ChemPath 3: Sodium and Fluid Balance Flashcards

1
Q

Define Hyponatraemia

A
  • Serum sodium <135 mmol/L
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2
Q

Which is the commonest electrolyte abnormality in hospitalised patients?

A

Hyponatraemia

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3
Q

Which hormone regulates water balance?

A

ADH

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4
Q

Outline how ADH works

A
  1. Synthesised in hypothalamus
  2. Secreted from posterior pituitary, acts on CD in the kidney
  3. Water retention through insertion of aquaporin 2 (AQA2)
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5
Q

Briefly explain the pathogenesis of hyponatraemia

A
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6
Q

Which receptors does ADH act on?

What happens once it has bound to these receptors?

A

V2 receptors in collecting duct –> insertion of AQA2

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7
Q

Where are V1 receptors found?

A
  1. Vascular smooth muscle
  2. Vasoconstriction – higher concentrations
  3. “Vasopressin”
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8
Q

What are the 2 main stimuli for ADH secretion?

A
  1. Serum osmolality (high) – mediated by hypothalamic osmoreceptors
  2. Blood volume/pressure (low) – mediated by baroreceptors in carotids, atria, aorta
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9
Q

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

A
  1. ADH only resorbs water, not any sodium
  2. –> Hyponatraemia
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10
Q

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

A

clinical assessment of volume status (Hypovolaemia, euvolemia, hypervolaemia)

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11
Q

What are the clinical signs of hypovolaemia?

A
  • Tachycardia
  • Postural hypotension
  • Dry mucous membranes
  • Reduced skin turgor
  • Confusion or drowsiness
  • Reduced urine output
  • Low urine Na+ (<20)
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12
Q

What is the normal range of urine Na?

A
  • Normal range = 40-220 mEq/L [<20 non-renal loss; >20 in renal loss)
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13
Q

What is the issue with using urine Na as a tool for assessing ?hyponatraemia?

A
  • Patients on diuretics may have urine Na that is not reliable (hypovolemic, but no hyponatraemia)
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14
Q

What are the clinical Signs of hypervolemia?

A
  • Raised JVP
  • Bi-basal crackles
  • Peripheral oedema
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15
Q

What does hyponatraemia in a hypovolaemic patient require?

A

requires more sodium than water loss

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16
Q

What are the causes of hyponatraemia in a hypovolaemic patient?

A
  • Diuretics
  • Diarrhoea and vomiting
17
Q

What is the difference between hypovolemic Hyponatraemia and dehydration?

A
  • Hypovolemic Hyponatraemia = loss of water and sodium (as opposed to dehydration = loss of just water)
18
Q

What is the pathophysiology of hypovolemic hyponatraemia?

A
  • Start euvolaemia and then a hypovolemia develops (quickly)
  • –> release of ADH à just water retention
  • –> dilutes [Na+] but not to same volume status as they were when euvolaemic
  • –> hyponatraemia + hypovolaemic
19
Q

What are the causes of hyponatraemia in a hypervolemic patient?

A
  • excess water,
  • excess ADH
  • Cardiac failure → low pressure → detected by baroreceptors → ADH release
  • Cirrhosis → vasodilated due to excess NO → low BP → baroreceptors → ADH release
  • Renal failure → not excreting enough water
20
Q

What are the causes of hyponatraemia in euvolemic patient?

A
  • Hypothyroidism à reduced contractility à reduced BP à ADH release
  • Adrenal insufficiency à less aldosterone à less Na+ reabsorption
  • SIADH –> AQA2 water retention –> inc. volume –> suppress RAAS –> less aldosterone –> less Na+ reabsorption
    • CNS pathology – stroke, haemorrhage, tumour
    • Lung pathology – pneumonia (Legionella), pneumothorax
    • Drugs – SSRI, TCA, PPI, carbamazepine, opiates
    • Tumours
    • Surgery
21
Q
  • What investigations would you order in a patient with euvolemic hyponatraemia?
A
  • Hypothyroidism → thyroid function tests
  • Adrenal insufficiency → short SynACTHen test
  • SIADH → plasma and urine osmolality → low plasma and high urine osmolality
    • Excess ADH = excess water = volume expansion → secretion for BNP → naturesis à euvolaemic
    • If sodium is high**, it’s a **pseudohyponatraemia (i.e. hyperlipidaemia, hyperproteinaemia)
22
Q

What is required for the diagnosis of SIADH?

