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PANRE > endocrine > Flashcards

endocrine Flashcards

1
Q

hpa

A

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!!

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2
Q

CRH

A

CRH is in hypo then ACTH made at pitutary gland and then ADRNEAL gland makes CORTISOL

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3
Q

GNRH

A

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!

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4
Q

secondary disorders

A

secondary and tertiary disrodes have LABS IN THE SAME DIRECTION

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5
Q

primary disorders

A

labs in opposite directs if the problems is the target organ!!

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6
Q

TSH

A

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

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7
Q

Free t4

A

ordered when tSh is abnormal

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8
Q

hashimoto’s ab

A

antithyroid peroxidase AB

anti thyroglobulin AB

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9
Q

grave’s disease ab

A

thyrodi sitmulating RECEPTOR ab

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10
Q

free t3

A

used to diagnosed hyperthyroidsim when TSH is low and T4 is STILL NORMAL!

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11
Q

normal ft4 and elevated tsh

A

subclinical hypothyroidism

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12
Q

low TSH plus normal FT4

A

subclinical hyperthyroidism

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13
Q

radioactive test

A

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

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14
Q

subclinical hypothyroid

A

levothyroixine- if patient develops hyperlipid, or tsh too high

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15
Q

hypothyroid

A

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

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16
Q

hyperthyroidism

A

HEAT intolerance, weight loss, skin warm, most, alpecia, goiter, hyperactivity, anxiety, inervous, diarrhea, hyperdefecation, tachy, plapitation, high output heart failure, no periods, hyper GLYCEMIA

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17
Q

euthyroid sick syndrome

A

surgery, malig, sepsis, cardiac- decreased t3/t4- but t3 ABNORMALLY LOW, decreased TSH too

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18
Q

thyroid storm

A

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!!!

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19
Q

myexdema crissis

A 
bradycardia, coma, hypothermia, hypoventilation, hypotensive, hypoGLYCEMIC, hypoNATREMIA
IV SYNTHROID (levo_, passive warming. DONT WARM THEM SO FAST!, normal saline
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20
Q

grave’s

A

pretibial myxedema!!- non pitting- pink to brown plques on shin
diffuse uptake!- radioactive iodine- MC therapy!!!

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21
Q

toxic multinodular goiter

A

patchy aras of both increased and decreased uptake= radioactive iodine!
methimazle: and ptu: AGRANULOCYSOIS!!! hepatitis
PTU preferred in pregnancy

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22
Q

medication induced

A

AMIODARONE- hypothryoidsim , OR LITHIUM!!!!!!

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23
Q

levothyroroxine

A

synthetic T4!!!!- monitor TSH every 6 week intervals!!!

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24
Q

thryoid nodules

A

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

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25
Q

thyorid carc

A

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

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26
Q

phosphate

A

opposite direction of calcium usually! in priary

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27
Q

hypercalcemia

A

stimulates calcitonin secretion- decreases blood calcium levels

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28
Q

primary hyperparathyroidism

A

too much TH- PARATHYORID ADENOMA MC!!!!!

lithium!!

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29
Q

secondary hyperparathyroidism

A

increased pth due to hypocalcemia or vitamin D deficiency (chronic kidney failure!!!) - mc common reason fo secondary!!- kidney covers vit D to usable form!

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30
Q

hypercalcemia

A

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!

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31
Q

hypoparathyroidism

A

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

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32
Q

osteoporosisi

A

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

33
Q

osteogenesis iperfecta

A

blue tinted sclera and preseile deafness- -genetic mutation

34
Q

renal osteodystrophy-

A

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)

35
Q

osteomalaci and rickets

A

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)

36
Q

adrenocortical insufficiency

A

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!!

37
Q

adrenal insufficiency

A

LACK OF CORTISOL!!!!- muscle ache, weak, fatigued, weight/appetite loss, nausea, vomiting , abd pain, heaache, sweating, HYPOGLYCEMIA- common in secondary!!!

38
Q

primary addison’s disease

A

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!

39
Q

diagnosis of adrenocort insufficiency

A

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!

