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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

Extended-matching questions (EMQs)
C. Intravenous fluid, low-dose fixed-rate insulin infusion
(0.05 units per kilogram per hour), antibiotics and lowmolecular-weight heparin
D. Glucagon, 1 mg intramuscularly.
E. Hydrocortisone, 100 mg intramuscularly.
F. Intravenous administration of 100 mL of 20%
dextrose.
G. Intravenous fluid, propranolol intravenously,
hydrocortisone intravenously and iodine and
propylthiouracil orally.
H. Intravenous fluid, hydrocortisone intravenously and T3
intravenously.
I. Intravenous fluid, hydrocortisone intravenously, insulin
and dextrose intravenously and 10 mL of 10% calcium
gluconate
Please select the appropriate treatment for the following
emergencies.
1. A 50-year-old diabetic patient, with reduced
consciousness, no intravenous access and a blood
glucose level of 2.2 mmol/L.
2. A 50-year-old woman with a background of
hypothyroidism and vitiligo, who presents profoundly
hypotensive. She has had unexplained nonspecific
symptoms, including abdominal pain. Her blood
glucose level is low, and her potassium level is raised.
3. A 70-year-old woman who comes to the emergency
department confused, dishevelled, hypotensive and
hypothermic.
4. A 70-year-old man with diabetes taking metformin
attends the emergency department confused,
hypotensive and with very high capillary blood
glucose level (35 mmol/L). He appears to be clinically
hypovolaemic.
5. A 65-year-old with metastatic breast cancer is
confused and has abdominal pain.
1. An 80-year-old woman presents with a hot, swollen
knee and no history of trauma. She is apyrexial, with
normal levels of inflammatory markers, and is taking
warfarin for metallic heart valve replacement, with a
latest international normalized ratio measurement of 6.
2. A middle-aged women with low mood and unspecific
symptoms of fatigue and widespread joint pain
presents to her general practitioner. On examination
the only finding is tenderness on palpation of muscles.
Blood test results are normal.
3. A 60-year-old man who drinks half a bottle of wine
a day presents with an acutely swollen, red first
metatarsophalangeal (MTP) joint and raised serum
creatinine level.
4. A 23-year-old woman presents with two swollen
fingers in her right hand, a swollen ankle and a
swollen wrist. She also has colitis and has had iritis in
the past.
5. A 20-year-old woman with morning stiffness of both
her wrists preventing her from playing the piano.
Blood tests show elevated levels of inflammatory
markers and that she is positive for rheumatoid factor.
Chapter35 Skin disease
Skin
A. Erythema multiforme.
B. Erythema nodosum.
C. Alopecia areata.
D. Aplasia cutis.
E. Gottron papules.
F. Koplik spots.
G. T-cell lymphoma.
H. Sotos syndrome.
I. Ehlers–Danlos syndrome.
J. Dermatitis herpetiformis.
Chapter34 Musculoskeletal system
A. Rheumatoid arthritis (RA).
B. Psoriatic arthritis (PA).
C. Septic arthritis.
D. Haemarthrosis.
E. Chondrocalcinosis.
F. Gout.
H. Reactive arthritis.
I. Osteoarthritis (OA).
J. Fibromyalgia.
K. Myositis.
Which of the conditions listed above is most likely to affect
joint pain as described below?
418
Which condition from the list above best matches the
descriptions below?
1. A 5-year-year-old with large hands and feet and high
arched palate who is noticed to have advanced bone
age on examination.
2. A 25-year old woman with coeliac disease who
developed vesicular lesions on her buttocks.
3. A 60-year-old man with tinea infection who is
complaining of a bald patch he developed following a
period of problems at work.
4. A 13-year-old boy with a 2-day history of swollen neck
glands, fever and malaise.
5. A 67-year-old man who has skin nodules that a few
months ago were diagnosed as mycosis fungoides.

Extended-matching questions (EMQs)
Chapter36 Haematological disorders
Haematological disorders
A. Polycythemia Vera.
B. Hodgkin lymphoma.
C. Multiple myeloma.
D. Myelodysplastic syndrome.
E. Non-Hodgkin lymphoma (NHL).
F. Chronic myeloid leukaemia (CML).
G. Essential monoclonal gammopathy.
H. Acute lymphoblastic leukaemia (ALL).
I. Acute myeloid leukaemia (AML).
J. Haemophilia B.
For each patient with a haematological disease, select the
most likely diagnosis.
1. A 5-year-old boy who presents to his general
practitioner with lethargy, weakness and petechial
rash. He is pale but afebrile and on examination
shows widespread lymphadenopathy and
hepatosplenomegaly.
2. A middle-aged man with Down syndrome presents
with a few months’ history of malaise, bone and joint
pain, and hepatosplenomegaly.
3. A 15-year-old male with a painless enlarged lymph
node in his neck. His medical history includes
treatment of Epstein–Barr virus infection last year.
There is no other lymphadenopathy, and biopsy
confirms lymphoma.
