Views
5 years ago

A Textbook of Clinical Pharmacology and Therapeutics

A Textbook of Clinical Pharmacology and Therapeutics

is sometimes caused by

is sometimes caused by drugs, notably the anticonvulsant carbamazepine, which stimulates ADH release from the posterior pituitary, and sulphonylureas, which potentiate its action on the renal collecting ducts. Antidiuretic hormone secretion results in a concentrated urine, while continued drinking (as a result of dietary habit) leads to progressive dilution of the plasma, which becomes hypo-osmolar and hyponatraemic. The plasma volume is slightly increased and urinary sodium loss continues. Some causes of SIADH resolve spontaneously (e.g. some cases of head injury), whereas others may improve after specific treatment of the underlying cause (e.g. following chemotherapy for small-cell carcinoma of the bronchus). Hyponatraemia that has arisen gradually can be corrected gradually by restricting fluid intake. This does not cause thirst (because the plasma is hypo-osmolar), but may not be well tolerated because of habit. Rapid correction of hyponatraemia to levels greater than 125 mmol/L is potentially harmful and is associated with central pontine myelinolysis, with resultant devastating loss of brainstem function. Demeclocycline inhibits adenylyl cyclase and renders the collecting ducts insensitive to ADH (thereby producing a form of nephrogenic diabetes insipidus). It has been used to treat SIADH. In common with other tetracyclines, it increases plasma urea levels and can produce deterioration of renal function and increased loss of sodium in the urine. Electrolytes and renal function must be monitored during treatment. VOLUME DEPLETION PRINCIPLES OF FLUID REPLACEMENT Volume depletion is seldom treated with drugs. Even in Addisonian crisis, where the definitive treatment is replacement with glucocorticoid and mineralocorticoid hormones, emergency treatment pivots on replacement of what is depleted, i.e. salt and water, usually in the form of adequate volumes of isotonic 0.9% sodium chloride solution (Chapter 40). The same is true of diabetic ketoacidosis, where the critical life-saving intervention is the rapid infusion of large volumes of isotonic saline, as well as insulin (Chapter 37). In patients with hypovolaemia due to acute and rapid blood loss, the appropriate fluid with which to replace is blood. In some situations, particularly when hypoalbuminaemia and oedema coexist with acute blood volume depletion, infusion of solutions of high-molecular-weight colloid (e.g. gelatin) may be preferable to isotonic saline. Anaphylactoid reactions are an unusual but severe adverse effect of such treatment. Lactate is metabolized aerobically with the production of bicarbonate and Ringer’s lactate solution is used to avoid hyperchloraemic acidosis. Bicarbonate-containing solutions for i.v. use are being developed. DIABETES INSIPIDUS AND VASOPRESSIN ‘Pure’ water deprivation (i.e. true dehydration) is much less common than loss of salt and water (i.e. desalination). Plasma VOLUME DEPLETION 277 osmolality rapidly increases if fluid intake is inadequate. This causes thirst, which leads to drinking and restoration of plasma osmolality, and to secretion of antidiuretic hormone (ADH, arginine vasopressin) by the posterior pituitary, which results in the formation of a small volume of concentrated urine. ADH combines with receptors coupled to G-proteins. The most physiologically important actions of vasopressin, including its antidiuretic effect, are mediated by V 2-receptors which are coupled to adenylyl cyclase. V 1-receptors activate the phosphatidyl inositol signalling system in vascular smooth muscle, mobilizing cytoplasmic calcium and causing vasoconstriction. Vasopressin renders the collecting ducts permeable to water. Consequently, water leaves the collecting ducts passively down its osmotic gradient from tubular fluid (which is hypotonic at the beginning of the distal tubule) into the highly concentrated papillary interstitium. This process results in the formation of a small volume of highly concentrated urine under the influence of vasopressin. Control of plasma osmolarity via thirst fails when a patient is denied oral fluid, usually because of surgery (‘nil by mouth’). Fluid must then be administered parenterally if dehydration with increased plasma sodium ion concentration is to be prevented. An isotonic (5%) solution of glucose is used in these circumstances, as the glucose is rapidly metabolized to carbon dioxide, leaving water unaccompanied by solute. Surgical patients also lose salt, but unless they have been vomiting or losing electrolyte-rich fluid from the gastro-intestinal tract via a drain or fistula, salt is lost at a lower rate than water. Consequently, post-operative patients are often given two or three volumes of 5% glucose for every volume of isotonic saline, adjusted in the light of serial serum electrolyte determinations. Diabetes insipidus is an uncommon disorder in which either the secretion of ADH is deficient (‘central’ diabetes insipidus which can follow neurosurgery or head injury or complicate diseases such as sarcoid that can infiltrate the posterior pituitary), or in which the sensitivity of the collecting ducts to ADH is deficient (‘nephrogenic’ diabetes insipidus). Nephrogenic diabetes insipidus is sometimes drug induced, lithium being a common cause. Severe nephrogenic diabetes insipidus is a rare X-linked disease caused by a mutation in the V 2-receptor gene. In such cases, exogenous vasopressin or desmopressin (see below) is ineffective. Paradoxically, thiazide diuretics (see above) reduce polyuria in nephrogenic diabetes insipidus by reducing the hypotonicity of fluid entering the distal tubule, and are combined with mild salt restriction. Dehydration is not a problem in diabetes insipidus provided the patient has access to water, because increasing plasma osmolality stimulates thirst. The consequent polydipsia prevents dehydration and hypernatraemia. However, patients with diabetes insipidus are at greatly increased risk of dehydration if they become unconscious for any reason (e.g. anaesthesia for an intercurrent surgical problem). Polydipsia and polyuria in central diabetes insipidus can be prevented by vasopressin. Treatment with ADH necessitates repeated injections. Currently, the usual treatment is therefore with a stable analogue, namely desamino-D-arginine vasopressin (DDAVP, desmopressin). This is sufficiently well

