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YEAR 5 - CHEMPATH > ChemPath: Sodium and Fluid Balance > Flashcards

ChemPath: Sodium and Fluid Balance Flashcards

1
Q

What is the underlying pathogenesis of hyponatraemia?

A

Excess water - concentration of sodium is lower

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2
Q

Which hormone controls water balance?

A

ADH (vasopressin)

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3
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.

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4
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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5
Q

What are the two main stimuli for ADH secretion?

Where are the receptors

A
  • high serum osmolality - mediated by hypothalamic osmoreceptors
  • low blood volume/pressure - mediate by baroreceptors in carotids, atria and aorta
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6
Q

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

A

Hyponatremia

(More water = Less sodium)

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7
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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8
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

hard to differentiate between hypo + euvolemia without urine Na+

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9
Q

What are clinical signs of hypervolaemia?

A
  • Raised JVP
  • Peripheral oedema
  • Bibasal crackles (on chest examination)
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10
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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11
Q

What are causes of hypovolaemia?

A
  • Diarrhoea
  • Vomiting
  • Diuretics
  • Salt losing nephropathy

NOTE: even though patient is hypovolemic the hyponatremia is still due to excess water because the drop in blood volume –> baroceptors –> release ADH –> reabsorb more water

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12
Q

What are causes of euvolaemic hyponatraemia?

A
  • Hypothyroidism
  • Adrenal insufficiency
  • SIADH
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13
Q

What are causes of hypervolaemic hyponatraemia?

A
  • Heart failure —> reduced CO –> low BP –> detected by baroceptors –> ADH release
  • Cirrhosis –> increase NO produced –> splanchnic vasodilation –> low BP –> baroceptors –> ADH released
  • Nephrotic Syndrome –> albumin lost in urine –> oncotic pressure lost from blood –> water moves into insteritium –> low BP –> baroreceptors –> ADH released
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14
Q

What are causes of hyponatraemia in a hypovolaemic patient?

A
  • Renal: diuretics
  • Extra-renal: diarrhoea, vomiting
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15
Q

What the causes of hyponatraemia in a hypervolaemic patient?

A
  • Cardiac failure
  • Cirrhosis
  • Renal failure
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16
Q

What are causes of hyponatraemia in a euvolaemic patient?

A
  • Hypothyroidism - due to reduction in CO detected by baroreceptors leading to ADH secretion
  • Adrenal insufficiency - cortisol needed for water excretion, aldosterone needed for sodium and water retention.
  • SIADH
17
Q

What are the causes of SIADH?

A
  • CNS pathology - infection, haemorrhage, stroke
  • Lung pathology - PE, SCLC, pneumonia, pneumothorax
  • DRUGS (SSRI, TCA, opiates, PPIs, carbamazepine)
  • Tumours - don’t forget breast exam
  • Surgery - acutely due to fluid adminstration during surgery
18
Q

What investigation is urgently required in suspected SIADH

A

CT head - to exclude brain/CNS pathology

CXR - to exclude lung pathology

to identify underlying cause - if nothing with these –> CT CAP

19
Q

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

A
  • Hypothyroidism: Thryoid function tests
  • Adrenal insufficiency: Short synacthen test
  • SIADH: Paired plasma and urine osmolality (low plasma & high urine osmolality)
20
Q

how does the short synACTHen test work

A

inject potent synthetic ACTH

if no corresponding rise in serum cortisol –> adrenal insufficiency

21
Q

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

A

Plasma osmolality - LOW

Urine osmolality - HIGH (>100)

High ADH –> resorbing lots of water
Circulating volume increase –> atria stretches –> ANP release –> excrete more Na+

22
Q

What does a diagnosis of SIADH require?

A
  • No hypovolaemia - urine Na+ has to be normal
  • No hypothyroidism - TFTs normal
  • No adrenal insufficiency - rise in cortisol following short synACTHen test
  • Reduced plasma osmolality
  • Increased urine osmolality (>100)
23
Q

How would you manage a hypovolaemic patient with hyponatraemia?

A

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

24
Q

How can saline be used for diagnostic purposes in hyponatremia

A

Give a very small amount of saline

If Na+ continues to fall –> indicates it is SIADH

If it starts to increase –> indicates its hypovolemic

25
Q

How would you manage a hypervolaemic patient with hyponatraemia?

A

Fluid restriction 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.

26
Q

How would you manage a euvolaemic patient with hyponatraemia?

A

Fluid restriction and treat the underlying cause (same as hypervolaemic patient with hyponatraemia)

27
Q

What are clinical symptoms of severe hyponatraemia?

A
  • Reduced GCS
  • Seizures

Seek expert help (treat with hypertonic 3% saline)

28
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.

29
Q

What is an important point to remember while correcting hyponatraemia?

A
  • Serum Na must NOT be corrected >4-6 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
30
Q

What is the treatment for SIADH?

A

Water restriction

PLUS (but both used rarely)

  1. Demeclocycline - reduces responsiveness of collecting tubule cells to ADH - but caution because nephrotoxic - monitor U&Es
    OR
  2. Tolvaptan (V2 receptor antagonist) - use cautiously as they work rapidly
31
Q

What are the main causes of hypernatraemia?

A
  • Unreplaced water loss
    • Gastrointestinal losses, sweat losses
    • Renal losses: osmotic diuresis, reduced ADH release/action (Diabetes insipidus/Vasopressin deficiency/resistance)
  • Patient cannot control water intake e.g. children, elderly
  • Diabetes insipidus
    • Not enough ADH
    • Resistant to ADH
  • Osmotic diuresis in uncontrolled diabetes mellitus
    • Loss of water leads to HHS
32
Q

What investigations would you order in a patient with suspected vasopressin deficiency/resistance?

Prev known as diabetes insipidus

A
  • Serum glucose (exclude diabetes mellitus)
  • Serum potassium (exclue hypokalaemia) - low K+ reduces action of ADH (vasopression resistance)
  • Serum calcium (exclude hypercalcaemia) - high Ca2+ reduces action of ADH (vasopressin resistance)
  • Plasma and urine osmolality
  • 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

How would you treat hypernatraemia?

A
  • Fluid replacement (not normal saline!!)
  • Treat the underlying cause
35
Q

What is the management of hypernatraemia?

A
  • Correct water deficit
    • 5% DEXTROSE (free water)
  • May need to correct extracellular fluid volume depletion/hypovolemia (especially if they’ve been vomiting)
    • 0.9% saline
  • Serial Na+ measurement
    • Every 4-6 hours
    • Risk of cerebral oedema is correction is too rapid –> seizures –> coma –> death

normal saline will NOT treat hypernatremia

36
Q

What are the effects of diabetes mellitus on serum sodium?

A

Variable:

  • 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

37
Q

What is the definition of hyponatraemia?

A

Sodium concentration <135 mmol/L

YEAR 5 - CHEMPATH (26 decks)

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