Electrolytes and phosphate Flashcards
(28 cards)
Sodium regulation
Serum Na+ determined by ratio of total ECF Na+ to total ECF water
Na+ concentrations regulated through changes in blood volume
Hypovolaemia -> RAAS is activated and angiotensin II and aldosterone stimulate sodium and water reabsorption in the kidney. Associated with increased ADH secretion which in turn stimulates water reabsorption
In hypervolaemia atrial natriuretic peptide (ANP) is secreted which decreased sodium and water reabsorption in the kidney.
Causes of decreased ECF sodium
Altered renal handling (increased excretion) - hypoadrenocorticism, ketonuria
Alimentary losses - vomiting, diarrhoea
Hypoadrenocorticism and sodium
Immune mediated destruction of adrenal glands
Often in young, female dogs
Leads to reduced cortisol and aldosterone production
Clinical signs: intermittent vomiting and diarrhoea, lethargy, abdominal pain, weight loss
Lack of aldosterone meanns that sodium and water are not reabsorbed in kindey and potassium is not excreted.
Hyponatraemia and hyperkalaemia
Ketonuria and sodium
Ketones produced in NEB or when glucose not able to get into cells due to lack of insulin
Ketones are filtered from circulation and not reabsorbed
They are anionic so require cations for electroneutrality, so are excreted with sodium and/or potassium
Causes of increased ECF water
Hyperglycaemia - Shifts water from ICF to ECF (osmotic effects)
Causes of hypernatraemia
Inadequate water intake - water deprivation or inadequate thirst response (hypothalamic lesion)
Pure water loss (respiratory) without intake - pyrexia, panting
Hypotonic fluid losses - diabetes insipidus (nephrogenic or central), osmotic diuresis
Consequences of hyponatraemia
Cells become hypertonic so water moves from ECF to ICF. Other solute move out of cells to compensate for this.
Associated with neurological signs (weakness, depression, seizures)
Consequences of hypernatraemia
Cells are hypotonic so water moves from ICF into ECF. Solutes leak back into cells to compensate.
If chronic then brain cells generate idiogenic osmoles to raise intracellular osmolality and retain water
Associated with neurological signs (weakness, depression, seizures)
Correction of hypernatraemia
Use IV fluids
Serum sodium should be monitored closely (hourly) and should not be corrected faster than 0.5mmol/L/hr to avoid development of cerebral oedema
Serum chloride concentrations
Influenced by serum sodium concentration and serum bicarbonate concentrations
Chloride maintains electric neutrality in response to changes in serum sodium and bicarbonate concentration
Should be interpreted in light of knowledge of serum sodium and acid base status
Chloride regulation
Reabsorbed with sodium in the proximal tubules
Also actively reabsorbed in the Loop of Hene which is inhibited by furosemide
Cells in the distal tubules secrete Cl- with H+ in acidosis and conserve Cl- in exchange for HCO3- in alkalosis
Causes of hypochloraemia with hyponatraemia
Same causes as hyponatraemia
Hypoadrenocorticism
Ketonuria
Alimentary losses
Causes of hypochloraemia with normonatraemia
Metabolic alkaloses
- vomting (loss of H+ and Cl-)
- furosemide therapy (loss of Cl-)
Accumulation of other anions
- ketoacidosis
- lactic acidosis
- ethylene glycol toxicity
Causes of hyperchloraemia with hypernatraemia
Same causes as hypernatraemia
Inadequate water intake
Pure water losses (respiratory) without intake
Hypotonic fluid losses
Causes of hyperchloraemia with normonatraemia
Consider potassium bromide administration
Alimentary or renal losses of bicarbonate (uncommon)
Regulation of serum potassium
Renal excretion
- excreted by cells in distal tubule, driven by aldosterone activity
- aldosterone secretion is stimulated by hyperkalaemia
- faster urinary flow rate promotes potassium excretion by maintaining downwards concentrating gradient
Change in distribution between ICF and ECF
- hyperkalaemia promotes uptake by cells
- hypokalaemia promotes release by cells
- adrenaline and insulin promote uptake by cells
Causes of hyperkalaemia
Pseudohyperkalaemia
Reduced renal excretion - AKI, urinary obstruction of leakage, hypoaldosteronism (hypoadrenocorticism, ACE-i)
Increased potassium intake - IV administration
Shifting from ICF to ECF - tissue necrosis, metabolic inorganic acidosis
Causes of pseudohyperkalaemia
Thrombocytosis (platelets release potassium during clotting)
Delayed serum separation
In vitro haemolysis (usually only mild unless japanese breed with high K+ red cells)
EDTA contamination (contains K+)
COnsequences of hyperkalaemia
Bradycardia and weakness
Correction of hyperkalaemia
Administration of IV fluids and furosemide to increase urinary flow rate and potassium excretion
If secondary to urinary blockage or leakage then resolve this
Detrimental effects on the heart can be reduced by administration of calcium gluconate and administration of insulin/glucose solutions to encourage K+ uptake
Causes of hypokalaemia
Decreased total body potassium
- reduced intake (anorexia)
- increased renal excretion (increased flow rate e.g. CKD, increased excretion of anions e.g. ketonuria, hyperaldosteronism)
- increased alimentary losses (diarrhoea)
Shifting of potassium into cells (minor effects)
- insulin therapy
- alkalosis
- endotoxaemia
Consequenses of hypokalaemia
Weakness and cervical ventroflexion in cats (due to lack of nuchal ligament)
Correction of hypokalaemia
Mild: corrected with potassium supplements in diet
Marked: IV administration of potassium supplemented fluids - ensure well mixed as high concentration can cause cardiac arrest and sudden death
Determinants of serum phosphate concentrations
Intestinal absorption, shifting of phosphate between ICF and ECF, and renal excretion
