NBME CBSE EXAM ACTUAL EXAM COMPLETE TEST
BANK QUESTIONS WITH DETAILED VERIFIED ANSWERS
(100% CORRECT ANSWERS) /ALREADY GRADED A+
A cellular adaptation characterized by increased gene activation leading to increased
numbers of structural proteins and organelles. - ANSWER: Hypertrophy
A cellular adaptation characterized by proliferation of stem cells leading to an
increased total number of cells. - ANSWER: Hyperplasia
A cellular adaptation characterized by a decrease in tissue mass due to decrease size
and/or number of cells. - ANSWER: Atrophy
Describe the cellular process of muscle atrophy? - ANSWER: Initially due to
decreased protein synthesis and loss of fibrills/cell mass.
Later stages there is apoptosis
A cellular adaptation characterized by replacement of one cell type with another in
response to stress. Reversible if stressor is removed. - ANSWER: Metaplasia
A cellular adaptation characterized by disordered cell growth with high malignant
potential. Reversible if stressor is removed. - ANSWER: Dysplasia
What are the hallmarks of reversible cell injury? - ANSWER: Na/K ATPase dysfunction
Membrane Blebbing
Chromatin Clumping
Decreased Protein synthesis (ribosome detachment)
What are the hallmarks of irreversible cell injury? - ANSWER: Membrane
Damage/Rupture
Rupture of Lysosomes
Leak of cytosolic enzymes into serum
Mitochondrial permeability (cytochrome C release and apoptosis)
Pyknosis-> Karyorrhexis -> Karyolysis
What is pyknosis? - ANSWER: Nucleus turns into blobs
"pick blobs"
What is karyorrhexis? - ANSWER: nuclear fragmentation
,What is Karyolysis? - ANSWER: dissolution of nucleus (sign of necrosis)
What is necrosis? - ANSWER: Disorganized cell death
This type of necrosis features cell shape and organ structure preservation due to
coagulation of proteins - ANSWER: Coagulative necrosis
Where is coagulative necrosis seen? - ANSWER: Wedge shaped infarcts of solid
organs
NOT the Brain or Pancreas
This type of necrosis features enzymatic lysis of cells and proteins due to release of
neutrophil enzymes - ANSWER: Liquefactive
When is liquefactive necrosis seen? - ANSWER: Brain infarcts
Abscesses
Pancreatitis
This type of necrosis is characterized by a coagulative necrosis that resembles tissue
mummification (dry form), commonly involving the lower extremities and GI tract.
Superimposed Liquefactive necrosis leads to the "wet" form. - ANSWER: Gangrenous
This type of necrosis is a combination of coagulative and liquefactive necrosis that
results in a "cottage cheese" like appearance of the affected tissue. - ANSWER:
Caseous Necrosis
When is Caseous Necrosis seen? - ANSWER: Most characteristic of granulomatous
inflammation in the lungs due to TB or fungal infection
This form of necrosis leads to the chalky white appearance of adipose tissue due to
the deposition of calcium in saponified fat. - ANSWER: Fat necrosis
When is fat necrosis seen? - ANSWER: Trauma to the breast and Acute Pancreatitis
This form of necrosis is characterized by leakage of protein into blood vessel walls. -
ANSWER: Fibrinoid
When is fibrinoid necrosis seen? - ANSWER: 1. Malignant HTN
2. Vasculitis
What type of hypersensitivity reaction is Fibrinoid necrosis? - ANSWER: Type III
,What is Apoptosis? - ANSWER: Energy (ATP) dependent cell death. The dying cell
shrinks and nucleus condenses / fragments in an organized manner.
(eosinophilic cytoplasm and basophilic nucleus)
Describe the intrinsic pathway of activation (Caspase-Apoptosis) - ANSWER: Occurs
in response to cellular injury that inactivates BCL2.
This allows Cytochrome C to leak out of the mitochondria and activate caspases to
chop up the cell
Describe the extrinsic pathway of activation (Caspase-Apoptosis) - ANSWER: FAS
ligand binds FAS death receptor on target cell leading to activation of caspases 8 &
10.
TNF/TNFR can also activate it.
Describe T-Cell mediated Caspase Apoptosis - ANSWER: CD8+ (cytotoxic) T-Cells
create pores in membranes via perforin secretion.
T-Cell granzymes enter cytoplasm and activate caspases.
This is how virally infected cells are killed.
