lecture 13

Question 1

Causes of Vascular injury to blood vessels

Answer 1

-trauma, surgical manipulation, prior thrombosis, atherosclerosis

Question 2

Stasis (flow of blood) (mainly cause venous thrombosis)

Answer 2

immobility - post op, plane
Pressure - (blockages) catheter, tumour obstruction
Increased viscosity - polycthaemia, dehydration, EPO

Question 3

Blood Hypercoagulability

mainly venous thrombosis

Answer 3

increased procoagulants
decrease in inhibitors
impaired fibrinolysis (rare)

Question 4

Deep vien thrombosis

• what is it caused by?
• what are the symptoms/signs of DVT, PE ?

Answer 4

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

Question 5

D dimer blood test

Answer 5

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

Question 6

Cancer linked to DVT

Answer 6

cancer can disrupt balance and cause thrombosis

• need to think of this as being a cause
• if anaemia is present - could be cancer

Question 7

Diagnosis of PE

Answer 7

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

Question 8

Thrombophilia

-KEY LEARNING POINT - she said it was a hint

Answer 8

• 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

Question 9

Inherited Thrombophilia

Answer 9

-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

Question 10

Factor V leiden

Answer 10

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

Question 11

Treatment PE and DVT

Answer 11

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

Question 12

Wafarin

Answer 12

• interacts with a lot of things e.g antibiotics,

- higher INR increases bleeding risk further

Question 13

Direct acting oral anticoagulants

Answer 13

• 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