endocrine Flashcards
hpa
TRH stimulates TSH then regulates thryoid gland to make T3 and T4
T3/T4 sensed by hypothalamas- increases TRH- then more TSH
negativ feedback: if thyroid hormone is too high- they inhibit BOTH HYPOTHALAMS AND PITUATRY tsh secretion!!
CRH
CRH is in hypo then ACTH made at pitutary gland and then ADRNEAL gland makes CORTISOL
GNRH
GNRH i hypothalm, FSH AND LH BY pitutary and OVARIES MAKES ESTROGEN, progesterone and small amount of teststerone, and in men- stimulates testes to produces TESTOSTERONE!
secondary disorders
secondary and tertiary disrodes have LABS IN THE SAME DIRECTION
primary disorders
labs in opposite directs if the problems is the target organ!!
TSH
best thyroid function test- initial test for suspected thyroid disease
also used to follow patients on thyroid hormone
LOW TSH—DECREASE DOSE OF LEVo
high tSh: increase dose of leveo
Free t4
ordered when tSh is abnormal
hashimoto’s ab
antithyroid peroxidase AB
anti thyroglobulin AB
grave’s disease ab
thyrodi sitmulating RECEPTOR ab
free t3
used to diagnosed hyperthyroidsim when TSH is low and T4 is STILL NORMAL!
normal ft4 and elevated tsh
subclinical hypothyroidism
low TSH plus normal FT4
subclinical hyperthyroidism
radioactive test
diffuse : grave’s disease or TSH secreting pitutary adnormal
decreased utake: THyROIDITIS- hypothyorid
hot nodule: toxic adnoema
multiple nodules: toxic multinodular goiter
cold nodules: rule out malig
subclinical hypothyroid
levothyroixine- if patient develops hyperlipid, or tsh too high
hypothyroid
cold intolerance, weight gain, dry thickened skin, loss of outer 1/3 eyebrow, goiter, nonpitting edema! sluggish, depression, decreased DTR, consti, anorexia, bradycardia, decresaed cardiac output, moenorrhagia, hypoglycemia
hyperthyroidism
HEAT intolerance, weight loss, skin warm, most, alpecia, goiter, hyperactivity, anxiety, inervous, diarrhea, hyperdefecation, tachy, plapitation, high output heart failure, no periods, hyper GLYCEMIA
euthyroid sick syndrome
surgery, malig, sepsis, cardiac- decreased t3/t4- but t3 ABNORMALLY LOW, decreased TSH too
thyroid storm
usually ater surgery, truama, infection, illness, preg
palpitations, tachy, atrial fibb, high fever, nausea, vomiting, psychosis, tremors
Propylthioracil or methimazole@!!!- ptu prevents peripheral conversation of t4 into t3.
BETA BLOCKRES!!! IV sodium iodide
IV GLUCOCORTICOSTEROIDS!!!- NO ASPIRIN!!!- COOLING BLANKETS!!!
myexdema crissis
bradycardia, coma, hypothermia, hypoventilation, hypotensive, hypoGLYCEMIC, hypoNATREMIA IV SYNTHROID (levo_, passive warming. DONT WARM THEM SO FAST!, normal saline
grave’s
pretibial myxedema!!- non pitting- pink to brown plques on shin
diffuse uptake!- radioactive iodine- MC therapy!!!
toxic multinodular goiter
patchy aras of both increased and decreased uptake= radioactive iodine!
methimazle: and ptu: AGRANULOCYSOIS!!! hepatitis
PTU preferred in pregnancy
medication induced
AMIODARONE- hypothryoidsim , OR LITHIUM!!!!!!
levothyroroxine
synthetic T4!!!!- monitor TSH every 6 week intervals!!!
thryoid nodules
most in women are BENIGN = follicular adenoma or cysts!!!
men and children - most likely malig- papillary CANCER MC in Women
asymptomatic.
most patients ARE EUTHyroid
benignnodules: follicular ADENOMA!!!!!
