Salbutamol Adrenaline Terbutaline Salmeterol Formoterol Fluticasone Budesonide Zafirlukast Montelukast Theophylline Omalizumab

short-acting B2-agonists (SABA). Used in acute asthma. Relaxes airways

Chlorothiazide Propranolol Atenolol Prazosin Nifidepine Captopril Enalapril Losartan Clonidine a-methyl dopa Propranolol Atenolol Verapamil Diltiazem Nifidepine Glyceryl trinitrate (GTN) Isosorbide-5-mononitrate Frusemide Venous dilatation Arterial dilatation Captopril Enalapril Losartan

LABA Slow onset LABA rapid onset Glucocorticoids with salmeterol Glucocorticoids with formoterol Orally activate. It s a cysteinyl leukotriene receptor antagonist Prophylactic use only as a preventer. cysteinyl leukotriene receptor antagonist Phosphodiesterase inhibitor Selectively binds to IgE. Inhibits IgE induced release of mast cells. Treating hypertension Diuretic. Acts on luminal side of distal tubule. Too weak for heart failure Beta adrenoceptor antagonists. Non selective B1, B2 Beta adrenoceptor antagonists. Cardioselective B1 Alpha adrenoceptor antagonists (vasodilator) calcium channel blockers (vasodilator). Selective vascular block. Acting on (rennin-angiotensin system) RAS system. ACE inhibitors. (kininase) Acting on (rennin-angiotensin system) RAS system. Angiotensin II receptor antagonist. Centrally acting agents. It s not a first line therapy. a 2 agonist. Centrally acting agents. It s not a first line therapy. a methyl NA
Drugs for angina, heart failure

Beta blockers. Non selective B1/B2. Prophylaxis Beta blockers. Selective B1 Calcium channel blockers. Vascular: cardiac selectivity 1:1 For heart Calcium channel blockers. Vascular: cardiac selectivity 7:1 For heart Calcium channel blockers. Vascular: cardiac selectivity 14:1 For dilating arteries Nitrates. Short acting. 1st pass metabolism so not given orally. Don t take with viagra Longer acting nitrate. Active metabolite. Given sublingually or orally. Diuretic reduces preload and O2 demand. Reduces preload. Inhibits NaCl reabsorption in loop of Henle. Vasodilator reduces O2 demand. Decrease venous return, decrease preload Vasodilator reduces afterload and O2 demand. Decrease TPR, decrease afterload. ACE inhibitors AT1 receptor antagonist

Milrinone Dobutamine Digoxin Metoprolol Carvedilol Cyclosporin

B1 adrenoceptor agonists. Positive inotrope increases SV, CO by increasing intracellular Ca. In heart cAMP increase cardiac muscle contractility. Phosphodiesterase inhibitors. Used for acute severe failure B1 stimulants. Used for acute severe failure. Cardiac glycosides. Increases contractility without increasing O2 consumption. Novel therapy. B blockers for heart failure. Used in early stages. Immunosuppressant therapies Calcinuerin inhibitors via cyclophilin. It binds to immunophilin, which binds to cyclophilin. Derived from borel. Side effect: nephrotoxicity. Calcinuerin inhibitors via FKBP. Derived from borel. Side effects: nephrotoxicity Binds to FKBP too. Inhibits mTOR. Side effects: Hepatotoxicity (liver damage) Glucocorticoids Anti-metabolites. Inhibits purine biosynthesis. Targets action on lymphocytes Antibodies. Derived from mice. Leads to T cell depletion and inhibition. Leads to T cell depletion and inhibition. Chimeric. Human Fc portion. Murine antigen binding site. Leads to T cell depletion and inhibition. Humanized. Murine complementary determining regions. Antibacterials Synthetic metabolic inhibitors (antibiotic) Amoxycilin+clavulanic acid. It is a novel antibiotic which bypasses resistance. Can be given with B lactams Penicilins/B lactams are inhibitors of cell wall synthesis.

Tacrolimus Sirolimus (rapamycin) Methylprednisolone Mycophenolate mofetil. Muronomab (OKT3) Basiliximab Daclizumab

Sulfonamides Augmentin Penicilins Cephalosporin Carbapenems Vancomycin Teicoplanin Tobramycin Neomycin Framycetin Tetracycline

Glycopeptides are inhibitors of cell wall synthesis. It acts earlier than B lactam. Resistance is emerging. Aminoglycosides are inhibitors of protein synthesis. Mainly for G-

Tetracyclines are inhibitors of protein synthesis as they block tRNA binding to ribosomes. They are useful for intracellular bacteria and malaria.

Doxycycline Minocycline Erythromycin Clarithromycin

Macrolides are inhibitors of protein synthesis for G+. Used for skin and respiratory infections.

