good for those whos exam is near - rizowana

[ArchivalUser]

seizure- nbme 4
#136548
docirb - 11/08/06 09:21

A 45-year-old man has had four episodes of involuntary twitching of the right foot. Following the last episodes, he had a tonic-clonic seizure. Which of the following structures on the left is the most likely origin of the seizure?

A ) Inferior frontal cortex

B ) Inferior temporal cortex

C ) Insular cortex

D ) Primary motor cortex

E ) Supplementary motor cortex
d?
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* Reeizure- nbme 4
#548724
uromle - 11/08/06 09:25

Ans D

[ArchivalUser]

nbme 5 block 1 q 46
#329028
silva - 08/17/08 16:08

what is the diagnosis?pls
26 y o woman with the multiple lesion in eye lid and nasal flare?
thanks
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* Re:nbme 5 block 1 q 46
#1423398
draga - 08/17/08 16:13

She has also hilary limphadenopathy so I thought it cuold be sarcoidosis(common skin lession are found in sarcoidosis) and answer b but I'm not shure at all
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* Re:nbme 5 block 1 q 46
#1423408
silva - 08/17/08 16:22

I agree with u but why should be the forign body the answer?
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* Re:nbme 5 block 1 q 46
#1423409
draga - 08/17/08 16:23

I ask my self same thing-I don't know
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* Re:nbme 5 block 1 q 46
#1423422
avandia - 08/17/08 16:48

when macrophages are transformed in to giant cells, have various
names in different organs.
Example-skin-Langhan's giant cells.
Lung-foreign body giant cells
iris-Touton's cells.
Bottom line-Foreign body giaint cells are transformed macrophages and are one of the
three types of giant cells and can be found in sarcoidosis.
GL
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* Re:nbme 5 block 1 q 46
#1423426
draga - 08/17/08 16:51

Thanks -it helps
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* Re:nbme 5 block 1 q 46
#1423535
silva - 08/17/08 20:12

http://images.google.com/imgres?imgurl=h...n%26sa%3DN
what do you think about this lesions/?dont you think it is similar to this q?

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[ArchivalUser]

NBME 2 Block 4 , Q40
#316900
vitf - 07/08/08 11:31

ans given is b..
but does angiotension produce bradycardia??
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* Re:NBME 2 Block 4 , Q40
#1373849
vitf - 07/08/08 14:49

anyone??
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* Re:NBME 2 Block 4 , Q40
#1374328
durham - 07/08/08 23:16

so you can prevent this by giving scopolamine
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* Re:NBME 2 Block 4 , Q40
#1374348
okt3 - 07/08/08 23:37

maybe angiotension, bradycardia is by reflex
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* Re:NBME 2 Block 4 , Q40
#1374450
vitf - 07/09/08 00:43

i havent read about bradycardia related to angiotensin anywhere, guess will have to follow exclusion rule here..
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* Re:NBME 2 Block 4 , Q40
#1423371
zoh - 08/17/08 15:49

norepinephrine produce vasoconstriction and reflex bradycardia which is reversed by atropin
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[ArchivalUser]

nbme5q
#319022
efi - 07/15/08 11:45

I did online and remember a qestion which I couldnt figure out at all. In GVHD which specific transplant gets benefits. lung(PHTN),BM(ALL),Kidney,liver.
Some body explain to me please. I couldnt even know how to associate it.
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* Re:nbme5q
#1381936
99hope - 07/15/08 11:47

BM(ALL)
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* Re:nbme5q
#1381940
99hope - 07/15/08 11:53


The reason is it because the Donor T cells recognize host tissue (ALL)and activate host CD4 and CD8 T cells Destroy in this case not normal calls but (ALL)


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* Re:nbme5q
#1381953
efi - 07/15/08 12:06

that is the way i saw it. in answer some of u post say lung.
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* Re:nbme5q
#1423362
zoh - 08/17/08 15:44

norepinephrine produce vasoconstriction and reflex bradycardia that can be reversed by atropin

[ArchivalUser]

NBME 6 block 1 q43
#325390
mdia - 08/04/08 17:10

Certain chromosomal abnormalities can result in rudimentary development of the cerebral hemispheres, which of the following labeled structures in the cross section of a normal brain stem is expected to be most underdeveloped as a result of such an anormaly?