What is the major cellular receptor disturbed by ischemia (mediating cell Damage) -
ANSWER: Na/K ATPase
Leads to high intracellular calcium
Which cells of the brain are most sensitive to ischemia? - ANSWER: Perkinje cells of
the cerebellum and pyramidal cells of the hippocampus/neocortex
What tissue of the heart is most susceptible to ischemia? - ANSWER:
Subendocardium
What zone of the liver is most susceptible to ischemia? - ANSWER: Zone 3
(surrounding the central venule)
What area of the GI tract is most susceptible to ischemia? - ANSWER: Splenic
Flexure/Rectum
A chemical species with an unpaired electron in outer orbit, which is capable of
scavenging electrons from cells and damaging them. - ANSWER: Free Radicals (ROS)
How do free radicals cause damage? - ANSWER: 1) Lipid membrane Peroxidation
2) protein modification
3) DNA Breakage
, Describe reperfusion injury - ANSWER: Blood returning to hypoxic organ leads to the
generation of ROS which further damage tissue.
Explains continual rise in cardiac troponins even after reperfusion of ischemic heart.
What is amyloid? - ANSWER: Misfolded protein that deposits in extracellular space
causing damage.
Beta pleated sheet with apple-green birefringence and congo red staining.
What is primary amyloidosis? - ANSWER: Systemic deposition of AL amyloid, derived
from misfolded immunoglobulin light chain
Associated with Multiple Myeloma
What is secondary amyloidosis? - ANSWER: Systemic deposition of AA protein,
derived from misfolded Serum Amyloid Associated Protein
Associated with Familial Mediterranian Fever syndrome (High SAA leads to increased
deposition)
What are the classic findings of Amyloidosis? - ANSWER: Nephrotic Syndrome
Cardiomyopathy
Tongue Enlargement
Describe Senile Cardiac Amyloidosis - ANSWER: Non-mutated serum transerythretin
deposits in heart. Usually asymptomatic, present in 25% over age 80.
Describe familial amyloid cardiomyopathy - ANSWER: deposition of MUTATED serum
transerythretin in cardaic tissue leading to restrictive cardiomyopathy
5% of African Americans
Describe the cells seen in acute inflammation - ANSWER: Neutrophils are first seen,
peak at 24 hr.
Macrophages peak at 2-3 days
What are the cardinal signs of inflammation? - ANSWER: Redness, swelling, heat,
pain, loss of function
What is the major inflammatory mediator(s) responsible for redness seen in
inflammation (due to inducing vasodilation and extravasation of cells/fluids. -
ANSWER: Histamine, Prostaglandins, Bradykinin
BANK QUESTIONS WITH DETAILED VERIFIED ANSWERS
(100% CORRECT ANSWERS) /ALREADY GRADED A+
A cellular adaptation characterized by increased gene activation leading to increased
numbers of structural proteins and organelles. - ANSWER: Hypertrophy
A cellular adaptation characterized by proliferation of stem cells leading to an
increased total number of cells. - ANSWER: Hyperplasia
A cellular adaptation characterized by a decrease in tissue mass due to decrease size
and/or number of cells. - ANSWER: Atrophy
Describe the cellular process of muscle atrophy? - ANSWER: Initially due to
decreased protein synthesis and loss of fibrills/cell mass.
Later stages there is apoptosis
A cellular adaptation characterized by replacement of one cell type with another in
response to stress. Reversible if stressor is removed. - ANSWER: Metaplasia
A cellular adaptation characterized by disordered cell growth with high malignant
potential. Reversible if stressor is removed. - ANSWER: Dysplasia
What are the hallmarks of reversible cell injury? - ANSWER: Na/K ATPase dysfunction
Membrane Blebbing
Chromatin Clumping
Decreased Protein synthesis (ribosome detachment)
What are the hallmarks of irreversible cell injury? - ANSWER: Membrane
Damage/Rupture
Rupture of Lysosomes
Leak of cytosolic enzymes into serum
Mitochondrial permeability (cytochrome C release and apoptosis)
Pyknosis-> Karyorrhexis -> Karyolysis
What is pyknosis? - ANSWER: Nucleus turns into blobs
"pick blobs"
What is karyorrhexis? - ANSWER: nuclear fragmentation
,What is Karyolysis? - ANSWER: dissolution of nucleus (sign of necrosis)
What is necrosis? - ANSWER: Disorganized cell death
This type of necrosis features cell shape and organ structure preservation due to
coagulation of proteins - ANSWER: Coagulative necrosis
Where is coagulative necrosis seen? - ANSWER: Wedge shaped infarcts of solid
organs
NOT the Brain or Pancreas
This type of necrosis features enzymatic lysis of cells and proteins due to release of
neutrophil enzymes - ANSWER: Liquefactive
When is liquefactive necrosis seen? - ANSWER: Brain infarcts
Abscesses
Pancreatitis
This type of necrosis is characterized by a coagulative necrosis that resembles tissue
mummification (dry form), commonly involving the lower extremities and GI tract.
