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A Textbook of Clinical Pharmacology and Therapeutics

A Textbook of Clinical Pharmacology and Therapeutics

Ranitidine has a similar

Ranitidine has a similar profile of minor side effects to cimetidine. There have been some very rare reports of breast swelling and tenderness in men. However, unlike cimetidine, ranitidine does not bind to androgen receptors, and impotence and gynaecomastia in patients on high doses of cimetidine have been reported to resolve when they were switched to ranitidine. Cardiovascular effects have been even more infrequently reported than with cimetidine. Small amounts of ranitidine penetrate the central nervous system (CNS) and (like, but less commonly than, cimetidine) it can (rarely) cause mental confusion, mainly in the elderly and in patients with hepatic or renal impairment. Drug interactions Ranitidine has a lower affinity for cytochrome P450 than cimetidine and does not inhibit the metabolism of warfarin, phenytoin and theophylline to a clinically significant degree. Choice of H2-antagonist All of the H2-receptor antagonists currently available in the UK are effective in peptic ulceration and are well tolerated. Cimetidine and ranitidine are most commonly prescribed and have been available for the longest time. Cimetidine is the least expensive, but in young men who require prolonged treatment ranitidine may be preferable, due to a lower reported incidence of impotence and gynaecomastia. Ranitidine is also preferable in the elderly, where cimetidine occasionally causes confusion, and also when the patient is on drugs whose metabolism is inhibited by cimetidine (e.g. warfarin, phenytoin or theophylline). Other H2-receptor antagonists available for use in the UK include famotidine and nizatidine, but they offer no significant advantage over ranitidine. PROTON-PUMP INHIBITORS The proton-pump inhibitors inhibit gastric acid by blocking the H � /K � -adenosine triphosphatase enzyme system (the proton pump) of the gastric parietal cell. Examples are omeprazole, esomeprazole, lansoprazole, pantoprazole and rabeprazole. The main differences, if any, appear to be in relation to drug interactions. As yet there do not appear to be any clinically significant drug interactions with pantoprazole, whereas omeprazole inhibits cytochrome P450 and lansoprazole is a weak inducer of cytochrome P450. The indications for proton-pump inhibitors include the following: • benign duodenal and gastric ulcers; • NSAID-associated peptic ulcer and gastro-duodenal erosions; • in combination with antibacterial drugs to eradicate H. pylori; • Zollinger–Ellison syndrome; • gastric acid reduction during general anaesthesia; • gastro-oesophageal reflux disease (GORD); • stricturing and erosive oesophagitis where they are the treatment of choice. DRUGS THAT ENHANCE MUCOSAL RESISTANCE PROSTAGLADIN ANALOGUES Misoprostol is a synthetic analogue of prostaglandin E1 which inhibits gastric acid secretion, causes vasodilatation in the submucosa and stimulates the production of protective mucus. Uses These include the following: PEPTIC ULCERATION 251 1. healing of duodenal ulcer and gastric ulcer, including those induced by NSAIDs; 2. prophylaxis of gastric and duodenal ulceration in patients on NSAID therapy. Adverse effects Diarrhoea, abdominal pain, nausea and vomiting, dyspepsia, flatulence, abnormal vaginal bleeding, rashes and dizziness may occur. The most frequent adverse effects are gastrointestinal and these are usually dose dependent. Contraindications Pregnancy (or desired pregnancy) is an absolute contraindication to the use of misoprostol, as the latter causes abortion. BISMUTH CHELATE Colloidal tripotassium dicitratobismuthate precipitates at acid pH to form a layer over the mucosal surface and ulcer base, where it combines with the proteins of the ulcer exudate. This coat is protective against acid and pepsin digestion. It also stimulates mucus production and may chelate with pepsin, thus speeding ulcer healing. Several studies have shown it to be as active as cimetidine in the healing of duodenal and gastric ulcers after four to eight weeks of treatment. It has a direct toxic effect on H. pylori and may be used as part of triple therapy. Bismuth chelate elixir is given diluted with water 30 minutes before meals and two hours after the last meal of the day. This liquid has an ammoniacal, metallic taste and odour which is unacceptable to some patients, and chewable tablets can be used instead. Antacids or milk should not be taken concurrently. Ranitidine bismuth citrate tablets are also available for the treatment of peptic ulcers and for use in H. pylori eradication regimes. Adverse effects Adverse effects include blackening of the tongue, teeth and stools (causing potential confusion with melaena) and nausea. The latter may limit dosing. Bismuth is potentially neurotoxic. Urine bismuth levels rise with increasing oral dosage, indicating some intestinal absorption. Although with normal doses the blood concentration remains well below the toxic threshold, bismuth should not be used in renal failure or for maintenance treatment.

