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Welcome to fkstpashlsโ€™s page.
Contributor score: 23


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 +3  visit this page (nbme20#17)
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Process of elimination is the only way to get this answer without Savant levels of autism, as some bowtie wearing doucher who wrote the question probably has.

Cancer is unilateral almost all the time, DM doesn't make sense for any reason, HTN itself wouldn't cause milky boobs, and mast cells degranulating doesn't make milky boobs either. So, and because many drugs can have milky boobs, you're left with drug effects by process of elimination.

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djinn  I dont think the autor was a savant. Also I think is right proccess to think "cancer" can be bilateral and malignant but the "drug" that causes this isnt HCT. This question is bad written. +1
hungrybox  According to Pathoma, galactorrhea is NOT associated with cancer ever (see 16.1 - breast pathology). +
djeffs1  according to strugglebus's numbers its more likely to be b/l cancer than thiazides... +




Subcomments ...

submitted by athleticmedic(18), visit this page
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Can anyone help explain to me why he has lower extremity hyperreflexia and upper extremity resting tremor? I can't find anything that associates those symptoms to Schizophrenia.

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krewfoo99  I think its because his hypothyroidism is being overtreated with levothyroxine. +
wasifp  So I respectfully disagree that he is being over treated because the TSH would drop below 0.5 if that was the case. His hyperreflexia and resting tremor along with mutism and staring are consistent with catatonia which is seen in severely schizophrenic patients. Catotonia can be both "excited" and "retarded". The excited aspect of his catatonia is the hella purposeless movement (eg, tremor) and his spasticity maybe actually be a manifestation of posturing seen in these patients. +3
fkstpashls  they're parkinsonian symptoms more than catatonia symptoms, though. +


submitted by ht3(25), visit this page
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If the chin is deviated to the right, then wouldn't the "mass" (which I assume is the tight SCM muscle) be on the LEFT side of the neck??

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cinnapie  Contraction of right SCM moves your chin to the left. I know its weird to think that the SCM kinda pushes the chin away but its how the origin and insertion of the muscle is. +3
fkstpashls  If you're slouching in bed with your mouth open wondering why you get rammed by another question, tense up your SCM on one side and you'll feel your jaw move to the opposite. +


submitted by notyourgangsta(0), visit this page
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this question does not feel complete. I think the correct diagnosis is compartment syndrome. If there is tightness and pain after an operation, compartment syndrome must be considered.

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etherbunny  ...in which case ultrasound would demonstrate vascular compression, so it's still a good option. However DVT is far more common with lower limb surgery and immobilisation (or was, before LMWH became a standard of care). +2
fkstpashls  Just adding to the above, because it initially got me on UW: just because they're getting LMWH doesn't mean they can't get a DVT, it's just much less likely. +1
jigermisker  I just read the question again. fixation was right leg, pain now is left leg. +5


submitted by seagull(1933), visit this page
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THe acid-base status of aspirin is always in the process of shifting from alkalosis to acidosis over a few hours. So relying on ABG is unreliable (in my opinion) for a quick answer.

Rule of thumb for aspirin toxicity: Fast respirations, tinnitus, kidney damage (increased creatinine).

This question she had a fast respiration rate.

---Not perfect but may help in a quick pinch-----

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fkstpashls  Yup, just adding a little bit to this: You can have a normal range pH but expect both primary resp alk and primary met acidosis afterwards to be present, making sure you have an elevated anion gap - if you have questions with the arrow shit to choose from. +


submitted by hello(429), visit this page
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This is the actual correct explanation:

PDA causes blood to flow from descending aorta to patent ductus arteriosus into pulmonary circulation ("right-to-left")

The "steal" from the aorta during diastole requires increased cardiac output to compensate to deliver adequate amount of blood to rest of body

Source: https://www.ncbi.nlm.nih.gov/books/NBK430758/

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fkstpashls  It's L to R +2


submitted by vonhippelindau(21), visit this page
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Itโ€™s acute alcohol consumption so fatty change more likely. Cellular swelling indicates alcoholic hepatitis which requires chronic alcohol consumption (See FA 2019 pg 385). At least thatโ€™s the logic I used to pick fatty change.

