18. The Adrenal Glands Flashcards

1
Q

What are the layers of the adrenal gland?

A

Capsule
Cortex - zona glomerulosa (mineralocorticoids), zona fasiculata (glucocorticoids), zona reticularis (glucocorticoids and androgens)
Medulla - chromatin cells

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2
Q

What do corticosteroids do?

A

Affect gene transcription

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3
Q

What are the types of corticosteroids?

A

Mineralocorticoids
Glucocorticoids
Androgens

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4
Q

Give an example of a mineralocorticoid

A

Aldosterone

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5
Q

Give examples of glucocorticoids

A

Cortisol
Corticosterone
Cortisone

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6
Q

Give examples of androgens

A

Dehyrdroepiandrosterone

Androstenedione - testosterone and oestrogens

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7
Q

Describe steroid hormones

A

Synthesised from cholesterol in adrenal glands and gonads
Lipid soluble hormones
Bind to receptors of the nuclear receptor family to modulate gene transcription

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8
Q

How do corticosteroids work?

A

Readily diffuse across plasma membrane
Bind to glucocorticoid receptors
Binding causes dissociation of chaperone proteins
Receptor ligand complex trans locates to nucleus
Dimerisation with other receptors can occur
Receptors bind to glucocorticoid response elements (GREs) or other transcription factors

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9
Q

Where is aldosterone synthesised and released from?

A

Zona glomerulosa of adrenal cortex

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10
Q

What is the carrier protein of aldosterone?

A

Mainly serum albumin and to a lesser extent transcortin

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11
Q

How does aldosterone work?

A

Aldosterone receptor is intracellular and exerts its actions by regulating gene transcription

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12
Q

What is the role of aldosterone?

A

Regulation of plasma Na+, K+ and arterial blood pressure
Main actions in distal tubules and collecting ducts where it promotes expression of Na+/K+ pump promoting reabsorption of Na+ and excretion of K+

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13
Q

What is primary hyperaldosteronism?

A

Too much aldosterone produced
Defect in adrenal cortex
Can be due to either bilateral idiopathic adrenal hyperplasia or aldosterone secreting adrenal adenoma (Conn’s syndrome)
Low renting levels

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14
Q

What is secondary hyperaldosteronism?

A

Too much aldosterone produced
Due to overactivity of renin-angiotensin-aldosterone system (RAAS)
Can be due to renin producing tumour or renal artery stenosis
High renin

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15
Q

What are the signs if hyperaldosteronism?

A
High BP
Left ventricular hypertrophy
Stroke
Hypernatraemia
Hypokalaemia
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16
Q

What is the treatment for hyperaldosteronism?

A

Depends on type
Aldosterone producing adenomas removed by surgery
Spironolactone (mineralocorticoid receptor antagonist)

17
Q

Where is cortisol synthesised and released from?

A

Zonal fasiculata in response to ACTH

Negative feedback o hypothalamus inhibits CRH and ACTH release

18
Q

What is the carrier protein of cortisol?

A

Transcortin

19
Q

How does the cortisol receptor exert its actions?

A

By regulating gene transcription

20
Q

What are the actions of cortisol?

A
Increased protein breakdown in muscles
Increased lipolysis in fat
Increased gluconeogenesis in liver
Resistance to stress
Anti-inflammatory effects
Depression of immune system
21
Q

What are the net effects of glucocorticoid on metabolism?

A

Increased glucose production
Breakdown of protein
Redistribution of fat

22
Q

What are the external causes of Cushing’s syndrome?

A

Prescribed glucocorticoids

23
Q

What are the endogenous causes of Cushing’s syndrome?

A

Benign pituitary adenoma secreting ACTH (Cushing’s disease)
Excess cortisol produced by adrenal tumour (Adrenal Cushing’s)
Non pituitary-adrenal tumours producing ACTH or CRH e.g. in small cell lung cancer

24
Q

What are the signs and symptoms of Cushing’s syndrome?

A
Plethoric moon-shaped face
Buffalo hump
Abdominal obesity
Purple striae
Acute weight gain
Hyperglycaemia
Hypertension
25
Q

What are the signs and symptoms of Addison’s disease?

A
Postural hypotension
Lethargy
Weight loss
Anorexia
Increased skin pigmentation 
Hypoglycaemia
26
Q

What is Addison’s disease?

A

Chronic adrenal insufficiency

Most common cause is destructive atrophy from autoimmune response

27
Q

Why does hyperpigmentation occur in Addison’s disease?

A
Decreased cortisol
Negative feedback on anterior pituitary reduced
More POMC required to syntheses ACTH
Increased POMC leads to increased MSH
MSH promotes melanin synthesis
28
Q

What is Addisonian crisis?

A

Life threatening emergency due to adrenal insufficiency

29
Q

What is addisonian crisis precipitated by?

A
Sever stress
Salt deprivation
Infection
Trauma
Cold exposure
Over exertion
Abrupt steroid drug withdrawal
30
Q

What are the symptoms of addisonian crisis?

A
Nausea
Vomiting
Pyrexia
Hypotension
Vascular collapse
31
Q

What is the treatment for addisonian crisis?

A

Fluid replacement

Cortisol

32
Q

What is male dehydroepiandrosterone (DHEA) converted to?

A

Testosterone in testes

After puberty this is insignificant since testes release for more testosterone themselves

33
Q

What do adrenal androgens do in females?

A

Promote libido and are converted to oestrogens by other tissues
After menopause this is only source of oestrogens

34
Q

What is phaeochromocytoma?

A

Chromatin cell tumour

Rare, catecholamine-secreting tumour

35
Q

What are the characteristics of phaeochromocytoma?

A
Severe hypertension
Headaches
Palpitations
Diaphoresis
Anxiety
Weight loss
Elevated blood glucose