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Comments ...

 +0  (nbme23#24)

Chronic Myelogenous Leukemia vs Leukemoid Reaction has a few differentiating features:

  • Basophilia can be seen in Myeloproliferative diseases such as CML. However, they are not seen in Leukemoid Reactions.

  • Leukocyte Alkaline Phosphatase (LAP) is often elevated in Leukemoid Reactions. But it will be decreased in CML because Abnormal cells don't make the normal enzyme.

  • Dohle Bodies are characteristic of Leukemoid Reactions. Not seen in CML.

As vshummy pointed out FA-2019 pg 424 has all this information as well as UWorld problem...I just can't seem to find the Q.ID. Maybe someone else can tag-team in.

 +0  (nbme23#37)

I had a pretty straight forward line of thinking for this. Cool discolored leg automatically rules out problems elsewhere (all the brain related choices). We know blood has been cut off to the left foot. Specifically, there is an embolus in the arterial blood supply. (Venous would lead to a warm foot)

If you take into account the acute episodes of palpitations, it is plausible to think that she had some sort of A-Fib triggering a blood clot to break off and be sent through the systemic circulation. It then got lodged in the femoral artery cutting off poor g-ma's blood.

 +1  (nbme23#22)

Visceral Leishmaniasis aka. "Kala-Azar"

Caused by Leishmania Donovani. (an intracellular protozoan)

Transmitted via the Phlebotomine Sand Fly.

Treated with Amphoterrible B. Can also use Sodium Stibogluconate, miltefosine, or paromomycin.

Will commonly be seen with pancytopenia, fever, and splenomegaly are the three big clues. Other symptoms you can see are night sweats, blackening of the skin, scaly skin, weakness, and substantial weight loss. This will kill ya if you don't get treatment.

usmlecharserssss  i got 2 leishmania questions 38 and 39 in 3rd block , both got incorrect because i thought no way they can do that (((((((

Subcomments ...

So a simpler way than all the math being done is understanding what CI means.

CI - range of values w/in which the true mean of the population is expected fall

So a CI of 95% will be more precise and have a narrow range compared to a CI of 99% will be less precise because its including more values in and result in a wider range.

So if CI of 95% is 110 to 116 then a CI of 99% has to be a range that is wider... 108 to 118

paulkarr  Glad I wasn't the only one to solve it this way...didn't even think to bother with the calculation. +  

submitted by sajaqua1(278),

Gynecomastia, spider angiomata, and hypogonadism (as well as palmar erythema) are all signs of excess estrogen. The liver in patients with hepatic disease is impaired and so cannot clear estrogen sufficiently. Six 12 oz beers daily (72 oz, or half a gallon) is too much, and is destroying his liver.

uslme123  No hepatosplenomegaly, ascites, or edema through me off. We that being said, I shied away from cirrhosis. I thought that he showed signed of depression, so I went with the thyroid. But who's to say he isn't injection anabolic steroids?! +1  
catch-22  The principle is you can get liver dysfunction without having HSM, ascites, etc. Liver disease is on a progressive spectrum. +3  
notadoctor  He likely has hepatitis B/C given his history of intravenous drug use. I believe both can have liver dysfunction but may or may not have ascites, whereas the type of damage we would expect from alcohol that would match this presentation would also show ascites. +  
charcot_bouchard  For Ascities u need to have portal HTN. Thats a must. (unless exudative cause like Malignancy) +1  
paulkarr  For anyone who needs it; the FA photo is kinda burned into my mind for these questions. NBME has some weird infatuation with this clinical presentation.. FA (2019) Pg: 383 "Cirrhosis and Portal HTN". +  

submitted by sympathetikey(479),

Any time you see fixed wide splitting of S2, smash ASD.

someduck3  I'm not 100% about this so take it with a grain of salt. But i was confused about why there would be a systolic murmur. I think its b/c prolonged ASD would eventually cause pulmonic stenosis which would present as a systolic murmur. But besides that I super agree with @sympathetikey +  
need_answers  https://www.youtube.com/watch?v=7hzabZ7YBr0 -smash, smash, smuh-ash +2  
usmlecharserssss  with airpods in 2012 +  
paulkarr  Low key was hoping for someone to try and argue this one... +  

submitted by water(14),

surprisingly, I actually learned this from the Magic School Bus when I was a kid. That's the only reason I got this right. Thanks Ms. Frizzle! :D

paulkarr  She taught me more than my med school professors did... +3  

Clodipogrel prevents platelet aggregation by blocking the ADP receptor. The ADP receptor is what is responsible for putting GpIIb/IIIa receptors on the surface of platelets. Without GpIIb/IIIa, the platelets cannot aggregate together.

