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 +0  (free120#13)

Calcium is low while PTH is high. It’s primary hyperparathyroidism (not secondary). Ans is branch of IJV.

mdmofongo  You’re right, how weird. But I guess following the Hx there is no other way to approach it? Not a fair question I would agree. Also the inferior thyroid artery does branch off of the thyrocervical trunk. The superior and middle veins of the thyroids drain into the IJV.
b1ackcoffee  I got that it must be some vein, I just didn’t know the tributaries. Oh well, anatomy fucks me again!

 +0  (free120#18)

Any good material for this and lymph node drainage in general? Is this common knowledge or low yield stuff?

mdmofongo  I got this question right thanks to the 100 high yield concepts of anatomy pdf, learn the lymph node drainage from there and you will be all right.

 +0  (free120#31)

confused why this is not autonomic dysfunction or hyponatremia due to sweating and why is this orthostatic hypotension?

mdmofongo  This one is tricky and come downs to choosing the “best” option. I can see why you were confused. However do note that in an autonomic dysfunction you will never present tachycardia as this patient does. I guess the key here is seeing how her BP normalizes once she is laying down? Sorry, this one is a kinda unusual presentation of Orthostatic hypo.
mamed  Not sure if this is correct thinking but how I got this right was: 1. She is hypovolemic 2. Likely retaining salt so water follows (ADH or just renal dynamics in general). This is how I ruled our hypokalemia and hyponatremia 3. If she is hyponatremic b/c sweating then why wouldn't she also be hypokalemic? so both have to wrong because both can't be right 4. Volume depletion ==> orthostatic hypotension

 +0  (free120#19)

I am wondering which parasite is this actually? --

mdmofongo  The clinical presentation sounds like a GI parasite, which are transmitted via fecal-oral route, so ingestion of soil would be the most sensible answer. All the other routes are of parasites with more severe or systemic infection.
b1ackcoffee  @mdmofongo I know this. But which parasite is this?
drblu92  The parasite is most likely Trichuris trichiura (human whipworm). Trichuriasis is often asymptomatic and adult forms can reach 2 cm in length (visible with naked eye). A lot more common in tropical areas but there have been cases in the southeastern US (ex: Kentucky). All other GI worms would present with either a fever or a cough. Treat with mebendazole or albendazole.

 +0  (free120#40)

from @melchior

From the UW ID 666 explanation, although type II pneumocytes normally differentiate into type I pneumocytes after proliferation, they do not differentiate in idiopathic pulmonary fibrosis due to altered cell signals and altered basement membrane, which is why type II pneumocytes are increased.

explanation by @benwhite_dotcom is incorrect


 +0  (free120#1)

If you are making fatty acid, you should not burn it simultaneously.


 +3  (nbme22#18)

as @mtfp said, NRTI need to be phosphorylated by HOST CELL thymidine kinase, mutation in viral kinase has no role in NRTI resistance.

Need to put as separate comment as wrong explanation is at top.


 +2  (nbme24#42)

Any good material to prepare for this kind of stuffs?

apurva  Lord Jesus

 +1  (nbme21#14)

exactly how does maternal hashimoto can cause cretinism?


 -1  (nbme21#4)

wrist extensors (tennis - backhand)--> lateral epicondyl wrist flexors (golf - think near shot - don't know what it's called) - medial epicondyl

b1ackcoffee  fucked formatting.




Subcomments ...

Calcium is low while PTH is high. It’s primary hyperparathyroidism (not secondary). Ans is branch of IJV.

mdmofongo  You’re right, how weird. But I guess following the Hx there is no other way to approach it? Not a fair question I would agree. Also the inferior thyroid artery does branch off of the thyrocervical trunk. The superior and middle veins of the thyroids drain into the IJV. +  
b1ackcoffee  I got that it must be some vein, I just didn’t know the tributaries. Oh well, anatomy fucks me again! +  


