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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2826_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Contents
- •Preface
- •Malignant disease
- •Rheumatology
- •Water and electrolytes
- •Renal disease
- •Cardiovascular disease
- •Respiratory disease
- •Intensive care medicine
- •Poisoning, drug and alcohol abuse
- •Endocrinology
- •Diabetes mellitus and other disorders of metabolism
- •The special senses
- •Neurology
- •Dermatology
- •Elderly medicine and frailty
- •Abbreviations
- •Medical emergencies
- •Symptom Based
- •System Based
- •Infectious diseases and tropical medicine
- •Gastroenterology and nutrition
- •Liver, biliary tract and pancreatic disease
- •Diseases of the blood and haematological malignancies
- •Significant websites
- •Guidelines and evidence-based medicine
- •Medical calculators
- •Chapter-specific websites
- •Legally Valid Consent
- •Capacity
- •Information disclosure
- •Obtaining consent
- •Special circumstances
- •Adults who lack capacity to consent
- •Advance decisions
- •Children
- •Teaching
- •Human immunodeficiency virus testing
- •End-of-life decisions including assisted dying
- •Cardiopulmonary resuscitation
- •Confidentiality
- •Communication
- •The medical interview
- •1. Building a relationship
- •2. Opening the discussion
- •3. Gathering information
- •4. Understanding the patient
- •5. Sharing information
- •6. Reaching agreement on management
- •7. Providing closing
- •Breaking bad news
- •Communication in difficult circumstances
- •When things go wrong
- •Complaints
- •Culture and communication
- •Patients with impaired faculties for communication
- •Medical record keeping
- •Team communication
- •2 Infectious diseases
- •Common investigations in infectious disease
- •Septicaemia
- •Pyrexia of unknown origin
- •Investigations
- •Management
- •Common Viral Infections
- •Clinical features
- •Complications
- •Management
- •Clinical features
- •Management
- •Diagnosis
- •Management
- •Herpes viruses
- •Herpes simplex virus (HSV)
- •Investigations
- •Management
- •Varicella zoster virus
- •Varicella (chickenpox)
- •Herpes zoster (shingles)
- •Epstein–Barr virus infection
- •Clinical features
- •Investigations
- •Management
- •Bacterial Infections
- •Lyme disease
- •Clinical features
- •Investigations
- •Management
- •Clinical features
- •Investigations
- •Management
- •Rickettsia
- •Management
- •Treatment of uncomplicated falciparum malaria
- •Prevention and control
- •Clinical features
- •Investigations
- •Management and prevention
- •Enterocolitis
- •Dengue fever
- •Schistosomiasis
- •Fever in the Returned Traveller
- •Approach to diagnosis
- •Investigations
- •Aetiology
- •Pathogenesis
- •Clinical features
- •Investigations
- •Miscellaneous Viral Infections
- •Zika
- •MERS Co-V
- •Clostridium difficile
- •Pathology and clinical features
- •Management
- •Prevention of C. difficile infection
- •Travellers’ diarrhoea
- •Clinical features
- •Treatment and prevention
- •Clinical features
- •Intestinal amoebiasis (amoebic dysentery)
- •Amoebic liver abscess
- •Investigations
- •Serology
- •Colonic disease
- •Liver disease
- •Differential diagnosis
- •Management
- •Pathophysiology and clinical features
- •Management
- •Prevention and control
- •Giardiasis
- •Clinical features
- •Investigations
- •Management
- •Helminthic Infections
- •Sexually Transmitted Infections
- •Gonorrhoea
- •Clinical features
- •Diagnosis
- •Management
- •Chlamydia urethritis
- •Genital ulcers
- •Syphilis
- •Early stages
- •Primary infection
- •Secondary infection
- •Late stages
- •Tertiary syphilis
- •Congenital syphilis
- •Treponemal tests.
- •Non-treponemal tests.
- •Diagnosis
- •Management
- •Routes of acquisition
- •Pathogenesis of HIV infection
- •Natural history of HIV infection
- •Clinical features
- •Diagnosis
- •Human Immuodeficiency Virus
- •Monitoring
- •Management
- •Conditions due to immunodeficiency
- •Fungi
- •Protozoal infections
- •Viruses
- •Bacterial infection
- •Neoplasia
- •Prevention and control
- •Prognosis
- •Therapeutics
- •Antibacterials
- •β-Lactam antibacterials
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •Cephalosporins
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •Aminoglycosides
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •Macrolides
- •Mechanism of action
- •Indications
- •Side effects
- •Metronidazole
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •Quinolones
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •Gastroenterology
- •Symptoms of Gastrointestinal Disease
- •Dyspepsia and indigestion
- •Dysphagia
- •Vomiting
- •Flatulence
- •Diarrhoea and constipation
- •Steatorrhoea
- •Abdominal pain
- •Investigation of Gastrointestinal Disease
- •Endoscopy
- •Oesophagogastroduodenoscopy (OGD, ‘gastroscopy’)
- •Sigmoidoscopy
- •Colonoscopy
- •Imaging
- •Plain X-rays
- •Ultrasound
- •Computed tomography (CT) scan
- •Magnetic resonance imaging (MRI)
- •Positron emission tomography (PET)
- •Contrast studies
- •Oesophageal physiology testing
- •The Mouth
- •Mouth ulcers
- •Non-infective
- •Infective
- •Oral white patches
- •The tongue
- •Periodontal disorders
- •Salivary gland disorders
- •The Oesophagus
- •Symptoms of oesophageal disorders
- •Gastro-oesophageal reflux disease (GORD)
- •Pathophysiology
- •Clinical features
- •Investigations
- •Management
- •Complications
- •Peptic stricture
- •Barrett’s oesophagus
- •Achalasia
- •Clinical features
- •Investigations
- •Management
- •Complications
- •Systemic sclerosis
- •Other oesophageal dysmotility disorders
- •Hiatus hernia
- •Benign oesophageal strictures
- •Oesophageal infection
- •Eosinophilic oesophagitis
- •Oesophageal perforation
- •Malignant oesophageal tumours
- •Pathology
- •Epidemiology and aetiological factors
- •Clinical features
- •Investigations
- •Management
- •Prognosis
- •Benign oesophageal tumours
- •The Stomach and Duodenum
- •Helicobacter pylori infection
- •Epidemiology
- •Clinicopathological features
- •Diagnosis of infection
- •Management
- •Peptic ulcer disease
- •Epidemiology
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Complications
- •Management of dyspepsia
- •Gastropathy
- •Gastritis
- •Gastric cancer
- •Epidemiology
- •Aetiology
- •Pathology
- •Clinical features
- •Investigations
- •Management
- •Prognosis
- •Other gastric tumours
- •Gastrointestinal Bleeding
- •Acute upper gastrointestinal bleeding
- •Aetiology
- •Management
- •Endoscopy
- •Post-endoscopy
- •Lower gastrointestinal bleeding
- •Management
- •Chronic gastrointestinal bleeding
- •Investigations
- •Management
- •The Small Intestine
- •Coeliac disease (gluten-sensitive enteropathy)
- •Aetiology
- •Clinical features
- •Investigations
- •Other investigations
- •Management
- •Complications
- •Dermatitis herpetiformis
- •Tropical sprue
- •Bacterial overgrowth
- •Clinical features
