NBME PATHOLOGY EXAM NEWEST 2024 WITH COMPLETE
QUESTIONS AND CORRECT VERIFIED ANSWERS (DETAILED
ANSWERS) ALREADY GRADED A+ 100% GUARANTEED TO
PASS CONCEPTS!!!
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.
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occurs when a regulating factor is withdrawn from a proliferating cell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.
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 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.
Gangrenous necrosis: - ANSWER-Dry (ischemic coagulative) and wet (infection).
Common in limbs and GI tract.
Reversible cell injury with O2: - ANSWER-low ATP synthesis, cellular swelling
because with no ATP there's impaired Na/K pump. Nuclear chromatin
clumping. Low glycogen. Fatty change. Ribosomal detachment (low protein
synthesis).
Irreversible cell injury: - ANSWER-nuclear pyknosis, karyolysis and karyorrhexis.
Ca2+ influx--> caspase activation. PM damage. lysosomal rupture.
mitochondrial permeability.
Areas of the brain susceptible to ischemia: - ANSWER-ACA / MCA / PCA
boundary areas. The watershed areas, or border zones, receive dual blood
supply from most distal branches of two arteries. However, systemic
QUESTIONS AND CORRECT VERIFIED ANSWERS (DETAILED
ANSWERS) ALREADY GRADED A+ 100% GUARANTEED TO
PASS CONCEPTS!!!
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.
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.
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 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.
Gangrenous necrosis: - ANSWER-Dry (ischemic coagulative) and wet (infection).
Common in limbs and GI tract.
Reversible cell injury with O2: - ANSWER-low ATP synthesis, cellular swelling
because with no ATP there's impaired Na/K pump. Nuclear chromatin
clumping. Low glycogen. Fatty change. Ribosomal detachment (low protein
synthesis).
Irreversible cell injury: - ANSWER-nuclear pyknosis, karyolysis and karyorrhexis.
Ca2+ influx--> caspase activation. PM damage. lysosomal rupture.
mitochondrial permeability.
Areas of the brain susceptible to ischemia: - ANSWER-ACA / MCA / PCA
boundary areas. The watershed areas, or border zones, receive dual blood
supply from most distal branches of two arteries. However, systemic
