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SEM 4: Haematology > Blood Coagulation, Haemostasis and Its Investigation > Flashcards

Blood Coagulation, Haemostasis and Its Investigation Flashcards

1
Q

What is haemostasis?

A

A protective process evolved in order to maintain stable physiology.

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2
Q

Why is infection important in haemostasis?

A

It is an important indicator of haemostasis. It changes the balance of haemostasis and leads to the formation of a clot.

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3
Q

What can happen when clots occur?

A

Clots forming in blood vessels going to organs result in the necrosis of certain areas of tissue

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4
Q

Describe the blood supply of the horseshoe crab

A

The blood supply consists of one main cell - haemolymph.

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5
Q

What are amebocytes in the haemolymph?

A
  • Proteins of the coagulation system
  • Proteins and peptides of the immune system
  • |f the crab has an infection, it could have antibodies around it.
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6
Q

What is disseminated intravascular coagulation (DIC)?

A

Too much clotting so the blood supply to areas has stopped.

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7
Q

How does antibodies combat DIC?

A
  1. The immune system works with the coagulation system to carry out the antibodies.
  2. The antibodies stop the infection from spreading to the important organs.
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8
Q

What are the life-preserving processes of haemostasis?

A
  • Respond to tissue injury
  • Curtail blood loss
  • Restore vascular integrity and promote healing
  • Limit infection
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9
Q

What are the four key components of haemostasis?

A
  • Endothelium
  • Coagulation
  • Platelets
  • Fibrinolysis
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10
Q

What makes a blood clot?

A
  • Fibrin mesh: proteins that come out of coagulation to strengthen the clot
  • Platelets: small and important in clotting - makes up a lot of the clot
  • Red blood cells: the biconcave shape is changed to help the mesh. If anaemic, there is more bleeding.
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11
Q

Give an overveiw of haemostasis

A
  1. Endothelial damage occurs
  2. The vessel constriction so less blood flow = less blood loss.
  3. Laminar flow of blood and platelets in the bloodstream
  4. Platelets stop when they reach the area of damage and adhere to the site. This stops blood loss.
  5. The fibrin enters.
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12
Q

What is primary haemostasis (phase 1 of the haemostatic system)?

A
  • Vasoconstriction (immediate)
  • Platelet adhesion (within seconds)
  • Platelet aggregation and contraction (within minutes)
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13
Q

What is secondary haemostasis (phase 2 of the haemostatic system)?

A
  • Activation of coagulation factors (within seconds)

- Formation of fibrin (within minutes)

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14
Q

What is fibrinolysis (phase 3 of the haemostatic system)?

A
  • Activation of fibrinolysis (within minutes)

- Lysis of the plug (within hours)

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15
Q

When does regeneration of tissues occur?

A

Occur after the clot has dissolved and leaves

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16
Q

Describe the process of primary haemostasis

A
  1. Endothelial damage occurs and the subendothelial is exposed to blood, collagen and tissue factor (these are not usually exposed).
  2. Platelet recognises the damaged site and sticks to the area - collagen due to vWF as the vWF is exposed when the blood cell globular structure unravels and platelets can stick.
  3. Platelets form a shape and release prothrombotic substances into the micro-environment. This stops the bleeding of the thrombotic state damaged vessels.
  4. The other platelets are joined. They become a template for the coagulation factors to release information. The phospholipid surface of platelet enables the coagulation of the factors to work better with each other.
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17
Q

What is vWF?

A

A protein with a multimeric structure that is hidden usually in the endothelium and released and unravelled when there is an increase in sheer stress or injury.

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18
Q

What happens to vWF when there is an injury?

A
  • Unravels and becomes active
  • Looks for collagen and starts to form a clot
  • Acts as the anchor between the platelet and the subendothelial collagen.
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19
Q

Briefly describe the role of platelets in haemostasis

A
  1. Primary haemostasis occurs when blood comes into contact with TF and collagen.
  2. Platelets are activated and release thrombotic factors causing the recruitment of more platelets. An aggregate forms and there is contraction.
  3. Secondary haemostasis starts to form. Fibrin will form on top of the activated platelets forming a platelet plug at the site of injury.
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20
Q

Describe the formation of the platelet plug in detail

A
  1. The vessel wall is damaged exposing signalling molecules such as TF and collagen.
  2. TF leads to the production of thrombin - this is the initiation step of the coagulation process
  3. The exposed signalling molecules attract platelets which attach to the subendothelial tissue - this is adhesion. (Primary haemostasis)
  4. Platelets are activated through the presence of thrombin and release further attractant chemicals that attract more platelets. This is secretion.
  5. New platelets bind to the adhered platelets and themselves become activated. This is aggregation. (Still primary haemostasis)
  6. Conformational change takes place during activation and the loose platelet plug contracts to form a dense adherent plug. (primary haemostasis)
  7. The activated platelets form an area of negatively charged phospholipid membrane at the site of injury so subsequent coagulation occurs if needed. (secondary haemostasis)
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21
Q

Which organ makes the coagulation factors?

A

The liver

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22
Q

What is the original waterfall hypothesis?

