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Comments ...

 +0  (free120#27)

No idea if this is the right logic but: Start with a punnett square. We know there are 4 alleles ass. with alpha-globins. TBH, i'm not sure why, but i think of them as received together. So i used the following nomenclature:

A/ B/ C/ D = normal Ao / Bo = abnormal.

Mom has one mutation, so AoBCD x ABCD Dad had two mutations, one on each chromosome (trans): AoBCD, ABoCD

Crossing them together:

AoBCD x AoBCD = Hit (two mutations, oppisite chromosomes) AoBCD x ABoCD = hit (two mutations, oppisite chromosomes) ABCD x AoBCD = non-hit ABCD x ABoCD = non-hit - therefore, 50% chance of having a trans mutation in the offspring.


 +1  (free120#29)

So mad.. these don't even look like neutrophils! They all have what look like are 2 lobes.

I couldn't make heads or tails of what they were. I ended up thinking they were eosinophils (bilobed), even if they weren't exactly fileld with granules lol.

So much pain.


 +0  (nbme21#10)

My dumbass thought it was Large Cell cancer, for which i had no associated paraneoplastic syndrome. Yay.


 +0  (nbme21#29)

This question is pretty dumb... I feel like if he was running 12 miles obviously his SymNS will be thru the roof already. My thinking was that the lightheadedness may be the result of sympathetic fatgue, and hence, could fall.

Obviously, ParaNS activity and Carotid impulse will decrease... But those who run know the bear of running long distances on a hot day.

an_improved_me  I always harken back to "don't overcomplicate these questions", but sometimes, NBME requires making some leaps of logic. The trick is knowing when the question requires such a leap... I haven;t gotten very good at that. +

 +0  (nbme21#37)

So i found this question ridiculous... the explanations provided did not really clear it up for me, but i think i understand it now (please correct me if i'm wrong).

First and foremost, I'm not even sure if this is truly a lineweaver-burke plot, since the X-axis is not 1/Km.

But, more generally, I tried to understand what happened at both extremes of [PLP] and Velocity.

PLP: Ask yourself: where on the graph is [PLP] highest? Well, if the X-axis is equal to 1/PLP, PLP would be at its highest at the value closest to 0 on the x-axis. (think: what is 1 divided by a billion? VERY CLOSE TO ZERO). This would correspond to a point along the y-axis for the enzymes activity. In other words, PLP is at its highest concentration at the graphs Y-intercept.

Remember what we also said: when the mutated enzyme is around lots of PLP, it basically functions like a nml enzyme. This means, that the Vmax of the mutated enzyme is equivalent to the Vmax of the normal enzyme. Therefore, The 1/Vmax of both enzymes are equivalent... at the y-intercept! This is big! If you get this far, then you can eliminate (A) and (D), since these graphs have different Y-intercepts (different V-maxes) for their respective enzymes.

Moving on...

Velocity (V): When V is at its highest (i.e. Vmax), the value of 1/V would be at its lowest. (Again: think of it practically: what is 1 divided by 1 billion? ~0!) Therefore, the value of 1/V is at its lowest when the y-axis is equal to 0. Therefore, The Vmax of this occurs when the y-axis is close to zero... Heres the thing tho.. these enzymes require different levels of PLP to operate at V-max. Remember, the V-max of the MUTATED enzyme will happen at a much HIGHER [PLP]. Or conversely, the V-max of the NORMAL enzyme will happen at a much LOWER [PLP]...

an_improved_me  Meaning, when we look at the X-intercept (when V is highest), the mutated enzyme will require more PLP. More PLP means a "lower" value on the x-axis (closer to zero) relative to the normal enzyme. +
an_improved_me  Putting it ALL together: y-intercept will be the same for both mutated/normal enzme x-intercept will be closer to 0 for the mutated enzyme, relative to the normal enzyme. The only answer that has both correct relationships is (B). I think i spent 5 minutes on this question trying to figure it out. I probably would have needed 10 minutes to actually get there. Hopefully now I can get it quicker if something like this shows up on the real thing. +

 +0  (nbme21#11)

Question: even if this pt did have myocardial rupture... is that even a cause of death? I feel like like the mechanism of death in myocardial rupture is cardiogenic shock; blow a hole in your heart, and suddenly it aint pumping so well. Just asking for future reference.


 +0  (nbme21#28)

ANother way to get at it is via elimination:

A. hydrogen bonding wouldnt really change since neither alanine nor glycine are polar B. Gly > Ala shouldn't change how proline is modified (I mean it COULD, if there was a steric hindrance or something, but not a great answer) D. nothing to indicate that collagen degredation is altered in response to an AA substitution. Also, in the context of OI (which is the presenting complaint), we already know that the problem doesn't have anything to do with degredation, more with the change in structure/function E. Honestly don't know.


 +0  (nbme21#26)

Fucking shit the cecum is not a part of the ascending colon


 +0  (nbme21#47)

Honest question: Why does it matter what pattern of inheritance it has? For all we know, its multi-factorial/can't be determined.

I feel like the easiest way to answer it is: acknowledging it is "uniformly fatal to males in-utero" = 0% chance for males; and legit just counting the fraction of females in generation III that have the disease = 4/6 ~50%.


 +0  (nbme21#37)

@blackcoffee;

Insulin does play a role in bringing back K+ into cells via modulation of K+/H+ exchange. This is because it helps to address the ketoacidotic state of the patient. By bringing pH closer to baseline, there is return of K+ into the cells, while H+ comes back out of the cells.

an_improved_me  However, you are right, in that too my knowledge, that is not the main way insulin influences K+; it is more via the NaATPase as you have mentioned. +

 +0  (nbme21#2)

Might be a dumb question but... Can patients normally breathin on their own if givne succinylcholine?

trazobone  Yes! Normal people will have an adequate level of pseudocholinesterase to break down the succinylcholine and eventually cease its effects. But if your question is, will succinylcholine still inhibit breathing in a normal person, yes it will. It will work to paralyze muscles (like your diaphragm) in both a normal person and in someone with the pseudocholinesterase deficiency. The main issue is the ability to eventually break down the succinylcholine and come out of the paralysis +

 +0  (nbme21#18)

I totally get how asking about suicide, and asking about it directly is important. But my confusion is how this answer doesn't provide any good segue. I went with "has it come as a surprise..." because i figured that would lend itself nicely to the patient opening up. When i feel it is appripriate, i would then bring up the conversation about self-harm, harming the baby, and suicide. But as its written, the patient tells you they feel shitty, and the physician very directly says "wow you feel pretty shitty". Seems very insensitive and not optimal for honest communication.

an_improved_me  Also, while i hear some people saying that making it seem like her problems aren't unique... well thats actually the point in a lot of conversations with patients-- making them feel not alone. I don't think i would feel great knowing that all other parents instantly love their kids, and have no problems taking care of them. Instead, I'd want to feel like whatever i'm feeling isn't abnormal and unnatural. "I feel like a bad parent"; "that's rare, most people feel like great parents" "thanks doc". Yikes. +

 +2  (nbme21#12)

I would have easily chosen granulomatous colitis... had i known it is the same thing as Crohns. Shout out to ignorance and its bliss.


