Welcome to almondbreezeโs page.
Contributor score: 110
Comments ...
peridot
Also, deer fly can transmit loa loa (FA 2019 p.159) in addition to F. tularensis
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almondbreeze
b/c pancreatic causes can form blood clot in splenic v, b/c splenic v runs behind pancreas
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Subcomments ...
almondbreeze
FA 2019 pg 248 pill-induced esophagitis : bisphosphonates, ferrous sulfate, NSAIDs, potassium chloroide, tetracyclines
+3
dbg
I seriously could not figure out whether those white opacities were actual lesions or reflections from the actual picture (flash light) ... mind went all the way maybe this is the shiny pleura so they're going after mesothelioma. smh
+10
dbg
shiny pleura with tiiiiny granulations if you look closely. but obviously was far off
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bullshitusmle
guys something I learned from NBMEs is that if there is a clinical vignette dont even look at the images they give you ,they are all useless and time-consuming
+1
goaiable
The way i narrowed it down was that the patient had signs of weight loss since three months whereas her cough developed recently (3 weeks). If the cancer arose in the lung then I think the cough or other pulmonary symptoms should emerge earlier.
+1
almondbreeze
FA2019 pg 669 in the lung, metastasis (usually multiple lesions) are more common the primary neoplasms. most often from breast, colon, prostate, and bladder ca.
+1
medstruggle
Doesnโt supine position compress IVC leading to decreased venous return? (This is the pathophys of supine hypotension syndrome.) There was a UWorld questions about this ...
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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 wouldnโt be the same postural compression.
+12
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
+3
yotsubato
You gotta be preggers to compress your IVC
+5
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.... ?
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urachus
wouldnt low aldosterone cause low plasma sodium? choice B
+5
kpjk
could it be that, while low aldosterone levels decrease plasma sodium levels- there is also decrease in blood volume(plasma),so there wont be a decrease in the "concentration" of sodium
+5
almondbreeze
FA 2019 pg 306 on Lt heart failure induced orthopnea - Shortness of breath when supine: increased venous return from redistribution of blood
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almondbreeze
if there was no HF, it would lead to increased CO --> decreased aldosterone
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theunscrambler
@peqmd thanks for sharing that. According to the presentation, the diuresis via ANP occurs (along with sodium), which is followed up by an increased in RAAS --> maintains sodium levels. This cycle can then continue. Slide 13.
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jj375
@urachus - Either BB or Sattar taught me this but I feel like it is often forgotten. "RAAS/Aldosterone affects blood volume, and ADH affects Na level". So Increasing aldosterone will increase blood levels however water follows the sodium so you will not get a change in sodium levels. ADH however does affect Na since aquaporins are bringing in water without affecting sodium levels.
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medstruggle
Doesnโt supine position compress IVC leading to decreased venous return? (This is the pathophys of supine hypotension syndrome.) There was a UWorld questions about this ...
+4
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 wouldnโt be the same postural compression.
+12
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
+3
yotsubato
You gotta be preggers to compress your IVC
+5
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.... ?
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urachus
wouldnt low aldosterone cause low plasma sodium? choice B
+5
kpjk
could it be that, while low aldosterone levels decrease plasma sodium levels- there is also decrease in blood volume(plasma),so there wont be a decrease in the "concentration" of sodium
+5
almondbreeze
FA 2019 pg 306 on Lt heart failure induced orthopnea - Shortness of breath when supine: increased venous return from redistribution of blood
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almondbreeze
if there was no HF, it would lead to increased CO --> decreased aldosterone
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theunscrambler
@peqmd thanks for sharing that. According to the presentation, the diuresis via ANP occurs (along with sodium), which is followed up by an increased in RAAS --> maintains sodium levels. This cycle can then continue. Slide 13.
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jj375
@urachus - Either BB or Sattar taught me this but I feel like it is often forgotten. "RAAS/Aldosterone affects blood volume, and ADH affects Na level". So Increasing aldosterone will increase blood levels however water follows the sodium so you will not get a change in sodium levels. ADH however does affect Na since aquaporins are bringing in water without affecting sodium levels.
