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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

Clinical examination
This nerve is tested simultaneously with the vagus nerve
(cranial nerve X).
Cranial nerve X (vagus nerve)
This has sensory and motor functions; it provides sensation to
the larynx, and motor innervation to the cricothyroid and the
muscles of the pharynx and larynx. It carries parasympathetic
nerve fibres to the bronchi, heart and gastrointestinal tract.
The glossopharyngeal nerve (cranial nerve IX) and vagus nerve (cranial nerve X) are tested simultaneously by assessment of palatal movement (ask the patient to say ‘Aah’).
Lesions cause reduced palatal elevation on the affected side,
with the uvula pulled towards the normal side.
Check for a gag reflex; this tests the sensory function of
the glossopharyngeal nerve and motor innervation of the
vagus nerve.
Cranial nerve XI (accessory nerve)
This provides motor innervation to some muscles of the
soft palate and larynx and the trapezius and sternocleidomastoid muscles. Test the function of this nerve by asking
the patient to shrug the shoulders, and resist as you attempt
to press them down. Then ask the patient to turn his or her
head against your resisting hand, and test the sternocleidomastoid muscle bulk.
Causes of glossopharyngeal, vagus and accessory nerve
palsies are summarized in Table2.21.
Cranial nerve XII (hypoglossal nerve)
This provides the motor supply to the styloglossus, hyoglossus and all intrinsic muscles of the tongue. Test this nerve by
asking the patient to open the mouth. Look for wasting and
fasciculation. This indicates a lower motor neurone lesion
of the tongue. Then ask the patient to protrude the tongue.
If the tongue deviates to one side, this suggests a hypoglossal nerve lesion. If it is a lower motor neurone lesion, the
tongue will deviate towards the side of the lesion; with an
upper motor neurone lesion it will deviate away from the
side of the lesion.
Table2.21 Causes of glossopharyngeal, vagus and
accessory nerve palsies
Anatomical site Examples
Central (brainstem) Tumour, infarction, syringobulbia,
motor neurone disease
Peripheral Tumour or aneurysm near the
jugular foramen, trauma of skull
base, Guillain–Barré syndrome,
poliomyelitis
CLINICAL NOTES
Upper motor neurone lesions are due to stroke,
tumour or motor neurone disease.
Lower motor neurone lesions affecting the
hypoglossal nerve are due to diseases in the
posterior fossa, skull base and neck, including
tumour, motor neurone disease, syringobulbia,
trauma and poliomyelitis.
Upper limb
Visual survey
When you are performing a neurological examination,
good inspection is key. Look carefully for:
• muscle wasting: seen with lower motor neurone lesions,
muscle disease and disuse;
• fasciculation: a feature of a lower motor neurone
lesion;
• scars, particularly from surgery;
• deformity, which may cause mononeuropathy by
entrapment and contractures may be the result of
neurological disease;
• tremor (Table2.22).
Tone
Reduced tone is a feature of a lower motor neurone lesion
or cerebellar lesion. Increased tone, hypertonia, is a feature
of an upper motor neurone lesion. Hypertonia may manifest itself as either spasticity or rigidity. ‘Spasticity’ describes
the sudden build-up of increased tone during the first few
degrees of passive movement. The resistance lessens as the
movement is continued, and this is characteristic of upper motor neurone lesions. This is often described as the
‘clasp-knife’ phenomenon. ‘Rigidity’ describes the sustained
resistance to passive movement seen in extrapyramidal conditions (e.g. parkinsonism). This may be described as ‘lead
pipe’ rigidity, and when associated with a tremor gives rise
to ‘cogwheel’ rigidity.
Table2.22 Causes of tremor
Type Features Causes
Resting Seen when patient
relaxed with hands
at rest
Postural Seen when hands
held outstretched
Intention Seen when patients
try to touch
examiner’s finger
with their own finger
Parkinsonism
Benign essential
tremor
Anxiety
Thyrotoxicosis
β2-Agonists
Cerebellar disease
28

The nervous system
n
Eversion (S1)Inversion (L4)
Shoulder adduction and
Shoulder abduction and
22
Power
All muscle groups should be tested and scored (Table2.23).
