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 +0  (nbme22#20)

Of all the options listed, there are two that function in eversion of the foot (and would cause this patient pain): the fibularis brevis and fibularis tertius.

At this point, NBME expects us to have some super asinine knowledge, but here's why (I think) the answer is brevis and not tertius. The brevis muscle runs over the lateral malleolus and therefore directly over this fracture. The tertius takes a different route into the foot, since it arises from the medial fibula and so it runs anterior to the lat malleolus and wouldn't cross the fracture site.


 +0  (nbme22#20)

Of all the options listed, there are two that function in eversion of the foot (and would cause this patient pain): the fibularis brevis and fibularis tertius.

At this point, NBME expects us to have some super asinine knowledge, but here's why (I think) the answer is brevis and not tertius. The brevis muscle runs over the lateral malleolus and therefore directly over this fracture. The tertius takes a different route into the foot, since it arises from the medial fibula and so it runs anterior to the lat malleolus and wouldn't cross the fracture site.


 +1  (nbme21#1)

To go through the other answers:
A and C) If she had some sort of hemolytic anemia caused by antibodies (i.e. positive Coombs test) or she had hemolysis, her reticulocyte count would be elevated B) No need to do a electrophoresis, you know she has sickle cell E) She has an elevated MCV, so she can't have iron-deficiency anemia


 +1  (nbme18#41)

Here's how I thought through this. problem with DCML (absent proprioception and vibration sense), problem with deep tendon reflexes (DRGs), ataxic gait (spinocerebellar pathway), mild weakness (motor neurons). The only thing that all of these pathways have in common is that they all use myelinated afferents.

I don't know if Guillan Barre would actually present like this, but you don't have to know what the illness is to figure the question out.


 +0  (nbme23#32)
  • A) GABA-A receptors let Cl- in
  • B) Glycine is used in the spinal cord as an inhibitory neurotransmitter; also lets Cl- in
  • C and E) Metabotropic glutamate receptors are G-protein coupled
  • Therefore, the only thing that could let Ca2+ in is NMDA receptors
thotcandy  according to this, 5HT3 is an ion channel (mainly Na and K, but some Ca) so that was kinda effy imo

 +0  (nbme23#45)

I also think that the point being made here is about mean arterial pressure (MAP), which is what autoregulatory systems actually change based on. Because he has increased MAP (due to increased DBP), the capillaries will constrict to maintain constant pressure/flow through the capillary bed.





Subcomments ...

It said it was fatal to males in utero, and the question asked about live born offspring. Since the males aren’t being born in the first place, I said 50% females and 0% males.

hungrybox  fuck i got baited +19  
jcrll  "live-born offspring" ← baited +8  
sympathetikey  Same :/ +  
arkmoses  smh +  
niboonsh  why is it 50% females tho? +2  
imgdoc  felt like an idiot after i figured out why i got this wrong. +1  
temmy  oh shit! +  
suckitnbme  This isn't exactly right as males can still be born as evidenced by individuals III 6,9,11. This basically an x-linked recessive disease. A carrier mother can still pass her normal X chromosome to a son (50% chance). It's just that the other 50% chance of passing an affected X chromosome results in death of the fetus in utero. Thus all males actually born will not be affected. +2  
makinallkindzofgainz  @suckitnbme, Correct, but if you're a live-born male, you 100% for sure do NOT have the disease, so the chance of a live-born male "being affected" is 0. +1  
spow  @suckitnbme it's not X-linked recessive, otherwise every single son would be affected and therefore have died in utero. It's X-linked dominant +  
qball  Jail-baited +  


Even though TSH producing adenomas mat also produce compression fractures they are far less common than ACTH producing tumors

spow  But if you had a TSH secreting adenoma, you would NOT have had weight gain (hyperthyroid = weight loss) +  


submitted by mahesh(0),

Osteosarcoma histological appearance. Paget disease is one of risk factor

spow  Looking back, I know it's osteosarcoma but the lung metastases made me think of Ewing's +  
makinallkindzofgainz  Ewing sarcoma is common in boys <15 years old. This patient is a 70 year old woman. The stem notes elevated periosteum and a sunburst pattern which are characteristic of osteosarcoma. +  


submitted by amarousis(15),

But doesn't subacute combined degeneration lead to impairment in DCML, spinocerebellar and corticospinal tract? I get the ataxic gait - DCML/spinocerebellar. But the sensation to pinprick, wouldn't that be the spinothalamic tract? That is not usually affected in subacute combined degeneration.

krewfoo99  It would affect the dorsal column tract and the spinothalamic tract. It wont affect the spinocerebellar tract (Thus Rombergs sign in B12 deficiency will be positive) All three of the tracts are affected in Friedrichs Ataxia +  
krewfoo99  Sorry. Just checked on FA. It will also affect the spinocerebellar tract +  
spow  Sensation to pinprick is DCML +  


submitted by sajaqua1(346),

The patient has a prior history of hysterectomy with bilateral salpingo-oophorectomy, and received external beam radiation to the pelvis. The patient now displays hydronephrosis and hydroureter, with distal ureteral narrowing bilaterally. The likeliest option is that we are seeing adhesions from previous surgery constrict the ureters, causing this.

E) Urothelial carcinoma (also called transitional cell carcinoma) is also a possibility. What makes this unlikely is the location: bilateral. The prior hysterectomy and bilateral salpingo-oophorectomy would leave scar tissue on both sides of the body, but the odds of urothelial carcinoma arising bilaterally are very slim.

