Station 5: Brief Clinical Encounters
Hints for the Brief Clinical Encounters Station
Headache (Idiopathic Intracranial Hypertension)
Rheumatoid Arthritis with Carpal Tunnel Syndrome
HINTS FOR THE BRIEF CLINICAL ENCOUNTERS STATION
•Station 5 is worth many marks in the exam, and it is crucial to dedicate a substantial proportion of revision time to it.
•Carefully read the instructions to candidates before entering the station, and brainstorm the specific questions you need to ask to help get the diagnosis.
•Formulate a structure for your focused clinical assessment.
•On entering the room, look closely for any clues to the diagnosis; ‘ spot diagnoses’ are common in this station.
•Generally, begin with an open question, but quickly become more focused after this. Establish a likely diagnosis (and differential) and then find out about specific complications.
•Examination generally involves looking for specific signs to clarify a diagnosis rather than following a set pattern – remember that the examination should be focused.
•Be sure to examine for evidence of complications/manifestations of the primary disorder.
•When presenting the case, give the likely diagnosis first, but have a differential available in case you are asked for this.
•Always ask about any specific concerns that the patient has, and provide a solution or explanation as appropriate.
•Addressing the patient’ s welfare and concerns is vital in this station.
This patient, a 25-year-old man, has been experiencing back pain (including pain at night), stiffness and fatigue. Please ask any relevant questions and proceed as appropriate.
FOCUSED HISTORY
1.Duration, timing (often have pain at night) and nature of backache; location of pain
2.Age and gender of patient (onset before 40 years and males affected more than females)
3.Morning stiffness: Duration (improves with exercise and worse with rest)
4.Falls, trauma and injuries to spine
5.Spinal deformity
6.Other joints affected: Sacroiliac joints, hips, knees, ribs
7.Family history of back problems
8.Neurological symptoms: Ensure no bladder/bowel disturbance (all histories of back pain), paraesthesia/numbness/limb weakness
9.Other features: Chest pain, breathlessness, eye symptoms (pain, redness, floaters), enthesitis, fatigue
10.Patient welfare/concerns: Deformity, genetic link, mobility aids
•Spine
•Ask the patient to stand up, back and front fully exposed (ensure that you preserve dignity).
•Kyphotic spine, compensatory hyperextension of the neck (‘ question mark’ posture).
•Reduced spinal movements: Rigid, immobile spine.
•Increased anteroposterior (AP) diameter of chest wall.
•Cardiac
•Listen to aortic area and left sternal edge for early diastolic murmur of aortic regurgitation.
•Chest
•Fine apical fibrotic crepitations
•Eyes
•Iritis, visual acuity check
•Gait
•Likely antalgic, will make the spinal deformity more obvious
QUESTIONS
1.What are the immunological associations with ankylosing spondylitis?
•Seronegative spondyloarthropathy
•HLA-B27 positive in > 90% of individuals
•Tumour necrosis factor (TNF)-? and interleukin (IL)-1 also implicated in disease activity
2.How is the diagnosis of ankylosing spondylitis made?
•Mainly clinical from history and examination with supporting radiological evidence
•Young patients (< 40), possible family history
•Plain radiograph – erosions and fibrosis/sclerosis of the sacroiliac joints, squaring of the vertebra (‘ bamboo spine’ ) due to ossification of the anterior longitudinal ligament and intervertebral spaces
•Blood tests: Raised erythrocyte sedimentation rate (ESR)/C-reactive protein (CRP) during active inflammation, normocytic anaemia
•Genetic testing: HLA-B27
3.What is the treatment for ankylosing spondylitis?
•No known cure: Mainly symptomatic
•Physiotherapy: Encourage increased exercise, physiotherapy and exercises for maintaining good posture
•Analgesia: Nonsteroidal anti-inflammatory drugs (NSAIDs), paracetamol and weak opioids
•Corticosteroid injections: For sacroiliitis and enthesitis
•Biological agents: TNF-? antagonists such as etanercept, adalimumab, infliximab, golimumab and certolizumab pegol (help slow disease progression)
•Treat complications such as iritis
•Treat osteoporosis with bisphosphonates to prevent spinal fractures
4.What are the extra-articular manifestations of ankylosing spondylitis?
•Respiratory: Restrictive lung defect/reduced lung capacity due to restricted chest wall movement and apical lung fibrosis.
•Cardiac: Chronic aortitis leading to aortic regurgitation, conduction defects and cardiomyopathy.
•Neurological: Atlantoaxial instability/dislocation and cauda equina syndrome.
•Eyes: Iritis and cataracts.
•Amyloidosis (secondary/amyloid A [AA]): Multisystem involvement, including hepatic and renal involvement.
•Coexistent inflammatory bowel disease is common.
PATIENT WELFARE AND CONCERNS
1.Adequate management of pain.
2.Concern regarding the impact upon activities of daily living – will this stop the patient working?
3.Cosmetic concerns regarding possible spinal deformity.
4.Is this inherited, and could I pass this onto my children doctor?
5.Is there a cure?
CANDIDATE EXPECTATIONS
1.Recognition of an inflammatory arthropathy, and in particular ankylosing spondylitis, from a detailed history
2.Awareness of the need to rule out ‘ red-flag symptoms’
3.Understanding of the extra-articular manifestations of inflammatory arthropathies
4.Examine for features of ankylosing spondylitis, including extra-articular manifestations, e.g. auscultate for aortic regurgitation and lung fibrosis
5.Explanation that treatment aims are to maintain a good quality of life and prevent disease progression and complications
REFERENCES
National Institute for Health and Care Excellence. (2013) Clinical knowledge summary: Ankylosing spondylitis. Available from http://cks.nice.org.uk/ankylosing-spondylitis#!scenariorecommendation:4. Accessed 5 July 2016.
National Institute for Health and Care Excellence. (2016) TNF-alpha inhibitors for ankylosing spondylitis and non-radiographic axial spondyloarthritis. Available from https://www.nice.org.uk/guidance/ta383/resources/tnfalpha-inhibitors-for-ankylosing-spondylitis-andnonradiographic-axial-spondyloarthritis-82602848027077. Accessed 5 July 2016.
This 65-year-old man has been having palpitations intermittently for the past 3 months. On one occasion, he attended the emergency department and was found to be in atrial fibrillation (AF) with rapid ventricular response. The team in the emergency department has given him some bisoprolol to slow the rate, and he attends your rapid access outpatient department to discuss anticoagulation.
FOCUSED HISTORY
1.Start by summarising the history and ensuring that the patient knows that the focus of the consultation will be to discuss anticoagulation.
2.Enquire about the risk factors for stroke, i.e. does this patient need anticoagulation?
3.Is the patient known to have hypertension?
4.Is the patient known to have diabetes?
5.Is the patient known to have heart failure?
6.Need to assess the patient’ s bleeding risk?
7.Prior history of gastrointestinal (GI) bleeding?
8.Prior history of liver disease?
9.Does the patient have any known renal problems?
10.Prior history of intracranial bleeding?
11.Does the patient have an active cancer?
12.Take an alcohol history.
13.Take a thorough drug history, including over-the-counter and herbal medications.
14.Social history is important. Contact sport should be avoided if the patient is to take anticoagulants.
FOCUSED EXAMINATION
•Observe for stigmata of bleeding/chronic liver disease.
•Check the patient’ s blood pressure.
•Look for clinical signs of cardiac failure.
