Anticoagulants and antiplatelet agents work to prevent clot formation through different mechanisms. Anticoagulants like heparin and warfarin prevent clotting by inhibiting coagulation factors, while antiplatelets like aspirin prevent platelet aggregation. Platelets play a key role in hemostasis, initially forming a platelet plug through adhesion and aggregation at the site of vascular injury. This is later stabilized by the coagulation cascade forming a fibrin clot. Anticoagulants and antiplatelets are used to prevent thrombus formation in conditions like heart attacks, strokes, and deep vein thrombosis.

1. Anticoagulants and Antiplatelet Agents
Antiplatelet
Antiplatelet: A substance that prevents platelet plugs from forming; this effect can help prevent cardiovascular
disease such as MI & strokes. Makes platelets slippery.
Antiplatelet agent; A drug that prevents clot formation by in inhibiting platelet aggregation.
Aspirin
Prophylaxis and treatment of cerebral ischemia and myocardial infarction, coronary stenting -low dose aspirin
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Acetylates and irreversibly inhibits COX enzymes
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Adverse effects: hemorrhagic stroke, GI bleeding, gastric ulcers, tinnitus, allergic reactions, interstitial nephritis-
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acute kidney injury, tinnitus
uses: prophylaxis against MI and TIAs
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precautions: GI/GU intracranial bleed; use of other OTC substances for analgesia; use in elderly
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Aspirin (antiplatelet)
inhibits platelet aggregation by inhibiting enzyme for thromboxane A2 synthesis
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dose: 81-325 mg daily
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effects last life of a platelet (about 7 days)
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at risk for cardiovascular disease
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THROMBUS VERSUS EMBOLUS
thrombus; blood clot formed in a blood vessel
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embolus; A clot that breaks lose and travels through the bloodstream. So moving clot
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involves a clot that is rich in fibrin.
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PLATELET RESPONSE TO VASCULAR INJURY
2 phases of hemostasis
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1) Primary hemostasis: rapid formation of platelet "plugs"
Involves the interaction of blood vessels and platelets to prevent blood loss
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The Blood vessels vasoconstriction decreased blood flow to the are
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Then the formation of a platelet plug (primary homeostatic plug) which adheres and aggregates at the injury site,
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temporarily stopping the bleeding.
components of primary hemostasis
1. Platelets (pro-clotting)
-Anucleate cells
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-Small fragments of megakaryocytes
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-Granules: alpha and delta
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-Cell surface adhesion molecules
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2. Vascular endothelium (anti-coagulant)
-Endothelial cells
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-Sub-endothelium
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Injury;
endothelial damage>transient vasoconstriction via neural stimulation reflex.
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Exposure;
VWF binds to exposed collagen
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Von Willebrand Factor;
a protein required for normal platelet formation and synthesized by the endothelial cells.
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Adhesion;

2. Reversible process Platelets adhere to the exposed subendothelial connective tissue (collagen and basement
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membrane)
aggregation;
Occurs following adhesion and activation of platelets and Platelets adhere loosely to one another Is reversible
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This process includes platelet adhesion, platelet activation, and platelet aggregation which results in the formation
of a platelet plug which temporarily stops the bleeding.
2) Secondary hemostasis: formation of thrombus (clot)
The substances released at the time of blood vessel injury initiate the clotting cascade (biochemical reaction of
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soluble coagulation proteins)
The circulating plasma clotting proteins interact to form an insoluble fibrin strands which stabilize the platelet
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plug (secondary homeostatic plug)
components of secondary hemostasis
Soluble plasma proteins
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Anticoagulants
Anticoagulant ; A substance that prevents or delays coagulation of the blood. Does not dissolve a clot.
Anticoagulant agent; Drug that inhibits coagulation, clot formation. Used as a prophylaxis, have no effect on an
already formed clot.
make platelets less sticky
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prevent clots
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Doesn't remove clots that already exist; make sure don't get bigger
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examples: Heparin (Parenteral); Coumadin (Oral); Enoxaparin (Parenteral); Xarelto (Oral); Pradaxa (Oral)
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Heparin (Injectable anticoagulant;
Heparin;
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activates antithrombin III, inhib x factor
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metabolized partially by liver,
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excreted mostly unchanged in urine
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impaired renal function prolongs heparin more than hepatic disease
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unable to cross membranes: pregnant women can take it
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not problematic for renal patients
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Low dose Heparin (SQ); neutralizes activated factor X, inhibition of prothrombin to thrombin, moderately
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effective
Higher dose Heparin (IV); inactivates thrombin , inhibit fibrin formation
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Heparin- indications; prevent/treat venous thrombosis, open heart surgery and renal dialysis: blood wants to clot
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when out of the body, DIC (disseminated intravascular coagulation): clotting/bleeding at same time. Pregnancy/
acute illness, acute myocardial: clots in coronary arteries; prevent infarction
IV: immediate coagulation
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SQ: more gradual, longer lasting
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very short half life (1.5 hours)
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mostly used in hospital
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prevents clots from forming
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ideal before surgery
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Warfarin sodium (Coumadin) (oral anticoagulant)
rapid and total absorption from GI
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metabolized by liver
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inhibits synthesis of Vit K dependent clotting factors: X, IX, VII
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takes several days of Rx to see prolongation of coagulation
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need to also be on heparin/lovenox at first
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3. Warfarin: indications
long term phophylaxis and Rx of venous thrombosis or PE
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manage possibility of embolization in a. fib, or prosthetic vascular device
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reduce risk of CVA and MI
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Warfarin antidote
Vitamin K
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may cause flushing or hypotension
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Indications: chronic anticoagulation for DVT/PE, stroke prevention in atrial fibrillation
Needs PT monitoring with INR; highly protein bound and unpredictable
Adverse effects: increased risk of bleeding, teratogenic, skin necrosis due to initial hypercoagulation because of
protein C and S inhibition
Vitamin K for delayed reversal, in acute conditions – fresh frozen plasma or prothrombin complex concentrate
Thrombolytic agent
A drug that dissolves the formed clot; "clot buster."
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Antifibrinolytic agent;
Causes clot formation.
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Fibrinolysis
Involves the interaction of circulating proteins that break down the clot and prevent further clotting.
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Alpha Granules; most numerous of the granules store many substances needed for hemostasis
Dense Granules; Smaller granules and fewer than alpha
The contents of both alpha and dense granules are released, promoting recruitment of additional platelets for the
platelet aggregate at the site of vascular injury.
Lysosomal Granules; Glycogen granules and mitochondria
Lipid-lowering agent with side effect:
flushing Niacin
Lipid-lowering agents with side effects: elevated LFTs, myositis Fibrates Statins (HMG-CoA inhibitors)
Lipid-lowering agent with best effect on ↑HDL Niacin
Lipid-lowering agent with best effect on ↓triglycerides/VLDL Fibrates
Lipid-lowering agent with best effect on ↓LDL/cholesterol Statins
These drugs lower LDL and TAGs, and raise HDL. Useful in hypertriglyceridemia.
Definitions of lipid-lowering medication. lowers blood cholesterol levels by inhibiting HMG-CoA reductase.