Electrolyte Imbalance Flashcards
causes of hyperkalaemia: intake
oral intake
blood transfusion
causes of hyperkalaemia: redistribution
acidosis
rhabdomyolysis
tumour lysis
causes of hyperkalaemia: urinary
renal tubular acidosis type 4 renal failure adrenal insufficiency diabetes K+ sparing diuretics
immediate management of hyperkalaemia
ABCDE
fluid resuscitation (enhance renal perfusion and elimination)
bloods: FBC, U&E, CK, ABG
monitoring: ECG and blood pressure
why do you give calcium in hyperkalaemia
cardiac protection: antagonises the membrane excitability of the heart
DOES NOT LOWER SERUM K+
how can K+ be moved back INTO cells
insulin/dextrose: stimulates Na+/K+ ATPase
salbutamol: indirectly stimulates Na+/K+ ATPase
how does HCO3 move K+ into cells
decreases the concentration of H+ in the ECF
increases IC Na+ via the Na+/H+ exchanger and facilitates K+ shift into cells via the Na+/H+ ATPase
IN ADDITION TO insulin/dextrose or salbutamol
HCO3 should not be administered at the same time as…
Ca2+
can cause precipitation
what is the role of resonium (K+ binders) in hyperkalaemia
calcium resonium acts as a cation exchange
negatively charged polymer that exchanges the cation for K+ cars the intestinal wall
SLOW ACTING
definition of hyperkalaemia
serum K= >5.5 mmol/L
moderate = >6
severe = >7
what is the relationship between hyperkalaemia and acidosis
acidosis causes increased H+ in ECF which inhibits Na+/H+ exchanger
less sodium in transported into the cell which inhibits the Na+/K+ ATPase from moving sodium OUT and potassium IN leading to increase [K+]
hyperkalaemia stimulates the Na+-K+ ATPase to move sodium OUT of the cell
increased EC sodium stimulates the Na+/H+ exchanger leading to acidosis
effects of increased potassium on the heart and ECG changes
reduced myocardial excitability
depression of pacemaking and conducting tissues
bradycardia, conduction blocks, cardiac arrest
mild: peaked T waves
moderate: wide, flat P wave, prolonged PR
severe: prolonged QRS with abnormal morphology, high-grade AV block with slow junctional and ventricular escape rhythms, conduction blocks (BBB, fascicular)
causes of hypokalaemia: intake
inadequate intake
causes of hypokalaemia: redistribution
alkalosis hypomagnesaemia glucose infusion periodic paralysis beta-agonists
causes of hypokalaemia: urinary
steroids DKA hyperaldosteronism Cushings renal tubular acidosis diuretics
causes of hypokaelamia: non-urinary output
upper GI: vomiting
Mid GI: fistula
lower GI: diarrhoea
other: sweat, burns, bleeding, RRT
how does alkalosis cause hypokalaemia
reduced H+ stimulates Na/H+ exchanger to move sodium into cells and H+ out of cells
increased IC sodium stimulates NaK ATPase to move sodium out of cells and potassium in
how does DKA cause hypokalaemia
potassium moves out of the cell due to acidosis but is lost in urine
how does hypomagesaemia cause hypokalaemia
reduces the intracellular potassium concentration and promoting renal potassium wasting
how do steroids cause hypokalaemia
promote renal potassium loss
where is the main site of K+ homeostasis
kidney (responsible of 90% of daily K+ loss)
definition of hypokalaemia
mild: 3.0-3.5
moderate: 2.5-3.0
severe: <2.5
symptoms of hypokalaemia
fatigue muscle cramps and weakness constipation rhabdomyolysis ascending paralyses resp failure arrhythmias medications
ECG signs of hypokalaemia
increased amplitude and width of P wave prolonged PR T wave flattening and inversion ST depression U waves frequent SV and V ectopics SVTs potential for ventricular arrhythmias (VT, VF, TdP)
management of hypokalaemia
replace Mg2+ (allows faster correction of hypokalaemia)
give potassium
10-20 mmol/hr if non-acute
