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
Diagnosis of SIADH
``` No Hypovolaemia No Hypothyroidism No Adrenal insufficiency Reduced plasma osmolality AND Increased urine osmolality (>100) ```
26
Hypovolaemic Hyponatraemia - Rx
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
Hypervolaemic/Euvolaemic Hyponatraemia - Rx
Fluid restriction | Treat the underlying cause
28
Severe hyponatraemia
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
SIADH - Rx
Demeclocycline- Reduces responsiveness of collecting tubule cells to ADH. Monitor U&Es (risk of nephrotoxicity). Tolvaptan - V2 receptor antagonist
30
Hypernatraemia - Main Causes
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
Suspected Diabetes Insipidus - Ix
``` Serum glucose (exclude diabetes mellitus) Serum potassium (exclude hypokalaemia) Serum calcium (exclude hypercalcaemia) Plasma & urine osmolality Water deprivation test +/- desmopressin ```
32
Hypernatraemia - Rx
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
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
34
Types of DI
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
Hypernataraemia - Clinical Features
Lethargy, thirst, irritability, confusion, coma, fits