ChemPath: Sodium and Fluid Balance Flashcards

1
Q

What level of serum Na delineates hyponatraemia

A

<135 mmol/L

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2
Q

What is the underlying pathogenesis of hyponatraemia?

A

Excess water - concentration of sodium is lower

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3
Q

Which hormone controls water balance?

A

ADH (vasopressin)

Synthesized in hypothalamus
Secreted from posterior pituitary
Acts on collecting duct in kidney

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4
Q

Describe how ADH controls water balance.

A

ADH is released from the posterior pituitary gland. It acts on V2 receptors on collecting ducts causing insertion of aquaporin-2 water channels. This causes increased water reabsorption.

Less important for water balance but ADH can also interact with V1 receptors in vascular smooth muscle causing vasoconstriction

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5
Q

What receptors may ADH (Vasopressin) work on?

A

V1 receptors:

  • On vascular smooth muscle
  • Causes vasoconstriction
  • This occurs at higher concentrations

V2 receptors:

  • On kidneys
  • Insertion of aquaporin-2 channels on collecting ducts
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6
Q

What are the two main stimuli for ADH secretion?

A
  • Serum osmolality - mediated by hypothalamic osmoreceptors (high osmolality = stimulus)
  • Blood volume/pressure - mediate by baroreceptors in carotids, atria and aorta (low pressure = stimulus)
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7
Q

What is the effect of increased ADH secretion on serum sodium?

A

Hyponatraemia - as ADH only reabsorbs water not any sodium. Lowering its concentration

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8
Q

What is the first step in the clinical assessment of a patient with hyponatraemia?

A
  • Clinical assessment of volume status
    • Look at hands
    • Head and neck
    • Peripheries
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9
Q

What are clinical signs of hypovolaemia?

A
  • Dry mucous membranes
  • Reduced JVP
  • Reduces tissue turgor
  • Tachycardia
  • Postural hypotension
  • Confusion/drowsiness
  • Reduced urine output
  • Low urine Na+ (\ <20)

If you are hypovolaemic, you need to hold onto sodium so urine sodium will be low → always remember to send off this test

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10
Q

What are clinical signs of hypervolaemia?

A
  • Raised JVP
  • Peripheral oedema
  • Bibasal crackles (on chest examination)
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11
Q

What is the most accurate measure of volume status

A

urine osmolality

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12
Q

What makes urine sodium uninterpretable?

A

Diuretics - these alter the kidney’s ability to retain salt

Must stop it and check 48 hours after.

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13
Q

What are causes of hypovolaemic hyponatraemia?

A

= small loss of water and large loss of sodium

  • Diarrhoea
  • Vomiting
  • Diuretics

Diarrhoea + Vomiting = Na+ released by enterocytes into digestive juices. However it is not reabsorbed as it is lost = hyponatraemia.

Explanation of how hypovolaemic hyponatraemia occurs in picture:

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14
Q

What are causes of hypervolaemic hyponatraemia

A

= large increase in water, no or small increase in sodium

  • Cardiac failure (low pressure detected by baroreceptors + leakage of water from capillaries to interstitial fluid (oedema) = ADH stimulation and release. )
  • Cirrhosis (vasodilation due to excess NO released resulting in low BP + leakage of water from capillaries to interstitial fluid (oedema) = ADH stimulation and release)
  • Renal failure (not excreting enough water leakage of water from capillaries to interstitial fluid (oedema) = ADH stimulation and release)
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15
Q

What are causes of euvolaemic hyponatraemia?

A

= Increase in water , no change to sodium (despite increas in water it is not “hypervolaemic” as there is no excess fluid in interstitial space so no oedema and no clinical signs of hypervolaemia.)

  • Hypothyroidism - reduced contractility resulting in decreased cardiac output and BP = ADH release
  • Adrenal insufficiency - less aldosterone released resulting in less Na+ reabsorption. Water remains as does not osmotically move with sodium into renal tubules.
  • SIADH (excess ADH release)
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16
Q

What are the causes of SIADH?

A
  • CNS pathology (stroke, haemorrhage, tumour)
  • Lung pathology (legionella pneumonia, pneumothorax)
  • DRUGS (SSRI, TCA, opiates, PPIs, carbamazepine)
  • Tumours
  • Surgery
17
Q

Explain how SIADH results in hyponatraemia

A

SIADH —> Excess ADH —> water retention —> increased volume —> suppress RAAS —-> less aldosterone —-> less Na+ reabsorption

18
Q

What investigations would you order in a patient with euvolaemic hyponatraemia?

