Nurs 6501 Advanced Pathophysiology Actual
Week 6 Midterm Exam 2026 Winter Quarter
Walden University | 100 Correctly Answered
Questions | Verified Exam Graded A+
Q1. Which cellular adaptation occurs in response to chronic irritation or stress?
A. Hyperplasia
B. Hypertrophy
C. Metaplasia
D. Atrophy
Answer: C
Rationale: Metaplasia is the reversible replacement of one differentiated cell type with
another (e.g., squamous in bronchial epithelium due to smoking). Hyperplasia (A) increases
cell number; hypertrophy (B) increases cell size; atrophy (D) decreases size/number.
Q2. The most common cause of cellular injury is:
A. Hypoxia
B. Toxins
C. Infection
D. Physical agents
Answer: A
Rationale: Hypoxia (ischemia, hypoxemia) is the leading cause of ATP depletion and cell
death. Toxins (B), infection (C), and physical (D) are secondary.
Q3. Free radicals cause cellular damage primarily by:
A. Lipid peroxidation of membranes
,B. Protein synthesis inhibition
C. DNA replication
D. Mitochondrial fusion
Answer: A
Rationale: ROS attack polyunsaturated fatty acids in membranes, causing chain reactions.
Protein (B) secondary; DNA (C) mutation; fusion (D) normal.
Q4. In reversible cell injury, the earliest ultrastructural change is:
A. Plasma membrane blebbing
B. Mitochondrial swelling
C. Nuclear chromatin clumping
D. ER dilation
Answer: A
Rationale: Blebbing reflects cytoskeletal disruption and ion imbalance. Mitochondrial
swelling (B) follows; nuclear (C) later; ER (D) variable.
Q5. Necrosis is characterized by:
A. Cell shrinkage and nuclear fragmentation
B. Cell swelling and membrane rupture
C. Orderly DNA degradation
D. Caspase activation
Answer: B
Rationale: Uncontrolled death with inflammation. Shrinkage/fragmentation (A) apoptosis;
orderly DNA (C) apoptosis; caspases (D) apoptosis.
Q6. The type of necrosis seen in myocardial infarction is:
A. Coagulative
B. Liquefactive
,C. Caseous
D. Fat
Answer: A
Rationale: Preserves tissue architecture due to protein denaturation. Liquefactive (B)
brain/abscess; caseous (C) TB; fat (D) pancreatitis.
Q7. Apoptosis is initiated by:
A. Intrinsic (mitochondrial) and extrinsic (death receptor) pathways
B. Only extrinsic
C. Only intrinsic
D. Lysosomal rupture
Answer: A
Rationale: Both converge on caspases. Lysosomal (D) autophagy/necroptosis.
Q8. The primary mediator of acute inflammation is:
A. Neutrophils
B. Macrophages
C. Lymphocytes
D. Mast cells
Answer: A
Rationale: First responders (6–24 hours). Macrophages (B) chronic; lymphocytes (C)
adaptive; mast (D) immediate.
Q9. The cardinal signs of inflammation include all EXCEPT:
A. Redness (rubor)
B. Swelling (tumor)
C. Pain (dolor)
D. Bradycardia
, Answer: D
Rationale: Rubor, tumor, dolor, calor (heat), functio laesa (loss of function). Bradycardia
(D) not a sign.
Q10. Histamine is released from:
A. Mast cells and basophils
B. Neutrophils
C. Eosinophils
D. Platelets only
Answer: A
Rationale: Preformed mediator causing vasodilation/edema. Others release different
mediators.
Q11. The complement protein that enhances phagocytosis is:
A. C3b
B. C5a
C. C3a
D. C1q
Answer: A
Rationale: Opsonin. C5a (B) chemotaxis; C3a (C) anaphylatoxin; C1q (D) classical
initiation.
