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submitted by xxabi(123),

ARBs result in the following changes: increased renin, increased Ang I, increased Ang II, decreased aldosterone and unchanged bradykinin

famylife  ...and just to clarify, they directly inhibit the Ang II receptor (AT1) https://www.drugs.com/mmx/losartan-potassium.html +  
kpjk  I had a doubt- that wouldnt increased RAA lead to increased serum aldosterone as well. Now I understand that since the receptors are blocked- even the receptors to increase aldosterone secretion by Ang II would also get blocked... +  


submitted by madojo(24),

FA 19 256

Does the drug SWIM? Phase 1 - small number of volunteers assess for Safety Phase 2 - moderate number of patients, does it Work Phase 3 - large number random assignment, with placebo, any Improvement? Phase 4 - hit the market, any unexpected side effects, can be withdrawn from Market

kpjk  just would like to make a small correction phase 3- not placebo, but a drug already present in market so to test if there is improvement over standard care phase 2- would have the placebo, to see if the drug is actually working thats why i got confused in this question couldnt phase 2 also have randomized,prospective double blinded study +  
kpjk  Sorry! Just saw FA- it says even placebo can be used in phase 3 +  


submitted by madojo(24),

FA 19 256

Does the drug SWIM? Phase 1 - small number of volunteers assess for Safety Phase 2 - moderate number of patients, does it Work Phase 3 - large number random assignment, with placebo, any Improvement? Phase 4 - hit the market, any unexpected side effects, can be withdrawn from Market

kpjk  just would like to make a small correction phase 3- not placebo, but a drug already present in market so to test if there is improvement over standard care phase 2- would have the placebo, to see if the drug is actually working thats why i got confused in this question couldnt phase 2 also have randomized,prospective double blinded study +  
kpjk  Sorry! Just saw FA- it says even placebo can be used in phase 3 +  


submitted by colonelred_(54),

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 ... +3  
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 +2  
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 +  


submitted by divya(10),

okay but where in the question is it asking whether it's intention to treat or per protocol or as treated???

are we to assume its ITT if they don't mention anything or the part of the question that says "primary analysis" the giveway to ITT??

kpjk  I had the same doubt. I think if we were to consider "per protocol" then answer would have to be a mash of options A and B. There is no option that would be right for per protocol +  


The thing is, the spinothalamic tract crosses 2 vertebral levels up and then decussates at the anterior white commissure to get from the right to the left, so how do I know which vertebral level I'd be working on this guy?

chris07  I think the assumption here is that we are dealing with the cord section at the level of the problem. The picture is incredibly misleading. You have to orient yourself. The dorsal columns F, E, A, B are facing the patient's posterior. Once you properly orient it in 3D space, you know that what's labeled "right" is actually the patient's left, and what's labeled "left" is his right side. Super confusing. +1  
sne  The input arises in a limb/part of body at the level of lesion, enters through the dorsal root (pictured between A and B), decussates and ascends at the anterior commissure, and finally synapses on the second order neuron in the lateral spinothalamic tract. So the spinothalamic tract is responsible for contralateral pain and temperature sensation. So AT THE LEVEL technically would be in the dorsal column +2  
nwinkelmann  also, @chris07, I think you're wrong about the labels being wrong on the image. Becuase the spinothalamic tract = contralateral pain and temperature, and the patient's pain is on the right side, you would want to target the left spinothalamic tract for pain relief, i.e. the area labeled H. The area labeled D would be the right spinothalamic, purely because that is how the image is labeled. If you assume the label is different, you will get it wrong. +4  
kpjk  @sne I don't think entering from the dorsal root would be between A and B. It would be part of the gray matter so, lateral to B and F +  


O type patients have preform IgG anti A anti B. Not IgM antibodies "Shortly after transfusion" raise up suspicion for anaphylaxis. no sign of hemolysis-> favor anaphylaxis due to IgA deficiency=> effector cell is Mast cells

eclipse  they have IgG and IgM +  
kpjk  if it had been anaphylaxis- there would have been urticaria and pruritis +  


This is a keloid. In normal wound healing type 3 collagen is first synthesized and then degraded by Matrix metalloproteinase (a collagenase which uses Zinc as a cofactor) and replaced by Type 1. In a Keloid an excessive amount of disorganized Type 3 collagen persists. Therefore the defect is in Collagen synthesis (Type 1 synthesis)

dulxy071  Wouldn't Granulation tissue be the (more correct) answer since the initial collagen laid down for wound healing is Type III collagen which is consistent of granulation tissue? Collagen is a vast for so many types of itself as we know +2  
kpjk  @dulxy071 she had a surgery 3 months ago healing was fine even uptill 6 weeks ago so the abnormality occurred during remodeling- when type 3 is replaced by type 1 collagen, so the answer wouldnt be granulation tissue +2  


submitted by step1soon(18),

The reported incidence of Caplan syndrome is 1 in every 100,000 people. This has been a declining number due to lower exposure to coal, asbestos, and silica. Prevalence of Caplan syndrome is higher in patients with silica exposure compared to the other causes. The first epidemiologic study undertaken by the Pneumoconiosis Research Unit observed an increased prevalence of RA amongst men with progressive massive fibrosis (PMF). Miall et al. found no increased prevalence of rheumatoid arthritis in miners when compared to a community where PMF and rheumatoid arthritis were prevalent and therefore concluded that the etiology of RA was not associated with exposure to dust or lung changes of complicated pneumoconiosis. There was a high prevalence rate of PMF and tuberculosis amongst miners and ex-miners with rheumatoid arthritis.[4][5]

Pathophysiology: An autoimmune condition is a phenomenon where one's body has inflammatory cells which attack its own tissue and, in the case of RA, the synovium. It is believed that in these patients, there is an alteration which causes the increased immune response to foreign materials in the lungs. There is immune hyperactivity that is sparked by silica in which monocytes and macrophages release cytokines such as interleukin-1 and granulocyte-macrophage-colony-stimulating factor and tumor necrosis factor alpha. The sharp edges of the silica also cause lysis of lysosomal proteases in macrophages. Lymphocytes are activated by the cytokines released by macrophages. This all leads to an autoimmune phenomenon through exposure to silica which is triggered in genetically predisposed individuals who have RA.

wouldn't the underlying disease be RA which is then causing bronchogenic carcinoma? I'm confused!!

kpjk  i dont think its RA, because they said xray shows new bone formation, where as RA would have erosion +  


submitted by monoloco(75),

This is the only choice that comes close to nicking the thoracic duct, specifically at its inlet, the left subclavian.

kpjk  why not midsternal thoracotomy? +  
wuagbe  because the thoracic duct ascends the thorax posteriorly, and enters venous circulation from behind. link to image: https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/thoracic-duct +1