Professional Documents
Culture Documents
H1-Antihistamines
* * * * * * * brompheniramine CHLORPHENIRAMINE DIPHENHYDRAMINE FEXOFENADINE hydroxyzine loratadine promethazine
H2-Antihistamines
* * * *
Antidegranulating drugs
* * CROMOLYN SODIUM nedocromil sodium
Eicosanoids
* * * * * * * alprostadil (PGE1) dinoprostone (PGE2) epoprostenol misoprostol MONTELUKAST zafirlukast ZILEUTON
Treatment of asthma
* -adrenergic agonists (non-selective, epinephrine; selective short-acting, ALBUTEROL, bitolterol, METAPROTERENOL; selective longacting, SALMETEROL) anticholinergics (IPRATROPIUM bromide) antidegranulating agents (CROMOLYN SODIUM, nedocromil sodium) anti-IgE antibody (omalizumab) glucocorticoids (BECLOMETHASONE, budesonide, flunisolide, FLUTICASONE) leukotriene inhibitors (MONTELUKAST, zafirlukast, ZILEUTON)
* * * * *
Bradykinin
* * aprotinin BRADYKININ
Antigout Drugs
* * * * * * * ALLOPURINOL COLCHICINE methylprednisolone NSAIDs (e.g. indomethacin, except aspirin) PREDNISONE PROBENECID SULFINPYRAZONE
ABCIXIMAB
ACETYLSALICYLIC ACID (aspirin)
argatroban CLOPIDOGREL
COBALAMIN (cyanocobalamin, hydroxocobalamin)
danaparoid sodium
darbepoetin alpha (NESP) DEFEROXAMINE desmopressin acetate (DDAVP)
LEPIRUDIN
protamine sulfate reteplase sodium ferric gluconate STREPTOKINASE tenecteplase TICLOPIDINE tirofiban TISSUE PLASMINOGEN ACTIVATOR(t-PA) thrombopoietin VITAMIN B-12 VITAMIN K WARFARIN SODIUM
Antiarrhythmic Drugs
ADENOSINE AMIODARONE Atropine -ADRENOCEPTOR ANTAGONISTS (e.g. METOPROLOL, SOTALOL) Bretylium CALCIUM CHANNEL BLOCKERS (e.g. DILTIAZEM, VERAPAMIL) digitoxin digoxin disopyramide disopyramide dofetilide flecainide ibutilide LIDOCAINE mexiletine PROCAINAMIDE propafenone QUINIDINE
Antianginal Drugs
ANTIPLATELET AGENTS (e.g. Clopidogrel) ADRENOCEPTOR ANTAGONISTS (e.g. PROPRANOLOL) CALCIUM CHANNEL BLOCKERS (e.g. NIFEDIPINE) VASODILATORS
Antihyperlipidemic Drugs
CHOLESTYRAMINE colestipol
ezetimibe FIBRIC ACID DERIVATIVES (e.g. GEMFIBROZIL, FENOFIBRATE) HMG CoA REDUCTASE INHIBITORS (e.g. ATORVASTATIN, LOVASTATIN, PRAVASTATIN) nicotinic acid
Respiratory Drugs
ALBUTEROL beclomethasone CROMOLYN SODIUM EPINEPHRINE flunisolide IPRATROPIUM BROMIDE isoproterenol sulfate metaproterenol nedocromil oxymetazoline phenylephrine pseudoephedrine salmeterol TERBUTALINE THEOPHYLLINE
Antimicrobial Agents
Narrow spectrum Penase-sensitive
Pen G NAFCILLIN AMOXICILLIN TICARCILLIN PEN V OXACILLIN AMPICILLIN
Extended spectrum
PIPERACILLIN
Monobactams
Aztreonam
Carbapenems
Imipenem with cilastatin
Cephalosporins
First generation
CEPHALEXIN
Second generation
CEFOXITIN
Third generation
CEFTRIAXONE
Fourth generation
CEFEPIME
Vancomycin
STREPTOGRAMINS
Quinupristin Dalfopristin (Synercid)
OXAZOLIDINONES MACROLIDES
Clarithromycin Azithromycin LINEZOLID Erythromycin
DOXYCYCLINE
MINOCYCLINE
Sulfonamides
Best urine solubility
SULFASOXAZOLE SULFAMETHOXAZOLE
Ciprofloxacin
Levofloxacin
Topical (burns)
SILVER SULFADIAZINE
TRIMETHOPRIM
Use as TRIMETHOPRIM - SULFAMETHOXZAOLE combo.