Azithromycin Roxithromycin Choramphenicol Quinolones Ofloxacin Rifampicin Sulfonamides Trimethoprim Lipopeptides (Daptomycin) Polypeptides Metronidazole Aciclovir

Treats conjunctivitis. Targets bacterial ribosomes 50S and host mitochondrial ribosomes Inhibitors of nucleic acid synthesis. They block chromosomal replication. Inhibitors of nucleic acid synthesis. Inhibitors of nucleic acid synthesis. Blocks mRNA synthesis Inhibitors of metabolic pathways. Block consecutive steps in folate synthesis. Inhibitors of cytoplasmic membrane function. Intereferes with nutrient uptake and ATP synthesis in G+ Inhibitors of cytoplasmic membrane function Broad spectrum of anaerobes and protozoa. Antivirals Herpesvirus treatment. Prodrug activated by viral thymide kinase. It blocks viral DNA synthesis by chian termination. (1st generation) Herpesvirus treatment Herpesvirus treatment Herpesvirus treatment . Topical use only Herpesvirus treatment. Effective for CMV HIV treatments. Nucleotide reverse transcriptase inhibitors (RTI) Non-nucleotide RTIs. Non-competitive inhibitors of RTI Protease inhibitors Treatment for hep C Antifungal Polyenes block cell membrane function. Binds to sterols. (Topical eye use.) Tablets, lozenges, cream, drops Azoles block ergosterol synthesis, increasing membrane permeability (topical, IV, oral) Topical and oral. Inhibits DNA synthesis. Combined with amphotericin B to decrease resistance. Inhibits mitosis by interfering with microtubules. Superceded by terbinafine (lamisil) Topical steroids. Suppresses cell migration Potency, IOP rise Potency, IOP rise Potency, penetration, IOP rise Topical NSAIDs. Inhibits formation of PG Delayed epithelial growth and wound healing

Valaciclovir Famciclovir Penciclovir Ganciclovir Azidothymidine (AZT) Tenofovir Nevirapine Nelfinavir Saquinavir Interferon+ribavirin Amphotericin B Nystatin Miconazole Fluconazole Flucytosine Griseofulvin

Dexamethasone Flurometholone Hydrocortisone Prednisolone Diclofenac Flubiprofen Ketorolac

Levocabastine Olopatadine Cromoglycate Lodoxamide Probenecid Frusemide

Histamine H1 antagonists For allergic conjunctivitis Histamine receptor antagonist and mast cell stabiliser. Mast cell stabilisation Treat allergic conjunctivitis and keratoconjunctivitis Drugs in the kidney Inhibits secretion of banned substances in sport Loop diuretics Thiazide diuretics. Inhibit Na/Cl- contransporter Potassium sparing diuretics Osmotic diuretics Cause renal toxicity. It s an antibiotic treating Gram negative infections Antineoplastic. Causes renal toxicity. Binds to neucleophilic cell components such as thiols in protein. antipsychotics Agonist at CNS 5-HT receptor induces schizophrenia like symtoms Glutamate receptor antagonists shown to induce schizophrenic like symptoms Antipsychotic drug. Classical. Antagonists at dopamine D2 receptor Atypical antipsychotic drug. More selective receptor antagonism. Blockade of 5-HT Antiepileptics Limits excitatory nerve activation. Reduces excitatory input Enhance GABA receptor activity. Enhance inhibitory input Inhibits metabolism Inhibits reuptake Ca channel blockers Endocrine Treatment of type 1 diabetes Treatment of type 2 diabetes. Stimulate the pancreas to make more insulin. Treatment of type 2 diabetes due to insulin resistance. Sensitize the body to insulin and decrease hepatic glucose production (Increase insulin-mediated peripheral glucose uptake) Decrease insulin resistance by making muscle and adipose cells more sensitive to insulin. Slows the absorption of starches. Block the enzymes that digest and promote absorption of starches in the small intestine Incretin mimetics and enhancer

Gentamicin Cisplatin

Lysergic acid diethylamide (LSD)

Chlorpromazine Haloperidol Clozapine Olanzapine Phenytoin Benzodiazepines (diazepam) Barbiturates Vigabatrin Tiagabine Ethosuximide Insulin Sulfonylureas (~ide) Meglitinides Biguanides

Thiazolidinediones (~glitazone) Alpha-glucosidase Inhibitors (Acarbose) Exenatide Sitagliptin

Pilocarpine Ecothiopate Atropine Cyclopentolate Acetazolamide Dorzolamide Ouabain Brimonidine Adrenaline Timolol Betaxolol Mannitol Glycerol Chlolingeric agonists Latanprost Phenylephrine Phentolamine Isoprenaline Propronalol Dobutamine Atenolol Salbutamol Clonidine Phentolamine Phenylephrine Prazosin Clonidine Yohimbine Cocaine Desipramine Moclobemide Botulinum toxin Physostigmine Neostigmine Organophosphates Nerve gas Tensilon=edrophonium d-tubocurarine (newer: vecuronium) Neostigmine Suxamethonium

