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5. Endocrinology > 16. Adrenal gland disorders > Flashcards

16. Adrenal gland disorders Flashcards

1
Q

What is adrenal insufficiency?

A

Adrenocortical insufficiency resulting in a reduction of mineralocorticoids, glucocorticoids and androgens.

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2
Q

Give 5 primary causes of adrenal insufficiency.

A
  1. Addison’s disease (autoimmune destruction of the adrenal cortex)
  2. Congenital adrenal hyperplasia (CAH)
  3. TB
  4. Adrenal metastases (lung, breast, kidneys)
  5. Drugs
  6. Adrenal haemorrhage
  7. Infection / opportunistic HIV infection (CMV, M. avium)
  8. Lymphoma
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3
Q

What is the commonest cause of primary adrenal insufficiency?
(common exam question!)

A
  1. Worldwide = TB
  2. In UK = Addison’s Disease (autoimmune adrenalitis)
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4
Q

Give 3 secondary causes of adrenal insufficiency.

A
  1. Hypopituitarism (damage to pituitary - low ACTH)
  2. Withdrawal from long term steroids.
    - Long-term steroid therapy suppressing the pituitary-adrenal axis - becomes apparent when steroids are withdrawn.
  3. Infiltration.
  4. Infection.
  5. Radiotherapy.
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5
Q

What is the affect of hypopituitarism on cortisol and ACTH levels?

A
  • Cortisol is low.
  • ACTH is low.
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6
Q

Give a tertiary cause of adrenal insufficiency.

A

Hypothalamus - low CRH
- Long term steroid use
- Withdrawal from steroids

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7
Q

Addison’s disease is describe as adrenal insufficiency - which part of the adrenal gland is destroyed? What hormones are affected?

A

The adrenal cortex.

Decreased production of mineralocorticoids (aldosterone), sex steroids and glucocorticoids (cortisol).

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8
Q

Give 6 signs + symptoms of adrenal insufficiency.

A
  1. Fatigue and tiredness
  2. Hypotension + postural hypotension + syncope
  3. Hyponatramia
  4. Hyperkalaemia
  5. Hypoglycaemia
  6. GI problems e.g. abdominal pain, nausea, vomiting,
  7. Weight loss + anorexia - thin appearance
  8. Hyperpigmentation - tanned
  9. Psychiatric symptoms e.g. confusion, depression, low self esteem, tearfulness
  10. Vitiligo and loss of body hair on females
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9
Q

Why does hypotension occur in adrenal insufficiency?

A

Decreased glucocorticoids
Decreased vascular responsiveness to Angiotensin II and Norepinephrine

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10
Q

Why does hyponatraemia occur in adrenal insufficiency?

A

Mineralcorticoid deficiency
Sodium ion loss
Decreased volume due to increased ADH secretion secondary to decreased cortisol

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11
Q

Why does hyperpigmentation occur in adrenal insufficiency?

A

ACTH stimulation of melanocyte activity

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12
Q

State whether Na+ and K+ levels would be high or low in someone with adrenal insufficiency.

A
  • Hyponatraemia -> Decreased Na+
  • Hyperkalaemia -> Increased K+

Lack of aldosterone
Less sodium is reabsorbed
Less potassium is excreted

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13
Q

What is Addison’s disease commonly misdiagnosed as?

A

Viral infection
or
Anorexia nervosa

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14
Q

Investigations for diagnosis of Addison’s disease

A

1) Bloods -> FBC & U+E
- ↓Na+ and ↑K+ -> due to ↓ aldosterone
- ↑Ca2+
- ↑Urea
- Adrenal cortex antibodies -> done secondary
- 21-hydroxylase adrenal antibodies -> done secondary

2) ↓ Glucose

3) Short Synactin (ACTH) stimulation test

  1. Measure cortisol - baseline
  2. Give IV/IM synthetic ACTH in the morning and measure cortisol again - 30 mins + 60 mins after
    = In healthy: should be double x2 = adrenal glands are healthy
  3. Positive for Addison’s if the cortisol decreases
    = Either the same as baseline or less than double
  4. Addison’s is excluded if cortisol after is > 550 nmol/L

4) Measure ACTH - on a different day:
- Primary cause: ACTH high -> Then: CT abdomen
- Secondary cause: ACTH low -> MRI brain

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15
Q

Would you observe decreased or increased levels of renin in primary adrenal insufficiency?