QUESTIONS
1.Do you know of any risk stratification tools that can be used to assess bleeding risk for patients on warfarin?
•The HASBLED score (see below).
•This takes into account hypertension, renal and liver failure, age, drug use, alcohol consumption, labile international normalised ratios (INRs) and medication usage that would predispose to bleeding (NSAIDs and antiplatelets).
•A score out of 9 is given and can be used to calculate bleeding risk. If the patient scores 3 or more, caution with anticoagulation is advised and regular review must be in place if a decision is taken to anticoagulate.
2.Do you know of a tool one can use to predict stroke risk for patients with AF?
•The CHA2DS2-VASc score (see below).
•This score is out of 9 and takes into account other stroke risk factors, including age, diabetes, hypertension and heart failure.
•The higher the score, the greater the risk of stroke.
•Dependent on the score, a percentage stroke risk per year for a patient can be given.
3.Under what circumstances would one use novel anticoagulants such as rivoroxaban as opposed to warfarin?
•The National Institute for Health and Care Excellence (NICE) guidelines suggest that novel oral anticoagulants (NOACs) can be used where appropriate. They are guidelines, and use will be clinician dependent and dependent on local guidelines. An example may be if a patient has mild cognitive impairment and has difficulty managing warfarin.
•Local guidelines may vary.
•If the patient cannot get to and from hospital for blood tests.
•If they have had a cardiovascular event while on warfarin with a subtherapeutic INR.
•If they have a labile INR.
4.List some disadvantages of novel anticoagulants?
•If the patient misses one dose, then they are not receiving the benefit; therefore, likely compliance must be assessed and the importance of this stressed.
•Not all are safe in renal failure, so this may need to be monitored if there are concerns. Dose will vary depending on estimated glomerular filtration rate (eGFR); consult the British National Formulary (BNF).
PATIENT WELFARE AND CONCERNS
1.Clear and concise explanation of the rationale behind the use of anticoagulation, i.e. risk versus benefit and, in the case of anticoagulation, why the benefit outweighs the risk
2.Need to counsel the patient on the risks of anticoagulation (drug– food interactions/noncontact sports/regular blood tests/dentists, etc.)
3.Appreciate that the risk may be unacceptable to a patient who has capacity.
CANDIDATE EXPECTATIONS
1.Ensure that you ask questions that will demonstrate that you are assessing the risk of stroke and the risk of bleeding.
2.Ensure that you thoroughly explain the risks surrounding anticoagulation, but remind the patient that these risks are outweighed by the benefits in stroke risk reduction.
3.Show an awareness of the patient’ s autonomy.
H – Hypertension uncontrolled (systolic BP < 160)
A – Abnormal renal function: Dialysis, transplant, Cr > 2.26 mg/dL or > 200 µ mol/L Abnormal liver function
S – Stroke: Prior history of stroke
B – Bleeding: Prior major bleeding or predisposition to bleeding
L – Labile INR: (Unstable/high INRs), time in therapeutic range < 60%
E – Elderly: Age > 65 years
D – Prior alcohol or drug usage history (≥ 8 drinks/week) Medication usage predisposing to bleeding: (Antiplatelet agents, NSAIDs) Each point scores 1
CHADSVASC
C – Congestive heart failure (or left ventricular systolic dysfunction) scores 1
H – Hypertension: Blood pressure consistently above 140/90 mmHg (or treated hypertension on medication) scores 1
A – Age ≥ 75 years scores 2
D – Diabetes mellitus scores 1
S – Prior stroke or transient ischaemic attack (TIA) or thromboembolism scores 2
V – Vascular disease (e.g. peripheral artery disease, myocardial infarction, aortic plaque) scores 1
A – Age 65– 74 years scores 1
S ex C ategory – Females score 1
REFERENCES
Lip GY, et al (2010). Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: The Euro Heart Survey on atrial fibrillation. Chest 137(2): 263– 72.
National Institute for Health and Care Excellence. (2014) Guidance CG180. Preventing stroke in people with atrial fibrillation. Available from http://pathways.nice.org.uk/pathways/atrialfibrillation#path=view%3A/pathways/atrial-fibrillation/preventing-stroke-in-people-with-atrial-fibrillation.xml&content=view-node%3Anodes-anticoagulation-treatment. Accessed 24 August 2016.
Pisters R, et al. (2010) A novel user-friendly score (HAS-BLED) to assess 1-year risk of major bleeding in patients with atrial fibrillation. Chest 138 (5): 1093– 100.
This patient has noticed his vision has become blurred at times. Please ask any relevant questions and proceed as appropriate.
FOCUSED HISTORY
1.Duration of symptoms: Has there been a progressive change rather than sudden onset?
2.Has there been any visual loss?
3.Assess diabetic control.
4.Other microvascular complications: Nephropathy, neuropathy, autonomic dysfunction.
5.Macrovascular complications: Peripheral vascular disease, ischaemic heart disease, stroke.
FOCUSED EXAMINATION
•Eyes
•Glasses
•Visual acuity (ideally using a Snellen chart)
•Pupillary reactions
•Eye movements
•Fundoscopy
•Cataracts, features of diabetic retinopathy (nonproliferative, proliferative, maculopathy, photocoagulation scars)
•Extras
•Evidence of neuropathy
•Ask for blood glucose measurement, urine dipstick for proteinuria and blood pressure
QUESTIONS
1.What are the features of nonproliferative diabetic retinopathy?
•Microaneurysms (dot haemorrhages)
•Blot haemorrhages
•Hard exudates
•Soft exudates (cotton wool spots)
2.What are the features of proliferative diabetic retinopathy?
•Features of nonproliferative diabetic retinopathy, with evidence of new vessel formation.
•Photocoagulation scars are evidence of treatment.
3.What are the features of diabetic maculopathy?
•Any features of diabetic retinopathy at or near the macula.
•Most commonly, there is circinate formation of hard exudates.
4.What effect does glycaemic control have on the risk of diabetic retinopathy?
•This was assessed by the UK Prospective Diabetes Study (UKPDS) and the Diabetes Control and Complications Trial (DCCT).
•These studies showed that better glycaemic control lowers the risk of retinopathy. For example, a 10% reduction in HbA1c is associated with a more than 40% reduction in the development of retinopathy.
5.What else can be done to lower the risk of retinopathy in type 2 diabetes?
•Optimal treatment of hypertension
6.How is peripheral (nonmacular) diabetic retinopathy managed?
•Background retinopathy does not need treatment but should be monitored.
•If preproliferative retinopathy is severe, laser treatment may be considered.
•Proliferative retinopathy requires laser treatment.
•Severe proliferative retinopathy may not respond to laser treatment and may require vitrectomy.
PATIENT WELFARE AND CONCERNS
1.Vision: Concerns of visual loss?
2.Prevention: Prevention of further deterioration?
3.Treatment: Is treatment possible?
CANDIDATE EXPECTATIONS
1.Recognition that diabetic retinopathy can be asymptomatic or can present with visual disturbance
2.Recognition of the features of diabetic retinopathy
3.Understanding of the stages of diabetic retinopathy
4.Formulate the correct diagnoses and convey this to the patient
5.Generate a management plan, recognising when urgent intervention is necessary to save vision
REFERENCES
Diabetes Control and Complications Trial Research Group. (1995) The relationship of glycemic exposure (HbA1c) to the risk of development and progression of retinopathy in the Diabetes Control and Complications Trial. Diabetes 44(8): 968– 83.
