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josefk
So, the fact the they're saying its a right dominant to me is a way to throw you off as it does not change what the LCX artery is supplying just where its coming from.
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covidclassof2022
Yes, i think so. When they say "pt has right dominant coronary circulation" its more of extra info you dont need to answer the question. Whether the pt has Left or Right Dominant Circulation, the LCX in the question should supply the left ventricle. I had to look this up too.
To clarify:
Left dominant: Posterior interventricular (descending) C.A comes off the circumflex (10% of people)
Right dominant: Posterior interventricular (descending) C.A comes off the right coronary artery (70% of people, more common, just like the patient in the stem)
Either way, the question asked about the LCX... which supplies the left ventricle.
+1
drdoom
^ voted best username
+1
covidclassof2022
Thank you. This is the second dedicated study period Ive had this year. In March we got notice that our test would be cancelled, 1 week before. I take pride in this suffering. :')
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drdoom
hand flapping ≠ asterixis
+2
Subcomments ...
zalzale96
Created an account just to up vote this answer
+5
cheesetouch
1998 journal via google " Myocardial injury after cardiac surgery with cardiopulmonary bypass may be related to free oxygen radical-induced lipid peroxidation"
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peteandplop
"Evidence suggests that reactive oxygen species (ROS) may play important roles in the pathogenesis in myocardial infarction [2]. Following ischemia, ROS are produced during reperfusion phase [3, 4]. ROS are capable of reacting with unsaturated lipids and of initiating the self-perpetuating chain reactions of lipid peroxidation in the membranes" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2274989/)
+1
mittelschmerz
Honestly the wording got me on this one. Great answer
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acerj
Also, you can rule out a few of the options to help justify this. Post MI you expect necrosis, not apoptosis. Remember, apoptosis is suicide, and necrosis is MURDER! Cell swelling is a sign of cellular injury, not cell shrinkage. The heart will undergo coagulative necrosis, not liquefactive necrosis. Also, protease inactivation by cytoplasmic free calcium is kind of nonsensical to me. Free calcium is more likely to cause cell injury via caspases (a form of proteases amongst other things), which is why calcium is usually bound up inside healthy cells.
+5
ownersucks
This question presentation is exactly how Sattar said in pathoma Ch2. Raise in cardiac enzyme following reperfusion
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amy
FA2020 305: Reperfusion injury: free radical and increased Ca influx--hypercontraction of myofibrils
There is increased cytoplasmic free calcium ions, but it induces hypercontraction, no protease inactivation.
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flapjacks
I believe Goljan mentions that the #1 cause of anemia in older adults is GI bleeds
+6
mark0polo
Also, B-thalassemia major would present in childhood, not in a 75 year old man
+3
sexymexican888
ALSO, #1 cause of Iron deficiency anemia in a older person -> colon cancer. HOWEVER, remember golijan ALSO SAID "GUYSSSS YOU THINK RBCs JUST TURN MICROCYTIC OVERNIGHT?! LIKE YOU HAVE IRON DEFICIENCY ANEMIA AND THEYRE ALL LIKE CHEERLEADERS AND GO 1,2,3 ->MICROCYTIC?! NO!! ITS NORMOCYTIC FIRST THEN MICROCYTIC EVENTUALLY" It was hilarious lol but yeah they dont really say how long he's been weak and had fatigue so its probably pretty recent, it takes a few days for the IDA to turn microcytic
+1
sexymexican888
Also an adult male (not elderly) with IDA -> peptic ulcer disease
+1
sexymexican888
ALSO IDA can be due to blood loss or dietary lack. Remember iron is VERY tightly regulated in the body and there's no real official way to get rid of it except bleeding (menstruation in females & sloughed of cells in the intestine that had ferritin stored) thats why male patients with hemochromatosis get HCC and all these horrible manifestations in their 40s cause getting rid of iron is actually hard unless you're underconsuming it or bleeding
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chaosawaits
I also thought those were some large looking microcytic RBCs
+1
chj7
Side note: CML should have high platelet counts (as most chronic myeloproliferative disorders). [FA 2020 P.433]
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amy
Thrombocytopenia indicates CML acceleration
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neurotic999
I got caught up between GI blood loss and B12 def. The RBCs were clearly hypochromic but they also seemed large for some reason. Also the other cell in the picture (PMN?) I assumed was a hypersegmented neutrophil and so I drifted toward B12.
