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MEH > 9. Adrenal Glands > Flashcards

9. Adrenal Glands Flashcards

1
Q

Outline the structure of the adrenal glands.

A

Outer capsule surrounding the cortex, central medulla.

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2
Q

What are the 3 regions of the cortex?

A

Zona glomerulosa
Zona fasciculata
Zona reticularis

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3
Q

What is secreted by the zona glomerulosa?

A

Mineralocorticoids - aldosterone

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4
Q

What is secreted by the zona reticularis?

A

Androgens - dihydroepitestosterone (DHEA) and androstenedione

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5
Q

What is secreted by the zona fasciculata?

A

glucocorticoids - cortisol

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6
Q

What is the role of the adrenal medulla?

A

contains chromaffin cells that synthesise adrenaline (80%) and noradrenaline (20%)

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7
Q

What are the precursors for corticosteroid synthesis?

A

Cholesterol

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8
Q

How do corticosteroids exert their effects?

A

Bind to cytoplasmic receptor, chaperone proteins dissociate and complex translocated to nucleus, dimerisation and binding to glucocorticoid response elements (GREs).

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9
Q

How is aldosterone transported in the blood?

A

Albumin mainly, some by transcortin

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10
Q

What is the main role of aldosterone?

A

Regulating electrolytes to maintain blood pressure and volume

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11
Q

What is the main action of aldosterone?

A

Promotes expression of the Na+/K+ pump in distal tubules and collecting ducts of nephron tubules.

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12
Q

How does increased expression of Na+/K+ transporter alter blood volume?

A

Increases uptake of Na+ and water. Increases K+ excretion.

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13
Q

What is the difference between primary and secondary hyperaldosteronism?

A

Primary - defect in adrenal cortex

Secondary - over activity of RAAS

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14
Q

What are possible causes of primary hyperaldosteronism?

A

Bilateral idiopathic adrenal hyperplasia (most common)

Aldosterone secreting adrenal adenoma

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15
Q

What is the name given to an Aldosterone secreting adrenal adenoma?

A

Conn’s syndrome

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16
Q

What can cause secondary hyperaldosteronism?

A

Renin producing tumour (rare)

Renal artery stenosis

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17
Q

What is a useful marker to distinguish between primary and secondary hyperaldosterone?

A

Renin levels.

Low in primary hyperaldosteronism, High in secondary hyperaldosteronism.

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18
Q

What clinical signs would you see in hyperaldosteronism?

A 
High blood pressure
LV hypertrophy
Stroke
Hypernatraemia 
Hypokalaemia
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19
Q

What drug can be used to treat hyperaldosteronism?

A

Spironolactone - mineralocorticoid receptor antagonist

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20
Q

What hormone is released by the anterior pituitary to stimulate cortisol release from adrenal glands?

A

ACTH

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21
Q

What carrier protein is bound to cortisol in the blood?

A

Transcortin

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22
Q

What hormone is released by the hypothalamus to stimulate ACTH release from the pituitary gland?

A

CRH - corticotropin releasing hormone

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23
Q

What are the main catabolic actions that cortisol causes?

A

Increased proteolysis in muscle
Increased gluconeogenesis in liver
Increased lipolysis

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24
Q

What stimulates the hypothalamus to release CRH?

A

Stress - pain, fever, low bp, hypoglycaemia

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25
Q

How does cortisol exert an anti-inflammatory response?

A

Inhibits macrophage activity and mast cell degranulation

Depresses immune response

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26
Q

Due to it’s anti-inflammatory effects, when can cortisol be prescribed?

A

After organ transplant

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27
Q

What disease is characterised by raised cortisol exposure?

A

Cushing’s disease

28
Q

What is a common exogenous cause of Cushing’s syndrome?

A

Prescribed glucocorticoids

29
Q

What are possible endogenous causes of Cushing’s?

A
  • Benign pituitary adenoma secreting ACTH
  • Adrenal tumour secreting cortisol
  • Non-pituitary-adrenal tumours secreting ACTH
30
Q

What is the name given to the condition caused by benign pituitary adenoma secreting ACTH?

A

Cushing’s DISEASE

31
Q

What is the name given to raised cortisol as a result of an adrenal tumour?

A

Adrenal cushing’s

32
Q

What non-pituitary-adrenal tumour has been known to secrete ACTH?

A

Small cell lung cancer

33
Q

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

A 
Moon-shaped face
Buffalo hump
Abdominal obesity
Purple striae 
Acute weight gain
Hyperglycaemia 
Hypertension
34
Q

By what mechanism does cortisol function to raise blood pressure?

A

Increases blood vessel sensitivity to vasoconstrictors.

35
Q

Give 2 examples of steroid drugs frequently prescribed.

