Anticoagulants

Najwa Najihah binti Salpad

(012015051954)
Anticoagulant Agent
• Interfere with proteins in the bloods that are involved with
the coagulation process
• Prevent formation of blood clots
• Maintain open blood vessel
• May prevent existing clots from getting larger
COAGULATION
• Process by which blood changes from liquid to gel, forming a
blood clot.
• Blood clots are made up of red blood cells, platelets, fibrin
and white blood cells. These components stick together and
form a clot
• Blood clots in the blood vessels can block the blood flow to
the heart muscle and can cause heart attack
• Block flow to the brain which can leads to stroke
Anticoagulant Drugs
• Heparin (Calciparine, Hepathrom, Lipo-Hepin)
• Warfarin (Coumidin, Panwarfin, Athrombin-K)
• Rivaroxaban (Xarelto)
• Dabigatran (Pradaxa)
• Apixaban (Eliquis)
• Edoxaban (Savaysa)
• Enoxaparin (Lovenox)
• Fondaparinux (Arixtra)
Mechanism of Action
1. Factor Xa inhibitors competitively inhibit the activation of factor X
2. Factor Xa inhibitors bind to the active site of factor Xa thus
preventing the formation of prothrombinase
3. Direct thrombin inhibitors bind directly to thrombin and prevent
fibrin formation as well as thrombin-mediated activation of factors
4. They also prevent thrombin-mediated activation of platelets,
inflammation, antifibrinolysis, and the anticoagulant protein C
5. Interfere with the synthesis of vitamin K and thus inhibits
activation of vitamin K-dependent clotting factors (II, VII, IX, X)
6. Also decreases the activity of protein C (activated by thrombin) –
responsible for some side effects
Adverse Effects
• Increase bruising
• can easily bleed/prolong nosebleed
• Bleeding gums
• Red or pink colored urine
• Stools turn red, dark brown or black
• Bleed more than normal during menstrual period
• Have a very bad headache or pain that doesn’t go away
Drugs Available in Malaysia
• Apixaban (Eliquis)
• Aspirin (Aceprin)
• Alteplase (Actilyse)
• Cardiprin 100
• Clopidogrel (Clopivid)
• Enoxaparin Na (Clexane)
• Prasugrel HCL (Effient)
• Rivaroxaban (Xarelto)
• Warfarin (Orfarin)
Anti-platelets
By Norafidah binti Mhd Idris (012015052436)
Physiology
Platelets are blood cells that help the
blood to clot and prevent bleeding.
When the body has a cut, scratch,
bruise or bleed, platelets go into
action and begin to work.
These platelet cells need thromoxane
A2 and adenosine; vitamin K specific
clotting factors (chemicals produced
by the body) to make them stick
together.
These chemicals are essentially the
glue that holds the blocks together to
make the clot.
Physiology
• Antiplatelet drugs are a
group of powerful medicines
that prevent blood clots.
• When you are wounded,
platelets arrive on the scene
and group together to form a
clot that stops the bleeding..
• But platelets can also group
when injury to a blood vessel
comes from the inside, as
may happen in an artery
affected by atherosclerosis.
 Drugs available in Malaysia
• Abciximab and Aspirin are a platelet aggregation inhibitors. It
works by blocking platelets from sticking together to form blood
clot.
• In Malaysia, aspirin for anti platelet can be obtained in
Aceprin(brand name).
Mechanism of
Action
Abciximab or Aceprin will binds
to glycoprotein (GP)
IIb or IIIa receptor on platelet
surface, thus preventing
binding of fibrinogen,
von Willebrand factor, and
other adhesive molecules to the
receptor sites leading to
inhibition of platelet
aggregation.
Abciximab
• Drug interaction with Anticoagulants (eg, warfarin, heparin),
dipyridamole, nonsteroidal anti-inflammatory drugs (NSAIDs)
(eg, ibuprofen), ticlopidine, or thrombolytics (tissue plasminogen
activators) because the risk of bleeding may be increased.
Aceprin
• Drug interactions with anticoagulants and corticosteroids.
 Adverse Effects

