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A Textbook of Clinical Pharmacology and Therapeutics

A Textbook of Clinical Pharmacology and Therapeutics

MYCOBACTERIUM LEPRAE

MYCOBACTERIUM LEPRAE INFECTION Leprosy manifests in two forms, lepromatoid (the organism being localized to skin or nerve) or lepromatous (a generalized bacteraemic disease that effects many organs, analogous to miliary tuberculosis). The main drugs used to treat leprosy are dapsone, rifampicin and clofazimine. The current World Health Organization (WHO) regimen for multibacillary leprosy is: 1. rifampicin, once a month; 2. dapsone, daily unsupervised given for 24 months; 3. clofazimine, daily unsupervised, plus a larger dose under supervision every four weeks. Other anti-lepromatous drugs include ofloxacin, minocycline, clarithromycin (see Chapter 43) and thalidomide. DAPSONE Uses Dapsone (4,4-diaminodiphenyl sulphone) is a bacteriostatic sulphone. It has been the standard drug for treating all forms of leprosy, but irregular and inadequate duration of treatment as a single agent has produced resistance. Dapsone is used to treat dermatitis herpetiformis, as well as leprosy, pneumocystis and, combined with pyrimethamine, for malaria prophylaxis. Mechanism of action Dapsone is a competitive inhibitor of dihydropteroate (folate) synthase, thereby impairing production of dihydrofolic acid. Adverse effects These include: • anaemia and agranulocytosis; • gastro-intestinal disturbances and (rarely) hepatitis; • allergy and rashes, including Stevens–Johnson syndrome; • peripheral neuropathy; • methaemoglobinaemia; • haemolytic anaemia, especially in glucose-6-phosphate dehydrogenase (G6PDH)-deficient patients. Pharmacokinetics Dapsone is well absorbed (�90%) from the gastro-intestinal tract. The t1/2 is on average 27 hours. It is extensively metabolized in the liver, partly by N-acetylation, with only 10–20% of the parent drug being excreted in the urine. There is some enterohepatic circulation. Drug interactions The metabolism of dapsone is increased by hepatic enzyme inducers (e.g. rifampicin) such that its t1/2 is reduced to 12–15 hours. Case history FURTHER READING MYCOBACTERIUM LEPRAE INFECTION 339 A 27-year old Asian woman presents to her physician with a history of streaky haemoptysis and weight loss for the past two months. Clinical examination is reported as normal. Her chest x-ray shows patchy right upper lobe consolidation and her sputum is positive for acid-fast bacilli. After having obtained three sputum samples, she is started, while in hospital, on a four-drug regimen, pyrazinamide (800 mg/day), ethambutol (600 mg/day), isoniazid (300 mg/day) and rifampicin (450 mg/day). She is also prescribed pyridoxine 10 mg daily (to reduce the likelihood of developing peripheral neuropathy secondary to INH). She tolerates the therapy well, without evidence of hepatic dysfunction, and her systemic symptoms improve. Three months later, when reviewed in the outpatient clinic, she has been off pyrazinamide and ethambutol for just over one month, and she complains of daily nausea and vomiting, and is found to be eight weeks pregnant. She is taking the low-dose oestrogen contraceptive pill and is adamant that she has been meticulously compliant with all of her anti-TB medications and the contraceptive pill. Question What therapeutic problem has occurred here and how can you explain the clinical situation? How could this outcome have been avoided? Answer Ethambutol, isoniazid, rifampicin and pyrazinamide are all inducers of hepatic CYP450 enzymes. Rifampicin is most potent. and affects many CYPs. Over a period of several weeks her drug therapy induced several CYP450 isoenzymes, especially CYP3A4, so that hepatic metabolism of oestrogen and progesterone was markedly enhanced, reducing their systemic concentrations and efficacy as contraceptives. Therefore, drug-induced hepatic CYP450 enzyme induction caused a failure of contraceptive efficacy and so the patient was ‘unprotected’ and became pregnant. The patient should continue on her anti-TB drug regimen, as there is no evidence that these agents are harmful to the developing fetus, except for streptomycin, which should never be given in pregnancy. This outcome could have been prevented by advising the patient to double her usual dose of her oral contraceptives while taking anti-TB therapy, and to take additional contraceptive precautions (e.g. barrier methods), or to abandon the pill altogether and use alternative effective contraceptive measures (e.g. an intrauterine contraceptive device) during her anti-TB drug treatment. Joint Tuberculosis Committee of the British Thoracic Society. Control and prevention of tuberculosis in the United Kingdom: code of practice 2000. Thorax 2000; 55: 887–901. Joint Tuberculosis Committee Guidelines 1999. Management of opportunist mycobacterial infections: Subcommittee of the Joint Tuberculosis Committee of the British Thoracic Society. Thorax 2000; 55: 210–8. Joint Tuberculosis Committee of the British Thoracic Society. Chemotherapy and management of tuberculosis in the United Kingdom: recommendations 1998. Thorax 1998; 53: 536–48.

