NBME 12 discussion

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1 v max 1 enzyme is 300 and 2 nd 30 compare the Km values

km1 is 10 times km 2
km1 is 1/10 km2
we cant compare


2 upregulation of which protects from ARDS is IL 10

3 which anti hypertensive restores back potassium other k sparing

4 a 14 years old brougt to physian because mostly sleeping withdrawn and complaining of abdomen pain 3 weeks , what history will u take first...should we recretion drug history....options school history , devlopmental, family history

5 a drug given in two patients obese and normal given same doses graph ploted with conc on y axis and time on x , slope of normal person is greater
compared to normal person drug x in obese has

greater VD/ lower bioavailability / higher clearance/ shorter absorption

6 pedigree given four genrations AD 1st genration gene seq 4 5 6 changes to 156 cause...is it recombination

7 cytoplasmic enzyme mutated at 127 alanine replaced by serine why reduction of enzyme activity

1. Vmax tells you only half of the story about Km. Km is the substrate concentration at 1/2 Vmax.

2. IL-10 is anti-inflammatory

3. K+ sparing diuretics and drugs interfering with the RAAS axis will increase K. This is not a perfect question because beta blockers can also increase K. (Or more clinically relevant, someone on continuous albuterol often develops hypo K.)

4. SUICIDE RISK. The kid is depressed. It is of academic interest only as to whether he has relatives with mood disorders. This guy might be planning to end his life in the next day/week/month, don't you think you'd want to uncover that and address it? I'll type it in all caps again if you think it helps. =)

5. Increased volume of distribution. You know that the half life is greater since it takes longer to reach steady state. Since steady states are equivalent, you know that the Clearance is equal. (Css = infusion rate / CL). You can study the half-life equation to convince yourself that if half-life is increased and drug clearance is constant, then Vd must be larger in the fatty.

6. Recombination.

7. Serine's can be phosphorylated as they contain a hydroxyl group. Asparagine's are N-glycosylated. I forget the other choices.

Hope this helps.

In the spinal cord slice, isn't the left anterior horn lesioned when the guy has weakness and muscle atrophy in the intrinsic muscles of his left hand? Missed 6 total, but if my life depended on it, I could not tell you what I'm missing in this Q. Other options are R and L CSTs and the R anterior horn.

thanks for answers ,i thought intrinsic muscle r supplied by cortico spinal then answer would be right C

my friend who is IMG took exam step1 today, and she got 20 questions exactly the same from nbme 12 form, which i thought is bit weird i was always under the impression that nbme are retired step questions

Originally Posted by titan25

thanks for answers ,i thought intrinsic muscle r supplied by cortico spinal then answer would be right C

I am weak at neuro, but here is my thought:

Atrophy implies LMN lesion, thus an anterior horn, nerve root, or peripheral nerve.

Primary motor neurons arise in contralateral cortex, decussate at pyramids, then descend in the lateral CST (ignoring trunk stabilizers in the anterior CST) on the same side as the anterior horns on which they synapse. An anterior horn lesion on the same side as the motor deficit would be expected. Thus, left intrinsic hand muscle atrophy implies left LMN lesion. If it's in the spinal cord, I would think that it's the anterior horn..

Am I doing of this wrong or is NBME? Anyone?

Edit: Alternatively if you got the right letter answer but don't want explain it, that would also be most helpful..

Originally Posted by ScubaStarved

I am weak at neuro, but here is my thought:

Atrophy implies LMN lesion, thus an anterior horn, nerve root, or peripheral nerve.

Primary motor neurons arise in contralateral cortex, decussate at pyramids, then descend in the lateral CST (ignoring trunk stabilizers in the anterior CST) on the same side as the anterior horns on which they synapse. An anterior horn lesion on the same side as the motor deficit would be expected. Thus, left intrinsic hand muscle atrophy implies left LMN lesion. If it's in the spinal cord, I would think that it's the anterior horn..

Am I doing of this wrong or is NBME? Anyone?

Edit: Alternatively if you got the right letter answer but don't want explain it, that would also be most helpful..

hey scuba

were there two answer choices in the anterior horn? If so, the more lateral choice would be the correct answer.

Originally Posted by Encephalectomy

hey scuba

were there two answer choices in the anterior horn? If so, the more lateral choice would be the correct answer.

Thanks a lot. Had been thinking that was the intermediolateral column and that the level was T1, but you are totally right. The intermediolateral column is more pointy.

