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Flashcards in Rheumatology Deck (29)
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1
Q

What is Felty syndrome?

A

RA + splenomegaly + neutropenia

2
Q

SOAP BRAIN MD

A

Serositis (pleuritis, pericarditis)
Oral ulcers
ANA +
Photosensitivity

Blood disorder - anaemia, leukopenia, thrombocytopenia
Renal disorder (proteinuria, haematuria)
Arthritis
Immunological - APLS, anti-dsDNA, anti-Smith
Neuro - seizures, psychosis

Malar rash
Discoid rash

(Generally need 4 out of 11 features)

3
Q

SLE.

a) Pathogenesis
b) Risk factors
c) Presentation - general symptoms
d) Diagnostic criteria
e) Joint involvement
f) Typical skin involvement
g) Overlap syndromes

A

a) Auto-immune connective tissue disease
b) - Chinese/SE Asian/Afro-Caribbean; female
c) Fever, fatigue, malaise, splenomegaly, lymphadenopathy, weight loss
d) SOAP BRAIN MD - need 4/11

e) - Inflammatory small-joint polyarthritis (morning stiffness, improves with use)
- May have reversible deformities (ie. Jaccoud’s arthropathy)

f) (note: all rashes may be photosensitive)
- Malar - butterfly on face; spares naso-labial folds
- Discoid - in sun-exposed areas; scaling
- Livedo reticularis - purple mottled reticular pattern
- Mild alopecia
- Vasculitic rashes

g) Other CTDs:
- vasculitis, myositis, APLS, Sjogren’s, scleroderma, Raynaud’s, etc.

4
Q

SLE management.

a) Investigations for suspected SLE
b) Non-drug management
c) Drug management
d) In pregnancy/ contraception

A

a) - Bedside: urine dip (and send for microscopy), ECG, pregnancy test
- Bloods: FBC (pancytopenia), CRP/ESR (raised), U+Es (renal involvement),
- Antibodies: ANA, dsDNA, Smith; cardiolipin and lupus anticoagulant (APLS); histone (drug-induced lupus), ANCA (vasculitis)
- Imaging: joint XR, ?renal USS
- Special tests: complement (C3 and C4 depletion), red cell microscopy, renal biopsy (lupus nephritis)

b) - Patient education: empowerment, self-management (avoid sun exposure), adherence to medication
- Allied health professionals: PT/OT/orthotics (and devices), nurses, counselling, social work, etc.

c) - Symptom control: analgesia, NSAIDs (beware in renal involvement) and steroids (topical, intra-articular, IM, oral)
- Hydroxychloroquine (antimalarial: 1st line in mild SLE)
- Cyclophosphamide and mycophenolate (used in life-threatening disease- eg. vasculitis, nephritis)
- Other DMARDs
- Biologics: eg. rituximab or belimumab (B-cell inhibitors)

d) - COCP contraindicated if: Hx of migraine, HTN, VTE or anticardiolipin antibody positive
- Pregnancy should be delayed until disease is quiescent for > 6 months
- Complications of SLE/APLS in pregnancy: worsens SLE, foetal loss and abnormality, maternal VTE
- If APLS in pregnancy - LMWH and aspirin

5
Q

Drug-induced lupus.

a) Common causes
b) Clinical features (vs. SLE)
c) Antibody associated
d) Management

A

a) Procainamide, chlorpromazine, methyldopa, hydralazine, isoniazid, d-penicillamine, anti-TNF drugs

b) Arthralgia most commonly (90%);
less end-organ damage than SLE; renal and central nervous system (CNS) involvement is uncommon

c) Anti-histone
d) Stop the offending drug and it should resolve

6
Q

Antiphospholipid syndrome (APLS).

a) 2 types and complications
b) Antibodies associated
c) Causes
d) Who should be screened?
e) Management

A

a) - Obstetric: recurrent miscarriage, stillbirth, IUGR, pre-eclampsia, pre-term birth, etc.
- Thrombotic: recurrent arterial/venous thrombosis

b) Anti-cardiolipin, anti-b2-glycoprotein I antibody
(+ lupus anticoagulant)

c) - SLE (30% have APL antibodies; not all have APLS)
- Other AI disease (RA, Bechet’s, seronegative SpA, etc.)

