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 +3  (nbme24#4)

Cryptococcal meningitis that is transferred through respiratory droplets

https://www.cdc.gov/fungal/global/cryptococcal-meningitis.html


mousie  http://www.sparknotes.com/biology/cellreproduction/cellcycle/section3/page/2/
fahmed14  Cyclins help regulate cell cycle phases. They help with checkpoints before progression to the next phase of a cell cycle. Therefore the checkpoint before mitosis would be in G2 and probably where mitotic specific cyclins are synthesized
artist90  https://en.wikipedia.org/wiki/Cyclin . 4 types of Cyclins and when they rise and fall.

 -2  (nbme24#18)

This was lateral medullar syndrome aka dorsolateral infarct of the PICA.



 +2  (nbme24#44)

I thought this was just referencing zollinger ellison, which would have elevated gastrin


 +6  (nbme23#20)

It was a type IV HSN reaction, which deals with T cells and that was the only answer that had t cells involved.

yogi  Poison Ivy/ oak /Sumak

 +3  (nbme23#15)

The pt had asthma (SOB, wakes up at night out of breath, has allergies). It asked for the precursor of leukotrienes, which is arachidonic acid. The prob gave him Montelukast or inhaled glucocorticoids.

ls3076  wtf is up with the phrasing of this question

 +3  (nbme23#24)

Hemochromatosis, aka "bronze diabetes". Cannot be Addison due to the hyperglycemia and normal BP

alexb  I missed this bc didn't notice it was a middle-aged guy w/ just 3 year hx of Type 1 DM.
tinydoc  I got it mixed up with primary adrenal insufficiency and the acth ⇒ hyperpigmentation.
maddy1994  testicular atrophy &hepatomegaly helped me out to eliminate the options..when i was left with ferritin and saw pigmentation it clicked that it is hemochromatosis
krewfoo99  Symptoms of Darkening of skin, liver dysfunction, diabetes, with testicular atrophy will always be hemochromatosis

 +2  (nbme23#10)

I chose this b/c its the most common pathogen for skin infections

seagull  same here
sympathetikey  Some bowlsheet

 +5  (nbme23#26)

2/3 1/25 1/4

He has a 2/3 chance of being heterozygous (not 2/4 b/c we know he for sure doesn't have CF)

1/25 chance in the population

1/4 chance of a heterozygous couple having a child with CF

welpdedelp  ok, so it messed up the formatting 0.66667 x 1/25 x 0.25
nwinkelmann  ugh... I ALWAYS forget about changing the carrier status to 2/3. Chance of affected individual = chance of father passing allele * chance of mother passing allele = 2/31/21/25*1/2 = 2/300 = 1/150.
zpatel  2/3(chance of heterozygous) * 1/25(meet carrier) * 1/2(chance of male to transfer affected gen) * 1/2(female to transfer affected gen) = 1/150

 +4  (nbme23#50)

30* 0.15. Think about it, there is x flow with an oxygen concentration of y--so to find out the delivery you just multiply them together.

yotsubato  One of those questions too simple to believe its actually the right answer
mimi21  Right, I was like this is too simple lol ! im not sure if this is also a good tip but I tend to look at the units they are asking for and double check my math to make sure I end up with them.
osgood-schlatter  what equation is it exactly?

 +7  (nbme23#1)

when a follicle doesn't rupture (aka anovulation) then it will form a cyst.

uslme123  n premenopausal women, simple adnexal cysts (image 1) that are <3 cm in diameter typically represent normal follicles or may be a corpus luteal cyst (these may appear simple or complex) and may be considered a normal finding. Even when up to 5 cm in diameter, these simple cysts are so commonly due to normal menstrual physiology that the Society of Radiologists in Ultrasound (SRU) does not recommend follow-up when asymptomatic

 +7  (nbme23#43)

It was the only peripheral lung cancer, its also more common in women. Metastasis would have shown multiple lesions

sympathetikey  Also, lung adenocarcinoma is the most common lung cancer overall, most common in women, and most common in non-smokers. I know she smoked in the past, but that's what tipped me off to it.
alexb  Yeah I literally picked SCC bc I knew she'd smoked in the past smh
maddy1994  20 years of non smoking history ,she wouldnt be at elevated risk for smoking related carcinoma.

