NBME 12 discussion

[titan25]

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4 a 14 years old brougt to physian because mostly sleeping withdrawn and complaining of abdomen pain 3 weeks , what history will u take first...should we recretion drug history....options school history , devlopmental, family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

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?

I'm pretty sure it was squamous cell ca. I just saw vocal cord and went w/ that (although I think only true vocal cords are squamous).

And that was the first time I'd heard of the word "viscus" too...

 

[Altruist]

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

2) Yeah there was definitely air under the right hemidiaphragm on the film, thus ruptured bowel. I'm not sure if it's the free air, or if it's the spilled abdominal contents that do the irritating... Probably only of academic interest anyway. Effect is the same.

9) UTI's can cause confusion in older folks, for sure. Could also (maybe) be uremia from the pressure back-up. Would depend on the question stem I suppose, if there was any indication of infection.

And that was the first time I'd heard of the word "viscus" too...

This kind of thing is, from the war stories, standard on the boards. They'll describe it in a way you haven't heard before, or use an old term (small non-cleaved cell lymphoma instead of Burkitt's, for example) that throws you off. I don't know how much you can prepare for that without doing a ton of low-yield reading, so just accept that you may have to puzzle out some answer choices and/or move on.

 

[bobsagat]

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.

Still looking for a solid answer on this one...

 

[SlaveOfTCMC]

Regarding the Hardy Weinberg:

The question asked about the WIFE... who was perfectly normal... (all that stuff about the husband's sister was irrelevant)

The normal population frequency of disease is 1/40,000

A short cut you use whenever disease frequency < 1/1000

Is that

HETEROZYGOUS carrier rate = 2q

Therefore, square root of 1/40,000 = 1/200

2q = 1/100= the answer.



The other one regarding the NNT was 100

The question asked "how many women need to have babies and treated to prevent a woman from getting ANY development disorder"

Using trace metals as the control group, it would have been"

2.3% - 1.3% = 1.0% absolute risk reduction

Then 1/0.01 = 100

 

[kastle6797]

Still looking for a solid answer on this one...

The answer was squamous cell carcinoma. The histology showed that the cancer was invasive, kind of hard to interpret, but the histology just didn't look organized enough to be in-situ or benign. Also, I think (memory is iffy) there were pink keratin pearls in the pic, indicating squamous cell origin as opposed to adenocarcinoma.

 

[SlaveOfTCMC]

Answered

 

[kastle6797]

Question: 13 YO boy with pruritic rash on right foot. No fever, chills, cold. Patient's family spent weekend at a lake. (Rash is on top of foot and moving sort of linearly). Treat with a. clindamyin, b. fluconazole, c. mebendazole, d. metronidazole, or e. prednisone?

Did anyone know what this was? I thought it was a fungus but fluconazole was wrong. Parasitic maybe?

 

[SlaveOfTCMC]

Question: 13 YO boy with pruritic rash on right foot. No fever, chills, cold. Patient's family spent weekend at a lake. (Rash is on top of foot and moving sort of linearly). Treat with a. clindamyin, b. fluconazole, c. mebendazole, d. metronidazole, or e. prednisone?

Did anyone know what this was? I thought it was a fungus but fluconazole was wrong. Parasitic maybe?

That serpiginous tunneling is probably scabies.

Thus mebendazole.

 

[ScubaStarved]

Posting photos and exact question stems will at the very least get you an email from SDN. It also makes it impossible for others to quote your post if they don't want to receive the same email. Finally, many of the questions being asked are answered on this page and the previous page (if they thread were longer, then fine, don't read anything yourself, but this one is 2 pages).

Slave:

1. If you've done clinical work, this is tough because low fecal elastase is the best (?) confirmation of chronic pancreatitis. However, the pain and malabsorption is from insufficient neutralization of stomach acid by the pancreas. (Whatever enzymes are secreted by the pancreas are inactive at low pH.)
2. Serum CK. It's Duchenne's.
3. Malrotation
4. UGT deficiency. All babies have this initially and negative Coombs rules out immune mediated hemolysis.
5. G. It IS the anterior horn, but the intrinsic hand muscles are located laterally.

 

[bobsagat]

1) A 56 year old man with alcoholism comes to the physician b/c of a 2 month Hx of increasingly severe stomach pain and increased volumes of foul smelling stool; he also has had a 9kg weight loss during this period. He has a Hx of multiple visits to the ER because of severe abdominal pain. He has consumed one bottle of red wine daily for 5 years. His temperature is 98.6F. Physical exam shows epigastric tenderness. His fasting serum glucose concentration is 150mg/dL. CT scan of abdomen shows pancreatic calcifications. The most likely cause of this patient's current symptoms is a DECREASE in which of the following?
A) Bile acid synthesis
B) Colonic bacteria
C) Duodenal pH
D) Fecal elastase (WRONG)
E) 7a hydroxylase activity

I put D as well, since it was my best guess about why he would have weight loss and foul-smelling stool. But if we're to exclude D, I think the best answer would be C. A tumor in the head of the pancreas would obstruct the gall bladder and pancreas from secreting bicarb into the lumen of the duodenum. Admittedly the duodenum also has brunner's glands, but maybe that's the etiology of epigastric tenderness in pancreatitis/pancreatic tumor? I don't understand why that would cause you to lose weight, though...

