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Comments ...

 +2  (nbme24#31)

My simple understanding is that pt's heart contractility is decreased due to MI => heart can't pump a lot of blood => increased backup flow into pulmonary vasculature => increased PCWP.

More blood in pulmonary vasculature => they will dilate in order to just keep all these blood => decreased pulmonary vascular resistance

Decreased cardiac output => peripheral vasoconstriction => increased systemic vascular resistance


 +0  (nbme24#8)

Albuterol - relaxes bronchial smooth muscle (short acting β2-agonist). For acute exacerbations. Can cause tremor, arrhythmia.


 +1  (nbme23#14)

More simple from FA 2019: Heparin-induced thrombocytopenia is due to development of IgG antibodies against heparin-bound platelet factor 4 (PF4) Antibody-heparin-PF4 complex activates platelets => thrombosis and thrombocytopenia

  • highest risk with unfractionated heparin

 +6  (nbme23#12)
  • binding to the MHC class II receptor and triggering the release of cytokines - superantigens

  • binding to the neuromuscular junction and prevention of ACh release - botulinum toxin

  • blockage of a GTP-binding protein resulting gin the accumulation of cAMP - pertussis toxin

  • blockage of presynaptic inhibition of spinal motor reflexes - tetanus toxin

  • prevention of protein synthesis by blocking elongation of the polypeptide chain - diphtheria toxin, Pseudomonas aeruginosa exotoxin A

thomasburton  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.
humble_station  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

 +0  (nbme23#7)

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


 +1  (nbme23#27)
  • children often exhibit sexual knowledge or behavior incongruent with their age.

  • abuser is known to victim, usually male

  • peak incidence 9-12 years


 +0  (nbme23#28)

Wilson disease => Fanconi syndrome => metabolic acidosis (type II (proximal) RTA)


 +1  (nbme23#16)

abnormal test result means that test detects cancer =>

  • 35 of 50 men with prostate cancer have abnormal test result => n of pts with cancer = 50. Test shows cancer in 35 men => TP=35 => we can calculate FN = 50-35 = 15

  • 20 of 100 men without prostate cancer have abnormal test results => FP =20 => we can calculate TN = 100-20=80

  • now we can calculate specificity = TN/(TN+FP) = 80/100 = 0.8 (in % will be 80%)

here is my 4/4 table: [https://www.reddit.com/r/usmlestep1/comments/ccul3w/biostat_question_from_nbme23/]

smc213  Exactly what I did!
smc213  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.

 +1  (nbme22#10)

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.



 +1  (nbme21#24)

FullSizeRender-04-07-19-11-28.jpg

sorry for the napkin, hope that will help someone

yb_26  tried to attach photo, sorry for that(




Subcomments ...

submitted by lsmarshall(191),

Urea Cycle Disorders > Isolated severe hyperammonemia (> 1000; i.e., no other severe metabolic disturbances

Ornithine transcarbamylase deficiency > (most common urea cycle dis.) orotic acidemia/aciduria, hyperammonemia

Organic Acidemias > Hyperammonemia, anion-gap acidosis, ketosis (from hypoglycemia)

Medium-chain acyl-CoA dehydrogenase deficiency > Hyperammonemia, hypoketotic hypoglycemia (seen in β-oxidation disorders, EXCEPT adrenoleukodystrophy)

Liver dysfunction > Hyperammonemia, LFTs messed up, older pt.

lsmarshall  Summary of metabolic issues relating to hyperammonemia +3  
seagull  i'm leaning towards Ornithine transcarbamylase deficiency. +2  
notadoctor  Not sure why this isn't considered a mitochondrial disorder since the issue is Ornithine transcarbamylase deficiency in the mitochondria? +1  
charcot_bouchard  if it was mitochondrial disorder no one would escape +  
wowo  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 +1  
artist90  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 +  
artist90  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? +  
yb_26  1) hyperammonemia is seen in all urea cycle disorders except arginase deficiency 2) organic acids directly inhibit urea cycle => hyperammonemia (from UWorld) +  
yex  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. +3  


submitted by snafull(1),

Can somebody explain why this is not a foreign body granuloma?

