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BRS Y2 > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

Define haemostasis

A

The cellular and biochemical process that enables cessation of bleeding in response to injury

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2
Q

What are the 3 roles of haemostasis?

A

To prevent loss of blood from intact vessels
To arrest bleeding from injured vessels
To enable tissue repair

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3
Q

What are the 4 mechanisms of haemostasis?

A

Vessel constriction
Primary haemostasis
Secondary haemostasis
Fibrinolysis

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4
Q

Describe the first mechanism of haemostasis

A

Vessel constriction occurs at the site of injury to limit blood flow, usually in vascular smooth muscle

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5
Q

Describe the second mechanism of haemostasis

A

Primary haemostasis is the formation of a temporary platelet plug, this occurs via:
Exposure of collagen on the endothelium wall at the site of injury
Platelets attach either directly via g1pIa receptor or indirectly via VWF and gp1b receptor
Platelets aggregate after release of contents, thromboxane is synthesised from arachidonic acid
This activates platelets by activating g1pIIb or IIa receptors

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6
Q

What are the 2 ways platelets attach at the endothelium wall? What receptors are involved?

A

Directly via g1pIa

Indirectly via VWF and gp1b receptor

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7
Q

What are the 3 components of primary haemostasis?

A

VWF
Platelets
Vessel wall

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8
Q

What content do platelets release?

A

ADP and thromboxane

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9
Q

What is thromboxane synthesised from?

A

Arachidonic acid

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10
Q

What is the 3rd mechanism of haemostasis?

A

Secondary haemostasis, this is the formation of a permanent platelet plug

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11
Q

What is the scientific term for secondary haemostasis?

A

Coagulation

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12
Q

What is the 4th mechanism of haemostasis?

A

Fibrinolysis, it involves breakdown of the fibrin clot and vessel repair so vessel integrity is restored

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13
Q

What is normal haemostasis the balance between?

A

Fibrinolytic factors and anticoagulant proteins vs coagulant proteins and platelets

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14
Q

What will a tip in the haemostatic balance cause either way?

A

Excess coagulant proteins/platelets= thrombosis

Excess fibrinolytic factors/anticoagulant proteins= bleeding

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15
Q

What are ways bleeding will occur?

A

Excess fibrinolytic factors/anticoagulant
Reduced nos of platelets and coagulant proteins, this could occur via
1) Reduced production (congenital or acquired)
2) Increased clearance or consumption (genetic or acquired)

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16
Q

What is the name of the condition where someone has low numbers of platelets?

A

Thrombocytopenia

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17
Q

What are the 3 main ways thrombocytopenia can arise?

A

Bone marrow failure causing reduced production
Increased clearance
Pooling and destruction in the spleen

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18
Q

How can bone marrow failure cause thrombocytopenia?

A

Leukaemia- white cells infiltrate the bone marrow and so platelets cannot be produced
B12 deficiency- causes megaloblastic anaemia so normal haemopoeisis ceases

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19
Q

How can accelerated platelets clearance manifest? Describe the pathophysiology of the conditions

A

ITP- platelets are destroyed in circulation by auto antibodies
DIC- small clots form all over the body in small vessels using up a lot of platelets

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20
Q

How does aspirin cause impaired platelet function?

A

It reversibly blocks the action if cyclo-oxygenase which reduces platelet aggregation

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21
Q

What drugs impair the function of platelets?

A

NSAIDs, clopidrogel, aspirin

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22
Q

How long does a dose of aspirin last?

A

7 days

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23
Q

How does clopidrogel impair platelet function?

A

Irreversibly blocks ADP receptor P2Y12 on platelet cell membranes

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24
Q

What is Glanzmann thrombothaenia?

A

Absence of GPIIb/IIIa receptors on platelets

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25
Q

What is Bernard Soullier syndrome?

A

Absence of GPIb receptors

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26
Q

What is storage pool disease?

A

A group of disorders where there is reduced granular contents in platelets

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27
Q

What are the 3 subcatagories of disorders of primary heamostasis?

