Chempath - Sodium and Fluid Balance Flashcards

1
Q

% of body that is water

A

60%

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2
Q

Intracellular:extracellular fluid ratio

A

2:1

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3
Q

Components of ECF

A

Intravascular, interstitial (largest components), transcellular (within epithelial lined spaces e.g. CSF, joint fluid, urine etc)

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4
Q

ECF solute components in comparison to ICF

A

More Na+ and Cl-
Less K+

Think of cells as primitive organisms that used to be in the sea –> need salty water to survive

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5
Q

Osmolality vs osmolarity

A
Osmolality = total number of particles in solution - measured with an osmometer, units = mmol/kg.
Osmolarity = calculated, units = mmol/l
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6
Q

Osmolarity calculation

A

2(Na+ + K+) + urea + glucose

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7
Q

Osmolar gap

A

Osmolality - osmolarity

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8
Q

Normal range for serum osmolality

A

275-295 mmol/kg

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9
Q

Sodium normal range

A

135-145 mol/l

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10
Q

Hyponatraemia =

A

excess extracellular water relative to Na+

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11
Q

Hyponatraemia - Rx

A

Treat underlying cause, not the hyponatraemia (unless severe (<125mmol/l)) AND symptomatic (chronic hyponatraemias may be asymptomatic). More dangerous to correct too quickly –> central pontine myelinolysis

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12
Q

Hyponatraemia - Symptoms

A

Nausea and vomiting (<134)
Confusion (<131)
Seizures, non-cariogenic pulmonary oedema (<125)
Coma (<117) and eventual death

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13
Q

Hormone that controls water balance

A

ADH (vasopressin) - acts on V2 receptors to insert aquaporin 2 into collecting ducts to increase water reabsorption

Also - V1 receptors:
Vascular smooth muscle
Vasoconstriction (higher concentrations)
Alternative name ‘vasopressin’

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14
Q

2 main stimuli for ADH secretion

A

Serum osmolality (mediated by hypothalamic osmoreceptors). Increase in osmolality –> increased thirst and ADH secretion.

Blood volume/pressure (mediated by baroreceptors in carotids, atria, aorta). Decrease in BP –> increase in ADH

Increased ADH –> increased water reabsorption –> relative hyponatraemia.

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15
Q

1st step in assessing hyponatraemic patient

A

Assessment of fluid status

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16
Q

Clinical signs of hypovolaemia

A
Tachycardia
Postural hypotension
Dry mucous membranes
Reduced skin turgor
Confusion/drowsiness
Reduced urine output
Low urine Na+ (<20) --> kidneys try to hold onto the sodium to hols onto the water
17
Q

Clinical signs of hypervolaemia

A

Raised JVP
Bibasal crackles (on chest examination)
Peripheral oedema

18
Q

Causes of hypovolaemia

A

Gastro and renal

Diarrhoea
Vomiting
Diuretics - especially thiazides
Salt losing nephropathy

19
Q

Causes of euvolaemia

A

Endo

Hypothyroidism
Adrenal insufficiency
SIADH

20
Q

Causes of hypervolaemia

A

“Three Failures”

Heart failure –> reduced CO –> reduced BP –> increased ADH secretion
Renal failure
Liver failure (cirrhosis) –> NO –> vasodilation –> reduced BP –> increased ADH secretion

21
Q

Difference between hypovolaemia and dehydration

A

Hypovolaemia - loss of water AND salt

Dehydration - loss of water

22
Q

Causes of SIADH

A

CNS pathology
Lung pathology
Drugs (SSRIs, TCAs, opiates, PPIs, carbamazepine)
Tumours - (small cell lung cancer, pancreatic, prostate, lymphoma)
Surgery

23
Q

Pseudohyponatraemia

A

Excess protein/lipid may be sensed by the machine as water - SODIUM WILL APPEAR DILUTED BUT OSMOLALITY WILL BE NORMAL. e.g. in multiple myeloma

24
Q

Euvolaemic hyponatraemia Ix

A

TFTs
Short syntACTHen test
Plasma & urine osmolality (SIADH will have low plasma & high urine osmolality)

25
Q

Diagnosis of SIADH

A
No Hypovolaemia
No Hypothyroidism
No Adrenal insufficiency
Reduced plasma osmolality AND
Increased urine osmolality (>100)
26
Q

Hypovolaemic Hyponatraemia - Rx

A

Volume replacement with 0.9% saline

Give 250 ml –> if sodium goes up then it was hypovolaemia, if it goes down then it was euvolaemia (can use diagnostically).

27
Q

Hypervolaemic/Euvolaemic Hyponatraemia - Rx

A

Fluid restriction

Treat the underlying cause

28
Q

Severe hyponatraemia

A

Reduced GCS
Seizures
Seek expert help (Treat with HYPERTONIC 3% SALINE)

Serum Na must NOT be corrected > 8-10 mmol/L in the first 24 hours
Risk of osmotic demyelination (central pontine myelionlysis)
quadriplegia, dysarthria, dysphgia, seizures, coma, death

29
Q

SIADH - Rx

A

Demeclocycline- Reduces responsiveness of collecting tubule cells to ADH. Monitor U&Es (risk of nephrotoxicity).
Tolvaptan - V2 receptor antagonist

30
Q

Hypernatraemia - Main Causes

A

Unreplaced water loss
Gastrointestinal losses, sweat losses
Renal losses: osmotic diuresis, reduced ADH release/action (Diabetes insipidus)

Patient cannot control water intake e.g. children, elderly

31
Q

Suspected Diabetes Insipidus - Ix

A
Serum glucose (exclude diabetes mellitus)
Serum potassium (exclude hypokalaemia)
Serum calcium (exclude hypercalcaemia)
Plasma &amp; urine osmolality
Water deprivation test +/- desmopressin
32
Q

Hypernatraemia - Rx

A

Fluid replacement
Treat the underlying cause

Correct water deficit - 5% DEXTROSE
Correct extracellular fluid volume depletion- 0.9% SALINE
Serial Na+ measurements - Every 4-6 hours

33
Q

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

34
Q

Types of DI

A

Cranial:
Lack of ADH
Causes: surgery, trauma, tumours
Rx - desmopressin

Nephrogenic:
Receptor defect - insensitivity to ADH
Causes: inherited channelopathies, lithium, demeclocycline
Rx - thiazide diuretics

35
Q

Hypernataraemia - Clinical Features

A

Lethargy, thirst, irritability, confusion, coma, fits