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Endocrine > Adrenal disease > Flashcards

Adrenal disease Flashcards

1
Q

Describe the production, regulation and function of mineralocorticoids

A

Aldosterone

  • Produced in the Zona Glomerulosa
  • Regulated by the Renin-Angiotensin system
  • Causes renal reabsorption of salt and water, therefore regulates BP
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2
Q

Describe the production, regulation and function of glucocorticoids

A

Cortisol/corticosterone

  • Produced in Zona Fasiculata
  • Regulated by ACTH from anterior pituitary (adrenocorticosteroid hormone)
  • Insulin antagonists, stimulate gluconeogenesis, lipolysis and proteolysis
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3
Q

Describe the production, regulation and function of adrenal sex hormones

A

DHEA/estradiol

  • Produced in the Zona Reticularis
  • ACTH from anterior pituitary
  • Only course of androgens in females
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4
Q

Describe the production, regulation and function of catecholamines

A
  • Produced in the medulla of the adrenal gland
  • Regulated by the sympathetic nervous system
  • Act on adrenergic receptors, particularly in the CV system to increase BP, RR, blood flow
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5
Q

What are the Clinical features of Cushing’s Syndrome?

A
  • Central obesity
  • Hypertension
  • Hyperglycaemia/diabetes
  • Easy bruising
  • Hirstuism
  • Abdominal striae
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6
Q

What is the pathophysiology of Cushing’s Disease

A

Excess circulating cortisol

  • Most common cause is a pituitary adenoma causing excess ACTH which cannot be turned off by negative feedback
  • Less commonly is adenoma/carcinoma or bilateral nodules of the adrenal gland
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7
Q

What investigations should be carried out to establish cortisol excess?

A

Dethamexasone suppression test

  • Potent glucocorticoid which should feedback to AP and halt ACTH and cortisol production
  • Cortisol levels will not drop in Cushings

24 hour urinary cortisol, late night saliva cortisol

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8
Q

What investigations should be carried out to establish the source of the cortisol excess?

A

Measure ACTH

  • If low: Adrenal imaging
  • If high: Pituitary imaging
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9
Q

What is the management of Cushing’s Disease?

A

Surgical removal of the source of excess cortisol

- transphenoidal removal of pituitary tumour

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10
Q

What are the clinical features of hypoadrenalism?

A
  • Bronze pigmentation of skin
  • Weight loss
  • Lethargy
  • Hypoglycaemia
  • Hypotension
  • Vomiting and diarrhoea
  • Disrupted biochemistry
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11
Q

What is the pathophysiology of hypoadrenalism?

A

Addisons disease is the most common cause. it is the autoimmune destruction of the adrenal cortex, causing reduced production of all 3 types of adrenal hormones.

Lack of negative feedback leads to increased CRH, ACTH and melanocyte stimulating hormone (ACTH precursor).

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12
Q

What investigation should be carried out to confirm adrenal insufficiency?

A

Short synacthen test

- Administer IV ACTH, blood cortisol will not rise in Addisons

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13
Q

What abnormal electrolytes would be seen in Addisons?

A
  • Low glucose
  • Low sodium (low aldosterone decreases reabsorption)
  • High potassium
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14
Q

What abnormal hormonal indicators would there be of adrenal insufficiency?

A
  • Low aldosterone, cortisol, and androgens
  • High ACTH and renin due to lack of negative feedback

Adrenal antibodies are also commonly present

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15
Q

What is the pharmacological treatment of Hypoadrenalism caused by Addisons?

A
  • Hydrocortisone to replace glucocorticoids, higher dose in the morning to try and mimic circadian rhythm
  • Fludrocortisone to replace mineralocorticoids
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16
Q

What is the pathogenesis of Congenital Adrenal Hyperplasia (CAH)?

A

An autosomal recessive disorder causing genetic defects in enzymes of the steroidogenic pathways. Lack of negative feedback causes increased ACTH and hyperplasia of the gland.
- Most commonly 21a-hydroxylase which affects aldosterone and cortisol production.

Steroidogenic pathway moves in direction away from defective enzyme

17
Q

What are the clinical features of 21a-hydroxylase deficiency in CAH?

A

Steroidogenic pathway shifts and causes an increase in androgens.
- Hypotension due to salt wasting and obesity

Females

  • Ambiguous genetalia
  • Amenhorrohea
  • Acne/hirtuism

Males
- Precocious puberty

18
Q

What investigations would be carried out in suspected CAH?

A

Short syACTHen test

- 21a-h deficiency would result in low cortisol and high 17a-h and androgens

19
Q

What is the pharmacological treatment of CAH

A

Glucocorticoid and mineralocorticoid replacement (hydrocortisone and fludrocortisone).

20
Q

What are the most common causes of primary aldosteronism?

A

Excess aldosterone due to:

  • Adrenal adenoma
  • Bilateral adrenal hyperplasia
21
Q

What are the clinical features of primary aldosteronism/

A
  • Hypertension
  • Hypokalaemia

Due to increases sodium/water retention by aldosterone

22
Q

What investigations should be carried out to diagnose primary aldosterone?

A

Hormone levels should show a high Aldosterone to Renin ratio

23
Q

What is the management of primary aldosteronism?

A
  • Surgical management: adrenalectomy

- Pharmacological management: potassium sparing diuretics (mineralocorticoid receptor antagonists) e.g. spinorolactone

24
Q

What is the pathophysiology of a phaeochromacytoma?

A

A (usually benign) neuroendocrine tumour of the chromatin cells of the adrenal medulla, causing an increase in catecholamines.

25
Q

What are the clinical signs of a phaeochromatoma?

A
  • Hypertension

- Episodes of pallor, palpitations, sweating, tremor and headache

26
Q

What is the management of a phaerochromacytoma?

A
  • Surgical removal of tumour

- Alpha blocker (phenoxybenzamine) pre-operatively

27
Q

From which amino acid are catecholamines synthesised?

A

Tyrosine

Endocrine (9 decks)

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