yb_26  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) +  


You know it’s an enveloped virus since it doesn’t hold up to acid or being dried. You know it causes a fever and a cough, while affecting the larynx. Only virus category that fits all that info is the coronavirus (causes SARS) from that list.

zelderonmorningstar  EBV doesn’t cause fever and cough? +  
zelderonmorningstar  Wow, just checked First Aid and it doesn’t list “cough” as a symptom of EBV. +  
drdoom  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. +7  
fulminant_life  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. +1  
nbmehelp  Can someone explain what not holding up to acid or being dried has to do with being enveloped? +  
yb_26  @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) +1  


yb_26  @at0xibolic, I think you won this competition on finding better picture lol thanks +2  


submitted by m-ice(122),

This woman has a lot of signs that point toward an intestinal parasitic infection: recent travel to Papua New Guinea, cough and alveolar infiltrates, high eosinophil count, and a stool sample that has a worm in it. Most likely the patient has a Strongyloides infection, as this is the intestinal parasite that shows larva on stool sample. Basically all intestinal parasites can be treated with Bendazole drugs, such as Thiabendazole. Praziquantel would be more appropriate for a worm or liver fluke infection.

fulminant_life  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 +3  
yb_26  they really should add Wikipedia in the list of top-rated review resources with A+ level of recommendation in FA2020))) +2  
usmile1  also a side note: cutaneous larva CURRENS is pathognomonic for strongyloides whereas Cutaneous larva MIGRANS is for ancylostoma braziliense or nectar Americanus +  


submitted by neonem(251),

This patient case sounds like he has iron deficiency anemia (anemia, low hematocrit, microcytic) from a GI bleed. To get this question right, you had to remember that the two major inherited GI cancer syndromes are FAP (due to mutation in APC gene, which is a tumor suppressor gene) and Lynch syndrome AKA hereditary non-polyposis colorectal carcinoma (HNPCC), caused by a mutation in a number DNA mismatch repair genes, of with MHS2 is a more common one.

The mechanisms of their carcinoma development are different; in FAP, tumors arise from a normal --> adenoma --> carcinoma sequence while in HNPCC, tumors arise from what's known as a microsatellite instability pathway, leading to spontaneous formation of a carcinoma (not preceded by a benign lesion like an adenoma)... You didn't need to know this to get this question right, but definitely good to know.

medpsychosis  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! +  
yb_26  I always get Li-Fraumeni and Lynch syndromes confused :/ +  


submitted by nwinkelmann(88),

Does anyone have a good explanation for why decreased levels of inhibin is wrong? From my understanding, inhibin and activin work together, in that inhibin binds and blocks activin leading to decreased feedback on hypothalamus and activin increases FSH and GnRH production.. thus, if you decrease inhibin then you would have increased activin which would lead to increased GnRH and FSH, right? I found one article talking about it in regards to puberty, but it seems to be a hypothesis/not confirmed at this point... is that why? But still... how do I rule it out on a test?

yb_26  I also picked decreased inhibin. may be it was one of the "experimental questions", which are not even counted on the real exam +  
artist90  Inceased FSH will lead to spermatogenesis and spermiogenesis NOT Increase in Testosterone which is causing increased Height of this pt +1  
artist90  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 +  
usmile1  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! +  


submitted by wonderboyg(5),

this patient's uterus was increased in size compared to a 12 week uterus. she had grape like structures and no fetus. this would indicate a hydatidiform mole. this patient also had no fetal parts so it would be a complete mole.

according to pathoma, a hydatidiform mole is an "abnormal conception characterized by swollen and edematous villi with proliferation of trophoblasts"

also in a complete mole, most villi are hydropic and trophoblasts will proliferate diffusely around these hydronic villi.

the sheetlike masses of syncytiotrophoblasts would indicate a choriocarcinoma.

