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Module 103: The Heart, Lungs and Blood > Theme 2: Lecture 7 - Thrombotic disorders > Flashcards

Theme 2: Lecture 7 - Thrombotic disorders Flashcards

1
Q

DVT

A

Deep vein thrombrosis

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2
Q

Describe how DVT happens

A
  • Due to activation of the clotting cascade in the veins when blood flow slows down
  • This will cause swelling of the leg
  • An embolus could break off and and travel to the lungs - life threatening
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3
Q

3 risk factors of Virchow’s triad

A
  • Circulatory stasis
  • Endothelial injury
  • Hypercoagulable state
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4
Q

Thrombotic risk factors

A
  • Post-operative, especially orthopaedic
  • Hospitalisation
  • Cancer
  • Pregnancy
  • Oral contraceptive pill
  • Long-haul flights
  • Obesity
  • i.v. drug abuse
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5
Q

Presentation of DVT

A
  • Can be no symptoms at all – clinically silent

- Unilateral calf swelling/ heat/ pain/ redness/ hardness

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6
Q

Differential diagnosis of DVT

A
  • cellulitis
  • Baker’s cyst
  • muscular pain
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7
Q

Cellulitis

A

a common, potentially serious bacterial skin infection

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8
Q

Baker’s cyst

A
  • A Baker’s cyst can form when joint-lubricating fluid fills a cushioning pouch (bursa) at the back of your knee.
  • A Baker’s cyst is a fluid-filled cyst that causes a bulge and a feeling of tightness behind your knee
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9
Q

How is DVT diagnosed

A

Doppler ultrasound

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10
Q

What is the likelihood of of having a DVT assessed by

A
  • D-dimer test

- Wells risk score

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11
Q

What do D-dimers indicate

A

activation of the clotting cascade

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12
Q

Negative predictive value

A
  • Represents the probability that a person does not have a disease or condition, given a negative test result.
  • NPV represents the proportion of individuals with negative test results who are correctly identified or diagnosed
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13
Q

What does a low wells score and a negative D-dimer test mean

A

There is a high negative predictive value for DVT, more than 99%

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14
Q

Initial treatment for above the knee DVT

A
  • Therapeutic anti-coagulation using sub-cut LMW heparin (such as tinzaparin or enoxaparin)
  • Dose of LMW heparin according to patient’s weight
  • LMW heparin used as a bridge before patient can be treated with warfarin
  • No monitoring required (but can use anti-Xa assay)
  • Ensure adequate EGFR > 30ml/min
  • Otherwise use iv unfractionated heparin (APTR 2.0)
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15
Q

Name 3 LMW heparin drugs

A
  • Tinzaparin
  • Enoxaparin
  • Dalteparin
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16
Q

EGFR

A

estimated glomerular filtration rate

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17
Q

What is an adequate EGFR

A

> 30mL/min

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18
Q

When is LMW heparin stopped for treating DVT

A

once the INR > 2.0 for 2 days

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19
Q

How long is the patient treated with anticoagulation after their first DVT

A

6 months

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20
Q

How long is the patient treated with anticoagulation after their 2nd DVT/PE

A

lifelong

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21
Q

How often is the INR monitored on treatment with anticoagulants

A

every 3 weeks

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22
Q

What should the INR be

A

between 2.0-3.0 (target of 2.5)

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23
Q

What drug is the patient switched to after the initial treatment with LMW heparin for DVT

A

oral warfarin

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24
Q

Clinical presentation of a micro emboli

A

asymptomatic

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25
Q

Classic symptoms of PE

A
  • pleuritic pain
  • dyspnoea
  • haemoptysis
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26
Q

haemoptysis

A

coughing up blood

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27
Q

What can a massive PE cause

A
  • syncope

- death

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28
Q

What is seen on examination of a patient with PE

A
  • tachycardia
  • tachypnoea
  • hypotension
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29
Q

Saddle embolus

A
  • A blockage of in one of the arteries of the lungs
  • An embolus that’s come from a deep vein in the leg, travelled to the lungs and impacted at the bifurcation of the pulmonary arteries
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30
Q

What are the investigations of a PE

A
  • CT pulmonary angiogram
  • V/Q scan
  • ECG
  • CXR
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31
Q

What is seen in a V/Q scan for PE

A
  • ventilation/perfusion radio-isotope scan
  • Underperfusion ~ V/Q mismatch
  • Limitation: underlying lung disease
  • rarely done
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32
Q

