Lecture 99 Overview of Adrenal Physiology Flashcards Preview

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Flashcards in Lecture 99 Overview of Adrenal Physiology Deck (22):

What hormones are produced by the adrenal cortex?

mineralocorticoid- aldosterone (Na+ reabsorption/K+ secretion; BP regulation)
glucocorticoids- (metabolic and anti-inflammatory effects in multiple tissues)
androgens- (DHEAS) androgeneic/virlizing (development of sex differenes) effects


What is the difference between a mineralocorticoid and a glucocorticoid?

gluco-no 3 OH's (cortisol)
mineral-2 OH's (aldosterone)


what are the three regions of the adrenal cortex? what do they produce?

from out to in
zona glomerulosa-aldosterone (mineralcorticoid)
zona fasciculata-cortisol (glucocorticoid)
zona reticularis-dehyroepiandrosterone (DHEA), androstenedione, testosterone (androgens)


what are the effects of glucocorticoids in bone, liver, muscle, kidney, muscle, GI,immune, behavior, fetal maturity? what disease occurs with excess amount in these tissues except kidney and fetal maturity? how does cortisol travel in the blood?

bone-increase osteoclasts and decrease osteoblasts bone resorption, excess-osteoporosis
liver-hepatic gluconeogenesis, excess-hyperglycemia
muscle-increase protein catabolism and decrease glucose uptake, excess-insuiln resistance, muscle breakdown
kidney-decrease renal free water clearance
muscle-decrease collagen and protein synthesis decrease wound healing and connective tissue, excess-easy bruising, thin muscle weakness
GI-decrease Ca2+ absorption; excess-osteoporosis
immune sys-decrease in immune molecules, excess-thymus and lymph immunosuppressive node involution
behavior-unknown mechanisms;excess-depression, psychosis
fetal maturity-increase in surfactant and maturity, increase in hepatic and GI enzyme systems
travels on CBG cortisol binding globulin


describe the production of cortisol

cholesterol gets converted to pregnenolone in glomerulosa. 17alpha hydroxylase converts pregnenolone to 17-hydroxypregnenolone which moves to fasciulata, here there are enzymes that convert 17-hydroxypregnenolone to cortisol.


what is the difference between Cushing syndrome and Cushing disease? name some causes of both.

Syndrome-only cortisol is high. DD, most common: exogenous glucocorticoids, others: adrenal adenoma, adrenal carcinoma, adrenal hyperplasia
Disease-both ACTH and cortisol are high.
other causes: ectopic ATCH syndrome (non-pituitary tumor i.e lung carcinoma) note cushing disease is specific to a pituitary tumor


what are some common causes of primary adrenal deficiency?

aka Addison's:
infection (TB, fungal)
cancer (metastatic)
infiltrative diseases
surgical resection; complete pharmacological adrenal block
enzymatic defect (Congenital Adrenal Hyperplasia, CAH)


What are some common causes of secondary adrenal deficiency?

hypopituitarism (pituitary adenoma, surgery, radiation, etc.)
hypothalamic injury
longstanding steroid therapy


what is the difference between primary (Addison's) and secondary adrenal deficiency

primary-cortisol levels low, ACTH levels high
secondary-both low


what is the enzyme that is deficient in congenital adrenal hyperplasia?

21-hydroxylase, without it you can produce cortisol (fasciculata) or aldosterone (glomerlosa). instead precursors get converted to androgens (pregnenolone (via 17-alpha hydroxylase) to 17-hydroxypregneolone (via 17,20 lyase) to DHEA (via various enzymes) to testosertone and estradiol)


How and where is aldosterone created?

glomerulosa: cholesterol enters zona glomerulosa to become pregnonolone which gets converted to progesterone via 13-beta hydroxylase and becomes aldosterone (via various enzymes)


what are the effects of mineralcorticoids? where in the kidney do they work?

increase renal Na+ absorption
increase plasma K+ secretion, increase plasma H+ secretion
DCT (distal convoluted tubule)


Describe the renin ang-ald-axis. name some drugs that inhibit this process.

the changes in pressure causes release of renin (from the kidney) which converts angiotensinogen (from the liver) to ANG I which then gets converted to ANG II (via ACE). ANGII acts on adrenal gland to release aldosterone which works to correct change in blood pressure
drugs-ACE-I blocks ANGI conversion to ANGII
ARB-blocks ANGII action on adrenal gland


name the causes of primary hyperaldosteronism. secondary hyperaldosteronism

primary-aldosteronoma (Conn syndrome), bilateral idiopathic hyperplasia, glucocorticoid-remediable aldosteronism (GRA)
secondary-hyperreninemia (renal a. sternosis, adrenal insufficiency, reninoma)


what are the signs and symptoms of cortisol excess?

weight gain hypertension diabetes edema
“moon facies” “buffalo hump”
hypokalemia weakness
hirsutism, abdominal striae, bruising depression


what are the signs and symptoms of cortisol deficiency?

fatigue hypotension
weakness orthostasis hyperpigmentation* hyponatremia weakness hyperkalemia* nausea/vomiting


What are the signs and symptoms of aldosterone excess?

hypertension hypokalemia edema fatigue weakness


what are the causes of primary aldosterone deficiency? secondary?

Primary-Addison disease, congenital adrenal hyperplasia, biosynthetic defects, medication-induced (spironolactone)
secondary- hyporeninemic hypoaldosteronism (type IV renal tubular acidosis (RTA); diabetic renal disease)


what are the signs and symptoms of aldosterone deficiency?

hypotension, hyperkalemia, fatigue, weakness


describe the mechanism of catecholamine biosynthesis, where does this occur?

occurs in adrenal medulla
tyrosine to DOPA (via tyrosine hydroxylase)
dihydroxyphenylalamine DOPA to Dopamine (via DOPA decarboxylase)
DA to norepinephrine (via dopamine-beta hydroslyase)
NE to epinephrine (via phentolamine-N- methyltransferase (PNMT)


what types of receptors are do catecholamines act on? what are their functions? which neural system controls them?

alpha-adrenergic receptors (NE>E)-increase gluconeogenesis, arteriolar constriction, muscle contraction growth hormone secretion, sweating, and pupil dilation. decreased insulin secretion
beta-adrenergic receptors (E>NE)-increased glycogenolysis, lipolysis and ketosis, arteriolar dilation, cardiac contractility (beta 1) muscle relaxation (beta 2), insulin secretion, renin secretion, thyroid hormone secretion. decrease glucose utilization.
under control of sympathetic nervous system


name the signs and symptoms of pheochromocytomas (neuroendocrine tumor of adrenal gland)? what is the classical triad? where are these commonly located?

hypertension+classical triad: headaches, palpitations, diaphoresis
located 90% intra-adrenal
10% extra adrenal