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endocrine system 1 > Clinical Aspects of the Adrenal Glands > Flashcards

Clinical Aspects of the Adrenal Glands Flashcards

1
Q

What types of adrenal disorders are there?

A
  • Hyperfunction
  • Hypofunction
  • Tumours
  • Functional symptoms
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2
Q

What is the common approach taken towards adrenal disorders?

A

clinical suspicion

test for assessing functional status

  • is it functioning
  • is it primary or secondary

what is the aetiology
- is it a tumour

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3
Q

What questions should you be thinking of if you suspect someone has an adrenal tumour?

A
  • can it be removed
  • additional chemotherapy/radiotherapy required
  • how can we follow the course of the disease
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4
Q

what can cause adrenal hypofunction

A

primary adrenal insufficiency
- addison’s disease

adrenal enzyme defects

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5
Q

Give an example of an adrenal enzyme defect which can result in primary adrenal insufficiency.

A

Congenital adrenal hyperplasia (most commonly 21-hydroxylase deficiency)

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6
Q

What can cause Addison’s disease?

A
  • Immune destruction (auto)
  • Invasion
  • Infiltration
  • Infection
  • Infarction
  • Iatrogenic
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7
Q

What is the greatest cause of adrenal failure in the UK?

A

> 85% caused by autoimmune Addison’s

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8
Q

What associated autoimmune diseases are common with Addison’s disease?

A
  • thyroid disease (20%)
  • type 1 DM (15%)
  • premature ovarian failure (15%)
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9
Q

What pathophysiology is found in Addison’s disease?

A
  • +ve adrenal autoantibodies to 21-OHase

- lymphocytic infiltrate of adrenal cortex

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10
Q

What are the common symptoms associated with Addison’s disease?

A
  • weakness, fatigue, anorexia, weight loss (100%)
  • skin pigmentation or vitiligo (92%)
  • hypotension (88%)
  • unexplained vomiting or diarrhoea (56%)
  • salt craving (19 %)
  • postural symptoms (12%)
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11
Q

What are the possible clues to the diagnosis of adrenal failure?

A
  • disproportion between severity of illness & circulatory collapse
  • unexplained hypoglycaemia
  • previous depression or weight loss
  • other endocrine features: hypothyroidism, body hair loss, amenorrhoea
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12
Q

What investigations should be carried out for adrenal insufficiency?

A

routine blood tests

  • U+Es
  • glucose
  • FBCs

random cortisol

  • > 450 nmol/l (not Addison’s)
  • <450nmol/l (adrenal status uncertain)
syacthen test (and basal ACTH)
-If suspicion high & patient unwell, treat with steroids and do Synacthen test later
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13
Q

How should adrenal insufficiency be treated?

A

glucocorticoid replacement

  • given in divided doses to ‘mimic normal diurnal variation’
  • hydrocortisone (20-30mg )
  • prednisolone (7.5mg)
  • dexamethasone (0.75mg)

mineralocorticoid replacement
- fludrocortisone (synthetic steroid)

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14
Q

What is fludrocortisone?

A

Synthetic steroid

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15
Q

What does fludrocortisone bind to?

A

Mineralocorticoid (aldosterone) receptors

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16
Q

How should fludrocortisone be administered?

A

50-300 micrograms daily

adjust dose according to:

  • clinical status (postural BP, oedema)
  • U&E
  • plasma renin level
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17
Q

Who needs special care when it comes to steroids and stress?

A
  • hypoadrenal patients on replacement steroids
  • patients on steroids in doses sufficient to suppress the pituitary adrenal axis
  • patients who have received such treatment during the previous 18/12
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18
Q

How should patients who require special care be managed with a short lived illness or stress?

A

Double glucocorticoid dose

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19
Q

How should patients who require special care be managed with a major illness or operation?

A
  • Especially if nil by mouth or GI upset
  • 100mg hydrocortisone iv stat
  • 50-100mg HC iv 8-hourly
  • As stress abates, reduce HC by 50% per day until back on usual replacement dose
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20
Q

What are the 3 important self-care rules for patients on steroids?

A
  • never miss steroid doses
  • double the hydrocortisone dose
  • if severe vomiting or diarrhoea, call for help without delay
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21
Q

Abnormalities of aldosterone can lead to?

A

Hypertension

22
Q

What are the endocrine causes of hypertension?

A

primary hyperaldosteronism

  • unilateral adenoma
  • bilateral hyperplasia

rarer causes

  • phaeochromcytoma
  • cushing’s syndrome
  • acromegaly
  • hyperparathyroidism
  • hypothyroidism
  • congenital adrenal hyperplasia
23
Q

What disorders are associated with hypersecretion of the adrenal cortex

A
  • Cushing’s syndrome

- Conn’s syndrome

24
Q

What condition is associated with hypersecretion of the adrenal medulla?