 +0  (nbme21#15)

Just to add another piece that i think may be worth considering.

Endoscopy is showing gastric varices specifically. In the cases I've encounterd gastric varices due to portal HTN, it relates to the connection between the splenic circulation and the epiplogic/short gastric veins (similar path i think for arterial circulation).

Consequently, gastric varices can be treated by altering the splenic (portal) circulation to a systemic circulation. In this case, the answer was l. renal.


 +0  (nbme21#25)

Since AgII also affects the proximal tubular Na+/H+ antiport, would (A) also be a correct answer if it didn't say "most effected"?


 +0  (nbme21#39)

I feel the wording is god-awful.

It makes it sound like cortisol increases the interaction between a given beta-agonist and its receptor. In reality, it increases the number of receptors, without changing the interaction between them. For me, this was an elimination of everything else, and choosing the least terrible answer.


 +0  (nbme21#40)

Question: based on what we know about the hypothalamic nuclei, would the effect mostly be ont he posterior or anterior nuclei?

Posterior = Heating, so is it being stimulated? Anterior = Cooling, so is it being inhibited?


 +0  (nbme21#43)

Initially i was stuck between embelectomy and fasciotomy, mainly because the pt did seem to have some symptoms of compartment syndrome: pain, pulseless, pallor, perishing cold (remember 6Ps) so i thought maybe fasciotomy could be an answer.

However, fasciotomy is something that would usually occur due to neurovascular compromise, which commonly happens from trauma. So i went with an embolus, since the pt had irregularly irregualr rhythm, prediposing to thrombus/embolus forming, with eventual occlusion.


 +1  (nbme24#35)

I figured since the answer was mis-spelled, it couldn't be the answer.


 +0  (nbme24#10)

clench my external sphincter any time i see answers with muscle names like mylohyoid, digastric, levator veli palatini...


 +0  (nbme24#42)

Another thing... Isn't it possible that both the sweat chloride test and the immunoreactive trypsin are just false +? Both of these tests have pretty low threshold for returning as a + response. Why can't it be possible that one allelic mutation is enough to cause a positive result in these tests, without actually signifying the pt has a disease? My only guess is that since two answers indicate that there could be a false positive, neither can be the right answer.


 +0  (nbme24#10)

What's all that anechoic stuff on the left side of the CT?


 +0  (nbme24#48)

Question i have is:

Does it matter if the cardiomypathy is eccentric vs. concentric? I feel like it might.

This pt likely has concentric cardiomypathy (i.e. diastolic), as others have mentioned, due to chronically untreated HTN. This leads to a decreased LV chamber size, and difficulty with myocardial relaxation. So my question is... If the problem in this pt is one of relaxation, and not so much of contraction. In this case, to me it would make sense to some extent, that LV EDV would actually be relatively decreased.

In fact, diastolic heart failure is associated with preserved EF (SV / EDV); this is both due to a decrease in SV and EDV.

I completely understand how EDV would increase in the ase of systolic (eccentric HF). The dilated heart can readily accept blood, but has problems pumping it out (i.e. decreased SV with an increased EDV. Let me know what you all think.

an_improved_me  I made a mistake above ^, this pt has a sytolic heart failure (despite chronic HTN...) as the question states it clearly ("echo shows decreased LV systolic function") +

 +2  (nbme24#40)

I feel like its these kinds of questions that really make a test-taker succeed. You could have studied your whole life for Step 1, and then...come up against a question like this. Its testing concepts that you're familiar with (e.g. Beta-thalassemia, genetics), but in a way that isn't something you'd ever directly learn. You have to stay calm, analyze what you know, what the question is asking, create a strategy to answer, and look at which answer is best.

I envy some of you!!


 +0  (nbme24#7)

I'm sorry but... where in the cytoscopy are the fibrovascular cores demonstrated? Are they visible?

an_improved_me  ok... i'm blind. it is literally just the projections... i thought I was missing some fine detail. +

 +0  (nbme24#30)

A question i more generally have is...

Is it possible that when you stratify the data, (i.e. comparing the effect that eating cookies has, in people who drink milk or people who do not drink milk) that the odds ratio will show significance for one but not the other?

Said differently, in the example above, could eating cookies in people who drink milk lead to a significant increase the risk of infection, but not in people who who didn't drink milk?

I've looked around in this comment thread, and have seen people mention the term "effect modification"; is that what my example above would show?

In other words, if eating cookies + drinking milk leads to a significant risk, but eating cookies + not drinking milk has no associated risk, would that mean that the milk has an "effect modification" on the risk of getting infection in people who eat cookies?


 +0  (nbme24#43)

Another thing to note: they could have made this question even trickier by asking whether or not you know which leads are associated with which arteries. This person had LAD and RCA stent placement. That means that they could have given you leads II, III, aVF (for RCA probs) or V1-V6, I, aVL (for LAD probs) and make you choose based on that.

This question was easier since all answers are regarding the RCA.


 +1  (nbme24#23)

The frustrating thing about this is that if you are familiar the biochem, you can get really stuck between D and E.

D would really be assocaited with SuccinylCoa Synthesis, as Methylmalonyl-Coa is the precurser to SuccinylCoa, which is an important gluconeogenic intermediary. Knowledge of biochem could make you think that the racemase is an important intermediary enzyme that is required for the MMA-mutase to even work (i.e. the product of PropionylCarboxylase is not the right chiral structure for it to work, hence the need for a racemase).

Ultimately, although the logic stands, I guess its better to go down the route of less logical leaps. It is better to know that hypoglycemia leads to neurogenic and neuroglycopenic Sx, the former being the autonomic response to increase glycemia. In that case, epi, which is an importnt hormone that metabolizes energy, is needed. PNMT generates Epi from NE.


 +2  (nbme24#26)

I think its also help to eliminate the other answers.

Adrenal fasciulata cells (producing adrenal androgens) can be eliminated b/c this pt has adrenal androgens in the normal ranges. If you wanted to make the leap that adrenal androgens could be peripherally converted to stronger androgens (testosterone/DHT), then the inciting adrenal androgens should also be elevated.

Glomerulosa: would produce aldosterone. Though we aren't given her aldo levels, her Sx wouldn't match a Conn's syndrome picture.

