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Comments ...

 +4  (nbme24#3)

The kid has gynecomastia due to puberty (excess testosterone → estrogen) This goes away naturally (apparently in 12 to 18 months)

I think you don't have to do blood tests because he has normal sexual development for his age and there are no other signs?

osler_weber_rendu  How does telling an "embarrassed kid" that he will have big tits for 12-18 months help?!
howdywhat  my exact thought, telling him that it will last for somewhere around a year and a half doesnt seem so reassuring

 +0  (nbme24#11)

Wasn't sure about others, but mammography for general population isn't recommended until 40

_yeetmasterflex  Also wouldn't mammography be secondary prevention since you'd look for asymptomatic disease already present?

 +2  (nbme24#7)

This was in NBME 20 as well. Its painless hematuria + papillary growth is showing transitional cell carcinoma This is associated with "Pee SAC": phenacetin, smoking, aniline dyes, and cyclophosphamide.

 +1  (nbme24#37)

I think what threw me off with this question was "serum T4" - wasn't sure if that meant total T4 or serum T4. Luckily, I don't think any of the other ones fit for either so I assumed it meant total T4 for which the answer makes sense

Subcomments ...

Why would it not be anemia of chronic disease with decreased serum transferrin concentration?

lispectedwumbologist  Nevermind I'm stupid as fuck I see my mistake +  
drdoom  be kind to yourself, doc! (it's a long road we're on!) +8  
step1forthewin  Hi, can someone explain the blood smear? isn't it supposed to show hypersegmented neutrophils if it was B12 deficiency? +  
loftybirdman  I think the blood smear is showing a lone lymphocyte, which should be the same size as a normal RBC. You can see the RBCs in this smear are bigger than that ->macrocytic ->B12 deficiency +9  
seagull  maybe i'm new to the game. but isn't the answer folate deficiency and not B12? Also, i though it was anemia of chronic disease as well. +  
vshummy  Lispectedwumbologist, please explain your mistake? Lol because that seems like a respectible answer to me... +  
gonyyong  It's a B12 deficiency Ileum is where B12 is reabsorbed, folate is jejunum The blood smear is showing enlarged RBCs Methionine synthase does this conversion, using cofactor B12 +  
uslme123  Anemia of chronic disease is a microcytic anemia -- I believe this is why they put a lymphocyte on the side -- so we could see that it was a macrocytic anemia. +  
yotsubato  Thanks NBME, that really helped me.... +  
keshvi  the question was relatively easy, but the picture was so misguiding i felt! i thought it looked like microcytic RBCs. I guess the key is, that they clearly mentioned distal ileum. and that is THE site for B12 absorption. +2  
sahusema  I didn't even register that was a lymphocyte. I thought I was seeing target cells so I was confused AF +  

submitted by ameanolacid(12),

Atherosclerosis is the MOST common cause of renal artery stenosis...with fibromuscular dysplasia being the SECOND most common cause (even though it is tempting to choose this option considering the patient's demographic).

xxabi  Is there a situation where you would pick fibromuscular dysplasia over atherosclerosis if given both options? Thanks for your help! +3  
baconpies  Atherosclerosis affects PROXIMAL 1/3 of renal artery Fibromuscular dysplasia affects DISTAL 2/3 of renal artery +13  
gonyyong  Why is there ↓ size in both kidneys? This threw me off +  
kateinwonderland  @gonyyong : Maybe because narrowed renal a. d/t atherosclerosis led to renal hypoperfusion and decrease in size? +  
drdre  Fibromuscular dysplasia occurs in young females according to Sattar Pg 67, 2018. +2  
davidw  Normally you will see Fibromuscular dysplasia in a young female 18-35 with high or resistant hypertension. She is older has a history type II DM predispose you to vascular disease and normal to moderate elevation in BP +1  

submitted by brethren_md(54),

Vitamin B12 is the distractor in this question because it also causes a broad-based, ataxic gait and decrease in vibration. But - Vitamin B12 will not have symptoms like Hemolytic Anemia (decreased hemoglobin, increased LDH). Vitamin E = answer, see below for explanation.

gonyyong  Also the MCV was normal, not megaloblastic like you would see in B12 deficiency +5  

They’re giving a lot of confusing extra information here, maybe to trip us up. They just want volume of distribution, simple as that.

