Clinical consultation viva facts Flashcards

1
Q

Besides apical fibrosis, are there any other causes in ankylosing spondylitis that could result in breathlessness?

A

Anaemia - may be related to a microcytic anaemia secondary to NSAID use or anaemia of chronic disease.

Mechanical restriction secondary to fusion of the spine causing a restriction.

Malignancy.

Cardiac causes: aortic regurgitation which has a known association with ankylosing spondylitis.

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2
Q

What investigations would you recommend in a patient you suspect has ankylosing spondylitis?

A

Bloods: CRP / ESR (for evidence of disease activity), FBC, UEs and LFTs (thinking about future treatments / NSAIDs). HLA-B27 test.

Imaging: XRs of spine and pelvis (looking for sacroiliitis and fusion in the spine). Consider MRI spine if XRs normal.

Special tests: pulmonary function tests (spirometry and transfer factor may differentiate pulmonary fibrosis from mechanical restriction), high-resolution CT, ECG, echo, observations including o2 sats

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3
Q

What pulmonary function abnormalities might you expect in a patient with ankylosing spondylitis and SOB?

A

I’d expect to see a restrictive pattern. That is a reduced FEV1 and FVC with a maintained ratio.

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4
Q

Is there any way to tell the difference between pulmonary fibrosis, and a mechanical restriction due to the thorax being fused, using PFTs?

A

Look closely at the transfer factor.

In mechanical restriction, would expect the transfer factor to be preserved due to the normal underlying lung, however in pulmonary fibrosis, would expect it to be reduced due to the underlying damaged lung.

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5
Q

What treatments are available for ankylosing spondylitis?

A

Non-pharmacological: patient education, physiotherapy, OT, hydrotherapy, smoking cessation, calculate BASDAI score (>4 = active disease)

Pharmacological: NSAIDs (ibuprofen / naproxen), MTX / sulfasalazine, anti-TNF agents in refractory disease (adalimumab / etanercept)

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6
Q

Do you know of any pre-treatment considerations before considering anti-TNF treatments?

A

Immunisations

Screening for latent or active TB (bloods / CXR)

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7
Q

How would you investigate a patient in hospital for whom you suspect has Crohn’s colitis?

A

Full set of observations - looking for signs of sepsis.

Bedside: stool sample for faecal calprotectin, stool culture

Bloods: FBC (anaemia), WCC and neutrophils (infection), U+Es (looking for signs of dehydration and the need for electrolyte replacement), and baseline LFTs.

Imaging: AXR (looking for evidence of dilatation).

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8
Q

How would you manage a patient presenting with an acute flare of Crohn’s disease?

A

Analgesia, IV hydrocortisone and IV abx dependent on baseline investigations.

IV fluid replacement and consider electrolyte replacement.

Start LMWH due to increased risk of VTE.

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9
Q

What complications of Crohn’s disease would prompt you to make a surgical referral?

A

Evidence of dilatation on the AXR.

Evidence of fistulating disease.

Refractory to full medical management.

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10
Q

How would you manage a patient hospitalised for an acute flare of Crohn’s disease on discharge?

A

IBD nurse and dietician input.

Long-term tapering dose of steroids.

Calcium and vit D replacement.

Refer to gastroenterology to consider escalation of treatment (anti-TNF agents).

Consider referral for flexible sigmoidoscopy.

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11
Q

What are the differences in endoscopic appearances of Crohn’s disease and UC?

A

Crohn’s: aphthous ulcers, cobble stoning, skip lesions, transmural inflammation. May be isolated involvement of the terminal ileum and normal rectum.

UC: more superficial inflammation, restricted to sub-mucosa or mucosa only, and evidence of crypt abscesses.

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12
Q

What would you receommend in terms of screening for malignancy in patients with IBD?

A

After 10 years of onset of symptoms, patients are recommended to have an index surveillance colonoscopy looking for signs of malignancy with appropriate biopsies.

