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all drugs first test

All Drugs First Test

by irarachel, Nov. 2014

Subjects: Pharmacology

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95 Cards in this Set

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Acetylcholine	Direct cholinergic agonists via Muscarinic receptor . – Postoperative atony – Glaucoma
Metacholine	Direct cholinergic agonists via Muscarinic receptor . – Postoperative atony – Glaucoma
Carbachol	Direct cholinergic agonists via Muscarinic receptor . – Postoperative atony – Glaucoma
Betanechol	Direct cholinergic agonists via Muscarinic receptor . – Postoperative atony – Glaucoma
Pilocarpin	Direct cholinergic agonists via Muscarinic receptor . –ophthalmic solution to treat Glaucoma
Muscarin	Direct cholinergic agonists via Muscarinic receptor . – Glaucoma
Physostigmine	Indirect cholinergic agonist Reversible inhibitor of acetylcholinesterase Increasing Acetylcholine concentration in blood. . – Atony of Bladder and Intestine, – Glaucoma.
Neostigmine	Indirect cholinergic agonist Reversible inhibitor of acetylcholinesterase Increasing Acetylcholine concentration in blood. . – Myasthenia Gravis – Postoperative atony of intestine and bladder
Pyridostygmine	Indirect cholinergic agonist Reversible inhibitor of acetylcholinesterase Increasing Acetylcholine concentration in blood. – chronic Myasthenia Gravis
Edrophonium	Indirect cholinergic agonist Reversible inhibitor of acetylcholinesterase Increasing Acetylcholine concentration in blood.
Donepezil	Indirect cholinergic agonist Reversible inhibitor of acetylcholinesterase Increasing Acetylcholine concentration in blood. . – Supportive care of Alzheimer’s
Rivastigmine	Indirect cholinergic agonist Reversible inhibitor of acetylcholinesterase Increasing Acetylcholine concentration in blood. . – Supportive care of Alzheimer’s
Parathion	Indirect cholinergic agonist Irreversible inhibitor of Cholinesterases – Used in agriculture as insecticides
Malathion	Indirect cholinergic agonist Irreversible inhibitor of Cholinesterases – Used in agriculture as insecticides
Tabun	Indirect cholinergic agonist Irreversible inhibitor of Cholinesterases – Nerve gasses.
Soman	Indirect cholinergic agonist Irreversible inhibitor of Cholinesterases – Nerve gasses.
Atropine	Muscarinic Receptor Antagonist – Painful Spasms(biliary and renal colic pain) – Bradycardia & Block, – Parkinsons Disease, – Poisonings ( of muscarin & anticholinesterase) – in anesthesiology– Prevention of respiratory	tract secretions, bronchospasm,
Benzatropine	Muscarinic Receptor Antagonist – Parkinson disease
Scopolamine / Hyoscine	Muscarinic Receptor Antagonist – antiemetic agent – prevention of motion sickness
Adiphenine,	Muscarinic Receptor Antagonist – antispasmodics
Oxyphenonium	Muscarinic Receptor Antagonist – antispasmodics
Ipratropium bromide	Muscarinic Receptor Antagonist – Bronchoconstriction – patients with heart disease – patients who not tolerate beta 2 agonists
Oxybutynine	Muscarinic Receptor Antagonist – Urinary incontinence (infantile enuresis)
Pirenzepine	Muscarinic Receptor Antagonist – peptic ulcers
Unfractionated heparin (UFH) / HMW heparin	Indirect thrombin inhibitors Heparin binds to antithrombin III (AT–III) and activate it The activated AT–III then inactivates thrombin & Xa & (VII, IXa,XIa,XIIa). The rate of inactivation by AT–III increases 1000–fold due to the binding of heparin. – acute deep vein thromosis – pulmonary embolism – prevent postoperative venous theombosis – pregnant women with prosthetic hart valves or with venous thromboembolism – coronary artery rethrombosis after thrombolytic treatment – prevent thrombosis in extracorporeal divices