Hypotension
Headache Nausea & Vomiting
Fever

Potentially Fatal: Bleeding (during the

1st 36 hr of admin); anaphylactic
bradycardia Back pain reactions
 Any
Any questions?
questions?
THROMTOLYTICS
THROMBOLYTICS
By NURUL KHAIRAH BT. ISMAIL (012015052434)
THROMBUS
• Is blood clot in the vein, artery or heart
• A blood clot can completely or partially block a blood vessel
• A blood clot can form;
1. blood flow is too slow
2. Clotting occurs when it is not needed
• It can happen in any common blood vessel
• Common type of thrombosis is blood clot in a vein in the leg
CAUSES
• Slow blood circulation
Prolonged physical inactivity
Contraction of leg muscle > blood pumped towards the heart >
if the muscle pump doesn’t work properly, blood will flow slowly
• Damaged wall of the blood vessel
• Changes in the composition of the blood
• Some hereditary disorders
RISK FACTORS
• Damage normally occurs in arteries and veins
• Usually due to;
1. Unhealthy eating habits
2. Smoking
3. Diabetes
4. High blood pressure
cause blood clots various
narrowing of form over the results of
the artery narrowing thrombosis
THROMBOLYTICS
• Thrombolytic = Thrombus therapy
• Treatment to;
1. dissolve dangerous clots in blood vessels
2. improve blood flow
3. prevent damage to tissues and organs
• Thrombolysis may involve the injection of intravenous (IV)
line or
• through a long catheter that delivers drugs directly to the
site of the blockage
• It also may involve the use of a long catheter with a
mechanical device attached to the tip that either removes the
clot or physically breaks it up.
MECHANISM OF ACTION
• Thrombolytic drugs dissolve blood clots by;
1. activating plasminogen, which forms a cleaved product called plasmin.
2. Plasmin is a proteolytic enzyme that is capable of breaking cross-links between fibrin
molecules, which provide the structural integrity of blood clots
3. Because of these actions, thrombolytic drugs are also called "plasminogen activators" and
"fibrinolytic drugs."

• 3 major classes of fibrinolytic drugs:

1. tissue plasminogen activator (tPA)
2. streptokinase (SK)
3. urokinase (UK)

• While drugs in these three classes all have the ability to effectively dissolve blood clots, they
differ in their detailed mechanisms in ways that alter their selectivity for fibrin clots.
• Derivatives of tPA are the most commonly used thrombolytic drugs,
especially for coronary and cerebral vascular clots
• Because of their relative selectivity for activating fibrin-bound
plasminogen
• Tissue plasminogen activator produces clot lysis through the following
sequence:
Plasmin is cleaved Fibrin molecules
Activates fibrin- from the are broken apart
tPA binds to fibrin on the
bound plasminogen by the plasmin
surface of the clot
plasminogen associated with and the clot
the fibrin dissolves

• Plasmin is a protease that is capable of breaking apart fibrin molecules,

thereby dissolving the clot
• However, it is important to note that plasmin also breaks down other
circulating proteins, including fibrinogen
 • SK is not a protease and has no enzymatic activity
• However, it forms a complex with plasminogen that releases plasmin
• Unlike tPA, it does not bind preferentially to clot-associated fibrin and therefore binds
equally to circulating and non-circulating plasminogen
• Therefore, SK produces significant fibrinogenolysis along with clot fibrinolysis
• For this reason, tPA is generally preferred as a thrombolytic agent over SK, especially
when used for dissolving coronary and cerebral vascular thrombi.
• Because SK is derived from streptococci, patients who have had recent streptococci
infections can require significantly higher doses of SK to produce thrombolysis.
Note!
• It is important to note that the efficacy of thrombolytic drugs depends on the age of the
clot
• Older clots have more fibrin cross-linking and are more compacted; therefore, older
clots are more difficult to dissolve
• For treating acute myocardial infarction, the thrombolytic drugs should ideally be given
within the first 2 hours. Beyond that time, the efficacy diminishes and higher doses are
generally required to achieve desired lysis.
DRUGS
• Tissue Plasminogen Activators
• This family of thrombolytic drugs is used in acute myocardial infarction, cerebrovascular
thrombotic stroke and pulmonary embolism. For acute myocardial infarctions, tissue
plasminogen activators are generally preferred over streptokinase.
• Alteplase (Activase®; rtPA) is a recombinant form of human tPA. It has a short half-life (~5
min) and therefore is usually administered as an intravenous bolus followed by an
infusion.
• Retaplase (Retavase®) is a genetically engineered, smaller derivative of recombinant tPA
that has increased potency and is faster acting than rtPA. It is usually administered as IV
bolus injections. It is used for acute myocardial infarction and pulmonary embolism.
• Tenecteplase (TNK-tPA) has a longer half-life and greater binding affinity for fibrin than
rtPA. Because of its longer half-life, it can be administered by IV bolus. It is only approved
for use in acute myocardial infarction.
• Streptokinase
• Streptokinase and anistreplase are used in acute myocardial infarction, arterial and
venous thrombosis, and pulmonary embolism. These compounds are antigenic
because they are derived from streptococci bacteria.
• Natural streptokinase (SK) is isolated and purified from streptococci bacteria. Its lack
of fibrin specificity makes it a less desirable thrombolytic drug than tPA compounds
because it produces more fibrinogenolysis.
• Anistreplase (Eminase®) is a complex of SK and plasminogen. It has more fibrin
specificity and has a longer activity than natural SK; however, it causes considerable
fibrinogenolysis.

• Urokinase
• Urokinase (Abbokinase®; UK) is sometimes referred to as urinary-type plasminogen
activator (uPA) because it is formed by kidneys and is found in urine. It has limited
clinical use because, like SK, it produces considerable fibrinogenolysis; however, it is
used for pulmonary embolism. One benefit over SK is that UK is non-antigenic;
however, this is offset by a much greater cost.
ADVERSE EFFECTS
• Major bleeding.
• Cardiac arrhythmias.
• Cholesterol embolus syndrome.
• Anaphylactoid reaction.
• Cerebrovascular accident.
• Intracraneal hemorrhage.