d) Thrombotic: < 50 years old with ischaemic stroke
- Obstetric: recurrent pregnancy loss (≥ 3)

e) - Conservative: healthy lifestyle (smoking, diet, etc.), pre-pregnancy counselling, manage other RFs
- APLS in pregnancy - LMWH and low-dose aspirin
- Non-pregnant: warfarin (switch to LMWH and aspirin if they become pregnant)

7
Q

Rheumatoid arthritis.

a) What is it?
b) Risk factors
c) Pattern of arthritis (site, number, features)
d) Tenosynovitis in RA - explain
e) Investigations in suspected RA
f) Give some poor prognostic factors in RA

A

a) Multisystem autoimmune disease, primarily causing an inflammatory arthritis (synovitis)

b) - Female, smoking, FHx, other AI disease
- Presence of RhF/ anti-CCP antibodies; HLA DR1 + DR4

c) - Usually symmetrical peripheral small-joint polyarthritis
- MCPJ, wrist, PIPJ, MTPJ; also elbows, knees, shoulders
- Inflammatory (red, hot, swollen, stiffness > 30 mins in the morning, improves with activity)

d) Tenosynovitis may be first sign - painful tendons and limited function, but joints non-inflamed (no synovitis)

e) - Bloods: FBC, CRP/ESR, uric acid, LFT/U+E (baseline)
- Antibodies: RhF (+/- anti-CCP), ?ANA, ?HLA-B27, etc.
- Imaging: XR hands and feet (peri-articular osteopenia, erosions, loss of joint space, soft tissue swelling)
- Aspirate any hot swollen joints - ?septic, ?gout

f) - Younger age of onset (< 30)
- Double sero-positive (RhF+ and anti-CCP+)
- Delay in starting DMARD (> 3 months)
- Persistently active disease
- Extra-articular features
- Early joint erosions on XR

8
Q

RA: extra-articular features

- head to toe

A
  • Neuro: peripheral nerve entrapment (eg. CTS), atlanto-axial subluxation (+ cervical myelopathy), polyneuropathy, mononeuritis multiplex.
  • Eyes: secondary Sjögren’s syndrome, scleritis and episcleritis.
  • Resp: pleural involvement, pulmonary fibrosis, Caplan’s syndrome
  • CV: ischaemic heart disease, pericarditis, endocarditis, vasculitis, Raynaud’s
  • Kidneys: analgesic nephropathy, amyloidosis (rare).
  • Liver: mild hepatomegaly and abnormal LFTs (more likely methotrexate-related)
  • Skin: subcutaneous nodules, rashes, nail fold infarcts, ulcers (especially in vasculitis/ Felty syndrome)
  • Haem: anaemia, Felty syndrome (neutropenia, splenomegaly), increased infections

Other: constitutional symptoms, thyroid disorders, osteoporosis, depression

9
Q

RA: classic signs on examination

- by site

A
  • Elbows: nodules, fixed flexion
  • Wrists: subluxation, fusion (if surgical - evident scar), deviation (ulnar or radial)
  • Dorsal: guttering, loss of furrowing between knuckles
  • Palmar: palmar erythema
  • Thumb: Z-deformity
  • Fingers: MCPJ subluxation (+/- tendon ruptures), MCPJ ulnar deviation, Boutonniere’s, swan-neck
10
Q

Rheumatoid nodules

a) Consistency
b) Common sites
c) What are they?

A

a) Rubber-like

b) - Subcutaneous: olecranon, finger joints
- Other: lung, heart, vocal cords

c) Granulomas

11
Q

RA management.

a) Indications for urgent rheumatology referral
b) Monitoring disease activity
c) Other things to check at annual review
d) Non-drug
e) Drugs
f) Surgery - indications (including urgent)
g) Surgery - types

A

a) - The small joints of the hands or feet are affected.
- > 1 joint is affected.
- Delay > 3 months between onset and presentation
(note: refer even if normal CRP/ESR and negative RhF)

b) Disease activity score (DAS-28):
- No. of tender/swollen joints (shoulders, elbows, wrists, MCPJ, PIPJ, knees)
- ESR
- Patient ‘assessment of global health’

c) - Assess compliance and for any complications
- Assess for: HTN (BP), coronary heart disease (QRISK), osteoporosis (DEXA/FRAX) and depression (PHQ-9); start therapies if necessary

d) Non-drug.
- MDT support: GP, rheumatologist, nurse specialist, PT, OT, dietician, podiatrist, pharmacist, social worker
- Devices (eg. walking aids, tap-turners, orthoses)
- Patient education and self-management
- Exercise