A
  1. Foreign substances and surface cause blood to coagulate because of the intrinsic pathway.
  2. The coagulation factors get activated and therefore, there is coagulation.
  3. Thrombin burst is achieved by other clotting factors getting activated.
  4. Activated thrombin causes other activating substances to be released.
  5. The intrinsic factor is important in getting the burst of the thrombin that causes the fibrin mesh to occur.
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23
Q

What happens if there is FVII deficiency or FXII deficiency?

A

FVII deficiency causes bleeding but FXII deficiency does not.

24
Q

What is the revised waterfall hypothesis?

A 
- Intertwined cascade 
 Each reaction requires: 
- Ca2+
- Phospholipid 
- +/- specific co-factors
25
Q

How is the revised cascade initiated?

A
  1. Activated factor 7 will stick to the tissue factor when there is bleeding
  2. The complex will then be activated by tissue factor 10.
  3. This goes on to form thrombin.
26
Q

What are the phases of coagulation?

A
  1. Coagulation is initiated when subendothelial tissue is exposed to the circulation at the site of injury.
  2. These tissues express TF on their surface and this binds to endogenous activated FVII (7).
  3. The complex binds small amounts of factor X (10) and FV (5) which starts to produce small quantities of thrombin.
  4. The thrombin activates platelets that are attracted to the site as well as plasma-borne clotting factors.
  5. The activated factors (including FVIII and FIX) enable the binding of activated FX and FV to the platelet surface.
  6. The platelets are activated causing a conformational change in their membrane exposing the “reaction site” necessary for the continuation of the process.
  7. This leads to the “thrombin burst” which produces large-scale fibrin and the development of a stable, effective clot.
27
Q

What is thrombin?

A

TF + factor 7

  • causes the recruitment of other factors
  • amplification is the most important
28
Q

Why is fibrinolysis important?

A

It encourages healing

29
Q

What is fibrinolysis?

A
  • Clot limiting, repair, and heal mechanism

- A series of tightly regulated enzymatic steps

30
Q

What are the main molecules in fibrinolysis?

A
  • Plasminogen
  • Tissue plasminogen activator (t-PA) and urokinase (u-PA)
  • Plasminogen activator inhibitor -1 and -2
  • a2-plasmin inhibitor
31
Q

Describe the process of fibrinolysis

A
  1. Plasminogen is the precursor. It is activated to plasmin by tissue plasminogen activator (t-PA) which enables the breakdown of the fibrin clot.
  2. Plasmin releases parts of the broken clot into the bloodstream.
  3. Cross-linked Fibrin will be degraded producing D-dimers. Fibrin degradation products (FDP) will be produced if there is non-cross linked fibrin or fibrinogen is not broken down.
  4. The body degenerates D-dimers.
32
Q

Why are D-dimers important clinically?

A

Elevated levels of D-dimers if someone has a clot as fibrinolysis occurs at the same time as clotting.

33
Q

What can be used in therapeutic thrombolysis for myocardial infarction?

A

tPA and a bacterial activator, streptokinase, are used in therapeutic thrombolysis for myocardial infarction (clot busters).

34
Q

When is therapeutic thrombolysis used?

A

Used in clots in the cerebral vessel or coronary vessel

35
Q

Why are plasminogen and tPA important?

A

They can chew up the clot, therefore, releasing it and causing minimal damage-therapeutic therapy.

36
Q

How is the haemostasis equilibrium balance maintained?

A
  • Turn off the coagulation factors and platelets as excess clotting isn’t desired.
  • Fibrinolysis does not achieve this because all it does is break up the clot.
37
Q

What is the function of anti-coagulants?

A

Turn off the coagulation factors to enable a balance to occur

38
Q

How does thrombosis occur?

A
  • Increase in coagulation factors, platelets, and decrease in fibrinolytic factors, anticoagulant proteins
  • If excess platelets present and the coagulation factor levels are elevated.
  • There is a mutation in the protein that causes there to be excess protein - more clotting - can cause thrombosis - DVT.
39
Q

What does chronic venous insufficiency cause?

A
  • Atropic changes
  • Hyperpigmentation
  • Ulceration
  • Infection
40
Q

How does bleeding occur?

A
  • Increase in fibrinolytic factors, anticoagulant proteins and decrease in coagulation factors, platelets
  • Opposite to thrombosis as no clotting factors, therefore, too much bleeding and fibrinolysis and deficiency in coagulation factors and platelets.
  • Will have bruising that is large
41
Q

What is ecchymosis?

A

Easy bleeding

- Virtually all bleeding disorders and often in normals

42
Q

What do coagulation tests show?

A
  • Coagulation tests determine if the clotting times are prolonged; if they are shows there’s a problem in the coagulation process.
43
Q

What do coagulation tests involve?

A
  1. Incubate plasma with reagents necessary for coagulation.
    • > Phospholipid, co-factors
    • > Trigger or activator
    • > Calcium
  2. Measure time taken to form fibrin clot
44
Q

What is the Prothrombin Time (PT) test?

