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NBME PATHOLOGY FINAL TEST BANK EXAM

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NBME PATHOLOGY FINAL TEST BANK EXAM [LATEST UPDATED]

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NBME PATHOLOGY
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Institution
NBME PATHOLOGY
Course
NBME PATHOLOGY

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Uploaded on
March 22, 2025
Number of pages
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Written in
2024/2025
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NBME PATHOLOGY FINAL TEST BANK EXAM
[LATEST UPDATED]


How does Fas initiate cell death? - ANSWER After it crosslinks with FasL, multiple
Fas molecules coalesce. This makes a binding site for a death domain.


Necrosis: - ANSWER 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: - ANSWER 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: - ANSWER 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: - ANSWER TB, systemic fungi, Nocardia. Tissue maintains a
cheese-like appearance. Tissue is a proteinaceous dead cell mass.


Fatty necrosis: - ANSWER Enzymatic--Pancreas. Saponification. Released fatty
acids interact with calcium to form soaps. Calc deposits appear dark on staining.
Nonenzymatic--breast trauma.

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Fibroid necrosis: - ANSWER Occurs in blood vessels. Henoch-Schonlein purpura,
Churg-Strauss syndrome. Malignant hypertension. Accumulation of amorphous,
basic proteinaceous substances resembling fibrin.


Gangrenous necrosis: - ANSWER Dry (ischemic coagulative) and wet (infection).
Common in limbs and GI tract.


Reversible cell injury with O2: - ANSWER 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).


Irreversible cell injury: - ANSWER nuclear pyknosis, karyolysis and karyorrhexis.
Ca2+ influx--> caspase activation. PM damage. lysosomal rupture. mitochondrial
permeability.


Areas of the brain susceptible to ischemia: - ANSWER ACA / MCA / PCA boundary
areas. The watershed areas, or border zones, receive dual blood supply from most
distal branches of two arteries. However, systemic hypoperfusion may cause
ischemia in these areas. **Hypoxic ischemic encephalopathy affects pyramidal
cells of the hippocampus and Purkinjie cells of the cerebellum.


Areas of heart: - ANSWER Subendocardium (LV)


Areas of kidney: - ANSWER Straight segment of the proximal tubule (medulla)
and thick ascending loop (medulla).
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Areas of liver: - ANSWER Area around central vein (zone III)


Areas of colon: - ANSWER splenish flexure, colon


Red infarct: - ANSWER Occur in loose tissues with multiple blood supplies such as
liver, lung, intestines.


Pale infarcts: - ANSWER Occur in solid tissues with a single blood supply such as
heart, kidney and spleen.


What is the first sign of shock? - ANSWER tachycardia.


Shock in the setting of DIC (disseminated intravascular coagulation) secondary to
trauma is likely due to... ? - ANSWER sepsis


What are the types of distributive shock? - ANSWER septic, neurogenic,
anaphylactic


Describe distributive shock: - ANSWER high output failure (low TPR, high CO, high
VR). Low PCWP. Vasodilation (warm, dry skin). Failure to increase BP with fluids IV.




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