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Welcome to zevvyt’s page.
Contributor score: 45


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 +1  visit this page (nbme22#31)
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You dont really need to know the murmur to get the question right, but I'm confused about the murmur. It sounds like Mitral Regurgitation. So why is it in the left sternal border and not the apex?

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madamestep  Maybe it's heard best at the apex, but you could also hear it at the LLSB? +

 -1  visit this page (nbme21#27)
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Of all the things they can test us on, they're testing our fucking Gadar??

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peridot  Don't mean to be an eager beaver but I thought it was pretty cool to get tested on our gaydar! I think that's an important thing to pick up on. As for their answer choices, I'm not always the biggest fan of those since I think there's more than one right way to do something... +4
yesa  @zevvyt I really don't think they are. I've done my internal medicine rotation and spent two weeks on solid onc where all my patients were terminal. It doesn't matter if the relationship is romantic or not, and the reason the friend should get to stay with the patient isn't so the friend can be updated on the patient's care/condition more easily--it's to provide comfort and companionship to the patient as she faces a constant uphill battle with her disease. The quality of the patient's life is contingent on such experiences/support if these are important to her. +1
sunnyside  Yikes... it's disconcerting reading this from a potential future colleague. Terrible joke if that's what you were going for. Boooo +

 +3  visit this page (nbme21#37)
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A= Caudate ( flanks Lateral Ventricle) B= Internal Capsule, between Thalamus and Lentiform Nucleus( Putamen, GP) C= Thalamus( Flanks 3rd Ventricle D= Temporal Lobe E= Occipital Lobe

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 +2  visit this page (nbme21#43)
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to me, this is a process of elimination question.

Fasciotomy and bosentan don't make sense.

Clopidogrel and aspirin kinda make sense, Except Treatment of DVT is not part of their clinical use. (Clopidogrel 429 and aspirin 475 of FA 2019).

So we're left w Embolectomy.

PS. Thrombolytics and Direct Factor Xa inhibitors are used for DVT

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personalpurposes  Yeah I dont think is going for a DVT though, the patient is presenting with "coolness and paleness" in her LE with absence of pulses". This is basically implying an arterial occlusion and thus an embolus in the ARTERIAL system. In a DVT we can say arterial supply is normal so we would feel a warm extremity with normal presentation. Either way I guess at the end of the day you could embolize the DVT clot too. +3
yhm17  And the mention of irregularly irregular rhythms clues you in that a clot was formed in the heart and embolized to the lower extremity arteries. +1




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submitted by bwdc(697), visit this page
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Leydig cells make testosterone. Leydig cell tumors aren’t always physiological active, but those that are can cause masculinization. Granulosa cell tumors, on the other hand, sometimes produce estrogen (which can lead to precocious puberty in young girls but otherwise may be occult). Teratomas are oddballs that typically have fat, hair, teeth, etc. Thecomas will not be on your test. Ovarian carcinoid is highly unlikely to show up on your test, but if it did, it would likely present with a classic carcinoid syndrome.

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sugaplum  FA 2019 page 632 +2
divakhan  because................"Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen" NBME 24 -#13 Qs explanations/comments on this website, has led me to choose this answer! :D +22
zevvyt  divakhan, thANK you i was hoping praying that someone would have written that +2
meja2  hahaha same!!!! I got this because of the explanations from NBME!! Thanks guyssssss +
meja2  **NBME 24 +


submitted by bwdc(697), visit this page
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Narcotic use for acutely painful conditions is both reasonable and important. Short-term use (immediately post-surgical) does not lead to long-term dependence (or so people have thought…). And yes, drugs addicts should also receive narcotics to control pain.