Further colonoscopic investigations are then carried out dependent on the patient’s risk level at that stage.

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13
Q

Describe the clinical features of pseudoxanthoma elasticum (PXE)

A

Skin: Small, yellowish papular lesions on skin.
Cutaneous laxity affecting neck, axillae, groin and flexural creases.

Eyes: ‘Peau d’orange’ on Bruch membrane of retina.
Angioid streaks on retina with retinal haemorrhages.

GI: gastric bleeding

Vascular: intermittent claudication, angina and MI, stroke. IC haemorrhage and SAH.

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14
Q

What is the genetic mutation associated with pseudoxanthoma elasticum?

A

Genetic disease that causes mineralisation of elastic fibres in some tissues.

Most signs are in the skin and eyes, and later in the blood vessels (premature atherosclerosis).

PXE is caused by autosomal recessive mutations in the ABCC6 gene.

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15
Q

Do you know of any risk stratification tools that can be used to assess bleeding risk for patients on warfarin?

A

HASBLED score: takes into account HTN, renal and liver failure, age, drug use, alcohol, labile INRS and anticoagulant use. Scored out of 9, if patient scores 3 or more, caution with anticoagulation is advised.

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16
Q

Do you know of a tool you can use to predict stroke risk for patients with AF?

A

CHA2DS2-VASc score

Score out of 9, the higher the score the greater the risk of stroke. Dependent on the score, a percentage stroke risk per year for a patient is given.

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17
Q

Under what circumstances would you use NOACs over warfarin?

A

Clinician-dependent and local guideline-dependent.

NOACs may be indicated if a patient struggles to attend appointments for blood tests, if they had a CV event on warfarin, if they have labile INRs, or cognitive impairment.

Disadvantages of NOAC: compliance is required (if miss a dose, do not receive benefit), not all are safe in renal failure.

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18
Q

How would you manage a patient with suspected ACS?

A

Bedside: o2 if hypoxic, BP both arms, 12-lead ECG, history and systems exam.

Bloods: IV access and send troponin, Hb, VBG, glucose, cholesterol and renal function.

Imaging: CXR (heart failure, mediastinal widening, consolidation).

If ACS diagnosis confirmed with CP, ECG changes and / or trop rise, I would give 300mg aspirin, analgesia, antiemetics, GTN spray, telemetry.

Start on beta-blockers, ACEi and a statin.

If NSTEMI / unstable angina, risk stratify with GRACE score which predicts 6-month mortality and use this to guide further management (i.e., the need for angiography, clopidogrel, anti-thrombin and glycoprotein II agents)

If STEMI, liaise urgently with nearest PCI team.

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19
Q

What medications are prone to causing oesophagitis?

A

NSAIDs, doxycycline, bisphosphonates.

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20
Q

What medications relax the lower oesophageal sphincter and predispose to reflux?

A

Nitrates
CCBs
Anticholinergics (TCAs)

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21
Q

What are the immunological associations with ankylosing spondylitis?

A

Seronegative spondyloarthropathy

HLA-B27 positive in >90% of individuals

TNF alpha and interleukin-1 also implicated in disease activity

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22
Q

Differential diagnosis for sacroiliitis?

A

Psoriatic arthritis

Enteropathic arthritis

Reactive arthritis

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23
Q

How is the diagnosis of ankylosing spondylitis made?

A

Mainly clinical from history and examination, with supporting radiological evidence.

Young patients <40y, possible FH.

Plain radiograph: erosions, fibrosis / sclerosis of SI joints, squaring of vertebrae ‘bamboo spine’.

Bloods: raised ESR / CRP, normocytic anaemia (of chronic disease)

Genetic testing: HLA-B27

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24
Q

What is the treatment for ankylosing spondylitis?

A

Physio, exercise, smoking cessation.

