NBME 12 discussion

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titan25

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4 a 14 years old brougt to physian because mostly sleeping withdrawn and complaining of abdomen pain 3 weeks , what history will u take first...should we recretion drug history....options school history , devlopmental, family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

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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
 
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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 :confused:
 
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..
 
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.
 
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.
 
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?
 
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?
 
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. :rolleyes:

"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]"
 
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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
 
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. :laugh:

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

"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.
 
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. :rolleyes:

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

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
 
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.
 
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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.
 
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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!
 
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?
 
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
 
2. Renin is secreted by juxtaglomerular cells.
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.
 
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?)
 
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.
 
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.
 
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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.
 
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?
 
congenital anomaly, NNT

was the answer 0?

I Think the question you are referring to was the NNT for folic acid treatment? i think the answer was 100.

NNT = 1/(CONTROL EVENT RATE - TX EVENT RATE)

NNT = 1/ARR
ARR = control event rate – tx event rate
ARR = .023 -.013 = 0.01
NNT = 1/0.01 = 100
 
1. experiment on effects of ATP in renal fxn --> inhibit mitochondria (no ATP). which nephron segment has the greatest decrease in Na reabsorption?

I know PCT is the major site but I thought it was mostly passive?

2. Pt with PMH of MS presents with a confusion, stupor, fever, dec respirations, low BP, dec lung volumes, clear to auscultation, minimal gag and distant breath sounds. There's arterial blood gas that shows respiratory acidosis.

what's the most likely cause?: UA obstruction, PE, ARDS, opioid OD

3. man with alcoholic cirrhosis, has petechia and easy bruising. labs show pancytopenia and MCV of 102, inc retics, what's the cause of pancytopenia?

hypersplenism, iron def, DIC, vit C def

4. for the hardy weinberg one, i still don't see how you go from incidence to 2pq? Sorry my brain isnt working

5. 3 yr old with bilat gluteal muscle weakness, intermittent pain in his legs at night, fracture of right fibula.

what confirms dx? ESR, serum creat kinase, hydroxyproline conc, Ig serum RF
 
1) Woman smells of piss. How do you confront?
I put: are you having any problems you're too embarrassed to talk about? would you be willing to talk about them today?
I think the right ans. is: I know this can be an embarrassing topic, but some ppl have difficulty holding their urine when they get older. Is this prb for you?

Not sure why my ans. is incorrect but was stuck b/t the two.

2) A CXR w/ hx of 3 days of shoulder/ab pain and acute peritonitis:
ileus, intraperitoneal abscess (incorrect), nephrolithiasis, perforated viscus, retained foreign body?

3) Jaundice due to mass @ pancreatic head. Tx:
cholecystectomy (incorrect), stent in common bile duct, stent in cystic duct?

4) Boy w/ abscesses in hair follicles. G+. Where is long-term carriage?
lips, mouth, nares, scalp, urethra

5) Necrosis of renal tubular cells w/o damage to stroma/glomeruli. What would happen to kidney if the pt survived?
Diffuse renal scarring (incorrect), renal atrophy, hyperplasia, hypertrophy, nl renal architecture

6) What causes neutrophil chemotaxis and oxidative metabolism?
Adenylyl cyclase, myeloperoxidase (incorrect), NADPH oxidase, PLC, PKC

7) (repeated from above me) Kid w/ R fibula fracture w/ bilateral gluteal weakness. What would confirm dx?
ESR, serum CK, serum hydroxyproline, serum Ig (incorrect), serum RF

8) Boy w/ periorbital edema, hypoalbuminemia, proteinuria and shows picture of a glomerulus:
Diabetic glomerulosclerosis, diffuse proliferative nephritis, focal GN, focal segmental glomerulosclerosis, membranous nephropathy (incorrect), minimal change, PIGN

9) Elderly man presents w/ confusion, distended bladder, enlarged prostate, elevated Cr and BUN. Dx?
BPH, bladder malignancy, neurogenic bladder (incorrect), renal cell ca., urolithiasis. My next guess would be BPH but I don't get why the confusion.

10) (repeated from above me) pt w/ petechiae, bruising, EtOH cirrhosis, portal htn - what causes his pancytopenia?
DIC, hypersplenism, Fe def, thiamine def. (incorrect), vitC def?

