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NBME PATHOLOGY FINAL EXAM 2024|BRAND VERIFIED NEW EXAM QUESTIONS AND DETAILED CORRECT ANSWERS ALL GRADED A+|GUARANTEED SUCCESS|LATEST UPDATE 2024

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NBME PATHOLOGY FINAL EXAM 2024|BRANDNEW VERIFIED EXAM QUESTIONS AND DETAILED CORRECT ANSWERS ALL GRADED A+|GUARANTEED SUCCESS|LATEST UPDATE 2024 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

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NBME PATHOLOGY FINAL EXAM
2024|BRAND VERIFIED NEW EXAM
QUESTIONS AND CORRECT ANSWERS
ALL GRADED A+|GUARANTEED
SUCCESS|LATEST UPDATE 2024

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

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