1|Page
NBME PATHOLOGY FINAL TEST BANK EXAM
NEWEST 2025 REAL EXAM COMPLETE 300
QUESTIONS AND CORRECT DETAILED ANSWERS
(VERIFIED ANSWERS) |ALREADY GRADED
A+||LATEST EXAM!!!
Apoptosis: - Answer-Programmed cell death. REQUIRES
ATP. Can occur via the intrinsic or extrinsic pathways, both
of which involve activation of cytosolic caspases which
mediate cellular breakdown. ***Unlike necrosis, apoptosis
does not involve significant inflammation. Involves
eosinophilic cytoplasm, cell shrinkage, pyknosis and
basophilia, membrane blebbing and karyorrhexis, and
formation of apoptotic bodies which are phagocytosed.
**DNA laddering is a sensitive indicator of apoptosis**
Occurs because during karyorrhexis endonucleases yield
180bp fragments.
Radiation therapy does what? - Answer-Causes apoptosis
of cancer cells because it causes formation of free radicals
which lead to dsDNA breakage. rapidly dividing cells like
skin and GI mucosa are highly susceptible to radiation-
induced apoptosis.
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Intrinsic pathway of apoptosis: what is its general purpose
/ when does it occur? - Answer-It's involved in tissue
remodeling in embryogenesis. Often occurs when a
regulating factor is withdrawn from a proliferating cell
population. For example, low IL-2 after completion of an
immunological reaction causes apoptosis of proliferating
effector cells. Also occurs in response to injury from
radiation, toxins, hypoxia,etc. Changes in proportions of
pro- and anti-apoptotic factors leads to an increase in
mitochondrial permeability and cyt c release.
BAK, BAX, Bcl-2: Which of these are pro- and which are
anti-apoptotic? - Answer-BAX and BAK are pro. Bcl-2 is
anti-apoptotic.
How does Bcl-2 function? - Answer-It prevents cyt c
release by binding to an inhibiting Apaf-1, which normally
INDUCES caspases.
What happens if Bcl-2 is overexpressed? - Answer-This
occurs in follicular lymphoma. Apaf-1 is over-inhibited
which leads to tumorigenesis because of lowered caspase
activation.
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Extrinsic pathway of apoptosis: 2 basic pathways? -
Answer-1. Ligand receptor interactions. FasL binding to
Fas (CD95). 2. Immune cell-->cytotoxic T-cell release of
perforin and granzyme B.
Where is Fas-FasL interaction required? - Answer-In
thymic medullary negative selection. Mutations in Fas
increases the numbers of circulating self-reactive
lymphocytes due to failure of clonal deletion. **Defective
fas-fasL interactions is the basis of autoimmune
disorders**
How does Fas initiate cell death? - Answer-After it
crosslinks with FasL, multiple Fas molecules coalesce.
This makes a binding site for a death domain.
Necrosis: - Answer-Exogenous injury causes enzymatic
degradation and protein denaturation of a cell. IC
components extravasate. **There's an inflammatory
process unlike apoptosis**
Coagulative necrosis occurs in the: - Answer-Caused by
ischemia or infarction typically. heart, liver, kidney. Occurs
in tissues supplied by end arteries. High cytoplasmic
, 4|Page
binding of acidophilic dye. Proteins denature first followed
by enzymatic degradation.
Liquefactive necrosis occurs in the: - Answer-brain,
bacterial abscess and pleural effusion. Occurs in CNS
because of high fat content there. Unlike coag necrosis,
enzymatic degradation due to release of lysosomal
enzymes occurs first.
Caseous necrosis: - Answer-TB, systemic fungi, Nocardia.
Tissue maintains a cheese-like appearance. Tissue is a
proteinaceous dead cell mass.
Fatty necrosis: - Answer-Enzymatic--Pancreas.
Saponification. Released fatty acids interact with calcium
to form soaps. Calc deposits appear dark on staining.
Nonenzymatic--breast trauma.
Fibroid necrosis: - Answer-Occurs in blood vessels.
Henoch-Schonlein purpura, Churg-Strauss syndrome.
Malignant hypertension. Accumulation of amorphous,
basic proteinaceous substances resembling fibrin.
