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Welcome to baja_blast’s page.
Contributor score: 91


Comments ...

 +0  (nbme18#13)

This man has a Meckel Diverticulum, which can cause hematochezia or melena. The 99mTc-pertechnetate scan used for diagnosis of Meckel Diverticula hinges on uptake of the radioactive compound by heterotopic gastric mucosa. FA 2019 p. 378.

The age of this patient threw me off. I would have thought that a Meckel Diverticulum would have presented earlier in life than 19 years old.


 +1  (nbme18#42)

The man in this question has hemochromatosis (bronzed skin, hepatomegaly, arthritis, increased iron content and cirrhosis on liver biopsy). Cirrhosis of any etiology is associated with hepatocellular carcinoma. FA2019 p. 386.

Basal Ganglia atrophy is associated w/ Wilson's disease (which can also cause cirrhosis and therefore hepatocellular carcinoma).

Hemochromatosis is associated with diabetes mellitus, not diabetes insipidus.


 +1  (nbme18#31)

I'm skeptical of this being Toxic Shock Syndrome, as the rash in TSS is usually described as being similar to that of a severe sunburn and, besides fever, there are no other associated TSS symptoms (hypotension, shock, vomiting, abnormal LFTs, etc). Moreover, questions about TSS usually mention nasal packing or a left-in tampon, both of which are absent in this three year old boy. You can read about TSS in FA 2019 on p. 135.

I think it's more likely that this is Bullous Impetigo, which is mentioned briefly on FA 2019 p. 470 as being caused by S. Aureus.

Either way, both are caused by S. Aureus so even if you thought this was TSS you should still get the right answer here.

cbreland  I agree with this explanation. Thought that they would make us decide between S aureus and GAS (bullous v. non-bullous impetigo) but seems like they went easy on us +1
jer040512  It sounded more like Scalded Skin Syndrome to me. I saw this in Amboss and thought i'd post it here. "SSSS belongs to the spectrum of diseases mediated by specific staphylococcal toxins, which also includes bullous impetigo, toxic shock syndrome (TSS), and Staphylococcus aureus food poisoning. Unlike TSS, SSSS does not have systemic manifestations (e.g., liver, kidney, bone marrow, and CNS involvement)!" +1
jer040512  It sounded more like Staph Scalded Skin Syndrome to me. Here's what i found on AMBOSS. SSSS belongs to the spectrum of diseases mediated by specific staphylococcal toxins, which also includes bullous impetigo, toxic shock syndrome (TSS), and Staphylococcus aureus food poisoning. Unlike TSS, SSSS does not have systemic manifestations (e.g., liver, kidney, bone marrow, and CNS involvement)! +
jer040512  It sounded more like Scalded Skin Syndrome to me. I saw this in Amboss and thought i'd post it here. "SSSS belongs to the spectrum of diseases mediated by specific staphylococcal toxins, which also includes bullous impetigo, toxic shock syndrome (TSS), and Staphylococcus aureus food poisoning." +
jer040512  I thought this was Scalded Skin Syndrome. Here's what I got from AMBOSS. SSSS belongs to the spectrum of diseases mediated by specific staphylococcal toxins, which also includes bullous impetigo, toxic shock syndrome (TSS), and Staphylococcus aureus food poisoning. Unlike TSS, SSSS does not have systemic manifestations (e.g., liver, kidney, bone marrow, and CNS involvement)! +

 +0  (nbme16#31)

Vinca alkaloids (e.g. vincristine, vinblastine) inhibit microtubule production and mitotic spindle assembly. They bind Beta-Tubulin and inhibit its polymerization into microtubules, arresting dividing cells in the M-phase of mitosis. FA 2019 p. 433.


 +1  (nbme16#34)

Lymphocytic infiltrate and collagen deposition are hallmarks of chronic inflammation. One might also observe plasma cells, macrophages, and angiogenesis. FA 2019 p. 217.

Worth noting is that of the Hepatitis viruses, Hepatitis C is the most likely to cause a chronic infection (C for Chronic).


 +5  (nbme15#48)

In this study, a placebo is not used on the control group. The experimental group gets dextromethorphan while the control group gets "no treatment". This results in procedure bias, as subjects in different groups are not treated the same. Blinding and use of a placebo reduce the influence of participants and researchers on procedures and interpretation of outcomes as neither are aware of group assignments.

See table on bias and study errors in FA 2019 p 260.


 -1  (nbme15#7)

Anyone know why this was Hydronephrosis and not Staghorn Calculus??

hchairston  There are no calculi in the image. The image shows a dilated ureter, you know it's a ureter because there is an opening into the hilum of the kidney. +2
prosopagnosia  Personally, I couldn't tell that the ureter was dilated without a comparison image. But what I did notice was the dilation of the renal calyces and severe renal atrophy which clued me into some ureteric obstruction --> Hydronephrosis. +1
trazobone  OK so I put ARPKD bc of chronic renal insufficiency and also i thought the dilated parts were cysts +1
shieldmaiden  Remember that for ARPKD both kidneys will be affected and it will involve the cortex as well as the medulla. If you notice, the cortex is intact +1

 +2  (nbme15#32)

Cocaine use in pregnancy is associated with low birth weight, premature membrane rupture and abruptio placentae. Click here for more.

FA 2019 p. 600 gives a list of drug effects during pregnancy.

cheesetouch  teratogens FA2018 p596 +1

 +1  (nbme15#8)

Vitamin B12 (Cobalamin) is absorbed in the terminal ileum along with bile salts. Remember that this inquires Intrinsic Factor from the stomach! Other answer choices are primarily absorbed in other components of the GI tract.

Folic acid = Duodenum, Jejunum ("small bowel" in FA)

Iron = Duodenum

Thiamine = Jejunum

Riboflavin = "upper small intestine" when dietary or large intestine for the riboflavin produced by gut microbiome. See this paper

See FA 2019 p. 368 for the high-yield absorption sites.


 +1  (nbme15#49)

Glucokinase expression is induced by insulin and helps to store glucose in the liver. FA 2019 p. 75


 +5  (nbme17#39)

Fibrosis pulls the airway open, increasing radial traction and decreasing resistance to airflow.

Here is a picture comparing fibrosis (increased traction) to emphysema (decreased traction) to a healthy lung.


 +4  (nbme17#0)

Gluconeogenesis primarily occurs in the liver, but enzymes for gluconeogenesis are also found in kidneys and intestinal epithelium. FA2019 p. 78


 +1  (nbme20#46)

The key bit in this question that makes the answer Cholecalciferol rather than 7-dehydrocholesterol is the nugget that the patient "rigorously avoids exposure to the sun." Conversion of 7-dehydrocholesterol to Cholecalciferol can only occur when the skin is exposed to sunlight. Therefore, decreased production of Cholecalciferol (D3) is the better answer.

This picture always helps me remember Vitamin D metabolism.