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masonkingcobra
Lamin looks like a "cross" and held up Jesus and the basal lamina is super important just like jesus (you bet there are people who believe this)
https://answersingenesis.org/biology/microbiology/laminin-and-the-cross/
+45
dr.xx
blasphemy @masonkingcobra
+1
luciana
I clearly confused lamin with laminin, now I know
+3
almondbreeze
picked tubulin but i guess tubulin makes up microtubules and therefore is spherical
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abkapoor
Also remember progeria is due to lamin a dysfunction, and progeria patients have messed up nuclei
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brise
@abkapoor the f is progeria? and do we need to know it for step?
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brise
@abkapoor omg jk jk wow
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masonkingcobra
Lamin looks like a "cross" and held up Jesus and the basal lamina is super important just like jesus (you bet there are people who believe this)
https://answersingenesis.org/biology/microbiology/laminin-and-the-cross/
+45
dr.xx
blasphemy @masonkingcobra
+1
luciana
I clearly confused lamin with laminin, now I know
+3
almondbreeze
picked tubulin but i guess tubulin makes up microtubules and therefore is spherical
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abkapoor
Also remember progeria is due to lamin a dysfunction, and progeria patients have messed up nuclei
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brise
@abkapoor the f is progeria? and do we need to know it for step?
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brise
@abkapoor omg jk jk wow
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wired-in
Patient has 5 yr h/o hep C, so it is chronic. Chronic inflammation is characterized by presence of lymphocytes & plasma cells while neutrophils is more characteristic of acute inflammation (Pathoma Ch. 2). AFP is within reference range so probably not HCC. Choice D, palisading lymphocytes & giant cells suggests granuloma which isn't typical of hep C.
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almondbreeze
Fa2019 pg 215, 217 on acute/chronic inflammation
+2
popofo
But doesn't AFP has not-so-high sensitivity for hepatocellular carcinoma (HCC)? If so, a negative result shouldn't be able to rule out HCC?
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popofo
But doesn't AFP has not-so-high sensitivity for hepatocellular carcinoma (HCC)? If so, a negative result shouldn't be able to rule out HCC?
+1
fatboyslim
HCC from hepatitis C usually takes decades to occur. This patient has only had HCV infection for 5 yeats
+1
portland2020
typically you would have a monocytic inflammatory infiltrate as described. The monocytes are an important component of the innate response. The monocytes can differentiate into macrophages.
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krewfoo99
Also in cirrhosis, the liver wont be enlarged or tender on palpation
+2
almondbreeze
@krewfoo99 Good job. accoring to FA2019 pg.368, congestive liver disease (hepatomegaly, ascites, varices, abdominal pain, liver failiure) seems to be the key in Budd-Chiari SD
+2
fatboyslim
Just to add, hepatic cirrhosis will have a shrunken and nodular liver.
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arcanumm
This makes sense have reading what your comment. I overlooked this and just assumed the GATC was a mutation that allowed the restriction enzyme to work on the mutant only.
+2
arcanumm
it makes even more sense when looking at "numerous small fragments." Methylation is truly the obvious answer here in retrospect.
+1
bgiri
DNAse can also cause a change in base by breaking down dna at the GATC sequence?
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almondbreeze
@bgiri Had the same reasoning - according to wiki, DNase catalyzes the hydrolytic cleavage of phosphodiester linkages in the DNA backbone, thus degrading DNA.
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sympathetikey
& Galactokinase deficiency would be much milder.
+9
smc213
Big was soybean formula not giving any issues. Soy-milk can be used as a substitute formula in patients with Classic Galactosemia since it contains sucrose (->fructose and glucose).
