Lecture 83 - Pituitary Disorders Flashcards
why is random plasma hormone testing not helpful?
what other tests should you consider if you suspect a deficiency in a hormone ?
If you suspect an excess of a hormone what should you consider?
hormones are cycling throughout the day (cortisol is lowest at midnight, peaks at 8am);
When suspecting hormone deficiencies, consider stimulation testing
For suspected hormone excess, consider suppression testing
inputs to the HPA axis that stimulates cortisol
what is the HPA axis?
Pain, pleasure, fear, anxiety, inflammation, hypoglycemia, depression
Hypothalamus –> CRH –> Pit —>ACTH –> Adnrenal —> Cortisol
Cortisol has negative feedback on levels of CRH and ACTH
what tests are are used to stimulate cortisol
cosyntropin (ACTH analog) test –
insulin tolerance test (ITT) – induces hypoglycemia which stimulates CRH
what the difference between primary and secondary adrenal insufficiency?
how can you differentiate between the two based on labs?
what is the best test for secondary hypothyroidism ?
Primary – due to direct adrenal failure (will have low cortisol, but high ACTH)
secondary – problem at the Pit or Hypothalamus (will have low CRH/ACTH + low cortisol)
secondary: ITT
Suspected Results for ITT and Cosyntropin tests for primary vs secondary adrenal insufficiencies?
Cosyntropin –
Primary – abnormal
Secondary - normal
ITT –
Primary – abnormal
secondary - abnormal
Cushing’s syndrome
whats the ddx for the etiology?
whats the most common exogenous etiology vs endogenous etiology
cortisol excess
Pitutiary adenoma (most common from endogenous)
Exogenous steroids (most common exogenous + overall cause) (such as those given for inflammatory)
Adrenal Tumor
Ectopic – Lung cancer (Small cell), carcinoid tumor
three bests diagnostic tests for hypercortisolism?
24 hour urine free cortisol (most specific)
Overnight 1 mg dexamethasone suppression test – should be low the next morning; but if Cushing’s state, then the cortisol will still be high
Midnight salivary free cortisol
tests for localization of the tumor
ACTH
if Adrenal – too much cortisol = negative feedback = low ACTH
If central/ectopic = normal or high ACTH
MRI - of brain
effects of too much cortisol
Cushing's features obesity moon facies poor bone and muscle strength Buffalo hump etc
what is Psueo-cushing state?
what can cause it?
Mild hypercortisolism in patients who have features of cushing’s
Hypercortisolism often seen in patients with clinical features
and
Generalized obesity
Active alcohol abuse
Depression
what is the thyroid axis
TRH –> TSH –> T3, T4
what is the most common cause of hypothyroid?
what is the level of TSH and T3/4?
in what other setting is the axis depressed?
how do you differentiate between primary and secondary hypothyroid based on labs ?
Hashimoto’s Disease
High TSH (b/c no neg feedback) Low T3, T4
Commonly depressed in very ll patients (neuro-endocrine response to severe illness)
Central (secondary) = low TRH, low T3, T4
Thyroid (primary) = low T3, T4 but high TRH
central vs primary hyperthyroidism:
how to you use labs to differentiate
whats the most common cause of primary hyperthyroid?
Central = High TSH, High T3, T4
Primary hyperthyroid (graves) = Low TSH, High t4, T3
Most common Primary = Graves Disease
what is Laron dwarfism? what are the GH labs?
what can these patients be treated with?
Normal GH levels
form of dwarfism in which the receptor is defective (therefore “effective” GH)
IGF1 (insulin like growth factor) is a possible treatment
beneficial effects of GH therapies for adults with GH deficeincy
Decreases in total and visceral body fat
Increase in muscle mass and bone density
Improved CV performance
Can help prevent HTN, Dyslipidemia, Insulin resistance, vascular effects, inflammation, osteoporesis
what is used as the surrogate marker for GH? when does it peak
IGF 1
rises up until ~20
then declines throughout life
why is it stupid to draw single dose of GH in the dx of GH disordres ?
GH secretion is pulsatile
for GH deficiency suspicion
describe the GH secretion test for the level of the pitutiary?
what is the stimulus at the level of the hypothalamus ?
Test Pituitary Function: block Somatostatin with Arginine;
stimulate GH with GHRH
Test Hypothalamic function:
ITT – in the stting of hypoglycemia;
acromegaly –
best diagnostic tests?
IGF1 levels
Glucose tolerance test (making the patient hyperglycemic should drop GH levels)
acromegaly –
Tx
□ Surgery
□ Radiation
□ Ocreotide (SST analog)
GH Antagonist: Pegvisomant (somavert)
prolactin – what inhibitors proflacin release?
Dopamine inhibits Prolactin
what factors promote the release of GH from the pituitary?
what factors inhibit it?
GHRH (from the hypothalamus) and Ghrelin (from the stomach) promote GH release
Somatostatin – inhibits GH release
GH excess before puberty is called _______
GH excess after puberty is called _____
Gigantism
Acromegaly
DDx of hyperprolactiemia
§ Dopamine Antagonists
§ Stalk effect – (anatomic/physiologic) block of dopamine
§ Hypothyrodism –> High TRH is a stimulator of prolactin
A clinical
tx of prolactinemia
§ Dopamine agonists – (cabergoline, bromocriptine)
Clinical consequences of hyper-prolactin
tx of prolactinemia
Clinical Consequences:
Amenorrhea in females (body things it might be pregnant)
hypogonadism in men
Dopamine agonists – (cabergoline, bromocriptine)
Clinical consequences of hyper-prolactin
tx of prolactinemia
Clinical Consequences:
Amenorrhea in females (body things it might be post partum)
hypogonadism in men
Dopamine agonists – (cabergoline, bromocriptine)