You will need to learn the root value for each movement
(Fig.2.3). Remember to compare muscle power of one side
with muscle power of the other side for each group.
Look for pronator drift by asking the patient to hold the
arms outstretched, hold the palms upward and close the
eyes. Marked weakness will be easily apparent. If an upper
motor neurone lesion affecting the parietal lobe is present,
the arm will drift downwards and the hand will pronate.
Coordination
Ask the patient to alternately touch his or her nose and your
finger. In cerebellar disease, there will be an intention tremor
and past pointing (i.e. the patient overshoots the examining clinician's finger consistently towards the side of the lesion). Ask
lateral rotation (C5)
medial rotation
(C6, C7, C8)
Table2.23 Medical Research Council grading system
for muscle power
Grade Features
0 No muscle contraction and no
movement at all
1 Muscle contraction visible, but no joint
movement
2 Movement only when gravity excluded
3 Movement can overcome gravity but
not resistance from the examiner
4 Movement can overcome gravity and
move against some resistance from
the examiner
5 Normal power against resistance
Elbow flexion
(C5, C6)
Elbow extension
(C7, C8)
Pronation (C6)
Supination (C6)
Wrist extension (C6, C7)
Intrinsic muscles of hand
(T1)
Wrist
flexion (C6, C7)
Hip flexion
(L2, L3)
Hip extension
(L4, L5)
Finger extensio
Finger flexion
(C8)
Dorsiflexion
(L4, L5)
Plantar flexion
(S1, S2)
(C7)
Knee flexion
(L5, S1)
Knee extension
(L3, L4)
Fig.2.3 Nerve roots for each muscle group movement.
29

Clinical examination
Supinator (C5, 6)
Left triceps
Biceps (C5, 6)
C7 C7
Front Back
(light touch, pressure)
(pain, temperature)
)
Dorsal columns
(C7, 8)
Fig.2.4 Eliciting reflexes. Upper limb tendon reflexes.
Right triceps (C7, 8)
the patient to tap one palm with alternating sides of the other
hand as quickly as possible (demonstrate to the patient what
you would like the patient to do). In cerebellar disease, this will
be slow and poorly coordinated and the action of the moving
hand has a high amplitude – this is dysdiadochokinesis.
Reflexes
Practice as often as you can. Test the biceps, triceps and supinator reflex, and learn the root value for the reflex (Fig.2.4).
Reflexes can be reduced, normal or increased. They will be
reduced or absent in lower motor neurone lesions, sensory
neuropathy and severe muscle disease (disruption of reflex
arc), and will be exaggerated in upper motor neurone lesions.
Sensation
Test each dermatome (Fig. 2.5) for the sensation of light
touch, pinprick (and temperature). Then, starting distally,
check vibration and joint position sense. Remember the different pathways these senses take (Fig.2.6). The tests for the
various sensory modalities are shown in Table2.24.
(joint position, vibration, pressure)
Dorsal
spinocerebellar
tract
(reflex, proprioception
Lateral
spinothalamic
tract
tract
Fasciculus
gracilis
Fasciculus
cuneatus
Anterior
spinothalamic
Fig.2.6 Anatomy of sensory pathways within the spinal cord.
Lower limb
Fig.2.5 Dermatomes of the upper limbs.
C3
C4
C5
30
T2 T2
T1 T1
C8 C8
C3
C4
C5
C6 C6
Visual survey
Like the upper limbs, look for wasting, fasciculation and scars.
Specific to the lower limb, take time to look at the feet. Look
for ulceration (may suggest a lack of pain reception). Look at
the soles, for pes cavus, high arched sole a feature of hereditary motor and sensory neuropathy type 1 (formerly known
as Charcot–Marie–Tooth disease) and Friedreich ataxia.
