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Haemostasis Flashcards

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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
What is Bernard Soullier syndrome?
Absence of GPIb receptors
26
What is storage pool disease?
A group of disorders where there is reduced granular contents in platelets
27
What are the 3 subcatagories of disorders of primary heamostasis?
Ones that affect platelets (reduced numbers of impaired function) or VWF or the vessel wall
28
What is von willebrand disease?
When there is reduced quantity or function of VWF
29
How is von willebrand disease inheroted?
Autosomal
30
What are the different types of von willebrand disease?
Type 1 an type 3 are deficiency | Type 2 is abnormal function
31
What are the 2 functions of VWF in haemostasis?
Bind to collagen at injury site and capture platelets | Stabilise factor VIII
32
What may be low if VWF is low?
Factor VIII
33
What are inherited conditions that affect the vessel wall and cause disorders of primary heamostasis?
Hereditary haemorrhagic telangiectasia, Ehlers Danlos Syndrome and other connective tissue disorders
34
What are acquired conditions that affect the vessel wall and cause disorders of primary heamostasis?
Steroid therapy Vasculitis Scurvy
35
How does bleeding occur with disorders of primary haemostasis?
Immediate bleeding that is prolonged with cuts Nose bleeds Gum bleeds Heavy menstrual bleeding
36
When do purpura appear?
If there are platelet or vascular problems
37
How does bruising change if there are disorders of primary haemostasis?
Bruising is spontaneous and may be easy
38
What is the difference between petechiae, purpura and ecchymosis?
Petechiae are < 3mm Purpura are 3-10mm Ecchymosis (bruises) are >10mm
39
What might severe VWD cause? Why?
Haemophilia like bleeding due to low factor VIII
40
What will APTT and PT (coagulation screens) in those with disorders of primary haemostasis be?
Normal
41
How are disorders of primary haemostasis treated if theres failure of production or function
Replace whats missing | Stop drugs eg aspirin and NSAIDs
42
How are disorders of primary haemostasis treated if theres immune destruction?
Immunosupression eg with prednisolone | Splenectomy in ITP
43
How are disorders of primary haemostasis treated if theres increased consumption?
Treat the cause | Replace whats necessary
44
How does desmopressin help as a haemostatic treatment?
It is a vasopressin analogue and increases stores of VWF
45
What is the normal range of platelets?
100-400 (x 10^9/L)
46
What is the other name for secondary haemostasis?
Coagulation
47
What is the role of coagulation
To generate thrombin (IIa) which converts fibrinogen to fibrin
48
What are the 3 tyoes of coagulation disorder?
Deficiency of coagulation factor production Dilution Increased consumption
49
How may deficiency of coagulation factors cause coagulation disorder?
Hereditary (haemophilia A or B) | Acquired (liver disease, anitcoagulant drugs eg warafrin and DOACs)
50
How does dilution cause coagulation disorder?
Acquired via blood transfusion where lots of RBCs are given but not enough plasma (they are now transfused together)
51
How does increased consumption cause coagulation disorder?
Acquired- commonly DIC or immune via antibodies
52
What factor is deficient in haemophilia A?
Factor VIII
53
What factor is deficient in haemophilia B?
Factor IX
54
How does factor deficiency in haemophilia lead to bleeding?
There is failure to generate fibrin to stabilise the platelet plug so it breaks away and causes bleeding
55
What is spontaneous joint bleeding called?
Haemarthrosis
56
What must you avoid in those with haemophilia?
Intramuscular injections
57
The absence of which factor is lethal?
Prothrombin (factor II)
58
How does bleeding occur with factor XI deficiency?
Bleeding occurs after trauma but not spontaneously
59
How does bleeding occur with factor XII deficiency?
It doesn't cause bleeding
60
How might liver failure affect haemostasis?
It results in reduced production of coagulation factors as most are synthesised in the liver
61
What is a marker of fibrinolysis? Why?
Raised D dimer, it is a product of the breakdown of fibrin
62
Describe bleeding patterns in disorders of coagulation
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
How does bleeding differ in coagulation disorders vs platelet/vascular disorders?
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
What pathway does prothrombin time measure? What factors does it involve
Extrinsic pathway, involves tissue factor and fcator VII
65
What pathway does activated partial thromboplastin time measure?
Intrinsic pathway
66
How is APTT measured?
Via contact activation using glass, silica or ellagic acid
67
When replacing missing coagulation factors, when is FFP given?
When you want to replace all coagulation factors
68
When replacing missing coagulation factors, when is cryopreciptate given?
To replace fibrinogen, factors VIII, XIII or VWF
69
When replacing missing coagulation factors, when are factor concentrates given? When can they not be given?
Given if you want to replace any singular factor but not available for factor V
70
What are some novel treatments for haemophilia?
Gene therapy Bispecific antibodies- bind to FIXa and FX to mimic the procoagulant fucntion of FVIIII RNA silencing
71
When is desmopressin effective?
It releases endogenous stores of VWF so only effective in mild conditions when these stores are present
72
What effect does tranexamic acid have?
Antifibrinolytic
73
What can cause high levels of fibrinolytic factors and anticoagulant proteins?
