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A Textbook of Clinical Pharmacology and Therapeutics

A Textbook of Clinical Pharmacology and Therapeutics

is the theoretical

is the theoretical concern of a ‘coronary steal’ effect in patients with ischaemic heart disease. Cerebral blood flow is little affected, and uterine tone is well preserved. Isoflurane has muscle-relaxant properties and potentiates non-depolarizing muscle relaxants. The rate of induction is limited by the pungency of the vapour. Fluoride accumulation is rare, but may occur during prolonged administration (e.g. when used for sedation in intensive care). SEVOFLURANE Sevoflurane is a volatile liquid used for induction and maintenance of general anaesthesia. It has a blood:gas solubility coefficient of 0.6 and an MAC of 2%. Cardiovascular stability during administration is a feature and it has gained popularity for rapid and smooth gaseous induction, with rapid recovery. A theoretical disadvantage is that it is 3% metabolized producing fluoride. It may also react with soda lime. In many centres in the UK it is the inhalational anaesthetic of first choice for most indications. DESFLURANE Desflurane is an inhalational anaesthetic. It has an MAC of 6% and a boiling point of 23.5°C, so it requires a special heated vaporizer. It has a blood:gas coefficient of 0.42 and therefore induction and recovery are faster than with any other volatile agents, allowing rapid alteration of depth of anaesthesia. Cardiovascular stability is good. It cannot be used for inhalational induction because it is irritant to the respiratory tract. NITROUS OXIDE Use Nitrous oxide is a non-irritant gas which is compressed and stored in pressurized cylinders. It is analgesic, but only a weak anaesthetic. It is commonly used in the maintenance of general anaesthetic in concentrations of 50–70% in oxygen in combination with other inhalational or intravenous agents. It can reduce the MAC value of the volatile agent by up to 65%. A 50:50 mixture of nitrous oxide and oxygen is useful as a self-administered analgesic in labour, for emergency paramedics and to cover painful procedures, such as changing surgical dressings and removal of drainage tubes. Adverse effects • When nitrous oxide anaesthesia is terminated, nitrous oxide diffuses out of the blood into the alveoli faster than nitrogen is taken up. This dilutes the concentration of gases in the alveoli, including oxygen, and causes hypoxia. This effect is known as diffusion hypoxia, and it is countered by the administration of 100% oxygen for 10 minutes. • Nitrous oxide in the blood equilibrates with closed gascontaining spaces inside the body, and if the amount of nitrous oxide entering a space is greater than the amount of nitrogen leaving, the volume of the space will increase. Thus pressure can increase in the gut, lungs, middle ear and sinuses. Ear complications and tension pneumothorax may occur. INHALATIONAL ANAESTHETICS 147 • Prolonged use may result in megaloblastic anaemia due to interference with vitamin B12 and agranulocytosis. • Nitrous oxide is a direct myocardial depressant, but this effect is countered indirectly by sympathetic stimulation. Pharmacokinetics Nitrous oxide is eliminated unchanged from the body, mostly via the lungs. Despite its high solubility in fat, most is eliminated within minutes of ceasing administration. Key points Inhaled anaesthetics Volatile liquid anaesthetics administered via calibrated vaporizers using carrier gas (air, oxygen or nitrous oxygen mixture): • halothane; • isoflurane; • sevoflurane; • desflurane. Gaseous anaesthetic • nitrous oxide. Key points Volatile liquid anaesthetics • All cause dose-dependent cardiorespiratory depression. • Halothane is convenient, inexpensive and widely used, but due to association with severe hepatotoxicity it has been superseded by sevoflurane (which is also associated with less cardiac depression) in the UK. Key points Commission on Human Medicines (CHM) advice (halothane hepatoxicity) Recommendations prior to use of halothane • A careful anaesthetic history should be taken to determine previous exposure and previous reactions to halothane. • Repeated exposure to halothane within a period of at least three months should be avoided unless there are overriding clinical circumstances. • A history of unexplained jaundice or pyrexia in a patient following exposure to halothane is an absolute contraindication to its future use in that patient. OCCUPATIONAL HAZARDS OF INHALATIONAL ANAESTHETICS There is evidence to suggest that prolonged exposure to inhalational agents is hazardous to anaesthetists and other theatre personnel. Some studies have reported an increased incidence of spontaneous abortion and low-birth-weight

