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PokerDoc

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Make them high yield and not absurd if possible.. but try to pick something people might have overlooked:


ok here goes nothing, my question:


Mutation in RAG-1 gene most likely causes: ?
 
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Fuzuli said:
Biological DMARDS (mainly infliximab, etanercept and adalimumab)

You are working for a clinical immunology laboratory, which is responsible for performing all immunophenotyping tests in your hospital. A sample of blood belonging to a 3 month old boy with recurrent fever attacks, sputum production and diarrhea arrives to the lab. His FACS results shows an increase in the number of cells having CD10+, CD19+, CD20+ phenotype, but a decrease of cells having markers of CD3, CD4, CD8, CD16 and CD56. What is the most common mode of transmission and the most common genetic abnormality assoicated with this patient?
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SCID (IL-2 Receptor deficiency), XLR due to Lack of T + NK cells only?
 
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knuckles said:
SCID (IL-2 Receptor deficiency), XLR due to Lack of T + NK cells only?
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Yes, that's correct.

A 40 year old woman with a known history of mitral stenosis arrives for her annual check-up. How would her auscultation findings change if her mitral stenosis had become more prominent?
 
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Oh that's a good one. I had a USMLE world question on this a while ago.

I believe it's the time between the closing of the aortic valve (S2) and the opening snap of the mitral valve. (A2-> OS) Therefore, more severe would be shorter time interval.


What's the best determination of the severity of a mitral regurgitation?
 
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knuckles said:
Oh that's a good one. I had a USMLE world question on this a while ago.

I believe it's the time between the closing of the aortic valve (S2) and the opening snap of the mitral valve. (A2-> OS) Therefore, more severe would be shorter time interval.


What's the best determination of the severity of a mitral regurgitation?
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Severe MR is defined by the level of regurgitation and loss of LV contractility seen by Doppler ECHO. Basically, if the rugurgitating area of orifice is >= 0.4 cm^2 , it's severe MR. Whether to operate or not depends on EF and ESD.
 
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A 4 year old girl is diagnosed with Wilms' tumor. After surgical resection of her right kidney, she's started on an 18 month chemotherapy course. During the course of her chemotherapy, she starts to have polyuria, polydipsia and failure to thrive. Her control hemogram shows WBC: 7000 with normal differentiation, Hb: 11.9, Plt: 253,000. Her biochemistry panel is: Glucose: 84 (fasting), BUN: 14, Cr: 0.45, AST: 24, ALT:19, Na:134, K:3.3, LDH: 400, Ca: 7,0, P: 1,9, uric acid: 2,1. Her urinary dipstick shows d: 1013, pH: 5, RBC: 0, WBC:0, protein: 2+, glucose: 2+. Capillary blood gas shows pH: 7.31, PaCO2: 30, HCO3-: 13. Her 24-hour urine sample reveals an increase in beta-2 microglobin, calcium, phosphorus, various aminoacids and sodium. What is the most likely etiology explaining her symptoms and lab findings?
 
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Fuzuli said:
A 4 year old girl is diagnosed with Wilms' tumor. After surgical resection of her right kidney, she's started on an 18 month chemotherapy course. During the course of her chemotherapy, she starts to have polyuria, polydipsia and failure to thrive. Her control hemogram shows WBC: 7000 with normal differentiation, Hb: 11.9, Plt: 253,000. Her biochemistry panel is: Glucose: 84 (fasting), BUN: 14, Cr: 0.45, AST: 24, ALT:19, Na:134, K:3.3, LDH: 400, Ca: 7,0, P: 1,9, uric acid: 2,1. Her urinary dipstick shows d: 1013, pH: 5, RBC: 0, WBC:0, protein: 2+, glucose: 2+. Capillary blood gas shows pH: 7.31, PaCO2: 30, HCO3-: 13. Her 24-hour urine sample reveals an increase in beta-2 microglobin, calcium, phosphorus, various aminoacids and sodium. What is the most likely etiology explaining her symptoms and lab findings?
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holy molly fuzuli, if you are actually coming up with these questions you should consider creating a qbank, 👍

on another notes, is it related to the platinum based drug cisplatin?

