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Year 3 - Medicine > D&E - Adrenal Axis > Flashcards

D&E - Adrenal Axis Flashcards

1
Q

Describe the adrenal axis.

A
  1. Hypothalamus secretes CRH.
  2. Cortisol stimulates anterior pituitary to release ACTH.
  3. ACTH stimulates the adrenal glands to release cortisol.
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2
Q

What are the actions of cortisol within the body?

A
  • increased alertness
  • inhibits the immune system
  • inhibits bone formation
  • raised blood glucose
  • increases metabolism
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3
Q

What is adrenal insufficiency?

A

The condition in which the adrenal glands do not produce enough steroid hormones, cortisol and aldosterone.

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4
Q

What is Addison’s disease?

A

Adrenal insufficiency when the adrenal glands have been damaged, resulting in reduce cortisol and aldosterone secretion.

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5
Q

What are the causes of secondary adrenal insufficiency?

A

Inadequate ACTH release from the pituitary:

  • pituitary adenomas
  • surgery to the pituitary
  • trauma
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6
Q

What is tertiary adrenal insufficiency?

A

Inadequate CRH release by the thalamus, usually a result of taking long-term oral steroids.

When exogenous steroids are suddenly withdrawn, the hypothalamus is not able to adequately replace with endogenous steroids.

This is why long-term steroids must be tapered slowly, to allow the adrenal axis to regain normal function.

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7
Q

Presentation of adrenal insufficiency.

A
  • fatigue
  • muscle weakness
  • muscle cramps
  • dizziness and fainting
  • thirst and craving salt
  • weight loss
  • abdominal pain
  • depression
  • reduced libido
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8
Q

What are the signs of adrenal insufficiency, and why do these occur?

A

Bronze hyperpigmentation of the skin due to excess ACTH. ACTH stimulates melanocytes to produce melanin.

Hypotension.

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9
Q

What are the biochemical findings in adrenal insufficiency?

A
  • hyponatraemia
  • hyperkalaemia
  • hypercalcaemia
  • hypoglycaemia
  • raised creatinine and urea (urea > creatinine = dehydration)
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10
Q

Which autoantibodies are associated with Addison’s disease?

A
  • adrenal cortex antibodies
  • 21-hydroxylase antibodies
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11
Q

What is the diagnostic test for pituitary insufficiency?

A

Short Synacthen test / ACTH stimulation test.

A dose of synthetic ACTH (Synacthen) is given in the morning, with blood cortisol checked before and after (30m, 60m) the dose.

The cortisol level should at least double in a healthy individual.

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12
Q

How is adrenal insufficiency managed?

A
  • hydrocortisone to replace cortisol
  • fludrocortisone to replace aldosterone

Patients are given a steroid card, ID tag and emergency letter to alert emergency services that they depend on steroids for life.

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13
Q

How are steroid doses altered during acute illness, for patients with adrenal insufficiency?

A

Doses are doubled during acute illness, to match the normal steroid response to illness.

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14
Q

What is Addisonian crisis?

A

An acute presentation of severe adrenal insuffieincy, where the absence of steroid hormones leads to life threatening emergency.

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15
Q

Presentation of Addisonian crisis?

A
  • reduced consciousness
  • hypotension
  • hypoglycaemia
  • hyponatraemia
  • hypokalaemia
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16
Q

What are the triggers for Addisonian crisis?

A
  • infection
  • trauma
  • acute illness
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17
Q

How should Addisonian crisis be managed?

A
  • ABCDE approach to initial assessment
  • IM hydrocortisone
  • IV fluids
  • correct hypoglycaemia (e.g. IV dextrose)
  • careful monitoring of electrolytes and fluid balance
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18
Q

Define:

a) Cushing’s syndrome

b) Cushing’s disease

A

a) prolonged elevated levels of cortisol within the body.

b) prolonged elevated levels of cortisol within the body, secondary to an ACTH-secreting pituitary adenoma, stimulating excess cortisol release from the adrenal glands.

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19
Q

Causes of Cushing’s syndrome.

A

CAPE

Cushing’s disease (pituitary adenoma ACTH releasing).

Adrenal adenoma (adrenal tumour secreting excess cortisol).

Paraneoplastic syndromes

Exogenous steroids (most common)

20
Q

Presentation of Cushing’s syndrome.

A
  • anxiety
  • depression
  • insomnia
  • round face
  • central obesity
  • abdominal striae
  • hirsutism
  • easy bruising
  • hyperpigmentation of skin
21
Q

What are the metabolic effects of Cushing’s syndrome?

A
  • hypertension
  • cardiac hypertrophy
  • T2DM
  • dyslipidaemia
  • osteoporosis
22
Q

Which paraneoplastic syndromes may cause Cushing’s syndrome?

A

Small cell lung cancer commonly causes ectopic ACTH release, stimulating excessive cortisol release from the adrenal glands.

23
Q

How is Cushing’s syndrome diagnosed?

A

Dexamethasone suppression test to diagnose Cushing’s syndrome caused by a problem inside the body.

24
Q

What is the normal physiological response to the dexamethasone suppression test?

A

Dexamethasone induces negative feedback upon the hypothalamus, reducing CRH output.

It also induces negative feedback on the anterior pituitary, reducing ACTH output.

Low CRH and ACTH output causes a low cortisol output by the adrenal glands.

