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Endocrinology > Adrenal physiology and pathology > Flashcards

Adrenal physiology and pathology Flashcards

1
Q

What hormones are synthesised in the cortex of the adrenal gland?

A

Mineralocorticoids
Glucocorticoids
Adrenal androgens

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2
Q

What hormones are synthesised in the medulla of the adrenal gland?

A

Catecholamines - adrenaline and noradrenaline

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3
Q

How is cortisol and androgen production regulated?

A

Regulated by hormones produced by hypothalamus and anterior pituitary gland

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4
Q

How is aldosterone production regulated?

A

Renin-angiotensin-aldosterone system

Plasma potassium

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5
Q

What triggers cortisol release?

A

Stress
Circadian rhythm
Illness

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6
Q

What is the pathway that triggers cortisol release?

A

Corticotrophin releasing hormone is released from the hypothalamus
CRH stimulates anterior pituitary to release ACTH
This acts on the adrenal cortex to produce cortisol

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7
Q

What are the 6 classes of steroid receptor?

A 
Glucocorticoid
Mineralocorticoid
Progestin
Oestrogen
Androgen
Vitamin D
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8
Q

What effects does cortisol have on the CNS?

A

Mood lability
Euphoria/psychosis
Decreased libido

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9
Q

What effects does cortisol have on bone/connective tissue?

A

Accelerates osteoporosis
Decreased serum calcium
Decreased collagen formation
Decreased wound healing

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10
Q

What immunological effects does cortisol have?

A

Reduced capillary dilatation/permeability
Reduced leucocyte migration
Reduced macrophage activity
Reduced inflammatory cytokine production

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11
Q

What effects does cortisol have on metabolism?

A

Carbohydrate: increases blood sugar
Lipid: increased lipolysis, central redistribution
Protein: increased proteolysis

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12
Q

What effects does cortisol have on the circulatory/renal system?

A

Increased cardiac output
Increased lood pressure
Increased renal blood flow and GFR

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13
Q

What are the 3 main principles in use of corticosteroids as treatment?

A

Suppress inflammation
Suppress immune system
Replacement treatment

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14
Q

What 3 main areas do corticosteroids have a role in the treatment of?

A

Allergic disease: asthma/anaphylaxis
Inflammatory disease: rheumatoid arthritis, ulcerative colitis, Crohns disease
Malignant disease

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15
Q

Where can mineralocorticoid receptors be found?

A

Kidneys
Salivary glands
Gut
Sweat glands

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16
Q

What does aldosterone regulate?

A

Sodium/potassium balance - K+/H+ excretion, increases Na+ reabsorption
Blood pressure regulation
Regulation of extracellular volume

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17
Q

What can cause primary adrenal insufficiency?

A

Addison’s disease
Congenital Adrenal Hyperplasia (CAH)
Adrenal TB/malignancy

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18
Q

What can cause secondary adrenal insufficiency?

A

Due to lack of ACTH stimulation
Iatrogenic (excess exogenous steroid)
Pituitary/hypothalamic disorders

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19
Q

What is the commonest cause of primary adrenal insufficiency?

A

Addison’s disease

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20
Q

What is Addison’s disease?

A

Autoimmune destruction of adrenal cortex resulting in insufficient secretion of cortisol and mineralocorticoids

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21
Q

What autoimmune conditions are associated with Addison’s disease?

A

Type 1 DM
Autoimmune thyroid disease
Pernicious anaemia

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22
Q

What are the features of Addison’s disease?

A 
Anorexia, weight loss
Fatigue/lethargy
Dizziness and low BP
Abdominal pain, vomiting, diarrhoea
Skin pigmentation
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23
Q

How can adrenal insufficiency be diagnosed?

A 
'Suspicious biochemistry' - decreased Na+, increased K+ and hypoglycaemia
Short synacthen test 
Increased ACTH
Adrenal autoantibodies
Increased renin, reduced aldosterone
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24
Q

What causes the skin pigmentation in Addison’s disease?

A

Increased ACTH

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25
Q

How is a short synacthen test performed?

A

Measure plasma cortisol before and 30 minutes after iv ACTH injection
Normal: baseline >250nmol/L, post ACTH >480

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26
Q

How should adrenal insufficiency be managed?

A

Hydrocortisone as cortisol replacement - if unwell, give iv first - usually 15-30mg daily in divided doses
Fludrocortisone as aldosterone replacement

27
Q

How much of the adrenal gland is destroyed before a patient becomes symptomatic?

A

> 90%

28
Q

What key differences are there clinically between Addison’s and secondary adrenal insufficiency?

A

No increased levels of ACTH so no skin pigmentation

Aldosterone unaffected

29
Q

What is Cushing’s syndrome?

A

Excess cortisol production, a disease with high mortality

30
Q

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

A 
Easy bruising
Facial plethora
Striae
Proximal myopathy
Osteoporosis
Buffalo hump
Hypertension
Thinning of skin
Euphoria
Psychosis
Moon face/red cheeks
Increased appetite
31
Q

What are the ACTH dependant causes of Cushing’s syndrome?

A

Pituitary adenoma
Ectopic ACTH production from carcinoid tumour
Ectopic CRH

32
Q

What are the ACTH independent causes of Cushing’s syndrome?

A

Adrenal adenoma
Adrenal carcinoma
Nodular hyperplasia

33
Q

How is Cushing’s syndrome diagnoses?

A 
Establishment of cortisol excess:
Overnight dexamethasone suppression test
24 hour urinary free cortisol
Late night salivary cortisol
Low dose dexamethasone suppression test
Repeat to confirm
34
Q

What is the commonest cause of cortisol excess?

