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Endocrine > Adrenal Physiology and Disorders > Flashcards

Adrenal Physiology and Disorders Flashcards

1
Q

How much do the adrenal glands weigh in a healthy adult?

A

4g

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2
Q

Where are corticosteroids synthesised?

A

In the adrenal cortex from cholesterol

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3
Q

What regulates cortisol and androgen production?

A

Hormones produced by the hypothalamus and pituitary gland

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4
Q

What regulates aldosterone?

A

Renin-angiotensin system and plasma potassium

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5
Q

What are the precursors of cortisol, which is produced in the adrenal cortex?

A

Corticotropin-releasing hormone (CRH) produced by the hypothalamus, adrenocorticotropic hormone (ACTH) produced in the anterior pituitary

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6
Q

What is the renin-angiotensin system activated in response to?

A

Decreased blood pressure = leads to production of angiotensin II which causes direct (vasoconstriction) and indirect (aldosterone) methods of BP elevation

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7
Q

What is the action of corticosteroids?

A

Bind intracellular receptors = receptor/ligand complex binds DNA to affect transcription

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8
Q

What are the six classes of corticosteroids?

A

Glucocorticoids, mineralocorticoids, progestin, oestrogen, androgen, vitamin D

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9
Q

What are some of the actions of cortisol?

A

Increases CO, BP, renal flow and GFR
Increases blood sugar, lipolysis and proteolysis
Central redistribution of fat, mood lability, euphoria/psychosis, decreased libido

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10
Q

How does cortisol affect the immune system?

A

Decreased capillary dilation/permeability, leucocyte migration, macrophage activity and inflammatory cytokine production

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11
Q

How does cortisol accelerate osteoporosis?

A

Decreases serum calcium wound healing and collagen formation

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12
Q

What are the three main clinical uses of corticosteroids?

A

Suppress inflammation, suppress immune system, replacement treatment

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13
Q

What are some conditions treated by corticosteroids?

A

Asthma, anaphylaxis, rheumatoid arthritis, ulcerative colitis, Crohn’s disease, malignancy

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14
Q

Where are the mineralocorticoid receptors for aldosterone located?

A

Kidneys, salivary glands, gut, sweat glands

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15
Q

What are the effects of aldosterone acting on mineralocorticoid receptors?

A

Na+/K+ balance = K+/H+ excretion, increases Na+ reabsorption

Blood pressure regulation, regulation of extracellular volume

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16
Q

What is adrenal insufficiency?

A

Inadequate adrenocortical function

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17
Q

What are some causes of primary adrenal insufficiency?

A

Addison’s disease, congenital adrenal hyperplasia, adrenal TB, malignancy

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18
Q

What are some causes of secondary adrenal insufficiency?

A

Due to lack of ACTH stimulation = excess exogenous steroid, pituitary/hypothalamic disorders

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19
Q

What is Addison’s disease?

A

Autoimmune destruction of adrenal cortex = most common cause of primary insufficiency, >90% destroyed before symptomatic, autoantibody positive in 70%

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20
Q

What are some other autoimmune conditions associated with Addison’s disease?

A

Type 1 diabetes, autoimmune thyroid disease, pernicious anaemia

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21
Q

What are some symptoms of Addison’s disease?

A

Anorexia, weight loss, fatigue/lethargy, dizziness and low BP, abdominal pain, vomiting, diarrhoea, skin pigmentation (due to increased ACTH)

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22
Q

How is adrenal insufficiency diagnosed?

A

Low Na+, high K+, hypoglycaemia, very high ACTH, very high renin, low aldosterone, short synacthen test

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23
Q

How is a short synacthen test carried out?

A

Measure plasma cortisol before and 30mins after IV/IM ACTH injection = normal baseline is >250nmol/L, normal post-ACTH is >550nmol/L

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24
Q

How is adrenal insufficiency treated?

A

Hydrocortisone as cortisol replacement, fludrocortisone as aldosterone replacement, educate patients on sick day rules and wearing identification

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25
Q

What are some features of hydrocortisone therapy as adrenal insufficiency treatment?

A

Given via IV if unwell, usually 15-30mg daily in divided doses, try to mimic diurnal rhythm

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26
Q

What must be monitored when giving fludrocortisone as part of treatment for adrenal insufficiency?

A

Blood pressure and potassium

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27
Q

How does hydrocortisone dose change when a patient with adrenal insufficiency is unwell but managing their illness at home?

