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
Albumin - synthesised by and utility as a marker of function?
synthesised by liver
Not a good marker as influenced by nutritional status and capillary leakage. Long half life
Clotting factors (10-14s) - synthesis? and reduced in?
Synthesised by liver, short half life so good measurement
Vit K deficiency in cholestasis can reduce factor production
Drug induced liver disease- type 1/2
Type 1 - usually dose dependent, oestrogen causes cholestasis, methotrexate causes hepatocyte damage
Type 2 - not dose dependent and immune mediated.
RBCs function, removal, increased and decreased by?
Carry O2 bound to Hb
Require B12/folate and iron
Removed by spleen
increased in polycythaemia and stress. Decreased in anaemia
Morphological anaemias - low, normal, high volume
normocytic, normochromic - anaemia of chronic disease microcytic, hypochromic (low MCV) - iron deficiency, sickle cell macrocytic (high MCV) - B12 or folate deficiency
Causes of anaemia
- iron deficiency (inadequate intake, excessive bleeding, malabsorption disorders, pregnancy
- B12 or folate deficiency (inadequate intake, malabsorption -coeliac disease or pernicious anaemia)
How is haematocrit measured?
MCV?
MCHC?
haemoglobin expressed as % of whole blood
Mean corposcular volume (average volume of RBCs)
Mean corposcular haemoglobin volume (haem in RBC as %)
PMN granulocytes and mononuclear cells
POLYMORPHONUCLEAR (PMN) granulocytes
Neutrophils – phagocytosis of bacteria and cell debris
Eosinophils – involved in allergy/inflammation
Basophils – involved in hypersensitivity reactions
MONONUCLEAR CELLS
Monocytes – macrophage precursors
Lymphocytes – cellular immunity and antibodies
WBC increase and decrease?
Increased in infection, malignancy (AML/CML),acute inflammation
Decreased in malignancy (leukaemia), chemotherapy, drug interactions
Neutropaenia
-makes up 50-70% of WBCs
Drugs:chemo, phenytoin, propylthiouracil, co-trimoxazole, clozapine
Platelets (thrombocytes) role, increased and decreased?
integral in clotting cascade, lifespan 8-14 days.
Increased:post splenectomy, myeloploriferative disorders(thrombocythaemia), inflammatory disorders
Decreased: bone marrow suppression - AIDS, SLE, drugs - gold, heparin
Thrombocytopenia - cause, symptoms, treatment
bone marrow failure, heparin-induced, drugs - valproate, MTX, H2 blockers
Symptoms - bleeding, bruising.
Treatment - support with platelets, tranexamic acid. Steroids, splenectomy, azathioprine
ESR - carried out
Measures the rate of fall of erythrocytes in a thin tube
RBC volume change in B12 deficiency?
RBC increases
Grave’s Disease?
cause of hyperthyroidism
Carbimazole effect on neutrophils?
reduce causing agranulocytosis
RBC volume in iron deficiency
RBC decreases
What causes numbness of fingers and tingling and burning in feet?
hypocalcaemia
potentially caused by diuretic and lansoprazole
treat with Adcal D3 bd
What drug combo (COPD) can cause hypokalaemia?
symptoms and treatment?
change bendro?
salbutamol (nebulised) + high dose prednisolone
symptoms - muscle cramps
treatment - oral Sando-K
change bendro to amlodipine
Post MI + Stroke?
Aspirin + clopidogrel Clopidogrel preferred If AF - warfarin after 2 weeks in STROKE Blood Pressure Cholesterol - BE AGGRESSIVE
