lecture 13 Flashcards
Causes of Vascular injury to blood vessels
-trauma, surgical manipulation, prior thrombosis, atherosclerosis
Stasis (flow of blood) (mainly cause venous thrombosis)
immobility - post op, plane
Pressure - (blockages) catheter, tumour obstruction
Increased viscosity - polycthaemia, dehydration, EPO
Blood Hypercoagulability
mainly venous thrombosis
increased procoagulants
decrease in inhibitors
impaired fibrinolysis (rare)
Deep vien thrombosis
- what is it caused by?
- what are the symptoms/signs of DVT, PE ?
Vessel itself is intact, but due to other disruptions, a clot forms with platelets blocking the vien (normally a leg vein)
- get swelling
- some can break off and travel up to the pulmonary arteries of the lung (when they get thinner)
- can be fatal
DVT - leg swelling, leg pain, oedema
PE - shortness of breath, chest pain, tachycardia, Tachypnoea
D dimer blood test
D dimer - is the breakdown products of fibrin
- use if in low prob for DVT
- if D dimer negative - then discharge
- if D dimer positive - then ultrasound
- Also get ultrasound if they are high probability
Cancer linked to DVT
cancer can disrupt balance and cause thrombosis
- need to think of this as being a cause
- if anaemia is present - could be cancer
Diagnosis of PE
classic symptom triad - pleuritic pain, shortness of breath, haemoptysis (blood in cough)
Signs - tachycardia, tacypnoea, hypoxia
Can do a CT scan
V/Q scan
- can die, or can get hypotension - need thormbolysis to break down the clot
- also can get see severe right heart strain due to back pressure from pulmonary arteries
Thrombophilia
-KEY LEARNING POINT - she said it was a hint
- Tendency to develop thrombosis
- Can be acquired or inherited
- manifested as venous thromboembolism
- some spontaneous -have genetic increased risk
- some are provoked events - surgery or trauma, immobility, hospitalisation, malignancy, pregnancy
Inherited Thrombophilia
-abnormal inhibitor function - resistance to activated protein C (factor 5 leiden)
-Deficiencey of inhibitors - antithrombin , protein C, protein S
Increased factor levels - prothrombin gene mutation, elevated factor VIII
Factor V leiden
Factor 5a enhances factor 10 activation
- activated protein C cleaves normal factor Va
- slows Xa production
- so if have bad protein C then cannot get inactive factor 5 and keep getting the clot
- may have helped survival in oldern days e.g not bleeding to death with pregnancy
APCr
-if have both carriers - then get a huge increase in risk of thrombosis
Treatment PE and DVT
Initially - heparin
Immediate effect
-heparine prolongs the APPT, antitrobin deificencey does not.??!
low molecular weight heparin
- similar to heparin, comes in injection, shorter chains of thormbin
- inhibits 10a
- subcutaneous better bioavailability
- come in prepackaged vials
- Enoxaparin 1mg/kg twice daily
- dont use appt to measure low molecular weight heparin
-basically are changing the bodys mechanisms around so can get clotting
Wafarin
- interacts with a lot of things e.g antibiotics,
- higher INR increases bleeding risk further
Direct acting oral anticoagulants
- same as warfarin for treatment of VTE
- superior for anticoagulation in atrial fibrillation - better stroke prevention with similar rates of bleeding
- people with kidney failure can accumulate high levels of this