Q12. Chronic inflammation is dominated by:
A. Mononuclear cells (macrophages, lymphocytes)
B. Neutrophils
C. Eosinophils
D. Basophils
Answer: A
Week 6 Midterm Exam 2026 Winter Quarter
Walden University | 100 Correctly Answered
Questions | Verified Exam Graded A+
Q1. Which cellular adaptation occurs in response to chronic irritation or stress?
A. Hyperplasia
B. Hypertrophy
C. Metaplasia
D. Atrophy
Answer: C
Rationale: Metaplasia is the reversible replacement of one differentiated cell type with
another (e.g., squamous in bronchial epithelium due to smoking). Hyperplasia (A) increases
cell number; hypertrophy (B) increases cell size; atrophy (D) decreases size/number.
Q2. The most common cause of cellular injury is:
A. Hypoxia
B. Toxins
C. Infection
D. Physical agents
Answer: A
Rationale: Hypoxia (ischemia, hypoxemia) is the leading cause of ATP depletion and cell
death. Toxins (B), infection (C), and physical (D) are secondary.
Q3. Free radicals cause cellular damage primarily by:
A. Lipid peroxidation of membranes
,B. Protein synthesis inhibition
C. DNA replication
D. Mitochondrial fusion
Answer: A
Rationale: ROS attack polyunsaturated fatty acids in membranes, causing chain reactions.
Protein (B) secondary; DNA (C) mutation; fusion (D) normal.
Q4. In reversible cell injury, the earliest ultrastructural change is:
A. Plasma membrane blebbing
B. Mitochondrial swelling
C. Nuclear chromatin clumping
D. ER dilation
Answer: A
Rationale: Blebbing reflects cytoskeletal disruption and ion imbalance. Mitochondrial
swelling (B) follows; nuclear (C) later; ER (D) variable.
Q5. Necrosis is characterized by:
A. Cell shrinkage and nuclear fragmentation
B. Cell swelling and membrane rupture
C. Orderly DNA degradation
D. Caspase activation
Answer: B
Rationale: Uncontrolled death with inflammation. Shrinkage/fragmentation (A) apoptosis;
orderly DNA (C) apoptosis; caspases (D) apoptosis.
Q6. The type of necrosis seen in myocardial infarction is:
A. Coagulative
B. Liquefactive
,C. Caseous
D. Fat
Answer: A
Rationale: Preserves tissue architecture due to protein denaturation. Liquefactive (B)
brain/abscess; caseous (C) TB; fat (D) pancreatitis.
Q7. Apoptosis is initiated by:
A. Intrinsic (mitochondrial) and extrinsic (death receptor) pathways
B. Only extrinsic
C. Only intrinsic
D. Lysosomal rupture
Answer: A
Rationale: Both converge on caspases. Lysosomal (D) autophagy/necroptosis.
Q8. The primary mediator of acute inflammation is:
A. Neutrophils
B. Macrophages
C. Lymphocytes
D. Mast cells
Answer: A
Rationale: First responders (6–24 hours). Macrophages (B) chronic; lymphocytes (C)
adaptive; mast (D) immediate.
Q9. The cardinal signs of inflammation include all EXCEPT:
A. Redness (rubor)
B. Swelling (tumor)
C. Pain (dolor)
D. Bradycardia
, Answer: D
Rationale: Rubor, tumor, dolor, calor (heat), functio laesa (loss of function). Bradycardia
(D) not a sign.
Q10. Histamine is released from:
A. Mast cells and basophils
B. Neutrophils
C. Eosinophils
D. Platelets only
Answer: A
Rationale: Preformed mediator causing vasodilation/edema. Others release different
mediators.
Q11. The complement protein that enhances phagocytosis is:
A. C3b
B. C5a
C. C3a
D. C1q
Answer: A
Rationale: Opsonin. C5a (B) chemotaxis; C3a (C) anaphylatoxin; C1q (D) classical
initiation.
Q12. Chronic inflammation is dominated by:
A. Mononuclear cells (macrophages, lymphocytes)
B. Neutrophils
C. Eosinophils
D. Basophils
Answer: A