Tone
This is best assessed with the patient relaxed on the bed, and
rolling patient’s leg from side to side. Then pick up the patient’s
knee to a flexed position and note how easy it is to flex the relaxed leg. Test for clonus, present with upper motor neurone
lesion. This is best elicited at the ankle through quick dorsiflexing of the foot of the patient. The patient’s foot will beat up and
down if clonus is present; more than five beats is significant.

The nervous system
Table2.24 Tests for different sensory modalities
Sensation Tested using Pathway Level of decussation
Pain Neurotip Lateral spinothalamic tract At level of sensory root within one spinal segment
22
Temperature Tuning fork for
Light touch Cotton wool Anterior spinothalamic tract At level of sensory root within several spinal
Vibration Tuning fork Posterior columns (fasciculus
Joint position
sense
Two-point
discrimination
cold
Move fixed
joints
Orange stick Posterior columns (fasciculus
Power
In the lower limbs, as for the upper limbs, test all muscle
groups and score them using the Medical Research Council
grading system for power (see Table2.23), and consider the
nerve roots (see Fig.2.3).
Lateral spinothalamic tract At level of sensory root within one spinal segment
segments
gracilis and fasciculus cuneatus)
Posterior columns (fasciculus
gracilis and fasciculus cuneatus)
gracilis and fasciculus cuneatus)
Medulla oblongata
Medulla oblongata
Medulla oblongata
Sensation
Test different modalities of sensation, as per the upper limb.
See Table 2.24. Look for patterns. Is there the glove and
stocking distribution sensation loss (a feature of diabetic
neuropathy), or is the sensation dermatomal (Fig.2.8).
Coordination
To check coordination in the lower limbs, ask the patient
to lift the leg, place the heel on the knee of the opposite leg
and gently run it down the shin and repeat this motion. In
cerebellar disease, this will be slow and clumsy.
COMMON PITFALLS
Make sure the patient does not just run the heel up
and down the shin. The movement should be down
the shin and then up in an arc back to the knee,
otherwise coordination is not being appropriately
assessed.
CLINICAL NOTES
A glove and stocking distribution does not follow
a dermatomal distribution but affects peripheral
nerves. When you are assessing the patient for
this, test sensation distally and work your way
proximally, noting a sensory level. Test the different
modalities of sensation, touch, pain, temperature
and proprioception in this way on both feet and
arms. Lower limbs are more commonly affected
than hands.
Reflexes
Test reflexes at the knee and ankle and check plantar responses. This is normally downgoing but will be upgoing
in upper motor neurone lesions, giving a Babinski response (see Fig.2.7).
HINTS AND TIPS
Reflexes can be hard to elicit, in particular the ankle
reflex. Ensure the patient is at ease and the muscle
is relaxed. Use of reinforcement techniques such as
asking the patient to clench the teeth or pull on clasped
hands when you are trying to elicit the reflex can help.
HINTS AND TIPS
When you are assessing proprioception (joint
position sense), it is best to start with the big toe.
Get the patient to close the eyes. Hold either side
of the interphalangeal joint and move the toe up
and down, telling the patient which is which to
orient the patient. Then move the toe and ask the
patient which way has it moved (up or down?) If the
patient lacks proprioception in the toe, move on
to the ankle. Loss of proprioception is commonly
seen in diabetes, and is a feature of dorsal column
disease.
31

Clinical examination
For upper limbs, ask the patient to clench his or her teeth as you tap the reflex
A
S1
L5
FrontBack
Biceps
supinator
Triceps
(C7, 8)
(C5, 6)
Knee
(L3, 4)
Ankle
(L5, S1)
B
‘Grip tightly as I
tap the ankle/knee’
C
Fig.2.7 Eliciting reflexes. (A) A simple way to remember root values of reflexes. (B) Testing ankle jerk with reinforcement.
(C) The normal response is a downgoing hallux. In an upper motor neurone lesion, the hallux dorsiflexes and other toes
fan out (the Babinski response).