A

Elevated renin in primary

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16
Q

What is the affect of primary adrenal insufficiency on cortisol and ACTH levels?

A
  • Cortisol is low.
  • ACTH is high.
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17
Q

Test for autoimmune Addison’s disease

A

21-hydroxylase adrenal autoantibodies will be +ve

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18
Q

An adrenal crisis is a common presentation of adrenal insufficiency. Give 3 features of an adrenal crisis.

A

Can happen if adrenal insufficiency is so bad OR remove steroids too quickly:

  1. Severe Hypotension + dehydration
  2. Abodminal pain and vomiting
  3. Skin hyperpigmentation
  4. Fatigue
  5. Fever
  6. Hypoglycaemia
  7. Hyponatraemia
  8. Hyperkalaemia
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19
Q

Treatment for an acute flare-up of Addison’s and in the long-term

A

Acute:
Hormone replacement - IM hydrocortisone
IV saline

Chronic:
Hydrocortisone and fludrocortisone
Patient should carry a steroid card/bracelet

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20
Q

Give 3 sick-day rules for an adrenal crisis.

A
  1. Always carry 10 x 10mg tablets hydrocortisone and CARD IF go into hospital.
  2. If unwell with fever or flu-like illness, take double dose of steroids
  3. If in doubt, double dose of steroids
  4. If vomiting or increasingly unwell, take emergency injection
    of hydrocortisone 100mg IM (SC)
  5. If unable to have injection, take hydrocortisone 20mg and
    repeat if vomit
  6. Go to emergency room / ring ambulance
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21
Q

What is Cushing’s syndrome?

A

Clinical state of signs/symptoms.
As a result of chronic glucocorticoid excess.
Loss of normal feedback mechanisms of the HPA-axis.
Loss of circadian rhythm of cortisol secretion.

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22
Q

What is Cushing’s disease?

A

A set of signs/symptoms resulting from inappropriate ACTH secretion from the pituitary.

ACTH dependent.

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23
Q

What are the 2 classes of Cushing’s syndrome?

A
  1. ACTH-dependent
    - Increased circulating ACTH from a pituitary / ectopic tumour with glucocorticoid excess
  2. ACTH-independent
    - Primary excess of cortisol secretion by an adrenal tumour or nodular hyperplasia with ACTH suppression
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24
Q

Give 3 causes of Cushing’s syndrome.

A
  1. Adrenal Tumour (adenoma or carcinoma).
  2. Pituitary tumour (Cushing’s disease).
  3. Exogenous steroids.
  4. Ectopic ACTH syndrome.
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25
Q

Give 2 ACTH-dependent causes of Cushing’s syndrome.

A
  1. Cushing’s disease
  2. Ectopic ACTH production
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26
Q

Give 2 ACTH-independent causes of Cushing’s syndrome.

A
  1. Adrenal adenoma/cancer
  2. Adrenal nodular hyperplasia
  3. Iatrogenic - STEROIDS
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27
Q

What is the main cause of Cushing’s syndrome?

A

Oral steroids

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28
Q

Give 3 signs of Cushing’s syndrome.

A
  1. Central obesity, moon face and buffalo hump
  2. Skin and muscle atrophy - muscle thinning -> proximal limb wasting (thin legs)
  3. Bruising
  4. Purple abdominal striae (stretch marks)
  5. Osteoporosis
  6. Pigmentation (in ACTH-dependent causes)
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29
Q

Give 3 symptoms of Cushing’s syndrome.

A
  1. Mood change - depression, lethargy, irritability, psychosis
  2. Weight gain
  3. Hypertension
  4. Loss of libido (if cause is hypopituitarism)
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30
Q

Investigations for suspected Cushing’s syndrome.

