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Comments ...

 +0  (nbme23#43)

According to Dr Sattar.. Adenocarcinoma is the most common cause of lung cancer in female non smokers.


 +0  (nbme23#42)

What of if the cancer is a urothelial cancer in the bladder due to radiation therapy. would it not cause similar signs

charcot_bouchard  Chance of bilateral ureteral ca is very rare. Also preincipal r/f for transitional cell ca is Smoking not radiation

 +0  (nbme23#27)

Dr Sattar talks about increase capillary permeability in the postcapillary venules and vasodilation in the arterioles as actions of histamine. That was what i thought of when i answered the questions.


 +0  (nbme21#8)

I agree with what has been said but also note that the patient called her internist to help her address the conflict between the two physicians which has gotten her worried. That is her desire. And from what i have gathered, where possible, the patients wishes should be met.


 +2  (nbme21#1)

Healthy people who get sick with parvovirus may have a subclinical illness with athralgias as the only symptom. But sickle cell patients and patients with decreases hematopoiesis will develop[ bone marrow failure because the virus affect the hematopoietic stem cells leading to aplastic crises and inability for the bone marrow to adequately compensate hence the low reticulocyte count. parvovirus causes..slapped cheeks in kids hydrops fetalis in fetus, aplastic crises in sickle cell and arthralgias in other patients.

henoch280  thanks. very helpful

 +0  (nbme21#10)

please help according to winters equation the patient has a normal anion gap

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
ergogenic22  in other words, winter's formula is not necessary for this question
the_sacramento_kings  lol unless you want to make sure its not A.
hello  @ergogenic22 Someone might use Winter's formula to rule out choice A.
maxillarythirdmolar  respiratory depression of alcohol should rule out "A"

 +1  (nbme21#27)

And never pick an option that makes you sound critical


 +1  (nbme21#27)

when in doubt, pick an open ended question. They give the patient an opportunity to express themselves with prompting from the doctor


 +0  (nbme21#40)

Almost failed this question but i kept hearing Dr Sattar screaming prostaglandin E2 FEEEEEEEVER


 +1  (nbme21#23)

IFN gamma stimulates macrophages to produce granulomas


 +0  (nbme21#43)

how i remember it for all granulomas formed by...IFN gamma Maintained by TNF alpha

Gamma forms alpha maintains (sustains it). That is why infliximab and etarnacept( TNF alpha inhibitors) will break down the granuloma if used.


 +0  (nbme21#42)

babies of diabetic moms end up being bigger and that may lead to shoulder dystocia

sahusema  If one of the answer choices was, "that baby gon be big lol" I would have gotten it right

 +0  (nbme21#48) i think the questions is trying to show the importance of unity among family members when there is a patient who is loved by both wife and kids. The duty of the doctor is to ensure the family is united in support of the patient the and in case there is still conflict regarding what to do, you use the hierarchy where wife comes first. i get it was a dumb but this was my logic

 +1  (nbme21#16) Type 2 pneumocytes produce stem cells and surfactant.

 +1  (nbme20#43)

i think it is not androgen insensitivity because the testosterone levels are normal. They should be high in AIS.





Subcomments ...

submitted by dr.xx(34),

right. he absolutely must remain in the waiting area so that he is at hand to attack his wife whenever her exam ends. go NBME!

meningitis  I guess it was all about not offering battering information in order to not make matters worse since he will figure out that the wife told on him.. Also, its a HUGE STRETCH but the only reason I thought he should stay in the waiting room was just in case the wife died they could detain him and call the police for questioning. +2  
temmy  Also, he should stay there because his wife did not grant him the permission to see him. Patients requests trumps. +  
nephcard  Doctor should not believe what wife told her. There may be some other reason for injury so batttering information should not be provided. But her wish of not letting her husband in should be fulfilled +  
charcot_bouchard  No. In real life patient lies. In Board ques they always tell the truth. Unless they make it very obvious. in fact its a board ques rule. So u believe her untill proven otherwise. +  
drdoom  The prevailing rule of American medicine and law is individual autonomy. No other person is granted “default access” or privilege to another person’s body—that includes the physician! The physician must receive consent from a (conscious) “person” before they become “a patient”. In the same way, the person (the patient) must give consent before anyone else is permitted to be involved in her care, spouses included! +  


submitted by cbrodo(12),

The posterior columns (Fasciculus cuneatus/Fasciculus gracilis) carry information to the brain regarding proprioception, vibration, discriminative touch and pressure. Physical exam findings suggest a lesion here (the spinothalamic tract carries pinprick/pain and temperature, and these were normal). Since the patient has abnormal findings in the lower extremities, and normal findings in the upper extremities, the answer is Fasciculus gracilis. This is because information from body areas below the level of T6 is carried by gracilis and information from body areas above the level of T6 is carried by cuneatus.