 +2  (nbme21#9)

Whole point of administering a SERM after breast cancer is to reduce risk of recurrence. Increased estrogen exposure is associated with increased risk of breast cancer (per FA 2019 p. 636). So you're looking for something that is an estrogen antagonist at the breast, which narrows it down to B and C right off the bat.





Subcomments ...

submitted by wishmewell(30),
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Tyhe rea iiersgcnbd oncesarvu nssui drmoneys FA( 1280 geap )265 NC VI is the smto cubpesielts ot uyrijn! CN VI is neddee to uctbad eth yee. eeht s astntipe ahve eovnuasrc nssui osthisombr radelte ot hte ,itoncnief ortdaic eocvusnar ustiaslf, siyccolalna ecrseadde raxyiallm asnes.toni daeceesdr eolncra sst,noaine henorr nysdoerm.

baja_blast  FA 2019 p. 530 +  


submitted by match95(48),
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eInumm rbiytncoephamoto A(F 721,0 gp 54)0 - cesaus rnusedotitc fo -tlnltaoeedybiapt mcxelpo yb peelsn daielng ot eadesecr in eattlepl QUNATYTI and nediascer ktresgeacmoyay on enob rrwmoa b.pysio

ellie0124  anti-GpIIb/IIIa antibodies +  
baja_blast  FA 2019 p. 419 +  
jurrutia  May be secondary to viral illness... +  


submitted by match95(48),
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ihTs owdul tujs be the nrolam pserseno fo our yiknsed ot hwne we 'ontd nridk twear hgeonu (aka sjtu )raml.on

laixPomr ueulbt si inoticos usceabe ew ear gaobenrisrb BHTO aN+ dna 2.OH

cMlaau sndae si chitopoyn uecabes it is ssgnien the dastli otlduvneoc butlue -- eht mots LUEIDT patr of the p.rnnoeh eeermbRm teh neeottnrcurcur acnexegh setyms - hickt dnicsegna bmli si glsnoi CNal (nueri sgte esls rncnteoceadt as it es).dcnas

rdylMaleu ncloeilcgt utcd si ietohpcnyr eucsaeb ew aer rebagibrnso lal teh eatwr gmnaki eht unire eorm arocttdceen.n



submitted by anechakfspb(27),

Sensation is decreased over the right lateral forearm and the man is unable to flex the right elbow. These are functions performed by the musculocutaneous nerve, which is labeled "E".

baja_blast  A) is the Median nerve (lesion here would cause loss of wrist flexion, carpal tunnel symptoms). B) is the Long Thoracic Nerve (lesion here causes winged scapula). C) is the Medical Cord. D) seems like it's probably the C8 nerve root, but that labeling is a little ambiguous. +  


submitted by wishmewell(30),
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I aws ocefdsun tbeween lpahA- nuSyelcni adn Tu.a isTh etpitna sha sskoiapnrn sdseseai adn htus we lodwu ees Aahpl nny.scleiu

auT is esen in atiepstn wtih sckiP dseeas,i aka onttpraoemrFol dneamtei DAN ihserzelam es.saide gea p 054. AF 2018

baja_blast  FA 2019 p. 508 +  


submitted by suckitnbme(164),

X-ray shows a fracture of the surgical neck of the humerus. This where the axillary nerve and the posterior circumflex humeral artery travels.

motherhen  Additionally, axillary nerve supplies sensory innervation for lateral aspect of shoulder. Radial does lateral elbow and musculocutaneous does lateral forearm. +  


submitted by aneurysmclip(134),

basically polycystic kidneys won't work properly, they've hinted at this with the s.creat of 4mg/dl. thus the kidney won't do what its supposed to do. REMEMBER to check whether they are asking SERUM changes or URINE changes

Kidneys normal function - reabsorb HCO3- , its not doing that now > decreased HCO3

PTH - would cause increased Calcium reabsorption in kidneys, but kidneys aren't able to reabsorb calcium > PTH responds to low calcium levels and levels increase

PO4 ties into PTH as well, PTH acts be DECREASING PO4 reabsorption. Since kidneys aren't working ie: not responding to PTH > there would be increase in PO4

pg32  Sometimes these questions are made more difficult by trying to decipher the order in which these changes happen (first cause). In my mind, whenever I see a question on renal insufficiency, I know that phosphate in the serum will increase. In response, Ca will decrease and in response to that, PTH will increase. Lastly and unrelated, HCO3 will decrease because the kidneys aren't absorbing HCO3 as they usually do. +10  
baja_blast  I also think there is decreased 1alpha hydroxylation of Vitamin D, which would increase PTH secretion +1  


submitted by breis(44),
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cptotcSoeucsr soengyP opr(gu A tp)ers has a sgereuntniap acunsig coks.h ihTs ntangie ihrngtrcyoeE ixnExoot A uacsse a oixcT i-hckoekls y:mdnreso Fr,eve a,shR hkc,oS etlrcaS Fre.ve

FA gp 331 10(2)9

extraordinr  correction: GAS erythrogenic toxin causes scarlet fever specifically in this question there is no reason for this child to have TSS +5  
loaloagubba  SpeA and SpeC toxin is erythrogenic toxin referred to here. +3  
baja_blast  Erythrogenic exotoxin A + Strep Pyogenes is responsible for BOTH Scarlet Fever and Toxic Shock Like Syndrome. It can also cause Necrotizing Fasciitis. It's definitely Scarlet Fever in this question but I just don't want people to get confused. FA2019 pages 133, 136 +  
baja_blast  Sorry, not A. Just Erythrogenic Exotoxin +. +  


submitted by breis(44),
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Seoccutrcsotp oeygPsn ropgu( A pre)ts sha a rnputasinege scnaigu ohkcs. sThi gnnaeit oeiErnrythcg xtoEonxi A ceusas a cioxT ci-kklsoeh myre:nsod eFv,er s,Rha khc,So etScral r.Fvee

FA gp 313 90)1(2

extraordinr  correction: GAS erythrogenic toxin causes scarlet fever specifically in this question there is no reason for this child to have TSS +5  
loaloagubba  SpeA and SpeC toxin is erythrogenic toxin referred to here. +3  
baja_blast  Erythrogenic exotoxin A + Strep Pyogenes is responsible for BOTH Scarlet Fever and Toxic Shock Like Syndrome. It can also cause Necrotizing Fasciitis. It's definitely Scarlet Fever in this question but I just don't want people to get confused. FA2019 pages 133, 136 +  
baja_blast  Sorry, not A. Just Erythrogenic Exotoxin +. +  


submitted by lamhtu(113),
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teSm uhsdlo mbyae ays mseo siosnle rae lctyi nad meos ear e.ortislcc traBse stem ot enbo is imedx tyep doiagcrnc ot A?F fI you go off eht emst iegnb uepylr yltc,i eon ldouc nhkit thirdoy cromcinaa si teh rcrecto riapyrm r.umto