What is seen in a CXR for PE

A
  • Usually normal
  • Linear atelectasis
  • Small effusions
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33
Q

atelectasis

A

collapse or closure of a lung resulting in reduced or absent gas exchange

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34
Q

What is seen in an ECG for PE

A
  • Sinus tachycardia
  • Atrial fibrillation
  • Right heart strain (RBBB)
  • Classic ECG trace SI, QIII, TIII (rare)
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35
Q

Alteplase

A

A tissue plasminogen activator

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36
Q

Treatment of massive PE

A
  • A tissue plasminogen activator e.g. alteplase

- iv unfractionated heparin

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37
Q

tissue plasminogen activator (tPA)

A
  • involved in the breakdown of blood clots

- catalyses conversion of plasminogen to plasmin

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38
Q

Treatment of standard PE

A
  • LMW heparin injections – e.g. tinzaparin
  • Warfarin (target INR 2.5) for 6 months
  • Consider underlying causes
  • LMW heparin is better if underlying cancer
  • IVC filters (inferior vena cava filter)
  • Consider a DOAC as an alternative
39
Q

inferior vena cava filter

A

small metal device that traps large clot fragments and prevents them from traveling through the vena cava vein to the heart and lungs

40
Q

Thrombophilia

A

clinical states in which you are prone to clot

41
Q

When is a thrombophilia screen considered

A

in young patients with spontaneous venous thromboembolisms

42
Q

Inherited causes of thrombophilia

A
  • Factor V Leiden (5% of people)

- Deficiency of natural anticoagulants: Anti-thrombin deficiency, Protein C deficiency, Protein S deficiency

43
Q

Acquired causes of thrombophilia

A

-Anti-phospholipid syndrome

44
Q

anti-phospholipid syndrom

A
  • Acquired cause of thrombophilia

- Auto immune disorder in which the bodies own antibodies attack your own phospholipids

45
Q

What is used to test for anti-phospholipid syndrome

A
  • Test for lupus anticoagulant using the dilute Russell viper venom time test (DRVVT)
  • Anticardiolipin antibodies
46
Q

Name 7 anti-thrombotic drugs/types of anti-thrombotic drugs

A
  • Warfarin
  • Heparin (unfractionated and LMW)
  • direct oral thrombin (factor IIa) inhibitor
  • direct oral factor Xa inhibitors
  • Anti-platelet drugs
  • fibrinolytic agents (thrombolytics)
47
Q

What does warfarin do

A
  • Vitamin K antagonist
  • Prevents γ-carboxylation of factors II, VII, IX, X -(Required for functional maturation of these factors)
  • Prolongs the extrinsic pathway (prothrombin time)
  • Also inhibits natural anticoagulants Protein C and S
48
Q

What is warfarin monitored by

A
  • international normalised ratio (INR)
  • Target INR usually 2.5 for DVT/PE and AF
  • Target 3.5 for recurrent VTE or metal heart valves
49
Q

Why can warfarin take 3 days to achieve therapeutic levels

A

half life of prothrombin (factor II) is 60 hours

50
Q

Warfarin interactions

A
  • Beware drug interactions due to cytochrome P450
  • Beware interaction with alcohol
  • Binding to albumin
  • Absorption of vitamin K from GI tract
  • Synthesis of vitamin K factor by liver
  • Hereditary resistance
51
Q

What do enzyme inhibitors of cytochrome P450 do in relation to warfarin

A

potentiate warfarin

52
Q

What do enzyme inducers of cytochrome P450 do in relation to warfarin

A

inhibit warfarin

53
Q

What does binge drinking do in relation to warfarin

A

potentiate warfarin

54
Q

What does chronic alcoholism do in relation to warfarin

A

inhibit warfarin

55
Q

Side effects of warfarin

A

-Teratogenic – therefore use LMW heparin in pregnancy
-Significant haemorrhage risk:
intra-cranial bleeds up to 1% per year
increased risk in elderly and with higher INR target
-Minor bleeding up to 20% per year
-Skin necrosis
-Alopecia

56
Q

Teratogenic

A

substances that may cause birth defects via a toxic effect on an embryo or foetus

57
Q

Alopecia

A

hair loss

58
Q

What do you give to reverse the effects of warfarin in a life threatening bleed

A
  • give activated prothrombin complex (e.g., Octaplex or Beriplex) which contains vitamin K dependent factors II, VII, IX and X
  • Dose is 25-50 units per kg depending on INR level
59
Q

examples of activated prothrombin complex

A
  • Octaplex

- Beriplex

60
Q

What else is given to reverse the effects of warfarin if it isn’t a life threatening bleed

