UNMC PATHOLOGY FINAL EXAM — 200
MCQs | QUESTIONS , ANSWERS &
RATIONALES
This exam covers the full scope of General and Systemic Pathology as examined at the
University of Nebraska Medical Center (UNMC) Final level, including:
General Pathology: Cell injury, death & adaptation; inflammation (acute & chronic);
tissue repair & wound healing; hemodynamic disorders (edema, thrombosis, embolism,
infarction, shock); neoplasia (nomenclature, carcinogenesis, tumor biology, metastasis);
genetic & pediatric diseases; immunopathology (hypersensitivity, autoimmunity,
immunodeficiency, transplant rejection); infectious diseases; environmental & nutritional
pathology
Systemic Pathology: Cardiovascular (IHD, cardiomyopathies, valvular disease, vascular
pathology); Respiratory (obstructive & restrictive lung disease, pneumonias, lung
tumors); GI (esophagus, stomach, intestines, IBD, tumors); Liver, biliary & pancreas;
Kidney & urinary tract; Female & male reproductive pathology; Breast pathology;
Endocrine pathology; Hematopathology (anemias, leukemias, lymphomas, bleeding
disorders); Musculoskeletal & soft tissue; CNS pathology; Skin pathology
200 MCQ QUESTIONS
SECTION 1: CELL INJURY, DEATH & ADAPTATION
1. A 55-year-old man with chronic alcoholism undergoes liver biopsy. Histology shows enlarged
hepatocytes with cytoplasmic vacuoles that displace the nucleus to the periphery. This change is
BEST described as:
A. Hydropic degeneration B. Fatty change (steatosis) C. Ballooning degeneration D. Glycogen
accumulation E. Amyloid deposition
(Correct Answer: B) Rationale: Fatty change (steatosis) is characterized by intracytoplasmic
accumulation of triglycerides appearing as clear vacuoles that push the nucleus to the cell
periphery. It is the most common hepatic response to alcohol. Hydropic change causes water
accumulation without nuclear displacement. Glycogen does not displace the nucleus in this
fashion.
,2. A 70-year-old woman with long-standing iron deficiency anemia has her peripheral smear
reviewed. The pathologist notes hypochromic, microcytic RBCs. Which adaptive cellular
response is MOST responsible for the marrow's attempt to compensate?
A. Hyperplasia B. Hypertrophy C. Metaplasia D. Dysplasia E. Atrophy
(Correct Answer: A) Rationale: Hyperplasia is an increase in cell number due to increased
proliferation of capable cells. The erythroid marrow undergoes hyperplasia to produce more
RBCs in response to anemia. Hypertrophy involves increase in cell size, not number; metaplasia
is a change in cell type; dysplasia represents disordered growth.
3. A renal tubular cell deprived of oxygen for 30 minutes is reperfused. Massive cell death
ensues — worse than during ischemia alone. The PRIMARY mediator of this reperfusion injury
is:
A. Complement activation B. Reactive oxygen species (ROS) C. Calcium influx D. Neutrophil
degranulation E. Mitochondrial permeability transition (MPT)
(Correct Answer: B) Rationale: Reperfusion injury is predominantly mediated by reactive
oxygen species generated upon reintroduction of oxygen to ischemic tissue. Xanthine oxidase
activity surges, generating superoxide. Calcium influx and MPT contribute, but ROS is the
primary driver. Neutrophils amplify injury but are not the primary initiator.
4. Electron microscopy of an ischemic cardiomyocyte shows flocculent densities in mitochondria
and membrane defects. These findings indicate:
A. Reversible cell injury B. Apoptosis C. Irreversible cell injury (necrosis) D. Fatty change E.
Hydropic degeneration
(Correct Answer: C) Rationale: Flocculent (amorphous) densities within mitochondria and
plasma membrane defects are ultrastructural hallmarks of irreversible cell injury. Reversible
injury shows only mitochondrial swelling without densities. Apoptosis shows chromatin
condensation and cell shrinkage without membrane breakdown early on.
5. A 6-year-old child has a mutation in FADD (Fas-associated death domain). Which process is
most likely impaired?