lae  thats also what I thought +6  
pg32  Yeah I didn't pick breast for the same reason. Then I didn't pick thyroid because I doubt serologic studies would be normal in thyroid cancer (if you check T3/T4 and TSH). So I went with avascular necrosis -_- +2  
lynn  in the FA index, the only things listed under lytic bone lesions are adult T cell lymphoma, langerhan histiocytosis, and multiple myeloma. Obviously there's more than that but those might be the main ones we need to know. You could also say that a giant cell tumor is also technically lytic, considering they describe it as "osteoclastoma." Idk. I thyroid but looking at FA, none of the thyroid carcinomas describe metastatic lytic lesions. Medullary carcinoma might be the one to confuse you, but it secretes calcitonin which inhibits osteoclasts, so it shouldn't cause resorp or lytic lesions. Right?? +1  
prp5c  just a different view - I was between avascular necrosis and metastatic carcinoma, but ended up going with metastatic carcinoma because I figured avascular necrosis of the lumbar and thoracic region would be hard since you'd have the artery of Adamkiewicz as a dual supply to the vertebrae? +1  
baja_blast  I only picked breast over thyroid because it specified "metastatic". I agree this definitely threw me off. According to Dr Sattar, breast cancer causes "mixed lytic/blastic lesions". Most all other bone mets are lytic w/ the exception of the prostate which causes blastic mets. +  


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hisT aveirs ngmao asstte ubt ni tosm of eth tessat a 21- yrea feer euesirz iorpde si ieeqrrud orf peitiepcl taipnset to teg htire liecens

baja_blast  Didn't realize I was in law school +12  


submitted by sympathetikey(1249),
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A lce,tyoecs also knnwo as a leprpdosa rlb,edad si a licadme ncnidtoio ni whihc a n'omwsa daedlbr egslub tnio rhe iaa.nvg mSeo yam aehv no omyst.pms Oehtr aym heva rlubeot tniatrgs naioiut,nr ruayirn it,ecennninoc or rteeuqfn .raniotinu poosClatiminc amy lindceu eutcrrenr arniryu cattr enocifitns nda iryruna etnnite.ro

/es/niyttkCgl/i.rwai.kwdppt/eoeiseo:hci

cbreland  How would you rule out uterine prolapse? +  
baja_blast  With a Uterine Prolapse you would see the uterus move down, into the vagina. With Cystocele you have the finding described in the question; bulge of anterior vaginal wall (which borders the bladder) into the vagina. Here's a pic to help illustrate: https://www.health.harvard.edu/media/content/images/cr/205345.jpg +  


submitted by masn8cc(2),

Can someone explain how they r/o aortic stenosis? because that could enlarge the LA and give the same sx of hoarseness etc. And the murmur also fits with AS

bmalamet  You would not see a "viable pulsation above the manubrium, which you should not confuse with a "brisk carotid upstroke" associated with aortic stenosis. +2  
nbmeanswersownersucks  "brisk carotid upstroke" is the description of a normal carotid pulse. Aortic stenosis has a slowly rising/late peaking upstroke since the stenosis impedes flow out of the LV. +4  
overa  AS affects the LV first. it isn't until later in the disease progression that there will be a significant enough enlargement of the LA to cause impingement of the LA. By the time the problem was that bad there would also be pulmonary findings of backed-up pressure (in my not so expert opinion). +  
305charlie94  Can anyone explain why the trachea is deviated in an aortic aneurysm? Made me think of a pneumothorax here +1  
baja_blast  ^It's basically mass effect. Aortic aneurism takes up space in the thorax, displacing the trachea to the right. Take a look at this CXR: https://radiopaedia.org/cases/thoracic-aortic-aneurysm-3?lang=us +3  


submitted by lsmarshall(393),
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yrbnenaSvotpi is teh etagrt fo nttpnmoaaessi enu(ttsa ;ix)ton seclum passsm era icetcsrihtarca. lOyn orhte narwse uyo hmtig sdcneiro is eyilersAstcnheloctea nesci eh si a mrefar dan uwbsdozzr oetfn rryac su to hte ormpsdie na..dl. tub tmspymso of a iihcogrnlec mtosr rea staebn.

vshummy  Synaptobrevin is a SNARE protein. Why they couldn’t just give us SNARE I’ll never know. +41  
yotsubato  Cause they're dicks, and they watched sketchy to make sure our buzzwords were removed from the exam +41  
yotsubato  Oh and they read FA and did UW to make sure its not in there either +34  
soph  This toxin binds to the presynaptic membrane of the neuromuscular junction and is internalized and transported retroaxonally to the spinal cord. Enzymatically, tetanus toxin is a zinc metalloprotease that cleaves the protein synaptobrevin, an integral neurovesicle protein involved in membrane fusion. Without membrane fusion, the release of inhibitory neurotransmitters glycine and GABA is blocked. -rx questions! +6  
qfever  So out of curiosity I checked out B) N-Acetylneuraminic acid It's sialic acid typical NBME +2  
alexxxx30  shocked they haven't started calling a "farmworker" a "drudge" <-- word I pulled from thesaurus. +2  
snripper  "You shouldn't memorize buzzwords. You gotta learn how to think." Lemme pick another random ass word that doesn't have anything to do with critical thinking skills and use it instead. +5  
mw126  Just as an FYI, there are multiple "SNARE" Proteins. Syntaxin, SNAP 25, Synaptobrevin (VAMP). From google it looks like Tetanospasmin cleaves Synaptobrevin (VAMP). Botulism toxin has multiple serotypes that target any of the SNARE proteins. +2  
wrongcareer69  Here's one fact I won't forget: Step 1 testwriters are incels +2  
baja_blast  FML +  
j44n  its not an ACH-E inhib because he doesnt have dumbell signs +  


submitted by neonem(549),
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aamltHsspio can tca kile TB dan aeucs vyartcai ienslos dna difliacce nosduel hitw iofrctbi sncrr.aig In nr,glaee nuifg rae abmeodttc yb yptehslyocm and agrsceph,aom tno sioipohnlse or soi.nleuhrpt

baja_blast  Asthma history got me and I put Eosinophils.... but in hindsight I should have noticed that the biopsy is specifically of the nodules. RIP. +1  


submitted by bingcentipede(208),

This is a peri-menopausal woman experiencing the typical symptoms of hot flashes and irregular periods. Decreased estrogen/progesterone production leads to vaginal atrophy and negative feedback onto the anterior pituitary, leading to increased FSH and LH hormones.

baja_blast  Menopause on FA2019 p. 622 +  


submitted by aoa05(21),

here are partial clinical manifestations of the right oculomotor nerve palsy:  the right pupil is 6 mm and nonreactive to light, and adduction of the right eye is impaired. The oculomotor nerve exits midbrain through the interpeduncular fossa and goes between the beginning of the posterior cerebral and superior cerebellar arteries. Rapture of an aneurysm in the posterior communicating artery near the beginning of the posterior cerebral artery may compress the oculomotor nerve and affect its function

medstudent  FA 2020 P. 516 +  
baja_blast  FA 2019 p. 529. +  


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uYo ohlsud eb niigkthn fo esmhogtin ekli crnsoc.Eeocut heTy dah a GU oeecprrdu adn tsbnqueues rdcciaa sss.eui

