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A Textbook of Clinical Pharmacology and Therapeutics

A Textbook of Clinical Pharmacology and Therapeutics

PEPTIC ULCERATION 249

PEPTIC ULCERATION 249 • With regard to drug therapy, several drugs (see below) are effective. Documented duodenal or gastric ulcerations Table 34.1: Typical triple therapy Helicobacter pylori eradication regime should be treated with an H2-blocker or proton-pump inhibitor. • Test for the presence of H. pylori by using the urease CLO test or antral biopsy at endoscopy. Lansoprazole Amoxicillin 30 mg bd • All suspected gastric ulcers should be endoscoped and biopsied to exclude malignancy, with repeat endoscopy following treatment, to confirm healing and for repeat biopsy. • The current recommendation in relation to H. pylori is summarized above. DRUGS USED TO TREAT PEPTIC ULCERATION BY REDUCING ACIDITY a Clarithromycin 1 g bd 500 mg bd } all for 1 week aMetronidazole 400 mg bd if patient is allergic to penicillin. Key points General management of peptic ulceration • Stop smoking. • Avoid ulcerogenic drugs (e.g. NSAIDs, alcohol, glucocorticosteroids). • Reduce caffeine intake. • Diet should be healthy (avoid obesity, and foods that give rise to symptoms). • Test for the presence of H. pylori. The choice of regimen used to eradicate H. pylori is based on achieving a balance between efficacy, adverse effects, compliance and cost. Most regimens include a combination of acid suppression and effective doses of two antibiotics. A typical regime for eradication of H. pylori is shown in Table 34.1. Eradication should be confirmed, preferably by urea breath test at a minimum of four weeks post-treatment. Non-steroidal anti-inflammatory drug-associated ulcer NSAID-related ulcers will usually heal if the NSAID is withdrawn and a proton-pump inhibitor is prescribed for four weeks. If the NSAID has to be restarted (preferably after healing), H2-receptor antagonists or proton-pump inhibitors or misoprostol (see below) should be co-prescribed. If H. pylori is present it should be eradicated. Key points Ulcer-healing drugs Reduction of acidity: • antacids; • H 2-blockers; • proton-pump inhibitors; • muscarinic blockers (pirenzapine). Mucosal protection: • misoprostol (also reduces gastric acid secretion); • bismuth chelate (also toxic to H. pylori); • sucralfate; • carbenoxolone (rarely prescribed). ANTACIDS Use and adverse effects Antacids have a number of actions which include neutralizing gastric acid and thus relieving associated pain and nausea, reducing delivery of acid into the duodenum following a meal, and inactivation of the proteolytic enzyme pepsin by raising the gastric pH above 4–5. In addition, it is thought that antacid may increase lower oesophageal sphincter tone and reduce oesophageal pressure. A number of preparations are available and the choice will depend on the patient’s preference, often determined by the effect on bowel habit (see Table 34.2). In general terms, antacids should be taken approximately one hour before or after food, as this maximizes the contact time with stomach acid and allows the antacid to coat the stomach in the absence of food. Drug interactions Magnesium and aluminium salts can bind other drugs in the stomach, reducing the rate and extent of absorption of antibacterial agents such as erythromycin, ciprofloxacin, isoniazid, norfloxacin, ofloxacin, pivampicillin, rifampicin and most tetracyclines, as well as other drugs such as phenytoin, itraconazole, ketoconazole, chloroquine, hydroxychloroquine, phenothiazines, iron and penicillamine. They increase the excretion of aspirin (in alkaline urine). H2-RECEPTOR ANTAGONISTS H2-receptors stimulate gastric acid secretion and are also present in human heart, blood vessels and uterus (and probably brain). There are a number of competitive H2-receptor antagonists in clinical use, which include cimetidine and ranitidine. The uses of these are similar and will be considered together in this section. Because each drug is so widely prescribed, separate sections on their individual adverse effects, pharmacokinetics and interactions are given below, followed by a brief consideration of the choice between them. Use 1. H2-receptor angonists are effective in healing both gastric and duodenal ulcers. A four-week course is usually