+1
ali_hassan
guys aplastic anemia has def. of all the cells; not the case here. CML i don't need to explain. B-thalassemia would present with target cells and simply have more manifestations than just weakness and fatigue and B12 would present with some neurologic symptoms like peripheral neuropathy. while knowing GI bleed is a common cause of bleeding in the elderly population, the answer was GI blood loss (i answered it correct through ruling out the rest)
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adong
A better way to think about it is insulin acts through MAPK which is a serine/threonine kinase
+1
amy
I intepretated Nuclear/Cytoplasmic shuttling would be the result of serine phosphorylation, so the reversible modification is only on serine phosphorylation, which lead to nuclear/cytoplasmic shuttling, but the shuttling itself is not under modification.
I got it wrong.
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hungrybox
Appreciate the effort but this is far too long to be useful.
+30
drachenx
hungrybox is a freaking hater
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drdoom
@drachenx haha, nah, coming back to this i realize i was probably over-geeking lol
+1
blueberrymuffinbabey
isn't the hydrogen bonding dependent on the hydroxylated proline and lysine? so that wouldn't really be the issue here since those aren't the aas being altered?
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drdoom
@blueberry According to Alberts’ MBoC (see Tangents at right), hydroxylysine and hydroxyproline contribute hydrogen bonds that form between the chains (“interchain”, as opposed to intra-chain; the chains, of course, are separate polypeptides; that is, separate collagen proteins; and interactions between separate chains [separate polypeptides] is what we call “quaternary structure”; see Tangent above). And in this case, as you point out, the stem describes a Gly->Ala substitution. That seems to mean two things: (1) the three separate collagen polypeptides will not “pack [as] tightly” to form the triple helix (=quaternary structure) we all know and love and (2) proline rings will fail to layer quite as snugly, compromising the helical conformation that defines an alpha chain (=secondary structure; the shapes that form within a single polypeptide).
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tadki38097
also you can't H bond with carbon, it's not polar enough
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amy
FA2020 P50 state: formation of procollagen(which is the triple helix structure) via hydrogen and disulfide. So A is incorrect bc there are no collagen molecules yet (2nd structure happens at procollagen level)
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drdoom
@amy triple helix is a quaternary structure (since triple helix is a shape that forms BETWEEN separate or “adult” pro-collagen/collagen peptides). Primary, secondary and tertiary structures are descriptions of a single polypeptide. Once you have 2 or more polypeptides interacting with each other (e.g., Hemoglobin molecule) you have quaternary structure.
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jotajota94
True! also, glycine is 1/3 of collagen alfa chains, so it makes sense that substitution with alanine (which is much bigger) would lead to disruption in the alpha helix formation.
+2
jotajota94
True! also, glycine is 1/3 of collagen alfa chains, so it makes sense that substitution with alanine (which is much bigger) would lead to disruption in the alpha helix formation.
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thepacksurvives
Glycine is small and bendy, which allows it to form the fibrils for the triple helix
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brasel
Also in general (FA 2018 pg 50) OI is from problems forming the triple helix which is secondary structure. Fortunately, they gave us something to reason with in the question (Gly->Ala)
+3
amy
Can someone help me understand why A is incorrect? FA2020 page 50: Triple helix of 3 collagen a chains is formed from procollagen via hydrogen and disulfide bond. Is this very similar to what A is decribing?
A. Decreased hydrogen-bond formation between collagen molecules.
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umpalumpa
The explanation given by wasabilateral could work if the question would say Gly-->Ala mutation. However, the question states that there is an Ala-->Gly mutation.
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bighead478
in FA it shows softening of the myocardium to happen at 3-14 days. Do you think this was overly misleading people (like me) into choosing myocardial rupture? I understand the histo features are consistent with < 24 hours, but the stem should also match this in every detail
+16
sbryant6
Myocardial rupture would not happen until 3-14 days. Since this shows signs of <24 hrs, the answer is arrythmia.
