Rheumatology Flashcards

1
Q

Common antibodies in SLE

A

ANA

Anti-smooth muscle

Anti-double stranded DNA

Antiphospholipid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Common antibodies in RA

A

Rheumatoid factor

Anti CCP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Common antibodies in Sjogren’s

A

Anti Ro

Anti La

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Common antibodies in Systemic Sclerosis

A

Limited = Anti Centromere

Diffuse = Anti Scl 70

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Polymyositis antibodies

A

Anti Synthetase

Anti-Jo1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Rheumatoid Arthritis

A

FM = 3:1, usually 30-50 years old at onset

Associated with HLA-DR4

Symmetrical, deforming, polyarthropathy
- Small joints mainly (70% have RA in wrist or hands)
- Spares DIPs
Morning stiffness
Slow onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Outline the American Classification Criteria for RA

A

= 4 components, A to D

A = joint involvement (type and number)

B = Serology (RF and anti CCP)

C = Acute phase reactants (CRP, ESR)

D = duration of symptoms (>6 weeks)

Score >6/10 = suggestive of RA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How would you investigate a patient in whom you suspect RA?

A

Bloods
- Routine FBC (?Felty’s), inflam markers, baseline U&Es
- RF (positive in 70%)
- anti CCP (positive in 70-80%, more specific)

Xrays of affected joints
- Loss of joint space, osteopaenia, subluxation, erosions

CXR –> HRCT if suspicious for fibrosis/nodules

Lung function tests

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Poor Prognostic Features for RA

A

RF positive
Anti-CCP antibodies
Poor functional status at presentation
HLA DR4 positive
Early erosions on xrays (<2 years)
Extra-articular features e.g. fibrosis
Insidious onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Possible Extra-Articular Features of RA

A

Can have multisystem involvement!

NEURO - peripheral neuropathy, mononeuritis multiplex

OCULAR - episcleritis, scleritis, keratoconjunctivitis

CARDIO - IHD, peri/myocarditis

RESP - pulmonary fibrosis (lower), effusions, nodules

HAEMATO - anaemia (secondary to chronic disease/NSAIDs), Felty’s syndrome, bone marrow suppression (secondary to MTX)

SKELETAL - osteoporosis

Increased risk of amyloidosis!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How would you manage a patient with RA?

A

MDT approach - rheumatologists, PT/OT

Exercise programme

Initial Rx = DMARD monotherapy (e.g. MTX) +/- prednisolone
Flares = PO/IV steroids
Biologic therapy e.g. Infliximab
- Indicated if on >2 DMARDs and 2 x DAS28 scores >5.1 at least 2 months apart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How can you monitor response to treatment in RA?

A

CRP &ESR

Disease Activity Score 28

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does MTX toxicity present? What can you give to treat this?

A

Bone Marrow Suppression
= symptoms of anaemia
= increased risk of infections (neutropaenia)
= bleeding/bruising (thrombocytopaenia)

Can also cause hepatitis

Rx = folinic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the main differences between Psoriatic Arthropathy and RA?

A

Psoriatic Arthropathy =
1) Asymmetrical (typically)

2) Negative RF, negative anti CCP

3) Nail changes e.g. pitting, oncholysis

4) Dactylitis

5) FHx/PMHx of psoriasis

6) F:M = 1:1

7) Skin change e.g. psoriatic plaques, koebner’s phenomenon
- Poor correlation with cutaneous psoriasis

8) Associated with HLA B27

9) More likely to affect DIPs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How would you manage a patient with Psoriatic Arthopathy?

A

MDT approach - rheum, derm, OT/PT

Mild Disease = NSAIDs

Moderate disease/little response to NSAIDs
= DMARDS e.g. MTX or sulfasalazine
= TNF inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which DMARD should you avoid using in Psoriatic Arthopathy?

A

Hydroxychloroquinne - can exacerbate psoriatic skin lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Differentials for Shortness of Breath in SLE / CTD

A

Multisystem disorders!

