NBME PATHOLOGY FINAL TEST BANK EXAM
NEWEST 2024 ACTUAL EXAM COMPLETE 300
QUESTIONS AND CORRECT DETAILED
ANSWERS
Leave the first rating
Terms in this set (223)
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
Apoptosis:
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.
Causes apoptosis of cancer cells because it causes
formation of free radicals which lead to dsDNA
Radiation therapy does
breakage. rapidly dividing cells like skin and GI
what?
mucosa are highly susceptible to radiation-induced
apoptosis.
, It's involved in tissue remodeling in embryogenesis.
Often occurs when a regulating factor is withdrawn
from a proliferating cell population. For example,
Intrinsic pathway of low IL-2 after completion of an immunological
apoptosis: what is its reaction causes apoptosis of proliferating effector
general purpose / when cells. Also occurs in response to injury from
does it occur? 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 BAX and BAK are pro. Bcl-2 is anti-apoptotic.
of these are pro- and
which are anti-apoptotic?
How does Bcl-2 It prevents cyt c release by binding to an inhibiting
function? Apaf-1, which normally INDUCES caspases.
This occurs in follicular lymphoma. Apaf-1 is over-
What happens if Bcl-2 is
inhibited which leads to tumorigenesis because of
overexpressed?
lowered caspase activation.
Extrinsic pathway of 1. Ligand receptor interactions. FasL binding to Fas
apoptosis: 2 basic (CD95). 2. Immune cell-->cytotoxic T-cell release of
pathways? perforin and granzyme B.
In thymic medullary negative selection. Mutations in
Fas increases the numbers of circulating self-
Where is Fas-FasL
reactive lymphocytes due to failure of clonal
interaction required?
deletion. *Defective fas-fasL interactions is the
basis of autoimmune disorders*
After it crosslinks with FasL, multiple Fas molecules
How does Fas initiate cell
coalesce. This makes a binding site for a death
death?
domain.
Exogenous injury causes enzymatic degradation
and protein denaturation of a cell. IC components
Necrosis:
extravasate. *There's an inflammatory process
unlike apoptosis*
, Caused by ischemia or infarction typically. heart,
liver, kidney. Occurs in tissues supplied by end
Coagulative necrosis
arteries. High cytoplasmic binding of acidophilic
occurs in the:
dye. Proteins denature first followed by enzymatic
degradation.
brain, bacterial abscess and pleural effusion. Occurs
Liquefactive necrosis in CNS because of high fat content there. Unlike
occurs in the: coag necrosis, enzymatic degradation due to
release of lysosomal enzymes occurs first.
TB, systemic fungi, Nocardia. Tissue maintains a
Caseous necrosis: cheese-like appearance. Tissue is a proteinaceous
dead cell mass.
Enzymatic--Pancreas. Saponification. Released fatty
acids interact with calcium to form soaps. Calc
Fatty necrosis:
deposits appear dark on staining. Nonenzymatic--
breast trauma.
Occurs in blood vessels. Henoch-Schonlein
purpura, Churg-Strauss syndrome. Malignant
Fibroid necrosis:
hypertension. Accumulation of amorphous, basic
proteinaceous substances resembling fibrin.
Dry (ischemic coagulative) and wet (infection).
Gangrenous necrosis:
Common in limbs and GI tract.
low ATP synthesis, cellular swelling because with no
Reversible cell injury with ATP there's impaired Na/K pump. Nuclear chromatin
O2: clumping. Low glycogen. Fatty change. Ribosomal
detachment (low protein synthesis).
nuclear pyknosis, karyolysis and karyorrhexis. Ca2+
Irreversible cell injury: influx--> caspase activation. PM damage. lysosomal
rupture. mitochondrial permeability.
ACA / MCA / PCA boundary areas. The watershed
areas, or border zones, receive dual blood supply
from most distal branches of two arteries. However,
Areas of the brain
systemic hypoperfusion may cause ischemia in these
susceptible to ischemia:
areas. **Hypoxic ischemic encephalopathy affects
pyramidal cells of the hippocampus and Purkinjie
cells of the cerebellum.
