Dipyramidole pharmacology (1)
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Dipyramidamole is a powerful coronary vasodilator that is no longer used due to its potential to cause coronary steal phenomenon. It dilates both large and small coronary vessels and abolishes autoregulation. Coronary steal phenomenon occurs when a coronary vasodilator is used in the setting of narrowed coronary arteries, shunting blood away from ischemic areas of the heart and worsening ischemia. While dipyramidamole has anti-platelet effects, it is not effective for angina due to the risk of coronary steal.
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Angina pectoris
Angina pectoris is caused by transient episodes of myocardial ischemia due to an imbalance in the myocardial oxygen supply-demand relationship. There are three main types of angina: stable angina, which is triggered by exertion and relieved by rest; unstable angina, which occurs at rest and is a medical emergency; and Prinzmetal angina, which occurs due to coronary artery spasm. Treatment strategies for angina include nitrates like nitroglycerin which relieve symptoms rapidly, calcium channel blockers which prevent calcium entry and relax blood vessels, beta blockers which reduce the heart's oxygen demand, and ranolazine which inhibits sodium channels to reduce the heart's work.
Critical Medications
This document provides summaries of common emergency medications used to treat critical patients. It lists indications, dosages, and considerations for oxygen, epinephrine, atropine, adenosine, amiodarone, dopamine, lidocaine, diltiazem, procainamide, nitroglycerine, magnesium sulfate, and calcium chloride. The document aims to describe the actions and importance of these frequently prescribed critical medications.
Chf ppn
Congestive heart failure is a condition where the heart cannot pump enough blood to meet the body's needs. It can be caused by impaired cardiac muscle contraction or an increased workload on the heart. There are two main types: systolic dysfunction where the weakened heart cannot contract properly, and diastolic dysfunction where the stiff heart cannot relax to allow chambers to fill with blood. Treatment involves drugs like diuretics, ACE inhibitors, beta-blockers, and vasodilators to reduce workload and improve pumping ability. Lifestyle changes like quitting smoking, weight control, exercise and medication adherence can help prevent disease progression.
Ranolazine
Ranolazine is a new antianginal drug that represents a new class of drugs. It partially inhibits fatty acid oxidation and shifts energy production to a more efficient carbohydrate oxidation during ischemia. It also inhibits late inward sodium currents, reducing calcium overload and improving diastolic function and myocardial perfusion. Ranolazine has been shown to reduce angina frequency and improve exercise ability with no effects on blood pressure or heart rate. Its benefits and mechanisms of action were discussed along with its indications, studies, and potential role in other conditions such as diabetes and cardioplegia.
Starling Case Report
The treatment for Mr. Starling's congestive heart failure condition included furosemide to reduce edema, captopril to decrease blood pressure, intravenous fluids to increase blood pressure, and dobutamine to increase contractility. While these treatments provided some improvement, his cardiac output was not improved so he was evaluated for cardiac transplantation. He ultimately received a heart transplant which involved removing his failing heart and implanting a donor heart to treat his end stage heart failure.
Diuretics, cardiovascular drugs, antiplatelets n anticoagulant.
The document discusses the sites of action and mechanisms of various classes of diuretic drugs. Osmotic diuretics like mannitol increase tubular lumen osmotic pressure, increasing water and electrolyte excretion. Carbonic anhydrase inhibitors reduce bicarbonate reabsorption and sodium-hydrogen exchange. Thiazide diuretics inhibit sodium-chloride symporters in distal convoluted tubules. Loop diuretics inhibit sodium-potassium-chloride symporters in the thick ascending limb of Henle's loop. Potassium-sparing diuretics inhibit sodium channels or aldosterone receptors to retain potassium while excreting sodium.
Antianginal drugs
Angina pectoris is a pain syndrome caused by an imbalance between myocardial oxygen supply and demand. There are three main types - stable angina, vasospastic angina, and unstable angina. Antianginal drugs work to reduce oxygen demand and increase supply. The main drug classes are organic nitrates, calcium channel blockers, and beta blockers. Nitrates like glyceryl trinitrate are rapidly converted to nitric oxide in smooth muscle cells, relaxing veins and arteries to decrease preload and afterload on the heart and increase blood flow to ischemic areas.
