Views
5 years ago

A Textbook of Clinical Pharmacology and Therapeutics

A Textbook of Clinical Pharmacology and Therapeutics

ASPIRIN

ASPIRIN (ACETYLSALICYLATE) Use Antiplatelet uses of aspirin are described in Chapters 29 and 30. As an antipyretic and mild analgesic it has similar efficacy to paracetamol. However, unlike paracetamol it also has antiinflammatory properties when used in high doses. Various preparations are available, including regular as well as buffered, soluble and enteric-coated forms. Enteric coating is intended to reduce local gastric irritation, but much of the gastric toxicity is due to inhibition of gastric mucosal prostaglandin biosynthesis (see below), rather than to direct gastric irritation. Consequently, slow-release preparations do not eliminate the adverse effects of aspirin on the gastric mucosa. Mechanism of action Aspirin inhibits prostaglandin biosynthesis, irreversibly acetylating a serine residue in the active site of cyclo-oxygenase (COX). There are two main isoforms, COX-1 and COX-2. COX-1 is a constitutive enzyme which is present in platelets and other cells under basal conditions. COX-2 is an inducible form, which is produced in response to cytokine stimulation in areas of inflammation and produces large amounts of prostaglandins. Acetylation of the serine in COX-1 active site prevents access of the endogenous substrate (arachidonic acid) to the active site, very effectively blocking thromboxane formation in platelets, as well as prostaglandin formation. Adverse effects and contraindications These include: • Salicylism – toxic doses of salicylates, including aspirin, cause tinnitus, deafness, nausea, vomiting, abdominal pain and flushing and fever. • Dyspepsia is common as is mild gastric blood loss. Severe blood loss from the stomach can be life-threatening. The mechanism is inhibition of gastric prostaglandin (PGE 2) biosynthesis. PGE 2 is the main prostaglandin made by the human stomach, which it protects in several ways: – inhibition of acid secretion; – stimulation of mucus secretion; – increased clearance of acid from the submucosa via local vasodilatation. Aspirin and other NSAIDs damage the stomach by impairing these protective mechanisms. Aspirin should not be given to patients with active peptic ulceration. • Aspirin-sensitive asthma occurs in approximately 5% of asthmatics (Chapter 33). It is associated with nasal polyps. Reactions to other chemically unrelated NSAIDs commonly occur in such individuals. Abnormal leukotriene (Chapter 33) production and sensitivity are implicated. In addition, aspirin and similar drugs can directly activate eosinophils and mast cells in these patients through IgE-independent mechanisms. • Reye’s syndrome, a rare disease of children, with high mortality, is characterized by hepatic failure and encephalopathy, often occurring in the setting of a viral illness (Figure 25.3). DRUGS USED TO TREAT MILD OR MODERATE PAIN 157 Figure 25.3: Histopathology of autopsy liver from child who died of Reye’s syndrome as a result of taking asprin. Hepatocytes are palestaining due to intracellular fat droplets. Plasma (acetyl) salicylate concentration (μg/mL) 60 45 30 15 Salicylate Acetylsalicylate 0 1 2 Time (h) 3 4 Figure 25.4: Plasma levels of salicylate and acetylsalicylate following 640 mg aspirin given orally, demonstrating rapid conversion of acetylsalicylate to salicylate. Pharmacokinetics Gastro-intestinal absorption is rapid. Aspirin is subject to considerable presystemic metabolism (to salicylate), so the plasma concentration of aspirin (acetyl salicylic acid) is much lower than that of salicylate following an oral dose (Figure 25.4). Some of the selectivity of aspirin for platelet cyclo-oxygenase is probably due to exposure of platelets to high concentrations of aspirin in portal blood, whereas tissues are exposed to the lower concentrations present in the systemic circulation. Salicylate is metabolized in the liver by five main parallel pathways, two of which are saturable (Michaelis–Menten kinetics) and is also excreted unchanged in the urine by a first-order process. This is summarized in Figure 25.5. The formation of salicylurate (in mitochondria) is easily saturable. Consequently,

158 ANALGESICS AND THE CONTROL OF PAIN Salicylate Michaelis-Menten First-order First-order First-order Michaelis-Menten Salicylurate (50%) Urinary salicylate (15%) salicylate has dose-dependent (non-linear) kinetics (Chapter 3) at high therapeutic doses or after overdose. Urinary elimination of salicylate is considerably influenced by pH, being more rapid in alkaline urine, which favours the charged (polar) anionic form that is not reabsorbed, rather than the free acid (Chapter 6). This property is utilized in the treatment of salicylate overdose by urine alkalinization and demonstrates the principle of ion trapping. (Chapter 54). Drug interactions Aspirin increases the risk of bleeding in patients receiving anticoagulants via effects on platelets, gastrotoxicity and, in overdose, by a hypoprothrombinaemic effect. Aspirin should not be given to neonates with hyperbilirubinaemia because of the risk of kernicterus as a result of displacement of bilirubin from its binding site on plasma albumin (Chapter 13). IBUPROFEN Ibuprofen has an approximately similar analgesic potency to paracetamol and, in addition, has useful anti-inflammatory activity, so it is an alternative to aspirin for painful conditions with an inflammatory component (e.g. sprains and minor soft tissue injury). It is also useful in dysmenorrhoea. It is a reversible cyclo-oxygenase inhibitor, but causes rather less gastric irritation than aspirin and other NSAIDs at normal doses, and is available over the counter in the UK and in many other countries. A suspension is available for use in children. It can cause other adverse reactions common to the NSAIDs, including reversible renal impairment in patients who are elderly or have cirrhosis, nephrotic syndrome or heart failure. It reduces the efficacy of antihypertensive medication and of diuretics by blocking formation of vasodilator and natriuretic prostaglandins in the kidney. For more detailed discussion of other common NSAIDs, which are widely used, see Chapter 26. TOPICAL NON-STEROIDAL ANTI-INFLAMMATORY DRUGS Salicyl acyl glucuronide (10%) Gentisic acid (5%) Several NSAIDs (including ibuprofen and piroxicam) are available as topical preparations. Systemic absorption does occur, but is modest. Their effectiveness in soft tissue injuries Salicyl phenolic glucuronide (20%) and other localized inflammatory conditions is also modest. They occasionally cause local irritation of the skin, but adverse effects are otherwise uncommon. NEFOPAM Use Figure 25.5: The main pathways of salicylate metabolism and excretion. Nefopam is chemically and pharmacologically unrelated to other analgesics. It is intermediate in potency between aspirin and morphine. Unlike NSAIDs, it does not injure the gastric mucosa. It is less of a respiratory depressant than the opioids and does not cause dependence. It is useful when opioidinduced respiratory depression is unacceptable. Neither tolerance nor drug dependence occur. Mechanism of action Nefopam is a potent inhibitor of amine uptake and potentiates descending pathways that operate the gate mechanism described above. Adverse effects and contraindications Nefopam has few severe (life-threatening) effects, although convulsions, cerebral oedema and fatality can result from massive overdose. It is contraindicated in patients with epilepsy, and also in patients receiving monoamine oxidase inhibitors (see below). It should not be used in acute myocardial infarction, as it increases myocardial oxygen demand and may be pro-dysrhythmogenic. Nefopam causes a high incidence of minor adverse effects, especially after parenteral use. These include sweating, nausea, headache, dry mouth, insomnia, dizziness and anorexia. Nefopam is contraindicated in glaucoma, and can cause urinary retention in men with prostatic hypertrophy. Pharmacokinetics Nefopam is rapidly absorbed following oral administration. It is extensively metabolized by the liver to inactive compounds excreted in the urine. Presystemic metabolism is substantial. Drug interactions Nefopam can cause potentially fatal hypertension with monoamine oxidase inhibitors (MAOIs) and potentiates the dysrhythmogenic effect of halothane.