Royal College of Ophthalmologists. (2012) Diabetic retinopathy guidelines. Available from https://www.rcophth.ac.uk/standards-publications-research/clinical-guidelines/. Accessed 5 July 2016. Stratton IM, et al. (2001) UKPDS 50: Risk factors for incidence and progression of retinopathy in type II diabetes over 6 years from diagnosis. Diabetologia 44(2): 156– 63.
UK Prospective Diabetes Study Group. (1998a) Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 38. BMJ ; 317(7160): 703– 13.
UK Prospective Diabetes Study Group. (1998b) Efficacy of atenolol and captopril in reducing risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 39. BMJ 317(7160): 713– 20.
This patient has been experiencing difficulty with closing their eyelids on one side. As a result, the eye is becoming dry and irritable. They are anxious to know the cause of the symptoms and what can be done. Please ask any relevant questions and proceed as appropriate.
FOCUSED HISTORY
1.Which eyelid is affected? What appears to be the problem? Does the eyelid shut at all, and if so, how much?
2.Duration of symptoms?
3.Are there any associated problems: speech, swallowing, taste or hearing impairment (tinnitus,* hyperacusis or deafness*)?
4.Any vertigo*/nausea*/vomiting or abnormality in gait* noted?
5.Any associated facial droop or distortion of the angle of mouth, change in taste?
6.Any recent viral (herpes) infection, surgery to the neck (parotid gland), inner ear or mastoid?
7.Medical history/family history: Neurofibromatosis ± acoustic neuroma with or without previous surgery.
*Be alert to these symptoms, as they may be indicative of acoustic neuroma.
FOCUSED EXAMINATION
•General
•Examine the patient at rest to assess facial symmetry.
•Any obvious drooping of the angle of the mouth, ptosis (unilateral). Ask patient to close their eyes. Assess ability to close fully. Is there a tarsorrhaphy scar?
•Movements
•Assess muscles supplied by facial nerve (demonstrate the movements yourself).
•Ask patient to squeeze their eyes tightly shut, raise their eyebrows, blow out their cheeks, smile and show you their teeth.
•Extras
•Look behind the ear for a mastoid surgery scar. Examine for any cranial scars from acoustic neuroma removal.
•Assess for any hearing disturbance (cranial nerve [CN] involvement).
•Assess gait (cerebellar/ataxic).
QUESTIONS
1.What are the causes of unilateral CN VII palsy?
•Upper motor neurone (UMN) lesion
•Cerebellopontine angle lesion (CNs V, VI, VII, VIII and loss of taste on anterior two-thirds of the tongue): Acoustic neuroma, meningioma
•Pontine lesion: Demyelination (multiple sclerosis [MS]), vascular lesion
•Lower motor neurone (LMN) lesion
•Bell’ s palsy: Most common cause; caused by herpes simplex type 1
•Ramsay Hunt’ s syndrome: Caused by herpes zoster virus
•Parotid gland tumour/surgery
•Facial neuroma
•Cholesteatoma
•Mononeuritis multiplex (diabetes, systemic lupus erythematosus [SLE], polyarteritis nodosa [PAN], sarcoid, amyloid, Wegener’ s granulomatosis): Remember WARDS PLC
•Trauma
2.What are the causes of bilateral LMN cranial nerve VII palsy?
•Motor neurone disease (MND).
•Guillain– Barré syndrome.
•Bilateral Bell’ s palsy.
•Myasthenia gravis.
•Sarcoidosis.
•Moebius syndrome (inherited rare form due to underdevelopment of cranial nerves VI and VII).
•Note that this question is another Practical Assessment of Clinical Examination Skills (PACES) ‘ classic’ .
3.Which condition is associated with an acoustic neuroma?
•Neurofibromatosis type 2: Defect on chromosome 22q12. This condition results in bilateral acoustic neuromas.
4.What is the management of an acoustic neuroma?
•Conservative: Observe the tumour size and growth.
•Radiotherapy: To retard tumour growth.
•Surgical resection.
PATIENT WELFARE AND CONCERNS
1.Aesthetic: Facial asymmetry secondary to the nerve palsy due to medical/surgical cause.
2.Will the facial nerve palsy resolve?
3.Is there any treatment for this?
4.Will the deafness resolve or will it be permanent? Is there any treatment for this?
CANDIDATE EXPECTATIONS
1.Obtain a thorough history of symptoms of a CN VII lesion.
2.Be aware of the range of causes leading to CN VII palsy.
3.Examine carefully to differentiate between UMN and LMN CN VII palsy.
4.Provide the patient with a clear explanation of the problem and the likely effects; e.g. if it is a Bell’ s palsy, there is a good chance of recovery. However, if it is a surgical consequence, then that is unlikely to be the case.
This 80-year-old male has been falling regularly at home. He has limited medical history (he has hypertension and diabetes mellitus, managed by his general practitioner [GP]) and hasn’ t ever been to hospital with the exception of having his appendix removed when he was 28. Please ask any relevant questions and proceed as you feel appropriate.
FOCUSED HISTORY
1.Need to establish exactly what occurs when the patient falls over. Does it sound like syncope or presyncope? Do they lose consciousness? If so, how quickly do they recover? (Need to be sure to rule out seizures.)
2.Ask about injuries postfall? Head injuries tend to indicate a loss of consciousness.
3.What environment are they in when they fall?
4.What had they been doing before each fall?
5.What are the precedent and antecedent symptoms?
6.How often do they fall?
7.Important: Past medical history/drug history will lead to many clues around the fall. For example, in this case the patient may be overtreated with antihypertensives and have postural hypotension or may have a sensory neuropathy from their poorly controlled diabetes.
8.Ask about their health in general. How far do they walk normally? (If they have severe osteoarthritis [OA], they are likely to have a degree of disuse myopathy and fall because of this.) What is their vision like? When was it last checked?
9.Ask about continence? Are they falling because they are rushing to the toilet because they have overactive bladder syndrome that is undiagnosed?
10.Make an enquiry about their social circumstances.
FOCUSED EXAMINATION
•General
•Comment on all/any injuries/bruises.
•Ask the patient to walk to assess gait (Parkinsonian/Marche à petits pas in vascular dementia).
•If possible, use your fundoscope to check for cataracts/look for signs of diabetic/ hypertensive retinopathy.
•Essential: Check postural blood pressure.
•Preform (or at least ask for) a finger-prick blood glucose check (note that diabetes can lead to both iatrogenic hypoglycaemia and autonomic neuropathy, which may result in falls).
•Look for proximal myopathy – common in older persons and often overlooked as a cause of falls.
•Cardiac
•Check pulse for arrhythmias.
•Listen for the murmur of aortic stenosis (syncope can be a symptom).
•Neurological
•Check for focal weakness/cerebellar signs.
•Examine for peripheral neuropathy that may be affecting sensory feedback.
QUESTIONS
1.How do you perform a lying and standing blood pressure?
•Lay patient down for 15 minutes and then take blood pressure.
•Stand patient.
•Take blood pressure at 1 minute.
•Take blood pressure at 3 minutes.
2.What constitutes a positive test?
•Systolic drop of 20 mmHg
•Diastolic drop of 10 mmHg
•Symptomatic patient (presyncopal)
3.What is the cause of this patient’ s fall?