Q: in which condition is the anti-cyclic citrullinated peptide related to?
 
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knuckles said:
RA.

What segment of small intestine absorbs the greatest amount of nutrients?
Click to expand...

GI is my crappiest section (pun win) so i'm gonna try this.. I'll say the ileum simply b/c stuff just aint done being processed when it enters the duodenum and the jejunum is never the right answer for anything.

but seriously.. im pretty sure its the ileum. sorta sure?





Why do boys have more GLUT5 receptors than girls?
 
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knuckles said:
thanks for killing this thread fuzuli
Click to expand...

Sorry about that 🙂

In retrospect, I should've given more clues; it's way too clinical in its present form. I've written the answer below, I hope it's helpful.

kryptik said:
holy molly fuzuli, if you are actually coming up with these questions you should consider creating a qbank, 👍

on another notes, is it related to the platinum based drug cisplatin?
Click to expand...

This question is actually based on a patient I've seen in wards. Here's the answer to the question:

This patient has metabolic acidosis with proteinuria (predominantly beta-2 microglobulin), glucosuria with normal blood glucose, aminoaciduria, increased uric acid excretion and loss of electolytes in urine. When considered together with her normal BUN and creatinine values, this indicates a proximal tubular pathology that spares renal glomerules. This condition is named as Fanconi syndrome. Fanconi syndrome can be acquired or inherited; in this instance, it's caused by ifosphamide - a chemotherapeutic that is commonly used in the treatment of pediatric solid tumors (like Wilms).
 
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Fuzuli said:
A 4 year old girl is diagnosed with Wilms' tumor. After surgical resection of her right kidney, she's started on an 18 month chemotherapy course. During the course of her chemotherapy, she starts to have polyuria, polydipsia and failure to thrive. Her control hemogram shows WBC: 7000 with normal differentiation, Hb: 11.9, Plt: 253,000. Her biochemistry panel is: Glucose: 84 (fasting), BUN: 14, Cr: 0.45, AST: 24, ALT:19, Na:134, K:3.3, LDH: 400, Ca: 7,0, P: 1,9, uric acid: 2,1. Her urinary dipstick shows d: 1013, pH: 5, RBC: 0, WBC:0, protein: 2+, glucose: 2+. Capillary blood gas shows pH: 7.31, PaCO2: 30, HCO3-: 13. Her 24-hour urine sample reveals an increase in beta-2 microglobin, calcium, phosphorus, various aminoacids and sodium. What is the most likely etiology explaining her symptoms and lab findings?
Click to expand...


2w6hqfr.gif
 
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An 3 year old girl presents with failure to thrive, foul smelling stools and bowing of her legs. Her mother tells that she was growing normally until 1 years of age. Her physical examination shows a pale child with dental problems, genu varum and costochondral swelling. Her height and weight is below 3rd percentile. Her blood work shows WBC: 8400 with normal differentiation, Hb/Hct: 10,1/30,4, MCV: 105,6, PLT: 199,000. Her physican suspects a malabsorption syndrome and orders fecal acid stercobilin test, which comes back positive. What is the most sensitive and specific serological test to confirm the diagnosis of this patient?
 
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Fuzuli said:
An 3 year old girl presents with failure to thrive, foul smelling stools and bowing of her legs. Her mother tells that she was growing normally until 1 years of age. Her physical examination shows a pale child with dental problems, genu varum and costochondral swelling. Her height and weight is below 3rd percentile. Her blood work shows WBC: 8400 with normal differentiation, Hb/Hct: 10,1/30,4, MCV: 105,6, PLT: 199,000. Her physican suspects a malabsorption syndrome and orders fecal acid stercobilin test, which comes back positive. What is the most sensitive and specific serological test to confirm the diagnosis of this patient?
Click to expand...

sounds like pancreatic insufficiency of some kind so lipase?
 
