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Year 2 Cardio > Haemostasis > Flashcards

Haemostasis Flashcards

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1
Q

What is haemostasis?

A

the cellular and biochemical processes that enables both the specific and regulated cessation of bleeding in response to vascular insult

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2
Q

What is haemostasis for?

A

Prevention of blood loss from intact vessels
Arrest bleeding from injured vessels
enable tissue repair

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3
Q

What are the stages of haemostasis?

A

Primary
Secondary
Fibrinolysis

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4
Q

What are the steps of haemostasis?

A

Vessel constriction
Formation of an unstable platelet plug
Stabilisation of plug with fibrin
Vessel repair and dissolution of clot

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5
Q

Why is it important to understand haemostatic mechanisms?

A

Diagnose and treat bleeding disorders

Control bleeding in individuals who do not have an underlying bleeding disorder

Identify risk factors for thrombosis

Treat thrombotic disorders

Monitor the drugs that are used to treat bleeding and thrombotic disorders

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6
Q

What is low platelets known as?

A

thrombocytopenia

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7
Q

What causes low platelets?

A

Bone marrow failure eg: leukaemia, B12 deficiency

Accelerated clearance eg: immune (ITP), Disseminated Intravascular Coagulation (DIC)

Pooling and destruction in an enlarged spleen

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8
Q

What causes impaired function of platelets?

A

Hereditary absence of glycoproteins or storage granules (rare)

Acquired due to drugs: aspirin, NSAIDs, clopidogrel (common)

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9
Q

What are conditions that impaired platelet function?

A

Glanzmann’s thrombasthenia
Bernard Soulier syndrome
Storage Pool diseas

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10
Q

What are the two functions of VWF?

A

Binding to collagen and capturing platelets
Stabilising Factor VIII
Factor VIII may be low if VWF is very low

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11
Q

What is VWD?

A

Von Willebrand disease
Hereditary decrease of quantity +/ function (common)
Acquired due to antibody (rare)

VWD is usually hereditary (autosomal inheritance pattern)
Deficiency of VWF (Type 1 or 3)
VWF with abnormal function (Type 2)

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12
Q

What is the third aspect that a defect in can affect haemostasis?

A

The vessel wall

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13
Q

What causes defects in the vessel wall?

A

Inherited (rare)

Hereditary haemorrhagic telangiectasia

Ehlers-Danlos syndrome

and other connective tissue disorders

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14
Q

What are the clinical features of primary haemostasis bleeding?

A

Immediate
Prolonged bleeding from cuts
Nose bleeds (epistaxis):prolonged > 20 mins
Gum bleeding: prolonged
Heavy menstrual bleeding (menorrhagia)
Bruising (ecchymosis), may be spontaneous/easy
Prolonged bleeding after trauma or surgery

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15
Q

What are petechia and purpura?

A

caused by bleeding under the skin

Purpura do not blanch when pressure is applied

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16
Q

What is a feature (to diagnose) of thrombocytopenia?

A

Petechia

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17
Q

What are tests for disorders of primary haemostasis?

A

Platelet count, platelet morphology

Bleeding time (PFA100 in lab)

Assays of von Willebrand Factor

Clinical observation

Note –coagulation screen (PT, APTT) is normal (except more severe VWD cases where FVIII is low)

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18
Q

What are the treatments if it is failure of production?

A 
Failure of production/function
Replace missing factor/platelets  e.g. VWF containing concentrates
 i) Prophylactic
ii) Therapeutic
Stop drugs e.g. aspirin/NSAIDs
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19
Q

What are treatments for immune destruction? (including ITP)

A

Immune destruction
Immunosuppression (e.g. prednisolone)
Splenectomy for ITP

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20
Q

What are treatments for increased consumption?

A

Treat cause

Replace as necessary

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21
Q

What are some additional haemostatic treatments?

A
  • Desmopressin (DDAVP)
    Vasopressin analogue
    2-5 fold increase in VWF (and FVIII)
    releases endogenous stores (so only useful in mild disorders)
  • Tranexamic acid
    Antifibrinolytic
  • Fibrin glue/spray
  • Other approaches e.g hormonal (oral contraceptive pill for menorrhagia)
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22
Q

What is the role of coagulation?

