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Clinical Pathology > Theme 7 Haematology: Thrombosis > Flashcards

Theme 7 Haematology: Thrombosis Flashcards

1
Q

What is Virchow’s triad?

A
  • stasis
  • vessel wall injury
  • hypercoagubility
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2
Q

What is thrombosis and why does it arise?

A

-abnormal clotting inside a blood vessel

occurs either because:

  • vascular endothelium damage (because blood is too sticky)
  • or because blood flow has been altered
  • this produces stasis which results in hypercoagulability
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3
Q

What is the usual primary abnormality that leads to arterial thrombosis?

A

atherosclerosis

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4
Q

What are the risk factors for arterial thrombosis?

A 
smoking
hypertension
hypercholesterolaemia
diabetes
family history
obesity
physical inactivity
age
male sex
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5
Q

What are thrombi predominantely composed of?

A

fibrin

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6
Q

What is the most common clinical manifestation of venous thrombosis?

A

DVT

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7
Q

what is VTE and what are the long term complications of VTE?

A
  • Venous thromboembolism
  • can develop chronic VTE
  • can develop post thrombotic syndrome (damage to the vein leads to reduction in flow, chronic swelling, chronic pain and leg ulceration
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8
Q

Why is hospital admission a risk factor for VTE?

A
  • because of the underlying condition
  • because of the fact they are immobile when they are in the hospital bed
  • definition includes any VTE within 90 days of discharge
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9
Q

What is NICE guidelines ‘care pathway’ for VTE?

A
  • consistent risk assessment
  • assess VTE risk and assess bleeding risk and balance
  • offer VTE prophylaxis if appropriate but not if there is risk of bleeding
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10
Q

What are the risk factors for VTE?

A
  • active cancer or cancer treatment
  • age > 60
  • critical care admission
  • dehydration
  • personal history of VTE
  • use of hormone replacement therapy
  • use of oestrogen containing contraceptive therapy
  • varicose veins with phlebitis
  • known thrombophilias
  • obesity
  • immobility
  • surgery
  • co morbidities
  • major trauma
  • pregnancy
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11
Q

Why does a heritable thrombophillia leave you at increased risk of VTE?

A

-deficiencies in factors in blood that protect us from having thrombus

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12
Q

Why do we use white stockings to prevent VTE?

A

They exert graduated pressure on the veins up the leg to keep the blood flowing in the right direction when they are immobile

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13
Q

What are the the options for prophylaxis against VTE?

A
  • low dose low molecular weight heparin

- fondaparinux (an alternative to heparin as it comes from pigs lungs or patients could be allergic)

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14
Q

What is rivaroxaban?

A
  • new anticoagulant

- direct inhibitor of FXa

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15
Q

How do heparins work?

A
  • by binding to the natural anti coagulant called antithrombin
  • antithrombin is an inhibitor of thrombin and FIIa and FXa
  • so this prevents blood clots
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16
Q

What is dabigatran?

A
  • new anticoagulant

- direct thrombin inhibitor

17
Q

How do we assess the clinical probability of VTE?

A

Wells score

18
Q

How can D-dimer levels diagnose VTE?

A

D dimers are break down products of fibrin which is with what that clots are made
so D dimers would be high in a patient with VTE

19
Q

How is the dose of LMWH decided for treatment of VTE?

A
  • doses are fixed by body weight

- usually once daily by s/c injection

20
Q

Explain the treatment pathway of an uncomplicated patient with DVT or PE

A
  1. treat with single dose LMWH
  2. Confirm diagnosis
  3. LMWH for 5 days
  4. Start warfarin
  5. Overlap warfarin and heparin until two consecutive therapeutic INR results
21
Q

what is a thrombophillia?

A

familial or acquired disorders of the haemostatic mechanism which are likely to pre dispose to thrombosis

22
Q

What are some examples of heritable thrombophilias?

A
  • antithrombin deficiency
  • protein C deficiency
  • protein S deficiciency
  • activated protein C resistance/ FV Leiden
  • dysfibrinogenaemia –> fibrin is not working properly
  • prothrombin 20210A
23
Q

What is anti phospholipid syndrome?

A
  • acquired thrombophilia
  • autoimmune disorder where patients develop autoantibodies against negatively charged phospholipids
  • this tips the balance towards the pro coagulant state
24
Q

What are the clinical features of thrombophilia?

A
  • DVT
  • PE
  • superficial thrombophlebitis –> thrombus forms in superficial veins often associated with inflammation
  • thrombosis of cerebral, axillary, portal, mesenteric veins
  • arterial thrombosis
  • obstetric complications
25
Q

What is the role of protein C and protein S?

A
  • Protein C is a natural anticoagulant that cleaves and breaks down activated factor V and VIII  factor V is a co factor in the common pathway and factor VIII is a cofactor in the intrinsic pathway
  • Protein S is a co factor for protein C
  • Protein C can also bind to thrombin so it can no longer act
26
Q

What is Factor V leiden?

A
  • a point mutation in the FV that codes for the pro-coagulation protein
  • at the point where protein C cleaves FV
  • so FV stays for longer as it cannot be activated by protein C
  • increases your chance of thrombosis
27
Q

What is the most common familial thrombophilia?

A

factor V leiden

28
Q

What is prothrombin 20210A?

A
  • point mutation in 3’ untranslated region of prothrombin gene
  • associated with increased prothrombin levels
  • 3 fold increase in venous thrombosis
29
Q

Thrombophilia screening:

  1. Who?
  2. When?
  3. Which tests?
A
  1. Who: Not indicated in unselected patients with VTE, younger patients, positive family history, if management will change
  2. When: Avoid confounding factors e.g acute VTE, on anticoagulants. Pregnancy and OCP also affect results
    - do not test unselected patients
    - do not test asymptoatic relatives
  3. Which tests: For selected patients with arterial events for recurrent miscarriage: antiphospholipid antibody screen only

Clinical Pathology (57 decks)

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