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 +2  (nbme24#10)

According to FA 2019 pg. 495 contraction of lateral pterygoids help lower the jaw, making the answer to this question seem counter intuitive. (Wouldn't you need the jaw to be open to slide the mandible back into the TMJ?) Consider, however, that the lateral LPs also facilitate protrusion of the jaw. Thus, their relaxation would make it easier to reduce the joint.

I found this video helpful for getting a visual of the LPs.

maria_danieli  i thought that when a TMJ dislocation isn't reduced quickly your muscles kind of contract in that position.. since in ATM dislocation your mouth is open you have a contracture of lateral pretygoids that prevents mouth's closure TMJ. to slide the mandible back you need to relax them otherwise the mouth won't close! Same as shoulder dislocation, you must act tempestively otherwise you'll need BZD to relax muscles could this be an explanation? +2
jj375  Agreed, it says that the person is drooling and has an "inability to elevate the jaw" therefore it is stuck in the lowered position --> a spasm of the Lateral pterygoid. I always remember it since its the only MUSCLE OF MASTICATION starting with an L there its the only one that LOWERs the mandible. Medial pterygoid, masseter, temporalis all help raise the mandible/jaw. Masseter also helps retracts the jaw. +

Subcomments ...

submitted by t123(20),

This question is really testing what the different types of diarrhea show. Key is "stool shows no abnormalities". In malabsorption, exudative, osmotic, and secretory diarrhea, your poop would be weird in some way. A motility disorder is the ONLY type here that would cause normal poop.

myoclonictonicbionic  How would stool be different in secretory or osmotic diarrhea? They state that he has loose stool which could also indicate osmotic/secretory diarrhea. I think they are trying to hint that he has diabetes for 26yrs therefore he has diabetes enteropathy and therefore motility issues +4  
takayasuarteritis  I'm with you on this. I think it's a myenteric nerve plexus issue from long-standing diabetes. +13  
drpee  Neuropathy makes sense for T1DM, I guess I just expected a motility issue to cause constipation rather than diarrhea... +13  

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tallerthanmymom  Wait... I swear we could treat hep C with Sofosbuvir and Ribavirin and that it is curable these days? +1  

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drdoom  prefer “patients with hx of substance abuse” over more conveniently typed but less redemptive “drug addict” +12  
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. +46  
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! +7  
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. +6  
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. +2  
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. +4  
llamastep1  I agree with anastomoses, cmon guys have you ever had serious pain? oral acetaminophen is NOT enough for that type of pain. +2  
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!! +  
topgunber  youd think after spending and borrowing every ounce possible that we were the ones paying for the tests +  

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tallerthanmymom  Can someone explain why it is an increase in risk rather than a decrease? Also, relative to what? Do we just assume it is relative to people who do not exercise regularly? +  
banana  Uncertain about this, but I think from my memory of the question that the above explanation should say "relative risk" and not odds ratio. The relative risk is the (number women fractured/total exposed)/(number women fractured/total unexposed):: therefore, >1 means that more women got fractured when they exercised. (FA 2020, 258) +1  
drpee  Same risk: RR = 1 (theoretical). Lower risk: RR < 1. Greater risk: RR > 1 +  
blah  I got confused by the question because I was bringing in my own biases (i.e. doesn't exercising decrease the risk of fractures in this population of women?). If you simply read the question as what does a RR>1 mean? No doubt you'll get the correct answer. +4  

submitted by nwinkelmann(294),
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drpee  TLD-Watch? Reducing sugars include galactose, lactose, and fructose. +4  

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jiya   why cant this be hand foot and mouth disease cause of coxsache +9  
drachenx  Also thought it was Hand-foot-mouth an RNA virus but I did consider Herpes. Changed because I thought Hand foot and mouth would be more common. +  
llamastep1  Hand foot mouth usualy involves all 3 places (hands, feet and mouth/perioral area) and the lesions on the hand arent localized to just one finger. +2  
aneurysmclip  Hand foot mouth disease affects palms and soles. ref: FA 2019 - 150 +3  
raffff  wouldnt the history also be different for coxsakie +  
focus  I think this image is trying to show the "dew drops on a rose petal" sign on Hermes, the god of Herpes on Sketchy Micro +1  
drpee  Google some images of HF&M disease. The small blisters look very different from herpetic whitlow. +  
drdoom  ^ ... some images of HF&M disease ... +  

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houseppary  Any guesses as to why he might have CKD at 4 y.o.? +1  
drpee  Possibly ARPKD? +  