A

Dose is doubled until they have recovered

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28
Q

What is the most common cause of secondary adrenal insufficiency?

A

Exogenous steroid use (iatrogenic) = often high dose prednisolone, dexamethasone or inhaled corticosteroid

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29
Q

What are the features of secondary adrenal insufficiency?

A

Similar to Addison’s except pale skin (no raised ACTH) and aldosterone production intact
Treat with hydrocortisone replacement

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30
Q

What is Cushing’s syndrome?

A

Excess cortisol secretion = high mortality, rare, more common in women, aged 20-40

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31
Q

What are the symptoms of Cushing’s syndrome?

A

Easy bruising, facial plethora, striae, proximal myopathy

32
Q

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

A

Pituitary adenoma (68%, Cushing’s disease), ectopic ACTH (12%, carcinoid), ectopic CRH (<1%)

33
Q

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

A

Adrenal adenoma (10%), adrenal carcinoma (8%), nodular hyperplasia (1%)

34
Q

How is cortisol excess established in Cushing’s syndrome?

A

Overnight dexamethasone suppression test, 24hr urinary free cortisol, late night salivary cortisol

35
Q

What is another test that can be used to diagnose Cushing’s syndrome?

A

Low dose dexamethasone suppression test

36
Q

What causes iatrogenic Cushing’s syndrome?

A

Prolonged high dose steroid therapy = usually oral therapy, can occur with high dose inhaled steroids or steroid injections

37
Q

What are some features of iatrogenic Cushing’s syndrome?

A

Chronic suppression of pituitary ACTH production, adrenal atrophy, most common cause of cortisol excess (negative feedback to anterior pituitary)

38
Q

What are some implications of iatrogenic Cushing’s syndrome?

A

Unable to respond to stress, need extra doses when ill, cannot stop suddenly, gradual withdrawl of steroid therapy if >4-6 weeks

39
Q

What causes primary aldosteronism?

A

Autonomous production of aldosterone independent of its regulators (ang II/K+) = commonest cause of secondary hypertension

40
Q

What are the cardiovascular actions of aldosterone?

A

Increases sympathetic outflow, increases cardiac collagen, cytokines and ROS synthesis, sodium retention, altered endothelial function (increases pressor responses)

41
Q

What are the features of primary aldosteronism?

A

Significant hypertension, hypokalaemia (30%), alkalosis

42
Q

What are the subtypes of primary aldosteronism?

A

Adrenal adenoma = Conn’s syndrome, 30% of cases
Bilateral adrenal adenoma = most common cause (60%)
Rare causes = genetic mutations, unilateral hyperplasia

43
Q

What can K+ channel mutations cause?

A

Adenomas and hereditary hypertension = mutations lead to loss of ion selectivity (Na+ entry and depolarisation)

44
Q

What is the function of the KCNJ5 channel?

A

Rectifying selective channel which maintains the membrane hyperpolarisation = somatic mutations identified at two key sites

45
Q

How is aldosterone excess confirmed in primary aldosteronism?

A

Measure plasma aldosterone and renin and express as ratio (ARR)

46
Q

What should be done is the ARR is raised in a patient with suspected primary aldosteronism?

A

If ARR raised (assay dependent) then investigate further with saline suppression test

47
Q

What result of a saline suppression test confirms the diagnosis of primary aldosteronism?

A

Failure of plasma aldosterone to suppress by >50% with 2L saline

48
Q

How is the subtype of primary aldosteronism conformed?

A

Adrenal CT for adenoma, sometimes adrenal vein sampling to confirm adenoma is source of aldosterone excess

49
Q

How is bilateral adrenal hyperplasia treated?

A

MR antagonists (e.g spironolactone, eplerenone)

50
Q

What is the main treatment for primary aldosteronism?

A

Surgery = unilateral laparoscopic adrenalectomy, only if adrenal adenoma and excess confirmed by vein sampling

51
Q

How effective is surgery as a treatment for primary aldosteronism?

A

Cure for hypokalaemia, cures 30-70% of hypertension

52
Q

What is congenital adrenal hyperplasia?

A

Rare conditions associated with enzyme defects in the steroid pathway = most common is 21 alpha hydroxylase deficiency (autosomal recessive)

53
Q

What are the variants of 21 alpha hydroxylase deficiency associated with congenital adrenal hyperplasia?

