ENDOCRINE LABS Flashcards
pancreas
diabetes diagnostic
- random blood sugar
- fasting blood sugar
random: 200 with DM symptoms
fasting: > or = 126 after 8hr fast (initial screening test)
pancreas
diabetes diagnostic
- oral glucose tolerance
- HgBA1C
oral glucose: glycemic response after 75mg glucose load, if 2 hrs post glucose >200
HgBA1C: 8-12 week gluc average >6.5 (also used to monitor tx)
diabetes guidelines for testing
- retest every 3 yrs when fasting glucose (FPG) <100 or A1C <5.7 (nl pt)
- retest 1-2 yrs when FPG is 100-125 or A1C 5.7-6.4
- counsel on smoking cessation, diet/exercise
- recommended screening >45 yrs or those w/multiple RFs
diabetes
- monitoring (3 ways)
point of care glucose
- monitoring before meals hypo or hyperglycemia (dexcom, freestyle libre)
microalbuminuria
- early marker of nephropathy
autoantibodies
- type 1—> pancreatic autoantibodies against 1 or more: GAD65 (MC), IA2, insulin, ZnT8
thyroid hormones
TRH
TSH
TRH- thyrotropin releasing hormone from hypothalamus, induces TSH
TSH- thyroid stimulating hormones, from ant pituitary, stimulates thyroid
thyroid hormones
T3
T4
free T4
TGB
T3- from thyroid
T4- from thyroid (thyroxine)
free T4- unbound to protein, better indicator of thyroid status
TGB- thyroid binding globulin, plasma protein for transport
iodine from dietary intake
anti thyroid antibodies
anti TPO: against protein in thyroid gland that produes thyroid hormones
(autoimmune thyroid ds)
anti TGL antithyroglobulin
present in BOTH hypo and hyper, must look at T3+4 and TSH to figure out which
radioactive iodine uptake test
- indication
- how does it work
pt takes radioactive iodine, can see when it is taken up
indication: determine underlyin cause of hyperthyroidism, eval thyroid nodules, and assess tx
hyperthyroidism (thyrotoxicosis)
- SS
- labs
- types
SS: nervousness, palpitations, muscle weakness, heat intolerance, wt loss, exophthalmos, fine tremor of hands
labs: low TSH, high Free T4
types: graves (autoimmune), toxic multinodular goiter, toxic adenoma
which medications can inc hyperthyroidism
amiodarone
lithium
hyperthyroidism
toxic multinodular goiter
- what is it, radioactive uptake?
- less severe
- normal to high radioactive uptake
- iodine localized to active nodules (patchy uptake)
function independent from TSH, benign
hyperthyroidism
toxic adenoma
- what is it, radioactive uptake?
- benign
- secretes thyroid hormone
- radioactive uptake local to adenoma (one spot)
hyperthyroidism
thyroiditis
- what is it, radioactive uptake?
- from viral infection
- eventually returns to normal (self limiting)
- NO radioactive uptake (thyroid is inflamed)
- can progress to hypothyroid
hyperthyroidism
painless thyroiditis
- what is it, radioactive uptake?
drug reaction (amiodarone or lithium)
- result in Low TSH, high free T4 and T3
- depressed radioactive uptake
hypothyroidism
- SS
- labs
infants– presents as cretinism
labs: inc TSH, low free t4
- high anti-TPO = hashimotos thyroiditis
SS
- dry hair, dry skin, cold intolerance, weight gain, constipation, hair loss, prolonged menstruation
adrenal cortex
- release?
