UNMC PATHOLOGY FINAL EXAM
version 2 — 200 MCQs | questions , answers
& rationales
Summary of Topics Covered:
Questions 1–10: Cell injury, adaptation, death
Questions 11–20: Inflammation & repair
Questions 21–30: Immunopathology & hypersensitivity
Questions 31–40: Neoplasia
Questions 41–50: Cardiovascular pathology
Questions 51–60: Respiratory pathology
Questions 61–70: Renal pathology
Questions 71–80: GI & hepatic pathology
Questions 81–90: Hematopathology
Questions 91–100: Endocrine pathology
Questions 101–110: Neuropathology
Questions 111–120: Reproductive & breast pathology
Questions 121–130: Musculoskeletal pathology
Questions 131–135: Vascular pathology
Questions 136–200: Advanced mixed pathology
📋 EXAM COVERAGE DESCRIPTION
This exam covers the following core Pathology domains as assessed at UNMC final
examinations:
General Pathology: Cell injury, death, adaptation, inflammation (acute & chronic),
wound healing, repair & regeneration
Immunopathology: Hypersensitivity reactions, autoimmune diseases,
immunodeficiency, transplant rejection, amyloidosis
Neoplasia: Tumor biology, oncogenes, tumor suppressors, carcinogenesis, invasion &
metastasis, tumor markers
Cardiovascular Pathology: IHD, cardiomyopathies, valvular disease, vascular
pathology, hypertension
Respiratory Pathology: Pneumonias, COPD, restrictive lung disease, lung tumors,
pulmonary vascular disease
Renal Pathology: Glomerulonephritides, tubular disorders, interstitial nephritis, renal
tumors, cystic diseases
GI & Hepatic Pathology: Peptic ulcer, IBD, colorectal carcinoma, cirrhosis, hepatitis,
hepatocellular carcinoma
, Hematopathology: Anemias, leukemias, lymphomas, myeloma, coagulation disorders
Endocrine Pathology: Thyroid, adrenal, pituitary, pancreatic disorders and tumors
Neuropathology: Degenerative diseases, CNS tumors, cerebrovascular disease,
demyelinating disorders
Reproductive & Breast Pathology: Cervical, endometrial, ovarian, testicular, and breast
pathology
Musculoskeletal Pathology: Bone tumors, metabolic bone disease, arthritis, soft tissue
tumors
SECTION 1: CELL INJURY, ADAPTATION & DEATH
1. A 45-year-old man with chronic alcohol use has an enlarged liver. Biopsy shows hepatocytes
with large, clear cytoplasmic vacuoles displacing the nucleus peripherally. Which of the
following best describes this change?
A. Hydropic degeneration B. Glycogen accumulation C. Steatosis (fatty change) ✅ (correct
answer) D. Ballooning degeneration E. Amyloid deposition
Rationale: Steatosis (fatty change) results from impaired lipid metabolism, commonly due to
alcohol. Fat accumulates as triglyceride vacuoles that displace the nucleus to the periphery.
Hydropic degeneration causes water accumulation (clear cytoplasm but nucleus is central).
Glycogen also displaces the nucleus but stains with PAS.
2. A cell undergoes a series of changes including nuclear chromatin condensation, cell shrinkage,
and membrane blebbing, ultimately resulting in phagocytosis of apoptotic bodies without
inflammation. Which pathway is most likely if cytochrome c is released from mitochondria?
A. Extrinsic pathway via Fas/FasL B. Receptor-mediated necrosis C. Intrinsic (mitochondrial)
apoptotic pathway ✅ (correct answer) D. Necroptosis E. Pyroptosis
Rationale: The intrinsic pathway is triggered by intracellular stress (DNA damage, oxidative
stress). Cytochrome c release from mitochondria activates the apoptosome (Apaf-1 + caspase-9),
leading to caspase-3 activation. The extrinsic pathway uses death receptors (Fas, TNFR), not
cytochrome c.