A 
Classical = salt-wasting, simple virilising
Non-classical = hyperandrogenaemia
54
Q

How is congenital adrenal hyperplasia diagnosed?

A

Basal (or stimulated) 17-OH progesterone

55
Q

What is the classical presentation of congenital adrenal hyperplasia?

A 
Males = adrenal insufficiency (often at 2-3 weeks), poor weight gain
Females = genital ambiguity
56
Q

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

A

Hirsute, acne, oligomenorrhoea, precocious puberty, infertility or sub-fertility

57
Q

How is congenital adrenal hyperplasia treated in children?

A

Timely recognition, glucocorticoid replacement, mineralocorticoid replacement in some, surgical correction, achieve maximal growth potential

58
Q

How is congenital adrenal hyperplasia treated in adults?

A

Control androgen excess, restore fertility, avoid steroid over-replacement

59
Q

What are the clues that someone has a phaeochromocytoma?

A

Labile hypertension, postural hypotension, paroxysmal sweating, pallor, sweating, tachycardia

60
Q

What are phaeochromocytomas?

A

Rare tumours = phaeochromocytomas when in adrenal medulla, paragangliomas when extra-adrenal (sympathetic chain)

61
Q

Why are phaeochromocytomas brown?

A

Chromaffin cells reduce chrome salts to metal chromium resulting in a brown colour reaction

62
Q

What are some features of phaeochromocytomas?

A

Potentially fatal, high rate of post-mortem diagnosis, insidious onset, incidental finding, family tracing, <0.1-1% of hypertensive cases in secondary care

63
Q

What are the differentials of phaeochromocytomas?

A

Angina, anxiety, carcinoid, thyrotoxicosis, insulinoma, menopause, arrhythmias, migraine, drug toxicity, alcohol withdrawl, pregnancy, hypoglycaemia, mastocytosis, autonomic neuropathy, factitious

64
Q

What is the classic triad of symptoms for phaeochromocytomas?

A

Occur in up to 90% = hypertension (50% paroxysmal), headache, sweating

65
Q

What are other symptoms of phaeochromocytomas?

A

Palpitations, breathlessness, constipation, anxiety, weight loss, flushing (rare)

66
Q

What are some signs of phaeochromocytomas?

A

Hypertension, postural hypotension (50%), pallor, bradycardia, tachycardia, pyrexia

67
Q

What are some signs of complications caused by a phaeochromocytoma?

A

LV failure, myocardial necrosis, stroke, shock, paralytic ileus of bowel

68
Q

What are some biochemical abnormalities associated with phaeochromocytomas?

A

Hyperglycaemia (adrenaline-secreting tumour), may have low K+, raised Hb concentration, mild hypercalcaemia, lactic acidosis (in absence of shock)

69
Q

Who should be investigated for phaeochromocytomas?

A

Family members with syndromes, resistant hypertension, age <50 with hypertension, classic symptoms, hypertension with hyperglycaemia

70
Q

How is catecholamine excess confirmed in phaeochromocytomas?

A

Urine 2x24hr catecholamines or metanephrins, plasma at time of symtpoms

71
Q

How is the source of catecholamine excess confirmed in phaeochromocytomas?

A

MRI of abdomen/body, MIBG, PET scan

72
Q

How are phaechromocytomas treated?

A

Full alpha and beta blockade, fluid and/or blood replacement, chemotherapy if malignant (radio-labelled MIBG), laparoscopic surgery

73
Q

How are alpha and beta blockades used to treat phaeochromocytomas?

A

Alpha blockade before beta blockade, phenoxybenzamine (alpha blocker), propanolol, atenolol or metoprolol (beta blockers)

74
Q

What kind of laparoscopic surgery is done for phaeochromocytomas?

A

Total excision of lesion when possible, surgical tumour de-bulking also done

75
Q

What are some extra elements of treatment for phaeochromocytomas?

A

Long term follow up, genetic testing, family tracing and investigation

76
Q

What are some clinical syndromes associated with phaechromocytomas?

A

MEN2, Von-Hipple Lindau syndrome, succinate dehydrogenase syndrome, neurofibromatosis, tuberose sclerosis

77
Q

What are the pitfalls of phaeochromocytoma diagnosis?

A

Catecholamines are also raised in heart failure, episodic catecholamine secretion so levels in plasma and urine may be normal

Endocrine (42 decks)

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