NBME PATHOLOGY EXAM WITH LATEST VERIFIED QUESTIONS AND 100% CORRECT ANSWERS GRADED A+
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Course
NBME PATHOLOGY
Institution
NBME PATHOLOGY
NBME PATHOLOGY EXAM WITH LATEST
VERIFIED QUESTIONS AND 100%
CORRECT ANSWERS GRADED A+
Apoptosis: - ANS-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 ...
NBME PATHOLOGY EXAM WITH LATEST
VERIFIED QUESTIONS AND 100%
CORRECT ANSWERS GRADED A+
Apoptosis: - ANS-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? - ANS-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.
Mestastatic calcification: - ANS-widespread, diffuse deposition of calcium in normal tissue secondary to
1. hypercalcemia: Primary hyperparathyroidism, sarcoidosis, hyper vitaminosis D or 2. High calcium-
phosphate product: chronic renal failure + secondary hyperparathyroidism, long term dialysis,
calciphylaxis, warfarin. The calcium in both cases deposits predominantly in the interstitial tissues of the
kidney, lungs, gastric mucosa (These tissues all lose acid quickly and high pH favors deposition). Patients
are normally NOT normocalcemic.
Where does leukocyte extravasation typically occur? - ANS-In post-capillary venules.
,What are the four steps of leukocyte extravasation at injury sites? - ANS-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? - ANS-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? - ANS-ICAM (CD54) on vessel--> CD18/11 integrins and LFA1/mac-1 on
leukocytes. VCAM (CD106) on vessels-->VLA4 integrins.
Intrinsic pathway of apoptosis: what is its general purpose / when does it occur? - ANS-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? - ANS-BAX and BAK are pro. Bcl-2
is anti-apoptotic.
How does Bcl-2 function? - ANS-It prevents cyt c release by binding to an inhibiting Apaf-1, which
normally INDUCES caspases.
What happens if Bcl-2 is overexpressed? - ANS-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? - ANS-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? - ANS-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? - ANS-After it crosslinks with FasL, multiple Fas molecules coalesce.
This makes a binding site for a death domain.
, Necrosis: - ANS-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: - ANS-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: - ANS-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: - ANS-TB, systemic fungi, Nocardia. Tissue maintains a cheese-like appearance. Tissue
is a proteinaceous dead cell mass.
Fatty necrosis: - ANS-Enzymatic--Pancreas. Saponification. Released fatty acids interact with calcium to
form soaps. Calc deposits appear dark on staining. Nonenzymatic--breast trauma.
Gangrenous necrosis: - ANS-Dry (ischemic coagulative) and wet (infection). Common in limbs and GI
tract.
Reversible cell injury with O2: - ANS-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).
Areas of the brain susceptible to ischemia: - ANS-ACA / MCA / PCA boundary areas. The watershed
areas, or border zones, receive dual blood supply from most distal branches of two arteries. However,
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