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89 Cards in this Set

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What is the daily Cardiovascular aspirin therapy level peri-operatively?
less than or equal to 325mg/day should be maintained.
Should anti-platelet drugs such as clopidogrel (Plavix) and prasurgrel (Effient) be continued before dental surgery? What patients are on these drugs?
Yes. Especially for patients with coronary stents. (both bare metal and drug eluting stents).
Should anti-platelet drugs such as clopidogrel (Plavix) and prasurgrel (Effient) be continued before dental surgery? What patients are on these drugs?
Yes. Especially for patients with coronary stents. (both bare metal and drug eluting stents).
Patients are usually on warfarin (Coumadin to prevent what complications from what two conditions? When is an INR required?
Warfarin is taken to prevent an emboli secondary to atrial fibrillation or deep vein thromboses (DVT's). An INR within 24 hours of a surgical procedure is required.
When performing complex restorative care, periodontal probing, SRP, non-surgical endo, what is a safe INR? a probably safe INR?
safe INR < 3
probably safe INR < 3.5
What are the recommended INR values for a single or limited number of non-surgical extractions? What is the INR for surgical extrations or more involved procedures?
Non surgical, single, or limited extractions INR preferably be 3 or less.

For surgical/involved, therapeutic INR of 2.5 or less.
When a patient is anti-coagulated for prevention of emboli secondary to prosthetic heart valves, what is an acceptable INR range
2.5-3.5
What is the protocol for patients taking enoxaprin (Lovenox) an injectable anticoagulant before a surgical procedure?
Enoxaprin should NOT be administered within 12 hours of the surgical procedure. Enoxaprin therapy is reinstituted asap after adequate hemostasis has been established.
How long do patients usually take fondaparinux (Atrixtra) for DVT prophylaxis after lower extremity orthopedic surgery? Should dental treatment be performed?
Usually patients take fondaparinux (Atrixtra) for 6-12 weeks after lower extremity orthopedic surgery. Dental treatment should be delayed if possible until therapy is no longer needed (6-12 weeks post surgery).
What is the mechanism of action for Fondaparinux (Atrixtra)?
Arixtra is a synthetic, highly sulfated pentasaccharide that binds to Anti-Thrombin II with a high affinity and causes a conformational change in ATIII significantly increasing the ability of ATIII to inactivate Factor Xa. (Anticoagulation drug)
How many half lives/how much time does it take for Fondaparinux (Atrixtra) to be metabolized?
3-5 half lives (2-4 days) following its last dose when patients have normal renal function.
What is Dabigatran (Pradaxa)?
Mechanism of action?
A direct thrombin inhibitor which inhibits both free and fibrin-bound thrombin.
What is the reason patients are normally taking Dabigatran (Pradaxa)? Should patient take these meds before dental treatment?
to prevent emboli secondary to atrial fibrillation. Patients with normal renal function should not take two doses of dabigatran (Pradaxa) prior to dental treatment.
What anesthetic injections should be avoided when working on a patient who is anti coagulated?
If possible, avoid IAN and PSA injections/block injections. Use infiltration techniques. Avaoid CN V-2.
What are platelets?
Platelets, or thrombocytes (from Greek θρόμβος, "clot" and κύτος, "cell"), are small, irregularly shaped clear cell fragments (i.e. cells that do not have a nucleus containing DNA), 2–3 µm in diameter,[1] which are derived from fragmentation of precursor megakaryocytes. The average lifespan of a platelet is normally just 5 to 9 days. Platelets are a natural source of growth factors. They circulate in the blood of mammals and are involved in hemostasis, leading to the formation of blood clots.
What is GP IIb/IIIa? It's main function?
They are receptors on platelets which are the "velcro" of the platelets. They aid in platelet aggregation (platelets binding to other platelets) to form the platelet plug.
What is Fibrin? What is it's function?
Fibrin (also called Factor Ia) is a fibrous, non-globular protein involved in the clotting of blood. It is polymerised to form a "mesh" that forms a hemostatic plug or clot (in conjunction with platelets) over a wound site. The "fishnet" of clotting. Activation of clotting factors leads to the conversion of fibrinogen to fibrin and fibrin in the presence of Factor XIII forms the clot
What is ASA (Aspirin)?
Aspirin (USAN), also known as acetylsalicylic acid (/əˌsɛtəlˌsælɨˈsɪlɨk/ ə-set-əl-sal-i-sil-ik; abbreviated ASA), is a salicylate drug, often used as an analgesic to relieve minor aches and pains, as an antipyretic to reduce fever, and as an anti-inflammatory medication.
What is Clopidogrel (Plavix)?