A
  1. Overnight (or 48 HR) low dose dexamethasone suppression test (DST):
    = do it to see if it’s primary or secondary cause
  • Negative result: Cortisol = low - Normal
  • Positive result: Cortisol = normal/high - Cushing’s Syndrome

If positive:
2. High dose dexamethasone suppression test (8 mg) + Test ACTH (in the morning):
- Cortisol low = Cushing’s Disease

  • Cortisol high + ACTH is high = Cushing’s Syndrome with Ectopic ACTH
    -> suggests ACTH-dependent cause - most likely from a lung tumour causing high cortisol - and warrants HDDT
  • Cortisol high + ACTH is low = Cushing’s Syndrome with adrenal adenoma
    -> suggests ACTH-independent -> warrant CT on adrenals -> adrenal tumor likely

Secondary investigations:
So if Cushing’s -> MRI of the brain
If ACTH low = Cushing’s syndrome -> CT abdomen
If ACTH high = Ectopic -> CT chest

  1. Late night salivary cortisol:
    - Loss of circadian rhythm
  2. 24 HR urinary free cortisol is raised
    - High (x3) should be high in 2/3 samples
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31
Q

Why would you not test for Cushing’s syndrome by taking random plasma cortisols?

A

Can be misleading - variation due to illness, time of day, and stress (e.g. venepuncture!)

32
Q

Management of Cushing’s syndrome

A
  1. Surgical removal of any pituitary tumours ± radiotherapy
    - Transsphenoidal pituitary adenomectomy
    - If surgery fails = pituitary irradiation
    - Last resort = bilateral adrenalectomy - monitor @ 6/12 months with ACTH + MRI
  2. Stop steroids if possible.
  3. Drugs to inhibit cortisol synthesis
    - E.G. metyrapone, ketoconazole and fluconazole when pre-op/awaiting affects of radiotherapy
33
Q

Give a sign of Cushing’s syndrome that is due to impairments in carbohydrate metabolism.

A

Diabetes mellitus.

34
Q

Give a sign of Cushing’s syndrome that is due to electrolyte disturbances.

A
  1. Sodium retention.
  2. Hypertension.
35
Q

People with Cushing’s syndrome may have immune dysfunction. Give a consequence of this.

A

Increased susceptibility to infection.

36
Q

Why is it important to take a drug history when speaking to someone with potential Cushing’s?

A

To exclude exogenous glucocorticoid exposure as a potential cause.

37
Q

Name 2 drugs that suppress cortisol synthesis and so can be used in the treatment of Cushing’s disease.

A
  1. Metyrapone.
  2. Ketoconazole.
38
Q

When might you see signs of hypercortisolism without Cushing’s disease?

A
  1. Pregnancy.
  2. Depression.
  3. Alcohol dependence.
  4. Obesity.
39
Q

Define Conn’s syndrome / Primary hyperaldosteronism.

A

Excess production of the hormone, aldosterone from the adrenal glands (hyperaldosteronism) due to an aldosterone-producing adrenal adenoma

40
Q

Give 2 main causes of primary hyperaldosteronism.

A
  1. Conn’s disease (adrenal adenoma)
  2. Bilateral adrenocortical hyperplasia
41
Q

What causes secondary hyperaldosteronism?

A
  1. Inappropriate activation of RAAS.
  2. Excess renin stimulation of zona glomerulosa from decreased renal perfusion in renal artery stenosis.
  3. Increased aldosterone + renin
  4. Accelerated hypertension.

Heart failure.
Obstruction.

42
Q

Explain the pathophysiology underlying Conn’s syndrome.

A
  1. Primary hyperaldosteronism
  2. Excess aldosterone production independent of RAAS activation
  3. Causes less renin release
  4. Causes H2O + sodium retention
  5. Causes potassium loss/excretion
  6. Causes hypertension -> high BP
43
Q

What hormone is raised in Conn’s syndrome and what hormone is reduced? Where are these hormones synthesised?

A
  1. Aldosterone is raised - synthesised in the zona glomerulosa
  2. Renin is reduced - synthesised by the juxta-glomerular cells
44
Q

Give the 2 main conditions seen in Conn’s syndrome that cause the symptoms observed.

