ENDO Flashcards
which hormones share common beta subunit
FSH LH TSH hCG
FLAT HUG
which ant pit glands are basophilic
B-FLAT FSH LH ACTH TSH
Prolactin and GH *(eosinophilic) pig
which pancreatic cells produce which hormone and location
Beta cells (INSIDE) - insulin alpha - glucagon (peripheral) gamma - somatostatin (interspirsed
preproinsulin syntheiszed where
RER…cleavage into “proinsulin” and stored in secretory granules
growth hormone stimulates linear growth and muscle mass through…
IGF 1
how does growth hormone affect insulin
increases insulin resistance
what hypothalamic hormone does prolactin inhibit
GnRH (prvents ovulation and spermatogenesis)
GH is strucutrally homologous to…
prolactin
prolactin secretion from ant pit inhibited by…
dopamine from tuberoinfundibular pathway hypothal
how does TRH affect prolactin
TRH increass prolactin (so can see this in hypthyroid states)
how can antipsychotics cause galacorhea
blocking dopamine which disinhibits prolactin
fertility and puberty emdiated by pulsatile release of what
GnRH
treatment acomegaly
somatostatin (decrases GH and TSH)
why can you see galactorrhea in hypothyorid
increased TRH = increased prolactin
excess mineral corticoids, dcreated cortisol and sexhormones
17ahydroxylaes deficiency
ambiguous genitalia HTN
17ahydroxlyase deficiency
lab value in 17ahydroxylase def
lower androgens
effects of cortisol
A BIG FIB
Appetitei increased
BP increased
Insulin resistance (diabetogenic)
Gluconeogenesis/lipolysis/proteolisis increased (decreased glucose utlization)
Fibroblast activity decasdd (poor wound healing, striae, decreased colagen)
Immune (decreased inflamm and immune response)
Bone (decerased osteoblasts
relation between exogenous corticosteroids and TB
can cause reactivation TB and candidiasis (blocks IL2)
if steroids decrease immune response and inflammation, why do you see nutrophilia
decreaeses WBC adhesion so more is floating around in blood
steroids and mast cells
blocks histamine relase
where does pituitary sit
sella turcia
functional vs non functional pit adenoma
functional - poduces hormones
non functional doesnt
MCC pituatry adenoma
prolactinoma
presentation prolactinoma females
galactorrhea, amenorrhea (anovulation due to no FSH, LH)
presentaiton prolactinoma male
decrased libido
headache
elvated GH adn IGF1
LACK of gluose suppression
growth hormone adenoma
rx growth hormone excess
ocretoide (somatostatin analog) blocks GhRH
what tumor in children can result in hypopit
craniopharyngioma (can present with bilateral hemianopsia too) big clue
poor lactation, LOSS OF PUBIC HAIR recently after postpartum bleeding
sheehan syndrome (increased susepctiblity of pituitary to uundergo infarction and hypoperfusion during postpartum bleeding, esp since it’s gotten bigger beause of pregnancy)
atrophy or compression of pituitary
empty sella
herniation of arachnoid or CSF into sella turcica
polyuria, polydipsia, hypernatremia and high serum osmoality, low urine osmolality
central diabetes inspidus
specific gravity of urine in diabetes insipidus
low (keep losing free water)
water depriv test in central DI
deprivation cauess they to keep peein g(still low urine osmolarity)
give ADH analog and urine osmolaitiy goes up)…able to concetrate urine and keep more water in
imparied renal responset o ADH
nephrogenic DI
bipolar person keeps peeing
lithium can cause nephrogenic DI
water depriv result nephrogenic DI
give ADH analog, no effect on urine osm (urine osm still low)
DI has what effect on serum osm
inncreases it (keeps losing free water)
SIADH does what to serum osm
decreases osm (keeps in too much watere)
Na and serum osmolality in SIADH
hyponatremia
low serum osm
what cancer can cause SIADH
small cell lung cancer
MOA demeclocycline
blocks ADH
so this medication causes nephrogenic DI
but treats
SIADH
hyperosmotic volume contraction
DI
why is the body still euvolemic in SIADH
bod responds to water retention by increassing ANP and BNP and decreasing aldosterone which will increase Na excretion into urine (hyperosmolar urine)…but further worsens SIADH hyponatremia
