to snoo-finity ... and beyond!
Welcome to yb_26's page.
Contributor score: 81
Not sure I agree with the second one, M.O.A for botulinum is cleave of SNARE protein preventing pre-synaptic ACH release. Think the second one almost describes something like sux or some other deporalising nicotinic drug.
You are right but to get the muscle spasms, trismus & seizures it has to inhibit GABA & Glycine release from Renshaw cells
Cleaving the snare proteins will cause paralysis
I googled the meaning of abnormal test results just to make sure.
A positive test is one in which the result of the test is abnormal; a negative test is one in which the test's result is normal.
median should be: 70 for group X ; 85 for group Y
median here is the avarage of Diastolic BP measured betweeen the 50 & 51 patients (since the number of patients in each group in even; Median= (n+1)/2 -> (100+1)/2= 50.5)
Group X = (70+70)/2 = 70
Group Y = (80+90)/2 = 85
tried to attach photo, sorry for that(
Summary of metabolic issues relating to hyperammonemia
i'm leaning towards Ornithine transcarbamylase deficiency.
Not sure why this isn't considered a mitochondrial disorder since the issue is Ornithine transcarbamylase deficiency in the mitochondria?
if it was mitochondrial disorder no one would escape
figure in OTC deficiency, they might have to explicitly mention the orotic aciduria AND typically presents earlier, around 24-48hrs of life after they've fed (at least per BB)
+ also per BB, propionic acidemia and MM acidemia have an onset of weeks to months and lead to build up of organic acids --> acidemia in addition to hyperammonemia (not sure why, but several aa enter the TCA cycle via propionyl CoA --> methylmalonyl CoA --> succinyl CoA, but now this is defunct d/t enzyme deficiencies...?). Anywho, propionic acidemia described on FA2019 p85, but doesn't list hyperammonemia
i think it cannot be Ornithine transcarbamylase deficiency bc it is XR disease. this pt has a healthy 2yr old brother which rules out X-linked recessive disease correct me if i m wrong
it is 100% Propionic acidemia Uworld Q-id: 1340. it is an exact copy question of uworld. i got it wrong bc i forgot these are organic acids. But i am still confused on 2 things
1-how does acidosis cause Hypoglycemia and Ketosis.
2-why is Ammonia elevated in these pts bc urea cycle will be fine?
1) hyperammonemia is seen in all urea cycle disorders except arginase deficiency
2) organic acids directly inhibit urea cycle => hyperammonemia (from UWorld)
According to UW, there is another question # 1341. This one refers to methylmalonic acidemia (ORGANIC ACIDEMIA). HYPOGLYCEMIA results from overall increased metabolic rate leading to increased glucose utilization and direct toxic (-) of gluconeogenesis by organic acids. The presence of hypoglycemia leads to increased free fatty acid metabolism that produces KETONES, resulting in a further anion gap met acidocis. Finally, organic acids also directly (-) the urea cycle, leading to HYPERAMMONEMIA.
because they mention scattered fragments of foreign material (pt presents 2 months after c-section, sutures are either removed in 1 week or dissolve in few weeks (depends on type of suture material)
Wow, just checked First Aid and it doesn’t list “cough” as a symptom of EBV.
EBV is not a “respiratory virus”; it’s a *B cell virus*. Even though you might associate it with the “upper respiratory tract” (=kissing disease), it doesn’t cause respiratory inflammation since that’s not its trope. B cells are its trope! That’s why EBV is implicated in Burkitt Lymphoma, hairy leukoplakia and other blood cancers. (EBV is also known as “lymphocryptovirus” -- it was originally discovered “hiding” in *lymphocytes* of monkeys.) So, EBV = think B cells.
EBV does cause pharyngeal and laryngeal inflammation along with fever, malaise, and cough and LAD. The only thing that pointed me away from mono and towards coronavirus was the patients age.
Can someone explain what not holding up to acid or being dried has to do with being enveloped?
