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A Textbook of Clinical Pharmacology and Therapeutics

A Textbook of Clinical Pharmacology and Therapeutics

CHOREA The

CHOREA The γ-aminobutyric acid content in the basal ganglia is reduced in patients with Huntington’s disease. Dopamine receptor antagonists (e.g. haloperidol) or tetrabenazine suppress the choreiform movements in these patients, but dopamine antagonists are best avoided, as they themselves may induce dyskinesias. Tetrabenazine is therefore preferred. It depletes neuronal terminals of dopamine and serotonin. It can cause severe doserelated depression. Diazepam may be a useful alternative, but there is no effective treatment for the dementia and other manifestations of Huntington’s disease. DRUG-INDUCED DYSKINESIAS • The most common drug-induced movement disorders are ‘extrapyramidal symptoms’ related to dopamine receptor blockade. • The most frequently implicated drugs are the ‘conventional’ antipsychotics (e.g. haloperidol and fluphenazine). Metoclopramide, an anti-emetic, also blocks dopamine receptors and causes dystonias. • Acute dystonias can be effectively treated with parenteral benzodiazepine (e.g. diazepam) or anticholinergic (e.g. procyclidine). • Tardive dyskinesia may be permanent. • Extrapyramidal symptoms are less common with the newer ‘atypical’ antipsychotics (e.g. olanzapine or aripiprazole). NON-DOPAMINE-RELATED MOVEMENT DISORDERS • ‘Cerebellar’ ataxia – ethanol, phenytoin • Tremor • β-Adrenoceptor agonists, e.g. salbutamol; • caffeine; • thyroxine; • SSRls, e.g. fluoxetine; • valproate; • withdrawal of alcohol and benzodiazepines. • vestibular toxicity – aminoglycosides; • myasthenia – aminoglycosides; • proximal myopathy – ethanol, corticosteroids; • myositis – lipid-lowering agents – statins, fibrates; • tenosynovitis – fluoroquinolones. TREATMENT OF OTHER MOVEMENT DISORDERS TICS AND IDIOPATHIC DYSTONIAS Botulinum A toxin is one of seven distinct neurotoxins produced by Clostridium botulinum and it is a glycoprotein. It is used by neurologists to treat hemifacial spasm, blepharospasm, cervical dystonia (torticollis), jaw-closing oromandibular dystonia and adductor laryngeal dysphonia. Botulinum A toxin is given by local injection into affected muscles, the injection site being best localized by electromyography. Recently, it has also proved successful in the treatment of achalasia. Injection of botulinum A toxin into a muscle weakens it by irreversibly blocking the release of acetylcholine at the neuromuscular junction. Muscles injected with botulinum A toxin atrophy and become weak over a period of 2–20 days and recover over two to four months as new axon terminals sprout and restore transmission. Repeated injections can then be given. The best longterm treatment plan has not yet been established. Symptoms are seldom abolished and adjuvant conventional therapy should be given. Adverse effects due to toxin spread causing weakness of nearby muscles and local autonomic dysfunction can occur. In the neck, this may cause dysphagia and aspiration into the lungs. Electromyography has detected evidence of systemic spread of the toxin, but generalized weakness does not occur with standard doses. Occasionally, a flu-like reaction with brachial neuritis has been reported, suggesting an acute immune response to the toxin. Neutralizing antibodies to botulinum toxin A cause loss of efficacy in up to 10% of patients. Botulinum B toxin does not cross-react with neutralizing antibodies to botulinum toxin A, and is effective in patients with torticollis who have botulinum toxin A-neutralizing antibodies. The most common use of botulinum is now cosmetic. AMYOTROPHIC LATERAL SCLEROSIS (MOTOR NEURONE DISEASE) Riluzole is used to extend life or time to mechanical ventilation in patients with the amyotrophic lateral sclerosis (ALS) form of motor neurone disease (MND). It acts by inhibiting the presynaptic release of glutamate. Side effects include nausea, vomiting, dizziness, vertigo, tachycardia, paraesthesia and liver toxicity. MYASTHENIA GRAVIS PATHOPHYSIOLOGY MYASTHENIA GRAVIS 129 Myasthenia gravis is a syndrome of increased fatiguability and weakness of striated muscle, and it results from an autoimmune process with antibodies to nicotinic acetylcholine receptors. These interact with postsynaptic nicotinic cholinoceptors at the neuromuscular junction. (Such antibodies may be passively transferred via purified immunoglobulin or across the placenta to produce a myasthenic neonate.) Antibodies vary from one patient to another, and are often directed against receptor-protein domains distinct from the acetylcholine-binding site. Nonetheless, they interfere with neuromuscular transmission by reducing available receptors, by increasing receptor turnover by activating complement and/or cross-linking adjacent receptors. Endplate potentials are reduced in amplitude, and in some fibres may be below the threshold for initiating a muscle action

