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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2683_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Series Editors’ foreword
- •Prefaces
- •Acknowledgements
- •Series Editors’ acknowledgements
- •History of the presenting complaint (HPC)
- •Past medical history (PMH)
- •Medications and allergies (DHX)
- •Family history (FHX)
- •Social history (SHX)
- •Systems review (SR)
- •General symptoms
- •Fatigue
- •Appetite
- •Weight change
- •Sweats
- •Pruritus (itching)
- •Sleep pattern
- •Cardiovascular symptoms
- •Chest pain
- •Shortness of breath (dyspnoea) and exercise tolerance
- •Loss of consciousness (syncope)
- •Palpitations
- •Ankle and calf swelling
- •Calf, thigh or buttock pain on exertion (claudication)
- •Respiratory symptoms
- •Dyspnoea
- •Cough
- •Sputum
- •Chest pain
- •Wheeze
- •Hoarse voice
- •Gastrointestinal disease
- •Abdominal pain
- •Dysphagia
- •Nausea and vomiting
- •Indigestion
- •Change in bowel habit or stools
- •Jaundice and itch
- •Abdominal swelling
- •Genitourinary symptoms
- •Dysuria
- •Change in urine appearance
- •Frequency and nocturia
- •Hesitancy
- •Contents
- •Loin pain
- •Incontinence
- •Menstruation
- •Discharge
- •Neurological symptoms
- •Headache
- •Dizziness and vertigo
- •Loss of consciousness
- •Visual disturbance
- •Altered hearing
- •General principles
- •Altered smell
- •Speech disturbance
- •Limb weakness, paraesthesiae and sensory loss
- •Metabolic and endocrine symptoms
- •Musculoskeletal symptoms
- •Pain
- •Weakness
- •Overview
- •The history
- •Presenting complaint (PC)
- •Visual survey
- •Position
- •Hands
- •Radial pulse
- •Blood pressure
- •Brachial and carotid artery
- •Jugular Venous Pressure
- •Face
- •Praecordium
- •Apex beat
- •Palpation
- •Auscultation
- •Summary
- •The respiratory system
- •Visual survey
- •Stiffness
- •Joint swelling
- •Disability
- •Skin symptoms
- •Rash
- •Pruritus
- •Precipitants
- •Haematological symptoms
- •Fatigue
- •Excessive bleeding or bruising
- •Recurrent infections
- •Glandular swelling
- •Conclusion of history taking
- •2 Clinical examination
- •ABCDE approach
- •Massive Blood Loss Protocol
- •General principles
- •Visual survey
- •Patient position, general behaviour and around the bed
- •Pallor
- •Cyanosis
- •Jaundice
- •Fluid status
- •Pigmentation
- •The face and body habitus
- •The hands
- •Hands
- •Nails
- •Tendons
- •Joints
- •Neuromuscular
- •Miscellaneous
- •The cardiovascular system
- •Position
- •Hands
- •Pulse
- •Blood pressure
- •Jugular venous pressure
- •Face and mouth
- •Trachea
- •Thorax
- •Inspection
- •Expansion
- •Tactile fremitus and vocal fremitus
- •Percussion
- •Auscultation
- •Summary
- •The abdomen
- •Visual survey
- •Position
- •Hands
- •Arms
- •Face and mouth
- •Neck
- •Trunk and back
- •Abdomen
- •Inspection
- •Palpation
- •Percussion
- •Auscultation
- •Concluding your examination
- •The nervous system
- •Visual survey
- •Cranial nerves
- •Cranial nerve I (olfactory nerve)
- •Cranial nerve II (optic nerve)
- •Cranial nerves III, IV and VI and eye movements
- •Cranial nerve III (oculomotor nerve)
- •Cranial nerve IV (trochlear nerve)
- •Cranial nerve VI (abducens nerve)
- •Cranial nerve V (trigeminal nerve)
- •Cranial nerve VII (facial nerve)
- •Cranial nerve VIII (vestibulocochlear nerve)
- •Cranial nerve IX (glossopharyngeal nerve)
- •Cranial nerve X (vagus nerve)
- •Cranial nerve XI (accessory nerve)
- •Cranial nerve XII (hypoglossal nerve)
- •Upper limb
- •Visual survey
- •Tone
- •Power
- •Coordination
- •Reflexes
- •Sensation
- •Lower limb
- •Visual survey
- •Tone
- •Power
- •Coordination
- •Reflexes
- •Sensation
- •Gait
- •Musculoskeletal examination
- •Visual survey
- •Look
- •Feel
- •Move
- •Assessment of disability
- •Hands
- •Skin and lymphadenopathy
- •Breast examination
- •Neck examination
- •3 Writing in the medical notes
- •General principles
- •Sample clerking
- •4 Chest pain
- •Introduction
- •History and examination findings
- •History
- •Type of chest pain
- •Onset and progression
- •Site and radiation
- •Nature of pain
- •Associated symptoms
- •Examination
- •Investigations
- •5 Shortness of breath
- •Introduction
- •History and examination findings
- •History
- •Onset
- •Severity
- •Precipitating and aggravating factors
- •Associated features
- •Other factors
- •Examination
- •Inspection
- •Palpation
- •Percussion
- •Auscultation
- •Investigations
- •Acute presentation
- •Chronic presentation
- •6 Cough and haemoptysis
- •Introduction
- •History and examination findings
- •History
- •Examination
- •Investigations
- •Bedside
- •Blood tests
- •Imaging
- •Further investigations
- •7 Palpitations
- •Introduction
- •History and examination findings
- •History
- •Causes and contributing factors
- •Examination
- •Investigations
- •8 Pyrexia of unknown origin
- •Introduction
- •History and examination findings
- •Investigations
- •Bedside investigations
- •Blood tests
- •Microbiology tests
- •Further investigations
- •Differential diagnosis
- •9 Abdominal pain
- •Introduction
- •History and examination findings
- •History
- •Examination
- •Ascertaining the underlying causes of abdomnal pain
- •Investigations
- •Bedside investigations
- •Blood tests
- •Imaging
- •Further investigations
- •10 Heartburn and indigestion
- •Introduction
- •History and examination findings
- •Investigations
- •Common investigations
- •Specialized investigations
- •11 Gastrointestinal bleed
- •Introduction
- •History and examination findings
- •History
- •Examination
- •Investigations
- •Bedside investigations
- •Blood tests
- •Further investigations
- •12 Change in bowel habit
- •Introduction
- •History and examination findings
- •History
- •Examination
- •Investigations
- •Bedside investigations
- •Blood tests
- •Imaging
- •Noninvasive
- •Invasive
- •Further investigations
- •13 Weight loss
- •Introduction
- •History and examination findings
- •History
- •Examination
- •Investigations
- •Blood tests
- •Imaging
- •14 Jaundice
- •Introduction
- •History and examination
- •History
- •Examination
- •Investigations
- •Haemolysis screen
- •Hepatocellular screen
- •Introduction
- •Micturition disturbances
- •History and examination findings
- •Examination
- •General appearance
- •Cardiovascular system
- •Abdominal examination
