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Endocrinology > Adrenals > Flashcards

Adrenals Flashcards

1
Q

What are the 3 zones of the adrenals and what do they produce?

A

GFR
Gets sweeter as you go deeper

Outer zone - zona glomerulus - produces aldosterone

Middle zone - zona fasiculata - produces cortisol

Inner zone - zone reticularis - produces sex steroids

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2
Q

Adrenal hormones are derived from …

A

Cholesterol

ACTH activates enzyme that converts cholesterol to pregnenolone –> aldosterone, cortisol, testosterone

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3
Q

Low aldosterone results in …

A

Lose Na+, lose water, hold onto K+ , hold onto hydrogen ions
= Hypovolaemia, hypotension, metabolic acidosis

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4
Q

Low cortisol results in …

A

Life threatening hypotension

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5
Q

What happens in CAH i.e. 21-hydroxylase deficiency?

A

21-hydroxylase deficiency –> defective conversion from 17-OHP to 11-deoxycortisol –> high 17-OHP –> high testosterone (shunt production towards testosterone)

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6
Q

How to diagnose CAH i.e. 21-hydroxylase deficiency?

A

High serum 17-OHP (screening test for suspected CAH)

ACTH stimulation test is gold standard confirmatory test
Give ACTH –> further rise in 17-OHP

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7
Q

What’s the difference between Classic adrenal hyperplasia and Non-classic adrenal hyperplasia?

A

Both are due to 21-hydroxylase deficiency

Classic adrenal hyperplasia

  • More severe form
  • 0% 21-hydroxylase activity –> 0 aldosterone and cortisol production. All production shunted towards testosterone.
  • Present in infancy with adrenal insufficiency and salt wasting. Females have ambiguous genitalia.

Non-classic adrenal hyperplasia

  • Less severe form and more common
  • 50% 21-hydroxylase activity –> reduced aldosterone and cortisol production and high testosterone
  • No salt wasting
  • Present in adolescent/young women as premature puberty, acne, hirsutism, irregular menses/amenorrhoea (similar to PCOS). Females have normal genitalia.
  • High serum 17-OHP + testosterone
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8
Q

What happens in 11-hydroxylase deficiency?

A

11-hydroxylase deficiency –> defective conversion from 11-deoxycorticosterone (weak mineralcorticoid activity) to corticosterone and 11-deoxycortisol (limited activity) to cortisol

Get overproduction of androgens

= females get ambiguous genitalia
= Hypernatraemia, hypokalaemia, hypertension due to increased mineralcorticoid activity from 11-deoxycorticosterone

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9
Q

How to diagnose 11-hydroxylase deficiency?

A

High serum 11-deoxycortisol
High androgens

If diagnosis is uncertain, can do ACTH stimulation test - would expect both to go up

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10
Q

Rx 11-hydroxylase deficiency

A

Cortisol replacement

Antihypertensives

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11
Q

Are adrenal masses generally benign?

A

Yes
Increases with age
Common incidental finding
Usually don’t produce hormones

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12
Q

What do we worry about when we see bilateral adrenal masses?

A

Metastasis

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13
Q

DDx adrenal masses

A

Adrenal adenomas - 75% non-functioning
Pheochromocytoma
Adrenal corticoid carcinoma
Metastasis

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14
Q

What characteristics in an adrenal mass point towards it being benign?

A

Small, usually ≤3cm, ≥6cm needs investigation

Homogenous texture, ≤10 housefield units tend to be benign. >10HU more likely to be ACC, pheo, mets

Round/oval, smooth margins

Usually solitary, unilateral (bilateral suggests mets)

Minimally vascular on CT (ACC, pheo, mets usually vascular)

High washout rate (compaerd to ACC, pheo, mets)

Isointense in relation to liver on MRI (others are hyperintense)

No necrosis, haemorrhage or calcification

Stable or very slow growth

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15
Q

What investigations might you do for an adrenal mass?

A

Non-contrast CT adrenals

1mg dexamethasone suppression test - give 1mg dex the night before then check cortisol at 8am. If high cortisol, it means the adrenal is producing it without ACTH

Aldosterone renin ratio - high aldosterone and suppressed renin tell us the adrenals are producing aldosterone on their own

Fasting plasma metanephrines - to exlude pheo

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16
Q

Should we biopsy adrenal masses?

A

No

Due to risk of spread if adrenal corticoid carcinoma

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17
Q

What tests to do in bilateral adrenal hyperplasia?

A

Serum 17-hydroxyprogesterone

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18
Q

When to do an adrenalectomy when there is an adrenal mass?

A

Suspect malignancy or if there is cortisol excess

Unilateral >6cm size
If 4-6cm, may choose to monitor growth every 6-12 months and consider surgery if growth is fast.

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19
Q

High aldosterone leads to…

A

Holds onto Na+, water, loses K+, hydrogen ions

= hypervolemia, hypertension, hypokalaemia, metabolic alkalosis

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20
Q

Causes of primary hyperaldosteronism

A

Bilateral adrenal hyperplasia (most common)
Adrenal adenoma (Conn syndrome)
Adrenal corticoid carcinoma (rare)

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21
Q

What drugs can affect aldosterone renin ratio?