Calcium channel blockers (cc bs)
This document discusses several calcium channel blocker drugs including verapamil, bepridil, diltiazem, nifedipine, amlodipine, felodipine, nimodipine, and nicardipine. It describes the mechanism of action, uses, and key details about each drug for treating conditions like hypertension, angina, and arrhythmias by blocking calcium channels and relaxing blood vessels and heart muscle. The drugs discussed include phenylalkylamine, dihydropyridine, and benzothiazepine classes of calcium channel blockers.
Pharmacology of Anti platelet drugs
This document discusses antiplatelet drugs used to treat arterial and venous thrombosis. It describes the role of platelets in arterial thrombosis, triggered by disruption of atherosclerotic plaque. Common antiplatelet drugs discussed include aspirin, clopidogrel, prasugrel, ticlopidine, dipyridamole, and glycoprotein IIb/IIIa inhibitors like abciximab and tirofiban. Their mechanisms of action, indications, and side effects are summarized. Clopidogrel resistance due to genetic factors is also mentioned.
Vasodilators
The document summarizes various vasodilator drugs including hydralazine, minoxidil, diazoxide, and sodium nitroprusside. It discusses the pharmacokinetics, pharmacodynamics, indications, contraindications and adverse effects of each drug. The drugs act by relaxing vascular smooth muscles through different mechanisms like opening potassium channels, causing vasodilation and reducing blood pressure and peripheral resistance. They may cause compensatory responses like increased heart rate and are often used with other drugs like beta blockers and diuretics.
Pharma seminar new version
The document discusses various drugs used to treat angina pectoris and myocardial infarction. It describes the classes of drugs which include nitrates, beta blockers, calcium channel blockers, nicorandil, aspirin, ACE inhibitors, and captopril. It explains the mechanisms of action, pharmacokinetics, indications, contraindications and side effects of these drug classes and examples like nitroglycerin, atenolol, nifedipine, verapamil, aspirin, and captopril.
Antihypertensive
This document summarizes various classes of antihypertensive and antianginal drugs. It describes 11 classes of antihypertensive drugs including diuretics, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, beta blockers, and others. It also describes 5 classes of antianginal drugs including nitrates, beta blockers, calcium channel blockers, potassium channel openers, and others. Specific drugs are provided within each class with details on mechanisms of action, indications, dosages, and side effects.
Antianginals
This document discusses antianginal drugs used to treat angina pectoris. It defines angina and describes different types. Antianginal drugs work by increasing myocardial oxygen supply or decreasing demand. Nitrates and calcium channel blockers increase supply by dilating coronary arteries. Beta blockers decrease demand by lowering heart rate and contractility. Combination therapy using these classes is common. The document also discusses mechanisms, administration, effects, and side effects of these major antianginal drugs.
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ANTI-ULCER DRUGS
PPIs have a short plasma half-life of around 1-2 hours, but they irreversibly inhibit the proton pump (H+/K+ ATPase enzyme) located in the parietal cells of the stomach. While the plasma concentration of the PPI falls quickly, the inhibition of acid production lasts much longer, up to 24 hours, because it takes time for new proton pumps to be synthesized to replace those that have been inhibited. This prolonged acid inhibition despite the short plasma half-life is why PPIs can be administered once daily to effectively reduce acid production over 24 hours.
Herbal drug technology
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Herbal drug technology unit 1
This document defines key terms related to herbal medicines and describes herbal materials, preparations, and products. It defines an herb as a plant used for medicinal purposes. Herbal medicines use plants to treat or prevent illness. Herbal medicinal products contain exclusively herbal substances or preparations as the active ingredient. Herbal preparations, such as extracts or tinctures, are the basis for finished herbal products and are produced through various extraction or processing methods. Finished herbal products consist of one or more herbal preparations from one or more plant sources, with or without additional excipients. The document also discusses good agricultural practices for cultivating medicinal plants, including organic farming and pest management techniques.
