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321 Cards in this Set
- Front
- Back
sx of pheochromocytoma vs neuroblastoma
|
pheochromocytoma will have episodic htn. Neuro does not
|
|
drainage of left adrenal vs right adrenal
|
left adrenal drains to left renal. Right adrenal drains directly to IVC
|
|
what pituitary hormones are made in basophils
|
BFLAT = FSH, LH, ACTH, TSH
|
|
what nucleus is responsible for secretion of ADH
|
supraoptic nucleus
|
|
what nucleus is responsible for secretion of oxytocin
|
paraventricular nucleus
|
|
what cranial hallmarks locate the pituitary gland
|
sella turcica near sphenoid bone
|
|
what gene products are made in the POMC gene
|
ACTH, MSH, beta-lipotropin, beta-endorphin
|
|
what gene are neurophysins made on
|
same gene as the hormone (secreted together - analogous to C peptide)
|
|
what hormones are secreted from anterior pituitary
|
FLAT PiG = FSH, LH, ACTH, TSH, Prolactin, GH
|
|
what pituitary hormones possess alpha subunit
|
FSH, LH, TSH, hCG (therefore these have some level of cross-reactivity)
|
|
secretion of what hormone is interrupted first in hypopituitary lesion
|
GNRH, then GH
|
|
what amino acids can stimulate GH
|
Arg, His
|
|
is GH secreted at constant levels throughout day
|
no, sleep increases GH, :. Diurnal cycle
|
|
stimulation tests are used for ____, suppression tests are used for ____
|
underactive gland vs hyperactive gland
|
|
in a pancreatic islet, where are the beta cells located
|
center of islet
|
|
in what part of the pancreas are most islets located
|
tail
|
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which cells do not require insulin for glucose uptake
|
BRICKL = brain, rbc, intestine, cornea, kidney, liver
|
|
where are GLUT2 receptors found
|
beta islet, liver, kidney, small intestine
|
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7 effects of insulin on metabolism (involving glucose, glycogen, gluconeogenesis, fat, systemic)
|
1. increase glucose uptake 2. glycogen synthesis 3. decreases gluconeogenesis 4. TG synthesis 5. causes sodium retention in kidney 6. increased protein in muscle 7. increased cellular uptake of potassium and amino acid
|
|
how does insulin affect gluconeogenesis
|
inhibition of glucagon. Insulin INCREASES glycolysis so that prevents gluconeogenisis
|
|
adrenergic effects on insulin
|
alpha stimulation decreases insulin. Beta stim increases insulin
|
|
where are GLLUT1 receptors found
|
RBC, brain
|
|
where are GLUT4 receptors found.
|
adipose, skeletal mm
|
|
defects in glucokinase will result in
|
impaired ability to sense glucose
|
|
what intracellular signaling pathway can antagonize insulin pathway
|
NFkappaB -> Ser/Thr kinase
|
|
review mechanism of beta cell sensor
|
p289
|
|
name a homolog of GH
|
prolactin
|
|
what regulates prolactin levels
|
promote by TRH, inhib by dopamine
|
|
what regulates GH levels
|
promote by GHRH, inhib by somatostatin
|
|
regulation of TSH levels
|
promote by TRH, inhib by somatostatin
|
|
effect of body weight on GnRH
|
decreased body weight decreases GnRH
|
|
what hormone regulates GnRH levels