A

Pheochromocytoma

25
Q

What is Cushing’s syndrome?

A

Excess corticosteroids

26
Q

What does Cushing’s syndrome cause?

A

Tissue breakdown
-causes weakness of skin, muscle & bone

Sodium retention
-may cause hypertension & heart failure

Insulin antagonism
-may cause diabetes mellitus

27
Q

What signs or symptoms may be present in Cushing’s syndrome?

A
  • central obesity
  • purple striae
  • plethoric faeces
  • osteoporosis
  • oedema
  • acne
  • easy bruisability
  • headaches
  • personality changes
  • hypertension
  • glucose intolerance
  • amenorrhoea or impotency
28
Q

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

A

75% cases: pituitary tumour (Cushing’s disease)

5% cases: ectopic ACTH secretion (eg lung carcinoid)

29
Q

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

A
  • 20% cases: adrenal tumour (adenoma or carcinoma)

- corticosteroid therapy (eg for asthma, IBD)

30
Q

How is hypercortisolism screened for?

A
  • 1mg overnight DEX suppression test

- 24hr urine free cortisol

31
Q

How is hypercortisolism diagnosed?

A
  • 24hr urine free cortisol

- low dose Dex test

32
Q

How is it determined if hypercortisolism is ACTH dependent or independent?

A

Paired morning-midnight ACTH cortisol

33
Q

How is it determined if the pituitary is involved in hypercortisolism?

A

High dose Dex test

34
Q

How is the cause of hypercortisolism localised?

A
  • MRI sella
  • CT adrenal
  • BIPSS
  • CT chest
35
Q

What is the pathophysiology of primary hyperaldosteronism?

A
  • aldosterone producing tumour
  • increase in blood volume, BP and urine K
  • decrease in renin
  • increase in A/R ratio
36
Q

How is primary and secondary hyperaldosteronism differentiated?

A

PA/PRA >20 : primary hyperaldosteronism

PA/PRA <20 : secondary hyperaldosetronism

37
Q

What can cause increased PRA and PAC?

A

Investigate for causes of secondary hyperaldosteronism

  • Renovascular hypertension
  • Diuretic use
  • Renin- secreting tumour
  • Malignant -Hypertension
  • Coarctation of Aorta
38
Q

What can cause decreased PRA with increased PAC?

A

Investigate for causes of Primary hyperaldosteronism

39
Q

What can cause decreased PRA and PAC?

A
  • congenital adrenal hyperplasia
  • exogenous mineralocorticoid
  • DOC-producing tumour
  • Cushing’s syndrome
  • 11 beta HSD deficiency
  • Liddle’s syndrome
40
Q

What are the screening tests for hyperaldosteronism?

A
  • Plasma renin activity (PRA) and plasma aldosterone concentration (PAC)
  • PAC/PRA> 20 with concomitant serum aldosterone >10ng/dl
41
Q

What are the confirmatory tests for hyperaldosteronism?

A

24hr urine aldosterone: >12ug/day

urinary sodium: >200mEq/day during 4 days of salt loading

42
Q

How is the aldosterone source established in hyperaldesteronism ?

A
  • CT scan of adrenal glands
  • upright posture test
  • plasma 18-hydroxycorticosterone
  • adrenal venous sampling if CT scan is inconclusive or discordant with posture test
43
Q

What is another name for hyperaldosteronism?

A

Conn’s syndrome

44
Q

What can cause Cushing’s syndrome?

A
  • adenoma
  • carcinoma
  • bilateral hyperplasia
45
Q

What can cause Conn’s syndrome

A
  • Adenoma

- Bilateral hyperplasia

46
Q

Why is pheochromocytoma referred to as the 10% tumour?

A
  • 10% extra-adrenal
  • 10% malignant
  • 10% multiple
  • 10% hyperglycaemia

(30% inherited origin)

47
Q

Pheochromocytoma is associated with paroxysmal attacks of….

A
  • Headache
  • Sweating
  • Palpitations
  • Tremor
  • Pallor
  • Anxiety/fear
48
Q

What is persistent in 70% of pheochromocytoma patients?

A

Hypertension

49
Q

What are >90% of congenital adrenal hyperplasia cases due to?

A

21-hydroxylase deficiency

50
Q

How can severe cases of congenital adrenal hyperplasia present?

A
  • Neonatal salt-losing crisis

- Ambiguous genitalia (girls)

51
Q

What incomplete defects can occur in congenital adrenal hyperplasia?

A
  • Pseudo-precocious puberty (boys)

- Hirsutism (women)

endocrine system 1 (25 decks)

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