CARDIAC - Pericarditis, pericardial effusion, IHD, cardiomyopathy

RESP - Pneumonia (increased risk of infections), pulmonary fibrosis, PE, pleural effusion
- Renal failure –> pulmonary oedema
- ARDS reaction to biologics

NEUROMUSCULAR - Myositis, GBS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Screening Questions for Connective Tissue Disease

A

1) Any rashes? Do they worsen in the sun? (PHOTOSENSITIVITY!)

2) Any hair loss?

3) Have you noticed any changes to your hands?

4) Do you suffer from dry eyes / dry mouth / ulcers?

5) Are you SoB?

6) Any difficulty swallowing? Any heartburn?

7) Any diarrhoea / weight loss?

8) Any muscle pain or weakness?

9) Any difficulty getting out of a chair/car?

10) How is this affecting your everyday life?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

SLE

A

Multisystem autoimmune disorder

Relapsing-remitting

F:M = 9:1, 20-40 year olds

Features (ACR diagnostic criteria =>4/11 present)
- Malar Rash
- Discoid rash
- Photosensitivity
- Oral ulcers
- Non-erosive arthritis (symmetrical, hands & knees commonly)
- Serositis e.g. pericarditis
- Renal disorder
- CNS disorder e.g. psychosis, seizures, GBS
- Haematological
- ANA +ve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How would you investigate a patient in whom you suspect SLE?

A

Bedside
- BP
- Urine dip, ACR and red cell casts

Bloods
- Routine FBC, U&Es, LFTs
- Inflammatory markers
- ANA (+ve in 99%)
- Anti dsDNA, ENAs, Antiphospholipid
- Complement
- CK (exclude myositis)

CXR

Echocardiogram

?Skin biopsy
?Renal biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How would you manage a patient in whom you suspect SLE?

A

MDT approach as multisystem disorder - rheum/derm/renal/cardio

First line = hydroxychloroquine +/- steroids

If internal organ involvement = IV cyclophosphamide
If lupus nephritis = MMF
If severe flare = ?IVIG

Managing Complications of SLE
- Antihypertensives (ACEIs/ARBs)
- Statins
- Warfarin/LMWH if secondary APS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How can you monitor for disease activity in SLE?

A

Urinary protein + blood
Urinary ACR
Urinary red cell casts

ESR
Anti dsDNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Sjogren’s Syndrome

A

Autoimmune disorder of exocrine glands

Can be primary or secondary to rheumatoid arthritis/other CTDs

F:M = 9:1

Increased risk of lymphoid malignancy (B-cell) - >40x!

Features
- Dry eyes
- Dry mouth (xerostomia)
- Vaginal dryness
- Arthralgia
- Recurrent parotitis –> bilateral enlarged parotid glands
- Raynaud’s
- Myalgia
- Sensory polyneuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How would you investigate a patient in whom you suspect Sjogren’s?

A

Bedside
- Schrimer’s test (litmus paper on lower eyelid)

Bloods
- Routine FBC, U&Es, LFTs
- RF (positive in 100%)
- Anti Ro (70% of primary SS)
- Anti La (30% of primary SS)

Salivary gland biopsy (definitive test)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How would you manage a patient with Sjogren’s?

A

Artificial saliva/tears

Long term f/u due to risk of malignancy (B cell lymphoma!!)

26
Q

What is Raynaud’s disease?

A

= exaggerated vasoconstrictive response of digital arteries to cold/stress

Can be primary or secondary to underlying CTD (scleroderma, SLE, RA)/leukaemia/drugs e.g. COCP

Features
- Painful cold hands & extremities
- White –> blue –> red
- Digital ulcers (if severe)

27
Q

Outline features which are more suggestive of Raynaud’s secondary to underling CTD

A

Onset > 40

Unilateral symptoms

Presence of autoantibodies

Features of systemic CTD e.g. joint pain, rashes, SoB

28
Q

How would you manage a patient with Raynaud’s disease?

