The Adrenal Glands Flashcards
1
Q
What are the 2 regions of the adrenal gland and their composition?
A
- cortex: glandular tissue derived from mesoderm (3 regions: outer zona glomerulosa, middle zona fasciculata and inner zona reticularis)
- medulla: sympathetic nervous system derived from the neural crest
2
Q
What hormones are secreted by the adrenal gland?
A
- zona glomerulosa: mineralcorticoids -aldosterone (maintain homeostasis of Na+, K+ and water)
- zona fasciculata:
glucocorticoids - cortisol and corticosterone (energy metabolism and glucose availability) - zona reticularis: gonadocorticoids - sex steroids (weak androgens)
- medulla: chromaffin cells secrete catecholamines
3
Q
Describe the blood supply of the adrenal gland
A
- receives blood by the superior, middle and inferior adrenal arteries which dip into the cortex with some reaching the medulla and then anastomosing under the capsule
- contains adrenocorticoids which influence adrenaline production
4
Q
Describe how steroid hormones are synthesised in the adrenal cortex and transported
A
- derived from cholesterol (from LDL in circulation)
- taken up by cells and converted to pregnenolone (rate limiting step and precursor of all hormones)
- can then be further converted until it forms its chosen hormone (depending on the factors it is exposed to)
- all hormones are lipid soluble and so can be carried around circulation attached to carrier proteins (eg. cortisol-binding globulins) which prolongs its half-life
5
Q
Describe the short-term stress response
A
- governed by hypothalamus and pituitary gland
- adrenaline and noradrenaline by sympathetic NS
6
Q
Describe the long-term stress response
A
- governed by hypothalamus stimulating the anterior pituitary gland to release ACTH
- results in release of cortisol (glucocorticoid) and aldosterone (mineralcorticoid) from the adrenal cortex
7
Q
Describe the functions and effects of cortisol
A
- synthesised and released in response to physical and mental stress
- maintain glucose levels keeping constant (mobilisation)
- maintain BP (monitor blood volume) to resist stress-related changes
(95% of glucocorticoid activity) - sensitises medulla to catecholamines
8
Q
Describe the activity levels of cortisol
A
- diurnal rhythm
- peaks in the morning at 6-8am
- is at its lowest around midnight-2am
- can be over-ridden by SNS in response to severe stress, and in disruption of the sleep-wake pattern
9
Q
Describe the physiological actions of cortisol
A
- major role is stimulating gluconeogenesis in liver: mobilising amino acid from muscle protein and increasing enzyme involved in amino acid conversion of glucose (eg. glycogen to glucose)
- increases liver protein synthesis
- muscle cell: inhibits protein synthesis, increases proteolysis to release amino acids into circulation to be taken in by liver to generate more glucose
- adipose cell: decreased lipogenesis and increased lipolysis to release glycerol into circulation to be taken in by liver for gluconeogenesis
- antagonises effects of insulin
- stabilises lysosomes (dampens immune response)
10
Q
Describe the role of the hypothalamus/pituitary in regulating cortisol release
A
- hypothalamus responds to stress which excites neurons within it
- stimulates release of CRF which induces anterior pituitary gland to synthesise and release ACTH which targets the adrenal cortex
- targets zona fasciculata to synthesise cortisol which is released to target tissue to carry out function
- stress is alleviated and cortisol levels feedback to the hypothalamus inhibiting further excitation and release
11
Q
List the clinical features of Cushing’s Syndrome (excess glucocorticoids)
A
- hyperglycaemia (due to gluconeogenesis and steroid diabetes)
- muscle wasting (due to proteolysis)
- increase in FFA (redistribution of fat to face and trunk)
- tissue oedema, hyperkalaemia, hypertension (water and Na+ retention)
- GIT ulceration (excess H+ and decreased mucus)
- immunosuppression
- decrease in protein synthesis
12
Q
What are the causes of Cushing’s Syndrome (excess glucocorticoids)
A
- ACTH-releasing pituitary tumour
- abnormal function of hypothalamus (high levels of CRH)
- ectopic ACTH-releasing tumour (eg. in lungs/pancreas/kidney)
- adrenal cortex tumour (hypersecretion of cortisol)
- clinical administration of glucocorticoid drugs
13
Q
What is the treatment for Cushing’s Syndrome?
A
- surgical tumour removal
- decrease glucocorticoid drug use
14
Q
Describe the main regulatory mechanism of aldosterone release
A
- high plasma K+ concentrations (detected by zona glomerulosa cells)
- can activate aldosterone release which acts on the kidney to decrease K+ (and also increase Na+ and water to maintain balance)
- therefore BP and blood volume also increases
- sends feedback to adrenal cortex
15
Q
Describe the RAAS involvement in aldosterone regulation
A
- aldosterone causes kidney to release renin which activates angiotensinogen to form angiotensin I
- gets converted to angiotensin II by ACE
- angiotensin II targets the adrenal glands to release more aldosterone, and acts on brain to release CRH (leading to ACTH release) and ADH