148 ANAESTHETICS AND MUSCLE RELAXANTS infants among female operating department staff. Although much of the evidence is controversial, scavenging of expired or excessive anaesthetic gases is now standard practice. INTRAVENOUS ANAESTHETICS UPTAKE AND DISTRIBUTION There is a rapid increase in plasma concentration after administration of a bolus dose of an intravenous anaesthetic agent; this is followed by a slower decline. Anaesthetic action depends on the production of sufficient brain concentration of anaesthetic. The drug has to diffuse across the blood–brain barrier from arterial blood, and this depends on a number of factors, including protein binding of the agent, blood flow to the brain, degree of ionization and lipid solubility of the drug, and the rate and volume of injection. Redistribution from blood to viscera is the main factor influencing recovery from anaesthesia following a single bolus dose of an intravenous anaesthetic. Drug diffuses from the brain along the concentration gradient into the blood. Metabolism is generally hepatic and elimination may take many hours. THIOPENTAL Use and pharmacokinetics Thiopental is a potent general anaesthetic induction agent with a narrow therapeutic index which is devoid of analgesic properties. Recovery of consciousness occurs within five to ten minutes after an intravenous bolus injection. The alkaline solution is extremely irritant. The plasma t1/2β of the drug is six hours, but the rapid course of action is explained by its high lipid solubility coupled with the rich cerebral blood flow which ensures rapid penetration into the brain. The shortlived anaesthesia results from the rapid fall (α phase) of the blood concentration (short t1/2α), which occurs due to the distribution of drug into other tissues. When the blood concentration falls, the drug diffuses rapidly out of the brain. The main early transfer is into the muscle. In shock, this transfer is reduced and sustained high concentrations in the brain and heart produce prolonged depression of these organs. Relatively little of the drug enters fat initially because of its poor blood supply, but 30 minutes after injection the thiopental concentration continues to rise in this tissue. Maintainance of anaesthesia with thiopental is therefore unsafe, and its use is in induction. Metabolism occurs in the liver, muscles and kidneys. The metabolites are excreted via the kidneys. Reduced doses are used in the presence of impaired liver or renal function. Thiopental has anticonvulsant properties and may be used in refractory status epilepticus (see Chapter 22). Adverse effects • Central nervous system – many central functions are depressed, including respiratory and cardiovascular centres. The sympathetic system is depressed to a greater extent than the parasympathetic system, and this can result in bradycardia. Thiopental is not analgesic and at subanaesthetic doses it actually reduces the pain threshold. Cerebral blood flow, metabolism and intracranial pressure are reduced (this is turned to advantage when thiopental is used in neuroanaesthesia). • Cardiovascular system – cardiac depression: cardiac output is reduced. There is dilatation of capacitance vessels. Severe hypotension can occur if the drug is administered in excessive dose or too rapidly, especially in hypovolaemic patients in whom cardiac arrest may occur. • Respiratory system – respiratory depression and a short period of apnoea is common. There is an increased tendency to laryngeal spasm if anaesthesia is light and there is increased bronchial tone. • Miscellaneous adverse effects – urticaria or anaphylactic shock due to histamine release. Local tissue necrosis and peripheral nerve injury can occur due to accidental extravascular administration. Accidental arterial injection causes severe burning pain due to arterial constriction, and can lead to ischaemia and gangrene. Post-operative restlessness and nausea are common. • Thiopental should be avoided or the dose reduced in patients with hypovolaemia, uraemia, hepatic disease, asthma and cardiac disease. In patients with porphyria, thiopental (like other barbiturates) can precipitate paralysis and cardiovascular collapse. PROPOFOL Uses Propofol has superseded thiopental as an intravenous induction agent in many centres, owing to its short duration of action, anti-emetic effect and the rapid clear-headed recovery. It is formulated as a white emulsion in soya-bean oil and egg phosphatide. It is rapidly metabolized in the liver and extrahepatic sites, and has no active metabolites. Its uses include: • Intravenous induction – propofol is the drug of choice for insertion of a laryngeal mask, because it suppresses laryngeal reflexes. • Maintenance of anaesthesia – propofol administered as an infusion can provide total intravenous anaesthesia (TIVA). It is often used in conjunction with oxygen or oxygenenriched air, opioids and muscle relaxants. Although recovery is slower than that following a single dose, accumulation is not a problem. It is particularly useful in middle-ear surgery (where nitrous oxide is best avoided) and in patients with raised intracranial pressure (in whom volatile anaesthetics should be avoided). • Sedation – for example, in intensive care, during investigative procedures or regional anaesthesia. Adverse effects • Cardiovascular system – propofol causes arterial hypotension, mainly due to vasodilation although there is some myocardial depression. It should be administered particularly slowly and cautiously in patients with hypovolaemia or cardiovascular compromise. It can also cause bradycardia, responsive to a muscarinic antagonist.

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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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  • Page 110 and 111: A case report has suggested a possi
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  • 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
  • Page 138 and 139: • pulmonary, retroperitoneal and
  • Page 140 and 141: CHOREA The γ-aminobutyric acid con
  • 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 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 •
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  • 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
  • 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
  • Page 190 and 191: esponsible for the strong predilect
  • Page 192 and 193: Ezetimibe Fat Muscle Dietary fat In
  • Page 194 and 195: educed). The risk of muscle damage
  • Page 196 and 197: ● Introduction 185 ● Pathophysi
  • Page 198 and 199: Each of these classes of drug reduc
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  • Page 204 and 205: Key points Drugs used in essential
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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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