- •Neurological examination
- •Investigations
- •Urine tests
- •Blood tests
- •Imaging
- •Further investigations
- •Haematuria
- •History and examination findings
- •Initial tests
- •Imaging
- •Other investigations
- •Proteinuria
- •16 Headache and facial pain
- •Introduction
- •History and examination findings
- •History
- •Solitary acute episode
- •Progressive headache
- •Recurrent episodic headache and facial pain
- •Chronic headache and facial pain
- •Examination
- •Investigations
- •Blood tests
- •Imaging
- •Introduction
- •History and examination findings
- •Investigations
- •Imaging
- •Further investigations
- •Differential diagnosis
- •Thyroid disease
- •Hypothyroidism
- •Aetiology
- •Clinical features
- •Investigations
- •Blood tests
- •Other
- •Imaging
- •Hyperthyroidism
- •Aetiology
- •Primary hyperthyroidism
- •Clinical features
- •Investigations
- •Subacute (de Quervain) thyroiditis
- •Thyroid malignancy
- •Papillary thyroid carcinoma
- •Follicular thyroid carcinoma
- •Anaplastic carcinoma
- •Medullary thyroid carcinoma
- •Primary thyroid lymphoma
- •Further reading
- •18 Loss of consciousness
- •Introduction
- •History and examination findings
- •History
- •Before the event
- •The event itself
- •After the event
- •Risk factors
- •Examination
- •Comatose patient
- •Patient with blackouts
- •Investigations
- •19 Confusion and delirium
- •Introduction
- •History and examination findings
- •History
- •Pattern of confusion
- •Underlying causes
- •Examination
- •Investigations
- •Bedside investigations
- •Blood tests
- •Further tests
- •20 Stroke and TIA
- •Introduction
- •Causes and pathophysiology
- •History and examination findings
- •History
- •Examination
- •Investigations
- •Bedside investigations
- •Blood tests
- •Imaging
- •Further investigations
- •Management
- •Acute treatment
- •Prevention
- •21 Lumps
- •Introduction
- •History and examination findings
- •Investigations
- •Differential diagnosis
- •Localized lymphadenopathy
- •Generalized lymphadenopathy
- •Splenomegaly
- •22 Focal neurological deficits
- •Introduction
- •History and examination findings
- •History
- •Pattern of deficit
- •Onset
- •Precipitants
- •Progression
- •Evidence of cause
- •Examination
- •The anatomical site of the lesion
- •The underlying cause
- •The resultant disability
- •Investigations
- •Bedside investigations
- •Blood tests
- •Cerebrospinal fluid analysis
- •Imaging
- •Further investigations
- •23 Dizziness and vertigo
- •Introduction
- •History and examination findings
- •History
- •Onset and pattern of vertigo
- •Aural symptoms
- •Neurological symptoms
- •Examination
- •Investigations
- •24 Back pain and joint pain
- •Introduction
- •History and examination findings
- •History
- •Ask about associated features:
- •Other important points to consider include:
- •Examination
- •Investigations
- •Bedside investigations
- •Blood tests
- •Imaging
- •Differential diagnosis
- •Joint disease
- •Back pain
- •25 Skin lesions and rash
- •Introduction
- •History and examination
- •History
- •Examination
- •Investigations
- •Differential diagnosis
- •Pigmented lesions
- •Scaly lesions
- •Vesicular lesions
- •Weepy or pustular lesions
- •Figurate erythema
- •Bullous lesions
- •Papular and nodular lesions
- •Photodermatoses
- •Maculopapular lesions
- •Ulcerated lesions
- •Petechial and purpuric lesions
- •Miscellaneous lesions
- •Introduction
- •History and examination findings
- •Investigations
- •Differential diagnosis
- •Platelet abnormality
- •Thrombocytopenia
- •Platelet dysfunction
- •Coagulation abnormality
- •Vitamin K deficiency
- •Factor deficiency
- •Acquired factor inhibitors
- •Vessel wall abnormalities
- •Hereditary
- •Acquired
- •27 Cardiovascular system
- •Coronary heart disease
- •General overview
- •Risk factors
- •Nonmodifiable risk factors
- •Family history
- •Ethnicity
- •Modifiable risk factors
- •Smoking
- •Poor nutrition
- •Hyperlipidaemia
- •Hypertension
- •Diabetes mellitus
- •Obesity
- •Pathophysiology
- •Clinical features
- •Investigations
- •Electrocardiogram
- •Exercise tolerance test
- •Echocardiography
- •CT coronary angiography
- •Nuclear imaging
- •Coronary angiography
- •Treatment
- •Lifestyle changes
- •Drug agents
- •Antiplatelet drugs
- •Nitrates
- •β-Blockers
- •Calcium channel blockers
- •Potassium channel activators
- •Angiotensin-converting enzyme inhibitors
- •Lipid-lowering drugs
- •Revascularization
- •Acute coronary syndrome
- •ST elevation myocardial infarction
- •General overview
- •Clinical features
- •Investigations
- •Management
- •Acute management
- •Non-ST elevation myocardial infarction and unstable angina
- •General overview
- •Clinical features
- •Investigations
- •Risk scoring
- •Management
- •Acute management
- •Subsequent inpatient management of patients with acute coronary syndrome
- •Complications of myocardial infarction
- •Cardiac failure and cardiogenic shock
- •Cardiac rupture
- •Mitral regurgitation
- •Arrhythmias and conduction disturbances
- •Supraventricular arrhythmias
- •Arrhythmias
- •General overview
- •Investigations
- •Sinus tachycardia
- •Atrial fibrillation
- •Aetiology and pathophysiology
- •Complications
- •Management
- •Atrial flutter
- •Paroxysmal supraventricular tachycardia
- •Atrioventricular reentry tachycardia
- •Atrioventricular nodal reentry tachycardia
- •Management
- •Ventricular tachycardia
- •Torsades de pointes
- •Ventricular fibrillation
- •Bradycardias
- •Sinus bradycardia
- •Sick sinus syndrome
- •Heart block
- •Antiarrhythmic drugs
- •Supraventricular arrhythmias only
- •Supraventricular and ventricular arrhythmias
- •Ventricular arrhythmias
- •Heart failure
- •General overview
- •Aetiology
- •Clinical features
- •Left-sided heart failure
- •Right-sided heart failure
- •Congestive cardiac failure
- •Investigations
- •Blood tests
- •Imaging
- •Other
- •Management of acute heart failure
- •Management of chronic heart failure
- •Drug treatment
- •Angiotensin-converting enzyme inhibitors
- •β-Blockers
- •Diuretics
- •Aldosterone antagonists
- •Hydralazine in combination with a nitrate
- •Digoxin
- •Ivabradine
- •Nondrug therapy
- •Implantable cardioverter defibrillator and cardiac resynchronization therapy
- •Left ventricular assist devices
- •Transplantation
- •Hypertension
- •General overview
- •Clinical features
