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Contributor score: 171

Comments ...

 +0  (nbme24#4)

FA 2017 states that extravascular hemolysis has jaundice where ABO incompatibility would not.

 +3  (nbme24#18)

Infliximab is a TNF-alpha inhibitor. from pubmed TNF-α has been demonstrated to have a central role in the host response against tuberculosis, including granuloma formation and the containment of disease (14,15). Notably, antibodies against TNF-α induced reactivation of tuberculosis

bigjimbo  TB can spread to psoas L1-2 often, which then goes to the actual L1-L2 vertebrae itself (Potts or osteomyelitis)

 +4  (nbme23#46)

medbullets has a nice pneumonic for the killed vaccines:

Rest In Peace Always:

Polio (Salk)
Hepatitis A

paulkarr  Also, the nice little puppet show from sketchy for those visual learners like me.
makinallkindzofgainz  just remembered that MMR is a live attenuated vaccine

 +2  (nbme22#40)

Prader Willi = Paternal deletion (partial or full). Noted for imprinting. Cousin to Angelmann (opposite deletion).

FA 2017: 25% of cases due to maternal uniparental disomy (two maternally imprinted genes are received; no paternal gene received).

drjungly  Physeo video explain this very clearly,

 +2  (nbme22#5)

according to medbullets link ns ss RNA must carry RNA dependent RNA polymerase (so that is out).

also, according to medbullets there are very few ds RNA viruses, so "most likely" will be ss. Also, RNA-dependent DNA polymerase = Reverse Transcriptase. Since HIV is a ss ps RNA virus with RT, they've described an HIV cousin. not sure beyond this.

nc1992  negative stranded can't be read by a translator so it needs to be transcribed into + first. Only then can it be used for protein. + is basically mRNA already. There's only one double stranded RNA family as far as I know- Reovirus so no encephalitis

 +9  (nbme22#14)

this image shows lymphocytic toxicity.

this image shows that the buildup of dATP inhibits RNR (ribonucleotide reductase), which inhibits the rest dNTP synthesis.

bonus image shows RNR is the target of hydroxyurea.

 +4  (nbme22#29)

pathogen: cryptococcus

Treatment options: Ampho B: binds ergosterol -> pores in fungal membrane -> leaks contents. can add Flucytosine: converted to 5-FU to inhibit nucleic acid synthesis

https://step1.medbullets.com/microbiology/104161/flucytosine https://step1.medbullets.com/microbiology/104158/amphotericin-b

 +7  (nbme22#37)

fibromuscular dysplasia in the left renal a. causes low flow resulting in low GFR. Chronic low GFR causes tubular atrophy. (excerpt and reference below).

Tubular atrophy is a general term that describes several patterns of chronic tubular injury with thickened tubular basement membranes, and clinically manifests as chronic kidney disease with decreased glomerular filtration rate. Increased extent of tubular atrophy and accompanying interstitial fibrosis correlates with worse prognosis. Proteinuria is variable, depending on cause.


 +6  (nbme22#12)

ranitidine blocks H2 receptor, which is Gs. Gs activates adenylyl cyclase -> +cAMP.

q: HAVe 1 M&M => H1, alpha1, V1, M1, M3 i: MAD 2 => M2, alpha2, D2 s: (everything else) => beta1, beta2, V2, D1 H2

I think this is from FA.

baja_blast  Yes; FA2019 p. 238

 +8  (nbme22#1)

apparently this is a common sequelae of abdominal trauma.

(from link below) Twenty-two of the 25 deaths were caused by blood loss. Two patterns of hepatic venous injury appeared to predominate: avulsion of the trunk of the right hepatic vein from the inferior vena cava and avulsion of the upper branch of the right hepatic vein.


 +1  (nbme22#40)

FA 2017: Characterized by massive proliferation of megakaryocytes and platelets. Symptoms include bleeding and thrombosis. Blood smear shows markedly increased number of platelets, which may be large or otherwise abnormally formed. Erythromelalgia may occur.

