they really copied and pasted this sh!t on nbme 6-8 huh? couldn't afford another heart sound smh
From UpToDate: For patients with SCLC, systemic chemotherapy is an important component of treatment, because SCLC is disseminated at presentation in almost all patients. For those with limited-stage disease, thoracic radiation therapy is used in combination with chemotherapy. Prophylactic cranial irradiation is often used to decrease the incidence of brain metastases and prolong survival. Prophylactic cranial irradiation and thoracic radiation may also be beneficial in those with a complete or partial response to initial systemic chemotherapy.
This is a case of late post-renal azotemia, as you can tell by the BUN/Cr ratio that is <15 and the 3 day history of pain. They also tell you that the hydronephrosis and lymphadenopathy are compressing the ureters so it makes sense that you would want to stent the ureters. The others are all in the wrong location: Foley catheter (penis), suprapubic tube (bladder), stent in renal arteries (self explanatory).
Pretty sure this is a case of Legionella. The fact that it didn't show up on culture but a "highly specialized" medium (in hindsight buffered charcoal yeast) yielded gram-negative rods put Legionella on my radar. The headache and dry cough also line up with it but the macrolides threw me off since I thought they were treated with fluoroquinolone. But the sketchy video for macrolides includes Legionella as a target so it worked out.
Plasmodium vivax/ovale have dormant stages where their hypnozoites can stay latent in hepatocytes and trigger malaria well after the initial infection. The only malarial drug that covers against this is primaquine. The answer choice is just worded funny - "exoerythrocytic malarial tissue stages" basically is the stage where they are in the liver/not in RBC, and chloroquine won't work for those.
"Finger-shaped" lesions is suggestive of a papilloma and the findings being on the vocal cords and epiglottis make this a laryngeal papilloma. Most common cause of laryngeal papillomas is HPV 6 and 11, per sketchy.
I also had no idea what the diagnosis was and purely went off elimination: Can't be fatty acid oxidation bc of the ketonemia, which you wouldn't be able to produce if that was the defect. Glycogen breakdown/synthesis are related to glycogen storage diseases, which the presentation didn't line up well with. Also I was thinking of a pathway that would incorporate glycerol, fructose and galactose which seemed more in line with gluconeogenesis/glycolysis. Between the last two, I went with faulty gluconeogenesis bc that would elad to his hypoglycemia. I don't know how legit or applicable that is to other questions, but thought I'd at least share in case anyone finds it helpful.
I knew it had to be X-linked because it said that it was fatal to males who have it in utero, but I had a hard time deciding between dominant and recessive. Ultimately it has to be X-linked dominant because the affected mother in the second generation gave birth to unaffected sons (which can't happen in X-linked recessive). That means the mother in question is heterozygous and her daughters will have a 50% chance of inheriting the disease while her sons have to be unaffected if they live, as previous posters mentioned. I didn't figure this out until way after the test...this one was a doozy. Still not sure that it's XLD because how come nobody in the first gen has it? Guessing it was a spontaneous mutation?
By default you should use intention to treat analysis b/c it's the most conservative.
You can answer by process of elimination. "Competitive interactions" makes you think stimulatory NT. Cross out GABA and glycine. In the cortex so glutamate. Metabotropic would mean there's second messengers involved and the receptor would not transmit calcium. Hence NMDA.
If you're confused by the systolic murmur look at FA2019 p.288. ASD can cause systolic ejection murmurs in the pulmonic location (can think of it as increase turbulent flow).
Of course the more important thing is fixed splitting so SMASH away.
In addition to what has already been said I think an important point in the question was regulatory adjustments which points more towards arteriolar regulation.
tricky image but question is asking more specifically about his visual complaints which is just "double vision" so IR entrapment is the best answer
I don't think you're supposed to know any complicated niche piece of knowledge. You have to infer that the pt has a skin lesion and is therefore prone to skin infections, most commonly from Staph aureus.