•Falls are almost always multifactorial, particularly if there is no syncope; e.g. in this case, he could be falling because he has dyspraxia secondary to vascular cognitive changes, a proximal myositis because of the statin his GP has given him for primary prevention and possibly a postural drop and sensory changes associated with his diabetes mellitus (autonomic neuropathy).
•You may not be expected to get the full diagnosis (it may beyond the scope of the station), but it is important that you demonstrate a holistic approach to the case.
4.What is the best approach to managing a patient with falls?
•Multidisciplinary team (MDT): The patient will need assessment by an occupational therapist (OT), physiotherapist, optometrist, pharmacist, nurse and geriatrician. A comprehensive geriatric assessment is often needed, and this will be performed by all of the above (and more). Of note, there is evidence that balance training and tai chi reduce the frequency of falls.
PATIENT WELFARE AND CONCERNS
1.Is the patient’ s home environment safe? They may well benefit from a home visit by the OT to review their environment.
2.Consider if is it safe for the patient to drive if syncope is the cause (see ethics case on driving regulations in Station 4).
CANDIDATE EXPECTATIONS
1.Being holistic is most important.
2.You are unlikely to cover every aspect, but you should demonstrate that you are thinking about multiple potential causes.
3.You need to demonstrate an awareness of common problems that older persons who fall face.
4.Aim to be proactive when presenting the case. If they are falling regularly and at risk of osteoporosis, have you considered bone protection?
REFERENCE
Gillespie LD, et al. (2009) Interventions for preventing falls in older people living in the community. Cochrane Database Syst Rev 15(2): CD007146.
HEADACHE (IDIOPATHIC INTRACRANIAL HYPERTENSION)
This 30-year-old lady with a family history of diabetes mellitus had a glucose tolerance test 6 months ago and was found to have impaired fasting glycaemia. Since then, she has been complaining of headaches and visual disturbance, getting much worse in the last 2 weeks. She does not usually wear glasses and wants to know what can be done to improve the symptoms.
FOCUSED HISTORY
1.Nature of visual disturbance: Diplopia or blurred vision, floaters/flashing lights, visual loss
2.Duration of visual disturbance: Stable or deteriorating
3.Effect on visual acuity: Any recent eye tests
4.Headaches: Worse in morning, on bending/coughing/sneezing/vomiting, nausea
5.Associated symptoms: Paraesthesia, weakness, hearing disturbance
6.Relevant other history: Weight loss/gain, obstructive sleep apnoea, drug history (vitamin A derivatives, tetracyclines, oral contraceptive pill)
FOCUSED EXAMINATION
•General
•Obesity, any obvious cranial nerve palsies
•Eyes
•Enlarged blind spot, ophthalmoplegia (abducens nerve palsy)
•Fundoscopy
•Assess for papilloedema and optic atrophy
•Extras
•Check for scars from ventriculoperitoneal (VP) shunts. Ask for blood glucose measurement and blood pressure.
QUESTIONS
1.What are the causes of papilloedema?
•Space-occupying lesion (tumour/abscess): Idiopathic intracranial hypertension (IIH)
•Hypertensive encephalopathy
•Infection: Encephalitis, meningitis
•Vascular: Intra-/extra-axial haemorrhage, venous sinus thrombosis
•Drugs: Tetracyclines, vitamin A derivatives
2.What are the fundoscopic features of papilloedema?
•Disc hyperaemia, blurred margins, absent venous pulsation
•Elevation of the disc with obscured vessels at the disc margin
•Loss of the cup with obscured vessels in the disc
•Bulging disc with all vessels obscured (this will eventually lead to optic atrophy)
3.What are the causes of optic atrophy?
•Congenital
•Friedreich’ s ataxia, Leber’ s hereditary optic neuropathy
•Acquired
•Vascular: Ischaemic (including temporal arteritis)
•Inflammatory: Multiple sclerosis, Devic’ s disease
•Compression: Optic nerve tumour, Graves’ ophthalmopathy, glaucoma
•IIH (untreated)
•Nutritional deficiencies: Vitamin B12, folate
•Toxins: Tobacco, alcohol, ethambutol, ethylene glycol, lead, cyanide, carbon monoxide
•Infective: Syphilis
4.What treatments can be used to treat IIH?
•Medical
•Weight loss if obese
•Stop any contributing medications
•Diuretics, e.g. acetazolamide
•Steroids: Beneficial in inflammatory conditions/causes
•Repeated lumbar punctures
•Surgical
•Optic nerve sheath decompression and fenestration is performed if vision is severely affected or threatened.
•Lumboperitoneal/ventriculoperitoneal shunt.
PATIENT WELFARE AND CONCERNS
1.Concerns regarding the visual disturbance: Could I lose my sight?
2.Concerns regarding the associated headache: Is this a brain tumour?
3.How can you be certain that this is a benign condition and that there is no sinister underlying pathology?
4.What are the treatment options? Would having a shunt inserted require brain surgery?
CANDIDATE EXPECTATIONS
1.Obtain a thorough history regarding the visual disturbances and headache.
2.Identify features suggestive of raised intracranial pressure and/or a space-occupying lesion, e.g. weakness/paralysis, seizures.
3.Carefully assess visual acuity, visual fields and ocular fundi.
4.Explain the likely diagnosis of IIH, but make the patient aware of the need to exclude a space-occupying lesion.
5.Explain that treatment strategies involve both medical and surgical options.
This patient has a tremor and weight loss. Please ask any relevant questions and proceed as appropriate.
FOCUSED HISTORY
1.Is there any history of weight loss despite normal or increased appetite (caveat – occasionally some gain weight)?
2.Does the patient suffer from heat intolerance?
3.Do they sweat excessively?
4.Is there any history of GI upset, specifically diarrhoea?
5.Do they suffer from tachycardia or palpitations?
6.If they are female, ask about their menstrual cycle and specifically about oligomenorrhoea?
7.Do they suffer from anxiety and/or irritability?
8.Do they have a goitrous thyroid swelling?
9.Eye symptoms: Excessive watering, grittiness, redness, puffiness, change in field of vision? Eye pain (exophthalmos)? Ensure that you ask about all these even if no obvious eye signs are seen.
10.Ask the patient if they are on any medication: Beta-blockers – for anxiety symptoms and tachycardia; carbimazole/propylthiouracil – to block production of T4 and T3.
FOCUSED EXAMINATION
•Initial impression: Wide staring anxious expression – possible proptosis. Anxious fidgety demeanour, a peripheral tremor and goitre point towards a diagnosis of hyperthyroidism.
•Hands and arms: Acropachy (clubbing – rarely found and must have Graves’ ophthalmopathy), sweaty palms, tachycardia/arrhythmia, fine tremor, proximal myopathy.
•Eyes: Observe from the side and above for degree of proptosis. Observe from the front for lid retraction, oedema and tearing, and perform eye movements for lid lag and opthalmoplegia.
•Eye signs from any cause of thyrotoxicosis: Lid retraction (see the white of the eye above and below the iris), lid lag.
•Graves’ ophthalmopathy: Reddened eyes, excessive lacrimation, periorbital oedema, proptosis, conjunctival oedema and ophthalmoplegia
•Neck: Thyroidectomy scar, observe goitre while swallowing water, palpate goitre (diffuse or nodular) and palpate while swallowing water, palpate nodes, percuss the retrosternal extent of the thyroid. Auscultation for thyroid bruit.
•Legs: Pretibial myxoedema (rarely found and must have Graves’ opthalmopathy).