Wnhe I haer fsto 1S, i nihkt tath eht patniet tsum vaeh adh a useis wiht teh cligosn of ertieh eth ltmira ro itspdiurc slaevv. gPnyali ,dsdo tshi hlouds be eht tamlri .vvael ouY laso ehre na elrya ctasiildo urm,rum os yuo itmgh eb gnnthiik lomvue dvoorael (.3)S

baja_blast  You're almost certainly right that it's mitral valve endocarditis. The murmur is accentuated by Expiration, consistent with lEft-sided murmurs. On the other hand, rIght-sided murmurs are accentuated by Inspiration. Note the capital letters for a handy trick. God Bless Dr. Jason Ryan. +2  


submitted by cassdawg(930),

Hairy cell leukemia is notable for staining tartrate-resistant acid phosphatase positive (TRAP positive) and for having hairy cytoplasmic projections [FA2020 p432].

If you did not know this, you could eliminate other answers based on the stem:

  • Lymphomas would have swollen lymph nodes
  • It mentions the lymphocytes as the issue and he has lymphocytosis, so you can eliminate the myelogenous leukemias and focus on the ones from the lymphocytic cell lines
  • Acute lymphoblastic leukemia most commonly occurs in children and is associated with immature B/T-cells that are TdT+, so you can eliminate this
  • Chronic myelogenous leukemia is slowly progressing and associated with smudge cells, so it also does not match the descriptors.
baja_blast  For the last bullet, I believe OP meant CLL instead of CML. +  


submitted by bingcentipede(208),

FA 2019, P. 304:

2-7 days following an MI, there can be a papillary muscle rupture, leading to mitral regurgitation. Thus the murmur in the answer, specifically the description of holosystolic and cardiac apex

baja_blast  A) describes Aortic Regurgitation. B) describes Mitral stenosis. C) describes Aortic stenosis. D) describes a PDA. +1  
beto  Can be VSD rupture too +  


submitted by cassdawg(930),

This is mesenteric artery stenosis causing postpranidal intestinal ischemia/angina. I definitely did not know this answering the question and I personally got to the answer by attempting to logically think through the symptoms:

  • Weight loss and abdominal pain in general pointed to intestinal ischemia of some sort and since most absorption of nutrients happens in the jejunum, ischemia there would cause weight loss. Jejunum is supplied by SMA
  • Bruit to me meant a larger vessel was blocked since to be able to hear it it has to be a pretty large vessel, SMA is one of the larger arteries listed
  • No liver symptoms (i.e. jaundice) so eliminated hepatic artery

If anyone has a better explanation please offer it.

deathcap4qt  great explanation for not knowing the answer! You're right in that it has to do with a vessel of a larger size. Generally Celia, SMA or IMA. pt hx of atherosclerosis should be a big hint. FA 2019 pg 380. +2  
nbmeanswersownersucks  SMA is the MOST COMMON vessel involved in ischemic bowel disease. +1  
baja_blast  I reasoned this out by remembering that the Abdominal Aorta was the most common place for atherosclerosis and picking the only option that branches off immediately from there. Not sure if that's what they were going for but it got me to the right answer. +1  
topgunber  i think thats a great explanation ^, namely because its possible obstruction at the other vessels may not cause symptoms due to collateral circulation. SMA on the other hand, if stenosed, would have a number of regions with ischemia- not to mention its involved in a watershed area. +  


submitted by andro(170),

Fatty Acid degradation
-Occurs in mitochondria or peroxisomes

First step - uptake of the fatty acids by the cell and addition of CoA to them

Second step - Uptake of the Fatty Acyl CoA molecule into the mitochondria by the Carnitine Shuttle *( which involves removal and then addition of the CoA molecule again to the fatty acid once inside the mitochondria)

Once in the mitochondria the fatty acid may undergo , Beta-oxidation ( a process in which a fatty acid is oxidized/cleaved at the Beta carbon to generate Acetyl CoA in several cycles )

An Acyl CoA dehydrogenase catalyzes the initial step .
Look out for Hypoketotic Hypoglycemia in defects of fatty acid degradation

The 2 main subtypes to be aware of are -a problem with the carnitine shuttle ( systemic carnitine deficiency) - or with an Acyl CoA dehydrogenase ( eg MCAD deficiency )

notyasupreme  It's actually funny because the question stem makes it seem like it's an MCAD deficiency (presence of dicarboxylic acid) and all the symptoms, but then treat it with MCAD. Whatever, I got it right but it just felt like a weird question to me. +2  
nbmeanswersownersucks  yeah I was confused too but I also think the negative serum carnitine is supposed to help r/o MCAD deficiency since that usually has elevated serum carnitine. +  
baja_blast  If Carnitine was an option here, how could we differentiate this from primary carnitine deficiency? Would it have been possible? +5  
melanoma  the presence of dicarboxylic aciduria is more related to mcad/lcad deficiency. the patient receives medium chain tryglicerides because he has the enzyme to metabolize it. +2  
melanoma  but no for the long chain +  
topgunber  just a few things, sure it sounds like mcad but lcad would present similarly, except in MCAD, giving medium chain triglycerides would worsen symptoms as compared with LCAD. + Similarly when fatty acids cant undergo Beta oxidation they undergo omega oxidation- which is why there is increased dicarboxlic acids (i.e. dont just jump for MCAD when you see dicarboxilic acids). Last of all it would be difficult to differentiate but if the patient were deficient in carnitine the treatment with MCADs would not show improvement because carnitine is required to shuttle the fatty acid into the MTs. +1  
topgunber  'a 'weird question' because my school never asked it' +1  


submitted by ergogenic22(301),
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oClo adn pael tseiteixrme lesru out ttevirsbdiui sescua nne,rueo(cig yhpnxsaia,al itecps).

lpoHmiyvcoe uwlod brscdeei a rcessop of evmuol ossl lein(gedb ro )oitrdaeydhn adn uwold tno eanilxp the ckrlaces ro uulrgaj veni sedosinit.n