- •Investigations
- •Management
- •Drug treatment
- •Angiotensin-converting enzyme inhibitors
- •Angiotensin II receptor blockers
- •Calcium channel blockers
- •Thiazide diuretics
- •β-Blockers
- •α-Adrenergic receptor blockers
- •Central acting agents
- •Vasodilators
- •Management of hypertension in pregnancy
- •Malignant (accelerated) hypertension
- •Valvular heart disease
- •General overview
- •Mitral stenosis
- •Clinical features
- •Management
- •Mitral regurgitation
- •Clinical features
- •Management
- •Mitral valve prolapse
- •Aortic stenosis
- •Clinical features
- •Management
- •Aortic regurgitation
- •Clinical features
- •Management
- •Tricuspid regurgitation
- •Pulmonary valve lesions
- •Miscellaneous conditions
- •Pericarditis and pericardial effusion
- •Clinical features
- •Management
- •Constrictive pericarditis
- •Cardiomyopathy
- •Hypertrophic obstructive cardiomyopathy
- •Dilated cardiomyopathy
- •Restrictive/infiltrative cardiomyopathy
- •Arrhythmogenic right ventricular dysplasia
- •Infective endocarditis
- •Clinical features
- •Management
- •Rheumatic fever
- •Major Jones criteria
- •Carditis (40%–50%)
- •Polyarthritis (80%)
- •Sydenham chorea (10%)
- •Erythema marginatum (5%)
- •Subcutaneous nodules (rare)
- •Management
- •Atrial myxomata
- •Congenital heart disease in adults
- •Acyanotic conditions
- •Atrial septal defect
- •Ventricular septal defect
- •Patent ductus arteriosus
- •Aortic coarctation
- •Aortic and pulmonary stenosis
- •Cyanotic conditions
- •Tetralogy of Fallot
- •Further reading
- •28 Respiratory system
- •Respiratory failure
- •General overview
- •Type I respiratory failure
- •Causes
- •Management
- •Type II respiratory failure
- •Causes
- •Management
- •Asthma
- •General overview
- •Aetiology
- •Pathophysiology
- •Clinical features
- •Investigations
- •Management
- •Emergency management
- •Long-term management
- •Chronic obstructive pulmonary disease
- •General overview
- •Aetiology
- •Cigarette smoking
- •α1-Antitrypsin deficiency
- •Occupation
- •Pathophysiology
- •Clinical features
- •Investigations
- •Management
- •Short-term management
- •Long-term management
- •Bronchiectasis
- •General overview
- •Clinical features
- •Investigations
- •Management
- •Pneumonia
- •General overview
- •Aetiology
- •Community-acquired pneumonia
- •Atypical pneumonia
- •Hospital-acquired pneumonia (nosocomial)
- •Aspiration pneumonia
- •Opportunistic pneumonia
- •Clinical features
- •Typical
- •Atypical
- •Investigations
- •Bedside
- •Imaging
- •Other tests
- •CURB65 score
- •Management
- •Pulmonary embolism
- •Clinical features
- •Investigations
- •Management
- •Lung cancer
- •General overview
- •Aetiology
- •Pathology
- •Clinical features
- •Paraneoplastic syndrome
- •Investigations
- •Tumour, Node, Metastasis (TNM) staging
- •Management
- •Tuberculosis
- •General overview
- •Pathogenesis
- •Pulmonary tuberculosis
- •Extrapulmonary tuberculosis
- •Clinical features
- •Systemic
- •Pulmonary
- •Extrapulmonary
- •Investigations
- •Management
- •Pneumothorax
- •General overview
- •Clinical features
- •Management
- •Pleural effusion
- •General overview
- •Clinical features
- •Investigations
- •Management
- •Interstitial lung disease
- •General overview
- •Aetiology
- •Known cause:
- •Unknown cause:
- •Clinical features
- •Investigations
- •Management
- •Idiopathic pulmonary fibrosis
- •Sarcoidosis
- •Occupational lung disease
- •Aspergillus and the lung
- •Hypoventilation syndromes and sleep-related respiratory disorders
- •General overview
- •Obstructive sleep apnoea syndrome
- •Obesity hypoventilation syndrome
- •Congenital hypoventilation syndrome
- •Acute respiratory distress syndrome
- •General overview
- •Management
- •Cystic fibrosis
- •General overview
- •Clinical features
- •Management
- •Further Reading
- •Upper gastrointestinal tract
- •Oesophageal disorders
- •Gastro-oesophageal reflux disease
- •Clinical features
- •Investigations
- •Management
- •Complications
- •Hiatus hernia
- •Sliding hiatus hernia
- •Rolling (or paraoesophageal) hiatus hernia
- •Barrett oesophagus
- •Eosinophilic oesophagitis
- •Oesophageal motility disorders
- •Achalasia
- •Oesophageal cancer
- •Clinical features
- •Investigations
- •Management
- •Gastroduodenal disorders
- •Gastroduodenitis and peptic ulcer disease
- •Clinical features
- •Investigations
- •Management
- •Upper gastrointestinal tract haemorrhage
- •Management
- •Gastric cancer
- •Clinical features
- •Management
- •Gastrointestinal stromal tumour
- •Small bowel disorders
- •Malabsorption
- •Coeliac disease
- •Bacterial overgrowth
- •Tropical sprue
- •Whipple disease
- •Neuroendocrine tumours of the bowel
- •Carcinoid tumours
- •Gastrinoma
- •Insulinomas
- •VIPomas
- •Glucagonomas
- •Lower gastrointestinal tract
- •Colorectal disorders
- •Colorectal neoplasia
- •Benign disease
- •Colorectal cancer
- •Screening
- •Diverticular disease
- •Clinical features
- •Investigations
- •Management
- •Clostridium difficile and pseudomembranous colitis
- •Lower gastrointestinal tract bleeding
- •Ischaemic colitis
- •Microscopic colitis
- •Irritable bowel syndrome
- •Clinical features
- •Investigations
- •Management
- •Nonulcer dyspepsia
- •Inflammatory bowel disease
- •General overview
- •Ulcerative colitis
- •Crohn disease
- •Hepatobiliary system
- •Gallbladder disorders
- •Gallstones and biliary colic
- •Clinical features
- •Investigations
- •Management
- •Acute cholecystitis
- •Clinical features
- •Investigations
- •Management
- •Recurrent cholecystitis
- •Biliary tract cancer
- •Cholangiocarcinoma
- •Gallbladder cancer
- •Cancer of the ampulla of Vater
- •Pancreatic disorders
- •Acute pancreatitis
- •Clinical features
- •Investigations
- •Management
- •Chronic pancreatitis
- •Investigations
- •Management
- •Pancreatic cancer
- •Clinical features
- •Investigations
- •Management
- •Liver disorders
- •Chronic liver disease
- •Established chronic liver disease
- •Hepatitis
- •Acute hepatitis
- •Acute viral hepatitis
- •Hepatitis A
- •Epidemiology
- •Hepatitis B
- •Hepatitis C
- •Investigations
- •Management
- •Autoimmune hepatitis
- •Alcoholic liver disease
- •Pathology
- •Clinical features
- •Investigations
- •Prognosis
- •Nonalcoholic steatohepatitis
- •Haemochromatosis
- •Investigations
- •Management
- •Primary biliary cholangitis