Originally Posted by ScubaStarved

Thanks a lot. Had been thinking that was the intermediolateral column and that the level was T1, but you are totally right. The intermediolateral column is more pointy.

yup, medial anterior horn is for medial muscles, lateral anterior horn is for lateral/limb muscles, which is why you only really have a boot shaped anterior horn in the parts of the cord that innervate the limbs

40 YO man allergic to grass has basophils taken out of peripheral blood, and incubated with anti-IgE Antibodies. What substance will be present after 1 minute?
Histamine, Leukotriene C4, D4, Major basic protein, prostaglandin D2?

Originally Posted by engineeredout

40 YO man allergic to grass has basophils taken out of peripheral blood, and incubated with anti-IgE Antibodies. What substance will be present after 1 minute?
Histamine, Leukotriene C4, D4, Major basic protein, prostaglandin D2?

I would guess histamine as major basic protein is eosinophils.

Originally Posted by Azadre

I would guess histamine as major basic protein is eosinophils.

Basophils don't release histamine?

Originally Posted by engineeredout

Basophils don't release histamine?

Basophils release histamine

Originally Posted by Azadre

Basophils release histamine

Ok thats my point. I thought that you bind the IgE with anti-IgE antibodies, the basophils don't degranulate, so what is left?

Originally Posted by engineeredout

Basophils don't release histamine?

Originally, I would also pick Histamine. But looking at the question more, I think it may be Major Basic Protein. Having IgE AB'S may prevent basophil release of acute phase reactants like Histamine and Leukortienes. But I think you would still have the late-phase response releasing Eosinophils. Does anyone know the correct answer for sure?

Originally Posted by engineeredout

Ok thats my point. I thought that you bind the IgE with anti-IgE antibodies, the basophils don't degranulate, so what is left?

MOA of Omalizumab, which is basically an IgE AB that prevents degranulation. I assume the question stem is describing this Rx, or something with a very similar MOA. Unfortunately, even after reading this, I'm not sold on what the answer is.

"Mechanism of action

Omalizumab inhibits the binding of IgE to the high-affinity IgE receptor FcεRI by binding to an epitope on IgE that overlaps with the site to which FcεRI binds. This feature is critical to omalizumab's pharmacological effects because a typical anti-IgE antibody can cross-link cell surface FcεRI-bound IgE and induce mediator release from basophils and mast cells. The epitope to which omalizumab binds is sterically hindered by the receptor when IgE is bound to the receptor and is therefore not accessible to omalizumab binding, preventing an inadvertent anaphylactic reaction. However, by binding to IgE in solution, omalizumab prevents IgE binding to cell surface receptor. Although the binding peptide sequence on IgE that is used to bind to low affinity IgE receptor (FcεRII) is different from the sequence used to bind to FcεRI, omalizumab, by steric hindrance, also prevents binding of IgE to FcεRII. Reduction in surface bound IgE on FcεRI-bearing cells limits the degree of release of mediators of the allergic response. Treatment with Xolair also reduces the number of FcεRI receptors on basophils in atopic patients.[5]"

Originally Posted by engineeredout

40 YO man allergic to grass has basophils taken out of peripheral blood, and incubated with anti-IgE Antibodies. What substance will be present after 1 minute?
Histamine, Leukotriene C4, D4, Major basic protein, prostaglandin D2?

That's a bizarre question o_O

Originally Posted by engineeredout

40 YO man allergic to grass has basophils taken out of peripheral blood, and incubated with anti-IgE Antibodies. What substance will be present after 1 minute?
Histamine, Leukotriene C4, D4, Major basic protein, prostaglandin D2?

Until this year, I don't think the omalizumab Ab was in UWorld.

Anyway, you are all overthinking it by 1000%. The IgE on this dude's mast cells and basophils is already attached to the FcEpsilon receptor. It needs to be crosslinked to cause degranulation. The added anti-IgE antibody accomplishes the crosslinking and causes degranulation --> histamine release.

(According to FA, basophils also have LTD4, but that's another issue altogether.)

Apparently omalizumab binds the FcEpsilon binding site on IgE, preventing its association with basophils/mast cells. Wikipedia it if you are so inclined.

Originally Posted by sgod34

Unfortunately, even after reading this, I'm not sold on what the answer is.