A) The patient had a hysterectomy, so the odds of recurrent cervical carcinoma are also incredibly low. C) and D) Urethral condyloma and urethral transitional cell papilloma are in the wrong location to account for bilateral urethral narrowing with hydroureter.

stinkysulfaeggs  Great explanation - just one addition. The retroperitoneal fibrosis could also be a direct consequence of the external beam radiation. It's linked to both causes. Either way, it's a better fit than urothelial carcinoma (in retrospect). +9  
spow  Why would the onset be 15 years later though? +1  
drzed  I was thinking the same thing @spow. I had put urothelial carcinoma, thinking that a field defect would result in bilateral tumor. +1  


submitted by yogi(11),

ITP - Platelet + Ab goes to spleen - Lysed - Low plt count.After splenectomy - usually plt count improve and Peripheral blood smear show - HJ bodies as a sign of asplenia ( nuclear remnants in RBC usually removed by spleen). If there was an accessory spleen (which was not functional when the main spleen was working) will take over the function gradually - HJ bodies will disappear and Plt starts to lyse - which has happened in this case scenario.

spow  But why are there no bite cells? Question stem states that there is normal morphology? That's why I didn't pick accessory spleen +2  
makinallkindzofgainz  Bite cells are seen when splenic macrophages take "bites" out of hemoglobin precipitates in G6PD deficiency, which doesn't have to do with our question. This patient had a splenectomy 3 months ago, 6 weeks later showed Howell-Jolly bodies (asplenia), and then today now has normal erythrocytes (spleen is working again somehow = accessory spleen) +  


submitted by chris07(30),

I'm guessing that since this is hashimoto's that a biopsy of the thyroid would show the thyroid gland completely engulfed by attacking lymphocytes. Over time though, wouldn't the thyroid be completely destroyed and fibrotic?

dr.xx  Progressive thyroid cell damage can change the apparent clinical picture from goitrous hypothyroidism to that of primary hypothyroidism, or "atrophic" thyroiditis. https://www.ncbi.nlm.nih.gov/books/NBK285557/ The pathological features are atrophic thyroid gland with lymphocytic infiltration and fibrous tissue replacing normal thyroid parenchyma. https://www.researchgate.net/publication/302196286_Atrophic_Thyroiditis +  
paulkarr  I was thinking that "Diffuse fibrosis" was trying to point to IgG4 Riedel Thyroiditis rather than Hashimoto's. +2  
spow  It's only been 10 months, per the question stem. This probably isn't long enough for fibrosis to be correct +  


submitted by momof21234(3),

the patient has asbestos which is restrictive (clue was pleural plaques) DLCO is decreased in intra-thoracic conditions (interstitial lung dz etc) and normal on extra-thoracic conditions (muscular issues)

usmlecharserssss  how FEV1/FVC is normal i cannot get that +1  
sammyj98  I think this is standard for restrictive lung diseases. In obstructive the airways collapse during expiration so it's hard to expire, but there's a long drawn out end to epiration as little by little it escapes, leading to a decreased FEV1/FVC. In restrictive pt's just aren't able to move and expand their lungs enough, so when they expire it's of a small volume, but there isn't any collapse involved. It's like a normal expiration just with a restricted volume, making the FEV1/FVC normal. +  
spow  @usmlecharserssss In restrictive lung diseases, the ratio is either normal or increased. +  
drzed  And the reason why FEV1/FVC is either normal or increased in restrictive lung disease is very simple: the FEV1 and FVC both decrease because you are restricting airflow, but the FVC will decrease MORE than the FEV1, and thus because the denominator is larger, the fraction either stays normal, or increases slightly Contrast this to obstructive lung disease where you have an obstruction to air FLOW, e.g. the FEV1 will decrease more than the FVC, leading to a low ratio by defition +  


submitted by neonem(366),

this patient has symptomatic aortic stenosis. This can be identified by the ventricular hypertrophy (to compensate for increased functional afterload from non-compliant aortic valve), midsystolic murmur and the location at the normal aortic area.

Per UpToDate on Clinical manifestations of Aortic Stenosis:

"Dizziness and syncope — Syncope occurs as a presenting symptom in approximately 10 percent of patients with symptomatic severe AS (or approximately 3 percent of all patients with severe AS) [3]. There are several proposed explanations for exertional dizziness (presyncope) or syncope in patients with AS, both of which reflect decreased cerebral perfusion. Exercise-induced vasodilation in the presence of an obstruction with fixed cardiac output can result in hypotension."

guillo12  What does "fixed cardiac output" signify? +  
usmleuser007  "fixed cardiac output" might mean that with the stenosis (ie. narrowed aortic valve) there is a limited or rather reduced cardiac output. Exercise would not increase cardiac output because the stenosis is caused by a mechanical (physical) rather than a biochemical process. Therefore, At any given moment the heart can not increase its output no matter how forcefully it contracts. +1  
fallot4logy  why not option A?arterial compression ? +1  
sunshinesweetheart  @fallot4logy LVH does not lead to coronary artery compression. only reallyyyy rarely will pulmonary artery dilation cause coronary artery compression. plus that would cause angina but probably wouldnt decrease cerebral bloodflow to syncope. her murmur + LVH point us toward aortic stenosis which does cause those --> fixed CO +  
drpatinoire  @fallot4logy LVH can cause coronary artery compression, but typically leading to coronary ischemia after exercise (i.e. stable angina in this patient). The question is asking what leads to her syncope. Syncope actually means her brain is lacking blood supply abruptly. +1  
rainlad  how do we rule out mitral valve prolapse in this case? +  
spow  @rainlad murmurs at the right upper sternal border are aortic in nature. Mitral murmurs are heard at left 5th intercostal at the midaxillary line. +