A

Gloves/hand warmers

1st line = CCBs (nifedipine)
2nd line = sildenafil

IV prostacyclin infusions if severe e.g. digital ulcers

29
Q

Systemic Sclerosis

A

Connective tissue disorder, characterised by thickening and fibrosis of the skin +/- systemic involvement

F:M = 3:1

3 patterns of disease
1) Scleroderma = localised skin thickening

2) Limited Cutaneous Systemic Sclerosis
= distal skin involvement, facial involvement, trunk spared
= Anti-Centromere
{CREST is a subgroup of this}

3) Diffuse Cutaneous Systemic Sclerosis
= Proximal skin involvement (above elbows and knees), trunk involved
= Anti Scl 70 abs

30
Q

Features of Systemic Sclerosis

A

Scleroderma

CREST
- Calcinosis
- Raynaud’s
- oEsophageal dysmotility
- Sclerodactyly
- Telangiectasia

Microstomia

Pulmonary involvement - ILD, pulmonary HTN

31
Q

What medical emergency are patients with Systemic Sclerosis at risk of? What can precipitate it, and what do we use to treat it?

A

Scleroderma renal crisis
= acute HTN and AKI
Can lead to pulmonary oedema, encephalopathy and renal failure

Common precipitant = steroids!

Rx = ACEIs

32
Q

How would you investigate a patient in whom you suspect Systemic Sclerosis?

A

Bedside
- BP
- Urine dip
- Lung function tests

Bloods
- Routine FBC, U&Es, inflammatory markers
- Autoantibodies
– ANA positive in 90%
– Anticentromere and anti Scl70
– Anti RNA polymerase III (increased risk of renal crisis)

Oesophageal studies/OGD (if features of oesophageal dysmotility)
CXR & HRCT (if features of ILD)
Echo

33
Q

How would you manage a patient with Systemic Sclerosis?

A

No curative treatment = symptomatic management mainly

Raynauds = CCBs etc

Cyclophosphamide has been shown to improve skin thickening, stabilise lung function and improve survival

PPIs

AVOID steroids!! (can precipitate a renal crisis)

34
Q

Causes of Gout

A

Main causes =
1) Diuretics
2) Alcohol
3) Trauma
4) CKD

Gout is secondary to increased serum urate concentration = either due to
1) Reduced uric acid excretion e.g. CKD, hyperparathyroidism, alcohol
2) Increased uric acid production e.g. MPD, cytotoxic drugs

35
Q

Clinical Features of Gout

A

Asymmetrical

70% 1st presentation = swollen, hot 1st MTP = Podagra
Other common sites = knee/ankle/wrist

“Flares” of joint pain and swelling, lasting 3-10 days
Often demonstrate diurnal pattern (worst at night!)

Tophi! e.g. ears

Monosodium urate crystals on joint aspirate (negatively bifringent)

36
Q

How would you manage a patient in whom you suspect gout?

A

Acute Rx
- NSAIDs or colchicine
- 2nd line = steroids
- Continue allopurinol if already on it
- Stop precipitating medications e.g. diuretics

Long-term Urate Lowering Therapy
- Offer if >2 attacks/year OR presence of erosions/tophi OR renal impairment secondary to calculi
- Offer for prophylaxis if on cytotoxics
= Allopurinol –> Febuxostat

Lifestyle Modifications
- Alcohol abstinence
- Weight loss
- Avoid high purine food e.g. seafood

37
Q

Key Questions for Acute Hot Joint

A

Onset - acute vs insidious
SOCRATES

Systemic features
Skin lesions

Previous history

Preceeding trauma
Preceeding infection e.g. UTI, STI, gastroenteritis

DHx
- Anticoagulation
- Recent course of steroids (AVN!!!)

37
Q

Pseudogout

A

Synovitis secondary to calcium pyrophosphate dihydrate crystal deposits

Associated with haemochromatosis, hyperparathyroidism, acromegaly

Knee most common joint affected

Weakly positive bifringent rhomboid crystals on aspirate

Rx = NSAIDs or IA/PO steroids

38
Q

How would you investigate a patient with an acutely swollen red hot joint?