"Mechanism of action

Omalizumab inhibits the binding of IgE to the high-affinity IgE receptor FcεRI by binding to an epitope on IgE that overlaps with the site to which FcεRI binds. This feature is critical to omalizumab's pharmacological effects because a typical anti-IgE antibody can cross-link cell surface FcεRI-bound IgE and induce mediator release from basophils and mast cells. The epitope to which omalizumab binds is sterically hindered by the receptor when IgE is bound to the receptor and is therefore not accessible to omalizumab binding, preventing an inadvertent anaphylactic reaction. However, by binding to IgE in solution, omalizumab prevents IgE binding to cell surface receptor. Although the binding peptide sequence on IgE that is used to bind to low affinity IgE receptor (FcεRII) is different from the sequence used to bind to FcεRI, omalizumab, by steric hindrance, also prevents binding of IgE to FcεRII. Reduction in surface bound IgE on FcεRI-bearing cells limits the degree of release of mediators of the allergic response. Treatment with Xolair also reduces the number of FcεRI receptors on basophils in atopic patients.[5]"

Bolded. It's a temporal thing. Omalizumab scavenges the circulating IgE before it can be captured by basophils.

Took the test today and histamine was the right answer.

Originally Posted by sgod34

MOA of Omalizumab, which is basically an IgE AB that prevents degranulation. I assume the question stem is describing this Rx, or something with a very similar MOA. Unfortunately, even after reading this, I'm not sold on what the answer is.

"Mechanism of action

Omalizumab inhibits the binding of IgE to the high-affinity IgE receptor FcεRI by binding to an epitope on IgE that overlaps with the site to which FcεRI binds. This feature is critical to omalizumab's pharmacological effects because a typical anti-IgE antibody can cross-link cell surface FcεRI-bound IgE and induce mediator release from basophils and mast cells. The epitope to which omalizumab binds is sterically hindered by the receptor when IgE is bound to the receptor and is therefore not accessible to omalizumab binding, preventing an inadvertent anaphylactic reaction. However, by binding to IgE in solution, omalizumab prevents IgE binding to cell surface receptor. Although the binding peptide sequence on IgE that is used to bind to low affinity IgE receptor (FcεRII) is different from the sequence used to bind to FcεRI, omalizumab, by steric hindrance, also prevents binding of IgE to FcεRII. Reduction in surface bound IgE on FcεRI-bearing cells limits the degree of release of mediators of the allergic response. Treatment with Xolair also reduces the number of FcεRI receptors on basophils in atopic patients.[5]"

I can see why the answer was histamine. The question probably wasn't asking specifically about omalizumab but rather any anti-IgE Ab, in which it would release histamine.

Originally Posted by ScubaStarved

Until this year, I don't think the omalizumab Ab was in UWorld.

Anyway, you are all overthinking it by 1000%. The IgE on this dude's mast cells and basophils is already attached to the FcEpsilon receptor. It needs to be crosslinked to cause degranulation. The added anti-IgE antibody accomplishes the crosslinking and causes degranulation --> histamine release.

(According to FA, basophils also have LTD4, but that's another issue altogether.)

Apparently omalizumab binds the FcEpsilon binding site on IgE, preventing its association with basophils/mast cells. Wikipedia it if you are so inclined.

Yeah, I think they added in the omalizumab question into UW only within the past couple of months; it's still a fairly easy question anyway.

That makes sense; you have to cross link 2+ IgE on the surface to release histamine

Just took this exam yesterday question: they said that a disease had an incidence of 1/40000 and they asked what are the chances that a guys wife is a carrier.
I figured if homozygous was 1/40000 then sq root of 40000 would be the carrier frequency... I was wrong and I have no clue what else it could be

p^2 + 2pq + q^2 == 1. 2pq is the carrier rate, which is obvious if you draw the allele table.

Originally Posted by ScubaStarved

p^2 + 2pq + q^2 == 1. 2pq is the carrier rate, which is obvious if you draw the allele table.

lol freaking Hardy Weinberg.....
thanks

deleting..

Q: man brought into the ER after having blunt trauma to abdomen in MVA. BP - 70/40 mmHG; P/E shows abdominal distention and diffuse tenderness in Left upper quadrant, bowel sounds decreased. which of the following sets occur as a result of sympathetic reflex compensation induced by this patients condition?

the answer choices are a bunch of mixed choices between: arterial constriction or dilation, venous constriction or dilation, and heart rate increased or decreased.

what would happen to this pt with increased sympathetic response...

Kid has pertussis, which turns the Gi subunit off, and increases AC.

I think. Glycolysis is low and gluconeogenesis is high.

Partial agonism

B. The mutation is the one at the beginning of the intron, the sequence of which is important for proper spliceosome formation. The FA page is actually good for this, but the details are subtle.