e) Drug.
- NSAIDs/ steroids - short-term
- Other analgesia
- DMARDs - methotrexate, sulfasalazine
- Biologics (after 2x trials of 6m of DMARDs fail to control): anti-TNF, CD-20 inhibitor, IL-6 inhibitor

f) - Urgent: cervical myelopathy, septic arthritis
- Other: worsening function or persisting pain, tendon rupture/imminent rupture, nerve entrapment (eg. CTS)

g) - Nerve decompression / cord decompression
- Fusion of joints
- Replacement of joints
- Tendon repairs/ tendon transfer

12
Q

Methotrexate.

a) MoA
b) Side effects
c) Monitoring
d) How to take?

A

a) Folate antagonist; cytotoxic (also chemotherapeutic)

b) Nausea (usually less if given SC), mouth ulcers
- More severe: hepatotoxicity, agranulocytosis, TERATOGENIC

c) - FBC, U+Es, LFTs (plus intermittent CRP/ESR)
- Women must be on contraception; pregnancy tests

d) Once per week (oral or SC)
- Give folic acid on day(s) not taking methotrexate (to reduce the side effects

13
Q

Biologics:

  • 4 main classes
  • give examples
  • give the diseases its used in
  • contraindications/cautions
A

TNF-inhibitors.

  • Etanercept, infliximab, adalimumab, certolizumab
  • Used in: RA, AS, IBD (inflix), PsA

Interleukin inhibitors.

  • IL-6: tocilizumab (used in: JIA, RA)
  • IL-12/23: ustekinumab (used in PsA)
  • IL-17: secukinumab (used in PsA)

B-cell (CD-20) inhibitors.

  • Rituximab, belimumab
  • Used in: NH lymphoma (B-cell lymphoma), RA, SLE

T-cell inhibitors.

  • Abatacept
  • Used in: RA

Biologics side effects.

  • Infection risk
  • Can activate latent TB or Hep B
  • Antibodies against drug produced - effect may wear off over time
14
Q

Ankylosing spondylitis.

a) What is it?
b) Causes/risk factors
c) Presentation
d) Possible signs o/e
e) Diagnostic criteria
f) Other investigations

A

a) Chronic seronegative spondyloarthropathy, primarily involving the axial skeleton (ie. sacroiliitis and spondylitis)
b) HLA-B27+, FHx, male, younger age (20 - 30)

c) - Inflammatory back/buttock pain
- Insidious onset/ relapsing-remitting pattern
- Systemic symptoms (eg. fever, weight loss, fatigue)
- Extra-articular symptoms

d) - Inspection - cervical kyphosis and loss of lumbar lordosis (question mark posture), buttock atrophy
- Palpation - tender sacro-iliac joints, tender entheses
- Movement - restricted lumbar flexion (< 5cm increase in Schober’s test indicates restriction); reduced chest
expansion

e) - At least one clinical finding of AS (inflammatory back pain, reduced lumbar flexion or chest expansion)
- Radiological findings (sacro-iliitis, etc.)

f) - Bedside: pulmonary function tests
- Bloods: FBC, ESR/CRP, antibodies (HLA-B27, RhF, ANA)
- Imaging: XR +/- MRI
- For complications (if suspected): DEXA (osteoporosis), ECHO (AR), CXR (fibrosis)

g) - Conservative: physiotherapy, hydrotherapy, encourage activity, monitor for complications, spinal extension and deep breathing exercises
- NSAIDs for symptom control
- Anti-TNF (etanercept or adulimumab; NOT infliximab) for severe AS not controlled by NSAIDs (note: classic DMARDs like methotrexate/5-ASAs don’t work in AS)
- Surgery if required

15
Q

Features of inflammatory pain.

A
  • Red hot, swollen, tender joints
  • Stiffness > 30 mins in the morning
  • Improves with activity
  • Worse/not relieved by rest
  • If back pain - insidious onset at age < 40 years
16
Q

AS: extra-articular features (6 As)

A
  • Anterior uveitis (occurs in 20 - 30%)
  • Apical lung fibrosis
  • Aortic regurgitation
  • Achilles enthesitis
  • Atlanto-axial subluxation (+ myelopathy)
  • Amyloidosis (rare) and IgA nephropathy
17
Q

AS: radiological findings

A

Early.
- Inflammation: sacro-iliitis / enthesitis

Later.