A

Full history

Bedside
- BP, temp (?fever)
- Urine dip

Bloods
- FBC, U&Es, LFTs,
- CRP
- Urate, LDH
- RF, anti CCP
- Blood cultures if suspect septic arthritis

Joint Xrays

Joint Aspirate
- WBC > 50,000 = treat as septic arthritis
- MC&S
- Cytology for crystals

?MRI of joint

39
Q

Contraindications to a joint aspirate

A

Prosthetic joint - aspirate in theatre

Overlying celluitis

Overlying psoriatic plaque (increased risk of septic arthritis)

Excess anticoagulation e.g. INR >3 / coagulopathy

40
Q

Ankylosing Spondylitis

A

HLA B27 associated spondyloarthropathy

Axial arthropathy - affects sacroiliac joints & spine

Lower back pain and stiffness
Worse in morning
Improves with exercise

Associated with IBD & psoriasis

41
Q

Extra-articular features of Ankylosing Spondylitis

A

The 8 As

Anterior Uveitis
Apical fibrosis
AV block
Aortic regurgitation
Amyloidosis
Arthritis
Achilles tendonitis
and cauda equina syndrome

42
Q

Clinical Tests for Ankylosing Spondylitis

A

Schober’s Test
= reduced lumbar spine forward flexion
- Mark 5cm below line between PSIS, and mark 10cm above
- Measure distance when bending forwards
- Diagnostic if <5cm increase in distance between 2 points (<20cm distance)

On forward flexion, >10cm distance between fingers and floor

Occiput to wall distance > 0cm

43
Q

Management of Ankylosing Spondylitis

A

Conservative
- Regular exercise & physio

Medical
- NSAIDS
- DMARDs only useful if peripheral joint involvement = sulphasalazine
- Anti TNF therapy e.g. adalimumab, etanercept
— Indicated if axial disease refractory to 2 different NSAIDs with 2 active disease flares 3 months apart
— Symptomatic relief, does not affect progression

44
Q

HLA B27 Associated Arthropathies

A

Ankylosing Spondylitis

Reactive Arthritis

Psoriatic Arthritis

45
Q

Reactive Arthritis

A

HLA B27 associated arthopathy

“Post dysenteric” e.g. shigella, salmonella, campylobacter
“Post STI” e.g. chlamydia

Occurs 2-6 weeks post infection
Asymmetrical oligoarthritis (<4 joints)

Urethritis
Dactylitis
Conjunctivitis/anterior uveitis

“Can’t pee, can’t see, can’t climb a tree”

Management = pain relief, usually resolves within 12 months

46
Q

Kocher Criteria for Septic Arthritis

A

1) Fever > 38.5

2) Non weight bearing

3) Raised ESR

4) Raised WBC

47
Q

Giant Cell Arteritis

A

Systemic granulomatous arteritis
Large-to-medium vasculitis

Usually > 50 years old, F>M
Associated with PMR

Rapid onset headache (unilateral) -Often localised to temporal region
Scalp tenderness
Jaw claudication
Diplopia –> visual disturbance
Painless loss of vision
Systemic features e.g. fever

48
Q

How would you investigate and manage a patient in whom you suspect GCA?

A

Bedside
- BP
- Fundoscopy

Bloods
- FBC, U&Es, LFTs
- ESR!
- Vasculitis screen e.g. ANA

?Temporal artery USS/biopsy - should NOT delay Rx

Treatment = high dose steroids to prevent blindness e.g. 60mg pred OD
Refer to rheumatology and ophthalmology

49
Q

Paget’s Disease

A

Disease of accelerated bone turnover

Typically affects skull, spine, pelvis and long bones of legs

Typical presentation = isolated raised ALP in older men with bone pain
Spontaenous fractures, bone deformities e.g. bowing of tibia

50
Q

Complications of Paget’s Disease

A

Bone deformities e.g. bowing of tibia, skull thickening

CN palsies due to bone thickening e.g. CN VIII compression –> deafness

Headaches

HTN, IHD, high output heart failure

Hypercalcaemia

51
Q

How would you investigate someone in whom you suspect Paget’s disease?