2) a 3 year old boy is brought to the ER by his mother because of severe pain in the right leg after he fell from the porch 30 minutes ago. He has a 6 month history of intermittent pain in his legs at night. His mother adds that he cannot keep up with his peers on the playground. Evaluation shows a fracture of the right fibula. There is also gluteal muscle weakness bilaterally. Measurement of which of the following is most likely to confirm Dx?

A) ESR
B) Serum CK activity
C) Serum hydroxyproline concentrations (WRONG)
D) Serum Ig concentrations
E) Serum Rheumatoid factor titer

No idea on this one.

3) A 24 year old man comes to the ED b/c of a 2 hour history of severe abdominal pain. HIs pulse is 110/min. Abdominal exam shows distension. An X-ray of the abdomen while the patient is sitting upright and an image from the upper GI series are shown. Based on the findings shown, this patient most likely has which of the following developmental anomalies?

A) Gastroschisis
B) Intestinal aganglionosis
C) Malrotation
D) Persistent vitelline duct
E) Situs inversus viscerum (WRONG)

I suppose there might be duodenal atresia, thus malrotation. But wouldn't that have presented neonatally?

I think C. Gastroschisis is obviously not correct because he's a grown dude, same with B and D. E isn't right because you can see the stomach on the correct side of the film.
I went with C because it looks like a large part of his abdomen is absent of bowel, which could be because of malrotation. The malrotation can predispose to volvulus, which looks right because there is clearly air on the left side of the film without any contrast in it.

4) A 3 day old female newborn is brought to the physician because of yellow eyes for 1 day. The newborn was delivered at term after an uncomplicated pregnancy. The newborn and her mother are both blood group A, Rh-positive. Physical exam shows scleral and factial icterus. Her serum total bilirubin is 6mg/dL, with a direct component of 0.5 mg/dL. Serum AST and ALT activities are within normal. A direct Coombs result is negative. Which of the following is the most likely cause of jaundice in the newborn.

A) Biliary atresia
B) G1P uridylytransferase deficiency
C) G6Pase deficiency
D) Immune hemolysis (wrong... I don't know why I chose that... all signs said it's not this... but I wasn't sure what else lead to indirect hyperbilirubinema)
E) UDP glucuronsyltransferase deficiency
F) Viral hepatitis

Physiologic jaundice of the newborn is an unconjugated hyperbilirubinemia due to deficiency of the enzyme in answer E. I don't know if the bilirubin level fits, but the rest of the presentation seems to. Nml LFT's rules out C, lack of bilious vomiting rules out A. As for ruling out jaundice from viral hepatitis or classic galactosemia, I'm not really sure... someone else jump in.

5) A 23 year old man has had progressive weakness and atrophy of the intrinsic muscles of the left hand during the past 3 months. The most likely cause is damage to which of the following?

It's not F, not the anterior horn.

I put F here, too. Isn't atrophic weakness a sx of an LMN lesion?

 

[bobsagat]

5. G. It IS the anterior horn, but the intrinsic hand muscles are located laterally.

Isn't G the IMLCC?

 

[SlaveOfTCMC]

Posting photos and exact question stems will at the very least get you an email from SDN. It also makes it impossible for others to quote your post if they don't want to receive the same email. Finally, many of the questions being asked are answered on this page and the previous page (if they thread were longer, then fine, don't read anything yourself, but this one is 2 pages).

Slave:

1. If you've done clinical work, this is tough because low fecal elastase is the best (?) confirmation of chronic pancreatitis. However, the pain and malabsorption is from insufficient neutralization of stomach acid by the pancreas. (Whatever enzymes are secreted by the pancreas are inactive at low pH.)
2. Serum CK. It's Duchenne's.
3. Malrotation
4. UGT deficiency. All babies have this initially and negative Coombs rules out immune mediated hemolysis.
5. G. It IS the anterior horn, but the intrinsic hand muscles are located laterally.

Point taken. Thank you for the help

 

[ScubaStarved]

Isn't G the IMLCC?

I got this question wrong also and another poster explained this to me on the first page of this thread, so it's kind of funny that I'm now answering it 30 posts later:

(Disclaimer: I suck at neuro.) The IML column is more pointy, and the ventral horn has "bulbs" at the cord levels corresponding to control of distal muscles (e.g. arm, leg, hand, foot). The more medial section of the ventral horn is present at all levels and innervates trunk muscles.

 

[bobsagat]

I got this question wrong also and another poster explained this to me on the first page of this thread, so it's kind of funny that I'm now answering it 30 posts later:

(Disclaimer: I suck at neuro.) The IML column is more pointy, and the ventral horn has "bulbs" at the cord levels corresponding to control of distal muscles (e.g. arm, leg, hand, foot). The more medial section of the ventral horn is present at all levels and innervates trunk muscles.

Just talked through it with a friend. The IMLCC starts at T1, and this is almost certainly the cervical cord. Facepalm.

