Physiology (Exam 2) Flashcards
Identify the (4) functional zones of the adrenal glands and the principal hormones secreted from each zone
(3) layers of adrenal cortex from outer to inner:
- Glomerulosa = aldosterone (salt)
- Fasiculata = cortisol (sugar)
- Reticularis = androgens (sex)
Adrenal medulla = Epinephrine and Norepinephrine
What (2) adrenal hormone biosynthetic pathways does 21-hydroxylase participate in?
Cortisol and Aldosterone synthesis. Becomes important when there is a deficiency.
What is DHEA-sulfate and how is it found in circulation?
DHEA-sulfate is a precursor to major sex hormones and 98% of it is bound to albumin in circulation.
(3) stimulating factors for release of CRH (cortisol-releasing hormone). Which is the primary?
Hypoglycemia (*primary);
Stress;
Diurnal rhythm (high cortisol in morning and low at night)
Negative feedback suppression of cortisol
elevated levels of cortisol inhibit both hypothalamic release of CRH and anterior pituitary release of ACTH
What is POMC and what is its clinical significance?
POMC = proopiomelanocortin. It is a precursor to the ACTH released by the anterior pituitary. It will be broken down into ACTH, an opiod, and a melanocyte stimulating factor.
Thus, high ACTH levels are associated w/ hyperpigmentation b/c of the concurrent melanocyte stimulation
(3) metabolic actions cortisol stimulates the liver to do
1) release glucose into the blood
2) use amino acids and fatty acids (from broken down protein in muscle and TAGs in fat) in Gluconeogenesis
3) store glucose as glycogen. Why?? B/c when cortisol is released, also have glucagon and epi that are all acting to break down glycogen. Thus, cortisol provides a substrate for them.
effects of low v. high doses of cortisol
low doses = permissive effect for NE and epi. Needed for the stress response high doses (pharmacological effects) = immunosuppression and anti-inflammatory
What is the anti-insulin effect of cortisol?
opposes glucose uptake by muscle and adipose tissue. Result is they break down their own protein and fat respectively to be used in gluconeogenesis
What effect can excess cortisol have in muscle?
can lead to muscle atrophy and weakness (through its anti-insulin effect)
How can high pharmacological doses of cortisol suppress the adrenocortical axis?
through negative feedback, high cortisol levels will turn off ACTH release. A decrease in ACTH can lead to decreased release of ALDOSTERONE b/c it indirectly affects maintenance of the adrenal gland
Addison’s Disease
insufficiency of the entire adrenal gland. Life-threatening b/c of lack of cortisol and aldosterone. Leads to hypotension (b/c no aldosterone) and poor muscle tone (b/c no cortisol)
(3) causes for Cushing’s Syndrome
a GROUP of sx related to high cortisol, may be due to:
- Cushing’s Disease = excess pituitary ACTH
- adrenal tumor
- ectopic ACTH
Adrenogenital syndrome, most common one and its sx
an enzyme deficiency w/ excess androgen production. Most common = 21-hydroxylase deficiency. Have low cortisol and high ACTH.
Sx = masculinization in developing female and precocity (unusually advanced) in developing male
How does 21-hydroxylase deficiency cause excess weak androgens?
With this deficiency, you don’t produce cortisol or cortisol is very low. Through negative feedback, this stimulates continuously high levels of ACTH, which will stimulate excess production of weak adrogens.
What is PNMT and why does it need cortisol?
PNMT is the enzyme that takes Norepinephrine and converts it to Epinpehrine. PNMT is activated by the cortisol draining from the adrenal cortex into the medulla. Thus, normal cortisol levels are needed to produce normal amounts of Epi!
Norepinephrine v. Epinephrine
Epi is made from NE using enzyme PNMT and cortisol in adrenal medulla.
However, NE is produced everywhere! The main source of NE in the blood is from its use as a SNS neurotransmitter
Chromaffin cells
Cells that synthesize catecholamines (80% Epi and 20% NE) in the adrenal medulla.
Pheochromocytoma
an unregulated NE producing tumor in the adrenal gland. Sx: hypertension (due to vasoconstriction), headache, perspiration, palpitations and anxiety
What is the MAIN effect of release of epinephrine?
to increase plasma glucose levels (by mobilizing glycogen from the muscle and liver). Epi also has fight or flight physiological responses
Catecholamines mechanism of action
since catecholamines can not diffuse through cell membranes, they act on membrane receptors (alpha and beta) to accomplish their action
(4) hormones stimulated by low glucose that work against insulin
Growth hormone Glucagon Cortisol Epinephrine *remember that cortisol is needed to stimulate PNMT to synthesize Epi
