Endo General Flashcards
What are steroids derived from
cholesterol
What are amines/AA derived from?
tyrosine
peptide hormone receptor location at target cell
plasma mem
steroid hormone receptor location at target cell
intracellular
peptide hormone speed of action
fast onset
steroid hormone speed of action
slow onset
Corticotropin-releasing hormone (CRH) is released from what gland?
fn?
hypothalamus
Fn: Stimulates adrenocorticotropic hormone (ACTH)
ACTH is released from what gland?
fn?
Anterior pituitary
Fn: Stimulates synthesis and secretion of cortisol, aldosterone, and androgens
Antidiuretic hormone (ADH) (also called arginine vasopressin, or AVP) is released from what gland?
fn?
Posterior pituitary
Fn: Increases water retention at kidney, vasoconstricts arterioles
Oxytocin is released from what gland?
fn?
Posterior pituitary
fn: Stimulates uterine contractions during labor, milk ejection in lactation
Aldosterone is released from what gland?
fn?
Adrenal cortex
Fn: Decreases urinary Na+ excretion, Increases urinary K+ and H+ excretion
Cortisol is released from what gland?
fn?
Adrenal cortex
Fn: Released in response to stress, Multiple metabolic actions
Insulin (β cell) is released from what gland?
fn?
Pancreas
Fn: Promotes storage of glucose as glycogen in liver and muscle
Promotes uptake of glucose and storage as triglyceride in adipose tissue and liver
Hormones circulate at (low/high) levels and bind to receptors with (low/high) affinity
Hormones circulate at LOW levels and bind to receptors with HIGH affinity
Hormone generally (can/cannot) cross cell membrane via diffusion
Hormone generally CANNOT cross cell membrane via diffusion
↑ receptor number when hormone level is low
Upregulation
when hormone level is high and/or continuous
Downregulation or desensitization
The plasma free hormone concentration is affected by:
- The rate of hormone secretion
- The rate of hormone elimination
- The extent of hormone binding to plasma proteins
What are the Trophic hormones?
GH: Growth Hormone ACTH: Adrenocorticotropic Hormone LH: Luteinizing Hormone FSH: Follicle Stimulating Hormone TSH: Thyroid Stimulating Hormone PRL: Prolactin
What hormone stimulates release of pancreatic enzymes and where is it released from?
Cholecystokinin (CCK) from Small Intestine
Where is GH produced & released?
anterior pituitary
What are the most abundant cells in the anterior pituitary?
somatotrophs
What is the MC pituitary cell to become malignant
somatotrophs
What do malignant somatotrophs produce?
GH & PRL
What occurs due to growth of a pituitary adenoma?
compresses infundibulum decreasing hypothalamic hormonal stimulation of anterior pituitary hormone release but also decreasing anterior pituitary hormones due to inability to suppress
How do GHRH neurons regulate GH production?
Positive feed-forward regulation
GHRH is released into hypo-physeal portal system and transported to somatotrophs causing GH release to secondary capillary plexus and to the body of the anterior pituitary
How is GH regulated by hypothalamic somatostain neurons?
Negative feed-forward regulation
Somatostain is released into hypophyseal portal system goes to somatotrophs and inhibits GH release
Fn of GH
Linear growth (soft tissue, visceral organ, muscle & bone) in growing ages Maintains lean body mass in adulthood
What is fetal growth mediated by?
IGF1 and IGF-2
How does GH work?
utilizes fat as main energy source
maximizes protein deposition for lean body mass
marks glucose for use by the brain
What contains the greatest number of GH receptors?
liver and cartilage
What is the effect on insulin when GH acts on fat and causes lipolysis and increased FA release?
antagonistic to insulin
GH action on AA
maximize AA and protein for lean body mass production
What is GH action on glucose metabolism?
antagonistic (so blood glucose levels increase)
What happens when there is excessive chronic GH release?
there is sustained increase in plasma glucose causing an increase in insulin and eventually insulin resistance and diabetogenesis
What causes GH excess?
pituitary adenoma
extrapituitary GH excess
excess GHRH
What hormones are secreted from the adrenal cortex?
corticosteroids
mineralocorticoids
androgens
What hormones are secreted from the adrenal medulla?
epinephrine
NE
What regulates glucocorticoid synthesis?
episodic secretion and circadian rhythm of ACTH
stress responsiveness of HPA axis
FB inhibition by cortisol on ACTH sectretion
When are ACTH burst most frequent?
in the AM
What are the physiological actions of glucocorticoids?
maintain blood glucose levels during fasting (increase during stress) by increasing liver synthesis of glucose and glycogen deposition
calcium homeostasis by slowing bone growth and inducing bone demineralization
What is the effect of glucocorticoids on: CV system Skeletal muscls CNS Immune system
CV: HEN with prolonged levels
Skeletal muscle: wasting with prolonged high levels
CNS: either excess fo insufficiency will cause alterations in mood, behavior and excitability
Immune: secreted in response to stress
What prevents glucocorticoids from interacting with the mineralocorticoid receptor?
11β-HSD2 will turn cortisol into cortisone so only the aldosterone can interact witht the MR
MR binds to cortisol with (high/low) affinity. MR target tissues express 11-betaHSD2 which (inactivates/activates) cortisol.
HIGH
INACTIVATES
What is the most active androgen?
testosterone
What is the consequence of 21-Hydroxylase deficiency?
Decreased cortisol and aldosterone
Hypoglycemia because of low cortisol
Loss of sodium because of mineralocorticoid deficiency Virilization because of excess androgen production
What is the consequence of 11β-Hydroxylase deficiency?
Excess mineralocorticoid activity
Hypoglycemia because of low cortisol
Salt and water retention
What is the consequence of 11β-HSD2 deficiency?
Decrease in glucocorticoid inactivation in mineralocorticoid- sensitive cells leading to excess mineralocorticoid activity
ACTH dependent causes of cushings
ACTH secreting tumors
CRH secreting tumors
ACTH independent causes of cushings
glucocorticoid secreting tumors
Causes of addison’s disease
primary adrenal insufficiency due to destruction of adrenal cortex
both mineralocorticoid and glucocorticoid deficiency
What is effect of Mifepristone at high doses on Glucocorticoid Function?
blocks the glucocorticoid receptor, blocks feedback regulation of HPA, increases ACTH and cortisol but blocks the action of cortisol at the receptor
What is effect of Spironolactone and Eplenerone at on Mineralocorticoid Function?
Inhibits binding of aldosterone to the MR