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MEH > 12 Adrenal Disorders > Flashcards

12 Adrenal Disorders Flashcards

1
Q

What is primary adrenal insufficiency (Addison’s disease) due to?

A

Arises due to destruction of adrenal gland or genetic defect in steroid synthesis

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2
Q

Clinical features of Addison’s disease/primary adrenal insufficiency

A
  • fatigue
  • weakness
  • anorexia + weight loss
  • nausea
  • abdominal pain
  • hyperpigmentation
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3
Q

How does Addison’s disease cause hyperpigmentation?

A
  • Insufficient adrenal function
  • Decreased cortisol
  • Negative feedback on ant. Pit reduced
  • More POMC needed to synthesis ACTH
  • More MSH produced&raquo_space; hyperpigmentation
  • ACTH at high level can stimulate receptors of MSH receptors
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4
Q

Clinical features of mineralocorticoid deficiency

A
  • dizziness
  • postural hypotension
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5
Q

Clinical features of glucocorticoid deficiency

A

Hypoglycaemia
hyperpigmentation due to ACTH excess due to reduced cortisol negative feedback

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6
Q

Causes of primary adrenal insufficiency/Addison’s diseas

A

Autoimmunity
infection
infiltrative processes

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7
Q

Investigations + results of primary adrenal insufficiency

A
  • U&Es
  • glucose levels
  • FBC
  • autoantibodies - (adrenal cortex ab/21-hydroxylase ab)
    .
  • hyponatraemia
  • hyperkalaemia
  • raised urea
  • hypoglycaemia
  • anaemia
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8
Q

Diagnosis of Addison’s disease

A

low 9am cortisol + simultaneously raised ACTH
ATCH/synacthen test for confirmation

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9
Q

Outline the short Synacthen test
What is it used to diagnose?

A
  • ACTH stimulation test
  • dose of synacthen given
  • blood cortisol checked before, 30 mins + 60 mins after
  • cortisol levels should at least double
  • failure to indicates adrenal insufficiency
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10
Q

What is long synacthen test used for?

A

to distinguish between primary adrenal insufficiency (high ACTH) + adrenal atrophy due to secondary adrenal insufficiency (low ACTH)

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11
Q

Management of Addison’s disease/primary adrenal insufficiency

A
  • Lifelong replacement of glucocorticoids (hydrocortisone) + mineralocorticoids (fludrocortisone)
  • Education to prevent crises - steroid card and bracelet, emergency HC injection if vomiting, emergency contract details for their endocrinology team
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12
Q

What is needed if a patient with Addison’s disease becomes ill?

A

double hydrocortisone dose until illness has resolved

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13
Q

What is secondary adrenal insufficiency?

A

ACTH deficiency due to hypopituitarism

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14
Q

Management of secondary adrenal insufficiency

A

hydrocortisone replacement

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15
Q

Difference in drug treatment of primary and secondary adrenal insufficiency

A

Both require hydrocortisone
fludrocortisone only in primary

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16
Q

what is Addisonian crisis?

A

Life threatening emergency due to adrenal insufficiency

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17
Q

What is Addisonian crisis caused by?

A

Severe stress
Salt deprivation
Infection
Cold exposure
Trauma
Over exertion
Abrupt steroid drug withdrawal

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18
Q

Clinical features of adrenal crisis

A

Collapse
Hypotension
Dehydration
Pigmentation
Coma
Vomiting
Pyrexia

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19
Q

What will blood tests show in renal crisis?

A

Low cortisol level
Low Na
High K

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20
Q

Treatment of Addisonian crisis

A

IV fluids
IV hydrocortisone 100mg
correct hypoglycaemia

21
Q

Why should long term steroids not be stopped abruptly?

A

long term steroids cause ACTH suppression so abrupt stoppage can cause adrenal crisis

22
Q

What is hyperaldosterionism?

A

Excessive aldosterone production

23
Q

What is Conn’s syndrome?

A

Adrenal adenoma that produces excessive aldosterone

24
Q

What is primary hyperaldosteronism due to?

A
  • defect in adrenal cortex
  • bilateral idiopathic adrenal hyperplasia - most common
  • aldosterone secreting adrenal adenoma (Conn’s syndrome)
  • low renin levels
25
Q

What is secondary hyperaldosteronism due to?