Ovarial Follicle cells: have the enzymatic machinery to produce androstenedione (theca cells, its downstream cholesterol product, DHEA, is not elevated) and estrogen (granulosa cells), which doesn't fit the clinical picture this pt has.

Acidophilic hormones (prolactin/GH) are not consistent with this pt clinical picture (like gigantism, galactorrhea)

Basophil (all the others) again, not consistent, even with the gonadotropic cells, since we see LH is low. That leaves you with (D), which as others have pointed out, is consistent with this pt's presentation.


 +0  (nbme19#9)

First recognizing her Dx just with Sx.

T1DM with confusion/sleepiness, tachycardia/tachypnea, hypotension and oliguria. All of this screams DKA with compensatory response. Confirmed by looking at her Glucose of 900.

She's given saline + insulin. Note: she would be given K+ if her K+ values were anything below 5meQ/L.

When you give insulin, you'll of course decrease glycemia, which will improve DKA. This will improve her acid/base metabolism back to normal (increase in bicarb, increase in pH). Consequently, pCO2, which was initially compensatory decreased (hyperventillation as a respiratory alkalosis). Insulin also activates Na/K+ pumps, leading to return to baseline (decrease).

Saline will help the pts hypovolemia, and consequently, her pre-renal azotemia (likely, we aren't giving Cr, but given her low volume state, we can assume its normal). Therefore, BUN will decrease, as RBC increases.


 +0  (nbme19#23)

More generally, i think PCWP increases due to tamponades ability to cause genererilzed equilibration of heart pressures across all 4 cardiac chambers. From the following link: https://www.mcgill.ca/criticalcare/teaching/files/pericardial-tamponade

"pericardial pressure is distributed equally among all chambers since pericardial fluid is free flowing. This reduces gradients between chambers throughout diastole. This is inconsequential in small effusions, but becomes hemodynamically significant in large effusions, in which greater pressure in the pericardium is transmitted to all four cardiac chambers, resulting in 'equilization of central pressures'"


 +1  (nbme19#22)

Also, to eliminate the other options:

Hypoventillation would have an increased pCO2 and decreased pO2.

High altitude wuold have low PO2, low pCO2 (Hyperevntillation)

V/Q mismatch would also have a low pO2 and high pCO2, since gases are exchanging.

Hyperventillation would have a normal PO2 and low PCO2


 +0  (nbme19#13)

Remember "Dude Is Just Feeling Ill, Bro", for the segments of the small intestine and what they reabsorb: Dude Is | Duodenum Iron Just Feeling | Jejunum Folate Ill, Bro | Ileum, B12 / Bile

Therefore, this person is at risk for losing lots of bile, and therefore fat, which predisposes to Fat-soluble Vitamin Defcieincy


 +0  (nbme19#0)

Pharyngeal arch question, or more easily understood as a DiGeorge question... The thymus arises from the 3rd arch, which is why in DiGeorge (loss of 3rd/4th) you have no thymus


 +0  (nbme19#46)

Feel like this question is actually pretty tough. I mean, I think of Pagets causing:

Enlarged Head (e.g. hats won't fit) Chalk stick fractures (we don't see any fractures on this guys X-rays, and his backpain is due to sclerosis of his vertebra [not fractures]) High output HF (due to AV shunts); Hearing difficulties (none of thet in his guy) Osteosarcoma

Only thing we're given is that he has verebral cortical thinning, which could be d/t lots of stuff. He's old (RF) and that's about it.


 +0  (nbme19#36)

i usually think about it as: a pt with multiple episodes of Sx similar to Heart attack that resolve on their own, and a completely benign workup.. >> panic disorder


 +0  (nbme19#6)

I guess a couple of key things are:

He is hyponatremic and shows signs of hyponatremia (tonic-clonic seizures, somnolence.

He shows signs of over-hydration (low specific gravity of urine, and low urine osmols).

He then is placed on fluid restriction, but breaks the test by not following doc orders.

The question isn't tricky so much by what it's asking, but more based on what it isn't telling. It does not tell you his fluid status, his urine ouput, his fluid input, what meds he is given, etc.





Subcomments ...

submitted by notadoctor(159),
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If uyo erwe kcust tbenwee oag(asmrlncnhimCodo)naatr dna Emrongnho(enicn)bad mrremebe macdesrnhnoo amy eeord the cerxto ubt can rnvee tsnvrdiuapi/ed eht er.xtoc I hitnk ihst wsa eht nostitdcnii the sonteuiq was gine.tst

an_improved_me  Also: Enchondromas are most common in young males (liek 20s) whereas chondrosarcoma are most commin in middle aged men (esp. hips) +  


submitted by mcdumbass(22),

I thought thought measuring a gas in the blood only measures partial pressure of dissolved gas in the blood

schistosite  Yeah, me too...the fact that they expect us to assume that HCO3- is counted in their measurement for CO2 concentration is absolutely absurd. +2  
happyhib_  they tell you measured is around 24 and 22 or some bs but give "mM"; if you look at the lab sheet HCO3 has a units in mM and normal is 22-28 = they are not just looking at partial pressure's. +1  
an_improved_me  Yea,.. Suprisingly in clinic, when you are measuring important parameters in the blood (think fish-bone diagram), you actually use HCO3- as an approximation for CO2 in the blood (so you use the value in CO2 when calculating like the anion gap or something) +  


This question is pretty dumb... I feel like if he was running 12 miles obviously his SymNS will be thru the roof already. My thinking was that the lightheadedness may be the result of sympathetic fatgue, and hence, could fall.

Obviously, ParaNS activity and Carotid impulse will decrease... But those who run know the bear of running long distances on a hot day.

an_improved_me  I always harken back to "don't overcomplicate these questions", but sometimes, NBME requires making some leaps of logic. The trick is knowing when the question requires such a leap... I haven;t gotten very good at that. +  


So i found this question ridiculous... the explanations provided did not really clear it up for me, but i think i understand it now (please correct me if i'm wrong).

First and foremost, I'm not even sure if this is truly a lineweaver-burke plot, since the X-axis is not 1/Km.

But, more generally, I tried to understand what happened at both extremes of [PLP] and Velocity.

PLP: Ask yourself: where on the graph is [PLP] highest? Well, if the X-axis is equal to 1/PLP, PLP would be at its highest at the value closest to 0 on the x-axis. (think: what is 1 divided by a billion? VERY CLOSE TO ZERO). This would correspond to a point along the y-axis for the enzymes activity. In other words, PLP is at its highest concentration at the graphs Y-intercept.