'dnot be ntrohw fof by hte olranm thare .dnusso

baja_blast  Raise your hand if you were also thrown off by the normal heart sounds. +6  
jmd2020  I think this question is poorly constructed. Cardiogenic shock would result in an INCREASE in SVR - this woman's BP is 70/40... +1  
drdoom  @jmd2020 low BP does not mean the SVR isn't increased — it /is/ increased! it's just that the heart is so effed up that even massively increased SVR is not enough to maintain good pressure +2  
drdoom  another way to explain: imagine you are losing blood volume at a constant rate (someone punched a tube into your aorta and draining you like a pig); at first, your heart would beat stronger (ionotropy) and faster (chronotropy) to maintain BP; at the same time, all your arterioles would constrict to maintain blood flow rates (and perfusion) to vital tissues ... but at some point you will have lost so much blood that all the ionotropy, chronotropy & SVR in the world could not save you or your BP .. your BP will plummet no matter what compensatory mechanisms your body has up its sleeve. +2  
drjo  Jugular venous distension clued me into cardiogenic shock (heart isn't pumping well resulting in back up) vs the others listed, esp since obstructive shock isn't an answer choice +  


submitted by cheesetouch(89),

A decrease in cell number means APOPTOSIS has occurred, thus the surviving tumor cells have a mutation which inhibits apoptosis

baja_blast  TGF-Beta helps regulate cellular differentiation, proliferation, and apoptosis +3  


submitted by moms(4),

In this case, the question is asking about Km and we know that Km is equal to the half of Vmax. So,

Vmax=2 (because is the higher number)

1/2 Vmax= 1

So the concentration is between 0.2 to 0.5.

baja_blast  FA 2019 p. 232 for a review +1  


submitted by cassdawg(930),

Total gastrectomy = absence of parietal cells

Parietal cells are necessary to secrete intrinsic factor which binds vitamin B12 to allow absorption.

Also his symptoms (which fit the description of subacute combined degeneration) are characteristic of B12 deficiency.

FA2020 p69 (insert sunglasses emoji here)

bingcentipede  The gastrectomy was also 10 years ago; it takes 3-4 years to deplete your hepatic B12 stores. +1  
baja_blast  Nice +  


What you can see is

1.Hyperkeratosis (thickened stratum corneum) 2.Parakeratosis (you can see the nuclei very clearly in the stratum corneum) 3.Dysplasia (notice keratinocytes hyperchromatic and large nuclei go up almost all the way to the top. This isnt so in normal skin)

all this fits actinic keratosis

cassdawg  Actinic keratosis is FA2020 p482 if anyone needs it! +4  
baja_blast  FA2019 p. 472 +1  
cheesetouch  Sweet name @osler_weber_rendu #represent #cureHHT +  


submitted by cassdawg(930),

T10 is the dermatome level for the umbilicus, hence the periumbilical discomfort (Landmark dermatomes FA2020 p510)

In appendicitis, the first pain is generalized referred pain and comes from stimulation of visceral afferents (which is why it is poorly localized). Pain eventually localizes as irritation to the parietal peritoneum occurs (FA2020 p383)

waitingonprometric  T10 for bellybutTEN dermatome. +5  
baja_blast  FA 2019 p. 498 for dermatomes and p. 377 for appendicitis +  


Metabolic acidosis because the arterial pH goes in the same direction as the bicarb and pCO2 (i.e. both pH and bicarb/pCO2 are decreased from normal); in primary respiratory acidosis/alkalosis the arterial pH goes in the opposite direction as the bicarb and pCO2.

Once you know that it is a primary metabolic acidosis, you have to check for concomitant respiratory disorders. Do this with Winter's formula:

expected pCO2 = 1.5(HCO3) + 8 +/- 2

so... expected pCO2 = 1.5(11) + 8 +/- 2 --> pCO2 = 24.5 +/- 2 = expected pCO2 is between 22.5-26.5, therefore, 23 is in the expected range, no concomitant respiratory process

baja_blast  Was looking for "Metabolic acidosis and respiratory acidosis" and was wondering why it wasn't a choice. Totally forgot about Winter's formula. Thanks!! +3  


submitted by tinyhorse(6),

Frankly pretty floored that anybody thought that this question contained enough information for someone to confidently answer it.

The question has you assume that both parents are heterozygotes at the locus. Why? I assume I'm missing some esoteric fact about P450 allele frequencies.

flapjacks  I got lucky guessing the same % chance that siblings share HLA markers +2  
baja_blast  I agree with OP seriously no idea how anyone could have gotten this right without totally guessing it. Am I missing something here?? +1  
snow_6  Personally I got this question wrong, partially due to me panicking in this question. Looked through it later and understood the following: - the pt. is homozygous i.e. AA; meaning each parent is heterozygous for the allele - if her sister is to have the same alleles, she is also homozygous i.e. AA - do the punnet square for Aa (mom) and Aa (dad) to get a homozygous allele of AA for only 25% of the time - based on the assumption that parents are heterozygous because question doesn't state any other extra information Only if i could've thought like this during the actual exam +  
sschulz2013  However, if one parent is homozygous and the other is heterozygous, then it works out that the sister will have the same allele 50% of the time, not 25%. So still not sure about the above answer. Don't think assuming the parents are both heterozygotes is something we should have to do. There is probably more to it than just that. +1  
j44n  the probability for being the same gene as a sibling thats homozygous is always 25% this has been on just about every practice NBME +  


submitted by cassdawg(930),

His low urine specific gravity combined with excessive thirst and urination indicates diabetes insipidus, which can be central (defect in the posterior pituitary production of ADH) or nephrogenic (kidney nonresponsive to ADH). (FA2020 p338)

Seeing as it asks us to ID the endocrine organ (and he does not have history indicative of nephrogenic, the less common variety), this indicates central diabetes insipidus and defect in posterior pituitary ADH production.

baja_blast  Posterior Pituitary produces ADH and Oxytocin. Anterior pituitary produces ACTH, TSH, FSH, LH, GH, and Prolactin +1  


submitted by haliburton(208),
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nirneaditi slobkc H2 ee,ptcorr ihwhc is Gs. sG ieatcvast lenyldya acylces -&g;t .cPA+M

q: HeVA 1 M;&paMm ;=&tg 1,H h1aalp, ,1V M,1 3i: M MDA 2 ;gt=& M,2 p2hl,aa :s2 D tehgynir(ve )else t&=;g e1bta, t,2aeb ,V2 1D 2H

I nhtik hist si from A.F

baja_blast  Yes; FA2019 p. 238 +  
medstudent  FA 2020 238 too. +  


submitted by drmohandes(84),
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srnftntrceeornaeeCu A0(921F p.g 42)5 = ordotc jepotcrs efengsli atubo oefvamrti or rteoh oprnttaim sspeorn onto itatenp g.(e. sentiEp td'ndi llki iflms.)eh

baja_blast  They really had mercy here by not also including Transference as an option.... phew. +  


submitted by welpdedelp(216),
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tI wsa juts insgka het nialepfs fo BCsR 12(0 a)yds

haliburton  If I'm reading this right, this is just a tricky dicky question. I think CO binds 200x stronger than O2. But if an O2 cycles through binding / unbinding 200 times before a CO gets kicked off, this should still clear the CO from that cell sooner or later. strange to think it is 1. essentially permanently trapped in a cell, and 2. doesn't kill you and can be treated with O2 to resolution within a few hours or a day. They must just be thinking, until that last RBC dies, you've got original CO in a circulating cell. but just a fraction (because you didn't die). not sure how that CO isn't just passed on during recycling, based on this line of thinking. +7  
link981  The question while stupidly written, asks how long the RBC's that carry the CO take to be removed from the circulation, not how long the CO takes to be removed from the RBC. Just asking the lifespan of RBCs in an stupidly complicated way. As we know, RBC's life span is about 120 days and then they are removed from our circulation. 120 days is about 4 months. Next time they will probably ask weeks or in hours, who knows? smh +6  
baja_blast  If that's what they're looking for why cant the NBME people just ask "How long does it take for RBCs to turn over?" Ridiculous. +1  