 +7  (nbme22#48)

no tonsilar tissue is a huge clue here. total lack of Ig which causes recurrent infections after 6mo (maternal IgG is gone). LN and tonsils are minor/non-existent. (FA 2017).

angelaq11  I totally hated this Q! I almost completely overlooked the "no tonsillar tissue", and thank God I didn't because that's the clue that made me change my answer. I had CGD (yeah, I know, S. pneumoniae not catalase +), but it said that he had muuultiple infections since birth. And I took to heart that "since birth" thing, because, isn't Bruton supposed to present with infections from around 6moa? I hope I don't screw this up next week

 +2  (nbme22#12)

warfarin inhibits the synthesis of factors II, VII, IX, X, C, and S by blocking reduction of oxidized vitamin K. The enzyme Epoxide Reductase is inhibited by warfarin. The reduced (active) form of vit. K is a cofactor for gamma-glutamyl carboxylase.

link981  So factors II, VII, IX, and X are precursor proteins? GTFO

 -6  (nbme22#45)

kaposi sarcoma. HHV8. violaceous (purple) lesions. advanced HIV CD4 < 200 (WHO).

yotsubato  Yeah thats the easy part. But the histology is whats hard

 +4  (nbme22#17)

FA 2017: H pylori is associated with gastric adenocarcinoma and MALT lymphoma

seagull  I might be mistaken but I also thought Epstein Bar Virus was also implicated in gastric lymphomas?

 +2  (nbme22#15)


a nice review of myotome and dermatome / reflexes

 +5  (nbme21#20)

Rabies attacks the nicotinic Acetylcholine receptor, and travels retrograde via dynein motors after binding AChR, according to FA.

 +12  (nbme21#31)

there are two essential fatty acids: linoleic = omega 6, and alpha-linoleic = omega 3.

lizard  Found in fish oils and are shown to lower triglyceride levels.
zpatel  alpha-Linolenic ==> omaga 3

 +1  (nbme21#13)

FA 2017: Chronic hypoxic pulmonary vasoconstriction results in pulmonary hypertension and RVH.

yotsubato  Yeah but in a chronic case this guy would produce more RBC and not be hypoxic anymore.

 +4  (nbme21#50)

this is a cervical spinal cord section. the cuneate fasciculus is intact (UE) vibration and proprioception, but the white section is the gracile fasciculus (LE) and is damaged. I think the lateral portion that is uneven is just natural/artifact.

arezpr  thorax section
guillo12  How do you know the gracile fasciculus is damage?!?!
cr  which parte of the image its damage?, the pink? or black?
usmile1  the pink park yes
d_holles  If you look at https://en.wikipedia.org/wiki/Gracile_fasciculus#/media/File:Spinal_cord_tracts_-_English.svg you can see that the closer to the center = legs, while further away = arms.
hyperfukus  i still don't see where the damage is lol! FML
hyperfukus  i finally figured it out lol that was a slow moment i hope im not this slow on step yikes!
angelaq11  @hyperfukus I had the same problem at first, marked it and then came back. If you remember, in the spinal cord the white matter and gray matter are "reversed" compared to the brain. That said, if the butterfly shaped region (ie, the gray matter) is colored (in this case) lilac and the rest (ie, white matter) is blackish, the only thing that is actually abnormal, is the region where the dorsal columns are, because it stains just like the normal gray matter. After that, you have to think about which fasciculus is damaged, the gracilis or the cuneatus. The gracilis is medial while the cuneatus is lateral (picture someone with glued legs and open arms). Hope this helped
azharhu786  Gracilus Fasciculus = Graceful legs

 +1  (nbme21#5)

wikipedia (apologies): The atmosphere is composed of 78% nitrogen and 21% oxygen. Since oxygen is exchanged at the alveoli-capillary membrane, nitrogen is a major component for the alveoli's state of inflation. If a large volume of nitrogen in the lungs is replaced with oxygen, the oxygen may subsequently be absorbed into the blood, reducing the volume of the alveoli, resulting in a form of alveolar collapse known as absorption atelectasis.