 

[SlaveOfTCMC]

Just talked through it with a friend. The IMLCC starts at T1, and this is almost certainly the cervical cord. Facepalm.

Makes sense since the sympathetics arise from the thoracic cord.

However, T1 is still controls medial arm. However, that would not exactly fit 'intrinsic hand muscle" which would be more C7 C8

 

[SlaveOfTCMC]

There was a beta thalassemia genetics question:

Basically they gave you the coding strand, bolded the exons then asked for a mutation where would lead to beta thalasemia.

None of the proposed changes would have lead to a nonsense mutation.

I narrowed it down to G-->A at codons 270ish and 670ish. (It had to be within the exons)

Apparently I chose the 270ish one and it was correct. I'm not entirely sure why though. Does anyone reclal this question?

 

[bobsagat]

Beta thal isn't due to a nonsense mutation, it's due to a mutation in "splicing sites or promoter sequences," according to FA pg 349.

The DNA NAs available to mutate were
A the very first one
B the one at the beginning of the first intron
C one in the middle of the second intron
D one at the end of the gene well after the third and final exon

(A)..exon/(B)intron/exon/int(C)ron/exon/intro(D)n

So, we're looking to introduce errors in promoters or splice sites. So, anything in the actual translated part of the gene is right out. (excludes C)
The tricky thing in looking back at this one is that I don't know for sure where transcription starts, but I can say that B is probably the best choice. You have to remember how introns are spliced out, looping out DNA in a lasso shape. Since either end of the intron contains the important sequence for that, you have to go with B.
I don't think you can necessarily exclude A or D because promoters can actually be within the coding region, but B is the best answer.

 

[ScubaStarved]

There was a beta thalassemia genetics question:

Basically they gave you the coding strand, bolded the exons then asked for a mutation where would lead to beta thalasemia.

None of the proposed changes would have lead to a nonsense mutation.

I narrowed it down to G-->A at codons 270ish and 670ish. (It had to be within the exons)

Apparently I chose the 270ish one and it was correct. I'm not entirely sure why though. Does anyone reclal this question?

This was a splice site mutation. Certain pairs of AA are well conserved and have some function in the spliceosome. FA covers this somewhat in the 2010 edition, but it is very subtle. QBank had another question about it. I would offer more help, but have forgotten so much in the last two weeks it's not funny. Basically an A, a G, or an AG pair is required somewhere..

 

[SlaveOfTCMC]

oh right. 5'AG GU3'

Therefore this must have been beta+ then.

 

[Altruist]

That serpiginous tunneling is probably scabies.

Thus mebendazole.

I got this one wrong on the day, but talking to a friend steered me to the right answer. The drug they're asking for is mebendazole (of the choices given), but it's cutaneous larva migrans, not scabies. This free article from the AAFP on pet-related infections includes a familiar-looking picture:
http://www.aafp.org/afp/2007/1101/p1314.html#afp20071101p1314-f1

This goes along with the question stem, which mentions the family just having come back from a trip to the lake. Cutaneous larva migrans is associated with playing barefoot on sand where dogs/cats have pooped.

 

[SlaveOfTCMC]

I got this one wrong on the day, but talking to a friend steered me to the right answer. The drug they're asking for is mebendazole (of the choices given), but it's cutaneous larva migrans, not scabies. This free article from the AAFP on pet-related infections includes a familiar-looking picture:
http://www.aafp.org/afp/2007/1101/p1314.html#afp20071101p1314-f1

This goes along with the question stem, which mentions the family just having come back from a trip to the lake. Cutaneous larva migrans is associated with playing barefoot on sand where dogs/cats have pooped.

Ah yes. Acyclostoma and Necator then

 

[hurdlepup]

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.

Can alanines be N-glycosylated too? b/c that was my concern... Also, how the heck do you remember this? Is this in FA somewhere that I have missed? Is there a pattern? Thanks!

 

[hurdlepup]

actually, i might have just partially answered my own question... it was that serines can be glycosylated and you lose a serine for an alanine in my concern...

still don't know if there is a pattern though...

 

[ScubaStarved]

Can alanines be N-glycosylated too? b/c that was the choice... Also, how the heck do you remember this? Is this in FA somewhere that I have missed? Is there a pattern? Thanks!

I don't think you're remembering the answer correctly, because the "N" of N-linked glycosylation stands either for Nitrogen or Asparagine (Asn, N). (I'm not actually sure which to be honest, but AFAIK only Asn in the sequence NXS or NXT can be glycosylated.)

This is in FA on the page about the Golgi network and post-translational modification. Most medical schools will lecture on the basis of enzyme active sites and membrane-bound receptor phosphorylation (multiple times each at my school) and should also explain a bit about the post-translational modification of proteins. I remember a little more about this topic because I spent one summer working on gp120's variable loops' N-glycosylation.

 

[kastle6797]

I got this one wrong on the day, but talking to a friend steered me to the right answer. The drug they're asking for is mebendazole (of the choices given), but it's cutaneous larva migrans, not scabies. This free article from the AAFP on pet-related infections includes a familiar-looking picture:
http://www.aafp.org/afp/2007/1101/p1314.html#afp20071101p1314-f1

This goes along with the question stem, which mentions the family just having come back from a trip to the lake. Cutaneous larva migrans is associated with playing barefoot on sand where dogs/cats have pooped.