Flucytosine Imidazoles
KETOCONAZOLE MICONAZOLE Terbinafine FLUCONAZOLE ITRACONAZOLE Voriconazole Griseofulvin
Antiviral Drugs
AMANTIDINE and Rimantadine ACYCLOVIR ZIDOVUDINE GANCICLOVIR FOSCARNET Didanosine Valacyclovir Efavirenz Indinavir Lamivudine Zanamivir Ribavirin Lopinavir Nelfinavir
Enfuvirtide
Stavudine
Antiparasitic Drugs
CHLOROQUINE MEFLOQUINE Quinine PRIMAQUINE PYRIMETHAMINESULFASOXINE (Fansidar) atovaquone
Antimalarial
Pneumocystis
TRIMETHOPRIM pentamidine SUFAMETHOXAZOLE Clindamycin plus primaquine
Toxoplasmosis
PYRIMETHAMINE plus sulfadiazine Pyrimethamine plus clindamycin
Trichomonas
Antihelminthic Drugs
METRONIDAZOLE
Flatworms
PRAZIQUANTEL
Filariasis
diethylcarbamazine ivermectin
Angiostroglyliasis
mebendazole
Trypanosomiasis
nifurtimox or
suramin
pentamidine
Giadiasis
metronidazole
Alkyating Agents
MECHLORETHAMINE CYCLOPHOSPHAMIDE busulfan Nitrosoureas (carmustine, lomustine) procarbazine 6-THIOGUANINE Cytosine arabinoside melphalan
Antimetabolites
METHOTREXATE 6-MERCAPTOPURINE Fludarabine Capecitabine 5-Fluorouracil gemcitabine
Natural Products
dactinomycin DAUNORUBICIN DOXORUBICIN BLEOMYCIN mitomycin C ETOPOSIDE (VP-16) VINBLASTINE asparaginase mitoxantrone Camptothecin analogs: irinotecan and topotecan paclitaxel/docetaxel amsacrine Imatinib
Antimitotics
VINCRISTINE
Miscellaneous
HYDROXYUREA CISPLATIN/ Carboplatin
Hormones
Estrogens Anti-estrogen (TAMOXIFEN) PREDNISONE flutamide leuprolide TACROLIMUS (FK506) goserelin
Immunosuppressives
azathioprine CYCLOSPORIN A
Adrenocorticoids
aldosterone aminoglutethimide androstenedione angiotensin (I, II & III) beclomethasone betamethasone dehydroepiandrosterone (DHEA) DEXAMETHASONE FLUDROCORTISONE fluocinonide HYDROCORTISONE (cortisol) ketoconazole METYRAPONE mifepristone (RU486) mitotane PREDNISOLONE triamcinolone trilostane
Gonadal Hormones
anastrozole bicalutamide
CLOMIPHENE CONJUGATED ESTROGENS (Premarin, estrone, equilin) cyproterone acetate danazol desogestrol DIETHYLSTILBESTROL drospirinone dutasteride ESTRADIOL (in saltsbenzoate, valerate, cypionate) ETHINYL ESTRADIOL ethynodiol exemastane fadrozole faslodex FINASTERIDE fluoxymesterone FLUTAMIDE formestane
ketoconazole letrozole MEDROXYPROGESTERONE megestrol acetate methyltestosterone mestranol methyltestosterone mifepristone (RU 486) nandrolone NORETHINDRONE norgestimate l-NORGESTREL OXANDROLONE oxymethalone phytoestrogens raloxifene spironolactone TAMOXIFEN TESTOSTERONE-salts (propionate, heptanoate, cypionate)
Thyroid/Parathyroid Drugs
alendronate, etidronate, pamidronate, risedronate calcium carbonate calcitonin calcitriol (1,25-dihydroxy Vitamin D3) cinacalcet cholecalciferol dihydrotachysterol ergocalciferol fluoborate fluoride iocetamic acid iopanoic acid LEVOTHYROXINE (T4) liothyronine sodium (triiodothyronine (T3) liotrix (T4 plus T3) lithium methimazole mithramycin (plicamicin) parathyroid hormone POTASSIUM IODIDE potassium perchlorate PROPYLTHIOURACIL radioactive iodide teriperatide (PTH 1-34) thiocyanate thyrotropin stimulating hormone (TRH) zoledronic acid
Uterine Drugs
carboprost DINOSPROSTONE dinoprostone ERGONOVINE MALEATE MAGNESIUM SULFATE misoprostol OXYTOCIN PROSTAGLANDIN E2 ritodrine terbutaline
Laxatives Drugs
bisacodyl docusate (dioctyl sodium sulfosuccinate) mineral oil polyethylene glycol lactulose MAGNESIUM HYDROXIDE methylcellulose
Antidiarrheal Drugs
atropine bismuth subsalicylate diphenoxylate LOPERAMIDE octreotide clonidine
Prokinetic Drugs
bethanechol cisapride ERYTHROMYCIN METOCLOPRAMIDE TEGASEROD ALVIMOPAN neostigmine
Priority toxic chemicals and antidotes which should be discussed PRIMARY DRUGS - All capital letters SECONDARY DRUGS - Small letters
