Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
38 Cards in this Set
- Front
- Back
|
Mechanism of action of aspirin
|
• Aspirin is an NSAID
• Aspirin irreversibly inhibits the enzyme, cyclooxygenase (COX) which, in platelets, prevents conversion of arachidonic acid to thromboxane A2, a stimulator of platelet aggregation • Why is low dose aspirin (≤ 325mg) a better antiplatelet than high-dose (anti-inflammatory doses of 650mg) aspirin? Higher doses inhibit not only COX but also inhibit a naturally occurring endogenous antiplatelet substance, prostacyclin (PGI2). Low-dose aspirin does not inhibit PGI2, thus the antiplatelet effects of low dose aspirin are even stronger than high-dose • Antiplatelet effects last for the life of the platelet (5 – 7 days) |
|
|
Therapeutic Uses of aspirin
|
• Common cardiac dose uses: primary prevention of stroke/MI, acute MI (chew & swallow), post-acute coronary syndrome (ACS), post-stent placement, secondary stroke prevention
Drug Interactions • Risk of GI ulceration/bleeding increases when combined with other NSAIDs • NSAIDs may block antiplatelet benefits of aspirin. This may be avoided by changing the administration timing or changing NSAIDs (must consult prescriber) • Risk of bleeding increases when combined with other antiplatelet drugs or anticoagulants. Risk of serious bleeding is 20% higher with combination ADP inhibitor + aspirin vs. aspirin alone |
|
|
3 types of ADP-inhibitor
|
clopidrogrel (Plavix®) (kloh PID oh grel)
prasugrel (Effient®) (PRA soo grel) ticagrelor (Brilinta®) (tye KA grel or) |
|
|
Mechanism of action of ADP- inhibitor
|
Mechanism of Action & Therapeutic Uses
• Platelet activation involves production of several substances, including adenosine diphosphate (ADP). These drugs inhibit ADP • More “powerful” than aspirin • Common uses include: post-acute coronary syndrome (ACS), post-stent placement, peripheral artery disease (PAD), & secondary stroke prevention |
|
|
Adverse Effects of ADP-inhibitors
|
Adverse Effects
• Does not directly cause GI bleeding like aspirin can; however, if GI bleeding does occur, the risk of death is just as high • Excessive bleeding |
|
|
Drug interaction of ADP-inhibitors
|
Drug Interactions
• Additive effect with other antiplatelet & anticoagulant drugs • NSAIDs increase the risk of serious GI ulceration/bleeding |
|
|
Discuss the therapeutic uses and drug interaction of Aggrenox
|
-Dipyridamole + aspirin (Aggrenox®) oral (dye peer ID a mole)
-FDA approved for secondary stroke prophylaxis -• Risk of GI ulceration/bleeding increases when combined with other NSAIDs • NSAIDs may block antiplatelet benefits of aspirin. This may be avoided by changing the administration timing or changing NSAIDs (must consult prescriber) • Risk of bleeding increases when combined with other antiplatelet drugs or anticoagulants. Risk of serious bleeding is 20% higher with combination ADP inhibitor + aspirin vs. aspirin alone |
|
|
List common triggers to platelet activation
|
Triggers of platelet activation: collagen (damaged tissue), epinephrine, thrombin (coagulation cascade), thromboxane A2 (arachidonic acid cascade), adenosine diphosphate (platelets
|
|
|
List the 3 doses of aspirin that are considered to be low dose or cardiac dose
|
81 mg baby aspirin, 162 mg Halfprin, 325 mg regular strength
|
|
|
Discuss the role of acid reducers and PPIs taken with antiplatelet drugs.
|
Acid reducers may be added to prevent GI ulcers: PPIs such as omeprazole (Prilosec) or acid-blockers such as ranitidine (Zantac)
|
|
|
List the adverse effects associated with cardiac dose aspirin and how these differ from higher dose aspirin (e.g. 650mg doses 4 times daily).
|
Cardiac dose ADRs: Upset stomach, GI discomfort, GI ulcers
Higher dose ADRs: Increased blood pressure, fluid retention, renal impairment |
|
|
Identify patients likely to be taking antiplatelet therapy.
|
This is a careful decision made between the prescriber & patient, taking into account the patient’s specific CV risk factors as well as GI bleed risk factors
-Antiplatelet therapy is not for everyone! Although aspirin is OTC, patients should not start taking it on their own without checking with their prescriber |
|
|
Primary Prvention
|
patients who have not yet experienced a stroke/MI, but are at increased risk. In these patients we are trying to prevent the first/primary event from occurring.
|
|
|
Secondary Prevention
|
patients who have already experienced issues with excessive clotting, stroke, TIA, MI, or angina. In these patients we are trying to prevent second events.