L1
S3
L1
S5
L2
S4
L2
S2
to walk. In clinical practice pay careful attention to how
your patient walks into your clinic room. Observe the symmetry of the gait, the smoothness, how comfortably the
patient turns and how many steps this takes, the height of
the step and whether there is any evidence of pain. To test
gait, ask your patient to walk for 2–3 m, turn and walk back,
then walk heel to toe (cerebellar ataxia) and finally stand on
L3
toes and on heels (any muscle weakness will now manifest
itself).
S2
L5
L4
Whilst the patient is standing, perform a Romberg
test. Do this by asking the patient to stand with the
eyes closed. This assesses posterior column function
(proprioception).
L5
Fig.2.8 Dermatomes of the lower limbs.
S1
PATIENT SAFETY
Gait
An immense amount of information can be gained by careful study of a patient’s gait; for this reason you may wish to
start your neurological examination by getting the patient
Make sure you are ready to catch the patient
should the patient become unsteady with the
Romberg test, and when asking the patient to walk.
32

Skin and lymphadenopathy
22
HINTS AND TIPS
Sensory testing is difficult and subjective. A
thorough inspection and examination of tone,
power, coordination and reflexes may help to
predict which sensory abnormality should be
expected.
MUSCULOSKELETAL EXAMINATION
When you are examining a joint, use a systematic look, feel,
move approach. Look around the bed and at the patient
as a whole, not just the joint in question. Diseases affecting the musculoskeletal system are discussed in detail in
Chapter24.
Visual survey
Look at the patient. Does the patient look well or ill?
Look for any evidence of systemic connective tissue
disorders, such as features of systemic sclerosis (microstoma, telangiectasia, sclerodactyly) or systemic
lupus erythematosus (butterfly rash), or evidence of
long-term steroid use (cushingoid facies, buffalo hump,
thin skin and bruising); see Chapter33. Note the patient’s posture (e.g. any kyphoscoliosis suggestive of
ankylosing spondylitis or osteoporosis) and any rashes
(e.g. psoriatic rash).
Look
• Deformity.
• Scars: previous surgery.
• Erythema: acute inflammation or infection.
• Swelling: osteophytes, gouty tophi, synovial
hypertrophy and acute inflammation.
• Muscle wasting: disuse, nerve entrapment,
mononeuritis multiplex or long-term steroid therapy.
• Is pain associated with movement?
• Is the joint stable? Are there intact ligaments and
supporting musculature?
Assessment of disability
It is very important to get an impression of how limiting the
joint problem is. For example, in a patient with rheumatoid
arthritis, ask the patient to undo some buttons or write their
name with a pen.
HANDS
Examining the hands makes up an important part of the
general musculoskeletal examination and can be very informative when you are looking for evidence of underlying arthritic diseases. It is common for you to be asked to
examine the hands. This should be performed in the same
way as examination of a joint, using the look, feel, move and
assessment of disability approach.
First get the patient to put his or her hands on a white
sheet or pillow. Take time to inspect the hands, nails and
elbows. Note any erythema, rashes, swelling, bony deformity, muscle wasting, scars and rheumatoid nodules (seen
at the back of the elbow). Feel across each joint in turn,
examining them for warmth and swelling. If they are swollen ask yourself if it is a spongy/boggy swelling or if it is
hard and bony. Assess power of movement of fingers and
wrist, in particular abduction of the thumb in the palmar
position, testing the median nerve, and abduction of the
fingers against resistance, testing the ulnar nerve, and interphalangeal extension of the thumb against resistance,
testing the radial nerve. Go on to examine the functional
use of the hand (e.g. ask the patient to undo a button or
pick up a pen). This is particularly important in neurological abnormalities and destructive arthritides (e.g.
rheumatoid arthritis).
HINTS AND TIPS
Feel
• Increased temperature: acute inflammation or
infection.
• Tenderness.
• Effusions.
• Crepitus on movement.
Move
• Assess both active (patient moves his or her own
limb) and passive movement (you move the
patient’s limb).
If the neck is normal, examine the jugular venous
pressure, listen to the carotid artery for bruits and
reexamine the patient for a cervical rib.