252 ALIMENTARY SYSTEM AND LIVER SUCRALFATE Use Sucralfate is used in the management of benign gastric and duodenal ulceration and chronic gastritis. Its action is entirely local, with minimal if any systemic absorption. It is a basic aluminium salt of sucrose octasulphate which, in the presence of acid, becomes a sticky adherent paste that retains antacid efficacy. This material coats the floor of ulcer craters, exerting its acid-neutralizing properties locally, unlike conventional antacid gels which form a diffusely distributed antacid dispersion. In addition it binds to pepsin and bile salts and prevents their contact with the ulcer base. Sucralfate compares favourably with cimetidine for healing both gastric and duodenal ulcers, and is equally effective in symptom relief. The dose is 1 g (one tablet) four times daily for four to six weeks. Antacids may be given concurrently. Adverse effects Sucralfate is well tolerated but, because it contains aluminium, constipation can occur and in severe renal failure accumulation is a potential hazard. Case history A 75-year-old retired greengrocer who presented to the Accident and Emergency Department with shortness of breath and a history of melaena is found on endoscopy to have a bleeding gastric erosion. His drug therapy leading up to his admission consisted of digoxin, warfarin and piroxicam for a painful hip, and over-the-counter cimetidine selfinitiated by the patient for recent onset indigestion. Question How may this patient’s drug therapy have precipitated or aggravated his bleeding gastric erosion? Answer NSAIDs inhibit the biosynthesis of prostaglandin E 2, as well as causing direct damage to the gastric mucosa. Warfarin is an anticoagulant and will increase bleeding. Cimetidine inhibits CYP450 enzymes and therefore inhibits the metabolism of warfarin, resulting in higher blood concentrations and an increased anticoagulant effect. OESOPHAGEAL DISORDERS REFLUX OESOPHAGITIS Reflux oesophagitis is a common problem. It causes heartburn and acid regurgitation and predisposes to stricture formation. NON-DRUG MEASURES Non-drug measures which may be useful include the following: 1. sleeping with the head of the bed raised. Most damage to the oesophagus occurs at night when swallowing is much reduced and acid can remain in contact with the mucosa for long periods; 2. avoiding: • large meals; • alcohol and/or food before bed; • smoking, which lowers the lower oesophageal sphincter pressure, and coffee; • aspirin and NSAIDs; • constricting clothing around the abdomen; 3. weight reduction; 4. bending from the knees and not the spine; 5. regular exercise. DRUG THERAPY Drugs that may be useful include the following: 1. metoclopramide, which increases oesophageal motility as well as being anti-emetic. It may also improve gastrooesophageal sphincter function and accelerate gastric emptying; 2. a mixture of alginate and antacids is symptomatically useful – the alginate forms a viscous layer floating on the gastric contents; 3. symptomatic relief may be obtained with antacids, but there is a risk of chronic aspiration of poorly soluble particles of magnesium or aluminium salts if these are taken at night; 4. H 2-antagonists; 5. proton-pump inhibitors are the most effective agents currently available for reflux oesophagitis and are the drugs of choice for erosive reflux oesophagitis. Case history A 25-year-old male estate agent complains of intermittent heartburn, belching and sub-xiphisternal pain which has been present on most nights for two weeks. It was particularly severe the previous Saturday night after he had consumed a large curry and several pints of beer. The symptoms were not improved by sleeping on two extra pillows or by taking ibuprofen. He smokes ten cigarettes daily. Examination revealed him to be overweight, but was otherwise unremarkable. Question Outline your management of this patient. Answer Life-style advice – stop smoking, lose weight and exercise, adopt a low-fat diet, avoid tight clothing, avoid large meals or eating within three hours of going to bed. Raise the head of the bed (do not add pillows). Avoid NSAIDs and excessive alcohol. Prescribe alginate/antacids. If there is an inadequate response or early relapse, prescribe an H 2-blocker or proton-pump inhibitor for six weeks. If symptoms have still not completely resolved, refer the patient for endoscopy.

