Biochemistry Hypo and Hyper natraemia Flashcards
2 interfaces:
- Cell membrane between intra and extra cellular
* Capillary epithelium between plasma and interstitial space
Cell membrane:
Balance of osmotic pressures →
• Intracellular potassium and associated anions balanced against the extracellular osmolality due to Sodium and its associated anions.
• It is this Osmotic balance that retains 2/3 of water insides cells.
= Osmi (k+) = Osmo (Na+)
Acute hyponatraemia Description
If there was an acute fall in extracellular Osmolality due to an acute fall in plasma Na concentration.
Fall in Na = fall is osmolality
Water → Will move towards the direction of higher osmolarity → Shift of water into the cells
Acute hyponatraemia Clinical features
Cerebral cellular oedema:
- Confusion (mild) – first sign
- Stupor
- Convulsions (most important)
- Coma
- Death (tentorial shift – coning)
Acute hyponatraemia Chronic Hyponatraemia
Sodium and extracellular osmolality falls slowly over weeks/months then there is a capacity to compensate by shifting the osmolar constituents to adjust for change.
Acute Hypernatraemia Description
Acute rise in extracellular Osmolality due to a rise in NA. Water will move towards the direction of higher osmolality → water leave cells
Acute Hypernatraemia Clinical features
Cerebral cellular dehydration accounts for acute hyernatraemia:
- Confusoin
- Stupor
- Convulsions (less often0
- Coma
Capillary endothelium function
Retain Plasma volume and interstial volume at the right levels
Governed by
Frank starling forces
Arterial end
Hydrostatic – water and electrolytes out arterial
Venous end
Colloid osmotic pressure drawing water back in at venous end
→ Small residual pressure exerted by large molecules (proteins mainly albumin)
Pathology
Reduction in albumin – nephrotic syndrome
Congestive cardiac failure – abnormal hydrostatic pressure gradient (accumulation of fluid in interstial space- oedema
Liver cirrhosis – abnormal albumin production and hydrostatic changes
Sodium and Water balance: Obligatory loss (unregulated inout)
- Skin (500 lm)
- Lungs (400 ml)
- Gut (100 ml)
- Kidney (UO) 500 m
Typical sources (regulated output): sodium and water
- Oxidation 400 ml
2. Dietary 1100 ml
Increased Fluid loss:
- Burns
- Fever
- Exercise
- Diarrhoea
- Vomiting
- Stomas
- Diabetes mellitus/insipidus
Pseudo Hyponatraemia explanation
Normally when we measure substance in plasma we assume that 1 L of plasma = 1 L of water.
→ E.g. Na in plasma 140 mmol/L
→ Homeostatic mechanisms regulates Na in plasma water
If patient has a negligible non water but with high lipid or immunoglobulin percentage of plasma not water will go up –less water per unit volume of plasma – less solvent for NA.
In plasma water 140 mol/L (still)
Total volume lower
If pseudo is suspected Measure
Osmolality – reflection of number of particles in the water. Despite the NA appearing low
ABG measurement of NA
Directly sense sodium concentration in plasma water (via electrode)
Compensated Hyponatraemia:
Description
If a patient has diabetes with a high extracellular glucose concentration. Not taken up to cells and not metabolism – how will this effect water?
Water moves out – dilutes other solutes present in plasma – therefore Na reduction
How does this effect Na levels
The high extracellular water dilutes other solutes present in plasma – therefore Na reduction
Compensated hyponatraemia always check
Glucose
Volume Depleted: Volume Expanded:
Renal Loss
Extra-Renal
Renal Loss
- Over diuresis
→ Thiazide diuretics – disproportionate loss of sodium - Intravascular volume depleted (excessive it can trigger ADH – this only protects WATER loss not Sodium loss) - Addison’s disease
Extra-Renal
Vomiting
Diarrhoea