Thanks for your help

 

[SlaveOfTCMC]

actually, i might have just partially answered my own question... it was that serines can be glycosylated and you lose a serine for an alanine in the question...

still don't know if there is a pattern though...

Reach back to your college biochemistry for this one...

As Scuba mentioned, the Nitrogen that is being glycosylated is on the side chain group. Thus Asn (and Gln in theory, but not sure if it happens in the cell)

LIkewise, Serine and Threonine have the side chain -OH groups be to -O glycosylated

 

[hurdlepup]

I don't think you're remembering the answer correctly, because the "N" of N-linked glycosylation stands either for Nitrogen or Asparagine (Asn, N). (I'm not actually sure which to be honest, but AFAIK only Asn in the sequence NXS or NXT can be glycosylated.)

This is in FA on the page about the Golgi network and post-translational modification. Most medical schools will lecture on the basis of enzyme active sites and membrane-bound receptor phosphorylation (multiple times each at my school) and should also explain a bit about the post-translational modification of proteins. I remember a little more about this topic because I spent one summer working on gp120's variable loops' N-glycosylation.

we had this stuff way back at the Fall of MS-1. and i'm not actually sure what AFAIK means...

so, I guess I see how losing a serine, which could be O-glycosylated, for an alanine, which cannot be glycosylated would result in losing glycosylation

Reach back to your college biochemistry for this one...

As Scuba mentioned, the Nitrogen that is being glycosylated is on the side chain group. Thus Asn (and Gln in theory, but not sure if it happens in the cell)

LIkewise, Serine and Threonine have the side chain -OH groups be to -O glycosylated

Thanks! I see the pattern now--all to do with the R-group!

 

[Scean]

1. Metaphyseal dysplasia due to single gene disorder caused my mutation in PTH receptor gene. Phenotype is "similar to that of acquired hyperparathyroidism." Mechanism?

Haploinsufficiency - wrong
Dominant Negative
Gain of function
Pleiotropy
Anticipation

I think i missed "aquired hyperparathryoidism" meaning here. I assumed that meant secondary; as in low calcium due to something (renal osteodystorphy) promoting PTH levels. So with that in mind I figured insufficient receptor, PTH doesnt work well, more out there. Insight?


2. So aripiprazole has what action compared to haloperidol on the dopamine receptors?

Reversible antagonism - wrong - didn't feel to good about it
Agonism
antagonism
inverse agonism
irreversible antagonist
partial agonism


3. Why is there reduced tactile fremitus in asthma kid?


4. Chronic peripheral neuropathy; enzyme histochemical staining shows fiber grouping. Most likely cause?

Altered trophic substance form innervating neuron - wrong
Altered muscle enzyme exprerssion due to damaged nerve fibers - correct?
Regeneration of muscle fibers
Re innervation of muscle fibers by regenerating axons
Selective loss of nerve fibers to type II muscle fibers


5. 73 year old w/ BPH, UTI +fever + chills +pain in flank + WBC + 100,000 colonies of gram + what is the causal organism?

Staphyloccus aureus - wrong
Streptococcus pyogenes
Enterococcus faecalis - would need a fistula and you'd see lots of other nasty stuff yea?


6. Lady with TIA's, cannot tolerate aspirin. Appropriate alternative?

Dipyramidal - wrong
Clopidogrel? -these were the two i narrowed
Acetaminophen
Ibuprofen
Tissue plasminogen activator


7. Lady gets to 10,000 ft ski resort. Dizzy, nausea, headache. Acetazolamide helps, how?

Stimulation of ion pumps in BBB - wrong
Direct action on resp centers, depressing ventilation
Direct action on resp centers, stimulate ventilation
Induction of metabolic acidosis, stimulate ventilation
Induction of metabolic alkalosis, depress ventilation
Stimulation of EPO

This one kid of bothered me. So her initial problem is alkalosis due to major reduction in PO2 at altitiude and subsequent increased RR blowing off CO2 = alkaline. Acetazolamide will help by creating some metabolic acidosis, but then what? Stimulating further respiration would be counter productive right? EPO would take a while. Direct action seemed a bit off to me. So i was left with ion pumps; I dunno.


8. Another carbonic anhydrase question - not my day. Didnt read this question fully though. CA deficiency in erythrocytes only; whats elevated in venous blood?

K+ wrong; i thought systemically, acidosis = H/K exchange
Ca
Cl
HCO3
Mg
Na



9. Lady with UMN issues. What helps?

Inhibit nicotinic-R in Renshaw - wrong
Activate GABA-R in muscle spindle afferents
Activate glutamate-R in gamma motoneurons
Activate serotonin-R in alpha motoneurons
Inhibit glycine-R in Golgi tendon afferents
Inhibition of (a)2-R in excitatory interneurons



10. Guy on steroids hurts his arm. Antecubital swelling and ecchymoses from antecubital fossa to mid forearm on anterior side, tender there also. Able to flex elbow actively, but unable to flex elbow or supinate against resistance. Injured muscle-tendon unit innervated by what?