250 ALIMENTARY SYSTEM AND LIVER Table 34.2: Antacids Antacid Features Adverse effects Sodium bicarbonate Rapid action Produces carbon dioxide, causing belching and distension; excess can cause metabolic alkalosis; best avoided in renal and cardiovascular disease Calcium carbonate High acid–neutralizing capacity Acid rebound; excess may cause hypercalcaemia and constipation Magnesium salts (e.g. Poor solubility, weak antacids; Diarrhoea dihydroxide, carbonate, the trisilicates inactivate pepsin; trisilicate) increase lower oesophageal sphincter tone, and may be of use in reflux Aluminium hydroxide Forms an insoluble colloid in Constipation; absorption of dietary the presence of acid, and lines phosphate may lead to calcium the gastric mucosa to provide a physical and chemical barrier; weak antacid, slow onset of action, inactivates pepsin depletion and negative calcium balance adequate. Nearly all duodenal ulcers and most gastric ulcers that are not associated with NSAIDs are associated with H. pylori, which should be eradicated (see above). Most regimens include an H 2-receptor antagonist or a proton-pump inhibitor. It is essential to exclude carcinoma endoscopically, as H 2-blockers can improve symptoms caused by malignant ulcers. Without gastric acid, the functions of which include providing a barrier to infection, patients on H 2-antagonists and proton-pump inhibitors are predisposed to infection by enteric pathogens and the rate of bacterial diarrhoea is increased. 2. Oesophagitis may be treated with H 2-antagonists, but proton-pump inhibitors are more effective. 3. In cases of acute upper gastrointestinal haemorrhage and stress ulceration, the use of H 2-blockers is rational, although their efficacy has not been proven. 4. Replacement of pancreatic enzymes in steatorrhoea due to pancreatic insufficiency is often unsatisfactory due to destruction of the enzymes by acid and pepsin in the stomach. H 2-blockers improve the effectiveness of these enzymes in such cases. 5. In anaesthesia, H 2-receptor blockers can be given before emergency surgery to prevent aspiration of acid gastric contents, particularly in obstetric practice (Mendelson’s syndrome). 6. The usual oral dose of cimetidine is 400 mg bd or 800 mg nocte, while for ranitidine it is 150 mg bd or 300 mg nocte to treat benign peptic ulceration. CIMETIDINE Cimetidine is well absorbed (70–80%) orally and is subject to a small hepatic first-pass effect. Intramuscular and intravenous injections produce equivalent blood levels. Diarrhoea, rashes, dizziness, fatigue, constipation and muscular pain (usually mild and transient) have all been reported. Mental confusion can occur in the elderly. Cimetidine transiently increases serum prolactin levels, but the significance of this effect is unknown. Decreased libido and impotence have occasionally been reported during cimetidine treatment. Chronic cimetidine administration can cause gynaecomastia, which is reversible and appears with a frequency of 0.1–0.2%. Rapid intravenous injection of cimetidine has rarely been associated with bradycardia, tachycardia, asystole or hypotension. There have been rare reports of interstitial nephritis, urticaria and angioedema. Drug interactions 1. Absorption of ketoconazole (which requires a low pH) and itraconazole is reduced by cimetidine. 2. Metabolism of several drugs is reduced by cimetidine due to inhibition of cytochrome P450, resulting in raised plasma drug concentrations. Interactions of potential clinical importance include those with warfarin, theophylline, phenytoin, carbamazepine, pethidine and other opioid analgesics, tricyclic antidepressants, lidocaine (cimetidine-induced reduction of hepatic blood flow is also a factor in this interaction), terfenadine, amiodarone, flecainide, quinidine and fluorouracil. 3. Cimetidine inhibits the renal excretion of metformin and procainamide, resulting in increased plasma concentrations of these drugs. RANITIDINE Ranitidine is well absorbed after oral administration, but its bioavailability is only 50%, suggesting that there is appreciable first-pass metabolism. Absorption is not affected by food.

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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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  • Page 256 and 257: PART VI THE ALIMENTARY SYSTEM
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  • Page 282 and 283: PART VII FLUIDS AND ELECTROLYTES
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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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