A
  • vitamin K

- fresh frozen plasma (contains all your clotting factors)

61
Q

What dose of vitamin K is given to reverse the effect of warfarin

A

2-10mg through iv/op depending on INR level (patient can become resistant to re-loading with warfarin)

62
Q

anti thrombin

A

small protein molecule that inactivates several enzymes of the coagulation system

63
Q

What is heparin

A
  • Mucopolysaccharide that works by potentiating anti-thrombin
  • Irreversibly inactivates factor IIa (thrombin) and factor Xa
64
Q

Is heparin safe in pregnancy

A

yes

65
Q

What are the two formulations of heparin

A
  • Unfractionated heparin

- Low molecular weight heparin

66
Q

How is unfractionated heparin administered

A
  • iv infusion
  • Not often used due to inconvenience of administration
  • Given i.v. with 5000U bolus and ~1000U/hour infusion
67
Q

How is LMW heparin administered

A
  • s.c injections

- very convenient

68
Q

How is dose of unfractionated heparin monitored

A

APTT ratio (APTR) with target of 2.0 x normal

69
Q

Why is unfractionated heparin safe in renal failure

A

unfractionated heparin is metabolised by the liver and not renally excreted

70
Q

What is used to partially reverse heparin if bleeding

A

protamine sulfate

71
Q

What is a rare complication from giving unfractionated heparin

A

heparin induced thrombocytopenia (HIT)

72
Q

heparin induced thrombocytopenia (HIT)

A
  • Suspect if platelet count falls on heparin
  • This is paradoxically a prothrombotic condition that can cause VTE
  • Diagnosis by doing a HIT screen and discontinuation of heparin
73
Q

What must the patient have to be able to have LMW heparin administered

A

creatinine clearance of over 30mL/min as LMW is excreted by the kidneys

74
Q

Benefits of DOACs

A
  • No monitoring
  • Flat dosing
  • Good safety profile
75
Q

What are the two classes of DOACs

A
  • direct thrombin (IIa) inhibitor

- direct factor Xa inhibitor

76
Q

When should DOACs not be used as a an alternative to warfarin

A

for cardiac valves

77
Q

Rivaroxaban

A
  • A DOAC
  • Direct factor Xa inhibitor
  • Causes irreversible anti-coagulation
78
Q

Indications for using rivaroxaban

A
  • VTE prophylaxis
  • Used for treatment of DVTs and PEs
  • Stroke prevention in atrial fibrillation
79
Q

What is an alternate anti-Xa drug to rivaroxaban

A

Apixaban (less affected by renal function)

80
Q

Dabigatran

A
  • A DOAC

- Direct thrombin (IIa) inhibitor

81
Q

Indications for using dabigatran

A
  • VTE prophylaxis
  • Used for treatment of DVTs and PEs
  • Stroke prevention in atrial fibrillation
82
Q

What can dabigatran be reversed by

A

Praxbind

83
Q

Dosing for dabigatran

A
  • Treatment dose is 150mg bd (bi daily)
  • Prophylactic dose is 110mg bd
  • Confirm creatinine clearance > 30ml/min
84
Q

Dosing for rivaroxaban

A

Dosing is 15mg bd for 3 weeks, then 20mg od (15mg od if CrCl is 15-50ml/min)

CrCl = Creatine clearance

85
Q

Name 5 anti-platelet drugs

A
  • Aspirin
  • Clopidogrel
  • Dipyridamole
  • Prostacyclin
  • Gloycoprotein IIb/IIIa inhibitors
86
Q

Aspirin

A
  • An anti-platelet drug

- cyclo-oxygenase inhibitor

87
Q

Clopidogrel

A
  • An anti-platelet drug

- ADP receptor blocker

88
Q

Dipyridamole

A
  • An anti-platelet drug

- inhibits phosphodiesterase

89
Q

Prostacyclin

A
  • An anti-platelet drug

- Stimulates adenylate cyclase

90
Q

Glycoprotein IIb/IIIa inhibitors

A
  • An anti-platelet drug

- used in angioplasty procedures

91
Q

What do fibrinolytic agents do

A

lyse fresh thrombi (usually arterial) by converting plasminogen to plasmin

92
Q

Name 3 fibrinolytic agents

A
  • Tissue plasminogen activator (e.g Alteplase)
  • Streptokinase
  • Urokinase
93
Q

When are fibrinolytic agents administered

A

Administered systemically in:

  • acute MI
  • recent thrombotic stroke
  • major PE
  • massive iliofemoral thrombosis

Module 103: The Heart, Lungs and Blood (51 decks)

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