A
  1. Hypertension
  2. Hypokalaemia
45
Q

Give 3 main signs/symptoms of Conn’s syndrome.

A
  1. Headache (due to hypertension)
  2. Muscle weakness (due to hypokalaemia)
  3. Polyuria (due to hypokalaemia)
  4. Tetany
  5. Nocturia
46
Q

What are the Na+ and Ka+ levels seen in patients with primary hyperaldosteronism / Conn’s syndrome?

A

High serum Na+

Low serum K+

47
Q

Primary hyperaldosteronism / Conn’s syndrome is normally asymptomatic and picked up on a routine test.
What test is this?

A

Testing BP - hypertension

48
Q

Investigations to confirm a diagnosis of Conn’s syndrome.

A
  1. Bloods - U+E:
    - Low Renin
    - High Aldosterone
  2. Plasma aldosterone : renin ratio can be used as an initial screening test
    - In primary -> high aldosterone with low renin
    - In secondary -> high aldosterone with high renin
    - Raised ratio of > 800 = indicates the need for further tests / imaging
  3. ECG for arrhythmia
  4. CT/MRI for adrenal cause -> primary cause

Renal Doppler ultrasound -> secondary causes
CT angiography / MRI -> secondary causes

49
Q

Before you begin to investigate primary hyperaldosteronism / Conn’s syndrome, what medications should you stop?

A

ACEi, beta-blockers, spironolactone, ARBs

50
Q

Treatment for primary hyperaldosteronism / Conn’s syndrome.

A
  1. Laparoscopic adrenalectomy (surgery)
  2. Aldosterone antagonist - spironolactone
51
Q

Give 4 ECG changes that you might see in someone with Conn’s syndrome.

A
  1. Increased amplitude and width of P waves.
  2. Flat T waves.
  3. ST depression.
  4. Prolonged QT interval.
  5. U waves.
52
Q

What is defined as hypokalaemia?

A
  • < 3.5 mmol/l
    • mild = 3 - 3.4 mmol/l
    • moderate = 2.5 - 2.9
    • severe <2.5 or symptomatic
53
Q

Give 3 causes of hypokalaemia.

A
  1. Diuretics.
  2. Vomiting/diarrhoea
  3. IV fluid without potassium
  4. Conn’s syndrome.
  5. Insulin.
54
Q

Give 5 symptoms of hypokalaemia.

A
  1. Muscle weakness.
  2. Hypotonia.
  3. Hyporeflexia.
  4. Palpitations.
  5. Tetany.
  6. Arrhythmia.
  7. Nausea and vomiting.
  8. Cramps.
  9. Constipation.
  10. Light-headedness.
55
Q

What ECG changes might you see in someone with hypokalaemia?

A
  1. Increased amplitude and width of P waves.
  2. Prolonged PR
  3. ST depression.
  4. Flat (small/inverted) T waves.
  5. Prominent U waves.
  6. QT prolongation.
56
Q

Treatment of hypokalaemia.

A

Mild - oral potassium supplement.
Severe - IV potassium (IV 40 mmol/L KCl in saline)

Never give as fast-stat bolus dose!!

57
Q

Define hyperkalaemia.

A

Mild -> 5.5 - 5.9
Mod -> 6.0 - 6.4
Severe - >6.5

58
Q

Give 3 causes of hyperkalaemia.

A
  1. Acute kidney injury (AKI) + Chronic kidney disease (CKD)
    - Renal impairment
  2. Medications:
    - Interfere with excretion: amiloride, spironolactone
    - Interfere with RAAS: ACEi, ARB, NSAIDs, heparin
    - Other: ciclosporin
  3. Metabolic acidosis
    - Hyperkalaemic renal tubular acidosis
  4. K+ sparing diuretics
  5. Mineralocorticoid deficiency (Addison’s)
  6. Burns
  7. Rhabdomyolysis (crush injury)
59
Q

Give 3 symptoms of hyperkalaemia.

A
  1. Weakness + fatigue.
  2. Flaccid paralysis.
  3. Depressed tendon reflexes.
  4. Palpitations.
  5. Tachycardia - fast irregular pulse.
  6. Chest pain.
  7. Light-headedness.
60
Q

What ECG changes might you see in someone with hyperkalaemia?