ACETAMINOPHEN N-ACETYL-L-CYSTEINE ACTIVATED CHARCOAL AIR POLLUTANTS ALCOHOLS (ETHANOL, METHANOL, ETHYLENE GLYCOL) ARSENIC CARBON MONOXIDE CHELATOR THERAPY (2,3DIMERCAPTOSUCCINIC ACID, DIMERCAPROL, EDETATE) cyanide AND ANTIDOTES DIG-SPECIFIC ANTIBODY FRAGMENTS GLUCAGON HEROIN IRON AND DEFEROXAMINE LEAD MERCURY METHYLENE BLUE NALOXONE SALICYLATES SODIUM BICARBONATE TRICYCLIC ANTIDEPRESSANTS SELECTED PESTICIDES (ANTICHOLINESTERASE, PRALIDOXIME[2-PAM])
PRIMARY DRUGS - All capital letters SECONDARY DRUGS - Small letters [Endogenous Agents] - [Inhalation and Intravenous Anesthesia] - [Local Anesthetics] - [Opioids] [Antitussives, Expectorants and Mucolytics] - [Drugs for Motor Disorders/Muscle Relaxants] [Antiepileptics] - [Hallucinogens] - [Mood Disorders] - [Sedative-Hypnotics] [Amphetamines, Anorexogenics and CNS Stimulants] - [Anxiolytics] - [Ethanol and Alcoholism] [Drugs of Abuse and Dependence] - [Drugs for Migraine] - [Drugs for Alzheimer's Disease]
Endogenous Agents
ACETYLCHOLINE (ACH) ADENOSINE TRIPHOSPHATE (ATP) aspartate (asp) Beta-Amyloid BRADYKININ DOPAMINE (DA) NOREPINEPHRINE dynorphins endocannabinoids beta-endorphin met-enkephalin
substance P
Local Anesthetics
BENZOCAINE bupivacaine cocaine levobupivacaine LIDOCAINE lidocaine/prilocaine eutectic mixture (EMLA) prilocaine PROCAINE ROPIVACAINE tetracaine
Opioids Agonists
CODEINE DIPHENOXYLATE fentanyl heroin loperamide MEPERIDINE METHADONE MORPHINE OXYCODONE d-propoxyphene combinations - opioids plus acetaminophen and ASA
Antiepileptics
LORAZEPAM PHENOBARBITAL PHENYTOIN primidone tiagabine topiramate VALPROIC ACID
Hallucinogens
atropine scopolamine
Antipsychotics
ARIPIPRAZOLE CHLORPROMAZINE (CPZ) CLOZAPINE fluphenazine HALOPERIDOL OLANZAPINE chloral hydrate diphenhydramine eszopiclone flurazepam oxazepam
Hypnotics
Anxiolytics Benzodiazepines
alprazolam chlorazepate chlordiazepoxide clonazepam
NonBenzodiazepine
AMITRIPTYLINE FLUOXETINE disulfiram ETHANOL
beta-adrenergic blocking agents BUSPIRONE
STEROIDAL ANTI-INFLAMMATORY DRUGS & DRUGS USED TO TREAT RHEUMATOID ARTHRITIS AND GOUT Steroidal anti-inflammatory drugs are also known as corticosteroids
Functions Anti-inflammatory Immunosuppressant Mechanisms of action Corticosteroids, being steroids, are highly lipophilic and can thus penetrate cell membranes fairly easily. They bind to intracellular receptors which modify gene transcription. Corticosteroids have wider ranging effects than NSAIDs because they inhibit a wider variety of enzymes by reducing their synthesis: Inhibit phospholipase A2 Inhibit COX 2 (not COX 1) Inhibit cytokine system Glucocorticoid
Glucocorticoid receptor
nGRE
Negative glucocorticoid response element Glucocorticoids bind to a glucocorticoid receptor in the cytosol. Once bound, the drug-receptor complex (in this case the negative glucocorticoid response element) goes into the cell nucleus and acts on the promoter region of a gene to block the transcription of cytokines, COX 2 and phospholipase A2. By inhibiting phospholipase A2 we are able to achieve a higher level of anti-inflammation by reducing the synthesis of all eicosanoids (both prostinoids and leukotrienes). The nGRE inhibits the transcription of certain genes. There is also the formation of a +GRE which increases the transcription and synthesis of lipocortin 1. Glucocorticoid
