Syndrome of Inappropriate ADH Flashcards

1
Q

Where is ADH produced?

A

Hypothalamus & secreted by posterior pituitary

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2
Q

ADH AKA?

A

Vasopressin

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3
Q

What does ADH do?

A

Stimulates water reabsorption from CDs in kidneys

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4
Q

What is SIADH?

A

Condition where there is inappropriately large amounts of ADH

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5
Q

What does inappropriately large amounts of ADH result in?

A

XS-ive water reabsorption in CD’s
|
Resulting in hyponatraemia, but water not usually enough to cause fluid overload therefore euvolemic hyponatraemia

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6
Q

Urine osmolality and urine sodium of patients with SIADH?

A

High urine osmolality

High urine sodium

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7
Q

General cause of SIADH?

A

Result of posterior pituitary secreting too much ADH or ADH may be coming from somewhere else eg sclc

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8
Q

Causes of SIADH?

A
  • Post-operative from major surgery
  • Infection (atypical pneumonia/lung abscesses)
  • Head injuries
  • Meds
  • Malignancy
  • Meningitis
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9
Q

Meds which can cause SIADH?

A
Thiazide diuretics 
Carbamazepine 
Vincristine 
Cyclophosphamide 
Antipsychotics 
SSRIs 
NSAIDs
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10
Q

Presnetation of SIADH?

A
  • Headache
  • Fatigue
  • Muscle aches and cramps
  • Confusion
  • Severe hyponatraemia leading to seizures
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11
Q

Initial diagnosis of SIADH?

A

Almost a diagnosis of exclusion

  • Clinical exam shows euvolaemia
  • U&Es show hyponatraemia
  • Urine Na and osmolality will be high
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12
Q

Excluding causes of hyponatraemia by?

A
  • Negative short synacthen test (excludes adrenal insufficiency)
  • No history of diuretic use
  • No diarrhoea, burns, fistula or XSive sweating
  • No XSive water intake
  • No CKD or AKI
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13
Q

What does a negative short synacthen test rule out?

A

Adrenal insufficiency

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14
Q

Establishing cause of SIADH?

A

CXR= 1st line for pneumonia, abscesses, lung cancer

If malignancy is sus= CT thorax/abdomen & pelvis & MRI brain

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15
Q

Management of SIADH?

A

Establish and treat cause

  • Essential to correct Na slowly to prevent central pontine myelinolysis
  • Fluid restriction
  • Tolvaptins & ADH receptor blockers
  • Demeclocycline
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16
Q

Rules when correcting Na in SIADH?

A

GO SLOW
-Aim for change in Na <10mmol/L/24Hours
TO PREVENT CENTRAL PONTINE MYELINOLYSIS

17
Q

Restrict fluids to?

A

500mls-1Litre

18
Q

Drugs for SIADH?

A

Tolvaptins & ADH receptor blockers: RAPID increase in Na

Demeclocycline: Tetracycline AB which inhibits ADH

19
Q

What is central pontine myelinolysis AKA?

A

Osmotic demyelination syndrome

20
Q

What is ODS usually caused by?

A

Complication f long term severe hyponatraemia (120

21
Q

What happens as blood Na decreases?

A

H2O will move by osmosis across BBB to cells to brain, causing brain swelling

22
Q

How does brain adapt to brain swelling when Blood Na decreases?

A

Reducing solutes in brain cells

This takes a few days but results in chronic hyponatraemia

23
Q

Osmolality and Na in CPM?

A

LOW osmolality

LOW Na

24
Q

What occurs when Na rapidly rises?

A

Water shifts out of brain causing 2 phases

25
Q

1st phase of CPM?

A
  • Due to electrolyte imbalance
  • Encephalopathic and confused
  • Symptoms - Headache, N/V
26
Q

2nd phase of CPM?

A

Due to demyelination of neurones especially in pons

  • Few days after rapid Na correction
  • May present as spastic quadriparesis, pseudobulbar palsy and cognitive behavioural changes
27
Q

Prevention of CPM is essential as there isn’t really treatment. True or false?

A

TRUE

Management = supportive