A
  • No hypovolaemia (euvolaemia)
  • No hypothyroidism
  • No adrenal insufficiency
  • Reduced plasma osmolality (resorbing lots of water) AND
  • Increased urine osmolality (>100) (concentrating the urine) – need to know this ref range
23
Q

What is the management of hypovolemic patient with hyponatraemia

A

volume replacement with 0.9% saline

24
Q

What is the Management of euvolaemic patient with hyponatraemia

A

fluid restrict (<750ml/day + ABx infusions) + treat underlying cause

25
Q

What is the Management of hypervolemic patient with hyponatraemia

A

fluid restrict (<750ml/day + ABx infusions) + treat underlying cause

26
Q

What are the signs of severe hyponatraemia?

A
  • Reduced GCS
  • Seizures
27
Q

What is the Tx for severe hyponatraemia?

A
  • Seek expert help – treat with hypertonic 3% saline
28
Q

What is the complication that arises from too rapid a correction of hyponatraemia?

A

Central pontine myelinolysis

  • a neurological condition involving severe damage to the myelin sheath of nerve cells in the pons
29
Q

What are the signs and symptoms of Central Pontine Myelinolysis?

A
  • Quadriplegia, dysarthria, dysphagia, seizures, coma, death
30
Q

What rate should hyponatraemia be corrected at?

A

not greater than 8-10mmol/L in the first 24 hours

31
Q

Which drug is used to Tx SIADH if fluid restriction is not enough?

A
  • Demeclocycline –> induce nephrogenic diabetes insipidus
  • Tolvaptan – V2 receptor antagonist
32
Q

How does Demeclocycline work?

A
  • Reduces responsiveness of collecting tubule cells to ADH
  • Monitor U&Es as risk of nephrotoxicity
33
Q

Define hypernatraemia

A
  • Serum [Na+] > 145mmol/L
34
Q

What are the main causes of hypernatremia?

A
  • 1st –> increase sodium intake AND/OR have a loss of water:
    • Increase in sodium:
      • Medical high intake (hypertonic saline, sodium bicarbonate)
      • Dietary high intake (salty infant formula, high dietary salt)
      • Conn’s syndrome (high aldosterone: renin ratio), BAH (high aldosterone: renin ratio)
      • Renal artery stenosis (low GFR from RAS à low BP at JGA à high renin à high aldosterone)
      • Cushing’s syndrome (overactivation of MR by cortisol à aldosterone-like effect)
    • Loss of water:
      • Renal losses:
        • Osmotic diuresis
        • Diabetes insipidus (less ADH action / release)
          • Insensitivity/lack to/of ADH à solitary water losses à hypovolaemia
          • Body compensates by resorbing more Na+ to reduce the water loss
          • Water loss persists and so you get a hypovolaemic hypernatraemia
      • Non-renal losses:
        • GI loss
        • sweat loss
  • 2nd –> maintain the low water intake:
    • Child / elderly / dementia
    • Fasting for surgery
    • Simply cannot keep up with losses
    • Busy nightshift and forget to drink
35
Q

What are the investigations for patient with suspected diabetes insipidus?

A
  • Serum glucose – exclude diabetes mellitus –> osmotic diuresis
  • Serum potassium – exclude hypokalaemia –> nephrogenic DI
  • Serum calcium – exclude hypercalcaemia –> nephrogenic DI
  • Plasma and urine osmolality –> exclude hyperaldosteronism (high plasma osmolality, low urine osmolality)
  • Water deprivation test (normal = concentrated urine, no ADH = carry on passing water – dilute urine)
36
Q

What is the management of hypernatraemia?

A
  • Fluid replacement → dextrose (if the patient is also hypovolemic, then 0.9% saline and 5% dextrose water)
  • Treat underlying cause

i.e.

  • Correct water deficit → 5% dextrose
  • Correct ECF volume depletion → 0.9% saline
  • Serial Na+ measurements → every 4-6 hours
37
Q

What are the effects of diabetes mellitus on serum sodium?

A
  • Variable
  • Hyperglycaemia draws water out of cells leading to hyponatraemia
  • Osmotic diuresis in uncontrolled diabetes leads to loss of water and hypernatremia