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q from the exam
#348662
cingular - 10/14/08 20:22

isolated smooth muscle = ACh is given, what will be secreted or made?
a) endothelin; b) NO synthase; c) Epithelial growth factor
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* Re:q from the exam
#1511869
dreeman - 10/14/08 21:41

..B
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* Re:q from the exam
#1511946
cingular - 10/14/08 22:09

can you explain why?
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* Re:q from the exam
#1511956
glia - 10/14/08 22:11

Ach stimulate EDRF/NO even when there is not parasympathetic innervation or m3 receptor on vessel.
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* Re:q from the exam
#1511979
mdsurgeon - 10/14/08 22:23

i think NO comes from endothelium but it diffuses to smooth muscle causing dilation. NO doesn't come directly from smooth muscle.
smooth muscle store endothelin in thier endoplasmic R. may be Ach causes release of endothelin from endoplasmic R

q from the exam
#348662
cingular - 10/14/08 20:22

isolated smooth muscle = ACh is given, what will be secreted or made?
a) endothelin; b) NO synthase; c) Epithelial growth factor
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* Re:q from the exam
#1511869
dreeman - 10/14/08 21:41

..B
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* Re:q from the exam
#1511946
cingular - 10/14/08 22:09

can you explain why?
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* Re:q from the exam
#1511956
glia - 10/14/08 22:11

Ach stimulate EDRF/NO even when there is not parasympathetic innervation or m3 receptor on vessel.
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* Re:q from the exam
#1511979
mdsurgeon - 10/14/08 22:23

i think NO comes from endothelium but it diffuses to smooth muscle causing dilation. NO doesn't come directly from smooth muscle.
smooth muscle store endothelin in thier endoplasmic R. may be Ach causes release of endothelin from endoplasmic R

* muscle contraction: conceptual link
#348465
warrior99 - 10/14/08 13:21

this is another site to help u understand muscle contractions, again with animations. u ll never forget the concept, believe me.
http://www.brookscole.com/chemistry_d/te...scles.html

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* Re:muscle contraction: conceptual link
#1510610
rockondoc - 10/14/08 14:55

hey good job warrior99..i just saw it and its really gr8..very nicelly presented basic concepts..thanks a lot!
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* Re:muscle contraction: conceptual link
#1510642
drstrider - 10/14/08 15:03

gr8 link
hats off to ya
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* Re:muscle contraction: conceptual link
#1510675
aspirantdoc98 - 10/14/08 15:13

Check this out:

http://highered.mcgraw-hill.com/sites/00...ction.html

and also:

http://highered.mcgraw-hill.com/sites/00...ction.html

Thanks.

synaptic transmission: a great link
#348441
warrior99 - 10/14/08 12:16

hello frens, i have found this great animation link that perfectly illustrates synaptic and neuromuscular transmission. check it out:-)

http://highered.mcgraw-hill.com/sites/00...iz_1_.html
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* Reynaptic transmission: a great link
#1510186
corona - 10/14/08 12:19

thanks warrior 99, great link.
BEST OF LUCK!
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* Reynaptic transmission: a great link
#1510309
warrior99 - 10/14/08 13:19

thanks corona. GL
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* Reynaptic transmission: a great link
#1510639
rockondoc - 10/14/08 15:02

hey thanx warrior
good luck!
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* Reynaptic transmission: a great link
#1510649
drstrider - 10/14/08 15:06

hey warrior gr8 job man
nxt tym around i'll b the first person to c ur threads..gud job
gl
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nbme q 111
#137619
myusmle - 11/10/06 21:36

A 25-year-old woman, gravida 1, para 0, who is Rh-negative, delivers a full-term Rh-positive neonate. The mother is given prophylactic anti-Rho(D) immune globulin immediately post partum. During her second pregnancy 3 years later, she is screened each trimester for Rho(D) antibodies. An indirect antiglobulin test done during the third trimester indicates the presence of anti-Rho(D) antibodies in her serum. Which of the following is the most likely mechanism for the occurrence of these maternal antibodies?