•Extras: Evidence of other autoimmune disease, especially vitiligo, as it is common and easily observed in PACES.
1.What are the causes of hyperthyroidism?
•Graves’ disease
•Toxic multinodular goitre
•Thyroid adenoma (toxic)
•De Quervain’ s thyroiditis (painful, fever at onset)
•Postpartum thyroiditis
•Drugs (amiodarone, rarely lithium)
2.What are the causes of a goitre?
•Nodular
•Multinodular goitre (especially iodine-deficient areas)
•Adenoma
•Carcinoma
•Diffuse
•‘ Simple’
•Graves’ disease
•Hashimoto’ s thyroiditis
•De Quervain’ s thyroiditis
•Thyroid lymphoma
3.What signs of thyroid disease are specific to Graves’ disease?
•Graves’ opthalmopathy – See above
•Thyroid acropachy
•Pretibial myxedema
4.What are the ‘ hyperthyroid emergencies’ ?
•Thyroid storm
•Exophthalmos causing fixed gaze, diplopia or decreased acuity or loss of colour vision (may lead to optic nerve compression)
•Cardiac failure (high output)
PATIENT WELFARE AND CONCERNS
•What treatment options are available?
•Is my condition curable?
•Is my condition life threatening?
CANDIDATE EXPECTATIONS
•Recognise early that the patient has thyroid disease.
•Assess the patient’ s thyroid status (hyper-/hypo-/euthyroid).
•Recognise signs specific to Graves’ disease.
•Be able to discuss treatment options with the patient and address their concerns.
This patient presents complaining of a neck lump. Please ask any relevant questions and proceed as you feel appropriate.
FOCUSED HISTORY
1.Ask the patient what their most concerning problem is.
2.Where in the neck is the lump? (Thyroid: Midline, and just above the clavicle; other lumps may be nodes; make sure you can describe the surface anatomy.)
3.How long has it been there? (Rapidly progressing lumps can be lymphoma or anaplastic thyroid carcinoma.)
4.Is the lump painful?
5.Does the patient suffer from dysphagia or dysphonia (hoarseness)?
6.Are there any other symptoms of thyroid disease?
•Over-/underactive
•Weight loss/gain, appetite
•Intolerance to heat/cold
•Mood instability, irritability
•Bowels: Diarrhoea/constipation
•Palpitations
7.Is there any family history of thyroid disease or malignancy?
8.Has there been any history of radiation exposure?
9.Is there any history of autoimmune disease? Type 1 diabetes mellitus, rheumatoid arthritis (RA), adrenal insufficiency, vitiligo, coeliac disease, pernicious anaemia, myasthenia gravis and multiple sclerosis
FOCUSED EXAMINATION
•General
•Evidence of hyperthyroid or euthyroid status, rarely hypothyroid
•Then proceed as per the hyperthyroidism case (hands, eyes, neck, legs)
•Additional extras
•Evidence of other autoimmune disease, especially vitiligo, as it is common and easily observed in PACES
QUESTIONS
1.What are the types of thyroid cancer?
•Papillary: Most common
•Follicular
•Medullary: Arise from parafollicular calcitonin-secreting C-cells
•Anaplastic: Most aggressive
•Lymphoma
•Metastases from other primaries (kidney most common)
2.What investigations are used to diagnose the cause of a thyroid mass?
•TSH, T3 and T4 (rarely malignant if thyroid dysfunction)
•Gold standard is ultrasound-guided fine needle aspiration (FNA)
•CT useful to show the extent of a goitre causing compressive symptoms to trachea, or staging for malignancy
PATIENT WELFARE AND CONCERNS
1.What is the cause? Is this a cancerous lump, and how will this be differentiated from something that is noncancerous?
2.Cosmetic: Address concerns about how this lump sticks out and if it will be fully treated. Will it need surgery?
3.Associated features: Hoarse voice, swallowing difficulties and symptomatic thyroid disease. Are these all treatable?
CANDIDATE EXPECTATIONS
1.Look out for any red-flag symptoms of malignancy, such as weight loss and strong family history. Poor prognostic indicators for thyroid malignancy include: rapid enlargement, hoarse voice, age, sex (male) and type of cancer (papillary carcinoma has the best outcome, anaplastic has the worst).
2.Thoroughly assess a thyroid mass and examine for any associated features of thyroid disease.
3.Aim to reach a diagnosis and convey this to the patient, along with the management plan that will follow. Address each of the different investigations and what these will help to elicit.
4.Address the patient’ s concerns, ranging from the concern that they may think that it’ s cancer to any cosmetic concerns. Reassure the patient that thyroid malignancy is just one of many causes of a thyroid mass, and is not the most common cause. However, you need to rule this out if there is nodule.
This 82-year-old female has recently been diagnosed with polymyalgia rheumatica and started on prednisolone tablets. She has a past history of chronic lower back pain for which she takes several painkillers. She has presented today with worsening backache and wants to know what more can be done about it. Of note, she is known to be diabetic.
FOCUSED HISTORY
1.Is the diabetes a red herring, or it is pertinent to the history?
2.Duration of current episode of back pain: Onset (acute/sudden or gradual worsening), severity (pain score), character, site and radiation. Has the pain ever been this severe in the past? Analgesic history.
3.Precipitating factors: Heavy lifting/fall/trauma.
4.Neurological symptoms: Paraesthesia/weakness or paralysis in lower limbs, bladder or bowel dysfunction.
5.Red-flag symptoms: Weight loss, nocturnal pain and fevers.
6.Relevant other history: Risk factors for osteoporosis (steroid use, immobility, family history), hypertension.
FOCUSED EXAMINATION
•General
•Examine patient standing: Obvious spinal deformity, skin/palmar pigmentation if pigmented appearance, central obesity, round face, thin skin, bruising
•Spine
•Palpate vertebrae to localise symptoms; assess spinal movements as far as able.
•Limbs
•Focused assessment of power in lower limbs, sensation and gait
•Extras
•State you would examine perineum for perianal sensation and anal sphincter tone. Ask for blood glucose measurement and blood pressure reading.
QUESTIONS
1.Assuming her back pain is caused by an osteoporotic fracture, should the patient in this case have medical management of osteoporosis?
•Patients with fragility fractures over the age of 75 should have treatment regardless of dual-energy X-ray absorptiometry (DEXA) results. Review the NICE guidance on this.
2.What are the risk factors for developing osteoporosis?
•Family history
•Disease associations: Cushing’ s syndrome, malabsorption, hyperparathyroidism, chronic inflammatory arthropathy
•Toxins: Excess alcohol or caffeine intake, smoking
•Prolonged immobility or inactivity
•Underweight
•Early menopause, late menarche, postmenopause, bilateral oophorectomy, hypogonadism in males
•Drugs: Prolonged steroid use (> 7.5 mg prednisolone daily for 6 months), prolonged use of low-molecular-weight heparin
3.What strategies can be used in the treatment of osteoporosis?
•Lifestyle changes: Nutrition, exercise
•Prevent falls: Appropriate footwear, OT/physio assessments (home adnum-justments), avoid sedative medications
•Drug therapies
•Reduce bone resorption: Bisphosphonates (zoledronic acid, ibandronic acid, alendronic acid), raloxifene (selective oestrogen reuptake inhibitor), calcitonin
•Aid new bone formation: Calcium and vitamin D supplements
•Reduce bone resorption and increase new bone formation: Strontium ranelate, teriparitide (recombinant parathyroid hormone [PTH]), denusomab (receptor activator of nuclear factor kappa-B ligand [RANKL] inhibitor)
PATIENT WELFARE AND CONCERNS
1.Concerns regarding the chronic back pain and the need for a diagnosis.
