Cardiac 4 & 5.txt

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  1. What are the main components of a lipid panel blood work?
    • Cholesterol
    • LDLs
    • HDLs
    • VLDLs-Triglycerides
  2. What are the drugs associated with HMG-CoA reductase inhibitors?
    "Statins" EX: Simvastatin (zocor)
  3. What is Atorvastatin (lipitor) MA? TU? AE? Dosing?
    • MA: Most effective drugs to lowering LDL. Reduction of LDL cholesterol. Elevation of HDL cholesterol. Reduction of triglyceride levels. Increased bone formation.
    • TU: Hypercholesterolemia. Primary and secondary prevention of CV events. Post MI therapy. Diabetes.
    • AE: Common : headaches, rash, GI disturbances (diarrhea, vomiting, etc). Rare: Myopathy/ rhabdomyolysis, hepatotoxicity, Peripheral neuropathy. May be some connection with Parkinson’s disease.
    • Dosing: Once a day, at night bc endogenous cholesterol synthesis increases at night.
  4. What are Nicotinic Acid (Niacin) MA? TU? AE?
    • MA: Effect on plasma lipoproteins. Reduces LDL and triglycerides. Increases HDL levels more effectively than any other drug. Decreases production of VLDLs.
    • TU: It decreases production of LDLs and VLDLs! which is the most important part.
    • AE: Skin (flushing - could be pretreat it w aspirin, and could be reduced with SR niacin) GI Hepatotoxicity (most likely slo-niacin) Hyperglycemia Gouty arthritis.
  5. What drugs are Bile Acid-binding sequestrates?
    Colesevelam (Welchol), cholestyramine (questran), colestipol (colestid)
  6. What are Colesevelam (welchol) MA? TU? AE?
    • MA: Reduction in LDL cholesterol by increasing LDL receptors on hepatocytes. Increase VLDLs (Tryglicerides) levels in some pts. Prevents reabsorption of bile acids.
    • TU: Reduces LDL cholesterol ( in junction with low-cholesterol diet and excersice) Controls hyperglycemia in persons with diabetes.
    • AE: constipation.
  7. Describe anticoagulants:
    • interfere with clotting factors in the clotting cascade.
    • Therapy is primarily prophylactic.
    • Prevent formation of new clots and extension of clots already present.
    • They do not dissolve existing clots.
    • Widely used in thrombotic disorders.
    • there are 2 types: Parental and Oral.
  8. Describe antiplalets:
    • Inhibit platelet aggregation.
    • Used to treat and prevent ischemic events.
    • Use to prevent clot formation.
  9. Describe thromboembolitic (thrombolytic):
    • Degrade fibrin strands and used to help dissolve an existing clot.
    • use when MI.
  10. What is heparin's MA? TU? AE? contraindications? antidote? labs?
    • MA: Enhances antithrombin Rapid-acting anticoaguant Administered by injection only (IV, or subQ)
    • TU: Preferred when pregnancy and when rapid anticoagulancy is required. PE (pulmonary embolism). Stroke evolving.  Massive deep venous thrombosis (DVT) Open-heart surgery. Renal Dialysis. Low-dose therapy postoperatively. Adjunct to thrombolytic therapy.
    • Contraindications: Thrombocytopenia. Uncontrollable bleeding. During and immediately after surgery of the eye, brain, or spinal cord.
    • Antidote: Protamine Sulfate.
    • Labs: aPTT (activated partial thromboplastin time)
  11. what is a parental anticoagulant drug?
    what is a oral one?
    • Parental: Heparin and enoxaparin (low molecular weight)
    • Oral: warfarin.
  12. What is enoxaparin advantages? TU? MA? AE? and antidote?
    • Advantages: Less lab monitoring needed. Less likely to cause thrombocytopenia. Half life longer — permits once daily dosing. Does not cross placeneta. DOC — port op. Composed of shorter molecules than heparin.
    • TU: Prevention of DVT following surgery. Treatment of established DVT. Prevention of ischemic complications in patients with unstable angina, non-Q wave MI, and STEMI.
    • MA: SubQ. Dosage based on body weight. Costs more than unfractionated heparin. Does not required monitoring; Can be given at home.
    • AE: Bleeding (but less than w heparin). Blacks stool. Dizziness. Immune-mediated thrombocytopenia. Severe neurologic injury for patients undergoing spinal puncture or spinal epidural anesthesia. Pruritis (itching)
    • Antidote: Protamine sulfate.
  13. what are Warfarin's CU? TU? AE? DI? Labs? antidote?
    • CU: Oral anticoagulant with delayed onset. blocks the biosynthesis of factor VII, IX, X and prothombin.
    • TU: Not useful in emergencies. Long-term prophylaxis of thrombosis (PE, thromboembolism, thrombosis)
    • AE: Hemorrhage (vitamine K for toxicity). Fetal hemorrhage and teratogenesis from use during pregnancy. Use during lactation. Black stool.
    • DI: Heparin. Aspirin. Acetaminophen. Drugs that increase anticoagulant effects. drugs that promote bleeding. drugs that decrease anticoagulant effects.
    • labs: Prothrombin time & (PT)INR
    • antidote: Vitamine K.
  14. What is the main drug use as an antiplalet?
  15. what is Aspirin's TU? AE?
    • TU: Ischemic stroke. TIA. Chronic stable angina. Unstable angina. Coronary stenting. Acute MI. Previous MI. Primary prevention of MI.
    • AE: Bledding. GI bleeding and hemorrhagic stroke. enteric-coated tables may not reduce the risk for GI bleeding.
  16. What group is streptokinase (streptase) and Alteplase (tPa) in?
    Thromboembolytic drugs (clot busters)
  17. What major AE of thromboembolytic drugs?
    • Bleeding.
    • hypotension.
    • fever.
Card Set:
Cardiac 4 & 5.txt
2014-10-01 01:08:56
cholesterol anticoagulants

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