+3
hello
@bighead478 You have to look at the whole picture. Histo shows preserved architecture, which indicates coagulative necrosis -- coagulative necrosis is a histo finding only in the first 24h.
The most common causes of MI-related sudden death are: arrythmia > cardiogenic shock (heart pump problem) > rupture.
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jcmed
I chose the rupture as well due to the timeline. Somebody gave me this advice the other day, NBME classically will give you an entire vignette leading you somewhere, and the what it asks will be something completely different; or in this case will give you a photo of something and will ask about the photo. They do what they want.
+5
athenathefirst
Anyone knows why it's not a cardiogenic shock if it was within 24 hours?
+5
zevvyt
It says "Mottling" which happens in the first day. If it was 3-14 days it would be yellow (p 302 2019). He can be having angina for 3 weeks leading up to an MI.
+2
amy
The stem of the question said "softening" which indicates 3-14 days (rupture ), and "mottling" which indicate 24h (arrthymia).
It seems from the picture in FA2020 page 305, coagulative necrosis would be there during both phases.
The cells in the picture are so small that it is hard to tell if it is purely neutrophil or if there are any macrophages.
Still seems like a very confusing stem to me.
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thisisfine
Same - the bleeding thing pushed me over to psoriasis as well. Oops.
+6
temmy
the distribution of the other lesions, forearm, face, ear, scalp..is not characteristic for psoriasis.
+8
hyperfukus
the scalp and ear are actually very common for psoriasis IRL the key is more of the fact that its in areas with UV exposure...actually UV Therapy is found to be helpful in treating some pts w/Psoriasis. Lastly the appearance and lots of things bleed if they were trying to go for auspitz sign it would have tiny dots of bright red blood with slightly touching it
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hyperfukus
oh last thing psoriasis itches! they said no itching
+7
drzed
Those locations may be common IRL, but on step 1, if they want you to think psoriasis, the illness script is going to be someone in their 30s (autoimmune age) with symmetric cutaneous plaques that have a silvery scale on the extensor surfaces.
In this case, the age and non-classic description (location, type of lesion) made me steer away from psoriasis.
+3
amy
Why not squamous cell carcinoma itself?
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amy
nevermind, I think the 8 year history explained it
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thisisfine
Same - the bleeding thing pushed me over to psoriasis as well. Oops.
+6
temmy
the distribution of the other lesions, forearm, face, ear, scalp..is not characteristic for psoriasis.
+8
hyperfukus
the scalp and ear are actually very common for psoriasis IRL the key is more of the fact that its in areas with UV exposure...actually UV Therapy is found to be helpful in treating some pts w/Psoriasis. Lastly the appearance and lots of things bleed if they were trying to go for auspitz sign it would have tiny dots of bright red blood with slightly touching it
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hyperfukus
oh last thing psoriasis itches! they said no itching
+7
drzed
Those locations may be common IRL, but on step 1, if they want you to think psoriasis, the illness script is going to be someone in their 30s (autoimmune age) with symmetric cutaneous plaques that have a silvery scale on the extensor surfaces.
In this case, the age and non-classic description (location, type of lesion) made me steer away from psoriasis.
+3
amy
Why not squamous cell carcinoma itself?
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amy
nevermind, I think the 8 year history explained it
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sbryant6
Atypical lymphocytes are CD8+ T cells, not CD4+. Remember that.
+17
mangotango
I remember this because Infectious Mononucleosis is caused by a virus (mostly EBV, sometimes CMV) and MHC Class I functions to present endogenous antigens (e.g. viral or cytosolic proteins) to CD8+ T cells. In comparison, MHC Class II is more involved with presenting exogenous antigens (e.g. bacterial proteins) to CD4+ T cells. // FA 2019, pg 100
+3
amy
I get the atypical T cell idea, but can someone help me understand why monocyte is not elevated in mononucleosis????
BTW, there are both heterophil positive(EBV) AND heterophil negative(CMV) mononucleosis, so patient can have - monospot test and still have mononucleosis...
