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Welcome to mdmikek89’s page.
Contributor score: -1


Comments ...

 +1  (nbme23#21)

Pulmonary barotrauma is a lung overexpansion injury that typically occurs when a diver fails to exhale properly, or holds their breath during ascent. Compressed gas in the lungs expands as the diver ascends and can cause the lungs to rupture if not exhaled


 -1  (nbme22#35)

Okay boys and girls this question is easier than you think.

Hypothalamus relays via the sympathetic nervous system to control the body when a new set point as been reached in lets say...fever...cause by....infection.

If the connection between the hypothalamus and spinal cord (mainly the sympathetic outflow) is cut, the thalamus cannot relay the body reaction of a fever, but the hypothalamus itself can still change the set point.

Boom

Within the brain, the autonomic nervous system is regulated by the hypothalamus. Autonomic functions include control of respiration, cardiac regulation (the cardiac control center), vasomotor activity (the vasomotor center), and certain reflex actions such as coughing, sneezing, swallowing and vomiting.

B-E occur as a result of a change in set point.

A happens to cause the B-E when a new set point is reached.


 -1  (nbme22#15)

Subacute lymphocytic thyroiditis Subacute lymphocytic thyroiditis is characterized by damage to follicular cells with lymphocytic infiltration resembling Hashimoto's thyroiditis instead of granuloma formation. Drugs: α-interferon, lithium, amiodarone, interleukin-2, tyrosine kinase inhibitors Autoimmune disease Postpartum thyroiditis: affects 5% of women during the postpartum period and is 3 times more common among women with type 1 diabetes mellitus.


 -2  (nbme22#15)

Y'all need some Amboss in your lives.

This is a benign or malignant question.

focal mass or density

irregular margins

calcifications

= malignant = carcinoma

CLICK AND GTFO


 +1  (nbme22#39)

The most common adverse effect of nitrates is headache. (60% of patients)


 -3  (nbme22#45)

Spindle cells....sarcoma or carcinoma

Kaposi *Sarcoma*...

Why y'all make this shit so complicated?

drdoom  This explanation only begs the question. (It's a tautology.) +1

 -5  (nbme20#20)

Y'all over complicate this shit so hard. Whether or not its Fanconi, it says Proximal Tubule defect. 85% of phosphate is reabsorbed here. If its defective, phosphate re-absorption is decreased.

hypophosphatemia

meddoc2023  Yes and sodium absorption would be affected too I believe because the PCT is affected +

 +0  (nbme20#2)

This question is testing whether you know the difference in who the virus infects. Notice it says 25 adults...Norovirus. Rota is preschoolers.





Subcomments ...

submitted by keycompany(311),
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yepT I ebiaseDt is ehadczrariect sa eht seoctruntdi fo aetarcinpc tlsesi iicsc(pleaylf beta sllc)e by .clTs-le eTh smto keilyl aseuc fro aygyecplhoim lnoowlfgi lninisu nstoniiirda,mta etorhe,erf is the nrodcseitut of aplah lcesl atth runosdur teh tabe cs.lel Tshi dluwo asceu saeeddcre lelsve fo niicrcautgl caglonug.

titanesxvi  I think rather that high insulin is going to block the release of glucagon +6  
melanoma  the answer is not correct +1  
melanoma  his answer +1  
prolific_pygophilic  I actually think this has some merit. I believe there is a U world question that talks about how very long history of T1DM (20 years in this patient) can progress to destruction of alpha cells and hence impaired release of glucagon and episodes of hypoglycemia. Thats how I reasoned it. The first answer is also possible. +  


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A amrnbloots si na emtiaurm R,CB so t'si daeelvte in aetsts fo csadrieen iooiepamhstse.

