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gaPe 417 fo atPamho
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-TG mtr:uo seonrtge exsecs
SL- u:tmro rengnaod eexscs
mr:aFobi nigeb,n tsbl,obfiasr sucea ge'ism neysdmro
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eeniKgp shti ni idnm orf uferut qoe.nstisu fI eon of eht nsraesw alutycal isft eht ll,ib 'otnd pkci eno ttha ru'eoy ont eusr of uaesceb eht eorccrt noe emses ynueki!ll gansb* eadh
Why si ti nto oraaivn ofellilc ecl?sl I tugtohh teh elaefm loanga fo reolitS nad Lgyeid is roagchuat/lensa .sellc
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.