MoD Flashcards
BCL-2 function
Main anti-apoptotic protein
Bim, Bid, Bad function
BH3 proteins: activate Bax/Bak channels (cause loss of cytochrome C, activation of capsases), also block BCL-2/BCL-X
Describe the extracellular apoptotic pathway
FasL (on T cells) binds to Fas, causing activation of “death receptors” in TNF family, leading to activation of caspases that degrade structural components of nuclear matrix. Fas can also activated Bid, inducing the intrinsic pathway.
Define Pyknosis. What broad change is it associated with?
Shrunken, hyper chromatic nucleus; necrosis
Define Karyolysis. What broad change is it associated with?
Fading of the nucleus; necrosis
Define Karyorrhexis. What broad change is it associated with?
Fragmentation of the nucleus; necrosis
List all changes associated with irreversible cell injury
Karyolysis, pyknosis, karyorrhexis, myelin figures, dilation of mitochondria (last 2 on EM)
What type of cellular adaptation precludes cell division? Give examples
Hypertrophy; uterine changes during pregnancy, cardiac myocytes (response to incr. workload)
What can cause atrophy? Give examples
Decr. inn., blood flow, hormonal stimulation, workload, nutrition, incr. pressure; old brain
What can cause hyperplasia? Give examples
Incr. hormonal or GF stimuli; endometrial changes in response to estrogen and lactating breast
What type of necrosis is uniquely associated with TB?
Caseous necrosis
Give an example of Fat necrosis
Pancreas: lipases split triglycerides into fatty acids which react with calcium to undergo saponification
Describe the mechanism of reperfusion injury
Restoration of blood flow causes surge in ROS and nitrogen, also inflammation (d/t hypoxic tissues expressing cytokines and adhesion molecules) with activation of the complement system
Describe abnormal intracellular accumulations seen in reperfusion injury
Exogenous substances like minerals, infectious agents; abnormal synthesis or metabolism of endogenous substances like A1AT, Mallory’s hyaline, neurofibrillary tangles in Alzheimers, amyloidosis
Describe the effect of mercuric chloride on GI intestinal cells
Incr. membrane permeability; can cause leakage of enzymes
Intracellular accumulations associated with hepatic steatosis
Triglycerides in hepatocytes
Intracellular accumulations associated with proteinuria
Protein droplets in tubules
Intracellular accumulations associated with A1AT deficiency
A1AT globules in liver
Diseases and deposition areas associated with “metastatic calcification”
Endocrine diseases (e.g. hypercalcemia caused by renal disease or parathyroid excess); areas of acid secretion like lung, kidney, stomach, pulm veins and systemic arteries
Gross and histologic hallmarks of acute inflammation
Edema; neutrophils
Phospholipase A2 function
Cleaves arachidonic acid from phospholipid cell membrane
PGI2 function
Vasodilation, incr. vasc permeability, pain (peripheral nerve ending sensitization), decr. platelet aggregation, “maintain GFR”
PGE2 function
Fever, vasodilation, incr. vasc permeability, pain (CNS + peripheral nerve ending sensitization), “maintain GFR,” “hyperalgesic”
Where does PGD2 come from? Effects?
Mast cells; vasodilation, incr. vasc permeability, attracts neutrophils