|
prolactin
|
|
tx for prolactinoma
|
dopamine agonist (eg bromocriptine)
|
|
effect of prolactin on dopamine synthesis
|
increases
|
|
3 functions of prolactin
|
1. milk production 2. inhibits ovulation 3. inhibits spermatogenesis
|
|
what nucleus in the hypothalamus secretes dopamine
|
arcuate
|
|
what could be cause of amenorrhea in pt 4-6mo postpartum
|
Sheehan's syndrome destroys pituitary -- so most likely GnRH, GH levels will be depressed
|
|
review steroid biosynthesis pathway
|
p291
|
|
regulated steps in steroid synthesis
|
StAR, desmolase
|
|
what type of enzyme is desmolase
|
CYP
|
|
what is mechanism of metopirone
|
inhibits 11b hydroxylase
|
|
hypertension, hypokalemia. Pseudohermaphrodite male, or female lacking 2* sex characteristics
|
17alpha
|
|
hypotension, masculinization, hyperkalemia, increased renin
|
21
|
|
masculinized, hypertension, decreased cortisol
|
11beta
|
|
how to tell quickly: 17alhpa vs 21 vs 11beta
|
1 in first digit = HTN; 1 in 2nd digit = masculization
|
|
5 main functions of cortisol
|
1. maintain blood pressure (upregulates alpha1 on arterioles) 2. decrease bone formatoin 3. anti-inflammatory 4. decreased immune function 5. increase gluconeogenesis, lipolysis, proteolysis
|
|
is corticol secreted at a constant level throughout day
|
diurnal variation (highest before waking)
|
|
how is cortisol anti-inflammatory
|
1. blocks phosopholipase A2 (arachadonic acid pathway) 2. decreases synthesis of adhesion molecules (which can cause increased neutrophils) 3. apoptosis of B cells 4. decreases eosiniphils 5. blocks NF kappa B which decreases TNFalhpa 6. blocks IL2
|
|
what hormones can decrease synthesis of adhesion molecules on blood vessels
|
cortisol, epi, norepi
|
|
increased what levels of what hormone can predispose to cataracts
|
cortisol
|
|
effect of cortisol on thyroid
|
1. blocks 5'-deiodinase 2. decreases TSHr on thyroid follicle
|
|
effect of cortisol on skin
|
decreases collagen -> stria
|
|
effect of PTH on serum Ca, phosphate and urine phosphate
|
increases serum calcium, decreases serum phosphate and increases urinary phosphate
|
|
4 effects of PTH on calcium and phosphate and vitamin D
|
1. increases bone resportion of calcium and phosphate 2. increased resportion of calcium in DCT 3. decreased kidney resporption of phosphate (excreted as cAMP) 4. increased 1alpha hydroxylase
|
|
effect of PTH on osteoblast
|
MCSF, RANKL expression
|
|
effect of Mg on PTH
|
less Mg means less PTH
|
|
causes of decreased Mg
|
DAAD = diarrhea, aminoglycoside, diuretic, alcohol abuse
|
|
another name for IL1
|
osteoclast activating factor
|
|
when is a negative calcium balance seen physiologically
|
pregnancy and lactation
|
|
vitamin D2 vs D3
|
D2 is from plants, D3 from sun exposure
|
|
what cells make calcitonin
|
parafollicular cells of thyroid
|
|
what endocrine hormones act through cAMP
|
FLAT CHAMP = FSH, LH, ACTH, TSH, CRH, hCG, ADH (V2), MSH, PTH, ALSO calcitonin, GHRH, glucagon, epinephrine
|
|
what signaling pathway does ANP use
|
cGMP
|
|
what signaling pathway does NO use
|
cGMP
|
|