the patient is pregnant so not doxy. azithro is alternative (see sketchy vid)
Dicumarol is in the coumarin family which includes warfarin. It helps if you think about warfarin's brand name Coumadin. Coumadin, coumarin, dicumarol...all the other derivatives have COUM it in some fashion
neuroendocrine cells doesn't always mean neural crest
literally know every single name they can possibly call this
from uworld: fibrates activate PPAR-alpha to increase LPL and decrease VLDL production
uworld says somewhere that testosterone increases hematocrit, increases LDL, and decreases HDL
got confused by the systolic pulsation of the liver but basically regurgitant blood from RV will go into RA > IVC > hepatic veins
hit the kidney so retroperitoneal. leaves only the duodenum and splenic flexure. kidneys are more lateral structures so splenic flexure (at turn of descending colon)
you need to add an amine (nitrogen) and most biochem processes from sugar --> amine requires glutamine
Super annoying they are using the same picture BUT you can answer with process of elimination. No mass in the picture so not nephroblastomatosis or RCC. 4 year old so not amyloidosis. Stem does not really cue you into membranous GN. Instead it talks about UTIs which would have inflammatory processes --> interstitial inflammation.
Cecum is intraperitoneal even though it's part of the ascending colon
Euthyroid sick syndrome = levels of T3 and/or T4 are abnormal, but the thyroid gland does not appear to be dysfunctional. The classical phenotype of this condition is often seen in starvation, critical illness, or patients in the intensive care unit. The most common hormone pattern is low total and free T3, elevated rT3, and normal T4 and TSH levels.
FA19 p.233 cortisol has a permissive effect on catecholamines
unequal BP/pulses in the arms is a big key for aortic dissection
Increased pressure is in the Bowman space (NOT the glomerular capillaries) so the only pathology listed that would cause backward build up of pressure is BPH
https://step-prep.org/tutoring/
what is "allergic nonhemolytic transfusion reaction"? i thought it was the febrile one, but febrile is listed separately
The positioning of the arm on presentation is different that what I was taught. I thought the arm was held in extension. I might be wrong here.
https://step-prep.org/tutoring/
Beck's triad: muffled heart sounds, jugular vein distension, and electrical alternans. This patient has cardiac tamponade. The fluid has to be removed.
A pericardial window is a cardiac surgical procedure to create a window from the pericardial space to the pleural cavity. The purpose of the window is to allow a pericardial effusion (usually malignant) to drain from the space surrounding the heart into the chest cavity.
i dont think it said she was on NSAIDs anywhere in the question stem and i thought that they had a synergistic effect with opioids, thus should be tried prior to changing opioid management.
how come this couldn't be decreased FSH? Doesn't estrogen have negative feedback on FSH/LH?
I get that the bruit = Renovascular disease. But why is it not hyperaldosteronism when there is hypertension + hypokalemia + elevated bicarb
https://step-prep.org/tutoring/
https://step-prep.org/tutoring/
https://step-prep.org/tutoring/
The stem says that he has a history of lower GI bleeding however upper endoscopy and colonoscopy show no abnormalities. With that said you can rule out all of the answers except for Angiodysplasia.
Angiodysplasia is confirmed with angiography. Tortuous dilatation of vessels that cause hematochezia.
FA2019 380
The question stem mentions 3 subsets of patients: a) Some patients were inconsistent with taking medication or "not adherent" to medication regimen b) Some patients discontinued the drug they were randomized to completely c) A subset of these patients in point 'b', who stopped the medication were then prescribe the medication from the comparison group.
The ultimate question however is regarding whether patients under point 'a'(as above) should be included or excluded.
Ideally this depends upon your study protocol. In essence you may have an 'Intention to treat protocol' or an 'Adherent protocol'. As part of an adherent protocol you only include patients or study subjects (as referred to in basic science research) you only include those patients that strictly followed the protocol and exclude everyone else. This is mostly how basic science protocols are designed.
With clinical research however being completely per protocol is difficult and that's where the intention-to-treat protocol apples. This is to accommodate the subjective nature of human subjects in clinical research. Following up with human subjects is but obvious harder than manually handling mice or pigs in the lab. So in such cases as long as the study team has followed protocol in contacting the patient and playing their role all patient data can be included even if there are some minor protocol deviations due to logistical issues. All these deviations need to be reported to the IRB ofcourse and specified in the manuscript in the most appropriate manner.
phenylpropanolamine is an alpha agonist that stimulates urethral smooth muscle contraction. - from uptodate, however, it also says it is not recommended treatment anymore
Coloboma is an eye abnormality that occurs before birth. They're missing pieces of tissue in structures that form the eye.
