Adrenal Gland Flashcards
what are the three zones of the adrenal cortex
zona glomerulosa, zona fasciculata, and zona reticularis
which zone(s) of the adrenal gland is/are controlled by the hypothalamus and pituitary
fasciculata and reticularis
which zone(s) of the adrenal gland is/are NOT controlled by the hypothalamus
zona glomerulosa (and the medulla, although it is not technically a zone)
what zone secretes glucocorticoids (cortisol and corticosterone)
zona fasciculata
what zone secretes the gonadal steroids (estrogen, progesterone, androgens)
zona reticularis
what secretes epineprhine and norepineprhrine?
the adrenal medulla
what zone secretes aldosterone
zona glomerulosa
what is the mechanism of action of aldosterone
it increases sodium retention/reabsorption, and inreases calcium, H, and K excretion (hypokalemia)
what induces aldosterone secretion
hyponatremia, hyperkaliemia, low extracellular fluid volume
regulation of glucocorticoid synthesis (sorry :( )
ACTH -> adrenal cortex -> cholesterol -> mitochondria -> pregnenolone synthesis -> SER -> 11-Deoxycortisol + 11- Deoxycorticosterone -> mitrochondria -> cortisol and corticosterone (glucocorticoids)
effects of excess glucocorticoids on carbohydrates
- causes hyperglycemia due to decreased affinity of insulin receptors to insulin
- promotes uptake of glu
- increases glycogen storage in liver (hepatomegaly)
effects of excess glucocorticoids on proteins
- reduces muscle mass
- thin and friable skin
- osteoporosis due to loss of bone matric proteins and calcium
effects of excess glucocorticoids on lipids
- fat mobilized to neck, shoulder and abdomen
- supraorbital fat pad
- lipolysis /hypercholesterolemia
effects of excess glucocorticoids on minerals
Na retention and K excretion (hypokalemia, Na:K ratio > 40:1)
Decreased Ca absorption
effects of excess glucocorticoids on water metabolism
increase excretion of water by interfering with ADH release (polyuria and polydipsia)
how does excess glucocorticoids cause metabolic alkalosis
increase loss of H ions
how does excess glucocorticoids cause anti-inflammatory effects
-stabilization of lysosomal membranes, decreased synthesis of proinflammatory prostaglandins, increase the number of circulating mature neutrophils
how are excess glucocorticoids immunosuppressive
decreases T lymphocytes and alters the ability of macrophages to take up and process antigens
what will a leukogram indicating stress show>
neutrophilia, lymphopenia, eosinopenia, monocytosis
What are the three classifications for hyperadrenocorticism (cushings disease)
- pituitary dependent (PDH)
- adrenocortical tumors (ADH)
- iatrogenic
what is the most common type of hyperadrenocorticism
PDH (pituitary dependent). Accounts for 80-85% of cases
Name some clinical manifestations of cushings disease
- polydipsia and polyuria
- polyphagia
- reduced muscle mass
- pot-bellies appearance
-alopecia
-fragile skin - muscle atrophy
-panting
What disease is the opposite of cushings disease?
addison’s disease (hypoadrenocorticism)
what is primary hypoadrenocorticism
an issue with the adrenal gland itself. leads to deficiency in cortisol and mineralocorticoids
what causes secondary hypoadrenocorticism
decreased secretion of ACTH, causing atrophy of the adrenal glands
in secondary hypoadrenocorticism, what are the expected levels of cortisol and mineralocorticoids?
cortisol will be low, mineralocorticoids will remain adequate/normal
clinical manifestations of hypoadrenocorticism
bradycardia due to hyperkalemia
shock due to hyonatremia
elevated urea/creatine due to decreased renal perfusion
acidosis
what tests do you use to diagnosis adrenal function
ACTH stimulation test, low dose dexamethasone test, high dose dexamethasone test
The post ACTH stimulation results beyond ___ indicates hyperadrenocorticism/ Cushing’s
disease
660
The post ACTH stimulation results below ___ indicates hypoadrenocorticism
55
what is the limitation to an ACTH stimulation test?
An exaggerated response to ACTH stimulation test may be obtained due to stress or
illness. Exogenous administration of steroids decreases both baselines as well as adrenal
responsiveness to ACTH
How does a low dose dexamethasone test work
First, a baseline level of cortisol is measured. Then a low
dose of dexamethasone is administered. Dexamethasone is a glucocorticoid and it will inhibit
production of ACTH from the pituitary and CRH from the hypothalamus in a normal animal. If
the normal feedback loop occurs, there will be ≤ 20nmol/ml of endogenous cortisol in the blood
for a prolonged period (for convenience we check cortisol level at 3h and 8 h post
dexamethasone injection). If there is > 40 nmol/ml of cortisol detected after the LDDT (at 3 h
and 8 h post injection), then hyperadrenocorticism will be confirmed. However, this test does not
predict origin of the disease (adrenal versus pituitary)
how does a high dexamethasone test work
Adrenal tumors are independent of pituitary control
and pituitary secretion of ACTH is already under inhibition. Therefore, administration of
dexamethasone should not inhibit cortisol production from neoplastic adrenal gland regardless
of dosage. PDH results from a pituitary tumor that chronically secretes ACTH, which in turn
causes adrenal hyperplasia. Chronic secretion of ACTH from a pituitary tumor can be inhibited
with higher doses of dexamethasone, leading to suppression of cortisol secretion from the
adrenal gland. Therefore, a dog that suppresses (to <50% the baseline cortisol concentrations
or <40 nmol/L) cortisol secretion in response to a high dose of dexamethasone (0.1-1.0 mg/kg
IV) is diagnosed with PDH and those with no suppression of cortisol level (see definition of
suppression above) are diagnosed with adrenal tumours. Therefore, this test can be used for
differentiating PDH versus AT
what are the two cell types in the adrenal medulla that are of nervous origin>
chromaffin cells and sympathetic ganglion cells
what type of cell secretes E or NE
chromaffin cells in the adrenal medulla
what amino acid are catecholamines synthesized from
tyrosine
what is the main stimulant for catecholamine release
stress
what enzyme is required for the synthesis for catecholamines>
hydroxylase
what enzyme is required to convert NE into E
Phenylethanolamine-N- methyltransferase enzyme.
chromaffin cells release catecholamines under the stimulation of ___-
acetylcholine from sympathetic neurons and by cortisol from the adrenal cortex
describe the synthesis and release of catecholamines
The enzyme hydroxylase is required for the synthesis of catecholamines. Norepinephrine is
synthesized in the chromaffin granules of chromaffin cells. Chromaffin cells that secrete
epinepherine synthesize this hormone from norepinephrine in the cytosol, using
Phenylethanolamine-N- methyltransferase enzyme. Epinephrine re-enters chromaffin granule
(probably to protect the animal from epinephrine effect). Chromaffin cells release
catecholamines under the stimulation of acetylcholine released from the sympathetic neurons
and by cortisol from the adrenal cortex. These agents increase intracellular calcium
concentration in the chromaffin cells, leading to the release of catecholamines