4. A 65-year-old Afro-Caribbean man presenting to
the emergency department with rib pain. His full
blood count (FBC) shows normocytic anaemia and
thrombocytopenia. His chest radiograph shows
multiple punched-out lesions on his ribs.
5. A 70-year-old woman is seen in the emergency
department with a 6-month history of progressively
worsening lethargy. Her FBC shows a raised white
blood cell count. Otherwise, she looks well, and
the only examination finding is the presence of
splenomegaly.
Chapter37 Infectious diseases
Infectious disease
A. Tuberculosis (TB).
B. HIV.
C. Plasmodium ovale.
D. Methicillin-resistant Staphylococcus aureus.
E. Plasmodium falciparum.
F. Mycobacterium avium.
G. Streptococcus pneumoniae.
H. Crohn disease.
I. Staphylococcus aureus.
J. Giardia lamblia.
For the following patient presentations, what is the most
likely diagnosis?
1. A 19-year-year-old freshman university student who
presents to her general practitioner with a short
history of shortness of breath, productive cough and
tiredness. She has found the symptoms limit her daily
living activities when she trying to attend all university
events. A chest X-ray reveals a 3-cm cavitating lesion
in the upper lobe of her right lung.
2. A 55-year old man with flu-like symptoms, new heart
murmur, aching joints and muscles, shortness of
breath and chest pain on taking a breath in and signs
of pericarditis on electrocardiogram.
3. A 60-year-old man with a recent history of weight
loss who presents to the emergency department with
fever, abdominal pain and watery diarrhoea. He is also
complaining of terrible flatus. Crohn disease would
cause a bloody diarrhoea.
4. A 35-year-old African man with fever, weight loss and
night sweats who has recently developed swelling in
his abdomen and is now unable to pass stool or flatus.
5. A 67-year-old with cirrhosis, fever and cough
who presents to the emergency department. He
is tachycardia and tachypnoeic with chest X-ray
showing right-sided patchy consolidation and leftsided pleural effusion.
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SBA answers
Chapter28 Respiratory system
1. A. A tension pneumothorax is a medical emergency
that requires immediate decompression (largebore cannula in the second intercostal space,
midclavicular line). It is a clinical diagnosis based on
the presence of all or some of the following features
on examination. The trachea is deviated away from
the affected side. Breath sounds will be absent or
diminished. Percussion note will be hyperresonant.
When the tension pneumothorax becomes
sufficiently large to compromise cardiovascular
function, venous return to the heart will be impaired,
resulting in a raised jugular venous pressure.
2. D. Tachycardia is a common finding in PE and the
most common EKG abnormality. Although the
S1Q3T3 pattern is often mentioned in textbooks,
it is encountered in less than 20% of PE cases.
Haemoptysis may well be a feature, but the most
common symptom is pleuritic chest pain. Treatment
depends on the cause, and ranges from 6months
of LMWH therapy (as would be the case here) to
lifelong warfarin therapy.
3. C. In severe asthma, intravenously administered
magnesium may be beneficial. Peak flow is a helpful
tool, especially when compared with the patient's
normal performance, in predicting severity. Peak
flow values of less than 33% of normal indicate a
life-threatening asthma attack. Blood gases are
a particularly important tool in the assessment of
severe asthma. A normal Pco2 level suggests the
patient is getting tired (it should be low because of
hyperventilation) and is not reassuring at all. Death is not
uncommon. There is no evidence to support the use of
intravenous bronchodilators over nebulized equivalents.
4. B. The CURB65 score is used to assess severity for
community-acquired pneumonia. Confusion, defined
as an abbreviated mini mental test score of less than
8, scores 1 point. A serum urea level of more than
7 mmol/L scores 1 point. A systolic blood pressure
of less than 90 mmHg scores 1 point. A respiratory
rate of more than 30 per minute scores 1 point. Age
greater than 65years scores 1 point. A score of 0
or 1 corresponds to mild pneumonia, a score of 2
corresponds to moderate pneumonia and a score
of 3–5 corresponds to severe pneumonia. Typically,
mild pneumonia is treated in the community,
moderate pneumonia is potentially treated in
hospital and severe pneumonia is definitely treated in
hospital, commonly with intravenous antibiotics.
5. B. Syndrome of inappropriate antidiuretic hormone
secretion and Eaton–Lambert myasthenic syndrome
are both associated with small cell lung cancer.
Squamous cell carcinoma may produce parathyroidrelated peptide, causing hypercalcaemia. The
mainstay of treatment is surgery, although patients
often present with metastases which commonly
occur in bone, the adrenal glands, brain and liver.
6. A. Amiodarone may cause lower zone pulmonary
fibrosis, particularly in the context of preexisting lung
disease. Other causes of lower zone fibrosis include
rheumatoid arthritis, asbestosis, idiopathic causes
and drugs such as methotrexate and nitrofurantoin.
7. E. There are four stages of CXR changes associated
with pulmonary sarcoidosis. Answer B is stage
1, answer C is stage 2, answer E is stage 3 and
answer D is stage 4. Pleural effusions are not a
feature in this classification.