- •Diagnosis
- •Management
- •Intestinal resection
- •Whipple’s disease
- •Miscellaneous Small Intestinal Conditions
- •Tuberculosis
- •Clinical features
- •Diagnosis
- •Management
- •Protein-losing enteropathy
- •Meckel’s diverticulum
- •Intestinal ischaemia
- •Tumours of the small intestine
- •Malignant tumours
- •Benign small bowel tumours
- •Carcinoid tumours
- •Pathology
- •Clinical features
- •Investigations
- •Management
- •Epidemiology
- •Aetiology
- •Genetic susceptibility
- •Environment
- •Inflammatory Bowel Disease
- •Host immune response
- •Pathology
- •Clinical features
- •Crohn’s disease
- •Ulcerative colitis
- •Radiology and imaging
- •Investigations
- •Differential diagnosis
- •Management
- •Medical
- •Induction of remission
- •Maintenance of remission
- •Surgery
- •Cancer in inflammatory bowel disease
- •Prognosis
- •Microscopic colitis
- •The Colon and Rectum
- •Constipation
- •Investigation
- •Management
- •Faecal incontinence
- •Diverticular disease
- •Aetiology
- •Clinical features
- •Management
- •Miscellaneous conditions
- •Megacolon
- •Ischaemic colitis
- •Adenomatous polyps
- •Colon polyps and the polyposis syndromes
- •Colorectal cancer
- •Epidemiology
- •Inheritance
- •Pathology
- •Clinical features
- •Investigation
- •Management
- •Prognosis
- •Screening
- •Diarrhoea
- •Mechanisms of diarrhoea
- •Osmotic diarrhoea
- •Secretory diarrhoea
- •Inflammatory diarrhoea (mucosal destruction)
- •Motility related
- •Approach to the patient with diarrhoea
- •Investigation
- •History
- •Examination
- •Investigations
- •Functional Bowel Disorders
- •The Acute Abdomen
- •Acute appendicitis
- •Epidemiology
- •Clinical features
- •Investigations
- •Differential diagnosis
- •Management
- •Complications
- •Acute peritonitis
- •Intestinal obstruction
- •The Peritoneum
- •Nutrition
- •Dietary requirements
- •Nutritional Support
- •Enteral nutrition
- •Total parenteral nutrition (TPN)
- •Monitoring of artificial nutrition
- •Refeeding syndrome
- •Disorders of BODY WEIGHT
- •Obesity
- •Anorexia nervosa
- •Therapeutics
- •Drugs for dyspepsia and peptic ulceration
- •Antacids
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •H2-receptor antagonists
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •Proton pump inhibitors
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •Constipation
- •Bulk-forming laxatives
- •Mechanism of action
- •Indications
- •Preparations and dose
- •Side effects
- •Cautions/contraindications
- •Stimulant laxatives
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •Osmotic laxatives
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •Bowel-cleansing solutions
- •Indications
- •Side effects
- •Diarrhoea
- •Side effects
- •Cautions/contraindications
- •Nausea and vomiting
- •Antihistamines
- •Indications
- •Mechanism of action
- •Side effects
- •Cautions/contraindications
- •Phenothiazines
- •Mechanism of action
- •Indications
- •Side effects
- •Domperidone and metoclopramide
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •5-HT3-receptor antagonists
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •Liver Biochemistry and Liver Function Tests
- •Other Investigations in Liver and Biliary Disease
- •Symptoms and Signs of Liver Disease
- •Jaundice
- •Haemolytic jaundice
- •Congenital hyperbilirubinaemia
- •Cholestatic jaundice
- •Investigations
- •Hepatitis
- •Viral hepatitis
- •Hepatitis A
- •Epidemiology
- •Clinical features
- •Investigations
- •Differential diagnosis
- •Management
- •Prophylaxis
- •Hepatitis B
- •Epidemiology
- •Viral structure
- •Acute HBV infection
- •Chronic HBV infection
- •Treatment of chronic infection: who to treat
- •Antiviral agents
- •Hepatitis B and HIV co-infection
- •Prophylaxis
- •Hepatitis D (delta or δ agent)
- •Hepatitis C
- •Hepatitis C virus
- •Chronic hepatitis C infection
- •Hepatitis E
- •Acute hepatic failure
- •Alcohol use
- •Screening for problem drinking
- •Consequences of alcohol use and dependence
- •Autoimmune hepatitis
- •Aetiology
- •Clinical features
- •Investigations
- •Treatment
- •Prognosis
- •Aetiology
- •Pathology
- •Clinical features
- •Non-Alcoholic Fatty Liver Disease
- •Cirrhosis
- •Investigations
- •Severity
- •Aetiology
- •Further investigations
- •Management
- •Prognosis
- •Portal hypertension
- •Aetiology
- •Clinical features
- •Variceal haemorrhage
- •Management
- •Ascites
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Complications
- •Portosystemic encephalopathy
- •Pathophysiology
- •Clinical features
- •Differential diagnosis
- •Investigations
- •Management
- •Hepatorenal syndrome
- •Hepatopulmonary syndrome
- •Liver Transplantation
- •Types of Chronic Liver Disease and Cirrhosis
- •Alcoholic cirrhosis
- •Primary biliary cholangitis
- •Epidemiology
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Prognosis
- •Secondary biliary cirrhosis
- •Hereditary haemochromatosis
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Prognosis
- •Wilson’s disease (hepatolenticular degeneration)
- •α1-Antitrypsin deficiency
- •Alcohol and the liver
- •Fatty change
- •Alcoholic hepatitis
- •Clinical features
- •Investigations
- •Management
- •Alcoholic cirrhosis
- •Aetiology
- •Clinical features
- •Investigations
- •Treatment
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Primary Sclerosing Cholangitis
- •Budd–Chiari Syndrome
- •Liver Abscess
- •Liver Disease in Pregnancy
- •Liver Tumours
- •Hepatocellular carcinoma (hepatoma)
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Prognosis
- •Benign liver tumours
- •Pathophysiology
- •Clinical presentation
- •Gallstones
- •Biliary pain
- •Clinical features
- •Investigations
- •Management
- •Acute cholecystitis
- •Clinical features
- •Investigations
- •Management
- •Chronic cholecystitis
- •Acute cholangitis
- •Clinical features
- •Investigations
- •Management
- •Common bile duct stones (choledocholithiasis)
- •The Pancreas
- •Pancreatitis
- •Acute pancreatitis
- •Pathogenesis
- •Clinical features
- •Investigation
- •Management
- •General supportive care
- •Complications
- •Chronic pancreatitis
- •Clinical features
- •Investigations
- •Treatment
- •Epidemiology
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Prognosis
- •Carcinoma of the Pancreas
- •Cancer of the bile ducts
- •Neuroendocrine Tumours of the Pancreas
- •5 Haematological disease
- •Anaemia
- •Microcytic anaemia
- •Iron deficiency
- •Causes of iron deficiency
- •Clinical features
- •Investigations
- •Differential diagnosis
- •Management
- •Anaemia of chronic disease
- •Sideroblastic anaemia
- •Macrocytic anaemia
- •Megaloblastic anaemia
- •Vitamin B12 deficiency
- •Pernicious anaemia
- •Epidemiology
- •Clinical features
- •Investigation of vitamin B12 deficiency
- •Differential diagnosis
- •Management
- •Folate deficiency
- •Clinical features
- •Investigations
- •Management
- •Prevention of neural tube defects with folic acid.