A

Any antihypertensives (works by volume depletion or vasodilation) –> increase renin

Low potassium –> decreases aldosterone
High potassium –> increases aldosterone

Aldosterone antagonists e.g. spironolactone, amiloride, epleronone

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22
Q

How does AKI affect aldosterone renin ratio?

A

AKI –> fluid and salt retention –> decrease renin

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23
Q

What’s the seated saline suppression test?

A

Give sodium loading –> expect aldosterone to go down –> if it doesn’t, you know its autonomous production = primary aldosteronism

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24
Q

What’s adrenal venous sampling and when do you do it?

A

Insert catheter through groin –> to left and right adrenal vein –> measure cortisol and aldosterone

Tells us which adrenal gland is the problematic one or whether its both

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25
Q

Right adrenal vein drains into….

Left adrenal vein drains into….

A

Right adrenal vein drains into IVC

Left adrenal vein drains into left renal vein

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26
Q

Rx primary aldosteronism

A

Aldosterone antagonist - spironolactone, epleronone, amiloride

Adenomas are usually surgically resected

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27
Q

Prognosis of adrenal corticoid carcinoma

A

Poor

5 year survival <15%

28
Q

How does adrenal corticoid carcinoma present?

A

1) Excess hormones
Usually 2+ hormones
Cortisol > androgens

2) Flank mass/pain

3) Incidental finding on imaging
- Very big - >6cm
- Heterogenous

29
Q

Rx adrenal corticoid carcinoma

A

1) Surgical resection

2) Mitotane
- Causes adrenal necrosis
- Improves survival and recurrence

3) Chemotherapy
- Slightly better progression of disease but no effect on survival

30
Q

Causes of secondary hyperaldosteronism

A

Renal artery stenosis
Fibromuscular hyperplasia in young people
Atherosclerosis in old people

Renal artery stenosis –> activation of the juxtaglomerular apparatus –> release renin –> converts angiotensinogen to ACEI –> ACEII –> activate adrenal gland to release aldosterone

31
Q

What would you expect the renin and aldosterone to be in secondary hyperaldosteronism?

A

High renin and aldosterone

32
Q

What would you expect the renin and aldosterone to be in primary hyperaldosteronism?

A

Low renin and high aldosterone

33
Q

When does cortisol level peak?

A

Morning

34
Q

Causes of high cortisol

A

Stress e.g. infection, trauma

Starvation/anorexic nervosa

Pregnancy

Alzheimer’s

Pseudocushing’s syndrome

Glucocorticoid resistance

Prenatal glucocorticoid excess

Pituitary tumour (Cushing’s disease)

Ectopic ACTH source e.g. small cell carcinoma

Adrenal tumour

Exogenous glucocorticoid

35
Q

What’s pseudocushing’s syndrome?

A

High cortisol but no tumour

Related to depression, ETOH excess or can be idiopathic

Lack of progression of Cushing’s features

36
Q

Clinical features of Cushing’s

A

Proximal muscle weakness

Moon facies, central adiposity, buffalo hump

Abdominal striae (>1cm pathognomonic for pregnancy or Cushing)

Hypertension + hypokalaemic + metabolic alkalosis (at very high levels, cortisol cross reacts with mineralcorticoid receptors)

Osteoporosis

Immunosuppression (late) especially prone to cellulitis

37
Q

Diagnostic approach to suspected Cushing’s disease

A

1) 24h urine cortisol or midnight salivary cortisol level or low dose dexamethasone test

2) Plasma ACTH
If low ACTH –> CT adrenals
If high ACTH
–> do high dose dexamethasone test (will tell us whether ACTH is coming from hypothalamus or ectopic)
–> CRH stimulation test - give CRH then measure ACTH and cortisol. Pituitary adenomas will respond by releasing more ACTH and cortisol. Ectopic source of ACTH and adrenal adenomas will not respond.
–> IPSS if both tests are inconclusive.

38
Q

What do you expect the adrenal glands to look like in excess exogenous glucocorticoids?

A

Bilateral adrenal atrophy (due to shut down of ACTH)

39
Q

What do you expect the adrenal glands to look like in ACTH secreting pituitary adenoma (Cushing’s)?

A

Bilateral adrenal hyperplasia

40
Q

What do you expect the adrenal glands to look like in ectopic ACTH secretion?

A

Bilateral adrenal hyperplasia

41
Q

What do you expect the adrenal glands to look like in primary adrenal adenoma?

A

One adrenal has adenoma/carcinoma
The other is atrophied (due to it being shut down by low ACTH)

OR

Bilateral adrenal hyperplasia

42
Q

Rx persistent Cushing’s

A

Irreversible options
Surgery

Radiotherapy

Mitotane

Reversible options 
Pasireotide 
Cabergoline 
Ketoconazole
Metyrapone
IV etomidate (emergency)
Mifepristone
43
Q

What happens in 17-hydroxylase deficiency?

