• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/52

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

52 Cards in this Set

  • Front
  • Back
anatomy surroundeing the pituitary
tumors lateral: cavernous sinus and may hit CN 3, 4, V1, V2, & 6
tumors superiod: hit optic chiasm
pituitary hormones from anterior lobe
GH
prolactin
ACTH
TSH
FSH
LH
pituitary hormones from posterior lobe
ADH
oxytociin
regulation of anterior pit hormone secretion
3 tiers of control
hypothalmic hormones traverse the portal system and impinge directly upon their respectivetarget cells
intrapituitary cytokinesand GF's regulatetropic cell function by paracrine & autocriine control
peripheral hormones exert negative feedback inhibition of respectivepit trophic hormone syn and secretion
hypothalmic pituitary disorders
hypothalmic disease
stalk interruption
pituitary tumors: mass effects
iatrogenic: surgery, radiation, steroids
invasive: other CNS, tumors, metastases
infarction: sheehan's diabetes
apoplexy: hemorrhage
infiltrative: hemochromatosis
trauma
immunologic: lymphocytic hypophysitis
genetic: Pit-1, prop-1 mutations
isolated ACTH
non-pituitary
hypothalmic disease
mass
infiltrative: sarcoidosis, langerhans histiocytosis
functional: steroids, illness, wt loss
non pituitary
cranioipharyngioma
rathke's cleft cyst
meningioma
carotid artery aneurysm
evalutation of hypothalmic-pituitary disorders
size/mass effect
- headache, nausea, vomiting
- visual disturbance: bitemporal hemianopsia

function: hypo or hyper
piuitary tumor subtypes
mostly lactotroph 40-50%: hyperprolactinemia

gonadotroph 15-40% : clinically non functioning; visual field loss & hypopituitarism

somatotroph 10-20% : acromegaly

corticotroph 10-15% : cushings disease

thyrotroph 1% : hyperthyroidism
prolactin actions
stimulates milk production from mammary gland
importnat for normal reproductive development
hyperprolactinemia
most common pituitary abnormality
frequent cause (25-40%) of female infertility
prolactin secretion
TRH and prolactin releaseing factor stimulate releasefrom anteerior lobe
- breast
- decrease LH, FSH -- decrease gonadal function/gonads
- other: lymphocytes, brain, tear ducts, nephron, gut, liver

decrease GnRH pulses causses dopamine release which inhibits prolactin secretion
how does hyperprolactinemia present in women
galactorrhea
amenorrhea or oliomenorrhea (by decrease GnRH pulses)
infertility
how does hyperprolactinemia present in men
more likely to present with headache, tumor
impotence, infertility
not galactorrhea or gynecomastia

tumors b/c suddle symptoms ignored
physiologic causes of hyperprolactinemia
stress: hypoglycemia, exercise, injury

sexual intercourse

estrogen: women>men; pregnancy; obesity

protein meal

nipple stimulation
pathologic causes of hyperprolactinemia
meds
untreated primary hypothyroidism: increase TRH
polycystic ovarian syndrome
RF
stalk compression or section: neurosurgery, empty sella, non pit CNA tumors
chest wall lesions: herpes zoster, chest contusion, mastitis
pituitary tumor
meds that cause pathologic hyperprolactinemia
antipsychotics
antidepressants
birth control pills
estrogen pills
pituitary tumor
prolactinoma
GH secreting
ACTH secreting
nonsecretory: large
prolactinomas
microadenoma: < 1 cm
- stable over time

macroadenoma: > 1 cm
- increase over time
- requires specific therapy

size & PRL concentration should decrease with therapy
specific therapy for macroadenoma (prolactinoma)
dopamine agonist
- bromocriptine : requires daily dosage
- cabergoline: fewer side effects, possibly more otent; can dose weekly
- surgery, radiation, or all of the above
indications for dopamine agonist therapy
infertility
amenorrhea: bone loss or osteoporosis
bothersome galactorrhea
decrease size of tumor: macroadenoma
hyperprolactinemia summary
common
- excluse hypothyroidism, meds, pregnancy

prolactin secreting tumors
- microademonas can be watched or treated and followed
- macro need tx: D aaonist, surgery and/or radiation therapy
GH axis
ghrelin (from stomach) & GHRH stimulate GH secretion

somatostatin from pancreas inhibi GH release

GH goes to liver and releases IGF-1 which goesto bone & muscle
GH also works directly at bone & muscle

IGF-1 is end organ functional GH; it is steady and this is what we measure
acromegaly
changing hands, feet (wider), head (lantern jaw), leonine facies, increase frontal sinuses, widened teeth

arthralgias

visual field disturbance

soft tissues grow: thyroid, heart, liver, etc
acromegaly presentation
hyperhidrosis
headache
hormone def
macroglossia
sleep apnea
dx of acromegaly
measurement of random GH not useful
- NI at times in acromegaly
- high following a normal pulse

