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Endocrine System > Adrenal Disorders > Flashcards

Adrenal Disorders Flashcards

1
Q

What hormones does the medulla produce?

A

Norepinephrine and epinephrine

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2
Q

What is the common approach for endocrine symptoms?

A

Clinical suspicion - test for assessing functional status - aetiology - if tumour - endocrine deficiency correction

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3
Q

Describe the hypathalmo- hypopituitary axis

A

If under stress the hypothalamus produces CRH which acts on anterior pituitary to stimulate ACTH
This stimulates adrenal gland to release cortisol
There is a short and long negative feedback loop

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4
Q

What enzyme is important in producing cortisol and aldosterone?

A

21-hydroxylase

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5
Q

What are 3 adrenal disorders leading to hypofunction?

A

Adrenal destruction - most common
Adrenal Dysgenesis
Impaired steroidogenesis

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6
Q

What disease causes primary adrenal insufficiency?

A

Addison’s disease - autoimmune destruction, invasion, infiltration, infection, iatrogenic

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7
Q

What causes adrenal enzyme defects?

A

Congenital adrenal hyperplasia - 21 hydroxylase deficiency

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8
Q

Describe autoimmune Addison’s disease

A

Positive adrenal autoantibodies
Lymphocytic infiltrate of adrenal cortex
Associated autoimmune diseases are common
More than 85% of adrenal failure

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9
Q

What are some common symptoms associated with primary adrenal failure?

A

Weakness, fatigue, weight loss
Skin pigmentation or vitiligo
Hypotension
Unexplained vomiting and diarrhoea
Salt craving
Postural symptoms

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10
Q

What are some possible clue to diagnosis of adrenal failure?

A

Disproportional between severity of illness and hypotension/ dehydration
Unexplained hypoglycaemia
Other endocrine features
Previous depression or weight loss

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11
Q

How is adrenal insufficiency diagnosed?

A

Bloods - U+E, glucose and FBC (low Na and high K)
Random cortisol (>450nmol/l adrenal status uncertain)
Synacthen test - 250mg of tetracosactin IM or IV (ACTH)

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12
Q

What tests should be done is adrenocortical insufficiency suspected?

A

Rapid ACTH stimulation test
If normal then excludes primary
If abnormal then Plasma ACTH
If elevated then primary
If supressed then secondary

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13
Q

Describe glucocorticoid replacement

A

Hydrocortisone (20-30mg), prednisolone and dexamethasone
Given in divided doses to mimic normal diurnal variation - more given in morning

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14
Q

Describe mineralocorticoid replacement

A

Synthetic steroid - fludrocortisone
Binds to mineralocorticoid (aldosterone) receptors
50-300 mg daily
Adjust dose according to clinical status, U+E and plasma renin level

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15
Q

Who needs special care when treating hypofunction?

A

Hypo-adrenal patients on replacement steroids
Patients on steroids
Patients who have received previous 18/12 treatment

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16
Q

What happens to treatment if minor short lived illness or stress?

A

Double glucocorticoid dose

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17
Q

What happens to treatment if major illness or operation?

A

100mg hydrocortisone IV stat
50-100 HC via IV every 8hrs

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18
Q

What are the 3 self acre rules for patients on steroids?

A

Never miss steroid dose
Double hydrocortisone dose in event of intercurrent illness
If severe vomiting or diarrhoea then call for help

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19
Q

What are some causes of primary hyperaldosteronism?

A

Unilateral adenoma and bilateral hyperplasia

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20
Q

What are some rarer endocrine causes for hypertension?

A

Pheochromocytoma, Cushing’s, acromegaly, hyperparathyroidism, hypothyroidism and congenital adrenal hyperplasia

21
Q

What causes hypersecretion from cortex of adrenal gland?

A

Cushing’s syndrome - cortisol and androgens
Conn’s syndrome - aldosterone

22
Q

What is a cause of hypersecretion from medulla of adrenal gland?

A

Pheochromocytoma - catecholamines

23
Q

What are the side effects of Cushing’s syndrome?

A

Weakness of skin, muscle and bone
Hypertension and heart failure
Diabetes mellitus

24
Q

Describe Cushing’s syndrome

A

Excess corticosteroids
Cortisol is a catabolic hormone so can cause tissue breakdown, sodium retention and insulin antagonism
Also immune system suppression

25
Q

What are some signs of Cushing’s syndrome?

