disorders of fluid and electrolyte balance Flashcards
Causes of hyponatremia - h20 retention
Usually H20 retention secondary to ecxcretion
(advanced renal failure. In absence of advanced renal failure, usually due to inability to suppress secretion of ADH
-can be because of hormonal changes such as cortisol deficiency, hypothyroidism
Causes of hyponatremia
Primary polydipsia [excessive water drinking]- often schizophrenia
What is pseudohyponatraemia
Artefactually low serum [Na+] resulting from volume displacement by massive hyperlipidaemia or hyperproteinemia
can be caused by hyperglycaemia or uncontrolled diabetes
How does pseudohyponatraemia present as
Plasma osmolality is normal
Plasma [Na+] is apparently low
Causes of hypernatremia
1) Mainly H20 loss (eg. diabetes insipidus, fever) + impaired thirst.
2) Na+ retention (eg. administration of hypertonic NaCl or NaHCO3-)
What is ECF [K+] controlled by
Uptake of K+ into cell
Renal excretion and extrarenal losses
What accounts for almost all K+ excretion
Abnormality in one/both of internal and external K+ balance in hypo/hyperkalaemia
Effect of increase in K+
↑[K°] –>depolarise membrane –> more excitable; but persistent depolarisation inactivates Na+ channels –> decreased membrane excitability –> impaired cardiac conduction/muscle weakness (paralysis).
Effect of decreased K+
low [K°] –> hyperpolarise membrane –> less excitable; but in cardiac myocytes –>membrane excitability due to removal of normal inactivation of Na+ channels
What does intracellular K+ affect
Protein and glycogen synthesis
What does a decrease in K+ reduce sensitivity to
ADH
Physiological factors influencing transcellular distribution of K+
Na+/K+ ATPase Catecholamines Plasma [K+] Exercise Insulin
Pathology al factors which influence transcelluler distribution of K+
Chronic diseases
Extracellular pH (decrease pH increases K+ etc)
Hyperosmolality (more water increases K+ movement out of cell)
Rate of cell breakdown
What does lack of insulin and b2 adrenoceptor antagonism do to plasma K+
Impairs but does not prevent K+ movement into cells
How do catecholamines influence trans cellular distribution of K+
B2 receptors increase K+ uptake into cells; activates Na+/K+ ATPase
When might there be increased rate of cell breakdown which would lead to increase in K+ release
Severe trauma e.g. burns, rhabdomyolysis
Causes of hypokalaemia
decreased net intake may contribute but rarely solely responsible
Increased entry into cells
Increased GI losses (vomiting diarrhoea)
How can there be increased entry into cells which may cause hypokalaemia
Alkalosis
Insulin (diabetic hyperglycaemia- K+ depleted already)
B2 adrenoceptor activation (adrenaline, stress, hypoglycaemia or inhalers)
Increased urinary losses
Increased sweat loss
What can cause increased urinary losses
Loop or thiazide like diuretics Vomiting Mineralocorticoid excess Renal tubular acidosis Rare hereditary disorders
How can vomiting cause hypokalaemia
Initially KHCO3- lose, Na+ reabsorbed
How can mineralocorticoid excess cause hypokalaemia
most often due to aldosterone-producing adrenal adenoma; usually results in metabolic alkalosis due to aldosterone stimulation of H+ATPase
How does type 1 renal tubular acidosis cause hypokalaemia
Decreased distal H+ secretion
Therefore increased K+ secretion for electroneutrality as Na+ is reabsorbed
How does type 2 renal tubular acidosis cause hypokalaemia
Decreased proximal HCO3- reabsorption
Therefore increased HCO3- loss in urine leads to increase in K+ secretion
How can hypokalaemia cause renal dysfunction
Polyuria, polydipsia
Increased ammoniagenesis
Increased HCO3- reabsorption (intracellular acidosis_