+4
oslerweberenu
Why can't this be glucose 6 phosphatase deficiency
Confused me
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almondbreeze
@oslerweberenu G6PD - increased RBC susceptibility to oxidant stress (eg, sulfa drugs, antimalarials, infections, fava beans) -> hemolysis; has nothing to do with presence of reducing sugar
+1
makinallkindzofgainz
@almondbreeze; Glucose-6-phosphatase deficiency is Von Gierke disease, they are not referring to G6PD deficiency (an entirely seperate disease)
+9
abhishek021196
Physiologic
neonatal jaundice
At birth, immature UDP-glucuronosyltransferase = unconjugated hyperbilirubinemia = jaundice/
kernicterus (deposition of unconjugated, lipid-soluble bilirubin in the brain, particularly basal
ganglia).
Occurs after first 24 hours of life and usually resolves without treatment in 1โ2 weeks.
Treatment: phototherapy (non-UV) isomerizes unconjugated bilirubin to water-soluble form.
+1
azharhu786
The water-soluble form is called Lumirubin.
+2
almondbreeze
a concept continuously emphasized by uw, but I get always wrong :'(
+4
raffff
why does the body make anp at all since its so useless
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makinallkindzofgainz
@raffff - at least BNP gives us a good marker for heart failure exacerbations :) thanks body!
+1
mannan
Yeah it's important clinically because it has a high sensitivity (if negative, rule out) for Heart failure.
+1
alimd
At the same time ANP inhibits renin release?
+1
freemanpeng
If it is High RAAS, Aldo must be High as well(AngII induce Aldo more than ADH). Then that would be SALT-WATER retention rather than PURE WATER retention. NO hyponatremia
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plaguedbyspleen
This patient is third-spacing and therefore has low effective circulating volume. I like to think that given his CV history, he is probably on an ACE inhibitor or something similar. So that leaves ADH to do its thing. Also high aldosterone saving salt isn't something we need to consider given the stem and answer choices.
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waterloo
Although history seems to point towards that, she has an enlarged thyroid, and in postpartum thyroiditis, thyroid usually normal in size (from FA). regardless either would have lymphocytes infiltrating.
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almondbreeze
b/c pancreatic causes can form blood clot in splenic v, b/c splenic v runs behind pancreas
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almondbreeze
info about ferruginous bodies being mf can't be found on FA/UW :'( they just say it's 'material'
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taediggity
FA 2020 677, FA 2019 659... mf?? mofos??
+3
69_nbme_420
Just to add: The question asks what cell type initiated the Fibrosis โ Alveolar macrophages engulf the particles and induce fibrosis (same pathophys for all Pneumoconiosis). Pathoma 2019 Pg 92
+10
alexv0815
"A small (< 3 ฮผm), golden-brown, dumbbell-shaped particle that contains iron. Most often seen in the alveolar septum in conditions such as asbestosis." amboss
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almondbreeze
thought his words on "think cheap" had to do with treatments - i.e. exercise
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alimd
Yes they are. There are so many trick questions
+1
skuutnasty
I chose leptin deficiency cuz I was tryna get fancy with it.
For anyone who is interested, however... according to UpToDate:
"Most people with obesity do not have any abnormalities in the leptin gene, their serum leptin concentrations are high reflecting their increased fat mass..."
Peace
+6
sunnyside
@skuutnasty should've just let me feel fancy, now i feel stupid :(
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carls14
aren't retinal cells a type of somatic cell? Why not is the mutation not considered in the somatic cell of the child?
+10
omerta
Although this mutation would be considered somatic, I believe the question is just asking you to be specific as to which cells. If you answered "somatic cells of the child," that's quite broad and could apply to almost anything.
+13
eacv
There is a Uworld qx that explain this in detail> ID: 863
+3
arcanumm
I read the answer options too fast so got this wrong. It is a somatic cell type, but somatic in general implies a higher risk for developing other cancers. The hint here is that the physician stated he is unlikely to develop any other neoplasms, so it is a specific double hit mutation in the retina.
