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Endocrine > Adrenal > Flashcards

Adrenal Flashcards

1
Q

How is ACTH regulated

A

Supressed by glucocorticoids

Stimulated by CRH, ADH and proinflammatory cytokines

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2
Q

Where does ACTH act

A

binds to melanocortin receptor 2 in adenocortical cells

acts by g protein coupled mechanism to induce steroidgenesis

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3
Q

When is ACTH tested

A

Measure at time based on disease in question

  • Insufficiency –> test at 8am when should be at highest
  • excess –> test at any time, nadir in evening best
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4
Q

Symptoms of Cushing syndrome

A

Central obesity, buffalo hump, moon face
Skin atrophy, easy bruising, striae, hyperpigmentation
Androgen excess - hirsuitism, increased libido
Proximal muscle weakness (most specific)
Osteoporosis
Psychiatric - depression, anxiety, irritability
Glucose intolerance
Increase risk of CVD, VTE, infection

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5
Q

What is pseudo cushings

A 
Conditions which are associated with hypercortisolism in absence of cushings syndrome eg.
Pregnancy
Severe obesity
PCOS
Major depression
Poorly controlled diabetes
Chronic alcoholism
Physical stress - illness
Malnutrition
Anorexia
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6
Q

What is most common cause of Cushings syndrome

A

Exogenous glucocorticoids

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7
Q

How to diagnosis hypercortisolism

A

Requires 2 first line tests to be abnormal

24h urinary free cortisol - avoid in renal failure
Midnight salivary cortisol - avoid in shift workers
Low dose dex suppression test - avoid in OCP, pregnancy and antiepileptics (false positive due to increased CBG)

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8
Q

When do you perform inferior petrosal sinus sampling?

A

In assessment of ACTH dependent Cushings
Most definitive test to determine between ectopic and pituitary source

Remember MRI provides no functional information
Only picks up 50% of tumours and small tumours may be incidentalomas

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9
Q

Causes of ACTH dependent Cushings (normal or high ACTH)

A

Cushings disease - pituitary adenoma
Ectopic ACTH - most commonly small cell lung ca
Ectopic CRH - rare
Iatrogenic/factitious administration of exogenous ACTH

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10
Q

Causes of ACTH independent Cushings syndrome (low ACTH)

A

Primary adrenocortical adenoma
Primary pigmented nodular adrenocortical disease
Bilateral macronodular adrenal hyperplasia
Iatrogenic/factitious - most common
Ectopic cortisol - rare, from ovarian tumours

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11
Q

Medical management options for Cushings

A

Consider if surgery delayed/contraindicated or unsuccessful
Ketoconazole - inhibits several steps of steroidgenesis
Metyrapone - inhibits 11B hydroxylase, step in cortisol synthesis
Mitotane - cytotoxic, used in adrenal carcinoma
Mifepristone
Pasireotide

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12
Q

Causes of secondary adrenal insufficiency

A

Exogenous withdrawal of glucocorticoids
Panhypopituaritism
Isolated ACTH deficiency - rare (autoimmune, genetic, medication related)

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13
Q

What are the zones of the adrenal cortex and what do they produce?

A

Zona glomerulosa - aldosterone
Zona fasciculata - cortisol
Zona reticularis - androgens

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14
Q

What parts of the adrenal cortex are under pituitary control?

A

Production of glucocorticoids and androgens

** Mineralocorticoids are regulated by renin angiotensin aldosterone system, not significantly affected by pituitary axis

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15
Q

How to test for glucocortioid excess

A

Dexamethasone suppression test

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16
Q

How to test for glucocorticoid deficiency

A

ACTH stimulation test

Insulin tolerance test - hypoglycaemia is strong stress signal to activate HPA axis

17
Q

How to test for mineralocorticoid excess

A

Renin and aldosterone levels

Load with Saline should suppress aldosterone

18
Q

How to test for mineralocorticoid deficiency

A

Renin activity will be increased

19
Q

Why is aldosterone not under ACTH controll

A

The zona glomerulosa is only zone that has CYP11B2 which is required for conversion of deoxycorticosterone to aldosterone

If it was expressed in other zones then aldosteone would be under control of ACTH - as seen in glucocorticoid remediable aldosteronism

20
Q

How does cortisol work

A

Binds to glucocorticoid receptrs
Acts on nucleus to enhance transcription of genes
Forms complexes which suppress proinflammatory genes