Superimposed Liquefactive necrosis leads to the "wet" form. - ANSWER: Gangrenous
This type of necrosis is a combination of coagulative and liquefactive necrosis that
results in a "cottage cheese" like appearance of the affected tissue. - ANSWER:
Caseous Necrosis
When is Caseous Necrosis seen? - ANSWER: Most characteristic of granulomatous
inflammation in the lungs due to TB or fungal infection
This form of necrosis leads to the chalky white appearance of adipose tissue due to
the deposition of calcium in saponified fat. - ANSWER: Fat necrosis
When is fat necrosis seen? - ANSWER: Trauma to the breast and Acute Pancreatitis
This form of necrosis is characterized by leakage of protein into blood vessel walls. -
ANSWER: Fibrinoid
When is fibrinoid necrosis seen? - ANSWER: 1. Malignant HTN
2. Vasculitis
What type of hypersensitivity reaction is Fibrinoid necrosis? - ANSWER: Type III
,What is Apoptosis? - ANSWER: Energy (ATP) dependent cell death. The dying cell
shrinks and nucleus condenses / fragments in an organized manner.
(eosinophilic cytoplasm and basophilic nucleus)
Describe the intrinsic pathway of activation (Caspase-Apoptosis) - ANSWER: Occurs
in response to cellular injury that inactivates BCL2.
This allows Cytochrome C to leak out of the mitochondria and activate caspases to
chop up the cell
Describe the extrinsic pathway of activation (Caspase-Apoptosis) - ANSWER: FAS
ligand binds FAS death receptor on target cell leading to activation of caspases 8 &
10.
TNF/TNFR can also activate it.
Describe T-Cell mediated Caspase Apoptosis - ANSWER: CD8+ (cytotoxic) T-Cells
create pores in membranes via perforin secretion.
T-Cell granzymes enter cytoplasm and activate caspases.
This is how virally infected cells are killed.
What is the major cellular receptor disturbed by ischemia (mediating cell Damage) -
ANSWER: Na/K ATPase
Leads to high intracellular calcium
Which cells of the brain are most sensitive to ischemia? - ANSWER: Perkinje cells of
the cerebellum and pyramidal cells of the hippocampus/neocortex
What tissue of the heart is most susceptible to ischemia? - ANSWER:
Subendocardium
What zone of the liver is most susceptible to ischemia? - ANSWER: Zone 3
(surrounding the central venule)
What area of the GI tract is most susceptible to ischemia? - ANSWER: Splenic
Flexure/Rectum
A chemical species with an unpaired electron in outer orbit, which is capable of
scavenging electrons from cells and damaging them. - ANSWER: Free Radicals (ROS)
How do free radicals cause damage? - ANSWER: 1) Lipid membrane Peroxidation
2) protein modification
3) DNA Breakage
, Describe reperfusion injury - ANSWER: Blood returning to hypoxic organ leads to the
generation of ROS which further damage tissue.
Explains continual rise in cardiac troponins even after reperfusion of ischemic heart.
What is amyloid? - ANSWER: Misfolded protein that deposits in extracellular space
causing damage.
Beta pleated sheet with apple-green birefringence and congo red staining.
What is primary amyloidosis? - ANSWER: Systemic deposition of AL amyloid, derived
from misfolded immunoglobulin light chain
Associated with Multiple Myeloma
What is secondary amyloidosis? - ANSWER: Systemic deposition of AA protein,
derived from misfolded Serum Amyloid Associated Protein
Associated with Familial Mediterranian Fever syndrome (High SAA leads to increased
deposition)
What are the classic findings of Amyloidosis? - ANSWER: Nephrotic Syndrome
Cardiomyopathy
Tongue Enlargement
Describe Senile Cardiac Amyloidosis - ANSWER: Non-mutated serum transerythretin
deposits in heart. Usually asymptomatic, present in 25% over age 80.
Describe familial amyloid cardiomyopathy - ANSWER: deposition of MUTATED serum
transerythretin in cardaic tissue leading to restrictive cardiomyopathy
5% of African Americans
Describe the cells seen in acute inflammation - ANSWER: Neutrophils are first seen,
peak at 24 hr.
Macrophages peak at 2-3 days
What are the cardinal signs of inflammation? - ANSWER: Redness, swelling, heat,
pain, loss of function
What is the major inflammatory mediator(s) responsible for redness seen in
inflammation (due to inducing vasodilation and extravasation of cells/fluids. -
ANSWER: Histamine, Prostaglandins, Bradykinin
