Drugs For The Treatment Of Coagulation Disorders PDF

 for the Treatment of Drugs Coagulation Disorders Introduction to Coagulation Disorders...

 for the Treatment of Drugs Coagulation Disorders Introduction to Coagulation Disorders (slot) formation excessive bleeding excessive thrombus pathological conditions i > - or are represent a breakdown of normal hemostatic mechanism /process carsieing bleeding to stop Blood Coagulation Cascade > - When vessel cells the blood vessel release chemicals that Injury to wall occurs , lining damagel Initiate the clotting process 3 major steps > - : ① Vasoconstriction : restrict blood loss ② Formation of platelet (bloodalls clottingm plug platelets involved collagen : in mu fibrils nu on injured vessel u of A Willebrand - Factor (blood glycoprotein) platelet , rate together ③ Blood coagulation : simulaneously , the path mation is , uted the on fibrin strands mmmation that resulting in mmm the platelet pluy into stabel clot , completing the coagulation process. The Cascade Coagulation involves factors (normally Inactive forms manymin exsist in > - ↳ during coagulation , they are minted 2 clotting > - pathways : Intrinsic pathway · : ↳ activated by Internal trauma to blood resses mmm s involves ↳ factors XII XI IX , , ↳ results A activation , in which result in as extrinsic Summary th , ultimately forming fibrin and completing clot.  Extrinsic pathway · : ↳ activated a bytrauma fissure release n factor begins ↳ when mmmged (TF) w which binds factor Ulla which activate , factor X ↳ X converts kombin to tambin which converts Eigen to #brin , the completing clot. Fibrinolysis process to fibrin clot to the size and spread of the dim m > - enzymatic clot also removes the clot has been repaired vessel > - the mmmmmmmmerely once t-PA activates to plasminogen plasmin > - which breaks down the clot ↳ inhibited once clot is dissolved Regulation of the Coagulation Cascade > - antithrombin 111 = small protein that functions as anticoagulant mum ↳ neutralises number of active cofactors clotting a in > ↳ keeps balence between and formation bleeding of Intravascular clots Thromboembolic Disease > - Coagulation disorder characterize byfoagulable states deep thrombosis (clot deep in thigh lower legs, ↳ E vein usually manifest veins in or , can ↳ pulmonary embolism /clot in one of the pulmonary arteries lang) in ↳ coronary artery disease Pharmalogical of Treatment of Thromboembolic Disease > - 3 classes antithrombotic agets : ①Anticoagulants : prevent or reduce coagulation blood minting in a vessel by Inoagulation cascade Laka-blinners) ② Antiplatelets : the aggregation Pete within blood vessel ⑤Thrombolytics : drugs that kenwanheady form clot (ALA clot busters) Anticoagulent Therapy thrombi aim-prevent formation of intravascular while minimizing tendancy to > - , bleed adverse effect of all major anticoagulants bleeding = > - ↳ first to look for thing 2 main anticoagulant therapeutics > - : ① Thrombin Inhibitors 1. Heparin and Low Molecular Weight Heparins (injected ↳ mod : Indirect Inhibition mummu finds antithrombinirombin III - immediate , enhancing it's action respose, acheived anticoagulation rapidely ↳ variable responce , degree of anticoagulation must be monitoral  2. Oral factor Xa Inhibitors ↳ increased compliance due to no injection > - be effective heparins may as as effects don't need to be monitored ② Warfarin Coral) ↳ widely prescribed ↳ Inexpensiveis effective relatively ↳ mod Inhibition of dependant factors le clotting = Vitamin - (vi IX , X , 11) ↳ cofactor In their synthesis , decreases of clotting ↳ the rate of synthesis cofactors Clinical Use of Anticoagulent Inherited disorders has deficite natural anticoagulant system · - > · acquired disorders - > a number of disorders leg. atrial fibrillation) put person & high risk for formation of venous thrombi of charfarin ↳ long use : - ↳ ↓ incidence of thrombotic events ↳ w/ artificial heart patients values (high risk of thrombosis) prophylaxis prophylactic during hip and knee replacement surgeries prevent · - > use Spreventative) thrombotic complications weight rain hmecular ↳ administered subcutaneously · Thrombeombolic disease - - treats overt thromboembolic disease ↳ venous thrombosis treated w/ in or weight heparin mmmolecular for first m 5-7 num days , then agent summed to oral warfarin - Triggers for > - Platelet prevention of thrombi formation w/ Aggregation drage reduces incidence of vascular events 3 tumm for platelet aggregation targets for drug action > - can be : ① membrane receptors on platelet that respond to norepinephrine thrombin , exterior of , and some prostaglandins initiating platelet aggregation , ② platelet produces App and prostaglandings (among other compounds) that can interact w/ ADP and protaglandin receptors on the surface of the platelet ③ platelet produces thromboxane Az , Cyclic AMP and calciumlons that act Inside the platelet to promote platelet adherence Antiplatelet Drugs ↳ target triggers for platelet formation to treatboembolic disease Initiates Platelet ↓ ① COX- 1 Inhibitors (aspirin( aggregation ↳ Major andin ↳ mod = reduces formation of thromboxane Al (TXA2) by irreversibly Inhibiting COX-1 (responsible for formation of prostaglanding > - therapeutic use = people at risk for stroke , heart attacks Ischemic vascular disease primary prevention for ↳ vascular events ② ADP Receptor Inhibitors (Clopidogrel ↳ mod = Inhibits App dependant activation of platelet by Irreversibly blocking ADD receptors on platelets myocardial ↳ clinical use = prevente recurrent stroke reduces , Ischemic Infarct , strone and following vascular surgeries ③ Platelet Glycoprotein 11B/11A Receptors (Absiximab) ↳ mod = Inhibition of IIBIIIA receptors on exterior of platelet , inhibiting aggregation ↳ therapeutic use = prevente coronary vessel occlusion in patients by pass surgery undergoing coronary  Thrombolytic Drugs ① Streptokinase moa protein that catalyzes of plasminogen to = conversion · plasmin to dissolve blood close ② Altpase · moa = human tissue plasminogen activator (t-PA) ↳ clinical use : · reduces of acute heart attack mortality · breaks fibrin formation of flasmin down by increasing summary : num already formal clot -> and thrombotic agent antiplatelets prevention of platelet aggregation > - slows clot formation > - anticoagulants Drugs > - In vitamin le Bleeding Disorders ↳ cofactor for synthesis of factors clotting -also used in warfarin overdose * for hemophilia where specific factors deficient , concentrated plasma , coagulation are fractions factors administered to the patient containing missing are