- •Primary sclerosing cholangitis
- •Wilson disease (hepatocellular degeneration)
- •Clinical features
- •Investigations
- •Management
- •Hepatic tumours
- •Benign tumours
- •Malignant tumours
- •Miscellaneous conditions
- •α1-Antitrypsin deficiency
- •Liver abscess
- •Budd–Chiari syndrome
- •Further reading
- •Haematuria and proteinuria
- •Proteinuria
- •Benign proteinuria
- •Pathological proteinuria
- •Overflow proteinuria
- •Clinical Features
- •Investigations
- •Urine
- •Blood tests
- •Imaging
- •Histological diagnosis
- •Acute kidney injury
- •Aetiology
- •Clinical features
- •Investigations
- •Urine
- •Blood tests
- •Other tests
- •Management
- •Hyperkalaemia
- •Acidosis
- •Pulmonary oedema
- •Renal replacement therapies
- •Supportive management
- •Summary
- •Chronic kidney disease
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Prevention of decline in renal function
- •Prevention of complications
- •Cardiovascular
- •Renal osteodystrophy
- •Acidosis
- •Anaemia
- •Hyperkalaemia
- •End-stage renal failure
- •Glomerular disease
- •Clinical features
- •Nephritic syndrome
- •Nephrotic syndrome
- •History
- •Investigations
- •Urine
- •Blood tests
- •Imaging
- •Renal biopsy
- •Management
- •Important primary and secondary glomerular diseases
- •Rapidly progressive glomerulonephritis
- •Antiglomerular basement membrane disease
- •IgA nephropathy
- •Lupus nephritis
- •Minimal change nephropathy
- •Focal segmental glomerulosclerosis
- •Membranous glomerulonephritis
- •Membranoproliferative glomerulonephritis
- •Poststreptococcal glomerulonephritis
- •Urinary tract infections
- •Lower urinary tract infections
- •Upper urinary tract infections
- •Clinical features
- •Investigations
- •Management
- •Renal calculi
- •General overview
- •Clinical features
- •Management
- •Urinary tract malignancies
- •Renal cell carcinoma
- •Transitional cell carcinoma
- •Prostatic carcinoma
- •Testicular cancer
- •Miscellaneous conditions
- •Adult polycystic kidney disease
- •Hepatorenal syndrome
- •Thrombotic microangiopathies
- •Sexually transmitted diseases
- •Chlamydia
- •Gonorrhoea
- •Syphilis
- •Further reading
- •Sodium and water balance
- •Hyponatraemia
- •Investigations
- •Hypernatraemia
- •Focal onset seizures
- •Normal awareness
- •Impaired awareness
- •Focal evolving to bilateral convulsive seizures
- •Generalized onset seizures
- •Tonic–clonic (grand mal) seizures
- •Absence attacks (petit mal)
- •Myoclonic seizure
- •Atonic or akinetic epilepsy
- •Aetiology
- •Hypokalaemia
- •Investigations
- •Management
- •Hyperkalaemia
- •Investigations
- •Management
- •Calcium balance
- •Hypocalcaemia
- •Hypercalcaemia
- •Investigations
- •32 Nervous system
- •Cerebrovascular disease
- •Stroke and TIA
- •Intracerebral haemorrhage
- •Subarachnoid haemorrhage
- •Clinical features
- •Investigations
- •Management
- •Subdural haematoma
- •Extradural haematoma
- •Headache
- •Migraine
- •General overview
- •Clinical features
- •Management
- •Cluster headache
- •Tension-type headache
- •Idiopathic intracranial hypertension
- •Trigeminal neuralgia
- •Persistent idiopathic facial pain (atypical facial pain)
- •Dementia
- •Epilepsy
- •General overview
- •Classification
- •Investigations
- •Bedside
- •Imaging
- •Electroencephalogram
- •Management
- •Drug treatment
- •First-line drugs
- •Second-line drugs
- •Withdrawing drugs
- •Other treatment
- •Status epilepticus
- •Pregnancy and epilepsy
- •Driving and work and epilepsy
- •Sudden unexpected death in epilepsy
- •Intracranial tumours
- •General overview
- •Clinical features
- •Raised intracranial pressure
- •Investigations
- •Management
- •Movement disorders
- •Parkinsonism
- •Clinical features
- •Tremor
- •Rigidity
- •Bradykinesia
- •Other features
- •Management
- •Drug therapy
- •Other therapy
- •Tremor
- •Essential tremor
- •Cerebellar tremor
- •Huntington Disease
- •Sydenham chorea
- •Other movement disorders
- •Multiple sclerosis
- •General overview
- •Pathogenesis
- •Clinical features
- •Optic neuritis
- •Diplopia
- •Sensory symptoms
- •Motor weakness
- •Cerebellar signs
- •Other manifestations
- •Investigations
- •Management
- •Central nervous system infection
- •Meningitis
- •General overview
- •Causative organisms
- •Clinical features
- •Meningism
- •Sepsis
- •Raised intracranial pressure
- •Investigations
- •Management
- •Encephalitis
- •Central nervous system abscess
- •Spinal cord infection
- •Spinal cord disorders
- •Spinal cord compression
- •Subacute combined degeneration of the cord
- •Syringomyelia and syringobulbia
- •Peripheral nervous system disorders
- •Peripheral neuropathy
- •Guillain–Barré syndrome
- •Clinical features
- •Investigations
- •Management
- •Entrapment/compression neuropathies
- •Neuromuscular disorders
- •Muscle disorders
- •Myotonic dystrophy (myotonia dystrophica)
- •Muscular dystrophy
- •Duchenne and Becker muscular dystrophy (pseudohypertrophic)
- •Facioscapulohumeral dystrophy (Landouzy–Dejerine syndrome)
- •Limb girdle dystrophy
- •Neuromuscular junction disorders
- •Myasthenia gravis
- •Clinical features
- •Investigations
- •Management
- •Lambert–Eaton myasthenic syndrome
- •Miscellaneous disorders
- •Motor neurone disease
- •Management
- •Horner syndrome
- •Bulbar and pseudobulbar palsy
- •Bell palsy
- •Further reading
- •Diabetes mellitus
- •Aetiology and Pathophysiology
- •Clinical features
- •Macrovascular disease
- •Microvascular disease
- •Diabetic retinopathy
- •Diabetic nephropathy
- •Diabetic neuropathy
- •Diabetic feet
- •Skin
- •Infections
- •Management
- •Diet and lifestyle
- •Oral hypoglycaemic agents
- •Biguanides
- •Sulphonylureas
- •Meglitinides; rapid-acting insulin secretagogues
- •Thiazolidinediones
- •Dipeptidyl peptidase 4 inhibitors
- •Glucagon-like peptide 1 agonists
- •Acarbose
- •Insulin
- •Diabetes and surgery
- •Diabetic emergencies
- •Hypoglycaemia
- •Diabetic ketoacidosis
- •Hyperosmolar hyperglycaemic state
- •Obesity and metabolic syndrome
- •Lipid disorders
- •Aetiology and pathophysiology
- •Primary hyperlipidaemia
- •Secondary hyperlipidaemia
- •Investigations
- •Management
- •Primary prevention
- •Secondary prevention
- •Drugs
- •Thyroid disease
- •Hypothyroidism
- •Management
- •Hyperthyroidism
- •Management
- •Antithyroid drugs
- •Radioiodine
- •Subtotal thyroidectomy
- •Thyroid emergencies