Some patients will take dual antiplatelet therapy: aspirin + an ADP inhibitor |
|
|
Discuss the general pathophysiology of venous thromboembolism.
|
• Stasis of blood; vessel damage; increased blood coagulability
• Platelet aggregation; platelet/fibrin clot formation • Inflammation is triggered: tenderness, swelling, redness • Pieces of thrombus may break loose & travel through circulation – emboli • Fibroblasts eventually invade the thrombus, scarring vein wall & destroying valves; valve damage is usually permanent & affects directional blood flow Post-thrombotic syndrome: long-term problems with leg swelling, aching, cramping, heaviness, itching/tingling, varicose veins, skin discoloration, leg ulcers, & reduced quality of life |
|
|
Discuss symptoms and complications of post-thrombotic syndrome
|
Post-thrombotic syndrome: long-term problems with leg swelling, aching, cramping, heaviness, itching/tingling, varicose veins, skin discoloration, leg ulcers, & reduced quality of life
|
|
|
Describe non-pharmacological preventive measures against VTE
|
• With documented DVT, mobilization and exercise of the lower extremity should be withheld 48 to 72 hours until appropriate medical therapy is implemented
• Early mobilization and passive exercise should be initiated as soon as the patient is medically stable following major medical illness or vascular injury. Therapy can begin in the intensive care unit • In high-risk individuals, patients, family members, and other caregivers should be educated in the recognition and prevention of DVT • Elastic compression stockings + mobilization for very low risk patients • Intermittent pneumatic compression devices – not as effective as anticoagulants; used when heparins are contraindicated or with heparins in high risk patients |
|
|
List the relative effectiveness of compression stockings vs. ICDs vs. heparins.
|
• Elastic compression stockings + mobilization for very low risk patients
• Intermittent pneumatic compression devices – not as effective as anticoagulants; used when heparins are contraindicated or with heparins in high risk patients |
|
|
List the signs of DVT
|
Pain, tenderness, and/or heaviness of the affected extremity
• Unilateral edema, warmth, and/or redness of calf or thigh • Increase in the venous pattern of collateral veins in the affected extremity • Low-grade fever of unknown origin |
|
|
List the signs of PE
|
Chest pain (often worse when taking a breath)
• Breathlessness • Apprehension (panic, feeling of doom) • Fever • Cough (dry cough or cough with blood) |
|
|
List the therapeutic uses of the heparins.
|
Prophylaxis of VTE: Low doses administered subcutaneously once or twice daily
-Treatment: Heparins do not break up the clot. Heparin blocks clotting so the body is able to effectively dissolve the clot on its own. Heparins are used to treat DVT, PE, ACS (MI & unstable angina), & acute ischemic stroke. UFH is dosed as continuous infusion IV. LMWH is dosed subcutaneously but at higher doses than are used for prophylaxis |
|
|
List the laboratory value monitored during heparin therapy and the purpose of monitoring CBC during therapy with heparin or low molecular weight heparin
|
Complete blood cell count (CBC) is monitored for signs of bleeding and HIT
-Activated partial thromboplastin time (aPTT) is monitored for continuous infusion UFH. aPTT measures the length of time it takes to form a clot. aPTT is not required for LMWH |
|
|
List the adverse effects associated w/ heparins
|
Excessive bleeding
-Heparin-associated thrombocytopenia (HAT) is a benign, transient, and mild phenomena, generally occurring within the first few days of treatment and recovers quickly -Heparin-induced thrombocytopenia (HIT) is a serious drug-induced auto-immune response requiring immediate discontinuation of the heparin -HIT & HAT are less likely to occur with LMWH |
|
|
List the risk factors for major bleeding during anticoagulation therapy.
|
Anticoagulation intensity (e.g. INR > 4.0)
-First few days & weeks of therapy initiation -Unexpected anticoagulant response -Age > 65 years old -Concurrent antiplatelet drug use -Concurrent NSAID use -History of gastrointestinal bleeding -Recent surgery/trauma to eye, brain, or spine -High risk for fall/trauma -Heavy alcohol use -Chronic renal failure |
|
|
List the contraindications against anticoagulation therapy.