 +8  (nbme23#44)

No diet deficiency, the patient had excess carotene due to his diet

sympathetikey  Would never have thought of that. Thanks
medschul  that's messed up dog
hpkrazydesi  Excess carotene in what way? sorry if thats a stupid question
davidw  this is directly from Goljan "Dietary β-carotenes and retinol esters are sources of retinol. β-carotenes are converted into retinol. (a) Increased β-carotenes in the diet cause the skin to turn yellow (hypercarotenemia). Sclera remains white, whereas in jaundice the sclera is yellow, which can be used to distinguish the two conditions. (c) Vitamin toxicity does not occur with an increase in serum carotene"
davidw  β-Carotenes are present in dark-green and yellow vegetables.
hyperfukus  ohhhh hellllll no
dashou19  When I was a little kid, I like to eat oranges, like I could eat 10 oranges at once, and after a few days, I could tell that I turned yellow...

 +1  (nbme22#1)

So I think that issue of wrist extension and/or finger drop would be more radial nerve. However, there was more proximal weakness, so it would be C7.

"7-8 lay them straight", the pt couldn't "lay them straight" so it would be C7 root

welpdedelp  *As an addition, median nerve involvement would have leaned more toward C8 than C7.
meningitis  Do you have anymore useful mnemonics for brachial plexus?
henoch280  FA pg 494 for mnemonics
winelover777  Doesn't look like there are many in FA 2019. S1/S2 - Buckle my shoe. L3/L4 - Shut the door. C5/C6 - Pick up sticks.

 +0  (nbme22#4)

This was SLE. https://step1.medbullets.com/msk/112039/systemic-lupus-erythematosus

Think: 1,2,3= S-L-E

Using ACID: Type III is for Immune Complexes


 -4  (nbme22#38)

Increased intracranial pressure that results in Cushing's triad of increased blood pressure, irregular breathing, and bradycardia. Thus, high CO2 induces cushing triad and if you give PP then it will reduced CO2, and then down regulate the sympathetic vasoconstriction. Originally the brain had so much CO2 that it spazzed out and tried to increase the BP in order to push more oxygenated blood to the brain.

https://pbs.twimg.com/media/CK3J5kZUsAAqSf-.jpg:large

lispectedwumbologist  "Bradycardia" 84 bpm lol
lispectedwumbologist  The hypertension in obstructive sleep apnea is due to increased sympathetic tone not increased intracranial pressure lmao
meningitis  @lispectedwumbologist : Be mature enough to correct him/her and move on, not laugh at him/her.


 +5  (nbme22#6)

It was just asking the lifespan of RBCs (120 days)

haliburton  If I'm reading this right, this is just a tricky dicky question. I think CO binds 200x stronger than O2. But if an O2 cycles through binding / unbinding 200 times before a CO gets kicked off, this should still clear the CO from that cell sooner or later. strange to think it is 1. essentially permanently trapped in a cell, and 2. doesn't kill you and can be treated with O2 to resolution within a few hours or a day. They must just be thinking, until that last RBC dies, you've got original CO in a circulating cell. but just a fraction (because you didn't die). not sure how that CO isn't just passed on during recycling, based on this line of thinking.
link981  The question while stupidly written, asks how long the RBC's that carry the CO take to be removed from the circulation, not how long the CO takes to be removed from the RBC. Just asking the lifespan of RBCs in an stupidly complicated way. As we know, RBC's life span is about 120 days and then they are removed from our circulation. 120 days is about 4 months. Next time they will probably ask weeks or in hours, who knows? smh

 +0  (nbme22#5)

Ok, so RNA dependent DNA polymerase is for reverse transcriptase... single stranded + use RNA dependent RNA polymerase. Can someone explain?