Remember what we also said: when the mutated enzyme is around lots of PLP, it basically functions like a nml enzyme. This means, that the Vmax of the mutated enzyme is equivalent to the Vmax of the normal enzyme. Therefore, The 1/Vmax of both enzymes are equivalent... at the y-intercept! This is big! If you get this far, then you can eliminate (A) and (D), since these graphs have different Y-intercepts (different V-maxes) for their respective enzymes.

Moving on...

Velocity (V): When V is at its highest (i.e. Vmax), the value of 1/V would be at its lowest. (Again: think of it practically: what is 1 divided by 1 billion? ~0!) Therefore, the value of 1/V is at its lowest when the y-axis is equal to 0. Therefore, The Vmax of this occurs when the y-axis is close to zero... Heres the thing tho.. these enzymes require different levels of PLP to operate at V-max. Remember, the V-max of the MUTATED enzyme will happen at a much HIGHER [PLP]. Or conversely, the V-max of the NORMAL enzyme will happen at a much LOWER [PLP]...

an_improved_me  Meaning, when we look at the X-intercept (when V is highest), the mutated enzyme will require more PLP. More PLP means a "lower" value on the x-axis (closer to zero) relative to the normal enzyme. +  
an_improved_me  Putting it ALL together: y-intercept will be the same for both mutated/normal enzme x-intercept will be closer to 0 for the mutated enzyme, relative to the normal enzyme. The only answer that has both correct relationships is (B). I think i spent 5 minutes on this question trying to figure it out. I probably would have needed 10 minutes to actually get there. Hopefully now I can get it quicker if something like this shows up on the real thing. +  


So i found this question ridiculous... the explanations provided did not really clear it up for me, but i think i understand it now (please correct me if i'm wrong).

First and foremost, I'm not even sure if this is truly a lineweaver-burke plot, since the X-axis is not 1/Km.

But, more generally, I tried to understand what happened at both extremes of [PLP] and Velocity.

PLP: Ask yourself: where on the graph is [PLP] highest? Well, if the X-axis is equal to 1/PLP, PLP would be at its highest at the value closest to 0 on the x-axis. (think: what is 1 divided by a billion? VERY CLOSE TO ZERO). This would correspond to a point along the y-axis for the enzymes activity. In other words, PLP is at its highest concentration at the graphs Y-intercept.

Remember what we also said: when the mutated enzyme is around lots of PLP, it basically functions like a nml enzyme. This means, that the Vmax of the mutated enzyme is equivalent to the Vmax of the normal enzyme. Therefore, The 1/Vmax of both enzymes are equivalent... at the y-intercept! This is big! If you get this far, then you can eliminate (A) and (D), since these graphs have different Y-intercepts (different V-maxes) for their respective enzymes.

Moving on...

Velocity (V): When V is at its highest (i.e. Vmax), the value of 1/V would be at its lowest. (Again: think of it practically: what is 1 divided by 1 billion? ~0!) Therefore, the value of 1/V is at its lowest when the y-axis is equal to 0. Therefore, The Vmax of this occurs when the y-axis is close to zero... Heres the thing tho.. these enzymes require different levels of PLP to operate at V-max. Remember, the V-max of the MUTATED enzyme will happen at a much HIGHER [PLP]. Or conversely, the V-max of the NORMAL enzyme will happen at a much LOWER [PLP]...

an_improved_me  Meaning, when we look at the X-intercept (when V is highest), the mutated enzyme will require more PLP. More PLP means a "lower" value on the x-axis (closer to zero) relative to the normal enzyme. +  
an_improved_me  Putting it ALL together: y-intercept will be the same for both mutated/normal enzme x-intercept will be closer to 0 for the mutated enzyme, relative to the normal enzyme. The only answer that has both correct relationships is (B). I think i spent 5 minutes on this question trying to figure it out. I probably would have needed 10 minutes to actually get there. Hopefully now I can get it quicker if something like this shows up on the real thing. +  


submitted by nwinkelmann(294),
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In caes nneyao si a eesdn sa I ma nad jsut dndti' trrdd/aeneuesemnmbr htwa tyxeacl xaoiyrrept wofl is = 1FE.V nI etisrcverit insdoocnt,i FVE1 is mlarno or eicsndrae eud to eeesadcdr VC.F eiasinItltrt fissiorb = sdenreiac yraaiw ahanmcrpey oscadflf udnaor the ,ysraawi hhicw si awth pvoisdre laiard .tctaoirn hTe etregar hte laaidr rt,aicont het lrweo het lpcsailnog re,ocf nda so iyoaxprrte fowl is sni.reaecd

champagnesupernova3  FEV1 is increased due to greater recoil of the lung tissue. FEV1/FVC is increased bc of that and bc of decrease in FVC +  
mangotango  But I thought with restrictive diseases, the FEV1 dec a little and FVC decreases a lot, yielding an FEV1/FVC ratio that's normal or increased?? +1  
an_improved_me  Yea the OP is wrong here. FEV1 does NOT equal expiratory flow rate. FEV1 is not a really a rate; its a volume of air pushed out in 1 second specifically. This will be decreased in a pt with ILD. This is because the volume of the lung decreases (due to increased elastic recoil). Expiratory flow rate (in this question) will be elevated, b/c of the answer stated. From uworld: "[fibrosis] causes increased lung elastic recoil, as well as airway widening due to increased outward pulling (radial traction) by surrounding fibrotic tissue. The resulting decrease in airway resistance leads to supernormal expiratory flow rates (higher than nromal when corrected for lung volume)". +  


submitted by assoplasty(94),
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I hktni teh pctocen hyet’re ntestig si eht eidrsnace BGT evsell in n,prceaygn adn otn sujt ymseiprtridyohh ni egr.aeln

Wehn ngenrceis orf orrhpeoyt,/hhdyiyspmi HTS evesll rae LAAWYS inyeerfetrlpal kdecech ueebcas yeht are remo ieistsenv ot tnueim efeendsficr in ./34TT tnefO isetm STH lvlees anc rdtsneameot a ncgeha eevn hwne /34TT llevse rae ni hte icnaclsbilu rneag. Teh lony ctinxepoe to hsit uwdol be ni garynnecp (and I esusg ebyam lriev ifur?ale I dtbou ehyt ulwdo kas hsti )hhtgou. igHh ngesroet slvele eesvntpr het ievlr form nrgbkaie odnw BG,T dlnaieg to cnsderaie TBG elvles in hte .ersmu hiTs bsndi to eerf ,T4 deneasircg the natmou of lbevlaaai free .T4 sA a esocymrapnot mhemc,ains STH vselel aer tnaeinrytsl recsdnaie nda hte TERA fo T4 niprocuotd si cseidraen to hisrneple siealnbe erfe T4 elsv.le revwoeH het OTATL mounta fo T4 is eiances.rd