A

Prednisolone

Dexamethasone

36
Q

What are steroid drugs often prescribed to treat?

A

Inflammatory disorders - asthma, IBD, RA, auto-immunity, organ transplant

37
Q

What is it important to remember about taking a patient off steroid drugs?

A

Dose must be reduced GRADUALLY to avoid crisis

38
Q

What is Addison’s disease characterised by?

A

Chronic adrenal insufficiency - decreased production of aldosterone, cortisol, and dehydroepiandrosterone

39
Q

What is the common cause of Addison’s disease?

A

Auto-immune destruction of the adrenal cortex

40
Q

Is Addison’s disease more common in men or women?

A

Women

41
Q

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

A 
Postural hypotension
Lethargy
Weight loss
Anorexia
Skin pigmentation
Hypoglycaemia
42
Q

Why is hyperpigmentation caused by Addison’s disease?

A

If cortisol levels are low,negative feedback will encourage more ACTH release from the hypothalamus. ACTH is derived from POMC, which also synthesises alpha-MSH. MSH stimulates melanin synthesis.
ACTH itself can also directly activate melanocortin receptors.

43
Q

What is an addisonian crisis?

A

Life threatening acute emergency due to adrenal insufficiency.

44
Q

What factors can trigger an addisonian crisis?

A

Severe stress, infection, trauma, cold exposure, over-exertion, salt deprivation, abrupt steroid withdrawal

45
Q

What are the symptoms of addisonian crisis?

A

nausea, vomiting, hypotension, vascular collapse, pyrexia

46
Q

How is addisonian crisis treated?

A

Fluids

Cortisol

47
Q

Which enzyme does the adrenal medulla use to convert noradrenaline to adrenaline?

A

N-methyl transferase

20% chromatin cells lack this enzyme and secrete NA.

48
Q

What is the name given to a chromatin cell tumour?

A

Phaeochromocytoma

49
Q

Why can a pheochromocytoma lead to life-threatening hypertension?

A

Massive adrenaline and noradrenaline release causing vasoconstriction

50
Q

What are the characteristics of phaeochromocytoma?

A 
Severe hypertension
Headaches
Palpitations
Anxiety
Weight loss 
Raised blood glucose
51
Q

If a patient has Cushing’s syndrome but their ACTH is suppressed, what does this tell you about the cause?

A

ACTH independent
Exogenous cushings - glucocorticoids taken
Adnrenal tumour secreting cortisol

52
Q

If a patient presents with Cushing’s syndrome and their ACTH is raised, what test can you do to help determine the cause?

A

Dexamethasone (corticosteroid) suppression test

53
Q

How does the dexamethasome suppression test work?

A

Dexamethasone should reduce ACTH by negative feed back to hypothalamus, thus reducing cortisol levels.In Cushing’s syndrome cortisol would not be supressed by a low dose of dexamethasone.

54
Q

If dexamethasone does lower cortisol levels, what is the likely cause of the Cushing’s?

A

Benign pituitary adenoma secreting ATCH

55
Q

If dexamethasone doesn’t lower cortisol levels, what is the likely cause of the Cushing’s?

A

Ectopic tumour producing ACTH

56
Q

Which disease is casued by an aldosterone secreting adrenal adenoma?

A

Conn’s disease

57
Q

Explain why purple striae are often seen in Cushing’s syndrome?

A

Central obesity from redistribution of fat stretches skin.

Increased proteolysis makes skin weaker and thinner

58
Q

Which time of day would be best to take a blood sample for cortisol measurement if Cushing’s syndrome is suspected?

A

Midnight - usually lowest cortisol levels.

59
Q

Name the synthetic analogue of ACTH used in an ACTH stimulation test.

A

Synacthen

60
Q

What is the ACTH stimulation test used for?

A

Test for Addison’s disease.

Synacthen would normally increase plasma cortisol. A normal response usually excludes Addison’s disease.

61
Q

Why might creatinine and urea levels be raised in a patient with Cushing’s disease?

A

Increased proteolysis

62
Q

How would you treat a patient with addison’s disease?

A

Prescribe glucocorticoids - hydrocortisone

63
Q

Explain why cortisol can have mineralocorticoid and androgen-like effects when present in high concentrations.

A

Steroid receptor hormology- all contain the same regions, so cortisol will bind with low affinity to the mineralocorticoid receptor at high levels.

64
Q

What enzyme is most commonly deficient in congenital adrenal hyperplasia?

A

21-hydroxylase - pathway producing both glucocorticoids and mineralocorticoids.

65
Q

Why does a deficiency in 21-hydroxylase lead to genital ambiguity in female infants?

A

Substrate for 21-hydroxylase is diverted to androgen synthesis, causing increased levels of DHEA and androstenedione.

MEH (19 decks)

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