@nbmehelp, the envelope consists of phospholipids and glycoproteins => heat, acid, detergents, drying - all of that can dissolve the lipid bilayer membranes => viruses will loss their infectivity (because they need an envelope for two reasons - to protect them against host immune system, and to attach to host cells surface in order to infect them)
@at0xibolic, I think you won this competition on finding better picture lol thanks
just to add to the explanation above," cutaneous larva currens" is a specific finding for strongyloides. Also the picture they used is the exact same one on wikipedia lol
they really should add Wikipedia in the list of top-rated review resources with A+ level of recommendation in FA2020)))
also a side note:
cutaneous larva CURRENS is pathognomonic for strongyloides whereas
Cutaneous larva MIGRANS is for ancylostoma braziliense or nectar Americanus
To make it even simpler, if you narrowed it down to FAP vs HNPCC and looked at the image provided in the question, you'd see it's less likely to be FAP due to absence of numerous polyps which would be expected. So HNPCC would be your best choice!
I always get Li-Fraumeni and Lynch syndromes confused :/
I also picked decreased inhibin.
may be it was one of the "experimental questions", which are not even counted on the real exam
Inceased FSH will lead to spermatogenesis and spermiogenesis NOT Increase in Testosterone which is causing increased Height of this pt
Inhibin B only has negative feeback on FSH not GnRH. see the diagram on the topic of semineferous tubules in FA. Testosterone has a negative feedback on BOTH LH and GnRH
Kind of like how nocturnal pulsatile GNRH release occurs during sleep to stimulate growth (FA page327), the same thing happens for puberty. Pg 325 in FA, "pulsatile GnRH leads to puberty and fertility." It doesn't explicitly state during sleep, but pulsatile release of GnRH leading to pulsatile release of LH and FSH will lead to puberty. Puberty starts in the brain, its onset really has nothing to do with decreased inhibin levels which happens in the testes. hope that makes sense!
Also, ball like masses of proliferating decidua, I think, means ectopic decidua, which can be seen in endometriosis, deciduocervicitis, and in the lymph nodes. Markedly dilated fetal blood vessels can be seen in rare complication of placentomegaly which could potentially lead to IUGR but could also result in a normal neonate.
@nwinkelmann no, ball-like masses of proliferating decidua are seen in endometrial papillary syncytial change
O-linked glycosylation of secreted and membrane bound proteins is a post-translational event that takes place in the cis-Golgi compartment after N-glycosylation and folding of the protein
amazing, thank you!
even if it would be steroid in the list, if NSAIDs are contraindicated => we give Colchicine, and if pt can't tolerate Colchicine as well => then we use steroids
uptodate - try to avoid steroid therapy in gout , in this case patient has aspirin (NSAID) allergy , so second line is Colchicine , not Allopurinol, which is for chronic management. This case is not RARE and a lot of people sits on Colchicine therapy even if they do not have NSAID problems. Colchicine also First line treatment for Familial Mediterranean Fever, prevent exacerbations.
To make sure, palpable Gallbladder is more in cholangiocarcinoma and Pancreatic Cancer? And if it were non-tender, could palpable gallbladder mean gallstones?
@meningitis, it is a Courvoisier sign of pancreatic adenocarcinoma: jaundice + palpable, nontender gallbladder
check UWorld #12299
great explanation, thanks for sharing!
To be even clearer, this sounds like **Fanconi syndrome, which has lead to Type II RTA**
To be even clearer: Wilson disease => Fanconi syndrome => type II (proximal) RTA
To be even clearer, you all have been pretty clear
To be even clearer, you all have been pretty clear
bacterial overgrowth is associated with iron deficiency, but also with Vit B12-deficiency, so I guess pts will have macrocytic anemia
100/120 = 83% roughly 80%
Not sure what lfsuarez and seagull above mean. Here is my explanation.
Specificity = TN/(TN+FP). This test gave 20 false positives out of 100 people, and only 15 true negatives out of 50 men.
