Sodium and fluid balance Flashcards

(38 cards)

1
Q

Cause of hyponatraemia

A

increased extracellular water

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2
Q

Hormone that controls water balance

A

ADH (vasopressin)

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3
Q

How does ADH control water balance

A

synthesised in the hypothalamus, 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

ADH acts on which receptors?

A

V1 receptors: On vascular smooth muscle, causes vasoconstriction at higher concentrations; V2 receptors: On kidneys, insertion of aquaporin-2 channels on collecting ducts.

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5
Q

Stimuli for ADH secretion

A

Serum osmolality is high - mediated by hypothalamic osmoreceptors; Blood volume/pressure (hypotension) - mediated by baroreceptors in carotids, atria and aorta.

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6
Q

Increased ADH effect on serum sodium

A

Hyponatraemia More water = Less sodium)

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7
Q

First step in assessing hyponatraemia

A

Clinical assessment of volume status: Look at hands, head and neck, peripheries.

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8
Q

Signs of hypovolaemia

A

Dry mucous membranes, reduced JVP, reduced tissue turgor, tachycardia, postural hypotension, confusion/drowsiness, reduced urine output, low urine Na+ (<20).

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9
Q

Signs of hypervolaemia

A

Raised JVP, peripheral oedema, bibasal crackles (on chest examination).

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10
Q

What makes urine sodium uniterpretable?

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

Causes of hyponatraemia in hypovolaemic patient

A

Renal: diuretics; Extra-renal: diarrhoea, vomiting.

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12
Q

Causes of hyponatraemia in hypervolaemic patient

A

Cardiac failure, cirrhosis, renal failure.

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13
Q

Causes of hyponatraemia in 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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14
Q

Causes of SIADH

A

CNS pathology, lung pathology, drugs (SSRI, TCA, opiates, PPIs, carbamazepine), tumours, surgery.

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15
Q

Investigations for euvolaemic hyponatraemia

A

Hypothyroidism: Thyroid function tests; Adrenal insufficiency: Short synacthen test; SIADH: Plasma and urine osmolality (low plasma & high urine osmolality).

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16
Q

Osmolality in SIADH

A

Plasma osmolality - LOW; Urine osmolality - HIGH (>100).

17
Q

Diagnosis of SIADH requirements

A

No hypovolaemia, no hypothyroidism, no adrenal insufficiency, reduced plasma osmolality, increased urine osmolality (>100).

18
Q

Management of hypovolaemic patient with hyponatraemia

A

Volume replacement with 0.9% saline

19
Q

Management of hypervolaemic patient with hyponatraemia

A

Fluid restriction and treat the underlying cause.

20
Q

Management of euvolaemic patient with hyponatraemia

A

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

21
Q

Clinical symptoms of severe hyponatraemia

A

Reduced GCS, Seizures

22
Q

Management of severe hyponatraemia

A

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

23
Q

Important point while correcting hyponatraemia

A

Serum Na must NOT be corrected >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.

24
Q

Drugs used to treat SIADH

A

Demeclocycline, Tolvaptan.

25
How Demeclocycline works
Reduces responsiveness of collecting tubule cells to ADH. Need to monitor U&Es (risk of nephrotoxicity).
26
How Tolvaptan works
V2 receptor antagonist. Very expensive.
27
Treatment for SIADH
Water restriction PLUS (but both used rarely) Demeclocycline (reduces responsiveness of collecting tubule cells to ADH - but caution because nephrotoxic) OR Tolvaptan (V2 receptor antagonist) - use cautiously as they work rapidly.
28
Main causes of hypernatraemia
Unreplaced water loss, Gastrointestinal losses, sweat losses, Renal losses: osmotic diuresis, reduced ADH release/action (Vasopressin deficiency/resistance), Patient cannot control water intake e.g. children, elderly.
29
Investigations for suspected VP deficiency
Serum glucose (exclude diabetes mellitus), Serum potassium (exclude hypokalaemia), Serum calcium (exclude hypercalcaemia), Plasma and urine osmolality, Water deprivation test - urine osmolality will fail to increase.
30
Presentation of VP deficiency
Polyuria and polydipsia.
31
Treatment for hypernatraemia
Fluid replacement and treat the underlying cause.
32
Management of hypernatraemia
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.
33
Effects of diabetes mellitus on serum sodium
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.
34
Definition of hyponatraemia
Sodium concentration <135 mmol/L.
35
severe hyponatraemia sodium concentration
<120 mmol/L
36
Investigations you need to do before you can make a diagnosis of SIADH
CXR, CT head, abdo, pelvis
37
hypernatraemia sodium concentration.
>145 mmol/L
38
Why does cirrhosis cause hyponatraemia?
Excess ADH secreted due to NO, this causes vasodilation - lower blood pressure which is detected by baroreceptors