Clopidogrel (INN) is an oral, thienopyridine class antiplatelet agent used to inhibit blood clots in coronary artery disease, peripheral vascular disease, and cerebrovascular disease. It is marketed by Bristol-Myers Squibb and Sanofi under the trade name Plavix. The drug works by irreversibly inhibiting a receptor called P2Y12, an adenosine diphosphate (ADP) chemoreceptor on platelet cell membranes. Adverse effects include hemorrhage, severe neutropenia, and thrombotic thrombocytopenic purpura (TTP).
What is Prasugrel (Effient)?
Prasugrel (marketing name Effient in the US, Efient in the EU and Prasita in India) is a platelet inhibitor developed by Daiichi Sankyo Co. and produced by Ube and currently marketed in the United States in cooperation with Eli Lilly and Company for acute coronary syndromes planned for percutaneous coronary intervention (PCI).Prasugrel is a member of the thienopyridine class of ADP receptor inhibitors, like ticlopidine (trade name Ticlid) and clopidogrel (trade name Plavix). These agents reduce the aggregation ("clumping") of platelets by irreversibly binding to P2Y12 receptors. Compared to clopidogrel, prasugrel inhibits adenosine diphosphate–induced platelet aggregation more rapidly, more consistently, and to a greater extent than do standard and higher doses of clopidogrel in healthy volunteers and in patients with coronary artery disease, including those undergoing PCI".[2]
What is Warfarin (Coumadin)
Warfarin (also known under the brand names Coumadin, Jantoven, Marevan, Lawarin, Waran, and Warfant) is an anticoagulant. While it may be one of many drugs popularly referred to as a "blood thinner" , this is a misnomer, since it does not affect the thickness or viscosity of blood. Instead, it acts on the liver to decrease the quantity of a few key proteins in blood that normally allow blood to clotWarfarin inhibits the vitamin K-dependent synthesis of biologically active forms of the calcium-dependent clotting factors II, VII, IX and X, as well as the regulatory factors protein C, protein S, and protein Z.[2][43]
What is INR?
The prothrombin time (PT) and its derived measures of prothrombin ratio (PR) and international normalized ratio (INR) are measures of the extrinsic pathway of coagulation. This test is also called "ProTime INR" and "INR PT". They are used to determine the clotting tendency of blood, in the measure of warfarin dosage, liver damage, and vitamin K status. PT measures factors I, II, V, VII, and X. It is used in conjunction with the activated partial thromboplastin time (aPTT) which measures the intrinsic pathway.
Dabigatran (Pradaxa)
Dabigatran (Pradaxa in Australia, Europe and USA, Pradax in Canada, Prazaxa in Japan) is an oral anticoagulant from the class of the direct thrombin inhibitors. It is being studied for various clinical indications and in some cases it offers an alternative to warfarin as the preferred orally administered anticoagulant ("blood thinner") since it does not require frequent blood tests for international normalized ratio (INR) monitoring while offering similar results in terms of efficacy. There is no specific way to reverse the anticoagulant effect of dabigatran in the event of a major bleeding event, unlike warfarin.
What are 4 general characteristics of Normal hemostasis physiologically?
1. Normal vessel wall integrity.
2. Adequate platelet plug formation.
3. Functioning coagulation system.
4. Normal fibrinolytic system.
After vascular injury, describe molecularly how the platelet plug is formed and it's timeline of forming.
Damage to the vessel wall exposes collagen causing the release of thrombin, von Willebrand's factor, ADP and epi. Causes platelet adhesion (1-2 seconds), platelet aggregation (10-20 seconds) then platelet plug formation (1-3 minutes).
What molecule helps bind platelets to the vessel wall via which receptor?
vWf binds platelet to vessel wall via GP Ib Receptor
During platelet plug formation which molecules activate the platelets to start forming the platelet plug?
Thrombin, ADP, epinephrine and exposed collagen.
During platelet plug formation what cofactors are released to help form the platelet plug?
Thromboxane A2 and Ca++ (Factor IV) are released.
What molecule "recruits" more platelets during plug formation? how do the platelets bind to each other/what receptor acts as the velcro.
Thromboxane A2 "recruits" more platelets. Platelets aggregate via GP IIb/IIIa receptor.
During normal hemostasis what is the series of events that occur after the platelet plug is formed to clot formation. Timeline?
after 1-3 minutes the platelet plug is formed, Thrombin (IIa) activates Fibrinogen to Fibrin causing platelet consolidation (3-5 mins). Fibrin in the presence of factor XIII forms the fibrin clot and stabilization (5-10 mins)
What is the factor involved in the common pathway of coagulation leading to clot formation?
Factor X is activated from the intrinsic and or extrinsic pathway. From Factor X Prothrombin is converted to thrombin --> Fibrinogen to Soluble Fibrin which interacts with Factor XIII to form the fibrin Clot.
What are the two hemostatic factors that promote clot formation?
vWf + collagen = platelet activation.