Drugs eg tPa and heparin
74
How does pulmonary embolism present?
Tachycardia, hypoxia, shortness of breath, chest pain, sudden death
75
How does DVT present?
``` Painful leg Swelling Red Warm Feeling like they've pulled a muscle ```
76
What triad is used in thrombosis?
Virchow's traid
77
What is virchow's traid?
Blood- dominant in venous thrombosis Vessel wall- dominant in arterial thrombosis Blood flow- dominant in both types of thrombosis
78
What is thrombophilia?
An increased risk of thromobosis
79
How does thrombophilia present?
Thrombosis at a young age Multiple thrombosis (may be spontaneous) Thrombosis even when anticoagulated
80
What might cause thrombophilia?
Reduced fibrinolytic factors, anticoagulant proteins, antithrombin, protein C or protein S Increased coagulant factors Increased platelets
81
What does protein C inactivate?
Factor Va and VIIIa
82
What does antithrombin inactivate?
Factor IIa and Xa
83
What factor is thrombin?
IIa and Xa
84
What is the name for reduced blood flow
Stasis
85
How does reduced blood flow affect blood?
It increases the risk of thrombosis
86
How is venous thrombosis prevented?
Assess and tackle personal risk factors | Prophylactic anticoagulant therapy
87
What drugs can be given for reducing risk of thrombosis? Briefly explain how hey work
Warfarin and DOACs- they lower procoagulant factors | Heparin- increases anticoagulant therapy
88
What are the indications for anticoagulant therapy
Therapeutic: venous thrombosis, atrial fibrillation, mechanical prosthetic heart valve Preventative: post-surgery, during hospital admission, during pregnancy
89
What class of molecule is heparin?
Glycosaminoglycan
90
How are long chains of heparin adminsitered?
Intravenously
91
How do long chains of heparin work?
They enhance antithrombin by changing its active site, this gives it a greater affinity for factor Xa and thrombin
92
What are long chain heparins targets (for increasing affinity between them and antithrombin)
Factor Xa | Thrombin
93
What does antithrombin inactivate?
Factors IXa, Xa and IIa (IIa is thrombin)
94
How is low molecular weight heparin administered?
Subcutaneously
95
How does low molecular weight heparin work?
It has anti Xa activity, does this by enhancing antithrombin
96
What is the main difference between the actions of low molecular weight heparin and long chain heparin?
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
What type of heparin doesnt need to be monitored? Why?
Low molecular weight heparin. It is less powerful and has a dose predictable effect
98
What is used to monitor the effects of heparin? Alongside the use of which type of heparin?
APTT (this will only be affected by long chain heparin though)
99
What is the method of action of warfarin?
It blocks vitamin K which is required to make clotting factors II, VII, IX, V, anticoagulant factors, protein C and protein S
100
What is the main downfall of warfarin?
It has a narrow therapeutic index that requires monitoring
101
What state does warfarin induce? How fast
An anticoagulant state, but slowly
102
Is warfarin reversible?
Yes
103
How is warfarin reversed slowly?
By vitamin K administration
104
How is warfarin reversed quickly?
Infusion of coagulation factors like prothrombin complex concentrate (contains factors II, VII, IX and X) or fresh frozen plasma
105
What are side effects of warfarin?
Bleeding (mostly minor) Skin necrosis Purple toe syndrome Embryopathy
106
When must warfarin not be given?
During pregnancy, especially during the first trimester as then it will kill the baby
107
How is warfarin monitored?
Via the international sensitivity index (ISI)
108
What will happen to INR to indicate a higher risk of bleeding?
It will increase
109
What are some reasons patients may be resistant to warfarin?
Lack of compliance Increased vitamin K in the diet Increased metabolism Reduced binding
110
What is the method of action of DOACs?
They directly inhibit factor Xa or thrombin
111
How does the onset/offset differ between warfarin and DOACS?
Warfarin is slow | DOACs is fast
112
How does the dosing differ between warfarin and DOACS?
Variable | Fixed
113
How does the effect on food between warfarin and DOACS?
Warfarin affects food | DOACs do not affect food
114
How do interactions differ between warfarin and DOACS?
Warfarin has many interactions | DOACs have few interactions
115
How does monitoring differ between warfarin and DOACS?
Warfarin requires monitoring | DOACs dont require monitoring
116
How does renal dependance differ between warfarin and DOACS?
Warfarin doesnt have renal dependance | Some DOACs have renal dependance
117
How does reversibility differ between warfarin and DOACS?
Warfarin is reversible via vitamin K and PCCs | There are specific antidotes to DOACs available
118
When are DOACs not given as first line treatment? Why?
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
When are DOACs given first line?
Venous thrombosis initial and long term treatment Atrial fibrillation Sometimes after surgery
120
When is LWMH given as first line treatment?
Following surgery During hospital admission During pregnancy
121
What is haemostasis a balance between?
Coagulant factors/platelets vs fibrinolytic factors/anticoagulant proteins
122
What are the 2 outcomes of a tip in the haemostatic balance?
Bleeding | Thrombosis

BRS Y2 (85 decks)

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