Thrombosis + RF Flashcards

1
Q

what is an arterial thrombosis, causes, RF’s and treatment

A

atherosclerosis of the vessel wall - - rupture of the plaque then platelet clog

smoking, hypertension, age, diabetes

platelet aggregation and platelet thrombi = vessel occlusion 
antiplatelet drugs such as aspirin
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2
Q

what is the pathogenesis of venous thrombosis

A

venous stasis

hypercoaguable states

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3
Q

what are thrombi clots made from

A

fibrin clots with a lesser role for platelet accumulation and aggregation

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4
Q

what is the treatment of venous thrombosis

A

anti-coagulation drugs

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5
Q

what is the most common venous thrombus

A

DVT

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6
Q

which type of DVT can cause sudden death

A

venous thromboembolism

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7
Q

what are the risk factors of DVT or PE

A

active cancer, dehydration, surgery, major trauma

obesity

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8
Q

what are the causes of VTE

A

balance is tipped in the blood between pro-coagulant and anti-coagulant
Virchow triad - stasis, vessel wall injury, hyper coagulability

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9
Q

what are examples of anticoagulant proteins

A

protein C, S, antithrombin 3, fibrinolytic system

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10
Q

what is the treatment for VTE

A

injection of LMW heparin or compression stockings - keeps pressure gradient in legs
anti Xa and antithrombin IIa

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11
Q

which drugs is used in VTE which affects Xa but not thrombin and vice vera

A

fondaparinux = Xa inhibitor

dabigatran = IIa (thrombin) inhibitor

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12
Q

what are the three methods of diagnosis of VTE

A

exclusive tests - through clinical assessment
wells score / D dimer test
ultrasound scanning - CT or VQ scan

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13
Q

what does the wells score and D dimer test measure for

A

low wells score means low chance VTE

elevated d dimer = active coagulation process and fibrinolytic system, has broken down

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14
Q

what does a VQ scan do

A

measure of ventilation perfusion mismatch

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15
Q

what is the management of first time VTE

A

warfarin

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16
Q

what is thrombophilia

A

familial or acquired disorder of haematological homeostasis likely to predispose thrombosis

imbalance weighted towards clotting

17
Q

what are some examples of heritable types of thrombophilia

A

antithrombin deficiency
protein c/s deficiency (loss of natural anticoagulant)
dysfibrinoganaemia - dysfunctional fibrinogen molecule

18
Q

what is an examples of acquired thrombophilia

A

antiphospholipid syndorme

19
Q

what does antithrombin work against

A

factor Xa and thrombin

20
Q

how does protein C affect thrombin

A

thrombin binds to thrombomodulin which activates protein C - this inhibits F Va and VIIIa

21
Q

what is the function of protein S

A

cofactor for the effects of activated protein C

22
Q

what do protein C / S require before activation

A

require Vit K for synthesis in the liver

23
Q

what is the most common acquired polymorphism producing anticoagulant deficiency

A

factor V leiden

24
Q

what is factor V leiden polymorphism and mechanism

A

most common familial thrombophilia
F V leiden is resistant to protein C and can’t be broken down = greater risk of VTE
single point mutation of G to A

25
Q

what does a mutation in prothrombin 20210A result in

A

increased prothrombin levels which causes 3x risk of VTE

26
Q

what is antiphopholipid syndrome

A

most common acquired thrombophilia

antiphospholipid antibodies with increased risk of thrombosis and recurrent foetal loss

27
Q

what disease has lupus anticoagulant

A

antiphospholipid syndrome

28
Q

what is heparin and the difference in subtype use

A

IV anticoagulant - activates antithrombin and inactivates FXa and FIIa (thrombin)

unfractional heparin (UFH) - natural form

LMWH - less adverse affects and longer half life

29
Q

how do you monitor effects of UFH vs LMWH

A

UFH - APTT

LMWH - FXa assay

30
Q

what is the risk of using heparin as treatment

A

heparin induced thrombocytopenia - use protamine sulphate to resolve