A) Anamnestic production of maternal anti-Rho(D) immunoglobulin

B) Intrauterine transplacental fetal-maternal hemorrhages during the second pregnancy

C) Residual circulating prophylactic anti-Rho(D) immunoglobulin

D) Transplacental passage of fetal IgG anti-Rho(D) antibodies


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* Re:nbme q 111
#554177
myusmle - 11/10/06 22:12

B ???????????
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* Re:nbme q 111
#554438
myusmle - 11/11/06 02:50

anymore inputs plz

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* Re:nbme q 111
#554447
umraojaan - 11/11/06 03:36

b

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* Re:nbme q 111
#555217
eu_phoria - 11/11/06 22:55

C???????
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* Re:nbme q 111
#555219
zarra - 11/11/06 23:01

ccc
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* Re:nbme q 111
#555222
eu_phoria - 11/11/06 23:05

thanks zara .. i was thinking its only me thiking otherwise ;-)
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* Re:nbme q 111
#555244
deric - 11/11/06 23:34

i am thinking b so waht is the answer
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* Re:nbme q 111
#555246
zarra - 11/11/06 23:34

eu_phoria why are u thinking C?

this is my reasoning - dont know if its right or wrong.

A) Anamnestic production of maternal anti-Rho(D) immunoglobulin --- b/c mom doesnt produce anti-Rho(D) antibodies - it is given to her via Rhogam (passive artifificial)

B) Intrauterine transplacental fetal-maternal hemorrhages during the second pregnancy -- it doesnt say in the question that she hemorrhaged during her second pregnancy. Plus I thought that maternal-fetal blood mix during delivery. Not before that. So no mixing her during second pregnancy -- mom is in third trimester of pregnancy, she has not delivered yet.

C) Residual circulating prophylactic anti-Rho(D) immunoglobulin -- because she was given rhogam after her first pregnancy (so its passive artificial b/c with rhogam your giving her anti-RHO antibodies)

D) Transplacental passage of fetal IgG anti-Rho(D) antibodies -- at the end of her first pregnancy, there was mixing of blood - and 1st babies RH D+ antigens went to mom, mom produces anti Rh D+ antibodies. Mom is given Rhogam b/c what Rhogam does is that it eliminates the Rh antigen that went into mom from 1st baby, so mom does not end up producing anti Rh D+antibodies.


What do you think?
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* Re:nbme q 111
#555257
eu_phoria - 11/11/06 23:52

right.. i have exactly same reasoning
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* Re:nbme q 111
#555258
nautilus - 11/11/06 23:52

It is B
Passive immunization is short lived..so no residual

2 nd pregnancy-->fetal-placental bleed in utero(most common in 2nd and 3rd trimester) is the reason Rhoham given in 28wks gestation (So active immunization doesnt develop)
and also pospartum with in 72 hrs for the same reason--prevention of active immunisation bcoz of any accidental exposure to fetal RBC


nautilus - 11/11/06 23:55

Zarra,
even an insignificant amount of maternal hemorrhage can can elicit immune response(need not be a clinically significant bleed),to be detected by mom r doc
Why would not moms body respond to any foriegn Ag(here fetal RBC) even before r after delivery?
So its B
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* Re:nbme q 111
#555264
zarra - 11/12/06 00:04

I dont know nautilus - you could be right. All I know from old questions and from what I understood from Kaplan - is that Rhogam is given at 28 weeks and post delivery. I dont know about blood mixing prior to delivery - but what you said makes sence, maybe thats why they give it at both 28 weeks and postpartum. However, they are talking about her second pregnancy - not first. So mom already has rhogam (anti Rho-D). So even if some small amount of mixing accours before delivery - say baby's blood gets into mom, then the anti Rho-D antigens in mom would lyse those cells right away in mom. If some of moms blood gets into baby - then the anti-Rho D antigens that baby has already been exposed to wont affect baby anyway ----- remember its the baby we have to worry about b/c baby forms new blood. With Rhogam given in first pregnancy - mom is protected with her anti Rho - antibodies (she wont attack her own blood type) and she is protected against her babies RhO+ blood b/c of the rhogam she recieved last time during her pregnancy. Thats why I dont think B can be the answer. I would go with C.
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* Re:nbme q 111
#555899
coolzone - 11/12/06 16:30

ans = A
please confirm
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* Re:nbme q 111
#556318
caps31382 - 11/13/06 07:52

c.......
if no residual anti rho immunoglobin was der then mother wud nevr ever produce anti bodies
against them .
if h'rrage then what wud hav been produced by mother is anti rho not antibodies to anti rho
HENCE CCCCCC
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* Re:nbme q 111
#556571
leschnyhan - 11/13/06 11:40

Can Anti rho immunoglobulin last for 3 years in mothers body?

