Adrenal Gland Flashcards by Emily Huff

what are the three zones of the adrenal cortex

zona glomerulosa, zona fasciculata, and zona reticularis

How well did you know this?

Not at all

Perfectly

which zone(s) of the adrenal gland is/are controlled by the hypothalamus and pituitary

fasciculata and reticularis

How well did you know this?

Not at all

Perfectly

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)

How well did you know this?

Not at all

Perfectly

what zone secretes glucocorticoids (cortisol and corticosterone)

zona fasciculata

How well did you know this?

Not at all

Perfectly

what zone secretes the gonadal steroids (estrogen, progesterone, androgens)

zona reticularis

How well did you know this?

Not at all

Perfectly

what secretes epineprhine and norepineprhrine?

the adrenal medulla

How well did you know this?

Not at all

Perfectly

what zone secretes aldosterone

zona glomerulosa

How well did you know this?

Not at all

Perfectly

what is the mechanism of action of aldosterone

it increases sodium retention/reabsorption, and inreases calcium, H, and K excretion (hypokalemia)

How well did you know this?

Not at all

Perfectly

what induces aldosterone secretion

hyponatremia, hyperkaliemia, low extracellular fluid volume

How well did you know this?

Not at all

Perfectly

regulation of glucocorticoid synthesis (sorry :( )

ACTH -> adrenal cortex -> cholesterol -> mitochondria -> pregnenolone synthesis -> SER -> 11-Deoxycortisol + 11- Deoxycorticosterone -> mitrochondria -> cortisol and corticosterone (glucocorticoids)

How well did you know this?

Not at all

Perfectly

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)

How well did you know this?

Not at all

Perfectly

effects of excess glucocorticoids on proteins

reduces muscle mass
thin and friable skin
osteoporosis due to loss of bone matric proteins and calcium

How well did you know this?

Not at all

Perfectly

effects of excess glucocorticoids on lipids

fat mobilized to neck, shoulder and abdomen
supraorbital fat pad
lipolysis /hypercholesterolemia

How well did you know this?

Not at all

Perfectly

effects of excess glucocorticoids on minerals

Na retention and K excretion (hypokalemia, Na:K ratio > 40:1)

Decreased Ca absorption

How well did you know this?

Not at all

Perfectly

effects of excess glucocorticoids on water metabolism

increase excretion of water by interfering with ADH release (polyuria and polydipsia)

How well did you know this?

Not at all

Perfectly

how does excess glucocorticoids cause metabolic alkalosis

increase loss of H ions

How well did you know this?

Not at all

Perfectly

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

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