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How does telling an "embarrassed kid" that he will have big tits for 12-18 months help?!
my exact thought, telling him that it will last for somewhere around a year and a half doesnt seem so reassuring
I thought it was reassuring in that the kid is being told this isn't permanent as well as that this isn't something serious. It's important to inform him about the prognosis.
"don't worry your gynecomastia isn't permanent, but the mental scars from the bullying you will receive in HS definitely will be :) good luck!"
@therealslimshady the gynecomastia is from the sudden surge of testosterone during puberty being converted into estrogen => more breast tissue.
My breasts are not rubbery nodules, thank you very much!
Also wouldn't mammography be secondary prevention since you'd look for asymptomatic disease already present?
USPSTF recommends starting screening at age 50. 40 by patient choice if there's risk factors.
@_yeetmasterflex thats a good point i didnt think about that
be kind to yourself, doc! (it's a long road we're on!)
Hi, can someone explain the blood smear? isn't it supposed to show hypersegmented neutrophils if it was B12 deficiency?
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
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.
Lispectedwumbologist, please explain your mistake? Lol because that seems like a respectible answer to me...
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
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.
Thanks NBME, that really helped me....
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.
I didn't even register that was a lymphocyte. I thought I was seeing target cells so I was confused AF
Leave it to NBME to find the palest macrocytes on the planet.
so i guess size is more important than color cause those are hypochromatic as fuck
The NUCLEUS of a lymphocyte should be the same size as a normal RBC, which is not the case here. Under normal circumstances RBCs are not as big as lymphocytes, so this is truly extraordinary = megaloblastic anemia.
Is there a situation where you would pick fibromuscular dysplasia over atherosclerosis if given both options? Thanks for your help!
Atherosclerosis affects PROXIMAL 1/3 of renal artery
Fibromuscular dysplasia affects DISTAL 2/3 of renal artery
Why is there ↓ size in both kidneys? This threw me off
@gonyyong : Maybe because narrowed renal a. d/t atherosclerosis led to renal hypoperfusion and decrease in size?
Fibromuscular dysplasia occurs in young females according to Sattar Pg 67, 2018.
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
@gonyyong there's bilateral renal artery stenosis. The decrease in size of both kidneys should be from atrophy due to lack of renal blood flow.
1 year ago, she did not present any physical or Lab abnormalities. This means she must not suffer fibromuscular dysplasia, otherwise she must have presented renal abnormalities for a long long time, or even before DM-2.
a little surprised that atherosclerosis leading to bilateral renal artery stenosis and shrunken kidneys could happen that quickly after everything was A okay the year prior
Also the MCV was normal, not megaloblastic like you would see in B12 deficiency
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)
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
Or, like a normal human, convert 4ug/mL into mg/L ... which is 4 mg/L. 80mg/4mg/L is 20L.
I hate NBME... I thought these stupid conversions were over after undergrad. Nope.
You do 1000000000s of these a day if you do any type of labwork o.O You just get used to it eventually
It looks like it was a type II RTA. The difference is incredibly subtle from the info given in this question.
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
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.
Another easy way to go about this one is the question tells you he has metabolic acidosis, the only that can happen with is Fanconi/Type2 RTA. The rest will cause hypokalemia and metabolic ALKALOSIS. (pg 586 FA)
Personally thought if they were going for Fanconi syndrome they would describe a lot more symptoms for the kid like growth failure or hypophosphatemic rickets but its NBME so.
Lol I guessed it exactly because of that
Never heard of that one before. Thanks!
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!
I actually think it's both prosopagnosia AND apperceptive agnosia. She is neither able to recognize her mother's FACE nor is she able to recognize objects w/o the help of other senses (apperceptive agnosia)
Yea couldn't remember the exact name but I just thought of three pathways (visual, somatosensation, and auditory) all converging somewhere/processor (probably somewhere in the temporal lobe...hippocampus?). Beyond the point, the pathways converge to an area which culminates in recognition.
Cut off one of the routes (in this case visual), the other two will still work. How is visual cut off? By the PCA not supplying the area leading to neuronal death resulting in varying loss of visual function depending on the area in the occipital lobe.
Agreed - I think I got this by thinking about tabes dorsalis (syphillis) and why it has hyporeflexia is due to dorsal root damage
I'm confused about why it wouldn't cause muscle atrophy. Isn't that a fever of LMN damage?
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
DRG you lose DTR
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