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Diabetes and Endocrinology YR3 > The Adrenal Gland Lecture > Flashcards

The Adrenal Gland Lecture Flashcards

1
Q

Anatomy of adrenal gland

A
  • 4-5g
  • 90% is cortex surrounding medulla
  • Arterial supply from renal arteries, aorta and inferior phrenic artery
  • Venous drainaing right –> IVC, left –> left renal vein

Venous drainage important to note for sampling

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2
Q

3 zones of cortex

A
  • Zona glomerulosa
  • Zona fasiculata
  • Zona reticularis

GFR

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3
Q

What does each zone produce?

A
  • G - mineralocorticoids (salt) Aldosterone under RAAS control
  • F - glucocorticoids (sugar) cortisol under ACTH control
  • R - androgens (sex) DHEA and andronstenedione under ACTH control
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4
Q

Significance of aldosterone not being under ACTH control

A

If have pituitary problem, aldosterone will not need to be replaced as won’t be affected

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5
Q

Normal amount of aldosterone and cortisol and DHEA daily

A
  • Aldosterone 100-150mcg/day
  • Cortisol - 10-20mg/day
  • DHEA - 10mg/day
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6
Q

Causes of mineralocorticoid deficiency

A
  • Congenital eg congenital adrenal hyperplasia 21-hydroxylase deficiency

Acquired:
* primary adrenal insuffiency,
* secondary due to low renin in renal tubular acidosis (diabetes)
* Drug induced eg heparin, ciclosporin

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7
Q

Treatment for mineralocorticoid deficiency

A

Fludrocortisone 50-100mcg / day

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8
Q

Cautions with fludrocortisone

A
  • Can cause fluid overload - HF caution
  • Can cause hypokalaemia
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9
Q

Adrenal insufficiency causes

A
  • Addisons
  • Congenital adrenal hyperplasia
  • Secondary - hypothalamic or pituitary dysfunction
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10
Q

Causes of primary adrenal insufficiency - acquired

A
  • Autoimmune
  • Malignancy (mets or lymphoma)
  • Infiltration - sarcoidosis, amyloidosis
  • Infection - TB, fungal, HIV
  • Vascular - haemorrhage, meningococcal septicaemia
  • Infarction - thrombosis
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11
Q

Causes of congenital primary AI

A
  • CAH
  • CLAH
  • Triple A syndrome
  • X linked adrenal leukodystrophy
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12
Q

Causes of primary AI iatrogenic

A
  • Bilateral adrenalectomy
  • Drugs - etomidate, ketoconazole, mitotane
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13
Q

Causes of secondary AI - more common than primary

A
  • Tumours
  • Infection
  • Infiltation
  • Isolated ACTH deficiency
  • Exogenous steroid use suppressing axis
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14
Q

Clinical features of AI - primary

A
  • Anorexia
  • Weight loss
  • Tiredness
  • Weakness
  • Hyperpigmentation
  • Dizziness and postural hypotension
  • N+V
  • Abdo pain
  • Arthralgia
  • Myalgia
  • Reduced libido and pubic hair
  • Salt craving
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15
Q

Secondary AI clinical features

A
  • Same as primary
  • BUT no hyperpigmentation as there is no increased ACTH to cause this - no mineralocorticoid deficiency
  • Low ACTH is the problem in secondary remember
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16
Q

Investigation for AI - findings

A
  • Hyponatraemia
  • Hyperkalaemia
  • Elevated urea
  • Anaemia
  • Eosinophilia
  • Hypercalcaemia (mild)
  • Hypoglycaemia
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17
Q

Investigations for AI

A
  • 9am cortisol (should be peak)
  • ACTH
  • TFTs
  • Short synacthen test
  • Renin - increased in primary
  • Adrenal antibodies
  • CT scan +/- biopsy?
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18
Q

What is SST?

A
  • 9am cortisol bloods
  • Administer ACTH
  • Do bloods 30mins and 60 mins after
  • Cortisol should double
19
Q

Treatment for AI

A
  • Glucocorticoid - hydrocortisone BD/TDS
  • Mineralocorticoid - Fludrocortisone
  • DHEA replacement? - not usually needed
20
Q

Advice for someone on replacement for AI

A
  • Sick day rules - double steroid dose
  • Steroid card
  • Emergency pack -has IM hydrocortisone if adrenal crisis, go to hospital if inject
21
Q

Management of adrenal crisis

A
  • O2
  • IV access
  • Fluids 0.9% NaCl
  • Dextrose in cases of hypoglycaemia
  • Hydrocortisone IV 100mg bolus then every 6hrs for 24-48hrs (then titrated down)
  • Fludrocortisone when HC dose less than 50mg

Be mindful of chronic hypoNa - no more than 10-15mmol/L in 24hrs

22
Q

Presentation of adrenal crisis

A
  • Hyponatraemia
  • Hyperkalaemia
  • Hypoglycaemia
  • Shock
23
Q

When to investigate for secondary causes of HTN?