Originally Posted by Merit2011

Q: man brought into the ER after having blunt trauma to abdomen in MVA. BP - 70/40 mmHG; P/E shows abdominal distention and diffuse tenderness in Left upper quadrant, bowel sounds decreased. which of the following sets occur as a result of sympathetic reflex compensation induced by this patients condition?

the answer choices are a bunch of mixed choices between: arterial constriction or dilation, venous constriction or dilation, and heart rate increased or decreased.

what would happen to this pt with increased sympathetic response...

Constriction of everything and increased HR. The large veins are said to be "capacitance vessels" and their elasticity decreases with exercise, hypovolemia, etc. An alpha-1 mediated effect, I think. This guy will be cold and has hypovolemic shock.

Contrast this scenario with a patient with shock due to infection (sepsis), who will have warm extremities due to pathologically dilated arterioles.

Few questions which I feel like I shouldn't have missed but did... oh well:

1. Man comes in because of infertility, he's 6ft2, BMI 24, PE shows small testes, semen shows no sperm - what's wrong?

Answer choices: chromosomal analysis of lymphocytes, cystic fibrosis mutation, DNA for trinucleotide repeats in FRAX, FISH analysis of subtelomeres (this was my answer), and SRY gene sequencing

2. Woman comes in with clear renovascular hypertension (increased renin in the right renal vein, normal in the left renal vein) probably due to renal artery stenosis, has slightly low potassium. Systemic HTN in this patient is mediated by a vasoconstricter released from which of the following?

Answers: adrenal medullary chromaffin cells, glomerular efferent arteriole, glomerular afferent arteriole, pulmonary vasculature, renal JGA cells (I had no idea what to put for this one because I thought it was Ang II... and none of these things actually make Ang II to my knowledge...)

3. 2 year old boy with hydrocephalus, CT shows cystic dilation of 4th ventricle, hypoplasia of cerebellar hemispheres, enlarged posterior fossa with high tentorium cerebelli; what part of neural tube in development was defective?

Answers: diencephalon, mesencephalon, metencephalon, prosencephalon, spinal cord, telencephalon (i thought this was straightforward aqueductal stenosis and ansewred mesencephalon, but i'm not sure)

4. 70 y/o male with 6 month history of abnormal sleep behavior, punches at the air and yells as if acting out his dreams but doesn't wake up, and often falls on the floor; no abnormality on neuro exam, what would you find in patient?

Answers: absent muscle atonia in REM, anterior cingulate mass lesion, major depressive disorder with psychotic features, left temporal EEG spikes, nocturnal hypoglycemia (no clue about this, i said left temporal EEG, but it could also be muscle atonia absent in REM)

5. 3 month old boy with hypoglycemia, hypoketonemia, lactic acidosis, and hypercholesterolemia 4 hours after feeding; giving glucagon does not increase blood glucose and only worsens lactic acidosis by increasing lactate; what enzyme deficiency is this?

Answers: Fructose 1,6 bisphosphatase, Galactose 1 phosphate uridyltransferase, glucose-6-phosphatase, alpha 1,4 glucosidase, MCAD deficiency (said MCAD deficiency, was between this and glucose-6-phosphate)

6. 22 y/o man faints while waiting for inoculations in line; his BP and pulse on fainting are 50 mmHg systolic and 45/min; on arousal BP and pulse were 88/min and 100/70; what is the cause?

Answers: aortic stenosis, hypertrophic cardiomyopathy, increased parasympathetic tone, third degree AV block, ventricular tachycardia (said HCM because of his age and maybe he had a syncopal episode, apparently that was wrong, so...)

The other mistakes I made were all inevitably stupid mistakes... these are the only ones I was confused on (ugh). Help is appreciated, thanks!

Originally Posted by ArcGurren

Few questions which I feel like I shouldn't have missed but did... oh well:

1. Man comes in because of infertility, he's 6ft2, BMI 24, PE shows small testes, semen shows no sperm - what's wrong?

Answer choices: chromosomal analysis of lymphocytes, cystic fibrosis mutation, DNA for trinucleotide repeats in FRAX, FISH analysis of subtelomeres (this was my answer), and SRY gene sequencing

2. Woman comes in with clear renovascular hypertension (increased renin in the right renal vein, normal in the left renal vein) probably due to renal artery stenosis, has slightly low potassium. Systemic HTN in this patient is mediated by a vasoconstricter released from which of the following?

Answers: adrenal medullary chromaffin cells, glomerular efferent arteriole, glomerular afferent arteriole, pulmonary vasculature, renal JGA cells (I had no idea what to put for this one because I thought it was Ang II... and none of these things actually make Ang II to my knowledge...)

3. 2 year old boy with hydrocephalus, CT shows cystic dilation of 4th ventricle, hypoplasia of cerebellar hemispheres, enlarged posterior fossa with high tentorium cerebelli; what part of neural tube in development was defective?

