Lecture 6 - adrenal gland Flashcards
what is another name for the adrenal gland?
The suprarenal gland.
How much does the adrenal gland weigh?
4g in adults.
How do they look?
They are glands but look like fatty tissue sitting superior to the kidneys.
What are the 2 main parts of the adrenal gland?
The adrenal medulla.
The adrenal cortex.
Describe the adrenal medulla?
- in the middle
- makes up 25% of full gland
- neuroendocrine (composed of neural tissue)
- controlled by sympathetic nervous system
- secretes catecholamines (amines)
- secretes epinephrine (adrenaline), norepinephrine and dopamine.
Describe the adrenal cortex?
- true endocrine gland
- made of 3 layers
- secretes steroid hormones (glucocorticoids - cortisol, mineralocorticoids - aldosterone, sex steroids - testosterone, progesterone and oestrogen).
- controlled by hypothalamus (CRH) and anterior pituitary (ACTH).
Which two hormones work together that are both secreted from the adrenal cortex?
Cortisol and aldosterone.
What is the adrenal cortex contribution to sex steroids?
Very minor.
They secrete all 3 hormones in males and females but in a very tiny number.
- In females the ovaries secrete lots of oestrogen and progesterone.
- In males the testes secrete lots of testosterone.
What are the 3 different layers of the adrenal Cortex?
Outer to inner
- zona glomerularis (aldosterone)
- Zona fasciculata (cortisol)
- zona reticulatis (sex hormones)
Why are different hormones secreted in the different layers of the adrenal gland?
Because different enzymes are found in each layer vital for hormone synthesis.
what are all steroid hormones derived from?
Cholesterol.
What steroid hormones is 21-hydroxylase needed to produce?
Aldosterone and cortisol. NOT the sex steroids.
What does a congenital defect in 21-hydroxylase cause?
- Adrenal hyperplasia.
- No production of aldosterone and cortisol (disruption of salt and glucose balance)
- Increased production of sex steroids (MALFORMED GENITALIA).
How does deficient 21-hydroxylase cause adrenal hyperplasia?
Because no cortisol can be produced so the negative feedback loop doesn’t work.
- CRH and ACTH (especially ACTH) continue to be secreted.
- This causes over stimulation of the adrenal gland.
How does 21-hydroxylase cause malformed genitalia?
The production of androgens (sex steroids) is not affected because it doesn’t need 21-hydroxylase.
There is more cholesterol due to no production of cortisol or aldosterone.
This leads to increase of all sex steroids - giving the baby too much of each genitalias characteristics.
How much of plasma cortisol is bound to plasma protein?
95% of it.
Only 5% is free.
What is the plasma protein for cortisol?
Cortisol binding globulin.
Which cells have receptors for cortisol?
ALL nucleated cells.
The receptors are intracellular (because cortisol is a steroid, lipophilic).
How does cortisol work?
It changes gene expression inside the nucleus and effects persist for a long time.
How long does the effects of cortisol last for?
Days or weeks.
When are glucocorticoids (cortisol) used clinically?
To manage inflammatory diseases like asthma or ulcerative colitis, or post organ transplant.
How does glucocorticoids (cortisol) switch off inflammation?
They alter gene expression.
- switch off coding for nitric oxide synthase and cyclo-oxygenase (these enzymes are needed in the inflammation pathway).
What hormone determines cortisol release?
ACTH
Adrenocorticotropic hormone.
When is most cortisol released?
In the early morning.
Random spikes in the afternoon due to daily stress.
When is least cortisol released?
In the evening.
What lasts for longer in the plasma, cortisol or ACTH?
Cortisol. IT is steroid so is bound to a carrier protein which protects it from enzyme degradation. ACTH is peptide so doesn’t bind to carrier protein. So isn’t protected from enzyme degradation.
Cortisol has the longer half life.
Why do we need cortisol in the morning?
- to increase BG to give skeletal muscles energy to make us stand up.
- to increase blood pressure to ensure blood still gets to out brain when we go from lying to standing.
What does cortisol have a permissive action on?
Glucagon (helps increase BG).
Aldosterone (increases binding of the adrenoreceptors)
side effects of glucocorticoid (steroid) therapy?
- suppressed immune system (increased severity and frequency of infection)
- increased protein catabolism (muscle wastage)
- increase in lipolysis (thin skin due to loss of percutaneous fat).
How to withdraw glucocorticoid (steroid) therapy?
Should be done slowly.
Increasing cortisol increases negative feedback - decreases CRH and ACTH - so no effect on adrenal gland - gland gets smaller.
- Gland needs time to grow again or will be adrenal insufficient.
What is the function of aldosterone?
It is involved in he renin-angiotensin-aldosterone system.
- it increases sodium uptake (which is followed by water)
- it stimulates potassium excretion
- rise in water = INCREASES BLOOD PRESSURE
Which cushings problem is more common?
Cushings disease
What is cushings syndrome caused by?
A primary disorder.
A tumour of the adrenal gland secreting too much cortisol.
What is cushings disease caused by?
A secondary disorder.
A tumour of the pituitary gland causing hyper secretion of ACTH which causes hyper secretion of cortisol as a result.
What are the characteristics of cushings syndrome and disease?
increased cortisol causes:
- increased proteolysis (increased protein breakdown causing muscle wastage and skinny arms and legs)
- fat deposits to the back of the neck, face and trunk (central obesity)
What is a disease caused by hypo secretion of the adrenal gland?
Addisons disease
What is Addisons disease?
Autoimmune attack on the adrenal gland.
Causing hypo secretion of all steroid hormones.
What are the results of Addisons disease?
- No permissive effect of cortisol on aldosterone (Low blood pressure)
What happens to pigmentation in primary Addisons disease?
hyperpigmentation.
- adrenal gland doesn’t produce cortisol (no negative feedback loop)
- increase in ACTH (there’s also an increase in MSH - melatonin secreting hormone) because they are made from the same precursor = hyperpigmentation.
What happens to pigmentation in secondary Addisons disease?
No change.
Problem is with lack of ACTH being made from the pituitary, so there’s also no increase in MSH.
What is Addisons crisis/adrenal crisis?
Life threatening hypotension and hypoglycaemia (due to the loss of cortisol and aldosterone).
What are pathologies of the adrenal medulla?
Pheochromocytoma
- rare neuroendocrine tumour found in the adrenal medulla.
- increase in catecholamines (epinephrine, norepinephrine, dopamine)
- increase in sympathetic nervous system response
- increase in BG (epinephrine), increase in HR, increase in Co and increase in BP.
- it can also be diabetogenic
How is pheochromocytoma treated?
It responds well to surgery.