paulkarr  Just adding that Clopidogrel irreversibly inhibits the P2Y12 receptor. This can be found in FA2019, pg 403. The other drugs in this category are: Prasugrel, ticagrelor, and ticlopidine. Ticlopidine is famous for causing Neutropenia and having an increased risk for TTP. +  

submitted by hello36654(0),

I understand why it's lung now, but I picked thyroid gland because often times thyroid tumors press on the parathyroid sitting above, which causes the parathyroids to secrete more Ca...can someone comment if they've read this too?

paulkarr  I personally have not read that, but I wouldn't be surprised by that fact. I think with these NBME problems though, if you can get the answer within one "step" that should be your choice. Here you can just go Squamous Cell Carcinoma with a direct action on serum calcium levels (via PTHrP). Thyroid requires a few more steps, (assuming your statement is true) so in the eyes of NBME, it ain't gonna be the right choice. Always follow the "KISS" logic! +  

submitted by nlkrueger(16),

why isn't, "0% blasts on the peripheral smear" right? is this the distinguishing future for acute leukemia?

lispectedwumbologist  Because you'll see some blast cells in a leukemoid reaction. It won't be 0%. +1  
paulkarr  Also, don't get confused with 0% Basophils. Basophils are seen in CML but not in Leukemoid reactions. I just went with LAP because they pointed it out in the lab values. Had that not been there, I would have chosen "0% basophils" +  

submitted by chris07(23),

I'm guessing that since this is hashimoto's that a biopsy of the thyroid would show the thyroid gland completely engulfed by attacking lymphocytes. Over time though, wouldn't the thyroid be completely destroyed and fibrotic?

dr.xx  Progressive thyroid cell damage can change the apparent clinical picture from goitrous hypothyroidism to that of primary hypothyroidism, or "atrophic" thyroiditis. https://www.ncbi.nlm.nih.gov/books/NBK285557/ The pathological features are atrophic thyroid gland with lymphocytic infiltration and fibrous tissue replacing normal thyroid parenchyma. https://www.researchgate.net/publication/302196286_Atrophic_Thyroiditis +  
paulkarr  I was thinking that "Diffuse fibrosis" was trying to point to IgG4 Riedel Thyroiditis rather than Hashimoto's. +1  

submitted by sugaplum(92),

This is ridiculous but I could never keep these straight so meet my family:
Achey grandpa Meynert
Dope cousin VT with a side Ho* (who's names are just initials) SNc
Uncle and aunt Raphe and sara Cousin Gabby always screaming Na-Na-Na
norepi reminds me of the color blue, so locus ceruleus

paulkarr  LOL. Achey Granpa Meynert. I'm gonna steal this from you. +  

submitted by nwinkelmann(154),

So, for some reason, neurotransmitters is something I've ALWAYS struggled with... probably because I wasn't taught it well so never really learned it, just learned enough for whatever exam. I just found this boo through NCBI and its FANTASTIC! It's from 2001 so might be old, but it was great. You can search through the book and find the chapters. I pretty much just went through all of the neurotransmitter chapter. https://www.ncbi.nlm.nih.gov/books/NBK10799/

My main take-aways: Glutamate = major excitatory neurotransmitter. Two types of receptors: 1) metabotropic, most of which are presynaptic Gi which leads to decreased NMDA receptor activity and risk of exocitotixicity, or postsynaptic Gq receptors that lead to increase Na+, K+, and decreased glutamate causes depolarization and increased Mg++ displacement and NMDA receptor activity and risk of exocitotxicity, and 2) ionotropic channels including NMDA and AMPA/kainate channels, which all allow nonspecific cation influx, but only NMDA allows Ca++ influx (and only in a voltage dependent manner after sufficient depolarization has displaced the inhibitor Mg++ ion in the channel).

GABA and glycine = inhibitory neurotransmitters. 1) GABA-A and GABA-C = ionotropic channels that lead to eflux of Cl-, and despite this causing depolarization, the neuron still stays below resting potential. GABA-A binding site for barbiturates, steroids, GABA, and picrotoxin = inside pore of channel. GABA-A binding site of benzodiazepines = outside of pore of channel. 2) Glycine channel is a very similar Cl- eflux channel. 3) GABA-B is a metabotropic channel that activates Gi leading to decreased cAMP which activates efflux K+ channels and inhibits Ca++ influx channels leading to hyperpolarization.

Biogenic amines = catecholamines dopamine (coordination of body movement, reward, motivation, reinforcement), norepinephrine (sleep, wakefulness, attention, feeding behavior, epinephrine (lowest concentration in CNS), plus serotonin (sleep, wakefulness, depression, anxiety, nausea) and histamine (arousal, attention, allergy, tissue damage, and may influence blood brain flow). Obviously, all of this is in addition to adrenergic neurotransmission and flight, fright, and fight response.