A
  1. Collect the sample for the test in a tube
  2. Take the calcium out and therefore, it cannot form a clot.
  3. Re-add the calcium when doing the test -> so you can test for coagulation.
  4. Trying to test the TF7a complex
  5. Clotting time takes 9-11 seconds
45
Q

What is the Activated Partial Thromboplastin Time (APTT) test?

A
  1. Use chemicals that have the right structure to cause the activation of the specific coagulation factors.
  2. Takes 30-40 secs
  3. If the APTT takes longer, then it shows that there are coagulation factors missing. In F5, 2, or 1.
46
Q

What is the Thrombin Time (TT) test?

A
  1. Sensitive to defects in the conversion of fibrinogen to fibrin.
  2. If the endpoint cannot form, it is difficult to validate the other results.
47
Q

Give an overview of coagulation pathways

A

The intrinsic pathway joins with the extrinsic pathway which forms the common pathway to form a fibrin clot.
APTT - 1. surface activating agent (e.g. kaolin), 2. phospholipid and 3. calcium to the intrinsic pathway, and PT - 1. Thromboplastin Tissue factor phospholipid and 2. Calcium to the extrinsic pathway to the common pathway
to form the fibrin clot in thrombin time (1. thrombin).

48
Q

What are the limitations of clotting time?

A

Clotting time is limited as only doing tests on the initial stages of the clotting process therefore, the information we retain is not that detailed.

49
Q

Describe the total testing process

A
  1. Transportation
  2. Analysis
  3. Report
  4. Proper order and test selection:
    - Interpretation and Clinical use of test results
    - Results will not be specific enough if the sample not collected properly.
50
Q

Describe blood sample collection for haemostasis testing

A
  • Accuracy of haemostasis laboratory tests depends on the quality of the specimen submitted.
  • Blood is anticoagulated with 3.2% (0.109 M) sodium citrate
  • Most tubes contain 0.3 mL anticoagulant and require 2.7 mLs of blood
  • Under filling the tube yields grossly inaccurate results.
51
Q

What are some pre-analytical errors that can occur?

A
  • Problems with the blue-top tube: partial fill tubes and vacuum leak and citrate evaporation
  • Biological effects: Hct >55 or <15 and Lipaemia, hyperbilirubinaemia and haemolysis
  • Problems with phlebotomy: Heparin contamination, wrong label, slow fill, underfill, vigorous shaking and difficult venepuncture
  • Laboratory errors: delay in testing, prolonged incubation at 37oC and Freeze/thaw deterioration
  • Minimise errors to get good reliable results
52
Q

Why are the mixing studies done?

A
  1. Do tests with plasma as well to see if there is anything in the plasma that is causing coagulation.
  2. If it is to do with a deficiency when we mix with control factors, all the coagulation factors will be replaced that are missing.
  3. The final tube will have everything in it if there is a deficiency in clotting factors because the control replaces the missing factors.
  4. In an inhibitor test, there are antibodies present rather than a deficiency which will cause a prolonged time. It will not be correct if there is antibodies present but there will be if there is a deficiency.
53
Q

Normal PT and Abnormal APTT. What is the most common inhibitor and factor deficiencies?

A

Mix with 50:50

  • If Abnormal: test for inhibitor activity
    • > Specific factors: VIII, IX and XI
    • > Non-specific: anti-phospholipid Ab
  • If Normal: test for factor deficiency
    • > Isolated deficiency in intrinsic pathway (factors VIII, IX, XI)
    • > Multiple factor deficiencies (rare)
54
Q

Abnormal PT and Normal APTT. What is the most common inhibitor and factor deficiencies?

A

Mix with 50:50

  • If Abnormal: test for inhibitor activity
    • > Specific: Factor VII (rare)
    • > Non-specific: Anti-phospholipid (rare)
  • If normal: test for factor deficiency
    • > Isolated deficiency of factor VII (rare); multiple factor deficiencies (common) (Liver diseases, vitamin K deficiency, warfarin, DIC)
55
Q

Abnormal Pt and Abnormal APTT. What is the most common inhibitor and factor deficiencies?

A

Mix with 50:50

  • If abnormal: test for inhibitor activity
    • > Specific: Factors V, X, II, I (rare)
    • > Non-specific: anti-phospholipid (common)
  • If normal: test for factor deficiency
    • > Isolated deficiency in common pathway: Factors V, X, prothrombin, fibrinogen and multiple factor deficiencies (common) - Liver disease, vitamin K deficiency, warfarin, DIC
56
Q

What happens if there is an issue with the thrombin time (TT)?

A
  • Abnormal: dysfibrinnaemia, abnormal fibrinolysis, and elevated FDPs
  • Normal: Von Willebrand’s disease, platelet disorder, FXIII deficiency, and Non-coagulation defect
57
Q

What will the D-dimer testing show?

A
  • A measure of the D-dimer, a fibrin degradation product
  • Found elevated in the situation of enhanced fibrinolysis (Thrombosis, DIC)
  • Not specific for thrombosis also elevated as an acute phase reactant
  • A negative result is useful if clinical suspicion of VTE is low

SEM 4: Haematology (8 decks)

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