FA 2019 p156 Does anyone know how to differentiate the picture labeled Trypanosoma brucei and cruzi?

footballa  This question is likely not important for two reason: They're both Trypansomastigotes, so of course they look almost the same. You can differentiate these two species clinically as they have very little clinical similarity in patient presentation. For these reasons there's little to no reason you would be expected to differentiate these two species by histology alone +2  
snripper  Does Chagas have recurrent fever? Because that's what pointed me to African Sleeping Sickness. +  
baja_blast  The history of travel to the Amazon is what pointed me to Cruzi over Brucei but agree it's a tough distinction to make here. In the absence of that detail I would have probably picked Tsetse fly. +1  


submitted by armymed88(47),
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eluoscG is tptd-rnscooera toin ensetrytcoe of IS vai miodus

toxoplasmabartonella  That makes that glucose needs to be given with sodium. But, what about bicarb? Isn't the patient losing lots of bicarb from diarrhea? +3  
pg32  Had the same debate. I knew glucose/sodium was the textbook answer for rehydration but also was wondering if we just ignore the bicarb loss in diarrhea...? +4  
makinallkindzofgainz  @pg32 - Sure, they are losing bicarb in the diarrhea, and yes this can effect pH, but it doesn't matter that much. You're not going to replace the bicarb for simple diarrhea in a stable, but hydrated previously healthy 12 year old. You're gonna give him some oral rehydration with a glucose/sodium-containing beverage. Don't overthink the question :) +2  
makinallkindzofgainz  *dehydrated +  
teepot123  salt and sugar, that's all the kid needs when ill simple +1  
mtkilimanjaro  Hm I put bicarb/K+ since thats lost in diarrhea, but I think the key thing in this Q is that its only 6 hours of acute diarrhea and nothing else. You would prob give bicarb and K+ in more "chronic" diarrhea over a few days or longer not just a few hours +1  


submitted by seagull(1403),
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otu of yu,iricost hwo may eplpoe wkne t?hsi o(tdn be syh ot sya you idd ro tddi?n)

yM yrovept aindocteu dni'td niaignr tshi ni m.e

johnthurtjr  I did not +1  
nlkrueger  i did not lol +  
ht3  you're definitely not alone lol +  
yotsubato  no idea +  
yotsubato  And its not in FA, so fuck it IMO +1  
niboonsh  i didnt +  
imnotarobotbut  Nope +  
epr94  did not +  
link981  I guessed it because the names sounded similar :D +14  
d_holles  i did not +  
yb_26  I also guessed because both words start with "glu"))) +27  
impostersyndromel1000  same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle. +1  
jaxx  Not a clue. This was so random. +  
ls3076  no way +  
hyperfukus  no clue +  
mkreamy  this made me feel a lot better. also, no fucking clue +1  
amirmullick3  My immediate thought after reading this was "why would i know this and how does this make me a better doctor?" +7  
mrglass  Generally speaking Glutamine is often used to aminate things. Think brain nitrogen metabolism. You know that F-6-P isn't an amine, and that Glucosamine is, so Glutamine isn't an unrealistic guess. +4  
djtallahassee  yea, I mature 30k anki cards to see this bs +4  
taediggity  I literally shouted wtf in quiet library at this question. +1  
bend_nbme_over  Lol def didn't know it. Looks like I'm not going to be a competent doctor because I don't know the hexosamine pathway lol +21  
drschmoctor  Is it biochemistry? Then I do not know it. +4  
snoochi95  hell no brother +  
roro17  I didn’t +  
bodanese  I did not +  
hatethisshit  nope +  
jesusisking  I Ctrl+F'd glucosamine in FA and it's not even there lol +  
batmane  i definitely guessed, for some reason got it down to arginine and glutamine +1  
waterloo  Nope. +  
monique  I did not +  
issamd1221  didnt +  
baja_blast  Narrowed it down to Arginine and Glutamine figuring the Nitrogen would have to come from one of these two but of course I picked the wrong one. Classic. +1  
amy  +1 no idea! +  
mumenrider4ever  Had no idea what glucosamine was +  
feeeeeever  Ahhh yes the classic Glucosamine from fructose 6-phosphate question....Missed this question harder than the Misoprostol missed swing +1  
surfacegomd  no clue +  
schep  no idea. i could only safely eliminate carbamoyl phosphate because that's urea cycle +  
kernicteruscandycorn  NOPE! +  
chediakhigashi  nurp +  
kidokick  just adding in to say, nope. +  
flvent2120  Lol I didn't either. I think this is just critical thinking though. The amine has to come from somewhere. Glutamine/glutamate is known to transfer amines at the least +1  


submitted by oznefu(20),
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I get taht eth snwrea is toccrer orf a srirevleeb urnjiy heewr rthee si llce sewglnil eaecusb fo the acidresne llcrtlarueian a+N dna +a2C deu ot perdiima KNa/ and opccramssila cemurtuil ctytiiva ...

uBt fi eerth rae aiednrcse cciraad yneezsm ni eht odbol cagnintidi elcl hedta adn beemamrn eam,dag ondtw’lu the laatelnulrrci sttleecolrye be lwo eicns yhte are eldsreea tion eht od?lbo

lord_voss  troponin = irreversible injury and membrane damage -> high extracellular concentration of Na+ and Ca++ causes both to move into cell through damaged membrane and high intracellular K+ leaves the cell +12  
rogeliogs  Question is asking about the changes in the myocardiocytes and my second interpretation was that they are asking the changes before they "rupture" and liberate their content in the blood producing increase enzymes in the patient. Therefore because is a ischemic process = reduction of O2 = low ATP = impairment of Na/K ATPase = increase Na-decrease K intracellular = block Ca/Na exchanger = increase Ca intracellular. the same effect as digoxin +4  
allodynia  What will happen to Na and ca conccentration when there is an irreversible injury? +  
baja_blast  @allodynia Pathoma pg. 4 has a really good summary of this. In short, Na+ and Ca2+ both increase intracellularly in an irreversible injury. +  


submitted by usmleuser007(370),
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1) VEB = rtktBui l,ampmhoy kHdgoni laphy,mom rgsoeapanlhnay rcmcon,aai 1° CSN mhomypal in( minrcomommouepids itesant)p

