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Haemostasis Flashcards

(44 cards)

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1
Q

What is haemostasis?

A

The body’s response to stopping of a haemorrhage.

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2
Q

What are the principles of normal haemostasis?

A
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3
Q

What are the critical steps in the clotting cascade?

A
  1. Contraction
    • severed artery contracts to decrease the pressure downstream
    • doesn’t occur in veins but the pressure is lower there
  2. Primary haemostatic plug
    • formed in seconds - minutes
    • platelets form at the hole of vessel and stick to the exposed connective tissue
  3. Secondary haemostatic plug
    • fibrin filaments stablise the platelet plug
    • forms after 30 minutes
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4
Q

What is the role of the vessel wall in haemostasis?

A
  • Vasoconstriction
  • Subendothelium traps platelets
  • Release of factors:
    • to oppose clotting:
      • tissue plasminogen activator (for fibrinolysis)
      • thrombomodulin (activates protein C)
    • to favour clotting:
      • von Willebrand factor
      • tissue factor
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5
Q

What is the role of platelets in the clotting cascade?

A
  • Stick to the exposed subendothelium, specifically von Willebrand factor
  • Aggregate with other platelets through cross-linking
  • Swell and change shape into sticky spheres
  • Secrete factors helping the platelet plug to grow
    • fibrinogen
    • ADP
    • thromboxane A2
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6
Q

What is the role of the platelet plug in the clotting cascade?

A

To control bleeding

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7
Q

What is clotting?

A

Process where blood becomes a solid mass after making contact with connective tissue.

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8
Q

What is the end result of the clotting system?

A

Production of enzyme thrombin which causes circulating blood plasma fibrinogen (soluble) to produce fibrin filaments (insoluble) which are deposited to trap RBC.

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9
Q

What is fibrinolysis?

A

An opposite system to clotting which causes the destruction of clots.

  • plasmin (enzyme) breaks down fibrin which is consumed by macrophages
  • can be natural or therpeutic
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10
Q

Which cells do not cause the clotting of blood upon contact?

A

Endothelial cells, WBC, unactivated platelets and RBC.

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11
Q

What are platelets?

A
  • Blood cell produced by megakaryocytes in the bone marrow
    • platelets bud off the cytoplasm of megakaryocytes
  • Normal platelet count = 150-400 x109/L
    • Platelet levels <10 x109/L to cause internal bleeding
  • Normal life span = 7-10 days
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12
Q

What are platelets activated by?

A
  • Collagen surfaces within extravascular areas
  • ADP
    • released by activated platelets and injured RBC to amplify the platelet response.
  • Thromboxane A2
  • Thrombin
    • from the clotting cascade
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13
Q

How does aspirin work as an anticoagulant?

A

Irreversibly inactivates cyclooxygenase which is responsible for producing thromboxane A2

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14
Q

What are therapeutic targets to prevent coagulation?

A

Mediating factors of thrombus formation e.g. vWF, fibrinogen, collagen, ADP, thromboxane, thrombin.

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15
Q

What is meant by the ‘clotting cascade’?

A

An amplification system that activates precursor proteins to generate thrombin (IIa).

  • thrombin converts fibrinogen into fibrin which enmeshes the platelet plug to make a stable clot.
  • Natural anticogulants inhibit clot formation
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16
Q

Give examples of natural anticoagulants

A
  • Protein C
  • Protein S
  • Antithrombin
  • Tissue factor pathway inhibitor
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17
Q

Give examples of therapeutic anticoagulants and antiplatelet

A

Anti platelet:

  • Aspirin
  • Clopidogrel

Anticoagulants:

  • Wafarin
  • Heparin
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18
Q

How does a clot aid wound closure?

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A
  • Platelets in the clot die, pulling fibrin by their actin myosin filaments
  • Clot retraction aids pulling the sides of the wound together to toughen the clot by squeezing out fluid.
19
Q

Where are coagulation factors made?

20
Q

List the coagulation factors

Study These Flashcards
A
  • Fibrinogen (F1)
  • Prothrombin (F2)
  • Factor 5
  • Factor 7
  • Factor 8
  • Factor 9
  • Factor 10
  • Factor 11
  • (Factor 12)
  • Factor 13
  • Tissue factor
21
Q

What are the plasmin activators?

Study These Flashcards
A

Plasmin circulates as a precursor - plasminogen

Activated by:

  • tissue plasminogen activator (tPA)
  • urokinase
  • streptokinase (produced by streptococci)
22
Q

What is APTT and what factors are involved?

Study These Flashcards
A

Activated Partial Thrombin Time

  • measures the time taken for a clot to form by the intrinsic pathway
  • Factors VIII, IX, XI, XII are affected
23
Q

What is PT?