Sorry that I can not past the picture, anyone knows what's the defect and why it's B??
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* Re:NBME 6 block 1 q43
#1408936
drkyhasan - 08/04/08 17:54

most common brainstem anomaly is pons
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* Re:NBME 6 block 1 q43
#1408951
mdia - 08/04/08 18:09

Thanks, drkyhasan! but why is B? what is B?
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* Re:NBME 6 block 1 q43
#1419825
goout - 08/13/08 17:36

why it's B? i thought it's E.
B is CNXII nuclei, how could it form from cerebral hemispheres?
confused....
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* Re:NBME 6 block 1 q43
#1419827
drkyhasan - 08/13/08 17:41

B is not a cranial nerver nucleus its the PONS
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* Re:NBME 6 block 1 q43
#1419828
drkyhasan - 08/13/08 17:42

its a cut section thru the pons
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* Re:NBME 6 block 1 q43
#1419854
akm07 - 08/13/08 18:16

isnt that cut section of upper medulla?
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* Re:NBME 6 block 1 q43
#1423122
drkyhasan - 08/17/08 05:31

sorry its a cut section thru upper medulla, question asks which part of the medulla will be under develloped as a result of anomalies of the cerebral hemispheres

Ans: corticospinal tract or dorsal column medial leminiscus
or E


sorry for the confusion

[ArchivalUser]

* nbme 5 q bloc1 ques 18
#325733
afdr - 08/05/08 19:40

at the answers that i hve it says the answers is E. can anyone explain that for me plz
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* Re:nbme 5 q bloc1 ques 18
#1410576
afdr - 08/05/08 20:34

any one plz
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* Re:nbme 5 q bloc1 ques 18
#1410688
analysis - 08/05/08 22:44

i think ans is either

C or D

more D because nowadays graft survival with TX is more than 10 yrs. may be this is the reason. longer time is the only benefit i can think.
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* Re:nbme 5 q bloc1 ques 18
#1410724
mdia - 08/05/08 23:12

I think it should be A
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* Re:nbme 5 q bloc1 ques 18
#1410856
vitaminb6 - 08/06/08 01:11

can u plz type the q
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* Re:nbme 5 q bloc1 ques 18
#1422672
drdeb - 08/16/08 13:06

i think its ©....... in type 1 DM there is autoimmune destruction of islet cells........ which will be prevented by thus GVHD.. any sugg??

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* Re:nbme 5 q bloc1 ques 18
#1422714
ilrep - 08/16/08 14:27

http://usmleforum.com/showthread.php?tid=319022.php

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[ArchivalUser]

NBME 6 block 1 q43
#327864
ilrep - 08/13/08 07:41

Certain chromosomal abnormalities can result in rudimentary development of the cerebral hemispheres, which of the following labeled structures in the cross section of a normal brain stem is expected to be most underdeveloped as a result of such an anormaly?

sorry can't put the picture here

the given ans is B, can someone pls explain what is B and how it is the ans.. thanks
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* Re:NBME 6 block 1 q43
#1419152
akm07 - 08/13/08 08:01

this is upper medulla. B is Xii nucleus then. i chose CST though(E)
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* Re:NBME 6 block 1 q43
#1419160
ilrep - 08/13/08 08:11

even i went for E

[ArchivalUser]

* NBME6-block3-Q11
#319454
durham - 07/16/08 14:03

I picked C. what is your opinion???
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* Re:NBME6-block3-Q11
#1383940
jazzblue - 07/16/08 14:31

ccc
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* Re:NBME6-block3-Q11
#1383951
pmle - 07/16/08 14:34

yes CC
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* Re:NBME6-block3-Q11
#1383960
durham - 07/16/08 14:36

thanks Jazzblue and pmle

would you check block3 Q23. how to treat the minor???
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* Re:NBME6-block3-Q11
#1383970
pmle - 07/16/08 14:39

