lecture 13 Flashcards Preview

BII > lecture 13 > Flashcards

Flashcards in lecture 13 Deck (13):

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


-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

-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



-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