130 MOVEMENT DISORDERS AND DEGENERATIVE CNS DISEASE potential, thus reducing the force of contraction of the muscle. The precise stimulus for the production of the antireceptor antibodies is not known, although since antigens in the thymus cross-react with acetylcholine receptors, it is possible that these are responsible for autosensitization in some cases. Diagnosis is aided by the use of edrophonium, a short-acting inhibitor of acetylcholinesterase, which produces a transient increase in muscle power in patients with myasthenia gravis. The initial drug therapy of myasthenia consists of oral anticholinesterase drugs, usually neostigmine. If the disease is non-responsive or progressive, then thymectomy or immunosuppressant therapy with glucocorticosteroids and azathioprine are needed. Thymectomy is beneficial in patients with associated thymoma and in patients with generalized disease who can withstand the operation. It reduces the number of circulating T-lymphocytes that are capable of assisting B-lymphocytes to produce antibody, and a fall in antibody titre occurs after thymectomy, albeit slowly. Corticosteroids and immunosuppressive drugs also reduce circulating T cells. Plasmapheresis or infusion of intravenous immunoglobulin is useful in emergencies, producing a striking short-term clinical improvement in a few patients. ANTICHOLINESTERASE DRUGS The defect in neuromuscular transmission may be redressed by cholinesterase inhibitors that inhibit synaptic acetylcholine breakdown and increase the concentration of transmitters available to stimulate the nictonic receptor at the motor end plate. Neostigmine is initially given orally eight-hourly, but usually requires more frequent administration (up to two-hourly) because of its short duration of action (two to six hours). It is rapidly inactivated in the gut. Cholinesterase inhibitors enhance both muscarinic and nicotinic cholinergic effects. The former results in increased bronchial secretions, abdominal colic, diarrhoea, miosis, nausea, hypersalivation and lachrymation. Excessive muscarinic effects may be blocked by giving atropine or propantheline, but this increases the risk of overdosage and consequent cholinergic crisis. Pyridostigmine has a more prolonged action than neostigmine and it is seldom necessary to give it more frequently than four-hourly. The effective dose varies considerably between individual patients. ADJUVANT DRUG THERAPY Remissions of myasthenic symptoms are produced by oral administration of prednisolone. Increased weakness may occur at the beginning of treatment, which must therefore be instituted in hospital. This effect has been minimized by the use of alternate-day therapy. Azathioprine (see Chapter 50) has been used either on its own or combined with glucocorticosteroids for its ‘corticosteroid-sparing’ effect. MYASTHENIC AND CHOLINERGIC CRISIS Severe weakness leading to paralysis may result from either a deficiency (myasthenic crisis) or an excess (cholinergic crisis) of acetylcholine at the neuromuscular junction. Clinically, the distinction may be difficult, but it is assisted by the edrophonium test. Edrophonium, a short-acting cholinesterase inhibitor, is given intravenously, and is very useful in diagnosis and for differentiating a myasthenic crisis from a cholinergic one. It transiently improves a myasthenic crisis and aggravates a cholinergic crisis. Because of its short duration of action, any deterioration of a cholinergic crisis is unlikely to have serious consequences, although facilities for artificial ventilation must be available. In this setting, it is important that the strength of essential (respiratory or bulbar) muscles be monitored using simple respiratory spirometric measurements (FEV 1 and FVC) during the test, rather than the strength of non-essential (limb or ocular) muscles. Myasthenic crises may develop as a spontaneous deterioration in the natural history of the disease, or as a result of infection or surgery, or be exacerbated due to concomitant drug therapy with the following agents: • aminoglycosides (e.g. gentamicin); • other antibiotics, including erythromycin; • myasthenics demonstrate increased sensitivity to nondepolarizing neuromuscular-blocking drugs; • anti-dysrhythmic drugs, which reduce the excitability of the muscle membrane, and quinidine (quinine), lidocaine, procainamide and propranolol, which may increase weakness; • benzodiazepines, due to their respiratory depressant effects and inhibition of muscle tone. TREATMENT Myasthenic crisis Myasthenic crisis is treated with intramuscular neostigmine, repeated every 20 minutes with frequent edrophonium tests. Mechanical ventilation may be needed. Key points Myasthenia gravis • Auto-antibodies to nicotinic acetylcholine receptors lead to increased receptor degradation and neuromuscular blockade. • Treatment is with an oral anticholinesterase (e.g. neostigmine or physostigmine). Over- or under-treatment both lead to increased weakness (‘cholinergic’ and ‘myasthenic’ crises, respectively). • Cholinergic and myasthenic crises are differentiated by administering a short-acting anticholinesterase, intravenous edrophonium. This test transiently improves a myasthenic crisis while transiently worsening a cholinergic crisis, allowing the appropriate dose adjustment to be made safely. • Immunotherapy with azathioprine and/or corticosteroids or thymectomy may be needed in severe cases. • Weakness is exacerbated by aminoglycosides or erythromycin and patients are exquisitely sensitive to non-depolarizing neuromuscular blocking drugs (e.g. vecuronium).

