Endocrine 3 Flashcards
(37 cards)
POMC processing
Glycosylation, acetylations, extensive proteolytic cleavage by pro-hormone convertases to produce tissue specific activity of different hormones.
Zona Glomerulosa
Secretes aldosterone to regulate plasmatic Na+.
Outermost layer of the cortex.
Zona Fasciculata
Secretes glucocorticoids (cortisol, cortisone…) to regulate glucose metabolism and the immune response. Middle layer of the cortex.
Zona Reticularis
Secretes sex steroids and dehyroepiandrosterone. Innermost layer of the cortex
Adrenal medulla function
Secretes epinephrine and norepinephrine to stimulate the sympathetic nervous system.
Center portion of the adrenal gland.
Glucocorticoids
Hormones that regulate glucose metabolism: cortisol, corticosterone, cortisone.
Biosynthesis of adrenocortical hormones
Stimulated by many hormones (ACTH, LH, and Angiotensin II, and FSH) at different points int he pathway to produce hormones such as cortisol, estradiol, testosterone.
All begin with cholesterol.
Cortisol secretion regulation
Regulated by light, peaks during the day.
Light -> SCN -> PVN -> anterior pituitary secretes ACTH, and subsequent cortisol secretion acts as negative feedback.
Stimulants of cortisol
Physical stress (trauma, exercise, fasting)
Emotional stress (anxiety, anticipation, novel situations).
Physiological effects of cortisol
- Liver, muscle, adipose
- Immune system, vascular
- increase GNG
- Increase breakdown, decrease synthesis, decrease uptake (of proteins and of glucose)
— Suppress immune response
— Enhance vascular responsiveness.
Permissive effects
Cortisol facilitates the actions of other hormones (like glucagon and epinephrine) on mobilisation of energy stores
Mineral corticoids
Increase Na+ reabsorption, increase K+ secretion, increase H+ secretion.
Adrenal androgens
Females - stimulates pubic hair growth and auxiliary hairs (adrenarche), and stimulates libido.
Males - same effect as testosterone.
Pathology of excess cortisol
Hyperglycemia (decreased glucose uptake)
Increased proteolysis (increased breakdown)
Muscle wasting
Central obesity
Poor wound healing
Striae
Dexamethasone suppression test
Low dose suppresses in individuals with no pathologies - confirms an issue.
High dose exerts negative feedback on the pituitary - determines location of issue.
Cushing’s syndrome vs Cushing’s disease
Syndrome - adrenal tumor that causes an excess of cortisol.
Disease - pituitary tumor that caused excess ACTH secretion that in turn increases cortisol.
Ectopic ACTH syndrome
Due to an ACTH secreting tumor causing increased ACTH levels and increased cortisol.
Tertiary adrenal deficiency
Occurs within the hypothalamus, decreased CRH release that does not respond to feedback of low cortisol.
Secondary adrenal deficiency
Occurs in the pituitary and causes low cortisol that acts on the hypothalamus to increase CRH levels but no change in ACTH release.
Primary adrenal deficiency
Occurs within the adrenal gland and causes a decrease in cortisol as well as aldosterone - extra symptoms include hyperkalemia, hyponatremia, and hypotension.
Addison’s disease
Due to dresctruction of the adrenal cortex and a lack of negative feedback means ACTH is in excess.
ACTH stimulates POMC processing to increase α-mash production, which causes hyperpigmentation.
21-hydroxylase deficiency
Interrupts production of adrenocortical hormones such that cortisol is absent and cannot suppress ACTH. Excess ACTH induces adrenal hyperplasia. Abnormal sexual development, treat with dexamethasone prenatally
Importance of maintaining blood glucose
Caloric intake is discontinuous but caloric needs are constant and variable. The body must balance nutrient availability and energy balance of intake vs. demand.
Insulin effects, release
Released during the FED state, produced by beta cells.
- increases glucose oxidation, glycogen synthesis, fat synthesis, protein synthesis.