8. C. The scenario described above is one of a lifethreatening asthma attack. The most important
features here are the considerable length of the
attack and the apparent lack of effective ventilation.
In the acute setting, the CO2 level would be low, with
an associated respiratory alkalosis (answers D and
E) due to hyperventilation. Once the patient gets
tired, Pco2 will be in the normal range (this is a bad
sign) and the pH will subsequently normalize.
9. E. Although Fio2 is highly dependent on respiratory
rate and oxygen flow rate through the delivery
system, it is useful to have a rough idea of the
concentrations of oxygen given. Inspired room air
has Fio2 of 21%, whereas a non-rebreather mask
at 15 L/min is as close to an Fio2 of 100% as
possible. Venturi masks have special valves that
closely regulate Fio2 and are commonly available
at concentrations of 28%, 35% and 40%. A simple
facemask delivering oxygen at 5 L/min delivers Fio2
of roughly 50%.
10. E. The history points to the diagnosis of
mesothelioma. The condition is usually caused by
industrial asbestos exposure, and may therefore
result in compensation for the patient and/or family.
It is a tumour of the pleura rather than the lung
parenchyma. Associated pulmonary asbestosis
is found in only approximately 15% of cases. The
prognosis is poor.
11. E. TB is an infectious disease caused by the
bacterium M. tuberculosis. Although the disease
can involve various organs, pulmonary TB is the
most common presentation. The drug regimen for
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SBA answers
pulmonary TB includes a combination therapy of
four drugs: rifampicin, isoniazid, pyrazinamide and
ethambutol. All four are taken for the first 2months.
After that only rifampicin and isoniazid are taken.
Streptomycin is no longer recommended as first-line
therapy for treatment of pulmonary TB.
12. C. This patient is acutely unwell. His respiratory
effort is inadequate, and he is at risk of suffering a
respiratory arrest if not treated. Urgent management
is required. Senior help should be sought. The
patient is achieving saturations of only 88%
despite high-flow oxygen. Although he is at risk
of carbon dioxide retention, hypoxia is more likely
to kill him first. The patient is septic with a high
temperature, and Sepsis Six management should be
commenced. Although the help of an anaesthetist
may be needed, lower-level interventions should be
tried first before endotracheal intubation. Although
answer E illustrates an appropriate logical approach
to management, this patient is too unwell and will
require a higher level of support.
13. D. An ABG test is extremely important in this case,
as the results will tell you whether the patient
is in respiratory failure, and if so, whether he is
retaining carbon dioxide. This will help guide your
treatment. In addition, it will give you other useful
information, such as sodium, potassium, lactate
and haemoglobin levels. CXR and blood tests will
also help establish the diagnosis. Raised levels
of inflammatory markers will suggest an infective
cause. Consolidation on a CXR will further support
the diagnosis. CXR showing pulmonary oedema
will point towards a cardiac cause of shortness of
breath. Urine dip is a simple bedside investigation
that can be very useful. A urinary tract infection
can be asymptomatic, especially in the elderly,
and urosepsis can be a cause of acute illness. CT
pulmonary angiogram would not be useful in the
first instance. Although a PE should be amongst
the differential diagnosis, the other tests would be
considered first.
14. A. CT pulmonary angiogram is the most sensitive
noninvasive test available for diagnosis of PE. It is
a scan that requires intravenous administration of
contrast media. These compounds are known to
be nephrotoxic. In a previously healthy individual,
with normal kidney function test results, the effect of
contrast medium is usually of no clinical significance;
however, in patients with preexisting renal
impairment, contrast medium can lead to contrast
nephropathy and worsening of kidney function.
15. D. Although Streptococcus pneumonia is the most
common pathogen causing community-acquired
pneumonia, in this case the history suggests
that the patient has an atypical pneumonia.
Legionella pneumophila is a bacterium that causes
Legionnaires disease. The organism’s natural
habitat is water. Human spread has been linked
to contaminated water reservoirs such as air
conditioning systems in hotels, office buildings, and
hospitals. Infection causes nonspecific symptoms.
Chapter29 Gastrointestinal and
hepatobiliary systems
1. C. Barrett oesophagus is usually asymptomatic.
Less than 1% of cases progress to adenocarcinoma
per year. It is characterized by metaplasia from
squamous to columnar epithelium in the distal part
of the oesophagus. The underlying cause is GORD,
which is typically managed medically with lifestyle
changes and proton pump inhibitors.
2. B. Pancreatitis is an inflammatory condition of the
pancreas most commonly caused by alcohol or
gallstones. The history of intermittent RUQ pain is
suggestive of biliary colic in a woman in her 40s. The
likelihood is thus that this is gallstone pancreatitis.
Severity can be assessed with the modified Glasgow
or APACHE-II scoring systems. The Rockall score is
used to predict mortality in gastrointestinal bleeding.