A

Ones that affect
platelets (reduced numbers of impaired function)
or VWF
or the vessel wall

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28
Q

What is von willebrand disease?

A

When there is reduced quantity or function of VWF

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29
Q

How is von willebrand disease inheroted?

A

Autosomal

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30
Q

What are the different types of von willebrand disease?

A

Type 1 an type 3 are deficiency

Type 2 is abnormal function

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31
Q

What are the 2 functions of VWF in haemostasis?

A

Bind to collagen at injury site and capture platelets

Stabilise factor VIII

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32
Q

What may be low if VWF is low?

A

Factor VIII

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33
Q

What are inherited conditions that affect the vessel wall and cause disorders of primary heamostasis?

A

Hereditary haemorrhagic telangiectasia, Ehlers Danlos Syndrome and other connective tissue disorders

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34
Q

What are acquired conditions that affect the vessel wall and cause disorders of primary heamostasis?

A

Steroid therapy
Vasculitis
Scurvy

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35
Q

How does bleeding occur with disorders of primary haemostasis?

A

Immediate bleeding that is prolonged with cuts
Nose bleeds
Gum bleeds
Heavy menstrual bleeding

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36
Q

When do purpura appear?

A

If there are platelet or vascular problems

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37
Q

How does bruising change if there are disorders of primary haemostasis?

A

Bruising is spontaneous and may be easy

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38
Q

What is the difference between petechiae, purpura and ecchymosis?

A

Petechiae are < 3mm
Purpura are 3-10mm
Ecchymosis (bruises) are >10mm

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39
Q

What might severe VWD cause? Why?

A

Haemophilia like bleeding due to low factor VIII

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40
Q

What will APTT and PT (coagulation screens) in those with disorders of primary haemostasis be?

A

Normal

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41
Q

How are disorders of primary haemostasis treated if theres failure of production or function

A

Replace whats missing

Stop drugs eg aspirin and NSAIDs

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42
Q

How are disorders of primary haemostasis treated if theres immune destruction?

A

Immunosupression eg with prednisolone

Splenectomy in ITP

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43
Q

How are disorders of primary haemostasis treated if theres increased consumption?

A

Treat the cause

Replace whats necessary

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44
Q

How does desmopressin help as a haemostatic treatment?

A

It is a vasopressin analogue and increases stores of VWF

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45
Q

What is the normal range of platelets?

A

100-400 (x 10^9/L)

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46
Q

What is the other name for secondary haemostasis?

A

Coagulation

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47
Q

What is the role of coagulation

A

To generate thrombin (IIa) which converts fibrinogen to fibrin

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48
Q

What are the 3 tyoes of coagulation disorder?

A

Deficiency of coagulation factor production
Dilution
Increased consumption

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49
Q

How may deficiency of coagulation factors cause coagulation disorder?

A

Hereditary (haemophilia A or B)

Acquired (liver disease, anitcoagulant drugs eg warafrin and DOACs)

50
Q

How does dilution cause coagulation disorder?

A

Acquired via blood transfusion where lots of RBCs are given but not enough plasma (they are now transfused together)

51
Q

How does increased consumption cause coagulation disorder?

A

Acquired- commonly DIC or immune via antibodies

52
Q

What factor is deficient in haemophilia A?

A

Factor VIII

53
Q

What factor is deficient in haemophilia B?

A

Factor IX

54
Q

How does factor deficiency in haemophilia lead to bleeding?

A

There is failure to generate fibrin to stabilise the platelet plug so it breaks away and causes bleeding

55
Q

What is spontaneous joint bleeding called?

A

Haemarthrosis

56
Q

What must you avoid in those with haemophilia?

A

Intramuscular injections

57
Q

The absence of which factor is lethal?

A

Prothrombin (factor II)

58
Q

How does bleeding occur with factor XI deficiency?

A

Bleeding occurs after trauma but not spontaneously

59
Q

How does bleeding occur with factor XII deficiency?

A

It doesn’t cause bleeding

60
Q

How might liver failure affect haemostasis?