A lack of cortisol suppression in response to dexamethasone suggests Cushing’s syndrome.

25
Q

What test would be used to:

a) exclude Cushing’s syndrome?

b) confirm suspected Cushing’s syndrome?

c) determine the cause of Cushing’s syndrome?

A

a) low-dose overnight test

b) low-dose 48-hour test

c) high-dose 48-hour test

26
Q

Describe the low-dose overnight, dexamethasone suppression test.

A

1mg dexamethasone is given at 10pm, and cortisol is checked at 9am the following morning.

A normal result is that the cortisol level is suppressed.

If cortisol is not suppressed, Cushing’s syndrome cannot be excluded.

27
Q

Describe the low dose 48-hour, dexamethasone suppression test.

A

0.5mg dexamethasone is taken QDS, starting at 9AM on day 1.

Cortisol is checked on day 1 (before the first dose) and day 3 (after the last dose).

A normal result is that the cortisol level on day 3 is suppressed.

If cortisol is not suppressed, this indicates Cushing’s syndrome.

28
Q

Describe the high dose 48-hour, dexamethasone suppression test.

A

2mg dexamethasone is taken QDS, starting at 9AM on day 1.

Cortisol is checked on day 1 (before the first dose) and day 3 (after the last dose).

The higher dose is enough to suppress the cortisol in Cushing’s syndrome caused by a pituitary adenoma (Cushing’s disease), but not when it is caused by an adrenal adenoma or ectopic ACTH.

29
Q

Besides dexamethasone suppression testing, how else can Cushing’s syndrome be investigated?

A

FBC (elevated WCC)

U&Es (hypokalaemia if adrenal adenoma is also secreting aldosterone).

MRI brain (pituitary adenoma)

CT chest (small cell lung cancer)

30
Q

Treatment of Cushing’s disease?

A

Transphenoidal removal of pituitary adenoma.

31
Q

Treatment of Cushing’s syndrome secondary to adrenal tumour?

A

Laparoscopic removal of adrenal tumour.

32
Q

What is a phaeochromocytoma?

A

A tumour of the Chromaffin cells of the adrenal glands that secretes excessive adrenaline.

33
Q

Give the genetic associations of phaeochromocytomas.

A
  • MEN 2
  • neurofibromatosis 2
  • Von Hippel-Lindau disease
34
Q

Presentation of phaeochromocytoma.

A
  • anxiety
  • sweating
  • headache
  • tremor
  • palpitations
  • hypertension
  • tachycardia

Symptoms are usually intermittent, as adrenaline is secreted in bursts in phaeochromocytomas.

35
Q

What are the complications of untreated phaechromocytomas?

A
  • hypertensive crisis
  • encephalopathy
  • hyperglycaemia
  • pulmonary oedema
  • cardiac arrhythmias
  • death
36
Q

How is phaechromocytoma diagnosed?

A
  • plasma free metanephrines*
  • 24-hour urine catecholamines

CT or MRI to look for tumour.

*breakdown product of adrenaline

37
Q

Why is serum catcholamine or serum adrenaline not useful in diagnosing phaeochromocytomas?

A

Catecholamines and adrenaline have a very short half life in the blood.

38
Q

What is the management of phaeochromocytomas?

A

Alpha blockers (phenoxybenzamine or doxazosin) initiated at diagnosis.

Beta blockers when established on alpha blockers.

Only definitive management is surgical removal of the tumour.

39
Q

What is hyperaldosteronism?

A

Excess levels of aldosterone.

Conn’s syndrome is an adrenal adenoma that produces too much aldosterone.

40
Q

What are the actions of aldosterone?

A
  • increase sodium reabsorption from the distal tubule
  • increase potassium secretion from the distal tubule
  • increase hydrogen secretion from the collecting ducts
41
Q

What is primary hyperaldosteronism?

A

Adrenal glands are directly responsible for producing too much aldosterone.

Serum renin will be low as the high blood pressure suppresses it.

42
Q

What are the causes of primary hyperaldosteronism?

A

Bilateral adrenal hyperplasia

Adrenal adenoma secreting aldosterone (Conn’s syndrome)

Familial hyperaldosteronism

43
Q

What is secondary hyperaldosteronism?

A

Excessive renin release stimulating the release of excessive aldosterone, due to disproportionately lower blood pressure in the kidneys.

44
Q

What are the causes of secondary hyperaldosteronism?

A

Disproportionately lower blood pressure in the kidneys causes excessive renin release:
- renal artery stenosis
- heart failure
- liver cirrhosis and ascites

45
Q

How is hyperaldosteronism screened for?

A

Aldosterone-to-renin ratio (ARR):

High aldosterone and low renin indicates primary hyperaldosteronism.

High aldosterone and high renin indicates secondary hyperaldosteronism.

46
Q

How is hyperaldosteronism investigated?

A
  • ACR
  • blood pressure (hypertension)
  • U&Es (hypokalaemia; hypernatraemia)
  • VBG (metabolic alkalosis)

To find the underlying cause:
- CT / MRI for adrenal tumour
- renal artery imaging
- adrenal vein sampling

47
Q

How is hyperaldosteronism managed?

A

Aldosterone antagonists to medically manage:
- eplerenone
- spironolactone

Surgical management includes removal of adrenal adenomas (Conn’s syndrome) and percutaneous renal artery angioplasty to treat renal artery stenosis.

Year 3 - Medicine (33 decks)

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