A. Necroptosis B. Extrinsic apoptosis C. Intrinsic apoptosis D. Pyroptosis E. Autophagy
,(Correct Answer: B) Rationale: FADD is an adapter protein critical to the extrinsic (death
receptor) apoptosis pathway. Upon Fas-FasL binding, FADD recruits procaspase-8 to form the
DISC (death-inducing signaling complex). Intrinsic apoptosis uses BAX/BCL-2/cytochrome c.
Necroptosis uses RIPK3/MLKL.
6. A biopsy shows dead cells with a preserved tissue outline, loss of nuclei, and intensely
eosinophilic cytoplasm. The underlying mechanism involves:
A. Enzymatic liquefaction by neutrophils B. Protein denaturation with preservation of cell
architecture C. Caseous transformation D. Fat saponification E. Gangrene with superimposed
infection
(Correct Answer: B) Rationale: This describes coagulative necrosis — the most common type.
Protein denaturation preserves the cell ghost/outline while enzymatic activity is halted. It is
typical of ischemic infarcts in solid organs (heart, kidney, spleen). Liquefactive necrosis (brain,
abscess) results from enzymatic digestion.
7. A 45-year-old with a pancreatic abscess has areas of necrosis appearing chalky-white and
soap-like. This represents:
A. Coagulative necrosis B. Caseous necrosis C. Fat necrosis D. Fibrinoid necrosis E. Gangrenous
necrosis
(Correct Answer: C) Rationale: Fat necrosis occurs when pancreatic lipases released during
pancreatitis digest peripancreatic fat. Free fatty acids combine with calcium to form calcium
soaps (saponification), appearing chalky-white grossly. Caseous necrosis is seen in TB with a
cheese-like gross appearance.
8. Which of the following best describes the mechanism by which BCL-2 overexpression
promotes tumor survival?
A. Activation of caspase-9 B. Inhibition of the mitochondrial permeability transition C.
Promotion of cytochrome c release D. Activation of BAX oligomerization E. Upregulation of
p53
(Correct Answer: B) Rationale: BCL-2 is an anti-apoptotic protein that prevents BAX/BAK
from forming pores in the outer mitochondrial membrane, thereby blocking cytochrome c release
and subsequent caspase-9 activation. Its overexpression (e.g., follicular lymphoma t[14;18])
blocks intrinsic apoptosis, promoting cell survival.
, SECTION 2: INFLAMMATION & REPAIR
9. A 25-year-old sustains a splinter wound. Within minutes, the area becomes red and warm. The
FIRST vascular event in acute inflammation is:
A. Increased vascular permeability B. Arteriolar vasodilation C. Transient vasoconstriction D.
Emigration of neutrophils E. Platelet aggregation
(Correct Answer: C) Rationale: The immediate vascular response to injury is a brief transient
vasoconstriction (seconds), followed by arteriolar vasodilation leading to increased blood flow
(causing redness/warmth). Increased permeability follows, causing edema (swelling). Leukocyte
emigration occurs later.
10. A biopsy from an area of chronic inflammation shows epithelioid macrophages, Langhans
giant cells, and central caseous necrosis. This pattern is called:
A. Suppurative inflammation B. Fibrinous inflammation C. Granulomatous inflammation D.
Serous inflammation E. Pseudomembranous inflammation
(Correct Answer: C) Rationale: Granulomatous inflammation is a specific form of chronic
inflammation characterized by collections of activated macrophages (epithelioid cells) often
surrounded by lymphocytes, with or without giant cells. Caseous necrosis is hallmark of
Mycobacterium tuberculosis granulomas. Suppurative inflammation involves neutrophilic
infiltration with pus.
11. Which complement component is MOST responsible for mast cell degranulation and
increased vascular permeability during anaphylaxis?
A. C3b B. C5a C. C3a and C5a (anaphylatoxins) D. C1q E. MAC (C5b-9)
(Correct Answer: C) Rationale: C3a and C5a are anaphylatoxins that bind mast cell receptors,
triggering degranulation and histamine release, causing increased vascular permeability and
smooth muscle contraction. C5a is more potent and also a powerful neutrophil chemoattractant.
C3b is an opsonin. MAC causes direct cell lysis.
12. A 30-year-old receives a deep laceration. Wound healing begins. On day 3, the wound is
primarily populated by which cell type?