Radial - wrong; i was thinking brachioradialis
Anterior interosseous
Median
Musculocutaneous
Ulnar



11. Still unclear on what would improve the lady taking a thiazide with improved BP but low K+

Atenolol - wrong
Furosemide
Losartan
Nifedipine
Prazosin


12. Septic arthritis in 18 year old kid; gram + stain picture shows what I think look like intracellular bugs

Ceftiraxone
Doxycycline - wrong
Genatmicin
Metronidazole
Vancomycin


13. Apparently autistic kid? 3 years old, 20 word vocab. Doesn't speak in sentences, points alot, no physical abnormalities. Kid is looking at reflex hammer instead of acknowledging mom's presence.

Inform her that the child will need special education - wrong
Further evaluation to determine cause of language delay
MRI
Reassure that this is normal
Advise to enroll in preschool early


14. Guy smokes 2 packs a day lives in basement apartment. Dizzie, headache, nausea for 4 hours. No physical abnormalities; what explains it?

Acidosis with heme dissociation shift right
Activation of nicotinic-R in locus caeruleus
Cerebral arteriolar constriction due to increased CO2 in blood
Competative inhibition of oxyhemeoglobin formation
Inactiation of cytochrome oxygenase by cyanide - wrong; seemed like a lot of cigs

Probably competitive inhibition - CO poisoning. I skimmed over the part that said it was WINTER - and basement apartments i guess only have space heaters right? Sure.



15. What else would you give to someone w/ acute hep C already receiving (a)IFN?

IL-2 - wrong
Infliximab
Levamisole
Ribavirin
Thlidomide


16. Guy with prostate cancer; Low back pain. Most appropriate drug MoA:

Activation of GnRH receptors - probably correct if given CONTINUOUSLY
Activation of LH receptors
Blockade of estrogen receptors
Blockade of FSH receptors -wrong, convinced myself T --> DHT was FSH stimualted
Inhibition of 11-B hydroxylase



Thoughts, or some scolding to get me motivated welcome

 

[sincity college]

Had a quick couple questions:

1.) 6th rib fracture and insert chest tube through which muscle? pec minor, rhomboid major, or serratus anterior

2.) Different isolates of influenza recovered than previous year. where is mutation? point mutation in matrix protein/ ribonucleoprotein. reassortment involving hemagglutin/ matrix protein / ribonucleoprotein

3) Breast mets, which protein when dysfunctional allows this? CD44, E-caherin, pepsin, RNAse

4) Quickest way to decrease sudden cardiac deaths? anti-smoking campaign, exercise program, water supply with aspirin, automatic defibrillators in public places, free stress management programs

5) How does dexamethasone promote differentiation of surfantant-producting cells? Is it nuclear receptors???

6) 26 yo F with 3 mo amenorrhea. Mom died. 15 lb weight loss. Cause? Altered GnRH pulses, increased E and P, decreased cholestrol, premature ovarian failure

7) 48 yo F pw 3d hx of fever 2wk hx of colicky lower abd pn. tender LLQ. Normo anemia with left shift. IV ab subside pain and fever. doc should recommend? avoid alcohol, find others in support group, yoga to decrease stress, high fiber diet

THANKS in advance!!! you guys are rockstars!

 

[Scean]

Had a quick couple questions:

1.) 6th rib fracture and insert chest tube through which muscle? pec minor, rhomboid major, or serratus anterior

2.) Different isolates of influenza recovered than previous year. where is mutation? point mutation in matrix protein/ ribonucleoprotein. reassortment involving hemagglutin/ matrix protein / ribonucleoprotein

3) Breast mets, which protein when dysfunctional allows this? CD44, E-caherin, pepsin, RNAse

4) Quickest way to decrease sudden cardiac deaths? anti-smoking campaign, exercise program, water supply with aspirin, automatic defibrillators in public places, free stress management programs

5) How does dexamethasone promote differentiation of surfantant-producting cells? Is it nuclear receptors???

6) 26 yo F with 3 mo amenorrhea. Mom died. 15 lb weight loss. Cause? Altered GnRH pulses, increased E and P, decreased cholestrol, premature ovarian failure

7) 48 yo F pw 3d hx of fever 2wk hx of colicky lower abd pn. tender LLQ. Normo anemia with left shift. IV ab subside pain and fever. doc should recommend? avoid alcohol, find others in support group, yoga to decrease stress, high fiber diet

THANKS in advance!!! you guys are rockstars!

1. serratus anterior. Level is above split of trachea (corina/carina?) so its pretty high and very lateral. Too lateral for pec, rhomboid not around there.

2. Influenzae have segmented genomes for reassortment. hemmaglutinin is a major source of immune defense (and subsequently, variation by the virus). H1N1 = hemagglutinin # Neuroaminidase #. hemagglutin is the ADHESION one; so yea immunity to that halts the infection before it starts. A change = lots of ppl infected.