Tissue factor causing clot formation (which is expressed after injury)
What two molecules are needed to cause platelet activation?
Exposed collagen (damaged vessel wall) + vWf.
There are molecules released from the endothelium which inhibit platelet activation/aggregation. What are two of them?
Prostacyclin and Nitric Oxide.
What are three anticoagulant factors which prevent clot formation during normal hemostasis?
Antithrombin III, protein S and Thrombomodulin.
What is the result of fibrinolysis?
Dissolving the clot during normal hemostasis.
What is the molecule that causes fibrinolysis?
Tissue Plasminogen activator.
What is a thrombosis? Is it common? What are the two different classes of thrombi?
Thrombosis = formation of unwanted clot within a blood vessel. It is the most common abnormality of hemostasis. There are Aterial and venous thrombi
What are three examples/diseases caused by Arterial Thrombi?
Coronary Artery disease (CAD)
Carotid Artery disease
Peripheral vascular disease (PVD)
What are two examples/complications of Venous thrombi?
DVT: Deep vein thrombosis
Atrial fibrillation
Arterial Thrombi are clots rich in what hemostatic molecule?
Platelet rich clots (the velcro)
Where do arterial thrombi normally form/occur? what are the three complications of arterial thrombi?
Arterial Thrombi are platelet rich clots which occur in medium sized arteries. Atherosclerosis is etiologic. Renders surface of endothelial cell thrombogenic and causes Coranary artery disease, Peripheral vascular disease and carotid disease.
What kind of drugs are given to treat arterial thrombi?
Anti-PLATELET drugs.
What are examples of anti-platelet drugs?
Aspirin, NSAID's, Clopidogrel, Prasugrel
Venous Thrombi are composed mainly of what hemostatic molecule?
Fibrin Rich clots (Fishnet)
Venous Thrombi occur in what areas? What are two examples of Venous thrombi complications?
Venous thrombi are fibrin rich clots which occur in areas of slow blood flow causing venous stasis in the lower extremities (DVT) and Atrial fibrillation can cause venous thrombi.
What type of medications are taken to treat venous thrombi? What are some specific examples?
Anticoagulant drugs are given to treat venous thrombi to dissolve the fibrin rich clot. Heparin, LMWH, Warfarin/Coumadin, Dibigantran (Pradaxa), Fondaparinux (Atrixtra)
List four drugs that are anti-coagulation drugs used to treat venous thrombi?
Heparin, LMWH, Warfarin/Coumadin,
Dibigantran (Pradaxa), Fondaparinux (Atrixtra)
What is an Emobolus?
Detached blood clot moving within the bloodstream.
What is the danger of emboli? what happens if the emboli lodges in a vessel?
Emboli occludes ARTERIAL vessels inhibiting blood flow. Loss of blood supply distal to the site of occlusion. Leads to tissue infarction (death of tissue due to lack of oxygen).
What are three examples of complications/deadly events that occur because of an embolus?
Myocardial Infarction (heart attack).
Ischemic stroke
Pulmonary emobolus (prohibits O2/CO2 exchange).
In four steps describe platelet activation to aggregation mechanism and role of thromboxane starting with the activation of platelets. (Arachidonic acid, Prostaglandin, COX1 are hints).
Activation of platelets (via vWf + exposed collagen) liberates arachidonic acid.
Arachidonic acid is converted to prostaglandin H2 via COX1
Prostoglandin H2 results in Thromboxane A2.
Thromboxane A2 promotes platelet aggregation.
How does Aspirin (ASA) inhibit platelet aggregation? How long is the platelet impaired?
ASA IRREVERSIBLY inhibits the conversion of arachidonic acid to Thromboxane A2 by the INHIBITION OF COX1.