SKIN AND LYMPHADENOPATHY
The clinical approach to rashes will be discussed in detail in Chapter25. When you are asked to look at a rash,
you will be awarded marks for giving a good description,
33

Clinical examination
even if you are unable to make a diagnosis. Remember to
describe:
• distribution: this can be diagnostic in itself
• shape
• size
• colour
• consistency
• temperature
• tenderness
• margins
• relation to the surface: raised, flat, or ulcerated
• fixation to underlying structures
When you are examining a patient for lymphadenopathy, it is
important to examine all lymph node sites (Fig.2.9). Always
examine the cervical lymph nodes standing behind the patient.
The causes of generalized and localized lymphadenopathy are
discussed in Chapter21. If lymphadenopathy is present, pay
special attention to examination of the spleen and liver.
BREAST EXAMINATION
Breast examination should be performed in women who have
symptoms of breast disease or when an underlying malignancy
is suspected. Occasionally it is also necessary in men. Follow
the systematic approach of inspection, palpation and movement. Pay close attention to the nipple. Is it inverted? Look for
overlying skin changes or dimpling. Palpate the breast moving
clockwise around the nipple, and feel for any masses. If any
masses are found, note the size, texture, regularity, tenderness
and whether they are fixed to the muscle (see Box2.8). Do
not forget that breast tissue extends into the axillae. Palpate
the breast for lymph nodes. Ask the patient to move his or her
hands behind the head; this can help assess whether the mass
is fixed to muscle. A breast examination must be approached
sensitively with a full explanation. Ask for a female chaperone;
this is important and helps put the patient at ease and protects
you against accusations of inappropriate behaviour.
NECK EXAMINATION
In clinical examinations, when you are asked to examine the
neck, there will usually be a thyroid mass or lymphadenopathy. However, do not forget the salivary glands, branchial
cyst, pharyngeal pouch, cervical rib, carotid body tumour and
cystic hygroma. Causes of lymphadenopathy are described in
Chapter21. Table2.25 lists the causes of thyroid enlargement.
First, look very carefully at the neck. Look for obvious
masses, scars, skin changes or deformity. If there is a mass
in the region of the thyroid gland, ask the patient to take a
sip of water into the mouth and then swallow—a goitre will
move upwards on swallowing. In addition, ask the patient to
open the mouth and then watch as the tongue protrudes—a
thyroglossal cyst will move upwards. Stand behind the patient to palpate the neck for a mass. If a mass is present,
assess its properties as described in Box2.8. Percussion is
useful to determine retrosternal extension of a goitre. Bruits
may be audible in the thyroid gland (thyrotoxicosis) or
carotid artery (atheroma). If you find a thyroid mass, you
should go on to assess thyroid status as shown in Table2.26.
Fig.2.9 Examination of lymph node sites.
34
Table2.25 Causes of thyroid gland enlargement
Form of
enlargement Causes
Diffuse
enlargement
(goitre)
Solitary
nodule
Idiopathic
Physiological: puberty, pregnancy
Autoimmune: Hashimoto and
Graves diseases
Iodine deficiency: endemic, e.g.
Derbyshire neck
Thyroiditis: de Quervain thyroiditis
(viral), Riedel thyroiditis (autoimmune)
Drugs: carbimazole, lithium,
sulphonylureas
Genetic: dyshormonogenesis
(Pendred syndrome)
Thyroglossal cyst
Prominent nodule in multinodular goitre
Adenoma
Cyst
Carcinoma (papillary, follicular,
anaplastic, medullary)
Lymphoma

Neck examination
22
Table2.26 Examination of thyroid status
Hyperthyroidism Hypothyroidism
Mood Irritability, anxiety Depression,
Weight Thinness Overweight
Hands Fine tremor,
Pulse Tachycardia, atrial
Face Lid lag, lid
Skin Pretibial
Neuromuscular Proximal
a
Feature that is specific to Graves disease.