A

It results in reduced production of coagulation factors as most are synthesised in the liver

61
Q

What is a marker of fibrinolysis? Why?

A

Raised D dimer, it is a product of the breakdown of fibrin

62
Q

Describe bleeding patterns in disorders of coagulation

A

Superficial cuts don’t bleed
Bruising is common
Spontaneous bleeding is deep eg into muscles and joints
Bleeding frequently restarts after stopping
Severe bleeding after injury that is delayed

63
Q

How does bleeding differ in coagulation disorders vs platelet/vascular disorders?

A

Platelet vascular: superficial bleeding into skin, bleeding is immediate after injury
Coagulation: Bleeding deep into joints and muscles, it is delayed after injury but severe

64
Q

What pathway does prothrombin time measure? What factors does it involve

A

Extrinsic pathway, involves tissue factor and fcator VII

65
Q

What pathway does activated partial thromboplastin time measure?

A

Intrinsic pathway

66
Q

How is APTT measured?

A

Via contact activation using glass, silica or ellagic acid

67
Q

When replacing missing coagulation factors, when is FFP given?

A

When you want to replace all coagulation factors

68
Q

When replacing missing coagulation factors, when is cryopreciptate given?

A

To replace fibrinogen, factors VIII, XIII or VWF

69
Q

When replacing missing coagulation factors, when are factor concentrates given? When can they not be given?

A

Given if you want to replace any singular factor but not available for factor V

70
Q

What are some novel treatments for haemophilia?

A

Gene therapy
Bispecific antibodies- bind to FIXa and FX to mimic the procoagulant fucntion of FVIIII
RNA silencing

71
Q

When is desmopressin effective?

A

It releases endogenous stores of VWF so only effective in mild conditions when these stores are present

72
Q

What effect does tranexamic acid have?

A

Antifibrinolytic

73
Q

What can cause high levels of fibrinolytic factors and anticoagulant proteins?

A

Drugs eg tPa and heparin

74
Q

How does pulmonary embolism present?

A

Tachycardia, hypoxia, shortness of breath, chest pain, sudden death

75
Q

How does DVT present?

A 
Painful leg
Swelling
Red
Warm
Feeling like they've pulled a muscle
76
Q

What triad is used in thrombosis?

A

Virchow’s traid

77
Q

What is virchow’s traid?

A

Blood- dominant in venous thrombosis
Vessel wall- dominant in arterial thrombosis
Blood flow- dominant in both types of thrombosis

78
Q

What is thrombophilia?

A

An increased risk of thromobosis

79
Q

How does thrombophilia present?

A

Thrombosis at a young age
Multiple thrombosis (may be spontaneous)
Thrombosis even when anticoagulated

80
Q

What might cause thrombophilia?

A

Reduced fibrinolytic factors, anticoagulant proteins, antithrombin, protein C or protein S
Increased coagulant factors
Increased platelets

81
Q

What does protein C inactivate?

A

Factor Va and VIIIa

82
Q

What does antithrombin inactivate?

A

Factor IIa and Xa

83
Q

What factor is thrombin?

A

IIa and Xa

84
Q

What is the name for reduced blood flow

A

Stasis

85
Q

How does reduced blood flow affect blood?

A

It increases the risk of thrombosis

86
Q

How is venous thrombosis prevented?

A

Assess and tackle personal risk factors

Prophylactic anticoagulant therapy

87
Q

What drugs can be given for reducing risk of thrombosis? Briefly explain how hey work

A

Warfarin and DOACs- they lower procoagulant factors

Heparin- increases anticoagulant therapy

88
Q

What are the indications for anticoagulant therapy

A

Therapeutic: venous thrombosis, atrial fibrillation, mechanical prosthetic heart valve
Preventative: post-surgery, during hospital admission, during pregnancy

89
Q

What class of molecule is heparin?

A

Glycosaminoglycan

90
Q

How are long chains of heparin adminsitered?

A

Intravenously

91
Q

How do long chains of heparin work?