NBME PATHOLOGY FINAL TEST BANK EXAM
NEWEST 2025 REAL EXAM COMPLETE 300
QUESTIONS AND CORRECT DETAILED ANSWERS
(VERIFIED ANSWERS) |ALREADY GRADED
A+||LATEST EXAM!!!
Apoptosis: - Answer-Programmed cell death. REQUIRES
ATP. Can occur via the intrinsic or extrinsic pathways, both
of which involve activation of cytosolic caspases which
mediate cellular breakdown. ***Unlike necrosis, apoptosis
does not involve significant inflammation. Involves
eosinophilic cytoplasm, cell shrinkage, pyknosis and
basophilia, membrane blebbing and karyorrhexis, and
formation of apoptotic bodies which are phagocytosed.
**DNA laddering is a sensitive indicator of apoptosis**
Occurs because during karyorrhexis endonucleases yield
180bp fragments.
Radiation therapy does what? - Answer-Causes apoptosis
of cancer cells because it causes formation of free radicals
which lead to dsDNA breakage. rapidly dividing cells like
skin and GI mucosa are highly susceptible to radiation-
induced apoptosis.
,2|Page
Intrinsic pathway of apoptosis: what is its general purpose
/ when does it occur? - Answer-It's involved in tissue
remodeling in embryogenesis. Often occurs when a
regulating factor is withdrawn from a proliferating cell
population. For example, low IL-2 after completion of an
immunological reaction causes apoptosis of proliferating
effector cells. Also occurs in response to injury from
radiation, toxins, hypoxia,etc. Changes in proportions of
pro- and anti-apoptotic factors leads to an increase in
mitochondrial permeability and cyt c release.
BAK, BAX, Bcl-2: Which of these are pro- and which are
anti-apoptotic? - Answer-BAX and BAK are pro. Bcl-2 is
anti-apoptotic.
How does Bcl-2 function? - Answer-It prevents cyt c
release by binding to an inhibiting Apaf-1, which normally
INDUCES caspases.
What happens if Bcl-2 is overexpressed? - Answer-This
occurs in follicular lymphoma. Apaf-1 is over-inhibited
which leads to tumorigenesis because of lowered caspase
activation.
,3|Page
Extrinsic pathway of apoptosis: 2 basic pathways? -
Answer-1. Ligand receptor interactions. FasL binding to
Fas (CD95). 2. Immune cell-->cytotoxic T-cell release of
perforin and granzyme B.
Where is Fas-FasL interaction required? - Answer-In
thymic medullary negative selection. Mutations in Fas
increases the numbers of circulating self-reactive
lymphocytes due to failure of clonal deletion. **Defective
fas-fasL interactions is the basis of autoimmune
disorders**
How does Fas initiate cell death? - Answer-After it
crosslinks with FasL, multiple Fas molecules coalesce.
This makes a binding site for a death domain.
Necrosis: - Answer-Exogenous injury causes enzymatic
degradation and protein denaturation of a cell. IC
components extravasate. **There's an inflammatory
process unlike apoptosis**
Coagulative necrosis occurs in the: - Answer-Caused by
ischemia or infarction typically. heart, liver, kidney. Occurs
in tissues supplied by end arteries. High cytoplasmic
, 4|Page
binding of acidophilic dye. Proteins denature first followed
by enzymatic degradation.
Liquefactive necrosis occurs in the: - Answer-brain,
bacterial abscess and pleural effusion. Occurs in CNS
because of high fat content there. Unlike coag necrosis,
enzymatic degradation due to release of lysosomal
enzymes occurs first.
Caseous necrosis: - Answer-TB, systemic fungi, Nocardia.
Tissue maintains a cheese-like appearance. Tissue is a
proteinaceous dead cell mass.
Fatty necrosis: - Answer-Enzymatic--Pancreas.
Saponification. Released fatty acids interact with calcium
to form soaps. Calc deposits appear dark on staining.
Nonenzymatic--breast trauma.
Fibroid necrosis: - Answer-Occurs in blood vessels.
Henoch-Schonlein purpura, Churg-Strauss syndrome.
Malignant hypertension. Accumulation of amorphous,
basic proteinaceous substances resembling fibrin.