heT nestoiuq is kasgni woh to nrcfoim yiiyhtopdhrsmre ni a natpnerg onawm -g-;&t ouy eend ot echkc EERF T4 slvlee eecsuab( teyh sulodh be aonrlm due to rmosenoctapy rno.sps)ee uYo atnnco hckec SHT yulsua(l laevdete in naepryngc ot acnptesome rof drcseaien BGT,) adn ouy nncota hccke aoltt 4T ellves (iwll be ei.dnae)crs uoY ogt teh awenrs hgtri ietehr awy ubt I nthki hist is a fifredten ioeasngrn twohr soigcier,dnn ceaseub eyht can sak thsi necopct ni rteho nstxteco fo setrhernseipy-,mog adn if they sidlet HS“T” sa an nrewas iecohc atth ouwdl be rcri.nceot

hungrybox  Extremely thorough answer holy shit thank u so much I hope you ACE Step 1 +8  
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. +1  
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. +1  
lovebug  Amazing answer! THX +  
an_improved_me  Just to add: Pregnancy is not an exception to using TSH in suspected hyperthyroid pregnant patients (not sure in hypothyroid); you would still get a TSH first, and if its unusually low, you would then proceed to measure T4 (free, total), and so on. https://www.uptodate.com/contents/hyperthyroidism-during-pregnancy-clinical-manifestations-diagnosis-and-causes?search=hyperthyroidism%20in%20pregnancy&source=search_result&selectedTitle=2~150&usage_type=default&display_rank=2#H994499 +  


9 lb isn't that big of a baby... I made it out okay. Definitely should've made the baby bigger to make the answer more clear

swagcabana  More than 8 lbs is by definition macrosoma +  
nifty95  Shawn Carter was born December 4th Weighing in at 10 pounds 8 ounces He was the last of my four children The only one who didn't give me any pain when I gave birth to him And that's how I knew that he was a special child +5  
an_improved_me  Legend +  


submitted by taway(31),
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oDse ydbyoan tnnresduda yhw ew are ldewoal ot rrneefeti hwit het cailnlci iieckgoimsdnan fo wot rtoeh apilsteicss ldt?yeric nWludto' atht duymd eth atrews neve meor by ignadd our nn?ooipi I to'dn see teh irnuegdynl icpiplner htta lsinpxae het aatoelnir in isht .ensawr

jcrll  I think it's about adding our opinion and more about seeing what the situation is because a patient contacted you in distress. The others are about contacting management off hearsay; that could also "muddy the waters," I Is this question also addressing quaternary prevention? +1  
meningitis  I agree with jcrll. My same thought process but then I changed it to psychiatric consultation in order to first attend the patient's distress and anxiety since it was hindering her decision making. Besides, the whole ordeal about her treatments and ineffectiveness was emotionally and physically exhausting her. +2  
vi_capsule  Referral is NEVER a answer +10  
tsl19  Going straight to the chair of the ethics committee without having spoken to the other physicians would be inappropriate because it would be jumping a bunch of steps in communication first - like jcrll said, you want to get the picture of what's going on from the other physicians first. Maybe the gynecologic oncologist isn't actually as opposed to palliative measures as the patient perceives him to be and thinks he's doing what the patient wants, etc. It could just be miscommunication, which you could help clear up without getting ethics involved ... better to start there. +10  
an_improved_me  Also, to add a little bit: internists on a healthcare team are the care coordinators. For any given problem a patient has, the internist is responsible for managing all the different aspects of a patients treatment. In this case, the intern has to manage the dissenting opinions of her different gynecologists. In other instances, an internist may have to manage the disagreement between a Surgeon vs. IR vs. Onc. +  


@blackcoffee;

Insulin does play a role in bringing back K+ into cells via modulation of K+/H+ exchange. This is because it helps to address the ketoacidotic state of the patient. By bringing pH closer to baseline, there is return of K+ into the cells, while H+ comes back out of the cells.

an_improved_me  However, you are right, in that too my knowledge, that is not the main way insulin influences K+; it is more via the NaATPase as you have mentioned. +  


submitted by sweetmed(144),
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hTe thmtcaiocce aofrstc rddocuep yb etcnsmooy nad tams llcse nda eht lloca daaosiaotvilnt teslsiamtu hceiprtnulio comxih.tesa ols,A eoehiadtnll llsec vcitoaaitn treuhrf ravtasegag eth imnatyorfmla seseopnr dna oitiragmn fo enlstopiu.rh isTh leads ot na iulxnf of nehliuoptrs .ylaclol

e:ercenrf m./Ccwm/t5i/b/ctl:wwth5/e/1vngonPirs.25nliscM1a.hpp2.

bronchophony  Why not complement activation? +1  
joyceeepan  the way i though about it was: you need antibodies (IgG/IgM) to activate the complement system. But there's no such a thing as an anti-gout antibody. (and it is not an infection neither) +1  
an_improved_me  Thats not exactly true for a couple reasons. I saw a UWorld question that said something along the lines of an ApoProtein being useful b/c it binds the urate crystals, and makes it less likely for the crystals to be opsinized/recognized by neutrophils. Therefore, Abs do play a role. Secondly, you can have activation of coplement via the alternative pathway, which does not require ABs. +  


submitted by nosancuck(87),
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yuo okwn woh it is dzee siob got dta lcaiaf USFHL edu to xarteeln sntautmili

dr.xx  please use standard English. I cannot understand a word of what you are saying. +8  
aishu007  FA pg 468, facial flushing due to external stimuli like spicy food. InAammatory fac ial skin disorder characterized by erythematous papules and pustu les 0 , but n<> comedones. May be associated with fac ial Rushing in response to external stimu li (eg, alcohol, heat). Phymatous rosacea can cause rhinophyma (bu lbous deformation of nose). +2  
madisonivy  https://madisonivy.online/ +  
madisonivy  madison ivy +  
an_improved_me  Didn't know Madison was getting her MD; same as Dr. Johnny Sins! +  


I totally get how asking about suicide, and asking about it directly is important. But my confusion is how this answer doesn't provide any good segue. I went with "has it come as a surprise..." because i figured that would lend itself nicely to the patient opening up. When i feel it is appripriate, i would then bring up the conversation about self-harm, harming the baby, and suicide. But as its written, the patient tells you they feel shitty, and the physician very directly says "wow you feel pretty shitty". Seems very insensitive and not optimal for honest communication.

an_improved_me  Also, while i hear some people saying that making it seem like her problems aren't unique... well thats actually the point in a lot of conversations with patients-- making them feel not alone. I don't think i would feel great knowing that all other parents instantly love their kids, and have no problems taking care of them. Instead, I'd want to feel like whatever i'm feeling isn't abnormal and unnatural. "I feel like a bad parent"; "that's rare, most people feel like great parents" "thanks doc". Yikes. +  


submitted by drschmoctor(95),

How does one differentiate factitious disorder from being thirsty w poor impulse control?