Answers: diencephalon, mesencephalon, metencephalon, prosencephalon, spinal cord, telencephalon (i thought this was straightforward aqueductal stenosis and ansewred mesencephalon, but i'm not sure)

4. 70 y/o male with 6 month history of abnormal sleep behavior, punches at the air and yells as if acting out his dreams but doesn't wake up, and often falls on the floor; no abnormality on neuro exam, what would you find in patient?

Answers: absent muscle atonia in REM, anterior cingulate mass lesion, major depressive disorder with psychotic features, left temporal EEG spikes, nocturnal hypoglycemia (no clue about this, i said left temporal EEG, but it could also be muscle atonia absent in REM)

5. 3 month old boy with hypoglycemia, hypoketonemia, lactic acidosis, and hypercholesterolemia 4 hours after feeding; giving glucagon does not increase blood glucose and only worsens lactic acidosis by increasing lactate; what enzyme deficiency is this?

Answers: Fructose 1,6 bisphosphatase, Galactose 1 phosphate uridyltransferase, glucose-6-phosphatase, alpha 1,4 glucosidase, MCAD deficiency (said MCAD deficiency, was between this and glucose-6-phosphate)

6. 22 y/o man faints while waiting for inoculations in line; his BP and pulse on fainting are 50 mmHg systolic and 45/min; on arousal BP and pulse were 88/min and 100/70; what is the cause?

Answers: aortic stenosis, hypertrophic cardiomyopathy, increased parasympathetic tone, third degree AV block, ventricular tachycardia (said HCM because of his age and maybe he had a syncopal episode, apparently that was wrong, so...)

The other mistakes I made were all inevitably stupid mistakes... these are the only ones I was confused on (ugh). Help is appreciated, thanks!

1. Klinefelter's, look for the Barr body in easily obtainable cells.

2. Pulm vasculature. I believe the idea is an outdated one (at least so we were told by lecturers), but ACE is present in high amounts at capillary beds. FA "covers" this in the renal chapter with a picture of the lungs in the AngII discussion. This was quite tricky, actually, and should serve as a reminder to read all choices.

3. That's Dandy-Walker and is from absent formation of the 4th vent. If I remember correctly, Met is the right answer. (e.g., no cerebellar vermis which arises from Met). Between Met and Myencephalon, I don't know how you would pick. Luckily Mye was not a choice.

4. No muscle atonia in REM. FA covers this fairly well in Behavioral chapter.

5. Took me a while to figure this one out, but you've copied it wrong. I had to go to my test to find this out. The boy has increased ketones and hepatosplenomegaly. Increased ketones rules out MCAD/LCAD and Carnitine transfer deficiencies. The time course is also much better for a disorder of gluconeogenesis than one of impaired FA oxidation.

6. Parasympathetic outflow is responsible for the vasovagal response (aka neurocardiogenic syncope), which is a fancy way of saying "fainting." People faint when anxious (giving blood, needles, etc.) and can experience warmth, nausea, and light-headedness prior to going out. Think about the important diagnostic points separating cardiac syncope (all the other causes listed) from fainting and seizures. This is more of a third year thing, admittedly. As a test taking skill, you should also note that all the others imply structural damage to the heart and would be unlikely in a young military recruit who is undergoing BT. Another place this skill is useful is in lung pathology questions: separate obstructive from restrictive answer choices, increased A-a gradient choices from normal A-a choices, increased AG met acidosis from normal AG choices, and so on.

Edit: Just wanted to add that these are tough questions and if you can minimize your careless errors on test day you'll likely do super. For my own education, what were you looking for with FISH of subtelomeres in the infertile man?

Originally Posted by ScubaStarved

For my own education, what were you looking for with FISH of subtelomeres in the infertile man?

not sure what arc was looking for necessarily (and i agree, those were all hard questions so good job!), but I guess isolated telomerase failure in the gonads could lead to aspermia (your stem cells and cancer cells express telomerase so that they can keep dividing forever, if you had deficient telomerase in your testis for some reason I guess that could make you infertile because your spermatogonia would stop dividing.)

thats my best stab at that answer choice anyways

somebody else got it

[QUOTE=BTC;10965734]2. Renin is secreted by juxtaglomerular cells.
[QUOTE]

I agree with all your other choices, except number 2. Yes, rein is released by JGA cells (which trigger low BP in the afferent), but since the question specifically asked where is the systemic vasoconstricter released from, I believe they specifically where looking for angiotensin, which is released from the lungs, and later converted to AT2 by ACE. Personally, I can't stand questions like this because it's somewhat hard to understand and interrupt what they exactly want to know on a topic that isn't very difficult in my opinion. I can think of ways to justify pulmonary vasculature, afferent, efferent and JGA cells to be the answer.