Analgesia: NSAIDS

Corticosteroid injections

Biologics: etanercept, adalimumab, infliximab (anti-TNF for axial disease once failed 2 NSAIDs at max dose for 4 weeks).

Treat complications such as iritis / osteoporosis. Liaise with other specialties for treatment of complications.

Calculate BASDAI score to guide management.

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25
Q

What are the extra-articular manifestations of ankylosing spondylitis? (7 A’s)

A

Anterior uveitis
Aortitis / aortic regurgitation
Apical fibrosis
AVN block
Amyloidosis (secondary)
Atlantoaxial dislocation
IgA nephropathy

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26
Q

What disease-scoring system can be used for ankylosing spondylitis?

A

Bath ankylosing spondylitis disease activity index (BASDAI)

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27
Q

What changes woudl you see on spine XR in ankylosing spondylitis?

A

Bilateral sacroiliac erosive changes with eventual fusion of the sacroiliac joint.

Syndesmophytes bridge multiple vertebrae causing a ‘bamboo spine’ appearance.

Squaring of vertebral bodies on lateral film.

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28
Q

What diagnostic criteria are used in rheumatoid arthritis?

A

ACRC: American College of Rheumatologists Criteria.

The criteria can be applied in those with synovitis and clinical suspicion of RA. Look at 4 areas: number and size of joints affected, duration of symptoms, serology (RF or anti-CCP) and ESR / CRP.

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29
Q

What are anti-CCP antibodies?

A

Antibody markers used for the diagnosis of rheumatoid arthritis.

Aid assessment of likely future progression to RA, in undifferentiated arthritis.

Prognostic value as a marker of erosive disease.

30
Q

What biological therapies are available for the treatment of RA?

A

TNF-alpha blockers: etanercept, infliximab, adalimumab (eia)

Anti-CD20 MABs: rituximab

IL-6 inhibitor: tocilizumab

31
Q

What treatments are available for RA?

A

Non-pharmacological: education, information leaflets, support groups, PT / OT, podiatry.

Medical: analgesia (pain ladder), intra-articular steroids. DMARDS (MTX / sulfasalazine, leflunomide, hydroxychloroquine).

Biologics: if 2x DMARDs fail: anti-TNF or anti-IL6

Surgical: joint replacement, joint fusion, tendon transfer

32
Q

Name some serious side effects associated with the use of biological therapies.

A

Opportunistic infections.

Activation of latent TB / progression to miliary TB.

Anaphylaxis.

Increased risk of skin cancer.

CNS demyelinating disorders.

33
Q

How is scleroderma classified?

A

Localised SS - local skin involvement without internal organ involvement

Limited SS (formerly CREST syndrome) - calcinosis, Raynaud’s, oesophageal dysmotility, sclerodactyly and telangiectasia. Skin changes limited to hands / arms / feet / neck / face.

Diffuse SS - skin changes proximal to elbows, knees, face or neck. Can develop pulmonary fibrosis, scleroderma renal crisis or cardiac involvement.

34
Q

What other organs, besides the skin, are involved in systemic sclerosis?

A

Kidneys: scleroderma renal crisis
GI tract: GI bleeding
Lungs: pulmonary fibrosis / HTN
Cardiac: pericardial effusions, myocardial fibrosis, conduction defects, CCF

35
Q

What treatment options are available for systemic sclerosis?

A

Non-pharmacological: education (scleroderma society), hand warmers, OT / SLT / smoking cessation.

Medical:
GI: prokinetics, antacids, PPIs, cyclical sbx for SIBO
Raynaud’s: CCBs, sildenafil, iloprost, bosentan
Skin / joint / lung: MTX, MMF, cyclophosphamide, LTOT
Renal: ACEi’s

Surgical: lung transplant, contracture release, excision of calcinosis.

36
Q

What immune tests can be used to help identify the cause of systemic sclerosis?

A

Limited SS: anti-centromere antibodies.

