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Y2 ENDOCRINOLOGY > Adrenal disorders > Flashcards

Adrenal disorders Flashcards

1
Q

Name the hormones synthesised in the adrenal cortex

A

Corticosteroids, mineralocorticoids - aldosterone, glucocorticoids - cortisol, sex steroids - androgens and oestrogen.

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2
Q

What is the precursor for all adrenal hormones?

A

Cholesterol

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3
Q

What term describes how cortisol is released in the body?

A

Diurnal rythmn

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4
Q

What are the consequences associated with adrenocortical failure?

A

Fall in BP, loss of salt in urine, increased plasma potassium. Fall in glucose due to corticosteroid deficiency, high ACTH, death due to severe hypertension

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5
Q

What type of adrenal failure is Addison’s disease?

A

Primary adrenal failure

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6
Q

What is Addison’s disease?

A

Where the adrenal cortex is destroyed either by autoimmunity or by tuberculosis of the adrenal glands

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7
Q

What are the 3 causes of adrenocortical failure?

A

Tuberculosis Addison’s disease, autoimmune Addison’s disease, Congenital adrenal hyperplasia

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8
Q

How does congenital adrenal hyperplasia result in adrenocortical failure?

A

Stops enzymes in the steroid synthetic pathway from working

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9
Q

What signs and symptoms are associated with Addison’s disease?

A

low BP, increased pigmentation, fatigue, low mood, muscle weakness, autoimmune vitiligo

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10
Q

what would you expect to see in the blood tests of someone with addisons disease?

A

low 9am cortisol, high ACTH

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11
Q

what is given to Addisons patients as a cortisol replacement?

A

prednisolone, 3-4mg once daily

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12
Q

what is more potent, cortisol or prednisolone?

A

prednisolone, 2.3x binding affinity than cortisol

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13
Q

what treatment is given to a patient with adrenal failure?

A

hydrocortisone 3x daily. prednisolone 3mg daily. fludrocortisone 50-100 mcg daily

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14
Q

what is congenital adrenal hyperplasia?

A

caused by 21-hydroxylase deficiency, born like an addisons patient, cortisol and aldosterone completely absent, hyperplasia of adrenal gland, can survive less than 24 hours

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15
Q

What are the three main different presentations of complete 21-hydroxylase activity?

A

1- as a neonate with a salt losing Addisonian crisis. 2- in utero foetus get steroids across placenta. 3- girls might have ambiguous genitalia (virilised by adrenal testosterone)

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16
Q

What problems can occur due to parial 21-hydroxylase deficiency?

A

hirsutism and virilisation in girls, precocious puberty in boys.

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17
Q

outline the pathophysiology of 11 hydroxylase deficiency?

A

11 deoxycorticosterone behaves like aldosterone. deficient in aldosterone and cortisol. excess sex steroids

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18
Q

what are the main problems that occur as a result of a 11 hydroxylase deficiency?

A

virilisation, hypertension, hypokalaemia

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19
Q

outline the pathophysiology of a 17 hydroxylase deficiency

A

deficient in cortisol and sex steroids, mineralocorticoids in excess

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20
Q

what are the main problems associated with a deficiency in 17 hydroxylase?

A

hypertension, low potassium, sex steroid deficiency no puberty/feminised, glucocorticoid deficiency

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21
Q

what is the function of aldosterone?

A

controls blood pressure, sodium and lowers potassium

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22
Q

what are the effects of ACTH on the adrenals?

A

side chain cleavage, activation of 3 hydroxysteroid dehydrogenase, 21 hydroxylase, 11 hydroxylase, 17 hydroxylase

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23
Q

why do patients with addisons disease have a good tan?

A

POMC is a precursor protein that is cleaved to form ACTH and MSH. therefore more ACTH means more MSH which stimulates the production of melanin

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24
Q

What is an enzyme?

A

Protein that’s catalyses a specific reaction

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25
Q

What are the two types of adrenocortical failure in terms of causation?

A

Adrenal glands are destroyed, enzymes in the steroid synthetic pathway not working

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26
Q

What are the consequences of adrenocortical failure?

A

Fall in BP, loss of salt in urine, increased plasma potassium, fall in glucose due to glucocorticoid deficiency, eventual death due to servere hypotension

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27
Q

pro-opio melanocortin (POMC) is synthesised where?

A

The pituitary

28
Q

What tests are done to diagnose Addisons?

A

9am cortisol, short synACTHen test

29
Q

What is a short synACTHen test?

A

Give 250 ug synacthen IM, measure cortisol response

30
Q

Why can we not just give once daily aldosterone to Addison’s patients?

A

The half life of aldosterone is too short for safe once daily administration

31
Q

What drug treatment is given to Addisons patients?

A

Fludrocortisone 50-100mcg daily or Prednisolone 2-4mg once daily or Hydrocortisone three times daily

32
Q

Why is Fludrocortisone a better drug treatment than Aldosterone for Addisons patients?

A

Fluorine does not exist in natural steroids so its presence slows the metabolism substantially, meaning half life of Fludrocortisone is a lot longer than Aldosterone

33
Q

Why can we prescribe a much lower dose of Prednisolone (2-4 mg daily) than hydrocortisone?