MCQs | QUESTIONS , ANSWERS &
RATIONALES
This exam covers the full scope of General and Systemic Pathology as examined at the
University of Nebraska Medical Center (UNMC) Final level, including:
General Pathology: Cell injury, death & adaptation; inflammation (acute & chronic);
tissue repair & wound healing; hemodynamic disorders (edema, thrombosis, embolism,
infarction, shock); neoplasia (nomenclature, carcinogenesis, tumor biology, metastasis);
genetic & pediatric diseases; immunopathology (hypersensitivity, autoimmunity,
immunodeficiency, transplant rejection); infectious diseases; environmental & nutritional
pathology
Systemic Pathology: Cardiovascular (IHD, cardiomyopathies, valvular disease, vascular
pathology); Respiratory (obstructive & restrictive lung disease, pneumonias, lung
tumors); GI (esophagus, stomach, intestines, IBD, tumors); Liver, biliary & pancreas;
Kidney & urinary tract; Female & male reproductive pathology; Breast pathology;
Endocrine pathology; Hematopathology (anemias, leukemias, lymphomas, bleeding
disorders); Musculoskeletal & soft tissue; CNS pathology; Skin pathology
200 MCQ QUESTIONS
SECTION 1: CELL INJURY, DEATH & ADAPTATION
1. A 55-year-old man with chronic alcoholism undergoes liver biopsy. Histology shows enlarged
hepatocytes with cytoplasmic vacuoles that displace the nucleus to the periphery. This change is
BEST described as:
A. Hydropic degeneration B. Fatty change (steatosis) C. Ballooning degeneration D. Glycogen
accumulation E. Amyloid deposition
(Correct Answer: B) Rationale: Fatty change (steatosis) is characterized by intracytoplasmic
accumulation of triglycerides appearing as clear vacuoles that push the nucleus to the cell
periphery. It is the most common hepatic response to alcohol. Hydropic change causes water
accumulation without nuclear displacement. Glycogen does not displace the nucleus in this
fashion.
,2. A 70-year-old woman with long-standing iron deficiency anemia has her peripheral smear
reviewed. The pathologist notes hypochromic, microcytic RBCs. Which adaptive cellular
response is MOST responsible for the marrow's attempt to compensate?
A. Hyperplasia B. Hypertrophy C. Metaplasia D. Dysplasia E. Atrophy
(Correct Answer: A) Rationale: Hyperplasia is an increase in cell number due to increased
proliferation of capable cells. The erythroid marrow undergoes hyperplasia to produce more
RBCs in response to anemia. Hypertrophy involves increase in cell size, not number; metaplasia
is a change in cell type; dysplasia represents disordered growth.
3. A renal tubular cell deprived of oxygen for 30 minutes is reperfused. Massive cell death
ensues — worse than during ischemia alone. The PRIMARY mediator of this reperfusion injury
is:
A. Complement activation B. Reactive oxygen species (ROS) C. Calcium influx D. Neutrophil
degranulation E. Mitochondrial permeability transition (MPT)
(Correct Answer: B) Rationale: Reperfusion injury is predominantly mediated by reactive
oxygen species generated upon reintroduction of oxygen to ischemic tissue. Xanthine oxidase
activity surges, generating superoxide. Calcium influx and MPT contribute, but ROS is the
primary driver. Neutrophils amplify injury but are not the primary initiator.
4. Electron microscopy of an ischemic cardiomyocyte shows flocculent densities in mitochondria
and membrane defects. These findings indicate:
A. Reversible cell injury B. Apoptosis C. Irreversible cell injury (necrosis) D. Fatty change E.
Hydropic degeneration
(Correct Answer: C) Rationale: Flocculent (amorphous) densities within mitochondria and
plasma membrane defects are ultrastructural hallmarks of irreversible cell injury. Reversible
injury shows only mitochondrial swelling without densities. Apoptosis shows chromatin
condensation and cell shrinkage without membrane breakdown early on.
5. A 6-year-old child has a mutation in FADD (Fas-associated death domain). Which process is
most likely impaired?