Colobomas affecting the iris, which result in a "keyhole" appearance of the pupil, generally do not lead to vision loss.
Colobomas involving the retina result in vision loss in specific parts of the visual field.
Large retinal colobomas or those affecting the optic nerve can cause low vision, which means vision loss that cannot be completely corrected with glasses or contact lenses.
Since there were "small amounts of meconium" I thought it couldn't be atresia. Turns out atresia isn't always absence of lumen, it can also be abnormal narrowing of lumen, allowing just a small amount to pass through...
Why is the answer fibularis brevis and not fibularis tertius? How do you distinguish between the two from this vignette?
From ShoryukenHadooken on reddit:
What the question is getting at is the sympathetic chain was spared. It was a terrible way of wording it.
Your anterior hypothalamus is responsible for cooling features and is under parasympathetic control. A lesion would cause hyperthermia.
Your posterior hypothalamus is responsible for heating when you're cold and to generate the Fever response and is under sympathetic control. A lesion would cause hypothermia.
In this question it is simply asking a person gets sick, hypothalamus was spared, what happens.
Answer: hypothalamus will still be able to elevate set body temperature to battle infection.
Hint: IF they give a question similar to this but reworded to include a lesion of the sympathetic fibers or of the hypothalamus, you would in turn NOT be able to generate a fever response to infection. The hypothalamus would be entirely under parasympathetic control
This adds more context to the fact the Q states that the sympathetics was spared
Male internal genitalia -> Intact SRY , testes, and testosterone.
No female internal genitalia -> Presence of MIF (antimullerian hormone) and intact Sertoli cell function.
Female external genitalia -> No androgen present, which is required for male external genitalia formation.
If both HCTZ and loop diuretics were provided as an answer choice, further clue that hctz would be the answer choice is the presentation of the patient "feeling funny". This suggests hypercalcemia (psychiatric overtones) which is a side effect unique to HCTZ.
The Q stem states FOXO is a transcription factor that responds to insulin signaling by altering the transcription of metabolic genes --> therefore, FOXO is a transcription factor involved in metabolism. This should make sense because insulin-receptor activation has a role in regulating metabolism.
This Q asks about reversible ways that insulin reguates FOXO transcrption factor activity.
Ubiquitin-mediated proteolysis is irreversible. Eliminate all choices except for B, D, and H.
Insulin-receptors function through PI3K signaling. PI3K signaling involves phosphorylation of serine --> serine phosphorylation is a reversible process. Eliminate H. FYI: protein/amino acid phosphorylation is always reversible.
You are left with choices B and D.
FOXO is a transcription factor --> transcription factors mediate gene activity by shuttling between the cytoplasm and nucleus. Regulating the location of FOXO transcription factor (i.e. cytoplasm vs. nucleus) will therefore reversibly modulate FOXO-mediated metabolic gene activity.
This leaves you with the correct answer: Choice B.
Lysine is used in elastin and collagen cross linking; it is cross linked by lysyl oxidase to make collagen fibers
Uworld specifically says that Psoas abscess means the patient will prefer flexion to avoid stretching the muscle. That's why Psoas did not make sense to me since the patient preferred extension, which would be stretching out the muscle.
On the other hand it's right on the vertebra and it's associated with TB.
Can anyone answer why this one can't be F. Beta thalasemia major? I was thinking becaues of his anemia and the "european descent" which includes the mediteranian europeans. Unless NMBE writers think that european only means the ones with extra white people lol
Physical exams showed tenderness of costophrenic angles, which are the places where the diaphragm (-phrenic) meets the ribs (costo-). Not the Costovertebral angle tenderness that we think to hint renal disease.I got confused with this point.
Anything upper lip + above โ basal cell carcinoma
Anything lower lip โ Squamous cell carcinoma
FA 2019 -pg 473
SPOILER SPOILER SPOILER
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This is LITERALLY the same photo they used to describe the 4-year-old boy with diffuse cortical necrosis from NBME 18. Can someone explain what's going on here
This is how my brain farted while I was doing this question.... I wanted to choose TBG deficiency, but I kept thinking that if TBG is deficient, that means there are less or no binding proteins in the blood. And how can the free T4 be normal? Shouldn't free T4 increase if there were less T4 binding protein? ...
they really copied and pasted this sh!t on nbme 6-8 huh? couldn't afford another heart sound smh