Enoxaparin	Indirect thrombin inhibitors Low–molecular–weight heparins (LMWH) binds to antithrombin III (AT–III) and activate it The activated AT–III then inactivates Xa The rate of inactivation by AT–III increases 1000–fold due to the binding of heparin. – acute deep vein thromosis – pulmonary embolism – prevent postoperative venous theombosis – pregnant women with prosthetic hart valves or with venous thromboembolism – coronary artery rethrombosis after	thrombolytic treatment – prevent thrombosis in extracorporeal divices
Dalteparin	Indirect thrombin inhibitors Low–molecular–weight heparins (LMWH) binds to antithrombin III (AT–III) and activate it The activated AT–III then inactivates Xa The rate of inactivation by AT–III increases 1000–fold due to the binding of heparin. – acute deep vein thromosis – pulmonary embolism – prevent postoperative venous theombosis – pregnant women with prosthetic hart valves or with venous thromboembolism – coronary artery rethrombosis after	thrombolytic treatment – prevent thrombosis in extracorporeal divices
Ardeparin	Indirect thrombin inhibitors Low–molecular–weight heparins (LMWH) binds to antithrombin III (AT–III) and activate it The activated AT–III then inactivates Xa The rate of inactivation by AT–III increases 1000–fold due to the binding of heparin. – acute deep vein thromosis – pulmonary embolism – prevent postoperative venous theombosis – pregnant women with prosthetic hart valves or with venous thromboembolism – coronary artery rethrombosis after	thrombolytic treatment – prevent thrombosis in extracorporeal divices
Nadroparin	Indirect thrombin inhibitors Low–molecular–weight heparins (LMWH) binds to antithrombin III (AT–III) and activate it The activated AT–III then inactivates Xa The rate of inactivation by AT–III increases 1000–fold due to the binding of heparin. – acute deep vein thromosis – pulmonary embolism – prevent postoperative venous theombosis – pregnant women with prosthetic hart valves or with venous thromboembolism – coronary artery rethrombosis after	thrombolytic treatment – prevent thrombosis in extracorporeal divices
Tinzaparin	Indirect thrombin inhibitors Low–molecular–weight heparins (LMWH) binds to antithrombin III (AT–III) and activate it The activated AT–III then inactivates Xa The rate of inactivation by AT–III increases 1000–fold due to the binding of heparin. – acute deep vein thromosis – pulmonary embolism – prevent postoperative venous theombosis – pregnant women with prosthetic hart valves or with venous thromboembolism – coronary artery rethrombosis after	thrombolytic treatment – prevent thrombosis in extracorporeal divices
Reviparin	Indirect thrombin inhibitors Low–molecular–weight heparins (LMWH) binds to antithrombin III (AT–III) and activate it The activated AT–III then inactivates Xa The rate of inactivation by AT–III increases 1000–fold due to the binding of heparin. – acute deep vein thromosis – pulmonary embolism – prevent postoperative venous theombosis – pregnant women with prosthetic hart valves or with venous thromboembolism – coronary artery rethrombosis after thrombolytic treatment – prevent thrombosis in extracorporeal divices
Hirudin	Direct acting thrombin inhibitors – blood coagulation disorders (varicose veins)
Lepirudin	Direct acting thrombin inhibitors – patients with HIT who require parental anticoagulant therapy. – acute coronary syndrom.
bivalirudin	Direct acting thrombin inhibitors – patients with HIT who require parental anticoagulant therapy. – acute coronary syndrom.