FNA with biopsy- best test to evaluate!
cold nodules- suspicious for malig
thyorid carc
papillary most common, least aggressive, exceelent high cure rate- radiation exposure
folliculr: distant mets common- slow growing
medullary: MEN 2 association - secrete calcitonin
anaplastic: WORST one!! - most aggressive- rapid growth
phosphate
opposite direction of calcium usually! in priary
hypercalcemia
stimulates calcitonin secretion- decreases blood calcium levels
primary hyperparathyroidism
too much TH- PARATHYORID ADENOMA MC!!!!!
lithium!!
secondary hyperparathyroidism
increased pth due to hypocalcemia or vitamin D deficiency (chronic kidney failure!!!) - mc common reason fo secondary!!- kidney covers vit D to usable form!
hypercalcemia
stones, bones, abd groans, spychoic moans, DEEP tendon reflex DECREASED!- qt shortened!!
surgery- parathyroidecotomy, vitamin D if secondary
kidney stones, painful fractures, constipation, decreased DTR!
hypoparathyroidism
postsurgical or AUTOIMMUne mc
accidental removal of parathyroid glds or autoimmune destruction of parathyroid gladn, increased DTR!!!
TROUSSEAu’s and chvosket’s signs!!
prolonged QT- less stimulation needed for heart, nerves and activation/contration!
facial nerve tap : chvosket’s: causes facial spasm!!
trousseua’s: inflation of bp cuff above systolic BP causes carpal spasm
calcium tx: vitamin D
iv calcium gluconate if severe
osteoporosisi
dexa scan shows T score less than -2/5
normal is more than 1.0
bisphosphonates!!- can cause pill esophagitis, jaw osteonecrosis, pathological femur fx
vitamin D
SERM- raloxfine- not associated with risk of endometrial cnancer
ESTROGEN!- increases risk of endometrial and breast cancer
osteogenesis iperfecta
blue tinted sclera and preseile deafness- -genetic mutation
renal osteodystrophy-
chronic kidney failure- less vitamin D- hypocalcemia, increased PTh= decreased mineralization!
increased phosphate, but hypocalcemia!! secondary hyperparathyoridism!
osteiitis fibroiss cystica: salt and pepper appearance of skull!!!
vitamin D- treatent- give active form! (calcitroil)
osteomalaci and rickets
due to vitamin D deficiecnce- less calcium and less phosphate–Soft bones!
decreased mineralization of bone osteoid only!!
osteoporosis- mineral and matrix loss is PROPORTIONAL!
corical thinning- mineralization decreased only!
bowing in children , bone pain in adulst
both calcium and phosphate DECREASED and incresaed alkaline phosphatase
give vitamin D (ergo)
adrenocortical insufficiency
secondary most common
primary: addison’s diase : adrenal gland destruction (LACK OF CORTISOL AND ALDOSTERONE!)- autoimune mc in USa
SECONDARy: pitutary failure of ACTH secretion (lack of CORTISOL only)!!!!- aldosterone still itact!!- EXOGENOUS steroid use- MC!!
adrenal insufficiency
LACK OF CORTISOL!!!!- muscle ache, weak, fatigued, weight/appetite loss, nausea, vomiting , abd pain, heaache, sweating, HYPOGLYCEMIA- common in secondary!!!
primary addison’s disease
lack of aldosterone, lack of sex hormone, INCREASED ACT!!
hyperpig- due to increased ACTH!!
decreased ALDOSTERONE: SO HYPOTENSION- orthostatic hypotension, HyPOnatremia (salt is not treasured- it is let go of), hypoglycemia!!!!
decreased sex hormones in women- no libido, amenorrhea, loss of axillary and pubic hair!
diagnosis of adrenocort insufficiency
high dose ACTH stiulation test: SCREEN!!!- (COSYntropin)- blood urine cortisol checked before and after
NORMAL- rise in blood/urine cortisol levels after ACTH given
ADRENAL insufficiency: little or NO INCREASE IN CORTISOL!