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drdoom  prefer “patients with hx of substance abuse” over more conveniently typed but less redemptive “drug addict” +18
sugaplum  I don't see why switching her to oral pain meds when she is ready would be incorrect. Clearly she is worried about being on the pain meds, I feel making a proclamation that she has a low risk of addiction would be profiling just because she doesn't have a history. The opioid epidemic also affects people who didn't have a previous history of drug abuse. Just a thought, not trying to push any buttons. Maybe I am thinking to hard about this, but I don't see the clear A vs B line for this question. +58
nbme4unme  @sugaplum I thought the exact same thing as you and chose the acetaminophen answer accordingly. I maintain that I am correct, my score be damned! +10
sushizuka  I had a similar question on UW and the explanation stated that the correct answer choice was the only one that addressed the patient's concern and answered her question. The rest were just alternative treatments, so they were incorrect. But I too answered with oral pain meds. +7
angelaq11  couldn't agree more with you all. I chose acetaminophen because opioid abuse is NO joke. The crisis is still going strong because of answers like this... +1
houseppary  I ruled out oral acetaminophen because they described in great detail the severity of her injuries, and indicated that she wasn't even fully conscious/aware when she asked this question about opioids. Rather than expose her to more pain, and possibly worsen her long-term pain prognosis, by switching to acetaminophen too early, in this case it makes sense to keep her comfortable because she's very seriously injured and not even fully lucid. It's kind to reassure her in this case. +3
anastomoses  I appreciate all of the passion for the opioid crisis, and the wording of the answer is definitely not ideal. However, PAIN is also very real, and there is no way acetaminophen alone would cut it in a case like this, not "as soon as she can take medications orally." Maybe I'm lucky to have 6 months in clinicals before STEP or had a mom who just went through urgent spine surgery for breast cancer mets, but there is a time and place for opioids and this is clearly one of them. Thank you for coming to my ted talk. +10
llamastep1  I agree with anastomoses, cmon guys have you ever had serious pain? oral acetaminophen is NOT enough for that type of pain. +3
sora  I r/o oral acetaminophen b/c she's post-op for major GI surgeries so you might want to avoid PO meds for a while +
melchior  As argument against the oral acetaminophen answer choice, it says "switch the patient to oral acetaminophen boldas soon as she can take the medication orallybold" This means you're just waiting for her swallowing inability from the facial fracture surgery to come back, which might not have much to do with her pain, and so it seems somewhat arbitrary. +
drpee  Maybe logically/clinically A is true, but this seems like a "patient communication" question to me and I could NEVER imagine A being a good way to phrase this point IRL. +2
zevvyt  Don't forget who pays for these tests: BIG PHARMA!! +1
topgunber  youd think after spending and borrowing every ounce possible that we were the ones paying for the tests +
yesa  Good pain control post-op is going to decrease risk of bad outcomes later. +


submitted by madden875(25), visit this page
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From Goljan:

Platelet problem = epistaxis, echymoses, petechia, bleeding from superficial scratches

Coagulation problem = late re-bleed, Menorrhagia, GI bleeds, hemarthroses

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step7777  Also that: Platelet problem = primary hemostasis = superficial bleeding Coagulation problem = secondary hemostasis = "deep" / internal bleeding +2
zevvyt  i thought I read that INR was 12 and got real confused on that question +
topgunber  is there a reason for the decreased PTT? or is that just a distraction +
justanotherimg  @topgunber It throwed me off as well, but I found this on google- Sometimes a traumatic or difficult blood collection may result in activation of the coagulation pathway in the sample, resulting in a shortened aPTT time. So I guess it was just a distraction. +
icrieeverytiem  It's still confusing. The decreased PT and PTT seemed like hypercoagulability and the only rationale to eliminate that is that he is asymptomatic. Unfortunately I picked DVT and lost an easy point. +1
athenathefirst  also is subungal hemorrhage seen in infective endocarditis? +


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

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lispectedwumbologist  Nevermind I'm stupid as fuck I see my mistake +2
drdoom  be kind to yourself, doc! (it's a long road we're on!) +21
step1forthewin  Hi, can someone explain the blood smear? isn't it supposed to show hypersegmented neutrophils if it was B12 deficiency? +1
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 +25
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... +9
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 +2
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. +4
yotsubato  Thanks NBME, that really helped me.... +1
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. +6
sahusema  I didn't even register that was a lymphocyte. I thought I was seeing target cells so I was confused AF +
drschmoctor  Leave it to NBME to find the palest macrocytes on the planet. +5
zevvyt  so i guess size is more important than color cause those are hypochromatic as fuck +
yesa  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. +1
weirdmed51  @yesa you mean ‘macrocytic’. For it to be ‘megaloblastic’ there had to be a hypersegmented neutrophil. +


submitted by tinydoc(276), visit this page
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This question is very sneaky, but in essence this is whats happening.

