NBME PATHOLOGY FINAL TEST BANK EXAM, THE
NEWEST 2024 ACTUAL EXAM COMPLETES 250+
QUESTIONS AND CORRECTS DETAILED ANSWERS|
ALREADY GRADED
Apoptosis:
- Correct 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?
- Correct 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.
Intrinsic pathway of apoptosis: what is its general purpose / when does it occur?
- Correct 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occurs when a regulating factor is withdrawn from a proliferating cell population.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?
- Correct Answer- BAX and BAK are pro. Bcl-2 is anti-apoptotic.
,How does Bcl-2 function?
- Correct Answer- It prevents cyt c release by binding to an inhibiting Apaf-1,
which normally INDUCES caspases.
What happens if Bcl-2 is overexpressed?
- Correct Answer- This occurs in follicular lymphoma. Apaf-1 is over-inhibited
which leads to tumorigenesis because of lowered caspase activation.
Extrinsic pathway of apoptosis: 2 basic pathways?
- Correct 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?
- Correct 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?
- Correct Answer- After it crosslinks with FasL, multiple Fas molecules coalesce.
This makes a binding site for a death domain.
Necrosis:
- Correct 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:
, - Correct Answer- Caused by ischemia or infarction typically. heart, liver, kidney.
Occurs in tissues supplied by end arteries. High cytoplasmic binding of acidophilic
dye. Proteins denature first followed by enzymatic degradation.
Liquefactive necrosis occurs in the:
- Correct 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:
- Correct Answer- TB, systemic fungi, Nocardia. Tissue maintains a cheese-like
appearance. Tissue is a proteinaceous dead cell mass.
Fatty necrosis:
- Correct Answer- Enzymatic--Pancreas. Saponification. Released fatty acids
interact with calcium to form soaps. Calc deposits appear dark on staining.
Nonenzymatic--breast trauma.
Fibroid necrosis:
- Correct Answer- Occurs in blood vessels. Henoch-Schonlein purpura, Churg-
Strauss syndrome. Malignant hypertension. Accumulation of amorphous, basic
proteinaceous substances resembling fibrin.
Gangrenous necrosis:
- Correct Answer- Dry (ischemic coagulative) and wet (infection). Common in
limbs and GI tract.
Reversible cell injury with O2:
NEWEST 2024 ACTUAL EXAM COMPLETES 250+
QUESTIONS AND CORRECTS DETAILED ANSWERS|
ALREADY GRADED
Apoptosis:
- Correct 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?
- Correct 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.
Intrinsic pathway of apoptosis: what is its general purpose / when does it occur?
- Correct 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?
- Correct Answer- BAX and BAK are pro. Bcl-2 is anti-apoptotic.
,How does Bcl-2 function?
- Correct Answer- It prevents cyt c release by binding to an inhibiting Apaf-1,
which normally INDUCES caspases.
What happens if Bcl-2 is overexpressed?
- Correct Answer- This occurs in follicular lymphoma. Apaf-1 is over-inhibited
which leads to tumorigenesis because of lowered caspase activation.
Extrinsic pathway of apoptosis: 2 basic pathways?
- Correct 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?
- Correct 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?
- Correct Answer- After it crosslinks with FasL, multiple Fas molecules coalesce.
This makes a binding site for a death domain.
Necrosis:
- Correct 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:
, - Correct Answer- Caused by ischemia or infarction typically. heart, liver, kidney.
Occurs in tissues supplied by end arteries. High cytoplasmic binding of acidophilic
dye. Proteins denature first followed by enzymatic degradation.
Liquefactive necrosis occurs in the:
- Correct 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:
- Correct Answer- TB, systemic fungi, Nocardia. Tissue maintains a cheese-like
appearance. Tissue is a proteinaceous dead cell mass.
Fatty necrosis:
- Correct Answer- Enzymatic--Pancreas. Saponification. Released fatty acids
interact with calcium to form soaps. Calc deposits appear dark on staining.
Nonenzymatic--breast trauma.
Fibroid necrosis:
- Correct Answer- Occurs in blood vessels. Henoch-Schonlein purpura, Churg-
Strauss syndrome. Malignant hypertension. Accumulation of amorphous, basic
proteinaceous substances resembling fibrin.
Gangrenous necrosis:
- Correct Answer- Dry (ischemic coagulative) and wet (infection). Common in
limbs and GI tract.
Reversible cell injury with O2:
