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[EDITED] YEAR 5: Chemical Pathology PM > ChemPath: Sodium and Fluid Balance > Flashcards

ChemPath: Sodium and Fluid Balance Flashcards

1
Q

How is osmolarity calculated?

A

2 (Na + K) + urea + glucose

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2
Q

What is the normal range for serum osmolarity?

A

275-295 mmol/kg

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3
Q

What is the underlying pathogenesis of hyponatraemia?

A

Excess water - concentration of sodium is lower

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4
Q

Which hormone controls water balance?

A

ADH (vasopressin)

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5
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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6
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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7
Q

What are the two main stimuli for ADH secretion?

A
  • Serum osmolality - mediated by hypothalamic osmoreceptors
  • Blood volume/pressure - mediate by baroreceptors in carotids, atria and aorta
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8
Q

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

A

Hyponatrium

(More water = Less sodium)

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9
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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10
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) - on admission before saline, if on diuretics, not useful

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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11
Q

What are clinical signs of hypervolaemia?

A
  • Raised JVP
  • Peripheral oedema
  • Bibasal crackles (on chest examination)
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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 hypovolaemia?

A
  • Diarrhoea
  • Vomiting
  • Diuretics
  • Salt losing nephropathy
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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
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17
Q

What are the causes of SIADH?

A
  • CNS pathology
  • Lung pathology
  • DRUGS (SSRI, TCA, opiates, PPIs, carbamazepine)
  • Tumours (most commonly SCLC)
  • Surgery
18
Q

What investigations would you order in a patient wih 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) [this is because urine gets concentrated]

20
Q

What is the diagnostic criteria for SIADH?

A
  • True hyponatraemia (<135)
  • Low serum osmolality (<270)
  • High urine sodium (>20)
  • No adrenal / thyroid / renal dysfunction (normal 9am cortisol and LFTs)
  • Clinically euvolaemic

I.e. diagnosis of exclusion

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 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 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?

A

If water restriction is insufficient:

  • Demeclocycline
  • Tolvaptan
28
Q

How does Demeclocycline work?

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 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) 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 / Mellitus [HHS])
  • Patient cannot control water intake e.g. children, elderly
32
Q

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

A
  • Serum glucose (exclude diabetes mellitus)
  • Serum potassium (exclue hypokalaemia)
  • Serum calcium (exclude hypercalcaemia)
  • Plasma and urine osmolality
  • Water deprivation test - urine osmolality will fail to increase
33
Q

Describe the results of the water-deprivation test

A

Normal:

  • Urine osmolality >600
  • U:P ratio >2

Primary polydipsia:

  • Urine concentrates but less than normal e.g. >400-600

Cranial DI:

  • Urine osmolality increases to >600 only after desmopressin

Nephrogenic DI:

  • No increase in urine osmolality even after desmopressin
34
Q

Describe cranial diabetes insipidus

A
  • Lack of / no ADH production
  • Causes: surgery, trauma, tumours
  • Mx: desmopressin
35
Q

Describe nephrogenic diabetes insipidus

A
  • Insensitivity to ADH (receptor defect)
  • Causes: lithium, demeclocycline, hypokalaemia, hypercalcaemia
  • Mx: thiazide diuretics
36
Q

What do patients with diabetes insipidus present with?

A

Polyuria and polydipsia

37
Q

How would you treat hypernatraemia?

A
  • Slow fluid replacement
  • Treat the underlying cause
38
Q

What is the management of hypernatraemia?

A
  • Correct water deficit
    • 5% DEXTROSE (free water)
  • May need to correct extracellular fluid volume depletion (especially if they’ve been vomiting)
    • 0.9% saline
  • Serial Na+ measurement
    • Every 4-6 hours
39
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

40
Q

What is the definition of hyponatraemia?

A

Sodium concentration <135 mmol/L

41
Q

How Hypothyroid causes hyponatraemia

A

Reduced Cardiac contractility

Increased ADH

[EDITED] YEAR 5: Chemical Pathology PM (27 decks)

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