Study These Flashcards
A

Prothrombin time

  • time take nfor a clot to form via the extrinsic pathway
  • Factor VII affected
24
Q

Which factors cannot confer whether the intrinsic or extrinsic pathway is affected?

Study These Flashcards
A

V, X, prothrombin and fibrinogen

25
What is von Willebrand factor involved in?
* Platelet adhesion * Platelet aggregation * Carries FVIII
26
What are fibrin degradation products?
D-dimer ## Footnote Increased in conditions where there is thrombosis e.g. DIC, DVT and pulmonary embolism
27
Why is there a risk of post operative thrombosis?
Fibrinolytic actvity drops after surgery and remains low for 7-10 days
28
What is the 'final fate' of a clot?
Clot becomes organised thorugh fibrous repair and is replaced by granulation tissue then a scar.
29
What is haemophilia?
A disease causing reduced clotting due to an impaired clotting cascade. Therefore, not enough fibrin is produced.
30
What is haemophilia A?
* Deficiency of factor VIII * decreased amounts or activity * Most common hereditary disease associated with serious bleeding * X-linked recessive * affects males and homzygous females * 1 in 5000 males affected * 30% of cases caused by new mutations * Mild form: 6-50% activity * Severe form: \<1% activity
31
What are symptoms of haemophilia?
* Easy bruising * massive haemorrhage after trauma * haemarthrosis * repeptitive bleeding can cause joint deformities * Bleeding from mucosal membranes * menorrhagia * epistaxis * bleeding gums * muscle haematomas * intracerebral haemorrhage
32
What are the chemical signs of haemophilia A?
* Normal platelet count * Normal bleeding time * Normal PT * Prolonged APTT
33
What are the types of coagulation factor disorders?
Congentital: * Haemophilia A (deficiency in Factor 8) * Haemophilia B (deficiency in Factor 9) Acquired * Liver disease * Vitamin K deficiency (affects factors II, VII, IX, X) * Anticoagulants
34
What is petechiae and how does it normally occur?
Pinpoint haemorrhages, caused by blood leaking from the capillaries - typical in vasculitis or abnormalities in the number and function of platelets
35
What is Von Willebrand's disease?
Common (1 in 150) autosomal dominant disorder affecting platelet adhesion to the endothelium. * Reduction in vWF production * vWF functions: * carries **factor VIII** * mediates platelet adhesion to the endothelium * causes reduced factor VIII amount or activity
36
What are the symptoms of von Willebrands disease?
* Skin and mucous membrane bleeding * epistaxis * gum bleeding * bruising * Prolonged bleeding after trauma * heavy periods * post surgery * post dental extraction The pattern of bleeding is similar to thrombocytopenia. Spontaneous joint or muscle bleeds are rare.
37
What are the symptoms of vessel wall abnormalities?
* Easy bruising * Spontaneous bleeding from vessels * Mainly affects the skin but can also affect mucous membranes
38
What is hereditary haemorrhagic telangiectasia (HHT)?
Congenital _autosomal dominant_ disorder causing **malformations of blood vessels.** * Arteirous venous malformations often occur in the nose and gut Symptoms: * epistaxis * telangiectasia (abnormal blood vessels as red or purple spots) Can lead to **iron-deficiency** **anaemia**. Also known as Osler-Weber-Rendu syndrome
39
How are vessel wall abnormalities characterised?
Congential: * HHT * Connective tissue disorders * Ehler's-Danlos Syndrome * Marfan's Syndrome Acquired: * Senile purpura * bruising in the elderly - vessels become more damaged with age * Steroids * weakens vessel wall * Infection * Measles * Meningococcal infection * Scurvy/Vit C deficiency * defective collagen production
40
What is disseminated intravascular coagulopathy?
* Microangiopathic haemolytic anaemia * Abnormal activating of coagulation * numerous microthrombi are formed in the circulation * clotting factors and platelets are consumed * leads to haemolytic anaemia High risk of thrombosis **_OR_** bleeding means it is difficult to treat
41
What would clotting test show in disseminated intravascular coagulopathy?
* raised PT/INR * raised APTT * low fibrinogen * raised D dimers/ fibrin degradation products
42
What is the histological presentation of DIC?
Intravascular haemolysis -\> schistocytes
43
What are the causes of DIC?
* Malignancy * Massive tissue injury e.g. burns * Infections * normally gram-negative sepsis * Massive haemorrhage and transfusion * ABO transfusion reaction * coagulation factors become diluted * Obstetric causes: * placental abruption * pre-eclampsia * amniotic fluid embolism
44
What are thrombophilias?
Acquired or congenital defects of haemostasis which increase a pts risk of thrombosis. Congenital causes: * deficiencies in natural anticoagulants * protein C * protein S * antithrombin * abnormal factor V Acquired causes: * antiphospholipid syndrome

Pathological Processes (9 decks)

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