2.The impact of the back pain on daily life and ability to work.
3.Is there a treatment, medical or surgical, other than simple analgesia, for the back pain/osteoporosis?
CANDIDATE EXPECTATIONS
1.Obtain a thorough history of the back pain and quickly rule out ‘ red-flag signs’ .
2.Rule out spinal cord compression in all patients presenting with worsening back pain.
3.Search for causes of osteoporosis if the patient has had an osteoporotic compression fracture leading to the back pain (in this case, possible Cushing’ s).
4.Thoroughly examine any deformity of the spine and the range of spinal movements. Check for any neurological deficit and offer to check for perianal sensation and tone.
5.Explain the likely diagnosis.
6.Explain that bisphosphonates are first-line agents in the management of osteoporosis, for both treatment and prevention of further fracture.
REFERENCE
National Institute for Health and Care Excellence. (2014). Guidance CG146. Osteoporosis: Assessing the risk of fragility fracture. Available from https://www.nice.org.uk/guidance/cg146. Accessed 24 August 2016.
This lady has been recently seen by her doctor for generalised aches and pains present for several months. She is now complaining of weakness in her limbs. She is housebound due to severe osteoarthritis and often does not go out for weeks at a time. Please ask any relevant questions and proceed as you feel appropriate.
FOCUSED HISTORY
1.What is the nature of the weakness? Is it symmetrical, and which limbs are affected? Is it proximal/distal/widespread?
2.How long has the weakness been present? How rapidly has it progressed?
3.Has there been any associated muscle wasting? Are the muscles tender?
4.Ask what impact the symptoms have on daily life to help decipher the pattern of weakness.
Proximal myopathy: Difficulty getting up out of chairs, washing and dressing, combing hair
Distal weakness: Difficulties with fine movements/tasks (writing, doing up buttons)
5.Which joints are involved? Any symptoms suggestive of synovitis?
6.Drug history: Prolonged steroid use, statin therapy, vitamin D supplement.
7.Sinister symptoms: Weight loss, fevers, speech/swallowing impairment, bladder/ bowel dysfunction.
FOCUSED EXAMINATION
•General
•Gait should be normal.
•There should not be any evidence of fasciculation on inspection.
•Observe any areas of muscle wasting/disuse atrophy.
•Evidence of trauma/deformity.
•Palpation
•Check that the muscles are not tender to palpation.
•Assess muscle power throughout each limb. Pay close attention for proximal muscle weakness; power will be reduced in affected areas, and the signs will be symmetrical.
•If a chair is available, ask the patient to sit on it and get up off it without using their hands.
•Extras
•Examine the spine for any obvious deformity.
•Examine the hands: Rule out dermatomyositis, rheumatoid disease.
•The differential diagnosis here is wide. A detailed drug history is crucial to eliminate a drug cause, for example, statin-induced myopathy. In a housebound individual who has little sunlight exposure, never forget vitamin D deficiency as a cause of proximal myopathy.
QUESTIONS
1.What are the manifestations of vitamin D deficiency?
•Rickets: Impaired growth and deformity of long bones in children
•Osteomalacia: Reduced bone mineralisation resulting in proximal muscle weakness
•Osteoporosis: Reduced bone density and increased fracture risk
2.What are the risk factors for vitamin D deficiency?
•Nutritional/poor dietary intake
•Malabsorption syndromes
•Reduced sunlight exposure
•Darker skin pigmentation
•Lack of vitamin D in breast milk
•Renal/liver impairment
•Enzyme-inducing medication (e.g. anticonvulsant medications)
3.What are the biochemical features of vitamin D deficiency?
•Reduced serum vitamin D levels
•Reduced serum calcium levels
•Reduced serum phosphate levels
•Raised alkaline phosphatase (ALP)
•Raised PTH (secondary hyperparathyroidism)
PATIENT WELFARE AND CONCERNS
1.What is the cause of the weakness? Is this reversible?
2.Will they lose their independent mobility?
3.Seriousness of the pathology: Is there an underlying sinister cause?
4.How long will the symptoms take to recover following initiation of treatment?
CANDIDATE EXPECTATIONS
1.Be aware of the range of differential diagnoses contributing to proximal muscle weakness.
2.The key in this case is to take a focused history around the causes of a proximal muscle weakness to help rule in/out a diagnosis.
3.Examine the important areas of each system that help confirm the diagnosis.
4.Formulate the correct diagnosis and convey this to the patient.
5.Reassure the patient that there are many causes of a proximal myopathy, and most of them are readily treatable; however, the main part of the management will be rehabilitation.
This patient has attended complaining of a significant change in the appearance of her nails. She is becoming increasingly distressed by the problem, which seems to be worsening despite several treatments by the GP. She has also noticed pain and swelling in her hands, which is impacting on her job as a seamstress.
FOCUSED HISTORY
1.Duration of symptoms
2.Nails: Colour, change in appearance, brittleness, extent of the nail involved, nail-bed involvement, number of nails involved, history of trauma, treatments tried by GP
3.Skin changes: Plaques/scales, pustules, sites of skin involvement, itchy/dry skin
4.Joints: Sites of arthritis (hands, feet, spine, hips), swelling, tenderness, deformity
5.Impact of illness on lifestyle
6.Family history of psoriasis/arthritis
FOCUSED EXAMINATION
•Hands
•Nail changes: Discolouration, pitting, onycholysis, hyperkeratosis of nail bed
•Joints
•Polyarthritis, distal interphalangeal joint arthritis, arthritis mutilans
•Skin
•Inspect the back, abdomen, extensor and flexor surfaces, scalp and posterior aspect of ears
•Plaque psoriasis: Shiny, scaly, white plaques
•Guttate: Numerous widespread, erythematous small ‘ teardrop’ lesions
•Pustular: Widespread red pustules (often tender)
•Flexural: Plaques/areas of inflammation at limited sites
•Other joints
•Spine and sacroiliac joint involvement
•Asymmetrical oligoarthritis (examine joints highlighted in history)
QUESTIONS
1.What are the causes of psoriasis?
•Possibly immune-mediated via T-cell-stimulated cytokine release causing excess proliferation and production of skin cells within the dermis
•Genetic susceptibility: Major histocompatibility complex (MHC) antigen mediated
•Poststreptococcal infection (especially guttate form)
•Drug related
2.What treatments are used in the management of psoriasis?
•Moisturising creams
•Topical treatments: Coal tar, dithranol, steroids (usually short term), vitamin D analogues (calcipotriol) and calcineurin inhibitors (e.g. tacrolimus cream)
•Phototherapy: ultraviolet B (UVB)
•Photochemotherapy: Psoralen and ultraviolet A (PUVA)
•Medications
•Oral steroids
•Disease-modifying antirheumatoid drug (DMARDs): Methotrexate and ciclosporin are most commonly used
•Vitamin A analogue: Acitretin
•Biological agents: Anti-TNF therapy, e.g. adalimumab, and monoclonal antibodies, e.g. infliximab
3.How is psoriatic arthritis managed?
•In patients with psoriatic arthritis who also have severe skin/nail disease, collaboration should take place between rheumatology and dermatology, as systemic therapy may address both areas.