The accidental removal of the PTH glands during thyroidectomy ⇒ ↓ PTH

PTH normally: --in bone: ↑ removal of Ca²⁺ and Phophate from bone --in kidneys: ↑ Ca²⁺ reabsorption and ↓ PO₄³⁻ reabsorption --↑ conversion of 25, Hydroxyvitamin D to 1,25 Hydroxyvitamin D (Calcitriol - active form) via ↑ activity of 1-a Hydroxylase deficiency

Therefore a ↓ PTH would lead to:

⇒ ↑ PO₄³⁻ ⇒ ↓ Ca²⁺ ⇒ ↓ 1,25 Hydroxyvitamin D

The question is sneaky (much like the rest of this exam) because someone who isnt focusing really hard or in a rush might pick the option C where phophate is ↑ and PTH is ↓ BUT ↓ 25 hydroxyvitamin D

This is wrong as only 1,25 hydroxyvitamin D would be decreased, the conversions before this are done by the skin (sunlight) and liver.

I really wish they would stop making the questions confusing PURELY for the sake of making them confusing. Isnt it enough that we have to know this ridiculous amount of information, without having them intentionally making it harder by pointing you to 1 answer choice but changing a minute detail to make you answer wrong. Or using a random ass nomenclature for a disease to avoid making it too simple (PSGN = "proliferative GN")

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tinydoc  I literally got this wrong because I had the font zoomed in and assumed the 1 was on the line above like on uworld when it tries to squish the whole title in the same space x_X +1
hungrybox  Holy fuck they got me. They boomed me. The fucking NBME boomed me. +4
graciewacie9  Amen to the PSGN question. They got me on that one. lol +
msw  the psgn question is pinting to rapidly proliferating glomerulonephritis b/c the pt has developed acute renal failure within days of the insult +
msw  *pointing +
snoodle  HOLY GOD MY BRAIN FILLED IN THE 1. i had to read this explanation 4 times to finally see 25-hydroxyvitamin D and not 1,25. F U NBME +3
avocadotoast  this bs is prob why the question isnt on step 1 anymore +
zevvyt  so since conversion of 25 --> 1-25 is disrupted , would 25 be high? I know its not an answer choice, just wondering +2


submitted by lsmarshall(465), visit this page
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"Air droplets" sounds like respiratory (saliva or water) droplets. Inhalation of toxoplasma oocysts in cat feces isn't quite the same; not to say I know exactly what the oocysts are inhaled as (just microscopic dry cat poop particles?). Ingestion of undercooked meat to get the cysts is certainly a ROT for toxoplasma.

Toxoplasma as TORCH has triad of hydrocephalus, cerebral calcifications (intracerebral), and chorioretinitis. chorioretinitis can be in congenital CMV or toxoplasmosis. Periventricular calcifications are in CMV. Congenital CMV usually has hearing loss, seizures, petechial rash, “blueberry muffin” rash, chorioretinitis, and periventricular calcifications.

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usmile1  also note that toxoplasma can cause the "blueberry muffin" rash (also rubella can as well) +
raddad  So looking at the CDC website, it looks like "accidental ingestion of oocysts after touching cat feces" is the route you were talking about in the first paragraph, so inhalation of air droplets is wrong inherently. +2
zevvyt  is his small head common is Toxoplasma? +


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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.

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ankistruggles  Thanks! I agree with you. +1
brethren_md  Great explanation. +1
gonyyong  Agreed - I think I got this by thinking about tabes dorsalis (syphillis) and why it has hyporeflexia is due to dorsal root damage +10
duat98  I'm confused about why it wouldn't cause muscle atrophy. Isn't that a fever of LMN damage? +8
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 +5
zevvyt  DRG you lose DTR +2


submitted by notadoctor(175), visit this page
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Usual interstitial pneumonitis is the histological definition of Idiopathic pulmonary fibrosis. We know that this patient has pulmonary fibrosis because the question states that there is fibrous thickening of the alveolar septa. This question was just testing that we knew the other names for Pulmonary Fibrosis.

