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A Textbook of Clinical Pharmacology and Therapeutics

A Textbook of Clinical Pharmacology and Therapeutics

Table 54.2: Common

Table 54.2: Common indications for emergency measurement of drug concentration. Suspected overdose Effect on management Paracetamol Administration of antidotes – acetylcysteine or methionine Iron Administration of antidote – desferrioxamine Methanol/ethylene glycol Administration of antidote – ethanol or fomepizole with or without dialysis Lithium Dialysis Salicylates Simple rehydration or alkaline diuresis or dialysis Theophylline Necessity for intensive care unit (ITU) admission urea, creatinine, oxygen saturation and arterial blood gases. Drug screens are often requested, although they are rarely indicated as an emergency. Table 54.2 lists those drugs where the clinical state of a patient may be unhelpful in determining the severity of the overdose in the acute stages. In these, emergency measurement of the plasma concentration can lead to life-saving treatment. For example, in the early stages, patients with paracetamol overdoses are often asymptomatic, and although it only rarely causes coma acutely, patients may have combined paracetamol with alcohol, a hypnosedative or an opioid. As such, an effective antidote (acetylcysteine) is available, it is recommended that the paracetamol concentration should be measured in all unconscious patients who present as cases of drug overdose. When there is doubt about the diagnosis, especially in coma, samples of blood, urine and (when available) gastric aspirate should be collected. Subsequent toxicological screening may be necessary if the cause of the coma does not become apparent or recovery does not occur. Avoidable morbidity is more commonly due to a missed diagnosis, such as head injury, than to failure to diagnose drug-induced coma. PREVENTION OF FURTHER ABSORPTION Syrup of ipecacuanha is no longer recommended in the management of poisoning. Gastric aspiration and lavage should only be performed if the patient presents within one hour of ingestion of a potentially fatal overdose. If there is any suppression of the gag reflex, a cuffed endotracheal tube is mandatory. Gastric lavage is unpleasant and is potentially hazardous. It should only be performed by experienced personnel with efficient suction apparatus close at hand (see Table 54.3). If the patient is uncooperative and refuses to give consent, this procedure cannot be performed. Gastric lavage is usually contraindicated following ingestion of corrosives and acids, due to the risk of oesophageal perforation and following Table 54.3: Gastric aspiration and lavage INTENTIONAL SELF-POISONING 445 1. If the patient is unconscious, protect airway with cuffed endotracheal tube. If semiconscious with effective gag reflex, place the patient in the head-down, left-lateral position. An anaesthetist with effective suction must be present 2. Place the patient’s head over the end/side of the bed, so that their mouth is below their larynx 3. Use a wide-bore lubricated orogastric tube 4. Confirm that the tube is in the stomach (not the trachea) by auscultation of blowing air into the stomach; save the first sample of aspirate for possible future toxicological analysis (and possible direct identification of tablets/capsules) 5. Use 300 –600 mL of tap water for each wash and repeat three to four times. Continue if ingested tablets/capsules are still present in the final aspirate 6. Unless an oral antidote is to be administered, leave 50 g of activated charcoal in the stomach ingestion of hydrocarbons, such as white spirit and petrol, due to the risk of aspiration pneumonia. An increasingly popular method of reducing drug/toxin absorption is by means of oral activated charcoal, which adsorbs drug in the gut. To be effective, large amounts of charcoal are required, typically ten times the amount of poison ingested, and again timing is critical, with maximum effectiveness being obtained soon after ingestion. Its effectiveness is due to its large surface area (�1000 m 2 /g). Binding of charcoal to the drug is by non-specific adsorption. Aspiration is a potential risk in a patient who subsequently loses consciousness or fits and vomits. Oral charcoal may also inactivate any oral antidote (e.g. methionine). The use of repeated doses of activated charcoal may be indicated after ingestion of sustained-release medications or drugs with a relatively small volume of distribution, and prolonged elimination half-life (e.g. salicylates, quinine, dapsone, carbamazepine, barbiturates or theophylline). The rationale is that these drugs will diffuse passively from the bloodstream if charcoal is present in sufficient amounts in the gut or to trap drug that has been eliminated in bile from being re-absorbed (see below). Metal salts, alcohols and solvents are not adsorbed by activated charcoal. Whole bowel irrigation using non-absorbable polyethylene glycol solution may be useful when large amounts of sustained-release preparations, iron or lithium tablets or packets of smuggled narcotics have been taken. Paralytic ileus is a contraindication. SUPPORTIVE THERAPY Patients are generally managed with intensive supportive therapy whilst the drug is eliminated naturally by the body. After an initial assessment of vital signs and instigation of