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    A Textbook of Clinical Pharmacology

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    A Textbook of Clinical Pharmacology

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    This fifth edition is dedicated to

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    FOREWORD viii PREFACE ix ACKNOWLEDG

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    PREFACE Clinical pharmacology is th

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    PART I GENERAL PRINCIPLES

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    ● Use of drugs 3 ● Adverse effe

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    and acquired factors, notably disea

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

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    Dose ratio -1 100 50 The relationsh

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    ● Introduction 11 ● Constant-ra

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    In reality, processes of eliminatio

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    lood (from which samples are taken

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    ● Introduction 17 ● Bioavailabi

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    ROUTES OF ADMINISTRATION ORAL ROUTE

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    Transdermal absorption is sufficien

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    FURTHER READING Fix JA. Strategies

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    and thromboxanes are CYP450 enzymes

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    and lorazepam. Some patients inheri

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    Orally administered drug Parenteral

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    ● Introduction 31 ● Glomerular

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    ACTIVE TUBULAR REABSORPTION This is

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    DISTRIBUTION Drug distribution is a

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    Detailed recommendations on dosage

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    DIGOXIN Myxoedematous patients are

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    ● Introduction 41 ● Role of dru

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    25 20 10 Life-threatening toxicity

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    ● Introduction 45 ● Harmful eff

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    vagina in girls in their late teens

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    an anti-analgesic effect when combi

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    Case history A 20-year-old female m

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    METABOLISM At birth, the hepatic mi

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    lifelong effects as a result of tox

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    DISTRIBUTION Ageing is associated w

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    DIGOXIN Digoxin toxicity is common

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    FURTHER READING Dhesi JK, Allain TJ

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    Factors involved in the aetiology o

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    analgesic. Following its release, t

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    antibiotics, such as penicillin or

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    predisposes to non-immune haemolysi

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    ● Introduction 71 ● Useful inte

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    Response Therapeutic range Toxic ra

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    Table 13.1: Interactions outside th

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    Table 13.5: Competitive interaction

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    ● Introduction: ‘personalized m

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    Table 14.2: Variations in drug resp

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    lipoprotein (LDL) is impaired. LDL

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    Key points • Genetic differences

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    • Discovery • • Screening Pre

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    Too many statistical comparisons pe

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    ETHICS COMMITTEES Protocols for all

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    Table 16.1: Recombinant proteins/en

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    duration and benefit. Adenoviral ve

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    ● Introduction 97 ● Garlic 97

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    A case report has suggested a possi

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    including hypericin and pseudohyper

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    PART II THE NERVOUS SYSTEM

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    ● Introduction 105 ● Sleep diff

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    and daytime sleeping should be disc

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    Key points • Insomnia and anxiety

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    Box 19.1: Dopamine theory of schizo

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    The Boston Collaborative Survey ind

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    Oral medication, especially in liqu

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    e.g. interpersonal difficulties or

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    Partial response to first-line trea

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    Key points Drug treatment of depres

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    Case history A 45-year-old man with

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    Levodopa PRINCIPLES OF TREATMENT IN

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    • pulmonary, retroperitoneal and

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    CHOREA The γ-aminobutyric acid con

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    Cholinergic crisis Treatment of mya

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    ● Introduction 133 ● Mechanisms

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    absolute arbiter. The availability

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    Table 22.2: Metabolic interactions

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    FURTHER ANTI-EPILEPTICS Other drugs

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    Case history A 24-year-old woman wh

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    Assessment of migraine severity and

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    ● General anaesthetics 145 ● In

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    is the theoretical concern of a ‘

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    • Respiratory system - apnoea fol

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    Competitive antagonists (vecuronium

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    have also proved useful in combinat

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    ● Introduction 155 ● Pathophysi

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    ASPIRIN (ACETYLSALICYLATE) Use Anti

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    Key points Drugs for mild pain •

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    increases, correlating with the hig

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    • If possible, use oral medicatio

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    PART III THE MUSCULOSKELETAL SYSTEM

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    ● Introduction: inflammation 167

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    Chapter 33). All NSAIDs cause wheez

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    • Stomatitis suggests the possibi

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    Pharmacokinetics Allopurinol is wel

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    PART IV THE CARDIOVASCULAR SYSTEM

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    ● Introduction 177 ● Pathophysi

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    esponsible for the strong predilect

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    Ezetimibe Fat Muscle Dietary fat In