- •Differential diagnosis
- •Anaemia caused by marrow failure (aplastic anaemia)
- •Aetiology
- •Clinical features
- •Investigations
- •Differential diagnosis
- •Management
- •Haemolytic Anaemia
- •Inherited Haemolytic Anaemias
- •Membrane defects
- •Hereditary spherocytosis
- •Clinical features
- •Investigations
- •Management
- •Hereditary elliptocytosis
- •Haemoglobin abnormalities
- •Thalassaemia
- •β-Thalassaemia
- •Investigations
- •Management
- •α-Thalassaemia
- •Sickle syndromes
- •Sickle cell anaemia
- •Clinical features
- •Vaso-occlusion.
- •Anaemia.
- •Long-term problems.
- •Investigations
- •Management
- •Red cell concentrates.
- •Platelet concentrates
- •Sickle cell trait
- •Metabolic red cell disorders
- •Glucose-6-phosphate dehydrogenase deficiency
- •Acquired Haemolytic Anaemia
- •Autoimmune haemolytic anaemia
- •‘Warm’ autoimmune haemolytic anaemia
- •Clinical features
- •Investigation
- •Management
- •‘Cold’ autoimmune haemolytic anaemia
- •Clinical features
- •Investigation
- •Management
- •Drug-induced haemolysis
- •Non-immune haemolytic anaemia
- •Paroxysmal nocturnal haemoglobinuria
- •Mechanical haemolytic anaemia
- •Myeloproliferative Disorders
- •Polycythaemia
- •Polycythaemia vera
- •Clinical features
- •Investigations
- •Management
- •Secondary polycythaemia
- •Essential thrombocythaemia
- •Myelofibrosis (myelosclerosis)
- •Clinical features
- •Investigations
- •Management
- •Myelodysplasia
- •The Spleen
- •Splenomegaly
- •Blood Transfusion
- •Fresh frozen plasma
- •Cryoprecipitate
- •Factor VIII and IX concentrates
- •Albumin
- •Immunoglobulins
- •Neutrophil leucocytosis
- •Neutropenia
- •Vascular/platelet bleeding
- •Coagulation disorders
- •Blood groups
- •Procedure for blood transfusion
- •Complications of transfusing red blood cells
- •The White Cell
- •Neutrophils
- •Eosinophils
- •Monocytes
- •Lymphocytes
- •Haemostasis and Thrombosis
- •Haemostasis
- •Investigation of bleeding disorders
- •Platelet disorders
- •Immune thrombocytopenic purpura (ITP)
- •Investigation
- •Management
- •First-line therapy.
- •Second-line therapy
- •Thrombotic thrombocytopenic purpura (TTP)
- •Inherited coagulation disorders
- •Haemophilia A
- •Clinical features
- •Investigations
- •Management
- •Complications
- •Haemophilia B (Christmas disease)
- •von Willebrand’s disease
- •Clinical features
- •Investigations
- •Management
- •Acquired coagulation disorders
- •Vitamin K deficiency
- •Disseminated intravascular coagulation (DIC)
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Liver disease
- •Thrombosis
- •Arterial thrombosis
- •Prevention
- •Treatment
- •Venous thrombosis
- •Prevention
- •Treatment
- •Treatment of established thromboembolism
- •Ferrous sulphate.
- •Folic acid.
- •Hydroxocobalamin.
- •Cyanocobalamin.
- •Phytomenadione.
- •Menadiol sodium phosphate
- •Aspirin.
- •Clopidogrel.
- •Therapeutics
- •Oral iron
- •Indications
- •Preparations and dose
- •Side effects
- •Cautions/contraindications
- •Folic acid
- •Indications
- •Preparations and dose
- •Side effects
- •Cautions/contraindications
- •Indications
- •Preparations and dose
- •Side effects
- •Cautions/contraindications
- •Vitamin K
- •Mechanism of action
- •Indications
- •Preparations and dose
- •Side effects
- •Cautions/contraindications
- •Drugs affecting haemostasis
- •Antiplatelet agents
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •Thrombin inhibitors
- •Mechanism of action
- •Indications
- •Warfarin.
- •Drug interactions.
- •Alteplase.