  • Squaring of vertebral bodies
  • Bony bridges (syndesmophytes) form between adjacent vertebrae
  • Ossification of spinal ligaments and, in late disease,
  • Complete fusion of vertebral column (bamboo spine)
18
Q

Classic radiological findings.

a) OA
b) RA
c) Gout
d) Pseudogout
e) PsA
f) AS

A

OA.
- LOSS (loss of joint space, osteophytes, subchondral sclersosis, subchondral cysts)

RA.
- Loss of joint space, erosions, subluxations, peri-articular osteopenia, joint ankylosis/fusion

Gout.
- Punched out/lytic/rat bite lesions

Pseudogout.
- Chondrocalcinosis (calcific shadowing in joint space)

PsA.
- Pencil-in-cup deformity

AS.

  • Early: sacro-iliitis, enthesitis
  • Later: squared vertebral bodies, syndesmophytes, bamboo spine
19
Q

Seronegative spondyloarthropathies.

a) What are they?
b) Give the 5 types
c) Common features
d) Management
e) Features of PsA

A

a) Group of HLA-B27+ disorders characterised by axial and/or peripheral arthritis, enthesitis and extra-articular features (SPINE ACHE)
b) Ank Spond, PsA, reactive arthritis, enteropathic-associated, JIA

c) SPINEACHE
- Sausage digit
- Psoriasis
- Inflammatory back pain
- NSAID-responsive
- Enthesitis
- Arthritis
- Crohn’s/colitis
- HLA-B27 positive
- Eyes (anterior uveitis)

d) - Conservative: encourage activity. monitor for complications, physio/hydro, orthotics, etc.
- NSAIDs for symptom relief
- Corticosteroids for acute flare-ups
- DMARDs generally first line (not in AS)
- Biologics - 1st line in AS (eg. anti-TNF), and used in the others where DMARDs have been ineffective
- Antibiotics (+ NSAIDs/ steroids/ DMARDs in reactive arthritis)
- Surgery as required

e) - Arthritis mutilans (mainly in hands; joint destruction)
- DIPJ arthropathie
- Pencil In cup
- nail changes / skin lesions
- Other SpA changes (eg. Spondylitis)

20
Q

Gout.

a) What is it?
b) Risk factors
c) Presentation
d) Clinical sign classic for gout
e) Atypical presentations
f) Investigations

A

a) An acute inflammatory monosodium urate crystal arthropathy (usually monoarthropathy)

b) - Increased purine intake: meat, alcohol, seafood
- Impaired uric acid excretion: CKD, diuretics, diabetes
- Other: male, CHD

c) - Acute inflammatory monoarthritis
- Symptoms peak in < 24h; duration < 2 weeks
- 50% attacks 1st MTPJ (70% first attacks)
- Painful red, swollen, tender, unable to weight bear
- May have systemic sx (fever,

d) Tophi

e) - Tenosynovitis, bursitis and cellulitis
- Hyperuricaemia also causes uric acid kidney stones and increases risk of heart disease

f) - Bloods: FBC, CRP, ?cultures, uric acid
- Imaging: XR affected joint (?punched-out lesions)
- Special tests: joint aspirate - send for MC+S (must rule out septic arthritis) and polarised light microscopy (negatively birefringent needle-shaped monosodium urate crystals)

21
Q

Gout: management

a) Acute attack
b) Lifestyle advice for preventing recurrence
c) When to start prophylactic therapy
d) Options for prophylaxis
e) Other risk factors that should be managed
f) How to initiate preventive therapy
g) Advice for allopurinol and acute attacks

A

a) - Conservative: rest, ice, elevate
- NSAIDs (eg. naproxen) - beware in CKD and CCF
- Colchicine - preferred in CKD/CCF
- Steroids - where NSAIDs / colchicine are contraindicated or ineffective
- Canakinumab (IL-1 inhibitor) - where the above three classes are contraindicated or ineffective

b) - Weight loss, exercise, less alcohol
- Lower purine-rich foods (meat, seafood, beer)
- Avoid dehydration

c) After the 2nd attack (wait until 1 - 2 weeks after acute attack has resolved)

d) - Xanthine oxidase inhibitors: allopurinol, febuxostat
- Uricosurics (eg. sulfinpyrazone) - they increase renal excretion (but also risk of uric acid kidney stones)

e) - Avoid drugs causing hyperuricaemia (thiazides and loop diuretics, pyrazinamide, ethambutol, ciclosporin)
- Manage HTN, CKD, hyperlipidaemia and CVD

f) - Wait 1-2 weeks after acute episode has resolved
- Start at a low dose
- Co-prescribe colchicine/NSAIDs for 3 months to prevent acute episode
- Titrate up slowly and check renal function regularly
- Generally preventive therapy is continued for life

g) - Continue allopurinol at usual dose (do NOT stop it)
- Add in NSAIDs, colchicine, steroids or canakinumab