- •Thyrotoxic crisis (‘thyroid storm’)
- •Myxoedema coma
- •Parathyroid disease
- •Hypoparathyroidism
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Hyperparathyroidism
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Pituitary disorders
- •Hypopituitarism
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Pituitary tumours
- •Clinical features
- •Investigations
- •Management
- •Acromegaly
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Surgery
- •Radiotherapy
- •Medical therapies
- •Prognosis
- •Prolactin disorders
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Diabetes insipidus
- •Cranial diabetes insipidus
- •Nephrogenic diabetes insipidus
- •Management
- •Adrenal disorders
- •Cushing syndrome
- •Clinical features
- •Investigations
- •Management
- •Cushing disease
- •Adrenocortical tumours
- •Ectopic adrenocorticotrophic hormone syndrome
- •Addison disease
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Conn syndrome (primary hyperaldosteronism)
- •Clinical features
- •Investigations
- •Management
- •Phaeochromocytoma
- •Clinical features
- •Investigations
- •Management
- •Hypothalamus–pituitary–adrenal axis
- •Dynamic tests for cortisol excess
- •Tests for cortisol deficiency
- •Pituitary function tests
- •Miscellaneous endocrine conditions
- •Multiple endocrine neoplasia
- •Autoimmune polyendocrine syndrome
- •Congenital adrenal hyperplasia
- •Metabolic bone disease
- •Osteoporosis
- •Aetiology
- •Primary osteoporosis
- •Secondary osteoporosis
- •Clinical features
- •Investigations
- •Management
- •General principles
- •Drugs
- •Paget disease
- •Clinical features
- •Investigations
- •Management
- •Bisphosphonates
- •Calcitonin
- •Surgery
- •Osteomalacia
- •Aetiology
- •Clinical features
- •Investigations
- •Biochemistry
- •Imaging
- •Management
- •Renal osteodystrophy
- •Management
- •Further reading
- •34 Musculoskeletal system
- •Osteoarthritis
- •Pathology
- •Clinical features
- •Management
- •Rheumatoid arthritis
- •Pathology
- •Clinical features
- •Management
- •Spondyloarthropathies
- •Ankylosing spondylitis
- •Pathology
- •Clinical features
- •Management
- •Reactive arthritis
- •Pathology
- •Clinical features
- •Management
- •Psoriatic arthritis
- •Enteropathic arthropathies
- •Crystal arthropathy
- •Gout
- •Pathology
- •Clinical features
- •Management
- •Pseudogout
- •Connective tissue disorders
- •Systemic lupus erythematosus
- •Pathology
- •Clinical features
- •Treatment
- •Systemic sclerosis
- •Pathology
- •Clinical features
- •Management
- •Polymyositis and dermatomyositis
- •Pathology
- •Clinical features
- •Management
- •Sjögren syndrome
- •Vasculitis
- •General overview
- •Eosinophilic granulomatosis with polyangiitis
- •Granulomatosis with polyangiitis
- •Henoch–Schönlein purpura
- •Kawasaki disease
- •Microscopic polyangiitis
- •Polyarteritis nodosa
- •Behçet disease
- •Polymyalgia rheumatica and giant cell arteritis
- •Polymyalgia rheumatica
- •Giant cell arteritis
- •Antiphospholipid syndrome
- •35 Skin disease
- •Skin manifestations of systemic disease
- •Diabetes mellitus
- •Inflammatory bowel disease
- •Coeliac disease
- •Hyperthyroidism
- •Malignant disease
- •Sarcoidosis
- •Rheumatic fever
- •Neurofibromatosis
- •Lyme disease (borreliosis)
- •Hyperlipidaemia
- •Skin disease
- •Psoriasis
- •Clinical features
- •Management
- •Eczema/dermatitis
- •Clinical features
- •Management
- •Acne vulgaris
- •Actinic keratosis
- •Seborrhoeic keratosis
- •Herpes simplex
- •Herpes (varicella) zoster
- •Lichen planus
- •Erythema multiforme
- •Stevens–Johnson syndrome and toxic epidermal necrolysis
- •Pemphigus vulgaris and bullous pemphigoid
- •Erythema nodosum
- •Vitiligo
- •Pyoderma gangrenosum
- •Neoplastic disease
- •Basal cell carcinoma
- •Squamous cell carcinoma
- •Malignant melanoma
- •Infections
- •Impetigo
- •Cellulitis
- •Necrotizing fasciitis
- •36 Haematological disorders
- •Anaemia
- •Diagnosis
- •Management
- •Iron replacement
- •Vitamin B12 and folate replacement
- •Blood transfusion
- •Splenectomy
- •Erythropoietin
- •Causes of anaemia
- •Anaemia of chronic disease
- •Clinical features
- •Management
- •Haemolytic anaemia
- •Clinical features
- •Management
- •Sickle cell anaemia
- •Clinical features
- •Management
- •Thalassaemia
- •Clinical features
- •Management
- •Aplastic anaemia
- •Clinical features
- •Management
- •Leukaemia
- •Acute lymphoblastic leukaemia
- •Aetiology
- •Pathology
- •Clinical features
- •Treatment and prognosis
- •Acute myeloid leukaemia
- •Aetiology
- •Pathology
- •Clinical features
- •Treatment and prognosis
- •Chronic lymphocytic leukaemia
- •Aetiology
- •Pathology
- •Clinical features
- •Treatment and prognosis
- •Chronic myeloid leukaemia
- •Aetiology
- •Pathology
- •Clinical features
- •Treatment and prognosis
- •Multiple myeloma
- •Aetiology
- •Pathology
- •Clinical features
- •Treatment and prognosis
- •Lymphoma
- •Hodgkin disease
- •Aetiology
- •Pathology
- •Clinical features
- •Treatment and prognosis
- •Non-Hodgkin lymphoma
- •Aetiology
- •Pathology
- •Clinical features
- •Treatment and prognosis
- •Myelodysplastic syndromes
- •Classification
- •Clinical features
- •Management
- •Myeloproliferative disease
- •Polycythaemia vera
- •Essential thrombocythaemia
- •Primary myelofibrosis
- •Bleeding disorders
- •Haemophilia A
- •Haemophilia B (Christmas disease)
- •Von Willebrand disease
- •Immune thrombocytopenia
- •Disseminated intravascular coagulation
- •Aetiology
- •Pathology
- •Clinical features
- •Treatment and prognosis
- •Thrombotic disorders and thromboembolism
- •Aetiology
- •Pathology
- •Clinical features
- •Treatment and prognosis
- •Thrombotic thrombocytopenic purpura
- •Haemolytic uraemic syndrome
- •37 Infectious diseases
- •General overview
- •HIV and AIDS
- •Epidemiology and aetiology
- •Pathology
- •Clinical features
- •Primary HIV infection
- •Clinical stage 1
- •Clinical stage 2
- •Clinical stages 3 and 4
- •Treatment and prognosis
- •Prevention
- •Malaria
- •Epidemiology and aetiology
- •Pathology
- •Clinical features
- •Treatment and prognosis
- •Prevention
- •Diarrhoeal disease
- •Drug-resistant bacteria
- •Other resistant bacteria
- •38 Drug overdose and abuse
- •General overview
- •Common presentation, investigations and management
- •History
- •Examination
- •How ill is the patient?