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joonam  Hey bro, thank you so much for your contributions on these free 120 questions. Your advice on test taking strategies for step 1 have been very helpful. +21  
luciana  "Elaborated enzymes by H. pylori may also contribute directly to epithelial cell injury. Ammonia produced through urease activity may be toxic to gastric epithelial cells. H. pylori protease and lipase degrade gastric mucus and disrupt the phospholipid-rich layer at the apical epithelial cell surface, allowing for cell injury from back diffusion of gastric acid." +2  
luciana  I got tricked :( Thought the damage was due to destruction of local somatostatin cells with increased gastrin and acid production... but this is actually the mechanism of duodenal ulcers development related to H. pylori But makes sense, so thats how the somatostatin producing cells are destroyed lol +4  
drpee  "Hyperacidity and gastric ulcer development" is also sort of true, but this is hinting at the mechanism for DUODENAL ulcer development from H Pylori. Irritation in the stomach leads to G Cell hyperplasia, increasing acid secrection which causes downstream ulceration. +5  
itsalwayslupus  Did anyone else pick the hyperacidity answer just because the correct answer had "local tissue destruction" in it? I figured that H. Pylori was non-invasive, so would not directly damage the tissue it is localized too +5  
cbreland  @itsalwayslupus exact same thoughts over here +  

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drpee  Also question suggests a negative Nikolsky sign ("The blisters do not easily break"). This suggests BP over PV. +3  

submitted by anu(4),
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yhw is otpoin D ) rehet is na nresdacei kihlliodoe fo ttasilltysiac ntfcniigsia gworn ?

micray  There is a decreased likelihood of statistically significant findings due to the much higher threshold (lower p-value). +3  
drpee  The lower you make your p-value, the harder it will be to prove the relationship. That's why I always go with a p-value of .49 in my research. +1  
lba9587  Because BOTH values are significant. PValue of Less than or equal to 0.05 is significant. +  

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charcot_bouchard  But they grouped them based on dosaged? +  
keyseph  I think the key thing here is that the participants were told what treatment they would be receiving. This is in line with an open-labeled clinical trial. Open-labeled clinical trials can still be randomized and do not need a control (as in this case). +6  
drpee  Yeah, bad question IMO. Open-labeled trial can also be randomized... Since they didn't tell us how participants were selected for each group perhaps that's why C is better than D? +1  

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ihsT is a abd uon.stqei taltlePe igengaagrto temi ibgen m,olran ko ifen I acn ese tuB FVW isezbastli rcotaf 8 dan doyu' ees an sniecrea in TTP strf(i inel netx to FWV ni tsFri d.)Ai yWh is rithe TTP nlra?mo

a1_antitrypsin  Totally agree, and they give you a slight increase in PT instead +  
mambaforstep  yeah but if they gave you an increase in PTT then Hemophilia A could have been a valid answer choice. so they prob showed a nl PTT to differentiate vWF dz from hemophlia A +  
drpee  VWD only sometimes presents with a slightly increased PTT. Don't let those anki facts steer you wrong... Plus all the other answers make no sense. Afibrinogenemia? That means literally no fibrinogin (PT and PTT would be infinitely increased). Hemophelia? Or vitamin K deficiency? Those are coagulation factor disorders so they would present with deep bleeding and large bruising. (Unlike platelet disorders, including VWD, which present with mucosal bleeding, petechiae, and heavy menses). VWD is actually the ONLY one that makes sense. +5  
cbreland  I get why it's not afibrinogenemia (which is what I picked), but still don't understand how VWD is right. You have normal PTT and normal platelet aggregation (both of which should be abnormal). Is the only thing leading us to VWD is it being a primary bleeding issue? Again, my answer made no sense, but VWD in this context, seems way out there +  
osteopathnproud  I agree with you @cbreland once I noticed I had to bend lab values for any answer choice then in my head most of them were possible. I took a step back and answer with the most common bleeding disorder, vW disease. Funny thing is when I retook it to check my answers, I had time to overthink and got it wrong. +  
aakb  the anki facts never steer you wrong! my zanki cards say "Low vWF in von Willebrand disease impairs platelet {{c1::adhesion}}" (Gp1B binds to vWF) not platelet aggregation (GpIIbIIIa binds to fibrinogen). additionally it says you can have either a normal or increase PTT. in this case the PT is not increased. It is decreased a little, which I assume is fine esp w an INR of 1.0 +  
lebabs  Shut up +  

submitted by monoloco(136),
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lilyo  Vasoconstriction of the EFFERENT arteriole actually leads to increased GFR. It selective VASODILATION of the efferent arteriole effect of ACE inhibitors since they undo Angiotensin II actions. This patient already has rescued renal blood flow due to bilateral renal artery stenosis, the addition of an ACE inhibitor further decrease GFR prompting an increase in renin due to loss of negative feedback. +2  
drpee  We should always expect GFR to drop a little after adding an ACE-inhibitor due to efferent arterial vasodilation. For this reason we should also expect Renin levels to rise via tubuloglomerular feedback. So it's not really the reaction to the ACE inhibitor that gives this away as RAS (which is why I got it wrong). I think what we are expected to be looking at it are lab values: Hypokalemia, and secondary hyperaldosteronism. +  
stepwarrior  ACE inhibitors would actually have the opposite effect of AT-II, and result in efferent dilation. But the actual mechanism of increased renin activity per UWorld is lack of systemic vasoconstriction by AT-II leading to blood shunting away from the kidney. +