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* Re:nbme q 111
#1425720
rizowana - 08/19/08 18:21

what is the answer here? all these people made me more confused.
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* Re:nbme q 111
#1425746
drtariq - 08/19/08 18:42

It should be c
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* Re:nbme q 111
#1425849
rkmehta - 08/19/08 22:01

here question stem clearly tells c z screened 4 anti rh ab each trimester...c must b negative in 1st n 2nd trimester...n bcm +ve in 3re..so it must b minor feto maternal bleed...which hs caused fetal celll 2 enter maternal circulation n produce ab....
so ans z bbbb

NBME 5, block 1, Q31
#329641
drtilakpasala - 08/19/08 19:07

A patient with blood group O undergoing an operation for repair of an aortic aneurysm is mistakenly transfused with a group A unit of packed red blood cells. He immediately goesinto shock. A blood sample is markedly hemolyzed. Which of the followin is the primary mechanism of hemolysis?

a) Action of properdin to cleave C3
b) Action of C5-9 comple of complement
c) Activation of factor XII(Hageman factor)
d) Production of C5a to stimulate phagocytosis
e) Release of histamine by the action of C5a

can you explain why as well.

regards
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* Re:NBME 5, block 1, Q31
#1425788
analysis - 08/19/08 20:24

DDDDDD
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* Re:NBME 5, block 1, Q31
#1425791
physician1 - 08/19/08 20:33

. it could be A
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* Re:NBME 5, block 1, Q31
#1425793
rsvr - 08/19/08 20:46

this is what i think not sure--hemolysis---preformed Ab to RBC---type 2 hypersensivity, Ag-Ab complex and complement activation occurs, with eventual progression to cell lysis through formation of the "membrane attack complex". so i i think b is the ans ,
please feel free to give ur views if u think this is wrong
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* Re:NBME 5, block 1, Q31
#1425794
raju2008 - 08/19/08 20:49

I think B.serum has IgM which destroy RBC by MAC by C5-9.

NBME 5 section 1 discussion
#329548
rsvr - 08/19/08 12:25

guys anyone interested in discussion, please contribute , it will help us form a correct ans list to the new forms of NBME so that it will help everyone

cd u please look at these Q and share ur views
The Q nos are 14, 18, 20, 25, 26, 31, 33, 35 in form 5 section 1, it wd help if you cd give reasons to ur choices

thanks a lot
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* Re:NBME 5 section 1 discussion
#1425430
drtilakpasala - 08/19/08 13:16

hey rsvr...i would be interested....even i felt some of the answers hovering around were wrong...

i am having some doubts with 6, 10, 18, 20, 31, 33, 36, 39, 40, 41, 45, 47 let me know if you have any of these ans/explanation.

just ans couple of yours

q 14...the ans is B. that is the premotor cortex....where planning of the motor activity takes place....it is in connection with cerebellum (from lateral hemisphere)

q 26...site of pineal gland...posterior part of the midbrain....so its perinauds syndrome (tumour of the pineal gland) compresses the vertical gaze centre....leading to vertical gaze palsy.

q 35...ans D....muscle is a permanent cell(can not replicate...no hyperplasia in contrast to labile cell which can), it undergoes hypertrophy i,e increase in organelles. the actin bit was a guess as these are filaments and hypertrophied muscles doesnt seem to change its length.

hope that helps...

if you want discuss nbme 5 and 6....email me we could do it quickly on skype or yahoo..
email: drtilakpasala@googlemail.com

regards

thanks so much for your help,i appreciate it!

nbme q 92
#137593
myusmle - 11/10/06 21:26

A 48-year-old man with a long history of alcohol abuse has painless vomiting of large amounts of bright red blood. Heart rate is 110/min and blood pressure is 80/0 mm Hg. He dies despite rapid transfusion of packed erythrocytes. At autopsy, the source of the hemorrhage is found in the lower esophagus. A photograph of the site is shown. Which of the following mechanisms most likely caused the hemorrhage?



