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
Volume Expanded:
No oedema
Oedema
No oedema
SIADH
Hypothyroid
UNa>20
Rx – Normal Saline
Oedema
Nephrotic Cirrhosis
CCF
UNa <10
Rx – fluid restriction
SIADH
Inappropriate action of ADH
Causes of Inappropriate ADH Secretion (SIADH) →
Neoplasia
Pulmonary disorders
Neurological disorders 0 dsmage hypothalamus
Neoplasia
Bronchogenic carcinoma
Pancreatic carcinoma
Lymphoma
Pulmonary disorders
Pneumonia Tuberculosis Bronchiectasis Positive pressure ventilation Acute exacerbation of COPD (reduction with sodium)
Neurological disorders - damage hypothalamus
Encephalitis (basal)
Meningitis (basal)
Head Injury
Porphyria (toxic)
Causes of Hypernatraemia →
Inadequate water intake Impaired water retention Loss of hypotonic fluids Excessive sodium intake Increased sodium retention
Inadequate water intake
- Lack of water (not available)
- Inability to drink (coma)
- Loss of thirst
Impaired water retention
Diabetes insipidus Osmotic diuresis (very common due to hyper glycaemia)
Loss of hypotonic fluids
Sweat
Hyperventilation
Watery diarrhoea
Burns
Excessive sodium intake
Intravenous fluids
Drugs (e.g. IV antibiotics)
Increased sodium retention
Primary hyperaldosteronism (Conn’s Syndrome)
Diabetes insipidus:
→ Deficiency in ADH
Causes if Diabetes Insipidus →
Cranial
Nephrogenic
Cranial types
Idiopathic
Secondary
Idiopathic
Familial (autosomal dominant)
Sporadic
Secondary
Trauma (accidents, surgery) Tumours (craniopharyngioma, pit, adenoma) Granuoma (sarcoid, histocytosis X) Infection (encephalitis, meningitis) Vascular (aneurysm, hypoxia, vasculitis) Autoimmune
Idiopathic
Familial (autosomal dominanant)
Sporadic
Secondary:
Drugs/Toxins Metabolic Vascular Pyelonephritis After ATN
Secondary: Drugs and Toxins
Demeclocycine – used to treat SIADH
Lithium
Metabolic
Hypercalcaemia
Hypokalaemia
Amyloid
Vascular
Sickle cell disease