+7
almondbreeze
wouldn't she have any possibility of developing osteosarcoma as well? :(
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almondbreeze
did some reading and it seems like osteosarcoma only occurs in familial retinoblastoma with RB mutation
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brise
But how can a 5 year old get two mutations to get retinoblastoma? In 5 years?! Obviously doctor is probably wrong LOL
+1
jaramaiha
The difference between familial and sporadic mutations dealing with Rb is that in this case he only had one hit so that only one eye is affected. In other words, if he would have been born with the familial type, he would present with Rb in both eyes and also be predisposed to osteosarcoma. In this instance he only has Rb in one eye having only a one hit mutation in his right eye. When the stem says this is the first mutation it's implying that he wasn't born with the familial type so to obtain a second mutation over the course of his lifetime would be rare.
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brise
@jaramiaha I believe it still falls into a two hit mutation, but both were sporadic. But you are right about being unilateral.
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jaramaiha
Sorry I'm just getting back to this. Been on the grind and taking my exam Monday fingers crossed but I found the section I was thinking about when I first wrote this. In Pathoma chapter 3 page 27 (in the 2018 edition) located in the end of the section discussing tumor suppressor genes. It talks about the sporadic mutation in Rb(both hits being somatic) is characterized by unilateral retinoblastoma. While germline mutation results in familial retinoblastoma (2nd hit is somatic), characterized by retinoblastoma and osteosarcoma.
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abhishek021196
One-third of all retinoblastomas are hereditary : RB1 gene mutations are present in all of the body's cells, including reproductive/germ (sperm or eggs) cells - k/as germline mutation/gametic mutation : mutations in the cells from which egg or sperm cells develop. These patients thus have higher risk of developing cancers in other body parts as well and can also pass these mutations to their offspring. The other two-thirds of retinoblastomas are non-hereditary, which means that RB1 gene mutations are present only in retinal cells of that eye and do not occur in the germline - k/as somatic
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abhishek021196
continued to my previous comment - These patients do not have risk of developing cancer in other body parts and as they do not occur in the germline, they cannot be passed on to offspring via the ovum or sperm.
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carls14
aren't retinal cells a type of somatic cell? Why not is the mutation not considered in the somatic cell of the child?
+10
omerta
Although this mutation would be considered somatic, I believe the question is just asking you to be specific as to which cells. If you answered "somatic cells of the child," that's quite broad and could apply to almost anything.
+13
eacv
There is a Uworld qx that explain this in detail> ID: 863
+3
arcanumm
I read the answer options too fast so got this wrong. It is a somatic cell type, but somatic in general implies a higher risk for developing other cancers. The hint here is that the physician stated he is unlikely to develop any other neoplasms, so it is a specific double hit mutation in the retina.
+7
almondbreeze
wouldn't she have any possibility of developing osteosarcoma as well? :(
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almondbreeze
did some reading and it seems like osteosarcoma only occurs in familial retinoblastoma with RB mutation
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brise
But how can a 5 year old get two mutations to get retinoblastoma? In 5 years?! Obviously doctor is probably wrong LOL
+1
jaramaiha
The difference between familial and sporadic mutations dealing with Rb is that in this case he only had one hit so that only one eye is affected. In other words, if he would have been born with the familial type, he would present with Rb in both eyes and also be predisposed to osteosarcoma. In this instance he only has Rb in one eye having only a one hit mutation in his right eye. When the stem says this is the first mutation it's implying that he wasn't born with the familial type so to obtain a second mutation over the course of his lifetime would be rare.
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brise
@jaramiaha I believe it still falls into a two hit mutation, but both were sporadic. But you are right about being unilateral.
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jaramaiha
Sorry I'm just getting back to this. Been on the grind and taking my exam Monday fingers crossed but I found the section I was thinking about when I first wrote this. In Pathoma chapter 3 page 27 (in the 2018 edition) located in the end of the section discussing tumor suppressor genes. It talks about the sporadic mutation in Rb(both hits being somatic) is characterized by unilateral retinoblastoma. While germline mutation results in familial retinoblastoma (2nd hit is somatic), characterized by retinoblastoma and osteosarcoma.