Vd = [drug administered] ÷ [plasma drug concentration]

First convert it all to g/L because this is how the answer will be:

administered: 80 mg = 0.08 g plasma concentration: 4 ug/ml = 0.004 g/L


Vd = 0.08 grams ÷ 0.004 g/L = 20 L

Clearance of drug is not a huge factor because the half life is so long that the drug is distributing before significant clearance occurs.

gonyyong  I think the distribution half-life and elimination half-life was saying that by the time you checked, it had fully distributed (10 half-lifes) and had not been cleared yet (super long half-life) +7  
soph  1000ug= 1mg and 1g=1000000ug so then 4ug/ml * 1g/ 1000000ug= 0.000004 g/ml 0.000004g/ml * 1000ml/L= 0.004 g/L 80mg*1g/1000mg= 0.08 g vd= 0.08g/ 0.04g/l =20L +2  

submitted by seagull(545),

I thought this was a type 1 RTA but I was wrong. Any suggestions?

seagull  It looks like it was a type II RTA. The difference is incredibly subtle from the info given in this question. +1  
gonyyong  He has Fanconi syndrome which is generalized reabsorption defect in PCT which leads to metabolic acidosis and hypophosphatemia → can lead to rickets Also, does lead to type II RTA +7  
duat98  Also the proximal tubule is the place with the highest phosphate absorption rate. That's why PTH works here mostly and a little bit in the distal tubule. +3  

submitted by lsmarshall(230),

PCA stroke can cause "prosopagnosia" which is the inability to recognize familiar faces. Caused by bilateral lesions of visual association areas, which are situated in the inferior occipitotemporal cortex (fusiform gyrus). The ability to name parts of the face (e.g., nose, mouth) or identify individuals by other cues (e.g., clothing, voices) is left intact.

Without knowing that, remembering occipital lobe is involved in 'visual stuff' broadly, including image processing and this patient is having issues with understanding images should be enough to get to the answer.

gonyyong  Lol I guessed it exactly because of that +1  
sympathetikey  Never heard of that one before. Thanks! +1  
karthvee  This is not prosopagnosia, but instead a case of apperceptive agnosia. Wiki: "...patients are more effective at naming two attributes from a single object than they are able to name one attribute on each of the two superimposed objects. In addition they are still able to describe objects in detail and recognize objects by touch." Although, lesions tend to be in the occipito-parietal area so PCA again is the answer! +1  

The answer is hyporeflexia because the afferent arc of the muscle stretch reflex has to go through the dorsal rami and dorsal root ganglia. Dumb question, I know, but it’s the only answer that made sense. If you hurt the DRG, you not only lose afferent somatic sensory fibers, you also lose the sensory bodies involved in the various reflexes.

You can also get hyporeflexia from damaging the efferent neurons that innervate the muscle (like a LMN), but as you know these are in the anterior horn and ventral rami.

ankistruggles  Thanks! I agree with you. +  
brethren_md  Great explanation. +  
gonyyong  Agreed - I think I got this by thinking about tabes dorsalis (syphillis) and why it has hyporeflexia is due to dorsal root damage +1  
duat98  I'm confused about why it wouldn't cause muscle atrophy. Isn't that a fever of LMN damage? +1  
charcot_bouchard  Muscle atrophy wont occur because alpha motor neuron is intact. Motor control of Corticospinal tract on this is intact. so no atrophy. u can move shiti/ But remeber muscle spindle that is responsible for INITIATING stretach reflex send Ia fibre to DRG from where it synapse with Alpha motor neuron. if DRG is damage ur muscle is fine but u cant initiate strech reflex. areflexia +  

submitted by neonem(306),

I think the idea here is that if you take someone off a PPI, if there's no neoplasm or any problem with gastrin production then you should see it go down from baseline due to more negative feedback of gastric acidity. If not, you probably have a neoplasm that's just making tons of gastrin, such as in the case of Zollinger-Ellison syndrome.

gonyyong  I thought it was that if you are taking a PPI, you will see elevated gastrin regardless of it you have a gastrinoma. Thus to confirm diagnosis, you make them stop taking it, then re-measure gastrin → if it's still high, you have confirmed. If it's normal, it's something else +10