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Old 09-02-2012
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GIT Intestinal Cellular Injury

A 56 yr old woman comes to a physician for diffuse mid abdominal pain..on p/e however, she has unimpressive pain on palpation..her lab values are remarkable for leukocytosis...if the pt. is untreated, which of the following characteristics would most likely be found in her intestinal cells..?

a) chromatin condensation at nuclear periphery
b) cytoplasmic shrinkage
c) lack of inflammation
d) myelin figures
e) membrane bound apoptotic bodies....

need some explanation.....
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Old 09-02-2012
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it was a nice Q so I cheated a bit before I concluded the answer....

the pt. is most prolly havin Gastroenteritis n hence will have intestinal cell necrosis....

a b e are features of apoptosis

c is wrong coz there will be some inflammation even if it is a non infective cause like ibd etc...

left with d...

but i had to google wat that is...
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Old 09-02-2012
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Default Myelin figures

I remember only one thing about myelin figure is that they are present in reversible injury. Where as A, B, E signifies apoptosis (as mentioned above)

It would be good that you explain more about myelin figures and all apototisis stages. As i always have one or other doubt in it.
One day i will infect these microbes and they will search for "Anti-MEbiotic"....
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Old 09-02-2012
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Post D is the right answer

well , the correct answer is D) Myelin figures

exclusion method------A,B,C,E deals with apoptosis .easily excluded

explanation------pt. is suffering from classic case of ischemic bowel disease----ischemic bowel disease involves severe abdominal pain with no significant abdominal findings....ischemic changes most commonly leads to necrosis than programmed cell death(apoptosis)

it's really complex pathological process of hypoxic cell injury....i'll try to explain it briefly,but i may be correct me if i'm wrong....

Reversible changes-----hypoxic cell injury leads to decrease in ATP (coz, no oxygen for oxidative phosphorylation)
--only glycolysis takes place with activation of PFK(only 2ATP is produced)
--lactic acidosis( decreased pH---lead to denaturation of proteins)
--impairment of Na+-K+ -ATPase pump----Na+ and water permeability increases(cell swelling)
--ribosomal detachment(decrease protein synthesis)
--plasma membrane blebs

These above changes are often revertible if we given oxygen again...but sometimes, cells with damaged tissue will paradoxically die when oxygen is given------called as reperfusion injury(by free radicals/inflammation/complement activation)------ultimately leading to cell death via necrosis or apoptosis(irreversible processes)

Necrosis----is inflammatory process with absent nuclei and karyolysis
( nuclear fading---chromatin dissolution),
-mitochondrial permeability increases leading to vacuolization(myelin figures)-----myelin figures are composed of lipid bilayer resembling myelin sheath..found in cytoplasm or mitochondria vacuoles
-denaturation of enzymes and proteins,lysosomal lysis/rupture takes place..(due to severe lactic acidosis)....leading to autolysis(enzymatic degradation of cell) of cell..

Apoptosis----it is programmed cell death with absence of inflammatory involves caspase activation(via impaired Ca2+-ATPase pump--leading to influx of Ca2+).....

2 pathways......1) Extrinsic----TNF,FAS mediated apoptosis--CD95 acts as cellmembrane receptor--its activation(via TNF/FAS) lead to A)phospholipase stimulation releasing macrophages and phagocytosis (or)
B)caspase activation leading to DNA fragmentation(karyorrhexis---chromatin condensation into periphery,cytoplasmic shrinkage)---leads to formation of apoptotic bodies

2)Intrinsic------free radical injury with mitochondrial permeability---leads to cytochrome C release into cytosol.(along with APAF-1,an apoptosome)---caspase activation...act on P53/Bax/Bac----apoptosis

but, regarding myelin figures.....ROBBINS say it's the part of necrosis(which is irreversible process)...but rest other books say it's reversible.....
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Cell-Biology-, Gastrointestinal-Tract-, Pathology-, Step-1-Questions

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