,3. A pathologist examining a myocardial infarct 24 hours old notes preserved tissue architecture
but deeply eosinophilic cells with pyknotic nuclei and loss of cytoplasmic detail. This pattern is
most consistent with:
A. Liquefactive necrosis B. Caseous necrosis C. Fat necrosis D. Coagulative necrosis ✅
(correct answer) E. Gangrenous necrosis
Rationale: Coagulative necrosis preserves tissue architecture (ghost outlines) due to protein
denaturation. It is characteristic of ischemia in solid organs (heart, kidney, spleen). Liquefactive
necrosis destroys architecture (seen in brain infarcts and abscesses). Caseous necrosis (TB)
shows cheese-like debris with complete architecture loss.
4. A 30-year-old woman living at high altitude has increased red blood cell count. Her physician
explains this is a normal physiological adaptation. Which type of cellular adaptation is this?
A. Hypertrophy B. Hyperplasia ✅ (correct answer) C. Metaplasia D. Dysplasia E. Atrophy
Rationale: Hyperplasia is an increase in cell number in response to a stimulus (here, hypoxia
stimulating erythropoietin release). Hypertrophy is an increase in cell size. RBCs are terminally
differentiated and cannot hypertrophy, but erythroid precursors can proliferate.
5. A biopsy of the esophagus of a patient with chronic GERD shows replacement of normal
stratified squamous epithelium with columnar epithelium containing goblet cells. This is an
example of:
A. Dysplasia B. Anaplasia C. Hyperplasia D. Metaplasia ✅ (correct answer) E. Hypertrophy
Rationale: Metaplasia is the reversible replacement of one differentiated cell type with another.
In Barrett's esophagus, squamous epithelium is replaced by intestinal-type columnar epithelium
(with goblet cells) in response to chronic acid injury. This is a premalignant condition.
6. Free radical injury causes cell damage via all of the following mechanisms EXCEPT:
A. Lipid peroxidation of membranes B. Protein cross-linking and fragmentation C. DNA strand
breaks D. Activation of caspase-independent apoptosis ✅ (correct answer) E. Oxidative
modification of nucleotides
Rationale: Free radicals cause damage by lipid peroxidation, protein modification, and DNA
damage. Caspase-independent apoptosis is mediated by AIF (apoptosis-inducing factor) from
, mitochondria — while reactive oxygen species can trigger apoptosis, this is not a direct
mechanism of free radical injury per se and is the least direct of the listed options.
7. Which of the following findings is MOST characteristic of irreversible cell injury?
A. Cellular swelling B. Loss of microvilli C. Ribosomal detachment from RER D. Amorphous
densities in mitochondria ✅ (correct answer) E. Membrane blebs
Rationale: Amorphous (flocculent) densities in mitochondria represent denatured proteins and
lipids and are a hallmark of irreversible injury. All the other options (swelling, loss of microvilli,
ribosomal detachment, blebs) can occur in reversible injury.
8. A 60-year-old man with ischemic heart disease dies. Autopsy reveals pale, waxy myocytes
with absent nuclei and striations but preserved cell outlines. The most likely time since infarction
is:
A. 30 minutes B. 4–12 hours ✅ (correct answer) C. 3–5 days D. 1–2 weeks E. 1 month
Rationale: Coagulative necrosis with loss of nuclei and striations but preserved outlines begins
to appear at 4–12 hours. At 30 minutes, changes are only ultrastructural. At 3–5 days, neutrophils
and macrophages are prominent. At 1–2 weeks, granulation tissue forms.
9. Lipofuscin, the "wear and tear" pigment, is best described as:
A. An exogenous pigment deposited in macrophages B. A product of hemoglobin breakdown C.
Undigested material from oxidative damage to cellular membranes ✅ (correct answer) D. A
calcium deposit in aging cells E. A product of myelin degeneration
Rationale: Lipofuscin is a golden-brown granular pigment composed of lipid-protein complexes
formed by peroxidation of polyunsaturated lipids. It accumulates in lysosomes of aging cells
(liver, brain, heart) and is a marker of cellular aging and oxidative stress.
10. Which of the following correctly pairs the type of calcification with its pathological
mechanism?