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Hiptage presentation for pharmacognosy and phytochemistry
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iron preparation
This document discusses iron and iron deficiency. It provides information on:
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3. Oral iron is usually sufficient to treat iron deficiency anemia, though parenteral iron may be needed in cases of malabsorption or intolerance. Different oral and parenteral iron preparations are available.
corticosteroid drugs and its uses
Corticosteroids are steroid hormones produced in the adrenal cortex. There are two main types: glucocorticoids which help regulate metabolism and mineralocorticoids which regulate salt and water balance. In 1949, cortisone was discovered to help treat rheumatoid arthritis, leading researchers like Hench, Kendall, and Reichstein to win the Nobel Prize for their work on corticosteroid hormones. Since then, many synthetic corticosteroids have been developed with varying durations of action and potencies. Corticosteroids have wide-ranging anti-inflammatory and immunosuppressive effects useful for treating many conditions.
Gastric proton pump inhibitor
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Anti-diabetic drugs with structures and uses
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Anticancer agents in medicinal chemistry
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Oral and injectable contraceptive steroids
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Treatment of gout
This document discusses drugs used to treat gout. It begins by describing gout as a metabolic disorder characterized by high uric acid levels in the blood. It then discusses drugs to treat acute gout attacks such as NSAIDs, colchicine, and corticosteroids. It also discusses drugs to treat chronic gout and prevent future attacks, including allopurinol, probenecid, and newer drugs. It notes complications if gout is not properly treated and measures for prophylaxis such as urate-lowering drugs and lifestyle changes.
Bioassay vasopressin digitalis ACTH
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Processing problems in tablet manufacturing
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Warfarin
Warfarin is an oral anticoagulant that prevents blood clotting by inhibiting vitamin K, which is necessary for the production of various clotting factors. It is commonly used to prevent potentially life-threatening conditions such as deep vein thrombosis, pulmonary embolism, myocardial infarction, and stroke. As an oral coumarin anticoagulant, warfarin works by antagonizing vitamin K to control and prevent thromboembolic disorders.
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Dipyramidole pharmacology (1)
- 2. Dipyramidamole Powerful coronary vasodilator Obsolete – not used these days It dilates both conducting vessels & resistance vessels and abolishes auto regulation. However, it is not effective in angina because of Coronary steal phenomenon.
- 3. CORONARY STEAL PHENOMENON Coronary steal is a phenomenon where an alteration of circulation patterns leads to a reduction in the blood flow directed to the coronary circulation. It is caused when there is narrowing of the coronary arteries and a coronary vasodilator is used – "stealing" blood away from those parts of the heart. This happens as a result of the narrowed coronary arteries being always maximally dilated to compensate for the decreased upstream blood supply. Thus, dilating the resistance vessels in the coronary circulation causes blood to be shunted away from the coronary vessels supplying the ischemic zones, creating more ischemia..
- 4. Uses
- 5. MECHANISM OF ACTION Dipyridamole likely inhibits both adenosine deaminase and phosphodiesterase, preventing the degradation of cAMP, an inhibitor of platelet function. This elevation in cAMP blocks the release of arachidonic acid from membrane phospholipids and reduces thromboxane A2 activity. Dipyridamole also directly stimulates the release of prostacyclin, which induces adenylate cyclase activity, thereby raising the intraplatelet concentration of cAMP and further inhibiting platelet aggregation.
- 7. Absorption 70% ( when given orally ) Metabolism Dipyridamole is metabolized in the liver to the glucuronic acid conjugate and excreted with the bile. Half life 40 mins Excretion Through urine Clearance - 2.3-3.5 mL/min/kg Pharmacokinetics
- 8. Side effects Headache Diarrhoea Vomiting Flushing Rashes, itching Dizziness Uses Dipyramidamole has vasodilator & anti-platelet action. It is used in Post-MI & Post-stroke to prevent coronary & cerebral thrombosis. It is used to prevent blood clots after heart valve replacement.