Specificity also equals 1-FPrate, and here the FP rate seems 20% so 100%-20%=80%.
abnormal test result means pt has cancer =>
TP = 35, FN = 15 (50-35), FP=20, TN =80 (100-20) => specificity = TN/(TN+FP) = 80/100 = 0.8 (in % will be 80%)
true negatives are 80 out of 100, not 15 out of 50
If you replace the values from the question in the table of page 257 of FA 2019, yb_26 explanation is correct. Abnormal test = patient has cancer = test +
Question says 35/50 men with prostate cancer (so all 50 have cancer) only 35 have abnormal test results, meaning that TP=35 (disease + test +) and FN= 15 (disease + test - because they do have cancer but the test was not abnormal for them ).
20/100 men without prostate cancer have abnormal test results meaning all 100 DONT have cancer but 20 show that they have cancer when its not true so FP=20 (disease - test +) and TN =80 (disease - test -)
Agreed. I'm pissed though because PGE2 mediates pain, which is why I picked it.
If im not mistaken, the question describes unstable angina. Unstable angina is due to thrombosis with incomplete occlusion. So, yes TXA2 is responsible for the thrombus that is causing the symptoms in this patient. I'm also pissed because I also went straight for the PGE2
hahah, seems like all in same boat like me
thromboxane A2 is also vasoconstrictor, so my thoughts were about vasospastic angina
same I went for pgE2 ... I M PISSED
same I went for pgE2 ... I M PISSED
Went for PGE2 ... shit
I went for leukotriene B4, what the hell was I doing....SHIT
I picked Leukotrine B4 thinking that the neutrophil infiltration was the source of the pain, seems wrong lol.
Sometimes it helps me to think of it in a general, non med school textbook kind of way. When answering, I narrowed it down to PGE2 and TXA2 as well. Then I asked myself, if someone is experiencing chest pain, would I recommend Aspirin or Advil? That's helped on a few over the counter pharm questions.
same here I M PISSED PGE2
Maybe PGE2 isint the answer because it mediates pain and fever during episodes of acute inflammation? Thus making TXA2 more likely.
ditto on the looked at it for 2 seconds and went PGE2
PPIs are not antacids!
They are just asking about side effect of statins, not about treatment of hypothyroidism
Hypothyroidism is just a red herring.
statins cause both hepatotoxic and mypopathy so I want for hepatotoxic:( I thought usmle expects different stuff
Hm, what do you mean by "normal compensation?" Are you talking about the bicarb should be increased? Are you saying that a normal compensation would be metabolic alkalosis? Would metabolic alkalosis be an increase in bicarb?
How do you know which one has bigger contribution in this situation where there's increased CO2 and decreased HCO-, both indicating acidosis??
normal kidney compensation would be an increase in bicarb reabsorption => increased serum bicarb. This pt has low serum bicarb => concurrent metabolic acidosis
Thats myosatellite cells. Satellite cells are also glial cells that form around damaged nerve cells and lie close to neuron bodies in the CNS
acetylcholinesterase inhibitors are used in treatment of urinary retention, not urinary frequency
http://medresearch.in/index.php/IJPR/article/view/782/1271 This explains a case in an infant. "Respiratory depression and coma after overdosage have been shown to be reversible by injection of naloxone . Owing to its structural similarity to opioid, loperamide toxicity can be reversed by using Nalaxone which is a specific opioid antagonist acts competitively at opioid receptors. Naloxone hydrochloride is usually given intravenously for a rapid onset of action which occurs within 2 minutes."
FA 2019: "Loperamide has poor CNS penetration" - so it still penetrates => can cause respiratory depression
Also maybe because the blood brain barrier in a baby is not developed as well as in an adult.
yeah, i’ve never heard of antiphospholipids increasing PT time ...
Not sure if that little detail was to throw us off. I think the point of the question was to ID antiphospholipid syndrome based on the clinical criteria (spontaneous abortion + thrombosis)
I actually went down a rabbit hole with this one recently - essentially in vitro findings =/= in vivo findings, clot-wise with anti-phospholipid antibodies.