Platelet Aggregation is IMPAIRED FOR THE LIFE of the platelet.
How does Aspirin affected the risk of thrombosis? platelet activity? How is bleeding time affected?
Risk of (arterial) thrombosis DECREASED.
Platelet activity DECREASED
Bleeding time INCREASED up to 10 minutes.
What is the mechanism of NSAIDs other than Aspirin?
non-ASA NSAIDs REVERSIBLY inhibit the conversion of arachidonic acid to Thromboxane A2 by the inhibition of COX1.
With NSAIDs, How long is platelet activity affected?
Platelet activity is inhibited for 3-4 half lives of the specific NSAIDs (this is when the effect is functionally gone). At this point platelet activity is functionally restored. Different NSAIDs have different half lives.
What are five NSAID's that aren't ASA. What are their approximate half lives? After 4 half lives how much drug is eliminated?
4 half lives = 94% drug elimination.
Ibuprofen 2 hrs
Naproxen sodium (Alieve) 15 hrs
Ketoprofen 2 hrs
Flurbiprofen 7 hrs.
Diclofenac 2.5 hrs
NSAIDs should not be taken within how many hours of ASA?
Why?
2 hours
Not really sure, maybe because they interfere with ASA inhibition of platelets.
Is COX1 or COX2 critical to Thromboxane A2 synthesis?
COX1
Do COX2 inhibitors interfere with ASA inhibition of platelets? What's a cox2 inhibitor?
NO
Celebrex
What are 3 Thienopyridine drugs? Are they anti-platelet or anti-coagulation?
Anti-Platelet drugs
Clopidogrel (Plavix)
Prasugrel (Effient)
Ticlopidine (Ticlid) rarely used.
What's the mechanism of Thienopyridines?
IRREVERSIBLY inhibit ADP chemoreceptors (P2Y-12) on platelet cell membranes. Inhibits platelet AGGREGATION by blocking GPIIb/IIIa pathway.
What type of drug is Clopidogel? half life? any reversal drugs? complications?
Clopidogrel (Plavix) is a Thienopyridine. It's a prodrug requiring metabolism. Has a very long half life. No antidote for prolonged bleeding.

Complications: Thrombocytopenic purpura, neutropenia.
What type of drug is Prasugrel (Effient)? How does it compare to clopidogrel (Plavix)?
Theinopyridine. Newer anti-platelet drug. Prodrug.

Action is more rapid and consistent than clopidogrel (Plavix). Also lower incidence of ischemia but may have increased risk of fatal bleeding.
What are anti-platelet drugs such as ASA and Theinopyridines used to manage?
Acute coronary syndrome
Percutaneous coronary intervention such as angioplasty and stent placement.
Coronary Artery disease
Peripheral vascular disease,
Cardio vascular disease
post-stent placement (all arterial thrombi diseases)
Should a patient continue anti-platelet drugs when receiving dental care?
ASA and Thienopyridines should be maintained! especially for Drug Elutingn Stents!!! (DES)
Thrombin is aka what factor?
Thrombin converts what to what?
Thrombin = Factor IIa
Thrombin (IIa) facilitates the conversion of Fibrinogen (I) to Fibrin.
What is Fibrin?
Fibrin is a glycoprotein which forms a "Fishnet" clot matrix by cross linking platelets.
The Intrinsic system is activated by what factor? What test is used to evaluate it? What two drugs work on the intrinsic system?
Factor XII activates it.
evaluated by PTT
Heparin and LMWH
What is the Mechanism of action of Heparin/LMWH?
Heparin and LMWH INHIBIT Thrombin. Combines with anti-thrombin III to change conformation of anti-thrombin III. Anti-ThrombinIII then INHIBITS factor Xa and Thrombin (IIa).
What are the important factors of the extrinsic system?
How is it evaluated?
What drug works on it?
Factors VII, X, II (prothrombin)
PT = INR
Warfarin = Coumadin
What are two other drugs (besides heparin and LMWH) that are thrombin inhibitors?
Dabigatran (Pradaxa): Direct thrombin inhibitor.

