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Body Systems > Haematology II > Flashcards

Haematology II Flashcards

1
Q

What are the phases of the haemostatic response?

A
  • vasoconstriction
  • platelet adhesion and aggregation
  • clotting/coagulation phase
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2
Q

What does vasoconstriction do?

A

Help to control blood flow to a damaged area and limits blood loss

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3
Q

What does the coagulation phase take place on?

A

the primary platelet plug

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4
Q

How do the clotting phases communicate?

A
  • through continuous feedback and feedforward

- one phase doesn’t have to stop for the other to start

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5
Q

Give features of platelets

A
  • Small, oval, no nucleus (limited lifespan)
  • 2-3 um in diameter
  • Contains granules (allow platelets to take part in haemostasis
  • Produced from Myeloid cell line
  • Lives for about 7-10 days
  • Variety of function essential to the normal process of haemostasis
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6
Q

How are platelets produced?

A
  • they are produced from the cytoplasm of Megakaryocytes
  • The cytoplasm fragments and produces platelets
  • One megakaryocyte can produce about 4000 platelets
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7
Q

Where is thrombopoietin (TPO) produced?

A
  • Mainly in the liver

- some in the kidneys

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8
Q

What controls the production of platelets?

A
  • number of platelets already in circulation

- low number of platelets leads to increased thrombopoietin which increases platelet formation

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9
Q

What does thrombopoietin do?

A

regulates the differentiation of megakaryocytes and platelet formation

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10
Q

What happens when platelets are exposed to collagen?

A
  • platelet adhesion (binding) takes place)

- this causes platelets to be activated. They change shape, secrete granule content and activate GPllb/lla

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11
Q

What happens after the platelet activation phase?

A
  • serotonin is released which leads to vasoconstriction
  • Thromboxane A2 and ADP are released which leads to platelet aggregation phase (ADP causes the platelets to swell so they come into contact with other platelets)
  • Platelet phospholipid is released which leads to the blood coagulation cascade
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12
Q

What is the coagulation phase

A

The endpoint. The conversion of soluble plasma protein to the insoluble rigid polymer fibrin

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13
Q

Why can’t the fibrin clot be broken down the same way as the platelet plug was?

A

It is insoluble

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14
Q

What is released when there is damage to blood vessel surface?

A

Tissue factor

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15
Q

What are the different pathways in the coagulation phase?

A
  • Extrinsic
  • Intrinsic
  • Common: intrinsic and extrinsic come together to activate factor X
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16
Q

What happens when clotting factors/coagulation enzymes are activated and how can you tell it has been activated?

A
  • Activated when they are taking part in production of a clot
  • turns the clotting factors into an enzyme
  • once this has been activated it activates the next in the sequence
  • When there is an ‘a’ at the end of the clotting factor name it shows it has been activated
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17
Q

What happens with the extrinsic pathway?

A
  • activated by exposure of tissue factor on damaged blood vessel surface
  • exposes tissue factor to the circulation
  • comes into contact and binds with factor VII and forms tissue-factor - FVIIa complex
  • this then binds to FX and activates it turning it into FXa
  • fast pathway
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18
Q

What happens with the intrinsic pathway

A
  • Negatively charged collagen activates the clotting factors that come into contact with it
  • Factor XII activated to become XIIa
  • Platelet factor 3 released by aggregated platelets forming on the surface of the damaged blood vessel wall
  • This allows allow activation of Factor VIII and factor IX which combine together (Factor X activator complex) to allow activation of FX to FXa
  • Slightly slower than extrinsic pathway
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19
Q

What does prothrombinase consist of?

A

FXa and FCa as co-factors

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20
Q

What happens in the common pathway?

A
  • Prothrombin is activated to from thrombin
  • Thrombin converts fibrinogen to fibrin
  • we then produce out fibrin clot
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21
Q

Thrombin plays a big part in the feedback process. What clotting factors does it activate?

A
  • FVIII and FIX which then allows them to take part in the intrinsic pathway
  • FV to take part in the common pathway
  • Also activates platelets which allows them to produce the platelet plug on which the fibrin clot can form
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22
Q

Why will any disorder that decreases Ca2+ concentration impair blood clotting?

A

Because calcium is needed for almost every part of the clotting process

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23
Q

What is vitamin K necessary for?

A

production of certain clotting factors in the liver including prothrombin

24
Q

What are the anticoagulants we have in normal plasma>

A
  • Antithrombin: inhibits thrombin (among other factors) that is not bound to fibrin
  • Heparin - released by basophils and mast cells - co-factor that accelerates the actions of antithrombin
  • both work on the intrinsic pathway
25
Q

What is fibrinolysis?

A

When the fibrin clot is broken down

26
Q

What happens in fibrinolysis?

A
  • You have large amounts of plasminogen incorporated into your clot that are inactive until they get a signal indicating it is time to break the clot down
  • When plasminogen is activated plasmin is produced
  • plasminogen is activated by TPA which converts plasminogen to plasmin
  • happens about two days after the clot forming and happens over several days until the clot is dissolved
27
Q

What is plasmin?

A

Fibrin digesting enzyme

28
Q

How many blood group systems do we have and how are they determined?

A
  • 35 blood group systems

- genetically determined by antigens on red blood cell membrane

29
Q

What are the blood groups of most clinical significance?

A

ABO and Rh (D) blood group systems

30
Q

What are the different ABO blood groups and their characteristics?

A
  • A: A antigen, Anti-B antibodies
  • B: B antigen, Anti-A antibodies
  • AB: A and B antigens, No antibodies
  • O: None, Anti-A and Anti-B antibodies
31
Q

When are antibodies for the ABO blood group produced?