what endocrine hormones act through IP3
|
GOAT = GnRH, oxytoxin, ADH (V1), ATII, TRH
|
|
where are thyroid receptors located
|
nuclear
|
|
where are steroid receptors located
|
cytoplasmic
|
|
what kinase Is intrinsic tyrosine kinase associated with
|
MAP kinase
|
|
what pathway is receptor-associated tyrosine kinase (NOT INTRINSIC TYROSINE KINASE) associated with
|
JAK/STAT
|
|
what signals use receptor associated tyrosine kinase
|
GH, prolactin, IL2
|
|
what signals use intrinsic tyrosine kinase
|
growth factors (eg insulin, PDGF, IGF, etc )
|
|
effect of increased sex hormone binding globulin on men
|
gynecomastia
|
|
effect of decreased sex hormone binding globulin on women
|
hirsutism
|
|
5 functions of thyroid hormone
|
1. bone growth (synergy with GH) 2. increase beta1 in heart 3. CNS maturation and mental alertness 4. increases na/k pump (BMR) 5. glyogenolysis, gluconeogenesis, lipolysis
|
|
effect of beta blockers on thyroid hormone
|
indirectly can reduce symptoms, but also bb inhibits 5' iodinase
|
|
relationship between thyroid and muscle growth
|
see decreased type 2 muscle in hypothyroid (increased breakdown elevates CK)
|
|
relationship of thyroid on fat levels
|
thyroid increases LDLr
|
|
effect of hypothyroid on bone growth
|
bone age < chronological age
|
|
name things which can increase thyroxine binding globulin
|
estrogen (ie pregnancy, ocp)
|
|
name things which can decrease thyroxine binding globulin
|
hepatic failure, androgen
|
|
causes of cushing
|
in order of mc: STEROIDS, pituitary adenoma = cushing's dz, ectopic acth, adrenal adenoma, carcinoma or hyperplasia
|
|
best screening test for cushing
|
24 hour cortisol
|
|
dexamethasone suppression on healthy person
|
low dose will suppress cortisol
|
|
dexamethasone suppression on pituitary adenoma
|
only high dose will suppress
|
|
dexamethasone suppression on ectopic acth tumor
|
cannot be suprressed
|
|
dexamethasone suppression on adrenal tumor
|
cannot be suppressed
|
|
skin changes with thinning and purple stria
|
cushing
|
|
osteoporosis, amenorrhea, muscle weakness, and recurrent infection
|
cushing
|
|
why does increased cortisol result in muscle weakness
|
gluconeogenesis results in breakdown
|
|
why is there increased fat in cushing
|
increased glucose results in insulin release
|
|
what is nelson's syndrome
|
bilateral adrenectomy results in enlargement of existing pituitary adenoma
|
|
pt develops bitemporal hemianopsia and galactorrhea after adrenal tumor was excised
|
nelson's syndrome
|
|
ACTH levels in: iatrogenic cushings, cushing dz, ectopic acth tumor, adrenal tumor
|
low, high, highest, low
|
|
causes of 2* hyperaldosteronism
|
anything which causes kidney to perceive low volume state (less CO like CHF, fluid compartment shift like ascites/cirrhosis, nephrotic syndorme, renal artery stenosis, etc)
|
|
renin levels in conn's syndrome vs 2* hyperaldosteronism
|
low renin in conn's, high in 2*
|
|
causes of addisons
|
usually autoimmune, but TB or met
|
|
2* adrenal insufficiency vs addison's
|
2* = just less acth, don't see hyperpigmentation and kyperkalemia.
