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Yr3 Medicine- Endocrinology > Addison's Disease > Flashcards

Addison's Disease Flashcards

1
Q

What is adrenal insufficiency?

A

Adrenal glands do not produce enough steroid hormones- particularly cortisol & aldosterone

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2
Q

What is Addison’s disease?

What is an alternative name for Addison’s disease?

State common causes of Addison’s disease

A
  • Specific condition/cause of adrenal insufficiency where adrenal galnds have been damaged resulting in reduction of secretion of steroid hormones (we are particularly bothered about the decreased secretion of aldosterone & cortisol).
  • Also called primary adrenal insufficiency
  • Causes:
    • Autoimmune (80% of cases in UK)
    • TB (commmonest cause worldwide)
    • Adrenal metastases
    • Adrenal haemorrhage (Waterhouse Frederickson syndrome, anti-phospholipid syndrome)
    • Congential (late onset adrenal hyperplasia)
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3
Q

What is secondary adrenal insufficiency?

State some common causes of secondary adrenal insufficiency

A
  • Inadequete ACTH secretion resulting in low stimulation of adrenal glands and hence decreased release of steroid hormones
  • Common causes secondary adrenal insufficiency:
    • Steroids (most common)
    • Due to loss or damage to pituitary gland e.g:
      • Surgery to remove pituitary tumour
      • Infection
      • Loss of blood flow to pituitary
      • Radiotherapy
      • Sheehan’s syndrome
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4
Q

What is Sheehan’ syndrome?

A

Massive blood loss in childbirth which leads to pituitary necrosis

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5
Q

What is tertiary adrenal insufficiency?

A
  • Inadequete CRH release by hypothalamus resulting in decreased ACTH secretion and hence decreased adrenal steroid horone production
  • Usually a result of withdrawing long term (>3 weeks) steroids too quickly; hypothalamus has been supressed due to exogenous steroids and if you remove the exogenous steroids too quickly the hypothalamus doesn’t ‘wake up’ faste enough and endogenous steroids are not adequetely produced. This is why you must taper down long term steroids slowly.
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6
Q

State some risk factors for developing Addison’s disease

A
  • Female sex
  • Adrenal haemorrhage (due to thromboembolic & hypercoagulable states for which you may be taking anticoagulants)
    • Sepsis (e.g. meningococcal sepsis, Waterhouse Frederickson syndrome)
    • Antiphospholipid syndrome
  • Other autoimmune conditions
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7
Q

State some symptoms of Addison’s disease

A
  • Fatigue
  • Nausea
  • Anorexia & weight loss (>90%)
  • Arthralgia & myalgia/cramps
  • Weakness- generalised
  • Abdo pain
  • Diarrhoea/constipation
  • Reduced libido
  • Depression
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8
Q

State some signs of Addison’s disease

A
  • Bronze hyperpigmentation to skin & membranes (often see pigmented palmar creases & buccal mucosa)
  • Hypotension (particularly postural hypotension)
  • Vitiligo
  • Hypoglycaemia
  • Loss of pubic & axillary hair (in women)
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9
Q

Explain why someone with Addison’s has hyperpigmentation (2 reasons)

A
  • Decreased adrenal steroid hormones causes ACTH to increase- via negative feedback. ACTH is produced from POMC. One of breakdwon products of ACTH is alpha-MSH. Alpha MSH is involved in melanin synthesis
  • ACTH can also stimulate melanocytes directly to produce melanin
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10
Q

Explain why someone with Addison’s disease will have reduced libido

A
  • Less ACTH
  • Less stimulation of adrenal glands
  • Adrenal glands produce androgens which have a role in libido
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11
Q

Discuss what investigations you would do if you suspect Addison’s disease, include:

  • Bedside
  • Bloods
  • Imaging
A

Bedside

  • Short synacthen test: see if synthetic ACTH can increse cortisol

Bloods

  • FBCs: may show anaemia & eosinophilia
  • U&Es: check K+ and Na+, urea may be high
  • Serum cortisol (early morning): see if low
  • ACTH: see if low or high
  • Adrenal autoantibodies: check for autoimmune cause
  • Renin: if mineralocorticoid production is low, renin will be high to compensate (in Addison’s. Not in secondary adrenal insufficiency)
  • Aldosterone: assess mineralocorticoid status

Imaging

  • CT/MRI adrenals: check for infection, haemorrhage, metastases etc.. Find underlying cause
  • MRI pituitary: check for pituitary pathology
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12
Q

State the biochemical hallmarks for Addison’s disease

A
  • Hyponatraemia
  • Hyperkalaemia
  • Raised urea
  • Hypoglycaemia
  • Mild anaemia
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13
Q

Explain why pts with Addison’s have raised urea

A
  • Aldosterone deficiency
  • Decreased reabsorption of Na+ and water
  • Decreased circulating volume
  • Decreased GFR
  • Decreased clearance of urea
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14
Q

What autoantibodies do you test for if you suspect Addison’s?