A. Necroptosis B. Extrinsic apoptosis C. Intrinsic apoptosis D. Pyroptosis E. Autophagy
,(Correct Answer: B) Rationale: FADD is an adapter protein critical to the extrinsic (death
receptor) apoptosis pathway. Upon Fas-FasL binding, FADD recruits procaspase-8 to form the
DISC (death-inducing signaling complex). Intrinsic apoptosis uses BAX/BCL-2/cytochrome c.
Necroptosis uses RIPK3/MLKL.
6. A biopsy shows dead cells with a preserved tissue outline, loss of nuclei, and intensely
eosinophilic cytoplasm. The underlying mechanism involves:
A. Enzymatic liquefaction by neutrophils B. Protein denaturation with preservation of cell
architecture C. Caseous transformation D. Fat saponification E. Gangrene with superimposed
infection
(Correct Answer: B) Rationale: This describes coagulative necrosis — the most common type.
Protein denaturation preserves the cell ghost/outline while enzymatic activity is halted. It is
typical of ischemic infarcts in solid organs (heart, kidney, spleen). Liquefactive necrosis (brain,
abscess) results from enzymatic digestion.
7. A 45-year-old with a pancreatic abscess has areas of necrosis appearing chalky-white and
soap-like. This represents:
A. Coagulative necrosis B. Caseous necrosis C. Fat necrosis D. Fibrinoid necrosis E. Gangrenous
necrosis
(Correct Answer: C) Rationale: Fat necrosis occurs when pancreatic lipases released during
pancreatitis digest peripancreatic fat. Free fatty acids combine with calcium to form calcium
soaps (saponification), appearing chalky-white grossly. Caseous necrosis is seen in TB with a
cheese-like gross appearance.
8. Which of the following best describes the mechanism by which BCL-2 overexpression
promotes tumor survival?
A. Activation of caspase-9 B. Inhibition of the mitochondrial permeability transition C.
Promotion of cytochrome c release D. Activation of BAX oligomerization E. Upregulation of
p53
(Correct Answer: B) Rationale: BCL-2 is an anti-apoptotic protein that prevents BAX/BAK
from forming pores in the outer mitochondrial membrane, thereby blocking cytochrome c release
and subsequent caspase-9 activation. Its overexpression (e.g., follicular lymphoma t[14;18])
blocks intrinsic apoptosis, promoting cell survival.
, SECTION 2: INFLAMMATION & REPAIR
9. A 25-year-old sustains a splinter wound. Within minutes, the area becomes red and warm. The
FIRST vascular event in acute inflammation is:
A. Increased vascular permeability B. Arteriolar vasodilation C. Transient vasoconstriction D.
Emigration of neutrophils E. Platelet aggregation
(Correct Answer: C) Rationale: The immediate vascular response to injury is a brief transient
vasoconstriction (seconds), followed by arteriolar vasodilation leading to increased blood flow
(causing redness/warmth). Increased permeability follows, causing edema (swelling). Leukocyte
emigration occurs later.
10. A biopsy from an area of chronic inflammation shows epithelioid macrophages, Langhans
giant cells, and central caseous necrosis. This pattern is called:
A. Suppurative inflammation B. Fibrinous inflammation C. Granulomatous inflammation D.
Serous inflammation E. Pseudomembranous inflammation
(Correct Answer: C) Rationale: Granulomatous inflammation is a specific form of chronic
inflammation characterized by collections of activated macrophages (epithelioid cells) often
surrounded by lymphocytes, with or without giant cells. Caseous necrosis is hallmark of
Mycobacterium tuberculosis granulomas. Suppurative inflammation involves neutrophilic
infiltration with pus.
11. Which complement component is MOST responsible for mast cell degranulation and
increased vascular permeability during anaphylaxis?
A. C3b B. C5a C. C3a and C5a (anaphylatoxins) D. C1q E. MAC (C5b-9)
(Correct Answer: C) Rationale: C3a and C5a are anaphylatoxins that bind mast cell receptors,
triggering degranulation and histamine release, causing increased vascular permeability and
smooth muscle contraction. C5a is more potent and also a powerful neutrophil chemoattractant.
C3b is an opsonin. MAC causes direct cell lysis.
12. A 30-year-old receives a deep laceration. Wound healing begins. On day 3, the wound is
primarily populated by which cell type?