CRH stimulation test: differences the cause
primary (ADRENAL CAUSE_ increased ACTH levels but LOW CORTISOL!- czu adrenals aren’t working
secondary: low ACTH AND LOW CORTISOL!- pitutary can’t produce ACTH!
tx for adrenocort insufficiency
only glucocorticoids in 2ndry: hydrocortisone, pred dexa
mineralocorticoid and gluco in primary: fludrocortisone (only for primary)
during illness/surgery/high fever
increase the corticosteroids to recreate normal adrenal gland response
addisonian crisis
stressful event makes adrenal insuf worse- ABRUPT WITHDRAWL OF GLUCOCORTICOIDS most common cause!!!
SHOCK~!!!!, hypotension, hypovolemia!! hyponatremia, hyperkalemia, hypoglycemia!!
iv fluids, dsns if hypoglycemic, iv hydrocortisone, fludrocortisone
cushing’s syndrome
CORtisol excess
cushing’s DISEASE: specifically due to pitutary increased ACTH secretion!!!
moon facies, buffalo hump, supraclivuclar fat pad,s central obesity, thin extremities,bruising, striae (skin atrophy), hyperpigmentation- too much acth, HTN, weight gain, hypokalemia!! androgen excess
TOO much high dose corticosteroids most common cause!!!
cushing disease
pitutary adenoma- secretes ACTH
ectopic acth
acth secreting- small smell lung cancer
adrenal tumor
cortisol-secreting ADRENAL ADENOMA
test for cushing’s syndrome
low dose dexa suppression test: dexa more potent than cortisol- normal woluld be cortisol supression- in cushing sydnrome- no suppresion
24 hour urinary free cortisol levels!!- increased in cushing’s syndrome!!!
differential test for cushing’s
high dose dexa suppression test: ACTH from pitutary is only partially resistant to glucocorticoid negative feedback!— suprresion:cushing’s disease- so pitutary secreting ACTH is the reason
if not suppressed: adrenal or ectopic ACTH producting TUMOR
CAN ALSO DO ACTH levels: in cushing’s disease: increased ACTH or ectopic production
decreased ACTH in adrenal tumors!!—too much cortisol suppresses ACTH
hyperaldolsteronism
ADRENAL hyperplasia!!
Aldosterone: Glomerulosa
Cortisol : fasciculata:
Estrogen: R (reticularis)
primary: idiopathic bilateral adrena l hyperplasia- mc
or CONN’s syndrome- adrenal aldosteronma in zona GLOmerulosa!!
2ndry: due to increased RENIN– due to renal artery stnossis!
gets rid of the potassium, keeps the sodium: HTN, hypokalemia, headches,
peheochromocytoma
increased metanephrine and vanillylmadndelic acid- adrenalacetomy
alpha blockade and then beta blockers
PHENOXYbenamine or PHEntolamine and thenbeta blockers!!
don’t initiate with beta blockers before alpha
anterior pitutary tumors
MICROADENOMAS that are functinoal!!- hypersecretion!!
prolactinoma: most common type
somatotropinoma: growth hromone secreting —> acromegaly and gigantism!!- DM and GLUCOSE INTOLERANCE!!- GH increases glucose!!
diagnosis: insulin like growth factor is increased
ACTH tumor: increases ACTH- cushing’s disease and hyperpig
TSH secreting adneoma
acromegaly treatmnet
TSS and bromocriptine!! (dopamiene agonist DECREASES GH production) OCTREotide: somatostatin analog that inhibits GH SECRETION!
dopamine
INHIBITS prolactin release
so treatment is bromocriptine for prolactinomas!
DKA
hyperglycemia, dehydration, ketones- high anion gap and POTASSium DEFICIT!!!
abd pain
kussmaul’s respiration- deep continuus respirations, fruity breath
hyperosmolar hyperglycemic syndrome
potassium deficity, no ketones, dehydration- INCREASED OSMOLARITY!!
mental status cahnge1
tx for DKA and hhs
isotonic NS, insulin, potassium!!!!!!!!!!!! potassium deficit present in both!!!
