Haemostasis Flashcards

1
Q

Define haemostasis?

A

The body’s normal physiological response to prevent bleeding / haemorrhage.

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2
Q

What are the essential components of haemostasis ?

A
  • blood vessels
  • platelets
  • coagulation factors
  • anticoagulant factors
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3
Q

What is the normal lifespan of platelets ?

A

7-10 days

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4
Q

What can haemostasis be divided into ?

A

1) primary haemostasis
- platelet plug formation
2) secondary haemostasis - coagulation cascade

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5
Q

Outline the process of primary haemostasis

A
  1. Damage to blood vessel which initially results in vasoconstriction.
  2. PLATLET ADHESION : Platelets begins to adhere to exposed collagen on blood vessels via vWF.
  3. PLATLET ACTIVATION : Platelets secrete ADP ( helps additional platelets to adhere to injury site ) thromboxane and other substances to become activated and activate other platelets. This helps to activate the clotting cascade.
  4. PLATLET PLUG : Platelets aggregate to form platelet plug.
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6
Q

Outline the process of secondary haemostasis ( the clotting cascade )

A
  1. Prothrombin is converted into thrombin. This occurs via the clotting factor X ( also known as prothrombinase).
  2. Thrombin now works to convert fibrinogen into soluble fibrin fibres which forms a mesh that traps more platlets and RBC - producing a clot.
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7
Q

Where are majority of clotting factors and anticoagulants made ?

A

The liver

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8
Q

Name a few coagulation factors

A

Fibrinogen

Prothrombin

Factor 5,7,8,9,10,11,11,13

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9
Q

Name a few anticoagulants ( natural )

A

Protein C

Protein S

Antithrombin 111( prevents prothrombin turning into thrombin)

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10
Q

What is the Von willebrand factor ?

A

An adhesion glycoprotein that circulates in plasma. It is synthesised by endothelial cells and megakaryocytes. It mediates adhesion of platelets to the subendothelial at sites of vascular damage.

Moreover , it is a carrier and stabiliser of circulating factor V111 (8)

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11
Q

Why is the vessel wall important in haemostasis ?

A
  1. Vasoconstriction
  2. Production of Von willebrands factor (vWF)
  3. Essential for platlet adhesion
  4. Carrier and protector of factor 8.
  5. Exposure of collagen and tissue factor which initiates activation of clotting factors
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12
Q

What is the role of natural anticoagulants?

A

Stop further coagulation

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13
Q

What is fibrinolysis

A

Enzymatic breakdown of fibrin

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14
Q

Outline the process of. Fibrinolysis

A

In order to break down a clot , plasminogen an inactive precursor is activated by natural tPA. Plasminogen is then converted into plasmin.

Plasmin is used to convert fibrin into D dimers.

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15
Q

What is haemophilia A ?

A

A congenital coagulation factor disorder

X linked recessive inheritance

This is where there is a lack of factor 8 ( V111)

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16
Q

At what age is haemophilia A diagnosed ?

A

Diagnosed pre nasally or soon after birth if family history.

17
Q

What are clinical problems associated with haemophilia A ?

A

Bleeding into muscles and joints

Bruising very easily

18
Q

What abnormalities would you expect to see in the blood results of a patient with haemophilia A ?

A

Increased APTT time.

( activated partial thromboplastin time) - indicates that clotting is taking longer to occur.

19
Q

How do you treat haemophilia A ?

A

Treat with recombinant factor V111 ( 8) Or DDAVP.

20
Q

What is haemophilia B ?

A

A congenital coagulation factor disorders

X linked recessively inherited

Congenital reduction in factor 1X (9)

21
Q

What is more common , haemophilia A or B ?

A

A

22
Q

What is Von willebrand disease ?

A
  • very common disease . Usually autosomal dominant.
  • because Von Willebrand factor carries factor V111 (8) and mediated platlet adhesion to endothelium , this could lead to abnormal platlet adhesion to vessel wall and reduce factor V111 amount.
23
Q

What are clinical symptoms of Von willebrand’s disease ?

A
  • platlet associated bleeding
  • skin and mucous membranes bleeding
  • gum bleeding
  • bruising very easily
  • prolonged bleeding after trauma , heavy periods , post surgery bleeding and post dental extraction bleeding.

JOINT / MUSCLE BLEEDS ARE RARE!

24
Q

What is DIC ( disseminated Intravascular coagulopathy)

A
  • type of microangiopathic haemolytic anaemia
  • this is where there is pathological activation of coagulation. Therefore numerous microthrombi are formed in circulation. This leads to consumption of clotting factors and platlets. As RBC try to move through small vessels , they get damaged because of the clots.
  • there is usually raised APTT ( takes longer to clot) , low fibrinogen and raised D dimers.
  • can develop thrombosis or bleeding due to lack of clotting factors as they are getting used up
25
Q

What are the triggers for DIC ?

A

ACQUIRED ONLY.

Malignancy

Massive tissue injury eg burns

Infections eg gram negative sepsis

Massive haemorrhage

ABO transfusion reaction

Obstetric causes

26
Q

What is thrombophilias?

A

These are acquired or congenital defects of haemostasis which can increase a patients risk of thrombosis.

Congenital causes include deficiency in natural anticoagulants such as protein C , protein S and antithrombin and abnromal factor V.

Acquired conditions involve anti phospholipid syndrome.

THESE ARE RARE.

27
Q

What are congenital problems with vessels ?

A

Hereditary haemorrhage is telangiectasia ( HHT)

This is autosomal dominant , dilated micro vascular swellings increase with time which could lead to GI haemorrhage which can lead to iron deficiency anaemia.

28
Q

What are a few acquired problems with vessels ?

A
  1. Taking steroids
  2. Infections such as malaria and measles
  3. Scurvy can cause defective collagen production.
29
Q

What are clinical symptoms of vessel wall abnormalities?

A

Easy bruising

Spontaneous bleeding from small vessels

Skin mainly affected

Can be mucous membranes affected too

30
Q

What drug is commonly given for patients who qualify thrombolysis? And what are the side effects for this treatment ?

A

Altoplase - given IV.
A trans plasminogen activator (artificial form)

Bleeding from mucosal membranes - eg from teeth , nose . Mucous membranes tend to be very rich and vascular.

31
Q

For patients who do not qualify for thrombolysis , what medication do we administer ?

A

Aspirin - because this is an anti-platlet aggregation