what chemo drug can cause SIADH
cyclophsphamide
transporter that mediates glucose uptake in skeletal muscle cells
GLUT4
TSH function
stimulates small amt of T3 and lots of T4
relationship of reverse T3 and T4
peripheral T4 floating around gets converted to rt3
how is t4 converted to t3 in peripheral tisssue
5’deiodinase
what inhibits peripheral t4 to t3 conversion
glucocorticoids
wolff chaikoff effect
excess iodine will temporarily inhibit thyroid peroxidase which will decrase iodine organification and deccrease t3/t4 production
what mediates oxidation of I to I2
thyroid perioxidase
how to form MIT and DIT
I2 + thyroglobuiln (tyrosine residues)
what couples DIT and MIT together
thyroid perioxidase
what iodinates thyroglobulin to form MIT and DIT
thyroid perioxidase
which binds nuclear reeptor at greater affinity t3 or t4
t3
target PTU and methimazole
PTU porpylthiouracil - thyroid peroxidase and 5 deiodinase
methimazole - inhibits thyroid peroxidase only
which antithyroid med blocks peripiheral conversion t4-t3
PTU Prevents Peripheral conversion
teratogen in early pregnancy thyroid med
methimazole (meth is a teratogen)
adverse affect PTU
hepatotoxicity (so use it in later pregnancy instead of meth)
anterior neck mass, mobile
thyroglossal duct
oremnant of thyrglossal duct
foramen cecum (remember thyroid starts and tongue andmoves donward)
baswe of tongue mass
lingual throid
how does thyroid icrease basal metabolic rate
via increasing Na K ATPase!!!!!! and increasing B1 adrenergic receptors
how does thyroid affect cholesterol and glucose
hypocholesterolemia
hyperglycemia
thyroid incerases gluconeogenesis and glygogenolysis (icnreased sugar in blood)
Igg autantibody TSH receptor (stimualtes
Graves disease (increased produciton adn release of TH)
hyper thyroid, diffuse goiter, exophtalmos and pretibila myxedma
grave disease
dough like appearance on shin
pretibial myxedema which will increase fibroblast secretion of GLYCOASMINOGLYCANS which will increase osmotic muscle swelling and muscle inflmattion
graves hypersensitivity
type II
HADR3 HLA B8
graves disseae
how does T4 decrase TSH
downregulated TRH on anterior pit so it will not produce as much TSH
rx graves
5 Ps propanolol propylthiouracil prednsolen (steroids) potassium iodide
“hot” enlarged thyroid gland
multinodular goiter (work independently of TSH and increase relase of t3 t4
iodine deficient patient who is given iodine causes thyrotoxicosis
thyrotoxicosis
mental retardation, short stature, coarse facila features
proatruding umblicus
protuberant tomgue
cretinism
myxedema
doughy skin due to increased glycosaminoglycans
low thyroid can cause what to choleserol
hypercholetolemia
HLA DR5
hashimotos
how does hashiotos present
initla hyperthyroidism (as thyroid follicles are destroyed) then ebcomes euthyroid then hypothyroid
low T4 and higher TSH
histologic hallmark hashimotos
Hurthle cells
lymphoid aggregates with germinal centr
lmyphoid aggregates with germinal centers
hashimotos
incresaed risk for marginal non hodgkin lymphoma B cell
thyroiditis after viral infection with TENDER thyroid
subacute gran thyroditis
hard as wood non tender thyroid
reidel fibrosing thyrodisi
thyroid replaced by fibroid tissue
how does thyroid cancer look on iodine radio uptake studies
DECREASED UPTAKE (SO DO A Fine needle BIOPSY …IF IT’S COLD)
graves or nodular goiter will have increaesed uptake (hot)
fibrous capsul solitary growth thyroid (most are cold) no capsular or vascular invasion
thyroid adeoma
benign
MCC thyoird cacinoma
thyroid carcinoma
histologic hallmark papillary thyroid
orphan annie eyes
empty nuclei with WHITE CENTRAL CELARING
empty uclei with white central celaring
papillaryy
histologic hall marks of papillary thyroid
Papi and Moma adoptee Orphan Annie
papillary
psamomma bodies
orphan annie eys
RAS mutation
follicular carcinoma
invasion of thtroid capsule and vasculature uniform follicles
follicular CARCINOMA
what thyroid carcinoma likes to spread to blood
folicular
