Flashcards in Endo-Repro L7 Adrenal Glands Deck (33):
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3 major structural components:
1. Capsule
2. Cortex (90% of adrenal gland)
3. Inner Medulla
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Medulla developed from
Neural crest cells, which migrate into ganglion → mesodermal cortex.
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Adrenal vasculature:
→ Inferior phrenic artery and renal artery → plexus of arterioles that leads into channels called sinusoids.
No venous return medulla → hormones taken from cortex into medulla that requires cortisol.
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Zona glomerulosa
Mineralcorticoids e.g. aldosterone
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Zona fasiculata
Glucocorticoids e.g. Cortisol and small amounts of andorgens
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Zona reticularis
Androgens (eg. DHEA) and small amounts of androgens
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Medulla
Catecholamines
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Sympathetic innervation of chromaffin cells:
Stimulated by sympathetic NS T7-T9 bypassess coeliac ganglion and preganglionic axon synapses on a chromaffin cell stimulated medulla.
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Neurosecretory cells
storage vesicles in the cytoplasm which have no axons but release directly into the circulation.
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1. ANS exerts
direct control over chromaffin cells, therefore hormone release occurs rapidly (<1 min)
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Adrenaline:
1. 50% bound to albumin
2. T0.5 → 10 min
3. All form adrenal medullary chromaffin cells
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Noradrenaline:
1. 50% bound ot albumin
2. T0.5 <15 min
3. Mostly form postganglionic sympathetic neurons
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Functions of adrenal medullary catecholamines →
adrenaline is the strongest agonist for both alpha and beta adrenoceptors ( same for noradrenaline).
1. Act as a peripheral amplifier of the nervous system
2. Enhance ‘fight-flight’ response
3. Does not augment the action of insulin and does no inhibit glucagon actions
4. Does not promotes anabolic effects
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Alarm response: coronary blood flow and adreno-medullary catecholamines
1. Increased Cardiac output (Beta1)
2. Increased peripheral resistance (alpha1)
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1. Increased Cardiac output (Beta1)
a. Increased heart rate
b. Increased systolic force
c. Increased stroke volume
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2. Increased peripheral resistance (alpha1)
a. Increased vasoconstriction
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Alarm response: metabolic effects of adrenaline (counterregulatory hormone):
1. Adipose tissue = fatty acid release and ketogenesis
2. Skeletal Muscle and protein breakdown = gluconeogenesis
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Mineralocorticoids
Sodium (water) retention and potassium elimination.
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Glucocorticoids
Metabolic control, stress, actions on the immune system.
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Weak androgens
Low significance in adult male, libido in female.
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Adrenocortical hormones:
Mineralocorticoids
Glucocorticoids
Weak androgens
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Hypothalamo-pituitary-adrenal (HPA) axis activation results in glucocorticoid release →
1. Stress and diurnal rhythm stimulates hypothalamus.
2. Hypothalamus releases CRH and ADH which act on the anterior pituitary
3. Anterior pituitary releases ACTH
4. ACTH stimulates adrenal cortex to release cortisol
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Functions of glucocorticoids:
1. Metabolic
2. Cardiovascular
3. Immunologic
4. Homeostatic
5. Musculoskeletal → enhance renal calcium excretion
6. Arousal and mood
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Disorders affecting glucocorticoid:
Cushings Syndrome
collection of symptoms and physical signs caused by chronic glucocorticoid excess
See symptoms in lecture.
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Causes of cushings
1. Exogenous steroid use:
2. 1. Oral or topical administration
3. Most common cause (overall)
1. Used for treatment of inflammatory disorders and glucocorticoid defiency
2. Exogenous steroid use suppresses HPA axis and leads to atrophy of adrenal cortex
3. Other drugs can be used to suppress cortisol synthesis (e.g. Metyrapone)
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Endocrine challenge test:
1. Response of normal patients and those with Cushing’s DISEASE to a n injection of CRH → increased ACTH as patient’s pituitary more responsive. (CHECK)
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Disorders affecting glucocorticoid production:
Adrenocortical deficiency → deficient producton of glucocorticoids mineralcorticoids
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1. Destruction or dysfunction of the adrenal cortex- primary adrenocortical defiency
a. Causes:
i. Addison’s disease (autoimmune) or adrenal haemorrhage
1. Mineralcprticoids and glucocorticoids low
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2. Deficient pituitary ACTH (secondary adrenocortical deficiency
a. Causes:
i. Withdrawal from prolonged glucocorticoid therapy
1. Mineralcorticoids normal, glucocorticoids low
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Addison’s disease: symptoms
Weakness and fatigue
Anorexia and weight loss
Hyperpigmentation
Hypotension
GI disturbances
Salt craving
Amenorrhea; loss of axillary and pubic hair
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Adrenocortical insufficiency: diagnosis:
1. Urinary and plasma adrenocortical steroids
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2. Assessments of pituitary-adrenal axis function
a. CRH challenge test
b. ACTH challenge test
c. Primary or secondary defect? – Measure basal plasma ACTH levels
i. V high ACTH (Primary adrenal insufficiency)
ii. Low ACTH (Secondary adrenal insufficiency)
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