Team Oct & Nov................Sep25th - genius123

[ArchivalUser]

same here genius..u seem quite ready for exam and still haven`t taken date?? that`s a point to freak out for us novices

[ArchivalUser]

someone please explain me what is the difference between constrictive and restrictive pericarditis...i tend to believe they are one and the same always..

[ArchivalUser]

genius123 & okt3 you guys are corrects..... thanks genius123 wish you the same =0)...dshikha i wont be taking all the NMBE prob just 2 as they are expensive along with all the other exams we have to pay for ..i will take one nbme soon & see how i do based on that i will decide to postpone...then i willl take another NBME rt before the step1 ..i think that should be good enough ..but if you can only take one that should be fine too alot of ppl just take one & see how they score & where they stand...on the otherhand if u can afford 2 NBME exams then go for it it will pay off in the end...right now i just feel like i forgot everything in FA i have to keep on revising its driving me crazy ...oh well i guess thats life ...GL to all of you ..happy studying lol

[ArchivalUser]

lol bergkamp,i am perfectionest,wil do it this week inshallah
stil has to do three more nbme!

regarding long QT interval=
Congenital
Aquired:
*drugs as u guys mentioning(of course amiadarone which leads to torsades as wel)and actually many antiarrythmiacs can do that but esp class III,thioridazine ,tricyclics.
*myocardial ischemia
*electrolyte abnormality

for torsades t/m=yes bergkamp i/v B blocker +i/v Magnesium(after stopping the drug of course)

[ArchivalUser]

@genius..hope some of ur qualities rub off on me too

[ArchivalUser]

i think u r talking about "constrictive pericarditis" and "restrictive cardiomyopathy"bergkamp,difficult to distinguish clinically for a cardiologist as wel,so dont blame urself
as u must be knowing the causes and pathology of both,i hope
wel clinically,
1.pul pressures r lower in constrisction as compared to restrictive

2.reduced left vent filling on insp in constrictive

3.LV diastolic pressure and rt ven dias pre are same in cons while LV diastolic greater in restrictive coz of greater pul HT.

[ArchivalUser]

u r doing actually pretty good bergkamp,and i am flattered by ur commentsi was just kiddin regarding being perfectionistof course i want to go wel prepared no doubt,but its just that i hav som other commitments and responsibilities as wel and need little time.thnx .

dshikha,u can do downloaded but at least one on line,GL to u.

Wolff parkinson white syndrome=

Accessory conduction pathway from atria to ventricle(bundle of kent)bypassing AV node.As a result ventricles begin to partially depolarize,giving rise to delta wave on ECG.May lead to reentry current leading to SVT.

[ArchivalUser]

Evolution of MI:

A) First Day= no changes in first 2-4hrs. After 4hrs there is coagulative necrosis - contraction bands visible, release of necrotic contents into bloodstream & begining of neutrophil emigration

B) 2-4 Days= RISK FOR ARRHYTHMIA- tissue surrounding infarct shows acute inflammation, hyperemia (dilated vessels), neutrophil emigration, & muscle shows extensive coagulative necrosis

C) 5-10 Days= RISK FOR FREE WALL RUPTURE- presence of outer zone (ingrowth of granulation tissue), macrophages & neutrophils

D) 7 Weeks= RISK FOR VENTRICULAR ANEURYSM- recanalized artery & contracted scar complete

[ArchivalUser]

INCLUSIONS:

Negri bodies are characteristic cytoplasmic inclusions in neurons infected by rabies virus.

Yellow fever: Councilman bodies (acidophilic inclusions) may be seen in liver.

Alcoholic hepatitis: Mallory bodies (intracytoplasmic eosinophilic inclusions)

Acute promyelocytic leukemia (M3):Auer rods are peroxidase-positive cytoplasmic inclusions in granulocytes and myeloblasts.

Chlamydiae: cytoplasmic inclusions seen on Giemsa or fluorescent antibody“stained smear.

[ArchivalUser]

thanks for he explanation genius..and that li`ll word of praise raises hopes in me