11) med that decreases preload and increases coronary flow has what mechanism?
Ca conductance (incorrect), cAMP synthesis, cGMP synthesis, K conductance, PG synthesis, Na conductance

12) man playing golf exp severe chest pain. tachypnic, tachycardic, pallor/diaphoresis, crackers heard halfway up bases of lungs
bunch of ups/downs for hydrostatic/oncotic pressure. I picked decrease oncotic pressure in pulmonary artery b/c I thought that would increase the driving force of fluid to enter the lungs but don't really know what's going on here


Thx in advance!
 
1. experiment on effects of ATP in renal fxn --> inhibit mitochondria (no ATP). which nephron segment has the greatest decrease in Na reabsorption?

I know PCT is the major site but I thought it was mostly passive?

2. Pt with PMH of MS presents with a confusion, stupor, fever, dec respirations, low BP, dec lung volumes, clear to auscultation, minimal gag and distant breath sounds. There's arterial blood gas that shows respiratory acidosis.

what's the most likely cause?: UA obstruction, PE, ARDS, opioid OD

3. man with alcoholic cirrhosis, has petechia and easy bruising. labs show pancytopenia and MCV of 102, inc retics, what's the cause of pancytopenia?

hypersplenism, iron def, DIC, vit C def

4. for the hardy weinberg one, i still don't see how you go from incidence to 2pq? Sorry my brain isnt working

5. 3 yr old with bilat gluteal muscle weakness, intermittent pain in his legs at night, fracture of right fibula.

what confirms dx? ESR, serum creat kinase, hydroxyproline conc, Ig serum RF

1. I think the Na absorption is passive at the luminal end but at the basolateral side, Na/K ATPase is driving all Na transport so it's PCT b/c that's where most of Na is reabsorbed.

4. HW incidence of homozygous recessive = q^2 so you take the # and square root it to get q. 1-q = p. Incidence of heterozygous is 2pq and you just solved for p and q. I think the calculation came out to:

1/40000 = incidence --> q = 1/200 --> p = 1-q = 1-(1/200) = 199/200 (essentially 1)
q = 1/200
p = 1
2pq = heterozygous incidence = 1/100
 
1) Woman smells of piss. How do you confront?
I put: are you having any problems you're too embarrassed to talk about? would you be willing to talk about them today?
I think the right ans. is: I know this can be an embarrassing topic, but some ppl have difficulty holding their urine when they get older. Is this prb for you?

Not sure why my ans. is incorrect but was stuck b/t the two.

2) A CXR w/ hx of 3 days of shoulder/ab pain and acute peritonitis:
ileus, intraperitoneal abscess (incorrect), nephrolithiasis, perforated viscus, retained foreign body?

3) Jaundice due to mass @ pancreatic head. Tx:
cholecystectomy (incorrect), stent in common bile duct, stent in cystic duct?

4) Boy w/ abscesses in hair follicles. G+. Where is long-term carriage?
lips, mouth, nares, scalp, urethra

5) Necrosis of renal tubular cells w/o damage to stroma/glomeruli. What would happen to kidney if the pt survived?
Diffuse renal scarring (incorrect), renal atrophy, hyperplasia, hypertrophy, nl renal architecture

6) What causes neutrophil chemotaxis and oxidative metabolism?
Adenylyl cyclase, myeloperoxidase (incorrect), NADPH oxidase, PLC, PKC

7) (repeated from above me) Kid w/ R fibula fracture w/ bilateral gluteal weakness. What would confirm dx?
ESR, serum CK, serum hydroxyproline, serum Ig (incorrect), serum RF

8) Boy w/ periorbital edema, hypoalbuminemia, proteinuria and shows picture of a glomerulus:
Diabetic glomerulosclerosis, diffuse proliferative nephritis, focal GN, focal segmental glomerulosclerosis, membranous nephropathy (incorrect), minimal change, PIGN

9) Elderly man presents w/ confusion, distended bladder, enlarged prostate, elevated Cr and BUN. Dx?
BPH, bladder malignancy, neurogenic bladder (incorrect), renal cell ca., urolithiasis. My next guess would be BPH but I don't get why the confusion.