Argatroban	Direct acting thrombin inhibitors – prophylaxis and treatment of thrombosis in patients with heparin–induced thrombocytopenia (HIT)
Warfarin	Inhibits the synthesis of the active forms of: • vitamin K–dependent clotting factors: II, VII,	IX , X • protein C, protein S – prophylaxis of thrombosis and embolism in many disorders
Coumarin	Inhibits the synthesis of the active forms of: • vitamin K–dependent clotting factors: II, VII,	IX , X • protein C, protein S – prophylaxis of thrombosis and embolism in many disorders
Rivaroxaban	Directly inhibit X factor – prevent venus tromboembolism, after hip and knee surgery
Dabigatran	Direct inhibitor of II factor – prevent venus tromboembolism, after hip and knee surgery
Tissue plasminogen activator (tPA) / Alteplase	Dissolve blood clots by: Activat the conversion of plasminogen to plasmin Plasmin hydrolyzes Fibrin to Fibrin degradation products (FdP) – acute myocardial infarction (within 12h of onset). – Acute thrombotic stroke (within 3 h of onset) – – deep vein thrombosis – pulmonary embolus – acute arterial thromboembolism
Streptokinase (SK)	Dissolve blood clots by: Activat the conversion of plasminogen to plasmin Plasmin hydrolyzes Fibrin to Fibrin degradation products (FdP) – acute myocardial infarction (within 12h of onset). – Acute thrombotic stroke (within 3 h of onset) – – deep vein thrombosis – pulmonary embolus – acute arterial thromboembolism
Urokinase (UK)	Dissolve blood clots by: Activat the conversion of plasminogen to plasmin Plasmin hydrolyzes Fibrin to Fibrin degradation products (FdP) – acute myocardial infarction (within 12h of onset). – Acute thrombotic stroke (within 3 h of onset) – – deep vein thrombosis – pulmonary embolus – acute arterial thromboembolism
Aspirin	Irreversibly inhibits cyclooxygenase COX1 in platelets and thereby blocks the formation of thromboxane A2 – prophylactic treatment of transient cerebral ischemia. – reduce the incidence of recurrent myocardial infarction – decrease mortality in pre– and post myocardial infarct patients
Clopidogrel	ADP receptor inhibitors – patients in whom aspirin is not tolerated when – dual antiplatelet therapy is desirable
Ticlopidine	ADP receptor inhibitors – Patients in whom aspirin is not tolerated when – dual antiplatelet therapy is desirable
plasugrel	ADP receptor inhibitors – patients in whom aspirin is not tolerated when – dual antiplatelet therapy is desirable
Abciximab	Glycoprotein IIB/IIIA inhibitors – prevention of cardiac ischemic complications. – unresponsive unstable angina – prophylactic use in myocardial infarction
Tirofiban	Glycoprotein IIB/IIIA inhibitors
Vorapaxar	Inhibit trombin receptor on platelets
Cimetidine	H2 receptor antagonist – Reducing intragastric acidity – Peptic ulcer disease – Gastro esophageal reflux disease – Dyspepsia Stress ulcer prophylaxis – Gastroduodenal ulcers
Ranitidine	H2 receptor antagonist – Reducing intragastric acidity – Peptic ulcer disease – Gastro esophageal reflux disease – Dyspepsia Stress ulcer prophylaxis – Gastroduodenal ulcers
Famotidine	H2 receptor antagonist – Reducing intragastric acidity – Peptic ulcer disease – Gastro esophageal reflux disease – Dyspepsia Stress ulcer prophylaxis – Gastroduodenal ulcers
Nizatidine	H2 receptor antagonist – Reducing intragastric acidity – Peptic ulcer disease – Gastro esophageal reflux disease – Dyspepsia Stress ulcer prophylaxis – Gastroduodenal ulcers
Omeprazol	Proton pump inhibitors – Reducing intragastric acidity – Peptic ulcer disease – Gastro esophageal reflux disease – Dyspepsia Stress ulcer prophylaxis – Gastroduodenal ulcers
Lansoprazole	Proton pump inhibitors – Reducing intragastric acidity – Peptic ulcer disease – Gastro esophageal reflux disease – Dyspepsia Stress ulcer prophylaxis – Gastroduodenal ulcers
Rabeprazole	Proton pump inhibitors – Reducing intragastric acidity – Peptic ulcer disease – Gastro esophageal reflux disease – Dyspepsia Stress ulcer prophylaxis – Gastroduodenal ulcers
Pantoprazole	Proton pump inhibitors – Reducing intragastric acidity – Peptic ulcer disease – Gastro esophageal reflux disease – Dyspepsia Stress ulcer prophylaxis – Gastroduodenal ulcers
Esomeprazole	Proton pump inhibitors – Reducing intragastric acidity – Peptic ulcer disease – Gastro esophageal reflux disease – Dyspepsia Stress ulcer prophylaxis – Gastroduodenal ulcers