  • Page 2 and 3:

    A Textbook of Clinical Pharmacology

  • Page 4 and 5:

    A Textbook of Clinical Pharmacology

  • Page 6 and 7:

    This fifth edition is dedicated to

  • Page 8 and 9:

    FOREWORD viii PREFACE ix ACKNOWLEDG

  • Page 10 and 11:

    PREFACE Clinical pharmacology is th

  • Page 12 and 13:

    PART I GENERAL PRINCIPLES

  • Page 14 and 15:

    ● Use of drugs 3 ● Adverse effe

  • Page 16 and 17:

    and acquired factors, notably disea

  • Page 18 and 19:

    100 Effect (%) 0 0 5 10 1 10 100 (a

  • Page 20 and 21:

    Dose ratio -1 100 50 The relationsh

  • Page 22 and 23:

    ● Introduction 11 ● Constant-ra

  • Page 24 and 25:

    In reality, processes of eliminatio

  • Page 26 and 27:

    lood (from which samples are taken

  • Page 28 and 29:

    ● Introduction 17 ● Bioavailabi

  • Page 30 and 31:

    ROUTES OF ADMINISTRATION ORAL ROUTE

  • Page 32 and 33:

    Transdermal absorption is sufficien

  • Page 34 and 35:

    FURTHER READING Fix JA. Strategies

  • Page 36 and 37:

    and thromboxanes are CYP450 enzymes

  • Page 38 and 39:

    and lorazepam. Some patients inheri

  • Page 40 and 41:

    Orally administered drug Parenteral

  • Page 42 and 43:

    ● Introduction 31 ● Glomerular

  • Page 44 and 45:

    ACTIVE TUBULAR REABSORPTION This is

  • Page 46 and 47:

    DISTRIBUTION Drug distribution is a

  • Page 48 and 49:

    Detailed recommendations on dosage

  • Page 50 and 51:

    DIGOXIN Myxoedematous patients are

  • Page 52 and 53:

    ● Introduction 41 ● Role of dru

  • Page 54 and 55:

    25 20 10 Life-threatening toxicity

  • Page 56 and 57:

    ● Introduction 45 ● Harmful eff

  • Page 58 and 59:

    vagina in girls in their late teens

  • Page 60 and 61:

    an anti-analgesic effect when combi

  • Page 62 and 63:

    Case history A 20-year-old female m

  • Page 64 and 65:

    METABOLISM At birth, the hepatic mi

  • Page 66 and 67:

    lifelong effects as a result of tox

  • Page 68 and 69:

    DISTRIBUTION Ageing is associated w

  • Page 70 and 71:

    DIGOXIN Digoxin toxicity is common

  • Page 72 and 73:

    FURTHER READING Dhesi JK, Allain TJ

  • Page 74 and 75:

    Factors involved in the aetiology o

  • Page 76 and 77:

    analgesic. Following its release, t

  • Page 78 and 79:

    antibiotics, such as penicillin or

  • Page 80 and 81:

    predisposes to non-immune haemolysi

  • Page 82 and 83:

    ● Introduction 71 ● Useful inte

  • Page 84 and 85:

    Response Therapeutic range Toxic ra

  • Page 86 and 87:

    Table 13.1: Interactions outside th

  • Page 88 and 89:

    Table 13.5: Competitive interaction

  • Page 90 and 91:

    ● Introduction: ‘personalized m

  • Page 92 and 93:

    Table 14.2: Variations in drug resp

  • Page 94 and 95:

    lipoprotein (LDL) is impaired. LDL

  • Page 96 and 97:

    Key points • Genetic differences

  • Page 98 and 99:

    • Discovery • • Screening Pre

  • Page 100 and 101:

    Too many statistical comparisons pe

  • Page 102 and 103:

    ETHICS COMMITTEES Protocols for all

  • Page 104 and 105:

    Table 16.1: Recombinant proteins/en

  • Page 106 and 107:

    duration and benefit. Adenoviral ve

  • Page 108 and 109:

    ● Introduction 97 ● Garlic 97

  • Page 110 and 111:

    A case report has suggested a possi

  • Page 112 and 113:

    including hypericin and pseudohyper

  • Page 114 and 115:

    PART II THE NERVOUS SYSTEM

  • Page 116 and 117:

    ● Introduction 105 ● Sleep diff

  • Page 118 and 119: and daytime sleeping should be disc
  • Page 120 and 121: Key points • Insomnia and anxiety
  • Page 122 and 123: Box 19.1: Dopamine theory of schizo
  • Page 124 and 125: The Boston Collaborative Survey ind
  • Page 126 and 127: Oral medication, especially in liqu
  • Page 128 and 129: e.g. interpersonal difficulties or
  • Page 130 and 131: Partial response to first-line trea
  • Page 132 and 133: Key points Drug treatment of depres
  • Page 134 and 135: Case history A 45-year-old man with
  • Page 136 and 137: Levodopa PRINCIPLES OF TREATMENT IN
  • Page 138 and 139: • pulmonary, retroperitoneal and
  • Page 140 and 141: CHOREA The γ-aminobutyric acid con
  • Page 142 and 143: Cholinergic crisis Treatment of mya
  • Page 144 and 145: ● Introduction 133 ● Mechanisms
  • Page 146 and 147: absolute arbiter. The availability
  • Page 148 and 149: Table 22.2: Metabolic interactions
  • Page 150 and 151: FURTHER ANTI-EPILEPTICS Other drugs
  • Page 152 and 153: Case history A 24-year-old woman wh
  • Page 154 and 155: Assessment of migraine severity and
  • Page 156 and 157: ● General anaesthetics 145 ● In
  • Page 158 and 159: is the theoretical concern of a ‘
  • Page 160 and 161: • Respiratory system - apnoea fol
  • Page 162 and 163: Competitive antagonists (vecuronium
  • Page 164 and 165: have also proved useful in combinat
  • Page 166 and 167: ● Introduction 155 ● Pathophysi
  • Page 170 and 171: Key points Drugs for mild pain •
  • Page 172 and 173: increases, correlating with the hig
  • Page 174 and 175: • If possible, use oral medicatio
  • Page 176 and 177: PART III THE MUSCULOSKELETAL SYSTEM
  • Page 178 and 179: ● Introduction: inflammation 167
  • Page 180 and 181: Chapter 33). All NSAIDs cause wheez
  • Page 182 and 183: • Stomatitis suggests the possibi
  • Page 184 and 185: Pharmacokinetics Allopurinol is wel
  • Page 186 and 187: PART IV THE CARDIOVASCULAR SYSTEM
  • Page 188 and 189: ● Introduction 177 ● Pathophysi
  • Page 190 and 191: esponsible for the strong predilect
  • Page 192 and 193: Ezetimibe Fat Muscle Dietary fat In
  • Page 194 and 195: educed). The risk of muscle damage
  • Page 196 and 197: ● Introduction 185 ● Pathophysi
  • Page 198 and 199: Each of these classes of drug reduc
  • Page 200 and 201: AT 1 receptor) produce good 24-hour
  • Page 202 and 203: Table 28.2: Examples of calcium-cha
  • Page 204 and 205: Key points Drugs used in essential
  • Page 206 and 207: Case history A 72-year-old woman se
  • Page 208 and 209: Assess risk factors Investigations:
  • Page 210 and 211: Persistent ST segment elevation Thr
  • Page 212 and 213: Mechanism of action GTN works by re
  • Page 214 and 215: Because of the risks of haemorrhage
  • Page 216 and 217: Intrinsic pathway XIIa XIa the acti
  • Page 218 and 219:

    that the pharmacodynamic response i

  • Page 220 and 221:

    used with apparent benefit in acute

  • Page 222 and 223:

    ● Introduction 211 ● Pathophysi

  • Page 224 and 225:

    The drugs that are most effective i

  • Page 226 and 227:

    therapeutic plasma concentration ca

  • Page 228 and 229:

    ● Common dysrhythmias 217 ● Gen

  • Page 230 and 231:

    BASIC LIFE SUPPORT CARDIOPULMONARY

  • Page 232 and 233:

    arrest. The electrocardiogram is li

  • Page 234 and 235:

    should be given to insertion of an

  • Page 236 and 237:

    Drug interactions Amiodarone potent

  • Page 238 and 239:

    effect when treating sinus bradycar

  • Page 240 and 241:

    Case history A 24-year-old medical

  • Page 242 and 243:

    PART V THE RESPIRATORY SYSTEM

  • Page 244 and 245:

    CHAPTER 33 THERAPY OF ASTHMA, CHRON

  • Page 246 and 247:

    STEP 5: CONTINUOUS OR FREQUENT USE

  • Page 248 and 249:

    Adenylyl cyclase Table 33.1: Compar

  • Page 250 and 251:

    Drug interactions Although synergis

  • Page 252 and 253:

    use in asthma has declined consider

  • Page 254 and 255:

    α 1-antitrypsin deficiency, neutro

  • Page 256 and 257:

    PART VI THE ALIMENTARY SYSTEM

  • Page 258 and 259:

    ● Peptic ulceration 247 ● Oesop

  • Page 260 and 261:

    PEPTIC ULCERATION 249 • With rega

  • Page 262 and 263:

    Ranitidine has a similar profile of

  • Page 264 and 265:

    Vestibular stimulation ? via cerebe

  • Page 266 and 267:

    cortical centres affecting vomiting

  • Page 268 and 269:

    • in hepatocellular failure to re

  • Page 270 and 271:

    Ciprofloxacin is occasionally used

  • Page 272 and 273:

    withdrawal), small doses of benzodi

  • Page 274 and 275:

    Table 34.7: Dose-independent hepato

  • Page 276 and 277:

    ● Introduction 265 ● General ph

  • Page 278 and 279:

    dinucleotide (NAD) and nicotinamide

  • Page 280 and 281:

    Table 35.1: Common trace element de

  • Page 282 and 283:

    PART VII FLUIDS AND ELECTROLYTES

  • Page 284 and 285:

    ● Introduction 273 ● Volume ove

  • Page 286 and 287:

    Key points Diuretics Diuretics are

  • Page 288 and 289:

    is sometimes caused by drugs, notab

  • Page 290 and 291:

    or with potassium-sparing diuretics

  • Page 292 and 293:

    Greger R, Lang F, Sebekova, Heidlan

  • Page 294 and 295:

    PART VIII THE ENDOCRINE SYSTEM

  • Page 296 and 297:

    ● Introduction 285 ● Pathophysi

  • Page 298 and 299:

    in prefilled injection devices (‘

  • Page 300 and 301:

    Metformin should be withdrawn and i

  • Page 302 and 303:

    FURTHER READING American Diabetes A

  • Page 304 and 305:

    deficiency. Potassium iodide (3 mg

  • Page 306 and 307:

    fertility. It is contraindicated du

  • Page 308 and 309:

    ● Introduction 297 ● Vitamin D

  • Page 310 and 311:

    effective in life-threatening hyper

  • Page 312 and 313:

    Further reading Block GA, Martin KJ

  • Page 314 and 315:

    Table 40.1: Actions of cortisol and

  • Page 316 and 317:

    injection may be useful, but if don

  • Page 318 and 319:

    CHAPTER 41 REPRODUCTIVE ENDOCRINOLO

  • Page 320 and 321:

    elease by the pituitary via negativ

  • Page 322 and 323:

    Treatment with depot progestogen in

  • Page 324 and 325:

    infusion using an infusion pump to

  • Page 326 and 327:

    significant proportion of men who r

  • Page 328 and 329:

    with symptoms caused by the release

  • Page 330 and 331:

    FURTHER READING Birnbaumer M. Vasop

  • Page 332 and 333:

    PART IX SELECTIVE TOXICITY

  • Page 334 and 335:

    ● Principles of antibacterial che

  • Page 336 and 337:

    2. transfer of resistance between o

  • Page 338 and 339:

    Pharmacokinetics Absorption of thes

  • Page 340 and 341:

    Mechanism of action Macrolides bind

  • Page 342 and 343:

    asic quinolone structure dramatical

  • Page 344 and 345:

    Case history A 70-year-old man with

  • Page 346 and 347:

    PRINCIPLES OF MANAGEMENT OF MYCOBAC

  • Page 348 and 349:

    Pharmacokinetics Absorption from th

  • Page 350 and 351:

    MYCOBACTERIUM LEPRAE INFECTION Lepr

  • Page 352 and 353:

    POLYENES AMPHOTERICIN B Uses Amphot

  • Page 354 and 355:

    therapy is adequate though more fre

  • Page 356 and 357:

    NUCLEOSIDE ANALOGUES ACICLOVIR Uses

  • Page 358 and 359:

    Table 45.3: Summary of available ac

  • Page 360 and 361:

    Uses Interferon-α when combined wi

  • Page 362 and 363:

    ● Introduction 351 ● Immunopath

  • Page 364 and 365:

    Table 46.1: Examples of combination

  • Page 366 and 367:

    NON-NUCLEOSIDE ANALOGUE REVERSE TRA

  • Page 368 and 369:

    FUSION INHIBITORS Uses Currently, e

  • Page 370 and 371:

    salvage therapy include azithromyci

  • Page 372 and 373:

    ● Malaria 361 ● Trypanosomal in

  • Page 374 and 375:

    Pharmacokinetics Chloroquine is rap

  • Page 376 and 377:

    Table 47.2: Drug therapy of non-mal

  • Page 378 and 379:

    ● Introduction 367 ● Pathophysi

  • Page 380 and 381:

    Table 48.1: Classification of commo

  • Page 382 and 383:

    Polymorph count/mm 3 (a) (b) 10 000

  • Page 384 and 385:

    doses are used to prepare patients

  • Page 386 and 387:

    Adverse effects Methotrexate Inhibi

  • Page 388 and 389:

    Table 48.7: Summary of clinical pha

  • Page 390 and 391:

    Table 48.9: Summary of the clinical

  • Page 392 and 393:

    Plasma membrane Signal transduction

  • Page 394 and 395:

    Table 48.10: Monoclonal antibodies

  • Page 396 and 397:

    INTERFERON-ALFA 2B Interferon-alfa

  • Page 398 and 399:

    PART X HAEMATOLOGY

  • Page 400 and 401:

    ● Haematinics - iron, vitamin B 1

  • Page 402 and 403:

    one marrow to produce red cells. Th

  • Page 404 and 405:

    EPO Erythroid precursors Erythrocyt

  • Page 406 and 407:

    Therapeutic principles The extent o

  • Page 408 and 409:

    PART XI IMMUNOPHARMACOLOGY

  • Page 410 and 411:

    ● Introduction 399 ● Immunity a

  • Page 412 and 413:

    Key points Antigen recognition Expr

  • Page 414 and 415:

    Table 50.1: Novel anti-proliferativ

  • Page 416 and 417:

    Key points Treatment of anaphylacti

  • Page 418 and 419:

    DRUGS THAT ENHANCE IMMUNE SYSTEM FU

  • Page 420 and 421:

    PART XII THE SKIN

  • Page 422 and 423:

    ● Introduction 411 ● Acne 411

  • Page 424 and 425:

    DERMATITIS (ECZEMA) PRINCIPLES OF T

  • Page 426 and 427:

    SPECIALISTS ONLY SPECIALISTS ONLY E

  • Page 428 and 429:

    TREATMENT OF OTHER SKIN INFECTIONS

  • Page 430 and 431:

    effect of too high a dose of UVB in

  • Page 432 and 433:

    PART XIII THE EYE

  • Page 434 and 435:

    ● Introduction: ocular anatomy, p

  • Page 436 and 437:

    to cause pupillary dilatation, name

  • Page 438 and 439:

    Table 52.3: Antibacterial agents us

  • Page 440 and 441:

    Table 52.6: Common drug-induced pro

  • Page 442 and 443:

    PART XIV CLINICAL TOXICOLOGY

  • Page 444 and 445:

    ● Introduction 433 ● Pathophysi

  • Page 446 and 447:

    Table 53.2: Central nervous system

  • Page 448 and 449:

    which provide anonymized data to th

  • Page 450 and 451:

    Peak plasma levels after smoking ci

  • Page 452 and 453:

    Key points Acute effects of alcohol

  • Page 454 and 455:

    FURTHER READING Goldman D, Oroszi G

  • Page 456 and 457:

    Table 54.2: Common indications for

  • Page 458 and 459:

    Table 54.5: Antidotes and other spe

  • Page 460 and 461:

    Commission on Human Medicines (CHM)

  • Page 462 and 463:

    Note: Page numbers in italics refer

  • Page 464 and 465:

    atrial fibrillation 217, 221 digoxi

  • Page 466 and 467:

    Cushing’s syndrome 302 cyclic ade

  • Page 468 and 469:

    5-fluorouracil 375-6 fluoxetine, mo

  • Page 470 and 471:

    children 54 diazepam 108 iron prepa

  • Page 472 and 473:

    non-steroidal anti-inflammatory dru

  • Page 474 and 475:

    puberty (male), delay 314 puerperiu

  • Page 476:

    tolerance 9, 433 benzodiazepines 10

A-Textbook-of-Clinical-Pharmacology-and-Therapeutics-5th-edition
World Journal of Gastrointestinal Pharmacology and Therapeutics
World Journal of Gastrointestinal Pharmacology and Therapeutics
World Journal of Gastrointestinal Pharmacology and Therapeutics
World Journal of Gastrointestinal Pharmacology and Therapeutics
World Journal of Gastrointestinal Pharmacology and Therapeutics
World Journal of Gastrointestinal Pharmacology and Therapeutics
World Journal of Gastrointestinal Pharmacology and Therapeutics
Clinical Pharmacology and Therapeutics
World Journal of Gastrointestinal Pharmacology and Therapeutics
Role of Quantitative Clinical Pharmacology in Guiding Drug
[+][PDF] TOP TREND Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy [NEWS]
Experience In Using PBPK Models in Clinical Pharmacology Reviews
ReadOnline Soliman s Auricular Therapy Textbook: New Localizations and Evidence Based Therapeutic Approaches M.D. Nader Soliman PreOrder
Diagnosis and pharmacological management of Parkinson's - SIGN
Prescribing and Pharmacology of Controlled Drugs: Critical Issues ...
An Anatomico-Clinical Overview - Advances in Clinical ...
NEWS - The Journal of Clinical Endocrinology & Metabolism
HIV/AIDS Treatment and Care : Clinical protocols for the European ...
2012 EDUCATIONAL BOOK - American Society of Clinical Oncology
A textbook of pharmacology and therapeutics, or, The action of ...
CLINICAL PHARMACOLOGY AND THERAPEUTICS FOR THE ...
O - Journal of Pharmacology and Experimental Therapeutics
Pharmacology and therapeutics, clinical trial - Dermage
O - Journal of Pharmacology and Experimental Therapeutics