3. E Cadherin --> cadherins are calcium dependent components of Demosomes which are cell-cell adhesions (vs hemidesmosomes which use integrins and are cell-BM adhesion)

4. Defibrillators all over the place. Effect almost immediate. excercise, stress, smoking all help; but more long term/big picture.

5. yea, steroid = nuclear receptor

6. I actually cant remember what I put; there were a couple quesitons on this. Maybe grief/depression --> low dopa/sertonin --> more prolactin --> less GnRH? or was it primary ovarian (i think there was a question for each)

7. High fiber. normo-Anemia = GI bleed, colicky due to ischemic large bowel (splenic flexure), necrotic tissue infected for fever. Large bowel infarct - local pain vs small bowel is diffuse. Alcohol would be cirrhosis RUQ instead of LLQ


My thoughts. I'm pretty confident on most of em', ha.

 

[sincity college]

Scean,

1) Gain of function - not really sure why, its right though - my reasoning what that if you have acquired hyperparaT, there was something in the genetics that causes up regulation of the gene which is usually a gain of function mutation?
2) partial agonism - it doesnt bind the D2 receptors as tightly and has fast dissociation from them
3) asthma because wheezing and its a kid. only thing i know of that has increased tactile fremitus is pneumonia
4) Re innervation of muscle fibers by regenerating axons ( i think)
5) E.faec causes UTIs, other listed G+s dont
6) Clopidogrel, dipyramidal is used for intermittment claudication by inhibiting PDE and increasing cAMP; clopidogrel inhibits aggregation like aspirin
7) Induction of metabolic acidosis, stimulate ventilation to comp for resp alkalosis, your body is normally going to do this, but drug as prophalaxsis does it quicker by eliminating HCO3. You want to stimulate your resp drive to get more oxygen in blood
8) Cl, venous blood as more CO2, if no CA, then it cant be converted into HCO3 which is transported out of RBC in exchange for Cl (Chloride shift), if this doesnt occur, CL builds up
9) Activate GABA-R in muscle spindle afferents, not sure why, my reasoning was GABA is inhibitory and want relaxation?
10) Musculocutaneous, its the flexor
11) losartan - diuretic + ARB/ACE is first line
12) ceftriaxone - for N gonorrhea diplocci
13) Further evaluation to determine cause of language delay - should be at 900 words, seems a bit early to Dx mental ******ation
14) Competative inhibition of oxyhemeoglobin formation, i believe from CO buildup
15) Ribavirin - standard treatment in inf + ribavirin
16) I got this one wrong

 

[SlaveOfTCMC]

16. Guy with prostate cancer; Low back pain. Most appropriate drug MoA:

Activation of GnRH receptors - probably correct if given CONTINUOUSLY
Activation of LH receptors
Blockade of estrogen receptors
Blockade of FSH receptors -wrong, convinced myself T --> DHT was FSH stimualted
Inhibition of 11-B hydroxylase
[/QUOTE]

Leuprolide continuously because prostate cancer is sensitive to testosterone.

Eliminate that signaling.

MOreover, this was NOT marked WRONG on expanded feedback for me

 

[Scean]

alright, alright, alright - thank for the responses

 

[Scean]

Some additional thought about that PTH receptor mutation quesiton:

I guess the fact that it is a metaphyseal dysplasia indicates that calcium is being rapidly reabsorbed from it and not staying put from the epiphyseal growth out towards the metaphysis?

My real problem is that I was thinking acquired hyperparahthyriod means calcium is LOW but in this case calcium must be HIGH due to a gain of function, highly active, receptor that is reabsorbing any calcium laid down in that plate causing the dysplasia.

 

[SpunkySpunk]

Girl with horner's and neck mass resection. Post synaptic sym fibers from sup cerv ganglion dmged?

Alzheimer woman, forgetful, problems with learning/naming. Lesion where? Hippocampal formation?

Chronic periph neuropathy: enzyme staining shows fiber grouping. What the deal is?
I put selective loss of n fibers --> T2 mm fibers.
is it: altered musc enzyme expresion due to dmg n fibers
or altered trophic substance from innerv n.

Chick with MS. Resp acidosis. Aspiration pna?

That alcoholic with chronic pancreatitis, severe stomach pain and malabsorption was a bitch.

 

[ThereHeIs]

From above...

2. So aripiprazole has what action compared to haloperidol on the dopamine receptors?

Reversible antagonism - wrong - didn't feel to good about it
Agonism
antagonism
inverse agonism
irreversible antagonist
partial agonism

The answer is partial agonism. Reference baby katzung 9th ed. pg 252 in the chart.

 

[MsKrispyKreme]

I have a few questions, guys.

-funky prevalence graph --> was the answer 2?
-pic of glomerulus stained with elastin --> was it chronic graft rejection?
-lost in the desert for 2 weeks --> what happens to F-2,6-BP, glucose-6-phosphatase, PEPCK, and pyruvate kinase? (arrows question)
-chlordiazepoxide overdose and alcohol (slow reacting pupils & decreased bowel sounds) --> what happens to PO2, PCO2, and pH?
-graph of insulin-stimulated vs. unstimulated (?) transport of glucose in myocytes --> which graph was correct?

Thanks!