A

Prednisolone is more potent than cortisol, has a 2.3x higher binding affinity

34
Q

How long can you survive with a complete 21-hydroxylase deficiency?

A

Less than 24 hours

35
Q

In a complete 21-hydroxylase deficiency which hormones will be completely absent?

A

Aldosterone and cortisol

36
Q

Which hormones are deficient in a 11-hydroxylase deficiency?

A

Cortisol and aldosterone

37
Q

Which hormones are in excess in a 11-hydroxylase deficiency?

A

Sex steroids and testosterone and 11-deoxycorticosterone

38
Q

What are the main problems associated with a partial 11-hydroxylase deficiency?

A

Virilisation, hypertension and low potassium

39
Q

What are the clinical features associated with Cushing’s?

A

High cortisol, central obesity, moon face, red striae, proximal myopathy, osteoporosis, diabetes, hypertension, buffalo hump fat pad, hypokalaemia

40
Q

What are the four causes of Cushing’s?

A

Taking too many steroids, pituitary dependent Cushing’s, ectopic ACTH from lung cancer, adrenal adenoma secreting cortisol

41
Q

What are the 3 tests used to diagnose Cushing’s?

A

24h urine collection for urinary free cortisol. Blood diurnal cortisol levels. Low dose dexamethasone suppression test

42
Q

What is the low dose dexamethasone test for Cushing’s?

A

0.5mg 6 hourly for 48 hours, normal response is suppression of cortisol to zero, any form of Cushing’s will fail to do so

43
Q

Two medications can be givens to Cushing’s patients to combat the hyper secretion of Cortisol?

A

Metyrapone or ketoconazole

44
Q

What is the drug target for Metyrapone?

A

11beta-hydroxylase

45
Q

Outline the mechanism of action of Metyrapone

A

Inhibits action of 1a beta-hydroxylase therefore steroid synthesis in the zona fasciculata is arrested at the 11-deoxycortisol stage

46
Q

What affect does 11-deoxycortisol have on the hypothalamus and pituitary gland?

A

Has no negative feedback effect

47
Q

When is Metyrapone normally prescribed?

A

To control Cushing’s syndrome prior to surgery or to control Cushing’s symptoms after radiotherapy

48
Q

How is Metyrapone used to control Cushing’s syndrome prior to surgery?

A

Aim for mean serum cortisol 150-300nmol/L. This improves patients symptoms and promotes better post-op recovery

49
Q

What are the unwanted actions associated with use of Metyrapone?

A

Hypertension on long-term administration.
Hirsutism

50
Q

What is the drug target of Ketoconazole?

A

Blocks 17alpha-hydroxylase inhibiting cortisol production

51
Q

When is Ketoconazole usually prescribed to Cushing’s patients?

A

Treatment and control of symptoms prior to surgery

52
Q

What are the unwanted actions associated with the use of Ketoconazole?

A

Liver damage, possibly fatal therefore liver function has to be monitored weekly, clinically and biochemically

53
Q

The treatment for Cushing’s depends on what?

A

The cause of the Cushing’s

54
Q

What are the treatment options for Cushing’s?

A

Pituitary surgery (transsphenoidal hypophysectomy), bilateral adrenalectomy, unilateral adrenal to my for adrenal mass

55
Q

What is Conns syndrome?

A

Benign adrenal cortical tumour (zona glomerulosa) causing excess aldosterone

56
Q

What leads to a diagnosis of Conns syndrome?

A

Tests showing primary hyperaldosteronism and a suppressed renin-angiotensin system

57
Q

What treatment is available for Conns syndrome?

A

MR antagonists - spironalactone and Epleronone

58
Q

Outline the primary mechanism of action of Spironolactone

A

Is converted into several active metabolites, including canrenone, a competitive antagonist of the mineralcorticoid receptor (MR). Blocks sodium resorption and potassium excretion in the kidney tubules

59
Q

What are the adverse effects associated with the use of Spironolactone?

A

Menstrual irregularities and gynaecomastia

60
Q

Outline the primary mechanism of action of Epleronone

A

Acts as a mineralocorticoid antagonist

61
Q

Why is Epleronone better tolerated than spironolactone?

A

Has a similiar affinity to MR, less binding to androgen and progesterone receptors

62
Q

What are phaeochromocytomas?

A

Tumours of the adrenal medulla which secrete catecholamines (adrenaline/ nor-adrenaline)

63
Q

What are the clinical features of phaeochromocytomas?

A

Hypertension in young people , episodic severe hypertension after abdominal palpitation, high adrenaline (can cause ventricular fibrillation and death)

64
Q

How are phaeochromocytomas managed?

A

Need surgery but patient needs careful preparation as anaesthetic can precipitate hypertensive crisis.

65
Q

Before surgery to treat a phaeochromocytoma how is the patient prepared as to avoid anaesthetic precipitating a hypertensive crisis?

A

Alpha blockade is first step, patient may need IV fluid, beta blockade then added to prevent tachycardia

Y2 ENDOCRINOLOGY (13 decks)

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