I chose cardiogenic edema, but I believe this is incorrect because there is no heart failure risk at this time, so the purpose of the PEEP is certainly not to push out fluid.

bighead478  doesn't there have to be an airway obstruction (mucus, foreign object etc.) in order for this to happen? 100% O2 without any airway obstruction should not cause absorption atelectasis, right?
iloveallpotatoes  And Tension Pneumothorax is wrong bc PEEP would furthur exacerbate that.
hyperfukus  @iloveallpotatoes yea i realized that now after getting it wrong :(
plzhelp123  @bighead478, they are using a cuffed endotracheal tube and mechanically ventilating this patient which is creating an iatrogenic "obstruction" and as @haliburton mentioned, having a high FiO2 leads to over-absorption by the blood which leads to absorption atelectasis if no other gas is allowed to enter/there is no communication with atmospheric pressure during expiration. Thus, we add positive end-expiratory pressure which keeps alveoli open at the end of expiration to prevent collapse

 +8  (nbme21#4)

EF2 is translational elogation factor 2, which is necessary for protein synthesis.

sympathetikey  I. Am. So. DUMB.
nala_ula  same :(

 +13  (nbme21#2)


"People with pseudocholinesterase deficiency may not be able to move or breathe on their own for a few hours after [fast-acting drugs, such as succinylcholine and mivacurium] are administered.

ragacha  THX

 +3  (nbme21#28)

FA 2017: Fibrate ADRs include myopathy increased risk with statins, cholesterol gallstones

yotsubato  How is that NOT posterior to middle concha? bad question
sympathetikey  @yotsubato - That would have been if it was the spehnoid sinus (I got it wrong too btw)
niboonsh  this is a good video if u need a visual https://www.youtube.com/watch?v=mf7rY1VNy70
sahusema  Sphenoethmoidal RECESS not sphenoethmoidal SINUS

 +3  (nbme21#35)

This is water intoxication. https://www.ncbi.nlm.nih.gov/pubmed/1877579

thisisfine   Agreed! It's along the lines of those marathon runners who collapse questions. Nothing but water for 24 hours = getting rid of too much sodium.
temmy  are we just going to ignore the diarrhea for 3 days? what is its significance
kard  Temmy, We aint Ignoring the Diarrhea, Actually the most likely electrolytes to get lost with it is sodium> chloride> potassium> bicarbonate... Plus the Water intoxication -> HYPONATREMIA
bronchophony  why not hypoglycemia?
saulgoodman  Because glucose is not an electrolyte, it does not conduct electricity in solution. The question is asking "Which of the following electrolyte abnormalities".

 +3  (nbme21#33)

from AAFP ED of mixed organic and psychogenic origin is common. Psychogenic causes are more likely when the patient has normal erections with masturbation or when nocturnal penile tumescence is normal.

yotsubato  Couldnt a psychogenic cause reduce libido?
home_run_ball  "Testosterone concentration is within the reference range" and the fact that he has no difficulty masturbating = normal libido. Low testosterone would contribute to low libido And if he had low libido he would have difficulty masturbating
home_run_ball  whoops meant to comment on the other comment

 -2  (nbme21#10)

FA 2017: Urinary cyanide-nitroprusside test is diagnostic. not sure how to know that it was a red color, but maybe just the fact that red seemed like a positive test result.

link to more background but not necessarily helpful for this question

nobody  "Detection of cystine in urine: cyanide reduces cystine to cysteine → Cystine turns red and becomes detectable when it comes into contact with nitroprusside. If the test is negative, the presence of cystinuria is unlikely." - AMBOSS

 +4  (nbme21#18)

Bullous pemphigoid antigen must be hemidesmosome. FA: bulla are "bullow" the dermis (subepidermal blister). BP also yield "tense" bulla.

seagull  I love how this cant be straight forward. All the other proteins are either subunits of desmosomes or cytoskeletal components. Because I know molecular biology that well on top of the majority of medicine....FML
cienfuegos  @seagull: excellent comment, literally loling right now
cienfuegos  or sobbing and threatening to hold my breath if they don't make it stop

 +1  (nbme21#38)

I chose G-CSF because the granulocytes seemed to me more of a risk than the moderate anemia. Erythropoietin seems like an appropriate choice as well but G-CSF more critical.

kentuckyfan  I think it's also because he has an infection (since he was prescribed antibiotics) boosting the immune system is more important than increasing platelet count E) or RBC count A)