|
|
2 ways to dx addisons
|
1. cortrosyn stimulation test (detect cortisol production) 2. mitopirone test (detect acth)
|
|
how to dx addisons vs waterhouse friedrichsen
|
waterhouse is acute, with some sx of DIC and septicemia
|
|
dx of pheochromocytoma
|
urinary vma is elevated
|
|
tx for pheo
|
phenoxybenzamine, w/ surgery
|
|
sx of episodic hyperadrenergic sx
|
paroxysmal bp, pain (headache), perspiration, palpitation, panic/pallor
|
|
where does neuroblastoma occur
|
anywhere along sympathetic chain
|
|
why might you see neutrophilic leukocytosis in pheo
|
epinephrine decreases adhesion molecules
|
|
what paraneoplastic product can pheo secrete
|
epo
|
|
rule of 10's for pheo
|
malig, bilat, extra-adrenal, calcify, kids, familial
|
|
urinary labs in pheo vs neuroblastoma
|
pheo = vma, neuro = hva
|
|
what gene is overexpressed in neuroblastoma
|
nmyc
|
|
histological finding of neuroblastoma
|
homer wright pseudorosette
|
|
what marker is neuroblastoma positive for
|
bombesin
|
|
what dz is neuroblastoma assoc w
|
opsoclonus-myoclonus
|
|
facial myxedema and macroglossia
|
hypothyroid
|
|
reflexes in thyroid dz
|
increased in hyperT
|
|
GI effects in thyroid dz
|
hyper = diarrhea. Hypo = constipation
|
|
hla association of hashimoto
|
dr5
|
|
mcc of hypothyroid
|
hashimoto
|
|
ddx of thyrotoxicosis
|
all hyperthyroid dz, early hypothyroid can present as thyrotoxicosis
|
|
painless goiter with hypothyroid
|
reidel's thyroiditis
|
|
histology of hashimoto
|
hurthle cells (epithelial cell), lymphocytic infiltrate w/ germinal centers
|
|
most common location of cretinism
|
china
|
|
endemic vs sporadic cretinism
|
endemic = iodine deficiency. Sporadic = defect in t4 formation or developmental failure in thyroid formation
|
|
cold intolerance, weight gain, and decreased appetite after flulike illness
|
de quervain (subacute) thyroiditis
|
|
what type of hypothyroid has granuloma formation
|
de quervain (subacute) thyroiditis
|
|
thyroid is replaced by fibrous tissue
|
reidel's thyroiditis
|
|
macrophage and eosinophils in hypothyroidism
|
reidel's thyroiditis
|
|
prognosis of someone with de quervain's thyroiditis
|
self limited
|
|
tx for graves dz
|
need glucocorticoids (antithyroid cannot reverse opthalmopathy)
|
|
tender hypothyroidism
|
de quervain (subacute) thyroiditis
|
|
hypothyroidism with jaw pain
|
de quervain (subacute) thyroiditis
|
|
complication of thyrotoxicosis
|
fatal arrythmia
|
|
how to tx thyroid storm
|
bb, antithyroid
|
|
pathogenesis of toxic multinodular goiter
|
some follicular cells stop responding to TSH (mutation in TSH receptor) -> hot nodules that are not malignant
|
|
jod-basedow effect
|
giving iodine deficient pt iodine produces thyrotoxicosis
|
|
do thyroid cancers change thyroid status
|
no
|
|
most common thyroid cancer
|
papillary
|
|
complication of hashimoto
|
lymphoma (usally NHL)
|
|
orphan annie nuclei w/ thyroid cancer
|
papillary
|
|
what type of thyroid cancer has psommama bodies
|
papillary
|
|
which type of thyroid cancer is associated with radation
|
pipillary
|
|
mechanism of invasion: papillary vs follicular
|
lymphatic vs hematogenous
|
|
thyroid cancer with amyloid
|
medullary
|
|
thyroid cancer in iodine deficient areas
|
follicular
|
|
most common cause of 1* hyperparathyroid
|
adenoma
|
|
adenoma vs hyperplasia for all endocrine gland
|
adenoma results in heterogeneity for size (one part is big, other parts are atrophied from negative feedback). Hyperplasia = diffuse enlargement
|
|
sx of hyperPT
|
stones (hypercalciuria), bones (hypophospatemia and hypercalcemia -> osteitis fibrosa cystica, osteoporosis, osteomalacia), groans (gastrin secretion due to calcium, pancreatitis), moans (calcium related)
|
|
labs in 1* hyperpth
|
increased pth, alp, and increased camp in urine
|
|
how to dx hyperPT based on anatomy
|
primary is an adenoma. Secondary is usually hyperplasia
|
|
where is subperiosteal thinning in osteitis fibrosa cystica
|
medial phalanges 2&3
|
|
1* vs 2* hyperpt
|
2* = LOW calcium and HIGH phosphate
|
|
review hypoPT graph
|
p299
|
|
mcc of hypopt
|
1. surgical excision 2. autoimmune 3. digeorge 4. low magnesium
|
|
what is chvostek's sign
|
tapping of facial n leads to contraction
|
|
what is albrights hereditary osteodystrophy? Inheritance?