)2 BHV ma&p; VCH = cptelelloaurHa arcnaiomc

H)-H38V = Kpsiao acosram

4) H=PV erliCcav adn /elnalaenip cimoaranc seytp( 6,1 1)8, aedh and ncek aeccrn

5) H. lyopri = Gircast ncaeoacaidrnom nad LMAT lahmyopm

)6 1L-HVT = ultAd Telc-l eoaym/laelimkmphu

)7 evirL uelfk olnhior(csC ninsessi) = ihgaCoolnocrinmaca

8) shotcaSmios uoamihbmtea = arBeddl cncare u(saumqso )lcel

some0217710  Aren’t both H.pylori and EBV associated with gastric lymphoma? +3  
baja_blast  You're right that EBV is associated with gastric lymphomas, but this is specifically asking about marginal zone lymphoma (or MALToma) which is associated with H. Pylori, not EBV. https://www.ncbi.nlm.nih.gov/pubmed/11552717 +1  


submitted by joha961(43),
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ntaenaMicne deso = C(ss * LC * t) / F

... eewhr t is spdeael item enwbeet sesdo on(t vtleaner hree ecnsi ’tsi octnusinou nu)fosini nad F si lioitbyaiiabavl i(wchh is 0%10 ro .10 here ceubesa tis’ nievg )V.I

nrots​tCa iwht olinagd o:eds

(ssC * Vd) / F

... erewh Vd si eluvom of .utnortdiibsi

yotsubato  So do we just have to memorize this... +9  
gh889  yep +12  
drschmoctor  @yotsubato Not necessarily. I can't remember a formula to save my life. The Css is the amount you want in the blood. The clearance is the fraction removed per unit time. Since we want to maintain a steady state, we only need to replace what is removed. Thus, maintenance dose = amount present * fraction removed. +8  
mambaforstep  https://www.youtube.com/watch?v=gnqOUmNhmdg good & short explanation +1  
castlblack  I remember CLoCk Time as in check the clock time to give the next dose Cl = clearance, C = concentration and T = half life. I have never had to use F. +21  
baja_blast  This is on p. 233 in FA 2019. +  


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ghouthlA erhte ear no ecciipfs hrsepe tdo,rniicsa a FCS pelan iwht yotlms scoktlueey cteisidan a rvail itncfoeni sa( lewl sa hte molnra uclgs.o)e oS ouy cna urel uto B,T esrsosoaiuicondr dna ibcla.tare grrskBi/iuzkdenni insg are ldtaree ot ietgisinm,n utb eenv fi you do'tn wokn htaw otshe ,ear the oqseunti assy tath heter is na nobmaatrliy in the TLAEORMP beol (iiignsenmt = eg.mis)nne inlepthasciE oulwd eb eht sebt rnswae, siceplyela seauecb eHrpes sainpEtilhce tfsafce teh aoretlmp oebl.

taediggity  Also look for Kluver-Bucy like symptoms in the stem +1  
mambaforstep  why? +  
b1ackcoffee  I agree with everything but normal glucose. Glucose here is NOT normal. to quote wiki "The glucose level in CSF is proportional to the blood glucose level and corresponds to 60-70% of the concentration in blood. Therefore, normal CSF glucose levels lie between 2.5 and 4.4 mmol/L (45–80 mg/dL)." +  
baja_blast  NBME reference table gives normal CSF glucose to be 40-70 mg/dL. As far as I'm concerned, for the purposes of the exam the reference table is probably a better source than wiki. +4  


submitted by bhangradoc(21),
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The u-lPave is ilasaylcb ptye 1 reo,rr dan etyh peek eht -plaevu the asme ta( 5)&;.0lt in hotb snervsoi fo teh persmneei.tx yB nrgcsiaein unbrme of snaptite in het rgoup, they craisnee reowp fo teh syu,td hcihw sdeercu eytp II .orerr

jfny21  Thank you +1  
baja_blast  For more, FA 2019 p. 262 goes over Type I and II errors. +  


submitted by neonem(549),
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loohAcl ltawidrhwa dsela ot a spcehipatkvyryyelaeiti-i-tmcht sydomnre tiwh et,osrmr N,TH msoanini, GI ,stupe pasrs,ieihdo and mlid gtnaotaii 633- oursh raeft hte atsl dkinr. reeTh is a lriamsi, tub ulslayu litshygl rlte,a oaelrvp of iwwdahatrl rieeszus 468- shoru fetar het salt kdi.nr

baja_blast  p. 558 in FA 2019. +  
cp87  p 547 FA 2019. Hallucinations are usually tactile. +  


submitted by sympathetikey(1249),
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tDirce tgoibnAlnliu = Dcteir Cmboso Tste

eDttecs toiaibdens uobdn iltrdeyc to C.BsR yisHmseol somt ellkiy edu to ihogesntm in the duefnarsts lodob n(ot usre hyw it toko 4 kesew henw Tepy 2 SH si ospduspe ot be kureciq tbu w./)e

ergogenic22  there is a delayed onset hemolytic transfusion reaction which should be evaluated with direct cooms test. https://www.ncbi.nlm.nih.gov/books/NBK448158/ +5  
hungrybox  such a dumb question wtf +25  
sonichedgehog  takess longer due to slow destruction by RES +  
baja_blast  Dang, I didn't know that was the same thing as a direct Coombs test. I guess it makes sense in hindsight. Thanks! +  
sars  Theres a UWORLD question with a table displaying the different types of hemolytic reactions. Don't know the question ID. Agree with delayed hemolytic transfusion reaction due to formation of antibodies against donor non ABO antigens. Typically presents as an asymptomatic patient or mild symptoms (jaundice, anemia). Different from an acute hemolytic transfusion reaction, which is against ABO antigens. +1  
tomatoesandmoraxella  The Uworld table is in question 17780 +1  


submitted by lilyo(69),
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kTae a kool at AF g26p.3 rof tenarn asestg fo seauxl vltdeme.oenp

baja_blast  (This is the right page for FA 2019) +1  


submitted by hayayah(1056),
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sian'cnoF si a rlgezediane rtrbapeionso ceedft in TCP sicnaug eerscidan ixtonerec of oinam c,asdi scogeul, –H3,OC and 3P4,–O dan lal stbuessnca eerbarbods yb eht .PTC

baja_blast  FA2019 p. 581. Fanconi syndrome causes a type 2 (proximal) renal tubular acidosis +1  


submitted by ankirin(3),

What is esophageal spasm and how would it present differently?

