Assorted Electrolytes Flashcards
what are the main electrolytes?
Na+ K+ Ca2+ Mg2+ PO42-
homeostasis
requires the maintenance of water, pH and electrolytes within a narrow range to be conducive to life
1/3 reduction in K+
paralysis
unable to generate APs
1/2 Ca2+
tetanic skeletal muscle contractions
main calcium ion location
extracellularly
main magnesium ion location
intracellular
main phosphate ion location
intracellular
Na+
determinant in controlling ECF volume and water distribution
kidneys are major route of excretion
changes affect BP and intracellular fluid composition and volume
Na+ in kidney
freely filtered in glomerulus
reabsorbed in PCT, LoH and DCT so less than 1% is excreted in urine
homeostasis of plasma Na+
ADH secretion due to increased blood osmolality
reduced BP triggers ANP production and RAAS and ADH secretion
act on kidney to promote water and sodium rabsorption
hyponatraemia
<135mmol/L
serum osmolality important
isotonic and hypertonic hyponatraemia
possible alterations in other plasma components impacting Na+ concentration
high or normal serum osmolality
low serum osmolality
hypotonic hyponatraemia
true alteration in sodium concentration
presentation of hypotonic hyponatraemia
hypovolaemia
euvolaemia
hypervolaemia
pathophysiology of hypovolaemia
decreased water and Na+
excessive renal or extrarenal water and Na+ loss
euvolaemia
increased water retention
hypervolaemia
presence of oedema or ascites
increase in bodily water and sodium
causes of hypovolaemia
from diuretics, vomiting and diarrhoea
causes of euvolaemia
due to hypothyroidism
or adrenal insufficiency
causes of hypervolaemia
due to heart failure and renal disease
symptoms of hyponatraemia
headache
lethargy
dizziness
confusion
intervention for hyponatraemia
treat underlying cause
causes of hypernatraemia
reduction in bodily water
increased loss of water or decreased intake
rarely sodium gain
hypernatraemia
rarer
>145mmol/L
increased plasma osmolality
how can hypernatraemia present
euvolaemia
hypovolaemia
hypervolaemia
patient’s at high risk of hypernatraemia
fragile condition
restricted access to water - mental health, unconcious, small children
impaired thirst perception
common causes of hypernatraemia
dehydration not drinking enough diarrhoea kidney dysfunction diuretics
symptoms of hypernatraemia
thirst
fever
dry mucous membranes
restlessness
intervention for hypernatraemia
depends on underlying cause
K+
forms basis of resting membrane potential
sodium potassium pump
3 sodiums moved outside and 2 potassiums moved inside cell
resting membrane potential
small leak of potassium to outside of cell until equilibrium reached
what maintains K+ balance?
kidneys
renal handling of K+
freely filtered through glomerulus
reabsorbed along tubules - only 10% excreted
which cells are involved in reabsorption of K+
principal cells
intercalated cells
in DCT and collecting duct
activity of intercalated cells
K+/H+ transport with ATPase pump
K+ reabsorbed and H+ excreted stimulated by acidosis and low K+ concentration
activity in principal cells
ENaC
coupled channels reabsorb Na+ and secrete K+
stimulated by aldosterone, increased K+ conc and alkalosis and increased tubular flow
hypokalaemia
due to increased potassium uptake into cells or increased elimination of K+
causes of hypokalaemia
alkalosis diarrhoea vomiting renal loss diuretics reduced reabsorption of Na+ insulin administration hyperaldosteronism
symptoms of hypokalaemia
decreased neuromuscular excitability - muscle weakness decreased tone in smooth muscle delayed ventricular repolarisation bradycardia AV block
clinical features of hypokalaemia
membrane hyperpolarisation
parameters for hypokalaemia
<3.5mmol/L
intervention for hypokalaemia
oral or slow IV K+ administration
hyperkalaemia
movement of K+ from intracellular to extracellular environment or decreased excretion
parameters for hyperkalaemia
> 5.3mmol/L
common causes of hyperkalaemia
tissue damage
acidosis
aldosterone impairment
symptoms of hyperkalaemia
increased neuromuscular irritability restlessness intestinal cramping diarrhoea loss of muscle tone and paralysis in severe cases