|
type of pseudohypoPT, AD, kidney can't respond to PTH.
|
|
sx of pseudohypoPT
|
short stature, shortened 4th and 5th digits
|
|
mcc pituitary adenoma
|
prolactinoma
|
|
what is cabergoline
|
dopamine agonist (eg bromocriptine)
|
|
when is GH normally increased
|
stress, exercise, hypoglyemia. has diurnal cycle so at night
|
|
dx of acromegaly
|
increased serum IGF. Fail to suppress GH w/ glucose tolerance
|
|
what pituitary hormones help to promote insulin resistance
|
GH, thyroid, cortisol
|
|
tx for acromegaly
|
ostreotide + surgery
|
|
risk of death with gigantism
|
every organ gets bigger including heart -> cardiomyopathy
|
|
causes of central DI
|
pituitary tumor, trauma, surgery, histiocytosis X
|
|
causes of 2* nephrogenic DI
|
hypercalcemia, lithium, demeclocycline (ADH antagonist)
|
|
how to dz between psychogenic, central, and nephrogenic DI
|
water deprivation test -- in dz, osm will not go up. Then desmopressin can distinguish central vs nephrogenic
|
|
serum osmolarity in di
|
>290
|
|
tx for nephrogenic DI
|
thiazide (helps to push out electrolytes) and amiloride and indomethacin
|
|
DI: damage to pituitary stalk vs hypothalamus
|
pituitary stalk -> transient DI. Hypothalamus -> permanent
|
|
causes of SIADH
|
1. ectopic ADH (eg small cell) 2. any CNS issue 3. any pulmonary issue 4. Drugs (eg cyclophosphamide)
|
|
in SIADH, what is total amount of sodium relative to normal
|
decreased, because body responds to excess ADH by decreasing aldosterone :. Throws out salt and keeps potassium.
|
|
Complication of SIADH
|
seizures
|
|
tx for siadh
|
demeclocycline (ADH antagonist), water restrict
|
|
what is demeclocycline
|
adh antagonist
|
|
what type of diabetes assoc w dka
|
dm1
|
|
what type of dm assoc w hyperosmolar coma
|
dm2
|
|
mcc death in dm
|
MI
|
|
2 pathogenetic mechanisms in dm
|
1. nonenzymatic glycosylation leading to small vessel dz and large vessel atherosclerosis 2. osmotic dmg
|
|
what types of cells do not have sorbitol dehydrogenase
|
schwann cells, lens, retina, kidneys
|
|
dm: leukocytic infiltrate vs amyloid deposit
|
dm2 has amyloid. Dm1 has leukocytic
|
|
polyuria, polydipsia, polyphagia, weight loss
|
dm1>>dm2
|
|
hla association of dm1
|
dr3,4
|
|
what triggers dka
|
some stressful condition increases insulin requirements
|
|
effect of insulin on capillary LPL
|
increases it
|
|
effect of insulin on hormone sensitive LPL in adipocytes
|
decreases it
|
|
intracellular K+ in DKA
|
decreased
|
|
why is there nausea and vomiting in dka
|
gets rid of acid
|
|
cbc in dka
|
leukocytosis
|
|
tx for dka
|
k and mg, insulin, fluids, and glucose
|
|
rule of 1/3 for carcinoid
|
1/3 met, 1/3 present with 2nd malignancy, 1/3 multiple
|
|
what is secreted by carcinoid
|
serotonin
|
|
tx for carcinoid
|
octreotide
|
|
heart murmurs seen with carciniod syndrome
|
TIPS = tricuspid insufficiency, pulmonic stenosis
|
|
why doesn't carcinoid syndrome occur in tumor confined to GI
|
5ht goes first pass metabolism in liver
|
|
4 sx of carcinoid syndrome
|
BFDR - bronchospasm, flushing, diarrhea, right sided heart dz
|
|
mc tumor in appendix
|
carcinoid tumor
|
|
dx of carcinoid syndrome
|
5hiaa in urine
|
|
what is Z-E associted with
|
MEN1
|
|
why do you see diarrhea in Z-E
|
acid inhibits lipase which causes malabsoprtion
|
|
management of pt with unusual hypoglycemia
|
get a c peptide level (distinguish b/w exogenous insulin and insulinoma)
|
|
what needs to be r/o in pt w abd pain, gallstone, constipation, and diarrhea
|
somatostatinoma
|
|
why do you see diarrhea in somatostatinoma
|
somatostatinoma blocks CCK, so get fatty diarrhea
|
|
why is there an increased risk of gastric adenocarcinoma in somatostatinoma
|
blockage of gastrin leads to achlorydia
|
|
which islet cell tumor is not malignant
|
insulin
|
|
what needs to be r/o in pt w DM, necrotic erythema, anemia
|
glucagonoma
|
|
are ketones elevated in hyperosmolar coma
|
no
|
|
gluclose levels DKA vs hyperosmolar coma
|
>300, >800
|
|
do you see kuusmal respirations in hyperosmolar coma or DKA
|
DKA
|
|
wermer's syndrome vs werner's syndrome
|
werner's is an adult progeria w/ DNA repair defect. Wermer's is MEN1
|
|
3 locations of MEN1
|
pituitary, parathyroid, pancreas
|
|
3 locations of MEN2A
|
parathyroid, pheochromocytoma, medullary thyroid
|
|
sipples syndrome
|
men2a
|
|
