Adrenal glands Flashcards
what are the zones of the adrenal cortex glands+ what do they release (6)
zona glomerlosa=mineralocorticoids
zona fasiculata=glucocorticoids
zone reticularis = androgens
the zones are within the adrenal cortex
Adrenal Medulla :
1-Chromaffin cells–>NE,E
2-Medullary veins
3-Splanchnic nerves
describe the cicadian rhythm of cortisol and it control via CRH ,ACTH
what cells release —-
-stress acts on hypothalamus ( CRH –>anterior pituitary ->corticotropes –>ACTH–>zona fasicualta –>cortisol
( night time = low ACTH before you sleep , higher when u wake
- We check cortisol defficiency at 8am
- Cortisol excess =Midnight levels
How is cortisol transported, what happens when cortisol is high , in terms of tests ?
- Transcortin
- When it is high Transcortin is saturated quickly and free cortisol increases , Urinary free cortisol is also high
What actions do glucocorticoids have?
4
- Muscle ( loss of AA to make glucose)
- Liver (Gluconeogenesis , glycogenesis )
- Fat cell =lipolysis )
- Immune system = suppressed
why is cortisol is a permissive hormone
It needs to be present for glucagon, adrenaline, and growth hormone to work.
Cortisol = very important in glucose homeostasis
- it is also required for the expression of adrenergic and angiotensin 2 receptor expression
causes of Glucocorticoid excess
1-Anterior pituitary tumor (Cushing’s disease = Increases CRH, negative feedback to hypothalamus fails)
2- Hypothalamic tumor ( more CRH)
3- adrenal tumor (More ACTH)
4- Iatrogenic Cushing’s syndrome = due to excessive use of exogenous glucocorticoids
Cushing syndrome mnemonic
- > Central obesity and thin limbs, Comedones (acne)
- > Urinary free cortisol
- > Suppressed immunity
- > Hyperglycemia, hypercholesterolemia, hypertension, -hypercortisolism
- > Iatrogenic (increased exogenous corticosteroids)
- > Noniatrogenic
- > Glucose intolerance, -growth retardation
What is the treatment for Cushing’s disease?(2)
- Cushings disease is due to a tumor in pituitary
- Resection of the anterior pituitary tumor
Outline RAAS
Decrease in BP
1) JG cells = secrete renin
2) ANG1–ANG2 VIA ACE:
- Vasoconstriction of arterioles
- Adrenal cortex = ALDOSTERONE ( increases na+ in kidney and water reabsorption )
Actions of aldosterone, where is it secreted from?
Secreted from zona glomerulosa (mineralocorticoid) :
1) Increased Na+/H2O re-absorption
2) Increased K+/H+ secretion
3) BV and BP increases
aldosterone deficiency indications
3
1) increases the loss of na+ and h20 in urine
2) Renal retention of K+= hyperkalemia = cardiac excitability and ventricular fibrillation
3) Renal retention of H+= metabolic acidosis
Primary hyperaldosteronism
- What is it called
- What happens
CONN'S DISEASE Due to adrenal adenoma aldosterone increases : Na+ retention, total body water increases , ECF increases , BP increases : -HT -HK -metabolic alkalosis
Primary adrenocortical insufficiency
- lack of glucocorticoids
- lack of mineralocorticoids
- Lack of adrenal androgen
Insufficiency = Addison’s disease
Destruction of both Adrenal cortices :
Mainly due to autoimmune response
Lack of Glucocorticoids :
- Hypoglycemia
- Reduction in fat/protein metabolism
- Poor exercise tolerance
- Poor stress tolerance =DEATH
Lack of mineralocorticoids (aldosterone):
1-Na+ decreases , K++H+ increases
2-CO goes down =shock =DEATH will kill u first!
3-Hypovolemia
Lack of adrenal androgens:
no real serious consequences
(mood)
Addisons disease signs and symptoms
FATIGUED mneumonic
Fatigue
Antibodies (ie: anti-adrenal, antithyroid, anti-parietal cell
Triad: hyponatremia, hypokalemia, azotemia (increased blood urea nitrogen)
Increased pigmentation of skin and tongue
Gastrointestinal: weight loss, anorexia
Nausea and vomiting
Eosinophilia (high levels of eosinophils), neutropenia (too few neutrophils)
Decreased blood pressure
Effects of adrenaline an sympathetic NS
1-pupils dilate 2-lower saliva= dry mouth 3-Increases HR 4-relaxes bronchi 5-directs blood away from GIT