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aneurysmclip  Nbme back at it again +37
pg32  Is it still considered idiopathic pulmonary fibrosis is it appears to have been caused by an atypical pneumonia? +1
zevvyt  Why not Sarcoidosis? Wouldn't Sarcodosis also be a chronic inflamation with fibrous thickening? +2
swagcabana  UIP is a better answer. Sarcoid is a leap in logic, usual interstitial pneumonitis is textbook histological definition of idiopathic pulmonary fibrosis. The biopsy has no mention of noncaseating granulomas and the clinical picture is not consistent with an inflammatory process. You have to focus on the better answers, try not to get caught up in the "why nots?" Calling this sarcoidosis is like someone coming in with prototypical asthma and jumping to eosinophilic granulomatous with polyangiitis. Sure its a possibility but its definitely not likely. +7
mangotango  I picked “diffuse alveolar damage” with Pulmonary Fibrosis in mind but these are actually key words for ARDS :/ +5
zevvyt  thank you swagcabana! Very good explanation and strategy! +


submitted by welpdedelp(270), visit this page
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It was scabies, which is transmitted person-operon.

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welpdedelp  **person-person lol +9
suckitnbme  NBME loves their scabies +23
dentist  did you get scabies from "burrows" and "night itching" +1
pg32  My question is where do you get scabies originally? I knew it was transmitted person-to-person, but thought it has to originate somewhere (a pet possibly?) so I went with pets. The internet only seems to say that you get scabies from another person with scabies, so the question remains: where do people contract scabies from? +1
leaf_house  @pg32 , long quote: + "Sarcoptes scabiei mites seek the source of stimuli originating from the host when they are off the host but in close proximity to it. This behavior may facilitate their finding a host if they are dislodged from it and contaminate the host environment. Thus, direct contact with an infested host may not be required for humans and other mammals to become infected with S. scabiei. In the case of human scabies, live mites in bedding, furniture, toys, and clothing can be a source of infection. Sarcoptes scabiei var. hominis have been recovered from laundry bins in a nursing home." + from here: https://parasitesandvectors.biomedcentral.com/articles/10.1186/s13071-017-2234-1 +1
zevvyt  to summarize leafhouse: Fomites +3
surfacegomd  FA 2020 p.161 "transmission through skin-to-skin contact (most common) or via fomites" +1


submitted by keycompany(351), visit this page
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Nitrogen balance is a measurement of protein metabolism in the body. A negative nitrogen balance indicates muscle loss, as increased amounts of amino acids are being metabolized to produce energy. This increases the amount of nitrogen secreted from the body. Because the amount of nitrogen you are taking in is less than the amount of nitrogen you are secreting, you have a negative nitrogen balance.

This man is malnourished, edematous, cachetic, and has hypoalbuminemia. These clinical findings point to protein malnutrition (Kawashkior Disease), which causes edema due to decreased serum oncotic pressure. Low oncotic pressure in this case is due to protein loss, and hence a negative nitrogen balance.

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drdoom  Nice! +23
dubywow  I knew your last sentence and suspected Kwashiorkor. It's just everything else I did not know. I have not heard or thought of muscle/protein changes in terms of "nitrogen balance" before... and that's why I got this wrong. Nice explanation! +3
macrohphage95  I agree with you in first part but i dont think it has any relation to kwashirkor. It is simply due to cachexia which causes muscle destruction through the proteasome pathway .. +5
zevvyt  also, it says that his albumin is low. +
ankigravity  A few other points related to nitrogen balance. Any patient who is growing (i.e., children, people working out and building muscle) are in positive nitrogen balance and arginine becomes an essential amino acid. +1
drdoom  @ankigravity Wow, this is technically correct! (Didn’t realize “essential” doesn't mean “cannot be synthesized by the body” but rather ”cannot be synthesized in sufficient amounts”; so what qualifies as essential is a bit of a moving target! Thanks!) +
drdoom  Here's the definition from MeSH: “Amino acids that are not synthesized by the human body in amounts sufficient to carry out physiological functions. They are obtained from dietary foodstuffs.” https://meshb.nlm.nih.gov/record/ui?ui=D000601 +
imgdoc  I don't think this has to do with kwashiokor like macrohphage95 suggested. This is cachexia secondary to lung cancer, TNF-alpha increases and causes proteasomal destruction of proteins. This guy is also not intaking enough proteins so negative nitrogen balance is the answer explained above +


submitted by amphotericin(11), visit this page
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I put constipation because I thought the medication being described might be CCB: can someone explain why nitrates over CCB?

