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12 Adrenal Disorders Flashcards

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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
Causes reduced cortisol + aldosterone

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2
Q

Clinical features of Addison’s disease/primary adrenal insufficiency

A
  • fatigue
  • weakness
  • anorexia + weight loss
  • nausea + vomiting
  • hyperpigmentation (especially palmar creases)
  • loss of pubic hair in women
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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 also 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

low aldosterone
- 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 disease

A
  • Autoimmunity (most common)
  • infection e.g. TB, HIV
  • antiphospholipid syndrome
  • metastases e.g. bronchial carcinoma
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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
  • 9am cortisol levels: low 9am cortisol + simultaneously raised ACTH
  • short 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, sick day rules
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12
Q

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

A

double hydrocortisone dose, same fludrocortisone dose
Or
IM hydrocortisone if vomiting

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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
  • Sepsis or surgery causing acute exacerbation of chronic insufficiency
  • Salt deprivation
  • Infection e.g. gastroenteritis
  • Trauma
  • Over exertion
  • Abrupt steroid drug withdrawal
  • inadequate sick day rule management
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18
Q

Clinical features of adrenal crisis

A
  • confusion
  • Collapse
  • Hypotension
  • Dehydration
  • convulsions
  • 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
Hypoglycaemia
Metabolic acidosis

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20
Q

Treatment of Addisonian crisis

A
  • IV 1L 0.9% sodium chloride IV over 15-20 mins
  • IV hydrocortisone 100mg single dose or 50mg IM/IV bolus every 6 hours
  • correct hypoglycaemia
  • give PO steroid replacements after 24 hours
  • identify + treat precipitating cause
  • education of sick day rules + encourage use of steroid alert cards/bracelets
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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

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22
Q

What is hyperaldosterionism?

A

Excessive aldosterone production

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23
Q

What is Conn’s syndrome?

A

Adrenal adenoma that produces excessive aldosterone

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24
Q

What is primary hyperaldosteronism due to?