kai  kick Goals (gracilis) with your feet Cook and eat (cuneatus) with your hands +2  
temmy  i remember gracilis is for legs by saying i have graciously long legs and they are inside while arms can spread out to remember their orientation on the spinal cord +  
jess123  I remember it as gracilis = grass so feet haha +  
link981  Just to add found on page 492 on FA 2018. +  
charcot_bouchard  Hey Temmy, I can spread my legs too :) +  
maxillarythirdmolar  I can't feel GRACIE's ~fine touch~ as she ~vibrates~ my balls. +  


submitted by hipster_do(2),

I’m going to say it’s X linked agammaglobulinemia rather than SCID, but the difference between these two are tiny but this is why I think it’s the former:

  • Boy (increased risk but both BA and SCID are x linked)
  • Recurrent bacterial infections but don’t mention diarrhea or thrush which is in SCID
  • Timeline is after 6 months, so the mother’s antibodies wore off.

SCID should be immediately because they just don’t have the IL2 receptors. CVID shows up when they’re 20-40 years old. You get absent germinal centers in both. No mention of absent thymic shadow which is in SCID.

placebo079  “Uniformly” low is also a clue; in CVID they are not. +  
tea-cats-biscuits  This makes sense, though what really threw me off was that in Classic Bruton’s Agammaglobulinemia there’s near-zero B counts though (or at least that’s what FA and UTD says, “Absent B cells in peripheral blood” FA 116, 2018). The Q says the leukocyte count was normal though. Wouldn’t the leukocyte count include lymphocytes in the differential? And wouldn’t lymphocytes be low due to the near complete lack of B cells in peripheral circulation if it was BA? +  
partybrockk  @tea-cats-biscuits Bruton’s is a failure of B cells to /MATURE/. So you get normal lymphocyte counts, decreased levels of immunoglobulins, and absent germinal centers. +  
tea-cats-biscuits  @partybrockk That makes sense to me, but I keep getting hung up on how that’s not what either FA or UTD says about the classic lab findings of XLA. UTD specifically says this: “Laboratory findings include hypogammaglobulinemia/agammaglobulinemia, deficient antibody responses to immunizations, and absent or markedly reduced B cells in the blood,” and I previously quoted FA. I suppose it doesn’t really matter, but it’s definitely a bit frustrating unless I’m missing something about how absent B cells in the blood wouldn’t correlate to a decreased lymphocyte count ... +  
temmy  please correct me if i am wrong cos i might be but my logic was there is decreases immunoglobulin uniformly meaning the B cells are uniformly absent and since they develop in the germinal center, the germinal center will be absent. +  


submitted by dubchak7(0),

They suggest Misoprostol to counteract NSAIDs... Why not PPIs?

hayayah  PPI's don't have many side effects! If the question didn't involve the diarrhea side effect the answer would have been to give her a PPI. +  
tsarcoidosis  I guess one takeaway is that PPIs don't directly cause diarrhea, but they do increase the risk for C-diff, which causes diarrhea. +2  
usmleuser007  PPI side-effects: + increased risk for C. diff + Increased risk for resp infections + can cause hypomagnesia + decrease absorption of (Ca2+, Mg2+, & iron) + increased risk of osteoporotic hip fractures (d/t low serum calcium) +  
temmy  The patient got severe gastric burning and discomfort as an effect of the drug. My logic was since the patient was taking an NSAID it had to be a COX 1 inhibitor that destroys the protective barrier of the GI mucosa due to inhibition of prostaglandin so we needed to treat with a drug that will regenerate prostaglandin and prostaglandin is a vasodilation which might be the reason for the diarrhea. +  


Androgens cause acne. Testosterone is a better answer than Androstanediol b/c the Testosterone is associated with puberty, Androstanediol is more associated with the adrenal glands.

meningitis  I chose Testosterone but I almost chose GnRH because it is surged when starting puberty and therefore increases everything downstream. +1  
temmy  When answering the question, i thought to myself that if GnRH is correct, LH will be too cos GnRH stimulates the Leydig cells via LH to release testosterone. That left testosterone as the best answer because it had the most direct effect. +1  


submitted by drdre(4),

Page 506 FA 2019 describes headaches.