A

They enhance antithrombin by changing its active site, this gives it a greater affinity for factor Xa and thrombin

92
Q

What are long chain heparins targets (for increasing affinity between them and antithrombin)

A

Factor Xa

Thrombin

93
Q

What does antithrombin inactivate?

A

Factors IXa, Xa and IIa (IIa is thrombin)

94
Q

How is low molecular weight heparin administered?

A

Subcutaneously

95
Q

How does low molecular weight heparin work?

A

It has anti Xa activity, does this by enhancing antithrombin

96
Q

What is the main difference between the actions of low molecular weight heparin and long chain heparin?

A

Low molecular weight heparin is not long enough to wrap around both antithrombin and thrombin so it only has anti Xa activity and is therefore less powerful. Long chain heparin is more powerful and has both anti Xa and thrombin activity

97
Q

What type of heparin doesnt need to be monitored? Why?

A

Low molecular weight heparin. It is less powerful and has a dose predictable effect

98
Q

What is used to monitor the effects of heparin? Alongside the use of which type of heparin?

A

APTT (this will only be affected by long chain heparin though)

99
Q

What is the method of action of warfarin?

A

It blocks vitamin K which is required to make clotting factors II, VII, IX, V, anticoagulant factors, protein C and protein S

100
Q

What is the main downfall of warfarin?

A

It has a narrow therapeutic index that requires monitoring

101
Q

What state does warfarin induce? How fast

A

An anticoagulant state, but slowly

102
Q

Is warfarin reversible?

A

Yes

103
Q

How is warfarin reversed slowly?

A

By vitamin K administration

104
Q

How is warfarin reversed quickly?

A

Infusion of coagulation factors like prothrombin complex concentrate (contains factors II, VII, IX and X) or fresh frozen plasma

105
Q

What are side effects of warfarin?

A

Bleeding (mostly minor)
Skin necrosis
Purple toe syndrome
Embryopathy

106
Q

When must warfarin not be given?

A

During pregnancy, especially during the first trimester as then it will kill the baby

107
Q

How is warfarin monitored?

A

Via the international sensitivity index (ISI)

108
Q

What will happen to INR to indicate a higher risk of bleeding?

A

It will increase

109
Q

What are some reasons patients may be resistant to warfarin?

A

Lack of compliance
Increased vitamin K in the diet
Increased metabolism
Reduced binding

110
Q

What is the method of action of DOACs?

A

They directly inhibit factor Xa or thrombin

111
Q

How does the onset/offset differ between warfarin and DOACS?

A

Warfarin is slow

DOACs is fast

112
Q

How does the dosing differ between warfarin and DOACS?

A

Variable

Fixed

113
Q

How does the effect on food between warfarin and DOACS?

A

Warfarin affects food

DOACs do not affect food

114
Q

How do interactions differ between warfarin and DOACS?

A

Warfarin has many interactions

DOACs have few interactions

115
Q

How does monitoring differ between warfarin and DOACS?

A

Warfarin requires monitoring

DOACs dont require monitoring

116
Q

How does renal dependance differ between warfarin and DOACS?

A

Warfarin doesnt have renal dependance

Some DOACs have renal dependance

117
Q

How does reversibility differ between warfarin and DOACS?

A

Warfarin is reversible via vitamin K and PCCs

There are specific antidotes to DOACs available

118
Q

When are DOACs not given as first line treatment? Why?

A

To those with mechanical prosthetic heart valves because they aren’t effective, warfarin is given instead
They aren’t given in pregnancy as they aren’t safe
For medical thromboprophylaxis as they arent effective

119
Q

When are DOACs given first line?

A

Venous thrombosis initial and long term treatment
Atrial fibrillation
Sometimes after surgery

120
Q

When is LWMH given as first line treatment?

A

Following surgery
During hospital admission
During pregnancy

121
Q

What is haemostasis a balance between?

A

Coagulant factors/platelets vs fibrinolytic factors/anticoagulant proteins

122
Q

What are the 2 outcomes of a tip in the haemostatic balance?

A

Bleeding

Thrombosis

BRS Y2 (85 decks)

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