hyoid  The only thing I can think of is that HIV is a (+)-sense single-stranded RNA virus that relies on an RNA dependent DNA polymerase (reverse transcriptase) to synthesize DNA.
haliburton  according to [medbullets link](https://step1.medbullets.com/step1-microbiology/104196/rna-viruses_) ns ss RNA must carry RNA dependent RNA polymerase (so that is out). also, according to medbullets there are very few ds RNA viruses, so "most likely" will be ss. Also, RNA-dependent DNA polymerase = Reverse Transcriptase. Since HIV is a ss ps RNA virus with RT, they've described an HIV cousin. not sure beyond this.
some0217710  Can’t think of any retroviruses outside of HIV and HTLV and they’re both +ssRNA

 +3  (nbme22#3)

It was a Ferruginous bodies--> asbestosis. Ferruginous bodies are believed to be formed by macrophages that have phagocytosed and attempted to digest the fibers.


 +1  (nbme22#23)

This is Lambert-Eaton, which improves with movement as compared to Myesthenia gracias whichh worsens with movement

sbryant6  Lambert-Eaton is typically associated with Small Cell Lung Cancer. Since there was no mentino of that, I was thrown off. Such is the difference between UWorld and NBME I guess.

 +4  (nbme22#22)

It was scabies, which is transmitted person-operon.

welpdedelp  **person-person lol




Subcomments ...

Why do you give IV leucovorin with intrathecal methotrexate? Wouldn’t MTX lose its efficacy since leucovorin reverses the effects of MTX?

colonelred_  MTX will still work but yes some purine/pyrimidine synthesis can still occur. You often give leucovorin to decrease adverse effects of MTX. +  
welpdedelp  ok I have a question, leucovorin is the same as folic acid...so why give one over the other? +  
lsmarshall  Leucovorin, folinic acid, is a modified version of THF and enter folate metabolism where THF is, after the point where methotrexate takes its effect. I have a pharm. card that says "toxic effects on normal cells may be reduced by administration of folinic acid (a.k.a. leucovorin or citrovorum factor), which is **preferentially taken up by normal cells versus tumor cells**." +2  


Can someone please explain this? What is the diagnosis here?

welpdedelp  I thought it just as it was, polyneuropathy is supposed to be a burning pain affecting the extremities, he might have acute intermittent porphyria. He was too young and didn't fit ALS due to the rapid onset. No loss of pain in the arms so it couldn't be syringomelia. Wasn't asymmetric so couldn't be polio. Didn't have anything resembling Parkinson. +4  


Whats the difference between “heterozygous null mutation in B globin gene” and “heterozygous mutation known to cause 50% decrease in B globin gene function of one allele”?

welpdedelp  I interpreted "null" as meaning full deletion while the other heterozygous mutations was only a 50% decrease in the function. One child would inherit 1 null mutation and 1 50% mutation, which would leave them with a 25% functional gene. +2  


Why is duodenal lumen incorrect? I thought pancreatic enzymes (chymotrypsin, carboxypeptidase) would be located here.

colonelred_  Enterokinase actives trypsinogen and is located closer to the intestinal mucosal (“brush border”). +  
drdoom  Yeah, @colonelred is right. @medstruggle: the duodenal lumen (and the pancreatic /proteases/ you mention) is the site where pancreatic enzymes (“endopeptidases”) cleave large polypeptides into smaller bits. It is at the BRUSH BORDER where the smallest kinds of peptides (dipeptides, tripeptides) are broken down into their amino acids, which finally can be co-transported with Na+ into the intestinal cell. I think about it this way: stomach acid denatures and “opens up” proteins (without any specific cleavage); pancreatic enzymes then cleave denatured polypeptides into smaller bits; brush border enzymes finally break down tiny peptides into absorbable amino acids. +  
welpdedelp  http://1.bp.blogspot.com/-UDdBiBiEgec/UzM61mV4pTI/AAAAAAAABRA/_qCG05fliGk/s1600/VBN.PNG +6  
drdoom  Nice schematic, @welpdedelp +  


submitted by colonelred_(48),

Looked it up and found that because you’re in a supine position for a long time you’re going to have increased venous return which leads to increased CO. This negatively feedsback on RAAS, leading to decreased aldosterone. As a result, you’re going to have increased diuresis which leads to decreased blood and plasma volume.