A

to generate thrombin (IIa), which will convert fibrinogen to fibrin

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23
Q

What would a deficiency in any coagulant factor cause?

A

Deficiency of any coagulation factor results in a failure of thrombin generation and hence fibrin formation

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24
Q

What are hereditary causes of coagulation factor production?

A

Factor VIII/IX: haemophilia A/B

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25
What are acquired causes of disrupted coagulation factor production?
Liver disease Anticoagulant drugs Warfarin Direct Oral Anticoagulants (DOACs)
26
What are acquired causes of dilution causing disorder of coagulation?
Blood transfusion
27
What are acquired causes of increased consumption?
Disseminated intravascular coagulation (DIC) – common | Immune – autoantibodies – rare
28
Wha are the features of inherited coagulation disorders?
``` Haemophilia A (Factor VIII deficiency) Haemophilia B (Factor IX deficiency) sex linked 1 in 104 births Others are very rare (autosomal recessive) ```
29
What should be avoided in patients with haemophilia?
IM injections
30
Why are different coagulation factor deficiencies not all the same?
Factor VIII and IX (Haemophilia) Severe but compatible with life Spontaneous joint and muscle bleeding Prothrombin (Factor II) Lethal Factor XI Bleed after trauma but not spontaneously Factor XII No bleeding at all
31
Why does liver failure cause coagulation disorders?
Most coagulation factors are synthesised in the liver
32
Why does dilution produce coagulation disorders?
Red cell transfusions no longer contain plasma | Major haemorrhage requires transfusion of plasma as well as red cells and platelets
33
What are the features of increased consumption?
Generalised activation of coagulation – Tissue factor Associated with sepsis, major tissue damage, inflammation Consumes and depletes coagulation factors Platelets consumed - thrombocytopenia Activation of fibrinolysis depletes fibrinogen – raised D-dimer (a breakdown product of fibrin) Deposition of fibrin in vessels causes organ failure
34
What are the clinical features of coagulation disoders?
superficial cuts do not bleed (platelets) bruising is common, nosebleeds are rare spontaneous bleeding is deep, into muscles and joints bleeding after trauma may be delayed and is prolonged Bleeding frequently restarts after stopping
35
What are the tests for coagulation disorders?
Screening tests (‘clotting screen’) Prothrombin time (PT) Activated partial thromboplastin time (APTT) Full blood count (platelets) Coagulation factor assays (for Factor VIII etc) Tests for inhibitors
36
What are the different types of factor replacement therapy?
Fresh Frozen Plasma Cryoprecipitate Factor Concentrates Recombinate forms of FVIII and FIX
37
What are the features of FFP?
Contains all Coagulation factors
38
What are the features of cryoprecipitate?
Rich in Fibrinogen, FVIII, VWF, Factor XIII
39
What are the features of factor concentrates?
Concentrates available for all factors except factor V. | Prothrombin complex concentrates (PCCs) Factors II, VII, IX, X
40
Wen are recombinant forms of FVIII and FIX used?
‘On Demand’ to treat bleeds | Prophylaxis to prevent bleeds
41
How to disorders of thrombosis present?
Pulmonary embolism | Deep vein thrombosis
42
What are the features of PE?
``` Tachycardia Hypoxia Shortness of breath Chest pain Haemopysis Sudden death ```
43
What are the features of DVT?
``` Painful leg Swelling Red Warm May embolise to lungs Post thrombotic syndrome ```
44
What type of thrombosis are PE and DVT?
Venouse
45
What is thrombosis?
``` Intravascular coagulation Inappropriate coagulation Venous (or arterial) Obstructs flow May embolise to lungs ```
46
What is Virchow's triad?
``` Three contibutpry factors to thrombosis Blood (dominant in venous) Vessel wall (dominant in arterial) Blood flow (both) ```
47
What is thrombophilia?
Increased risk of thrombosis
48
What is indicative of thrombosis?
Thrombosis at young age ‘spontaneous thrombosis’ Multiple thromboses Thrombosis whilst anti-coagulated
49
What are anticoagulant proteins?
Antithrombin Protein C Protein S
50
What is the role of vessel wall in thrombosis?
