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Pathological Processes > Haemostasis > Flashcards

Haemostasis Flashcards

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?

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?

A

Liver

20
Q

List the coagulation factors

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?

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?

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?

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?

A

V, X, prothrombin and fibrinogen

25
Q

What is von Willebrand factor involved in?

A
  • Platelet adhesion
  • Platelet aggregation
  • Carries FVIII
26
Q

What are fibrin degradation products?

A

D-dimer

Increased in conditions where there is thrombosis e.g. DIC, DVT and pulmonary embolism

27
Q

Why is there a risk of post operative thrombosis?

A

Fibrinolytic actvity drops after surgery and remains low for 7-10 days

28
Q

What is the ‘final fate’ of a clot?

A

Clot becomes organised thorugh fibrous repair and is replaced by granulation tissue then a scar.

29
Q

What is haemophilia?

A

A disease causing reduced clotting due to an impaired clotting cascade. Therefore, not enough fibrin is produced.

30
Q

What is haemophilia A?

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
Q

What are symptoms of haemophilia?

A
  • 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
Q

What are the chemical signs of haemophilia A?

A
  • Normal platelet count
  • Normal bleeding time
  • Normal PT
  • Prolonged APTT
33
Q

What are the types of coagulation factor disorders?

A

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
Q

What is petechiae and how does it normally occur?

A

Pinpoint haemorrhages, caused by blood leaking from the capillaries - typical in vasculitis or abnormalities in the number and function of platelets

35
Q

What is Von Willebrand’s disease?

A

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
Q

What are the symptoms of von Willebrands disease?

A
  • 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
Q

What are the symptoms of vessel wall abnormalities?

A
  • Easy bruising
  • Spontaneous bleeding from vessels
  • Mainly affects the skin but can also affect mucous membranes
38
Q

What is hereditary haemorrhagic telangiectasia (HHT)?

A

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
Q

How are vessel wall abnormalities characterised?

A

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
Q

What is disseminated intravascular coagulopathy?

A
  • 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
Q

What would clotting test show in disseminated intravascular coagulopathy?

A
  • raised PT/INR
  • raised APTT
  • low fibrinogen
  • raised D dimers/ fibrin degradation products
42
Q

What is the histological presentation of DIC?

A

Intravascular haemolysis -> schistocytes

43
Q

What are the causes of DIC?

A
  • 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
Q

What are thrombophilias?

A

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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