inheritance of MEN
|
ad
|
|
3 locations of MEN2B
|
pheochromocytoma, medullary thyroid, mucosal neuroma
|
|
when MEN is associated with marfanoid habitus
|
MEN2b
|
|
what are the rapid acting insulins
|
lispro, aspart, regular
|
|
what are the long acting insulins
|
glargine, detemir
|
|
what is tolbutamide
|
1g sulfonylurea
|
|
what is chlorpromaide
|
1g sulfonylurea
|
|
what is glimepiride
|
2g sulfonylurea
|
|
tx for life threatening hyperkalemia
|
insulin
|
|
what type of insulin should be used with dka
|
regular
|
|
which diabetes drugs can cause hypoglycemia
|
2g sulfonylurea, meglitinide
|
|
which diabetes drug can cause disulfram like effects
|
1g sulfonylurea
|
|
mechanism of sulfonylurea
|
closes k+ channel in beta cell, which depolarizes it
|
|
are secretagogues useful in dm1
|
no
|
|
toxicity of metformin
|
lactic acidosis :. CI in renal failure or contrast dye
|
|
mechanism of metformin
|
decreases gluconeogenesis, increases glycolysis and peripheral uptake of glucose
|
|
mechanism of thiazolidinedione
|
increases insulin sensitivity by binding to PPAR-gamma
|
|
toxocity of thiazolidinediones
|
weight gain, hepatotox, CV tox, edema
|
|
what type of drug is glitazone
|
thiazolidinedione
|
|
what type of drug is miglitol
|
alpha glucosidase inhibitor
|
|
what type of drug is pramlintide
|
amylin analog that decreases glucagon
|
|
what is amylin
|
a small peptide hormone secreted with insulin that decreases glucagon secretion, promotes satiety, and delays gastric empty
|
|
what is exenatide
|
GLP-1 analog that increases insulin after meal
|
|
toxicity of pramlintide
|
nausea, diarrhea. REMEMBER that pramlintide is not a meglitinide
|
|
what diabetic drug is associated with pancreatitis
|
glp-1 analog
|
|
what are best weight loss drugs
|
sibutramine, orlistat
|
|
mechanism of propylthiouracil and methimazole
|
1. inhibits organification and coupling 2. PTU can also inhibit 5' deiodinase
|
|
what endocrine drug can cause agranulocytosis
|
propylthiouracil, methimazole
|
|
what endocrine drug can cause aplastic anemia
|
proyplthiouracil, methimazole
|
|
what endocrine drug is a teratogen
|
methimazole
|
|
what endocrine drug can be used in turner syndrome and prader willi
|
gh
|
|
what endocrine drug can cause photosensitivity
|
demeclocycline
|
|
what endocrine drug can cause abnormalities of bone and teeth
|
demeclocycline
|
|
what are long acting gc's
|
dexamethasone, beclomethasone
|
|
effect of glucocorticoids on sleep
|
can cause insomnia (stress hormone remember)
|
|
what receptor do somatomedins act through
|
TRK receptor
|
|
4 effects of growth hormone
|
1. decreases glucose uptake (anti-insulin) 2. increases lipolysis 3. increases protein synthesis 4. promotes IGF
|
|
effect of alpha AG on ADH
|
inhibits it
|
|
effect of alcohol on ADH
|
inhibitis it
|
|
what drugs can stimulate ADH
|
narcotics, opiate, antineoplastic, cyclophosphamide, 1g sulfonylurea
|
|
causes of elevated phosphate
|
CRF, child, 1* hypoPT, pseudohypoPT
|
|
causes of decreased phosphate
|
1. parathyroid axis dysfunction: hypovitamin D, 1* hyperP, PTHrP; 2. alkalosis; 3. insulin Rx in DKA
|
|
what factors stimulate glucagon
|
decreased glucose, increased AA's, CCK, NE/E, Ach
|
|
does glucagon act on muscle
|
no, THEREFORE NO PROTEOLYSIS
|
|
triad of hand schuller christian
|
skull lysis + central DI + exophthalmos
|
|
causes of pituitary hypofunction
|
null adenoma (assoc w/ MEN1), craniopharyngioma, infarct (sheehan), autoimmune (women related to preg)
|
|
effect of craniopharyngioma vs pituitary adenoma on pituitary
|
cranio will usually be hypofunction, adenoma has hyperfunction
|
|
effect of excess prolactin in males
|
inhibition of GnRH results in impotence
|
|
GH adenoma can result in
|
cardiomyopathy
|
|
in hypothyroid, will thyroid shrink or grow
|
either grow (i.e. hashimoto) or stay the same
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|
what types of hypothyroid have painful gland? Painless?
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subacute is very painful. Reidel and hashimoto are painless
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what is the usual cause of subacute thyroiditis
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viral
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postpartum hypothyroid