CCC,,for Q23
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* Re:NBME6-block3-Q11
#1383973
jazzblue - 07/16/08 14:40

ccc
STD is among the situations that allow medical intervention without parent notification
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* Re:NBME6-block3-Q11
#1383984
durham - 07/16/08 14:45

thanks for the explanation
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* Re:NBME6-block3-Q11
#1422514
zoh - 08/16/08 06:39

ans is BBBBBBBBBBBBBBBBBBBBBB

[ArchivalUser]

nbme 6 blk 3
#328629
nisa - 08/15/08 16:37

an 18 yr old man had an appendectomy , 2wks later the abdominal incision has healed well & has a pink,shiny,granular apperance.which is most likely finding on examination of tissue obtained from helaing area.

angiogenesis

epitheloid cells

fibrinoid necrosis

granulamatous inflammation

ischaemic injury


pls someone give the correct ans and reason
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* Re:nbme 6 blk 3
#1422003
nisa - 08/15/08 16:45

hello pls reply
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* Re:nbme 6 blk 3
#1422012
rizowana - 08/15/08 16:52

aaa
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* Re:nbme 6 blk 3
#1422026
draga - 08/15/08 17:08

a-cause 2 week after incision there is granulacion tissue=kolage type 3(by fibroblast) and capillary proliferation=angiogenesis.after a month it will be a scar=kolagen type 1
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* Re:nbme 6 blk 3
#1422038
drtilakpasala - 08/15/08 17:14

i guess the answer is A. granulation (inflammation) is the confusing option.

hope below helps

regards

Primary wound healing or healing by first intention occurs within hours of repairing a full-thickness surgical incision. This surgical insult results in the mortality of a minimal number of cellular constituents.

Following tissue injury via an incision, the initial response is usually bleeding. The cascade of vasoconstriction and coagulation commences with clotted blood immediately impregnating the wound, leading to hemostasis, and with dehydration, a scab forms. An influx of inflammatory cells follows, with the release of cellular substances and mediators. Angiogenesis and re-epithelization occur and the deposition of new cellular and extracellular components ensues.

Initial phase - Hemostasis

Following vasoconstriction, platelets adhere to damaged endothelium and discharge adenosine diphosphate (ADP), promoting thrombocyte clumping, which dams the wound. The inflammatory phase is initiated by the release of numerous cytokines by platelets. Alpha granules liberate platelet-derived growth factor (PDGF), platelet factor IV, and transforming growth factor beta (TGF-b), while vasoactive amines such as histamine and serotonin are released from dense bodies found in thrombocytes. PDGF is chemotactic for fibroblasts and, along with TGF-b, is a potent modulator of fibroblastic mitosis, leading to prolific collagen fibril construction in later phases. Fibrinogen is cleaved into fibrin and the framework for completion of the coagulation process is formed. Fibrin provides the structural support for cellular constituents of inflammation. This process starts immediately after the insult and may continue for a few days.

Second phase - Inflammation

Within the first 6-8 hours, the next phase of the healing process is underway, with polymorphonuclear leukocytes (PMNs) engorging the wound. TGF-b facilitates PMN migration from surrounding blood vessels where they extrude themselves from these vessels. These cells "cleanse" the wound, clearing it of debris. The PMNs attain their maximal numbers in 24-48 hours and commence their departure by hour 72. Other chemotactic agents are released, including fibroblastic growth factor (FGF), transforming growth factors (TGF-b and TGF-a), PDGF, and plasma-activated complements C3a and C5a (anaphylactic toxins). They are sequestered by macrophages or interred within the scab or eschar.5

As the process continues, monocytes also exude from the vessels. These are termed macrophages. The macrophages continue the cleansing process and manufacture various growth factors during days 3-4. The macrophages orchestrate the multiplication of endothelial cells with the sprouting of new blood vessels, the duplication of smooth muscle cells, and the creation of the milieu created by the fibroblast. Many factors influencing the wound healing process are secreted by macrophages. These include TGFs, cytokines and interleukin-1 (IL-1), tumor necrosis factor (TNF), and PDGF.