No mention of lupus anticoagulant, anticardiolipin, or anti Beta 2 antibodies. FA mentios prolonged PTT but nothing on PT. What a piece of shit question. But thanks to the dudes above who explained it
UWorld mentioned "prolong aPTT (and sometimes PT)" in APS
@yb_26 Can u please tell the QID because the one I have seen it says, "Although patients often have prolonged ptt (because the antiphospholipid interferes with ptt test), pt is normal."
this one is the best, thank you!
you're definitely not alone lol
And its not in FA, so fuck it IMO
I guessed it because the names sounded similar :D
I also guessed because both words start with "glu")))
same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle.
Not a clue. This was so random.
this made me feel a lot better.
also, no fucking clue
My immediate thought after reading this was "why would i know this and how does this make me a better doctor?"
Generally speaking Glutamine is often used to aminate things. Think brain nitrogen metabolism. You know that F-6-P isn't an amine, and that Glucosamine is, so Glutamine isn't an unrealistic guess.
yea, I mature 30k anki cards to see this bs
I literally shouted wtf in quiet library at this question.
I stand corrected @yb_26. Brainfart moment 🙈
I chose atherosclerosis because they said “radial artery is non-pulsatile but remains palpable even as the cuff is inflated”--> my reasoning was that normally you can’t feel the artery anymore once you overflate the cuff bc this occludes blood flow and arteries are squishy (compliant); BUT if you had atherosclerosis, which is literally a hardening, you would not be able to compress the artery, and neither would you expect the normal radial (outward) expansion of an artery during systole. (that is, the pulses!)
I think athero is just a subtype of arteriosclerosis. Also my thought process was (like Lila) if something were to not be palpable then it would have to collapse and athero prevents this from happening.
FA 2019, page 299: types of Arteriosclerosis: arteriolosclerosis and Mockenberg sclerosis.
then on page 300: Atherosclerosis - form of arteriosclerosis caused by buildup of cholesterol plaques.
Gemfibrozil is a CYP450 inhibitor causing an increase drug concentration of statin which would lead to the adverse side effect of myopathy. Not sure about niacin in combination with statin but believe this would be more likely to occur. Hope this helps!
yes, it can be seen with niacin and esetemibe as well, according to UWorld. But first choice in such questions is always fibrates.
number one no-go combi is statin+fibrate here
tried to attach photo, sorry for that(
tried to attach photo, sorry for that(
narrowed down to MDD and restless leg then convinced myself that elderly are at higher risk for MDD than RLS. Is that valid reasoning?
Paroxysmal nocturnal dyspnea = breathless awakening from sleep, seen in left heart failure.
It is not a paroxysmal nocturnal hemoglobinuria.
no, decreased CO => peripheral vasoconstriction => SVR will be increased
No SVR will increase due to RAAS and SAN thats why we decrease afterload in HF treatment ( ACEI, ARBs )
Wouldn't pulmonary vascular resistance also be decreased here due to pulmonary vasodilation in the setting of an MI?
@snafull: my initial thought is that we would see pulmonary vasoconstriction because of the relatively low oxygen tension (that results from the low cardiac output).
Never had heard of that one. Just a good guess. Thanks!
IgE-independent mast cell degranulation can also be caused by radiocontrast agents, some antibiotics (vancomycin)
it was a u world question
thiazolidinediones (pioglitazone) increase insulin sensitivity (in muscles and liver) through activation of peroxisome proliferator-activated receptor-gamma (PPAR)
I think they are asking about primarily mechanism of action, that's why it is E
UW explanation regarding the genes upregulated
1. GLUT4: insulin responsive on adipocytes/skeletal
increases G uptake
2. adiponectin: cytokine
secreted by adipocytes
increases # of
adipocytes and stims
3. PPAR family also
plays significant role
in pathogenesis of
Also, I think the word uptake shouldn't be right when speaking about insulin, it does increase insulin sensitivity and therefore glucose uptake