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abrupt onset of postpartum autoimmune. NO GERMINAL FOLLICLES
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myxedema in graves vs hypothyroid
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graves is pretibial, hypo is more periorbital or in larynx (hoarse voice)
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digital swelling and clubbing w/ hyperthyroid
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graves
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what is euthyroid sick syndrome
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depressed thyroid hormones (but increased rT3) even though thyroid appears to be fine
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difference b/w type I and type II vitamin D dep rickets
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type I has less dihydroxy vitamin D, type I has more
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why is there increased alzheimer's disease with metabolic syndrome
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because increased insulin saturates proteases, which keeps them from working on beta amyloid
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what is the cause of insulin resistance
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insulin resistance is directly caused by increased FFA's and TG's, which acts directly on receptors
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what is polyglandular deficiency
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kind of like a MEN where multiple endocrine glands are dysfunctional. Type 1 = AR, no HLA, Addisons + hypoPT + mucocutaneous candidiasis. Type 2 = AD, HLA DR, Addison's + Hashimoto + DM1
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review hyperPT dx chart at end of notes
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goljan notes
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what can increase activity of desmolase
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ACTH
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what GAG is deposited into myxedma of graves
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hyaluronic acid
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what is volume status in SIADH
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NORMAL, because early hypervolemia is corrected by decreased aldosterone (which may cause hyponatremia and hyperkalemia)
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htn, low renin, metabolic alkalosis, hypokalemia
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1* aldosteronism
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where is the receptor for glitazones located
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intracellular
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does 21-alpha hydroxylase always produce salt wasting
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no
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kid w/ increased growth, virilization, increased testosterone and 17-hydroxyprogesterone
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CAH (21 alpha), not Leydig tumor cuz 17-hydroxyprogesterone is not increased in those
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tx for gestational diabetes
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regular insulin
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what bone is adjacent to pituitary gland
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sphenoid bone
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what is the nernst equation
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rmp = ln (out / in)
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effect of prolactin on arcuate nucleus
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stimulates, i.e. stimulates dopamine release to exert negative feedback
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tx for 21-hydroxylase deficiency
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give steroids, which suppresses acth and decreases steroids
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sx of 17 vs 21 vs 11 CAH
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1 in 1st digit = hypertension. 1 in 2nd digit = masculization.