A

Decreased androgens and cortisol

  • Primary amenorrhoea and lack of pubic hair in females
  • Pseudohermaphroditism in males

Get increased weak mineralcorticoid (11-DOC) –> hypertension, mild hypokalaemia. Low aldosterone.

44
Q

Rx for 21-hydroxylase deficiency

A

Mineralcorticoids

Glucocorticoids

45
Q

Rx for 17-hydroxylase deficiency

A

Glucocorticoids

Sex steroids

46
Q

Causes of adrenal insufficiency

A

Acute

  • Abrupt withdrawal of steroids
  • Adrenal haemorrhage
  • Pituitary problem (secondary adrenal insufficiency) - pituitary tumour, tumour of the hypothalamic-pituitary region, pituitary radiation, lymphocytic hypophysitis
  • Hypothalamus problem (tertiary adrenal insufficiency)

Chronic (Addison’s)

  • Autoimmune destruction (associated with other autoimmune disease such as Hashimoto’s thyroiditis)
  • TB, HIV
  • Metastatic carcinoma e.g. from lung
  • Congenital - congenital adrenal hypoplasia, ACTH resistance
47
Q

Clinical features of adrenal insufficiency

A

Low cortisol –> hypotension, weakness, diarrhoea, vomiting, abdo pain, hypoglycaemia

Postural hypotension is a very specific sign - drop BP, raised HR on standing

Low mineralcorticoids –> lose water, lose Na+, retain K+, keep hydrogen ions –> hypovolaemia, hyponatraemia, hyperkalaemia, metabolic acidosis

Features of high ACTH –> stimulates melanocytes –> hyperpigmentation (takes time)

48
Q

What clinical feature helps distinguish primary from secondary adrenal insufficiency?

A

Hyperpigmentation from too much ACTH (primary insufficiency)

49
Q

Rx adrenal insufficiency

A

1) hydrocortisone or cortisone or pred
- Don’t give dex as it doesn’t have mineralcorticoid effect.

2) Fludrocortisone
- Monitor electrolytes, renin

50
Q

Symptoms of adrenal crisis

A

Cardinal symptom is hypotension

Anorexia, nausea, vomiting, weakness, fatigue, abdo pain, diarrhoea, confusion, coma, fever

51
Q

Who gets adrenal crisis?

A

Undiagnosed people with adrenal insufficiency having an infection

People with adrenal insufficiency who fails to stress dose

Bilateral adrenal infarction/haemorrhage

52
Q

How much do you stress dose in someone with adrenal insufficiency who is unwell?

A

Triple dose for 3 days
- Hydrocortisone 100mg stat then 50mg Q6H until stable and tolerating oral intake

Particularly if there is infection, fever

If they can’t take tablet, then IM/SC hydrocortisone 100mg emergency injection kit (tie people over for 12 hours before they can present to ED) or prednisolone/hydrocortisone suppository

53
Q

Labs in adrenal crisis

A

Low sodium
High potassium
Low glucose
High calcium

54
Q

Autoimmune Addison’s disease is often associated with …

A

T1DM

55
Q

Adrenal medulla - its main function is …

A

Produces catecholamines (adrenaline and noradrenaline)

56
Q

Clinical features of pheochromocytoma

A

Due to increased serum catecholamines

Episodic HTN
Headache
Palpitations
Tachycardia 
Sweating
57
Q

How to diagnose pheochromocytoma?

A

Serum metanephrine (usually pretty good) or 24h urine metanephrine

If >2 fold elevation above ULN, localise with adrenal/abdominal MRI or CT +/- I-MIBG (nuclear med scan with iodine)

Consider genetic testing

58
Q

Rx pheochromocytoma

A

Pre-op preparation
Alpha blockade - phenoxybenzamine, prazosin

Beta blockade - propanolol, atenolol, labetalol

If possible, beta blockade must not be started in patients until alpha blockade has been established.
- Can cause dramatically elevated BP, due to unopposed alpha-adrenoreceptor stimulation

Then… Surgery

59
Q

What syndrome is pheochromocytoma associated with?

A

MEN2A and 2B
Neurofibromatosis type 1
Hippel-Lindau disease

60
Q

Why do we check cortisol in the morning?

A

Diurnal

Peaks at 8am

61
Q

Rx adrenal crisis

A

IV hydrocortisone 100mg then 50mg Q6H until stable + intravascular volume expansion

Hydrocortisone preferred as the 1st line therapy because at higher dose (>60-80mg), it also has mineralcorticoid effect, hence bypass the need to worry about starting fludrocortisone initially

62
Q

Rx CAH i.e. 21-hydroxylase deficiency

A

Glucocorticoid
Mineralcorticoid

New: gene therapy (coming)

63
Q

Adrenal incidentaloma DDx

A

Cortisol or aldosterone secreting adenoma (14%) - most common
Phaeochromocytoma (7%)
Adrenalcortical carcinoma or metastatic carcinoma (4%)

64
Q

Do all primary hyperaldosteronism cause hypokalaemia?

A

NO

30% have normal K

65
Q

What is the most common cause of primary aldosteronism related hypertension?

A

Bilateral idiopathic hyperplasia 60%

Aldosterone producing adenoma 30%

Endocrinology (9 decks)

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