22
Q

Pseudogout.

a) What is it?
b) Risk factors
c) Presentation
d) Investigations
e) Management

A

a) An acute inflammatory crystal arthropathy caused by calcium pyrophosphate deposition

b) - Increasing age, arthritis (OA, RA, etc.), dialysis, long-term steroid use
- Endocrine: hypothyroid, hyperparathyroid, haemochromatosis, acromegaly, etc.
- Precipitants: dehydration, intercurrent illness

c) - Acute* inflammatory mono/oligoarthropathy
- Most commonly knees; also wrists, shoulders, ankles, hands and feet
- Painful, red, swollen, tender (usually milder than gout)
- May have systemic symptoms

*Note: may have chronic or asymptomatic calcium pyrophosphate deposition (chondrocalcinosis)

d) - Bloods: FBC, CRP, ?cultures, uric acid
- XR: chondrocalcinosis
- Joint aspirate: for MC+S, and polarised light microscopy (positively birefringent rhomboid-shaped intracellular calcium pyrophospate crystals)

e) - Conservative: rest, ice, analgesia
- Acute: NSAIDs, colchicine, steroids
- Chronic: no good evidence; can use NSAIDs (+ PPI), colchicine, methotrexate, low-dose steroids

23
Q

Vasculitis.

a) What is it?
b) Large vessel (ie. aorta and major branches)
- types? - presentation?
c) Medium vessel vasculitides
d) Small vessel vasculitides
e) Investigations
f) Management
g) Complications

A

a) A group of disorders characterised by inflammation of blood vessels

b) - Types: GCA, Kawasaki, Takayasu (rare)
- Presentation: end organ ischaemia (eg. stroke/TIA), aneurysm, dissection

c) GPA (ENT bleeding, GN), Churg-Strauss (asthma, sinusitis), GCA, Kawasaki (Fever BURNS)
d) HSP, autoimmune disease (eg. RA), hypersensitivity, infective causes (eg. endocarditis)

e) - Bedside: urine dip
- Bloods: FBC, ESR, U+Es, LFTs, serology (eg. Hep)
- Antibodies: ANA, ANCA, RhF,
- Imaging: CXR, ECHO (especially ?Kawasaki), renal USS
- Special tests: ?renal biopsy, ?complement, ?skin biopsy

f) - Steroids in the acute phase
- Immunosuppression: cyclophosphamide
- Mycophenolate in ANCA-associated vasculitis
- Treat any underlying secondary cause
- IVIg or plasmapheresis in refractory cases
- Aspirin + IVIg in Kawasaki disease
- Manage complications (eg. renal failure - dialysis)

g) - Renal insufficiency
- Digital gangrene
- Pulmonary haemorrhage
- CNS infarction
- Arterial or venous thrombosis or dissection
- Subglottic stenosis

24
Q

GCA.

a) What does it affect?
b) Risk factors
c) Presentation
d) Signs o/e
e) Investigations
f) Histological finding on biopsy
g) Initial management
h) Further management + recurrence management
i) Complications

A

a) A medium-large vessel vasculitis, predominantly affecting the carotid artery and its branches
b) Age > 50, female, coexistent PMR, FHx

c) - Headache (temporal), scalp tenderness, facial pain
- Ischaemic: transient visual symptoms, jaw claudication
- Systemic: fever, malaise, fatigue, weight loss, PMR (bilateral proximal muscle pain and stiffness)

d) Temporal artery: prominent, beaded, tender, pulseless
- Fundoscopy: ?pale optic disc
- Fever
- Scalp/ shoulder tenderness

e) - Bloods: FBC (anaemia, thrombocytosis), ESR
- ?CT head (stroke)
- ?Slit-lamp examination
- Temporal artery biopsy

f) Mononuclear cell infiltration or granulomatous inflammation, usually with multinucleated GIANT CELLS