A
  • If less than 40
  • Resistant to medication
  • Hypokalaemia
24
Q

Causes of mineralocorticoid excess

A
  • Primary aldosteronism (Conns - adenoma, bilateral hyperplasia, GRA)

-

  • Secondary - RTA, renovascular, cirrhosis, CHF, nephrotic syndrome, renin secreting tumour (all increases renin)

Other:
* Liqourice
* Ectopic ACTH
* Exogenous

25
Q

Most common cause primary hyperaldosteronism

A

Bilateral hyperplasia

26
Q

What is GRA?

A

Glucocorticoid-remediable Aldosteronism
When ACTH activates aldosterone instead of RAAS

27
Q

Presentation of hyperaldosteronism

A
  • Under 40
  • Resistant hypertension
  • Hypokalaemia
28
Q

Investigations for hyperaldosteronism

A
  • Aldosterone renin ratio
  • Saline infusion - usually suppresses
  • Fludrocortisone suppression
  • Captopril supression
  • Genetic testing if GRA
  • Localise - CT/MRI, adrenal venous sampling, radiolabelled sampling
29
Q

Things that can effect aldosterone renin ratio

A
  • Beta blockers can cause false +ve
  • ACEi can cause false -ve
  • Spironolactone needs to be stopped 4-6 weeks prior test
30
Q

Treatment primary hyperaldosteronism

A
  • Surgery - laparascopic adrenalectomy
  • Medical - mineralocorticoid receptor antagonists eg spironolactone, eplerenone
31
Q

GRA management

A
  • Low dose dexamethasone - suppress the ACTH
32
Q

Causes of Cushings syndrome ACTH independent

A
  • Adrenal adenoma
  • Adrenal carcinoma
  • Bilateral micro/macronodular hyperplasia
33
Q

Associated features of Cushings syndrome - systemic

A
  • HTN
  • DM
  • Osteoporosis
  • Recurrent infections
34
Q

Investigations for Cushings syndrome

A
  • 24hr urine free cortisol - x2
  • Overnight dexamethasone suppression test
  • Salivary cortisol
  • Midnight cortisol
  • Low dose DMT or HDDT
  • ACTH, serum K, CRH
  • CT adrenal if points to this

Step1 - find raised cortisol, step 2 check ACTH, step 3 adrenals

35
Q

Treatment for Cushings syndrome adrenal

A
  • Adenoma - unilateral adrenalectomy
  • Carcinoma - surgery, chemo, adrenolytic agents
  • Bilateral hyperplasia - bilateral adrenalectomy
36
Q

What is phaechromocytoma?

A
  • Tumour arising from adrenal medulla
  • 10% bilateral, 10% FH, 10% malignant
37
Q

When to screen for phaechromocytoma?

A
  • Young pts with HTN
  • Adrenal incidentaloma
  • Unexplained HF
  • Hypertensive crisis during general anaesthesia
38
Q

Gene mutations associated with phaechromocytoma

A
  • Multiple endocrine neoplasia (MEN)
  • VHL - Von Hippel Lindau
  • NF - neurofibromatosis
  • SDH - tumour supressor mutation
  • MAX
  • TMEM
39
Q

Investigation for phaechromocytoma

A
  • 24hr urine catacholamines/metanephrines
  • Plasma metanephrines (more sensitive, less specific)
  • Localise - CT, MRI, MIBG, FDG PET
40
Q

Management of phaechromocytoma

A
  • Alpha blockade (FIRST) eg Phenoxybenzamine
  • Beta blockage
  • Monitor BP, haematocrit and fluid status
  • Surgical resection when stable
41
Q

Management of phaechromocytoma crisis

A
  • ICU admission
  • Ventilation may be needed due to extreme hypoxia
  • Alpha blockade with phenoxybenzamine and prazosin
  • Correct IV volume - IV fluids and high salt
  • Beta blockade after adequate alpha
  • Surgical removal
42
Q

Why alpha blockade before beta?

A

Avoid unapposed alpha adrenergic activity

43
Q
A

Diabetes and Endocrinology YR3 (28 decks)

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