Endo-Repro L7 Adrenal Glands

Question 1

3 major structural components:

Answer 1

1. Capsule
2. Cortex (90% of adrenal gland)
3. Inner Medulla

Question 2

Medulla developed from

Answer 2

Neural crest cells, which migrate into ganglion → mesodermal cortex.

Question 3

Adrenal vasculature:

Answer 3

→ 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.

Question 4

Zona glomerulosa

Answer 4

Mineralcorticoids e.g. aldosterone

Question 5

Zona fasiculata

Answer 5

Glucocorticoids e.g. Cortisol and small amounts of andorgens

Question 6

Zona reticularis

Answer 6

Androgens (eg. DHEA) and small amounts of androgens

Question 7

Medulla

Answer 7

Catecholamines

Question 8

Sympathetic innervation of chromaffin cells:

Answer 8

Stimulated by sympathetic NS T7-T9 bypassess coeliac ganglion and preganglionic axon synapses on a chromaffin cell stimulated medulla.

Question 9

Neurosecretory cells

Answer 9

storage vesicles in the cytoplasm which have no axons but release directly into the circulation.

Question 10

1. ANS exerts

Answer 10

direct control over chromaffin cells, therefore hormone release occurs rapidly (<1 min)

Question 11

Adrenaline:

Answer 11

1. 50% bound to albumin
2. T0.5 → 10 min
3. All form adrenal medullary chromaffin cells

Question 12

Noradrenaline:

Answer 12

1. 50% bound ot albumin
2. T0.5 <15 min
3. Mostly form postganglionic sympathetic neurons

Question 13

Functions of adrenal medullary catecholamines →

Answer 13

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

Question 14

Alarm response: coronary blood flow and adreno-medullary catecholamines

Answer 14

1. Increased Cardiac output (Beta1)

2. Increased peripheral resistance (alpha1)

Question 15

1. Increased Cardiac output (Beta1)

Answer 15

a. Increased heart rate
b. Increased systolic force
c. Increased stroke volume

Question 16

2. Increased peripheral resistance (alpha1)

Answer 16

a. Increased vasoconstriction

Question 17

Alarm response: metabolic effects of adrenaline (counterregulatory hormone):

Answer 17

1. Adipose tissue = fatty acid release and ketogenesis

2. Skeletal Muscle and protein breakdown = gluconeogenesis

Question 18

Mineralocorticoids

Answer 18

Sodium (water) retention and potassium elimination.

Question 19

Glucocorticoids

Answer 19

Metabolic control, stress, actions on the immune system.

Question 20

Weak androgens

Answer 20

Low significance in adult male, libido in female.

Question 21

Adrenocortical hormones:

Answer 21

Mineralocorticoids
Glucocorticoids
Weak androgens

Question 22

Hypothalamo-pituitary-adrenal (HPA) axis activation results in glucocorticoid release →

Answer 22

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

Question 23

Functions of glucocorticoids:

Answer 23

1. Metabolic
2. Cardiovascular
3. Immunologic
4. Homeostatic
5. Musculoskeletal → enhance renal calcium excretion
6. Arousal and mood

Question 24

Disorders affecting glucocorticoid:

Cushings Syndrome

Answer 24

collection of symptoms and physical signs caused by chronic glucocorticoid excess
See symptoms in lecture.

Question 25

Causes of cushings

Answer 25

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)

Question 26

Endocrine challenge test:

Answer 26

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)

Question 27

Disorders affecting glucocorticoid production:

Answer 27

Adrenocortical deficiency → deficient producton of glucocorticoids mineralcorticoids

Question 28

1. Destruction or dysfunction of the adrenal cortex- primary adrenocortical defiency a. Causes:

Answer 28

i. Addison’s disease (autoimmune) or adrenal haemorrhage | 1. Mineralcprticoids and glucocorticoids low

Question 29

2. Deficient pituitary ACTH (secondary adrenocortical deficiency a. Causes:

Answer 29

i. Withdrawal from prolonged glucocorticoid therapy | 1. Mineralcorticoids normal, glucocorticoids low

Question 30

Addison’s disease: symptoms

Answer 30

``` Weakness and fatigue Anorexia and weight loss Hyperpigmentation Hypotension GI disturbances Salt craving Amenorrhea; loss of axillary and pubic hair ```

Question 31

Adrenocortical insufficiency: diagnosis:

Answer 31

1. Urinary and plasma adrenocortical steroids

Question 32

2. Assessments of pituitary-adrenal axis function

Answer 32

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)

Question 33

Therapeutic uses of glucocorticoids:

Answer 33

1. Replacement therapy in Addison’s (patients also require life-long mineralcorticoid theory) 2. Acute inflammatory disease (e.g. asthma, eczema) 3. Chronic inflammatory disease (e.g. rheumatoid arthritis) 4. Neoplastic disease 5. Immunosuppression (e.g. organ transplant) 6. Emergency medicine