20 mol/10 min If life-threatening
causes of hypermagnesaemia
iatrogenic (Mg infusion)
urinary: panel failure increases risk of accumulation
definition of hypermag
> 2.2 mmol/l
toxic >4 mmol/
which other electrolyte disturbances is hypermag associated
hyperkal
hypocalc
symptoms of hypermag
> 4
muscle weakness, hyporeflexia, N+V, hypotension due to vasodilation
10
coma, hypoventilation, neuromuscular paralysis, cardiac arrhythmia, bradycardia, death
ECG changes in hypermag
increased PR and QTc
prolonged QRS
peaked T waves and flattened P waves
complete AV block and asystole
management of hypermag
dialysis is best
calcium chloride 10% treats life threatening arrhythmia
forced diuresis (IV saline and furosemide)
hypomag causes: intake
TPN
malabsorption
alcoholism
hypomag cause: redistribution
insulin
hungry bone syndrome
hypomag causes: urinary output
RTA
diuretics
polyuria from any cause
hypomag causes: non-urinary output
upper GI: NG suction
lower GI: diarrhoea
hypercalcaemia
definition hypomag
<0.75 mmol/l
pathophysiology of hypomag
Mg deficiency leads to drop in ICF K+ and rise in ICF Na+
elevation in resting potential and a rise in inward Ca2+ current
this causes enhanced neurological and cardiac irritability
magnesium is required for potassium reabsorption by the kidneys
ASSOCIATED WITH HYPOKAL AND HYPOCALC
symptoms of hypomag
Trousseau and Chvostek signs weakness/fatigue vertical nystagmus tetany seizures reversible blindness arrhythmia (TdP) hypokalaemic ECG vit D deficiency PTH resistance
management of hypomag
resus: treat dysrhythmias, seizures etc
Iv magnesium replacement/oral
correct other electrolyte abnormalities (hypokal and hypocalc)
potassium-sparing diuretic is renal wasting
causes of hypercalc: intake
Ca2+ vitamin A or D hypomag hypovolaemia TPN
causes of hypercalc: redistribution
immobilisation malignancy hyperparathyroidism sarcoid litium adrenal insufficiency endocrine causes (thyrotoxicosis, acromegaly, phaeo)
urinary causes of hypercalc
thiazides
how is free ionised Ca2+ concentration related to pH
inversely related
increase in pH results in decreased Ca2+
how does vitamin D help calcium absorption
cholecalciferol is formed in the skin
liver converts it to 25-hydroxycholecalciferol
kidney proximal tubules convert that to 1,25-dihidroxycholecalciferol
helps calcium absorption in the intestine
controlled by parathyroid hormone
roles of vitamin D
increases intestinal absorption of Ca2+
increases renal Ca2+ reabsorption
mobilises bone Ca2+ and PO4
which electrolyte states impact parathyroid secretion
increased PTH: hypocalc and hypomag
decreased PTH: hypercalc and hypermag
what are the functions of PTH
mobilises Ca2+ from bone
increases renal Ca2+ reabsorption
increases renal PO4 excretion
increases formation o 1,25-dihydroxycholecalciferol
action of calcitonin
antagonist of PTH
secreted from thyroid gland in response to hypercalc, catecholamines, gastrin
inhibits the mobilisation of bone Ca2+, increases renal Ca2+ and PO4 excretion
what are the most common causes of hypercalc
malignancy (inappropriate release of PTH-related peptide from tumour cells - lung, breast, prostate, colon, T-cell malignancies) post-hypocalc hypercalc adrenal insufficiency prolong immobilisation Mg2+ metabolism disorder TPN hypovolaemia iatrogenic
hypercalc symptoms
stones, bones, groans and moans
GI: smooth muscle relaxation = constipation, anorexia, nausea, vomiting
neuro: lethargy, hypotonia, confused, coma
renal: polyuria, dehydration, stone, dehydration
CVS: arrhythmia
investigations in hypercalc
confirm malignancy/bony involvement (R, CT etc)
assess bone turnover (ALP)
assess PTH
management of hypercalc