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seracen  Wouldn't nitrates be a faster acting drug here? That was my take-away anyway. One is more acute, the other for long term maintenance. +4
suckitnbme  I also believe it's because CCBs have minimal effect on venous beds and would not cause a significant decrease on preload. +3
beto  decrease of cardiac preload is another word of Venodilation, so Nitrates primarly venodilators. CCB dilate arteria more than veins +1
zevvyt  also, verapamil is the one that causes constipation. But Verampamil is non-dyhydropiridine, so it works more on the heart than the vessels +3
nowherekid139  CCB- decrease afterload by vasodilating arteries by acting on smooth muscle (remember arteries are muscular, veins are flimsy) Nitrates- decrease preload by vasodilating veins Hope that helps! +


submitted by cellgamesgojan(43), visit this page
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The patient suffered from Immune Thrombocytopenia. autoantibodies against the glycoproteins GP2B/3A.

On labs, you’ll see: increase in megakaryocytes; on the question stem they’re described as “rare but large.” Megakaryocytes are not suppressed.

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ergogenic22  isolated thrombocytopenia (low platelets) should be highly suggestive of ITP https://www.aafp.org/afp/2012/0315/p612.html +3
pg32  I agree that in ITP you will see an increase in megakaryocytes, but where did you see that in the stem? Platelets being, "rare but large" doesn't mean megakaryocytes, does it? Also... can anyone explain why she was anxious but alert and had petechiae distal to the blood pressure cuff? +
meryen13  @pg32, I'm not too sure about the "anxious but alert" but I think they might wanted to mention she is oriented so in case there was no lab values, you would guess that she is not extremely anemic or something. and about the petechia with the cuff and the tooth brushing bleeds, that is a sign of platelet problems because its a superficial bleed. if you saw deep bleeds like joint bleedings, think about coagulation pathway problems (like hemophilia) +2
zevvyt  "rare" means thrombocytopenia. "Large" means there are megakaryocytes to make up for the thrombocytopenia +2
lovebug  FA2019, page419 +1


submitted by cantaloupe5(87), visit this page
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Histology showed coagulative necrosis (preserved architecture of myocardial fibers) with neutrophil infiltration which hinted that the MI was within 24 hours. Most likely cause of death within first 24 hours of MI is arrhythmia. Myocardial rupture would also be visible on gross appearance of the heart, which they described in the stem.

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bighead478  in FA it shows softening of the myocardium to happen at 3-14 days. Do you think this was overly misleading people (like me) into choosing myocardial rupture? I understand the histo features are consistent with < 24 hours, but the stem should also match this in every detail +16
sbryant6  Myocardial rupture would not happen until 3-14 days. Since this shows signs of <24 hrs, the answer is arrythmia. +3
hello  @bighead478 You have to look at the whole picture. Histo shows preserved architecture, which indicates coagulative necrosis -- coagulative necrosis is a histo finding only in the first 24h. The most common causes of MI-related sudden death are: arrythmia > cardiogenic shock (heart pump problem) > rupture. +
jcmed  I chose the rupture as well due to the timeline. Somebody gave me this advice the other day, NBME classically will give you an entire vignette leading you somewhere, and the what it asks will be something completely different; or in this case will give you a photo of something and will ask about the photo. They do what they want. +5
athenathefirst  Anyone knows why it's not a cardiogenic shock if it was within 24 hours? +5
zevvyt  It says "Mottling" which happens in the first day. If it was 3-14 days it would be yellow (p 302 2019). He can be having angina for 3 weeks leading up to an MI. +2
amy  The stem of the question said "softening" which indicates 3-14 days (rupture ), and "mottling" which indicate 24h (arrthymia). It seems from the picture in FA2020 page 305, coagulative necrosis would be there during both phases. The cells in the picture are so small that it is hard to tell if it is purely neutrophil or if there are any macrophages. Still seems like a very confusing stem to me. +


submitted by mcl(671), visit this page
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Deltoid is innervated by axillary nerve, which comes from roots C5/C6. Actions of the deltoid include abduction of the upper extremity.