 +0  (nbme21#50)

my notes from UWORLD: andes aegypti mosquito = dengue south, southeast asia, pacific islands, carribean, americas HA, retro=orbital pain, joint pain, muscle ache. petechiae, purpura, epistaxis, melena, throbocytopenia leukpoenia, hemoconcentration

thomasalterman  Dengue is an arbovirus. The important hints are that she was traveling in endemic (tropical) and that she has **excruciating pain in the joints and muscles**. This is why dengue is aka "break-bone fever"
sam  Same vector
sam  Same vector

 +1  (nbme21#15)

i think this is because bilirubin is a soluble liver breakdown product of heme, but has not entered the intestine/colon for gut bacteria conversion to stercobilin or urobilin. urobilin in urine is normal.

 +4  (nbme21#19)

Peri- or postpartum cardiomyopathy (PPCM) is a rare, life-threatening heart disease of unclear origin and is characterized by heart failure of sudden onset between the final weeks of pregnancy and 6 months after delivery. link to pubmed The clinical picture of PPCM corresponds to a dilated cardiomyopathy (DCM) with signs of severe heart failure.

maxillarythirdmolar  For anyone wanting to understand why^ the tl;dr is that prolactin gets cleaved into two toxic metabolites. Treatment is something like bromocriptine (and therefore no more breast feeding) to stop prolactin release. Lastly, you can treat with regular HF meds.

 +8  (nbme21#16)

FA 2017: Secrete surfactant from lamellar bodies. Also serve as precursors to type I cells and other type II cells. Proliferate during lung damage.

teepot123  fa 19 pg 647

 +9  (nbme21#10)

Small cell lung cancer causes SIADH. Location + exclusionary clues.

mcl  To expand, SIADH may also result in euvolemic hyponatremia. This is because, as we know, ADH increases absorption of water and therefore initially results in an increased circulating volume. However, this results in increased stretch of the atria and subsequent secretion of ANP. ANP (atrial natriuretic peptide) then results in loss of sodium and water.

 -5  (nbme20#8)

FA 2017: 3° syphilis disrupts the vasa vasorum of the aorta with consequent atrophy of vessel wall and dilatation of aorta and valve ring. May see calcification of aortic root, ascending aortic arch, and thoracic aorta. Leads to “tree bark” appearance of aorta. Can result in aneurysm of ascending aorta or aortic arch, aortic insufficiency.

 +8  (nbme20#19)

resonant sound is normal. hyperresonant with overexpansion. tactile fremitus is increased /c solid mass or fluid, and decreased with air/fluid level or overexpansion. prolonged expiratory phase -> obstructive conditions.

 +0  (nbme20#39)

Mycoplasma pneumoniae cold agglutinins, no response to amoxicillin.

FA 2017: Classic cause of atypical “walking” pneumonia (insidious onset, headache, nonproductive cough, patchy or diffuse interstitial infiltrate). X-ray looks worse than patient. High titer of cold agglutinins (IgM), which can agglutinate or lyse RBCs. Grown on Eaton agar. Treatment: macrolides, doxycycline, or fluoroquinolone (penicillin ineffective since Mycoplasma have no cell wall). ABC = Africa, Blindness, Chronic infection. D–K = everything else. Neonatal disease can be acquired during passage through infected birth canal. No cell wall. Not seen on Gram stain. Pleomorphic A. Bacterial membrane contains sterols for stability. Mycoplasmal pneumonia is more common in patients < 30 years old. Frequent outbreaks in military recruits and prisons. Mycoplasma gets cold without a coat (cell wall).

johnthurtjr  Have you mixed Chlamydia in with Mycoplasma?
smc213  I mean the Q stem is not about Chlamydiae, but Chlamydiae does lack the classic PTG cell wall d/t decreased muramic acid = beta-lactam abx ineffective. FA 2018 p.148

 +0  (nbme20#4)

FA 2017: Infects B cells through CD21. Atypical lymphocytes on peripheral blood smear G —not infected B cells but reactive cytotoxic T cells. ⊕ Monospot test—heterophile antibodies detected by agglutination of sheep or horse RBCs. Use of amoxicillin in mononucleosis can cause characteristic maculopapular rash.

zup  misread the "accounts for" question as what's the reason for the atypical lymphocytes. So I answered "virus infected B lymphocytes." Anyone else misread it like that?
nala_ula  Shit, I misread that too and I noticed it now. Nerves get the best of us!
stevenorange  If the question is ask what is the atypical lymphocyte in the brain , than it should be the infected B cell, RIGHT?

