Adrenal - cortex stuff! Flashcards
What does corticotrophin releasing hormone (CRH) do?
stimulates corticotrophs to release ACTH
decrease in which hormone causes the symptoms of decreased pubic and axillary hair and decreased libido in females?
decreased androgens
When is the greatest secretory activity of cortisol?
MORNING
21 b-hydroxylase deficiency effect on ACTH?
ACTH levels are HIGH (due to no cortisol)
high ACTH = trophic effect on adrenal gland (GROWTH OF GLAND)
What is the only thing that inhibits corticotrophin releasing hormone (CRH)
cortisol
17a-hydroxylase deficiency
(hyper/hypo)tension
(hyper/hypo)kalemia
metabolic (alkalosis/acidosis)
hypertension
hypokalemia
metabolic alkalosis
(same as conn syndrome except there is LESS aldosterone… effects from increased 11-DOC and corticosterone)
Conn syndrome is caused by:
an aldosterone-secreting tumor
Why is skin pigmentation normal with secondary and tertiary adrenocortical insufficiency but hyperpigmented in primary adrenocortical insufficiency (Addisons)
2/3: normal because ACTH is not over secreted from pituitary (hypothalamus and pituitary are the problems)
primary: hyperpigment because ACTH is over secreted from pituitary due to low cortisol from the adrenal gland which is the problem
(a-MSH is the reason for pigmentation which is a derivative of ACTH)
Why are renin levels low in Conn syndrome?
Due to the hypertension caused by aldosterone.
Only aldosterone is increased due to the tumor
Why does the adrenal gland enlarge with 21 b-hydroxylase deficiency
trophic effect on adrenal gland from high levels of ACTH (due to lack of cortisol)
What layers of the cortex contain desmolase
all layers
zona glomerulosa
zona fasiculata
zona reticularis
decrease in which hormone causes the symptoms of hypoglycemia, weight loss, and muscle weakness in Addison’s disease?
decreased cortisol
What is the LEAST important secretagogue for aldosterone synthesis?
ACTH
21 b-hydroxylase deficiency leads to:
(hyper/hypo)natremia
(hyper/hypo)glycemia
hyponatremia (no aldosterone!)
hypoglycemia (no cortisol!)
What causes hyperpigmentation of skin on elbows, knees, nipples, and scars in Addison’s disease?
increased ACTH —> increased a-MSH fragment
increased ACTH caused by low cortisol because only cortisol is the inhibitor of CRH —> which keeps ACTH stimulated
cortisol (and androgens) levels in the blood reflect a ______ and _______ release of ACTH
circadian and pulsatile release of ACTH
What are androgens responsible for in women?
- axillary hair
- pubic hair
- libido
What are the results of a 21 b-hydroxylase deficiency in utero?
masculinization of female penis-like clitoris scrotum-like labia deep voice increased muscle mass amenorrhea hirsutism
cortisol effects on bone:
decrease calcium absorption —> decrease plasma calcium —> mobilizes calcium from bone —> inhibits bone formation —> bone loss
(no calcium taken up from GI or kidneys, so the bones release calcium to make up for the decrease in plasma calcium which causes the bones to be deficient and cannot form new bone cells)
decrease in which hormone causes the symptoms of hyperkalemia, hypotension, metabolic acidosis, and salt craving in Addison’s disease?
decreased aldosterone
Which part of the adrenal gland responds to SHORT term stress?
medulla
Why are adrenal androgens referred to as 17-ketosteroids?
because they have a ketone at C17
cortisol effect on:
protein:
lipids:
glucose uptake:
protein CATABOLISM (synthesis is decreased)
lipoLYSIS (provides glycerol)
decreased glucose uptake by tissue (more in blood)
What does aldosterone bind to to stimulate sodium and water reabsorption? and potassium and H+ secretion?
intracellular mineralcorticoid receptor (MR1)
which binds to a mineralcorticoid responsive element (MRE)
How is secretion of ACTH enhanced during periods of stress?
increased AMPLITUDE of CRH burst
NOT frequency
cortisol action on the cardiovascular system:
2
- with catecholamines regulates blood pressure
2. up-regulates a-1 receptor responsiveness
What is the SECOND most important secretagogue for aldosterone synthesis?
increase is plasma K+ concentration
NOT ACTH!