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Fuzuli said:
It doesn't explain her anemia.
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well you said she had a macrocytic anemia.. a pancreatic insufficiency would lead decreased stimulation of intrinsic factor production and malabsorption of b12 along with the ADEK vitamins.. that could still explain her anemia cant it? And the decreased absorption of vitamin D could lead to Rickets causing her bow-legged deformity..

i still think its pancreas
 
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PokerDoc said:
well you said she had a macrocytic anemia.. a pancreatic insufficiency would lead decreased stimulation of intrinsic factor production and malabsorption of b12 along with the ADEK vitamins.. that could still explain her anemia cant it? And the decreased absorption of vitamin D could lead to Rickets causing her bow-legged deformity..

i still think its pancreas
Click to expand...
cystic fibrosis?

Fuzuli you will have to start giving us options 🙂
 
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kryptik said:
cystic fibrosis?
Click to expand...

could be, it would explain the malabsorption; i didnt realize CF could have that late of a presentation though? Wouldn't you have failure to pass meconium, and non-normal development in year 1?
 
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PokerDoc said:
GI is my crappiest section (pun win) so i'm gonna try this.. I'll say the ileum simply b/c stuff just aint done being processed when it enters the duodenum and the jejunum is never the right answer for anything.

but seriously.. im pretty sure its the ileum. sorta sure?





Why do boys have more GLUT5 receptors than girls?
Click to expand...

Haha it's the jejunum. I had a UWorld question asking where the majority of fat was absorbed and it was jejunum.

I did a little research and apparently the jejunum absorbs the majority of nutrients. Seems like trivial knowledge though.
 
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knuckles said:
Haha it's the jejunum. I had a UWorld question asking where the majority of fat was absorbed and it was jejunum.

I did a little research and apparently the jejunum absorbs the majority of nutrients. Seems like trivial knowledge though.
Click to expand...

i thought the jejunum only absorbs the most water.. but that nutrients were mostly ileum? like all your vitamins, bile, b12, etc. do you have a link to a source on this?
 
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PokerDoc said:
well you said she had a macrocytic anemia.. a pancreatic insufficiency would lead decreased stimulation of intrinsic factor production and malabsorption of b12 along with the ADEK vitamins.. that could still explain her anemia cant it? And the decreased absorption of vitamin D could lead to Rickets causing her bow-legged deformity..

i still think its pancreas
Click to expand...

Pancreatic insufficiency does not cause decreased stimulation of IF production. The role of pancreas is in pancreatic proteases, which cleave R protein from the IF-B12 complex. In adults, severe chronic pancreatitis can cause vitamin B12 deficiency, but it is not typical for pancreatic insufficiencies seen in children (such as CF).

I've looked back at Nelson to see if I've missed anything, but it does not list pancreatic insufficiency as one of the etiologies of vitamin B12 deficiency. But your reasoning is correct: Her problems arise from B12 and D deficiency (among other things).

As for the question, the answer is a type of IgA.
 
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Fuzuli said:
Pancreatic insufficiency does not cause decreased stimulation of IF production. The role of pancreas is in pancreatic proteases, which cleave R protein from the IF-B12 complex. In adults, severe chronic pancreatitis can cause vitamin B12 deficiency, but it is not typical for pancreatic insufficiencies seen in children (such as CF).

I've looked back at Nelson to see if I've missed anything, but it does not list pancreatic insufficiency as one of the etiologies of vitamin B12 deficiency. But your reasoning is correct: Her problems arise from B12 and D deficiency (among other things).

As for the question, the answer is a type of IgA.
Click to expand...


ah; i see now....hmm so IgA deficiency complicating celiac sprue or something?
 
