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4. Metabolism > 18. Disorders of the Adrenal Cortex > Flashcards

18. Disorders of the Adrenal Cortex Flashcards

1
Q

What are the three layers of the adrenal cortex?

A

Glomerulosa (salt), fasciculata (sugar), reticularis (sex hormones).

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2
Q

What levels do mineralocorticoids control?

A

Na and water in, K out.

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3
Q

How do steroid hormones work?

A

They act on the intracellular receptors and enter the nucleus to alter DNA transcription.

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4
Q

What happens in a deficiency of mineralocorticoid?

A

Low sodium, dehydration and high potassium.

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5
Q

What happens in an excess of mineralocorticoid?

A

High sodium, hypertension, low potassium.

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6
Q

What is the action of glucocorticoid?

A

Increased glucose production, breakdown of protein and redistribution of fat,

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7
Q

What can a deficiency of glucocorticoid cause?

A

Low glucose, weight loss, nausea and hypotension.

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8
Q

What can an excess of glucocorticoid cause?

A

High glucose, weight gain, increased appetite, hypertension and cushingoid.

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9
Q

What us congenital enzyme deficiency?

A

A rare paediatric condition which lowers Na and raises K levels. It’s a medical emergency.

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10
Q

What are the three steps in the hypothalamus-pituitary-adrenal axis?

A

Hypothalamus, pituitary and the end organ - adrenal.

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11
Q

What is the precursor to ACTH that’s secreted?

A

POMC.

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12
Q

How is POMC converted to ACTH?

A

POMC is cleaved into ACTH and MSH (melanocytes stimulating hormone).

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13
Q

What could cause a sudden, unexplained pigmentation?

A

Excess ACTH.

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14
Q

What can primary adrenal failure cause?

A

Addison’s disease.

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15
Q

What happens in primary adrenal failure?

A

There is high ACTH levels, but a lack of negative feedback. This means there are increased precursors to ACTH produced and MSH causes pigmentation.

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16
Q

How can an excess of ACTH affect the hypothalamo-pituitary-adrenal axis?

A

Causes more cortisol to be produced and released from the adrenal gland. This causes ACTH-dependent Cushing’s.

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17
Q

What causes ACTH independent Cushing’s?

A

A cortisol secreting adrenal tumour.

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18
Q

How can an adrenal tumour affect ACTH levels?

A

It lowers them.

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19
Q

What could the cause of corticosteroid excess be?

A

Cushing’s disease, ectopic ACTH, primary adrenal tumour or exogenous steroids.

20
Q

When should cortisol levels be checked with suspected Addison’s disease?

A

In the morning where cortisol will be at its maximum.

21
Q

When should cortisol levels be measured for suspected Cushing’s disease?

A

At midnight, where cortisol will be at its minimum.

22
Q

What can the synacthen test be used for?

A

Primary adrenal failure, disease of the adrenal cortex, cortisol response to synthetic ACTH.

23
Q

What is involved in the ACTH-stimulation test?

A

Inducing stress, namely hypoglycaemic stress caused in the insulin stress test.

24
Q

How can corticosteroid deficiency be tested for?

A

Morning cortisol, stimulating HPA axis, synacthen test primary adrenal failure or insulin tolerance test pituitary ACTH deficiency.

25
Q

How is a corticosteroid excess tested for?

A

Midnight cortisol, dynamic suppression test. Dexamethasone is given, a failure to suppress cortisol levels suggests Cushing’s syndrome.

26
Q

What is the five year mortality rate of untreated Cushing’s disease?

A

50%.

27
Q

What causes Addison’s disease?

A

Auto immune destruction of the adrenal cortex. It could also be caused by TB or surgical removal of the pituitary. All three corticoid levels go down.

28
Q

What are the specific clinical features of Addison’s disease?

A

Pigmentation and postural hypotension (dizzy when they stand up).

29
Q

How is Addison’s disease treated?

A

With hydrocortisone or fludrocortisone.

30
Q

What are the biochemical features of Addison’s disease?

A

Low sodium, high potassium, high urea and low glucose.

31
Q

How is Addison’s disease confirmed?

A

Morning cortisol, short synacthen test, ACTH tested, plasma renin and adrenal antibodies tested.

32
Q

What happens in secondary adrenal failure?

A

Inadequate ACTH production and suppression of the HPA axis.

33
Q

What can cause suppression of the HPA axis?

A

Long term steroid use.

34
Q

What can abrupt withdrawal of steroids lead to?

A

Hypo-adrenal crises. Hypotension, hypoglycaemia, hyponatraemia, hyperkalaemia, severe dehydration and eventually death.

35
Q

How is a hypoadrenal crisis treated?

A

Correction of electrolytes, IV fluids and glucose and IV hydrocortisone.

36
Q

What can cause Cushing’s syndrome?

A

Pituitary source, adrenal tumour or ectopic ACTH.

37
Q

What are the clinical features of Cushing’s disease?

A

Central weight gain, change in appearance, depression, insomnia, menstrual disturbance and or libido. Also thin skin, easy bruising, hair growth, acne and muscle weakness.

38
Q

How is Cushing’s syndrome diagnosed?

A

Exclude pseudocushing’s using midnight cortisol levels. Also low dose DST and 24-hour urinary free cortisol.

39
Q

How is Cushing’s syndrome treated?

A

Trans-sphenoidal surgery, pituitary irradiation, medical treatment, bilateral adrenalectomy.

40
Q

What can happen as a result of an adrenalectomy?

A

Nelsons syndrome. Lack of negative feedback, uncontrolled pituitary growth, very high ACTH levels and increased pigmentation.

41
Q

What is congenital adrenal hyperplasia?

A

An autosomal recessive rare endocrine disorder.

42
Q

What are the clinical features of CAH?

A

Virilisation of female baby (ambiguous genitalia), neonatal salt losing crisis, hypotension, hypoglycaemia, hyponatraemia and hyperkalaemia.

43
Q

How is CAH investigated?

A

Androstenedione levels are high, testosterone levels are high and ACTH levels are high.

44
Q

How is CAH treated?

A

With steroids.

45
Q

Where are the adrenal glands found?

A

On top of (ad) the kidneys (renal).

4. Metabolism (22 decks)

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