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Welcome to trazabone’s page.
Contributor score: 14

Comments ...

 +10  (nbme24#2)
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henrtniOi arrlnoasasecambt ciceinyedf. roalyCmob ophpaehst )P(C is esuhtdn ot yeiidirpnm esystihsn ;-&-gt earciensd ocirto ciad routicpond SCP( ouy dlwuo not ees ctrioo e)dmic.aai raUe leycc aosl hnibteiid t&g--; esniercad miamano v.leles

savethewhales  Sidenote, OTC deficiency is the only X-linked recessive urea cycle deficiency (all others are autosomal recessive) and it's the most common +2

 +1  (nbme24#16)
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Knydie akmse 2,15- odyyhrx nvaiitm .D cy 2(tlrriox)y5d-ohalic itv D liloc)c(dia si aemd ni het il,vre dan ahtrydorampsophiiy ldowu otn decaesre tis sevlel sa ti tsca to senaiecr ha-l1pa ohayleydsxr in eht knediy ot resiecna otricciall srneottioncanc g--t&; pt/pshhCeaoa asiobtprrnoe form het eobn nad mlals

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. +1
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 +

 +2  (nbme24#5)
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My aurednnnsidgt is hatt fi ernspta are aneedrtul yb bdloo ot hoest ,eaetfdfc ew ssueam tath they are tno rcriersa (ni the srseevice ).eacs Teefehrro, fi we vaeh a amle fhaetr cefaeftd wtih xdline-k ssereiecv redarim ot a r-encor,airn r'teshe no ywa nay fo shi gffpionsr lwoud eb cad.tffee

I"f one pntrae is not a erra,ric hten a ilhdc can ynol tehrnii a iaessed laelle fomr hte rtohe ert.nap nI ehtse ,msolprbe we cna aseusm that yan uvildanidi irmyarng itno eth fmaliy si ont a r ierr."

linwanrun1357  If we assume that they are not carriers (in the recessive case) Then how came it can be AR?!! +1
catscan1979  ^exactly what's said above here. I think x-linked recessive is the least likely, but not impossible. +2

Subcomments ...

submitted by medstruggle(12),
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anC seonmeo aeplnxi yhw oesd hits aetiptn have eihlp?kyaoma

colonelred_  Catecholamines activate the Na/K pump, which will drive K inside. +11  
trazabone  Read online that catachelamines are released following tonic clonic seizures. Besides that, BP of 180/100 could indicate that catecholamines are circulating. +1  
fulminant_life  This mechanism is why giving albuterol for hyperkalemia works +8  
nbmehelp  Why does this guy have increased catecholamines tho +  
johnson  His SNS activity is seriously increased --> increased catecholamines. +  
nbmehelp  Why is his SNS activity increased? Is the BP literally the only hint? +  
youssefa  Alcohol withdrawal creates a hyper- catecholaminergic state + Seizures do that as well. +5  
water  My best guess is that withdrawal puts the body in a state of stress (same for seizures) and with stress you have release of catecholamine which we'll see in the BP and the hypokalemia. +3