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seagull  Seems like fatty change would require more than 1 weekend. I choose swelling since it's reversible and seems like something with a quick onset. +51
nc1992  I think it's just a bad question. It should be "on weekends" +17
uslme123  https://webpath.med.utah.edu/LIVEHTML/LIVER145.html +27
uslme123  So his hepatocytes aren't dying ( ballon degeneration ) vs just damaged/increased FA synthesis due to increased NADH/citrate +1
sympathetikey  @seagull I agree! +
et-tu-bromocriptine  It's not in pathoma, but I have it written in (so he or Dr. Ryan may have mentioned it) - Alcoholic hepatitis is generally seen in binge drinkers WITH A LONG HISTORY OF CONSUMPTION. +1
linwanrun1357  Do NOT think the answer of this question is right. Cell swelling make more sense! +1
fkstpashls  some asshole in suspenders and a bowtie definitely wrote this q, as I've seen both acute swelling and fatty change be used to describe one episode of drinking. +15
msw  short term ingestion of as much as 80gm of alcohol (six beers) over one to several days generally produces mild , reversible hepatic steatosis . from big robin 8th edition page 858. Basically to develop alcoholic hepatitis with cellular swelling etc you have to have sustained long term ingestion of alcohol while steatosis can develop with a single six cap . hope that helps . ps i got it wrong too . +3
msw  six pack8 +
mariame  After even moderate intake of alcohol, lipid droplets accumulate in hepatocytes increasing with amount and chronicity of alcohol intake. (...) Fatty change is completely reversible if there is abstention from further intake of alcohol. The swelling is caused by accumulation of fat, water and proteins. Therefore this will occur later. From big Robins 9th pg842. +
l0ud_minority  Just thinking about this Alcohol is a Mitochondrial poison which would lead to stress uncoupling of oxidative phosphorylation and cellular swelling. I got it wrong with that logic though which is frustrating. +


submitted by hyoscyamine(59), visit this page
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FA pg 217. Too much oxygenation can cause free radical damage leading to retinopathy of prematurity

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mmm21  Okay i might be retarded, but why i canโ€™t understand that they r asking about the thing that is damaged ? ๐Ÿ˜‚๐Ÿ˜‚ +8
sahusema  Seriously! The question says "the goal of treatment is the protection of which of the following structures?" If too much O2 damages the retina, how is this treatment supposed to be protective to the retina? +2
ratadecalle  I think too much oxygen would be with the ventilator having a high FiO2 setting, which they don't mention here but I'm guessing thats the thing they're controlling to avoid oxygen toxicity? +2
burak  they didn't give the patient fio2 100%, question asks the reason for it. but in a very stupid way +31
naught  Supplemental O2 may also cause bronchopulmonary dysplasia or intraventricular hemorrhage (germinal matrix, located in subventricular zone NOT choroid plexus) +1
fkstpashls  92-95% isn't high, but it's enough to get everything else oxygenated. Because it's not 100% high flow the retinas don't over-vascularize and lead to damage/hemorrhage, and shit like that. +1
soccerfan23  In other words....the question is basically asking why they gave the patient a fio2 of 92-95% instead of 100%. The reason is because 100% oxygen would lead to retinopathy of prematurity. The lower 92-95% oxygen levels protect the retina from damage. The wording of the question sucks tho imo. +3
randi  FA 2019 p210 under Free radical injury examples +
umpalumpa  from NATURE https://www.nature.com/articles/7211475#:~:text=Several%20recent%20studies%20have%20shown,high%2Doxygen%20saturation%20and%20ROP.&text=It%20seems%20that%20a%20SaO,in%20a%20high%2Doxygen%20saturation.: Several recent studies have shown a relationship between a high-oxygen saturation and ROP. It seems that a SaO2>93% increases the risk for severe ROP and need for therapy +


submitted by dr.xx(176), visit this page
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Among the most prevalent hematologic abnormalities in patients with rheumatologic disorders are the anemia of chronic disease (ACD), a mild anemia that is generally asymptomatic, and iron deficiency anemia.

In iron-deficiency anemia, the TIBC would higher than 400โ€“450 mcg/dL because stores would be low.

Patients with RA occasionally have concurrent iron deficiency anemia and ACD. When this occurs, the hemoglobin level usually drops to below 9.5 g/dL, and the MCV is less than 80.

https://www.uptodate.com/contents/hematologic-manifestations-of-rheumatoid-arthritis

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sympathetikey  Got the right answer too, but man, that whole "1 month after starting therapy" almost threw me off. +1
fkstpashls  all I do is put the wrong answer when I'm between two. Fuck +1


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