oiloydrdcehohhaoizrt si DCO rfo crpNoenhegi eDtaibse susdpiiin sebuace it dycarpxliaoal cuessa an icensaer ni PB yb scrnaeingi idousm oprbasonit and thus rweta pnai,trobso athoPma sexipnal thsi yi.ecnl
nDssspeorime is iorecncrt secbaeu uopn ngsatif lf(udi ctrtsnor)eii AHD is aencedris amingne HAD si egibn arledese lelCynatr but si nto wrnkiog in the kineyds ta eht 2V escrroetp fo het lleitpahie lraen eslcl ta cgeCnllito ct.du
nO that tn,eo ioidmAelr is esdu rfo iumLiht dicuend epnngihcero DI.
gnccairdo ot tupeatod hzidasite sucae a ldim epvlmychoio state tush royu PCT lilw ees omer aN dan 2OH &-tg-; yb iipercpnl that teh PCT ylsaaw oarsbsbre %60 fo thaw ti sese, ti llwi ebrrasob omer tarew dna Na.
ttePina sha erngcnpohie isDbetea .nupIdiiss Oen of het nrtmeatets si lichidyda.orrzotehH
Just to add thought process. Pt has excessive thirst, and urinating frequently but his Serum osmolality is increased...which means he has to omuch solute in his blood and his ADH is not working.
ADH not working can be due to Central DI or Nephrogenic DI. Central DI is when pt has lack of ADH but in this vignette they say the ADH is increased --> must be nephrogenic.
I don't think you need to know that HCTZ paradoxically works for nephrogenic. I think you can save time and just memorize FA's tx choices for Nephrogenic DI - HCTZ, amiloride, and indomethacin. You could argue it's good to know mechanisms, but I think knowing the drug names and their MOA, you'd be able to figure it out if they went for a 4th order reasoning (there's already enough thinking to do in this question)