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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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  • Page 92 and 93: Table 14.2: Variations in drug resp
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  • Page 96 and 97: Key points • Genetic differences
  • Page 98 and 99: • Discovery • • Screening Pre
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  • Page 102 and 103: ETHICS COMMITTEES Protocols for all
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  • Page 106 and 107: duration and benefit. Adenoviral ve
  • Page 108 and 109: ● Introduction 97 ● Garlic 97
  • Page 110 and 111: A case report has suggested a possi
  • Page 112 and 113: including hypericin and pseudohyper
  • Page 114 and 115: PART II THE NERVOUS SYSTEM
  • Page 116 and 117: ● Introduction 105 ● Sleep diff
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  • Page 120 and 121: Key points • Insomnia and anxiety
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  • 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 142 and 143: Cholinergic crisis Treatment of mya
  • Page 144 and 145: ● Introduction 133 ● Mechanisms
  • Page 146 and 147: absolute arbiter. The availability
  • Page 148 and 149: Table 22.2: Metabolic interactions
  • Page 150 and 151: FURTHER ANTI-EPILEPTICS Other drugs
  • Page 152 and 153: Case history A 24-year-old woman wh
  • Page 154 and 155: Assessment of migraine severity and
  • Page 156 and 157: ● General anaesthetics 145 ● In
  • Page 158 and 159: is the theoretical concern of a ‘
  • Page 160 and 161: • Respiratory system - apnoea fol
  • Page 162 and 163: Competitive antagonists (vecuronium
  • Page 164 and 165: have also proved useful in combinat
  • Page 166 and 167: ● Introduction 155 ● Pathophysi
  • Page 168 and 169: ASPIRIN (ACETYLSALICYLATE) Use Anti
  • Page 170 and 171: Key points Drugs for mild pain •
  • Page 172 and 173: increases, correlating with the hig
  • Page 174 and 175: • If possible, use oral medicatio
  • Page 176 and 177: PART III THE MUSCULOSKELETAL SYSTEM
  • Page 178 and 179: ● Introduction: inflammation 167
  • Page 180 and 181: Chapter 33). All NSAIDs cause wheez
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  • Page 184 and 185: Pharmacokinetics Allopurinol is wel
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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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    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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