Third phase - Granulation

This phase consists of different subphases. These subphases do not happen in discrete time frames but constitute an overall and ongoing process. The subphases are "fibroplasia, matrix deposition, angiogenesis and re-epithelialization".4

In days 5-7, fibroblasts have migrated into the wound, laying down new collagen of the subtypes I and III. Early in normal wound healing, type III collagen predominates but is later replaced by type I collagen.

Tropocollagen is the precursor of all collagen types and is transformed within the cell's rough endoplasmic reticulum, where proline and lysine are hydroxylated. Disulfide bonds are established, allowing 3 tropocollagen strands to form a triple left-handed triple helix, termed procollagen. As the procollagen is secreted into the extracellular space, peptidases in the cell wall cleave terminal peptide chains, creating true collagen fibrils.

The wound is suffused with GAGs and fibronectin produced by fibroblasts. These GAGs include heparan sulfate, hyaluronic acid, chondroitin sulfate, and keratan sulfate. Proteoglycans are GAGs that are bonded covalently to a protein core and contribute to matrix deposition.

Angiogenesis is the product of parent vessel offshoots. The formation of new vasculature requires extracellular matrix and basement membrane degradation followed by migration, mitosis, and maturation of endothelial cells. Basic FGF and vascular endothelial growth factor are believed to modulate angiogenesis.

Re-epithelization occurs with the migration of cells from the periphery of the wound and adnexal structures. This process commences with the spreading of cells within 24 hours. Division of peripheral cells occurs in hours 48-72, resulting in a thin epithelial cell layer, which bridges the wound. Epidermal growth factors are believed to play a key role in this aspect of wound healing.

This succession of subphases can last up to 4 weeks in the clean and uncontaminated wound.

Fourth phase - Remodeling

After the third week, the wound undergoes constant alterations, known as remodeling, which can last for years after the initial injury occurred. Collagen is degraded and deposited in an equilibrium-producing fashion, resulting in no change in the amount of collagen present in the wound. The collagen deposition in normal wound healing reaches a peak by the third week after the wound is created. Contraction of the wound is an ongoing process resulting in part from the proliferation of the specialized fibroblasts termed myofibroblasts, which resemble contractile smooth muscle cells. Wound contraction occurs to a greater extent with secondary healing than with primary healing. Maximal tensile strength of the wound is achieved by the 12th week, and the ultimate resultant scar has only 80% of the tensile strength of the original skin that it has replaced.

[ArchivalUser]

nbme question
#328562
draga - 08/15/08 14:19

68 years old woman come into a hospital with gross hematuria,during hospitalisation she develops aphasia and right hemiparesis and slips into coma.two days later she dies.The most probably cause is:
a)polycistic renal disease
b)renal cell carcinoma
c)papilary necrosis
d)renal infarction
e)renal metastasis

I would really need some help with association of stroke like Sy and gross hematuria...
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* Re:nbme question
#1421836
orthop - 08/15/08 14:20

aaa. Ruptured berry aneurysm becos of HTN in APCKD
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* Re:nbme question
#1421843
mydream270 - 08/15/08 14:22

polYcystic kidney disease assiciated with with berry aneurysm in LINDAU DIEASE.
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* Re:nbme question
#1421861
draga - 08/15/08 14:29

but there was a picture and it didn,t seem at all like ADPKD-I woudn't miss polycistic kidney..
That why I'm confused-cause picture didn't match with berry aneurisam rupture and Polycist.kidney

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* Re:nbme question
#1421908
atosa - 08/15/08 14:49

may be B,renal cell carcinoma can cuz gross hematuria,also ranal ca------>incr EPO--->thrombotic event---> LFT middle cerebral a------>aphasia &Rt hemiparesis,
Renal cell ca can also be 2ndry 2 ADPKD,?????????????????
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* Re:nbme question
#1421911
rkmehta - 08/15/08 14:51

den der wud b renal cell ca...
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* Re:nbme question
#1421965
drkyhasan - 08/15/08 16:01

the patient is 68 so APKD would be unlikely, pt would present at an earlier age, renal cell ca. could be a probable cause.
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* Re:nbme question
#1422019
klm25 - 08/15/08 17:00

aaaaaa