nwinkelmann  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. +1  
yb_26  @nwinkelmann no, ball-like masses of proliferating decidua are seen in endometrial papillary syncytial change +  


submitted by step420(18),

Integral membrane proteins are found within the plasma membrane and span the whole length across. The inside of the membrane is very hydrophobic due to the long carbon chains. Extensive hydrophobic interactions between the protein side chain and the lipid tails will help anchor the protein in the membrane.

yb_26  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 +  


submitted by sajaqua1(198),

Posterior cord syndrome occurs due to infarction of the posterior half of the spinal cord, from occlusion of the posterior spinal artery. Our patient presents with decreased sensation to pinprick below the level of the knees as well as walking with a wide-based gait, likely indicating loss of proprioception. The patient is also anemic with hyper-segmented neutrophils.

Hypersegmented neutrophils are typically caused by an inability to make enough DNA, caused by a lack of necessary precursors and vitamins including B9 (folate) and B12 (cobalamin). If the patient is folate deficient, we see elevated homocysteine deficiency. If the patient is B12 deficient, we see elevated methylmalonic acid and homocysteine levels. Hyperhomocysteinemia can increase thrombosis. Thrombosis in the posterior spinal artery can cause posterior cord syndrome. In addition, lack of vitamin B12 impairs myelin formation and leads to Subacute Combined Degeneration, which affects the Spinothalamic tract (accounting for decreased pinprick sensation), Corticospinal Tract, and Dorsal Column-Medial Lemniscus Tract (accounting for the reduced proprioception.

A) Anterior cord syndrome- loss of motor command, as well as bilateral loss of heat and pain, the patient has not lost motor function, so it cannot be this. B) Central cord syndrome- presents as a combination of motor and sensory loss, usually with bladder dysfunction. This patient does not display motor loss or bladder dysfunction. C) Hemicord syndrome- Also called Brown-Sequard, this is complete injury to either the left or right side of the spinal cord. It presents with motor dysfunction and reflex dysfunction ipsilaterally at the level of the lesion; loss of upper motor command below the lesion ipsilaterally (spastic paresis); loss of dorsal column-carried sensation ipsilaterally at and below the lesion; and loss of pain and temperature sensation contralaterally 2 to 3 vertebra below the lesion. E) Segmentary syndrome- a congenital failure to develop part of the spinal cord. The new onset of symptoms at 82 years old makes this an unlikely diagnosis,.

yb_26  amazing, thank you! +  


submitted by sympathetikey(301),

Acute gout treatment:

  1. NSAIDs
  2. Steroids
  3. Colchicine

I, like a dumby, misread -zone for -sone, thinking it was steroid picked that. For anyone who cares, Sulfinpyrazone competitively inhibiting uric acid reabsorption in the proximal tubule of the kidney.

Source: https://en.wikipedia.org/wiki/Sulfinpyrazone

yb_26  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 +  


submitted by joonam(7),

Acute or chronic inflammation of gallbladder. Murphy sign: inspiratory arrest on RUQ palpation due to pain. Pain may radiate to right shoulder (due to irritation of phrenic nerve).􏰁ALP if bile duct becomes involved (eg, ascending cholangitis).

meningitis  To make sure, palpable Gallbladder is more in cholangiocarcinoma and Pancreatic Cancer? And if it were non-tender, could palpable gallbladder mean gallstones? +2  
yb_26  @meningitis, it is a Courvoisier sign of pancreatic adenocarcinoma: jaundice + palpable, nontender gallbladder +1  


submitted by mguan1993(2),

For completeness sake, could someone explain the other wrong answer choices in graph form? I can easily visualize the right answer but for some reason can't picture the other choices

yb_26  check UWorld #12299 +  


submitted by nwinkelmann(88),

Per pathologyonlines.com

Leukoplakia = risk factors include male gender, 40-70 years old, smoking, White patch or plaque, 5 mm or more, on oral mucous membranes that cannot be removed by scraping, not due to another disease entity such as lichen planus or candidiasis and not reversed by removal of irritants and lesion must be considered precancerous until proven otherwise. Premalignant lesion transformation would lead to invasion of the submucosa.