- •Is there any evidence to suggest an underlying cause?
- •Have any complications occurred?
- •Investigations
- •Management
- •Supportive care
- •Preventing absorption
- •Increase elimination of drug
- •Specific antidotes
- •Psychiatric and social assessment
- •Paracetamol overdose
- •Illegal drugs
- •Alcohol misuse and withdrawal
- •Alcohol withdrawal
- •Wernicke encephalopathy/Korsakoff psychosis
- •Long-term treatment
- •Further reading
- •Self-Assessment
- •SBA answers
- •EMQ answers
- •Index

Urinary symptoms and haematuria
Decision algorithm for the investigation and referral of haematuria.
Visible haematuria (VH)
Plasma creatinine/eGFR
Exclude transient cause
including UTI
Symptomatic nonvisible
haematuria (s-NVH)
Urology assessment
• Imaging and cystoscopy
Non-visible haematuria (NVH)
Exclude transient causes, including UTI
Asymptomatic non-visible haematuria (a-NVH)
Blood pressure
Plasma creatinine/eGFR
Send urine for ACR or PCR
≥40 yrs <40 yrs
All of:
• eGFR ≥60 ml/min AND
• ACR <30 or PCR <50 AND
• BP <140/90
2 of 3 dipstick tests positive
YesNo Stop
Normal Abnormal
Any one of:
• eGFR <60 ml/min
• ACR ≥30 or PCR ≥50
• BP ≥140/90
Nephrology assessment
No cause established
Primary care monitoring
Annual assessment (whilst haematuria persists) of BP, eGFR and ACR/PCR
Referral or re-referral to urology if:
• Development of VH or s-NVH
Referral to nephrology if:
• Significant or increasing proteinuria (ACR >30 or PCR >50)
• eGFR <30 ml/min (confirmed on at least 2 readings and without an identifiable
reversible cause)
• Deteriorating eGFR (by >5 ml/min fall within 1 year, or >10 ml/min fall within 5 years)
N.B. Direct referrals between urology and nephrology will depend on local commissioning guides
Cause establishedCause established
Fig.15.3 Decision algorithm for the investigation and referral of haematuria. BAUS/RA Guidelines: Initial assessment of
haematuria July 2008. ACR, Albumin/creatine ratio; BP, blood pressure; eGFR, estimated glomerular filtration rate, PCR,
protein/creatinine ratio; UTI, urinary tract infection.
98

Introduction
1515
Imaging
In urological practice, imaging is of most use when you suspect structural lesions. Renal tract ultrasound scanning is
useful to assess the size and cortical structure of the kidney
and visualize the ureters and bladder to guide further imaging. This may include:
• Abdominal CT scan: to visualize the kidneys,
adjacent organs and other abdominal masses.
Noncontrast CT of the kidneys/ureters/bladder is
now the gold standard for the diagnosis of renal
calculi (99% sensitive).
• Abdominal magnetic resonance imaging is superior to
CT for some solid lesions and for staging of renal cell
carcinoma.
Other investigations
• Cystoscopy: bladder lesions.
• Ureteroscopy: ureter lesions.
RED FLAG
Visible asymptomatic haematuria in patients older
than 45years and persistent nonvisible haematuria
in patients older than 60years needs urgent
urological investigation to exclude a renal tract
malignancy (see Fig.15.3).
Proteinuria
Small amounts of proteinuria can occur in non-renal disease such as urinary tract infection and with vaginal mucus; however, significant proteinuria of more than 1 g/day
usually indicates primary renal pathology. Proteinuria is
discussed in further detail in Chapter30.
Chapter Summary
• Urinary symptoms include symptoms of irritation, such as frequency and dysuria or
obstructive symptoms, including hesitancy, poor stream, postmicturition dribbling and
incomplete voiding.
• Polydipsia and polyuria can be driven by high glucose levels, hypercalcaemia and
diabetes insipidus.
• Diabetic insipidus can be cranial or nephrogenic; focus your history taking and
examination on potential causes.
• Haematuria can occur from anywhere in the urogenital tract. It can be classified into visible
and nonvisible, painful and painless. Painless visible haematuria in patients older than
45years and persistent nonvisible haematuria in patients older than 60years should
prompt urological referral to exclude an underlying malignancy.
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Headache and facial pain
16
INTRODUCTION
Headache is one of the most common presenting symptoms. There are often few clinical signs, and the history
is the main diagnostic tool. Many different pathological
processes can result in headache and facial pain. The
International Headache Society classification divides
headache into primary (where the headache is itself the
disease; e.g. migraine), secondary (where the headache is
due to other conditions; e.g. infection, trauma, vascular
disorder) and other headaches, facial pains and cranial
neuropathies.
The differential diagnosis of headache and facial pain is
summarized in Table16.1.
History and examination findings
History
Characteristics of the headache will point towards the
diagnosis.
Solitary acute episode
This pattern is seen in vascular events, infection and
trauma. It may also be the first presentation of the other
causes of headache.
Subarachnoid haemorrhage presents with a sudden onset of severe pain ‘as if someone had hit them on the head’.
Often most severe occipitally, it usually reaches maximal
severity at onset or within seconds. Nausea, vomiting, neck
stiffness and photophobia can occur and can result from
meningeal irritation. Subarachnoid haemorrhage can be
associated with altered level of consciousness, seizures and
focal neurological deficits.
Seizures, focal neurological signs and symptoms of raised
intracranial pressure (see later) can also result from cerebral
venous sinus thrombosis. Causal factors include inherited
disorders of coagulation, pregnancy, oral contraceptive pill
use, dehydration, extension of local infection (e.g. of paranasal sinuses or middle ear) and severe intercurrent illness.
Dissection of a carotid or vertebral artery can also cause a
sudden onset of pain associated with focal neurology.
Patients with infective meningitis present with a short
history of headache, symptoms of infection (malaise, fever,
rigors), symptoms of meningeal irritation (vomiting, photophobia, neck pain and/or stiffness) and possibly a rash
or altered mental state. ‘Aseptic’ meningitis that can occur
because of tuberculosis or carcinoma presents in a more
subacute manner and can go unnoticed. Encephalitis, acute
inflammation of the brain, may present with headache, fever and altered mental status.