10) (repeated from above me) pt w/ petechiae, bruising, EtOH cirrhosis, portal htn - what causes his pancytopenia?
DIC, hypersplenism, Fe def, thiamine def. (incorrect), vitC def?

11) med that decreases preload and increases coronary flow has what mechanism?
Ca conductance (incorrect), cAMP synthesis, cGMP synthesis, K conductance, PG synthesis, Na conductance

12) man playing golf exp severe chest pain. tachypnic, tachycardic, pallor/diaphoresis, crackers heard halfway up bases of lungs
bunch of ups/downs for hydrostatic/oncotic pressure. I picked decrease oncotic pressure in pulmonary artery b/c I thought that would increase the driving force of fluid to enter the lungs but don't really know what's going on here


Thx in advance!

1) I was stuck between the 2 as well. Picked the latter one eventually. I'm not really sure why that one was right, but I picked it because it was a polite way of addressing her issue more directly than the first.

2) I think I saw some air in the peritoneum on the CXR. Might have been hallucinating but I went with perforated viscus because I thought some of the contents might have irritated the diaphragm, leading to the shoulder pain.

3) This question implies that the pancreatic head is obstructing something leading to jaundice. The common bile duct is adjacent to the pancreatic head and is likely to be obstructed.

4) Thought of Staph Aureus. Located in the nose.

5) ATN. As far as I know, everything should go back to normal if they live in most cases.

6) I wasn't really sure about this. I didn't think it was either myeloperoxidase or NADPH oxidase. Since PKC is linked to PLC, I chose adenylate cyclase.

7) Thought this was Duchenne's w/ the fibular fracture as a distractor. Picked serum CK.

8) Kid w/ nephrotic syndrome. Most common cause is minimal change disease w/ no changes of glomerulus on LM.

9) I thought it was BPH. Confusion can be because he has an UTI. I think infections can cause delirium in old folks.

10) Hypersplenism. Only thought this because the other things didn't fit and enlarged spleen= more space to store blood cells --> decreased peripheral counts. I learned in heme that enlarged spleens can cause thrombocytopenia so it seemed close enough.

11) cGMP. NO causes venodilation and vasodilation (depending on which drug you use). Venodilation should decrease preload and vasodilation should dilate the coronary arteries to increase flow.

12) He's having a MI. He has cardiogenic edema due to pump failure (increased hydrostatic pressure).

Just my thoughts. Feel free to correct me.
 
10) Hypersplenism. Only thought this because the other things didn't fit and enlarged spleen= more space to store blood cells --> decreased peripheral counts. I learned in heme that enlarged spleens can cause thrombocytopenia so it seemed close enough.
That's correct, and also the same reason you can get anemia in cases of cirrhosis.

There was one that confused me:
60-year old man with a history of smoking and persistent hoarseness, he has a lesion on his vocal cord that is biopsied and the histology is shown. What is the dx?
(vocal cord polyp, adenocarcinoma, adenoma, squamous cell carcinoma, squamous cell papilloma)

I think one of the pictures was zoomed in to show an intact basement membrane, so I wanted to put squamous carcinoma in situ but it wasn't an answer choice. Polyps and papillomas are usually exophytic while this one was invading downward, so I excluded those... I think I went with sq carcinoma, but I didn't get the expanded feedback so I don't know if that's right or not.

Also, what the hell is a viscus?
 
1) Woman smells of piss. How do you confront?
I put: are you having any problems you're too embarrassed to talk about? would you be willing to talk about them today?
I think the right ans. is: I know this can be an embarrassing topic, but some ppl have difficulty holding their urine when they get older. Is this prb for you?

Not sure why my ans. is incorrect but was stuck b/t the two.
The choice you picked is incredibly non-specific (she probably has more than one concern which may be embarrassing) and would lead to confusion AND gives her an out by suggesting she can discuss the issue at another time. In the limited time you have to address people's issues, be direct. This includes asking about suicide in a depressed person, alcohol use in a suspected drinker, domestic abuse, adolescent sex and drug use, and so on. It is far, far more awkward to bring these things up in an indirect manner and you will get burned on step 1 and 2 (and observed clinical encounters if your school has them) if you avoid these topics or handle them poorly.
 
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