A
  • Hypothyroidism: Thryoid function tests
  • Adrenal insufficiency: Short synacthen test
  • SIADH: Plasma and urine osmolality (low plasma & high urine osmolality)
19
Q

Will osmolality of plasma and urine be high or low in SIADH?

A

Plasma osmolality - LOW

Urine osmolality - HIGH (>100)

20
Q

What does a diagnosis of SIADH require?

A
  • No hypovolaemia
  • No hypothyroidism
  • No adrenal insufficiency
  • Reduced plasma osmolality
  • Increased urine osmolality (>100) - must know this range
21
Q

How would you manage a hypovolaemic patient with hyponatraemia?

A

Volume replacement with 0.9% saline - this removes the stimulus for ADH secretion

22
Q

How would you manage a hypervolaemic patient with hyponatraemia?

A

Fluid restriction (<750ml/day) and treat the underlying cause.

Do NOT give saline as the patient will just hold onto the water and exacerbate the hyponatraemia → giving saline won’t address the issue causing ADH secretion if it’s a tumour etc.

23
Q

How would you manage a euvolaemic patient with hyponatraemia?

A

Fluid restriction (<750ml/day) and treat the underlying cause (same as hypervolaemic patient with hyponatraemia)

24
Q

What are clinical symptoms of severe hyponatraemia?

A
  • Reduced GCS
  • Seizures

Seek expert help (treat with hypertonic 3% saline)

25
Q

How is severe hyponatraemia managed?

A

Can give boluses of hypertonic 3% saline but only if patient has low GCS or fitting.

DO NOT GIVE 3% saline if alert and orientated.

26
Q

What is an important point to remember while correcting hyponatraemia?

A
  • Serum Na must NOT be correct >8-10 mmol/L in the first 24 hours
  • Risk of osmotic demyelination (central pontine myelinolysis)
    • Presents a few days later with quadriplegia, dysarthria, dysphagia, seizures, coma, death
27
Q

What drugs are used to treat SIADH and when are they used?

A

If water restriction is insufficient:

  • Demeclocycline
  • Tolvaptan
28
Q

How does Demeclocycline work? What must you monitor when using it?

A
  • Reduces responsiveness of collecting tubule cells to ADH
  • Need to monitor U&Es (risk of nephrotoxicity)
29
Q

How does Tolvaptan work?

A
  • V2 receptor antagonist
  • Very expensive
30
Q

What is the definition of hyponatraemia?

A

Sodium concentration <135 mmol/L

31
Q

What are the main causes of hypernatraemia?

A

1) Increase in sodium AND/OR have a loss of water
- Increase in sodium:
- medical high intake (hypertonic saline, sodium bicarb)
- dietary high intake (salty infant formula, high dietary salt)
- Conn’s syndrome
- Renal artery stenosis (low GFR = low BP and JGA = high renin + aldosterone)
- Cushing’s syndrome
- Loss of water
- Renal losses (Diabetes insipius, osmotic diuresis)
- Non-renal losses: GI or sweat

2) Patient cannot control water intake e.g. children, elderly, fasting for surgery,

32
Q

What investigations would you order in a patient with suspected diabetes insipidus?

A
  • Serum glucose (exclude diabetes mellitus which can cause osmotic diuresis)
  • Serum potassium (exclue hypokalaemia which can cause nephrogenic DI)
  • Serum calcium (exclude hypercalcaemia which can cause nephrogenic DI)
  • Plasma and urine osmolality (exclude hyperaldosteronism - high plasma osmo, low urine osmo)
  • Water deprivation test - urine osmolality will fail to increase
33
Q

What do patients with diabetes insipidus present with?

A

Polyuria and polydipsia

34
Q

Causes of nephrogenic DI

A

Hypercalcaemia
Hypokalaemia
Lithium
Sickle cell anaemia

35
Q

How would you treat hypernatraemia?

A
  • Fluid replacement with dextrose (if patient is also hypovolaemic then 0.9% saline then 5% dextrose water)
  • Serial Na+ measurements every 4-6 hours
  • Treat the underlying cause
36
Q

What are the effects of diabetes mellitus on serum sodium?

A

Variable as the following processes occur:

  • Hyperglycaemia draws water out of the cells leading to hyponatraemia
  • Osmotic diuresis in uncontrolled diabetes leads to loss of water and hypernatraemia

This varies from person to person - based on which factor is pre-dominating