•The following guidance is targeted at predominantly peripheral arthritis (axial disease is managed more similarly to ankylosing spondylitis):
•NSAIDs
•DMARDs: Methotrexate, sulfasalazine, leflunomide, ciclosporin
•Biologics: Infliximab, etanercept, adalimumab, golimumab
PATIENT WELFARE AND CONCERNS
1.Cosmetic/aesthetic concerns regarding plaques, nail changes and joint involvement
2.Impact of arthropathy on job
3.Curative or symptomatic control only
4.Duration of treatment (particularly immunosuppression) – short course versus lifelong
5.Number of medications needed to control/abate symptoms
6.Long-term effects and risks of newer biological agents – susceptibility to infection, risk of malignancy
CANDIDATE EXPECTATIONS
1.Take a relevant history regarding the nails and skin lesions.
2.Obtain a detailed history for arthritis.
3.Be able to differentiate rapidly from the history whether this is likely to be an inflammatory or degenerative joint problem.
4.Examine the psoriatic plaques appropriately commenting on colour, location, size of area and distribution affected, using correct terminology.
5.Explain the diagnosis to the patient of psoriasis and the possible association between psoriasis and arthropathy.
6.Explain there are both local and systemic treatments that can be used to control symptoms.
REFERENCES
Coates LC, et al. (2013) The 2012 BSR and BHPR guideline for the treatment of psoriatic arthritis with biologics. Rheumatology (Oxford) 52(10): 1754– 7.
DermNetNZ. (2015) Treatment of psoriasis. Available from http://www.dermnetnz.org/scaly/psoriasis-treatment.html. Accessed 5 July 2016.
National Institute for Health and Care Excellence. (2012) Guidance CG153. Psoriasis: Assessment and management. Available from https://www.nice.org.uk/guidance/Cg153. Accessed 5 July 2016.
RHEUMATOID ARTHRITIS WITH CARPAL TUNNEL SYNDROME
This patient has been complaining of a recent history of dropping objects. Ask any relevant questions and proceed as you feel appropriate.
FOCUSED HISTORY
1.Which hand is dominant?
2.One or both hands affected?
3.Duration of symptoms: Worsening or stable.
4.History of trauma or injury to hand/arm/shoulder.
5.Associated pain/numbness/paraesthesiae (including distribution).
6.Joint synovitis, muscle wasting, early morning stiffness.
7.Extent of weakness: Functional limitations, impact on quality of life (QOL)/ activities of daily living (ADLs).
8.Any other joint involvement?
9.Constitutional symptoms: Fever, weight loss.
10.Any other system involvement?
11.Drug history.
12.Family history of RA or autoimmune conditions.
FOCUSED EXAMINATION
•General
•Evidence of rheumatoid arthritis, acromegaly, thyroid disease or pregnancy
•Hands
•Symmetrical arthropathy
•Thenar eminence wasting
•Deformity: Ulnar deviation, metacarpophalangeal joint (MCPJ) subluxation, swan neck, boutonniè re, Z-thumb
•Evidence of scars from previous tendon release or nerve decompression surgery
•Palpation
•Hand, wrist and elbow joints: Check for evidence of active synovitis.
•Movements
•Test specifically the lumbricals, opponens pollicis, abductor pollicis brevis and flexor pollicis brevis.
•Assess function: Doing up a button, gripping a key and opening a door handle.
•Neurological
•Phalen’ s and Tinel’ s tests to assess the median nerve
1.What are the diagnostic criteria for rheumatoid arthritis?
American College of Rheumatologists Criteria (2010)
Classification criteria for RA (Score-based algorithm: Add score of Categories A– D. A score of ≥ 6/10 is needed for classification of a patient as having definite RA.) |
||
A. Joint involvement |
||
|
1 large joint |
0 |
|
2-10 large joints |
1 |
|
1-3 small joints (with or without involvement of large joints) |
2 |
|
4-10 small joints (with or without involvement of large joints) |
3 |
|
>10 joints (at least one small joint) |
5 |
B. Serology (at least one test result is needed for classification) |
||
|
Negative rheumatoid factor (RF) and negative anticitrullinated protein antibody (ACPA) |
0 |
|
Low-positive RF or low-positive ACPA |
2 |
|
High-positive RF or high-positive ACPA |
3 |
C. Acute-phase reactants (at least one test result is needed for classification) |
||
|
Normal CRP and normal ESR 0 |
0 |
|
Abnormal CRP or normal ESR 1 |
1 |
D. Duration of symptoms |
||
|
< 6 weeks |
0 |
|
≥ 6 weeks |
1 |
2.What are anticyclic citrullinated peptide (anti-CCP) antibodies?
•Antibody markers used for the diagnosis of rheumatoid arthritis
•Aid assessment of likely future progression to RA, in undifferentiated arthritis
•More sensitive (~70%– 75%) and specific (~95%– 98%) than immunoglobulin (Ig) M rheumatoid factor antibodies
•Prognostic value as marker of erosive disease
3.What biological therapies are available for the treatment of rheumatoid arthritis?
•TNF-? blockers: Infliximab, adalimumab, etanercept
•Monoclonal B-cell (anti-CD20) antibodies: Rituximab
•IL-6 inhibitor: Tocilizumab
4.What are the serious side effects associated with the use of biological therapies?
•Opportunistic infections: Fungal, bacterial, viral (e.g. severe infection with varicella-zoster virus).
•Activation of latent TB ± progression to miliary TB.
•Anaphylaxis.
•Increased risk of skin cancer.
•Central nervous system demyelinating disorders (anti-TNF).
•Anti-TNF and rituximab should not be used in Stage 3/4 NYHA heart failure.
1.Concerns regarding the impact of an inflammatory arthropathy on daily life and the possible cosmetic effects of deformities
2.Concerns regarding systemic extra-articular manifestations
3.Impact of DMARDs/biological agents and their side effects
4.Risks to offspring in terms of passing on the condition and their chances of developing rheumatoid arthritis in the future
CANDIDATE EXPECTATIONS
1.Obtain a thorough history regarding the extent of joint involvement and duration of symptoms that clearly points to a diagnosis of inflammatory arthritis.
2.Ascertain the impact of symptoms on daily life. Can the patient still function as normal?
3.Thoroughly examine all affected joints. Assess active synovitis and identify any associated extra-articular manifestations.
4.Explain the likely diagnosis of rheumatoid arthritis.
5.Explain that management is a multidisciplinary team approach with physiotherapists, occupation therapists and nurse specialists involved, etc. Treatment strategies include anti-inflammatory agents, disease-modifying agents and biological agents. (There are NICE criteria for guidance on biologics use.)
REFERENCE
Funovits J, et al. (2010) The 2010 American College of Rheumatology/European League Against Rheumatism classification criteria for rheumatoid arthritis: Methodological report phase l. Ann Rheum Dis 69: 1589– 95.
This patient has been complaining of colour changes in her fingers and difficulty moving them. Please ask any relevant questions and proceed as appropriate.
FOCUSED HISTORY
1.How long have these symptoms been going on for?
2.Have they noticed any changes in their skin over the fingers or elsewhere in the body?
3.Any discolouration of the skin anywhere on the body?
4.Any red patches (telangiectasiae)?
5.Any hard deposits anywhere, especially the fingers?
6.Any shortness of breath that is new or that is getting worse?