Diffuse SS: anti-Scl-70 antibodies

Mixed CTD: U1-RNP (SS, SLE, polymyositis)

37
Q

What is the typical histological subtype of pulmonary fibrosis in patients with systemic sclerosis?

A

Non-specific interstitial pneumonia (NSIP subtype).

38
Q

Would you use steroids in systemic sclerosis?

A

No - very little chance of benefit, increases the patient’s risk of infections and renal crisis.

39
Q

What are the features of non-proliferative diabetic retinopathy?

A

Microaneurysms
Blot haemorrhages
Hard exudates
Soft exudates

40
Q

What are the features of proliferative diabetic retinopathy?

A

Features of non-proliferative diabetic retinopathy, but with evidence of new vessel formation.

Photocoagulation scars are evidence of treatment.

41
Q

What are the features of diabetic maculopathy?

A

Any features of diabetic retinopathy at or near the macula.

Most commonly, there is circinate formation of hard exudates.

42
Q

Besides good glycaemic control, what else can be done to lower the risk of retinopathy in T2DM?

A

Optimal treatment of hypertension.

43
Q

List some causes of hyperthyroidism.

A

Graves’ disease
Toxic multinodular goitre
Thyroid adenoma
De Quervain’s thyroiditis
Postpartum thyroiditis
Drugs (amiodarone, lithium)

44
Q

What are the causes of a goitre?

A

Nodular: multinodular goitre, adenoma, carcinoma.

Diffuse: simple, Graves’, Hashimoto’s thyroiditis, de Quervain’s thyroiditis, thyroid lymphoma

45
Q

What signs of thyroid disease are specific to Graves’ disease?

A

Graves’ ophthalmopathy
Thyroid acropachy
Pretibial myxoedema

46
Q

What are the ‘hyperthyroid emergencies’?

A

Thyroid storm.

Exophthalmos causing fixed gaze / optic nerve compression.

High output cardiac failure.

47
Q

What are the different types of thyroid cancer?

A

Papillary: most common
Follicular
Medullary
Anaplastic: most aggressive
Lymphoma
Metastases from other cancers (kidney most commonly)

48
Q

What investigations are used to diagnose the cause of a thyroid mass?

A

TFTs: TSH, T3 and T4.

Gold-standard is USS-guided fine needle aspiration (FNA).

CT can be useful to show the extent of a goitre causing compressive symptoms, or for staging of malignancy.

49
Q

Who is eligible for medical management of osteoporosis?

A

All patients with fragility fractures >75 years should have treatment regardless of DEXA results.

50
Q
A
51
Q

What are the risk factors for developing osteoporosis?

A

Family history
Cushing’s syndrome
Alcohol + smoking
Deconditioning / prolonged immobility
Underweight
Early menopause
Drugs: prolonged steroid use

52
Q

What treatment strategies are used for osteoporosis?

A

Lifestyle: nutrition, exercise.

Prevent falls: appropriate footwear, OT / PT, home adjustments, avoid polypharmacy.

Medical:
- Bisphosphonates (IV zol, aledronic acid)
- Calcium and Vit D optimisation
- Denosumab if reduced CrCl
- Teriparitide in special cases

53
Q

What are the causes of a unilateral 7th cranial nerve palsy?

A

UMN:
Cerebellopontine angle lesion
Pontine lesion

LMN:
Bell’s palsy - caused by HSV1
Ramsay Hunt syndrome
Parotid gland tumour
Facial neuroma
Cholesteatoma
Mononeuritis multiplex
Trauma

54
Q

What are the causes of bilateral LMN 7th cranial nerve palsy?

A

MND
Guillain-Barre syndrome
Bilateral Bell’s palsy
Lyme disease
Myasthenia gravis
Sarcoid
Moebius syndrome

55
Q

What condition is associated with an acoustic neuroma?

A

Neurofibromatosis type 2: defect on 22q12. This condition results in bilateral acoustic neuromas.