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abhishek021196
One-third of all retinoblastomas are hereditary : RB1 gene mutations are present in all of the body's cells, including reproductive/germ (sperm or eggs) cells - k/as germline mutation/gametic mutation : mutations in the cells from which egg or sperm cells develop. These patients thus have higher risk of developing cancers in other body parts as well and can also pass these mutations to their offspring. The other two-thirds of retinoblastomas are non-hereditary, which means that RB1 gene mutations are present only in retinal cells of that eye and do not occur in the germline - k/as somatic
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abhishek021196
continued to my previous comment - These patients do not have risk of developing cancer in other body parts and as they do not occur in the germline, they cannot be passed on to offspring via the ovum or sperm.
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john055
it looks like the patient has new onset erythema which points to infection and I think neutrophils make sense. I myself have marked angiogenesis but I did it offline. Is angiogenesis the right answer ?
+1
almondbreeze
according to FA 2019 pg217, neutrophil is present during inflammatory phase- i.e. only up to 3d after the wound. After that we have the proliferative phase with granulation tiss. and angiogenesis, epithelial cell proliferation, dissolution of clot, and wound contraction (involved cells: fibroblasts, myofibroblasts, endothelial cells, keratinocytes, mf)
+1
waterloo
mitchell_to_lakers They are asking why is the incision erythematous and slightly warm. When someone is red, Dr. Sattar says that's because blood is going there. Fibrosis isn't a mechanism where someone's tissue will appear red and warm, it's collagen deposition.
+7
srmtn
is not infected, is healing. normally when healing is a little warm and erythematous because of angiogenesis.
+3
john055
it looks like the patient has new onset erythema which points to infection and I think neutrophils make sense. I myself have marked angiogenesis but I did it offline. Is angiogenesis the right answer ?
+1
almondbreeze
according to FA 2019 pg217, neutrophil is present during inflammatory phase- i.e. only up to 3d after the wound. After that we have the proliferative phase with granulation tiss. and angiogenesis, epithelial cell proliferation, dissolution of clot, and wound contraction (involved cells: fibroblasts, myofibroblasts, endothelial cells, keratinocytes, mf)
+1
waterloo
mitchell_to_lakers They are asking why is the incision erythematous and slightly warm. When someone is red, Dr. Sattar says that's because blood is going there. Fibrosis isn't a mechanism where someone's tissue will appear red and warm, it's collagen deposition.
+7
srmtn
is not infected, is healing. normally when healing is a little warm and erythematous because of angiogenesis.
+3
meningitis
Thank you for your explanation!
One question: How about the serine phosphorylation? Is it answered by pure memorization that the FOXO TF is serine phosphorylated, or is it a general fact that all TF's are serine-threonine phosphorylated?
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tsl19
I'm not sure, but it may be as simple as this: ubiquitin-mediated proteolysis is irreversible, but both N/C shuttling and phosphorylation are generally reversible processes.
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didelphus
I also guessed that FOXO must be a part of the PI3K pathway, since insulin regulates metabolism through PI3K and the question stem specifically mentions that. Phosphorylation is a major part of that pathway, so even indirectly phosphorylation would regulate FOXO. Frustrating question.
+21
alexb
According to wikipedia (https://en.wikipedia.org/wiki/FOXO1) phosphorylation of FOXO1 is irreversible. This is referring to phosphorylation of serine residues on FOXO by Akt, which occurs in response to insulin. But the NBME answer suggests it's reversible. What's up?