Table16.1 Differential diagnosis of headache and facial pain (see Chapter32)
Pattern Causes
Solitary acute episode Infection: meningitis, encephalitis, abscess
Vascular event: intracranial haemorrhage (especially subarachnoid), venous sinus
thrombosis, occasionally infarction (especially if arterial dissection occurred)
Trauma
First migraine or benign thunderclap headache
Progressive headache Raised intracranial pressure (including idiopathic intracranial hypertension)
Giant cell arteritis
Episodic headache/facial pain Migraine
Cluster headache and other trigeminal autonomic cephalalgias
Trigeminal neuralgia
Coital cephalalgia
Chronic headache/facial pain Tension headache/analgesic rebound headache
Postherpetic neuralgia
Head injury
Paget disease of the skull
Other causes of facial pain Dental problems
Temporomandibular joint
Ears/nose/sinuses
Cervical spine
Eye—especially acute or intermittent angle-closure glaucoma
Myocardial ischaemia (rarely)
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Headache and facial pain
Cerebral abscess may cause fevers, rigors, headaches,
seizures and symptoms of raised intracranial pressure as the
lesion enlarges. The infection may have spread from a local
or distant primary focus, such as lung (bronchiectasis, abscess), heart (endocarditis), middle ear or sinuses (paranasal
sinusitis).
Acute angle-closure glaucoma can cause a severe
headache associated with blurred vision, eye pain, cloudiness of the cornea, conjunctival injection and a dilated
pupil. There may be nausea and vomiting. It should be
considered in hypermetropic, middle-aged or elderly
patients. It may occur intermittently with repeated acute
attacks.
Progressive headache
A headache that comes on gradually over days or weeks and
increases in severity is often a feature of a ‘space- occupying
lesion’ (such as a tumour or abscess), idiopathic intracranial
hypertension, chronic subdural haematoma or hydrocephalus. Hydrocephalus can be due to either blockage of
cerebrospinal fluid (CSF) flow (‘noncommunicating’, e.g.
haemorrhage, cysts, malformations) or failure of CSF reabsorption (‘communicating’, e.g. following meningitis or subarachnoid haemorrhage).
In these, the headache results from raised intracranial
pressure, and has the characteristic features shown below.
CLINICAL NOTES
SYMPTOMS OF RAISED INTRACRANIAL
PRESSURE
• Headache worse on coughing, sneezing,
stooping down.
• Headache worse in the morning.
• Visual disturbance due to papilloedema.
• Nausea and vomiting.
• Diplopia (false localizing cranial nerve VI palsy).
Headache associated with temporal arteritis is also of
gradual onset; however, the nature of it is different from
that described above. The condition predominantly affects older people (mean age at onset is over 70 years).
Presentation is with superficial headache overlying the
temporal arteries; scalp tenderness which may be exacerbated by brushing or combing the hair is often present.
Jaw claudication, and occasionally tongue claudication,
may arise because of inflammation of the branches of
the external carotid artery. Visual loss may be temporary
(amaurosis fugax) or permanent if the ciliary or central
retinal arteries are affected. Weight loss, anorexia, fever
and proximal muscle stiffness (but not tenderness) may
also occur.
HINTS AND TIPS
Consider temporal arteritis in any patient older than
50years with a headache.
Recurrent episodic headache and facial pain
Migraine and cluster headaches present with episodes of
pain (often severe) interspersed with long symptom-free
periods. Paroxysms of pain are also a feature of trigeminal
neuralgia and other cranial neuralgias.
Although, classically, migraine is preceded by aura,
migraine without aura is more common. Premonitory
symptoms precede both types, occur hours to days before
the migraine and include fatigue, nausea and sensitivity to light and noise. Aura can consist of visual features
(positive, e.g. flickering lights, spots or lines, or negative, e.g. visual loss), sensory symptoms (paraesthesiae
or numbness), speech disturbance and focal neurology.
These symptoms can occur with or without a headache,
and are fully reversible. The headache can be unilateral
or bilateral. It is often pulsating in nature, and can be
associated with nausea, photophobia, phonophobia and
aversion to physical activity. The attack resolves spontaneously after 4–72 hours in adults.
Cluster headache is a severe unilateral pain centred
around one eye. The pain lasts for 15–180 minutes if untreated, and occurs up to eight times per day for several
weeks, often waking the patient from sleep. There may be
ipsilateral nasal congestion or rhinorrhoea, and the eye can
become watery and red; miosis and ptosis can also develop,
and occasionally will become permanent. Symptom-free
periods of many months occur between attacks. Cluster
headache is more common in men, and may be precipitated
by alcohol.
Trigeminal neuralgia is characterized by paroxysms of
lancinating pain in the distribution of cranial nerve V. It is
often stimulated by the touching of ‘trigger zones’ on the
face such as the lips, or by eating or drinking, but can occur spontaneously. The pain does not occur during sleep.
Spontaneous remissions can last several months.
Chronic headache and facial pain
Persistent pain is a feature of postherpetic neuralgia, posttraumatic headache, Paget disease of the skull and tension
headache.
Postherpetic neuralgia is persistent burning pain in
the distribution of the trigeminal nerve that develops
following infection of the nerve by varicella zoster virus
(commonly known as ‘shingles’). Facial scarring is usually
apparent, and the pain may disturb sleep. It is uncommon
in the young.
Tension-type headache is often described as ‘a tight
band around the head’. It is most often constant and
102

Eyes
— Papilloedema
— Subhyaloid haemorrhage
— Horner's syndrome
— 3rd, 6th cranial nerve palsies
— Optic atrophy
Meningism
— Neck stif
— Kernig sign
— Brudzinski’
TMJ
—
Tenderness and
Temporal artery
movement
fness
s sign
Introduction
— Tenderness
— Loss of pulsation
Sinuses and teeth
— Dental hygiene
— Sinus tenderness
Cervical spine
— Movement and
tenderness
Pulse and
blood pressure
— Septic shock
— Cushing reflex
1616
Fig.16.1 Examining the patient with headache and facial pain. AVM, Arteriovenous malformation; TMJ,
temporomandibular joint.
bilateral, and tends to be worse towards the end of the day
or at times of stress.
Following head injury, a few patients develop persistent
headache, like a tension headache. It is associated with
poor memory and concentration, dizziness, irritability and
symptoms of depression.
People in whom headache developed or worsened
while they were using analgesic medication for more than
3months may have a medication-overuse headache. It can
occur with practically any of the medications commonly
used for treatment of headache including NSAIDs, paracetamol, aspirin and triptan, opioid and ergot drugs.
Examination
On examination, look for evidence of the pathological processes, such as raised intracranial pressure and meningism.
General
— Altered consciousness
level
— Photophobia
— Phonophobia
— Fever
— Audible bruit over AVM
— Facial herpetic scarring
— Purpuric rash
— Focal neurological
signs
— Paget disease/bony
deformity
Focal neurological deficits, if present, help to determine
the site of the lesion. Fig.16.1 summarizes the examination
approach.
CLINICAL NOTE
SIGNS OF RAISED INTRACRANIAL PRESSURE
• Papilloedema.
• False localizing sign (ipsilateral then bilateral
cranial nerve VI palsy).
• Altered level of consciousness.
• Bradycardia with hypertension (the Cushing
reflex – a late sign); may indicate imminent brain
herniation and death.