Cluster

  • Unilateral
  • 15 mins to 3 hours
  • Periorbital pain with lacrimation and rhinorrhea
  • Tx: Sumatriptan

Migraine

  • Unilateral
  • 4 to 72 hours
  • Pulsating pain with nausea, photophobia, phonophobia, may have "aura"
  • CN V, meninges or blood vessel irritation
  • Tx: NSAIDS, triptans, dihydroergotamine

Tension

  • Bilateral
  • 4 to 6 hours
  • Band-like pain
  • Tx: analgesics, NSAIDS, acetaminophen

drdre  yay formatting fail +  
drdoom  @drdre, next time try hitting enter twice ("start a new paragraph") before beginning a list. +  
temmy  cluster mostly seen in men +  


submitted by neonem(227),

This is a case of acute gout. Monosodium urate crystals are taken up by neutrophils, leading to an acute inflammatory reaction. T-cells aren't really involved in gout (more rheumatoid arthritis).

hungrybox  Great explanation! So frustrating that I got this wrong, should have been easy. +1  
temmy  the way i thought about it was how did the neutrophils get there? the answer is via increased vascular permeability +2  
nor16  they, unfortunately, did not ask " how did neutrophils get there" but " whats the cause of the swelling " not to confuse with " what causes the swelling " +  


It said it was fatal to males in utero, and the question asked about live born offspring. Since the males aren’t being born in the first place, I said 50% females and 0% males.

hungrybox  fuck i got baited +5  
jcrll  "live-born offspring" ← baited +2  
sympathetikey  Same :/ +  
arkmoses  smh +  
niboonsh  why is it 50% females tho? +  
imgdoc  felt like an idiot after i figured out why i got this wrong. +  
temmy  oh shit! +  


submitted by sympathetikey(252),

The whole "picks at the lesion...causes some bleeding", made me think Psoriasis. Should have gone with Actinic Keratosis based on the patient history (lots of sun exposure).

Actinic Keratosis

Premalignant lesions caused by sun exposure. Small, rough, erythematous or brownish papules or plaques. Risk of squamous cell carcinoma is proportional to degree of epithelial dysplasia.

thisisfine   Same - the bleeding thing pushed me over to psoriasis as well. Oops. +1  
temmy  the distribution of the other lesions, forearm, face, ear, scalp..is not characteristic for psoriasis. +1  
hyperfukus  the scalp and ear are actually very common for psoriasis IRL the key is more of the fact that its in areas with UV exposure...actually UV Therapy is found to be helpful in treating some pts w/Psoriasis. Lastly the appearance and lots of things bleed if they were trying to go for auspitz sign it would have tiny dots of bright red blood with slightly touching it +1  
hyperfukus  oh last thing psoriasis itches! they said no itching +  


submitted by neonem(227),

Major risk factor for aortic dissection is hypertension, and in this case might be due to cocaine use, which causes marked hypertension. Dissections cause a tear in the tunica intima -- blood can flow backwards into the pericardium and cause tamponade. This manifests as crackles in the lung due to poor left ventricular function (filling/diastolic problem due to compression).

forerofore  there is another clue, the man has diminished pulses in just one arm, which means that the left subclavian artery must be involved somehow, and an aortic dissection would be the best answer explaining this. +3  
temmy  please why is there where a diastolic mumur? +1  
whoissaad  @temmy Aortic dissection especially near the root of aorta can lead to dilatation of the aortic valves, which can lead to Aortic regurgitation (diastoic murmur at left sternal border) +2  
garibay92  Does anyone know why is this patient's tepmerature elevated? +  
ratadecalle  @garibay92, not important for this question I think but cocaine can cause malignant hyperthermia +1  


submitted by aishu007(1),

can anyone explain why enterococcusfaecalis is the answer here?

