Syndrome of inappropriate antidiuretic hormone syndrome (SIADH) Flashcards

1
Q

What is syndrome of inappropirate antidiuretic hormone syndrome (SIADH)?

A

Increased antidiuretic hormone (ADH) release from posterior pituitary or an ectopic source

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2
Q

What are some of the neurological causes of SIADH?

A

Meningitis, encephalitis, or cerebral abscess
Intracranial haemorrhage e.g. subarachnoid or subdural
Stroke

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3
Q

What are some of the malignant causes of SIADH?

A

Small cell carcinoma of the lung (most common)

Others: breast cancer, head + neck tumours are rarer causes

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4
Q

What are some of the infectious causes of SIADH?

A

Pneumonia

Tuberculosis

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5
Q

What are some of the endocrine causes of SIADH?

A

Hypothyroidism

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6
Q

What are some of the drugs that can cause SIADH?

A

SSRIs + TCAs
Proton pump inhibitors
Carbamazepine
Sulfonylureas (glimperide + glipizide)

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7
Q

What are some of the miscellaneous causes of SIADH?

A

Porphyria

Positive end-expiratory pressure

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8
Q

What is classified as mild SIADH and what are the symptoms?

A

Mild (130-135 mmol/L)

Nausea, vomiting, headache, lethargy

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9
Q

What is classified as moderate SIADH and what are the symptoms?

A

Moderate (125-129 mmol/L)

Weakness, muscles aches, confusion, ataxia

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10
Q

What is classified as severe SIADH and what are the symptoms?

A

Severe (<125 mmol/L)

Reduced consciousness, seizures, respiratory arrest

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11
Q

What is the role of ADH in the body?

A

ADH is responsible for free water reabsorption by acting on the collecting ducts of the kidneys resulting in water retention (but not reabsorption of the solutes)

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12
Q

What does an increase in ADH result in?

A

Increase in free water retention and therefore dilution of the blood and a decrease in solutes in the blood

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13
Q

Why are patients with SIADH typically euvolaemic?

A

Water distributes throughout the entire intravascular and extravascular compartment

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14
Q

In SIADH why is there a continuous ADH production irrespective of serum osmolarity?

A

SIADH results in a loss of an effective feedback mechanism, resulting in low serum sodium + relatively high urinary sodium with concentrated urine

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15
Q

What is classified as hyponatremia?

A

Sodium concentration < 135 mmol/L

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16
Q

What does it mean if a patient is euvolaemic?

A

Patient has normal circulatory or blood fluid volume within their body

17
Q

Clinical features in SIADH depend on degree of what?

A

Hyponatraemia + rate of change in serum sodium levels

18
Q

What is the essential diagnostic criteria for SIADH?

A
Low plasma osmolarity <275 mOsm/kg
High urine osmolarity > 100 mOsm/kg
High urine sodium >30 mmol/L
Clinical euvolaemia
Exculsion of glucocorticoid deficiency or hypothyroidism (rare)
19
Q

In health people why should low serum osmolarity cause low urine osmolarity?

A

Kidney attempts to retain solute

20
Q

What is the management of acute onset (<48 hrs) hyponatraemia?

A

Hypertonic (3%) saline

21
Q

What is the management of chronic onset (>48 hrs) hyponatraemia?

A

Correction should not occur too quickly - aim for maximum increase of 10 mmol/L per day

22
Q

What is the management of chronic onset (>48 hrs) hyponatraemia in mild to moderate asymptomatic cases?

A

Fluid restriction

23
Q

What is the management of chronic onset (>48 hrs) hyponatraemia in severe or symptomatic cases?

A

Demeclocycline or ADH receptor antagonists (e.g. tolvaptan) may be considered

N.B. Guidelines differ

24
Q

What are some of the complications of SIADH?

A

Cerebral odema

Central pontine myelinolysis

25
Q

How does SIADH cause central pontine myelinolysis?

A

Rapid correction of sodium can cause osmotic demyelination, particularly in chronic hyponatraemia

Therefore slow correction is vital

26
Q

What are the symptoms of central pontine myelinolysis?

A

Tremors, dysarthria, quadriplegia, opthalmoplegia, seziures + extra pyramidal symptoms

May result in ‘locked-in syndrome’ - patients are awake but unable to verbally communicate or move

27
Q

How is a diagnosis of central pontine myelinolysis made?

A

MRI

28
Q

How does SIADH result in cerebral odema?

A

Hyponatraemia lowers the osmolarity of the blood causing an osmotic shift of water into the brain tissue with subsequent odema + risk of herniation