Final Exam Flashcards - MI and Stroke
Myocardial Infarction (Heart Attack)
-Occurs when the blood supply to the heart is interrupted causing cell death
Stroke
-Occurs when brain cells are deprived of oxygen or are damaged by sudden bleeding into the brain
Pharmacotherapy For Stroke and MI
- Reduce formation of blood clots
- Control the buildup of lipids and plaque
Antithrombotics
- Drugs that control the rate of clot formation or cause clot dissolution
- Include: Antiplatelets, Anticoagulants, and thrombolytics
Antiplatelet Drugs
- Platelets cluster at the site of injury and stick to damaged cell wall
- Platelets are activated by natural substances in the blood
- Activated platelets attract more platelets to the region
- Fibrin combines with platelets to strengthen the clot
Aspirin MOA
- Blocks the COX enzyme which reuduces plaque formation
- Inhibits platelet aggregation
abciximab/tirofiban/eptifbatide MOA
-Blocks the final pathway of platelet aggregation
ticlopidine & clopidogrel MOA
- Interferes with platelet adhesion and aggregation
- Decreases the concentration of fibrinogen
dipyridamole MOA
- Inhibits platalet aggregation
- Is a coronary vasodilator
Antiplatelet ADR’s
- Bleeding
- Skin rash or itching
- Stomach pain
- Pain at the injection site
Anticoagulants
- heparin is derived from pig intestines or cow lungs
- LMWHs are produced by separating heparin fragments
- There are oral and parenteral agents
Warfarin
- VERY NARROW TI
- Many drug and dietary interactions
- alcohol, cranberry, and grapefruit decrease metabolism
- Vitamin K decreases anticoagulant activity or warfarin and is the antidote for overdose
Antiplatelet and Anticoagulant Tech Note!
- Antiplatelets should NOT be combined with anticoagulants without medical supervision
- Nonprescription drugs such as NSAIDS, vitamin supplements, and herbs can also cause interactions
Anticoagulants ADR’s
- Excess anticoagulation and bleeding
- Dizziness and fainting
- Irritation at injection site
- Rash or red spots on skin
- Bleeding of gums, nose, etc
Thrombolytics
- Dissolve blood clots
- Administered in early stages of stroke to open blood vessels to the brain
Hyperlipidemia
-Treatment of hyperlipidemia is a principal focus for prevention of cardiovascular disease. emphasis is on Reducing LDL levels and raising HDL levels
LDL
Promotes:
- Plaque buildup in arteries
- Atherothrombosis
- Vasoconstriction
HDL
- Reduces LDL-c
- Has protective anti-inflammatory properties
- Acts as an antioxidant
Antihyperlipidemics
Drug therapy can decrease LDL and triglycerides and increase HDL by:
- Interfering with cholesterol synthesis (Statins)
- Increasing elimination in bile (Bile acid sequestrants)
- Acting on LDL metabolism (fibrates)
HMG CoA Reductase Inhibitors (Statins)
- Common Ending: “statin”
- Inhibit cholesterol synthesis
- Decrease LDL clearance and have anti-inflammatory action
- Usually dosed at bedtime
- Major grapefruit interaction (atorvastatin, lovastatin, and simvastatin)
Statin ADR’s
- Myositosis
- Liver dysfunction
- Rhabdomyolisis
- Diarrhea
- Gas
- Headache
- Joint pain
- N/V
- Stomach pain
- Tiredness
Fibric Acid Derivatives (Fibrates)
- Increase clearance of the very low density lipoprotein (VLDL) so less is available to convert to LDL
- Less effective than statins
Bile Acid Sequestrants
- Promote intestinal clearance of cholesterol by fecal elimination
- Are drugs of choice in pregnancy
- Produce bloating and gas
- Should be administered at least 1 hour before or 4 hours after other medications
- Lower body levels of fat-soluble vitamins
Nicotinic Acid Derivatives
- Niacin is vitamin B3
- Niacin is much less effective than statins
- Niacin is MOST effective for increasing HDL
Cholesterol Absorption Inhibitors
-Prevents cholesterol absorption through intestinal villi