g) - No ischaemic symptoms: 40 mg prednisolone daily
- Ischaemic symptoms: 60 mg
- Visual disturbance: admit for IV methypred

h) - Aspirin 75 mg (+ PPI) to reduce risk of stroke
- Once symptoms and ESR improve, reduce steroid by 10 mg every 2 weeks to 20 mg, then in 2.5 mg steps, then 1 mg, etc.
(generally stop taking steroids after 18 - 24 months)
- Recurrence: increase to level at which symptoms were previously controlled (rarely need the max dose)

i) - Of GCA: stroke, vision loss, arterial dissection or aneurysm
- Of steroids: osteoporosis, infection, myopathy, bruising, HTN, weight gain, diabetes, psych (hypomania, agitation, etc.)

25
Q

PMR.

a) What is it? (vs. myositis)
b) Risk factors
c) Presentation
d) Investigations
e) Management
f) Monitoring

A

a) Inflammatory condition characterised by bilateral pain + morning stiffness of shoulders, neck and pelvic girdle
(vs. myositis - predominantly weakness, rather than pain)

b) As for GCA: age > 50 (mean: 73), female, FHx

c) - Bilateral pain + morning stiffness of shoulders, neck and pelvic girdle; tender to touch
- Acute onset; may have systemic upset
- Functional limitation: eg. hair, stair and chair
- Look out for GCA symptoms!!!

d) - Inflammatory markers: ESR or CRP (normal does not exclude PMR; if steroid-responsive can still diagnose)
- FBC, U+Es, LFTs, bone profile, protein electrophoresis, TFTs, CK, RhF, anti-CCP ANA, etc.
- ?imaging - CXR, USS shoulders or hips

e) - Screen for adverse effects to steroids before starting (DM, HTN, history of PUD, osteoporosis, psych history)
- Initiate steroids at 15mg daily, reduce gradually over a period of weeks and months (12.5, 10, 9, 8, etc.)
- Maintenance dose of 2.5 - 5 mg until symptom-free
- Usual total duration of treatment = 18 - 24 months
- Prescribe AdCal (+ BPs if > 65 or other fracture risk)
- Recurrence: increase to level at which symptoms were previously controlled (rarely need the max dose); if recurrent relapse, consider starting methotrexate

f) - PMR/ GCA symptoms
- Adverse effects of steroids (infection, weight gain, diabetes, HTN, osteoporosis, psych, etc.)
- Monitor bone health: DEXA scans (and BP therapy if required)

26
Q

FIbromyalgia.

a) What is it?
b) Risk factors
c) Presentation
d) Features o/e
e) Investigations
f) Management
g) Common associated conditions

A

a) Chronic idiopathic pain disorder, thought to be due to dysregulated pain perception
b) Female (10x more likely), age 20 - 50, FHx, chronic pain disease, stress, Hx of trauma (physical, sexual, psychological, etc.)

c) - Chronic (> 3 months) “pain all over” - commonly lower back, legs, neck, shoulders, headaches
- Sleep disturbance, morning stiffness, paraesthesiae, light-headedness or dizziness, fluctuations in weight.
- Cognitive issues (eg, memory disturbance, difficulty with word finding), anxiety and depression

d) 11 out of 18 tender points on body (minimal pressure)

e) - FBC, ESR, TFTs, RhF, ANA
- ?imaging
- Note: be careful not to over-investigate

f) Non-drug.
- MDT approach: GP, rheumatologist, chronic pain specialist, psychologists, psychiatrists, PT, OT, etc.
- Patient education
- Exercise - aerobic + strength training (slowly increase intensity of exercise; if symptoms worsen, cut back on exercise until symptoms improve)
- CBT, relaxation, IAPT, fibromyalgia support group, counselling etc.

Drugs.

