Pituitary Gland Flashcards
what is the infundibulum?
the stalk that attaches the hypothalamus to the pituitary gland (sits in the sella turcica)
what hormones does the anterior Pit secrete?
ACTH, TSH, LH, GH, FSH, PRL
what hormones does the posterior pit secrete?
oxytocin and ADH
what does the intermediate lobe produce?
melanocyte-stimulating hormone that controls skin pigmentation
GH excess
benign pituitary adenoma, a mixed cell tumor, or ectopci tumors (islet cell type) or MEN type I
what does a pit. adenoma secrete?
> 1 cm, stimulates GH release that then stimulates the relase of insulinlike growth factors from the liver
what accounts for 10-15% of pituitary tumors?
somatotrph-producing tumors
what are mixed cell tumors often associated with?
PRL secretion
what is gigantism?
occurs in children prior to closure of the epiphyses and causes excess growth of long bones (super rare)
what is acromegaly
causes enlargement and elongation of the hands, feet and jaw and internal organs
when is the onset of acromegaly?
in the 30s so it doesn’t affect long bones
what are other features of acromegaly?
- increased risk of DM. HTN, CAD
- doughy, moist hands
- macroglossia
- carpal tunnel syndrome,
- deep, coarse voice
- obstructive sleep apnea
- goiter
- HTN and cardiomegaly
- weight gain and insulin resistance
- arthralgias and arthritis
- colon polyps
- hyperhidrosis
- cystic ance
- acanthosis nigrican
- HA
- spinal stenosis
- tmeproal hemainopsio
- decreased libido
- ED
- menstural abnormalites
what is a common organ finding upon dx of acromegaly?
overt heart failure w/ dilated left ventricle and reduced EF
dxof GH excess
if IGF-1 is elevated fivefold, them suggests adnemoa
PRL levles are also measure
-randome GH levels aren’t accurate
what would a 1 hour glucose tolerance test show?
failure of GH to decrease to 2 ug/L after 75 g loading dose
what is the modality of choice when dx GH excess?
MRI- negative scan virtually r/o GH pit adenoma
skull radography often shows enalarged sella and thickened skull
what might an xray of the hands and feet reveal?
tufting of the terminal phalanges
tx of GH excess?
somatostatin analogs
ocreotide and lanreotide are inhibiory and may decrase tumor size
what can be used for pts that fail surger?
DA agonist like cabergoline or bromocriptine 9supress GH levels)
what is the most successful surger in pts w/ GH blood levels below 50 and tumors no larger than 2 cm?
transphenoidal microsurger
what ist he best measure of surgical success in GH excess?
normilization of IGF-I
what is pegvisomant?
a GH receptr antagonist that blocks hepatic IGF-1 production- sx relieft
Diabetes Inspidus
-insipid- tasteless (as opposed to sweet0mellitus)
what is DI caused by?
deficiency of or resistance to vasopressin (ADH)
at what serum osmoloatlity level does max antidiuresis occur?
295
at what serum osmolaltiy does thirst kick in?
290
what specifica gravity do DI pts hang out around?
1.00
what is primary DI?
genetic or sporadic
what can secondary DI be caused by?
hypothalamic or pituitary pathology caused by tumor, anoxic encephalopathy, surgery, accidental head trauma, infxn, sarcoidosis, multifocal langerhangs cell granulomatosis or metastatic dz
what are the four types of DI?
hypothalmaic, nephrogenic, transient, primary polydipsia
what are the clinical features of DI?
polydipsia, polyuria, and a dilute urine
- intense thrist w/ fluid intake of 2 to 20 L/da
- craving for ice water
- large volume polyuria
- hypernatreumoa
- dehydration
-unremitting enuresis
what are features of central (hypothalamic) DI?
inability to produce and secrete vasopression (levels will be low)
- commonly occurs after head trauma or brain surgery
- can be inhertited
- may lack “osmostat”
- repsoneds to desmopressin
what are features of nephorogenic DI?
kidney unalbe to respond to vasopressin (levels are high)
- associated w/ CKD, lithium toxcicity, hypercalcemia, hypokalema
- may be inheroted
- abnormal receptors in kidneys
- NO response to desmopressin
what is transient DI?
- pregnance and puerperium
- rapid destruction/breakdown of vasopression
what is primary polydipsia?
disorder of thirst mechanism- ADH levels low
dx studies of DI
clinical judgement
- serusm osmolality high, urine osmolality low
- BUM may be low,
- uric acid elevlabed
- serum sodium can be N or high
- may need supervised vasopressing challenge test
- MRI- mass lesion
tx of DI
desmopressin acetate in central DI or transient DI
mild cases of DK?
none
what else can central and nephrogenic DI respond to?
HCTZ, K or amiloride supplementaion
what does nephrogenic DI respond to?
indomethacin +/- desporessin, HTZ, amiloride
