Physiology 2058 Blood Flashcards
Total body water
60% of BW- ECF and ICF
Red blood cells
Mature cells non nucleated, unusual biconcave shape
RBC/ erythrocyte production
Begins in utero, 6-7 months bone marrow takes over - all for children, sternum, vertebrae, ribs and pelvis for adults
Requirements for RBC production
Adequate nutrition, protein, vitamins B12 folic acid, hormone- erythropoietin released by kidney,
lack of RBC and/ or hb- anaemia- reduced O2 carrying capacity
Sequence of events in RBC production
Erythropoiesis
2.5 million RBC’s/ second
120 day lifespan
Old RBC’s removed from blood by phagocytic cells in liver, spleen and bon marrow- iron recycled back in Hb production
Role of erythropoietin in production
accent to high altitude will initiate a physiological increase in RBC production to combat lack of O2, synthetic EPO available, EPO in sport doping
Control of RBC production
Tissue oxygen levels decline - release of EPO- increased mitotic rate and acclerated maturation, increased numbers of circulating RBC, improved oxygen content of blood, tissue oxygen levels rise
Function of RBC
Contain Hb, oxygen trasnport, CO2 transport, blood buffer - maintain normal pH
Structure of HB
4 polypeptide chains, in foetus - HbF binds O2 easier than HbA, each linked to one haem molecule
Each haem contains one iron atom to which O2 associates
Haemoglobinopathies- abnormal Hb- sickle cell disease
Oxyhemoglobin dissociation curve
Decreased p50 (increased affinity)- decrease temp, PCO2, increase pH
Increased P50- (decreased affinity)- increase temp, PCO2, decrease pH
RBC breakdown
lifespan 120 days- fragile, trapped in spleen, haem separated from globin, globin recycled as AA, haem breakdown yields iron- recycled, yields biliverdin and bilirubin
Anaemia causes
Sickle cell disease - genetic - symptoms in children- sickle cell haemolytic anaemia - sickled cells are fragile- blood transfusion need- cells trapped in microcirculation - obstruct blood flow - ischemia and pain, jaundice, stroke , resp symptoms
Blood groups
Determined by antigen present on red cell membrane, blood group O RH- -> no antigens to react with patients plasma
Rh +/-
Type A
Antigen A
Anti body B
Type B
Antigen B
Antibody A
Type AB
Antigen AB
Antibody - none
Type O
Antigen - none
Antibody AB
Blood transfusion
typed and cross match in serum
Rhesus incompatibility in pregnancy
If mother is Rh- and baby Rh+
Rh- produce antibodies to antigen D if contact is made with Rh+
Treatment injection of anti D- casues inactivation of any Rh antigen in maternal blood, doesn’t produce antibodies that can cross placenta and agglutinate with baby’s RBC
Role of platelets
Damage to endothelium allows platelets to bind to exposed collagen, von willebrand factor increases bond by binding collagen and platelets, they stick to collages and release ADP, serotonin and thromboxane A2- platelet release rxn
Clotting process
local vasoconstriction- reduce blood loss,
tissue thromboblastin activates extrinsic pathway while exposure of collagen activates intrinsic pathway,
prothrombin converted to thrombin by enzyme prothrombinase
Calcium ions and Vit K essential for normal clotting