adrenal cortex and medulla, lect 18/19 Flashcards
where is the adrenal glands located
sits on the kidneys
function of mineralocorticoids
regulate salt and water retention at the kidney
function of glucocorticoids
increase plasma glucose levels
the adrenal gland is actually composed of what two glands
- adrenal cortex
- adrenal medulla
the adrenal cortex is composed of what three layers? What hormone does each layer secrete
- zoma glomerulosa (outmost layer): aldosterone
- zona fasciculata: cortisol
- zona reticularis: sex steroids (androgens)
what hormones does the adrenal medulla secrete
epinephrine and norepinephrine
hormones secreted from the cortex are derived from what compound
cholesterol
List the regulation steps that cause the release of adrenal cortex hormones
- hypothalamus secretes corticotropin-releasing hormone (CRH) which acts on corticotrophs of AP
- anterior pituitary releases adrenocorticotropic hormone (ACTH)
- adrenal cortex secretes cortisol, aldosterone, and adrenal androgens
corticotropin releasing hormone acts on what cells types in the anterior pituitary
corticotrophs -> cause secretion of ACTH
ACTH has what two functions
- activates cholesterol desmolase which acts on cholesterol to form pregnenolone, a product that then can differentiate into hormones
- stimulates adrenal gland growth
function of cholesterol desmolase
- precursor for all adrenocortical steriods is cholesterol
- first step in synthesis is conversion of cholesterol to pregnenolone by desmolase
- all 3 layers contain cholesterol desmolase which is stimulated by ACTH
cortisol has what negative feedback mechanisms
- directly inhibits CRH at hypothalamus
- inhibits action of CRH on corticotrophs decreasing ACTH release
CRH released from hypothalamus reaches the corticotrophs in the anterior pituitary and activates what messenger cascade
- G protein
- adenylyl cyclase/cAMP/PKA
- activation of L-type Ca2+ channels leads to an increase in Ca2+ that rapidly leads to the release of preformed ACTH
cortisol secretion follows what pattern
- a diurnal rhythm
- levels begin to increase during sleep, reach highest levels in the am
cortisol is released in response to what? What is the primary function?
- Stress
- effect of cortisol is to increase the availability of glucose which would protect the CNS from malnutrition or extreme fasting
cortisol increases synthesis of what
- gluconeogenesis -> increased blood glucose
- increased protein catabolism
- increases lipolysis, providing glycerol
- decreases glucose uptake by tissues
aldosterone is a mineralocorticoids that is synthesized in what layer
z. glomerulosa
what two enzymes are necessary in production of aldosterone from cholesterol
- cholesterol desmolase
- aldosterone synthase
why can’t z. glomerulosa produce glucocorticoids and androgens
- zone lacks 17a hydroxylase
what causes release of aldosterone
- a drop in ECF and blood pressure
- a rise in plasma K+
ACE is present in which organ
lung
function of aldosterone
- stimulates
- sodium reabsorption
- potassium secretion
- net effect: expansion of extracellular fluid
what adrenal cortex layer produces androgens
Z. reticularis
What enzymes are necessary in the production of androgens from cholesterol
- 17 a-hydroxylase
- 17,20 desmolase (lyase)
adrenal androgens are more significant in males or females
- in females, the cortex is the major source of androgens
- responsible for the development of pubic and axillary hair and for libido
- little signifance in males
adrogens produced from adrenal cortex is converted to testosterone in males in what organ
testes
primary dysregulation: disorders of adrenal cortex
disorder resides in the actual endocrine gland
secondary dysregulation: disorders of adrenal cortex
- dysfunction resides in pituitary
tertiary dysregulation: disorders of adrenal cortex
disturbance is explained by a hypothalamic defect
Differentiate between cushings syndrome and cushings disease
- cushings syndrome: primary adrenal hyperplasia -> ACTH levels are low
- cushings disease: defect caused by overactive anterior pituitary -> excess ACTH
clinical presentation
- hyperglycemia
- thin skin
- muscle wasting
- central obesity
- round face
- buffalo hump
- HTN
- cushing’s
- excess glucocorticoids and androgens
What is addison’s disease
- primary adrenocortical insufficiency: autoimmune destruction of gland
- decreased synthesis in all adrenocorticol hormones
- loss of cortisol
- loss of aldosterone
- loss of androgens
clinical presentation
- hypoglycemia during stress, anorexia, weight loss, weakness
- hyperkalemia, hypotension, mtabolic acidosis
- in females: decreased pubic and axillary hair, decreased libido
addisons disease
what is secondary adrenocortical insufficiency
- insufficient CRH or failure of corticotrophs to adequately secrete ACTH
- plasma ACTH levels are low
- clinical features relate to cortisol and androgen deficiency
- aldosterone levels are usually normal
what is conn’s syndrome
- aldosterone secreting tumor -> aldosterone hypersection
- increased Na+ reabsorption -> HTN
- increased K+ secretion -> hypokalemia
- increased H+ secretion -> metabolic alkalsosis
- low renin levels
what is adrenogenital syndrome
- hypersecretion of adrenal androgens
- masculinizing conditions in females
- deepened voice
- increased muscle mass
- amenorrhea
- hirsutism
- cliotral enlargement
- acne
what does 21 B-hydroxylase deficiency cause
- cortex does not produce glucocorticoids or mineralocorticoids
- steroid intermediates build up and are converted to androgens -> androgenital syndrome
- ACTH levels are high, because of lack of feedback control or cortisol on the pituitary
what does 17a-hydroxylase deficiency cause
- glucocorticoids and androgens are not produced
- steroid intermediates build up -> promote mineralocorticoids production -> overproduction of mineralocorticoids
-
HTN inhibits renin secretion
- aldosterone levels are low because of the symptoms of corticosterone excess
synthesis of epi and NE is regulated by
- sympathetic stimulation
cortisol activates what molecule that converts NE into epi
phenylethanolamine-N-methyltransferase
catecholamine effects on metabolism
- epi mobilizes fuels in times of STRESS to sustain glucose production for use by CNS
- skeletal muscle -> increased glycogenolysis
- liver -> increased glycogenolysis
- adipose tissue -> increased lipolysis
