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A Textbook of Clinical Pharmacology and Therapeutics

A Textbook of Clinical Pharmacology and Therapeutics

Chapter 33). All NSAIDs

Chapter 33). All NSAIDs cause wheezing in aspirin-sensitive individuals. COX-2 inhibitors increase cardiovascular events, limiting their usefulness. Unfortunately, they were aggressively marketed to elderly people many of whom were not at high risk for gastro-toxicity and this has led to the withdrawal of agents that would have been valuable for a more carefully targeted patient population. It is unclear how much, if any, cardiovascular risk is associated with conventional NSAIDs, but it is possible that this is, at a maximum, similar to certain COX-2selective drugs. NSAIDs cause hepatitis in some patients. The mechanism is not understood, but the elderly are particularly susceptible. Different NSAIDs vary in how commonly they cause this problem. (Hepatotoxicity was one of the reasons for the withdrawal of one such drug, benoxaprofen, from the market.) Aspirin is a recognized cause of hepatitis, particularly in patients with systemic lupus erythematosus. Aspirin and ibuprofen are covered in Chapter 25). Other important NSAIDs are covered below. INDOMETACIN Use Indometacin has a powerful anti-inflammatory action, but only a weak analgesic action. It is used to treat rheumatoid arthritis and associated disorders, ankylosing spondylitis and acute gout. Adverse effects are common (approximately 25% of patients). Adverse effects Gastric intolerance and toxicity, renal and pulmonary toxicities occur, as with other NSAIDs (see above). Headache is also common; less often light-headedness, confusion or hallucinations arise. Pharmacokinetics Indometacin is readily absorbed by mouth or from suppositories. It undergoes extensive hepatic metabolism. Both the parent drug and inactive metabolites are excreted in the urine. Drug interactions The actions of antihypertensive drugs and diuretics are opposed by indometacin. Triamterene, in particular, should be avoided, because of hyperkalaemia. NAPROXEN Use Naproxen is used rheumatic and musculoskeletal diseases, acute gout and dysmenorrhoea. Mechanism of action Naproxen is approximately 20 times as potent an inhibitor of COX as aspirin. An additional property is inhibition of leukocyte migration, with a potency similar to colchicine. DISEASE-MODIFYING ANTIRHEUMATIC DRUGS 169 Adverse effects Naproxen causes all of the adverse effects common to NSAIDs. Key points NSAIDs • Inhibit cyclo-oxygenase (COX). • Examples include indometacin, naproxen and ibuprofen. • Uses: – short term: analgesia/anti-inflammatory; – chronic: symptomatic relief in arthritis. • Adverse effects: – gastritis and other gastrointestinal inflammation/bleeding; – reversible renal impairment (haemodynamic effect); – interstitial nephritis (idiosyncratic); – asthma in ‘aspirin-sensitive’ patients; – hepatitis (idiosyncratic). • Interactions: – antihypertensive drugs (reduced effectiveness); – diuretics: reduced effectiveness • COX-2-selective drugs may have reduced gastric toxicity, but increase cardiovascular thrombotic events. GLUCOCORTICOIDS Glucocorticoids are discussed in Chapters 40 and 50. Despite their profound effects on inflammation (they were the original ‘wonder drugs’ of the 1950s), they have such severe long-term effects that their use is now much more circumscribed. Prednisolone is generally preferred for systemic use when a glucocorticoid is specifically indicated (e.g. for giant-cell arteritis, where steroid treatment prevents blindness). A brief course of high-dose prednisolone is usually given to suppress the disease, followed if possible by dose reduction to a maintenance dose, given first thing in the morning when endogenous glucocorticoids are at their peak. A marker of disease activity, such as C-reactive protein (CRP), is followed as a guide to dose reduction. Intra-articular steroid injections are important to reduce pain and deformity. It is essential to rule out infection before injecting steroids into a joint, and meticulous aseptic technique is needed to avoid introducing infection. A suspension of a poorly soluble drug, such as triamcinolone, is used to give a long-lasting effect. The patient is warned to avoid over-use of the joint should the desired improvement materialize, to avoid joint destruction. Repeated injections can cause joint destruction and bone necrosis. DISEASE-MODIFYING ANTIRHEUMATIC DRUGS Disease-modifying antirheumatic drugs (DMARDs) are not analgesic and do not inhibit COX, but they do suppress the