A

Iatrogenic Cushing’s syndrome

35
Q

What usually causes iatrogenic Cushing’s syndrome?

A

Prolonged high dose steroid treatment
eg. treatment for asthma, rheumatoid arthritis, inflammatory bowel disease, transplants
This causes chronic suppression of pituitary ACTH production and adrenal atrophy

36
Q

What should happen to the dose of steroid a patient takes when undergoing surgery or if ill, when they have ACTH suppression?

A

Increased doses of steroid as they are unable to respond normally to illness or stress

37
Q

What is primary aldosteronism?

A

Autonomous production of aldosterone independent of its regulators

38
Q

When should you suspect a secondary cause of hypertension?

A

Young patient

Resistant hypertension

39
Q

What clinical signs would make you consider primary aldosteronism in a patient with hypertension?

A

Resistant hypertension
Hypokalaemia
Alkalosis

40
Q

What cardiovascular actions does aldosterone have?

A 
Increased sympathetic outflow
Increased cardiac collagen
Increased blood pressure
Increased left ventricular hypertrophy
Increased atheroma development
Sodium retention
41
Q

What is Conn’s syndrome?

A

An adrenal adenoma causing primary aldosteronism

42
Q

What is the most common cause of primary aldosteronism?

A

Bilateral adrenal hyperplasia

43
Q

What are some of the rarer causes of primary aldosteronism?

A

Genetic mutation

Unilateral hyperplasia

44
Q

How is primary aldosteronism diagnosed?

A

Step 1: confirm aldosterone excess
Measure plasma aldosterone and renin and express as ratio (ARR-aldosterone to renin ratio)
If ratio > 750 then investigate further with saline suppression test
Failure of plasma aldosterone to suppress by > 50% with 2 litres of normal saline confirms PA
Step 2: confirm subtype
Adrenal CT to demonstrate adenoma
Sometimes adrenal vein sampling to confirm adenoma is true source of aldosterone excess

45
Q

What are surgical management options for primary aldosteronism?

A

Unilateral laparoscopic adrenalectomy - only if adrenal adenoma (and excess confirmed in adrenal vein sampling)
Cure of hypokalaemia
Cures hypertension in 30-70% cases

46
Q

What therapy can be given for treatment of bilateral adrenal hyperplasia causing primary aldosteronism?

A

Mineralocorticoid receptor antagonists (spironolactone or eplerenone)

47
Q

What is the most common cause of congenital adrenal hyperplasia?

A

21α hydroxylase deficiency

48
Q

What is congenital adrenal hyperplasia?

A

Any of several autosomal recessive diseases associated with enzyme defects in the steroid pathway

49
Q

What is the classical presentation of congenital adrenal hyperplasia in males?

A

Adrenal insufficiency at around 2-3 weeks

Poor weight gain

50
Q

What is the classical presentation of congenital adrenal hyperplasia in females?

A

Genital ambiguity

51
Q

What are some of the non-classical features of congenital adrenal hyperplasia?

A 
Hirsutes 
Acne
Oligomenorrhoea
Precocious puberty
Infertility or sub-fertility
52
Q

What three areas does the adrenal cortex consist of?

A

Zona glomerulosa
Zona fasciculate
Zona reticularis

53
Q

What is a phaeochromocytoma?

A

A rare tumour of adrenal gland tissue, found either in the adrenal gland or in the sympathetic chain

54
Q

What are the symptoms of phaeochromocytoma?

A 
Hypertension - 50% paroxysmal
Headache
Sweating
Palpitations
Breathlessness
Constipation
Anxiety/Fear
Weight loss
Flushing – uncommon
Incidental finding on imaging
Family tracing
55
Q

What is the name given to an extra-adrenal phaeochromocytoma?

A

Paraganglioma

56
Q

What are the signs of phaeochromocytoma?

A 
Hypertension
Postural hypotension in 50% cases
Pallor
Bradycardia and Tachycardia
Pyrexia
57
Q

What are the signs of complications from phaeochromocytoma?

A 
Left ventricular failure
Myocardial necrosis
Stroke
Shock
Paralytic ileus of bowel
58
Q

What is the classical triad presentation of phaeochromocytoma?

A

Hypertension
Headache
Sweating

59
Q

What are the biochemical abnormalities seen in phaeochromocytoma?

A

Hyperglycaemia – adrenaline secreting tumours
May have low potassium level
High haematocrit – i.e. raised Hb concentration
Mild hypercalcaemia
Lactic acidosis – in absence of shock

60
Q

Why is phaeochromocytoma known as the 10% tumour?

A 
10% malignant
10% extra-adrenal [probably 20-30%]
10% bilateral
10% associated with hyperglycaemia
10% in children
10% familial (but probably 25%)
61
Q

How is phaeochromocytoma diagnosed?

A

Catecholamine excess confirmed - plasma & urine
Source of catecholamine excess found - MRI Scan
Abdomen
Whole body
MIBG – meta-iodobenzylguanidine
PET Scan

62
Q

How should phaeochromocytoma be treated?

A 
Full α and β- blockade: phenoxybenzamine and atenolol or metoprolol
Fluid and/or blood replacement
Careful anaesthetic assessment
Surgical - laparoscopic
Total excision wherever possible
Tumour de-bulking
Chemotherapy if malignant
Radio-labelled MIBG
Long-term follow-up 
Genetic testing
Family tracing and investigation
63
Q

What syndromes is phaeochromocytoma associated with?

A 
Multiple Endocrine Neoplasia II
Von-Hippel-Lindau syndrome
Succinate dehydrogenase mutations
Neurofibromatosis
Tuberose sclerosis

Endocrinology (12 decks)

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