Lipocortin 1 is an endogenous anti-inflammatory agent. Normally, phospholipase A2 is inactive and must be activated for it to breakdown phospholipids into arachidonic acid. If it were always active, cell membranes would be constantly breaking down. Lipocortin 1 binds to the inactive phospholipase A2 and keeps it inactive. Normally, inflammation will activate protein kinase C which converts lipocortin 1 into an inactive form It then releases phospholipase A2 which can now become active. Corticosteroids act to increase the synthesis of lipocortin. Note that the inflammatory system is still active (we have done nothing to inhibit it) and so it is still acting to inactivate lipocortin. However, since at the same time, we are stimulating the synthesis of active lipocortin at a faster rate, there will be a net increase in lipocortin levels. Lipocortin is thus more likely to hold phospholipase A2 in an inactive form. Also, there is reduced synthesis of phospholipase A2 which makes it even better, because lots of lipocortin can find and bind easily with small levels of PLA2.
Uses Usage of these drugs are associated with a higher level and more severe adverse effects. Anti-inflammatory E.g. Asthma. Local inhalation of beclomethasone. Topical (local)administration to a specific site E.g. On the skin, or eyes A topical administration is useful to try and diminish the systemic side effects Rheumatoid arthritis Treated with prednisolone This is a systemic treatment and is often used only as a last resort. We tend to use NSAIDs as the first resort. Adverse effects Suppression of endogenous glucocorticoid synthesis. High levels of steroids negatively feed back on the pituitary to decrease the release of ACTH from the anterior pituitary. ACTH, apart from stimulating the release of adrenal hormone, is also trophic to the adrenal cortex. Hence, reduced ACTH will eventually lead to atrophy of the adrenal glands. If we try to remove steroid treatment, we often get symptoms similar to a withdrawal effect, e.g. fever, muscle pain If steroid treatment is initiated, it is often for life. In order to stop treatment, we need to slowly reduce the dosage over a long period of time to minimise withdrawal effects. Suppression of the response to infection or injury These drugs are immunosuppressants and also suppress wound repair due to the reduction in protein synthesis. E.g. For an eye infection, we may treat the inflammation but the micro-organisms which caused the inflammation is still around (because the bodys immune system has not responded to eliminate the organism) and so things can get worse. E.g. Sometimes a combination of steroid treatment with NSAIDs are given. NSAIDs may cause gastric ulceration and GIT disorders, but the steroids only exacerbate the adverse effects of NSAIDs because they suppress the repair of the ulcers. The point is that we must treat the cause, not the symptoms. We may be able to treat the inflammation associated with a wound but will not get any wound repair. Behavioural disturbances Cataract, glaucoma An increase in intraocular pressure is the normal response to steroidal treatment. Fluid and electrolyte disturbances. Similarity to aldosterone or cortisol increased reabsorption of Na, increased secretion of K. Metabolic effects Osteoporosis
Muscle wasting Due to mimicking the actions of cortisol. Hyperglycemia Inhibition of bone growth in children Steroids cause fusion of the epiphyseal plates. A lot of children are given steroids to treat asthma not good! The use of topical steroids is more desirable to reduce the systemic effects. Both NSAIDs and steroid treatment aim to treat the symptoms (reduce pain, inflammation and discomfort), but may not do a good job in treating the cause of the disease. Unless the cause is treated, the disease will keep on getting worse.