 +0  (nbme20#23)

[comment moved to subcomment]

Subcomments ...

submitted by lsmarshall(314),

I thought this was a trick question since skin cancers are the most common type of cancers overall. But actually among HIV patients, HIV-related cancers are much more common than non-HIV-related cancers (even skin cancers). EBV-induced primary CNS lymphoma is the only option that is AIDs-defining illness/cancer.

medskool123  why not hep B? i guess another whats the better answer ones... Just rem reading that it was more common with aids pts.. anyone have an idea about this? +1  
haliburton  Yes, I think CNS lymphoma as an AIDS defining illness wins the day. My thought was since SHE has AIDS it is most likely from IVDA, which has a high risk of HBV that could go undiagnosed for a long time. at 32, that might not be long enough to have HBV and get HCC (but with no immune system...?) +1  
yotsubato  God damn this is such BULLSHIT... +8  
trichotillomaniac  Why you gotta do me dirty like this NBME +1  

submitted by m-ice(235),

This girl has Mono caused by Epstein-Barr Virus. The symptoms are relatively vague, but lymphadenopathy like this would be common for Mono. The CBC shows elevated lymphocytes, implying this is not a bacterial illness, so viral is likely. Combined with the lymphadenopathy, this makes us worry about Mono. The Mono-Spot test for EBV is what the question is referring to when describing the sheep erythrocytes agglutinating. From there, this question requires that you know that in EBV infection, EBV infects B cells, but does not cause them to become abnormal. Instead, CD8 cells, which are actively trying to kill the B cells, become abnormal.

medskool123  NBME does trick now and then.. when they zig you zag. then when you think they are going to zag, they zig just to destroy yourself confidence. +10  
kylemax  The abnormal T-cells are known as Downey type II cells (Sketchy) +3  
haliburton  I was recognized EBV, then knew EBV infects Bc, and the atypical lymphocytes are Tc. Then I said CD8 are MHC1 for virii, and bingo bango, boom. +2  
trichotillomaniac  congrats you played yourself +3  
lilyo  Soooooooo EBV infested B- cells is not considered atypical WTFF?? +  
med4fun  They are atypical b/c usually you do not see a super high amount of CD8+ in peripheral blood. Now there are a ton to try to stop the infected cells. +  
aneurysmclip  oh and primary CNS lymphoma caused by EBV has T cells NOT B cells. I just try to remember the peripheral blood has atypical lymphocytes which are CD8+ T cells, and the CNS lymphoma is the opposite, ie; B cells +  

haliburton  ^^^ THIS ONE SHOWS DUCT ^^^ +3  

Why is the answer “granulation tissue”? I thought after 14 days you have a fully formed scar.

colonelred_  If you go back and look at the image you can see that it was highly vascular which is characteristic of granulation tissue. Scar tissue formation will be closer to 1 month, plus you will see lots of fibrosis on histology. +9  
sympathetikey  It's a bit misleading, for me, since you do see fibrosis intermixed with the granulation tissue, but granulation tissue was a better answer. +1  
haliburton  According to FA 2017: 3-14d: Macrophages, then granulation tissue at margins. 2wk to several months: Contracted scar complete. Dressler syndrome, HF, arrhythmias, true ventricular aneurysm (risk of mural thrombus). i'm getting pretty frustrated with NBME contradictions to FA, and FA omissions of content. this stuff is hard enough to get straight as it is. +1  
yotsubato  Thats cause the NBME exam writers read FA, then make questions not fit in with FA +4  
trichotillomaniac  This fits the timeline laid out in Pathoma! 1-3 wks = granulation tissue with plump fibroblasts, collagen, and blood vessels +7  

submitted by trazabone(10),

Kidney makes 1-25, hydroxy vitamin D. (calcitriol) 25-hydroxy vit D (calcidiol) is made in the liver, and hypoparathyroidism would not decrease its levels as it acts to increase 1-alpha hydroxylase in the kidney to increase calcitriol concentrations --> Ca/phosphate reabsorption from the bone and small intestine.

