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What are the main components of a lipid panel blood work?
- Cholesterol
- LDLs
- HDLs
- VLDLs-Triglycerides
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What are the drugs associated with HMG-CoA reductase inhibitors?
"Statins" EX: Simvastatin (zocor)
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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.
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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.
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What drugs are Bile Acid-binding sequestrates?
Colesevelam (Welchol), cholestyramine (questran), colestipol (colestid)
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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.
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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.
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Describe antiplalets:
- Inhibit platelet aggregation.
- Used to treat and prevent ischemic events.
- Use to prevent clot formation.
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Describe thromboembolitic (thrombolytic):
- Degrade fibrin strands and used to help dissolve an existing clot.
- use when MI.
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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)
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what is a parental anticoagulant drug?
what is a oral one?
- Parental: Heparin and enoxaparin (low molecular weight)
- Oral: warfarin.
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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.
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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.
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What is the main drug use as an antiplalet?
Aspirin.
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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.
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What group is streptokinase (streptase) and Alteplase (tPa) in?
Thromboembolytic drugs (clot busters)
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What major AE of thromboembolytic drugs?
- Bleeding.
- hypotension.
- fever.
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