I am wondering which parasite is this actually? --

mdmofongo  The clinical presentation sounds like a GI parasite, which are transmitted via fecal-oral route, so ingestion of soil would be the most sensible answer. All the other routes are of parasites with more severe or systemic infection. +  
b1ackcoffee  @mdmofongo I know this. But which parasite is this? +  
drblu92  The parasite is most likely Trichuris trichiura (human whipworm). Trichuriasis is often asymptomatic and adult forms can reach 2 cm in length (visible with naked eye). A lot more common in tropical areas but there have been cases in the southeastern US (ex: Kentucky). All other GI worms would present with either a fever or a cough. Treat with mebendazole or albendazole. +2  


submitted by mdmofongo(0),

Myeloperoxidase is the only one actually involved in making free radicals. Catalase makes H2O2 into water, Superoxide dismutase eliminates oxygen radicals, LDH makes lactate (no role in bacterial killing), and NO synthase, makes NO.

b1ackcoffee  I thought SOD also comes (second) after pathway (making h2o2) to make HO—Cl +  
mdmofongo  Now that I took a look at the pathway again you are right. Knowing this I’d say that free radicals of O2 still have a chance to cause some damage, as where Hydrogen peroxide just serves as a intermediate for free radical formation. Thus SOD deficiency leaves some bactericidal action but MPO leaves none? +  


submitted by doodimoodi(39),

Did no one notice that the Odds ratio on the top left is wrong? Am I missing something? If you calculate it, it's 6 just like the top right one....

mjmejora  thats actually really funny +  
yex  Because I said so, applies here... :-/ +  
doodimoodi  Cant believe we pay $60 for this crap +23  
aisel1787  best comment doodimoodi) +1  
b1ackcoffee  that fucking threw me off on exam. I was like is there an effect modification by "Not drinking milk". the fuck! +  


submitted by j000(-2),

i got this question wrong, but i think what this question is really asking is what happens in a systemic infection: which is fever

in systemic infection, the most obvious sign to look for is a fever, not necessarily shivering, sweating, heat production by brown fat, etc.

and how does fever occur? like someone already mentioned: pyogenes --> macrophages releasing IL1 and TNF which increases COX activity in hypothalamus perivascular cells, increase production of PGE2 in hypothalamus and reset the temperature set point.

i think the whole phrase "complete transection of the spinal cord superior to the level of sympathetic..." is a distraction. it just tells you that development of a fever has nothing to do with it

j000  development of a fever in systemic infection has nothing to do with sympathetic nervous flow, so even it's injured, fever would still occur. I think this question is just asking how does fever occur in inflammation/infection situation. +  
b1ackcoffee  So, how do you explain the actual fever by just changing the thermostat?? Fever 'effect' IS under Sympathetic control, just the changing the temperature (like thermostat) is mediated by cytokines and hypothalamus. +  
j000  oh i see what you mean, well i didn't know that, so thanks for clarifying that. however, based on your explanation, it would still get us to the right answer which is "alteration of thermostatic set point", not the fever effect itself. +  


submitted by mattnatomy(34),

Answer = Decreased libido; normal nocturnal erections

I believe what they were trying to indicate in this question was Psychological Sexual Dysfunction (aka - Performance Anxiety).

In this case, it wasn't so much the performance that worried the man, but he may be so focused on his health issues (post stroke), that he is unable to perform adequately. Therefore, his natural libido would be decreased. However, because it's psychogenic & not physiologic, he should still have normal nighttime erections.

b1ackcoffee  Wouldn't pshychological SD have normal libido and just performance anxiety? +  


Although there are no specific herpes indicators, a CSF panel with mostly leukocytes indicates a viral infection (as well as the normal glucose). So you can rule out TB, neurosarcoidosis and bacterial. Brudzinski/kernig sign are related to meningitis, but even if you don't know what those are, the question says that there is an abnormality in the TEMPORAL lobe (meningitis = meninges). Encephalitis would be the best answer, especially because Herpes Encephalitis affects the temporal lobe.