- •Side effects
- •Cautions/contraindications
- •Oral anticoagulants
- •Mechanism of action
- •Indications
- •Preparations and dose
- •Side effects
- •Contraindications
- •Direct oral anticoagulants (DOACs)
- •Mechanism of action
- •Preparations and indications
- •Side effects
- •Contraindications
- •Fibrinolytic drugs
- •Mechanism of action
- •Indications
- •Preparations and dose
- •Side effects
- •Contraindications
- •6 Malignant disease
- •Diagnosis of Malignancy
- •Cancer treatment
- •Chemotherapy
- •Radiotherapy
- •Endocrine therapy
- •Biological therapy
- •Myeloablative Therapy and Haemopoietic Stem Cell Transplantation (HSCT)
- •Oncological emergencies
- •The leukaemias
- •Aetiology
- •Acute leukaemia
- •Epidemiology
- •Clinical features
- •Investigations
- •Management
- •Treatment
- •Acute myeloid leukaemia
- •Acute promyelocytic leukaemia
- •Acute lymphoblastic leukaemia
- •Chronic myeloid leukaemia
- •Clinical features
- •Investigations
- •Management
- •Chronic lymphocytic leukaemia
- •Clinical features
- •Investigations
- •Management
- •Prognosis
- •The Lymphomas
- •Hodgkin’s lymphoma
- •Clinical features
- •Investigations
- •Differential diagnosis
- •Management
- •Non-Hodgkin’s lymphoma
- •Clinical features
- •Investigations
- •Management
- •The Paraproteinaemias
- •Multiple myeloma
- •Clinical features
- •Investigations
- •Management
- •Monoclonal gammopathy of undetermined significance
- •Management of pain
- •Palliation of nausea and vomiting
- •Care of the dying patient
- •Palliative Medicine and Symptom Control
- •7 Rheumatology
- •The Normal Joint
- •Musculoskeletal Symptoms
- •Common Investigations in Musculoskeletal Disease
- •Blood tests
- •Imaging
- •Synovial fluid analysis
- •Common Regional Musculoskeletal Problems
- •Back Pain
- •Lumbar back pain
- •Investigations
- •Management
- •Intervertebral Disc Disease
- •Acute disc disease
- •Clinical features
- •Investigations
- •Management
- •Chronic disc disease
- •Mechanical problems
- •Spondylolisthesis
- •Spinal stenosis
- •Neck pain
- •Epidemiology
- •Pathology and pathogenesis
- •Clinical features
- •Differential diagnosis
- •Investigations
- •Management
- •Osteoarthritis
- •Inflammatory Arthritis
- •Rheumatoid arthritis
- •Epidemiology
- •Aetiology and pathogenesis
- •Pathology
- •Clinical features
- •Non-articular manifestations
- •Investigations
- •Differential diagnosis
- •Management
- •Prognosis
- •The Seronegative Spondyloarthritis
- •Axial spondylarthritis
- •Clinical features
- •Investigations
- •Management
- •Psoriatic arthritis
- •Clinical features
- •Investigations
- •Treatment
- •Reactive arthritis
- •Clinical features
- •Investigations
- •Management
- •Enteropathic arthritis
- •Crystal Arthritis
- •Gout and hyperuricaemia
- •Epidemiology
- •Pathogenesis
- •Clinical features
- •Investigations
- •Management
- •Pseudogout (pyrophosphate arthropathy)
- •Investigations
- •Management
- •Infection of Bones and Joints
- •Septic arthritis
- •Clinical features
- •Management
- •Specific types of bacterial arthritis
- •Osteomyelitis
- •Autoimmune Rheumatic Diseases
- •Systemic lupus erythematosus
- •Epidemiology
- •Aetiology
- •Pathogenesis
- •Clinical features
- •Investigations
- •Management
- •Prognosis
- •Antiphospholipid syndrome
- •Clinical features
- •Management
- •Systemic sclerosis (scleroderma)
- •Aetiology
- •Clinical features
- •Limited cutaneous scleroderma (LcSSc, 70% of cases)
- •Diffuse cutaneous scleroderma (DcSSc, 30% of cases)
- •Investigations
- •Management
- •Prognosis
- •Polymyositis and dermatomyositis
- •Clinical features
- •Investigations
- •Management
- •Sjögren’s syndrome
- •Clinical features
- •Investigations
- •Management
- •‘Overlap’ syndrome and undifferentiated autoimmune rheumatic disease
- •Systemic Inflammatory Vasculitis
- •Polymyalgia rheumatica and giant cell arteritis
- •Clinical features
- •Investigations
- •Management
- •Takayasu’s arteritis
- •Polyarteritis nodosa
- •Kawasaki disease
- •Microscopic polyarteritis (polyangiitis)
- •Eosinophilic granulomatosis with polyangiitis
- •Henoch–Schönlein purpura
- •Cryoglobulinaemic vasculitis
- •Behçet’s disease
- •Diseases of Bone
- •Control of calcium and bone metabolism
- •Vitamin D
- •Parathyroid hormone
- •Osteoporosis
- •Aetiology
- •Clinical features
- •Investigations
- •Assessment of fracture risk
- •Management
- •Clinical features
- •Investigations
- •Treatment
- •Osteomalacia and vitamin D deficiency
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Therapeutics
- •Anti-inflammatories and pain relief
- •Paracetamol (acetaminophen)
- •Non-steroidal anti-inflammatory drugs
- •Mechanism of action
- •Indications
- •Examples of preparations and doses
- •Side effects
- •Gastrointestinal toxicity.
- •Other side effects
- •Cautions/contraindications
- •Drugs affecting bone metabolism
- •Bisphosphonates
- •Mechanism of action
- •Indications
- •Examples of preparations and doses
- •Side effects
- •Calcium
- •Indications
- •Examples of preparations and doses
- •Side effects
- •Vitamin D
- •Mechanism of action
- •Indications
- •Examples of preparations and doses
- •Side effects
- •Water and Electrolyte Requirements
- •Body Fluid Compartments
- •Distribution of extracellular fluid
- •Glucocorticoid-induced osteoporosis
- •Osteonecrosis
- •Paget’s disease
- •Aetiology
- •Intravenous fluids in clinical practice
- •Regulation of Body Fluid Homeostasis
- •Regulation of extracellular volume
- •Abnormalities of extracellular volume
- •Increased extracellular volume
- •Clinical features
- •Aetiology
- •Management
- •Decreased extracellular volume
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Plasma Osmolality and Disorders of Sodium Regulation
- •Regulation of body water content
- •Hyponatraemia
- •Hyponatraemia resulting from salt loss (hypovolaemic hyponatraemia)
- •Clinical features
- •Management
- •Hyponatraemia resulting from water excess (dilutional hyponatraemia)
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Central pontine myelinolysis
- •Hypernatraemia
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Disorders of Potassium Regulation
- •Hypokalaemia
- •Aetiology
- •Clinical features
- •Management
- •Hyperkalaemia
- •Aetiology
- •Clinical features
- •Management
- •Disorders of Magnesium Regulation
- •Hypomagnesaemia
- •Aetiology
- •Clinical features
- •Management
- •Hypermagnesaemia
- •Disorders of Acid–Base Balance
- •Respiratory acidosis
- •Respiratory alkalosis
- •Metabolic acidosis
- •Clinical features
- •Differential diagnosis (the anion gap)
- •Lactic acidosis
- •Diabetic ketoacidosis
- •Renal tubular acidosis
- •Uraemic acidosis
- •Metabolic alkalosis
- •Clinical features
- •Management
- •Therapeutics
- •Diuretics
- •Thiazide diuretics
- •Examples
- •Mechanism of action
- •Indications
- •Side effects
- •Loop diuretics
- •Examples
- •Mechanism of action
- •Indications
- •Side effects
- •Potassium-sparing diuretics and aldosterone antagonists
- •Examples
- •Mechanism of action
- •Indications
- •Side effects
- •9 Renal disease
- •Presenting Features Of Renal Disease
- •Dysuria
- •Polyuria and nocturia
- •Oliguria
- •Haematuria
- •Pain
- •Investigation Of Renal Disease
- •Blood tests
- •Glomerular filtration rate
- •Urine dipstick testing
- •Proteinuria
- •Haematuria
- •Glycosuria
- •Urine microscopy
- •White cells
- •Red cells
- •Casts
- •Bacteria
- •Imaging techniques
- •Transcutaneous renal biopsy
- •Glomerular Diseases
- •Normal glomerular structure
- •Pathogenesis and terms in glomerular disease
- •Classification and presentation of glomerulopathies
- •Aetiology
- •Nephrotic syndrome with ‘bland’ urine sediments
- •Nephrotic syndrome with ‘active’ urine sediments (mixed nephrotic/nephritic)
- •Clinical features
- •Differential diagnoses
- •Investigations
- •Management
- •General oedema
- •Specific treatment
- •Complications
- •Nephrotic Syndrome
- •Acute glomerulonephritis (acute nephritic syndrome)
- •Clinical features
- •Investigations
- •Management
- •Rapidly progressive glomerulonephritis
- •Urinary Tract Infection
- •Pathogenesis
- •Risk factors for UTI
- •Clinical features
- •Natural history
- •Investigations
- •Diagnosis
- •Treatment of single isolated attack
- •Recurrent infection.