40
Q

tx for adrenocort insufficiency

A

only glucocorticoids in 2ndry: hydrocortisone, pred dexa

mineralocorticoid and gluco in primary: fludrocortisone (only for primary)

41
Q

during illness/surgery/high fever

A

increase the corticosteroids to recreate normal adrenal gland response

42
Q

addisonian crisis

A

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

43
Q

cushing’s syndrome

A

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!!!

44
Q

cushing disease

A

pitutary adenoma- secretes ACTH

45
Q

ectopic acth

A

acth secreting- small smell lung cancer

46
Q

adrenal tumor

A

cortisol-secreting ADRENAL ADENOMA

47
Q

test for cushing’s syndrome

A

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!!!

48
Q

differential test for cushing’s

A

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

49
Q

hyperaldolsteronism

A

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,

50
Q

peheochromocytoma

A

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

51
Q

anterior pitutary tumors

A

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

52
Q

acromegaly treatmnet

A

TSS and bromocriptine!! (dopamiene agonist DECREASES GH production) OCTREotide: somatostatin analog that inhibits GH SECRETION!

53
Q

dopamine

A

INHIBITS prolactin release

so treatment is bromocriptine for prolactinomas!

54
Q

DKA

A

hyperglycemia, dehydration, ketones- high anion gap and POTASSium DEFICIT!!!

abd pain
kussmaul’s respiration- deep continuus respirations, fruity breath

55
Q

hyperosmolar hyperglycemic syndrome

A

potassium deficity, no ketones, dehydration- INCREASED OSMOLARITY!!

mental status cahnge1

56
Q

tx for DKA and hhs

A

isotonic NS, insulin, potassium!!!!!!!!!!!! potassium deficit present in both!!!

57
Q

DM

A

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

58
Q

Dm retinopathy

A

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!!

59
Q

hypoglycemia

A

brain dysfunction at 50

sx @60

60
Q

diagnosis

A

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!!!!

61
Q

goals for DM

A

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!

62
Q

biguanides

A

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

63
Q

pancreatic insulin release stimulated- hypoglycemia!

A

glypizide glyburide, glimipiride
hypoglycmeia!!!
weight GAIN! common side effect- sulfa allergy people can’t take this

64
Q

meglitidnides

A

stimulates panc beta cell release- repaglinide, netaglinides

hypoglycemia- mc side effect

65
Q

a-glucosidase inhibit

A

acarbose, miglitol = delays intestinal glucose absorption!
inbhitis amylase and alpha glucosidase hydrlase

hepatitis- flatulance, diarrhea, abd pain

66
Q

thazolidinediones

A

increaes insulin sensitivyt in peripheral receptor site- adipose and muscle tissues
fluid retension and EDMEA!!= cardiovscular tox with AVANDIA

67
Q

glucagon like petitede 1-

A

exenatide
liraglutide- slows gastric emptying
increses insulin secretion- mimics incretin!
hypoglycemia!!!- common side effect- injection!

68
Q

dpp 4 inhibitor

A

januvia- sitagliptin, gliptin! increases GLP-1

69
Q

sglt-2 inhibitor

A

flozin
increaes urinary glucse secretion!!
makes you thirst as side effects

70
Q

insulin

A

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!

71
Q

dawn phenomenon

A

rise in serum glucose levels between 2am -8am- due to nightly surge of counter regulatory hormones- given bedtime injection of nph!!!- growth hrmone

72
Q

samogyi effect

A

nocturnal hypoglycemia followed by rebound hyperglycemia- due to surge in growth hormone
prevent hypoglycemia!!!—decrease nph or give bedtime snack!!

73
Q

x-ray of wrist and left hand

A

used to determine bone age

74
Q

constitutional growth delay

A

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.

75
Q

insulin like growth factor 1- synthesized by liver

A

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.

76
Q

more than 1000 triglyceride

A

risk for pancreatitis

77
Q

hormones produced by hypothalamus

A

Corticotropin releasing hormone, thyrotropin releasing hormone, GH releasing hormone, somatostatin (GHIH), gonadotropin releasing hormone, and dopamine are produced in the hypothalamus.

78
Q

pitutary adenoma

A

micro- less than 10 mm- treat with meds with bromocriptine for small one for prolactinoma!
bigger than that- surgery

PANRE (18 decks)

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