Cardiovascular Flashcards
Thrombosis
is blood coagulation inside a vessel
Where can thrombosis occur
arterial circulation: high pressure, platelet rich
venous circulation: low pressure, fibrin rich
Normal bleeding time
2-9 minutes, 9-15 platlet dysfunction, 15+ critical
How to measure bleeding time
The time from the beginning of incision until the termination of bleeding is considered as the BT. A standard filter paper should be used every 30 seconds to draw off it until the blood completely stops
Arterial thrombosis-anatomy + symptoms
Coronary circulation- angina
Cerebral circulation- stroke syptoms
Peripheral circulation- pain in leg
Other territories- SMA- bellyache
Arterial thrombosis-etiology
Atherosclerosis
Inflammatory
Infective
Trauma
Tumours
Unknown- Platelet driven
Arterial thrombosis-Presentations
Myocardial infarction
CVA- cerebral vascular accident or stroke
Peripheral vascular disease
Others
Arterial thrombosis: treatment- coronary
Aspirin + other antiplatelets
Anticoagulants
Thrombolytic therapy: streptokinase tissue plasminogen activator
Reperfusion – Catheter directed treatments and stents
TPA generates plasmin, degrades fibrin- dissolve clots
Anticoagulants example and action
LMWH (low molecular weight heparins) and UFH (unfractionated heparin)- enhances antithrombin ability to inactive thrombin (factor IIa), factor Xa and factor IXa
Fondaparinux- inhibits factor Xa directly
Aspirin- thrombosis treatment
inhibits platelet function
Why is Fondaparinux used instead of heparin?
Rate of serious bleeding with Fondaparinux was much lower than with heparin because Fondaparinux has a lower half life
Arterial thrombosis: treatment- cerebral
Aspirin, other anti-platelets
Thrombolysis- Catheter directed treatments
Reperfusion
Why is heparin not used for strokes?
Limited efficacy and an increased risk of bleeding complications
Venous thrombosis-anatomy
Peripheral –Ileofemoral, femoro-popliteal
Other sites – Cerebral, Visceral
Fibrin driven
Venous thrombosis-diagnosis
Signs and symptoms-very non specific (specific= calf pain and chest pain/breathlessness)
Blood tests –D-dimer –sensitive but not specific- not used often for in patients
Imaging-usually required- ultrasound, or CT/MRI
Vichow’s triad
increased risk of vascular thrombosis- Hypercoagulability of blood, statis of flow+ Vessel wall injury/ Endothelial damage
What are the three components of Virchows triad?
intravascular vessel wall damage, stasis of flow, and the presence of a hypercoagulable state
Venous thrombosis-aetiology- Virchows triad blood flow
Immobilisation:
Surgery
Long haul flights
Trauma
Injury – physical, chemical
Venous thrombosis-aetiology- Virchows triad blood constituent
Mainly genetic
others:
Malignancy
Oestogens
Venous thrombosis-treatment
Heparin or LMWH
Warfarin
DOAC- main treatment for DVT
Endo-vascular- for longer clots in younger patients- clot destroyed or removed using catheter
Surgical- very rare
DOAC
direct oral anticoagulants
Warfarin action
Inhibits enzyme responsible for activating vitamin K, depletes body of functional vitamin K and reduce synthesis of vitamin K dependent factors clotting factors (10, 9, 7, 2)
When would the treatment of DVT be more aggressive?
DVT is very large, blocks major veins, or produces severe pain and swelling of the limb
Venous thrombosis-prevention
Mechanical or chemical thromboprophylaxis after risk assessment upon entrance to hospital
Also early mobilisation and good hydration