baja_blast  I had narrowed it down to that and the correct answer. I think the difference is that esophageal spasm tends to present with pain and dysphagia. FA 2019 p. 371, right at the top of the page. +  
orthonerd  Relating the phrase "diffuse painful contraction" to esophageal spasm has helped me remember the associated descriptions they go to. +  


submitted by hayayah(1056),
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nI yoenla,pscr ether is a edcrit nrtositnai form aklswneufse ot REM ples.e Biylsacal tndeias of inogg tghrohu het rlaye stseag dan ayldaulrg lnliagf nito a edep ep,les yuo tsju enddlsyu go mrfo geinb ewkaa ot engib in a edep ep.sle

kamilia20  FA2020 P497(Sleep physiology): Changes in narcolepsy: decrease REM latency. +1  
baja_blast  p. 485 for us plebs still using FA 2019 +  
randi  FA2019 p. 556 "nocturnal and narcoleptic sleep episodes that start with REM sleep (sleep paralysis)" +  


submitted by divya(58),
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Wyh si teerh rnrhaohrie ni iiopod aidh?warlwt dAn aosl, if slinsumatt eikl iaecnoc aecsu aslan ritoscasi,ntcnovo u'tondlhs oiidop iwhatadrlw od eht a?mes

the_enigma28  Mechanism of opioid-induced rhinorrhoea, lacrimation, stomach cramps and diarrhoea is actually muscarinic receptor effects, rather than alpha adrenergic blockade caused by cocaine, causing nasal vasoconstriction. +1  
baja_blast  Symptoms of Opioid Withdrawal can be remembered with the phrase "anxious, hot, and moist" per SketchyPharm Opiods. Rhinorrhea is one way people can be "moist" during opioid withdrawal, but they can also sweat excessively and lacrimate too. +1  


submitted by tinydoc(223),
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Nuietphaocr iPan refta kesrot is ncltare Pots tkoers niap oymneSdr

auedsc by ltraenatlocar tmahlcai lsiosne

gP. 405 9FA1

chandlerbas  agreed! more specifically damage to the VPL +6  
docshrek  Pg. 403 FA 19. +  
baja_blast  Both commenters above got the page wrong; it's FA 2019 p. 503. +4  
teepot123  looooool ^ what were the odd of both being wrong +  
mumenrider4ever  Pg. 515 FA 2020 +  
bbr  503 in 2019 Interesting that its seen in 10% of strokes. Starts with allodynia ---> neuropathic pain. +  


submitted by est88(17),
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yPeuvtar iaensK tecefd daels ot dedcresea PTA galeidn to gridi BsRC nad atxer acrslvua r.ydylossih enaesIdrc lselve fo B-PG3,2 rseescade boenliomgh tfnfaiyi fro O2.

baja_blast  FA 2019 pg 414 +1  


submitted by temmy(126),
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lpaees elph cindgoarc to entsriw oauientq eht ntteiap ahs a anomrl oinan gpa

ergogenic22  winter's formula is to look at the compensation to see if it is appropriate. PCO2 = 1.5[HCO3-] + 8 +/- 2 In this case, 1.5* 10 (Pt's bicarb) +8 +/-2 = 21 to 25 Pt's PO2 is 23, so compensation is appropriate. If PCO2 was below 21, it would be concomitant respiratory alkalosis +5  
ergogenic22  in other words, winter's formula is not necessary for this question +2  
the_sacramento_kings  lol unless you want to make sure its not A. +1  
hello  @ergogenic22 Someone might use Winter's formula to rule out choice A. +  
maxillarythirdmolar  respiratory depression of alcohol should rule out "A" +  
baja_blast  Isn't the low pCO2 enough to rule out A? +1  


submitted by benzjonez(42),
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AF 2810 .p 069. eucpstS arelturh unryji if oblod is seen ta the eurtrlha .metaus imnaecsMh fo ooriptsre urtrlahe nrijyu = livpce aerfc,urt hwihc we ese in tish tpiate.n errUthla irztotiectenhaa si yatlrileve diecoctr.anntiad

hyperfukus  thank you! +  
baja_blast  Understood, but is there anything in the question that rules out BPH specifically? I honed in on the words "most likely" and saw he was 60. I guess I overthought it but I'd appreciate any insight as to what if anything in the Q makes that definitively wrong. +  
daddyusmle  I think the question stem, with the trauma and fractures, points you in the direction of membranous urethral trauma. Pelvic fractures are more associated with urethra damage than prostate damage, although they're right next to each other, and I can see why someone would choose prostate hypertrophy. Also, I'm not sure if bleeding is associated with BPH. +  
mumenrider4ever  FA 2020 pg. 627 +2  
nio5021  could someone explain why urethral stricture is incorrect? +  
nio5021  According to mayo clinic, strictures can be caused by trauma to pelvis as well. Would strictures be more likely if this patient had some sort of procedure done? https://www.mayoclinic.org/diseases-conditions/urethral-stricture/symptoms-causes/syc-20362330 +  
eghafoor  @nio5021: "Trauma to the anterior urethra is often from straddle injuries. This can occur with a sharp blow to the perineum. This type of trauma can lead to scars in the urethra ("urethral stricture"). These scars can slow or block the flow of urine from the penis. Trauma to the posterior urethra almost always results from a severe injury. In males, posterior urethral trauma may tear the urethra completely away below the prostate" Source: https://www.urologyhealth.org/urologic-conditions/urethral-trauma#:~:text=Trauma%20to%20the%20anterior%20urethra,of%20urine%20from%20the%20penis. +  
eghafoor  The key for this question was recognizing that the pelvis was fractured = unique only to posterior urethral injuries (FA 2020 p. 627), and after was to realize that you'd have an urethral disruption/tear +  


submitted by hyoscyamine(55),
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AF 3.g7p.2 qsuaoumS lecl irnmccaoa oscruc ni eth prupe /23 fo speusohag eehswra eomcncrainodaa cusocr ni hte lisdat .13/ nSeic iths wsa ni the imd aeug,possh sit msuausoq clle macrn.cioa yeK refteau fo oumsasqu llec omnracaic si kaeitnr pra.lse

turtlepenlight  can remember it as wearing a pearl necklace (upper 2/3 of throat-ish) +4  
baja_blast  Patient is also a heavy smoker and drinker. In the absence of GERD this should raise suspicion for SCC of esophagus over Adenocarcinoma. +1  
lovebug  Is there anyone who can explain about C)Intra-cytoplasmic pigment? what is this?;; +  
misrao  @lovebug I'm thinking Negri bodies in rabies +  


submitted by thotcandy(74),

What is there that rules out deltoid? overhead abduction is >15' so shouldn't that point more towards deltoid?

baja_blast  Deltoid only does abduction from 15 to 90 degrees. So not overhead. +  
donttrustmyanswers  With that logic, supraspinatus only does abduction form 0-15 +7  
rina  the positive empty can test is the biggest thing "pain and weakness with abduction, particularly with simultaneous shoulder internal rotation" - that tells you it has to be one of the SITS muscles (supraspinatus, infraspinatus, teres minor, subscapularis), not the deltoid. tenderness in the right deltoid region tells you it's the supraspinatus which is right underneath the deltoid muscle +1  


submitted by krewfoo99(88),
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hprineipnEe atsc mtsoyl no eBat tsep.roerc aetB pteorsecr era G poeclud.

baja_blast  Alpha receptors are also G-coupled and are another potential site of action for Epinephrine (at high doses according to SketchyPharm Sympathomimetics) +