Pseudocyst formation is not an early complication—
it tends to occur after 2–6weeks. Although a serum
amylase level of 1400 U/mL is high, occasionally a
perforated viscus may present in a similar manner
with serum amylase concentrations higher than
1000 U/mL.
3. E. A large upper GI tract bleed is a medical
emergency and should be initially managed
according to advanced life support principles of
airway, breathing and circulation. Fluid resuscitation
is a priority. Blood results may show a raised urea
level (secondary to red cell ingestion) and may
initially show a normal haemoglobin concentration as
there has been no chance for haemodilution in the
very acute setting. The investigation of choice is an
oesophagogastroduodenoscopy. Rebleeding carries
immediate mortality of 40%.
4. B. Transmural inflammation, perianal lesions and skip
lesions are all features of Crohn disease. Ulcerative
colitis is less common in smokers, the converse of
which is true for Crohn disease. Pseudopolyps are
associated with ulcerative colitis.
5. D. The symptoms described here are suggestive
of a left-sided tumour. The more distal the disease,
the more likely it is to cause a change in bowel
habit. Tenesmus is suggestive of rectal disease.
Right-sided tumours typically present late and may
present as iron-deficiency anaemia. More than 90%
of tumours can be resected surgically.
6. D. Pseudomembranous colitis is a serious
infection, commonly hospital acquired. It is
caused by the toxins produced by C. difficile. As
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SBA answers
is the case for all forms of colitis, toxic dilatation
of the colon is a complication. Diagnosis of C.
difficile infection is made by toxin-positive stool
culture; pseudomembranous colitis is diagnosed
endoscopically. Prevention is predominantly through
hand washing using soap and water (to eliminate the
bacterial spores) and careful use of antibiotics. Initial
treatment is with orally administered metronidazole
or orally administered vancomycin.
7. D. IBS is a diagnosis of exclusion that can be made
only once organic causes have been excluded (such
as coeliac disease, inflammatory bowel disease).
The condition is more common in females between
the ages of 20 and 40years. Symptoms include
central or lower abdominal pain, commonly relieved
by defecation, abdominal bloating and altered bowel
habit. Rectal bleeding is not a feature. Treatment
may require input from dieticians, surgeons,
psychiatrists or gynaecologists, and is not always
successful.
8. B. Gallstones are commonly asymptomatic. Their
incidence increases with age, parity, raised BMI and
they are more common in females. Occasionally, a
large gallstone can erode through the gallbladder
into the adjacent duodenum, causing a gallstone
ileus. A minority of gallstones are radio-opaque
owing to their composition: they commonly
contain cholesterol and/or bile salts. Charcot triad
(RUQ pain, jaundice and rigors) is suggestive of
cholangitis.
9. C. Hepatitis A may relapse, but does not cause
chronic hepatitis. Hepatitis B transmission is
parenteral, and infection may be complicated by
hepatocellular carcinoma. Hepatitis C is usually
asymptomatic in the acute phase. Hepatitis E is
transmitted via the faecal–oral route.
10. D. Intussusception affects children more commonly
than adults. In 20% of cases there may be
redcurrant jelly stool, although this is a late sign.
Melaena is stool containing metabolized blood
(indicating an upper gastrointestinal tract bleed).
Fatty stool (or steatorrhoea) or putty-coloured
stool is a feature of obstructive jaundice or
chronic pancreatitis. Watery stool is common in
gastroenteritis.
11. A. Although portal hypertension and
hypoalbuminaemia have some effect on fluid
retention, renal sodium handling has the greatest
effect. It is thought that aldosterone plays an
important role in the mechanism, and it may be that
renal sensitivity to aldosterone is enhanced in liver
cirrhosis. There is no suggestion of inferior vena cava
or lymphatic obstruction in this clinical scenario.
12. C. Cases of acute pancreatitis should be referred
to the surgical team. Initial management is
rapid fluid replacement; provided there are no
contraindications, the patient should receive at least
3 L in the first 12 hours, and electrolyte replacement,
analgesia and antiemetics if indicated. Chronic
pancreatitis is referred to the medical team unless a
surgical cause is identified.
13. D. HBV infection is present when the test for HBsAg
is positive. Chronic infection is diagnosed if this
persists for more than 6months. Anti-HBc is present
if the patient has immunity against the pathogen,
either active (with a vaccine) or passive (due to
previous infection). HCV infection is present if the
test for HCV antibody is positive.
HBV
core
Anti-
Anti-HBc HBsAg
Acute infection + + – +
Chronic infection + + – –
Active
immunization
Passive
immunization
– – + –
+ – + –
HBs
antibody
IgM
14. D. This patient has ascites on a background of
alcoholic liver disease. The exact mechanism
of why patients develop ascites is not fully
understood; however, sodium and water balance
is thought to play a role. Spironolactone is an
aldosterone antagonist which, amongst other
functions, promotes diuresis and hyponatraemia.
Spironolactone was found to work better in
reducing ascites than other types of diuretics,
for instance furosemide (a loop diuretic). It is
important to remember that spironolactone can also
cause hyperkalaemia, and as such, monitoring is
important.
Antibiotics are indicated if the patient is suspected of
having spontaneous bacterial peritonitis, which can
be a complication in patients with cirrhosis.
β-Blockers, unless contraindicated, are given to
patients with portal hypertension.