- •Management
- •UTI in pregnancy
- •Abacteriuric frequency or dysuria (‘urethral syndrome’)
- •Bacterial prostatitis
- •Tuberculosis of the urinary tract
- •Tubulointerstitial Nephritis
- •Acute tubulointerstitial nephritis
- •Chronic tubulointerstitial nephritis
- •Hypertension and the Kidney
- •Essential hypertension
- •Renal hypertension
- •Bilateral renal disease
- •Renovascular disease
- •Options for renal artery imaging
- •Management
- •Aetiology
- •Calcium stones
- •Uric acid stones
- •Infection-induced stones
- •Cystine stones
- •Clinical features
- •Differential diagnosis
- •Investigations
- •Management
- •Renal Calculi and Nephrocalcinosis
- •Nephrocalcinosis
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Epidemiology
- •Clinical and biochemical features
- •Urinary Tract Obstruction
- •Acute Kidney Injury
- •Investigation of the uraemic emergency
- •Investigations
- •Management
- •Prognosis
- •Aetiology
- •Chronic Kidney Disease
- •Clinical features and investigations
- •Differentiating AKI from CKD
- •Management
- •Renoprotection
- •Reduce cardiovascular risk
- •Correction of complications
- •Referral to a nephrologist
- •Renal Replacement Therapy
- •Dialysis
- •Haemodialysis
- •Peritoneal dialysis
- •Haemofiltration
- •Complications of all long-term dialysis
- •Transplantation
- •Cystic Renal Disease
- •Solitary and multiple renal cysts
- •Autosomal-dominant polycystic kidney disease
- •Clinical features
- •Diagnosis
- •Management
- •Medullary sponge kidney
- •Tumours of the Kidney and Genitourinary Tract
- •Renal cell carcinoma
- •Clinical features
- •Investigations
- •Management
- •Prognosis
- •Urothelial tumours
- •Clinical features
- •Investigations
- •Management
- •Diseases Of The Prostate Gland
- •Benign enlargement of the prostate gland
- •Clinical features
- •Investigations
- •Management
- •Prostatic carcinoma
- •Clinical features
- •Investigation
- •Management
- •Screening
- •Clinical features
- •Investigations
- •Treatment
- •Testicular Tumour
- •Urinary Incontinence
- •Normal bladder physiology
- •Stress incontinence
- •Urge incontinence
- •Overflow incontinence
- •Neurological causes
- •Chest pain
- •Dyspnoea
- •Palpitations
- •Syncope
- •Other symptoms
- •Investigations in Cardiac Disease
- •The chest X-ray
- •ECG waveform and definitions (Fig. 10.5)
- •The Electrocardiogram
- •Exercise electrocardiography
- •24-hour ambulatory taped electrocardiography
- •Tilt testing
- •Echocardiography
- •Cardiac nuclear imaging
- •Cardiac computed tomography
- •Cardiovascular magnetic resonance
- •Positron emission tomography
- •Cardiac catheterization
- •Cardiac Arrhythmias
- •General principles of management of arrhythmias
- •Sinus rhythms
- •Sinus arrhythmia
- •Bradycardias and heart block
- •Sinus bradycardia
- •Neurally mediated syndromes
- •Heart block
- •Atrioventricular block
- •Bundle branch block
- •Supraventricular tachycardias
- •Sinus tachycardia
- •Atrioventricular junctional tachycardias
- •Atrioventricular nodal re-entry tachycardia (AVNRT)
- •Atrioventricular reciprocating tachycardia (AVRT)
- •Symptoms
- •Acute management
- •Long-term management
- •Atrial tachyarrhythmias
- •Atrial fibrillation
- •Management
- •Assessment for anticoagulation
- •Atrial flutter
- •Ventricular tachyarrhythmias
- •Ventricular ectopic premature beats (extrasystoles)
- •Sustained ventricular tachycardia
- •Non-sustained ventricular tachycardia
- •Ventricular fibrillation
- •Long QT syndrome
- •Cardiac arrest
- •Aetiology
- •Pathophysiology
- •Venous return (preload)
- •Outflow resistance (afterload)
- •Myocardial contractility
- •Neurohormonal and sympathetic system activation: salt and water retention
- •Natriuretic peptides
- •Antidiuretic hormone (vasopressin)
- •Clinical features
- •Symptoms
- •Signs
- •Investigations
- •Treatment of chronic heart failure
- •Heart Failure
- •Drug treatment
- •Non-pharmacological treatment
- •Acute heart failure
- •Clinical features
- •Management
- •Irreversible risk factors for coronary artery disease
- •Potentially changeable risk factors
- •Estimation of cardiovascular risk
- •Ischaemic Heart Disease
- •Angina
- •Clinical features
- •Diagnosis
- •Investigations
- •Management
- •Acute coronary syndromes
- •Clinical features
- •Treatment of NSTEMI and unstable angina
- •Risk stratification
- •ST segment elevation myocardial infarction (STEMI)
- •Clinical features
- •Investigations
- •Management
- •Complications (Table 10.10)
- •Disturbances of rate, rhythm and conduction (p. 411)
- •Post-ACS drug therapy and assessment
- •Epidemiology
- •Clinical features
- •Investigations
- •Treatment
- •Rheumatic Fever
- •Chronic rheumatic heart disease
- •Valvular Heart Disease
- •Prosthetic heart valves
- •Mitral stenosis
- •Aetiology
- •Pathophysiology
- •Symptoms
- •Signs
- •Investigations
- •Management
- •Mitral regurgitation
- •Aetiology
- •Pathophysiology
- •Symptoms
- •Signs
- •Investigations
- •Management
- •Prolapsing (‘floppy’) mitral valve
- •Aetiology
- •Clinical features
- •Investigation
- •Management
- •Aortic stenosis
- •Aetiology
- •Pathophysiology
- •Symptoms
- •Signs
- •Investigations
- •Management
- •Aortic regurgitation
- •Aetiology
- •Pathophysiology
- •Symptoms
- •Signs
- •Investigations
- •Management
- •Tricuspid and pulmonary valve disease
- •Infective endocarditis
- •Aetiology
- •Pathology
- •Clinical features
- •Investigations
- •Diagnostic criteria
- •Management
- •Surgery
- •Pulmonary Heart Disease
- •Pulmonary hypertension
- •Aetiology

The Acute Abdomen 123
• An erect chest X-ray may show air under the diaphragm with a perforated
viscus, but its absence does not exclude perforation. Plain abdominal
X-ray shows dilated loops of bowel and fluid levels in obstruction.