Micro = Varies histologically from acanthosis, hyperkeratosis, dysplasia or carcinoma in situ (associated with lymphocytes and macrophages). This article explains it much better and has pictures: https://emedicine.medscape.com/article/1840467-overview#a6. Based on this article and the pictures, I'd say the histo slide in the question is at least moderate squamous dysplasia.

Hairy Leukoplakia = White, confluent patches of fluffy (hairy) mucosa, bilateral, along lateral tongue, and associated with HIV+ patients (AIDS may appear within 2 - 3 years) but actually due to EBV infection

Histo = Hyperkeratotic oral mucosa due to piling of keratotic squamous epithelium, Cowdry type A intranuclear inclusions, Balloon cells with margination of chromatin (nuclear beading); EBV present in clear cells of spinous layer, variable koilocytosis, superimposed Candida infection, without inflammatory response.

From pictures (and this video: https://youtu.be/Shx61qKuIv8 timestamp 1:22), hairy leukoplakia has a lightly stained band of cells "ballon cells" in the stratum spinosum which is where the EBV lives. It looks much different than the histo slide shown in the question.

yb_26  great explanation, thanks for sharing! +  
shriya goyal  great explanation thanks +  
cathartic_medstu  on point +  


submitted by sympathetikey(301),

Keys were the:

-Glucosuria

-Phosphaturia

-Amino aciduria

Those should be re-absorbed by the PCT, so if they're not, Type 2 RTA.

lamhtu  To be even clearer, this sounds like **Fanconi syndrome, which has lead to Type II RTA** +3  
yb_26  To be even clearer: Wilson disease => Fanconi syndrome => type II (proximal) RTA +  
charcot_bouchard  To be even clearer, you all have been pretty clear +  
charcot_bouchard  To be even clearer, you all have been pretty clear +  


submitted by notadoctor(56),

Celiac sprue is a malabsorption syndrome that results in steatorrhea and results in iron deficiency anemia. As far as I'm aware, none of the others result in iron deficiency anemia. (I had Bacterial overgrowth as a close second but I don't believe that's associated with iron deficiency).

yb_26  bacterial overgrowth is associated with iron deficiency, but also with Vit B12-deficiency, so I guess pts will have macrocytic anemia +  
nor16  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3099351/. Vit B12 is key here, moreover, no bloating (IBS and bacterial overgrowth with bloating). bacterial overgrowth is a close one! +  


submitted by lfsuarez(65),

20 of the 100 men without prostate cancer have abnormal test results.

Specificity = FP/FP+TN = 20/100 = 0.8 = 80%

seagull  almost. 100/120 = 83% roughly 80% +  
amirmullick3  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%. +3  
yb_26  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 +2  
bulgaine  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 -) +  


submitted by jrod77(12),

I think they might be describing angina...not sure. TXA2 is responsible for platelet aggregation,so it may be contributing to thrombosis, thus ischemia to the cardiac tissue.

sympathetikey  Agreed. I'm pissed though because PGE2 mediates pain, which is why I picked it. +8  
he.sanchez14  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 +  
vik  hahah, seems like all in same boat like me +  
yb_26  thromboxane A2 is also vasoconstrictor, so my thoughts were about vasospastic angina +  
shriya goyal  same I went for pgE2 ... I M PISSED +  
shriya goyal  same I went for pgE2 ... I M PISSED +  
youssefa  Went for PGE2 ... shit +  
need_answers  I went for leukotriene B4, what the hell was I doing....SHIT +1  
hopsalong  I picked Leukotrine B4 thinking that the neutrophil infiltration was the source of the pain, seems wrong lol. +  
bballhandler11  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. +1  
ususmle  same here I M PISSED PGE2 +  


submitted by yotsubato(255),

This patient is unresponsive to many antiacids. They dont specify which ones, but the question is basically asking which antiacid is the strongest. That would be PPIs, which inhibit gastric H K ATPase

yb_26  PPIs are not antacids! +1  


submitted by mousie(82),

why does treatment of hypothyroid (with levothyroxine I'm assuming) increase risk for myopathy? I chose it simply bc its a common adverse effect of statins but I don't really understand how treating hypothyroidism at the same time would have anything to do with it ??? help please!

