Endocrinology Flashcards
additional finding in kallman syndrome
RENAL AGENESIS in 50%
growth hormone deficiency in adults
RARELY have symptoms, subtle signs - central obesity - increased LDL and CH levels - reduced lean mass
GH levels low
NOT that helpful since GH is pulsatile and maximum at night
confirming low GH
no response to arginine infusion
no response to GHRH
prolactin levels low confirmatory Dx
no response to TRH
metyrapovnse normally causes…
ACTH to rise, since inhibits 11 beta hydroxyls, thus decreasing output of the adrenal gland
before starting thyroxine what should you do,, for panhypopituitarism,,,,
CORTISONE before thyroxine
additional info for PC acromegly
carpal tunnel body odour colonic polyps arthralgias HTN
what can give a similar picture as acromegaly
GH abuse
best initial test for acromegaly
IGF-1
when should MRI be done in acromegaly
AFTER laboratory identification of acromegaly
what is co-secreted with GH
PRL
possible drugs for tx of acromegaly
cabergoline: DA agonist, inhibits GH release
octreotide or lanreotide: somatostatin inhibits GH release
PEGVISOMANY
PEGVISOMANT
GH receptor antagonist– inhibits IGF release from the liver
physiologic causes of hyperPRL
- pregnancy
- intense exercise
- renal insufficiency
- increased chest wall stimulation
- cutting pituitary stalk– no dopamine– no inhibition of PRL
drug causes of hyperPRL
- antipsychotic meds
- methyldopa
- metoclopramide
- opiods
- TCA’s
- verapamil
ONLY CCB to cause hyperPRL
VERAPAMIL
first thing necessary to do if patient has hyperPRL
PREGNANCY TEST
work up for hyperPRL
- TFTs
- Bun/Cr (since kidney insuff elevates PRL)
- LFTs (since cirrhosis elevates PRL)
which dopamine agonist is preferred for tx of hyperPRL
CABERGOLIN
when to tx hypothyroidism
High TSH (X2) + normal T4
when to decide on thyroid replacement in hypothyroidism
anti-TPO when TSH high, and T4 normal
involuted non palpable thyroid
exogenous thyroid hormone use
low TSH and decreased RAIU
- subacute thyroiditis– painful
- painless “silent” thyroiditis
- exogenous thyroid hormone use
tx of silent thyroiditis
NONE
tx of subacute thyroiditis
ASPIRIN
which thiourea drugs is preferred for hypthyeroidism
METHIMAZOLE
tx of graves opthalmopathy
STEROIDS
what must you do if FNA says follicular adenoma
REMOVE SURGICALLY– since can’t tell if benign or malignant from FNA alone
90% of hypercalcemia seen in
CANCER PATIENTS
tx of hypercalcemia of malignancy
saline
bisphosphonates
—— if not working yet–> CALCITONIN
how to tx hypercalcemia from granulomatous disease/ sarcoidosis
PREDNISONE
how long does it take for bisphosphonates to work
SEVERAL DAYS
bone effects imaging for hyperPTH
DEXA is greater than bone xr
imaging of neck for hyperPTH
dont pre-op for planning surgery
3 new random causes of hypocalcemia
- hypoMg: since need magnesium to cause release of PTH
- renal failure
- low albumin: causes decrease in 0.8 calcium
low albumin causing hypocalcemia
decrease total calcium
normal free calcium= ASYMPTOMATIC
EKG for hypocalcemia
PROLONGED QT
extra tid bits of info for cushings
- erectile dysfunction in men
- cognitive disturbance–> psychosis
- polyuria
best initial test for hypercortisolism
24-hr urine cortisol– more specific
next best test for hypercortisolism
1mg overnight DXM
FP’s with 1 mg overnight DXM suppression test
- depression
- alcoholism
- obesity
best initial test for determining the cause/location of hypercortisolism
ACTH level
ACTH level in cushing disease
increased
ACTH level in cushing syndrome
decreased
ACTH level increased, now what
MRI brain
negative MRI brain for cushings, now what
inferior petrosal sinus sampling for ACTH, possibly after stimulating with CRH
general endocrine rule
confirm the lab results first, THEN do imaging
cushing disease suppression test
YES suppresses
cushing syndrome/ cancer
NO doesn’t suppress
labs in cushings
hyperglycemia hyperlipidemia HYPOKalaemia metabolic alkalosis LEUKOCYTOSIS
why is adrenal crisis from the pituitary less common?
because the pituitary makes ACTH, which has a very little role in regulating aldosterone
labs in hypoadrenalism
hypoglycemia hyponatremia HIGH BUN HYPERkalaemia metabolic acidosis EOSINOPHILIA
what type of white cell is elevated in hypoadrenalism
EOSINOPHILS
dx or tx of adrenal crisis more important
TX
which steroid should we give when patient with hypoadrenalism has postural instability
fludrocortisone– has sufficient aldosterone-like effect
steroid in adrenal crisis
hydrocortisone– LIFE SAVING
best initial test for phaeo
24hr urine metanephreines, VMA
after biochemical testing for phaeo
CT adrenals
location of phaeo outside the adrenals imaging,
MIBG scanning
dx of DM
2 FBG > 125
1 random glucose >200 + symptoms
OGTT– increased glucose
HbA1c> 6.5%
goal HbA1c level in DM
less than 7%
which diabetes drugs cause weight loss
incretin mimetics
nateglinide, repaglinide
stimulators of insulin release, but don’t contain sulfa
onset: rapid acting insulin
5-15 minutes
peak action: rapid acting insulin
1 hour
duration: rapid acting insulin
3-4 hours
onset: short acting insulin
30-60 minutes
peak action: short acting insulin
2 hours
duration: short acting insulin
6-8 hours
onset: intermediate acting insulin
2-4 hours
peak action: intermediate acting insulin
6-7 hours
duration: intermediate acting insulin
10-20 hours
onset: long acting insulin
1-2 hours
peak action: long acting insulin
1-2 hours
duration: long acting insulin
24hrs
DKA presentation
in BOTH DMT1 and DMT2
potassium replacement DKA
replace potassium when levels are approaching normal
what factor indicates severity of DKA
serum bicarb (if very low, risk of death)
