Endocrine Flashcards
steroid hormones
cortisol (adrenal cortex); estrogen, progesterone (ovaries); testosterone (teestes)
amino acid hormones
catecholamines (epinephrine, norepi, dopamine), tyrosine and thyroxine (thyroid)
protein hormones
insulin, peptides
water-soluble hormone transport
free, unbound; SHORT ACTING RESPONSE (catabolized by enzymes)
lipid soluble
bound, small amt in free or active form; RAPID AND LONG LASTING RESPONSE (pass easily through lipid membrane of cell)
hypothalamus: base of the brain; connected to anterior pit by ______ and connected to posterior pit by _____
anterior pituitary by portal blood vessels; posterior pit by nerve tract
HPA produces a number of hormones, one of which is somatostatin, what does it do?
inhibits release of GH and TSH
gonadotropin-releasing hormone (GnRH) releases
LH and FSH from anterior pituitary
CRH causes release of _____
ACTH
Substance P from the hypothalamus does what?
inhibition of ACTH
Posterior pituitary hormones
ADH - released when plasma osmolality is high or plasma volume is low - water reabsorption in the kidneys
oxytocin - causes uterine contractions and milk ejection in lactating women
anterior pit hormones, ACTH
ACTH - activated by CRH from hypothalamus - target organ is the adrenal cortex - increase steroidogenesis - increase in cortisol, aldosterone
melanocyte-stimulating hormone (MSH) from the anterior pituitary
target organ: pigment cells
function: promotes secretion of melanin and lipotropin - makes skin darker
LH from ant pit - target organ in M and W? function?
target organ in W is granulosa cells (follicular cell); LEYDIG for LH cells (men)
function: ovulation, PROGESTERONE production (women); testicular growth, testosterone production (men)
FSH from ant pit - target organ M, W? function?
target organ: granulosa cells (women); SERTOLI for FSH cells (men)
function: follicle maturation, ESTROGEN production (women); spermatogenesis (men)
Growth hormone target organ? controlled by two hormones from the hypothalamus?
target organ: liver, bone, muscle
controlled by: GHRH (growth hormone releasing hormone): increases secretion
somatostatin: inhibits GH
precursor to triiodothyronine
thyroid hormone (TH)/thyroxine/T4
regulates metabolic rate of all cells and processes cell growth
triiodothyronine (T3)
pancreas is both ______ and ______ gland
endocrine (glucagon and insulin) and exocrine (digestive enzymes) gland
Islets of Langerhans of pancreas secretes
glucagon and insulin - help regulate carb metabolism
alpha cells of pancreas secrete
glucagon
beta cells of pancreas secrete
insulin and amylin
delta cells (d cells) of pancreas secrete, and what is this essential in?
somatostatin - essential in carb, fat, and protein metabolism; may prevent excess insulin secretion
SNS stimulates which cells in pancreas
alpha cells to release glucagon bc need energy for fight or flight
PSNS stimulates which cells in pancreas
beta cells bc need insulin, secretion of pancreatic juices
“rest and digest”
where does insulin come from
comes from beta cells and synthesized from proinsulin
function of insulin
it is an anabolic hormone that promotes synthesis of proteins, lipids, and nucleic acids
facilitates intracellular transport of K+, phosphate, and magnesium into cells
secretion of insulin is regulated by chemical, hormonal, and neural control; promoted by? diminished by?
promoted by increased blood glucose levels, increased amino acids, PSNS (vagal) stimulation of beta cells
diminished in low blood glucose levels, high levels of insulin negative feedback, SNS stimulation of alpha cells (epinephrine), hypokalemia (negative feedback)
insulin effect in the liver
inhibits glycogenolysis, inhibits gluconeogenesis, inhibits ketogenesis
insulin effects on the muscle
promotes protein synthesis, increase AA transport into m. cells, promotes glycogenesis
insulin effect on fat:
increase fatty acid synthesis, promotes triglyceride storage into fat cells, decrease lipolysis
brain and blood cells do not require ______ for glucose transport
insulin
amylin: co-created w/insulin by beta cells
effect?
antihyperglycemic effect by delaying nutrient uptake, suppressing glucagon secretion after meals, has satiety effect
glucagon function
released by alpha cells or lining GI - SNS, low glucose levels activate
function: acts on the liver and increases blood glucose by stimulating glycogenolysis and gluconeogenesis
adrenal medulla has ______ cells that release what?
has Chromaffin cells (pheochromocytes) cells of medulla that release catecholamines - epinephrine/adrenaline, norepi: fight or flight
promotes hyperglycemia
SIADH most common cause is
ectopic secretion of ADH
SIADH clinical manifestations
euvolemic hypotonic (dilutional) hyponatremia
increased total body water, increased ECF, total body sodium is unchanged, and edema = absent!
urine hyperosmolar, sermum hypoosmolar
types of DI
neurogenic (not enough made by brain), nephrogenic (kidneys don’t respond - genetic x),
dipsogenic/psychogenic - excessive fluid intake - lowers plasma osmolarity to the point that it falls below the threshold for ADH secretion
hyperpituitarism commonly caused by
benign, slow-growing pituitary adenoma
acromegaly cause? mortality r/t? clinical manifestations?
GH hypersecretion in adulthood - mostly caused by slowly progressive pituitary adenoma
connective tissue proliferation, bony proliferation, symptoms of diabetes, CNS symptoms (h/a, seizure activity, visual disturbances, papilledema - swollen optic nerve)
primary vs secondary hyperthyroidism/thyrotoxicosis
primary: dysfunction of thyroid gland
secondary: conditions that cause alterations in pituitary or hypothalamic functioning; alters TSH or thryotropin-releasing hormone (TRH) production
Grave’s disease - cause and clinical manifestations
type II autoimmune hypersensitivity that causes hyperthyroidism
ophthalmopathy - exophthalmos: increased secretion of hyaluronic acid, orbital fat accumulation, inflammation, and edema of the orbital contents
diplopia
pretibial myxedema (Graves’ dermopathy): leg swelling “orange peel appearance”
toxic multinodular goiter - cause, and clinical manifestations?
several hyperfunctioning nodules secrete thyroid hormone - same symptoms as hyperthyroidism but occurs slowly and w/o exophthalmos & pretibial myxedema
primary hypothyroidism caused by
inability of thyroid gland to produce TH
iodine deficiency (endemic goiter): most common worldwide
autoimmune thyroiditis: Hashimoto disease is most common in the US
primary hyperparathyroidism
caused by adenoma usually, excess secretion of PTH and hypercalcemia, normal feedback mechanisms: elevated serum levels of calcium fail to normally inhibit the release of PTH by the parathyroid gland
secondary hyperparathyroidism
from another disease process - CKD, vit D or calcium deficiency
-calcium will be low and PTH high
tertiary hyperparathyroidism
high PTH and calcium from long standing secondary hyperparathyroidism
clinical manifestations of hypoparathyroidism - what signs?
remember it can be caused by alcohol and low Mg levels
clinical manifestations: hypocalcemia, lowering the threshold for nerve and muscle excitation – muscle spasms, hyperreflexia, tonic-clonic convulsions, laryngeal spasms, death from asphyxiation
*Chvostek and Trousseau sign
remember that glucagon is secreted by
pancreatic alpha cells
glucagon is increased in both type I and type Ii
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