NSG 3280 Pathophysiology Exam 2
NSG 3280 Pathophysiology Exam 2
NSG 3280 Pathophysiology Exam 2
Accurate Exam Coverage Area
1. Cellular Adaptation, Injury, and Death — atrophy, hypertrophy, hyperplasia,
metaplasia, dysplasia; reversible vs. irreversible injury; ATP depletion;
coagulative, liquefactive, caseous, and fat necrosis; apoptosis versus necrosis
1 3 4
2. Inflammation and Tissue Repair — acute vascular response; histamine,
prostaglandins, leukotrienes; neutrophil versus macrophage predominance;
chronic inflammation; wound healing phases 3 8
3. Immune System Function and Disorders — innate versus adaptive immunity;
active versus passive immunity; IgM, IgG, IgE, IgA roles; Type I–IV
hypersensitivity reactions; autoimmune mechanisms 2 11 13
4. Infection and Infectious Disease — endemic, epidemic, pandemic terminology;
modes of transmission; sepsis pathophysiology; fever mechanisms 2
5. Fluid, Electrolyte, and Acid-Base Imbalances — metabolic acidosis/alkalosis;
respiratory acidosis/alkalosis; sodium-potassium pump failure; isotonic versus
hypertonic/hypotonic fluid shifts 3 5
, 6. Hematologic Alterations — anemia of chronic kidney disease; erythropoietin
deficiency; transfusion reactions; coagulopathy; DIC mechanisms 1 11 14
7. Cardiovascular Pathophysiology — RAAS and blood pressure regulation; heart
failure with reduced versus preserved ejection fraction; myocardial infarction
and troponin; atherosclerosis; pulmonary embolism origin 1
8. Endocrine Pathophysiology — Type 1 versus Type 2 diabetes mellitus
mechanisms; diabetic ketoacidosis; polyuria-polydipsia-polyphagia triad; insulin
resistance 1 3
9. Renal and Genitourinary Pathophysiology — chronic kidney disease
consequences; anemia from EPO deficiency; acid-base derangements; uremic
toxin effects 1 14
10. Respiratory Pathophysiology — asthma as reversible airway obstruction;
airway remodeling; silent chest in severe asthma; chronic hypoxemia and cor
pulmonale 13 14
NSG 3280 Pathophysiology Exam 2
Questions 1–250: Multiple Choice with Answers and Rationales
1. A patient with chronic hypertension develops thickening of the left ventricular
wall. Which cellular adaptation does the nurse recognize as the primary
mechanism?
,A. Atrophy
B. Hypertrophy
C. Hyperplasia
D. Metaplasia
Answer: B
Rationale: Hypertrophy is an increase in cell size that allows the heart to
compensate for increased afterload. Atrophy is shrinkage, hyperplasia is
increased cell number, and metaplasia is replacement of one mature cell type with
another . 4
2. A 68-year-old patient with a 40-pack-year smoking history develops
squamous metaplasia of the bronchial epithelium. Which statement best
explains this cellular change?
A. The cells have undergone malignant transformation with uncontrolled
proliferation
B. The ciliated columnar epithelium has been reversibly replaced by stratified
squamous epithelium
C. The bronchial cells have increased in size due to chronic irritation
D. The number of normal ciliated cells has increased in response to smoke
exposure
Answer: B
Rationale: Metaplasia is the reversible replacement of one differentiated cell type
with another in response to chronic irritation. Smoking causes pseudostratified
, ciliated columnar epithelium to transform into stratified squamous epithelium,
which is more resistant but loses mucociliary function . 4
3. During ischemic cell injury, which intracellular event occurs first and triggers
the subsequent cascade of damage?
A. Plasma membrane rupture with leakage of cellular contents
B. Nuclear pyknosis with chromatin condensation
C. Decreased ATP synthesis from failed oxidative phosphorylation
D. Mitochondrial swelling with calcium influx
Answer: C
Rationale: Decreased ATP synthesis is the earliest biochemical event in ischemia.
Without oxygen, oxidative phosphorylation fails immediately, leading to sodium-
potassium pump failure, cellular swelling, and eventually irreversible membrane
damage . 4
4. A patient sustains a crushing injury to the thigh and twelve hours later the
muscle tissue shows preserved tissue architecture with denatured proteins.
Which type of necrosis is present?