increase excretion - IV fluids - loop diuretics (decrease absorption in Loop of Henle) - steroids (inhibits effects of Vit D) reduce release - calcitonin bisphosphonates (inhibit osteoclasts)
causes og hypocalc: intake
Ca2+
vitamin D
phenytoin (increased metabolism of vitamin D)
causes of hypocalc: redistribution
alkalosis citrate toxicity hyperphosphataemia pancreatitis tumour lysis syndrome rhabdomyolysis decreased bone turnover hypoPTH drus
causes of hypocalc: urinary
ethylene glycol
cis-platin
protamin
loop diuretics
causes of hypocalc: non-urinary
bleeding
plasmapheresis
citrate RRT
history in hypocalc
personal numbness paraesthesias muscle cramps mild mental status changes (irritability) siezures tetany collapse
examination in hypocalc
Chvostek sign (tapping facial nerve anterior to ear causes facial muscle spasm) trousseau sign (inflate BP cuff, traps median nerve, carpal spasm) arrhythmias (long QT) heart failure
management of hypocalc
treat cause oral Ca2+ replace Mg2+ vitamin D IV calcium - symptomatic ionised <0.8 mmol CCB overdose hypermag hypocalc with high inotrope requirement massive transfusion post cardiopulmonary bypass
causes of hyperphos
renal failure
increased renal reabsorption
cellular injury with release (tumour lysis, rhabdomyolysis, haemolytic, ischaemic gut)
medication
clinical features of hyperphos are related to…
hypocalc precipitation of Ca2+ (nephrolithiasis) decreased vit D muscle cramps tetany hyperreflexia seizures prolonged QT
management of hyperphos
limit phosphate intake
chance urinary excretion (saline, acetazolamide)
dialysis
oral calcium binders
causes of hypophos: intake
malnutrition phosphate binders vitamin D malabsorption TPN
causes of hypophos: redistribution
referring syndrome
insulin in DKA
causes of hypophos: urinary
diuretics
osmotic diuresis
hyperPTH
proximal tubular dysfunction (Fanconi syndrome)
relationship between PTH and phosphate
PTH increases phosphate and Ca2+ release from bone, but increases excretion in kidney by inhibiting reabsorption in the proximal tubule
vitamin D from the kidneys acts on jejunum to increase absorption of Ca2+ and phosphate
symptoms of hypophos
SOB ventilator dependence weakness altered mental state heart failure symptoms shock
definition of hyponat
mild: 125-134
moderate: 120-124
severe: <120
types of Hyponatremia
hypoosmolar/hypotonic
iso-osmolar
hypertonic
causes of hypotonic/hypoosmolar Hyponatremia
solute depletion/dilution
hypovolaemic: loss of H2O and Na from the ECF - increased ADH secretion - decreased free H2O excretion and H2O retention - hyponat
euvolaemic: SIADH, psychogenic polydipsia, hypotonic IVF therapy, adrenal insufficiency, hypothyroidism
hypervolaemic: increase in total body Na+ and H2O but H2O is out of proportion to Na+
how to differentiate between renal and non-renal hypovolaemic hyponat
urinary Na+ <10 mmol = extra-renal (kidney is reabsorbing Na+ so there is less in the urine)
urinary Na+ >20 mmol = renal (kidney should be holding on to Na+ if hypovolaemic)
causes of SIAADH
MAD CHOP malignancy ADH secretion (ectopic) drugs (SSRIs, ecstasy) CNS disease hormone deficiency (hypothyroidism, adrenal insufficient) others pulmonary
causes of isotonic hyponat
aka pseudohyponatramia
marked hyperproteinaemia or hyperlipidaemia causes the lipid proportion of plasma to increase meaning there is a relative decrease in sodium
causes of hypertonic hyponat
osmotically active particles in the plasma induces movement of H2O from the ICF to ECF, meaning the serum Na+ decreases
can be caused by glucose, mannitol, sorbitol, radio contrast
inability to excrete H2O will initially lower osmolality ut increased urea will cause it to normalise