Ultrasound examination is useful in the diagnosis of acute cholecystitis,
cholangitis, appendicitis and gynaecological conditions such as ruptured
ovarian cyst and ectopic pregnancy. Spiral CT scan is the most accurate
modality in the investigation of the acute abdomen but is usually reserved
for patients with inconclusive or negative ultrasound results.
• Surgical intervention with a laparoscopy or laparotomy may be necessary
depending on the diagnosis.
Acute appendicitis
Acute appendicitis occurs when the lumen of the appendix becomes
obstructed by a faecolith.
Epidemiology
It affects all age groups but is rare in the very young and very old.
Clinical features
The typical clinical presentation is the onset of central abdominal pain which
then becomes localized to the right iliac fossa (RIF), accompanied by anorexia
and sometimes vomiting and diarrhoea. The patient is pyrexial, with tenderness and guarding in the RIF due to localized peritonitis. There may be a
tender mass in the presence of an appendix abscess.
Investigations
The white cell count, C-reactive protein and ESR are raised, but these are
not specific. Ultrasonography may show an inflamed appendix and can also
show an appendix mass. CT is highly sensitive and specific, and has reduced
removal of histologically normal appendices by 90%.
Differential diagnosis
Non-specific mesenteric lymphadenitis, terminal ileitis due to Crohn’s disease or Yersinia infection, acute salpingitis in women, inflamed Meckel’s
diverticulum and functional bowel disease can all mimic acute appendicitis.
Management
The treatment is surgical, with removal of the appendix either by open surgery or laparoscopically. An appendix mass is treated conservatively initially
with intravenous fluids and antibiotics and later appendicectomy.
Complications
Complications may arise from gangrene and perforation, leading to localized
abscess formation or generalized peritonitis.

124 Gastroenterology and nutrition
Acute peritonitis
Localized peritonitis occurs with all acute inflammatory conditions
of the gastrointestinal tract, and management depends on the underlying
condition, e.g. acute appendicitis, acute cholecystitis.
Generalized peritonitis occurs as a result of rupture of an abdominal
viscus, e.g. perforated duodenal ulcer, perforated appendix. There is a sudden
onset of abdominal pain which rapidly becomes generalized. The patient is
shocked and lies still, as movement exacerbates the pain. A plain abdominal
X-ray may show air under the diaphragm; serum amylase must be checked
to exclude acute pancreatitis.
Intestinal obstruction
Intestinal obstruction is either mechanical or functional.
Mechanical (see Table 3.17) The bowel above the level of the obstruction is
dilated, with increased secretion of fluid into the lumen. The patient complains of
colicky abdominal pain, associated with vomiting (occurs earlier with small bowel
than large bowel obstruction) and absolute constipation (occurs earlier with large
bowel than small bowel obstruction). On examination there is distension and
‘tinkling’ bowel sounds. Small bowel obstruction may settle with conservative
management (i.e. nasogastric suction and intravenous fluids to maintain
hydration). Large bowel obstruction is treated surgically.
Functional This occurs with a paralytic ileus, which is often seen in
the post-operative stage of peritonitis or of major abdominal surgery, or in
association with opiate treatment (acute colonic pseudo-obstruction, Ogilvie’s
syndrome). It also occurs when the nerves or muscles of the intestine are
damaged, causing intestinal pseudo-obstruction. Unlike mechanical obstruction,
pain is often not present and bowel sounds may be decreased. Gas is seen
throughout the bowel on a plain abdominal X-ray. Management is conservative.
THE PERITONEUM
The peritoneal cavity is a closed sac lined by mesothelium. It contains a little
fluid to allow the abdominal contents to move freely. Conditions which affect
the peritoneum include:
• Infective (peritonitis)
• Secondary to gut disease, e.g. appendicitis, perforation
• Chronic peritoneal dialysis
• Spontaneous (associated with cirrhotic ascites)
• Tuberculous
• Neoplasia
• Secondary deposits, e.g. from ovary
• Primary mesothelioma
• Vasculitis: connective tissue disease.

Nutrition 125
Table 3.18 Protein, energy and water requirement of normal
and hypercatabolic adults
Metabolic state Nutritional
Protein (g/kg)
Nitrogen (g/kg)
Energy (kcal/kg)
Water (mL/kg)
requirements
Normal
1
0.17
25–30
30–35
Hypercatabolic
2–3
0.3–0.45
35–50
30–35
NUTRITION
Dietary requirements
Food is necessary to provide the body with energy. The average daily requirement (Table 3.18) of a 55-year-old female in the UK is 8100 kJ (1940 kcal),
and a 55-year-old man is 10 600 kJ (2550 kcal). This is at present made up of
about 50% carbohydrate, 35% fat, 15% protein ± 5% alcohol. In developing
countries, however, carbohydrate may be >75% of the total energy input,
and fat <15% of the total energy input. Energy requirements increase during
periods of rapid growth, such as adolescence, pregnancy and lactation and
with sepsis.
Body weight is maintained at a ‘set point’ by a precise balance of energy
intake and total energy expenditure (the sum of the resting or basal metabolic
rate, physical activity, and the thermic effect of food eaten). Weight gain is
almost always due solely to an increase in energy intake which exceeds
total energy expenditure. Occasionally weight gain is due to a decrease in
energy expenditure, e.g. hypothyroidism, or fluid retention, e.g. heart failure
or ascites. On the other hand, weight loss associated with cancer and chronic
diseases is due to a reduction in energy intake secondary to a loss of appetite
(anorexia). In a few conditions, such as sepsis and severe trauma, there is an
increase in energy requirements (hypercatabolic or hypermetabolic) which
will result in a negative energy balance if there is no compensatory increase
in energy intake.
A balanced diet also requires sufficient amounts of minerals and vitamins.
In the developed world vitamin deficiency is rare except in specific groups,
e.g. alcohol dependent and patients with small bowel disease, and patients
with liver and biliary tract disease, who are susceptible to deficiency of the
fat-soluble vitamins (A, D, E, K). Deficiencies of the B vitamins riboflavin
and biotin are rare in all patient groups. Dietary deficiency of vitamin B6
(pyridoxine, pyridoxal and pyridoxamine) is also extremely rare, but drugs

126 Gastroenterology and nutrition
(e.g. isoniazid and penicillamine) that interact with pyridoxal phosphate may
cause deficiency and a polyneuropathy.
NUTRITIONAL SUPPORT
Patients should be screened for nutritional status on admission to hospital
and during their stay:
• Patients should be asked about recent weight loss, their usual weight
and whether they have been eating less than usual.
• Their weight and height should be recorded and body mass index (BMI)
calculated (weight [kg]/height [m]2). The acceptable range of BMI is
20–25 kg/m2 for men and 19–24 kg/m2 for women.
