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R - Endocrine Physiology (Megan) > Lecture 6 - adrenal gland > Flashcards

Lecture 6 - adrenal gland Flashcards

1
Q

what is another name for the adrenal gland?

A

The suprarenal gland.

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2
Q

How much does the adrenal gland weigh?

A

4g in adults.

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3
Q

How do they look?

A

They are glands but look like fatty tissue sitting superior to the kidneys.

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4
Q

What are the 2 main parts of the adrenal gland?

A

The adrenal medulla.

The adrenal cortex.

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5
Q

Describe the adrenal medulla?

A
  • 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.
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6
Q

Describe the adrenal cortex?

A
  • 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).
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7
Q

Which two hormones work together that are both secreted from the adrenal cortex?

A

Cortisol and aldosterone.

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8
Q

What is the adrenal cortex contribution to sex steroids?

A

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.

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9
Q

What are the 3 different layers of the adrenal Cortex?

A

Outer to inner

  • zona glomerularis (aldosterone)
  • Zona fasciculata (cortisol)
  • zona reticulatis (sex hormones)
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10
Q

Why are different hormones secreted in the different layers of the adrenal gland?

A

Because different enzymes are found in each layer vital for hormone synthesis.

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11
Q

what are all steroid hormones derived from?

A

Cholesterol.

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12
Q

What steroid hormones is 21-hydroxylase needed to produce?

A

Aldosterone and cortisol. NOT the sex steroids.

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13
Q

What does a congenital defect in 21-hydroxylase cause?

A
  • Adrenal hyperplasia.
  • No production of aldosterone and cortisol (disruption of salt and glucose balance)
  • Increased production of sex steroids (MALFORMED GENITALIA).
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14
Q

How does deficient 21-hydroxylase cause adrenal hyperplasia?

A

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.
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15
Q

How does 21-hydroxylase cause malformed genitalia?

A

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.

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16
Q

How much of plasma cortisol is bound to plasma protein?

A

95% of it.

Only 5% is free.

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17
Q

What is the plasma protein for cortisol?

A

Cortisol binding globulin.

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18
Q

Which cells have receptors for cortisol?

A

ALL nucleated cells.

The receptors are intracellular (because cortisol is a steroid, lipophilic).

19
Q

How does cortisol work?

A

It changes gene expression inside the nucleus and effects persist for a long time.

20
Q

How long does the effects of cortisol last for?

A

Days or weeks.

21
Q

When are glucocorticoids (cortisol) used clinically?

A

To manage inflammatory diseases like asthma or ulcerative colitis, or post organ transplant.

22
Q

How does glucocorticoids (cortisol) switch off inflammation?

A

They alter gene expression.
- switch off coding for nitric oxide synthase and cyclo-oxygenase (these enzymes are needed in the inflammation pathway).

23
Q

What hormone determines cortisol release?

A

ACTH

Adrenocorticotropic hormone.

24
Q

When is most cortisol released?

A

In the early morning.

Random spikes in the afternoon due to daily stress.

25
Q

When is least cortisol released?

A

In the evening.

26
Q

What lasts for longer in the plasma, cortisol or ACTH?

A

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.

27
Q

Why do we need cortisol in the morning?

A
  • 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.
28
Q

What does cortisol have a permissive action on?

A

Glucagon (helps increase BG).

Aldosterone (increases binding of the adrenoreceptors)

29
Q

side effects of glucocorticoid (steroid) therapy?

A
  • 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).
30
Q

How to withdraw glucocorticoid (steroid) therapy?

A

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.

31
Q

What is the function of aldosterone?

A

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
32
Q

Which cushings problem is more common?

A

Cushings disease

33
Q

What is cushings syndrome caused by?

A

A primary disorder.

A tumour of the adrenal gland secreting too much cortisol.

34
Q

What is cushings disease caused by?

A

A secondary disorder.

A tumour of the pituitary gland causing hyper secretion of ACTH which causes hyper secretion of cortisol as a result.

35
Q

What are the characteristics of cushings syndrome and disease?

A

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)
36
Q

What is a disease caused by hypo secretion of the adrenal gland?

A

Addisons disease

37
Q

What is Addisons disease?

A

Autoimmune attack on the adrenal gland.

Causing hypo secretion of all steroid hormones.

38
Q

What are the results of Addisons disease?

A
  • No permissive effect of cortisol on aldosterone (Low blood pressure)
39
Q

What happens to pigmentation in primary Addisons disease?

A

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.

40
Q

What happens to pigmentation in secondary Addisons disease?

A

No change.

Problem is with lack of ACTH being made from the pituitary, so there’s also no increase in MSH.

41
Q

What is Addisons crisis/adrenal crisis?

A

Life threatening hypotension and hypoglycaemia (due to the loss of cortisol and aldosterone).

42
Q

What are pathologies of the adrenal medulla?

A

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
43
Q

How is pheochromocytoma treated?

A

It responds well to surgery.

R - Endocrine Physiology (Megan) (10 decks)

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