DM
type i: pacretic beta cell destruction- can’t make insulin- young adults- autoimmune bta cell destruction
type II: insulin resitance and relation impairemnet of insulin secretion , genetic and environmental, weight gain and decreased physical activity is risk factors!
polyuria , polydipsia, polyphagia, weight loss
Dm retinopathy
microaneursms, hard exudates, blood (dot or flame shaped hemorrhages), cotton wool spots, neovascularations, macular edema- centr al vision loss
nephropathy: microalbuminaria- first sign!!!- ace inhibitors!!
hypoglycemia
brain dysfunction at 50
sx @60
diagnosis
fasting plasma more than 126 two ocassions- gold standard
2 hour glucose tolerance test: more than 200
3 hour glucose tolerance test: gold standard for gestational
hemoglobin a1c more than 6.5
or random plasma more than 200!!!!
goals for DM
hgb a1c less than 7, prepradial 80-130, post- less than 180!
lipid control: less than 100, hdl more than 40, tg less than 150!
biguanides
metforming- decreases hepatic glucose production, lactic acidosis- don’t give if hepatic or renal impariement- stop metformin 24 h before giving iodinated contraste and resume 48 h after monitoring creatinine
pancreatic insulin release stimulated- hypoglycemia!
glypizide glyburide, glimipiride
hypoglycmeia!!!
weight GAIN! common side effect- sulfa allergy people can’t take this
meglitidnides
stimulates panc beta cell release- repaglinide, netaglinides
hypoglycemia- mc side effect
a-glucosidase inhibit
acarbose, miglitol = delays intestinal glucose absorption!
inbhitis amylase and alpha glucosidase hydrlase
hepatitis- flatulance, diarrhea, abd pain
thazolidinediones
increaes insulin sensitivyt in peripheral receptor site- adipose and muscle tissues
fluid retension and EDMEA!!= cardiovscular tox with AVANDIA
glucagon like petitede 1-
exenatide
liraglutide- slows gastric emptying
increses insulin secretion- mimics incretin!
hypoglycemia!!!- common side effect- injection!
dpp 4 inhibitor
januvia- sitagliptin, gliptin! increases GLP-1
sglt-2 inhibitor
flozin
increaes urinary glucse secretion!!
makes you thirst as side effects
insulin
rapid acting- lispro, aspart- same time of meal given
short acting: regular: given 30-60 mins prior to meal
nph: insulin for half day or overnight- intermediate
long acting: detemire, glargine: 1 full day- basal!
dawn phenomenon
rise in serum glucose levels between 2am -8am- due to nightly surge of counter regulatory hormones- given bedtime injection of nph!!!- growth hrmone
samogyi effect
nocturnal hypoglycemia followed by rebound hyperglycemia- due to surge in growth hormone
prevent hypoglycemia!!!—decrease nph or give bedtime snack!!
x-ray of wrist and left hand
used to determine bone age
constitutional growth delay
Constitutional growth delay is the most common cause of short stature, and delayed puberty. It is characterized by a normal growth velocity, a bone age that is below chronological age, and normal growth hormone production. In boys, low levels of testosterone are also characteristic.
insulin like growth factor 1- synthesized by liver
Insulin-like growth factor 1
The insulin-like growth factors are proteins with high molecular sequence similarity to insulin. Insulin-like growth factor 1 (IGF-1) is mainly secreted by the liver as a result of stimulation by growth hormone. IGF-1 is important for both the regulation of normal physiology, as well as a number of pathological states.
more than 1000 triglyceride
risk for pancreatitis
hormones produced by hypothalamus
Corticotropin releasing hormone, thyrotropin releasing hormone, GH releasing hormone, somatostatin (GHIH), gonadotropin releasing hormone, and dopamine are produced in the hypothalamus.
pitutary adenoma
micro- less than 10 mm- treat with meds with bromocriptine for small one for prolactinoma!
bigger than that- surgery