6. I actually cant remember what I put; there were a couple quesitons on this. Maybe grief/depression --> low dopa/sertonin --> more prolactin --> less GnRH? or was it primary ovarian (i think there was a question for each)

Altered GnRH pulses is correct.

Girl with horner's and neck mass resection. Post synaptic sym fibers from sup cerv ganglion dmged?

Alzheimer woman, forgetful, problems with learning/naming. Lesion where? Hippocampal formation?

Chronic periph neuropathy: enzyme staining shows fiber grouping. What the deal is?
I put selective loss of n fibers --> T2 mm fibers.
is it: altered musc enzyme expresion due to dmg n fibers
or altered trophic substance from innerv n.

Chick with MS. Resp acidosis. Aspiration pna?

That alcoholic with chronic pancreatitis, severe stomach pain and malabsorption was a bitch.

-yes, post-synaptic sympathetic neurons from the superior cervical ganglion
-hippocampal formation
-reinnervation of mm. fibers by regenerating axons
-i didn't get this one correct. (i chose upper airway obstruction for some reason.) now that i think about it, it might be opioid overdose --> pain management for MS. i dunno.

 

[kstreet]

Question from the test

A 22 yo man who is a militar recruit is brought to the doc 15 min after fainting while waiting in line to receive vaccinations. Immediately after he fainted, his pulse was 45/min and his systolic was 50 mmHg. His pulse is now 88/min and bp is 100/70. Physical exam shows no abnormalities. What was the cause of the syncope?

A. Aortic Stenosis
B. Hypertrophic Cardiomyopathy
C. Increased Parasympathetic Tone
D. 3rd degree AV block
E. Ventricular Tachycardia

 

[kstreet]

A 54 yo woman comes to the doc for a follow up exam. 2 months ago she was dx'd with hypertension and rx'd with hydrochlorothiazide. BP today is 150/100 compared with 165/108 two months ago, and serum K is 3.2 vs 4.5 two months ago. Addition of which of the following medications is most likely to further decrease bp and restore K to normal?

A. Atenolol
B. Furosemide
C. Losartan
D. Nifedipine
E. Prazosin


A 25 yo man is lost in the desert for 1 week with plenty of water but no food, what changes in enzyme activity and molecule concentrations in live is most likely in this pt.

Up and Down arrows for

Fructose 2,6, bisphosphate
Glucose 6-phosphatase
PEP Carboxykinase
Pyruvate Kinase


Thanks for the help!

 

[Sheldor]

Question from the test

A 22 yo man who is a militar recruit is brought to the doc 15 min after fainting while waiting in line to receive vaccinations. Immediately after he fainted, his pulse was 45/min and his systolic was 50 mmHg. His pulse is now 88/min and bp is 100/70. Physical exam shows no abnormalities. What was the cause of the syncope?

A. Aortic Stenosis
B. Hypertrophic Cardiomyopathy
C. Increased Parasympathetic Tone
D. 3rd degree AV block
E. Ventricular Tachycardia

Parasympathetic tone! Presumably afraid of shots, so the thought of receiving one activated the PSNS --> Vagus --> Bradycardia and syncope

A 54 yo woman comes to the doc for a follow up exam. 2 months ago she was dx'd with hypertension and rx'd with hydrochlorothiazide. BP today is 150/100 compared with 165/108 two months ago, and serum K is 3.2 vs 4.5 two months ago. Addition of which of the following medications is most likely to further decrease bp and restore K to normal?

A. Atenolol
B. Furosemide
C. Losartan
D. Nifedipine
E. Prazosin

So they have lost potassium and they need to lower the blood pressure more. So you want a drug that will both lower BP and raise potassium. I believe the answer is Losartan beacuse you block ANG II, which means less aldosterone which means a lower BP, and less K+ secretion.

 

[kstreet]

One more question:

A 30 yo woman has unusually heavy menstrual bleeding and intermittent gingival hemorrhages. She has multiple bruises. LAb studies show

Hemoglobin 13.3
Hematocrit 40%
Leukocytes 5000
Platelets 25,000
PT 12 sec
PTT 34 sec

Peripheral blood smear shows normochromic normocytic erythrocytes w/o anisopoikilocytosis. A photo is shown. What's the most likely dx?

A. Acquired aplastic anemia
B. Acute leukemia
C. DIC
D. ITP
E. TTP

 

[hypnix]

One more question:

A 30 yo woman has unusually heavy menstrual bleeding and intermittent gingival hemorrhages. She has multiple bruises. LAb studies show

Hemoglobin 13.3
Hematocrit 40%
Leukocytes 5000
Platelets 25,000
PT 12 sec
PTT 34 sec

Peripheral blood smear shows normochromic normocytic erythrocytes w/o anisopoikilocytosis. A photo is shown. What's the most likely dx?

A. Acquired aplastic anemia
B. Acute leukemia
C. DIC
D. ITP
E. TTP

I believe D. PT and PTT normal. Platelet count low.

 

[kstreet]

I believe D. PT and PTT normal. Platelet count low.

Def makes sense. Thank you! During the test, got thrown off by the pic and ignored the values in the lab.

