Blood Flashcards

1
Q

3 Major functions of blood

A
  1. Transport substances around the body (e.g. O2, CO2, heat)
  2. Role in immune response (through phagocytes)
  3. Coagulation/prevents bleeding (carries platelets, endothelial cells and other substances that are vital in clotting)
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2
Q

Composition of blood

A
  1. Plasma (55%)
    - Makes up 1/5 of extracellular fluid
    - Composed of water (90%) and solutes (~10%, incl. proteins, nutrients, waste, respiratory gases)
  2. Cells (45%)
    - RBCs or erythrocytes
    - WBCs or leukocytes
    - Platelets or thrombocytes
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3
Q

3 main groups of plasma proteins

A

1) Albumins - maintain osmotic pressure, buffer blood, transport insoluble substances
2) Globulins - Mostly antibodies
3) Fibrinogen - precursor of fibrin during blood coagulation

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4
Q

What is the haematocrit/packed cell volume (PCV)?

Is it higher in females or males?

A
  • The amount of red blood cells making up blood

- Higher in males

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5
Q

What are the 2 types of stem cells in blood cell formation?

- What 3 main types of blood cells do they differentiate into?

A
  1. Myeloid stem cell. Differentiates into:
    - Erythrocytes/RBCs; and
    - Platelets
  2. Lymphoid stem cell. Differentiates into:
    - WBCs
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6
Q

Blood cells and their main function

A
  • 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
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7
Q

Physical features of RBCs

A
  1. Biconcave disk shape - large SA:V ratio
    - allows for efficient diffusion of gases for transport
  2. Flexibility
    - for movement through narrow capillaries
  3. Contain large amounts of Hb
    - for O2 transport
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8
Q

Production and destruction of RBCs

- How is it regulated

A

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

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9
Q

What is anaemia

  • What measurement would you use to determine if someone was anaemic?
  • causes
A
  • 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
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10
Q

How does erythropoietin increase performance?

A

Stimulates erythrocyte production → increased O2 capacity → increase performance

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11
Q

Platelets:

  • Structure
  • Production (name and stimulus)
A
  • Small, irregular spindels/ oval discs that assume various shapes on contact
  • Formation of platelets = thrombopoiesis (stimulated by thrombopoietin)
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12
Q

Platelet functions

A
  • Haemostasis: stops blood flow

- blood coagulation

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13
Q

Haemostasis stages

A

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)

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14
Q

Formation of a platelet plug

A
  1. Tissue/vessel damage
  2. Collagen exposed due to altered endothelium
  3. Platelets aggregate, agglutinate and adhere (form platelet plug)
  4. Mediators released (ADP and thromboxane A2) - vasoconstriction + platelet aggregation
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15
Q

Describe blood clot formation

- What is the precursor for activation of stage 2?

A

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
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16
Q

What factors oppose clot formation?

A
  1. Smooth endothelial surface (prevents platelets adhering)
  2. Endothelium releases:
    i) Prostacyclin and/or nitric oxide: vasodilation
    ii) TFPI: inhibits the extrinsic pathway
  3. Antithrombins (e.g. heparin): inhibit thrombin from activating fibrin
  4. Blood thinning drugs (warfarin, aspirin)
17
Q

Blood clot dissolution (fibrinolysis)

  • What does thrombin act with?
  • Causes?
  • What activates it?
A
  • Thrombin acts with t-PA (+ Factor XII and lysosomal enzymes) to convert plasminogen into plasmin, which hydrolyses fibrin to break down the blood clot.
18
Q

What determines blood transfusion compatibility?

Which antibodies will be present in each of the blood groups?

A
  • 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
19
Q

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
A
  • 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
20
Q

Which cells phagocytose broken down RBCs?

A

Macrophages in the lining of blood vessels

21
Q

Which intrinsic factors do haemophiliacs most commonly have a genetic absence of?

A

factors 8, 9 or 11 (a, b or c)