priapism  Best I can guess is that both S. aureus and E. faecalis can cause UTI, but S. aureus is described as having clusters where as the other Gm+ cocci are in chains +3  
nala_ula  My doubt here in this question is the fact that Enterococcus faecalis is a normal gut microorganism that causes these different symptoms of sickness after genitoruinary or gastrointestinal procedures... but in this question there is no mention of any procedures. +  
fez_karim  its says chains, so not staph. only other is entero +  
temmy  according to first aid, staph aureus is not one of the high yield bugs for UTIs +  
temmy  uti bugs are E.Coli Staph saprophyticus Klebsiella pneumonia Serratia Marcescens Enterococcus Proteus mirabilis Pseudomonad aeruginosa +  
privatejoker  Where in FA 2019 does it list that C.coccus is specifically in chains? +  
privatejoker  E.Coccus* i mean +  


submitted by aishu007(1),

can anyone explain why enterococcusfaecalis is the answer here?

priapism  Best I can guess is that both S. aureus and E. faecalis can cause UTI, but S. aureus is described as having clusters where as the other Gm+ cocci are in chains +3  
nala_ula  My doubt here in this question is the fact that Enterococcus faecalis is a normal gut microorganism that causes these different symptoms of sickness after genitoruinary or gastrointestinal procedures... but in this question there is no mention of any procedures. +  
fez_karim  its says chains, so not staph. only other is entero +  
temmy  according to first aid, staph aureus is not one of the high yield bugs for UTIs +  
temmy  uti bugs are E.Coli Staph saprophyticus Klebsiella pneumonia Serratia Marcescens Enterococcus Proteus mirabilis Pseudomonad aeruginosa +  
privatejoker  Where in FA 2019 does it list that C.coccus is specifically in chains? +  
privatejoker  E.Coccus* i mean +  


submitted by mcl(167),

Not sure if this is the right way to think about it, but if PT and PTT are both prolonged, this most likely means there is a problem with the common pathway (aka factor X).

temmy  exactly...i just thought the problem has to be where they meet or somewhere similar to both..hence the common pathway 12(PTT Heparin) 7 (PT, Warfarin) 11 9 10 5 2 1 In my head, both sides are looking for the perfect 10 +  


In the great words of Dr Sattar:

"Prostaglandin E2 mediates feeeeeeeeeever"

NSAIDs --> block prostaglandin syn

thisisfine   This is all I heard in my head +1  
temmy  Me it was so weird +  


submitted by yotsubato(207),

Why is his Libido normal? It's totally expected that he may have reduced libido after his wife died 2 years ago from some horrible prolonged illness.

nala_ula  perhaps it's more to do with the fact that he can get erections when masturbating, outside of nocturnal erections which are not mediated by sexual desire. So his libido must be intact since he has sexual desire evident in being able to masturbate. +  
nala_ula  At least, that's the way I saw it. +  
home_run_ball  "Testosterone concentration is within the reference range" and the fact that he has no difficulty masturbating = normal libido. Low testosterone would contribute to low libido And if he had low libido he would have difficulty masturbating +  
thisisfine   The way I made the decision about normal vs. decreased libido is also that he presented to his doctor due to difficulty maintaining an erection while trying to have sex - meaning he has the libido to try to have sex. Does that make sense? +1  
btl_nyc  It also says there are no signs of depression, which would cause the low libido after his wife died. +  
temmy  two years is a enough time to mourn...just saying +  
temmy  thisisfine, it makes absolute sense. That is the same way i saw it +  
dr_jan_itor  He misses his wife man, isn't ready for other women. Psychogenic ED. physically hes fine (can crank his meat) +  


submitted by yotsubato(207),

Why is his Libido normal? It's totally expected that he may have reduced libido after his wife died 2 years ago from some horrible prolonged illness.

nala_ula  perhaps it's more to do with the fact that he can get erections when masturbating, outside of nocturnal erections which are not mediated by sexual desire. So his libido must be intact since he has sexual desire evident in being able to masturbate. +  
nala_ula  At least, that's the way I saw it. +  
home_run_ball  "Testosterone concentration is within the reference range" and the fact that he has no difficulty masturbating = normal libido. Low testosterone would contribute to low libido And if he had low libido he would have difficulty masturbating +  
thisisfine   The way I made the decision about normal vs. decreased libido is also that he presented to his doctor due to difficulty maintaining an erection while trying to have sex - meaning he has the libido to try to have sex. Does that make sense? +1  
btl_nyc  It also says there are no signs of depression, which would cause the low libido after his wife died. +  
temmy  two years is a enough time to mourn...just saying +  
temmy  thisisfine, it makes absolute sense. That is the same way i saw it +  
dr_jan_itor  He misses his wife man, isn't ready for other women. Psychogenic ED. physically hes fine (can crank his meat) +  


submitted by didelphus(14),

Any idea why hyperchloremia isn't an answer? The diarrhea would cause an normal anion gap (hyperchloremic) metabolic acidosis.

