The Adrenal Glands Flashcards
location
just above the kidneys
Adrenal gland anatomy
central medulla, outer cortex, completely unconnected
Outer cortex
produces three major classes of steroid hormones synthesized from cholesterol
Glucocorticoids
mineralocorticoids
androgens
Three concentric zones of the cortex
Differ in the major steroid hormones they secrete
Zona glomerulosa - aldosterone
Zona fasciculata - cortisol
Zona reticularis - adrenal androgens
Adrenal medulla produces
catecholamine hormones
Cells of the medulla are derived from
nervous system
is an extension of the nervous system
Principal cell type of the medulla
Chromaffin cell
Cortisol
the major glucocorticoid
production controlled from the pituitary via ACTH secretion
increases gluconeogenesis
has anti-inflammatory properties
acts on renal tubules to increase sodium reabsorption and excretion of potassium
21 carbons
Aldosterone
the major mineralocorticoid
controlled by the renin-angiotensin system
acts on renal tubules to increase sodium reabsorption and excretion of potassium
21 carbons
Adrenal androgens
production controlled by pituitary ATCH
mimic the effects of testosterone on secondary sexual characteristics
females: constitute the major androgens produced
most common: DHEA, a precursor for gonadal hormones
lab testing: DHEA-S level (sulfated form)
19 carbons
Renin
converts angiotensinogen to angiotensin I
secreted by the juxtaglomerular kidney cells in response to a decrease in blood pressure
angiotensin converting enzyme (ACE)
convers angiotensin I to angiotensin II
angiotensin II causes
vasoconstriction, increase in blood pressure, more blood passes through the kidneys
causes increase in aldosterone production –> more sodium reabsorption –> more blood volume –> more potassium excretion
ACE inhibitors
work the renin-angiotensin system to regulate blood pressure
Cushing’s (Hypercortisolism) syndrome
a disease of the adrenal cortex
causes: adrenal tumor, adrenal hyperplasia, ectopic production of ACTH by a non-pituitary tumor, exogenous glucocorticoids
signs: loss of diurnal variation
Cushing’s disease
a type of Cushing’s syndrome where the cause is overproduction of ACTH by a pituitary adenoma
Laboratory diagnosis of Cushing’s
serum cortisol: + reagents allowing coritsol to release from its binding proteins –> total cortisol
urine gives an indication of the amount of free cortisol
saliva: free cortisol, only collected at midnight
24 hour urine cortisol: give dexamethasone suppression test and measure serum. Normal: suppression of ACTH, cortisol will decrease through negative feedback. Cushing’s: cortisol is not suppressed
Hyperaldosteronism - primary
Conn’s syndrome
tumor in adrenal cortex producing aldosterone
results in high plasma sodium, low plasma potassium, high plasma and urine aldosterone, low plasma renin
Secondary hyperaldosteronism
Renin-secreting tumor of the kidney
Results in high plasma sodium, low plasma potassium,high plasma and urine aldosterone, high plasma renin
Adrenal insufficiency (Addison’s disease)
major cause: autoimmune
result: low cortisol and aldosterone, high ACTH
low sodium and high potassium in blood
ACTH is a small polypeptide (39 aas) that fragments from a large molecule that also makes melanocyte stimulating hormone –> dark complexion
Congenital adrenal hyperplasia (CAH)
inherited enzyme defects in the adrenocortical steroid synthesis pathway
defect at the 21-hydroxylase enzyme
excess pituitary ACTH production, impaired cortisol and aldosterone synthesis
negative feedback is lost
uncontrolled stimulation of adrenal cortex tissue and excess synthesis of all steroids
high levels of adrenal androgens
Diagnosis of CAH
measure 17-OH progesterone, the substrate for 21-hydroxylsae
The Adrenal Medulla
central portion of the adrenal gland
comes from ectodermal/neural crest
secretes catecholamines
catecholamines
cause changes that are normally associated w/ fight or flight when bound to adrenergic receptors on target cells
