earliest electron-microscopic sign that the cell has passed the “point of
no return.” These densities represent precipitated calcium–phosphate complexes and
denatured mitochondrial proteins, indicating permanent loss of oxidative
,phosphorylation. Clumping of chromatin (A) and ribosomal detachment (B) occur earlier
but are still compatible with recovery if the injurious stimulus is removed.
Plasma-membrane blebbing (C) is a surface change that can be reversible.
2
A 4-year-old boy with sickle-cell disease develops acute vaso-occlusive pain. Which
pathophysiologic process is most responsible for the vascular obstruction?
A.
Increased red-cell affinity for oxygen
B.
Polymerization of deoxygenated hemoglobin S
C.
Excessive production of 2,3-bisphosphoglycerate
D.
Up-regulation of endothelial nitric-oxide synthase
Correct Answer: B
Rationale: Deoxygenated HbS molecules polymerize into long rigid fibers that distort the
erythrocyte into a sickle shape; these inflexible cells obstruct small vessels and produce
ischemic pain. Increased oxygen affinity (A) would inhibit sickling, not promote it.
Elevated 2,3-BPG (C) shifts the curve rightward but does not initiate obstruction.
Up-regulation of eNOS (D) would vasodilate vessels and lessen, not cause, obstruction.
3
,A 55-year-old woman with long-standing rheumatoid arthritis has progressive dyspnea.
High-resolution CT shows honeycombing and traction bronchiectasis. Which
inflammatory cell type drives this fibrotic remodeling?
A.
Neutrophils releasing elastase
B.
Activated macrophages secreting TGF-β1
C.
Mast cells producing histamine
D.
Eosinophils releasing major basic protein
Correct Answer: B
Rationale: Macrophage-derived transforming growth factor-β1 is the principal cytokine
that stimulates fibroblast proliferation and collagen deposition, leading to honeycomb
fibrosis. Neutrophil elastase (A) causes tissue destruction but is not the primary
fibrogenic signal. Mast-cell histamine (C) increases vascular permeability acutely.
Eosinophil major basic protein (D) is cytotoxic to epithelium but plays a lesser role in
progressive fibrosis.
4
, A child with cystic-fibrosis has a 3-bp deletion in the CFTR gene that removes
phenylalanine at position 508. Which post-translational event causes the
chloride-channel defect?
A.
Failure of glycosylation in the Golgi apparatus
B.
Premature degradation in the proteasome
C.
Abnormal phosphorylation by protein kinase A
D.
Blockade of ATP binding to the nucleotide-binding domains
Correct Answer: B
Rationale: ΔF508-CFTR protein misfolds in the ER, is recognized by quality-control
chaperones, and is retro-translocated to the cytosol for proteasomal degradation; thus
no mature channel reaches the apical membrane. Glycosylation (A) is not the primary
defect. Phosphorylation (C) is normal if the protein were present. ATP binding (D) is
intact in the few channels that do reach the membrane.
5
Laboratory values for a comatose patient are: Na 132 mEq/L, K 4.8 mEq/L, Cl 100
mEq/L, HCO3 8 mEq/L, PaCO2 18 mmHg, glucose 38 mg/dL. Which pathophysiologic
process best explains the acid–base status?
Midterm Exam | ACTUAL EXAM | Questions &
Verified Answers | Latest Update –
Chamberlain University
1
Which intracellular change is the earliest microscopic indicator of irreversible cell injury?
A.
Clumping of nuclear chromatin
B.
Detachment of ribosomes from rough endoplasmic reticulum
C.
Plasma-membrane blebbing
D.
Mitochondrial swelling with amorphous densities
Correct Answer: D
Rationale: Mitochondrial swelling followed by the appearance of amorphous, flocculent
densities is the earliest electron-microscopic sign that the cell has passed the “point of
no return.” These densities represent precipitated calcium–phosphate complexes and
denatured mitochondrial proteins, indicating permanent loss of oxidative
,phosphorylation. Clumping of chromatin (A) and ribosomal detachment (B) occur earlier
but are still compatible with recovery if the injurious stimulus is removed.
Plasma-membrane blebbing (C) is a surface change that can be reversible.
2
A 4-year-old boy with sickle-cell disease develops acute vaso-occlusive pain. Which
pathophysiologic process is most responsible for the vascular obstruction?
A.
Increased red-cell affinity for oxygen
B.
Polymerization of deoxygenated hemoglobin S
C.
Excessive production of 2,3-bisphosphoglycerate
D.
Up-regulation of endothelial nitric-oxide synthase
Correct Answer: B
Rationale: Deoxygenated HbS molecules polymerize into long rigid fibers that distort the
erythrocyte into a sickle shape; these inflexible cells obstruct small vessels and produce
ischemic pain. Increased oxygen affinity (A) would inhibit sickling, not promote it.
Elevated 2,3-BPG (C) shifts the curve rightward but does not initiate obstruction.
Up-regulation of eNOS (D) would vasodilate vessels and lessen, not cause, obstruction.
3
,A 55-year-old woman with long-standing rheumatoid arthritis has progressive dyspnea.
High-resolution CT shows honeycombing and traction bronchiectasis. Which
inflammatory cell type drives this fibrotic remodeling?
A.
Neutrophils releasing elastase
B.
Activated macrophages secreting TGF-β1
C.
Mast cells producing histamine
D.
Eosinophils releasing major basic protein
Correct Answer: B
Rationale: Macrophage-derived transforming growth factor-β1 is the principal cytokine
that stimulates fibroblast proliferation and collagen deposition, leading to honeycomb
fibrosis. Neutrophil elastase (A) causes tissue destruction but is not the primary
fibrogenic signal. Mast-cell histamine (C) increases vascular permeability acutely.
Eosinophil major basic protein (D) is cytotoxic to epithelium but plays a lesser role in
progressive fibrosis.
4
, A child with cystic-fibrosis has a 3-bp deletion in the CFTR gene that removes
phenylalanine at position 508. Which post-translational event causes the
chloride-channel defect?
A.
Failure of glycosylation in the Golgi apparatus
B.
Premature degradation in the proteasome
C.
Abnormal phosphorylation by protein kinase A
D.
Blockade of ATP binding to the nucleotide-binding domains
Correct Answer: B
Rationale: ΔF508-CFTR protein misfolds in the ER, is recognized by quality-control
chaperones, and is retro-translocated to the cytosol for proteasomal degradation; thus
no mature channel reaches the apical membrane. Glycosylation (A) is not the primary
defect. Phosphorylation (C) is normal if the protein were present. ATP binding (D) is
intact in the few channels that do reach the membrane.
5
Laboratory values for a comatose patient are: Na 132 mEq/L, K 4.8 mEq/L, Cl 100
mEq/L, HCO3 8 mEq/L, PaCO2 18 mmHg, glucose 38 mg/dL. Which pathophysiologic
process best explains the acid–base status?