15. D. You would expect a positive result for ketones on
a urine dip in diabetic ketoacidosis. Abdominal aortic
aneurysm can present as abdominal pain or back
pain. Although the patient presents with signs and
symptoms suggestive of an inflammatory process,
any blood passed rectally should be investigated for
a possibility of cancer.
16. B. Diarrhoea would cause loss of bicarbonate with
the stool and a high level of chloride in the blood and
therefore lead to normal anion gap metabolic acidosis.
Raised anion gap metabolic acidosis can occur
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SBA answers
because of excess acids in the body (e.g., diabetic
ketoacidosis, lactic acidosis, salicylate toxicity).
Metabolic acidosis with respiratory compensation is a
possibility; however, the respiratory rate is then likely to
be raised as the patient is breathing fast to try to blow
off carbon dioxide.
Chapter30 Renal, genitourinary and sexual
health medicine
1. D. Pulmonary oedema, severe acidosis, resistant
hyperkalaemia and symptomatic uraemia
(i.e., uraemic pericarditis) are all indications for
emergency haemodialysis/haemofiltration in the
context of AKI. In this case the patient has an
AKI from hypovolaemia and is at risk of having a
background of hypertension. His AKI is very likely
to have been made worse by his continuing use of
an angiotensin-converting enzyme inhibitor during
the time of hypovolaemia and hypotension. In
terms of needing to start dialysis, there is no cut-off
value for creatinine, urea or bicarbonate level that
would necessitate starting emergency dialysis.
Hyperkalaemia resistant to medical treatment
(this is the key) is an urgent indication for starting
dialysis.
2. A. The first EKG feature of raised potassium level
is tented T waves. At higher potassium levels the
following changes occur: small or absent P waves,
prolonged PR interval (progressive paralysis of atria)
broadened QRS complex, atrioventricular block
giving a bradycardia and, eventually, sinusoidal
waveform (this is commonly followed by ventricular
fibrillation and needs immediate senior input and
management). U waves are seen on an EKG in
association with hypokalaemia, hypocalcaemia
and hypomagnesia. This man’s potassium level
is 6.4 mmol/L, and the most usual features
would be peaked T waves. It is important to take
account of his normal potassium readings. If
the patient generally has a low potassium level,
then 6.4mmol/L may result in more myocardial
dysfunction and pose a greater risk to the patient.
3. A. The triad of nephrotic syndrome is
hypoalbuminaemia (<30 g/L), nephrotic range
proteinuria (PCR >300 mg/mmol or 24-hour
protein loss of >3 g) and peripheral oedema. It is
associated with increased risk of infections, (from
immunoglobulin loss), increased risk of thrombosis
(from loss of protein C and protein S) and high
cholesterol level but this does not make up the triad.
This young boy is most likely to have minimal change
disease. It is generally very steroid responsive.
High cholesterol level is quick to normalize, and
thrombotic tendency is less than in other forms of
nephrotic syndrome.
4. E. AKI, active urinary sediment and haemoptysis
suggests a pulmonary–renal disease. This includes
ANCA-associated vasculitis and Goodpasture
disease. Important serological tests to help support
diagnosis would be an ANCA titre and anti-GBM.
In these conditions, CRP level is likely to be raised
but would not help narrow down the diagnosis.
Anti-streptolysin O titre greater than 200IU suggests
recent streptococcal infection; complement levels
are generally normal in ANCA-associated vasculitis.
5. C. Small scarred kidneys on ultrasound scan best
support the likelihood that this is CKD. With
any blood test measuring creatinine level, an
eGFR will be estimated. However, to define CKD
requires the presence of a low eGFR measured
on at least two separate occasions 3months
apart. GFR should not be used in AKI. Anaemia
is common in CKD but can occur in many other
disease processes. Hydronephrosis and prostatic
hypertrophy would be more in keeping with an
AKI. A monoclonal paraprotein on electrophoresis
is suggestive of myeloma, which can lead to AKI
and if untreated CKD.
6. E. CKD is commonly caused by hypertension.
Proteinuria is associated with a more rapid
progression of renal dysfunction. Blood pressure
should be reduced to below 140/90 mmHg but with
a stricter target of 130/80 mmHg in the context
of significant proteinuria or diabetes. Decreased
production of erythropoietin combined with impaired
iron utilization results in normochromic normocytic
anaemia. Impaired renal excretion of potassium and
phosphate must be balanced by decreased oral
intake. High phosphate level can lead to increased
rate of atherosclerosis, so phosphate levels are
treated to bring this value down to the normal
range.
7. B. This is the classic presentation of pyelonephritis.
Sending midstream urine for culture and blood
cultures is important before antibiotic treatment is
started. This should be done urgently. Any female
of childbearing age presenting with abdominal
pain must have a pregnancy scan to rule out an
ectopic pregnancy; this would be less likely though
to present with fevers unless the ectopic had
ruptured. A full blood count would likely show a
raised white cell count in keeping with infection. The
preferred imaging modality would be an ultrasound
scan. This could show evidence of pyelonephritis,
abscess or hydronephrosis. A dimercaptosuccinic
acid scan maybe useful further down the line if
complications of pyelonephritis were considered,
to look for scarring. If there was a strong suspicion
of renal calculi, a noncontrast CT scan would be
performed—an abdominal X-ray would not be
indicated in this scenario.