A

Central obesity, proximal weakness, easy bruising, hypertension, purple striae, oedema, thin skin, and moon face

26
Q

What can cause ACTH dependant or independent Cushing’s disease?

A

Dependent - pituitary tumour or ectopic ACTH secretion
Independent - adrenal tumour

27
Q

What is the approach to hypersortisolism?

A

Overnight Dex test or 24hr urine free cortisol to screen and confirm
To see if ACTH dependent - paired morn midnight ACTH cortisol
To see if pituitary or not then high Dex test
MRI and CT for localisation

27
Q

What is the normal range for 24hr urinary free cortisol?

A

14-135 nmol/24hr

28
Q

What is the treatment for Cushing’s syndrome?

A

Surgery to remove causative tumour
Medical
RT
Bilateral adrenalectomy

29
Q

What is the medical treatment for Cushing’s syndrome?

A

Adrenal hormone synthesis inhibitors - ketoconazole and Metyrapone
Destroy adrenocortical cells - mitotane

30
Q

Describe Conn’s syndrome

A

Aldosterone excess production
Adenoma or bilateral hyperplasia
Aldosterone - water and sodium retention and K excretion

31
Q

Describe the pathophysiology of primary hyperaldosteronism

A

Aldosterone producing tumour increases blood volume, blood pressure and urine K+
Renin gives angiotensinogen then angiotensin I then II
So increased Aldosterone and decreased renin

32
Q

What is the screening for hyperaldosteronism?

A

Plasma PA/PRA ration
Primary hyperaldosteronism - Ratio is over 20
Secondary or essential - Ratio is under 20

33
Q

What are 2 signs of hyperaldosteronism?

A

Hypertension and hypokalaemia

34
Q

What does decreased plasma renin activity and increased aldosterone conc. suggest?

A

Primary hyperaldosteronism

35
Q

What does increased PRA and PAC suggest?

A

Secondary hyperaldosteronism

36
Q

What does decreased PRA and PAC suggest?

A

Congenital adrenal hyperplasia
Cushing’s syndrome
DOC producing tumour

37
Q

What is the conformation test for hyperaldosteronism?

A

24hr urine aldosterone . 12 ug/day
Urinary sodium >200mEq
During 4 days of salt loading

38
Q

What tests help to establish aldosterone source?

A

CT scan of adrenal glands
Upright posture test
Plasma 18-hydroxycorticosterone

39
Q

Describe pheochromocytoma

A

Rare tumour of adrenal glands producing too much catecholamines - norepinephrine and epinephrine
Get hypertension, headache, sweating, palpitations, tremor, pallor and anxiety (paroxysmal attacks)

40
Q

What are some types of pheochromocytoma?

A

MEN II
MEN III
Von Hippel Landau Syndrome

41
Q

How is a suspected pheochromocytoma investigated?

A

24 hr urine - total metanephrines and catecholamines
If normal then re check later
If 2 fold elevation then CT/MRI for localisation
Also consider 123-IMIBG scan

42
Q

What is tested for in pheochromocytoma - genetic testing?

A

PHEOs/ PGLs - this leads to the metabolic problem giving tumour growth

43
Q

What is the preoperative preparation for removal of pheochromocytoma?

A

Non selective alpha blocker
Beta blockers may also be needed
When trying to take tumour out - if touched could release large amounts of catecholamines into bloodstream

44
Q

What test should be done if there is clinical suspicion of adrenal mass?

A

Free metanephrine in plasma or urine
1mg Dexamethasone suppression test
If hypertension then K and ALD/PRA ratio

45
Q

How is an adrenal mass tested to see if malignant or benign?

A

Unenhanced CT
Chemical shift MRI
Then delayed enhanced CT
Surgery if malignant and if benign surgery depends on size (>6cm)

46
Q

Why does a deficit in 21-hydroxylase cause adrenal hyperplasia?

A

Lack of enzyme inhibits synthesis of cortisol
So removes negative feedback on ACTH and CRH
Increased ACTH secretion is responsible for enlargement

47
Q

Describe congenital adrenal hyperplasia

A

90% of cases are 21 hydroxylase deficiency
Severe cases - neonatal salt losing crisis and ambiguous genitalia
Incomplete - hirsutism and pseudo-precocious puberty

Endocrine System (23 decks)

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