We know little about the role of the vessel wall in venous thrombosis. Many proteins active in coagulation are expressed on the surface of endothelial cells and their expression altered in inflammation (TM, EPCR, TF)
51
What are the risk factors for venous thrombosis?
Age Genetic Environmental
52
How to you prevent thrombosis?
Assess and prevent risks | Prophylactic anticoagulant therapy
53
How do you reduce the risk of recurrence?
lower procoagulant factors e.g.: warfarin, DOACs increase anticoagulant activity e.g: heparin
54
When is therapeutic anticoagulation used?
Venous thrombosis Initial treatment to minimise clot extension/embolisation (< 3 months) Long term treatment to reduce risk of recurrence Atrial fibrillation: 800 per 100 000 population potentially eligible in 1 year To reduce risk of embolic stroke Mechanical prosthetic heart valve
55
When is thromboprophylaxis used?
following surgery, during hospital admission, during pregnancy
56
What are the main features of heparin?
Naturally occurring glycosaminoglycan Produced by mast cells of most species Porcine products used in UK Varying numbers of saccharides in chains – differing lengths - Long chains - Unfractionated (UFH) – intravenous administration, short half life - Low molecular weight (LMWH) – subcutaneous administration
57
What are the actions of unfractionated heparin?
Enhancement of Antithrombin Changing the active site of antithrombin Far greater affinity for target proteases (FXa and thrombin) Inactivation of thrombin (Hep binds AT + Thrombin) Inactivation of FXa (Hep binds AT only) (Inactivation of FIXa, FXIa, FXIIa)
58
What is the action of low-molecular weight heparin?
Predominantly against FXa | Shorter chains are not long enough to wrap around thrombin and antithrombin
59
What is the effect of unfractionated heparin on test?
Prolongation of APTT
60
How does Warfarin work?
Competes with Vitamin K – complicated metabolism Many dietary, physiological and drug interactions Narrow therapeutic index and requires monitoring Reduces production of functional coagulation factors Induces an anticoagulated state slowly Reversible
61
How is the action of Warfarin reversed?
Reversed slowly by Vit K administration – takes several hours to work Reversed rapidly by infusion of coagulation factors: PCC (Prothrombin Complex Concentrate- contains Factors II, VII, IX and X) FFP (Fresh Frozen Plasma)
62
What are side effects of Warfarin?
``` Bleeding Minor 5% pa Major 0.9 – 3.0% pa Fatal 0.25% pa Skin Necrosis Purple toe syndrome Embryopathy – Chondrodysplasia punctata ```
63
What are the features of skin necrosis?
Skin Necrosis Severe Protein C deficiency 2-3 days after starting Warfarin Thrombosis predominantly in adipose tissues
64
What are the features of purple toe syndrome?
Disrupted atheromatous plaques bleed | Cholesterol emboli lodge in extremities
65
What is chondrodysplasia punctata?
Early fusion of epiphyses | Warfarin teratogenic in 1st trimester
66
How do you monitor warfarin?
International Sensitivity Index Indicates sensitivity of particular thromboplastin for warfarin Unanticoagulated normal INR = 1.0 Target INR usually 2-3
67
What can cause resistance to warfarin?
Lack of patient compliance Measure warfarin levels Proteins Induced by Vitamin K Absence (PIVKA) Diet, Increased Vit K intake Increased metabolism Cyt P450 (CYP2C9) Reduced binding (VKORC1)
68
What would you give for initial treatment to minimise clot extension (< 3 months)?
DOAC or LMWH for first few days followed by DOAC or warfarin
69
What would you give for long term treatment to reduce risk of recurrence?
DOAC or warfarin
70
What would you give for AF?
DOAC or warfarin
71
What would you give for mechanical prosthetic heart valve?
Warfarin (DOACs not effective and should be avoided)
72
What would you give following surgery?
LMWH or DOAC
73
What would you give during pregnancy?
LMWH (DOACs not safe in pregnancy)
74
How would you tip the balance towards venous thrombosis?
Decreased fibrinolytic factors Decreased anticoagulant factors Increase coagulant factors Increase platelets
75
How would you tip the balance towards
Increased fibrinolytic factors Increased anticoagulant factors Decrease coagulant factors Decrease platelets

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