56
Q

How would you perform a lying and standing BP?

A

Lie patient down for 15 minutes and take BP.

Stand patient up.

Take BP at 1 minute, then again at 3 minutes.

Positive test = systolic drop of 20 or diastolic drop of 10, or presyncope.

57
Q

Differential diagnosis for a fall?

A

Falls are almost always multifactorial.

Visual: cataracts, visual field impairment
MSK: arthritis, deconditioning
Neurological: epilepsy, stroke, PD
Cardiac: arrhythmia, postural hypotension
Medications: polypharmacy, antihypertensives
Cognitive: delirium / confusion
Environmental: poor lighting, rugs, stairs, mobility aids
Incontinence

58
Q

What is the best approach to managing a patient with recurrent falls?

A

MDT approach: PT, OT, pharmacist, nurse and geriatrician.

Comprehensive geriatric assessment.

Balance training reduces frequency of falls (evidence-based).

59
Q

What are the causes of papilloedema?

A

SOL (tumour / abscess)
Idiopathic intracranial hypertension
Hypertensive encephalopathy
Infection
Vascular: venous sinus thrombosis
Drugs: tetracyclines

60
Q

What are the fundoscopic appearances of papilloedema?

A

Elevation of the disc with obscured vessels at disc margin.

Loss of cup.

Bulging of disc with all vessels obscured.

61
Q

What are the causes of optic atrophy?

A

Freidreich’s ataxia
Vascular (GCA)
MS, neuromyelitis optica
Optic nerve tumours, Graves’ ophthalmopathy, glaucoma
B12 / folate deficiency
Syphilis

62
Q

What treatments can be used to treat idiopathic intracranial hypertension?

A

Medical: weight loss, stop offending meds, acetazolamide, steroids, therapeutic LP.

Surgical: optic nerve sheath decompression and fenestration. LP / VP shunt.

63
Q

What are the manifestations of vitamin D deficiency?

A

Rickets
Osteomalacia
Osteoporosis

64
Q

What are the biochemical features of vitamin D deficiency?

A

REDUCED vitamin D, calcium and phosphate levels.

RAISED alk phos and PTH (secondary hyperparathyroidism).

65
Q

What is the difference between a ‘medical’ and a ‘surgical’ third nerve palsy?

A

Medical 3rd nerve palsy tends to be pupil sparing, and surgical 3rd nerve palsies tend to have a dilated pupil.

This is because surgical 3rd nerve palsies are due to compressive effects on the sympathetic fibres that supply the iris. The pupil will be dilated early in a surgical palsy.

66
Q

What are the medical causes of a 3rd nerve palsy?

A

Diabetes
Infection
Demyelinating disease (MS)
Autoimmune disease
Cavernous sinus thrombosis

67
Q

What are the surgical causes of a 3rd nerve palsy?

A

Aneurysm, post-neurosurgery, trauma, congenital cause.

68
Q

Why does an oculomotor nerve palsy lead to ptosis?

A

In addition to supplying the intrinsic muscles of the eye, the oculomotor nerve also supplies levator palpebrae superioris.

69
Q

What are the causes of psoriasis?

A

Immune-mediated via T-cell stimulated cytokine release.

Genetic susceptibility.

Post-strep (guttate).

Drug-related.

70
Q

What treatments are used in the management of psoriasis?

A

Topical treatments: emollients, coal tar, dithranol, steroids, vit D analogues (calcipotriol) and topical tacrolimus.

Phototherapy: UVB and PUVA.

Medications: oral steroids, MTX and ciclosporin, acitretin, adalimumab and infliximab.

71
Q

How is psoriatic arthritis managed?

A

Collaboration must take place between dermatology and rheumatology as systemic therapy may address both areas.

For predominantly peripheral arthritis:
- NSAIDs
- DMARDs: MTX, sulfasalazine, leflunomide, ciclosporin
- Biologics: infliximab, etanercept, adalimumab