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SBA answers
8. A. Females are at increased risk of UTI as a result
of a shorter urethra with its meatus closer to the
anus. The condition will affect 25–35% of women
at least once. UTIs are commonly asymptomatic;
they should still be treated regardless of being
asymptomatic in pregnancy. Infection is common
and hard to clear in the context of long-term
placement of a urinary catheter. Intermittent selfcatheterization is a good solution to this problem.
A simple UTI may ascend the ureters and cause
pyelonephritis.
9. C. The most likely diagnosis is indomethacininduced interstitial nephritis. The diagnosis would
be confirmed by renal biopsy. Use of indomethacin
should be stopped, and the patient might benefit
from oral steroids. Interstitial nephritis tends to
present with AKI and blood and protein on urine
analysis. NSAID-related interstitial nephritis is an
exception and can present with nephrotic syndrome
and fevers. The key to treatment is recognizing the
culprit drug and stopping its use. Membranous
nephropathy is not associated with NSAIDs or
surgical procedures. Acute tubular necrosis is often
due to prolonged hypotension, and would result in a
raised creatinine level, not a nephrotic presentation.
There are no other features to suggest lupus
nephritis. FSGS would be unlikely to give such a
rapid onset of nephrotic syndrome, and would tend
to be associated with nonvisible haematuria.
Chapter31 Fluid balance and electrolyte
disturbances
1. A. Sarcoidosis can cause hypercalcaemia.
Bisphosphonates can be used to treat
hypercalcaemia but such treatment should be
started only after aggressive fluid resuscitation,
which may be sufficient to control the calcium
level. The cause of the hypercalcaemia needs to
be investigated. The most common causes are
from hyperparathyroidism and malignancy. Ionized
calcium level is the relevant value, and correction for
albumin should be done (although most laboratories
now will give you the corrected calcium level).
Malignancy is a common cause of hypercalcaemia,
with common culprits including myeloma and those
that metastasize to bone; lung, breast, kidney,
thyroid and prostate cancer.
2. C. He has the classic features of polydipsia and
polyuria, and needs water, hence his aggression.
Lithium therapy is the likely cause, and it can lead to
a nephrogenic diabetes insipidus. This will result in
ADH not being able to act appropriately on the distal
collecting duct, resulting in free water excretion
(i.e., large volumes of dilute urine, with low urinary
sodium level), which is inappropriate in the context
of a high plasma osmolality and high serum sodium
level. Conn’s syndrome refers to excess production
of the hormone aldosterone from the adrenal gland.
This abnormality can be caused by hyperplasia or
by an aldosterone producing tumour. This tends
to give the clinical picture of hypertension, high
sodium level (although rarely this high) and low
potassium level. Polyuria and polydipsia are not a
feature. Addison disease is adrenal insufficiency
(i.e., low cortisol/ aldosterone level), and is not a
cause of hypernatraemia (biochemically associated
with hyperkalaemia and low glucose level). Cushing
disease and Cushing syndrome result in a high level
of cortisol. Cushing disease specifically refers to
when this is secondary to an adrenocorticotrophic
hormone (ACTH) secreting pituitary tumour.
Cushing syndrome can be caused by exogenous
glucocorticoids e.g., medications, or any tumour
outside the pituitary gland that produces or results
in the production of excess cortisol by the adrenal
gland. This is associated with a mild hypernatraemia,
hypokalaemia and hypertension, although again
polydipsia and polyuria are not a clinical feature.
Ingestion of salt tablets is possible, but again there
is no mention of this in the vignette, and it would not
cause a polyuria.
3. A. SIADH is a diagnosis of exclusion. The first
step in evaluating hyponatraemia is to assess
the patient’s fluid status. SIADH requires that the
patient is euvolaemic, and that thyroid function,
adrenal function, renal function and liver function
are normal. To make the diagnosis, the patient must
be hyponatraemic, with a serum osmolality which
is low and an inappropriately high urine osmolality
(perform paired tests), and urinary sodium level
should be inappropriately high. A fluid deprivation
test is a test to confirm the presence of diabetes
insipidus but is rarely performed. Fluid restriction
is the treatment for SIADH, although this is not
how the condition is diagnosed. If fluid restriction
is not successful, then other treatments such as
demeclocycline or tolvaptan can be trialled. A high
cortisol level is a feature of Cushing syndrome/
disease. A dexamethasone test is a dynamic test,
looking to see whether exogenous steroid can
suppress the cortisol production. A short Synacthen
test is a dynamic test for Addison disease; it
investigates whether synthetic adrenocorticotrophic
hormone can stimulate the adrenal gland to
produce mineralocorticoid/glucocorticoid, the
latter being measured with the cortisol level (see
Chapter34).