charcot_bouchard  this is the problem bet uw and nbme. in uw it would be for sure a gotcha ques. but in nbme they are usually looking for most obvious. also look what they are asking "most likely". baby would dev low Na before acidosis. Thats my 2 cents +2  
temmy  hyperchloremia will not account for the seizure that brought the patient to the hospital. seizures according to first aid is caused by hypocalcemia and hyponatremia +  
cry2mucheveryday  Children with diarrhoea who drink large amounts of water or other hypotonic fluids containing very low concentrations of salt and other solutes, or who receive intravenous infusions of 50% glucose in water, may develop hyponatraemia. This occurs because water is absorbed from the gut while the loss of salt (NaCl) continues, causing net losses of sodium in excess of water. The principal features of hyponatraemic dehydration are: there is a deficit of water and sodium, but the deficit of sodium is greater; serum sodium concentration is low (<130 mmol/l); serum osmolality is low (<275 mOsmol/l); the child is lethargic; infrequently, there are seizures. https://rehydrate.org/diarrhoea/tmsdd/2med.htm#CONSEQUENCES%20OF%20WATERY%20DIARRHOEA +  
cry2mucheveryday  Also, why is this being given formula...? May be lactase deficiency...which leads to osmotic diarrhea...leads to hyponatremia(goljan) Aren't newborns supposed to be kept on exclusive breast milk till 6 months?? +  
hello  @cry2mucheveryday Don't read too much into it. The fact that the baby is receiving formula isn't relevant to answering the Q. Btw, not everyone breast feeds. Additionally, the Q wouldn't make much sense if it said "they ran out of breastmilk"... +  
hello  @cry2mucheveryday Being on formula then the parents running out of formula is more of a clue for water intoxication. This is typically the scenario that water intoxication presents. However, I suppose if for some reason the baby was being breastfed and the parents switched to exclusively waterfeeding (and no other foods), then water intoxication would also result. +  


submitted by haliburton(74),

This is water intoxication. https://www.ncbi.nlm.nih.gov/pubmed/1877579

thisisfine   Agreed! It's along the lines of those marathon runners who collapse questions. Nothing but water for 24 hours = getting rid of too much sodium. +  
temmy  are we just going to ignore the diarrhea for 3 days? what is its significance +  
kard  Temmy, We aint Ignoring the Diarrhea, Actually the most likely electrolytes to get lost with it is sodium> chloride> potassium> bicarbonate... Plus the Water intoxication -> HYPONATREMIA +  


just a hunch.... Omeprazole is always the right answer

nala_ula  Famotidine is an H2 blocker which really only stops acid secretion via the stimulation of H+/K+ ATPase by histamine, but it still has vagus and gastrin stimulation. If you use Omeprazole, you get irreversible inhibition of the pump itself which stops the secretion of acid even if there is histamine, gastrin, vagus stimulation. +3  
temmy  what about the healing of her mucosa. Is that not the action of prostaglandin?. That threw me off cos according to FA, misoprostol increases secretion of the gastric mucosa +3  
cry2mucheveryday  same doubt..marked miso +  
sahusema  I guess because misoprostol is more associated with treatment of NSAID related ulcers and PPIs are 1st line DOC for GERD? +1  


submitted by yo(21),

This occurred within 6 hours and caused some pulmonary edema and respiratory distress after a transfusion caused by the donor's anti-leukocyte antibodies just destroying the recipients neutrophils and respiratory endothelial cells.

while allergic/anaphylaxis can cause respiratory arrest and shock it has a somewhat different picture, no wheezing, itchiness or whatever and according to first Aid it happens within minutes to 2-3 hours which is at least double what we're seeing here. also beware of IgA deficient people in this choice.

PE, eh I don't think it affects Pao2 that often much according to this super duper high yield resource. but uhh yeah doesn't feel PE kinda question https://emedicine.medscape.com/article/300901-workup#c12

pneomina, right after all the infusion business and no mention of fever or anything? Nah.

go to page 114 of first aid. I'm pretty sure we need to know our infusion/transplant crap because it just keeps coming up in uworld but this whole exam is a crapshoot.

