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MELS302 > Anticoagulation > Flashcards

Anticoagulation Flashcards

1
Q

Where is tissue factor pathway inhibitor synthesised and what activates it

A

Endothelial cells
Activated by X

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2
Q

What does tissue factor pathway inhibitor inhibit

A

TF-VII complex and factor X

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3
Q

What activates the protein C pathway

A

Thrombin binding to membrane protein thrombomodulin in normal vessels (low grade thrombin always being made)

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4
Q

How does activated protein C affect fibrinolysis

A

It enhances fibrinolysis by inhibiting tissue plasminogen activator inhibitor

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5
Q

How does protein C inhibit coagulation

A

Protein C binds to its cofactor protein S and inhibits factor 5 and 8

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6
Q

What factors does the protein C pathway inhibit

A

Factor V and VIII

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7
Q

What does antithrombin inhibit

A

Thrombin
Factors 9, 10, 11
(12, kallikrein, plasmin)

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8
Q

Half life of antithrombin

A

2-3 days

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9
Q

What does antithrombin need to work

A

Heparin
Antithrombin and thrombin/factors have binding sites that fit each other but heparin is needed to facilitate binding

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10
Q

When does fibrinolysis start

A

A few hours after fibrin cross linking

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11
Q

Fibrinolysis components

A

Plasminogen
Tissue plasminogen activator
Plasminogen activator inhibitor 1

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12
Q

What does plasmin do

A

Digests fibrinogen, fibrin, factor 5/8

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13
Q

What does tissue plasminogen activator do

A

Hydrolyses plasminogen to plasmin (bound/free)

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14
Q

Where is urokinase made

A

Urinary tract epithelial cells
Monocytes and macrophages

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15
Q

What does urokinase do

A

A minor plasminogen activator

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16
Q

When are D dimers found

A

Inflammation
Malignancy
Older age
Recent surgery
Trauma
Childbirth

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17
Q

What is the high negative predictive value for D dimers and DVT

A

D dimers will increase in many conditions along with DVT - would be very high if DVT is present along with other factors
A negative D dimmer result means it definitely can’t be DVT

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18
Q

Virchows triad for thrombophilia

A

Endothelial injury
Abnormal blood flow
Hypercoagulability

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19
Q

Consequences of thrombosis

A

Ischaemia
Embolisation

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20
Q

Arterial thrombosis most common cause

A

Rupture of an atherosclerotic plaque

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21
Q

General risk factors for arterial thrombosis

A

Diabetes
High BP/cholesterol
Older age
Male
High CRO
Smoking

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22
Q

Haemostatic risk factors for arterial thrombosis

A

Heparin induced thrombocytopenia
Antiphospholipid antibodies

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23
Q

Consequences of a DVT

A

Pulmonary embolus
Varicose veins
Post thrombotic syndrome

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24
Q

Inherited risk factors for DVT/venous thrombosis

A

Antithrombin deficiency
Protein S/C deficiency
Factor V Leiden
Prothrombin mutation

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25
Q

Acquired risk factors for DVT

A

Tissue injury
Immobilisation
Antiphospholid antibodies
Malignancy
Pregnancy
Obesity
HIT
AGE

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26
Q

What is factor V Ledien

A

An inherited thrombophilia (risk factor for DVT)
Mutated factor V resists cleavage by APC to stop coagulation so it just keeps going

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27
Q

Tests for Factor V Leiden

A

APC resistance assay is a screening test to test ability of PrC to prolong APTT from factors 5 and 8 activation
Confirm with genetic testing

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28
Q

Prothrombin G20210A

A

Increased prothrombin levels due to mutation in promoter region
Need genetic testing

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29
Q

How more likely are you to get DVT with Factor V Leiden

A

Hetero - 3x
Homo - 18x

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30
Q

How is antithrombin deficiency acquired

A

Liver disease (less is made)
Consumption from DIC, sepsis, nephrotic syndrome, malignancy, chemo drugs, transfusion reaction, sepsis

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31
Q

When does inherited antithrombin deficiency appear

A

Less than 40 years old

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32
Q

Two types of antithrombin deficiency

A

Type 1: quantitative
Type 2: qualitative so decreased function

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33
Q

Antithrombin functional assay (kinda like an enzyme assay) explain the substrate equation

A

Patient AT sample with thrombin and heparin (to speed it up) to make AT-thrombin complex with residual thrombin

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34
Q

Antithrombin deficiency indicator equation

A

Substrate with residual thrombin from first step
These products are measured for change in absorbance