4. B. Bendroflumethiazide is a thiazide diuretic; it acts
on the distal collecting tubule and causes sodium
and potassium excretion. Through its mode of
action it can lead to hyponatraemia. This would be
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SBA answers
the first agent whose use should be stopped, and if
necessary an alternative antihypertensive should be
used. Omeprazole and citalopram can both cause
a syndrome of inappropriate secretion of antidiuretic
hormone. These would be the next medications
whose use you should consider stopping if the
situation does not improve after discontinuation of
use of the thiazide. Levothyroxine and bisoprolol are
not causes of hyponatraemia.
5. B. Prolonged hypokalaemia can cause a
nephrogenic diabetes insipidus and polyuria
through distal tubular dysfunction. Abdominal
pain is a feature of hypercalcaemia. There is no
direct correlation between electrolyte disturbances
and urinary infections. Seizures are a feature
of severe hyponatraemia and hypocalcaemia.
Perioral numbness is a feature of hypocalcaemia.
Eponymous signs of hypocalcaemia include
Chvostek sign and Trousseau sign. Vomiting
is a cause of hypokalaemia, and with a level of
2.6 mmol/L she is likely to be symptomatic. An EKG
should be performed, and potassium should be
replaced along with any low level of magnesium.
This should be done in an inpatient environment as
she is at risk of cardiac arrhythmias.
6. D. This is a feature of hypocalcaemia. Peaked
T waves are the first abnormality seen in
hyperkalaemia; at higher potassium levels this
could cause sinusoidal wave form. A delta wave is
a slurring slow rise of the initial upstroke of the QRS
complex which is seen with preexcitation syndromes
such as Wolff–Parkinson–White syndrome. J
waves can be seen with hypercalcaemia and more
commonly hypothermia.
Chapter32 Nervous system
1. E. Facial weakness is usually due to an upper motor
neurone lesion which spares the forehead. As
this patient is taking warfarin, CT scan is required
urgently to rule out haemorrhage. If haemorrhage is
present and the international normalized ratio (INR)
is raised, the effects of warfarin should be reversed
with prothrombin complex concentrate. Ischaemic
strokes can occur in patients taking warfarin if the
INR is subtherapeutic for a prolonged period, or
occasionally if the INR is therapeutic. Haemorrhage
accounts for around 20% of strokes.
2. C. Meningitis is not as likely as migraine—the
patient is afebrile and the visual symptoms would
be atypical. A minority of SAHs are preceded by a
'sentinel bleed' but visual warning symptoms are not
typical. β-Blockers are sometimes used for migraine
prophylaxis. Patients with cluster headache are
typically restless, as opposed to those with migraine.
Triptans are effective for acute migraine.
3. B. Symptoms are asymmetrical in onset;
symmetrical onset implies an alternative diagnosis
such as the Parkinson plus syndromes. He is young,
and a dopamine agonist is often preferred as firstline therapy in younger patients. A radioiodine scan
may be helpful if the diagnosis is in doubt, but is not
required. Rigidity is one of the cardinal features of
parkinsonism, the others being tremor, bradykinesia
and postural instability.
4. D. Optic neuritis is commonly due to MS, but it can
occur in isolation or can be due to other disorders
such as infection or vasculitis. Colour vision is
usually affected more. In 90% of patients the vision
gradually improves over weeks to months following
the initial event. The risk of developing MS following
an episode of optic neuritis is higher if white matter
lesions are present on MRI. MS typically occurs
between the ages of 20 and 40years.
5. E. The purpuric rash is most likely to occur in
meningococcal infection. Streptococcus pneumoniae
is a common cause but does not usually cause
a purpuric rash. Listeria is more common in the
elderly, people with alcoholism and newborns.
Lumbar puncture is required but not immediately,
and the presence of severe headache, confusion
and vomiting should warn you of raised intracranial
pressure. Treatment with intravenous ceftriaxone
or benzylpenicillin is urgently required along with
supportive measures and notification of the intensive
care team (ITU).
6. D. It is commonly referred to as a 'false localizing
sign'. The headache is typically worse in the
morning. The Cushing reflex is a late sign consisting
of hypertension and bradycardia. Fundoscopy
should be performed to look for papilloedema if
raised ICP is suspected. Nausea and vomiting may
occur; abdominal pain is not a feature.
7. E. MND is slightly more common in men. It does not
affect the sensory nerves or the extraocular muscles.
Prognosis is poor; survival beyond 5years is very
rare. It usually causes a mixture of upper and lower
motor neurone signs.
8. C. Mortality associated with subarachnoid
haemorrhage is 50%. Only 30% are preceded by
a sentinel headache. As well as hydrocephalus,
other causes of decreasing Glasgow Coma Scale
score are vasospasm and rebleeding. Treatment is
with good fluid intake, analgesia and nimodipine.
Neurosurgery may be required.
9. C. Metastases are more common than primary
tumours. If primary tumour is suspected, stereotactic
biopsy is required. Meningiomas, when small, can
be simply observed. Surgery is often successful.
Glioblastomas are aggressive tumours with a poor
prognosis. Breast cancer, as well as lung and skin
cancer, commonly metastasizes to the brain.