A

Bloods
- Routine FBC, U&Es, LFTs - looking for raised ALP
- Calcium profile (normal)
- C-telopeptide = marker of bone turnover and progression of disease

Plain xrays

Technetium bone scan (high uptake areas)

52
Q

Management of Paget’s

A

Analgesia

Bisphosphonates if
- Bony pain
- Skull/long bone deformity
- Fractures

Calcitonin can be used if refractory to bisphosphonates/contraindicated

53
Q

Side Effects of Bisphosphonates

A

Bone pain
Hypocalcaemia

Oesophagitis/GI ulcers

Fever/flu-like symptoms

Osteonecrosis of the jaw!

54
Q

Sarcoidosis

A

Multisystem granulomatous disorder

Non caseating granulomas on biopsy

KEY FEATURES
- Fever, malaise, weight loss
- Erythema nodosum
- Lupus pernio
- Heerford’s syndrome = PUFF
– Parotid enlargement
– Uveitis
– Fever
– Facial nerve palsy
- SoB (pulmonary involvement)

MULTISYSTEM = neuro to cardiac to lung to renal involvement

55
Q

Poor prognostic features of Sarcoidosis

A

Insidious onset > 6 months

Absence of erythema nodosum

Extrapulmonary features

CXR stage III-IV

Afro-Caribbean

Increasing age

56
Q

How would you investigate someone in whom you suspect Sarcoidosis?

A

Bedside
- BP
- Urine dip

Bloods
- FBC, U&Es, LFTs
- Calcium profile
- ACE

CXR - ?hilar lymphadenopathy ?features of fibrosis
?HRCT

Biopsy of LNs

Spirometry

57
Q

How would you manage a patient with Sarcoidosis?

A

MDT approach, refer to rheumatology

If asymptomatic, no Rx required

Analgesia

Steroids if:
- Progressive CXR/PFT changes
- Cardiac or neuro involvement
- Hypercalcaemia
- Uveitis

58
Q

Ehler Danlos Syndrome

A

Autosomal dominant CTD, mostly affecting type III collagen
= increased elasticity of skin and muscle tissue

Features
- Elastic, fragile skin
- Atrophic scars
- Hypermobility and joint dislocation
- Easy bruising
- Aortic regurg/dissection
- MVP
- Angioid retinal streaks
- Poor wound healing
- Prolapses/hernias

Increased risk of SAH

59
Q

Polymyositis

A

Inflammatory myopathy

Causes = idiopathic, CTD or malignancy

F:M = 3:1

Features
- Symmetrical proximal muscle weakness
- Raynaud’s
- Resp muscle weakness
- ILD
- Dysphagia
- Dysphonia/dysarthria

Anti-Jo1 antibodies

Rx = Steroids

60
Q

Dermatomyositis

A

Inflammatory myopathy

Causes = idiopathic, CTD or malignancy (lung, breast, ovarian)

Skin Features (usually precedes myopathy)
- Periorbital heliotrope rash
- Gottron’s papules (red papules on dorsal aspect of fingers)
- Photosensitivity rash

Features
- Symmetrical proximal muscle weakness
- Raynaud’s
- Resp muscle weakness
- ILD
- Dysphagia
- Dysphonia/dysarthria

Anti-Mi2 antibodies

Rx = Steroids

61
Q

How would you investigate a patient in whom you suspect myositis?

A

Blood
- FBC, U&Es
- LFTs - AST and ALT often raised (markers of muscle)
- CK
- ANA
- Anti-Jo1 and Anti Mi-2

EMG

Muscle biospy

Consider investigating for underlying malignancy e.g. CT TAP, tumour markers