4.5 Endocrine adrenal Flashcards
adrenal gland location?
basically on top of kidneys; paired
adrenal gland structure?
outer cortex
inner medulla
3 layers of adrenal cortex?
1) zona glomerulosa = outer layer
2) zona fasciculata = middle layer
3) zona reticularis = inner layer
what two layer of cortex of overlap in function?
fasciculata and reticularis
zona glomerulosa secretes?
mineralocorticoids
most prevalent mineralocorticoids? does what?
aldosterone; regulates Na and K balance and helps to regulate BP
zona fasciculata secretes?
glucocorticoids
most prevalent glucocorticoids? does what?
cortisol; regulates nutrient metabolism
*basically does same things as aldosterone
zona reticularis secretes what? does what?
sex steroids
- these weak androgens are only significant when in excess
- contribute to male secondary sex characteristic development when in excess
ALL adrenal cortical hormones are synthesized from?
cholesterol
medula secretes?
epi and nor (catecholamines)
aldosterone comes from?
cortex zona glomerulosa outter layer
cortisol comes from?
cortex zona fasciculata middle layer
adrenal androgens come from?
cortex zona reticularis inner layer
what is the main stimulus for aldosterone secretion?
MOST IMPORTANT IS HIGH K+ LEVELS
**less important is low Na+ levels
mineralocorticoids normal actions? (aldosterone)
1) re-absorption of Na+! and Cl- and water
2) regulation of BV, BP, electrolyte balance
what is hyperkalemia?
having a HIGH concentration of K+ so aldosterone is secreted!!!!!
when aldosteron absorbs NA+, it is exchanged for?
K+, H+, Cl-
K+ and H+ are important for?
K= resting membrane potentuals H= acidity in lood
define hyperadrenalism
tumor of zona glomerulosa that increase aldosterone secretion causing HYPERALDOSTERONISM
what is hyperaldosteronism?
when you put out more aldosterone than what is typical
symptoms of major hyperaldosteronism
hypertension= rasingin BV and BP as a result of Na retention
symptoms of minor hyperaldosteronism
1) alkalosis= secreting of H+ ioons, more basic blood
2) neuromuscular paralysis= deals with resting membrane potential
- -retain more Na+ in exachnge for K+; causes
describe neuromuscular paralysis in regards to a minor hyperaldosteronism symptom
eals with resting membrane potential
–retain more Na+ in exchange for K+; typically have more K+ inside cells anyway BUT having even lower K+ outside of cells causes an efflux of K+ back out. this makes INSIDE more -; so resting potential is HYPER-POLARIZED (further from threshold so harder to excite)
aldosterone in excess primary effect?
increase Na and derease K+ reabsorption
aldosterone in excess secondary effect
1) moderate hypertesion due to fluid retention
2) mild alkalosis (due to increase H+ excretion with Na reabsorption)
3) neuromuscular paralysis =hyperpolarised RP/hard to excite
aldosterone deficiency primary effect
decrease in Na reabsorption
increase in K+ reabsorption
* causes low BP and acidic blood, cardiac is weak, hyPERkalemia bc K+ higher than normal outside of cell making it TOO EASY to excite cell
aldosterone deficiency secondary effect
1) dehydration and shock (no fluid reabosrption)
2) mild acidosis (derease H+ excretion, Na resorption)
3) cardiac weakness (due to increase K+ reabsorption, hyperkalemia >hyPOpolarized RP > smaller AP spike > weaker contraction
glucocortioids (cortisol) normal action?
mobilization of nutrients! raised blood nutrient levels!
cortisol is anabolic or catabolic?
catabolid; breaks stuff down more ti increase nutrient levels
cortisol has what effect on gluconeogenesis in liver, lipolysis and protein catabolism?
INCREASES ALL 3! breakdown of nutrients to increase nutrient level in blood
stress increases ACTH levels which will affect?
cortisol levels (BOTH are stress hormones)
how is the way the liver uses glucose different from other tissues?
in other tissues, cortisol tries to increase blood nutrients by breaking thigsn down… in the liver it is the opposite and stores glucose as glycogen
we can become ___ for having to much cortisol. why?
diabetic
*because an increased in blood glucose levels- only happens if hyperglycemic for a long period of time =adrenal diabetes
cortisol in excess increases?
1) blood glucose levels =adrenal diabetes due to B cell burnout
2) protein catabolism
3) fat mobilization and utilization
4) RBC production leading to polycythemic condition
polycythemic condition
increased concentraion of hemoglobin
- aka STRESS polycythemia
- caused by excess cortisol
extremely high levels of cortisol (either endo or exo) do what?
1) suppress immune system by decreasing gamma globulin production
- - GOOD with transplant surgeries
2) decreases inflammation and stabilizes lysosomes by decreasing the release of inflammatory agents
pharmacological doses of ______ are useful for treatment of inflammatory disease sucj as asthma and rheumatoid arthritis?
glucocorticoids
what is gaisbocks syndrome?
aka stress polycythemia
*INCREASE in RBC production due to higher metabolism due to stress
hyperadrenalism causes?
by a tumor located WITHIN one or more of the cortical layers
tumor of zona fasciculata (or reticularis) causes?
an increase in cortisol causing CUSHING’S disease
what is cushings disease?
causes?
symptoms?
appearance?
- caused by excess cortisol
- increase fat mobilization and redeposition in face and trunk
- increase protein catabolism= muscles wasting via protein breakdown (SKINNY legs)
- inflammatory and immune response is poor (sores and wounds)
- **MOONFACE and BUFFALO HUMP
cortisol deficiency decreases?
1) gluconeogensis
2) fat mobilization
3) protein catabolism
4) resistance to stress
* **cortical typical does all these things, but when deficient it does LESS
cortisol deficiency increases? does what?
ACTH secretion which INCREASES skin pigmentation!
(less cortisol= less -feedback on ant pit= increase ACTH= increase skin color with melanocytes =excess melanin around scars/pressure points)
common disease with hypoadrenalism?
addison’s disease
addison’s disease is usually caused by ?
glandular atrophy die to autoimmune disease, TB or cancer… hypoadrenalism
symptoms from a decrease in both aldosterone and cortisol? addison’s disease
- fluid and electrolyte imbalance = shock = LIFE THREATENING BC INSUFFICIENT CIRCULATION
- decreased ability to withstand stress - not life threatening
- increase in skin pigmentation (in ACTH, decr cortisol)
examples of androgens?
DHEA
DHEAS
androstenedione
androstenedione (weak androgens) can be converted to?
testosterone in peripheral tissues (skin, fat, liver) to INCREASE their androgenic activity
androgens regulated by?
ACTH, but adrenal androgens do not inhibit ACTH
androgens in males vs females?
- *males= amount of androgens from adrenals is insignificant compared to testes
- *females= adrenal derived testosterone may be important in maintaining pubic hair, axillary hair, libido, and possible skeletal muscles
hyperadrenalism caused by?
tumor in zona reticularis (or fasciculata) increases adrenal androgens
symptoms of hyperadrenalism
1) masulinization of female
2) early sexual development in male
hypoadrenalism caused by?
usually caused by hypopituitarism (decrease in ACTH)
**is RARE
symptoms of hyperadrenalism in males vs females
- *males = none
* *females= less body hair, less muscle mass low libido
libido
sexual desire