sympathetikey  Don't mind me. Just sippin my dumb ass soda over here. +63  
someduck3  The term "Normoblast" isn't even in first aid. +36  
link981  NBME testing your knowledge of synonyms. Have to know 15 descriptive words of the same thing I guess. +19  
tinydoc  I wish they would stop making it so every other question I know the answer and I can't find it among the answer choices because they decided to use some medical thesaurus on us. +18  
qball  Metamyelocytes = Precursor to neutrophils Siderophages = hemosiderin-containing macrophage aka heart failure cells +8  
llamastep1  Theres a UWorld question about Parvovirus B19 that mentions "giant pronormoblasts" that helped me make the connection +6  
fexx  I got it right but would it hurt them to put RBCs? Medicine is hard as it is. No need to make the exams more complicated. I doubt my pt is ever going to as me if his/ her normoblasts are going to increase if they go hiking in the mountains +6  
nerdstewiegriffin  I can guarantee you this Q was written by some sadistic PhD examiner +13  


submitted by drschmoctor(98),

I got thrown off thinking about nitric oxide synthesis occurring in the endothelial cells and NO diffusing to nearby smooth muscle cells. This does occur, though the cGMP the question asks about is a downstream effect of the NO in the smooth muscle cell.



submitted by lfsuarez(143),
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sThi ntaipte repessnt ihtw a mlasl clel acimocran whchi si vyre nmmooc ofr apra eolnicaspt .eonsmdrsy nI thsi aesc the cceanr is gnicusa .SDAIH ollnyeDcieecm si a yntreclictea btoniaitic tath si soal udse to trtae ADHSI

gabeb71  To add to ^ It is widely used (though off-label in many countries including the United States) in the treatment of hyponatremia (low blood sodium concentration) due to the syndrome of inappropriate antidiuretic hormone (SIADH) when fluid restriction alone has been ineffective. Physiologically, this works by reducing the responsiveness of the collecting tubule cells to ADH. The use in SIADH actually relies on a side effect; demeclocycline induces nephrogenic diabetes insipidus (dehydration due to the inability to concentrate urine). +14  
qball  And for you Sketchy people Demeclocycline is in GI/Endocrine ADH one with the bicycle and that "vaptans" are first line. +3  


submitted by keycompany(311),
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ilraAtoent fo teh arteiohtmtsc ste niotp si a liaohtaymphc opcerss emedaidt yb lnarisgdonatps dan si epdnneednti of hte cttyeampsih vrsoeun ssmtey.

,B ,C D, dna E lla qererui ctyhitepmsa seevnr to ietllci a ss.epnore

pg32  Can anyone explain the mechanism behind shivering and the sympathetic nervous system? +2  


submitted by keycompany(311),
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C/0tiswow.9t/bl5vmlmai6cneigPn/8s.w.pn/hrh0Mc/:/tc2.p

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It is seplobsi atht ire: tae)h Teh l-yweiciospftci fo shti etst aemns it is lsoa lealbpacpi ot eelsishcrtoroas ton( juts ) MA)b hTe BNME einrtorccyl melsiip ttha MA si anehicbenlatrg itwh ircessreo.lashot

bubbles  This was my reasoning, too. I thought this was Mockenberg for sure +  
hello  I don't think think it's a type. According to 2 other comments: "It's atherosclerosis because it said “radial artery is NON-pulsatile BUT REMAINS PALPABLE even as the cuff is inflated”--> normally, you can’t feel the artery when the cuff is overinflated b/c overindlation occludes blood flow and arteries are squishy (compliant); BUT if you had atherosclerosis, which is literally hardening, you would not be able to compress the artery, and neither would you expect the normal radial (outward) expansion of an artery during systole. (that is, the pulses!): "If if something were to not be palpable then it would have to collapse -- atheroclerosis prevents this vessel collapse." +17  
arcanumm  I agree, I just reasoned that atherosclerosis would not be thicker when the lumen is blocked. I don't think they were going for Mockenberg at all. +  
arcanumm  would be thicker +  
drzed  Atherosclerosis isn't common in the radial artery though... it's common in the abdominal aorta + coronary, popliteal, and carotid arteries. I am not going to assume a guy has radial artery atherosclerosis when he is in his 80s without a dyslipidemia syndrome over monckeberg calcification! +  
haydenelise  Would've thanked you for your explanation @mdmike if it hadn't included the "whoever upvoted this is dumb" comment. What a turd lol +4  


submitted by keycompany(311),
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h9on.itsil/8M/t.we5cl2nhiPw/b.:C6n0vpcma./mcw/s/rtp0g