Originally Posted by ScubaStarved

1. Klinefelter's, look for the Barr body in easily obtainable cells.

2. Pulm vasculature. I believe the idea is an outdated one (at least so we were told by lecturers), but ACE is present in high amounts at capillary beds. FA "covers" this in the renal chapter with a picture of the lungs in the AngII discussion. This was quite tricky, actually, and should serve as a reminder to read all choices.

3. That's Dandy-Walker and is from absent formation of the 4th vent. If I remember correctly, Met is the right answer. (e.g., no cerebellar vermis which arises from Met). Between Met and Myencephalon, I don't know how you would pick. Luckily Mye was not a choice.

4. No muscle atonia in REM. FA covers this fairly well in Behavioral chapter.

5. Took me a while to figure this one out, but you've copied it wrong. I had to go to my test to find this out. The boy has increased ketones and hepatosplenomegaly. Increased ketones rules out MCAD/LCAD and Carnitine transfer deficiencies. The time course is also much better for a disorder of gluconeogenesis than one of impaired FA oxidation.

6. Parasympathetic outflow is responsible for the vasovagal response (aka neurocardiogenic syncope), which is a fancy way of saying "fainting." People faint when anxious (giving blood, needles, etc.) and can experience warmth, nausea, and light-headedness prior to going out. Think about the important diagnostic points separating cardiac syncope (all the other causes listed) from fainting and seizures. This is more of a third year thing, admittedly. As a test taking skill, you should also note that all the others imply structural damage to the heart and would be unlikely in a young military recruit who is undergoing BT. Another place this skill is useful is in lung pathology questions: separate obstructive from restrictive answer choices, increased A-a gradient choices from normal A-a choices, increased AG met acidosis from normal AG choices, and so on.

Edit: Just wanted to add that these are tough questions and if you can minimize your careless errors on test day you'll likely do super. For my own education, what were you looking for with FISH of subtelomeres in the infertile man?

1. Thanks very much for your help and support. I'm not really sure what I was looking for in that question to be honest, I picked the answer which most closely suggested a chromosomal analysis; I knew it wasn't cystic fibrosis, Fragile X, etc. This is like the second time I've forgotten that Klinefelter's = Barr body on some question so I'mma write that down and never forget.

2. I actually picked pulmonary vasculature initially b/c of ACE production in the lungs but didn't think Ang II was made from there either... this question was kinda mean but oh well, now I know, lol

3. That makes a whole lot more sense; guess I need to review my brain embryology as well

4. Obviously I need to reread the behavioral part of FA too, I was considering that one and then picked another one (fml)

5. ARGH I read it as hypoketonemia, fml. I should probably slow down when reading this sort of question, I sort of sped through it -___-

6. I think I was thrown off b/c I've read somewhere that HCM can also cause syncope from the outflow obstruction, but I guess the "nervous" situation was more of a giveaway for vasovagal syncope.

And thanks again - I know for a fact the other questions I got wrong were because I think I had a headache while doing it so my score should easily have been 10 points higher than it was... oh well, I have about a week to make sure I shore up the extra stuff to study and I'll have to work triple hard to avoid stupid mistakes on exam day.

I had another question from the exam which I'm still not sure about:

40 y/o woman comes in with joint pain, swelling of her PIP, wrist, knees, increased ESR with a normocytic normochromic anemia; serum is positive for rheumatoid factor, what would you see in the synovium?

Answers: All up/down arrows, with complement, segmented neutrophils, IL-1, TNF

I know it has a chronic infiltrate of plasma cells/lymphocytes, but I'm at a loss for the IL-1 and TNF (both increased since inflammatory?)

Originally Posted by ArcGurren

I had another question from the exam which I'm still not sure about:

40 y/o woman comes in with joint pain, swelling of her PIP, wrist, knees, increased ESR with a normocytic normochromic anemia; serum is positive for rheumatoid factor, what would you see in the synovium?

Answers: All up/down arrows, with complement, segmented neutrophils, IL-1, TNF

I know it has a chronic infiltrate of plasma cells/lymphocytes, but I'm at a loss for the IL-1 and TNF (both increased since inflammatory?)

Complement down, PMNs, IL1 and TNF up.

Originally Posted by ScubaStarved

Complement down, PMNs, IL1 and TNF up.

Thanks once again!