medstruggle  Doesn’t supine position compress IVC leading to decreased venous return? (This is the pathophys of supine hypotension syndrome.) There was a UWorld questions about this ... +2  
tea-cats-biscuits  @medstruggle *Supine position* decreases blood pooling in the legs and decreases the effect of gravity. *Supine hypotension syndrome*, on the other hand, seems specific to a pregnant female, since the gravid uterus will compress the IVC; in an average pt, there wouldn’t be the same postural compression. +1  
welpdedelp  this was the exact same reasoning I used, but I thought the RAAS would inactivate which would lead to less aldosterone and less sodium retention +1  
yotsubato  You gotta be preggers to compress your IVC +1  
nwinkelmann  Could you also think of it in a purely "rest/digest" vs "fight/fright/flight" response, i.e. you're PNS is active, so your HR and subsequently your CO is less? But the explanation given above does make sense. Also because I think just saying someone is one bed rest leaves a lot up for interpretation, maybe not with this patient because his pelvis is broken, but lots of people on bed rest aren't lying flat.... ? +1  
urachus  wouldnt low aldosterone cause low plasma sodium? choice B +  


submitted by welpdedelp(75),

2/3 1/25 1/4

He has a 2/3 chance of being heterozygous (not 2/4 b/c we know he for sure doesn't have CF)

1/25 chance in the population

1/4 chance of a heterozygous couple having a child with CF

welpdedelp  ok, so it messed up the formatting 0.66667 x 1/25 x 0.25 +  
nwinkelmann  ugh... I ALWAYS forget about changing the carrier status to 2/3. Chance of affected individual = chance of father passing allele * chance of mother passing allele = 2/31/21/25*1/2 = 2/300 = 1/150. +  
zpatel  2/3(chance of heterozygous) * 1/25(meet carrier) * 1/2(chance of male to transfer affected gen) * 1/2(female to transfer affected gen) = 1/150 +  


submitted by welpdedelp(75),

So I think that issue of wrist extension and/or finger drop would be more radial nerve. However, there was more proximal weakness, so it would be C7.

"7-8 lay them straight", the pt couldn't "lay them straight" so it would be C7 root

welpdedelp  *As an addition, median nerve involvement would have leaned more toward C8 than C7. +1  
meningitis  Do you have anymore useful mnemonics for brachial plexus? +  
henoch280  FA pg 494 for mnemonics +  
winelover777  Doesn't look like there are many in FA 2019. S1/S2 - Buckle my shoe. L3/L4 - Shut the door. C5/C6 - Pick up sticks. +  


submitted by bobson150(3),

The wording of this question confused me. This is asking "which of these vessels is the high pressure system" right? So the high pressure superior rectal is causing increased pressure into the inferior rectal?

welpdedelp  Superior rectal comes from the inferior mesenteric vein which comes from the splenic vein --> portal veins Thus, this dude had cirrhosis so it would "back-up" into the superior rectal vein. FA 2018: p360 +5  
nc1992  Superior rectal not superior mesenteric. Took me a minute +  
hyperfukus  ugh am i ever gonna get these right EVER +2  
titanesxvi  why not the inferior mesenteric, since the superior rectal drains there +  
thomasburton  @titanesxvi think it is because question says direct which is why superior rectal +1  
lilyo  thomasburton, so are they asking what vessels do internal hemorrhoids directly drain into? The order is Superior rectal vein--> Inferior mesenteric vein--> portal vein. +  
thomasburton  Yes exactly, so they do eventually reach IMV but not 'directly' +  


submitted by welpdedelp(75),

It was scabies, which is transmitted person-operon.

welpdedelp  **person-person lol +