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
How do you diagnose SIADH?
No hypovolaemia, no hypothyroidism, no adrenal insufficiency, reduced plasma osmolality and increased urine osmolality (>100!!!!1)
26
Management of pt with hypovolaemic hyponatraemia
VOlume replacement with 0.9% saline
27
Management of pt with euvolaemic hyponatraemia
Fluid restrict + treat underlying cause
28
Management of pt with hypervolaemic hyponatraemia
Fluid restrict + treat underlying cause
29
What are two main signs of severe hyponatraemia and how is this treated?
Seizures and reduced GCS. Mx by seeking expert advice + 3% hypertonic saline
30
At what rate must serum sodium be correcteD?
8-10mmol/L in the first 24 hrs
31
If sodium serum is corrected too quickly what can this lead to?
Central pontine myelinolysis
32
What drugs are used to treat SIADH if fluid restriction is inefficient?
Demeclocycline or tolvaptan
33
What is demeclocyline's MOA?
Reduces responsiveness of collecting tubule cells to ADH, induces a nephrogenic diabetes insipidus
34
What do you need to monitor in pts taking demeclocycline?
U&Es as can cause nephrotoxicity
35
Tolvaptan MOA
V2 receptor antagonist
36
What is hypernatraemia caused by?
Unreplaced water loss
37
What are the causes of hypernatraemia?
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
Causes of nephrogenic DI
Hypercalcaemia, hypokalaemia, lithium, SCA
39
What investigations are done for nephrogenic DI?
Serum glucose --> diabetes melltius --> osmotic diuresis Serum potassium --> hypokalaemia --'> nephrogenic DI Serum calcium Plasma and urine osmolality (Exclude hyperaldosteronism) Water deprivation test
40
How do you treat hypernatraemia?
GIVE 5% DEXTROSE AS WILL REPLACE FLUID WITHOUT GIVING ADDED SALT
41
E.G. 70-year old man, 3-day history of diarrhoea, altered mental status, dry mucous membranes. Serum Na is 168mmol/L
* Correct water deficit → 5% dextrose * Correct ECF volume depletion → 0.9% saline * Serial Na+ measurements → every 4-6 hours
42
What is the relationship between diabetes mellitus and sodium?
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