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. +1  


submitted by mdrahimi7(-2),

The answer must be protein regulation not structure ! First of all you know that cystic fibrosis can have several mutation 1.severe splicing defect In which cftr protein is normal but less in concentration due to 3 types of mutation 1_ promotor box defect and leading to less transcription 2_ premature stop codon 3- and reading frame mutation All these mutation leading to less synthesis of normal cftr protein.The second type of mutation is 3 bade deletion that ctfr protein problem is in folding 3. The mutation is in those part of protein which regulates its function like nucleotide binding domain and regulatory domain Actually to clear more this protein has three part Regulatory domain, Nucleotide bonding domain and transmembrane part . And type 4 mutation is that transmembrane part of protein is defective channel will be made but work less. Now as you can see in the first picture that i sent you actually in(( bronchial and respiratory part)) the cftr protein is present that it normally you know that it secrets cl and inhibits na channel on membrane until na +chlorine absorb the h2o to soften the mucus so it means normally in respiratory system this protein secrets cl and regulate the function of na channel. Now according the respiratory problem that the patient had it points to this point that the mutation of this cftr leads to this that this protein can't secret cl +can't regulate the function of na channel so So the type of mutation occurring to this person is with the regualtory part not the structure (cftr protein is present but can't work in this way to secret cl and regulate the na channel. Because you can see that patient mutation of cftr is not so severe (if it was sever I mean the structure of protein has the problem so according this matter that cftr protein are present in different system of our body in respiratory,gis, other salivary gland , liver complication , heart complication , sweat gland all these systoms will be effected ) but the baby just it has problem in respiratory system and sweat gland so it is mild when it is mild so the mutation should be in this way that either structurally cftr is present but less in number or cftr protein is present but the problem is with the regulatory party that just it can't secrete the cl and can't regulate the function of na channel as you can see in this patient respiratory and sweat gland. Finished😊

b1ackcoffee  I thought the same and got it wrong, but answer is conditioning me NOT to overthink and keep it simple. +  


submitted by taway(22),

This question is phrased strangely, but it's essentially asking "what would happen if this woman's hypothyroidism became uncontrolled over the course of her pregnancy?"

currently her TSH is good --> well-controlled hypothryoidism HYPOTHETICAL high TSH --> her hypothyroidism must NOT be well-controlled (due to disruption of the T3/T4/TRH/TSH endocrine axis)

So, now that we understand that the question is asking "what would happen if her hypothyroidism was uncontrolled?"

Answer: cretinism

I think that this question is phrased atrociously, but far be it from me to criticize the USMLE licensing board...

yotsubato  I think that this question is phrased atrociously, Just like the rest of the NBME +5  
b1ackcoffee  exactly how does maternal hashimoto can cause cretinism? +  


submitted by dr.xx(101),

Henderson-Hasselbach Equation: pH = 6.1 + log(HCO3 / (0.03 * PaCO2)); so here, pH = 6.92 => Acute (uncompensated) primary respiratory acidosis, with metabolic acidosis

sbryant6  calculator can't do logs yo. +5  
usmlecrashersssss  lmfao +  
b1ackcoffee  wow, sherlock! +  


wrist extensors (tennis - backhand)--> lateral epicondyl wrist flexors (golf - think near shot - don't know what it's called) - medial epicondyl

b1ackcoffee  fucked formatting. +  


submitted by tsp(0),

Is the woman in the first generation 1(2) not affected because of incomplete penetrance?1(2) has to have the trait for the disease to develop in the future generation.

b1ackcoffee  disease developed due to germline mosaicism (mutation in of the oocyte) +  


submitted by divakhan(1),
This is not XLD, its XLR disease (FA 2020 page 59)

Here, the mother is homozygous for the mutation therefore she displays the disease.

We see that,

  1. It skips generations
  2. Males are more severely affected (die in utero)
  3. Females are affected (only when homozygous)

Here we see, that mother can pass defective X chromosome to 50% females & other 50% will be carriers (healthy X chromosome from father, defective from mother) For males, Mother passes defective X chromosome so they die (only 1 X chromosome)

For the males who are living (III 6,11 shown in pedigree), they have been lucky to survive due to mosaicism! ;)

b1ackcoffee  don't you think you are going through too many hoops (assumptions)? male survive due to mosaicism? Better chance is disease started due to germline mosaicism and it IS XLD. btw the disease is incontinentia pigmenti (not necessary to know). your second last para doesn't make sense, read again with fresh mind and perspective. +  


submitted by h0odtime(31),
  • Normocytic Intrinsic Hemolytic Anemia: Reticulocyte >>2.5%
  • PEP --> Pyruvate (last step of Glycolysis) second ATP producing step
  • Mature RBC require pyruvate kinase without it they depend on the anaerobic generation of ATP
  • With insufficient ATP, all active processes in the cell come to a halt. Sodium potassium ATPase pumps are the first to stop: increase intracellular K+, water leaves cell with Na+. Cell Shrinks & dies. Body is deficient in RBC + destroyed by lack of ATP = Hemolytic Anemia
  • Inheritance: AR
b1ackcoffee  ermm . buddy, stopping NaKATPase causes RISE in intracellular Na, cell SWELLS and dies. +  


submitted by madojo(93),

Know your STD's baby ;-) (going through every other choice on this question):