yb_26  They are just asking about side effect of statins, not about treatment of hypothyroidism +3  
mjmejora  Hypothyroidism is just a red herring. +  
ususmle  statins cause both hepatotoxic and mypopathy so I want for hepatotoxic:( I thought usmle expects different stuff +  


submitted by armymed88(15),

A little math here.. pH is low --> acidosis pCO2 is high --> respiratory Normal compensation should be roughly a 1 (acute) to 4(chronic) increase in bicarb per every 10 increase in pCO2.. Its lower here, so clearly not compensated and indicated additional drop in bicard --> add on metab acidosis

hello  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? +1  
kateinwonderland  How do you know which one has bigger contribution in this situation where there's increased CO2 and decreased HCO-, both indicating acidosis?? +  
yb_26  normal kidney compensation would be an increase in bicarb reabsorption => increased serum bicarb. This pt has low serum bicarb => concurrent metabolic acidosis +  


submitted by armymed88(15),

Of these options available, Schwann cells would be the only cells present in the PNS. Astrocytes, microglia and oligos are all CNS cells Satellite cells are in the muscle and serve to aid in muscle repair and regeneration

yb_26  Thats myosatellite cells. Satellite cells are also glial cells that form around damaged nerve cells and lie close to neuron bodies in the CNS +2  


submitted by enbeemee(4),

would an acetylcholinesterase inhibitor work as well to relieve the symptoms? but just because he's 73yo, we're supposed to assume it's due to BPH and give an a1 inhibitor?

yb_26  acetylcholinesterase inhibitors are used in treatment of urinary retention, not urinary frequency +1  


submitted by d_holles(34),

This question confused me bc I thought loperamide could not cross the BBB and therefore could not cause respiratory depression (mu-opioid agonism at the brainstem results in CNS/respiratory depression, 1). But @dr.xx is correct in noting that ↓ RR and CNS depression in the Pt should call for an mu-opioid antagonist rather than bethanchol (cholinomimetic) to treat constipation.

  1. https://anesthesiology.pubs.asahq.org/article.aspx?articleid=2675905
nwinkelmann  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 [6]. 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." +  
yb_26  FA 2019: "Loperamide has poor CNS penetration" - so it still penetrates => can cause respiratory depression +1  
whoissaad  Also maybe because the blood brain barrier in a baby is not developed as well as in an adult. +  


submitted by hayayah(394),

Pregnancy + Hx of thrombosis --> think antiphospholipid syndrome

The PT and PTT are prolonged d/t interference from the antibodies to phospholipids. Thrombin time normal.

Had to find research articles about it so take it from here and don't waste your time...

monoloco  yeah, i’ve never heard of antiphospholipids increasing PT time ... +3  
goldenwakosu  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) +1  
johnthurtjr  I actually went down a rabbit hole with this one recently - essentially in vitro findings =/= in vivo findings, clot-wise with anti-phospholipid antibodies. +1  
link981  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 +3  
yb_26  UWorld mentioned "prolong aPTT (and sometimes PT)" in APS +1  


submitted by monoclonal(6),

http://i.imgur.com/3fZ2AaE.png

This image shows the multiple veins which drain breast tissue. easy visual. (to easy to miss it, but i did)

yb_26  this one is the best, thank you! +1  
canyon_run  very nice! +  


submitted by seagull(413),

out of curiosity, how may people knew this? (dont be shy to say you did or didnt?)