NEWEST 2024 ACTUAL EXAM COMPLETE 300
QUESTIONS AND CORRECT DETAILED
ANSWERS
Leave the first rating
Terms in this set (223)
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
Apoptosis:
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.
Causes apoptosis of cancer cells because it causes
formation of free radicals which lead to dsDNA
Radiation therapy does
breakage. rapidly dividing cells like skin and GI
what?
mucosa are highly susceptible to radiation-induced
apoptosis.
, It's involved in tissue remodeling in embryogenesis.
Often occurs when a regulating factor is withdrawn
from a proliferating cell population. For example,
Intrinsic pathway of low IL-2 after completion of an immunological
apoptosis: what is its reaction causes apoptosis of proliferating effector
general purpose / when cells. Also occurs in response to injury from
does it occur? 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 BAX and BAK are pro. Bcl-2 is anti-apoptotic.
of these are pro- and
which are anti-apoptotic?
How does Bcl-2 It prevents cyt c release by binding to an inhibiting
function? Apaf-1, which normally INDUCES caspases.
This occurs in follicular lymphoma. Apaf-1 is over-
What happens if Bcl-2 is
inhibited which leads to tumorigenesis because of
overexpressed?
lowered caspase activation.
Extrinsic pathway of 1. Ligand receptor interactions. FasL binding to Fas
apoptosis: 2 basic (CD95). 2. Immune cell-->cytotoxic T-cell release of
pathways? perforin and granzyme B.
In thymic medullary negative selection. Mutations in
Fas increases the numbers of circulating self-
Where is Fas-FasL
reactive lymphocytes due to failure of clonal
interaction required?
deletion. *Defective fas-fasL interactions is the
basis of autoimmune disorders*
After it crosslinks with FasL, multiple Fas molecules
How does Fas initiate cell
coalesce. This makes a binding site for a death
death?
domain.
Exogenous injury causes enzymatic degradation
and protein denaturation of a cell. IC components
Necrosis:
extravasate. *There's an inflammatory process
unlike apoptosis*
, Caused by ischemia or infarction typically. heart,
liver, kidney. Occurs in tissues supplied by end
Coagulative necrosis
arteries. High cytoplasmic binding of acidophilic
occurs in the:
dye. Proteins denature first followed by enzymatic
degradation.
brain, bacterial abscess and pleural effusion. Occurs
Liquefactive necrosis in CNS because of high fat content there. Unlike
occurs in the: coag necrosis, enzymatic degradation due to
release of lysosomal enzymes occurs first.
TB, systemic fungi, Nocardia. Tissue maintains a
Caseous necrosis: cheese-like appearance. Tissue is a proteinaceous
dead cell mass.
Enzymatic--Pancreas. Saponification. Released fatty
acids interact with calcium to form soaps. Calc
Fatty necrosis:
deposits appear dark on staining. Nonenzymatic--
breast trauma.
Occurs in blood vessels. Henoch-Schonlein
purpura, Churg-Strauss syndrome. Malignant
Fibroid necrosis:
hypertension. Accumulation of amorphous, basic
proteinaceous substances resembling fibrin.
Dry (ischemic coagulative) and wet (infection).
Gangrenous necrosis:
Common in limbs and GI tract.
low ATP synthesis, cellular swelling because with no
Reversible cell injury with ATP there's impaired Na/K pump. Nuclear chromatin
O2: clumping. Low glycogen. Fatty change. Ribosomal
detachment (low protein synthesis).
nuclear pyknosis, karyolysis and karyorrhexis. Ca2+
Irreversible cell injury: influx--> caspase activation. PM damage. lysosomal
rupture. mitochondrial permeability.
ACA / MCA / PCA boundary areas. The watershed
areas, or border zones, receive dual blood supply
from most distal branches of two arteries. However,
Areas of the brain
systemic hypoperfusion may cause ischemia in these
susceptible to ischemia:
areas. **Hypoxic ischemic encephalopathy affects
pyramidal cells of the hippocampus and Purkinjie
cells of the cerebellum.
