Thrombosis Flashcards
Thrombosis
Formation of a solid mass of blood within the circulatory system
That solid mass is called a thrombus
Virchow’s triad
How a thrombus forms
Occurs when there is an abnormality in Vessel Wall, Blood flow, and blood components
Abnormality in the vessel wall - damage
Can be caused by -
Atheroma formation
Direct injury - could have come about through trauma - or by toxins causing that injury e.g. oxidative stress from toxins from cigs
Inflammation - e.g. vasculitis can lead to endothelial damage
Abnormality with blood flow
Problem that can occur is stasis (slowing of blood)
Occurs in veins more than arteries as flow is quicker in arteries so more likely to happen in slow movement
Veins also have valves which can also cause turbulent flow in its own right - due to occlusion of the vein at the valve points - so when closed gravity causes an element of back flow, which may contribute to turbulent flow formation
Abnormalities with blood components
Hyper coagulative states (sticky blood):
E.g. in smokers, pregnancy, post op patients, cancer patients and in trauma/burn patients
Arterial vs venous thrombosis
Arterial Thrombus:
These look pale and granular
- due to the lines of Zhan -
in high flow areas you get pattens/lines of RBC and platelets+fibrin
Venous thrombus:
These are soft, gelatinous, a deep red colour and have a higher cell content
Thrombosis and Fibrinolysis
Thrombosis -
Have both an intrinsic and extrinsic fibritic system present to form a clot
Intrinsic system involves activation of factors 2,8,9,11
Extrinsic system involves activation of factors 5, 7 10
These both activate Factor 10 / X which activates Factor Xa
Factor Xa converts Prothrombin to thrombin
Which converts Fibrinogen to fibrin which contributes to the platelet plug
Fibrinolysis -
tPA (tissue plasminogen activator) activates plasminogen
Plasminogen is converted to plasmin which breaks down the clot and fibrin
The fibrin degradation produces some products e.g. D dimers can be detected in blood tests, which are broken down by macrophages and neutrophils
Outcomes / complications of thrombus forming
Lysis - Most likely to occur when thrombi are small
Complete dissolution of thrombus occurs
Fibrinolytic system is active
Blood flow is re-established - most positive outcome
Propagation - Progressive spread of thrombosis
Distally in arteries - goes towards peripheries
Proximally in veins - comes back towards heart and lungs
Organisation - Reparative process
Ingrowth of fibroblasts and capillaries (similar to granulation tissue)
Lumen remains obstructed
Recanalisation - Blood flow re-established but usually incompletely due to still present occulsion of the blood vessel
One or more channels formed through organising thrombus
Embolism - Part of thrombus breaks off
Travels through the bloodstream
Can lodge at a distant site e.g. lungs or peripheral arteries
Effect of thrombosis on a tissue
Venous thrombosis e.g. in deep vein thrombosis
congestion
oedema
ischaemia (limited blood supply)
infarction (no blood supply) (depends on the size of the thrombus)
Can occur in the leg, arm , pelvis, brain etc…
Arterial thrombosis -
ischaemia
infarction
depends on the site (coronary embolus could lead to heart failure) and collateral circulation (end tissue doesn’t have any collateral circulation)
Embolism
Embolism is the blockage of a blood vessel by solid, liquid or gase at a site distant from its origin
>90% of emboli are thrombo-emboli
Thromboembolism – Arteries and Veins - Passes from the systemic veins pass to the lungs = pulmonary thromboemboli.
Pass from the heart pass via the aorta and lodge in the renal, mesenteric, and other arteries, resulting in bowel ischaemia, renal infarction etc.
Pass from atheromatous carotid artery to the brain leading to ischaemic stroke.
Pass from atheromatous abdominal aorta to the arteries of the legs leading to acute limb ischaemia
Predisposing factors fir a Deep vein thrombosis
If the patient has had a spell of Immobility/bed rest
Or in Post-operative care
Pregnancy and post-partum - as well as using Oral contraceptives
Severe burns
Cardiac failure
Disseminated cancer
Pulmonary thromboembolism
If its a large fragment then can block the whole pulmonary artery —> sudden death
A small fragment can get lodged in the peripheral artery —> pulmonary infarct
A smaller fragment can block tiny vessels can lead to pulmonary hypertension
Complications -
Massive PE >60% reduction in blood flow is rapidly fatal (especially saddle emboli)
Major PE - medium sized vessels blocked. Patients short of breath +/- cough and blood stained sputum
Minor PE - small peripheral pulmonary arteries blocked. Asymptomatic or minor shortness of breath
However Recurrent minor PEs lead to pulmonary hypertension
Other types of embolism
Embolism can be - Air Amniotic fluid Nitrogen Medical equipment Tumour cells Fat Bone marrow
Prophylaxis (prevention of) DVT/ PE
In a population identify high risk patients
LMW / inject heparin (anti coagulative agent) sub-cutaneously
Mobilise early and keep mobilising
Leg compressions during surgery and after -
TED stockings
‘Flowtron’ boots
Treatment of thrombus / thromboemboli
Clot Busters –streptokinase, ateplase (recombinant tPA)
Intravenous heparin type drugs
Newer generation NOAC (noval oral anticoagulants):
Dabigatran Rivaroxaban Apixaban Edoxaban - these are all Anti factor Xa drugs
Filters in IVC, devices in left atria to stop thrombus formation etc.
Embolectomy (legs etc for acute limb ischaemia)
Oral warfarin