● Antifungal drug therapy 340 ● Antiviral drug therapy (excluding anti-HIV drugs) 344 CHAPTER 45 FUNGAL AND NON-HIV VIRAL INFECTIONS ANTIFUNGAL DRUG THERAPY INTRODUCTION Fungi, like mammalian cells but unlike bacteria, are eukaryotic and possess nuclei, mitochondria and cell membranes. However, their membranes contain distinctive sterols, ergosterol and lanesterol. The very success of antibacterial therapy has created ecological situations in which opportunistic fungal infections can flourish. In addition, potent immunosuppressive and cytotoxic therapies produce patients with seriously impaired immune defences, in whom fungi that are nonpathogenic to healthy individuals become pathogenic and cause disease. Table 45.1 summarizes an approach to antifungal therapy in immunocompromised patients. Sites of action of antifungal drugs are summarized in Figure 45.1. Table 45.1: An approach to antifungal drug therapy in the immunocompromised host ● Interferons and antiviral hepatitis therapy 348 Glucan in cell wall Ergosterol in cell membrane DNA and RNA in nucleus Griseofulvin inhibits cell division and reproduction of fungal cells Fungal cell Flucytosine inhibits synthesis of fungal DNA and RNA Figure 45.1: Sites of action of antifungal drugs. Amphotericin B and nystatin bind with ergosterol and disrupt cell membrane Fluconazole, other azoles, and terbinafine inhibit synthesis of ergosterol and disrupt cell membrane Caspofungin inhibits synthesis of glucan and disrupts cell wall Fungal infection Drug therapy for superficial infection Drug therapy for deep-seated infection Candida Nystatin – topical Clotrimazole – topical Amphotericin B with or without flucytosine Miconazole – topical Fluconazole – oral or i.v. Fluconazole – oral Itraconazole or voriconazole oral Caspofungin if failing azole therapy Aspergillus Amphotericin B i.v. (liposomal) Voriconazole or caspofungin if failing azole therapy Cryptococcus Amphotericin B plus flucytosine or fluconazole i.v. (oral continuation therapy) Disseminated histoplasmosis Itraconazole or amphotericin B i.v. (or fluconazole) Disseminated coccidiomycosis Fluconazole or amphotericin B i.v. (plus flucytosine) or itraconazole Blastomycosis Amphotericin B i.v. or itraconazole

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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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    Mechanism of action GTN works by re

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    Because of the risks of haemorrhage

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    Intrinsic pathway XIIa XIa the acti

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    that the pharmacodynamic response i

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    used with apparent benefit in acute

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    ● Introduction 211 ● Pathophysi

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    The drugs that are most effective i

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    therapeutic plasma concentration ca

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    ● Common dysrhythmias 217 ● Gen

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    BASIC LIFE SUPPORT CARDIOPULMONARY

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    arrest. The electrocardiogram is li

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    should be given to insertion of an

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    Drug interactions Amiodarone potent

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    effect when treating sinus bradycar

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    Case history A 24-year-old medical

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    PART V THE RESPIRATORY SYSTEM

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    CHAPTER 33 THERAPY OF ASTHMA, CHRON

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    STEP 5: CONTINUOUS OR FREQUENT USE

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    Adenylyl cyclase Table 33.1: Compar

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    Drug interactions Although synergis

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    use in asthma has declined consider

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    α 1-antitrypsin deficiency, neutro

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    PART VI THE ALIMENTARY SYSTEM

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    ● Peptic ulceration 247 ● Oesop

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    PEPTIC ULCERATION 249 • With rega

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    Ranitidine has a similar profile of

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    Vestibular stimulation ? via cerebe

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    cortical centres affecting vomiting

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    • in hepatocellular failure to re

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    Ciprofloxacin is occasionally used

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    withdrawal), small doses of benzodi

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    Table 34.7: Dose-independent hepato

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    ● Introduction 265 ● General ph

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    dinucleotide (NAD) and nicotinamide

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    Table 35.1: Common trace element de

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    PART VII FLUIDS AND ELECTROLYTES

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    ● Introduction 273 ● Volume ove

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    Key points Diuretics Diuretics are

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    is sometimes caused by drugs, notab

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    or with potassium-sparing diuretics

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    Greger R, Lang F, Sebekova, Heidlan

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    PART VIII THE ENDOCRINE SYSTEM

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    ● Introduction 285 ● Pathophysi

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    in prefilled injection devices (‘

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  • Page 334 and 335: ● Principles of antibacterial che
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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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