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 +0  (nbme21#14)

exactly how does maternal hashimoto can cause cretinism?


 +0  (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 ...

submitted by taway(16),

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 +3  
b1ackcoffee  exactly how does maternal hashimoto can cause cretinism? +  


submitted by dr.xx(93),

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. +3  
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(15),
  • 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(50),

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(1),

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(220),
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(43),

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. +