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35
Q

Explain the proportional stuff in antithrombin deficiency assay

A

Change in absorbance is proportional to residual thrombin which is inversely proportional to antithrombin amounts

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36
Q

What factors increase in pregnancy to make it a hypercoagulable state

A

vWF
Fibrinogen
Factors 5,8,9,10,12
Plasminogen/Dimer

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37
Q

What decreases in pregnancy

A

Factor 11 and protein S (less anticoagulation)

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38
Q

What are many miscarriages (15-60%) the result of

A

Thrombophilia

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39
Q

What happens to APTT and PT in pregnancy

A

Hypercoagulable so shorter times

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40
Q

Pregnancy leads to a greater increase in what

A

DIC
thromboembolism
VTE risk is 100x greater in labour

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41
Q

Type 1 HIT

A

Benign
Recover in couple days
Mild thrombocytopenia (100-150)

42
Q

Type 2 HIT

A

Heparin induced antibody forms after 7-14 days
Rapid fall in platelets below 100 over 2-5 days

43
Q

Who gets TYPE 2 HIT

A

Those being treated with UFH

44
Q

Complications of type 2 HIT

A

MI
Stroke
VTE

45
Q

Test for Type 2 HIT

A

Platelet aggregation induced by heparin in vivo

46
Q

What must all patients on heparin be monitored for

A

Thrombocytopenia

47
Q

What are the antiphospholipid antibodies

A

Antibodies that bind to protein-phospholipid complexes

48
Q

What is antiphospholipid antibodies associated with

A

Lupus anticoagulant
ACL
APS (antiphospholipid syndrome)
Venous/arterial thrombosis
Recurrent miscarriage

49
Q

Alloimmune antibodies (antiphospholipid)

A

From infections or drugs
Disappears in less than 12 weeks
Could cause a prolonged APTT not correcting

50
Q

Autoimmune antiphospholipid antibodies

A

Primary - idiopathic
Secondary to other autoimmune disease like lupus

51
Q

How do antiphospholipid antibodies cause clotting too much

A
  1. Antibodies interact with ECs promoting coagulation and inflammation
  2. TF expression increases on ECs and monocytes which promotes WBC activation
  3. Antibodies bind to platelet binding proteins on platelets which promotes platelet aggregation
  4. Antibodies interfere with coagulation factors inhibiting anti coagulation and fibrinolysis
52
Q

Tests for thrombotic risk

A

FBC (increase viscosity, marked thrombocytosis)
Protein S/C functional assay of activity
Antithrombin functional assays
HIT SCREEN

53
Q

What is a lupus anticoagulant

A

An anticoagulant in vitro but prothrombotic in vivo
It blocks thromboplastin in tests leading to high APTT/PT that don’t correct

54
Q

What is needed after a prolonged APTT/TCT in lupus anticoagulant when it doesn’t correct

A

Phospholipid sensitive functional clotting tests where excess phospholipids will correct the prolonged results - this is phospholipid neutralisation

55
Q

Where does Russell’s viper venom time act

A

On factor 10

56
Q

How to test for anticardiolipin antibodies

A

Immunoassays detect antibodies against cardiolipin and beta 2 glycoprotein 1
Ab titre = how much at risk for thrombosis

57
Q

What is cardiolipin and beta 2 glycoprotein 1

A

Cardiolipin is a component of the inner mitochondrial membrane
B2G1 is an app lipoprotein that binds cardiolipin

58
Q

Lab testing for inherited thrombophilia - how common is it

A

Not common as results don’t influence patient management

59
Q

When is lab testing for inherited thrombophilia done

A

People younger than 40 presenting with unprovoked thrombosis and a family history of thrombosis

Children with purpura fulminans (protein C/S deficiency likely)

Pregnant women with previous VTE due to minor provoking factor or relative with one

60
Q

What does unfractioned heparin do

A

Reduces risk of venous and arterial thromboembolism
Prevents thrombi forming/extending

61
Q

When is UFH given in high doses

A

Cardiac bypass surgery
Haemodialysis

62
Q

Unfractioned heparin dosage

A

IV = high dose
Subcutaneous injection = low dose

63
Q

How is unfractionated heparin inactivated/excreted

A

Inactivated by the liver
Excreted in urine
Half life of 1hr via IV and 2hr via SC

64
Q

Is heparin and warfarin used together

A

Yes heparin is needed while starting warfarin after a DVT/PE as it can induce a prothrombiotic state