What is secondary adrenocortical insufficiency?
failure of corticoptrophs to adequately secrete ACTH
pituitary problem
The overall metabolic effect of cortisol is to increase _________ by enhancing _________
blood glucose
gluconeogenesis
cortisol has what effect on insulin sensitivity? Why?
decreased sensitivity to glucose
goal is to have increased BLOOD glucose, insulin would decrease blood glucose by putting it in the cell
Cushing’s syndrome
cortisol levels =
ACTH levels =
Cushing’s syndrome
cortisol levels = HIGH
ACTH levels = LOW
17a-hydroxylase deficiency
aldosterone =
cortisol =
androgens =
aldosterone = decreased cortisol = none androgens = none
cortisol effect on connective tissue and muscle
inhibits fibroblast proliferation
inhibits collagen formation
skin thins
impaired connective tissue support of capillaries
increased proteolysis in muscle —> weakness
What are 2 other terms for newborn females with androgenital syndrome from 21 b-hydroxylase deficiency
female pseudohermaphrodite
contra-sexual development
21 b-hydroxylase deficiency would cause an increase in __________ and a decrease in ___________
increased androgens
decreased cortisol and aldosterone
What three things does ACTH do in the adrenal gland
- growth of adrenal gland
- transfers cholesterol into mitochondria
- activates desmolase to convert cholesterol to pregnenolone
What is the most important secretagogue for aldosterone synthesis?
angiotensin 2 — RAAS system
NOT ACTH!
Free cholesterol is transferred to the mitochondria, and then to the innter mitochondrial membrane by:
steroidgenic acute regulatory protein (StaR)
Conn syndrome effect on:
Sodium
Water
Potassium
H+
Sodium - reabsorption = HYPERnatremia
Water - retention = HYPERtension
Potassium - secretion = HYPOkalemia
H+ - secretion = metabolic ALKALosis
What stimulates aldosterone? (two things)
- decrease in BP
2. decrease in ECF volume
What is tertiary adrenocortical insufficiency?
insufficient CRH
hypothalamus problem
Why is androgen synthesis in the adrenal cortex not as important for males as females
major source of male androgens is from the testes
Which part of the adrenal gland responds to PROLONGED stress?
cortex
Which adrenocortical hormones are decreased in Addison’s disease?
cortisol
aldosterone
androgens
because there is autoimmune destruction of the adrenal gland
Where is cholesterol derived from? (3 places)
What is the MAIN source?
- LDL particles from diet (MAIN)
- hydrolysis of cholesterol esters from vesicles
- de novo synthesis from acetyl CoA
How can you detect 21 b-hydroxylase deficiency in a lab test?
presence of 17-ketosteroids in the urine
too much cortisol = muscle weakness, how?
not enough cortisol = muscle weakness, how?
too much = proteolysis in muscle
not enough = due to hypoglycemia
Cushing’s syndrome =
Cushing’s disease =
Cushing’s syndrome = adrenal hyperplasia
Cushing’s disease = overactive pituitary or ACTH secreting cells in lung
both = too much cortisol and too much androgens
What 3 types of steroids are produced by the adrenal gland?
- glucocorticoids
- mineralcorticoids
- androgens
How does cortisol inhibits ACTH release?
INDIRECTLY! NOT DIRECTLY! NEED TO KNOW!!!!!
cortisol inhibits CRH —> decreased CRH = decreased ACTH
Cushing’s disease/syndrome
symptoms:
hyperglycemia proteolysis thin skin --- "striae" muscle wasting central obesity moon face buffalo hump hypertension virilization
YOU KNOW THESE ALREADY
cortisol effect on immune system
synthesis of lipocortin —> inhibits phospholipase 2 —> inhibits release of prostaglandins and leukotrienes
inhibits IL-2 —> inhibits release of histamine and serotonin
How big is the adrenal gland? (length and weight)
length = 3-5 cm
weight 1.5-2.5 grams
What is the large gene that ACTH is derived from?
POMC
proopiomelanocortin
Why are aldosterone levels NORMAL in secondary and tertiary adrenocortical insufficiency but NOT in primary adrenocortical insufficiency (Addisons)
2/3 : normal because aldosterone is stimulated by RAAS and adrenal gland is not the problem
primary: low because adrenal gland is the problem and not making the aldosterone
What stimulates corticotrophs to release ACTH
corticotrophin releasing hormone (CRH)
Where are AT2 receptors and potassium channels found in the adrenal cortex?
zona glomerulosa
Why is aldosterone decreased in 17a-hydroxylase deficiency
all progesterone is converted into 11-deoxycorticosterone (because cortisol and androgens cannot be made)
11-deoxycorticosterone builds up, and so does corticosterone, both of which act as mineral corticoids which produce HYPERTENSION
aldosterone inhibited during hypertension because RENIN is inhibited and RAAS system is the MOST IMPORTANT SECRETAGOGUE FOR ALDOSTERONE
aldosterone effect on:
Sodium
Water
Potassium
H+
Sodium - reabsorption = HYPERnatremia
Water - retention = HYPERtension
Potassium - secretion = HYPOkalemia
H+ - secretion = metabolic ALKALosis
Cushing’s disease
cortisol levels =
ACTH levels =
Cushing’s disease
cortisol levels = HIGH
ACTH levels = HIGH
Which arteries supplies the adrenal gland?
suprarenal arteries (superior, middle, and inferior)
