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NBME PATHOLOGY EXAM NEWEST ACTUAL EXAM
TEST BANK| 2 LATEST VERSIONS (VERSION A & B) WITH 550
REAL EXAM QUESTIONS AND CORRECT DETAILED
ANSWERS (VERIFIED ANS WERS) ALREADY GRADED A+|
PATHOLOGY NBME FINAL EXAM PREP|| BRAND NEW!!
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. 1 / 4
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pg. 2 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 2 / 4
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pg. 3 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 3 / 4
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pg. 4 Where does leukocyte extravasation typically occur? - ANSWER - In post-capillary venules.
What are the four steps of leukocyte extravasation at injury sites? - ANSWER - 1. Margination and rolling 2. Tight binding 3. diapedesis (where it slips between endothelial cells to get out) and 4. Migration (chemotactic signals cause the cell to move through the interstitium to the site of injury / inflammation).
How does margination and rolling occur? - ANSWER - E/P selectins and GlyCAM-1 and CD34 on vessels; sialyl lewis X molecules on leukocyte which interact with the selectins and L-selectin on the leukocyte which interacts with the Gly-CAM1 and CD34 on the vessels.
How does tight binding occur? - ANSWER - ICAM (CD54) on vessel-- > CD18/11 integrins and LFA1/mac-1 on leukocytes. VCAM (CD106) on vessels-->VLA4 integrins.
How does diapedesis occur? - ANSWER - PECAM-1 (CD31) on vessels--> PECAM-1 (CD31) on leukocytes
How does migration occur? - ANSWER - the vasculature releases
chemotactic products in response to bacteria: C5a, IL-8, LTB4,
kallikrein, plt activating factor
How do free radicals damage the cell? - ANSWER - via membrane lipid peroxidation, protein modification, and DNA breakage.
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