A
  • Adrenal cortex antibodies
  • 21-hydroxylase antibodies
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15
Q

Describe the short synacthen test

A
  • Ideally performed in morning
  • Measure baseline plasma cortisol
  • Give synacthen (250ug) IM
  • Measure plasma cortisol 30 minutes after synacthen
  • Failure of cortisol to rise indicates Addison’s disease
    • Some say failure to make cortisol double baseline= Addisons. Some say if cortisol is not >550nmol/L it is Addison’s.
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16
Q

There is also a long synacthen test; however, this is rarely used anymore.

  • Describe the long synacthen test
  • Explain why it is rarely used anymore
A
  • Involves giving an infusion of ACTH over a long period. Then same principle of measuring cortisol.
  • It was originally used to distinguish between primary adrenal insufficiency and adrenal atrophy secondary to prolonged understimulation in secondary adrenal insufficiency.
    • Addison’s= no cortisol response
    • Adrenal atrophy (secondary to secondary adrenal insufficiency)= prolonged ACTH eventually gets adrenals going again & cortisol rises

Now we simply measure ACTH and this helps us determine the underlying cause. ACTH high in Addisons, ACTH low in adrenal atrophy secondary to secondary adrenal insuffiency.

17
Q

Discuss the teratment for Adrenal insufficiency

A
  • Replacement steroids (titrated to signs, symptoms & electrolytes)
    • Hydrocortisone= glucocorticoid hormone used to replace cortisol
    • Fludrocortisone= mineralocorticoid used to replace aldosterone
    • NOTE: don’t need to replace mineralocorticoids in secondary adrenal failure
  • Pts given a steroid card & emergency ID tag
  • Androgen replaement with dihydroepiandrosterone if decreased libido
18
Q

Pts with Addison’s may have to alter their steroid intake dependent on their daily activities; state some situations in which pts may have to alter their steroids

A
  • Increase hydrocortisone uptake before strenous exercise (add 5-10mg to daily intake)
  • Double hydrocortisone in febrile illness, injury or stress (fludrocortisone can stay the same)
  • Show how to use IM injections in case vomitting prevents them taking steroids orally
19
Q

How are corticosteroids usually taken in Addison’s disease? (i.e. how much taken when)?

A

Usually split into two doses (BD)

Most of it taken in morning

20
Q

State some potential complications of Addison’s disease

A
  • Addisonian crisis
  • Secondary Cushing’s (over-replacement of glucocorticoids)
  • Treatment related hyeprtension
21
Q

Does Addison’s decrease life expectancy?

A

Decreases life expectancy by 11yrs for men, 3yrs for women

22
Q

What is an Addisonian crisis/adrenal crisis?

Describe the typical presentation of someone having an Addisonian crisis

A

Acute, life threatening presentation of severe Addison’s (absence of steroid hormones). Present with:

  • Reduced consciousness
  • Hypotension
  • Hypoglycaemia
  • Hyponatraemia
  • Hyperkalaemia
  • Weak
  • Confused
23
Q
A
24
Q

Who do Addisonian crisises usually present in?

A
  • First presentation of Addison’s disease
  • Pt with known Addison’s who has withdrawn, forgotten steroids
  • Pt with known Addison’s who has had infection, trauma or acute illness
25
Q

Should you wait to perform investigations & establish definitive diagnosis before treating someone with suspected Addisonian crisis?

A

NO- it requires immediate treatment as it is a life threatening condition

26
Q

Discuss the treatment for an Addisonian/adrenal crisis

A
  • Investigations (BUT REMEMBER: do not wait for results & definitive diagnosis before commencing treatment):
    • Cortisol
    • ACTH
    • U&Es
    • FBC
    • VGG (glucose)
    • ECG (as raised [K+] can cause arrhythmias. Give calcium gluconate if needed)
    • Investigations to identify source of infection is suspect infection is the cause
  • IV hydrocortisone 100mg stat, then 100mg every 6-8hrs (can be changed to oral steroids after 72hrs if pt is stable)
  • May need fludrocortisone (often not needed as high dose hydrocortisone has weak mineralocorticoid effects)
  • IV fluids: bolus of 500ml to support BP, continue until stable for slower IV fluids
  • Monitor & correct hypoglycaemia
  • Antibiotics is suspect infection
  • Intensive monitoring

Yr3 Medicine- Endocrinology (9 decks)

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