IGF-1: somatomedin C
- integrated measure of GH levels
- high in acromegaly: best screening test

oral glucosetolerance test
- normal suppress GH to < 1
- acromegalics do not suppress

head MRI scan
if you think there is hormone overproduction, what test do you do
suppression test

also can measure when should be low, to demonstrate overproduction
if you think hormone levels are too low, what do you do
measure when should be high
measure cortisol in am
secretion of GH in normal adult
pulsatile
mostly at night
GH secreting tumors summary
gigantism or acromegaly: based on timing

dx: increase IGF 1 and abnormal GH response to OGTT

dx late: largetumorwith multiple hormone def

tx may require surgery +/- radiation +/- GH antagonist
ACTH cortisol axis
CRH stimulates ACTH which goes to medulla and releases epi & NE; also goes to cortex and releases aldosterone, androgens, cortisol

end hormones negative feedback to hypothalamus & pituitary
cushing syndrome : clinical S/S
centripetal obesity: buffalo hump, moon facies
DM, HTN
mood affect
easy bruising
purple striae
proximal muscle weakness
hypokalemia
androgens: acne, hisrutism, menstraul irregularities
dx of cushing sndrome
high cortisol
- 24 UFC (urinary free cortisol)
- midnight salivary cortisols (should be low at this time)
- 1 mg dexamethasone suppression test (cortisol should go to 0 if normal)

after cushing confirmed, ACTH to determine level of problem
cushing's syndrome
exogenous: most common

endogenous
- ACTH dependent: pituitary or ectopic
- ACTH independent: adrenal
cushing syndrome tx
surgey

medical with inhiitors of steroidogenesis
- ketoconazole

all will have adrenal insufficiency as result of tx
hypopituitarism
gonadotropin: hypoonadism, infertility

ACTH: fatigue, ab pain, weakness (low cortisol)

TSH: secondary hypothyroidism

prolactin: failure of lactation postpartum

GH kids: short stature, adults, fatigue, weakness, LGM, increased fat mass
dx of hypopituitarism
TSH: low FT4, normal TSH
- beward of normal TSH asonly screen

ACTH: low cortisol & ACTH
- ACTH stim test, insulin tolerance test if not contraindicated

LH FSH: low testosteron,e LH, FSH, estradiol
- hypogonadotropic hypogonadism E2 not needed if menses normal

GH: IGF-1 suggestive if low
- GH reserve testing ITT

prolactin: no reserve testin necessary

AVP : AM urine for osmolality, serum Na, further evaluation if symptoms of DI
- unmasking of DI with cortisol replacement
multiple hormone failure
think hypopituitarism

def of 1 or more pt hormones: anterior more than posterior

causs: tumor, iatrogenic (surgery), trauma, autoimmune hypophysitis, infarction

if one hormone def, look for others

check hormones b4 surgery or anticipated stress
post pit
arginine vasopressin = AVP = ADH

disorders:
- DI: too little action
- SIADH: too much action (blood like water)
AVP action
V2R on collecting tubue of kidney
- insertion of AQP2 water channel into apicalmembrane of CD epithelial cell
- passivewater reabsorption
- along osmotic gradient

V1aR on vascular smooth muscle cell
- AVP mediated vasoconstriction

V1bR on ant pit corticotrophs
-regulation of ACTH secretion
Stimulus for AVP release
increase pOsm: 280-285
- small increase in pOsm : 1-2% really increases AVP
- max conc urine when AVP is 5 pg/ml
- pOsm 290-295
- >10 mOsm above osmotic threshold

decrease p Vol

decrease BP: via Baroreceptors in carotid A's and aortic arch; relatively weak stimuli

nausea, vomiting, pain meds, AI I, opiods
back up mechanism for water absorption
thirst

increase p Osm at 295 (higher than AvP)

via osmoreceptors in hypothalamus and wall of 3rd ventricle
DI
polyuria without osmotic stimuli
24 hr urine volume > 50 ml/kg
spec gravity < 1.010
Uosm < 300
DI presentation
no free water reabsorption
polyuria
polydipsia 5-10 L / day
DI dx
symptoms : polyuria, polydipsia, volume depletion

increasae serum Na with copious dilute urine

confirm with water deprivation test
DI causes
neurogenic: decrease AVP secretion: trauma, idiopathic

nephrogenic: decrease AVP action despite increase in concentration
- genetic, sickle cell anemia, lithium therapy
DI tx
free water intake by pt (drnk to thirst) or free water admin by provider, monitor serum Na

neurogenic: replace AVP
- temporary: aqueous AVP by SQ injection
-long term: long acting AVP analog: DDAVP (nasal spray or oral) once or twice daily

nephrogenic: AVP admin won't work
- hydrochlorothiazide: increases absorption of water in proximal tubule independent of aVP
- treat underlying cause: stop lithium
SIADH
ADH secreted in absence of hyperosmolar or hypovolemic (hypotensive) stimuli

CNS/hypothalmic: trauma, degenerative, vascular neoplastic

drugs: stimulate ADH secreion

neurogenic: pain, nausea

benign/malignant pulmonary disease
- pneumonia, emphysema, small cell
drugs that can induce SIADH
chlorpropamide
carbamazepine
vincristine
vinblastin
cyclophosphamide
phenothiazines
tricyclics
SSRI
SIADH clinical
S/S of hyponatremia
depends on acuteness
lethargy, malaise
nausea, vomiting
confusion, mental status changes
seizures

low serum osm, concentrated urine
natriuresis due to expansion of ECF
- increase in GFR, ANP, suppression of RAA axis
no edema
SIADH dx
hypoosmolar hyponatremia, euvolemic
ADH excess is appropriate in CHF, ascites, nephrosis, hypovolemia, hypercortisolism, hpocortisolism
low serum osm
concentrated urine
U Na > 20 mEq/L

excluse hypothyroidism, adrenal insufficiency, & diuretics
- must perform thyroid tests & ACTH stimulation test
SIADH tx
fluid restriction
treat underlying problem
AVP R inhibitor: conivaptan, tolvaptan ; if hyponatremia not responding to fluid restriction