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PokerDoc said:
ah; i see now....hmm so IgA deficiency complicating celiac sprue or something?
Click to expand...

It doesn't have to be with IgA deficiency (Although celiac is indeed associated with IgA deficiency).

Fat malabsorption with B12 and D deficiency is typically seen in Celiac disease. It is due to introduction of gluten containing foods in diet, so think about when babies are given additional food besides breast milk (that explains the 1 year old part). The doctor already shown fat malabsorption for you, so the next step would be to order anti-tissue transglutaminase (TTG) and/or anti-endomysium IgA antibody test, together with serum IgA levels, because of the possible IgA deficiency. Therefore, the answer would be "Anti-TTG IgA and/or anti-endomysium IgA; together with total serum IgA"
 
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PokerDoc said:
i thought the jejunum only absorbs the most water.. but that nutrients were mostly ileum? like all your vitamins, bile, b12, etc. do you have a link to a source on this?
Click to expand...

I've looked up this in Ganong's physiology. There's a table in Gastrointestinal Physiology chapter which compares upper, mid and lower small intestine with colon and there's a note written in the end that says "upper" mainly refers jejunum. According to this table, water and fat soluble vitamins (except B12), long chain fatty acids, Ca2+, Fe2+, Cl- and SO4 are mostly absorbed from jejunum. Conversion of LCFAs to TGs is mostly done in jejunum as well.
 
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Fuzuli said:
I've looked up this in Ganong's physiology. There's a table in Gastrointestinal Physiology chapter which compares upper, mid and lower small intestine with colon and there's a note written in the end that says "upper" mainly refers jejunum. According to this table, water and fat soluble vitamins (except B12), long chain fatty acids, Ca2+, Fe2+, Cl- and SO4 are mostly absorbed from jejunum. Conversion of LCFAs to TGs is mostly done in jejunum as well.
Click to expand...

the_more_you_know.jpg



I feel like this is gonna be on my test now.. GI has just been killing me, i really hope i get this question now.
 
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Dude , I just went through a block of UWorld GI questions and got raped. I thought GI was one of the easier sections. UWorld just turned my world upside down. Lung and Cardio were way easier.
 
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i seem to do fine on UW GI but the hepatobiliary questions have killed me.. they separate it on UW.
 
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PokerDoc said:
yeah i remember that question.. got that wrong haha
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was that the one with the girl with abdominal pain after a sudden weight loss? SMA syndrome? All I can say is thank you to my first year anatomy professor, he loved that question and it was on my anatomy final?
 
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theres more than one answer to the orotic aciduria question.. I cant remember off the top of my head, I remember getting a UW question wrong because i picked OTC since itsthe most common but it was wrong in the context of the question..

I think its orotate phosphoribosyltransferase as well, in pyrimidine synthesis right?
 
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PokerDoc said:
theres more than one answer to the orotic aciduria question.. I cant remember off the top of my head, I remember getting a UW question wrong because i picked OTC since itsthe most common but it was wrong in the context of the question..

I think its orotate phosphoribosyltransferase as well, in pyrimidine synthesis right?
Click to expand...

Yes but that doesn't have ammonia.
 
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In simple terms, confounding bias is when the independent variable that you are looking at doesn't affect the outcome at all but appears to. An effect modification is when more than one independent variable affects the outcome in a non-additive way and the magnitude of the association you see is not because of a single factor.

Example of confounding: women on average are shorter than men and more women wear dresses. So if you look at 2 groups of people with different average heights, you might conclude that wearing dresses cause short height. However, if you separate your groups into separate genders you find that among women and among men, wearing of dresses do not correlate with height at all. Thus, if you take the confounding factor out by stratifying your sample based on that factor, you lose the association.

