Pituitary Disease - SIADH Flashcards

1
Q

Function of ADH.

A
  1. Produced in Hypothalamus.
  2. Secreted by Posterior Pituitary Gland.
  3. Stimulates water resorption in the collecting ducts in the kidneys.
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2
Q

What is SIADH?

A

Syndrome of Inappropriate ADH Secretion.

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3
Q

Pathophysiology of SIADH.

A
  1. Excessive ADH - Excessive Water Resorption in Collecting Ducts.
  2. Hyponatraemia (Dilution).
  3. Euvolaemic Hyponatraemia.
  4. High Urine Osmolality and High Urine Sodium.
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4
Q

Clinical Features of SIADH (5).

A
  1. Headache.
  2. Fatigue.
  3. Muscle Aches/Cramps.
  4. Confusion.
  5. Severe Hyponatraemia - Seizures, Reduced Consciousness.
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5
Q

Aetiology of SIADH (2) - MAIN.

A
  1. Posterior Pituitary Overproduction.

2. Ectopic Production.

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6
Q

Aetiology of SIADH (6).

A
  1. Post-Operative.
  2. Infection e.g. Atypical Pneumonia, Lung Abscess.
  3. Head Injury.
  4. Medications.
  5. Malignancy - SCLC.
  6. Meningitis.
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7
Q

Investigations of SIADH.

A
  1. Diagnosis of Exclusion.
  2. Euvolaemic Hyponatraemia.
  3. High Urine Osmolality and High Urine Sodium.
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8
Q

Differentials of Hyponatraemia to Exclude (5).

A
  1. Adrenal Insufficiency - Short Synacthen Test.
  2. History of Diuretic Use.
  3. Diarrhoea, Vomiting, Burns, Fistulae, Excessive Sweating.
  4. Excessive Water Intake.
  5. CKD/AKI.
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9
Q

Management.

A
  1. Identify Underlying Cause.
  2. Fluid Restriction (500ml-1L).
  3. Tolvaptan.
  4. Demeclocycline (not anymore).
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10
Q

What is Tolvaptan?

A

ADH Receptor Blocker - rapid increase in Sodium, but requires close monitoring of Sodium levels every 6 hours.

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11
Q

What is Central Pontine Myelinolysis?

A

Osmotic Demyelination Syndrome - a complication of long-term severe hyponatraemia being treated too quickly.

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12
Q

Pathophysiology of Central Pontine Myelinolysis (4).

A
  1. Serum Sodium falls.
  2. Water moves by osmosis across blood-brain barrier.
  3. Brain tries to adapt by reducing solutes in brain cells
  4. If Sodium levels rapidly rise, water will rapidly shift out of the brain cells.
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13
Q

Phases of Central Pontine Myelinolysis (2).

A
  1. 1st - Electrolyte Imbalance - Encephalopathy and Confusion and Headache.
  2. 2nd - Demyelination of Neurones in Pons - Spastic Quadriparesis, Pseudobulbar Palsy, Cognitive Behavioural Changes.
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14
Q

Prognosis of Central Pontine Myelinolysis.

A

Supportive.

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