  • Bacterial vaginosis caused by gardnerella vaginallis. Se a thin, off white discharge and fishy smell (fish in the garden). There's no inflammation Lab findings: pH greater than 4.5 (just like trichomoniasis), and a positive whiff test with KOH. Stem will say something about malodorous discharge and show the infamous CLUE CELLS if we are lucky. Not the answer for this question obviously because we would not expect vesicles with this bacterial disease.

  • Candidiasis is going to be your thick cottage cheese discharge, with inflammation. normal pH see pseudohyphae. Treat with topical nystatin, or oral fluconazole unless you're pregnant than use Clotrimazole. Again not going to see any vesicles.

  • Chancroid per uworld is associated with Haemophilus ducreyi you will have a Deep purulent painful ulcer with suppurative lymphadenitis. Will be told that patient has painful inguinal nodes, there may be multiple deep ulcers with gray-yellow exudate. You do cry with H. duCRYi This wouldn't be true for what our patient has in this question because we aren't told of any inguinal adenopathy. a link to a chancroid VDA

  • Chlamydia trachomatis causes lymphogranuloma venereum which is small shallow ulcers, painless, but then the large painful coalesced inguinal lymph nodes aka BUBOES. Compared with gonnorhea the discharge is more thinner and watery. Again not the case here as its painful and no mention of any BUBOOESS. The discharge in gonorrhea is more thicker. Both lead to PID, treat for both because confection is common. With both patient may have some sort of pain or burning sensation upon urination. Sterile pyuria though for both.

  • Condyloma accuminatum is a manifestation of HPV 6 + 11 (genital warts). They look like big cauliflowers. This is in contrast to Condyloma lata that you see in syphillis which is just a flatter latte brown looking macule.

  • Genital Herpes (the answer to the question) will present with multiple painful superficial vesicles or ulcerations with constitutional symptoms (fever, malaise) Just fits better than all the other choices I ran through.

  • Syphillis is the painless chancre. UW describes it as a single, indurated well circumscribed ulcer, with a clean base. See corkscrew organisms on DF microscopy. Keep in mind other painless ulcers are lymphogranuloma venereum of clamydia (but the buboes are whats painful not the ulcer), and granuloma inguinale (donovanosis - klebsiella granulomatis) but whats hallmark about this one is that its painless without lymphadenopathy

In short, be safe.

drdoom  this write-up is AWESOME ... but it also made me vomit. +  
b1ackcoffee  This is awesome, writeup, not the stds. +  


submitted by saqeer(0),

a little misleading her increase in weight made it seem as if she had low thyroid hormone and tyrosine is a precursor.

b1ackcoffee  but hypothyroidism would decrease the height. +  


submitted by usmleuser007(278),
1. "Three HAL fans will try meth"
    a. Threonine = Three 
    b. Histidine; Arginine; Lysine = HAL
    c. Phenylalanine = fans
    d. Valine; Isoleucine; Leucine = will
    e. Tryptophan = try
    f. Methionine = meth
pparalpha  Thanks! Good mnemonic +1  
b1ackcoffee  best mnemonic +  


submitted by drzed(87),

Perhaps this is an incorrect way of thinking about this, but I always associate the virulence of Strep pneumo to its capsule, but I only associate the K capsular antigen of E. coli to meningitis (recall that E. coli has other specific virulence factors like fimbriae for UTI).

So basically, I figured that the capsule of Strep pneumo is involved in more disease processes (MOPS) than the capsule of E. coli (mostly meningitis), and thus I chose Strep.

b1ackcoffee  You are right, this is INCORRECT way. Capsule helps in hematogenous spread by protecting from phagocytosis causing sepsis, meningitis, pneumonia, i.e. more systemic infections. +  


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