Fondaparinux (Arixtra): increases the ability of Anti-Thrombin to inactivate Factor Xa
What are the Vitamin K dependent coagulation factors?
II, VII, X, IX
II = prothrombin
X = common pathway factor
What are the differences b/w Heparin and LMWH?
Heparin: Mixture of straight chain GAG's, wide range of MWs

LMWH: subset of Heparin molecules (MWs < 6000)
What's the big picture goal of heparin and LMWH? What are they used to prevent? What are they used to treat?
They limit the expansion of the Thrombus by preventing Fibrin formation! Employed to prevent venous thrombosis, rethrombosis. Treatment/prevent thrombotic disease: DVT, PE, Acute MI (angioplasty, stent placement).
Heparin:
How is it administered?
Origin?
Mech?
Anticoagulation?
What test is used to evaluate?
Whereis it used?
Half life?
Bridge therapy?
What drug is used to reverse it's effects?
Complications?
Injectable, rapid acing
Bovine, porcine origin (possible hypersensitivity).
Combines with ATIII, changes conformation and inhibits Factor Xa and Thrombin (IIa)
Variable anticoagulation.
Monitor/adjust via a PTT
Used in hospital settings.
Very short half life: Inhances peri-operative clotting.
May be used for "bridge therapy" for warfarin = coumadin
Reversed rapidly by protamine sulfate.
Complications: thrombocytopenia, undesired bleeding
LMWH. Trade names?
Mech?
Doses?
onset?
Predictable?
When is it used?
Bridge therapy?
Enoxaprin = Lovenox
Complexes with ATIII, inactivates Xa (does not bind aggressively to thrombin IIa)
usually dosed once or twice per day. 1.5mg/kg
More predictable anticoagulation vs heparin.
Weight adjusted dose.
Used on outpatient basis after orthopedic surgery.
May be used as bridge therapy for warfarin.
Dabigantran (Pradaxa)
Mechanism?
Influenced by what physiological system?
What condition is treated with it?
Protocol with dental surgery?
Direct thrombin inhibitor: inhibits free and bound thrombin.
Influenced by kidney function: creatine clearance.
Indicated for A-fib.
Usually, two doses should be with held prior to dent-alveolar surgery, restart after adequate hemostasis, no lab test.
Fondaparinux (Atrixtra)
Mechanism?
Reversal agent?
When is it used?
Protocol with dental surgery?
Binds to Anti thrombin with high affinity, causes a conformational change in AT which significantly increases the ability of Anti-thrombin to inactivate Factor Xa.
No reversal agent.
Typically used following lower extremity orthopedic surgery for 6-12 weeks.
Elective dental care usually deferred.
What is the mechanism of Coumadin/Warfarin?
Inhibits Vitamin K epoxide reductase, therefore Vitamin K is NOT regenerated which is needed for factors II, VII, X, and IX and coagulation is retarded.
How is warfarin/coumadin transported in the blood?
drug interactions?
How is coagulation levels tested?
Onset, full effect and offset times?
How is it's effects reversed?
Rapidly and completely absorbed. 99% bound to plasma albumin. May be displaced by other drugs or food with high vitamin K levels.
Evaluated by INR = PT
Onset = 8-12 hrs
Full effect = 2-4 days
Offset = 2-4 days
may be reversed with Vitamin K but this could take up to 24 hours.
How do you test the intrinsic/extrinsic system and what drugs are evaluated with these tests?
PTT: activated partial thromboplastin time. Normally 25-35 seconds. Evaluates the intrinsic system and activity of heparin/LMWH (II, X). Measures factors I, II, V, VIII, IX, X, XI, XII.

Prothrombin Time PT/INR evaluates the extrinsic system. normal 12-14 seconds. Evaluates activity of Warfarin/Coumadin (II, VII, IX, X)
What is INR?
How is it calculated?
International normalized raio. Used to compare PT from one lab to another.
INR = Patients PT/Mean lab PT adjusted by international sensitivity index.

With INR everyone speaks the "same language"
What drugs should you NOT prescribe with warfarin/coumadin?
ASA, SNSAIDs, propoxyphene.
Antifungal agents: fluconazole.
Cephalosporins, erythromycins, TCN, metronidazole, quinalones, sulfa drugs.
When on Warfarin/coumadin what should you prescribe your patients for post op pain? What should you not prescribe them?
Mild pain: acetaminophen
Severe pain: Vicodin (acetaminophen + opioid).
Do NOT perscribe ASA or NSAIDs due to effect on platelets.
What are two clot stabilizing drugs that retard fibrinolysis?
Aminocaproic acid = Amicar
Tranexamic acid = Cyclokapron
What is the mechanism of Aminocaproic acid/amicar?
Inhibits plasminogen activators and plasmin.
Orally administered prior to surgery and five days post op
Tranexamic acid/Cyclokapron, what is the mechanism?
Competitively inhibits plasminogen and directly inhibits plasmin.
Some patients have factor deficiency's. Specific factor replacements are available. What is used to treat vW disease?
Desmopressin (DDAVP)