Sucralfate (Aluminium hydroxide and sulfated sucrose complex)	Binds to positively charged glycoproteins at the ulcer base Forms complexes that protect mucosa against pepsin and hydrogen anions – Promoting mucosal defense – Peptic ulcer disease
Bismuth chelate (tripotassium dicitratobismuthate)	Coating ulcer base Adsorbing pepsin Stimulating bicarbonate synthesis Enhancing local prostaglandin levels Antimicrobial activity – Promoting mucosal defense – Peptic ulcer disease
Aluminum hydroxide Magnesium hydroxide Calcium salts Carbonate Sodium	Antiacids buffer gastric acid – Peptic ulcer disease
Metoclopramide	Prokinetic drugs (motility stimulants) Dopamine antagonists – Non–ulcer dyspepsia Non–specific or cytotoxic – induced nausea and vomiting
Domperidone	Prokinetic drugs (motility stimulants) Dopamine antagonists – Non–ulcer dyspepsia Non–specific or cytotoxic – induced nausea and vomiting
Psyllium husk Methylcellulose Agar Bran	Bulk–producing agents – Laxative, constipation
Docusate Glycerin suppository Mineral oil	Stool softeners/ Surfactans – Occasional constipation – Anorectal conditions that make passage of firm stool painful
Saline: Sodium phosphate Magnesium citrate Magnesium hydroxide Magnesium sulfate	Hydrating agent (osmotic) – Constipation
Bisacodyl Senna Aloe vera Castor oil	Stimulant laxatives – Constipation
Dolasetron	5HT3 receptor antagonist – Post–operative & cytoxic drug induced nausea and vomiting
Granisetron	5HT3 receptor antagonist – Post–operative & cytoxic drug induced nausea and vomiting
Ondansetron	5HT3 receptor antagonist – Post–operative & cytoxic drug induced nausea and vomiting
Palonsetron	5HT3 receptor antagonist – Post–operative & cytoxic drug induced nausea and vomiting
Droperidol	Dopamine antagonists – Neoplastic disease vomiting and diarrhea – Radiation sickness – Opioids – Cytotoxic drugs – General anesthetics
Haloperidol	Dopamine antagonists – Neoplastic disease vomiting and diarrhea – Radiation sickness – Opioids – Cytotoxic drugs – General anesthetics
Chlorpromazine	Dopamine antagonists – Neoplastic disease vomiting and diarrhea – Radiation sickness – Opioids – Cytotoxic drugs – General anesthetics
Promethazine	Dopamine antagonists – Neoplastic disease vomiting and diarrhea – Radiation sickness – Opioids – Cytotoxic drugs – General anesthetics
Prochlorperazine	Dopamine antagonists – Neoplastic disease vomiting and diarrhea – Radiation sickness – Opioids – Cytotoxic drugs – General anesthetics
Thietylperazin	Dopamine antagonists – Neoplastic disease vomiting and diarrhea – Radiation sickness – Opioids – Cytotoxic drugs – General anesthetics
Opiates: Loperamide Diphenoxylate Codeine	Antimotility agents – Diarrhea
Prophanteline Dicyclomine	Anticholinergic drugs – Diarrhea
Kaolin Pectin Chalk Charcoal Methyl cellulose	Adsorbents – Diarrhea
Benzocaine Chloroprocaine Cocaine Procaine Tetracaine	Inhibition of sodium influx through sodium–specific ion channels in neuronal cell membrane→ no action potential →signal conduction is inhibited – Local anesthetics – Lidocaine is used as antiarrhythmic drug
Bupivacaine Lidocaine Mepivacaine Prilocaine Ropivacaine Articaine	Inhibition of sodium influx through sodium–specific ion channels in neuronal cell membrane→ no action potential →signal conduction is inhibited – Local anesthetics –Lidocaine is used as antiarrhythmic drug
Theophylline (methylxanthines)	Non–specific inhibition of phosphodiesterase enzymes –COPD –Asthma
Cromoglicate (cormolyn)	Mast cell stabilizers Prevent release of histamine from mast cells – preventive of asthma
Nedocromil (Tilade)	Mast cell stabilizers Prevent release of histamine from mast cells – preventive of asthma
Montelukast	Leukotriene receptor antagonists – Preventive treatment in asthma
Zafirlukast	Leukotriene receptor antagonists – Preventive treatment in asthma
Pranlukast	Leukotriene receptor antagonists – Preventive treatment in asthma
Zileuton	Leukotriene receptor antagonists – Preventive treatment in asthma
Omalizumab	IgE blocker – Severe allergic asthma that does not respond to other drugs
Methotrexate	Antimetabolite of folic acid –Treatment of cancer Autoimmune disease
Flucitasone	Inhaled Glucocorticoids/ corticosteroids – Preventive treatment in asthma
Budesonide / Beclomethasone	Inhaled Glucocorticoids/ corticosteroids – Preventive treatment in asthma
Flunisolide	Inhaled Glucocorticoids/ corticosteroids – Preventive treatment in asthma
Triamcinolone	Inhaled Glucocorticoids/ corticosteroids – Preventive treatment in asthma