ATP and other purines = excitatory transmission, co-released with other small-molecule neurotransmitters. Adenosine isn't classically considered a neurotransmitter because it isn't stored/released in Ca++ dependent manner, but derived from ATP before having an excitatory potential.

Acetylcholine = major neurotransmitter involved in neurotransmission via muscarin and nicotinic receptors.

Peptide neurotransmitters = commonly released as propeptide larger precursors that are cleaved by specific enzymes that were in the same neurotransmitter vesicle upon release. Five types = brain/gut peptides, opioid peptides, pituitary peptids, hypothalamic releasing hormones, and those not classified. Examples = precursor that gives rise to substance P (hippocampus, neocortex, and GIT and released from small diameter PNS C fibers that transmit pain and temperature information, powerful hypotensive, inhibited by opioid peptides), neurokinin A, neuropeptide K, and neuropeptide gamma, and opioid peptides including plant alkaloids (like morphine), synthetic opioid derivatives, and endorphins, dynorphins, and enkephalins. In general opioid peptides are depressants (i.e. analgesia mechanism), involved in complex behaviors (sexual attraction, aggressive/submissive behaviors), and implicated (though not definitive) in psychiatric disorders.

Overall, neurotransmitters = type types: small-molecule transmitters and neuropeptides, where small-molecules transmitters are faster and mediate rapid synaptic transmission (i.e. androgen SNS fight/flight/fright quick response), where as neuropeptides (along with biologic amines and some small molecule transmitters) are slower and mediate gradual, prolonged neurotransmission.

Some pictures: http://tmedweb.tulane.edu/pharmwiki/doku.php/overview_of_cns_neurotransmitters, https://www.semanticscholar.org/paper/Targeting-GABAB-receptors-for-anti-abuse-drug-Phillips-Reed/a049643bb25c8631e0267a40182e6d310d1f31fb/figure/0, and https://www.bluelight.org/xf/threads/difference-between-gaba-a-and-gaba-b.733916/#lg=_xfUid-1-1562540128&slide=0

sweetmed  This is amazing. thank you +  
sweetmed  This is amazing. thank you +  
paulkarr  Woah... +  

submitted by haliburton(116),

medbullets has a nice pneumonic for the killed vaccines:

Rest In Peace Always:

Polio (Salk)
Hepatitis A

paulkarr  Also, the nice little puppet show from sketchy for those visual learners like me. +  

submitted by d_holles(59),

Even tho FA and SketchyMicro doesn't mention it, both Anaplasma and Ehrlichosis are carried by Robin of Ixodes.

bulgaine  FA 2019 does mention it P 149 +  
charcot_bouchard  Ehrlichia - Lone star tick +1  
paulkarr  "Lyme Disease caused by Borrelia Burgdorferi, which is transmitted by the ixodes deer tick (also vector for Anaplasma spp. and protozoa babesia)." FA 2019, Pg 146 +  

submitted by hayayah(536),

Femfibrozil is a fibrate, used for lowering TG levels.

mousie  I also chose Gemfibrozil too because its the best TG lowering drug listed but I can see where there might be some red flags for this drug in the way they asked the question... 40 year old obese woman with some upper abdominal pain ..... HELLO GALL STONES which is a common adverse outcome of Fibrates. +4  
uslme123  Well I didn't wanna give a fat, forty, female, that smokes a fibrate. So a statin, for me, was the best next option. +3  
whoissaad  Used same reasoning to choose statins. Fibrates are the main drug of choice for hypertriglyceridemia but given her symptoms, statins made more sense. Why do they do this to us... +  
roaaaj  what a tricky question! there are multiple factors should be taken in consideration.. she has triglyceridemia which put her in risk of pancreatitis, and most importantly atherosclerotic disease, and all of that would outweigh the risk of giving her gallstone. +  
paulkarr  Yeah I had statins selected initially because "statins are always the answer" but when I saw them stating first line "recently diagnosed with hyper TG" I figured this follow-up was purely to address that. So Fibrate is the best move. +1  

submitted by nlkrueger(16),

.... would we really take the word of a friend who definitely can't be confirmed? I feel like this is misleading

