Electrolytes Flashcards
Potassium
Intracellular or Extracellular
Hormones affecting
Intracellular
Insulin and Adrenaline (B agonists) move K intracellular
Aldosterone moves into collecting duct
Why do ACE inhibitors cause hyperkalemia
ACE converts Angiotensin I to Angiotensin II which increases the release of aldosterone from the adrenal cortex = Less K excretion
Causes of hyperkalemia (5)
Renal causes: AKI, Chronic kidney disease, Type 4 RTA eg Diabetic nephropathy
Drugs: ACEi/ARBs, Beta-blockers, NSAIDs, K+ sparing diuretics eg Spironolactone, Heparin, etc Mineralocorticoid deficiency (Addison’s disease)
Exogenous K - Supplements, bananas
Endogenous K - Tumour lysis syndrome, Rhabdomyolysis, trauma, burns.
Shift from intracellular to extracellular space - Acidosis e.g. DKA
ECG changes in hyperkalaemia
Tall tented T waves Long PR Flat P waves Broad QRS Sine waves - Late sing. Cardiac arrest imminent
Symptoms of hyperkalaemia.
Often asymptomatic Palpitations/ chest pain Bradycardia/ Heart block Tachypnoea Muscular weakness/ paralysis Generalized weakness/ fatigue Depressed tendon reflexes Cardiac arrest
Management of hyperkalaemia
For K+ 5.5 – 6.0 mmol/L: Stop K sparing drugs and
restrict dietary or IV potassium intake.
K+ 6.0 – 6.5 mmol/L with no ECG Changes: Oral Calcium Resonium 15g 3-4 times a
day in water. Prescribe lactulose 10-20 ml qds with
it. It takes around 10 hours for effect.
K+> 6.5 mmol/L or >6.0 mmol/L
with ECG Changes - 10ml 10% calcium gluconate IV over 5 minutes.
Insulin IV &; Salbutamol nebs drives K into cells+ 50ml 50% dextrose.
Use central access if available, otherwise use a large
peripheral vein.
Look for normalisation of ECG on cardiac monitor.
ECG changes in hypokalaemia
Flattened & inverted T waves;
Increased amplitude and width of the P wave
Prolongation of the PR interval
ST depression
Prominent U waves
Arrhythmias: VT, VF, Torsades de Pointes.
Hypokalaemia features
Often asymptomatic until arrest.
Weakness, fatigue, constipation, muscle cramping, palpitations.
Causes of hypokalaemia
Decreased intake: anorexia nervosa,
malnutrition, chronic alcoholism,
inappropriate IV therapy.
Transcellular shift: insulin, beta-agonists,
theophylline, re-feeding syndrome.
Renal loss: diuretic therapy, mineralocorticoid
excess/therapy, aminoglycosides, alkalosis,
renal tubular acidosis, magnesium depletion.
Extrarenal loss: Chronic D&V, laxative abuse,
fistula, villous adenoma.
Extra renal loss vs renal loss
Urine potassium < 10 indicates extra-renal loss, urine
potassium > 20 indicates renal loss.
Nb. If extra-renal K+ loss (e.g. vomiting /diarrhoea)
is associated with dehydration this can stimulate
aldosterone release which will increase renal K+ loss
Management of hypokalaemia
Treat the cause, in general oral K+ is
preferred. In severe and potential life threatening
hypokalaemia the rate of K+ infusion should not
exceed 20 mmol/h.
If secondary to low Mg then give Mg replacement –
otherwise potassium may be refractory to treatment
Management of Hypomagnesemia
≤ 0.5 mmol/L - IV infusion (peripheral or central) magnesium sulphate 20 mmol
(5g) in 500 ml 0.9% saline or 5% dextrose over 12
hours for 3-5 days.
With life threatening symptoms ( e.g seizures,
arrhythmias): IV bolus of 8mmol MgSO4 (2g) over
10-15 minutes followed by infusion as stated above.
Nb. Mg can accumulate in the kidneys so needs to be reduced and monitored in CKD
Maintenance requirements
Water
Na
K
20-25ml/kg/day
1mmol/kg/day
1mmol/kg/day
Features of hyponatraemia
Rarely occur below 120mmol/L
Result from movement of water into brain cells causing cerebral oedema
Headache, confusion, convulsions and coma
Causes of hyponatraemia
Dilutional - Heart failure, liver failure, renal failure, hypoalbuminaemia
Hypovolemia (Determine difference by Na in urine)
- Renal - Diuretics, Osmotic diuresis (hyperglycemia), adrenocortical insufficiency.
- Extra renal - Haemorrhage, vomiting, burns, diarrhoea.
Magnesium and potassium levels in hyponatraemia
Must be checked as low levels can stimualte ADH release and cause a dilutional hyponatrraemia
Central pontine myelinolysis
Areas of demyelination causing quadriparesis, respiratory arrest, pseudobulbar palsy, mutisum and seizures.
Caused by rapid overcorrection of Na
Management of hyponatremia resulting from water excess
Treat underlying cause
Restrict fluid to 1L and review diuretics
Acute hyponatraemia with neurological symptoms
- Infuse hypertonic saline (3%) at a rate of 1-2ml/kg/hour
- Aim to raise Na by 8-10 mols in the first day and 8 mols /day therafter
- Frusimide to encourage excretion of free water.
- Hypertonic saline is CI in fluid overload - Instead give mannitol
Hypernatraemia What Causes Features Management
> 145mmol/L
Poor intake of water or water loss in excess sodium
Nausea, vomiting, fever, confusion
If mild correct over 48 hours with 5% Dex. If severe >170mmol - Correct with normal saline.
