Chem path 3: Sodium and fluid balance Flashcards

1
Q

What is the commonest abnormality in hospitalised patients?

A

Hyponatraemia

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2
Q

What is the underlying pathogenesis in hyponatraemia?

A

Excess extracellular water

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3
Q

What hormone is responsible for water balance and how does it act on the kidney?

A

ADH, acts on V2 receptors in collecting duct cells by inserting AQ2 channels

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4
Q

Where are V1 receptors found and how does ADH act on them?

A

Vascular smooth muscle, ADH –> vasoconstriction at higher concentrations

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5
Q

What are the two main stimuli for ADH secretion?

A

Increased osmolality and reduced blood volume/pressire

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6
Q

What are serum osmolality and blood pressure/volume mediated by, respsectively?

A

Osmoreceptors and baroreceptors

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7
Q

Where are osmoreceptors and baroreceptors found, respectively?

A

Osmoreceptors - hypothalamus

Baroreceptors - Carotids, aorta, atria

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8
Q

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

A

Assess their volume status

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9
Q

What is the most reliable clinical sign of hypovolaemia?

A

Low urine Na+ (<20)

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10
Q

In which cohort of patients is urine Na+ not a reliable clinical marker of hypovolaemia?

A

patients on diuretics as they will have a high urine sodium regardless

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11
Q

What are the clinical features of hypervolaemia?

A

Raised JVP
Bibasal crackles
Peripheral oedema

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12
Q

Causes of hypovolaemic hyponatraemia

A

Diarrhoea/vomiting
Diuretics
Salt losing nephropathy

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13
Q

Euvolaemic hypoantraemia

A

Hypothyroidism
SIADH
Adrenal insufficiency

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14
Q

Hypervolaemic hyponatraemia

A

Cirrhosis
Nephrotic syndrome/renal failure
Heart failure

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15
Q

What does a urine sodium <20 indicate and what does one >20 indicate?

A

if <20, suggests the hyponatraemia is not due to renal causes >20 suggests due to renal causes

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16
Q

How does cardiac failure cause hypervolaemic hyponatraemia?

A

Low pressure is detected by the baroreceptors –> ADH release

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17
Q

How does cirrhosis cause hypervolaemic hyponatraemia?

A

Release of vasodilators e.g. NO which results in low pressure which is detected by baroreceptors –> ADH release

18
Q

How does renal failure cause hypervolaemic hyponatraemia?

A

Not excreting enough water. CKD results in urinary protein loss and hence oedema. This lower circuilating volume activates RAAS which results in sodium retention. This in turn causes ADH release –> water retention and hypervolaemic hyponatraemia

19
Q

How does hypothyroidism cause euvolaemic hyponatraemia?

A

Reduced cardiac contractility –> reduced BP –> ADH release

20
Q

How does SIADH cause hyponatraemia?

A

Excess AQ2 insertion in collecting duct –> water retention and increased blood volume –> suppresses RAAS –> less aldosterone –> less Na+ reabsorption

21
Q

Causes of SIADH

A

Lung cancer, pneumonia (legionella), CNS pathology, stroke, drugs (SSRIs, TCA, PPI, carbamazepine), surgery

22
Q

Why does SIADH cause a euvolaemic hyponatraemia and not hypervolaemic?

A

Excess ADH = excess water = volume expansion → secretion for BNP → naturesis –> euvolaemic

23
Q

What are two causes of pseudohyponatraemia?

A

Hyperlipidaemia and hyperproteinaemia

24
Q

What happens to the urinary sodium in patients with heart failure?

A

Urinary sodium low as there will be secondary hyperaldosteronism causing sodium retention

25
Q

How do you diagnose SIADH?

A

No hypovolaemia, no hypothyroidism, no adrenal insufficiency, reduced plasma osmolality and increased urine osmolality (>100!!!!1)

26
Q

Management of pt with hypovolaemic hyponatraemia

A

VOlume replacement with 0.9% saline

27
Q

Management of pt with euvolaemic hyponatraemia

A

Fluid restrict + treat underlying cause

28
Q

Management of pt with hypervolaemic hyponatraemia

A

Fluid restrict + treat underlying cause

29
Q

What are two main signs of severe hyponatraemia and how is this treated?

A

Seizures and reduced GCS. Mx by seeking expert advice + 3% hypertonic saline

30
Q

At what rate must serum sodium be correcteD?

A

8-10mmol/L in the first 24 hrs

31
Q

If sodium serum is corrected too quickly what can this lead to?

A

Central pontine myelinolysis

32
Q

What drugs are used to treat SIADH if fluid restriction is inefficient?

A

Demeclocycline or tolvaptan

33
Q

What is demeclocyline’s MOA?

A

Reduces responsiveness of collecting tubule cells to ADH, induces a nephrogenic diabetes insipidus

34
Q

What do you need to monitor in pts taking demeclocycline?

A

U&Es as can cause nephrotoxicity

35
Q

Tolvaptan MOA

A

V2 receptor antagonist

36
Q

What is hypernatraemia caused by?

A

Unreplaced water loss

37
Q

What are the causes of hypernatraemia?

A

Loss of water: renal losses e.g. osmotic diuresis, diabetes insipidus. non-renal losses e.g. GI, sweat loss. Increase in sodium: Medical, dietary, Conn’s, BAH, RAS, Cushing’s

38
Q

Causes of nephrogenic DI

A

Hypercalcaemia, hypokalaemia, lithium, SCA

39
Q

What investigations are done for nephrogenic DI?

A

Serum glucose –> diabetes melltius –> osmotic diuresis
Serum potassium –> hypokalaemia –’> nephrogenic DI
Serum calcium
Plasma and urine osmolality (Exclude hyperaldosteronism)
Water deprivation test

40
Q

How do you treat hypernatraemia?

A

GIVE 5% DEXTROSE AS WILL REPLACE FLUID WITHOUT GIVING ADDED SALT

41
Q

E.G. 70-year old man, 3-day history of diarrhoea, altered mental status, dry mucous membranes. Serum Na is 168mmol/L

A
  • Correct water deficit → 5% dextrose
  • Correct ECF volume depletion → 0.9% saline
  • Serial Na+ measurements → every 4-6 hours
42
Q

What is the relationship between diabetes mellitus and sodium?

A

It is variable as hyperglycaemia will draw water out of cells leading to hyponatraemia however osmotic diuresis in uncontrolled diabetes leads to loss of water and hypernatraemia