Nutritional supplementation is required in those patients who cannot eat,
should not eat, will not eat or cannot eat enough. It is necessary to provide
nutritional support for:
• All severely malnourished patients (indicated by a BMI less than 15 kg/m2)
on admission to hospital
• Moderately malnourished patients (BMI 15–19 kg/m2) who, because of
their physical illness, are not expected to eat for 3–5 days
• Normally nourished patients not expected to eat for 7–10 days.
Enteral nutrition is cheaper, more physiological and has fewer complications
than parenteral (intravenous) nutrition, and should be used if the gastrointestinal
tract is functioning normally. With both enteral and parenteral nutrition a
complete feeding regimen consisting of fat, carbohydrates, protein, vitamins,
minerals and trace elements can provide the nutritional requirements of the
individual (see Table 3.18). Ideally a multidisciplinary nutrition support team
should supervise the provision of artificial nutritional support.
Enteral nutrition
Foods can be given by:
• Mouth
• Fine-bore nasogastric tube for short-term enteral nutrition
• Percutaneous endoscopic gastrostomy (PEG): this is useful for patients
who need feeding for longer than 2 weeks
• Percutaneous jejunostomy where a tube is inserted directly into the
jejunum either endoscopically or at laparotomy.
A polymeric diet with whole protein, carbohydrate and fat is usually used;
an elemental diet composed of amino acids, glucose and fatty acids may be
used for patients with CD.
Total parenteral nutrition (TPN)
Parenteral nutrition may be administered via a feeding catheter placed
in a peripheral vein or a silicone catheter placed in the subclavian vein.

Nutritional Support 127
Table 3.19 Complications of total parenteral nutrition
Catheter related: sepsis, thrombosis, embolism and pneumothorax
Metabolic, e.g. hyperglycaemia, hypercalcaemia
Electrolyte disturbances
Liver dysfunction
Central catheters must only be placed by experienced clinicians under
strict aseptic conditions in a sterile environment. These catheters should
only be used for feeding purposes, and not the administration of drugs or
blood to reduce the risk of introducing infection. Complications of TPN are
given in Table 3.19.
Monitoring of artificial nutrition
Patients receiving nutritional support should be weighed twice weekly, and
they require regular clinical examination to check for fluid overload or depletion. Patients receiving nutritional support in hospital initially require daily
measurements of urea and electrolytes and blood glucose. More frequent
measurement of blood glucose is indicated in patients beginning TPN. Liver
biochemistry, calcium and phosphate are measured twice weekly. Serum
magnesium, zinc and nitrogen balance (see below) are measured weekly. The
frequency of biochemical monitoring is adjusted according to the patient’s
clinical and metabolic status.
It is necessary to give 40–50 g of protein per 24 hours to maintain nitrogen
balance, which represents the balance between protein breakdown and
synthesis. The aim of any regimen is to achieve a positive nitrogen balance,
which can usually be obtained by giving 3–5 g of nitrogen in excess of output.
The amount of protein required to maintain nitrogen balance in a particular
individual can be calculated from the amount of urinary nitrogen loss, using
the formula:
N2 loss (g/24 h) = Urinary urea (mmol/24 h) × 0.028 + 2
Urinary nitrogen × 6.25 = grams of protein required
(most proteins contain about 16% nitrogen)
Most patients require about 12 g of nitrogen per 24 hours, but
hypercatabolic patients require about 15 g/day.
Refeeding syndrome
The refeeding syndrome occurs within the first few days of refeeding by
the oral, enteral or parenteral route. It is underrecognized and can be fatal.
It involves a shift from the use of fat as an energy source during starvation

128 Gastroenterology and nutrition
to the use of carbohydrate as an energy source during refeeding. With the
introduction of artificial nutrition and carbohydrate by any source, insulin
release is augmented and there is rapid intracellular passage of phosphate,
magnesium and potassium resulting in hypophosphataemia, hypomagnesaemia, and hypokalaemia. Phosphate is an integral part of cellular machinery.
Deficiency results in widespread organ dysfunction (muscle weakness,
rhabdomyolysis, cardiac failure, immune suppression, haemolytic anaemia,
thrombocytopenia, coma, hallucinations, fits). Thiamine deficiency can be
precipitated. Patients at risk of refeeding are underweight (e.g. anorexia
nervosa, alcohol-dependent syndrome) or those with recent rapid weight loss
(5% within preceding month), including patients after treatment for morbid
obesity. These at-risk patients should receive high-dose vitamin B and C,
e.g. Pabrinex® beginning before feeding, and begin feeding at 25%–50% of
estimated calorie requirements, increasing by 100 calories per day. Serum
phosphate, magnesium, calcium, potassium, urea and creatinine, body
weight and evidence of fluid overload should be checked daily for the first
week, and electrolyte deficiencies corrected as necessary.
DISORDERS OF BODY WEIGHT
Obesity
Obesity, defined as an excess of body fat contributing to comorbidity, is an
increasingly common problem in developed and developing countries. It is
defined as a BMI of 30 kg/m2 or greater. Overweight is defined as a BMI of
25–30 kg/m2 and may be associated with a mildly increased risk of complications that have been identified in obese patients. In almost all obese individuals
weight gain is a result of increased energy intake and energy expenditure is
normal or indeed increased. In a few conditions, e.g. hypothyroidism, weight
gain is due at least in part to reduced energy expenditure. Obese patients are
at risk of a premature death, mainly from diabetes, ischaemic heart disease,
and cerebrovascular disease. Obesity is also associated with an increased
risk of hypertension, hyperlipidaemia, obstructive sleep apnoea, osteoarthritis
of the knees and hips, fatty liver disease, gallstones and an increased cancer
risk. Weight reduction can be achieved with a reduction in calorie intake and
an increase in physical activity, although this is often difficult to achieve. A
10% loss of body weight (i.e. 10 kg in a 100 kg person) is associated with
a fall in blood pressure and a reduced risk of diabetes and overall mortality.
Drug treatment such as orlistat, an inhibitor of pancreatic lipase and hence
fat digestion, may be used in the severely obese patient. Bariatric surgery is
increasingly performed in patients with morbid obesity (BMI >40 kg/m2) or
patients with a BMI >35 kg/m2 and obesity-related complications, after conventional medical treatment has failed. The techniques used are restrictive,
such as gastric banding (which restricts the ability to eat) or intestinal bypass
(which reduces the ability to absorb nutrients) or a combination (Roux-en-Y).

Therapeutics 129
Anorexia nervosa
Anorexia nervosa is a psychological illness, predominantly affecting young
females and characterized by marked weight loss (BMI <17.5 kg/m2), intense
fear of gaining weight, a distorted body image and amenorrhoea. Patients
with anorexia nervosa control their body weight by a process of semi-starvation and/or self-induced vomiting (bulimia) and may develop consequences of
undernutrition. Treatment is complex and should be undertaken in a specialist
eating disorders unit.
THERAPEUTICS
Drugs for dyspepsia and peptic ulceration
Antacids
Mechanism of action
Main effect is to neutralize gastric acid. Alginate-containing antacids (e.g.