A. Liquefactive necrosis
B. Caseous necrosis
C. Fat necrosis
D. Coagulative necrosis
NSG 3280 Pathophysiology Exam 2
NSG 3280 Pathophysiology Exam 2
Accurate Exam Coverage Area
1. Cellular Adaptation, Injury, and Death — atrophy, hypertrophy, hyperplasia,
metaplasia, dysplasia; reversible vs. irreversible injury; ATP depletion;
coagulative, liquefactive, caseous, and fat necrosis; apoptosis versus necrosis
1 3 4
2. Inflammation and Tissue Repair — acute vascular response; histamine,
prostaglandins, leukotrienes; neutrophil versus macrophage predominance;
chronic inflammation; wound healing phases 3 8
3. Immune System Function and Disorders — innate versus adaptive immunity;
active versus passive immunity; IgM, IgG, IgE, IgA roles; Type I–IV
hypersensitivity reactions; autoimmune mechanisms 2 11 13
4. Infection and Infectious Disease — endemic, epidemic, pandemic terminology;
modes of transmission; sepsis pathophysiology; fever mechanisms 2
5. Fluid, Electrolyte, and Acid-Base Imbalances — metabolic acidosis/alkalosis;
respiratory acidosis/alkalosis; sodium-potassium pump failure; isotonic versus
hypertonic/hypotonic fluid shifts 3 5
, 6. Hematologic Alterations — anemia of chronic kidney disease; erythropoietin
deficiency; transfusion reactions; coagulopathy; DIC mechanisms 1 11 14
7. Cardiovascular Pathophysiology — RAAS and blood pressure regulation; heart
failure with reduced versus preserved ejection fraction; myocardial infarction
and troponin; atherosclerosis; pulmonary embolism origin 1
8. Endocrine Pathophysiology — Type 1 versus Type 2 diabetes mellitus
mechanisms; diabetic ketoacidosis; polyuria-polydipsia-polyphagia triad; insulin
resistance 1 3
9. Renal and Genitourinary Pathophysiology — chronic kidney disease
consequences; anemia from EPO deficiency; acid-base derangements; uremic
toxin effects 1 14
10. Respiratory Pathophysiology — asthma as reversible airway obstruction;
airway remodeling; silent chest in severe asthma; chronic hypoxemia and cor
pulmonale 13 14
NSG 3280 Pathophysiology Exam 2
Questions 1–250: Multiple Choice with Answers and Rationales
1. A patient with chronic hypertension develops thickening of the left ventricular
wall. Which cellular adaptation does the nurse recognize as the primary
mechanism?
,A. Atrophy
B. Hypertrophy
C. Hyperplasia
D. Metaplasia
Answer: B
Rationale: Hypertrophy is an increase in cell size that allows the heart to
compensate for increased afterload. Atrophy is shrinkage, hyperplasia is
increased cell number, and metaplasia is replacement of one mature cell type with
another . 4
2. A 68-year-old patient with a 40-pack-year smoking history develops
squamous metaplasia of the bronchial epithelium. Which statement best
explains this cellular change?
A. The cells have undergone malignant transformation with uncontrolled
proliferation
B. The ciliated columnar epithelium has been reversibly replaced by stratified
squamous epithelium
C. The bronchial cells have increased in size due to chronic irritation
D. The number of normal ciliated cells has increased in response to smoke
exposure
Answer: B
Rationale: Metaplasia is the reversible replacement of one differentiated cell type
with another in response to chronic irritation. Smoking causes pseudostratified
, ciliated columnar epithelium to transform into stratified squamous epithelium,
which is more resistant but loses mucociliary function . 4
3. During ischemic cell injury, which intracellular event occurs first and triggers
the subsequent cascade of damage?
A. Plasma membrane rupture with leakage of cellular contents
B. Nuclear pyknosis with chromatin condensation
C. Decreased ATP synthesis from failed oxidative phosphorylation
D. Mitochondrial swelling with calcium influx
Answer: C
Rationale: Decreased ATP synthesis is the earliest biochemical event in ischemia.
Without oxygen, oxidative phosphorylation fails immediately, leading to sodium-
potassium pump failure, cellular swelling, and eventually irreversible membrane
damage . 4
4. A patient sustains a crushing injury to the thigh and twelve hours later the
muscle tissue shows preserved tissue architecture with denatured proteins.
Which type of necrosis is present?
A. Liquefactive necrosis
B. Caseous necrosis
C. Fat necrosis
D. Coagulative necrosis