A. Dystrophic calcification — elevated serum calcium ✅ (correct answer) B. Metastatic
calcification — occurs in dead/dying tissue C. Dystrophic calcification — occurs in dead/dying
version 2 — 200 MCQs | questions , answers
& rationales
Summary of Topics Covered:
Questions 1–10: Cell injury, adaptation, death
Questions 11–20: Inflammation & repair
Questions 21–30: Immunopathology & hypersensitivity
Questions 31–40: Neoplasia
Questions 41–50: Cardiovascular pathology
Questions 51–60: Respiratory pathology
Questions 61–70: Renal pathology
Questions 71–80: GI & hepatic pathology
Questions 81–90: Hematopathology
Questions 91–100: Endocrine pathology
Questions 101–110: Neuropathology
Questions 111–120: Reproductive & breast pathology
Questions 121–130: Musculoskeletal pathology
Questions 131–135: Vascular pathology
Questions 136–200: Advanced mixed pathology
📋 EXAM COVERAGE DESCRIPTION
This exam covers the following core Pathology domains as assessed at UNMC final
examinations:
General Pathology: Cell injury, death, adaptation, inflammation (acute & chronic),
wound healing, repair & regeneration
Immunopathology: Hypersensitivity reactions, autoimmune diseases,
immunodeficiency, transplant rejection, amyloidosis
Neoplasia: Tumor biology, oncogenes, tumor suppressors, carcinogenesis, invasion &
metastasis, tumor markers
Cardiovascular Pathology: IHD, cardiomyopathies, valvular disease, vascular
pathology, hypertension
Respiratory Pathology: Pneumonias, COPD, restrictive lung disease, lung tumors,
pulmonary vascular disease
Renal Pathology: Glomerulonephritides, tubular disorders, interstitial nephritis, renal
tumors, cystic diseases
GI & Hepatic Pathology: Peptic ulcer, IBD, colorectal carcinoma, cirrhosis, hepatitis,
hepatocellular carcinoma
, Hematopathology: Anemias, leukemias, lymphomas, myeloma, coagulation disorders
Endocrine Pathology: Thyroid, adrenal, pituitary, pancreatic disorders and tumors
Neuropathology: Degenerative diseases, CNS tumors, cerebrovascular disease,
demyelinating disorders
Reproductive & Breast Pathology: Cervical, endometrial, ovarian, testicular, and breast
pathology
Musculoskeletal Pathology: Bone tumors, metabolic bone disease, arthritis, soft tissue
tumors
SECTION 1: CELL INJURY, ADAPTATION & DEATH
1. A 45-year-old man with chronic alcohol use has an enlarged liver. Biopsy shows hepatocytes
with large, clear cytoplasmic vacuoles displacing the nucleus peripherally. Which of the
following best describes this change?
A. Hydropic degeneration B. Glycogen accumulation C. Steatosis (fatty change) ✅ (correct
answer) D. Ballooning degeneration E. Amyloid deposition
Rationale: Steatosis (fatty change) results from impaired lipid metabolism, commonly due to
alcohol. Fat accumulates as triglyceride vacuoles that displace the nucleus to the periphery.
Hydropic degeneration causes water accumulation (clear cytoplasm but nucleus is central).
Glycogen also displaces the nucleus but stains with PAS.
2. A cell undergoes a series of changes including nuclear chromatin condensation, cell shrinkage,
and membrane blebbing, ultimately resulting in phagocytosis of apoptotic bodies without
inflammation. Which pathway is most likely if cytochrome c is released from mitochondria?
A. Extrinsic pathway via Fas/FasL B. Receptor-mediated necrosis C. Intrinsic (mitochondrial)
apoptotic pathway ✅ (correct answer) D. Necroptosis E. Pyroptosis
Rationale: The intrinsic pathway is triggered by intracellular stress (DNA damage, oxidative
stress). Cytochrome c release from mitochondria activates the apoptosome (Apaf-1 + caspase-9),
leading to caspase-3 activation. The extrinsic pathway uses death receptors (Fas, TNFR), not
cytochrome c.