278 NEPHROLOGICAL AND RELATED ASPECTS absorbed through the nasal mucosa for it to be administered intranasally. It is selective for V 2-receptors and lacks the pressor effect of ADH. Desmopressin is also used for nocturnal enuresis in children over seven years old, and intravenously in patients with von Willebrand’s disease before undergoing elective surgery, because it increases circulating von Willebrand factor. It also increases factor VIII in patients with mild/moderate haemophilia. Key points Volume depletion • Volume depletion can be caused by loss of blood or other body fluids (e.g. vomiting, diarrhoea, surgical fistulas). • Replacement should be with appropriate volumes of crystalloid or blood in the case of haemorrhage. • Excessive renal loss of salt (e.g. Addison’s disease) or water (e.g. diabetes insipidus) can be due to renal or endocrine disorders and requires appropriate treatment (e.g. fludrocortisone in Addison’s disease, desmopressin in central diabetes insipidus). DISORDERED POTASSIUM ION BALANCE HYPOKALAEMIA Hypokalaemia commonly accompanies loss of fluid from the gastro-intestinal tract (e.g. vomiting or diarrhoea), or loss of potassium ions into the urine due to diuretic therapy (see above). Hypokalaemia in untreated patients with hypertension is suggestive of mineralocorticoid excess (e.g. Conn’s syndrome, liquorice abuse). Bartter’s syndrome is a rare cause of severe hypokalaemia that should be considered in normotensive children who are not vomiting. Severe hypokalaemia causes symptoms of fatigue and nocturia (because of loss of renal concentrating ability), and can cause dysrhythmias. Mild degrees of hypokalaemia (often associated with diuretic use) are generally well tolerated and of little clinical importance. Risk factors for more serious hypokalaemia include: 1. high-dose diuretics, especially combinations of loop diuretic and thiazide; 2. other drugs that cause potassium loss/redistribution (e.g. systemic steroids, chronic laxative treatment, high dose β 2-agonists); 3. low potassium intake; 4. primary or secondary hyperaldosteronism. POTASSIUM REPLACEMENT There are two ways to increase plasma potassium concentrations: potassium supplements, or potassium-sparing diuretics. POTASSIUM SUPPLEMENTS Potassium salts may be given orally as either an effervescent or slow-release preparation. Diet can be supplemented by foods with a high potassium content, such as fruit and vegetables (bananas and tomatoes are rich in potassium ions). Intravenous potassium salts are usually given as potassium chloride. This is used either to maintain body potassium levels in patients receiving intravenous feeding, or to restore potassium levels in severely depleted patients (e.g. those with diabetic ketoacidosis). The main danger associated with intravenous potassium is hyperkalaemia, which can cause cardiac arrest. Potassium chloride has the dubious distinction of causing the highest frequency of fatal adverse reactions. Potassium chloride solution is infused at a maximum rate of 10 mmol/hour unless there is severe depletion, when 20 mmol/hour can be given with electrocardiographic monitoring. Particular care is needed if there is impaired renal function. Potassium chloride for intravenous replacement should be dilute whenever possible (e.g. mini-bags of prediluted fluid); strong potassium solutions (the most dangerous) should be restricted to areas such as intensive care units where patients may need i.v. potassium while also severely restricting fluid intake. POTASSIUM-SPARING DIURETICS An alternative to potassium supplementation is to combine a thiazide or loop diuretic with a potassium-retaining diuretic (see above). Potassium-retaining diuretics are better tolerated than oral potassium supplements. Key points Disordered K � metabolism • Hypokalaemia is caused by urinary or gastro-intestinal K � loss in excess of dietary intake, or by a shift of K � into cells. Diuretics are often the cause. Endocrine causes include Conn’s syndrome. β 2-Agonists shift K � into cells. • Mild hypokalaemia is often unimportant, but severe hypokalaemia can cause dysrhythmias. Hypokalaemia increases digoxin toxicity. • Emergency treatment (e.g. in diabetic ketoacidosis) involves intravenous replacement, which requires close monitoring (including ECG). • Foods rich in K � include fruit and vegetables. Oral K � preparations are unpalatable and not very effective. • K � -retaining diuretics are used to prevent hypokalaemia. They predispose to hyperkalaemia, especially in patients with impaired renal function or with concomitant use of K � supplements, ACEI or NSAIDs. HYPERKALAEMIA Hyperkalaemia in untreated patients suggests the possibility of renal failure or of mineralocorticoid deficiency (e.g. Addison’s disease). Most commonly, however, it is caused by drugs. Hyperkalaemia can develop either with potassium supplements

  • 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 168 and 169:

    ASPIRIN (ACETYLSALICYLATE) Use Anti

  • 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 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
Clinical Pharmacology of Sleep
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
Diagnosis and pharmacological management of Parkinson's - SIGN
An Anatomico-Clinical Overview - Advances in Clinical ...
2012 EDUCATIONAL BOOK - American Society of Clinical Oncology
CLINICAL PHARMACOLOGY AND THERAPEUTICS FOR THE ...
CLINICAL PHARMACOLOGY THERAPEUTICS
Pharmacology and therapeutics, clinical trial - Dermage