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
Endocrine vs nerves
1-Nerves only innervate localised effect
2-Hormones = slow and delayed, CNS = fast
3-Adrenal stimulation has general effects
Catecholamines case study (4) -what are they -where are they made -what triggers them
1) Derived from tyrosine
2)NE, E, Dopamine
Chromaffin cells in the adrenal medulla secrete catecholamines into the blood via exocytosis.
2)TRIGGER IS STRESS
the hypothalamus activates sympathetic nerves, adrenal medulla, and catecholamines :
FIGHT OR FLIGHT
what a/b receptors do each NE, E have an affinity for?
Generally A1,2 = greater affinity for NE»_space; Adrenaline
B1,2,3= Adrenaline > NE
What is adrenomedullary dysfunction?
How can it come around?
Symptoms?
1-Tumour which secretes catecholamines
- HT
- Headache
- Sweating
- Palpitations
- Chest pain
- Anxiety
- Glucose intolerance
- Increased Metabolic rate
adrenocortical cells
1- Cortisol
2- Aldosterone
3- Androgens