A
  • due to over activity of RAAS (excessive renin) > excessive aldosteron release
  • renal artery stenosis
  • heart failure
  • liver cirrhosis + ascites
  • high renin levels
26
Q

Signs/symptoms of hyperaldosteronism

A

High BP
Stroke
Left ventricular hypertrophy
Hypernatraemia
Hypokalaemia
Headaches
Fatigue
Muscle wekaness

27
Q

Treatment of hyperaldosteronism

A
  • Primary - aldosterone producing adenomas removed by surgery
  • Spironoalactone/eplerenone
  • treating the underlying cause
28
Q

What is the best way to distinguish between primary and secondary hyperaldosteronism?

A

primary - low renin levels
secondary - high renin levels

29
Q

What is Cushing’s syndrome?

A

Features of prolonged high levels of glucocorticoids in the body (cortisol)

30
Q

Causes of Cushing’s syndrome

A
  • prolonged steroid use
  • benign pituitary adenoma secreting ACTH (Cushing’s disease)
  • excess cortisol produced by adrenal tumour (adrenal Cushing’s)
  • non pituitary-adrenal tumours producing ACTH (paraneoplastic syndromes) e.g. SCLC
31
Q

What is Cushing’s disease?

A

Pituitary adenoma secreting excessive ACTH > cortisol release

32
Q

Clinical features of Cushing’s syndrome

A
  • moon face
  • central obesity
  • purple abdominal striae
  • enlarged fat pad on upper back
  • hirsutism
  • easy bruising + poor skin healing
  • hyperpigmentation
  • proximal limb muscle wasting
33
Q

Why do patients with Cushing’s syndrome have purple striae?

A

Central obesity from fat redistribution due to cortisol stress the the skin
Weak + thin skin increases proteolysis > purple striae

34
Q

Investigations of Cushing’s syndrome + what for

A
  • dexamethasone suppression test
  • MRI - pituitary adenoma
  • CT chest - SCLC
  • CT abdomen - adrenal tumours
  • FBC - high WBC
  • U&E - low K if adrenal adenoma is secretomg aldosterone
35
Q

What do we do to diagnose Cushing’s?

A

Dexamethasone suppression test
lack of cortisol suppression indicates Cushing’s syndrome

36
Q

What are the three types of dexamethasone suppression test?

A

low dose overnight
low dose 48 hour
high dose 48 hour

37
Q

what is the action of dexamethasone?

A

suppresses secretion of ATCH > lowers cortisol

38
Q

Treatment of Cushing’s syndrome

A

Removal of underlying cause:
- trans-sphenoidal removal of pituitary adenoma
- surgical removal of adrenal tumour/tumour producing ectopic ACTH
.
- adrenalectomy with life long steroid replacement therapy
- metyrapone: reduces production of cortisol

39
Q

What is done when surgical removal of the causative tumour of Cushing’s syndrome isn’t possible?

A

adrenalectomy with life long steroid replacement therapy

40
Q

More on dexamethasone suppression test

A
41
Q

What is phaeochromocytoma?

A

Chromaffin cell tumour > secrete adrenaline + noradrenaline

42
Q

What is a paraganglioma?

A

extra-adrenal pheochromocytoma

43
Q

Characteristics of phaeochromocytoma

A
  • severe hypertension
  • headaches
  • palpitations
  • excessive sweating
  • weight loss
  • anxiety + panic attacks
44
Q

What can untreated phaeochromocytomas cause?

A
  • hypertensive crisis
  • encephalopathy
  • hyperglycaemia
  • pulmonary oedema
  • cardiac arrhythmias
45
Q

Investigations of phaeochromocytoma

A
  • plasma free metanephrines
  • 24-hour urine catecholamines
  • CT or MRI to look tumour
  • genetic testing incl. 1st degree relatives
46
Q

What are metanephrines?

A

Breakdown product of adrenaline

47
Q

Management of phaeochromocytoma

A
  • surgical excision
  • alpha blockers e.g. phenoxybenzamine or doxazosin
  • B blockers when established on a blockers to reduce risk of hypertensive crisis
48
Q

A patient presents with hypertension and hypokalaemia, what could the diagnosis be?

A

Hyperaldosteronism
Cushing’s syndrome ?

49
Q

What time of day would be best to take a blood sample to measure cortisol levels and why?

A

Midnight
Blood cortisol levels are normally at their lowest around midnight

MEH (23 decks)

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