|
Active bleeding; active GI ulcers
-Hemophilia or other hemorrhagic tendencies Severe liver disease -Severe thrombocytopenia Malignant (uncontrolled & very high) HTN |
|
|
List the mechanism of action of warfarin
|
• Vitamin K is required for the liver to synthesize many of the clotting factors involved in the coagulation cascade (factors II, VII, IX, X & protein C & S)
• Warfarin alters the structure of these vitamin K dependent clotting factors making them less effective. • It acts as a Vitamin K antagonist/blocker • Therapeutic window is very, very narrow |
|
|
List the therapeutic uses of warfarin
|
Prophylaxis against DVT/PE in patients with
• Recent DVT or PE x a few months • Recent large anterior MI x a few months • Major surgeries (e.g. coronary artery bypass, orthopedic) x a few months • Chronic atrial fibrillation • Tissue valves or valvular disease • Mechanical prosthetic valves |
|
|
List the adverse effects of warfarin
|
• Excessive minor & major bleeding
• GI: loss of appetite, N/V, stomach cramps, diarrhea • Warfarin-induced skin necrosis (purple toe syndrome) |
|
|
List the drug interactions of warfarin
|
• Many, many cytochrome p450 interactions & protein binding interactions
• NSAIDs are absolutely contraindicated with warfarin • Even cardiac dose aspirin should ONLY be taken if specifically instructed to do so by the prescriber • Vitamin K interactions are a concern. Interactions with vitamin K containing foods and vitamin K containing supplements. Some calcium / osteoporosis supplements contain vitamin K; green tea; green leafy vegetables |
|
|
List the antidotes for warfarin
|
• Vitamin K injection: phytonadione (Aquamephyton®) (fye toe na DYE one)
• Vitamin K oral: phytonadione (Mephyton®) • Onset of action is slow because body must make more clotting factors to reverse the bleeding • For immediate reversal fresh frozen plasma must be used (contains clotting factors) |
|
|
List foods rich in vitamin K and patient instructions for vitamin K in the diet.
|
Vitamin K in diet: avoid bingeing on foods high in vitamin K like green leafy vegetables. Patients do not have to avoid ALL foods that contain vitamin K. The key is to keep their intake of vitamin K containing foods relatively steady from day to day
|
|
|
List OTC products likely to contain “hidden” NSAIDs and/or vitamin K.
|
Do not use aspirin or other NSAIDs. Many cough & cold products contain aspirin and/or NSAIDs so patients should check labels of all OTC products carefully before use. Rarely a patient may be told by the prescriber to take low dose daily aspirin WITH the warfarin. As long as the prescriber is aware of the warfarin, it’s OK. Even in these cases patients should not take any more than 81 mg aspirin per day
|
|
|
Interpret the meaning of an elevated INR vs. a low INR.
|
High INR means blood has a high tendency of clotting
Low INR means blood has problems clotting |
|
|
Describe key concepts of patient instructions/education for persons taking warfarin.
|
Minimal alcohol, Do not take other NSAIDS, minimize Vitamin K consumption, avoid pregnancy
|
|
|
List the signs and symptoms of bleeding
|
-Signs & symptoms of bleeding: blood in urine or stools, blood in stools usually looks black/tarry rather than red, bloody nose, bruising, bleeding gums, cuts that will not stop bleeding. Patient should contact prescriber if any of these symptoms occur
|
|
|
List the signs and symptoms of clots
|
Signs & symptoms of clots: shortness of breath, chest pain, pain, tenderness, swelling in legs. Patient should contact prescriber if any of these symptoms occur
|
|
|
List the pain medications safe to take with warfarin and those that are contraindicated.
|
NSAIDS are a no no. Should not take more than 81 mg. Consult the DR.
|
|
|
30. Discuss differences between warfarin and the newer oral anticoagulants, dabigatran & rivaroxaban
|
Comparing warfarin to the newer oral anticoagulants
• Warfarin drug cost is less expensive, but must monitor INR • Newer oral anticoagulants do not have vitamin K interactions • All the oral anticoagulants have various drug interactions and narrow therapeutic windows |
