16. Acromegaly and Hyperprolactinemia Flashcards
acromegaly and hyperprolactinemia are both due to problems with what part of the endocrine system?
pituitary gland (specifically anterior pit)
what are some physical exam findings of acromegaly?
coarse facial features, prominent brow, large tongue, doughy hands, small goiter, skin tag on back, normal strength and reflexes, small/soft testes
why might some pts with acromegaly have poor sleep?
enlarged tongue causes sleep apnea
how would you test whether GH release is due to a primary or secondary cause?
glucose load -> should suppress GH release.
If primary, GH release is not dependent on upstream signals, will not suppress with glucose
If secondary, GH release is responding to signals, should suppress with glucose load.
GH vs IGF1: which is better to measure in serum for status of GH release?
best to measure serum IGF-1, since GH oscillates naturally over 24 h period. IGF1 has longer half life.
three therapeutic options for acromegaly?
surgery, radiation, medical therapy
describe the surgical options for acromegaly
transnasal adenectomy (removal of the tumor through the nose) subfrontal craniotomy (through the skull if needed for large tumors)
when would we recommend radiation as treatment for acromegaly?
if tumor has invaded the cavernous sinus, dangerous to remove surgically
what drug therapy do we have for acromegaly?
dopaminergic agonists (bromocryptine, cabergoline) long-acting somatostatin analog (octreotide)
why would a dopamine analog work in reducing a GH releasing tumor?
the cells for prolactin and GH originate from the same line embryologically, share suppressibility by dopamine
secondary v primary amenorrhea?
primary: someone who is the age that they should be menstruating, but has never started
secondary: once menstruated, but has now stopped.
what is the most common cause of secondary amenorrhea?
pregnancy! don’t forget to check beta-hCG
if menopause, what would be levels of gonadotropins?
HIGH
a cause of hyperprolactinemia that does not concern the Prolactin axis?
hypothyroid.
pathway: thyroid hormones (T4, T3) are decreased, so TRH is not suppressed
excessive TRH yields hyperprolactinemia
Prolactin: 2 major functions?
stimulate breast milk
disable pregnancy when lactating (via inhibiting GnRH release, causing gonad insensitivity to LH)
Hyperprolactin: presentation in females?
galactorrhea, mens irregularity, infertility
Hyperprolactin: presentation in males?
galactorrhea, visual field abnl, headache, impotense, EOM paralysis, ant pit malfunction
(men tend to present later, with bigger tumor, with more sx)
most common cause of hyperprolactin?
pituitary tumor: prolactinoma
Prolactinoma: three sequelae?
- infertility
- osteoporosis due to lack of estrogen
- mass effects of tumors (neuro)
Prolactinoma: treatment options?
- surgical
- medical with long-acting dopa agonists)
- radiation
Prolactinoma; what is preferred treatment?
med treatment. surgical removal tends to fail after several years with tumor recurrence.
meds are usually Preg X, so some women will do surgery in order to reduce tumor for a few years and avoid meds when preg, then begin meds when tumor recurs
describe the embryological lineage of pituitary endocrine cells. what precursors give rise to what endocrine cells? what transcription factors are involved?
Precursor 1 yields ACTH cells tsn factor PROP1 yields Precursor 2 Precursor 2 yields FSH/LH cells tsn factor Pit1 yields Precursor 3 Precursor 3 yields TSH cells and GH cells GH yields PRL cells
If there is a mutation in the transcription factor PROP1, what ant pit cells would still be made?
only ACTH cells
If there is a mutation in Pit1 transcription factor, what ant pit cells would be made/what would be absent?
Present: ACTH, FSH/LH cells
Absent: TSH, GH, PRL cells