170 ANTI-INFLAMMATORY DRUGS AND THE TREATMENT OF ARTHRITIS inflammatory process in inflammatory arthritis. Their mechanisms are generally poorly understood. They are used in patients with progressive disease. Response (though unpredictable) is usually maximal in four to ten weeks. Unlike NSAIDs, DMARDs reduce inflammatory markers (historically, it was this effect that led to them being referred to as ‘diseasemodifying’). It is difficult to prove that a drug influences the natural history of a relapsing/remitting and unpredictably progressing disease, such as rheumatoid arthritis, but immunosuppressants retard the radiological progression of bony erosions. DMARDs are toxic, necessitating careful patient monitoring, and are best used by physicians experienced in rheumatology. Rheumatologists use them earlier than in the past, with close monitoring for toxicity, with the patient fully informed about toxic, as well as desired, effects. This is especially important since many of these drugs are licensed for quite different indications to arthritis. In terms of efficacy, methotrexate, gold, D-penicillamine, azathioprine and sulfasalazine are similar, and are all more potent than hydroxychloroquine. Methotrexate (Chapter 48) is better tolerated than the other DMARDs, and is usually the first choice. Sulfasalazine (Chapter 34) is the second choice. Alternative DMARDs, and some of their adverse effects, are summarized in Table 26.1. GOLD SALTS Use Gold was originally introduced to treat tuberculosis. Although ineffective, it was found to have antirheumatic properties and has been used to treat patients with rheumatoid arthritis since the 1920s. Sodium aurothiomalate is administered weekly by Table 26.1: Disease-modifying antirheumatic drugs (DMARDs) deep intramuscular injection. About 75% of patients improve, with a reduction in joint swelling, disappearance of rheumatoid nodules and a fall in C-reactive protein (CRP) levels. Urine must be tested for protein and full blood count (with platelet count and differential white cell count) performed before each injection. Auranofin is an oral gold preparation with less toxicity, but less efficacy than aurothiomalate. Treatment should be stopped if there is no response within six months. Mechanism of action The precise mechanism of gold salts is unknown. Several effects could contribute. Gold–albumin complexes are phagocytosed by macrophages and polymorphonuclear leukocytes and concentrated in their lysosomes, where gold inhibits lysosomal enzymes that have been implicated in causing joint damage. Gold binds to sulphhydryl groups and inhibits sulphhydryl–disulphide interchange in immunoglobulin and complement, which could influence immune processes. Adverse effects Adverse effects are common and severe: Drug Adverse effects Comments • Rashes are an indication to stop treatment, as they can progress to exfoliation. • Photosensitive eruptions and urticaria are often preceded by itching. • Glomerular injury can cause nephrotic syndrome. Treatment must be withheld if more than a trace of proteinuria is present, and should not be resumed until the urine is protein free. • Blood dyscrasias (e.g. neutropenia) can develop rapidly. Immunosuppressants: Blood dyscrasias, carcinogenesis, Methotrexate is usually the first-choice azathioprine, methotrexate, opportunistic infection, alopecia, DMARD ciclosporin nausea; methotrexate also causes mucositis and cirrhosis; ciclosporin causes nephrotoxicity, hypertension and hyperkalaemia Sulfasalazine Blood dyscrasias, nausea, rashes, First introduced for arthritis, now used colours urine/tears orange mainly in inflammatory bowel disease (Chapter 34) Gold salts Rashes, nephrotic syndrome, Oral preparation (auranofin) more blood dyscrasias, stomatitis, convenient, less toxic, but less effective than diarrhoea intramuscular aurothiomalate Penicillamine Blood dyscrasias, proteinuria, urticaria Antimalarials: chloroquine, Retinopathy, nausea, diarrhoea, See Chapter 47 hydroxychloroquine rashes, pigmentation of palate, bleaching of hair

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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

  • 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
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  • Page 140 and 141: CHOREA The γ-aminobutyric acid con
  • Page 142 and 143: Cholinergic crisis Treatment of mya
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  • 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
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  • Page 160 and 161: • Respiratory system - apnoea fol
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  • Page 170 and 171: Key points Drugs for mild pain •
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  • Page 178 and 179: ● Introduction: inflammation 167
  • 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
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  • Page 206 and 207: Case history A 72-year-old woman se
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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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    Metformin should be withdrawn and i

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    FURTHER READING American Diabetes A

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    deficiency. Potassium iodide (3 mg

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    fertility. It is contraindicated du

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    ● Introduction 297 ● Vitamin D

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    effective in life-threatening hyper

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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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