This document discusses drugs used to treat angina pectoris. It begins by defining terms related to coronary artery disease and angina. It then describes various classes of antianginal drugs including nitrates, beta-blockers, calcium channel blockers, and piperazineacetamide. For each drug class, it discusses mechanisms of action, indications, pharmacokinetics, contraindications, adverse effects, drug interactions, and nursing considerations. The document also covers lipid-lowering agents including bile acid sequestrants, HMG-CoA reductase inhibitors, cholesterol absorption inhibitors, fibrates, and niacin. It provides details on the mechanisms, indications, and side effects of each lipid-lower
This document discusses drugs used to treat angina pectoris. It begins by defining terms related to coronary artery disease and angina. It then describes various classes of antianginal drugs including nitrates, beta-blockers, calcium channel blockers, and piperazineacetamide. For each drug class, it discusses mechanisms of action, indications, pharmacokinetics, contraindications, adverse effects, drug interactions, and nursing considerations. The document also covers lipid-lowering agents including bile acid sequestrants, HMG-CoA reductase inhibitors, cholesterol absorption inhibitors, fibrates, and niacin. It provides details on the mechanisms, indications, and side effects of each lipid-lower
This document discusses drugs used to treat angina pectoris. It begins by defining terms related to coronary artery disease and angina. It then describes various classes of antianginal drugs including nitrates, beta-blockers, calcium channel blockers, and piperazineacetamide. For each drug class, it discusses mechanisms of action, indications, pharmacokinetics, contraindications, adverse effects, drug interactions, and nursing considerations. The document also covers lipid-lowering agents including bile acid sequestrants, HMG-CoA reductase inhibitors, cholesterol absorption inhibitors, fibrates, and niacin. It provides details on the mechanisms, indications, and side effects of each lipid-lower
Terminology Angina pectoris – chest pain, caused by the imbalance between oxygen being supplied to the heart muscle and demand for oxygen by the heart muscle Atheroma – plaque in the endothelial lining of arteries Atherosclerosis – narrowing of the arteries caused by buildup of atheromas. Coronay Artery Disease – characterized by progressive narrowing of coronary arteries Myocardial Infarction – end result of vessel blockage in the heart, leads to ischemia and then necrosis of the area cut off from the blood supply. Stable Angina – pain due to imbalance of myocardial oxygen supply and demand that is relieved by rest. Unstable Angina - pain due to imbalance of myocardial oxygen supply and demand that persists even at rest. Coronary Artery Disease Coronary Artery Disease Antianginal Agents Helps restore the appropriate supply and demand ratio in oxygen delivery to the myocardium when rest is not enough. Improve blood flow through the following mechanisms: Dilate blood vessels – increase the supply of oxygen Decrease the work of the heart - decrease the demand of oxygen Antianginal Agents Nitrates
Beta-Blockers
Calcium Channel Blockers
Piperazineacetamide Nitrates Short Acting – Nitroglycerine Long Acting – Isosorbide Dinitrate (Isordil) and Isosorbide Mononitrate (Imdur) Mechanism of Action Relax and Dilate veins, arteries and capillaries allowing increase blood flow through the coronary vessels. Dilates the Veins more than the Arteries Dilation of arteries leads to a decrease in SVR thus leading to a drop in blood pressure thus decreasing the afterload Dilation of veins also leads to pooling of blood in veins and capillaries decreasing preload Indication Prevention and Treatment of attacks of Angina Pectoris Pharmacokinetics: Nitroglycerine Sublingual Check under the tongue Have the patient take a sip of water before taking the medication Caution patient not to swallow the drug Encourage the patient to alternate sides of the tongue Transbuccal Check the inside of the cheeks Caution the patient not to swallow the drug Transdermal When applying a new patch, always clean the are every after removing the old transdermal patch. Intravenous Amyl Nitrate – inhalational ISDN/ISMN – oral forms Contraindications and Cautions Allergy to nitrates Severe anemia – decrease in cardiac output could be detrimental in patients who already has a decrease ability to deliver oxygen Head trauma/cerebral hemorrhage – relaxation of blood vessels could further aggravate the bleeding Pregnancy and lactation Caution Hepatic and renal failure Hypotension/hypovolemia Conditions that limit cardiac output (e.g. cardiac tamponade) Adverse Events Adverse events are related to vasodilation CNS Headache, dizziness, and weakness GI Nausea, vomiting and incontinence Cardiovascular Hypotension, reflex tachycardia, syncope and antianginal Transdermal patch Contact dermatitis Local hypersensitivity reaction Clinically Important Drug-Drug Interaction Ergot derivatives – increases the risk of hypertension and decreased antianginal effect Heparin – decreases therapeutic effect of heparin Sildenafil – causes serious hypotension and cardiovascular events Nursing Consideration Assessment Assess for contraindications or cautions Perform physical assessment to establish baseline status before and after beginning therapy Skin inspection Assess the complaint of chest pain Assess the neurologic status Obtain ECG as ordered to evaluate the heart rate and rhythm Monitor laboratory results Nursing Consideration Nursing Diagnoses Decreased cardiac output related to vasodilation and hypotensive effects Risk for injury related to CNS or cardiovascular effects Ineffective tissue perfusion related to hypotension Deficient knowledge regarding the drug therapy Nursing Consideration Implementation Give sublingual preparations under the tongue or in the buccal pouch end encourage the patient not to swallow. Ask the patient if the tablets fizzles or burns Instruct the patient that a sublingual dose may be repeated in 5 minutes if relief is not felt for a maximum of 3 doses Give sustained release form with water, caution not to chew or crush the drug Rotate the sites of topical forms to decrease the risk of skin abrasions and breakdown Make sure that the translingual spray is used under the tongue and not inhaled Beta-Blockers MOA: blocks the stimulatory effects of the sympathetic nervous system this results in the following: Decrease in the excitability of heart Decrease in the cardiac output Decrease in the cardiac oxygen consumption Lowering of blood pressure Indications: Long term treatment of angina pectoris caused by atherosclerosis Used in combination with nitrates to increase exercise tolerance Calcium Channel Blockers MOA: inhibit the movement of calcium ion across the membranes of myocardial and arterial muscle cells, altering the action potential and blocking muscle cell contraction. Decreases the preload and afterload which decreases cardiac workload and decrease oxygen consumption Indication: Treatment of prinzmetal angina Treatment for chronic angina, effort associated angina and hypertension Lipid-Lowering Agents ROGER JOSEPH II R. JECINO, R.N., M.D. Bile Acid Sequestrants Drugs: Cholestyramine, colestipol, colesevelam Mechanism of action Bind with bile acids in the intestine to form an insoluble complex that is then excreted in the feces. Indications Used to reduce serum cholesterol in patients with primary hypercholesterolemia (manifested by high cholesterol and high LDL) Pharmacokinetics Not absorbed systematically Act while in the intestine and excreted directly in the feces Bile Acid Sequestrants Contraindications and cautions: Hypersensitivity reaction Complete biliary obstruction Abnormal intestinal function Pregnancy and lactation Adverse effect Vitamin A and D deficiency Increased bleeding tendency due to decrease absorption of vitamin K Drug to drug interaction Bile acid sequestrants decreases or delays the absorption of thiazide, digoxin, warfarin, thyroid hormones, and corticosteroids. If to be taken should be 1 hour before or 4-6 after the BAS. HMG-CoA Reductase Inhibitors Drugs: Simvastatin, Atorbastatin, Rosuvastatin MOA: Blocks the early rate limiting enzyme (HMG CoA Reductase) in the synthesis of cellular cholesterol Indications: For patients with high cholesterol and LDL Prevention of Myocardial Infarction in patient with multiple risk factors Pharmacokinetics: Absorbed in the GI tract and undergo first pass metabolism Excreted through the feces and urine Effective at night Crosses the placenta and is present in milk HMG-CoA Reductase Inhibitors Contraindication and Cautions: Hypersensitivity
Active liver disease and alcohol liver disease
Pregnancy and lactation Adverse Events: Most common: Flatulence, abdominal pain, cramps, nausea, vomiting and constipation Increased concentrations of liver enzymes Acute Liver Failure Rhabdomyolysis Cholesterol Absorption Inhibitors Drugs: ezetimibe MOA: decrease the absorption of dietary cholesterol from the brush border of the small intestine Indication: adjunct to diet and exercise to lower cholesterol Pharmacokinetics: absorbed well after oral administration, metabolized in the liver and small intestine and excreted in the urine and feces Contraindications: hypersensitivity reaction, when used with statin it should not be used during pregnancy and lactation or with severe liver disease Adverse effect: Mild abdominal pain and diarrhea – most common Fibrates Drugs: Fenofibrate and Gemfibrozil MOA: stimulate the breakdown of lipoproteins from the tissue and their removal in the plasma. Fenofibrate – inhibits the triglyceride synthesis in the liver, resulting in reduction of LDL Indication: used for patient with high Triglyceride Gemfibrozil – inhibits peripheral breakdown of lipids, Indication: used for patient with high triglyceride and LDL and also in patient with low HDL. Vitamin B3 (Niacin) Inhibits the release of free fatty acids from adipose tissue, increases the rate of triglyceride removal from the plasma. Reduces LDL and Triglyceride levels Increases HDL levels Decreases the levels of apoprotein Side effect: cutaneous flushing, nausea and abdominal pain Increases uric acid and may predispose patient to GOUT Thank You
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