 

[whoknows2012]

Its gotta be ITP because...

aplastic anemia will present with pancytopenia

acute leukemia you will see blasts in the smear

DIC has prolonged PT and PTT

Also with normal PT and PTT, and vastly decreased platelets (along with easy bruising and bleeding) it seems to be the only answer choice that fits the clinical vignette. Im too lazy to look up how TTP presents but I'd assume also with elevated PT and PTT?

 

[kstreet]

Its gotta be ITP because...

aplastic anemia will present with pancytopenia

acute leukemia you will see blasts in the smear

DIC has prolonged PT and PTT

Also with normal PT and PTT, and vastly decreased platelets (along with easy bruising and bleeding) it seems to be the only answer choice that fits the clinical vignette. Im too lazy to look up how TTP presents but I'd assume also with elevated PT and PTT?

TTP would be decreased PC and increased BT with schistocytes and increased LDH with renal, CNS, fever, microangiopathic hemolytic anemia, thrombocytopenia

 

[winkleweizen]

question...lady with jaundice and mass at head of pancreas. Which procedure releaves the jaundice?

Cholecystectomy
stent into common bile duct
stent into hepatic duct
stent into main pancreatic duct
Stent into cystic duct
placement of transjugular portosystemic shunt

Had no clue..

Also the one where The guy was stroked out with a CT of the head. I put Cholesterol plaque. Was the Most predisposing factor Hypertension?

And finally

THe guy undergoes a laparscopic cholecystectomy. Which thing cant the surgeon inspect?

Ileum
Jejunum
Pancreas
stomach
transverse colon(wrong).

I originally had pancreas but changed it.

 

[kstreet]

question...lady with jaundice and mass at head of pancreas. Which procedure releaves the jaundice?

Cholecystectomy
stent into common bile duct
stent into hepatic duct
stent into main pancreatic duct
Stent into cystic duct
placement of transjugular portosystemic shunt

Had no clue..

Also the one where The guy was stroked out with a CT of the head. I put Cholesterol plaque. Was the Most predisposing factor Hypertension?

And finally

THe guy undergoes a laparscopic cholecystectomy. Which thing cant the surgeon inspect?

Ileum
Jejunum
Pancreas
stomach
transverse colon(wrong).

I originally had pancreas but changed it.

Head of the pancreas obstructs CBD.

I think the other question is asking about what is retroperitoneal. Pancreas is mostly retroperitoneal.

 

[winkleweizen]

Head of the pancreas obstructs CBD.

I think the other question is asking about what is retroperitoneal. Pancreas is mostly retroperitoneal.

THanks ya


Mother F. I knew it was getting at retroperitoneal but for some reason i was thinking transverse was retro and the ascending and descending werent. Got it mixed up

 

[Scean]

A 54 yo woman comes to the doc for a follow up exam. 2 months ago she was dx'd with hypertension and rx'd with hydrochlorothiazide. BP today is 150/100 compared with 165/108 two months ago, and serum K is 3.2 vs 4.5 two months ago. Addition of which of the following medications is most likely to further decrease bp and restore K to normal?

A. Atenolol
B. Furosemide
C. Losartan
D. Nifedipine
E. Prazosin


A 25 yo man is lost in the desert for 1 week with plenty of water but no food, what changes in enzyme activity and molecule concentrations in live is most likely in this pt.

Up and Down arrows for

Fructose 2,6, bisphosphate
Glucose 6-phosphatase
PEP Carboxykinase
Pyruvate Kinase


Thanks for the help!

on the fasting one, this is liver specific right? I'm gonna go with:

At a week you are pretty well spent and mostly using keto acids yea?
Hmm so you definitely are NOT doing glycolysis - so

F2,6BP down
Pyruvate kinase down

But are you doing gluconeogenesis? I think you still are.

G6Pase up
PEPCK up


opinions welcome

 

[RapplixGmed]

Section 1:
29. Women doesn't have menstral period for 3 months. Lost 20lbs weight since mother's death. Is it altered GnRH hormone pulses or premature ovarian failure?

Section 2:
9. 30 weeks Pregnant women with lower left sternal border murmur and splitting of S2 that is more pronounced with inspiration. What is the best explanation? Is this a normal physiologic response? (sounds normal to me... like a high output cardiac murmur and a normal split S2)

21. Boy has coughing, wheezing and rapid breathing? Upper respiratory infection 2 days ago. Inspiratory/Expiratory wheezes. Decreased tactile fremitus. Asthma or Bronchitis? Leaning towards post-infectious bronchitis but not sure.


Section 3:
43. How does nictine stimulate pleasure and addition? Via the opiod receptors in the midbrain or dopmaine in the nucleus accumbens?

Section 4:
18. A 6 hour old female newborn has a harsh systolic murmur at the left upper sternal border. Findings on physical examination are otherwise unremarkable. Three hours later, the murmur has a diastolic component. Twelve hours later, there is no murmur, and ultrasonography discloses no cardiac abnormalities. Whcih fo the following is the most likely cause of the murmur.
Is this typical of PDA? What explains the switch between the systolic and diastolic if so?