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drdoom
@amy mononucleosis ≠ monocytes. Mono-nucleosis refers to the increase of mono-nuclear cells (lymphocytes) in the blood, as opposed to polymorpho-nuclear or “segmented” white blood cells like neutrophils, basophils, or eosinophils—which all have their nuclei divided into 2 or more “lobes” (multilobar cells). “Mono-nucleosis” just refers to an increase in the blood of those cells with a “single, unlobulated/unsegmented” nucleus = lymphocytes.
+1
amy
In case anyone is wondering:
Fat stranding: "Fat stranding refers to an abnormally increased attenuation in fat. Acute conditions that cause fat stranding include peritonitis; inflammation, infection, or ischemia of the bowel; perforation of colon cancer; inflammation associated with pancreatitis or cholecystitis; trauma; and surgery.
Creeping fat (the one associate with Crohn disease): mesenteric fat wrap around the bowel wall, causing it to thicken
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uroosisyed5
Which makes sense if we think about the pathophys of elevated Cl- and Na intracellularly. Both of these ions go up inside the cells due to the retention of the misfolded proteins in the RER.
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lilyo
I actually disagree with this reasoning. The pathophysiology in CFTR is not due to accumulation of misfolded proteins. It is due to decreased/absent ATP gated transmembrane Chloride channel. According to Uworld, the miscoded protein is detected by the Endoplasmic Reticulum. The abnormal protein is targeted for destruction by the proteasome and never reaches the cell surface. There is NO retention of misfolded protein, there is degradation of misfolded protein and therefore absence of chloride channels on the membrane. This is what leads to impaired removal of salt from the sweat as well as decreased NaCl in mucus. I dont think the answer should be ER. Can anyone tell me if I am missing something here that makes the answer ER as opposed to cytoplasm? Because the way I see if is misfolded proteins go form the ER into the cytoplasm to reach the proteasome and then be destructed. Uworld questions ID are 805, 802, 1514, and 1939.
+19
drdoom
@lilyo The CFTR is a transmembrane protein. Like all proteins, its translation begins in the cytosol; that said, CFTR contains an N-terminus “signal sequence”, which means as it is being translated, it (and the ribosome making it!) will be transported to the Endoplasmic Reticulum.^footnote! As it gets translated, its hydrophobic motifs will emerge, which embeds the CFTR protein within the phospholipid bilayer of the ER itself! That means the protein will never again be found “in the cytosol” because it gets threaded through the bilayer (which is, in fact, how all transmembrane proteins become transmembrane proteins at the cell surface -- they have to be made into transmembrane proteins in the ER first!).
+11
drdoom
@lilyo (continued) So, yes, ultimately, these misfolded proteins will be directed toward a proteasome for degradation/recycling, but that will happen as a little vesicle (or “liposome”); the misfolded protein, in this case, is not water-soluble (since, by definition, it has hydrophobic motifs which get “threaded through” a bilayer to create the transmembrane pattern), which means you won’t find it in the cytosol.
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drdoom
^footnote! : The movement of active* ribosomes from the cytosol to the Endoplasmic Reticulum is why we call that area of ER “rough Endoplasmic Reticulum (rER)”; on electron microscopy, that section was bespeckled with little dots; later, we (humans) discovered that these dots were ribosomes!
+1
drdoom
* By “active ribosomes”, I just mean ribosomes in the process of converting mRNA to protein! (What we call “translation” ;)
+1
wrongcareer69
How many goddamn ways are they going to test us on CF. I'm so over this!
+2
furqanka
also in FA, under alpha 1 antitrypsin, its says 'Misfolded gene product protein aggregates in hepatocellular ER". might be the same concept.
+9
joanmanuel26
According to Kaplan; All proteins that are synthesized in the ER must fold correctly in order to be transported to the golgi aparatus and then to their final destinations. If the mutation cause a misfolded protein, the result will be the loss of the protein function and, in some cases, accumulation of the protein in the ER.
+1
drdoom
@lilyo Thinking about this more. You will not find the (misfolded) protein in the cytosol. The misfolded protein may be inside a proteasome—and a proteasome may live in the cytosol—but the misfolded protein itself will never appear in the cytosol. The products of its degradation might (constituent amino acids or small peptides) but if you had an antibody for the misfolded protein and asked it “Where is the misfolded protein?”, the antibody would answer: “Most of what I could find appears to be in the rER.”