therealslimshady  If you're asking how to rule out diabetes insipidus, I think it's because: Diabetes insipidus is caused by a lack of ADH effect, so they will be peeing out too much water, thus making them dehydrated and hyperosmolar (thirsty). This CHF patient is presenting with signs of fluid overload +3  
an_improved_me  I think that ADH also has affects on central structures that increase thirst? Or is that only Angiotensin II? +  


submitted by neonem(571),
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loatSol si a eytp III ricaartyhtmhni K+( lbgncaokhe-cni)ln tath lsoa sah b-rblotackee ctiatvyi pTey( II ymiacrrit)hntah. sThi xpelanis eth eeedadcrs tatrehrea adn odolb rpureses t-(a1eb bgkolnci vic,atiyt) wiht eth QT tnpnoalirogo - all epty III ADAs cusae TQ r.noltpgiaono

abhishek021196  Would like to add that the IA antiarrythmics = Quinidine, Disopyramide, Procainamide also prolong QT interval and can lead to tosades de Pointes and they would most likely present with Cinchonism (headache, tinnitus with quinidine), reversible SLE-like syndrome (procainamide), HF (disopyramide), thrombocytopenia. The decreased HR and BP point towards Sotalol. +4  
armageddon_oh  Im glad you can regurgitate sketchy but none of those drugs were options here. It's as simple as which of these can cause torsades. +6  
an_improved_me  Lol why the salt ^? I'm sure to some people, this was a useful reminder of the side-effect profile of these drugs (spaced repetition), and was likely helpful for the poster (again, spaced repetition) Its all love! +4  


Question i have is:

Does it matter if the cardiomypathy is eccentric vs. concentric? I feel like it might.

This pt likely has concentric cardiomypathy (i.e. diastolic), as others have mentioned, due to chronically untreated HTN. This leads to a decreased LV chamber size, and difficulty with myocardial relaxation. So my question is... If the problem in this pt is one of relaxation, and not so much of contraction. In this case, to me it would make sense to some extent, that LV EDV would actually be relatively decreased.

In fact, diastolic heart failure is associated with preserved EF (SV / EDV); this is both due to a decrease in SV and EDV.

I completely understand how EDV would increase in the ase of systolic (eccentric HF). The dilated heart can readily accept blood, but has problems pumping it out (i.e. decreased SV with an increased EDV. Let me know what you all think.

an_improved_me  I made a mistake above ^, this pt has a sytolic heart failure (despite chronic HTN...) as the question states it clearly ("echo shows decreased LV systolic function") +  


submitted by mousie(220),
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is hist autuesbc dicdrnoiaest socadeasit pfrt-bMeronomeeaivlair NG?

jus2234  The question describes how he had a strep infection 15 days ago, and now this is poststreptococcal glomeruloneprhitis, which can also be described as proliferative glomerulonephritis +10  
seagull  The question would be too fair if it just said PSGN. Instead we need to smell our own farts first. +68  
yotsubato  And they used terminology NOT found in FA +5  
water  who said they were limited to FA? +2  
nbmehelp  FA uses the common nomenclature and the fact most of our other resources use the same nomenclature for this, I think we can agree that is is the accepted terms. If they're gonna decide not to use the nomenclature that most medical students are taught then they should provide their own study materials at that point for us to use. The test shouldn't be this convoluted for no reason. +8  
alimd  Ok. They can use terminology whatever they want. But BUN-CR>20 is CLEARLY prerenal right? +  
an_improved_me  I think you're talking passed each other. The fact of the matter is that NBME doesn't really care how we prepare. It cares to stratify students using whatever stupid metrics it deems necessary. It's not limited to first-aid, and that doesn't mean that it shouldn't be. +  


submitted by cmun777(28),

I think the key on this question is recognizing how much "most time-efficient" jumps out in the question stem - a pretty unique thing to be specifically asking. Going off that and the fact they want to look at exposure -> outcome, by far the fastest approach would be to find people who currently have the dz in question and then just ask them if they have a previous exposure aka case-control.

an_improved_me  I feel like you just described a prospective cohort? Find ppl with the disease (same populatin and outcome), and then see if they had a similar risk factor; then follow them to see if they had a risk factor. Case-control would be: Have two groups of people, some with the Dx, others without. See if there is a difference in proportion that have/don't have a risk factor Someone please correct me if i'm wrong? +  


I'm sorry but... where in the cytoscopy are the fibrovascular cores demonstrated? Are they visible?

an_improved_me  ok... i'm blind. it is literally just the projections... i thought I was missing some fine detail. +  


submitted by happysingh(45),
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,so eth eyK rsdwo atht no eno si ignotienmn : nnguicmctomia ylacsordphueh

eht ohthpyasp goes like isht :

an iylmatnmrfoa sgiettn ,(.ie. ncsidoauhabr ehmerhr)aog ieydl rsifsobi / rarsgnci of hte drcahnaio aangsroituln ;t=&g dapmerii FCS dnegriaa

het yek snopit / ncpeosct heyt aer igrnyt to tste rhee : 1. do ouy kwno htaw anncicgiummto rpdyhloeuchas wthiotu( hmte litlneg ouy shoet dsr)ow 2. do oyu ownk t'hwsa hte oyogslhtiphayop f(o atminoicungmc )yudrpsehalhco is ?

potentialdoctor1  Exactly. To add to this, communicating hydrocephalus can be subdivided as follows: Normal-pressure hydrocephalus: Chronic/gradual decrease in CSF reabsorption at arachnoid granulations, usually due to calcification due to aging. CSF accumulates slowly, so ventricles are able to widen without causing an important increase in intracranial pressure. Symptoms occur due to compression of periventricular white matter tracts ---> Wacky, wobbly, wet High-pressure hydrocephalus: Acute decrease in CSF reabsorption at arachnoid granulations, usually due to inflammatory state in the subarachnoid space (eg, meningitis, sub-arachnoid hemorrhage). CSF accumulates suddenly, causing an acute-onset increase in intracranial pressure +7  
sunshinesweetheart  not to take away from your perfect explanations, but if it were a woman with neck stiffness and fever (rather than circle of willis rupture) that could lead to increased CSF production, right? I think that's the only case where CSF production would increase. Also I think decr absorption in arachnoid granulations in that situation as well so it'd be a shit question +  
peqmd  If anyone like me also got "decreased absorption in choroid plexus", as their wrong answer it's because the choroid plexus doesn't "absorb" it produces. +9  
alienfever  FA 19 p510 +2  
alienfever  If anyone chose F, communication hydrocephalus is caused by decreased absorption and not increased production. FA 19 p510. +1  
an_improved_me  So she has a leaking aneurysm for how long.. gets it repaired, and then within 2 days has an inflammatory response that leads to decreased CSF absorption at arachnoid granulation... Is it the bleeding associated with the aneurysm causing it? The surgery? I'm inclined to say the latter, given that it happens coincidently after the surgery, and not for however long it was leaking beforehand. Thats what tripping me up. +  