65
Q

What is the therapeutic target for VTE using UFH

A

APTT should be 1.5-2.5x the baseline or ULM

66
Q

What affects UFH efficacy

A

People have different anti thrombin levels
Liver and renal issues
Brands

67
Q

What does UFH make a complex with

A

Anti thrombin
Thrombin
Factor X (9 and 11 lesser)

68
Q

Complications of UFH therapy

A

Haemorrhage
Osteoporosis
HIT

69
Q

Who is most likely to get haemorrhage using UFH

A

IV dose
Already have weird coagulation/thrombocytopenia
GI lesions or cerebral bleeding risk

70
Q

What to do if haemorrhage happens on UFH

A

Stop heparin and give protamine sulphate
This is strongly basic and binds and inactivates heparin

71
Q

Why is low molecular weight heparin better

A

Reduced bleeding risk
Less anti platelet effect/anti IIa effect
Reduced HIT
No monitoring required unless renal failure then do anti X assay o

Platelet check once a month

72
Q

LMWH vs UFH method

A

LMWH is smaller so cannot be complexes with as many factors (only works on antithrombin and factor X)
UFH works on thrombin, AT, factor X and 9/11 so more aggressive

73
Q

What does warfarin do

A

Blocks vitamin K epoxide reductase (VKOR) inhibiting electron transport
So factors 2,5,7,9 are made but can’t bind to platelet phospholipids so can’t function in coagulation

74
Q

Therapeutic range for warfarin

A

Very narrow

75
Q

How is warfarin given

A

Orally, absorbed in the GI tract
Mostly bound to protein

76
Q

Half life of warfarin

A

20-60hrs
Given once a day

77
Q

What effects warfarin metabolism

A

Other drugs being metabolised by the liver as it can displace warfarin from albumin increasing its effects
Diet
Liver function

78
Q

Protein C affected by warfarin

A

Protein C has the shortest half life so it falls quickly first leading to an intial procoagulant state
Leads to risk of thrombosis and warfarin induced skin necrosis in the first few days so need to give heparin with it

79
Q

How to monitor warfarin

A

Using INR
PT is strongly influenced by thromboplasin nature

80
Q

What does PT detect the reduced activity of

A

Thrombin, factor 7 and 10

81
Q

What does ISI stand for

A

international sensitivity index
On commercial products standardised against an IRP

82
Q

What is an INR

A

International normalised ratio

83
Q

INR calculation

A

(PT time of patient/PT time of mean) ^ ISI

84
Q

Target INR for warfarin treatment of DVT/PE/Afib/APS

A

2.0-3.0

85
Q

Target INR for warfarin on arterial grafts/prosthetic valves and some APS

A

2.5 -3.5

86
Q

How long are people on warfarin

A

3-6 months
Longer for prophylaxis

87
Q

What happens when INR>4

A

Bleeding risk increases
Stop warfarin and give IV vitamin K
Replace coagulation factors with prothrombinex and FFP

88
Q

Can you take warfarin if pregnant

A

No
Fetal malformations if used in the first trimester
Use heparin instead

89
Q

How does dabigatran work

A

Direct thrombin inhibitor
Taken orally

90
Q

What should be monitored with dabigatran

A

Renal functional
As not metabolised by the liver and kidney excretes it all
Creatinine should be above 30

91
Q

Contradicted dabigatran for who

A

Patients older than 75 yrs or with renal impairment

92
Q

Half life of dabigatran

A

13 hrs but longer with renal impairment

93
Q

When is dabigatran used

A

Prophylaxis for VT post stroke/embolism
Prophylaxis and treatment for DVT and PE

94
Q

Dabigatran lab test

A

Prolonged APTT/PT
Very high TCT not corrected
ECT, hemoclot thrombin inhibitor assay

95
Q

Antidote for dabigatran

A

Idarucizumab

96
Q

When is praxabind used

A

Emergency surgery, uncontrolled bleeding life threatening

97
Q

How does praxabind work

A

It is a monoclonal antibody fragment which directly inhibits the drug

98
Q

How is fibrinolytic therapy given - local admin

A

Injected into the occluded coronary artery
Reduced bleeding risk

99
Q

List 3 fibrinolytic agents

A

Urokinase
Streptokinase
Tissue plasminogen activator

100
Q

What does tissue plasminogen activator do

A

Recombinant DNA product which converts plasminogen to plasma.
Used to minimise MI size

101
Q

What does streptokinase do

A

Forms a complex with plasminogen and converts it to plasmin
This is a bacterial product so can’t use often

102
Q

What does urokinase do

A

A plasminogen activator

MELS302 (6 decks)

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