which carcinomas like to spread to blood
follicular
RCC
HCC
malignant proliferation of C cells
medullary carcinoma
hypocalcemia and thyroid mass
medullary carcinoma
malignant cells in amyloid stroma
medulary carcinoma thyroid
assocation familial medulary carcinoma
MEN 2A 2B
RET oncogene mutations
mutation Men 2A and 2B
ret mutation oncogene
undifferentiated malignant tumor of thyroid
anaplastic carcinoma (similar to reidel’s but seen in ELDERLY)
REIDELS SEEN IN YOUNG
congo red staining thyroid mass
medullary
amyloid has malignant cells in it
increasd calcitonin thyroid mass
medullary
MOA clomiphne
estrogen recepo modulation (decreases negative feedback inhibition of hpothalamus) there bincreaseing LH and FSH
genital lesion painful ulcer with ragged border and grey exudate with inguinal lymphadenopatyh
chancroid H ducreyi *curved gram neg rod)
camp signaling hormones
FLAT ChAMP FSH LH ACTH TSH CRH hcG ADH MSH PTH
how will Mg affect PTH
like Ca
low Mg = High PTH
high mg -> low PTH
how does PTH affect cAMPin urine
high PTH will increase cAMP in urine because it actiavtes kidney cells via Gs mechanism
how will PTH affect bone
cystic bone spaces with brown fibrous tissue hyper parathyroidsim)
consisting of osteo clasts and hemosierin
tourssea sign
hypocalcemia
fill bP cuff and get muslces spasms
tap on
higher than normal Ca levels required to suppress PTH (excessive renal Ca uptake
familial hypocalciuric hypercalcima
due to defective G coupled Ca ensing receptor
inflammation islets
t1dm
ketones
by hydroxybutryate and acetoacetate
mechanism t2dm
decrased numbers of insulin receptors!! = insulin resistance
aymloid deposits in islet cells
T2DM (islets are overworked)
marker t2dm
islet amyloid polypeptide deposits
elderly comes in with high glucose levels, hypotension and coma ABSENT KETONES
HYPEROSMOLAR non ketototic coma
how does diabetes cause cardiac complications
nonenzymatic gltosylation of larg medium sized vessels leads to athersceloriss in large vessles, leasds to hyaline arterioloscleorisis (kidny)
how is peripheral neuropathy caused in diabetes
osmotic damge to schwann cells (hyperglycemia increases glucose to SORBITAL metabolism faldose B which can deposit and cause damage)
marker insulinoma
C peptide
marker exogenous insulin
high insulin LOW C PEPTIDE
achlorhydria, cholelithiasis ans steatorrhea
somatostatinoma no gastric acid no contration of gallbladder galls tones no fat digestion
water diarrhea hypokalemia
VIPoma
abodinal striae cushings mcechaniem
cortisol inhibits collagen syntehsis
how does cushing cause HTN
increase up regulatio nof a1 receptors
cortisol inhibits ….
il2
histamine
phoslipase a2
bilateral adrenal atrophy
eogenous corticosteroids (steroids inhibits ACTH which will decrease stimulation of adernals)
high cortisol, low acth
exogenous glucocorticoids or adrenal tumor
high cortisol, high actch, high dose suppresses dex suppresses acth, CRH increass ACTH and cortisol
pituitary adeoma (cushing disease)
high cortisol high actch, high dose doesn’t dex doesn’t suppress actch, CRH stimulation doesn’t incerase ACTH and cortisol
ectopic ACTCH secretion (ct chest abdomen or pelvis)
hypernatremia, hypokalemia, metabolic alkaosis HTN
hyperaldostronism
HTN
secondary hyperaldosteronism causes
renovascular hypertension (activates RAAAS system) , renin producing tumors and edma
salt wasting and precocious puberty…clitormegaly in females
21 hydroxylase ef SHUNTING SEX
decreased cortisol increased ACTH, low aldosterone = HYPOTENSION
precocious puberty clitromegaly NO SALT WASTING
11 hydroxylase deficiency
excess mineralocortoids but no cortisol and sex steroids, ambiguous genitalia and sexual development HTN
17a hydroxylase
salt wasting
hyponatremia, hyperkalemia
due to decreased aldosterone
clle type medullary adrenal
chromaffin cells
brown tumor of adrenla medulla
pheochromocytoma
what to give before taking out pheochomo
pehnoxybenzamine (irreverisble a antagonist) follwoed by b blockers to prevent massive surge of catecholamines and hypertensive crisis