lispectedwumbologist  All the other answer choices make you come across as an asshole. Easy way to ace ethics questions is to just not be an asshole +2  
seagull  I would be a bigger asshole when the family came I'n after I pulled the plug...opps...but the friend said +7  
dr.xx  The patient has no wife, children, or close relatives... +1  
nwinkelmann  @lispectedwumbologist this is going to be my technique, because I've gotten a couple of these wrong, but I completely agree with everyone else's sentiments of suspicion of going off what a friend said without any confirmation about state of advance directives, etc. It's really dumb. +1  
paulkarr  With these questions; you have to take what NBME says at face value. If it says no family, he really does have no family. This friend is also claiming that the 78 y/o said this about himself, so we know it's the patients wishes rather than someone else's wishes for him. (A son saying he can't let go of his father yet despite the patient's DNR type of situation). +  
suckitnbme  I think the point here isn't that we would take the patient off the ventilator because the friend said so. The answer is saying "Thank you for your input, we will take that into consideration." It's completely non-committal. +3  

submitted by yotsubato(416),

Was it just me, or did "age at onset in years" appear RIGHT above the number of patients, rather than the mean. Which confused me for a good 3 minutes.

fulminant_life  Definitely was the same for me. I was so confused for like 5 mins +5  
d_holles  dude i almost didn't get the question bc of this ... i thought the age of onset was the actual age of onset (36) +3  
mellowpenguins  Are you serious. NBME strikes again with shitty formatting. +1  
yex  OMG!! Now I just realized that. Super confused and also thought onset of age was 36. :-/ +1  
monkey  what is 36 supposed to be? +  
thomasburton  Think the number of people in that group +1  
paulkarr  Yup...was looking at it for a good 3 min before just doing the "fuck it..it's gotta be 99" +  
arcanumm  Age of Onset is the Title of the table, which I didn't figure out until after exam was over. What terrible formatting. +  

submitted by sympathetikey(479),

Biggest clue was that there was no time frame given. Therefore, this seems to be a "slice in time" study, which lines up with cross sectional study.

tamey  and also among the other answer choices cross sectional study is the only one thats used for population study +  
paulkarr  Damn, epi at it again... +1  

submitted by smc213(61),

To be completely clear!

This patient has Cystinosis a rare autosomal recessive lysosomal storage disorder and most common cause of Fanconi syndrome in children. Cystinosis is systemic and leads to cystine crystal deposits in cells and tissues throughout the body.

Although Wilsons disease can lead to FS, the crystals in the corneas does not correlate with Wilsons disease.
More info: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4841061/

highyieldboardswards  Thank you! You are a legend for figuring this out! +  
paulkarr  Appreciate you. +  

Increased Levels of Myeloid cells ( Erythrocytosis, thrombocythemia, and granulocytosis) plus Dizziness and Headache increase the suspicion for Polycythemia vera.

Low EPO in PV due to Negative feedback on EPO release by kidney.

dentist  This is where the timing of everything in the question trips me up. FA say PV mechanism is increase EPO (2019, p299) +  
paulkarr  Different types of Polycythemia have different effects on EPO levels. "Appropriate Absolute" and "Inappropriate Absolute" will both increase EPO levels (Inappropriate is caused by this EPO increase). Where as Polycythemia Vera has decreased EPO levels due to the negative feedback loop. FA2019 pg 425 hooks it up nicely. +1  

submitted by mousie(105),

help with this one please.... is this because he has hyperTG AND Cholesterol AND chylomicrons.. only LL deficiency would explain all of these findings? I chose LDL R deficiency because I guess I though it would cause all of them to increase but is this type of deficiency only associated with high LDL?

sympathetikey  First off, do yourself a favor and check this out - https://www.youtube.com/watch?v=NJYNf-Jcclo The LDL receptor is found on peripheral tissues. It recognizes B100 on LDL, IDL, and VLDL (secreted from the liver). Therefore, an issue with that would cause an increase in those, but mainly LDL. Since in this question we see that Triglycerides and Chylomicrons are elevated, that points towards a different problem. That problem is in the Lipoprotein Lipase receptor. This is the receptor that allows tissues to degrade TGs in Chylomicrons. So, if it's not working, you get increased TGs and Chylomicrons. Additionally, you get eruptive xanthomas, which are the yellow white papules the question refers to. +4  
davidw  There is much easier way go to page 94 in first aid. This kid has Type 1 Hyper-Chylomicronemia which is I) Increased Chylomicrons, Increase TG and Increased Cholesterol. It can be either Lipoprotein Lipase or Apolipoprotein CII Deficiency +7  
bulgaine  The video sympathetikey referred to only mentions pancreatitis in type IV but according to page 94 of FA 2019 it is also present in type I Hyper-chylomicronemia which is what the question stem is referring to with the abdominal pain, vomiting and increased amylase activity +  
dentist  thats not the only difference in that video.... +  
paulkarr  Pixorize has a set of videos on all the lipid disorders that made it a breeze to answer. Pixorize is basically sketchy but for biochem and other basic science subjects. +