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Gastrointestinal Block > SIADH and Diabetes Insipidus > Flashcards

SIADH and Diabetes Insipidus Flashcards

1
Q

ADH is produced in the ______ and secreted by the ______.

It stimulates ______ reabsorption from the CDs in the kidneys.

A

hypothalamus, posterior pituitary, water

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2
Q

What is SIAD?

A

A condition where there is inappropriately large amounts of ADH

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3
Q

Compare primary vs secondary SIADH

A

Primary: posterior pituitary secreting too much ADH

Secondary: ADH coming from elsewhere ie. small cell lung cancer

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4
Q

Pathophysiology of SIADH?

A

↑ ADH = ↑ H20 reabsorption in CD

Dilutes Na in the blood but not enough to cause fluid overload → Euvolaemic Hyponatraemia

Less water excreted by kidneys, so urine becomes more concentrated → High urine Na and osmolality

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5
Q

Symptoms of SIADH?

A

Symptoms are non-specific

  • Headache
  • Fatigue
  • Muscle aches and cramps
  • Confusion
  • Severe hyponatraemia can cause seizures and reduced consciousness
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6
Q

List 4 causes of SIADH

A
  • Medications (most common)
  • Surgery
  • Infection (esp atypical pneumonia and lung abscesses)
  • Head injury
  • Malignancy (small cell lung cancer)
  • Meningitis
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7
Q

List 4 drugs known of cause SIADH

A
  1. Thiazide diuretics
  2. Carbamazepine
  3. Vincristine
  4. Cyclophosphamide
  5. Antipsychotics and SSRIs
  6. NSAIDSs
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8
Q

How is an initial diagnosis of SIADH made?

A

No test to directly measure ADH activity so diagnosis is based on:

  • Clinical examination → will show euvolaemia
  • U+Es → will show hyponatraemia
  • Urine sodium and osmolality will be high
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9
Q

List 4 differentials for hyponatraemia

A
  1. Adrenal insufficiency
  2. Diuretic use
  3. Diarrhoea, vomiting, burns, fistula or excessive sweating
  4. Excessive water intake
  5. CKD or AKI
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10
Q

If you suspect pneumonia, lung abscess or lung cancer, what investigation will you perform?

A

Chest xray

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11
Q

If you suspect malignancy, what investigation will you perform?

A

CT TAP and MRI brain

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12
Q

Management of SIADH?

A
  1. Correct Na slowly
  2. Fluid restriction (to 500mls-1litre)
  3. ADH receptor blockers ie. Tolvaptan
  4. Demeclocycline (tetracycline antibiotic) rarely used anymore
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13
Q

Why is it important to correct Na slowly in SIADH?

A

To prevent central pontine myelinolysis (osmotic demyelination syndrome)

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14
Q

What is CMP

A

A complication of long term severe hyponatraemia (< 120 mmols/l) being treated too quickly (> 10 mmol/l increase over 24 hours)

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15
Q

Pathophysiology of CMP?

A
  1. ↓ blood Na causes H20 to cross BBB by osmosis
  2. brain adapts by ↓ its solutes to prevent oedema (takes a few days)
  3. In hyponatraemia, brain cells have a ↓ osmolality
  4. when fluid is restored to fast, blood Na levels ↑ rapidly, so H20 moves out of brain cells into blood
  5. this causes destruction of myelin (2 phases of symptoms)
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16
Q

What is the first phase of symptoms in CPM?

Why?

A

Due to electrolyte imbalance

Presents as encephalopathic and confused

17
Q

What is the second phase of symptoms in CPM?

Why?

A

Due to demyelination of neurones in pons a few days after rapid correction (risk of death)

Present as:

  • spastic quadriparesis
  • pseudobulbar palsy
  • cognitive and behavioural changes
18
Q

What is Diabetes insipidus?

A

A condition characterised by either a decreased secretion of ADH from pituitary or an insensitivity to ADH

19
Q

What are the 2 types of Diabetes insidious and how do they differ?

A

Cranial - hypothalamus does not produce ADH for pituitary to secret

Nephrogenic - collecting ducts of the kidneys do not respond to ADH

20
Q

What is Primary polydipsia?

A

Patient has a normally functioning ADH system, but they are drinking excessive quantities of water leading to excessive urine production

They don’t have diabetes insipidus

21
Q

List 4 causes of cranial DI

A
  1. Idiopathic
  2. Head injury
  3. Pituitary or brain surgery
  4. Brain tumour
  5. Brain infections (meningitis, encephalitis, TB)
22
Q

List 4 causes of Nephrogenic DI

A
  1. Congenital
  2. Lithium
  3. Intrinsic kidney disease
  4. Hypokalaemia and hypercalcaemia
23
Q

What gene mutation is associated with congenital nephrogenic DI?

A

AVPR2 gene on the X chromosome that codes for the ADH receptor

24
Q

List 4 clinical features of DI

A
  • Polyuria
  • Polydipsia
  • Dehydration
  • Postural hypotension
  • Hypernatraemia
25
Q

List 3 Investigations for DI

A
  1. Low urine osmolality (< 700)
  2. High serum osmolality (>295)
  3. Water deprivation test
26
Q

What is the gold standard investigation to diagnose DI?

A

The water deprivation test

Also known as the desmopressin stimulation test

27
Q

Explain the Water Deprivation Test

A
  1. patient should avoid taking in any fluids for 8 hours - “fluid deprivation”
  2. urine osmolality is measured and synthetic ADH is administered
  3. 8 hours later urine osmolality is measured again
28
Q

Water deprivation test findings indicative of cranial vs nephrogenic DI

A

Cranial:

  • Before deprivation urine osmolality is LOW
  • After ADH urine osmolality is HIGH

Nephrogenic DI:

  • Before deprivation urine osmolality is LOW
  • After ADH urine osmolality is LOW
29
Q

What findings on the water deprivation differentiate indicate primary polydipsia?

A

HIGH before deprivation and after ADH

In PP, 8 hours of water deprivation will cause urine osmolality to be HIGH even before ADH is given

30
Q

Management of DI?

A
  1. Treat underlying cause (If possible)
  2. Cranial DI: Desmopressin
  3. Nephrogenic DI: thiazides and NSAIDs, low salt/protein diet, high dose desmopressin

Gastrointestinal Block (26 decks)

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