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    educed). The risk of muscle damage

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    ● Introduction 185 ● Pathophysi

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    Each of these classes of drug reduc

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    AT 1 receptor) produce good 24-hour

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    Table 28.2: Examples of calcium-cha

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    Key points Drugs used in essential

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    Case history A 72-year-old woman se

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    Assess risk factors Investigations:

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    Persistent ST segment elevation Thr

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    Further reading Block GA, Martin KJ

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    Table 40.1: Actions of cortisol and

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    injection may be useful, but if don

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    CHAPTER 41 REPRODUCTIVE ENDOCRINOLO

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    elease by the pituitary via negativ

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    Treatment with depot progestogen in

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    infusion using an infusion pump to

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    significant proportion of men who r

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    with symptoms caused by the release

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    FURTHER READING Birnbaumer M. Vasop

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    PART IX SELECTIVE TOXICITY

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    ● Principles of antibacterial che

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    2. transfer of resistance between o

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    Pharmacokinetics Absorption of thes

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    Mechanism of action Macrolides bind

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    asic quinolone structure dramatical

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    Case history A 70-year-old man with

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    PRINCIPLES OF MANAGEMENT OF MYCOBAC

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    Pharmacokinetics Absorption from th

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    MYCOBACTERIUM LEPRAE INFECTION Lepr

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    POLYENES AMPHOTERICIN B Uses Amphot

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    therapy is adequate though more fre

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    NUCLEOSIDE ANALOGUES ACICLOVIR Uses

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    Table 45.3: Summary of available ac

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    Uses Interferon-α when combined wi

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    ● Introduction 351 ● Immunopath

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    Table 46.1: Examples of combination

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    NON-NUCLEOSIDE ANALOGUE REVERSE TRA

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    FUSION INHIBITORS Uses Currently, e

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    salvage therapy include azithromyci

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    ● Malaria 361 ● Trypanosomal in

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    Pharmacokinetics Chloroquine is rap

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    Table 47.2: Drug therapy of non-mal

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    ● Introduction 367 ● Pathophysi

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    Table 48.1: Classification of commo

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

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    doses are used to prepare patients

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    Adverse effects Methotrexate Inhibi

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    Table 48.7: Summary of clinical pha

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    Table 48.9: Summary of the clinical

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    Plasma membrane Signal transduction

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    Table 48.10: Monoclonal antibodies

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    INTERFERON-ALFA 2B Interferon-alfa

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    PART X HAEMATOLOGY

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    ● Haematinics - iron, vitamin B 1

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    one marrow to produce red cells. Th

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    EPO Erythroid precursors Erythrocyt

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    Therapeutic principles The extent o

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    PART XI IMMUNOPHARMACOLOGY

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    ● Introduction 399 ● Immunity a

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    Key points Antigen recognition Expr

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    Table 50.1: Novel anti-proliferativ

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    Key points Treatment of anaphylacti

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    DRUGS THAT ENHANCE IMMUNE SYSTEM FU

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    PART XII THE SKIN

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    ● Introduction 411 ● Acne 411

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    DERMATITIS (ECZEMA) PRINCIPLES OF T

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    SPECIALISTS ONLY SPECIALISTS ONLY E

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    TREATMENT OF OTHER SKIN INFECTIONS

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    effect of too high a dose of UVB in

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    PART XIII THE EYE

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    ● Introduction: ocular anatomy, p

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    to cause pupillary dilatation, name

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    Table 52.3: Antibacterial agents us

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    Table 52.6: Common drug-induced pro

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    PART XIV CLINICAL TOXICOLOGY

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    ● Introduction 433 ● Pathophysi

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    Table 53.2: Central nervous system

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    which provide anonymized data to th

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    Peak plasma levels after smoking ci

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    Key points Acute effects of alcohol

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    FURTHER READING Goldman D, Oroszi G

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    Table 54.2: Common indications for

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    Table 54.5: Antidotes and other spe

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    Commission on Human Medicines (CHM)

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    Note: Page numbers in italics refer

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    atrial fibrillation 217, 221 digoxi

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    Cushing’s syndrome 302 cyclic ade

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    5-fluorouracil 375-6 fluoxetine, mo

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    children 54 diazepam 108 iron prepa

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    non-steroidal anti-inflammatory dru

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    puberty (male), delay 314 puerperiu

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    tolerance 9, 433 benzodiazepines 10

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