A
  • bilateral idiopathic adrenal hyperplasia - most common
  • aldosterone secreting adrenal adenoma (Conn’s syndrome)
  • low renin levels
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25
What is secondary hyperaldosteronism due to?
- due to over activity of RAAS (excessive renin) > excessive aldosteron release - renal artery stenosis - heart failure - liver cirrhosis + ascites - **high renin levels**
26
Signs/symptoms of hyperaldosteronism
High BP Stroke Left ventricular hypertrophy Hypokalaemia > muscle weakness Headaches Fatigue
27
electrolytes and acid base balance in hyperaldosteronism
hypernatraemia hypokalameia metabolic alkalosis
28
Investigations of hyperaldosteronism
- first line: **plasma aldosterone/renin ratio** - followed by: **high resolution CT abdomen + adnreal vein sampling**
29
Treatment of hyperaldosteronism
- Primary - aldosterone producing adenomas removed by **surgery - laparoscopic adrenalectomy** - ***Spironoalactone***/***eplerenone*** - treating the underlying cause
30
What is the best way to distinguish between primary and secondary hyperaldosteronism?
**aldosterone/renin ratio** primary - **low renin levels** secondary - **high renin levels**
31
What is Cushing's syndrome?
Disorder caused by prolonged high levels of glucocorticoids in the body (cortisol)
32
when in the day is cortisol at its highest?
9am
33
Causes of Cushing's syndrome
- prolonged steroid use (most common cause) - benign pituitary adenoma secreting ACTH (Cushing’s disease) - non pituitary-adrenal tumours producing ACTH (paraneoplastic syndromes) *e.g. SCLC* - excess cortisol produced by adrenal tumour/adenoma (adrenal Cushing’s)
34
What causes of Cushing's sydnrome cause hyperpigmentation?
Cushing's disease (high ACTH) NOT exogenous steroids or adrenal adenoma
35
What is Cushing's disease?
Pituitary adenoma secreting excessive ACTH > cortisol release
36
Clinical features of Cushing's syndrome
- moon face - central obesity - purple abdominal striae - enlarged fat pad on upper back - hirsutism - easy bruising + poor skin healing - proximal limb muscle wasting - insomnia
37
metabolic effects of cushing's sydnrome
- hypertension - cardiac hypertrophy - hyperglycemia> type 2 diabetes mellitus - hyperlipidaemia - osteoporosis
38
Why do patients with Cushing’s syndrome have purple striae?
Central obesity from fat redistribution due to cortisol stress the the skin Weak + thin skin increases proteolysis > purple striae
39
Investigations of Cushing's syndrome + what for
- **dexamethasone suppression test** - **24 hours urinary free cortisol** - **bedtime salivary cortisol** - **MRI** - pituitary adenoma - **CT chest** - SCLC - **CT abdomen** - adrenal tumours - **FBC** - high WBC - **U&E** - low K if adrenal adenoma is secreting aldosterone too
40
outline 24 hours urinary free cortisol
24 hours worth of urine collected and tested for cortisol levels cumbersone + does not indicate underlying cause
41
What do we do to diagnose Cushing’s?
*Dexamethasone* suppression test lack of cortisol suppression but ACTH suppression indicates Cushing's syndrome
42
What are the three types of dexamethasone suppression test?
low dose overnight low dose 48 hour high dose 48 hour
43
what is the action of *dexamethasone*?
negative feedback onto the pituritary gland suppresses secretion of ACTH> lowers cortisol
44
what should a high dose dexamethasone suppression test show in: - Cushing's disease - ectopic ACTH syndrome - Cushing's syndrome due to other causes *e.g. adrenal adenoma*
- **Cushing's disease (*pituitary adenoma*)**: suppressed cortisol + ACTH - **ectopic ACTH syndrome**: not suppressed cortisol + ACTH - **Cushing's syndrome due to other cause *e.g. adrenal adenoma***: not suppressed cortisol, suppressed ACTH
45
Cushing's disease findings of low dose vs high dose dexamethasone suppresion test
- low dose: does not suppress ACTH or cortisol - high dose: suppression ACTH + cortisol
46
Findings of dexamethasone suppression test in normal person: - baseline ACTH, - cortisol after low dose test - cortisol after high dose test
- **baseline ACTH**: normal - **cortisol after low dose test**: low - **cortisol after high dose test**: low
47
Findings of dexamethasone suppression test in adrenal adenoma: - baseline ACTH, - cortisol after low dose test - cortisol after high dose test
- **baseline ACTH**: low - **cortisol after low dose test**: high - **cortisol after high dose test**: high
48
Findings of dexamethasone suppression test in pituitary adenoma (Cushing's disease) - baseline ACTH, - cortisol after low dose test - cortisol after high dose test
- **baseline ACTH**: high - **cortisol after low dose test**: high - **cortisol after high dose test**: low
49
Findings of dexamethasone suppression test in ectopic ACTH: - baseline ACTH - cortisol after low dose test - cortisol after high dose test
- **baseline ACTH**: high - **cortisol after low dose test**: high - **cortisol after high dose test**: high
50
Treatment of Cushing's syndrome
Removal of underlying cause: - **trans-sphenoidal removal of pituitary adenoma** - **surgical removal of adrenal tumour/tumour producing ectopic ACTH** . if not possible: - **bilateral adrenalectomy with life long steroid replacement therapy** - ***metyrapone***: reduces production of cortisol
51
What drug can be used in Cushing's syndrome?
metyrapone reduces cortisol production
52
What is done when surgical removal of the causative tumour of Cushing's syndrome isn't possible?
adrenalectomy with life long steroid replacement therapy
53
What is phaeochromocytoma?
Chromaffin cell tumour > secrete adrenaline + noradrenaline
54
What is a paraganglioma?
extra-adrenal pheochromocytoma
55
Characteristics of phaeochromocytoma
- severe hypertension - headaches - palpitations - excessive sweating - weight loss - anxiety + panic attacks
56
What can untreated phaeochromocytomas cause?
- hypertensive crisis - encephalopathy - hyperglycaemia - pulmonary oedema - cardiac arrhythmias
57
Investigations of phaeochromocytoma
- **24-hour urine metanephrines** - plasma free metanephrines - CT or MRI to look tumour - genetic testing incl. 1st degree relatives - MEN type II
58
What are metanephrines?
Breakdown product of adrenaline
59
Management of phaeochromocytoma
- **surgical excision** - **alpha blockers** *e.g. phenoxybenzamine or doxazosin* - **B blockers** when established on a blockers to reduce risk of hypertensive crisis
60
A patient presents with hypertension and hypokalaemia, what could the diagnosis be?
Hyperaldosteronism Cushing’s syndrome ?
61
Why does addisonian crisis cause hypoglycaemia?
- in healthy people, cortisol is produced by adrenal glands as stress response - increasing rate of hepatic gluconeogenesis, inhibits cellular uptake of glucose to maintain glucose levels + reducing cellular insulin sensitivity - in addisonian crisis there is a depletion of cortisol - the above mechanism of impaired > less glucose in blood > hypoglycaemia

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