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Headache and facial pain
CLINICAL NOTES
SIGNS OF MENINGISM
• Irritability: with a preference for a quiet,
darkened room.
• Neck stiffness and photophobia.
• Positive Kernig sign: spasm and pain in
hamstrings on knee extension.
• Positive Brudzinski sign: neck flexion causes hip
and knee flexion.
• Delirium, fever and petechial rash: may be
present in infectious meningitis.
CLINICAL NOTE
SUBARACHNOID HAEMORRHAGE
Look for subhyaloid (retinal) haemorrhage, bruit of
an arteriovenous malformation and a cranial nerve
III palsy caused by direct pressure from a posterior
communicating artery aneurysm.
CLINICAL NOTE
SIGNS OF TEMPORAL ARTERITIS
• Temporal artery tenderness.
• Loss of temporal artery pulsation – there may be
overlying erythema.
• Optic atrophy (seen as optic disc pallor).
• Low-grade pyrexia.
Investigations
An algorithm for the investigation of the patient with headache and facial pain is shown in Fig.16.2. Investigations include the following.
Blood tests
• Full blood count: normochromic normocytic anaemia
suggests chronic disease (e.g. temporal arteritis,
tuberculous meningitis); leucocytosis in infection.
• Erythrocyte sedimentation rate: high in temporal
arteritis but may also be raised in infection and
malignancy.
• Clotting studies may be important in the context of
intracerebral bleeding.
Imaging
• CT or magnetic resonance imaging scans of the head:
presence of blood, space-occupying lesion (tumour,
abscess) or hydrocephalus. Contrast enhancement may
help determine the nature of a lesion.
• CT angiography, magnetic resonance angiography
or digital subtraction angiography: to identify the
precise cause (e.g. berry aneurysm or arteriovenous
malformation) in subarachnoid haemorrhage.
Further tests (Fig.16.2)
• Temporal artery biopsy: temporal arteritis. This is a
definitive test but, as there is often patchy vascular
involvement (‘skip lesions’), a negative result does not
exclude the diagnosis.
• Lumbar puncture: this should never be performed
when raised intracranial pressure is a possibility, as
it may cause cerebellar tonsil herniation (‘coning’).
CSF should be sent to the laboratory for assessment of
glucose and protein, microscopy, culture and cytology
(see Chapter22). CSF sampling and spectrophotometry
may also diagnose subarachnoid haemorrhages not
detected on CT.
• Visual fields: these should be serially measured in
patients with idiopathic intracranial hypertension
(because of the risk of optic nerve infarction).
• Electroencephalography: herpes simplex encephalitis
shows abnormal patterns.
• Intraocular tonometry: pressure will be raised in
glaucoma.
Chapter Summary
• Tension headache is the most common type of headache.
• The history and examination are the most useful diagnostic tools in a patient presenting
with headache.
• Brain imaging is not routinely performed in patients with no worrying features.
• Raised intracranial pressure is a contraindication to performing a lumbar puncture.
104

Headache
Facial pain
History
Examination
Introduction
1616
Suggestive of
temporal arteritis
ESR
Temporal artery biopsy
CSF
Leucocytosis
Meningitis
Diagnosis unclear
or suggestive of
intracranial disease
CT head scan
or MRI scan
Normal Abnormal
Lumbar
puncture
Xanthochromia
Subarachnoid
haemorrhage
Benign intracranial
Diagnosis clear
Migraine
Tension headache
Coital cephalagia
Cluster headaches
Temporomandibular
joint pain
Blood
Tumour
Abscess
Hydrocephalus
High CSF
pressure
hypertension
Dural sinus
thrombosis
Angiography
Berry aneurysm
Arteriovenous
malformation
No abnormality
Fig.16.2 Algorithm for the investigation of the patient with headache and facial pain. CSF, Cerebrospinal fluid; CT,
computed tomography; ESR, erythrocyte sedimentation rate; MRI, magnetic resonance imaging.
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Goitre, thyroid disease and
thyroid malignancy
INTRODUCTION
‘Goitre’ means an enlarged thyroid gland. It may be a single
enlarged gland or composed of a single nodule or multiple
nodules. The leading cause of a goitre worldwide is iodine
deficiency; in the United Kingdom, where iodine is added
to foods as a supplement, autoimmune conditions (e.g.
Hashimoto thyroiditis and Graves disease) are the most
common causes. Thyroid nodules are common, and are
often incidental findings on ultrasonography or at autopsy.
In adults, only around 5% of these nodules are malignant.
Thyroid nodules are less common in children but a greater
proportion are malignant.
History and examination findings
Most patients are asymptomatic. The goitre may be noticed
by someone else or may be seen by the patient in the mirror.
The history taking should aim to reveal any features of compression from the goitre, whether the metabolic function of
the gland is altered and to elucidate whether a malignant
cause is likely:
• Local symptoms: ask about dysphagia, dyspnoea and
hoarseness.
• Symptoms of hypothyroidism or hyperthyroidism.
• Previous or current use of goitrogenic drugs (e.g.
lithium, amiodarone).
• Diet, lack of iodine or conversely very high iodine
intake (e.g. seaweed); both can lead to goitre formation.
• Exposure to environmental factors such as previous
radiotherapy or environmental radiation such as fallout
from the Hiroshima or Chernobyl disasters, or living
in an area of high volcanic activity such as Iceland or
Hawaii (all are risk factors for benign and malignant
thyroid nodules).
• Family history: ask about a history of goitre (suggesting
autoimmune disease) or of thyroid cancer (suggesting
familial thyroid cancer or multiple endocrine
neoplasia).
• Smoking (the evidence is conflicting but smoking is
certainly a risk factor for other malignancies which
may cause neck lumps).
• Duration of goitre and rate of change: long-standing
goitres suggest benign disease.
• Tenderness: subacute thyroiditis.
• Pregnancy/menopause (associated with thyroid
enlargement).
Physical examination should look for:
17
CLINICAL NOTES
The incidence of thyroid cancer peaks between
30 and 50years and is around three times more
common in women.
• signs related to the patient's thyroid status;
• whether the goitre is smooth or nodular;
• whether there are nodules and whether these are
multiple nodules or a single nodule;
• whether the nodule is hard or soft, regular or
irregular and fixed or mobile, and whether there is
lymphadenopathy.
HINTS AND TIPS
On examination, ask the patient to drink some
water, and note the thyroid moving as the patient
swallows. Does the mass move with swallowing? If
it does, this suggests it is part of the thyroid. Look
for enlargement and asymmetry. Stand behind a
seated patient and use your fingers to examine the
gland as the patient swallows. Feel for lumps and
tenderness. Percuss down below the thyroid onto
the anterior chest wall to detect any retrosternal
thyroid mass.
RED FLAGS
The presence of stridor, signifying partial airway
obstruction, requires immediate referral.
Other red flags include any child with a thyroid
nodule, unexplained hoarseness or voice change
associated with a goitre, a painless rapidly
enlarging thyroid mass and a thyroid mass in a
patient with a history of previous radiation therapy.
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