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seagull  I hope everyone memorized every single part of the brachial plexus and all the roots of each, No detail let untouched!!! +31
mcl  In case anyone else has purged the whole brachial plexus from your memory (like me), this is a great resource linked by another user. https://geekymedics.com/nerve-supply-to-the-upper-limb/ +12
zevvyt  I thought it was radial since he lost sensation in his thumb. If Radial is C5-T1, wouldn't that be included in C5-C6? +3
alimd  they force us to know brachial plexus like the holy bible +2
skonys  the brachial plexus gives me the traumies +1


submitted by skip_lesions(17), visit this page
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Can't histamine also cause swelling or is it just not involved in the pathology of gout?

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zevvyt  yes. Histamine causes vasodilation and increased vessel permeability. But it's not involved in Gout. Gout is more about Neutrophils and Macrophages activating eachother and not really about Mast cells. +5


submitted by notadoctor(175), visit this page
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Usual interstitial pneumonitis is the histological definition of Idiopathic pulmonary fibrosis. We know that this patient has pulmonary fibrosis because the question states that there is fibrous thickening of the alveolar septa. This question was just testing that we knew the other names for Pulmonary Fibrosis.

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aneurysmclip  Nbme back at it again +37
pg32  Is it still considered idiopathic pulmonary fibrosis is it appears to have been caused by an atypical pneumonia? +1
zevvyt  Why not Sarcoidosis? Wouldn't Sarcodosis also be a chronic inflamation with fibrous thickening? +2
swagcabana  UIP is a better answer. Sarcoid is a leap in logic, usual interstitial pneumonitis is textbook histological definition of idiopathic pulmonary fibrosis. The biopsy has no mention of noncaseating granulomas and the clinical picture is not consistent with an inflammatory process. You have to focus on the better answers, try not to get caught up in the "why nots?" Calling this sarcoidosis is like someone coming in with prototypical asthma and jumping to eosinophilic granulomatous with polyangiitis. Sure its a possibility but its definitely not likely. +7
mangotango  I picked “diffuse alveolar damage” with Pulmonary Fibrosis in mind but these are actually key words for ARDS :/ +5
zevvyt  thank you swagcabana! Very good explanation and strategy! +


submitted by meningitis(644), visit this page
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LPS found in outer membrane of gram ⊝ bacteria (both cocci and rods). Composed of O antigen + core polysaccharide + lipid A (the toxic component).

Activates Macrophages and induces TNFalpha release -> Hypotension and fever.

Pg 133 Endotoxin.

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zevvyt  and just to note answer b) "induction of histamine release" DOES happen , but it's not the "Initial Event" that the question asks for +1
unknown001  there you go, another introducer of confusion who dislikes straightforward questions +


submitted by cantaloupe5(87), visit this page
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Recurrent kidney stones should include hyperparathyroidism on your differential, couple that with gastrinoma and you’re looking at MEN 1. Lipomas are also associated with MEN 1.

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sympathetikey  Yeah, I probably should have went with that. Just got thrown off, since I know that usually the serum calcium levels for someone with Calcium kidney stones is normal. +1
snoochi95  i understand the link to MEN 1, but why are we checking the calcium level? +1
cmun777  I feel like it's important to get a baseline of where the calcium is at for two reasons: 1. if the patient does indeed have MEN 1 it would be good to know if she has high calcium levels and possible Parathyroid etiology 2. You're putting the patient on a PPI which are known to decrease calcium levels and increase risk of osteoporosis for both these possible factors/concerns it would be good to see where calcium is currently at +6
zevvyt  Couldn't a Pituatary tumor secrete ACTH, causing high cortisol? +2
lola915  Patient has symptoms of a gastrinoma (Zollinger-Ellison Syndrome)- patients present with diarrhea, epigastric pain, duodenal and jejunal ulcers. Associated with MEN1 syndrome. +


submitted by tinydoc(276), visit this page
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infarcts would be a more peripheral wedge shape

abcess wouldnt be invasive to the surrounding area i think.

