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Pathological Processes > Intro To Haemostasis > Flashcards

Intro To Haemostasis Flashcards

1
Q

What is haemostasis?

A

Consequence of a tightly regulated process, maintains fluid status in normal vessels, whilst permitting rapid formation of a haemostatic clot at a site of vascular injury

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2
Q

What are the 3 components of haemostasis?

A

Vascular wall
Platelets
Coagulation cascade

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3
Q

What are the 3 basic processes of haemostasis?

A
  1. Contraction of vessel wall - decrease the pressure downstream
  2. Formation of platelet plug at site
  3. Formation of fibrin clot to stabilise platelet plug into a blood clot
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4
Q

What happens when a vessel is injured with regards to platelets?

A

Adhesion
Activation/secretion
Aggregation

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5
Q

Describe platelet adhesion

A

Happens in seconds
Damage to vessel wall, exposure underlying tissues, platelets adhere to collagen via Von Willebrand factor/receptor

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6
Q

Describe platelet activation/secretion

A

Secrete granules containing ADP, thromboxane and other substances to become activated and activate other platelets.
Involved in activation of the clotting cascade.
Provide some coagulation factors by secretion from internal stores.

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7
Q

Describe platelet aggregation

A

Cross linking of platelets to form a platelet plug (seconds to minutes)
Provides some stability but is friable

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8
Q

What are the 3 basic tests for clotting defects?

A

All performed on platelet poor plasma (centrifuged):
Activated partial thromboplastin time (APTT)
Prothrombin time (PT)
Thrombin time (TT)

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9
Q

What will APTT assess?

A

Intrinsic pathway
If prolonged, suggests a deficiency in one or more of factors VIII, IX, XI or XII

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10
Q

What is a deficiency in VIII also called?

A

Haemophilia A

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11
Q

What is a deficiency in IX also called?

A

Haemophilia B

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12
Q

What does PT assess?

A

Extrinsic pathway
Most commonly due to a factor VII deficiency

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13
Q

What are the natural anticoagulants?

A

Protein C, S and antithrombin

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14
Q

Describe the mechanism of activated protein C (APC)

A

Thrombin binds to an endothelial cell receptor called thrombomodulin.
The resulting complex activates protein C
This then inactivates facts VIIIa and Va
Protein S is a cofactor for APC

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15
Q

Describe the mechanism of antithrombin III

A

Plasma protein that inactivates thrombin and several other clotting factors
Activated by heparin on the surface of endothelial cells
Prevents the spread of a clot by rapidly inactivating clotting factors that are carried away from the immediate site of the clot by the flowing blood

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16
Q

What is tissue factor pathway inhibitor?

A

Poses clot formation
Acts in the initiation phase of clotting
Secreted mainly by endothelial cells
Binds to tissue factor-factor VIIa complexes and inhibits the ability of these complexes to generate factor Xa

17
Q

What is thrombocytopenia?

A

Deficiency of platelets in the blood resulting in bleeding into the tissues, bruising and slow blood clotting after injury.
Platelet count of less than 100. X 10^9/L is classified as thrombocytopenia

18
Q

At what platelet count does spontaneous bleeding occur?

A

Less than 20 x 10^9/L.

19
Q

Ow does thrombocytopenia present?

A

Purpura
Petichiae
Mucosal bleeding
Epistaxis
Menorrhagia

20
Q

How can the causes of thrombocytopenia be classified as? Give an example for each

A

Decreased production of platelets e.g. due to bone marrow infiltration by malignancy
Decreased platelet survival e.g. immunologic destruction
Sequestration e.g. in hypersplenism
Dilutional e.g. due to massive blood transfusions (blood stored for >24 hrs dont contain platelets)

21
Q

What are the complication of haemophilia?

A

Muscle haematomas
Recurrent haemarthroses
Joint pain and deformity
Prolonged bleeding post dental extraction
Life threatening post-operative and post-traumatic bleeding
Intracerebral haemorrhage

22
Q

What is the difference between Haemophilia A and B?

A

No difference in presentation

However, haemophilia A is due to a lack of factor VIII. Haemophilia B is due to reduction in factor IX.

Both are X-linked recessive

23
Q

How are Haemophilia A and B treated?

A

A treated with recombinant factor VIII or DDAVP.

B treated with infusions of recombinant factor IX

Both A and B result in prolonged APTT and normal PT

24
Q

describe Von Willebrand disease

A

Relatively uncommon
Usually autosomal dominant
Reduced factor VIII amount/activity

Bleeding tendency is mild and often goes unnoticed until additional stress in most patients
Excessive bleeding from wounds e.g. dental
Menorrhagia
Prolonged bleeding time in the presence of a normal platelet count
Spontaneous bleeding from mucous membranes

25
Q

What are the complications of vessel wall abnormalities?

A

Easy bruising
Spontaneous bleeding from small vessels
… In the skin mainly
… Can be in the mucous membranes

26
Q

What are the congenital causes of vessel wall abnormalities?

A

Hereditary haemorrhagic Telangiectasia (HHT):
Autosomal dominant
Dilated Microvascular swellings increase with time
GI haemorrhage can lead to on deficiency anaemia

Connective tissue disorders - Ehlers Danlos

27
Q

What are the acquired causes of vessel wall abnormalities?

A

Senile Purpura
Steroids
Infection e.g. measles, meningococcal infection
Scurvy - vitamin C deficiency causing defective collagen production

28
Q

What is Disseminated Intravascular Coagulopathy (DIC)?

A

Type of microangiopathic haemolytic anaemia
Pathological activation of coagulation
Numerous microthrombi are formed in the circulation -> clotting factors and platelets are used up, haemolytic anaemia
Failure of haemostasis -> haemorrhage

29
Q

What are the clotting test results with DIC?

A

Usually raised PT/INR
Raised APTT
Low fibrinogen
Raised D dimers/fibrin degradation products

30
Q

How is DIC acquired?

A

There must always be a trigger e.g.
Malignancy
Massive tissue injury e.g. burns
Infections - usually gram negative sepsis
Massive haemorrhage and transfusion
ABO transfusion reaction
Obstetric causes

31
Q

Describe thrombophilias

A

Can be congenital or acquired
Congenital - deficiency in natural anticoagulants (Protein c, s and antrithrombin)
- abnormal factor V - resistance to APC
Acquired causes induce antiphospholipid syndrome (due to antiphospholipid antibodies)

Pathological Processes (6 decks)

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