thrombotic disorders Flashcards

1
Q

what are the 3 elements of haemostasis

A

1y haemostasis

blood coagulation

fibrinolysis

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2
Q

3 parts of 1y haemostasis

A

vasoconstriction - at the site of endothelial insult

platelet adhesion - to exposed sub-endothelial collagen through GP Ia

platelet aggregation - through release of thromboxane and subsequently ADP

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3
Q

what triggers 1y haemostasis

A

tissue damage

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4
Q

2 main parts of coagulation

A

insoluble fibrin formation

fibrin cross linking

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5
Q

what is a thrombus

A

clot that arises in the wrong place

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6
Q

what is thromboembolism

A

movement of clot along a vessel

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7
Q

virchow’s triad

A

stasis

hypercoagulability

vessel damage

–> thrombosis

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8
Q

examples when components of virchow’s triad may be upset

A

stasis - bed rest, travel

hypercoagulability - pregnancy, trauma

vessel damage - atherosclerosis

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9
Q

3 main types of thrombosis

A

arterial
venous
microvascular

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10
Q

what is an arterial clot

A

‘white clot’ - platelets and fibrin

results in ischaemia and infarction

2y to atherosclerosis

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11
Q

examples of arterial thromboembolism

A

coronary thrombosis - MI, unstable angina

cerebrovascular TE - stroke, TIA

peripheral embolism - acute limb ischaemia

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12
Q

risk factors for arterial thrombosis

A
age 
smoking 
sedentary lifestyle
HT
DM
obesity 
hypercholesterolaemia 

FHx

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13
Q

management of arterial thrombosis

A

1y prevention - lifestyle modification, treatment of vascular risk factors

acute presentation - thrombolysis, anti-platelet/anticoagulant drugs

2y prevention - treatment of identified risk factors

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14
Q

what is a venous thrmobus

A

‘red thrombus’ - fibrin and red cells

results in back pressure

principally due to stasis and hypercoagulability

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15
Q

examples of venous thromboembolism

A
limb DVT
PE
visceral venous thrombosis 
intracranial venous thrombosis 
superficial thrombophlebitis - superficial veins
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16
Q

risk factors for venous thrombosis

A
stasis/hypercoagulability: 
increasing age 
pregnancy 
Hormonal therapy - HRT/COCP
tissue trauma 
immobility 
surgery 
obesity 
systemic disease
FHx
17
Q

systemic disease linked to venous thrombosis

A
cancer
myeloproliferative neoplasm (MPNs)
AI disease: 
- IBD
- connective tissue disease e.g. SLE
- antiphospholipid syndrome: arterial and venous thrombosis
18
Q

diagnosis of venous thrombosis

A

pretest probability scoring: Wells score, Geneva score

lab testing if pretest probability low - D dimer

imaging if low pretest probability but +ve D dimer; pts w/ high pretest probability go straight to imaging

19
Q

imaging for venous thrombosis

A

doppler US for upper and lower limb veins

long images and suspected PE: V/Q scan, CT pulmonary angiogram - gold standard for PE

20
Q

why is CT pulmonary angio gold standard for imaging PE

A

gives you detail on the clot pattern as well as whether there is evidence of right heart strain and anatomical detail

21
Q

aims of management for venous thrombosis

A

prevent clot extension

prevent clot embolisation

prevent clot recurrence in long term treatment

22
Q

drug treatment for venous thromboembolism

A

anticoagulants - LMWH, coumarins (warfarin), DOACs (prevent clot extending but don’t break down the clot)

thrombolysis only in selected cases e.g. massive PE (streptokinase, tenecteplase, alteplase)

23
Q

heritable thrombophilia

A

common:
factor V Leiden
prothrombin G20210A

rare:
antithrombin deficiency - highest thrombogenicity
protein C deficiency
protein S deficiency

24
Q

factor V Leiden and pathway

A

in the presence of thrombin, protein C is activated (promoted by thrombomodulin)

activated protein C w/ protein S subsequently inhibits activated factor VIII and V

25
what happens if an individual has factor V Leiden mutation
actions of activated protein C in inhibiting factor V are blocked activated protein C resistance means there is an ongoing drive towards thrombin generation and fibrin clot formation
26
naturally occurring anticoagulants and deficiency
anti-thrombin protein C and S deficiency of either means factor VIIIa and Va aren't inhibited their drive towards thrombin and fibrin generation continues
27
antithrombin deficiency
antithrombin potentiates the formation of complexes between heparin and serine protease and therefore has a direct blocking effect on thrombin if antithrombin is deficient then thrombin generation continues and you get fibrin clot formation
28
clinical utility of heritable thrombophila
majority aren't predictive of recurrent event screening of asymptomatic family members not recommended - wouldn't commence long term anticoagulation anyway unless they develop VTE limited thrombophilia screening restricted to high risk heritable thrombophilia (antithrombin deficiency)
29
what are microvascular thrombus
platelets and/or fibrin results in diffuse ischaemia principally in DIC
30
what is DIC
disseminated intravascular coagulation diffuse systemic coagulation activation; consumption of platelets and clotting factors leeding to bleeding activation of coagulation leading to microvascular thrombosis deposition
31
when does DIC occur and what does it cause
septicaemia, malignancy, eclampsia tissue ischaemia: gangrene, organ failure