Blood Flashcards
3 Major functions of blood
- Transport substances around the body (e.g. O2, CO2, heat)
- Role in immune response (through phagocytes)
- Coagulation/prevents bleeding (carries platelets, endothelial cells and other substances that are vital in clotting)
Composition of blood
- Plasma (55%)
- Makes up 1/5 of extracellular fluid
- Composed of water (90%) and solutes (~10%, incl. proteins, nutrients, waste, respiratory gases) - Cells (45%)
- RBCs or erythrocytes
- WBCs or leukocytes
- Platelets or thrombocytes
3 main groups of plasma proteins
1) Albumins - maintain osmotic pressure, buffer blood, transport insoluble substances
2) Globulins - Mostly antibodies
3) Fibrinogen - precursor of fibrin during blood coagulation
What is the haematocrit/packed cell volume (PCV)?
Is it higher in females or males?
- The amount of red blood cells making up blood
- Higher in males
What are the 2 types of stem cells in blood cell formation?
- What 3 main types of blood cells do they differentiate into?
- Myeloid stem cell. Differentiates into:
- Erythrocytes/RBCs; and
- Platelets - Lymphoid stem cell. Differentiates into:
- WBCs
Blood cells and their main function
- Neutrophils: immunity (phagocytosis)
- Eosinophils: allergic reactions
- Basophils: Anticoagulant
- Monocytes: transform into macrophages when in tissue (phagocytic cells)
- Lymphocytes: Secrete antibodies
- Platelets: coagulation
- erythrocytes: transporting gases
Physical features of RBCs
- Biconcave disk shape - large SA:V ratio
- allows for efficient diffusion of gases for transport - Flexibility
- for movement through narrow capillaries - Contain large amounts of Hb
- for O2 transport
Production and destruction of RBCs
- How is it regulated
Erythropoiesis (production)
1. Decrease in RBCs
2. Kidney senses decrease in O2 levels and releases erythropoitin (EPO)
3. Bone marrow stimulated to produce RBCs
- Requires: folic acid, vitamin B12, thymine, iron
Destruction
- Caused by end of life span or excess RBCs
- Broken apart and removed by macrophages
- Bilirubin transported to liver and excreted in bile (if not excreted –> jaundice)
- Other components (AAs, iron) recycled
What is anaemia
- What measurement would you use to determine if someone was anaemic?
- causes
- a decrease in conc. of Hb, and thus a decreased O2 carrying capacity of blood
- If Hb conc. was less than normal (approx. 150g/L):
Men = less than 130g/L
Women = less than 115g/L - Can be caused by:
1. ↓ RBC production
2. ↑ RBC destruction
3. Chronic blood loss
How does erythropoietin increase performance?
Stimulates erythrocyte production → increased O2 capacity → increase performance
Platelets:
- Structure
- Production (name and stimulus)
- Small, irregular spindels/ oval discs that assume various shapes on contact
- Formation of platelets = thrombopoiesis (stimulated by thrombopoietin)
Platelet functions
- Haemostasis: stops blood flow
- blood coagulation
Haemostasis stages
Stage 1
- Constriction of blood vessels; stops blood flow to area; immediate and short-lived response
- formation of a platelet plug
Stages 2 and 3
- Formation of blood clot (supported by platelets)
Formation of a platelet plug
- Tissue/vessel damage
- Collagen exposed due to altered endothelium
- Platelets aggregate, agglutinate and adhere (form platelet plug)
- Mediators released (ADP and thromboxane A2) - vasoconstriction + platelet aggregation
Describe blood clot formation
- What is the precursor for activation of stage 2?
1) Converging of intrinsic and extrinsic pathway at Factor X
- intrinsic pathway has all components in the blood
- extrinsic pathway requires substances in the tissue surrounding the blood (thus requires damage to the wall of a blood vessel)
2) Calcium ions catalyse the activation of factor X; cause
3) activation of thrombin (from prothrombin via prothrombin activator complex); cause
4) activation of fibrin (from fibrinogen)
5) Fibrin mesh formed (blood clot): RBCs enmeshed in fibrin ‘net’
- activation of stage 1
What factors oppose clot formation?
- Smooth endothelial surface (prevents platelets adhering)
- Endothelium releases:
i) Prostacyclin and/or nitric oxide: vasodilation
ii) TFPI: inhibits the extrinsic pathway - Antithrombins (e.g. heparin): inhibit thrombin from activating fibrin
- Blood thinning drugs (warfarin, aspirin)
Blood clot dissolution (fibrinolysis)
- What does thrombin act with?
- Causes?
- What activates it?
- Thrombin acts with t-PA (+ Factor XII and lysosomal enzymes) to convert plasminogen into plasmin, which hydrolyses fibrin to break down the blood clot.
What determines blood transfusion compatibility?
Which antibodies will be present in each of the blood groups?
- RBCs have membrane antigens that are genetically inherited
- plasma has antibodies to the opposite antigens
- Type A = anti-B antibodies
- Type B = anti-A antibodies
- Type O = anti-A and anti-B antibodies
- Type AB = doesn’t have either
Rhesus system
- What are individuals w/ D-antigen?
- When does Anti-Rh antibodies slowly develop?
- Why can rhesus factor be a problem in pregnancy?
- How to prevent this
- Individuals w/ D-antigen are rhesus positive (85% of the population)
- No pre-formed natural antibodies
- Anti-Rh antibodies slowly develop when Rh- patient receives Rh+ blood
- Rhesus factor can be a problem in pregnancy (Rh- mother/Rh+ fetus); not for first pregnancy but not for the following, bc the mother would now have anti-D antibodies.
- To prevent antibody development, give mother anti-D antibody at first delivery
Which cells phagocytose broken down RBCs?
Macrophages in the lining of blood vessels
Which intrinsic factors do haemophiliacs most commonly have a genetic absence of?
factors 8, 9 or 11 (a, b or c)
