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submitted by hyoscyamine(21),

FA pg 217. Too much oxygenation can cause free radical damage leading to retinopathy of prematurity

mmm21  Okay i might be retarded, but why i can’t understand that they r asking about the thing that is damaged ? 😂😂 +2  
sahusema  Seriously! The question says "the goal of treatment is the protection of which of the following structures?" If too much O2 damages the retina, how is this treatment supposed to be protective to the retina? +  
ratadecalle  I think too much oxygen would be with the ventilator having a high FiO2 setting, which they don't mention here but I'm guessing thats the thing they're controlling to avoid oxygen toxicity? +  
burak  they didn't give the patient fio2 100%, question asks the reason for it. but in a very stupid way +2  
naught  Supplemental O2 may also cause bronchopulmonary dysplasia or intraventricular hemorrhage (germinal matrix, located in subventricular zone NOT choroid plexus) +  


submitted by neonem(257),

Major risk factor for aortic dissection is hypertension, and in this case might be due to cocaine use, which causes marked hypertension. Dissections cause a tear in the tunica intima -- blood can flow backwards into the pericardium and cause tamponade. This manifests as crackles in the lung due to poor left ventricular function (filling/diastolic problem due to compression).

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. +3  
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) +3  
garibay92  Does anyone know why is this patient's tepmerature elevated? +  
ratadecalle  @garibay92, not important for this question I think but cocaine can cause malignant hyperthermia +1  


submitted by assoplasty(39),

I think the concept they’re testing is the increased TBG levels in pregnancy, and not just hyperthyroidism in general.

When screening for hypo/hyperthyroidism, TSH levels are ALWAYS preferentially checked because they are more sensitive to minute differences in T3/T4. Often times TSH levels can demonstrate a change even when T3/T4 levels are in the subclinical range. The only exception to this would be in pregnancy (and I guess maybe liver failure? I doubt they would ask this though). High estrogen levels prevents the liver from breaking down TBG, leading to increased TBG levels in the serum. This binds to free T4, decreasing the amount of available free T4. As a compensatory mechanism, TSH levels are transiently increased and the RATE of T4 production is increased to replenish baseline free T4 levels. However the TOTAL amount of T4 is increased.

The question is asking how to confirm hyperthyroidism in a pregnant woman --> you need to check FREE T4 levels (because they should be normal due to compensatory response). You cannot check TSH (usually elevated in pregnancy to compensate for increased TBG), and you cannot check total T4 levels (will be increased). You got the answer right either way but I think this is a different reasoning worth considering, because they can ask this concept in other contexts of hyper-estrogenism, and if they listed “TSH” as an answer choice that would be incorrect.

hungrybox  Extremely thorough answer holy shit thank u so much I hope you ACE Step 1 +3  
arkmoses  great answer assoplasty, I remember goljan talking about this in his endo lecture (dudes a flippin legend holy shit) but it kinda flew over my head! thanks for the break down! +2  
whoissaad  you mean total amount of T4 is "not changed"? 2nd para last sentence. +  
ratadecalle  @whoissaad, in a normal pregnancy total T4 is increased, but the free T4 will be normal and rest of T4 bound to TBG. If patient is hyperthyroid, total T4 would still be increased but the free T4 would now be increased as well. +  
maxillarythirdmolar  To take it a step further, Goljan mentions that there are a myriad of things circulating in the body, often in a 1:2 ratio of free:bound, so in states like this you could acutally see disruption of this ratio as the body maintains its level of free hormone but further increases its level of bound hormone. Goljan also mentions that you'd see the opposite effect in the presence of steroids and nephrotic syndromes. So you could see decreased total T4 but normal free T4 because the bound amounts go down. +  


submitted by rocmed(-2),

Can't renal cell carcinoma cause invasion of the renal artery, obstructing blood flow (resulting in a bruit), thereby upregulating RAAS and increasing blood pressure?

rocmed  And isn't smoking also a risk factor for RCC? +  
lispectedwumbologist  It is but RCC tends to present later in life (6th or 7th decade). In a 55 year old smoker, atherosclerosis of the renal artery is am much more common cause of bruits +  
seagull  Hypertension is also a risk factor of an atherosclerosis leading to more inflammation. Eventually dilation (aneurysm) might occur... if im wrong then ignore this +1  
seagull  Hypertension is also a risk factor of an atherosclerosis leading to more inflammation. Eventually dilation (aneurysm) might occur... if im wrong then ignore this +  
illogical  Renal Cell Carcinoma has a tendency to invade the Left Renal **Vein** (Pg 134, Pathoma 2018). Thus it has an association w/ obstructed drainage of the Left Spermatic Vein leading to a varicocele. Renal artery stenosis is more commonly due to atherosclerosis (almost 85-90%) or fibromuscular dysplasia. +8  
ratadecalle  With RCC and renal vein invasion you would see B/L lower edema and venous collaterals in the abd wall (Uworld). Also he has a severe headache and confusion which are signs of a hypertensive emergency. +  


submitted by dragon3(4),

What's the difference between reactive granulocytosis vs lymphocytosis?

whossayin  Yes I’m at a loss for this one too. Still can’t figure out how we’re expected to differentiate those based on this slide shown. The only logical explanation that I can think of is that reactive lymphocytes may be seen in LYMPHOMAS as opposed to granulocytes which are seen in LEUKEMIAS Such a shitty way to trick us, hah! +  
henoch280  reactive lymphocytes are seen in EBV infection. you would see lymphocytes in the slide not neutrophils FA2018 pg 165 +3  
whossayin  That makes sense.. but was the question talking about EBV infections or hematological malignancies? Just a vague question I wasn’t really sure what exactly was it trying to teach us, I guess the reactive lymphocytosis just threw me off! Anyways, thanks for the clarification buddy! +  
ratadecalle  They way I thought about it was: Granulocytes: multi lobed nucleus Lymphocytes: single lobe +2  
hello  @whossayin - it's not reactive lymphocytosis because there are no buzzword type symtoms of EBV in the Q stem. Also, reactive lymphocytes look way different. +