A
  1. Small/no P wave
  2. Prolonged PR
  3. Wide QRS
  4. Tall tented/ peaked T waves.
61
Q

What makes hyperkalaemia a medical emergency?

A

Causes cardiac hyperexcitability, leading to ventricular fibrillation and cardiac arrest.

62
Q

Treatment of hyperkalaemia.

A
  1. ABCDE
  2. 12 lead ECG
    - >7 or ECG change or syptomatic = urgent Rx
  3. Reduce potassium
    - Stop supplemental potassium: consider stopping digoxin and BB
  4. Protect cardiac membrane
    - 10ml 10% calcium gluconate IV (ECG change in 2 mins - only lasts 1 hour)
    - If no improvement: repeat every 10 mins up to 50ml
  5. Shift potassium into cells
    - Insulin infusion + glucose (10U insulin + 25g glucose)
    - Check CBG before during and after
    - Reduction by 1.0 in 15mins Lasts for 60 mins
    - 10-20mg nebulised salbutamol reduction 0.5 in 15 mins
    - Recheck U+E at 2 hours
  6. Remove potassium from body
    - Calcium resonium + lactulose - removal from GI (15g 3-4x daily)
  7. Haemodialysis
    - If still resistant
63
Q

Management of patient with severe hyperkalaemia in acute terms.

A

Give insulin - drives potassium into cells.
Give it with glucose.

64
Q

Why is glucose given along with insulin for severe hyperkalaemia?

A

To avoid hypoglycaemia.

65
Q

explain what ‘artefactual’ hyperkalaemia is

A

if patient is well, but shows hyperkalaemia the test should be repeated - may have been an artefactual result due to:
contamination with potassium EDTA anticoagulant in FBC bottles; thrombocythaemia; delayed analysis (potassium leads out of RBCs).

66
Q

Why do you give nebulised salbutamol, insulin and calcium gluconate to treat hyperkalaemia?

A
  1. Calcium gluconate
    - Increases the threshold potential
    - Restores normal gradient between that and the resting membrane potential
    - Protects heart, but doesn’t change K+ levels
  2. Insulin
    - Forces potassium back into cells - give with glucose.
  3. Salbutamol
    - Lowers serum potassium levels by promoting movement of potassium back into cells.
67
Q

Define phaeochromocytoma.

A

Rare catecholamine-producing adrenal tumour in the adrenal medulla.
Secrete autonomously from SNS.

68
Q

Which cells do phaechromocytomas arise from?

A

Sympathetic paraganglia cells - collections of chromaffin cells.

69
Q

Where are phaeochromocytomas usually found?

A

In the adrenal medulla

70
Q

What is the 10% rule of phaeochromocytomas?

A

10% are malignant, 10% are extra-adrenal, 10% are bilateral and 10% familial.

71
Q

Describe the classic triad of clinical features of phaeochromocytomas.

A
  1. Episodic headache
  2. Sweating
  3. Tachycardia / palpitations
72
Q

Other than the classic triad, give 5 other symptoms of phaeochromocytoma.

A
  1. Hypertension.
  2. Palpitations.
  3. Tremor.
  4. Arrhythmia.
  5. Confusion.
73
Q

What investigations might you do in order to diagnose someone with having a phaeochromocytoma?

A

Bloods
1. Raised WCC (white cell count)
2. Increased plasma metadrenaline and normetadrenaline.

74
Q

What is the main problem caused by phaeochromocytomas?

A

Life-threatening hypertension

75
Q

Treatment for phaeochromocytoma

A
  1. Pre-op alpha blocker
    - Phenoxybenzamine for 7-10 days to allow expansion blood volume
  2. Pre-op beta blocker
  3. Surgical removal of tumour.
  4. Post-op alpha blocker
    - Use propanolol
  5. Monitor with 24 hour catecholamines + VMA 2 weeks after surgery
76
Q

Management of phaeochromocytomas for hypetensive emergencies/crisis

A

Phentolamine or IV nitroprusside

5. Endocrinology (20 decks)

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