Oselr Sngi is a l,isin-ttyosievw wsecyfplo-tiic nigndfi fo ebkgroeMnc iAsolrrcsetloosrei )(AM cczheaiardter yb a" llepapba gulhatoh see,psllus iadlra earytr whlei eth PB ucff si tdnifeal evabo csilotsy eusp.e"srr

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bubbles  This was my reasoning, too. I thought this was Mockenberg for sure +  
hello  I don't think think it's a type. According to 2 other comments: "It's atherosclerosis because it said “radial artery is NON-pulsatile BUT REMAINS PALPABLE even as the cuff is inflated”--> normally, you can’t feel the artery when the cuff is overinflated b/c overindlation occludes blood flow and arteries are squishy (compliant); BUT if you had atherosclerosis, which is literally hardening, you would not be able to compress the artery, and neither would you expect the normal radial (outward) expansion of an artery during systole. (that is, the pulses!): "If if something were to not be palpable then it would have to collapse -- atheroclerosis prevents this vessel collapse." +17  
arcanumm  I agree, I just reasoned that atherosclerosis would not be thicker when the lumen is blocked. I don't think they were going for Mockenberg at all. +  
arcanumm  would be thicker +  
drzed  Atherosclerosis isn't common in the radial artery though... it's common in the abdominal aorta + coronary, popliteal, and carotid arteries. I am not going to assume a guy has radial artery atherosclerosis when he is in his 80s without a dyslipidemia syndrome over monckeberg calcification! +  
haydenelise  Would've thanked you for your explanation @mdmike if it hadn't included the "whoever upvoted this is dumb" comment. What a turd lol +4  


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uOr letilt nrifed hsa a vrrviaosuP ie,ifnnotc wchhi fnteics ieryothrd s,rroeuspcr ugsicna trtieuonpnri fo rheotyrtcey odn.rioctpu sThi si eth amse ywa ti ssuace dyoprhs teisfla ni nnurob bsebia adn tapiaslc nmaiea ni selick ,lcle e.ct

gainsgutsglory  I get Parvo has tropism for RBC precursors, but wouldn’t it take 120 days to manifest? +  
keycompany  RBCs don’t just spill out of the bone marrow every 4 months on the dot. Erythropoesis is a constant process. If you get a parvo virus on “Day 1” then the RBCs that were synthesized 120 days before “Day 1” will need to be replaced. They can’t be because of parvovirus. This leads to symptomatic anemia within 5 days because the RBCs that were synthesized 125-120 days before the infection are not being replaced. +27  
drdoom  @gainsgutsglory @keycompany It seems unlikely that “1 week” of illness can explain such a large drop in Hb. It seems more likely that parvo begins to destroy erythroid precursors LONG BEFORE it manifests clinically as “red cheeks, rash, fever,” etc. Might be overkill to do the math, but back-of-the-envelope: 7 days of 120 day lifespan -> represents ~6 percent of RBC mass. Seems unlikely that failure to replenish 6 percent of total RBC mass would result in the Hb drop observed. +  
yotsubato  He can drop from 11 to 10 hgb easily +3  
ls3076  Apologies if this is completely left-field, but I didn't think this was Parvovirus. Parvo would affect face. Notably, patient has fever and THEN rash, which is more indicative of Roseola. Thoughts?? +4  
hyperfukus  @is2076 check my comment to @hello I thought the same thing for a sec too :) +  
hyperfukus  also i think you guys are thinking of hb in adults in this q it says hb is 10g/dL(N=11-15) so it's not relatively insanely low +  
angelaq11  @Is3076 I completely agree with @hyperfukus and I think that thinking of Roseola isn't crazy, but remember that usually with Roseola you get from 3-5 days of high fever, THEN fever is completely gone accompanied by a rash. This question says that the patient has a history of 4 days of rash and 7 days of fever, but never mentioned that the fever subsided before the appearance of the rash. And Roseola is not supposed to present with anemia. +3  
suckitnbme  @Is3076 another point is that malar rash refers to the butterfly rash on the cheeks that is commonly seen in lupus, so the face is NOT spared. +