Example of effect modification: smoking and alcohol can both contribute to esophageal cancer and many people do both. You compare a population of smokers and a population of marathon runners and you find smoking apparently increases risk by 20x. However when you compare smokers and non-smokers at Alcoholics Anonymous, you find the risk increase of smoking on cancer is only 5x. If you go back to the first comparison and stratified the smokers and marathon runners by alcohol intake, you'll find that the real risk increase between smoking and cancer is 5x now.

Just to continue the chain, what's the mechanism of T wave inversion in an old infarct?
 
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jimmyboi said:
What disease is associated with advanced paternal age?
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Achondroplasia (relative risk [RR] = 8–12),

If achondroplasia is not among the answer choices:

Apert syndrome (RR = 9.5),
Pfeiffer syndrome (RR = 6),
Crouzon syndrome (RR = 8),
Neurofibromatosis I (RR = 3.7),
Retinoblastoma (RR = 3–5),
Down syndrome (RR = 1.37–4.5),
Tracheoesophageal fistula (RR = 2.55), and
Autism (RR = 5.75)
Waardenburg syndrome (RR=?)

Q1: Name the dermal muscles, their type and innervation?
Q2: What is Conjoint tendon made of?
Q3: What did Direct Inguinal hernial sac say to Indirect Inguinal hernial sac?
 
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Transposony said:
Achondroplasia (relative risk [RR] = 8–12),

If achondroplasia is not among the answer choices:

Apert syndrome (RR = 9.5),
Pfeiffer syndrome (RR = 6),
Crouzon syndrome (RR = 8),
Neurofibromatosis I (RR = 3.7),
Retinoblastoma (RR = 3–5),
Down syndrome (RR = 1.37–4.5),
Tracheoesophageal fistula (RR = 2.55), and
Autism (RR = 5.75)
Waardenburg syndrome (RR=?)

Q1: Name the dermal muscles, their type and innervation?
Q2: What is Conjoint tendon made of?
Q3: What did Direct Inguinal hernial sac say to Indirect Inguinal hernial sac?
Click to expand...


might be wrong.

1erector pili, smooth muscle, sympathetics?

2internal oblique and transversalis tendon

3"Tsk,Tsk, Look at you, following rules and stuff" or "I'm too big to fit through the hole"



Q. MCC of aseptic meningitis?
 
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Q2. which meningitis has more csf protein and why? Bacterial/viral?

Q3. which among gs,gi,gq are the somatostatin and glucagon receptor?
 
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voicesinmyhead said:
Q2. which meningitis has more csf protein and why? Bacterial/viral?
Click to expand...
Bacterial.
Normal proteins in csf 0.4g/L
In bacterial meningitis, the permeability of the microcirculation of brain increases, protens leak out in csf

voicesinmyhead said:
Q3. which among gs,gi,gq are the somatostatin and glucagon receptor?
Click to expand...
Gs

My question: why overuse of vocal cords results in their inflamation?
 
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Dr..Zainab said:
Bacterial.
Normal proteins in csf 0.4g/L
In bacterial meningitis, the permeability of the microcirculation of brain increases, protens leak out in csf


Gs

My question: why overuse of vocal cords results in their inflamation?
Click to expand...
I have no clue. Can anyone answer this?

Here is my question:

True of False?
Ganglionic blocking drugs prevent changes in heart rate elicited directly by beta1 or M2 agonists.
 
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voicesinmyhead said:
might be wrong.

1erector pili, smooth muscle, sympathetics?

2internal oblique and transversalis tendon

3"Tsk,Tsk, Look at you, following rules and stuff" or "I'm too big to fit through the hole"

Q. MCC of aseptic meningitis?
Click to expand...
Well done.
1. Arrector pili muscles, the walls of blood vessels, and the specialized muscle of genital skin, which includes the scrotum (dartos muscle), vulva and nipple (areolar smooth muscle).
Rest is same.
3. You are always Late(ral).

Q: What complement protein is involved in HUS?
 
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What causes opalascent plasma (as opposed to milky plasma in Chylomicronemia)
Throw me some tough GI qs I can handle them.
 
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