A

In relation to the environmental substances you are exposed to

32
Q

What would happen if type B blood cells came into contact with Anti-B antibodies>

A

the Anti-B antibodies would bind with the surface B antigen causing the to clog together (agglutination) and then this causes the red blood cells to break down – haemolysis

33
Q

How do you test for a blood type?

A

you put a serum of one blood in another and see if there is agglutination

34
Q

What would happen if you were exposed to a different blood group from your own?

A

Your red blood cells would break down

35
Q

What are the genetics behind blood group inheritance?

A
  • A and B genes are dominant and codominant

- O gene is recessive

36
Q

What are the two groups of the Rh (D) blood group and what is this determines by?

A
  • Rh negative (-) or Rh positive (+)

- Determined by presence or absence of the D antigen

37
Q

An Rh(-) individual will not usually contain anti-Rh (D) antibodies. What does getting the antibodies require and what does this happen by?

A

Sensitisation by exposure to Rh+ RBCs

This may happen by:

  • transfusion
  • pregnancy
38
Q

What is Haemolytic disease of the new born?

A
  • Rh- mother
  • Rh+ foetus
  • during pregnancy you are hopeful that the maternal and foetal blood don’t mix
  • during labour there is often mixing of the two circulations (haemorrhaging)
  • there is then maternal antibody production (anti-Rh)
  • normally takes about 72 hours for antibody production to reach a significant enough level to do damage
  • so it doesn’t do damage in the first pregnancy but antibodies will stay in the maternal circulation
  • So if the mother’s second pregnancy is with an Rh+ foetus as soon as their blood mixes the antibodies will attack the baby’s red blood cells and can cause significant anaemia
  • this could happen either during the pregnancy or during labour
39
Q

What are the important things to remember with blood donation and transfusion?

A
  • Blood donation rule: always give someone their own blood group (red blood cells) where positive
  • In an emergency – transfuse with O Rhesus negative: universal donor (No ABO antigens and no rhesus antigens so can’t be attacked)
40
Q

Platelets contain filaments of actin and myosin. What happens after a blood clot has formed?

A

platelet filaments contracts to shrink the clot and reduce the size of the break in the vessel wall

41
Q

What is platelet production called?

A

Thrombocytopoiesis

42
Q

Where does Thrombocytopoiesis take place?

A

In the red bone marrow

43
Q

What are the three substances that affect the rate of platelet formation and megakaryocyte activity?

A
  • Thrombopoietin (TPO)
  • Interlukin-6 a hormone that stimulates platelet formation
  • Multi-CSF which stimulates platelet production by promoting megakaryocyte formation and growth
44
Q

What happens during the vascular phase (vasoconstriction) of heamostasis?

A
  • The endothelial cells contract and expose the underlying basement membrane to the bloodstream
  • The endothelial cells begin releasing chemical factors and local hormones such as ADP, tissue factor and prostacyclin. Endothelial cells also release peptide hormones called endothelins which stimulate smooth muscle contraction and stimulate the division of endothelial cells, smooth muscle cells and fibroblasts to accelerate the repair process
  • In small capillaries endothelial cells on opposite sides of the vessel may stick together and prevent blood flow along the damaged vessel
45
Q

What happens at the start of the platelet phase?

A
  • phase the platelets attach to sticky endothelial surfaces, to the basement membrane to exposed collagen fibres
  • The attachment of platelets to exposed surfaces is called platelet adhesion. As more platelets arrive they stick to each-other as well this forms the platelet plug
46
Q

What do platelets release when they are activated?

A
  • ADP which stimulates platelet aggregation and secretion
  • Thromboxane A2 and serotonin which stimulates vascular spasms
  • Clotting factors
  • Platelet derived growth factor that promotes vessel repair
  • Calcium ions
47
Q

What is the growth of the platelet plug limited by?

A
  • Prostacyclin – a prostaglandin that inhibits platelet aggregation and is released by endothelial cells
  • Inhibitory compounds released by WBCs entering the area
  • Circulating plasma enzymes that break down ADP near the plug
  • Compounds that when abundant inhibit plug formation e.g. serotonin
48
Q

where does the extrinsic pathway begin?

A

Outside the bloodstream in the vessel wall?

49
Q

Where does the intrinsic pathway begin?

A

Inside the bloodstream

50
Q

What feedback system is involved with blood clotting?

A

Positive feedback system

51
Q

Thrombomodulin is released by endothelial cells. What does it do?

A

This protein binds to thrombin and converts it to an enzyme that activates protein C. Protein C is a plasma protein that inactivates several clotting factors and stimulates the formation of plasmin

52
Q

What does aspirin do in regards to blood clotting?

A

interferences with blood clotting and prolongs bleeding time. It inhibits platelets from producing prostaglandins and thromboxane A2 which stimulates new platelet activation and aggregation

53
Q

Where do we get half our daily vitamin K requirement from?

A

Our diet

54
Q

What does clot retraction do?

A

pulls the torn edges of the vessel closer together. This process reduces residual bleeding and stabilizes the injury site. It also reduces the size of the damaged area, making it easier for fibroblasts, smooth muscle cells and endothelial cells to complete repairs

55
Q

What are the surface antigens involved in blood groups?

A

Integral membrane glycoproteins

56
Q

What is a cross reaction or transfusion reaction?

A

is when during a transfusion an antibody meets its specific surface antigen and the RBCs agglutinate and may also haemolyze

57
Q

What does a compatibility test usually involve?

A
  1. A determination of blood type

2. A cross-match test

Body Systems (20 decks)

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