squamous cell is more centrally located

wasn't 100% sure but thats the best answer slthough stupid to give 0 symptoms and just a picture, nothing like an actual clinical scenario

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tsl19  Squamous cell is centrally located and has cavitation, which you can see in the pic. Similar to this one: https://webpath.med.utah.edu/LUNGHTML/LUNG068.html +8
zevvyt  I also didn't choose infarct cuz i think the lung would have a red infarct. +1


submitted by strugglebus(189), visit this page
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Hydrocodone/Methadone can lead to dependence--you avoid in long term use. NSAIDs you also avoid due to partial ineffectiveness in neuropathic pain as well as ulcer risk. TCA's are known to treat neuropathic pain very well (i.e. diabetes, ART therapy)

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champagnesupernova3  Drugs for neuropathic pain: TCAs, gabapentin and pregabalin +1
mangotango  SNRIs +
mangotango  also SNRIs* +1
zevvyt  methadone isn't a pain med(even though it's an opiate), it's used for opiate addiction. And hydrocodone is used for "moderate" pain and this person is in "severe" pain. +
shakakaka  Drugs for neuropathic pain: TCA, SNRI, Anticonvulsant, Opioids, Lidocaine, Capsaicin +1


submitted by stepbystep(1), visit this page
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does some mind explaining why this isn't a tear in the sciatic nerve?

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sugaplum  It is a very thick nerve, so I think it is hard to tear without physically cutting it. Also if it tore you would have tibial and common fibular nerve symptoms as well. You would see sensory numbness and tingling along the dermatome also the mechanism of injury is focused on spine so a disc rupture is more likely +1
zevvyt  I got this question wrong but I really like because it helped me get past a confusion I hadon this subject. If it were a tear, you'd see the loss of motor function that sugaplum was taling about(FA 444 2019). But if it's a herniation, like in this case, you see Radiculopathy/Sciatica symptoms that are on 446. +2


submitted by hayayah(1212), visit this page
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In order for a drug to be cleared by the kidney, it must first be filtered in the glomeruli. Drugs with a high VD have more of the drug in the tissue that are not available to filtered by the kidney. Drugs with high protein binding won't be filtered either. So you want a drug with low Vd and low binding if you want it cleared via the kidneys and urine.

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zevvyt  But a low VD corresponds to high Plasma Binding Concentration(FA 233, 2019). That's my main confusion with this question. +3
kevin  If it's high plasma binding, then it's low Vd. But, low VD doesn't necessarily require high plasma binding. Low Vd can simply be due to it being a large polar molecule +3
topgunber  So you the confusion is that VD of 1 means it stays in the circulation/ intravascular compartment. This would make you think that it would bind highly to protein in because of the low VD. But im assuming if it bound proteins it would not be cleared by the kidneys, so if this had a low VD (can be cleared at glomerulus) and if it bound plasma proteins weakly (allows the kidney to filter the substance) then it can be filtered into the tubular lumen. Now the pka. Bases when protonated (ph under their pka) become charged, while acids at ph under their pka get protonated are UNCHARGED, meaning in acidic urine acids become more lipophillic and can diffuse out of the tubular lumen. If we made the urine more basic, then we want to deprotonate the acid (ph higher than pka) so it will remain stuck in the tubular lumen as an ion. +


submitted by hayayah(1212), visit this page
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Acute interstitial renal inflammation. Pyuria (classically eosinophils) and azotemia occurring after administration of drugs that act as haptens, inducing hypersensitivity (eg, diuretics, NSAIDs, penicillin derivatives, proton pump inhibitors, rifampin, quinolones, sulfonamides).

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hungrybox  But how is a 2-year history acute? +4
jinzo  there is also " Chronic interstitial disease " +4
targetmle  i got it wrong because there wasnt rash, also there was proteinuria, doesnt it indicate glomerular involvement? +2
zevvyt  Got it wrong too cuz of that. But there can be proteinuria in nephritis, just not as much as in nephrotic syndrome. I guess that's confusing cuz this type of nephritis isn't grouped with the other nephritic conditions. +1
lovebug  FA 2019, Page 591. +


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