Hypomagnesaemia Causes Effect on K Effect on PTH Features Management
GI loss of Mg - Diarrhoea, malabsorption, bowel ressection (Most common)
Renal loss - Osmotic diuresis in DM, diuretics, alcohol abuse.
Increases renal K excretion (Hypokalaemia) Inhibits PTH (Hypocalcaemia)
Features related to hypokalaemia & hypocalcaemia
Oral supplements
Hypermagnesaemia
Rare and usually Iatrogenic occuring in patient with renal failure who have been given Mg containing antacids or laxatives.
Hypercalaemia
Usual cause
Other causes
Primary hyperparathyroidism or malignancy (Bone mets/multiple myeloma)
Nb if severe >3.5mmol cause is likely malignancy
Thyrotoxicosis, Addisons disease, excess vit D
Drugs - Thiazides - Reduced renal tubular excretion, Lithium - Increased PTH production.
Features of hypercalcaemia
Abdominal groans - Anorexia, nausea and vomiting, abdo pain, PUD, acute pancreatitis
Thrones - Polyuria, polydipsia, dehydration.
Stones - if long standing- Renal colic
Psychic overtones - Depression, dementia, confusion, memory
Muscle + CVS - Weakness, proximal myopathy, fatigue
HTN, *short QT
Ix of hypercalcaemia
High corrected Ca (<3 = PHPT, >3 = malignancy)
Albumin - high -> with high urea = dehydration
Alk phos - normal in myeloma (unless fracture healing), raised in bony mets
Calcitonin - B cell lymphoma
PTH - high = PHPT, low = granulomatous or adrenal
*XR - bone abnormalities, cysts, pathological fractures etc
Management of hypercalcaemia
Acute >3.5
0.9% saline - hydration and increase urinary excretion
Loop diuretic - furosemide for fluid overload
Post rehydration - IV bisphosphonates - pamidronate or zoledronic acid
If vit D toxicity, sarcoid, lymphoma - glucocorticoids
If secondary HPT = cinacalcet
If underlying kidney disease - haemodialysis
Causes of hypocalcaemia (4)
CKD (most common) resulting from reduced vit D secretion and phosphate retention.
Hypomagnesaemia (inhibits PTH)
Parathyroid sugery/radio
Vitamin D deficiency
Hypocalcaemia
Symptoms
Signs
Paresthesia: fingers, toes, mouth
Tetany (emergency)
Carpopedal spasm (wrist flexion and fingers drawn together)
Muscle cramps
Chvostek’s sign - latent tetany
Tap facial nerve face spasms
Trousseua’s sign - from increased neuromuscular excitability
Inflate a BP cuff above systolic - look for carpopedal spasm
Seizures
Prolonged QT (shortened in hyperCa)
Management of hypocalcaemia
Acute: seizures/tetany or <1.9
10ml 10% calcium gluconate slow IV infusion, repeat as necessary
Oral calcium
Monitor Ca
If hypomagnesaemia - correct otherwise Ca will not respond
Chronic: Ca and vit D
Osmolality calculation
Use in Hyponatraemia
2xNa + urea + Glucose
For true hyponataemia there must be a deficit in serum osmolality.
If Normal osmolality = High triglycerides, High total protein
If High = Hyperglycaemia
ALT vs ALP
ALT is found in high concentrations within hepatocytes and enters the blood following hepatocellular injury. It is, therefore, a useful marker of hepatocellular injury.
ALP is particularly concentrated in the liver, bile duct and bone tissues. ALP is often raised in liver pathology due to increased synthesis in response to cholestasis. As a result, ALP is a useful indirect marker of cholestasis.
A greater than 10-fold increase in ALT and a less than 3-fold increase in ALP = hepatocellular injury
A less than 10-fold increase in ALT and a more than 3-fold increase in ALP = cholestasis
Causes of isolated rise in ALP
Bony metastases / primary bone tumours (e.g. sarcoma)
Vitamin D deficiency
Recent bone fractures
Renal osteodystrophy
If there is a rise in ALP?
Another test?
If raised as well?
If not raised?
GGT
Suggestive of biliary epithelial damage and bile flow obstruction.
It can also be raised in response to alcohol and drugs such as phenytoin.
Non-hepatobiliary pathology. Alkaline phosphatase is also present in bone and therefore anything that leads to increased bone breakdown can elevate ALP.
Assessing liver function tests (4)
Serum bilirubin
Serum albumin
Prothrombin time (PT)
Serum blood glucose
Using stool and urine to determine cause of jaundice
Normal urine + normal stools = pre-hepatic cause
Dark urine + normal stools = hepatic cause
Dark urine + pale stools = post-hepatic cause (obstructive)
ALT:AST ratio
ALT > AST is seen in chronic liver disease
AST > ALT is seen in cirrhosis and acute alcoholic hepatitis
Anion Gap
Calculation
High
Normal
K+Na - Cl+Hco3
If the anion gap is raised, this suggests that there is increased production, or reduced excretion, of fixed/ organic acids e.g.
Lactic acid (sepsis, tissue ischaemia)
Urate (renal failure)
Ketones (diabetic ketoacidosis)
Drugs/ toxins (salicylates, methanol, ethylene glycol)
If there is a metabolic acidosis with a normal anion gap, then this is either due to loss of bicarbonate, or accumulation of H+ ions. Causes include: Renal tubular acidosis Diarrhoea Addison's disease Pancreatic fistula