  • Analgesia - paracetamol, NSAIDs, weak opioids (avoid strong opioids and steroids)
  • TCAs, SSRIs - amitryptilline and duloxetine useful as neuropathic analgesics as well as antidepressants

g) - Psych: depression, anxiety, PTSD
- Functional: IBS, non-cardiac chest pain, somatisation, non-epileptic seizures
- Pain disorders: eg. RA, SLE

27
Q

Systemic sclerosis (scleroderma).

a) What is it?
b) 2 basic types
c) Risk factors
d) Features in the skin
e) Other features
f) Antibodies
g) Monitoring investigations
h) Management
- non-drug
- disease-modifying
- complications (eg. renal crisis, PAH, Raynaud’s)
- surgical

A

a) Autoimmune disease of increased fibroblast activity, leading to increased collage deposition and fibrosis of the skin, vessels and internal organs

b) - Limited cutaneous SSc (CREST) - affects only the skin on the face, forearms and lower legs up to the knee
- Diffuse cutaneous SSc - also affects the skin of the upper arm, thighs + trunk; less common, higher mortality

c) FHx, may have infectious trigger (eg. parvovirus, EBV), vitamin D deficiency
d) Calcinosis, Raynaud’s, swelling of digits (non-pitting), sclerodactyly, telangiectasia, fingertip ulcers

e) - GI: heartburn, dysphagia, constipation
- Resp: pulmonary fibrosis, PAH
- CV: CHD, cardiac fibrosis, arrhythmias, impotence
- Renal: GN, scleroderma renal crisis
- MSK: myalgia, arthralgia, contractures, reduced ROM
- Overlap syndromes: eg. Sjogren’s

f) - ANA - sensitive but not specific
- Anti-topoisomerase (Scl-70) - associated with lung fibrosis, renal disease and poor prognosis
- Anti-centromere - associated with limited SSc and PAH

g) - Renal - U+Es, urinalysis
- Lung - pulmonary function tests, HRCT
- Heart - serum BNP, ECG, ECHO
- GI - endoscopy (if indicated)

h) - Non-drug: maintain ROM with gentle exercises, topical emollients, stop smoking, lose weight
- Drug: DMARD (eg. MTX)
- Arthralgia/myalgia: NSAIDs
- Raynaud’s: nifedipine (if severe - IV iloprost)
- PAH: sildenafil
- Renal crisis: ACE inhibitors
- Surgery: joint contractures

28
Q

Myositis (dermatomyositis/polymyositis).

a) What are they?
b) Risk factors
c) Presentation of polymyositis
d) Presentation of dermatomyositis - skin + other
e) Investigations
f) Management

A

a) Inflammatory proximal myopathies (+ rash in DM)
- There is also inclusion body myositis, but this disease may not have an inflammatory cause

b) - Malignancy

c) - Proximal muscle weakness - thighs, shoulders, neck (stair, chair, hair); progressive atrophy
- May affect pharyngeal muscles (dysphagia)
- Sparing of distal muscles (maintain dexterity), extraocular muscles and respiratory muscles
- Rarely have pain (more often cramps, aches)
- No rash, no neurological symptoms

d) - Myositis presentation, plus…
- Rash - violaecous rash in sun-exposed areas; Gottron papules on the finger extensors, heliotrope rash around eyes
- Other: systemic upset, ILD, cardiac disease

e) - Muscle-specific: CK (raised), EMG, muscle biopsy
- Antibodies: ANA, anti-Jo-1 (PM), ant-Mi-2 (DM)
- Cancer antigens: CA-125, CA-19-9
- Imaging: ?cancer - eg. CXR, CT CAP, etc.

f) - Non-drug: PT, OT, SALT, sun block (DM)
- Drug: steroids (topical or systemic), DMARDs, biologics
- Manage any underlying malignancy

29
Q

Raynaud’s.

a) What is it?
b) Risk factors
c) Triggers
d) Presentation

A

a) Paroxysmal vasospasm of the peripheral arterioles, leading to reduced blood flow, then cyanosis and finally vasodilation causing reactive hyperaemia

b) - Primary (onset < 30 usually): FHx, female, smoking
- Secondary: CTD (eg. scleroderma, SLE, myositis), vasculitis, RA, vibration injury, paraneoplastic

c) - Usually cold exposure
- Also: beta-blockers, emotions

d) - 3 stages: pallor, then cyanosis, then redness
- Accompanying numbness +/- pain
- Usually affects fingers or toes (may affect hands, legs)

e) - Clinical diagnosis
- Screen for secondary cause: FBC, ESR, ANA, etc.

f) - Non-drug: smoking cessation, avoid exposure to cold, wear heated mittens, avoid other triggers (eg. vibration, beta-blockers)
- Symptomatic: topical GTN
- Preventive: oral nifedipine
- Secondary: manage underlying cause (eg. scleroderma- DMARDs)
- Severe: IV iloprost infusion
- Surgical: angioplasty