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PATHOLOGY NBME Exam questions with correct answers.
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PATHOLOGY NBME Exam questionswith correct answers
Adaptation to stress - correct answer -Hypertrophy - due to increase size or cell adapts to increase
workload or hypertensive heart (LV enlarges)
hyperplasia - increase in number (glandular proliferation during pregnancy) it can occur together with
hypertrophy in uterus smooth muscle
Atrophy - decrease organ size due to oxygen deprivation or aging *(feature: intracytoplasmic vacuoles or
degraded organelles)*
Metaplasia - squamous metaplasia at squamocolumnar junction) due to chronic irritation *can become
dysplasia*
Hypoxia injuries - correct answer -Cellular swelling - increase intracelular Na and H2O and decrease
intracelular K+ *(Feature: hydropic change or large vacuoles on cytoplasm; ER or mitochondrial swelling)
are reversible damage*
Ribosome disaggregation - no protein synthesis
PKU stimulation- decrease pH result in clumping of nuclear chromatin
Cell death - *irreversible damage* massive calcium influx and mitochondria calcification
- myocardium infarct enzymes, LDH, CK and AST and myocardial necrosis proteins, troponin I/T and
myoglobin
free radical injury is - correct answer -Repercussion injury
Necrosis vs. Apoptosis - correct answer -Necrosis: bad, damage to nearby cells caused by lysis
,- coagulative: heat and kidney lose blood supply or ischemia *no nuclei and increase eosinopholia*
- *liquefactive: brain necrosis and liquification*
- caseous: TB granulomas, *cheese like appearance*
- *gangrenous: bowel loss of blood supply (dry or wet)*
- fibrinoid: wall of arteries fibrin deposits (vasculitis) *smudgy pink appearance*
- fat: pancreas release enzymes leading to necrosis *(lipid layden macrophages)*
Irreversible nuclear changes:
pyknosis - nucleons chromatin clumping, basophilic
kartorrhexis- chromatin fragmentation
karyolysis - chromatin fading
Apoptosis: good; for normal functioning of cell
- cell shrinkage (eosinophils and chromatin remnants by councilman bodies)
- *caspase activation 8 or 9 (extrinsic pathway)*
- *mitochondrial loss of GF deactivates BCL2 (anti apoptosis) this stimulate BAX (proapotothic) proteins*
Reversible changes - correct answer -Fatty changes - TAG accumulation in *liver*, heart and kidney due
to:
alcoholism
DM
malnutrition
obesity
Poisoning
,Hyaline changes - glassy eosinophilic appearance due to protein accumulation
Anthracosis - black pigment due to:
*carbon*
silica
iron dust
Pigment accumulation:
- melanin: keratinocytes cluster (tyrosine de defect or melanocytes)
- bilirubin: hemolytic, hepatocellular (liver parenchyma damage) or obstructive (intra or extra hepatic)
jaundices
- hemosiderin: iron pigments *(golden brown aggregates via Prussian blue)* within macrophages of
liver, BM, spleen
Hemosiderosis (hemosiderin within macrophages) due to alcohol; Hemochromatosis (hemosiderin
within parenchyma cells or *bronze diabetes*) with *high transferrin, increase iron and low TIBC*
Lipofusin - *wear and tear pigment in elders within hepatocytes* (brown atrophy)
Calcification - correct answer -Metastatic - hypercalcemia due to
hyperparathyroidism
increase vitamin D
osteolytic tumor that mobilizes calcium and phosphorus
excess calcium intake
Dystrophic - calcification in previous damaged tissue like *heart valve or atherosclerosis lesion*
Inflammation - correct answer -a response to an injury or tissue destruction:
, R ubor (*redness due to dilated blood vessels *)
D olor (*pain* mediated by *Bradykinin*)
C alor (due to increase blood flow)
T umor (swelling due to fluid accumulation)
F unctio laesa (loss function)
Acute inflammation - adhesion role is very important
selection - induce cytokines IL1 and TNF
L- selectin- induce NT to bind endothelial Glycam1
E and P selectins - endothelial express them to bind sialyl Lewis X and *P selectins stored in weibel
palade bodies and platelet alpha granules* *activated by histamine and thrombin*
integrins - LFA1, MAC1, VLA4 proteins
24hr - NT after bacteriana infarction
2-3 days - macrophages (in TB, brucellosis, typhus fever and salmonella infection)
*Lymphocytes* - viral infections (in influenza, mumps, mono, CML)
*Eosinophils* - in allergic or parasitic like asthma, fever (PAN, HL)
*Mast cells and Basophils* - histamine release (in CML and MPD)
cellular response to injury:
emigration
margination
pavementing
rolling
adhesion
*transmigration (PAM1 on leukocytes)*
chemotaxis - *C5a complement activator*
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