glucocorticoids: alter carb metabolism by inc glucogenesis and dec gluc utilization
mineralcorticoids: sodium conservation and potassium loss, influence retention or loss of fluid
sex steroids: androgens, progestogens, estrogens
ALL CHOLESTEROL BASED, synthesized by adrenals and gonads
adrenal cortex
ACTH and Cortisol
- what do they do
ACTH/corticotropin: regulates glucocorticoids and mineralocorticoids, secreted from ant pituitary
cortisol: highest in morning (4-8am), stress can blunt and reduce circadian rhythm
adrenal cortex
RAAS system
- renin released in response to dec blood sodium, volume, and/or pressure
- renin hydrolyzes angiotensin to produce angiotensin I
- rapidly converted to angiotensin II by ACE
- angiotensin II stimulates cells of the adrenal cortex to secrete aldosterone
angiotensin II is also a potent vasoconstrictor
adrenal cortex
cortisol testing
24 hr urinary excretion of cortisol
adrenal cortex
cushing syndrome
- what is it
- dx
- types
- disorder of excess cortisol production
Dx- low dose dexamethasone supression test
types:
- cushing disease: pituitary adenoma
- adrenal cushing syndrome: adrenal tumor
- cushing syndrome: lung carcinoma
cushings syndrome
low dose dexamethasone supression test vs. high dose results
low dose glucocorticoid given to suppress ACTH and then cortisol
- if its cushings syndrome there will be NO suppression and cortisol levels will be HIGH or nl
high dose test is done to determine cushings disease (pituitary tumor)
- if cortisol and ACTH levels are low with the HIGH DOSE test, it indicates cushings disease
adrenal cortex
cushings syndrome
SS
dec libido, obesity/wt gain, red/round face, osteoporosis, purple striae, HTN, CNS irritibaility/emotional disturbances, fat deposition on abdomen and back of neck, cardiac hypertrophy
females- amenorrhea, hirsutism
males- erectile dysfunc
moon face, buffalo hump, purple striae, truncal obesity (thin limbs, abdomen fat)
adrenal cortex
addisons ds- adrenal insufficiency
dx
ACTH stim test
- bolus of ACTH given, lack of rise in cortisol indicates adrenal insuff
addisons ds
SS
hyperpigmentation, low BP, weakness, wt loss, n/v/d, vitiligo
adrenal crisis- clin features
(addisonian crisis)
fever, syncope, convulsions, hypoglycemia, hyponatremia, severe v/d
SEVERE hypotension, nausea/vom, and electrolyte crash
adrenal cortex
dx for determining primary vs secondary adrenal insufficiency
CRH stim test
- checking if pituitary responds
- use if ACTH stim is abnormal to find the site of malfunction
primary–> elevated ACTH but NO cortisol
secondary–> low ACTH and cortisol
adrenal cortex
hyperaldosteronism and hypoaldosteronism
- aldosterone purpose
- clinical features/SS
aldosterone- responsible for sodium retention, potassium excretion and water resorp (blood volume control)
hyper: HTN, hypervolemia, LOW potassium
hypo: low blood volume, LOW sodium
adrenal medulla
produce catecholamines like epinehprine
- 2 min half life
adrenal medulla
pheochromocytoma
- what is it
- clinical features/SS
- how to dx
RARE, can be benign or malignant
- chromaffin cell tumor, secretes catecholamines
SS- HTN, palpitations, sweating, anxiety (like a constant shot of adrenaline/fight or flight)
dx- measure plasma metanephrines or urinary metanephrines and then find the tumor
parathyroid
- hormones
- feedback loops
- disorders alter calcium metabolism, effect bone
- PTH regulates calcium in extracellular fluids
inc in PTH–inc in serum calcium—dec in serum phosphorus
- nl or high calcium gives feedback to parathyroid to STOP PTH production
calcium and phosphorus usually fluctuate inversely
parathyroid gland
primary hyperparathyroidism
- causes
- labs
- clin features
- work up
excess PTH, high calcium
caueses: adenoma, hyperplasia, carcinoma
clin features: kidney stones, HTN, polyuria, constipation, depression, neuromusc dysfunc, recurrent pancreatitis, osteopenia
bones, groans, and kidney stones (high calcium)
work up: calcium, PTH, phosphorus
parathyroid gland
secondary hyperparathyroidism
- labs
- causes
- work up
chronic hypocalcemia, compensation with inc PTH
causes: vit D deficiency, renal ds
work up: high PTH w low calcium
hyperparathyroidism
vit D deficiency SS
depression, schizophrenia, asthma, wheezing, htn, coronary heart ds, type 1 DM, aches/weakness, rickets/osteoporosis
hypoparathyroidism
- mc cause
- clin features
- work up
mc with unintentional removal of parathyroid w thyroid surgery
ss - hypocalcemia causes numbness, tingling, low serum calcium levels, muscle spasms, convulsions
work up- PTH low, calcium low, high phosphorus
psuedohypoparathyroidism
resistance to the action of PTH
work up- high PTH, low calcium
NO response when given PTH
(genetic disorder)
parathyroid
osteoporosis vs. osteomalacia
osteoporosis
- dec bone mass
dx- bone mineral density study
tx- bisphosphonate
osteomalacia
- deficient mineralization from disturbance (lack of) in calcium and phosphorus
- rickets when before cessation of growth
- bones soften and weaken
testes and ovaries
- hormone path
hypothalamus–GnRH-pituitary—FSH LH—ovaries or testes
ovaries (granulosa cells)–estradiol
tests (leydig cells and sertoli cells)—testosterone
anterior pituitary
Growth hormone excess
excess in adults: acromegaly
excess in children: giantism
anterior pituitary
prolactin
milk production
posterior pituitary
ADH/vasopressin
- triggered by?
- neg feedback
triggered by inc in osmolality
ADH- binds to receptors on smooth muscle that induce vasoconstriction, inc BP and volume
- will inc volume retention
neg feedback- w/atrial natriuretic peptide
posterior pituitary
ADH- diabetes insipidus vs. SIADH vs. dehydration
diabetes insipidus: deficient in ADH—> inc serum Na, inc serum osmo, dec urine osmo
SIADH: ADH inc–> dec serum Na, dec serum osmo, inc urine osmo
dehydration: serum Na, osmo, and urine osmo all HIGH
insipidus- causes excessive thirst and urination due to an imbalance in the body’s ability to regulate water
