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PATH FINAL > ChemPath: Sodium and Fluid Balance > Flashcards

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 via V2 receptors

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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 sodium

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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 (as patient rehydrates by drinking 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: Loss of water + Na → hypovolaemia causing excess ADH release → increased water reabsorption (but not of Na+) hence hyponatraemia as ECF water level is increasing (albeit not as high as normal status hence still hypovol) but Na level is NOT matching

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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 but no capillary leakage = ADH release
  • Adrenal insufficiency - less aldosterone released resulting in less Na+ reabsorption.
  • SIADH (excess ADH release)
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16
Q

What are the causes of SIADH?

A
  • CNS pathology (any)
  • Lung pathology (any)
  • 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

SIADH excess fluid distributed equally across ICF and ECF but ultimately increased volume triggers natriuretic peptide release causing natriuresis (peeing Na) causing low Na in ECF.

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) - before thinking SIADH MUST RULE OUT hypothyroid and adrenal insufficiency.
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 -

As hypoNa is due to loss of fluid causing excess ADH. Giving NaCl replenishes lost fluid, with isotonic fluid (fluid that has appropriate amount of sodium in it). This shuts off ADH stimulation which is driving this hyponatraemia.

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 because if given in euvolemic or hypervolemic, NaCl will just increase ECF water content further increasing the disparity between water and sodium content and therefore worsening the hyponatraemia.

23
Q

How would you manage a euvolaemic patient with hyponatraemia?

A

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

Do NOT give saline because if given in euvolemic or hypervolemic, NaCl will just increase ECF water content further increasing the disparity between water and sodium content and therefore worsening the hyponatraemia.*

24
Q

What are clinical symptoms of severe hyponatraemia? How would you treat it?

A
  • Reduced GCS
  • Seizures
25
Q

How is severe hyponatraemia managed?

A

Can give boluses of hypertonic 2.7% saline but only if patient has low GCS or fitting.

DO NOT GIVE 2.7% 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

Aetiology either unreplaced water loss, sodium overload or water intake deficit

Unreplaced water loss = GI loss, Renal loss (diabetes insipidus, osmotic diuresis)

Sodium overload = iatrogenic, Cushing’s syndrome, Conn’s syndrome

Water intake deficit = abnormal thirst mechanism, child/frail elder

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 (exclude 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

Dextrose is hypertonic causing water to leave cells into ECF to increase water levels in ECF hence correcting water deficit.
0.9% NaCl is isotonic but manages to correct the volume depletion seen in hypernatraemia.

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

PATH FINAL (36 decks)

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