queezyfish  I'm confused about the phosphate level in questions like these. Decreased calcitriol would decrease phosphate absorption while PTH decrease lowers phosphate excretion. I'm assuming that the PTH decrease has the greater effect with serum phosphate levels? +1  
mousie  PTH = "Phosphate trashing hormone" if PTH is high Phosphate must be low - they are always opposite (unless d/t renal failure then Phosphate will be high - kidneys will be unable to get rid of phosphate) So low Ca d/t low PTH does not effect 25 H. Vit D ... only 1,25 H Vit D (active Calcitriol)? +4  
haliburton  Clarification because I was confused: PTH stimulates kidney to produce 1,25-(OH)2 D3 (calcitriol) via 1α-hydroxylase in proximal convoluted tubule. Therefore, without parathyroid glands, low PTH, 25,D is not converted and therefore not down (normal or up). phosphate "trashed" by PTH as eloquently stated above. +  
zbird  Here the primary defect is high up from the parathyroid gland, there is decresed or no PTH which normally trashes phosphate but not in this case so serum PHOSPHATE INCREASES and the serum calcium is low because PTH should have prevented the urine calcium so there is calciuria and no resorption from bone-LOW CALCIUM, Vitamin-D is independent of PTH so stays NORMAL +  

submitted by sajaqua1(389),

Wouldn't total AV nodal ablation destroy to autorhythmicity of the pacemaker? That would mean that below the AV node the rhythm would be provided by a ventricular foci, and those usually create wide QRS complexes.

haliburton  that was my reasoning as well. guess not. +  
yotsubato  Shitty NBME grammar strikes again. +1  
charcot_bouchard  No. No guys. Bundle of his located below AV node and it can generate impulse. it calls junction escape rhythm and narrow complex. Below this is purkinje, bundle branch & ventricular muscle. those are wide complex +5  
abhishek021196  Third-degree (complete) AV block The atria and ventricles beat independently of each other. P waves and QRS complexes not rhythmically associated. Atrial rate > ventricular rate. Usually treated with pacemaker. Can be caused by Lym3 disease +1  

submitted by welpdedelp(154),

Ok, so RNA dependent DNA polymerase is for reverse transcriptase... single stranded + use RNA dependent RNA polymerase. Can someone explain?

hyoid  The only thing I can think of is that HIV is a (+)-sense single-stranded RNA virus that relies on an RNA dependent DNA polymerase (reverse transcriptase) to synthesize DNA. +  
haliburton  according to [medbullets link](https://step1.medbullets.com/step1-microbiology/104196/rna-viruses_) ns ss RNA must carry RNA dependent RNA polymerase (so that is out). also, according to medbullets there are very few ds RNA viruses, so "most likely" will be ss. Also, RNA-dependent DNA polymerase = Reverse Transcriptase. Since HIV is a ss ps RNA virus with RT, they've described an HIV cousin. not sure beyond this. +  
some0217710  Can’t think of any retroviruses outside of HIV and HTLV and they’re both +ssRNA +1  

submitted by welpdedelp(154),

It was just asking the lifespan of RBCs (120 days)

haliburton  If I'm reading this right, this is just a tricky dicky question. I think CO binds 200x stronger than O2. But if an O2 cycles through binding / unbinding 200 times before a CO gets kicked off, this should still clear the CO from that cell sooner or later. strange to think it is 1. essentially permanently trapped in a cell, and 2. doesn't kill you and can be treated with O2 to resolution within a few hours or a day. They must just be thinking, until that last RBC dies, you've got original CO in a circulating cell. but just a fraction (because you didn't die). not sure how that CO isn't just passed on during recycling, based on this line of thinking. +5  
link981  The question while stupidly written, asks how long the RBC's that carry the CO take to be removed from the circulation, not how long the CO takes to be removed from the RBC. Just asking the lifespan of RBCs in an stupidly complicated way. As we know, RBC's life span is about 120 days and then they are removed from our circulation. 120 days is about 4 months. Next time they will probably ask weeks or in hours, who knows? smh +4  
baja_blast  If that's what they're looking for why cant the NBME people just ask "How long does it take for RBCs to turn over?" Ridiculous. +  

submitted by hayayah(884),

Secondary hyperparathyroidism (usually d/t chronic renal failure).