Originally Posted by ScubaStarved

Complement down, PMNs, IL1 and TNF up.

Is complement decreased because it is being used more? Thanks!

I received an email informing me that it is against the rules, so I am deleting any posts...

A couple of Qs if anyone has the time. Thanks a lot!


1) the fracture of fibular neck one: narrowed it down to 2, it was between:
a) pain over proximal fibula: absent ..... pain over distal fibula: present
b) pain over proximal fibula: present ..... pain over distal fibula: absent

I picked A) because, I thought if you sever a nerve, symptoms appear distal to the lesion. I'm assuming it's b) ... is my reasoning inverted?


2) Medulla cross-section slice.. pt. had ringing in right ear
- midline structures were medial lemniscus, inferior most was pyramids, so I'm assuming it was the lateral-most structures at the top of the pic. Was that pointing to the Vestibular nuclei? And would it be an ipsilateral lesion? R. lesion --> R. loss of hearing?

3) 6 year old boy coughing, wheezing, upper resp infection 2 wks ago, high pulse, high RR, insp and exp wheezes, decreased tactile fremitus
- was picking between asthma and atelectasis... picked atelectasis. why asthma?

4) newborn with harsh left upper sternal border murmur, 3 hours later.. diastolic component, 12 hours later.. no murmur --> I picked VSD w/ r-2-l shunt.. thought these were harsh systolic murmurs

5) Pedigree with the:
1 | 4
2 | 5
3 | 6

1| 1
2| 5
3| 6

I honestly have no idea how to approach this type of Q. Forget the answer, I don't even know what the fawk the numbers are referring to. Are they talking about 2 alleles separated by the "|" and different foci on them?? but aren't all foci on an allele inherited together? no fckin idea. If someone could even explain what the numbers mean... let alone the answer, I'd be very very grateful.

6) Duchenne hemizygous - hows it possible? I put 45,X since it's X linked, and thought he'd have "half" of expression as a result... resulting in a "hemizygous" phenotype

7) woman w/heavy menstrual bleeding + gingival hemorrhages. They gave a pic. of bone marrow. Had no idea wtf I was looking at. Only platelet counts were down.. so narrowed it to ITP and TTP --> picked TTP.

8) pancreatic cancer... was the answer low duodenal ph?

9) glycosylation of proteins for hepatocyte export.. where?

10) nerve regeneration after keratin gel --> wtf? I put undifferentiated stem cells

11) B-thalassemia mutations.. g->a mut at 246 leads to ATT... only way this can be a stop codon is if you find the complement in the reverse direction, leading to UAA --> but how can this be consistent, esp if the question underlines ATG, which basically shows u are looking at the (+) sense DNA equivalent of mRNA?

12) was gonna pick myxoma, but pt. was 18 and too young.. so I picked mural wall thrombus

13) AML patient w/bone marrow transplant.. symptoms 2 months later w/ pic.. can never tell if that red stuff is blood or eosinophils or some sort --> decreased function of what led to this condition?

14) integrin vs. iCAM-1? I picked integrin.. but that was wrong

15) transplant q: was it "i want to be sure i understand your concerns about getting a transplant"?


chromosome analysis of lymphocytes was tricky as hell.. I mean, why not epithelial cells or something!? ya know

and the ACE q, I did get right b/c I assumed it was a trick q. But ACE is made in the lung... ang I is made in the liver and converted to ang II. So I'd think the answer should have included a liver option.

1) the fracture of fibular neck one: narrowed it down to 2, it was between:
a) pain over proximal fibula: absent ..... pain over distal fibula: present
b) pain over proximal fibula: present ..... pain over distal fibula: absent

I picked A) because, I thought if you sever a nerve, symptoms appear distal to the lesion. I'm assuming it's b) ... is my reasoning inverted?

It's a Common Peroneal injury, so you loose the sensation near the bottom of the leg (dorsum of foot)

2) Medulla cross-section slice.. pt. had ringing in right ear
- midline structures were medial lemniscus, inferior most was pyramids, so I'm assuming it was the lateral-most structures at the top of the pic. Was that pointing to the Vestibular nuclei? And would it be an ipsilateral lesion? R. lesion --> R. loss of hearing?

I used motor is medial and sensory is lateral and I thought about where the vestibular nerve would come from, but I am terrible at neuroanatomy.

3) 6 year old boy coughing, wheezing, upper resp infection 2 wks ago, high pulse, high RR, insp and exp wheezes, decreased tactile fremitus
- was picking between asthma and atelectasis... picked atelectasis. why asthma?