Forgive me if I made a mistake/wrong about anything, I mostly got info from first aid. plz correct if there is a mistake, good luck.

hungrybox  we gonna make it bro +  
hungrybox  or sis +1  
nala_ula  I did the same, basically went through each one and the time of onset between each. Good luck on your tests!! +  
temmy  i don't think pulmonary embolism will cause bilateral lung infiltrate +1  


submitted by hungrybox(175),

Huntington's disease

  • anticipation: she has a similar disorder as her father but died earlier

Remember "HUNT 4 an animal, put it in a CAGe". Huntingtin gene found on Chromosome 4. CAG is the trinucleotide repeat:

  • Chorea, caudate nucleus
  • Ataxia
  • Gloomy (depression)
sbryant6  Side note: atrophy of the caudate nucleus leads to a widened anterior horn of the lateral ventricle. I've seen it worded both ways in UWorld. +3  
sbryant6  Side note: atrophy of the caudate nucleus leads to a widened anterior horn of the lateral ventricle. I've seen it worded both ways in UWorld. +  
foulari112  How would you differentiate this from Frontotemporal lobe dementia +  
temmy  Foulari 112..the ageof the patient and the anticipation cos her dad had it too. Also in frontotemporal pick, you will see personality changes where they act completely different vs huntington where they are aggressive and depressed. +  


AV Fistulas re-rout blood from the arterial system to the venous system, by-passing the Arterioles = Increase PL ---> INCREASE VR. All in all = Increase CO.

According to UWorld, the arterioles are a major source of resistance ... so bypassing the arterioles results in a decrease in Total Peripheral Resistance ... causing an increase in the rate and volume of blood returning to the heart. I am pretty sure there is more to the physiology behind this, but I hope this explained a little.

big92  "Immediately following creation, arteriovenous fistula (AVF) is associated with an increase in cardiac output (CO), achieved predominantly through a reduction in systemic vascular resistance, increased myocardial contractility, and an increase in stroke volume (SV) and heart rate. Over the following week, circulating blood volume increases in conjunction with increases in atrial and brain natriuretic peptides. These alterations are associated with early increases in left ventricular (LV) filling pressure with the potential for resultant impact on atrial and ventricular chamber dimensions and function." (PMID: 25258554) There's also another study by Epstein from the 1950s looking at the effects of AVF's effect on CO in men (PMID: 13052718). Apparently, the increase in resting CO is a big problem because it can lead to high-output cardiac failure (LVH). +3  
hungrybox  Jesus big92 you went in on the research lmao u must be MSTP +1  
temmy  big92 you are right. that is why pagets disease pagets have high output cardiac failure because of the av shunts. +  


submitted by hungrybox(175),

some wrong answers:

*makes sense b/c myeloblasts are precursors to granulocytes, which use MPO to fight off infections

temmy  Hungrybox aka life saver +  
hello  Thank you!!! +  


submitted by hungrybox(175),

other answers:

inhibition of H2 receptors: (for GERD) prevent gastric acid secretion (cimetidine,

inhibition of phosphodiesterases (PDE):

  • theophylline (asthma) inhibits cAMP PDE
  • -nafils (dick pills) for ED inhibit cGMP PDE

β2 agonists: (for asthma) cause bronchodilation

  • albuterol (short acting - A for Acute)
  • salmeterol, formoterol (long acting - prophylaxis)

(idk lymphocyte membrane stabilization)

hungrybox  H2 blockers are the -tidines +1  
yotsubato  > dickpills lol +5  
temmy  hungrybox, you are a life saver +1  
cienfuegos  Via FA: take H2 before you dine, think "table for 2" to remember H2 +  


submitted by moo(0),

if the lungs were clear to auscultation and the kid even said he doesn't want to be on the team anymore why couldn't it be malingering?

amarousis  malingering would be a conscious faking of symptoms to avoid being on the team. he wouldn't have the mid-systolic click and he would probably complain of his symptoms all the time and not just limited to during exertion. +  
temmy  malingering is also doing it for some external gain. which was not indicated in the stem +  
garibay92  Also, patients with asthma are usually asymptomatic at the time of physical exam unless they are examined precisely during the attack. +  


submitted by cantaloupe5(29),

Proccess of elimination for this one. Two you can eliminate immediately just from looking at the biochemical pathway chart. The other two required knowledge that eumelanin is more protective than pheomelanin (this is why redheads burn more easily). Because pheomelanin is less protective, there would be more not less ROS from sunlight.