Lab findings include ↑ PTH (response to low calcium), ↓ serum calcium (renal failure), ↑ serum phosphate (renal failure), and ↑ alkaline phosphatase (PTH activating osteoBlasts).

haliburton  also remember that in renal failure, 1-alpha-hydroxylase activity is down, so there will be less activation of 25-hydroxycholecalciferol to 1,25-hydroxycholecalciferol, which is a key mechanism causing hypocalcemia. +1  
cr  why not increased 25-hydroxycholecalciferol?, with the same logic haliburton explain +  
nala_ula  Increased phosphate, since the kidneys aren't working well, leads to the release of fibroblast growth factor 23 from bone, which decreases calcitriol production and decreased calcium absorption. The increase in phosphate and the decrease in calcium lead to secondary hyperparathyroidism. +1  
privatejoker  Probably a dumb question but how do we definitively know that the ALP is elevated if they give us no reference range in the lab values or Q stem? Everything stated above definitely makes sense from a physiological standpoint, I was just curious. +1  
fatboyslim  @cr the question asked "the patient's BONE PAIN is most likely caused by which of the following?" Increased levels of 25-hydroxycholecalciferol might exist in that patient, but it wouldn't cause bone pain. PTH causes bone pain because of bone resorption +1  
suckitnbme  @privatejoker ALP is included in the standard lab values +  
makinallkindzofgainz  @privatejoker ALP is listed under "Phosphatase (alkaline), serum" in the lab values +1  
pg32  Why does AlkPhos increase in renal osteodystrophy? The PTH would be trying to stimulate bone resorption (increase osteoCLAST activity), not bone formation (osteoBLAST activity). +  
drzed  @pg32 the only way to stimulate an osteoclast in this case (e.g. via PTH) is by stimulating osteoblasts first (thru RANKL/RANK interaction), thus ALP increases. +1  

I picked Crohn’s too. I think the severe constipation over 5 years distracted me.

haliburton  i think it is critical to remember that constipation is what caused the diverticulosis. +3  

submitted by nuts4med(6),

Anyone have an idea why the decreased arterial O2 saturation is incorrect? Assuming she has pulm edema since she has LE edema, wouldn't a lower O2 sat be expected too?

haliburton  I believe there would be no decrease in O2 saturation because oxygenated blood (high pressure) is shunted into deoxygenated circuit. As long as the lungs can keep up, this should increase venous oxygenation on average. +5  
hungrybox  ty both of you for this, was wondering the same thing +  
coxsack  O2 sat won’t change b/c you’re not adding deoxygenated blood to the arterial side. You’re just taking arterial blood and putting it into venous blood. Same reason why L->R cardiac shunts don’t decrease O2 sat (while in contrast, a R->L shunt would). +2  
hungrybox  just realized: the high pressure of the arterial system keeps out low-pressure venous blood in an AV fistula (probably obvious to most ppl but it was a eureka moment for me lol) +2  
chandlerbas  ya you wont have decreased arterial O2 sat because oxygenation of blood is perfusion limited (FA19 --654) therefore oxygenation of the blood happens within the first .3seconds of entering the pulmonary capillary that you could even handle having more deoxygenated blood enter +  

submitted by monoloco(113),

If you want to clear a drug, it is probably best that it not be bound to proteins (so that it gets filtered) and it has a low volume of distribution (so it isn't in the deep, hard to reach tissues).

kingtime9119  But that doesn't make sense. Page 233 of First Aid 2019 edition clearly states that being plasma protein bound creates the lowest volume of distribution, because not being bound to proteins increases the chance it will reach deep into the tissues before it reaches the kidneys. Discrepancy with First Aid? +  
haliburton  my reasoning was comparing two drugs, both with Vd of 1, the drug with the lower albumin binding would be cleared faster @kingtime. I don't think you're considering that A and B have equal Vd. +3  

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