7.Any chest pain, swelling of legs or palpitations?
8.Any heartburn or difficulty swallowing?
9.Any joint pains or stiffness?
10.Any generalised symptoms, such as fatigue, difficulty sleeping, depression, anxiety, weight loss and malaise?
FOCUSED EXAMINATION
•Hands
•Sclerodactyly (thickened, tight skin), calcinosis, evidence of Raynaud’ s, digital ulcers, telangiectasia.
•Assess the patient’ s hand function.
•In someone with colour change in hands/digital ulcers, always assess the pulses.
•Face
•Telangiectasiae, microstomia
•Lungs
•Fine end inspiratory crackles in keeping with pulmonary fibrosis or evidence of pulmonary hypertension (loud P2, parasternal heave, raised JVP, tricuspid regurgitation and peripheral oedema)
•Extras
•Ask for blood pressure and urine dip (renal failure)
QUESTIONS
1.How is scleroderma classified?
•Localised scleroderma
•Localised skin involvement without internal organ involvement
•Limited systemic sclerosis (SSc) (previously also known as CREST syndrome)
•Calcinosis, Raynaud’ s phenomena, oesophageal dysmotility, sclerodactyly, telangiectasiae
•Skin changes limited to hands, forearms, feet, neck and face
•Risk of pulmonary hypertension
•Diffuse systemic sclerosis
•Skin changes proximal to the elbows or knees, face or neck
•Can develop pulmonary fibrosis, scleroderma renal crisis or cardiac involvement
2.Which other organs are affected?
•Kidneys: Scleroderma renal crisis (occurs in 5%– 10% of SSc patients, who may present with an abrupt onset of hypertension, acute renal failure, headaches, fevers, malaise, hypertensive retinopathy, encephalopathy and pulmonary oedema)
•Lungs: Pulmonary hypertension, pulmonary fibrosis
•Cardiac: Pericardial effusions, myocardial fibrosis, conduction defects, congestive cardiac failure
3.What are the treatment options?
•Raynaud’ s: Calcium channel blockers, e.g. nifedipine, ARB, e.g. losartan, intravenous prostacyclin (iloprost), bosentan (a dual endothelin-1 receptor antagonist).
•Reflux/oesophageal dysmotility: Proton pump inhibitors, H2 antagonists.
•Hypertension/renal protection: ACE inhibitors.
•Skin/joint/lung: Immune modulation – steroids, steroid-sparing agents, cyclophosphamide.
•Surgical option includes digital sympathetomy.
•Smoking cessation is key.
4.What immune tests can be used to help identify the cause?
•Diffuse systemic sclerosis: Anti-SCL-70 antibodies (against topoisomerase I)
•Limited systemic sclerosis: Anticentromere antibodies
•U1-RNP: Indicative of a mixed connective tissue disorder (systemic sclerosis, SLE, polymyositis)
PATIENT WELFARE AND CONCERNS
1.Concerns regarding skin changes in hands
2.Is the reflux an unrelated separate issue to the Raynaud’ s/skin features?
3.What are the other complications of the condition, and are they treatable/curable?
4.What is the prognosis of the condition if there are cardiac, renal or pulmonary manifestations?
5.How will this condition affect life expectancy?
CANDIDATE EXPECTATIONS
•Obtain a thorough history of the skin features.
•Recognise that the patient has Raynaud’ s and look for an underlying cause of this.
•Realise that the Raynaud’ s is associated with underlying systemic sclerosis.
•Examine the hands and face and other systems that can be affected by systemic sclerosis.
•Explain the likely diagnosis and what investigations will need to be carried out to determine this.
•Explain the range of treatment options, depending on the severity of the disease and the importance of preventing disease progression.
THIRD NERVE PALSY OR PATIENT PRESENTING WITH DIPLOPIA
This 56-year-old male presents with diplopia, and his wife says his eye looks ‘ funny’ . He has brittle diabetes and hypertension. Take a focused history and perform a focused examination to determine the diagnosis and formulate a management plan.
FOCUSED HISTORY
1.When did this occur? (Note that it may be congenital.)
2.Describe the onset of diplopia (sudden vs. gradual).
3.Is there a specific direction of vision where the diplopia occurs?
4.Is there associated pain/headache?
5.Enquire about symptoms of raised intracranial pressure. Headache that is worse in the morning? Vomiting?
6.Need to review past medical history specifically focusing on diabetes/prior neurosurgery/multiple sclerosis/autoimmune disorders/hypertension.
FOCUSED EXAMINATION
•Note: Do not waste your time performing a full cranial nerve examination.
•Observe for unilateral ptosis, dilated pupil and deviation of the eye laterally and downward (due to unopposed actions of lateral rectus and superior oblique).
•Observe for stigmata of diabetes, e.g. finger-prick blood glucose testing.
•Formally examine eye moments and check cranial nerves IV and VI at the same time.
•If you suspect a surgical third nerve palsy, then perform (or mention that you would like to perform) fundoscopy to observe for signs of raised intracranial pressure (i.e. papilloedema).
•Be sure to differentiate (via your examination) whether this is ‘ medical’ third nerve palsy or a ‘ surgical’ third nerve palsy.
•A medical third nerve palsy will usually be pupil sparing, and surgical third nerve palsy will not
QUESTIONS
1.Explain the difference between a ‘ medical’ and ‘ surgical’ third nerve palsy?
•Medical third nerve palsy tends to be pupil sparing, and surgical third nerve palsies lead to a dilated pupil. This is because surgical third nerve palsies are due to compressive effects on the sympathetic fibres that run along the outside of the nerve bundle that go on to supply the iris. As such, the pupil will be dilated early in a surgical palsy (note that in a medical palsy, the pupil can also become dilated).
2.What are the medical causes of a third nerve palsy?
•Diabetes mellitus
•Infection
•Demyelinating disease
•Autoimmune disease
•Cavernous sinus thrombus
3.What are the surgical causes of a third nerve palsy?
•Aneurysm or bleed from the posterior communicating artery
•Postneurosurgery
•Posttrauma
•Congenital cause
4.Why does an oculomotor palsy lead to ptosis?
•In addition to supplying the intrinsic muscle of the eye, the oculomotor nerve also supplies levator palpebrae superioris.
1.Be sympathetic if talking about prognosis. Medical causes may partially resolve with time. Prognosis with surgical causes is variable.
2.If talking about reconstructive eye lid surgery in chronic oculomotor palsy cases, remain empathetic regarding the appearance.
CANDIDATE EXPECTATIONS
1.Demonstrate the signs of oculomotor palsy.
2.Differentiate between surgical and medical causes.
BRIEF CLINICAL ENCOUNTERS STATION SUMMARY
•It is crucial to dedicate substantial revision time to Station 5.
•Be sure to look out early for ‘ spot diagnoses’ .
•Any obvious signs may help guide towards a relevant history.
•In a case of back pain (such as ankylosing spondylitis), be sure to rule out spinal cord compression/cauda equine.
•There no set time to be spent on history and examination. This must be managed by the candidate on a case-by-case scenario. If there are likely to be many relevant signs, ensure that you demonstrate them.
•In cases of diabetes, always consider other micro- and macrovascular complications.
•Be able to assess a patient’ s thyroid status clinically.
•In a case of psoriasis, always look for evidence of arthritis.
•In any joint disorder, it is crucial to assess function.
•Take note of any patient concerns throughout and attempt to resolve them later in the consultation.