clinical features of hyperkalaemia
ECG changes
ventricular fibrillation
hyperventilation
interventions for hyperkalaemia
diet or medication adjustment
insulin and glucose administration
Ca2+ to treat ECG changes
danger of hyperkalaemia
arrhythmias causing cardiac arrest and death
increase in blood calcium levels
calcitonin released by thyroid
binds to receptors on osteoblast
increases osteoblast activity - Ca2+ deposition and reduced phosphate ions in ECF
increased excretion of Ca2+
decrease in blood calcium levels
PTH released and binds to receptors on osteoblasts causing increased release of Ca2+ and phosphate ions into ECF
increased reabsorption of calcium and increased excretion of phosphate
activates production of vitamin D
vitamin D
increases Ca2+ absorption and phosphate absorption
hypocalcaemia
<2.1 mmol/L
causes of hypocalcaemia
nutritional deficiency vit. D deficiency hypoparathyroidism kidney failure hyperventilation
symptoms of hypocalcaemia
confusion muscle spasm paraesthesia drowsiness coma
clinical features of hypocalcaemia
ECG prolonged QT interval
intervention for hypocalcaemia
long term oral calcium and/ or vitamin D
IV calcium in severe cases
phosphate and magnesium ion monitoring
hypercalcaemia
> 2.6mmol/L
causes of hypercalcaemia
hyperparathyroidism
excess vit. D
malignancy in bone
symptoms of hypercalcaemia
stones bones moans groans fatigue muscle weakness
clinical features of hypercalcaemia
shorten QT segment
depressed T waves\hypertension
kidney stones
interventions for hypercalcaemia
reduce dietary intake of Ca2+ and vit. D
medication or surgery to reduce PTH
phosphate role
essential part of biochemical systems - bones, buffers strongly associated with Ca2+ and Na+ phospholipids ATP regulate enzyme activity
hypophosphataemia
> 0.4mmol/L
causes of hypophosphataemia
reduced intestinal absorption (low vit. D or alcohol abuse)
primary hyperparathyroidism
osteomalacia
rickets
symptoms of hypophosphataemia
muscle weakness - diaphragm and cardiac contractility
confusion
hallucinations
convulsions
clinical features of hypophosphataemia
left shift of oxy-haem dissociation curve - reduced O2 transport
arrhythmias
heart failure
intervention for hypophosphataemia
oral phosphate therapy
IV phosphate
hyperphosphataemia
> 1.5mmol/L
causes of hyperphosphataemia
chronic kidney disease
symptoms of hyperphosphataemia
hypocalcaemia
due to calcium phosphate formation which precipitates in lungs, kidneys and joints
clinical features of hyperphosphataemia
similar to hypocalcaemia
intervention for hyperphosphataemia
reduce dietary phosphate
decrease intestinal reabsorption
dialysis
role of magnesium ions
enzymatic reactions needed for ATPase gene transcription bone remodelling neuromuscular stability
location of magnesium
intracellular
mostly in bones
some in muscle and soft tissue
magnesium regulation
by kidney, reabsorbed in loop of Henle mainly
magnesium disorders
often associated with other electrolytes - Na+/K+
hypomagnesaemia
<0.7mmol/L
causes of hypomagnesaemia
malnutrition defective gut absorption excessive gut or urinary loss alcoholism diuretics
symptoms of hypomagnesaemia
irritability tremor ataxia carpopedal spasm hyperreflexia confusion hallucinations convulsions
clinical features of hypomagnesaemia
progressive QRS complex widening
PR interval prolongation
flattened T waves
intervention for hypomagnesaemia
oral or IV replacement therapy
correct underlying cause
hypermagnesaemia
> 1mmol/L
hypermagnesaemia causes
kidney disease - chronic or acute
magnesium containing laxatives or antacids
symptoms of hypermagnesaemia
depressed skeletal muscle contraction and nerve functions hyporeflexia proceeding narcosis respiratory paralysis cardiac conduction defects
clinical features of hypermagnesaemia
ECG changes - prolonged QT interval
bradycardia
heart blocks
intervention for hypermagnesaemia
if renal function is normal - magnesium therapy stopped
if not peritonael dialysis or haemodialysis
heart failure patients
at risk of hyperkalaemia due to mineralocorticoid blockers for treatment
raised creatinine
can be secondary to hypercalcaemia due to calcium deposits in kidney