My poverty education didn't ingrain this in me.

johnthurtjr  I did not +  
nlkrueger  i did not lol +  
ht3  you're definitely not alone lol +  
yotsubato  no idea +  
yotsubato  And its not in FA, so fuck it IMO +  
niboonsh  i didnt +  
imnotarobotbut  Nope +  
epr94  did not +  
link981  I guessed it because the names sounded similar :D +4  
d_holles  i did not +  
yb_26  I also guessed because both words start with "glu"))) +2  
impostersyndromel1000  same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle. +  
jaxx  Not a clue. This was so random. +  
wolvarien  I did not +  
ls3076  no way +  
hyperfukus  no clue +  
mkreamy  this made me feel a lot better. also, no fucking clue +  


submitted by link981(32),

Histamine causes arteriole vasodilation, causing a buildup of blood in the capillaries. The increased blood in the capillaries will cause the pressure there to rise. Filtration is dependent on pressure, the higher the pressure, the more the filtration.

Remember blood flow: veins to venules to capillaries to arterioles to arteries

yb_26  agree in all, except the blood flow - it is right the opposite [https://teachmeanatomy.info/the-basics/ultrastructure/blood-vessels/] +1  
link981  I stand corrected @yb_26. Brainfart moment 🙈 +  


what is happening in this stem? unable to occlude the radial artery ? Can someone please explain?

lilamk  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!) +4  
mnemonia  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. +3  
yb_26  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. +  


submitted by luckeroo(2),

why was this gemfibrozil and not niacin? I was lucky and guessed, but I thought niacin combined could also trigger myopathy?

.ooo.   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! +  
yb_26  yes, it can be seen with niacin and esetemibe as well, according to UWorld. But first choice in such questions is always fibrates. +  
nor16  number one no-go combi is statin+fibrate here +  


submitted by yb_26(42),

FullSizeRender-04-07-19-11-28.jpg

sorry for the napkin, hope that will help someone

yb_26  tried to attach photo, sorry for that( +  


submitted by yb_26(42),

FullSizeRender-04-07-19-11-28.jpg

sorry for the napkin, hope that will help someone

yb_26  tried to attach photo, sorry for that( +  


submitted by hungrybox(216),

other answers:

  • narcolepsy: Associated with hypnogogic or hypnopompic hallucinations.
  • hypnoGO to sleep = night time hallucinations

  • paroxysmal nocturnal dyspnea: PNH is a hemolytic anemia. No signs of hemolytic anemia (hematuria, jaundice, dec. haptoglobin).

  • sleep apnea: Associated with obesity, loud snoring.

doingit21  narrowed down to MDD and restless leg then convinced myself that elderly are at higher risk for MDD than RLS. Is that valid reasoning? +  
yb_26  Paroxysmal nocturnal dyspnea = breathless awakening from sleep, seen in left heart failure. It is not a paroxysmal nocturnal hemoglobinuria. +1  


submitted by kentuckyfan(17),

I get why the mixed venous oxygen tension decreased. However,, isn't the systemic vascular resistance also decreased?

yb_26  no, decreased CO => peripheral vasoconstriction => SVR will be increased +2  
yssya1992  No SVR will increase due to RAAS and SAN thats why we decrease afterload in HF treatment ( ACEI, ARBs ) +2  
snafull  Wouldn't pulmonary vascular resistance also be decreased here due to pulmonary vasodilation in the setting of an MI? +  
cienfuegos  @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). +1  


submitted by neonem(251),

Morphine is a mu opioid agonist - one adverse effect of opioids is mast cell degranulation that is IgE-independent. Release of histamine is akin to an anaphylactic reaction --> pruritis, etc.

sympathetikey  Never had heard of that one. Just a good guess. Thanks! +  
yb_26  IgE-independent mast cell degranulation can also be caused by radiocontrast agents, some antibiotics (vancomycin) +  
temmy  it was a u world question +  


submitted by cr(1),

why not C?. It´s not supose that it improve the efectivity of insulin?

yb_26  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 +  
cienfuegos  UW explanation regarding the genes upregulated 1. GLUT4: insulin responsive on adipocytes/skeletal increases G uptake 2. adiponectin: cytokine secreted by adipocytes increases # of insulin responsive adipocytes and stims FA oxidation 3. PPAR family also plays significant role in pathogenesis of metabolic syndrome +