LAB DATA Flashcards
What is osmolality?
No. osmotic ions per unit solution mmol/kg
Hyponatraemia - symptoms and causes?
Symptoms- weakness <120mmol,
headache, nausea, cramps, confusion ( 90-105 )
then convulsions
Caused by water retention- CCF, renal disease, cirrhosis, ascites or certain drugs (SIADH)- carbamazepine, bendroflumethiazide, SSRIs
Hypernatraemia - symptoms and causes?
stupor, coma, lethargy
Insufficient water intake - elderly, young, sick
Sodium retention e.g. steroid use
Thirst is primary defence
Potassium importance?
Cation involved in resting membrane potential. Important in carbohydrate/protein, enzyme metabolism.
Hypokalaemia
muscle weakness, hypotonia, arrhythmias, muscle weakness in lower extremities
Cause- inadequate intake, N+V, diarroea, diuretics
Hyperkalaemia
muscle weakness, cardiac conduction abnormalities (VF if sudden increase, asystole if slow)
Cause - renal disease, tissue breakdown, k sparing diuretics, diabetic acidosis
Blood urea - organ failure it is involved in?
Endpoint of protein metabolism formed in liver, filtered in glomeruli. Hydration indicator.
Increased in RENAL failure, high protein intake, GI bleeding, dehydration, starvation.
Decreased in LIVER failure, poor protein diet, overhydration, pregnancy
Creatinine
eliminated by glomerular filtration, endpoint of muscle metabolism
Calcium- function, regulation, measurement
Most abundant mineral - 99% in bone as hydroxyapatite
Maintains cellular membrane, nervous cell excitability, muscle contractility.
Increased levels by PTH. 1,25-hydroxycholecalciferol controlling absorption, secretion, bone deposition/resorption.
Use corrected calcium - 1/3 is protein bound
Hypocalcaemia
Deficiency in Vit D or calcium, hypoparathyroidism, osteoporosis, chronic renal failure.
Numbness of fingers, tingling in lower extremities, thinning and loss of body hair, affects heart (ECG)
Hypercalcaemia
hyperparathyroidism, vit D OD, bone diseases
Signs - psychosis, fatigue, depression, GI disturbance, headache, weakness
Bilirubin
Signs of increased bilirubin
breakdown product of haemoglobin, almost completely bound to serum albumin. Taken up by liver cells where it is conjugated and excreted in bile
Cause increased -haemolyisis (drugs, infection, enzyme deficiency)
- hepatocellular damage
- cholestasis (obstruction to bile flow)
Build up leads to jaundice
ALP
occurs in liver, bone, gut, placenta
excreted in bile and markedly raised in obstructive jaundice
GGT
Microsomal enzyme, raised with ALP in cholestasis. Enzyme inducers cause increase (e.g. alcohol)
AST - organ cells?
ALT - organ cells?
liver, heart, skeletal muscle
ALT is liver specific
Increased- acute damage