I picked asthma I think because of the insp and exp wheeze (and that he is 6)


4) newborn with harsh left upper sternal border murmur, 3 hours later.. diastolic component, 12 hours later.. no murmur --> I picked VSD w/ r-2-l shunt.. thought these were harsh systolic murmurs

Continuous murmor that goes away: PDA

5) Pedigree with the:
1 | 4
2 | 5
3 | 6

1| 1
2| 5
3| 6

I honestly have no idea how to approach this type of Q. Forget the answer, I don't even know what the fawk the numbers are referring to. Are they talking about 2 alleles separated by the "|" and different foci on them?? but aren't all foci on an allele inherited together? no fckin idea. If someone could even explain what the numbers mean... let alone the answer, I'd be very very grateful.

They're chromosomes and the numbers are alleles. The point of the question is that you have an allele crossing over.

6) Duchenne hemizygous - hows it possible? I put 45,X since it's X linked, and thought he'd have "half" of expression as a result... resulting in a "hemizygous" phenotype
Wasn't the question about a woman who developed the symptoms in her 30s? I said she had unfortunate lyonization because the other answers didn't make as much sense.


7) woman w/heavy menstrual bleeding + gingival hemorrhages. They gave a pic. of bone marrow. Had no idea wtf I was looking at. Only platelet counts were down.. so narrowed it to ITP and TTP --> picked TTP.
When differentiating between ITP and TTP clinically, a useful marker is the shape of the RBC. The RBC was normal, so it's ITP.

8) pancreatic cancer... was the answer low duodenal ph?

Yep. I didn't necessarily agree with that one.

9) glycosylation of proteins for hepatocyte export.. where?
If I had to guess, golgi apparatus. I don't remember.

10) nerve regeneration after keratin gel --> wtf? I put undifferentiated stem cells
It helped direct schwan cell regeneration, I think.

11) B-thalassemia mutations.. g->a mut at 246 leads to ATT... only way this can be a stop codon is if you find the complement in the reverse direction, leading to UAA --> but how can this be consistent, esp if the question underlines ATG, which basically shows u are looking at the (+) sense DNA equivalent of mRNA?

It's not that you get a stop codon, you're removing the consensus sequence for intron removal.

12) was gonna pick myxoma, but pt. was 18 and too young.. so I picked mural wall thrombus

It's myxoma.

13) AML patient w/bone marrow transplant.. symptoms 2 months later w/ pic.. can never tell if that red stuff is blood or eosinophils or some sort --> decreased function of what led to this condition?
tcells because she was immunosuppreased from her bone marrow transplant.

14) integrin vs. iCAM-1? I picked integrin.. but that was wrong

Selectins bind to SiyalLewisx

15) transplant q: was it "i want to be sure i understand your concerns about getting a transplant"?

Probably

chromosome analysis of lymphocytes was tricky as hell.. I mean, why not epithelial cells or something!? ya know

He had klinefelter's I think, and any somatic cell can be used.

and the ACE q, I did get right b/c I assumed it was a trick q. But ACE is made in the lung... ang I is made in the liver and converted to ang II. So I'd think the answer should have included a liver option.

The active form is made in the lung.

thanks a lot! ^

so for the PDA one, I'm assuming it closed a few hours after, right? I didn't think you'd hear a murmur even a couple of hours after birth.. because I thought it closed immediately upon the first breath.

Originally Posted by hyrule

thanks a lot! ^

so for the PDA one, I'm assuming it closed a few hours after, right? I didn't think you'd hear a murmur even a couple of hours after birth.. because I thought it closed immediately upon the first breath.

Yeah, I guess so. What was wrong with the 20something who had the imaging done. I thought maybe he was aganglionic (that was wrong) but maybe it was malrotation.

Originally Posted by Azadre

Yeah, I guess so. What was wrong with the 20something who had the imaging done. I thought maybe he was aganglionic (that was wrong) but maybe it was malrotation.

malrotation i think

also lyonization vs. complete absence of 1 X chromosome - what's the difference?

is it that you'd automatically have turner's with XO? something we're just supposed to memorize?

Originally Posted by hyrule

also lyonization vs. complete absence of 1 X chromosome - what's the difference?

is it that you'd automatically have turner's with XO? something we're just supposed to memorize?

I think so.

congenital anomaly, NNT

was the answer 0?

Originally Posted by hyrule

congenital anomaly, NNT

was the answer 0?

Yeah, it was a mitochondrial disease.

Originally Posted by Azadre

Yeah, it was a mitochondrial disease.

are we talking about the same question? the biostats one.. with number needed to treat with folic acid vs. the other supplement