submitted by dbg(151),
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Ddi ynenoa lees ewdrno HAWT RUYPA"NMOL MOSYMT"PS is eth ntioesqu gerrienfr ot?? rTeeh si tieylrlal nto a egnsli mypotsm oinnmtdee in hte hwloe eget.invt No clek"acrs rahde ervo bhot gnlu iseldf" rea not posy.mmts eThy aer sngis ufdno yb the hiscny.iap

isSeyoulr ogtinudb het eohlw EBNM arbod etst wirrste htgir ow.n oD yhet eataelduqy rsivee terhi wk?or siTh si otn teh rtfsi niacelcht siemkat I lierzea on teh nwe mfros.

nbmehelp  Yup. Looking back its clear what they were trying to get at, but this definitely threw me off when I was taking the test bc I kept rereading the question looking for a specific symptom the pt had that they wanted me to explain. +2  
ergogenic22  I agree with you that the writers are whack but this question clearly says "diffuse crackles are heard over both lung fields" +2  
ergogenic22  i take that back i understand what you're saying +5  
peqmd  I think what are causing her pulmonary "signs" might be more accurate question. https://www.medicalnewstoday.com/articles/161858#sign-vs-symptom +1  
an_improved_me  I get where you anger is coming from.. They expect the students to pick up the most minor details as they may be relevant to an extremely vague and tedius questions and answers, but don't hold themselves to the same standard. +  


submitted by overa(16),

Presenilin... think "PREmature SENILE" for early-onset Alzheimer’s

an_improved_me  Gold!! +  


submitted by m-ice(340),
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HMG oCA caetredus hbiotsirin lkboc eth altbyii of het ybdo to pdoecru tsi now ehsrl.oteclo eTh v,leir eulbna ot akem sti now losltcoheer adn llsit dengein ot do tsi ojb fo animgk ,iineotplposr eneds ot tge it frmo woese.hrem ,So hte lrvie sraneiesc pniosreexs of LLD trecserop ot atke omer DLL otu fo teh bodlo fro rpciknage.ga

an_improved_me  just a quick addition: LDL is the main lipoprotein carrying cholesterl, hence the liver's selective increase in LDL receptors +  


submitted by yotsubato(1032),
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tWha swa oncfugsni fro me ni htsi tisnueqo swa atht he has na tecua ipseretntnoa. aTht dndit ekam eenss to em... He evdli 74 rsyea hwti rlane rayert essntosi adn own hsa ipesrehotnyn aeucbes of !it?

an_improved_me  Its hard to say when he had a clinically significant stenosis of the renal artery. He clearly has evidence of atherosclerotic CV disease, (MI 5 years ago), and so it's not necessarily suprising that he gets atherosclerosis elsewhere. Also not sure if the hypothyroidismis a clue to a risk factor for elevated LDL / Cholesterol, since thyroid is important for that (although he has been treated for it). +  


submitted by cassdawg(1165),

I love this question because we are all obviously trained radiologists...

In reality, rather than identifying every X-ray given and trying to match it to the question stem, the best way to approach this question is to identify what his most likely issue(s) and match to the general characteristic of an X-ray, going to the X-rays looking for these characteristics.

He is an alcoholic with foul smelling (ding anaerobic) sputum. Because he is an alcoholic he is at risk for aspiration pneumonia and anaerobic pulmonary abscesses from aspiration (which is why they mentioned the bouts of blacking out). So what are the characteristics of these diseases? Aspiration pneumonia is a lobar pneumonia which would present with lobar infiltration (see here for example). Pulmonary abscess would present with cavitation and an air-fluid line (see here for example with air fluid level pointed out and here for cavitation/abscess pointed again).

Thinking of this now approach the X-rays looking for specific findings. One has the air fluid level and cavitation, so that is the answer (it is an abscess). None of the others have lobar infiltrate and are either more diffuse or hilar so they should be ruled out.

an_improved_me  The even more frustrating part of this question is that they don't show an abscess in a more dependent region of the lung! +  


submitted by step12395(0),

could someone please explain why increased static lung compliance is wrong

an_improved_me  Increased compliance indicates an increased ability to maintain a certain volume at lower pressures. In other words, at equilibrium (static), the lung can hold volume at lower pressures. This is the oppisite of what would happen if physiologic levels of surfactant cannot be produced, since elastic recoil goes up (compliance goes down). In this case, certain volumes of fluid would correspond to higher pressures. +  


submitted by ajguard26(39),
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So ghuhlato iprsoMtolos DESO ernciaes umusc dooprincut and si eovrpgoesit-tratc dna( in AF sdeo taste ttah ti eedrsesac idac tnoo)c,dipru heybter andcgrseei tosmmpys adn idgnai in n,eghail rpelmzeoao si eht "emro orccr"et hceioc. iThs is uabcees lzmoeperoa is a -optnpumrop h,oniritbi ichwh will cta ryeldcit on eht toponr mpspu fo eht stchaom nad ersdecae eth nfdigofen netag roem ahtn teh sortlipmsoo l.lwi rh,eTeofre ti si het irtfs lnei udrg orf RG.DE

an_improved_me  These questions can be so frustrating... I mean most people know PPIs are your go to when considering GERD / peptic ulcer disease... but when you speicfically add "both relieving Sx ... promoting healing", why even add a drug that specifically and directly does both... I mean PPIs promote healing, but so indirectly. This hurts my heart +1  


submitted by okokok1(12),

although each answer choice can be used to treat Nausea and vomiting, only ondansetron is specifically used for chemo-induced nausea and vomiting.

an_improved_me  Actually, metoclosepramide can also be used (inhibits D2? receptors), but i think the important thing is that the initial N/V caused in chemo is d/t an increase in 5-HT3. Therefore, you first give a serotonin antagonist +  


How do the h/o renal cell carcinoma and removal of one kidney/adrenal correlate with occlusion of the hepatic vein?