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SBA answers
10. E. Syncope on exertion should prompt investigations
to look for aortic stenosis or hypertrophic
cardiomyopathy. Urinary incontinence and a few
jerks/twitches are commonly seen during syncope.
EKG is mandatory and may reveal arrhythmia. Biting
the side of the tongue is suggestive of a seizure.
11. C. Although the presentation could be due to a
space-occupying lesion, that there is a family history
of a similar presentation together with an early death
suggests that the condition is genetically linked.
The most likely diagnosis is Huntington disease.
Although Sydenham chorea and Wilson disease are
possibilities, these would normally present with other
signs and symptoms. Haloperidol causes tardive
dyskinesia.
12. A. Dopamine agonists are usually used first in
younger patients, whereas l-DOPA is the drug of
choice in older patients. Selegiline is a monoamine
oxidase B inhibitor and can be used in PD; however,
it would not be as first-line therapy. Carbidopa is
a peripherally acting l-DOPA metabolism inhibitor.
Propranolol can be used for treatment of essential
tremor but would not be helpful in PD.
13. C. This patient’s Glasgow Coma Scale score is
calculated as follows: eyes—2; voice–2; motor–4.
14. E. Pseudobulbar palsy is an upper motor
neurone disorder, whereas bulbar palsy is a lower
motor neurone disorder. Tongue wasting and
fasciculations is a lower motor neurone feature. All
the other presentations can occur in pseudobulbar
palsy.
15. A. Dermatomyositis is a connective tissue disorder.
Inflammation of the skin and muscle is one of the
characteristics. The rash present on the dorsal
aspect of the hands is known as ‘Gottron papules’.
Proximal muscle weakness and heliotrope rash are
also characteristic.
Chapter33 Metabolic and endocrine
systems
1. C. Diabetes may be diagnosed based on one
abnormal plasma glucose level of 11.1 mmol/L
or greater or fasting glucose level of 7 mmol/L or
greater in the presence of diabetic symptoms such
as thirst/polyuria. If the patient is asymptomatic,
two fasting glucose levels of 7 mmol/L or greater are
required or a fasting glucose level of 7 mmol/L or
greater followed by a positive oral glucose tolerance
test result (i.e., plasma glucose concentration of
11.1 mmol/L or greater 2 hours following an oral
75-mg glucose load). An HbA1c level of 48mmol/
mol or HbA1c fraction of 6.5% can also be used
to diagnose diabetes. Answer C fits this definition.
A random glucose level of 10.9 mmol/L warrants
further investigation. Answer D shows impaired
glucose tolerance and answer E shows impaired
fasting glucose.
2. D. Antibiotics are often required for underlying
infection, which is a common cause of DKA.
Patients are usually very dehydrated, and correction
of the fluid balance is the priority. In young patients,
particularly, overzealous fluid replacement can
precipitate cerebral oedema. Compensatory
hyperventilation (Kussmaul respiration) to 'blow off'
carbon dioxide is commonly seen. To diagnose
DKA it requires an acidosis (pH 7.3; reference range
pH 7.35–7.45), ketosis (serum ketone level greater
than 3 mmol/L or 2+ on urine dipstick) in a known
diabetic or hyperglycaemia (glucose level greater
than 11 mmol/L).
3. D. Type 1 diabetes requires treatment with
subcutaneously administered insulin and is usually
treated with a basal bolus regimen of four injections
per day. The aim is an HbA1c fraction between
6.5% and 7.5%. Type 2 diabetes can initially be
managed with oral medication. Metformin is the
first-line treatment but is contraindicated in renal
failure with an estimated glomerular filtration rate
of less than 30 mL/min per 1.73 m2, given the
risk of developing lactic acidosis. Sulphonylureas
often cause weight gain and can also cause
hypoglycaemia.
4. E. Osteoporosis is not painful until a fracture is
sustained. It is more common in women. Calcium,
phosphate and alkaline phosphatase levels should
be normal. A T score of less than −2.5 is diagnostic.
This is the standard deviation from the mean value
for a young adult and is calculated from the bone
mineral density measured on a dual-energy X-ray
absorptiometry scan. A Z score is also given which
is age matched.
5. A. Sarcoidosis is one cause of hypercalcaemia.
Malignancy, including myeloma, is a common cause.
Even if the calcium level quickly returns to normal
with treatment, it is important to find the underlying
cause. Ionized calcium level is the relevant value,
and correction for the albumin level should be done.
Hydration alone may normalize the calcium level;
bisphosphonates should be given only after the
patient has been treated with intravenous fluids
and should be administered only if rehydration is
insufficient. Allow time for the bisphosphonates to
lower the calcium level.
6. A. If present, the visual field defect is a bitemporal
hemianopia in acromegaly, with the pituitary
adenoma causing compression at the optic chiasm.
Prognathism is common, along with increased size
of the head, hands and feet. Hypogonadism and
hyperglycaemia are common.
7. C. The most common form of hypothyroidism
is primary hypothyroidism. Chronic autoimmune
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