palmar erythema,
sweaty palms,
acropachy
fibrillation
retraction,
exophthalmos,a
ophthalmoplegia,a
chemosis
myxoedema
(shins)
myopathy
a
a
a
slowness
Puffiness, anaemia,
Tinel sign (carpal
tunnel syndrome)
Bradycardia
Loss of outer third of
eyebrow, puffy eyes
and face causing
characteristic
appearance,
xanthelasmata
Dry, thin hair
Slow-relaxing ankle
jerks, cerebellar
signs
HINTS AND TIPS
When you are examining the hands, always look at
the elbows for a psoriatic rash, rheumatoid nodules
or gouty tophi. Most information can be gained from
inspection; do not rush this part of the examination.
Always ensure you do not cause the patient pain.
Ask them if their hands are painful before you start.
Chapter Summary
A good clinical examination relies on good communication. This is crucial to ensure your
patient knows what to expect, consents to the examination, feels as comfortable as
possible and understands what you are asking him or her to do. Take time to appropriately
position and expose your patient. A thorough inspection is key. This includes a visual sweep
of what is around the bed and of the patient, before focusing on the specific examination in
question. Adapt your examination to the clinical situation; it is not safe or appropriate to
perform a full thorough physical examination in a haemodynamically unstable patient when
a systematic A to E approach should be used.
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Writing in the medical notes
3
GENERAL PRINCIPLES
Writing in the medical notes includes any form of clinical
documentation that you undertake. It includes ‘clerking’ (a
written summary of the patient's history and examination),
recording the ward round, documenting discussions with
the patient, the patient’s friends and family or other healthcare professionals or any other communication relating to
patient care. Any documentation you make is a legal record,
and should be precise, complete and legible. You will see
many abbreviations in most medical notes you read, and
you will need to be familiar with the most common ones
(Table3.1). If you choose to use abbreviations, you should
consider if the meaning will be the same to other healthcare professionals, if they could be interpreted differently by
professionals in a different specialty or in a different hospital or if a nonmedically trained person were to read them.
Best practice is to avoid the use of abbreviations for these
reasons.
When you are documenting your clerking, the ‘history
of presenting complaint’ section is a useful place to document the most relevant positive and negative historical
points. Less relevant details can be recorded in their appropriate subsection. For example, in the case presented here,
the relevant negative historical points have been included in
the ‘history of presenting complaint’ rather than elsewhere
in the clerking.
At the end of the clerking, the salient points should be
emphasized in a summary statement. You should then compile a ‘problem list’. This is often forgotten by students and
junior doctors alike, but is invaluable in planning appropriate investigations and management. In some patients, it will
not be appropriate, or even possible, to take a full history
and perform a full clinical examination (e.g. in an emergency situation). We have outlined a clinical example.
As a student, it is good practice to be very thorough as it
helps you to learn the relevant questions and to avoid missing anything important. However, with practice, you will
learn to tailor carefully the clinical approach to each patient
based on individual, and often very different, needs.
Table3.1 Common abbreviations used in medical
documentation
Abbreviation Meaning
Titles
• OT
• PT
• RN
• SLT
Dosing
• OD
• OM
• ON
• BD
• TDS
• QDS
• PRN
Examination
• AE
• BS
• CN
• CP
• CR
• DIB
• HS
• MSK
• PEARLA
• SNT
• SOB
• WOB
Other
• CA
• CAMHS
• DNA
• FU
• GA
• RTA
• Occupational therapy/therapist
• Physiotherapy/physiotherapist
• Registered nurse
• Speech and language therapy/therapist
• Once daily
• Every morning
• Every night
• Twice daily
• Three times daily
• Four times daily
• Pro re nata (as required)
• Air entry
• Bowel sounds
• Cranial nerve
• Chest pain
• Capillary refill
• Difficulty in breathing
• Heart sounds
• Musculoskeletal
• Pupils equal and reactive to light and
accommodation
• Soft nontender
• Shortness of breath
• Work of breathing
• Cancer
• Child and Adolescent Mental Health
Services
• Did not attend
• Follow up
• General anaesthetic
• Road traffic accident
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