an_improved_me  looks like RCC may extend into the IVC with tumor thrombus leading to hepatic vein occlusion https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3193735/ +1  
an_improved_me  In general though, i don't think you need to know that... I think the important things are that: tells you there is widening of hepatic venules (which one can imagine is due to increased pressure) tells you that hepatic wedge pressure (estimate of portal pressure) is 30; portal pressure should be less than 5. therefore, elevated portal pressure in the absence of RA pressure indicates obstruction before the heart (in this case, budd chiari). Compare that to cardiac cirrhosis, which would have increased RA pressures AND increased portal venous pressures. +  
an_improved_me  Shit, and finally, since there are only mild increases in billi, AlkPhos, AST/ALT, i think that rules out cirrhosis. +  
an_improved_me  Add the fact that he doesn't have risk factors for cirrhosis (no drinking, smoking cigs, [would have loved to see a negative serology panel...], i think that also brings cirrhosis further down on your DDx +  
an_improved_me  Add the fact that he doesn't have risk factors for cirrhosis (no drinking, smoking cigs, [would have loved to see a negative serology panel...], i think that also brings cirrhosis further down on your DDx +  


How do the h/o renal cell carcinoma and removal of one kidney/adrenal correlate with occlusion of the hepatic vein?

an_improved_me  looks like RCC may extend into the IVC with tumor thrombus leading to hepatic vein occlusion https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3193735/ +1  
an_improved_me  In general though, i don't think you need to know that... I think the important things are that: tells you there is widening of hepatic venules (which one can imagine is due to increased pressure) tells you that hepatic wedge pressure (estimate of portal pressure) is 30; portal pressure should be less than 5. therefore, elevated portal pressure in the absence of RA pressure indicates obstruction before the heart (in this case, budd chiari). Compare that to cardiac cirrhosis, which would have increased RA pressures AND increased portal venous pressures. +  
an_improved_me  Shit, and finally, since there are only mild increases in billi, AlkPhos, AST/ALT, i think that rules out cirrhosis. +  
an_improved_me  Add the fact that he doesn't have risk factors for cirrhosis (no drinking, smoking cigs, [would have loved to see a negative serology panel...], i think that also brings cirrhosis further down on your DDx +  
an_improved_me  Add the fact that he doesn't have risk factors for cirrhosis (no drinking, smoking cigs, [would have loved to see a negative serology panel...], i think that also brings cirrhosis further down on your DDx +  


How do the h/o renal cell carcinoma and removal of one kidney/adrenal correlate with occlusion of the hepatic vein?

an_improved_me  looks like RCC may extend into the IVC with tumor thrombus leading to hepatic vein occlusion https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3193735/ +1  
an_improved_me  In general though, i don't think you need to know that... I think the important things are that: tells you there is widening of hepatic venules (which one can imagine is due to increased pressure) tells you that hepatic wedge pressure (estimate of portal pressure) is 30; portal pressure should be less than 5. therefore, elevated portal pressure in the absence of RA pressure indicates obstruction before the heart (in this case, budd chiari). Compare that to cardiac cirrhosis, which would have increased RA pressures AND increased portal venous pressures. +  
an_improved_me  Shit, and finally, since there are only mild increases in billi, AlkPhos, AST/ALT, i think that rules out cirrhosis. +  
an_improved_me  Add the fact that he doesn't have risk factors for cirrhosis (no drinking, smoking cigs, [would have loved to see a negative serology panel...], i think that also brings cirrhosis further down on your DDx +  
an_improved_me  Add the fact that he doesn't have risk factors for cirrhosis (no drinking, smoking cigs, [would have loved to see a negative serology panel...], i think that also brings cirrhosis further down on your DDx +  


How do the h/o renal cell carcinoma and removal of one kidney/adrenal correlate with occlusion of the hepatic vein?

an_improved_me  looks like RCC may extend into the IVC with tumor thrombus leading to hepatic vein occlusion https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3193735/ +1  
an_improved_me  In general though, i don't think you need to know that... I think the important things are that: tells you there is widening of hepatic venules (which one can imagine is due to increased pressure) tells you that hepatic wedge pressure (estimate of portal pressure) is 30; portal pressure should be less than 5. therefore, elevated portal pressure in the absence of RA pressure indicates obstruction before the heart (in this case, budd chiari). Compare that to cardiac cirrhosis, which would have increased RA pressures AND increased portal venous pressures. +  
an_improved_me  Shit, and finally, since there are only mild increases in billi, AlkPhos, AST/ALT, i think that rules out cirrhosis. +  
an_improved_me  Add the fact that he doesn't have risk factors for cirrhosis (no drinking, smoking cigs, [would have loved to see a negative serology panel...], i think that also brings cirrhosis further down on your DDx +  
an_improved_me  Add the fact that he doesn't have risk factors for cirrhosis (no drinking, smoking cigs, [would have loved to see a negative serology panel...], i think that also brings cirrhosis further down on your DDx +  


How do the h/o renal cell carcinoma and removal of one kidney/adrenal correlate with occlusion of the hepatic vein?

an_improved_me  looks like RCC may extend into the IVC with tumor thrombus leading to hepatic vein occlusion https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3193735/ +1  
an_improved_me  In general though, i don't think you need to know that... I think the important things are that: tells you there is widening of hepatic venules (which one can imagine is due to increased pressure) tells you that hepatic wedge pressure (estimate of portal pressure) is 30; portal pressure should be less than 5. therefore, elevated portal pressure in the absence of RA pressure indicates obstruction before the heart (in this case, budd chiari). Compare that to cardiac cirrhosis, which would have increased RA pressures AND increased portal venous pressures. +  
an_improved_me  Shit, and finally, since there are only mild increases in billi, AlkPhos, AST/ALT, i think that rules out cirrhosis. +  
an_improved_me  Add the fact that he doesn't have risk factors for cirrhosis (no drinking, smoking cigs, [would have loved to see a negative serology panel...], i think that also brings cirrhosis further down on your DDx +  
an_improved_me  Add the fact that he doesn't have risk factors for cirrhosis (no drinking, smoking cigs, [would have loved to see a negative serology panel...], i think that also brings cirrhosis further down on your DDx +  


Although the doctor should encourage talk between parents and patients, they have to allow for alone time with the patient for a more honest exchange. The doctor should also ask the patient their preference.

an_improved_me  Such a dumb question.. I thought doctors also encourage autonomy between younger patients. For sure you want patients to have privacy for questions regarding sexuality, but you should at least leave it up to the pt. +  


submitted by ajguard26(39),
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issamd1221  contralateral deficits +  
cbay0509  thank you +  
flapjacks  I think her 60 pack-year history suggests possible PAD and therefore loss of proprioception in the lower extremities, leading to an unfortunate distractor +  
an_improved_me  I don't understand why you would consider the propioceptive deficit a distractor... doesn't the DCML (which carries propioceptive information) project to the primary somatosensory cortex (via the VPL?). In this case, a lesion to the right anterior cerebral artery, which supplies both motor and sensory information to the lower limb would lead to somatosensory, propioceptive, and motor deficits. +