vascular system Flashcards
thrombosis: explain how a thrombus can form within a vein and identify the drugs used to treat deep vein thrombosis and pulmonary embolism
3 initial stages of thrombosis (small-scale thrombin production)
tissue factor -> prothrombinase complex -> antithrombin (AT-III)
initial stages of thrombosis (coagulation): tissue factor
tissue factor bearing cells activate factors X and V, forming a prothrombinase complex (fVa and fXa)
initial stages of thrombosis (coagulation): prothrombinase complex
prothrombinase complex activates factor II (prothrombin), creating factor IIa (thrombin); initiation stage of coagulation cascade
initial stages of thrombosis (anticoagulation): antithrombin (AT-III)
AT-III inactivates fIIa and fXa, regulating thrombin levels
4 mechanisms anticoagulants use to treat initial stages of thrombosis (first line of treatment); anticoagulants is generic term for drugs treating thrombosis, and specific term which targets coagulation factors
inhibit fIIa (same as antithrombin in body), inhibit fXa, increase activity of AT-III, reduce levels of other factors
example of fIIa inhibitor, and administration
dabigatran (direct-acting oral; causes GI bleeding)
example of fXa inhibitor, and administration
rivaroxaban (oral; maintenance treatment for DVT and PE)
2 classes of anticoagulants that increase activity of AT-III (fast onset of action, but not orally available)
heparin, low-molecular weight heparins
heparin administration and effects
IV, SC; activates AT-III and decreases fIIa and fXa (given for initial PE interim treatment - more effective than dalteparin so used in PE vs DVT)
low-molecular weight heparins example and effects
dalteparin (given initially as DVT or PE interim treatment, as work quickly); activate AT-III and decrease fXa
what factors is vitamin K required for
II, VII, IX, X
name a vitamin K antagonist, which therefore reduces levels of other factors, and administration and time of onset
warfarin (indirectly-acting oral, so slow onset of action (5-7 days) - maintenance treatment for DVT and PE)
in physiology, what are anti-coagulants balanced with, and how does change in thrombogenic conditions e.g. DVT/pulmonary embolism
balanced with pro-coagulants, but in thrombogenic conditions, pro-coagulants are higher than anti-coagulants
3 risk factors of Virchow’s triad (increase likelihood of thrombus formation)
rate of blood flow, consistency of blood, blood vessel wall integrity
in DVT/pulmonary embolism, describe rate of blood flow
slow/stagnating (e.g. due to immobility), with no replenishment of anti-coagulant factors and balance adjusted in favour of coagulation
in DVT/pulmonary embolism, describe consistency of blood
(not viscosity); natural imbalance between procoagulation (II, VII, IX, X) and anticoagulation factors; typically genetic
in DVT/pulmonary embolism, describe blood vessel wall integrity, and how hypertension increases risk of damage
damaged endothelia, so blood exposed to procoagulation factors; common in hypertension as blood hits endothelial cells more regularly, so more likely to get damaged
presentation of DVT and pulmonary embolism
swollen leg with pitting oedema and local tenderness (DVT) e.g. following immobility -> if embolises in lung (PE), chest pain, dyspnoea and tachypnoea
investigations of DVT
2-level Wells score (survey out of 10; higher the score, more likely the DVT); D-dimer test (tests for fibrin degradation products in blood); vein scan; confirmed by US
investigations for PE
CTPA (computed tomographic pulmonary angiography)