Aqueous in the eye Direct outflow. Muscarinic agonist. (mitotic) Can cause headaches due to cerebral vasodilation Indirect outflow. Muscarinic agonist (mitotic) Muscarinic antagonist (mydriatics). Impair outflow. Dilate Carbonic anhydrase inhibitor Blocks Na/K ATPase A2 agonists. Reduce aq production. Decrease blood flow Alpha and beta agonist. Reduce aq production B adrenoceptor antagonists. Oppose B2 dilation. Reduce NA/K ATPase activity. Decrease cAMP Hyperosmotic agents (systemic). Decrease production Improve aq outflow Uveoscleral outflow. Chemical signalling Alpha agonist (artery) Alpha antagonist (artery) Beta agonist (heart)B1 and B2 Beta antagonist (heart) B1 and B2 B1 adrenoceptor agonist. For heart failure B1 antagonist. For hypertension B2 adrenocepture. For asthma. A adrenoceptor agonist. Constrict BV A1 and A2 antagonist A1 agonist. All post junctional sites. Decongestant A1 antagonist. All post junctional sites. For Hypertension. A2 agonist. Prejunctional inhibits SNS. For hypertension A2 antagonist. Aphrodisiac Blocks neuronal reuptake, increasing NA Blocks MAO metabolism. Hence increasing NA NMJ Snare complexes don t form. Less ACh Anticholinesterase. Used to decrease IOP. More activity at parasympathetic NS Anticholinesterase. More activity at NMJ. Reserve effect of non-depolarising neuromuscular blockers Irreversible anticholinesterase Short acting anti-cholinesterase Non-depolarising skeletal muscle relaxant. Competitive antagonist Reverse antagonist effects Depolarising skeletal muscle relaxants. Binds to NicR, produces an initial reponse, then a functional block. Agonist. Neostigmine can further increase block

Hexamethonium Mepyramine Cimetidine Thioperamide Chlorpheniramine Promethazine Terfenadine Astemizole Cetirizine Loratidine Ranitidine (Zantac) Cimetidine (Tagamet) Sildenafil L-NAME (L-arginine analogues) Aspirin Paracetamol Codeine Morphine Morphine Ibupofen Naproxen Indomethecin Cocaine Procaine Lignocaine Bupivicaine Ropivicaine Benzocaine Tetrodotoxin Saxitoxin Aldosterone Cortisol Hydrocortisone Prednisolone Methylprednisolone Dexamethasone Beclomethasone Aurothiomalate Sulphasalazine Methotrexate Infliximab

Ganglion blocer. Autacoids and Peptides H1 mainly H2 mainly H3 mainly H1 receptor antagonists Sedative Sedative Non-sedative Non-sedative Newer non-sedative agents Newer non-sedative agents H2 receptor antagonist H2 receptor antagonist NO and PGs Blocks PDE. Hence increase cGMP and relaxation NOS inhibitors. Produces vasoconstriction and hypertension Analgesics and NSAIDs Sensitization of pain receptors in periphery Neurotransmission is central

Perception of pain is central NSAIDs: propionic acid Acetic acid imines. NSAID Local anaesthetics Aminoesters Aminoesters. Slow onset. Low potency. Short duration Aminoamides. Rapid onset, more potent Aminoamides. Long duration. Cardiac toxicity Aminoamides. Very long duration. Weak bases. Neutral Lethal toxins. Puffer fish Lethal toxins. Dinoflagellates DMARDS, glococorticoids Mineralocorticoid. Regulate water balance Glucocorticoid. Regulare carbohydrate, protein and lipid metabolism. Anti-inflammatory Glucocoritcoid activity: mineralocortocoid acitivity 1:1 4: 0.25. For rheumatoid arthritis. 5:0.25 18:<.01 Glucocorticoid for asthma. DMARDS (disease modifying anti-rheumatoid drugs). Gold compound DMARDs. Enteric coated DMARDS. Immunosuppressant. Competes with folate for DHFR, redeuced thymidine available for DNA synthesis. Anti-TNF therapy. TNF antibody

Etanercept Indomethacin Colchicine Allopurinol

Anti-TNF therapy. Treatment combined with methotrexate. Recombinant TNF receptor protein Treats gout. NSAIDs. Not aspirin. Decrease uric acid secretion. Acute treament Chronic and acute treatment. Interferes with tubulin. Prevents leukocyte migration Chronic treatment. Similar structure to hypoxanthine. Initially induces attack. Use Colchicine for prevention.