Gaviscon®, Mucogel®) form a ‘raft’ that floats on the surface of the stomach
contents to reduce reflux and protect the gastro-oesophageal mucosa.
Indications
Symptomatic relief in dyspepsia, gastro-oesophageal reflux and peptic ulceration. Healing of peptic ulcers is much less than with antisecretory drugs (see
below) and antacids should not be used for this indication.
Side effects
Magnesium-containing antacids tend to be laxative, whereas aluminiumcontaining antacids may be constipating; antacids containing both aluminium
and magnesium may reduce these colonic side effects.
Cautions/contraindications
Antacids may interfere with the absorption of other drugs and in general other
drugs should be given at least 1 hour before or after each dose of antacid.
The sodium content of some preparations, e.g. magnesium trisilicate mixture
(6.3 mmol/10 mL) and Gaviscon® Advance (4.6 mmol/10 mL; 2.25 mmol/
tablet) should be taken into account in patients on a ‘no added’ salt diet
(cardiac, renal or hepatic disease). Aluminium hydroxide is contraindicated in
hypophosphataemia. Constipating antacids (i.e. those containing aluminium)
should be avoided in liver disease.
H2-receptor antagonists
Mechanism of action
Reduce gastric acid secretion as a result of histamine H2-receptor blockade
(e.g. ranitidine, cimetidine).

130 Gastroenterology and nutrition
Indications
GORD, healing of benign gastric and duodenal ulcers, prevention of gastroduodenal damage in patients requiring intensive care, prevention of
NSAID-induced DUs, and in high doses prevention of GUs. However, for all
indications, PPIs are more effective and more commonly used in clinical
practice.
Side effects
Diarrhoea, altered liver biochemistry, headache, dizziness, rash. Rarely, other
side effects (see National Formulary).
Cautions/contraindications
Cimetidine retards oxidative hepatic drug metabolism by binding to microsomal cytochrome P450. It should be avoided in patients stabilized on
warfarin, phenytoin and theophylline (or aminophylline) but other interactions
(see National Formulary) may be of less clinical relevance.
Proton pump inhibitors
Mechanism of action
Inhibit gastric acid secretion by blocking the hydrogen/potassium–adenosine
triphosphate enzyme system (the ‘proton pump’) of the gastric parietal cell.
Examples include omeprazole, esomeprazole, lansoprazole.
Indications
GORD; healing of peptic ulcers; prevention of NSAID-induced peptic ulcers;
in combination with antibacterials for eradication of H. pylori; intravenously
and after endoscopic therapy to reduce re-bleeding rates in patients with
bleeding peptic ulcers; inhibition of gastric acid in pathological hypersecretory
conditions, e.g. gastrinoma; prevention of peptic ulcers in critically ill patients;
prophylaxis of acid aspiration during general anaesthesia; dyspepsia.
Side effects
Gastrointestinal disturbance (diarrhoea, nausea, vomiting), liver dysfunction,
hypersensitivity reactions, headache, skin reactions, increased risk of
gastrointestinal infections (due to reduced gastric acidity). Rarely, acute
kidney injury, deficiency of vitamin B12, calcium (leading to hip fracture) and
magnesium due to reduced intestinal absorption.
Cautions/contraindications
Omeprazole and esomeprazole competitively inhibit the CYP2C19 isoenzyme
(which metabolises clopidogrel to its active metabolite) and may reduce the
ability of clopidogrel to inhibit platelet aggregation. Omeprazole may decrease
the effect of warfarin, phenytoin and diazepam. Lansoprazole may increase

Therapeutics 131
the effect of warfarin, phenytoin and theophylline. Reduce dose in severe liver
disease. Proton pump inhibitors are also associated with an increased risk of
C. difficile infection as a result of altered pH of intestinal flora and therefore
should be discontinued if any concern about C. difficile infection.
Constipation
Treatment of constipation is initially with lifestyle changes and drugs are
reserved for use as second-line treatment. It may be necessary to use a combination of two different types of laxative, e.g. stimulant plus faecal softener.
All laxatives are contraindicated in intestinal obstruction or perforation, paralytic ileus, and severe inflammatory conditions of the gut such as CD and UC.
Bulk-forming laxatives
Mechanism of action
Agents such as ispaghula husk act to absorb water and increase faecal mass,
which stimulates peristalsis.
Indications
Treatment of slow-transit constipation and bulking of stool in patients with a
colostomy, diverticular disease and irritable bowel syndrome.
Preparations and dose
Unprocessed wheat bran is one of the most effective fibre laxatives, and
patients can add it to meals, e.g. cereal (2–6 tablespoons per day).
Side effects
Flatulence, abdominal distension.
Cautions/contraindications
Maintain adequate fluid intake to prevent faecal impaction; contraindications
(see above).
Stimulant laxatives
Mechanism of action
Stimulant laxatives (e.g. bisacodyl, senna, glycerin suppositories) act to
increase colonic motor activity.
Indications
Short-term treatment of constipation.
Side effects
Abdominal cramps, diarrhoea and hypokalaemia.

132 Gastroenterology and nutrition
Cautions/contraindications
Contraindications (see above).
Osmotic laxatives
Mechanism of action
Osmotic laxatives (e.g. lactulose, macrogols [polyethylene glycol], phosphate
enema) attract or retain water in the intestinal lumen, leading to softer stools
and improved propulsion.
Indications
Treatment of constipation. Lactulose is used in the treatment of hepatic
encephalopathy. Phosphate enemas are used to evacuate the bowel before
radiological procedures, flexible sigmoidoscopy and surgery.
Side effects
Abdominal distension, colic, nausea, local irritation after phosphate enema.
Cautions/contraindications
Contraindications (see above). May also cause electrolyte disturbance. Use
with caution in hepatic and renal impairment. Although magnesium ions
are absorbed poorly, similar to all osmotic ions some absorption does occur,
which can cause problems in patients with abnormal renal function.
Bowel-cleansing solutions
Indications
Bowel cleansing solutions (e.g. Fleet Phospho-soda®, Klean-Prep®, Moviprep®,
Picolax®) are used before colonic surgery, colonoscopy or radiological examination to ensure the bowel is free of solid contents. They are not treatments for
constipation. Bowel-cleansing agents are coupled with a low residue diet for at
least 3 days before the procedure, copious intake of water or other clear fluids
and cessation of all solid foods on the day before the procedure. All are contraindicated in bowel obstruction, perforated bowel or severe colitis and Moviprep®
is contraindicated in glucose-6-phosphate dehydrogenase deficiency.
Side effects
Nausea, vomiting, abdominal cramps. Occasionally dehydration and hypotension, electrolyte disturbance.
Diarrhoea
Most cases of acute diarrhoea are infective and will settle without treatment.
Oral rehydration salts (Dioralyte®), 1 sachet after every loose motion, are often
used especially in the elderly and children. Antidiarrhoeal agents (e.g. loperamide) relieve symptoms of acute diarrhoea but are not recommended routinely.
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