,3. A pathologist examining a myocardial infarct 24 hours old notes preserved tissue architecture
but deeply eosinophilic cells with pyknotic nuclei and loss of cytoplasmic detail. This pattern is
most consistent with:
A. Liquefactive necrosis B. Caseous necrosis C. Fat necrosis D. Coagulative necrosis ✅
(correct answer) E. Gangrenous necrosis
Rationale: Coagulative necrosis preserves tissue architecture (ghost outlines) due to protein
denaturation. It is characteristic of ischemia in solid organs (heart, kidney, spleen). Liquefactive
necrosis destroys architecture (seen in brain infarcts and abscesses). Caseous necrosis (TB)
shows cheese-like debris with complete architecture loss.
4. A 30-year-old woman living at high altitude has increased red blood cell count. Her physician
explains this is a normal physiological adaptation. Which type of cellular adaptation is this?
A. Hypertrophy B. Hyperplasia ✅ (correct answer) C. Metaplasia D. Dysplasia E. Atrophy
Rationale: Hyperplasia is an increase in cell number in response to a stimulus (here, hypoxia
stimulating erythropoietin release). Hypertrophy is an increase in cell size. RBCs are terminally
differentiated and cannot hypertrophy, but erythroid precursors can proliferate.
5. A biopsy of the esophagus of a patient with chronic GERD shows replacement of normal
stratified squamous epithelium with columnar epithelium containing goblet cells. This is an
example of:
A. Dysplasia B. Anaplasia C. Hyperplasia D. Metaplasia ✅ (correct answer) E. Hypertrophy
Rationale: Metaplasia is the reversible replacement of one differentiated cell type with another.
In Barrett's esophagus, squamous epithelium is replaced by intestinal-type columnar epithelium
(with goblet cells) in response to chronic acid injury. This is a premalignant condition.
6. Free radical injury causes cell damage via all of the following mechanisms EXCEPT:
A. Lipid peroxidation of membranes B. Protein cross-linking and fragmentation C. DNA strand
breaks D. Activation of caspase-independent apoptosis ✅ (correct answer) E. Oxidative
modification of nucleotides
Rationale: Free radicals cause damage by lipid peroxidation, protein modification, and DNA
damage. Caspase-independent apoptosis is mediated by AIF (apoptosis-inducing factor) from
, mitochondria — while reactive oxygen species can trigger apoptosis, this is not a direct
mechanism of free radical injury per se and is the least direct of the listed options.
7. Which of the following findings is MOST characteristic of irreversible cell injury?
A. Cellular swelling B. Loss of microvilli C. Ribosomal detachment from RER D. Amorphous
densities in mitochondria ✅ (correct answer) E. Membrane blebs
Rationale: Amorphous (flocculent) densities in mitochondria represent denatured proteins and
lipids and are a hallmark of irreversible injury. All the other options (swelling, loss of microvilli,
ribosomal detachment, blebs) can occur in reversible injury.
8. A 60-year-old man with ischemic heart disease dies. Autopsy reveals pale, waxy myocytes
with absent nuclei and striations but preserved cell outlines. The most likely time since infarction
is:
A. 30 minutes B. 4–12 hours ✅ (correct answer) C. 3–5 days D. 1–2 weeks E. 1 month
Rationale: Coagulative necrosis with loss of nuclei and striations but preserved outlines begins
to appear at 4–12 hours. At 30 minutes, changes are only ultrastructural. At 3–5 days, neutrophils
and macrophages are prominent. At 1–2 weeks, granulation tissue forms.
9. Lipofuscin, the "wear and tear" pigment, is best described as:
A. An exogenous pigment deposited in macrophages B. A product of hemoglobin breakdown C.
Undigested material from oxidative damage to cellular membranes ✅ (correct answer) D. A
calcium deposit in aging cells E. A product of myelin degeneration
Rationale: Lipofuscin is a golden-brown granular pigment composed of lipid-protein complexes
formed by peroxidation of polyunsaturated lipids. It accumulates in lysosomes of aging cells
(liver, brain, heart) and is a marker of cellular aging and oxidative stress.
10. Which of the following correctly pairs the type of calcification with its pathological
mechanism?
A. Dystrophic calcification — elevated serum calcium ✅ (correct answer) B. Metastatic
calcification — occurs in dead/dying tissue C. Dystrophic calcification — occurs in dead/dying