temmy  i don't understand this at all. i am completely blank...please help +1  
henoch280  @temmy. This question tests our knowledge on albinism which is normally a tyrosinase deficiency disease but the vignette states that the boy's albinism is caused by a genetic mutation in the TYRP1 gene which is shown in the biochemical pathway. A gene that helps in the synthesis of Eumelanin. Now you have to understand that all precursors before that gene is the pathway would still be available if not increased which make 2 of the options in the question wrong. you also have to understand this: (Eu)melanin = (normo)melanin i.e normal melanin which is protective to the skin, decreases reactive oxygen species and gives the dark pigments to the iris, choroid, skin, hair e.t.c. while (feo)melanin = (fake)melanin i.e pheomelanin, the one present in our patient here which is less protective again the uv rays, cannot pigment and cannot decrease ROS generated in the skin. i hope this helps +5  
eacv  @henoch280 thank u very much! I got it right by luck but now i do understand :D +  


submitted by neonem(227),

Morphine is a mu opioid agonist - one adverse effect of opioids is mast cell degranulation that is IgE-independent. Release of histamine is akin to an anaphylactic reaction --> pruritis, etc.

sympathetikey  Never had heard of that one. Just a good guess. Thanks! +  
yb_26  IgE-independent mast cell degranulation can also be caused by radiocontrast agents, some antibiotics (vancomycin) +  
temmy  it was a u world question +  


submitted by moneysacs(0),

Why is does a PDA after birth result in "higher than normal left ventricular cardiac output" over increased "right ventricular PO2"? Does the pulm artery --> aorta shunt become reversed after birth, so higher oxygen aorta blood would flow back into the right ventricle? I get that more blood would be pumped to the left ventricle, resulting in RVH/LVH, but don't understand the O2 bit.

usmleuser007  1) higher than normal CO b/c blood is shunted from aorta to pulmonary arteries. This blood is added to the volume that was pumped into the pulmonary arteries by the RV. Now when the oxygenated blood returns to the LA & LV, the O2 content would be greater d/t higher blood volume. Also for that same reason more blood is returning to the LV (d/t LV volume plus fraction of RV volume). This increased the CO. Right--> Left shunts have late cyanosis b/c the RV is pushing against the excess pressure generated by the LV. This leads to Eisenmenger Syndrome as RV enlarges and pushes against the pressure from the LV in the PDA. Thus shifting Left to right to right to Left and thus the late cyanosis +1  
temmy  The anatomy is aorta-pulmonary artery-pulmonary veins-left atrium-left ventricle Notice that the blood did not come across the right heart at all and because of the LEFT TO RIGHT shunt of the PDA, we add more volume to the LEFT side. Hence the increased left ventricular output +2  


submitted by ihavenolife(12),

Idk if it helps but I got it using the Hot T-Bone stEAK mnemonic

Hot -> IL 1 (Fever)

T cell stimulation -> IL 2

Bone marrow stimulation -> IL 3

IgE -> IL 4

IgA -> IL 5

aKute phase protein -> IL 6

temmy  cyclosporine inhibits transcription of IL2 +  


submitted by hayayah(330),

Down Syndrome Labs:

  • inc. nuchal translucency
  • inc. hCG
  • inc. inhibin
  • decreased AFP
  • decreased PAPPA
celeste  I remember this as Down Syndrome has high HI (hCg and inhibit) +5  
temmy  Thanks celeste. I'll remember Hi +1  


submitted by asdfghjkl(1),

Anyone know why IGF-1 wouldn't be increased as well? GHRH is stimulated in hypoglycemic states.

nala_ula  Honestly, it's something that has confused me for a while. Why is it that GH secretion is stimulated by hypoglycemia? I mean, it's literally called growth hormone (for growth!), and hypoglycemia, which is basically a "starvation" state, will stimulate this hormone? +  
shaeking  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3529368/ This might help answer your question. I basically didn't pick IGF-1 because it would increase the uptake of glucose leading to a worsen hypoglycemic state. Didn't have a true reason otherwise. +  
temmy  IGF-1 is regulated by insulin. so it will be decreased because insulin levels are also low. +  
nala_ula  thank you @shaeking! +  
nwinkelmann  I found this and it also explains to a more genetic/cellular level. Essentially, it says that starvation induces some factors that cause GH resistance and IGF1 suppression. +1  
nwinkelmann  Sorry forgot the link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2575072/ +