446 DRUG OVERDOSE AND POISONING appropriate resuscitation, repeated observations are necessary, as drugs may continue to be absorbed with a subsequent increase in plasma concentration. In the unconscious patient, repeated measurements of cardiovascular function, including blood pressure, urine output and (if possible) continuous electrocardiographic (ECG) monitoring should be performed. Plasma electrolytes and acid-base balance should be measured. Hypotension is the most common cardiovascular complication of poisoning. This is usually due to peripheral vasodilatation, but may be secondary to myocardial depression following, for example, α-blocker, tricyclic antidepressant or dextropropoxyphine poisoning. Hypotension can usually be managed with intravenous colloid. If this is inadequate, positive inotropic agents (e.g. dobutamine) may be considered. If dysrhythmias occur any hypoxia or hypokalaemia should be corrected, but anti-dysrhythmic drugs should only be administered in life-threatening situations. Since the underlying cardiac tissue is usually healthy (unlike cardiac arrests following myocardial infarction), prolonged external cardiopulmonary resuscitation whilst the toxic drug is excreted is indicated. Respiratory function is best monitored using blood gas analysis – a PaCO 2 of �6.5 kPa is usually an indication for assisted ventilation. Serial minute volume measurements or continuous measurement of oxygen saturation using a pulse oximeter are also helpful for monitoring deterioration or improvement in self-ventilation. Oxygen is not a substitute for inadequate ventilation. Respiratory stimulants increase mortality. ENHANCEMENT OF ELIMINATION Methods of increasing poison elimination are appropriate in less than 5% of overdose cases. Repeated oral doses of activated charcoal may enhance the elimination of a drug by ‘gastrointestinal dialysis’. Several drugs are eliminated in the bile and then reabsorbed in the small intestine. Activated charcoal can interrupt this enterohepatic circulation by adsorbing drug in the gut lumen, thereby preventing reabsorption and enhancing faecal elimination. Cathartics, such as magnesium sulphate, can accelerate the intestinal transit time, which facilitates the process. Orally administered activated charcoal adsorbs drug in the gut lumen and effectively leaches drug from the intestinal circulation into the gut lumen down a diffusion gradient. Although studies in volunteers have shown that this method enhances the elimination of certain drugs, its effectiveness in reducing morbidity in overdose is generally unproven. However, it is extremely safe unless aspiration occurs. Forced diuresis is hazardous, especially in the elderly, and is no longer recommended. Adjustment of urinary pH is much more effective than causing massive urine output. Alkaline diuresis (urinary alkalinization) should be considered in cases of salicylate, chlorpropramide, phenoxyacetate herbicides and phenobarbital poisoning, and may be combined with repeated doses of oral activated charcoal. Acid diuresis may theoretically accelerate drug elimination in phencyclidine and amfetamine/ ’ecstasy’ poisoning. However, it is not usually necessary, may be harmful and is almost never recommended. Table 54.4: Methods and indications for enhancement of poison elimination Method Poison Alkaline diuresis Salicylates, phenobarbital Haemodialysis Salicylates, methanol, ethylene glycol, lithium, phenobarbital Charcoal haemoperfusion Barbiturates, theophylline, disopyramide ‘Gastro-intestinal dialysis’ Salicylates, theophylline, quinine, via multiple-dose activated charcoal most anticonvulsants, digoxin Haemodialysis and, much less commonly, charcoal haemoperfusion are sometimes used to enhance drug elimination. Table 54.4 summarizes the most important indications and methods for such elimination techniques. In addition, exchange transfusion has been successfully used in the treatment of poisoning in young children and infants. The risk of an elimination technique must be balanced against the possible benefit of enhanced elimination. SPECIFIC ANTIDOTES Antidotes are available for a small number of poisons and the most important of these, including chelating agents, are summarized in Table 54.5. NALOXONE Naloxone is a pure opioid antagonist with no intrinsic agonist activity (Chapter 25). It rapidly reverses the effects of opioid drugs, including morphine, diamorphine, pethidine, dextropropoxyphene and codeine. When injected intravenously, naloxone acts within two minutes and its elimination half-life is approximately one hour. The plasma half-life of most opioid drugs is longer (e.g. 12–24 hours) and repeated doses or infusions of naloxone may be required. The usual dose is 0.8–1.2 mg, although much higher doses may be needed after massive opioid overdoses, which are common in addicts and especially after a partial agonist (e.g. buprenorphine) overdose, because partial agonists must occupy a relatively large fraction of the receptors compared to full agonists in order to produce even modest effects. Naloxone can precipitate withdrawal reactions in narcotic addicts. This is not a contraindication, but it is wise to ensure that patients are appropriately restrained if this is a risk. MANAGEMENT OF SPECIFIC OVERDOSES PARACETAMOL This over-the-counter mild analgesic is commonly taken in overdose. Although remarkably safe in therapeutic doses,

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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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    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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  • Page 422 and 423: ● Introduction 411 ● Acne 411
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  • Page 428 and 429: TREATMENT OF OTHER SKIN INFECTIONS
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  • Page 434 and 435: ● Introduction: ocular anatomy, p
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  • Page 444 and 445: ● Introduction 433 ● Pathophysi
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  • Page 448 and 449: which provide anonymized data to th
  • Page 450 and 451: Peak plasma levels after smoking ci
  • Page 452 and 453: Key points Acute effects of alcohol
  • Page 454 and 455: FURTHER READING Goldman D, Oroszi G
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  • Page 462 and 463: Note: Page numbers in italics refer
  • Page 464 and 465: atrial fibrillation 217, 221 digoxi
  • Page 466 and 467: Cushing’s syndrome 302 cyclic ade
  • Page 468 and 469: 5-fluorouracil 375-6 fluoxetine, mo
  • Page 470 and 471: children 54 diazepam 108 iron prepa
  • Page 472 and 473: non-steroidal anti-inflammatory dru
  • Page 474 and 475: puberty (male), delay 314 puerperiu
  • Page 476: tolerance 9, 433 benzodiazepines 10
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