21
Q

How does aldosterone work

A

Binds to mineralocorticoid receptor in DCT
Increases transcription of ENaC
Increased trafficking of ENaC to luminal surface where it increases Na reuptake

22
Q

Causes of mineralocorticoid excess

A

Primary hyperaldosteronism
- adrenal adenoma, micronodular hyperplasia and glucocorticoid remediable aldosteronism
Syndrome of apparent mineralocorticoid excess
Autonomous DOC secretion for adenocarcinoma
Congenital adrenal hyperplasia
Progesterone induced
Liddles syndrome

23
Q

Manifestations of mineralocorticoid excess

A

Hypertension - due to increased Na retention
Hypokalaemia - due to depletion
Metabolic alkalosis - due to H depletion

24
Q

How to confirm primary hyperaldosteronism

A

High plasma aldosterone level
Low Plasma renin level
Aldosterone:renin ratio high - greater than 555
Saline infusion test - fail to suppress aldosterone to less than 140
CT adrenal glands
Adrenal vein sampling - if older age (as higher likelihood of incidentaloma) or CT unclear

** If both renin and aldosterone are low
= look for cause of apparent mineralocorticoid excess and test urinary steroid metabolites

25
Q

Management of mineralocorticoid excess

A

Adrenalectomy
Aldosterone antagonist if not surgical candidate

If Liddles syndrome - use amiloride

26
Q

What is glucocorticoid remediable aldosteronism

A

Chimeric gene mutation crossover of CYP11B 1/2 genes which brings aldosterone under ACTH control

Consider if patients with family hx, young age and normal CT

Treat with dexamethasone - to suppress ACTH

27
Q

Approach to adrenal incidentaloma

A

Screen for hormone excess
- plasma metanephrines, cortisol tests, renin/aldosterone levels

CT to assess image phenotype
- benign suggested by size less than 3cm, attenuation less than 10 hounsfield units, contrast washout greater than 50% at 10mins

If hormone secreting, suspicious appearance or larger than 6cm, then consider adrenalectomy

28
Q

Features of primary adrenal insufficiency

A

Glucocorticoid deficiency - fatigue, weight loss, fever, myalgia, low BP, anaemia, hyponatraemia

Mineralocorticoid deficiency - abdo pain, nausea, vomiting, low BP, low Na, high K

Androgen deficiency - lack of energy, decreased libido, decreased hair growth

Hyperpigmentation - due to high ACTH causing stimulation of melanocytes

Note: hypoglycaemia not common in primary, more common in secondary

29
Q

How to diagnosis primary adrenal insufficiency

A

Early morning cortisol less than 80
Short synacthen test - cortisol less than 550

Primary = high ACTH, high renin, low aldosterone
Secondary = low/normal ACTH, normal renin, normal aldosterone
30
Q

Tests looking for cause of primary adrenal insufficiency

A

Adrenal autoantibodies - suggests autoimmune adrenalitis or autoimmune polyglandular syndrome

CT adrenal gland - look for infection, haemorrhage, infiltration, hyperplasia

Serum 17OH progesterone - looking for CAH

Very long chain fatty acids - X linked adrenoleukodystrophy

31
Q

Treatment of adrenal insufficiency

A

Hydrocortisone approx 20mg/day split to mimic diurnal rhythm (10-5-5)

Mineralocorticoid replacement required if hydrocortisone dose is less than 50mg (as otherwise has its own mineralocorticoid activity)

Patient education
- double dose if unwell for 3 days, need IV treatment if vomiting/surgery/trauma

32
Q

Most common mutation in CAH

A

21 hydoxylase deficiency (21OH) - causes 90-95% of CAH

Low glucocorticoid and mineralocorticoid hormones and raised ACTH which drives increased androgen synthesis

33
Q

Types of 21OH congenital adrenal hyperplasia

A

Severity of mutation dictates disease type

Classical (severe) - neonatal presentation, salt wasting crisis, severe virilization

Simple virilizing (moderate) - genital ambiguity, childhood presentation, precocious puberty, advanced bone age

Non classical (mild) - hirsuitism, oligomenorrhoea, acne, infertility, adolescent presentation

34
Q

How to diagnoses CAH

A

Measure serum or urinary steroid metabolites as they accumulate at site of enzyme block

In 21OH deficiency
- high 17OH progesterone and urinary preganetriol

Endocrine (6 decks)

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