+2
almondbreeze
could wiki be wrong on phosphorylation being irreversible? according to this article, it is a reversible process: regulation of FoxO transcription factors by reversible phosphorylation and acetylation (https://www.sciencedirect.com/science/article/pii/S0167488911000735#s0010)
some wiki info, however, is helpful : In its un-phosphorylated state, FOXO1 is localized to the nucleus, where it binds to the insulin response sequence located in the promoter for glucose 6-phosphatase and increases its rate of transcription. FOXO1, through increasing transcription of glucose-6-phosphatase, indirectly increases the rate of hepatic glucose production.[19] However, when FOXO1 is phosphorylated by Akt on Thr-24, Ser-256, and Ser-319, it is excluded from the nucleus, where it is then ubiquitinated and degraded. The phosphorylation of FOXO1 by Akt subsequently decreases the hepatic glucose production through a decrease in transcription of glucose 6-phosphatase.
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leaf_house
It seems like the phosphorylation from Akt leads to destruction, but maybe the assumption is that that phosphorylation step (excluding every other step of ubiquitin-proteosome pathway) is reversible, where proteolysis is final.
@niboonsh video is good but doesn't split this one.
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forerofore
there is another clue, the man has diminished pulses in just one arm, which means that the left subclavian artery must be involved somehow, and an aortic dissection would be the best answer explaining this.
+11
temmy
please why is there where a diastolic mumur?
+1
whoissaad
@temmy Aortic dissection especially near the root of aorta can lead to dilatation of the aortic valves, which can lead to Aortic regurgitation (diastoic murmur at left sternal border)
+9
garibay92
Does anyone know why is this patient's tepmerature elevated?
+1
ratadecalle
@garibay92, not important for this question I think but cocaine can cause malignant hyperthermia
+2
almondbreeze
judging by his heart murmur, he probably has marfan syndrome. that's the only place where FA talks about dissecting aneurysm
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turtlepenlight
did anyone else think it was weird his only sx was SOB? I always think of radiating pain as being a good clue for dissection
+3
cmun777
@almondbreeze his heart murmur is at the LSB (aortic regurg) and not consistent with MVP plus no other sx/indication of Marfan. I think the only association of RF you should think about in this question is the cocaine use and consequent HTN.
+1
ibestalkinyo
@turtlepenlight I agree. I chose another answer because I was like, there's no way this guy doesn't hurt if he's got a dissection.
+1
abk93
@whoissaad
but aortic regurgitation is a systolic murmur.
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calvin_and_hobbes
My guess is that the diastolic murmur is tricuspid stenosis as the tricuspid valve is the most common valve affected in patients who have IVDU
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almondbreeze
just to add : more agents causing such reaction - beta-lactams, sulfonamide, aminoglycoside
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drzed
Are those IgE dependent, or just allergic reactions (asking because the sketchy for beta-lactam penicillins mention acute interstitial nephritis as an allergic reaction)?
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almondbreeze
FA 2019 pg. 192: Do not take tetracyclines with milk (Ca2+), antacids (eg. Ca2+ or Mg2+), or iron-containing preparations b/c divalent cations inhibit drugs' absorption in the gut
+1
fatboyslim
This is also why tetracyclines are teratogenic and should not be given to children because tetracyclines chelate with the calcium in the teeth and cause tooth discoloration and inhibit bone growth in the fetus/growing child (Source: SketchyPharm)
+1
kevin
just remember fluoroquinolones also are prone to chelation. you know it's gonna pop up on the real one
+1
almondbreeze
FA 177 says Kaposi has lymphocytic inflammation whereas Bartonella spp has neutrophilic inflammation. I guess this does not apply when immunocompromised? But doesn't Bartonella usually affect the immunocompromised ppl?
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almondbreeze
Got it after seeing that she's immunocompetent
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Up to 80 percent of aortic aneurysms are caused by "hardening of the arteries" (atherosclerosis). Atherosclerosis can develop when cholesterol and fat build up inside the arteries. ... Elevated blood pressure through the aorta can then cause the aortic wall to expand and bulge.
https://www.uwhealth.org/heart-cardiovascular/aortic-aneurysm-causes-symptoms-and-concerns/10971
Also, FA 2019 pg300 says complications of atherosclerosis includes aneurysm