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what hormone has permissive effect on adrenergics to maintain blood pressure
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cortisol
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effect of pth on phosphate absorption in gut
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increases actually
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effect of decreased sex hormone binding globulin on women
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hirsutism
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effect of increased sex hormone binding globulin on men
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gynecomastia
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what is oxidation step in th synthesis
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conversion of i- to i2
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what is organification step in th synthesis
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putting i2 into thyroglobulin
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is thyroid hormone pro or anti insulin
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anti (increases glycogenolysis, gluconeogenesis and lipolysis)
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why is hypernatremia not seen in conn's syndrome
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aldosterone escape
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what can cause 2* hyperaldosteronism
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excessive RAAS activation due to decreased RBF from stenosis, CHF, CKD, cirrhosis, nephrotic syndrome (the last two have less protein which means edema and loss of plasma volume)
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what will happen to serum Na, K, H in addisons
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down, up, up
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why can pheochromocytoma cause a neutrophilic leukocytosis
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cuz catecholeamines decrease adhesion factor synthesis
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what is breakdown product of epinephrine
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metanephrines
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what is breakdown product of norepinephrine
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vma
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endocrine dz that can cause brittle hair vs fine hair
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hypo vs hyper thyroid
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hypothyroid with hard thyroid gland
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riedel
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what is proptosis
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pushing forward of eye
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myxedema contains what GAG
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hyaluronic acid
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subperiosteal thinning in medial phalanges
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osteitis fibrosa cystica
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will you see an adenoma in 2* hyperpth
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no, hyperplasia
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pth and serum calcium in osteoporosis
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normal
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cabergoline is used to tx
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prolactinoma (it is a dopamine agonist)
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how can you tx acromegaly
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surgery to remove pituitary adenoma, then octreotide (inhibits gh)
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secretions of what hormones may be increased in dm
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gh, epinephrine
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t/f: neg of small vessels may result in autoamputation
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no, only large vessels
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why might you see increased leukocytes in dka
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epinephrine
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intracellular k levels in dka
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depleted
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diabetes mellitus + necrolytic erythema + anemia
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glucagonoma
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which islet tumor is benign
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insulinoma
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what hypothyroid dz will have germinal follicles
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hashimoto
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autoimmune destruction of pituitary related to pregnancy
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lymphocytic hypophysitis
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effect of high thyroid on bone
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increases turnover so increased calcium
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does pheochromocytoma have a tendency to calcify
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10% of the time, so it can
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how does cortisol decrease bone formation (mechanism)
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decrease osteoblast function, increase osteoclast function
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first sx of insulin resistance
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increased baseline insulin
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|
positive ppd + hypotension
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addison's from tb
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jaundice + puffy faced + umbilical protrusion in newborn + hypotonia
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congenital hypothyroid
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|
what is the most important prognostic indicator in neuroblastoma
|
nmyc expression levels
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