A) Alcohol-induced esophagitis

B) Deficiency in hepatic synthesis of vitamin K-dependent coagulation proteins

C) Mechanical tearing of the esophageal mucosa during vomiting

D) Peptic ulceration of esophageal mucosa due to reflux of gastric acid

E) Transmission of portal hypertension to esophageal veins


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* Re:nbme q 92
#554072
myusmle - 11/10/06 21:42

E -- oesophageal varices -- long hist of alcohol abuse and painless vomiting of bright red blood .
anastomoses bet left gastric and azygous veins
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* Re:nbme q 92
#554437
rmansour - 11/11/06 02:50

I THINK IT'S CCC: MALLORY WEISS SYNDROME. THE ESOPHAGUS COULD RUPTURE IN THIS DISEASE IF HE RETCHES TO HARD AND LEAD TO DEATH. THE PHOTO ALSO SHOWED A LINEAR LIKE TEAR IN THE DISTAL ESOPHAGUS.

ESOPHAGEAL VARICES WOULD SHOW DILATED VEINS. THE LESION LOOKED LIKE A TEAR IN THE LOWER ESOPHAGUS DUE TO RETCHING, SO PROBABLY MALLORY WEISS.
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* Re:nbme q 92
#1425050
rizowana - 08/19/08 07:59

in the answer key it is e but i think its c.
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* Re:nbme q 92
#1425119
okt3 - 08/19/08 09:28

Hi rizo and everyone, this is the picture(I oversized), check the lower esophagus, and let me know if you stick with your answer C or change to E.

Download Link: http://www.sendspace.com/file/4lohbp


The has long history of alcohol abuse has painless vomiting of large amounts of bright red blood, is it esophageal varices rupture to due portal hypertension?


http://www.wrongdiagnosis.com/bookimages/12/4190.png


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* Re:nbme q 92
#1425146
rizowana - 08/19/08 09:51

okt3, i dont know why, still i am inclined to answer c.
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* Re:nbme q 92
#1425175
killmle - 08/19/08 10:12

why not E........??? esophageal varices esp in case of alcoholic, vomiting of blood & painless - doesnt thsi goes in favour esophageal varices???
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* Re:nbme q 92
#1425178
masha - 08/19/08 10:15

could be C
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* Re:nbme q 92
#1425302
greatscore - 08/19/08 11:54

I'm agree with rmansur the answer is C : the clinical symptoms are very similar in both , but if you look the endoscopy is very different the appearance of the Mallory Weiss syndrome and Esophageal varices. Let's take a look below in google image:

http://images.google.com/imgres?imgurl=h...n%26sa%3DN
http://www.pennhealth.com/health_info/pr.../18145.jpg



http://images.google.com/imgres?imgurl=h...n%26sa%3DG


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* Re:nbme q 92
#1425373
physician1 - 08/19/08 12:31

cccccccc
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* Re:nbme q 92
#1425464
rkmehta - 08/19/08 13:51

here it says large amt.so it must b varices.....in mallory weiss der wud b less amt of bleeding...n pt never get hopovolemic shock n die..
so ans z varices...eeeeee
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nbme 140
#137667
myusmle - 11/10/06 22:33

A 22-year-old woman is concerned about her risk for developing diabetes because her mother has type 2 diabetes mellitus. Which of the following is the primary defect thought to predispose individuals towards the development of type 2 diabetes mellitus?
A) Anti-insulin receptor antibodies

B) Autoimmune destruction of pancreatic β cells

C) Dysregulation of pancreatic β cells

D) Increased peripheral insulin resistance

E) Suppressed hepatic glycogen synthesis


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* Re:nbme 140
#554221
michaelis - 11/10/06 22:35

ddd
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* Re:nbme 140
#554251
pranju - 11/10/06 22:49

DDD
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* Re:nbme 140
#555206
mydream - 11/11/06 22:43

I would go for A.
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* Re:nbme 140
#555214
eu_phoria - 11/11/06 22:49

D..
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* Re:nbme 140
#555221
zarra - 11/11/06 23:02

dd
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* Re:nbme 140
#555320
leschnyhan - 11/12/06 01:54

D is ok for me

Hi mydream. can u explain y u think A is correct.
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* Re:nbme 140
#555406
drpardha - 11/12/06 07:30

The answer clearly is increases insulin resistance.

Type I DM - absolute insulin deficiency due to destruction of beta cells by autoimmune response

Type II DM - Two defects are seen here.
i) Insulin deficiency
ii) Insulin resistance.

The present world outbreak of DM is mainly due to Type II DM (90-95%)

drpardha
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* Re:nbme 140
#1425385
physician1 - 08/19/08 12:37

ddddddddd