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amy
FA2020 47: " Absent or dysfunctional SRP (signal recognition particle) results in accumulation of protein in the cytosol"
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drdoom
@amy, that’s a good point but it assumes the protein is otherwise normal, i.e., not misfolded or “abnormal” in some other way
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amy
The dorsal vs ventral is confusing!
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waterloo
I Dont know what you mean by low EVV. But here's my thought process.
This pt lost lots of water, and when someone takes a laxative causing them to have diarrhea that will lead to metabolic acidosis. A buffering mechanism for the decreased bicarb in the blood is for H+ to leave cells and K+ to go into the cells. So he has to have hypokalemia (low K+ in serum). They gave him IV fluids, so his BP should be headed back to normal. I would think his RAAS will chill out. But it takes time to correct the acidosis, you're kidney won't just immediately stop reabs bicarb so you're body will still be buffering against the acidosis (H+ out of cell, K+ in).
+2
waterloo
sorry, I wrote increased bicarb, I meant DECREASED bicarb in the blood. And also should have written "you're kidney won't just immediately START reabs new bicarb" My Bad, wasn't trying to add to confusion.
+1
drdoom
i think by `EVV` author meant `ECV` (extracellular volume). @waterloo, appreciate the explanation but think something is off: loss of HCO3- via diarrhea should result in acidemia, which would oppose the presumption of ``H+ leaving cell, K+ going in´´.
+2
waterloo
hey so sorry, I must have been super tired posting this. Can't believe I made so many mistakes. Read over it again, and it sounds like gibberish. Wish there was a way to delete. My bad.
+1
waterloo
I think I tried to explain too hard. Looking at this question again, I think really the only this is when you lose that much volume, you lose bicarb and K+. Nothing really to do with acid-base. My b.
+1
castlblack
EVV = effective vascular volume. Thank you for trying to help but I still don't understand. I still agree with my above mechanism as correct. Whether or not it's most correct idk.
+1
amy
what about the long steamy bath? He also sweat a lot, and profuse sweating is going to cause hyponatremia?
+1
helppls
thats what I was thinking as well^^^ I figured he was sweating out a lot of NaCl
+1
icrieeverytiem
The Q mentions that he feels better after an infusion of fluids so I assumed any hyponatremia that he had must've been resolved.
+1
ht3
you're definitely not alone lol
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yotsubato
And its not in FA, so fuck it IMO
+1
link981
I guessed it because the names sounded similar :D
+18
yb_26
I also guessed because both words start with "glu")))
+30
impostersyndromel1000
same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle.
+1
jaxx
Not a clue. This was so random.
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mkreamy
this made me feel a lot better.
also, no fucking clue
+1
amirmullick3
My immediate thought after reading this was "why would i know this and how does this make me a better doctor?"
+10
mrglass
Generally speaking Glutamine is often used to aminate things. Think brain nitrogen metabolism. You know that F-6-P isn't an amine, and that Glucosamine is, so Glutamine isn't an unrealistic guess.
+6
taediggity
I literally shouted wtf in quiet library at this question.
+2
bend_nbme_over
Lol def didn't know it. Looks like I'm not going to be a competent doctor because I don't know the hexosamine pathway lol
+25
drschmoctor
Is it biochemistry? Then I do not know it.
+5
jesusisking
I Ctrl+F'd glucosamine in FA and it's not even there lol
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batmane
i definitely guessed, for some reason got it down to arginine and glutamine
+3
baja_blast
Narrowed it down to Arginine and Glutamine figuring the Nitrogen would have to come from one of these two but of course I picked the wrong one. Classic.
+2
feeeeeever
Ahhh yes the classic Glucosamine from fructose 6-phosphate question....Missed this question harder than the Misoprostol missed swing
+1
schep
no idea. i could only safely eliminate carbamoyl phosphate because that's urea cycle
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flvent2120
Lol I didn't either. I think this is just critical thinking though. The amine has to come from somewhere. Glutamine/glutamate is known to transfer amines at the least
+1
Circumflex artery(LCX) and Obtuse marginal artery(OMA) supply left ventricles ONLY. Acute marginal artery (AMA) supplies right ventricle ONLY.