Anti rheumatoid drugs NSAIDs are the first line of defense Alternatively, specific drugs used to treat the rheumatoid arthritis can be used. These drugs do not have general anti-inflammatory effects. The drugs are often known as Slow acting anti rheumatoid drugs (SAARDs) or Disease modifying anti rheumatoid drugs (DMARDs). The following drugs used for rheumatoid arthritis are effective but we do not know their mechanism of action. Gold compounds Aurothiomalate Intramuscular injection Auranofin Oral, less common lymphocyte proliferation lysosomal enzyme release superoxide production neutrophil chemotaxis IL-1 synthesis May take months to see a beneficial effect. Adverse effects: Commonly allergic type reactions at the skin and mucous membranes Renal injury Blood dyscrasias (any adverse change in blood function) Chloroquine Is used in the treatment of malaria An anti-inflammatory only in rheumatic disease Less adverse systemic effects but tends to seriously affect the eyes The cornea of the patient undergoing this treatment needs to be monitored carefully. Retinopathy which occurs may be irreversible, causing blindness. Very slow onset (months) Sulphasalazine A combination of sulphonamide and salicylate A free radical scavenger? Free radicals cause cell injury and inflammation Has marked GI irritation and so is only available with an enteric coating. Methotrexate Immunosuppresant Folate antagonist Also used to treat cancer (see lecture enzymes 1) Penicillamine Adverse effects similar to gold compounds. Not as effective, most probably be obsolete soon. All these drugs are slow releases, with the effects being seen in weeks to months. Once the effects are observed, they will slow the disease progress, not just treating the inflammation.
Drugs used in the treatment of gout Gout is due to an accumulation of uric acid (a breakdown product of adenosine). High concentrations of uric acid leads to crystallisation and deposition in the synovium of joints, resulting in arthritic pain. Acute treatment of gout involves: NSAIDs (but NOT aspirin because aspirin inhibits the excretion of uric acid) Colchicine Glucocorticoids Chronic treatment involves: Allopurinol Colchicine Probenecid Adenosine
Synovial deposition (inflammation, classically in the big toes) Colchicine An antimitotic agent. It interferes with tubulin, which prevents leukocyte migration Reduced leukocytes in the synovial joints affected by gout would reduce the pain and discomfort as a result of the cytokines released by neutrophils. Can be used as an acute treatment Also can be used as a chronic treatment as prevention (prohpylacticaly) in conjunction with allopurinol. Allopurinol An analogue of hypxanthine It thus competitively inhibits the enzyme xanthine oxidase, preventing hypoxanthine from binding. The product of allopurinol with xanthine oxidase is alloxanthine. Alloxanthine is an irreversible inhibitor of xanthine oxidase. Thus, there is decreased synthesis of uric acid and the concentrations fall. Probenecid A uricosuric agent (increases the excretion of uric acid) It inhibits the tubular reabsorption of uric acid in the kidneys It has a limited use, not as effective as allopurinol It is used when a person has an inability to excrete uric acid (in most patients, an increased uric acid is mainly due to an increase in production and so allopurinol is better suited).