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3rd year MDEMO > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Soft tissue diseases

A

Tendonitis - tennis elbow lateral, golf elbow medial, achilles
Enthesitis
Mechanical back pain
Repetitive strain injury

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2
Q

Degenerative diseases

A

Osteoarthritis
Cervical spondylosis
Osteoporosis

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3
Q

Inflammatory diseases

A 
Connective tissue diseases
Rheumatoid arthritis
Polymyalgia rheumatica
Vasculitis
Seronegative spondyloarthropathies (AS, psoriatic arthritis, reactive arthritis)
Crystal arthritis
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4
Q

Key points to ask in a joint history

A
  1. Pain
  2. Swelling
  3. Reduced ROM/functionality
  4. Stiffness
  5. Deformity
  6. Weakness
    + if connective tissue disease - rashes, Raynaud’s, fatigue, dry eyes/mouth, hair loss, pleurisy/pericarditis history, PE/DVT history
    + if spondyloarthropathies - back pain (inflammatory), iritis/uveitis, dactylitis, psoriasis, IBD
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5
Q

Spondyloarthropathies

A

= inflammatory arthritises that aren’t RA
Types of inflammatory arthritis that affect vertebral column (+ the eye, the bowel, skin and nails, the urogenital tract, ligament and tendon entheses)
Seronegatives do not express rheumatoid factor in the blood
HLA-B27 association

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6
Q

Mechanical back pain

A

Acute onset
20-55 years typically (but can be any age)
Exacerbated by movement, relieved by rest
Due to damage to a specific part of the spine
‘sharp/stabbing pain’
NSAIDs don’t help the pain
Unilateral or bilateral pain

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7
Q

Inflammatory back pain

A

Insidious/chronic onset >3 months
<40 years age
Relieved by activity, worsened by inactivity or sleep
Due to chronic inflammation of parts of the spine
‘dull/aching/gnawing pain’
Strong familial link due to HLA-B27
NSAIDs give considerable relief
Usually bilateral, can have alternating buttock pain

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8
Q

Investigating inflammatory arthritis

A 
FBC (normochromic normocytic anaemia - chronic inflammation)
CRP/ESR
X ray (may take years to show changes)
MRI (gold standard, often unneccessary)
Joint aspiration if monoarthritis
? test for HLA B27?
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9
Q

Rheumatoid arthritis features

A

MCP, PIP, wrist
Deformities - Z thumb (swan from MCP/boutonniere from CMC), ulnar deviation at MCPs, radial deviation at wrist, prominent ulnar head, mallet finger (DIP), boutonniere (PIP), swan neck
Hard nodules, bilateral
Early morning stiffness worse on rest
Night time pain
Acute/subacute presentation
Extra-articular - scleromalacia, reticular nodular haziness in lungs, vasculitis (ulceration, rashes, periphery necrosis), Raynaud’s, dry eyes/mouth, systemic weight loss/fever/malaise

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10
Q

Pathology of RA

A

Inflammation of the synovium (synovitis)
Chronically, -> generalised cartilage loss, so joint space narrowing, as well as osteoporosis of the bone near the joint (juxta-articular osteoporosis)
Synovial cells overgrow and eat into bone, forming erosions

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11
Q

RA antibodies

A

Rheumatoid factor - present in 1/20 normally, but 1/2 in RA

anti-CCP - everyone with RA has, rarely in normal population (better)

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12
Q

DAS-28 score

A

In RA, disease activity score
28 joints - if swollen/painful, ESR/CRP, global analogue scale for pain and wellness
To determine eligibility for biologics (>5.1 and 2 failed DMARDs)

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13
Q

RA epidemiology

A

More common in women

30s-50s common first onset (can be any age)

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14
Q

Psoriatic arthritis features

A 
Often asymmetrical
DIPs mostly, also PIPs, MCPs, wrist, equivalent joints in feet
Skin changes (70% have first) - skin lesions and nail changes
Other features - dactylitis, achilles tendon enthesitis, plantar fasciitis, extreme fatigue, 'pencil in cup' erosive changes, telescoping
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15
Q

Subtypes of psoriatic arthritis

A

Arthritis mutilans – telescoping of digits, destruction of all joints in finger so becomes floppy and useless
Asymmetric oligoarthritis – 3 or fewer joints affected
Asymmetric polyarthritis – more than 3 joints affected
Rheumatoid-like symmetrical polyarthritis
Distal interphalangeal joint disease

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16
Q

Pathology of PA

A

Autoimmune inflammation of epidermis
Triggers cytokine storm, excessive proliferation of keratinocyte skin cells, skin thickening
(mostly will have psoriatic skin lesions before the development of psoriatic arthritis)

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17
Q

Epidemiology of PA

A

Equal in men and women

Commonly in 40-50s

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18
Q

Ankylosing spondylitis features

A

Arthropathy of vertebral column + sacroiliac joints also (40% have peripheral joint arthritis also, usually asymmetrical)
Stiffness, reduced ROM and lower back pain in inflammatory pattern
At advanced stage, ‘question mark posture’ – historic outcome only
 Lumbar lordosis flattening
 Thoracic kyphosis increasing
 Cervical lordosis
May then get fixed flexion at hip in response to the spine
Features not be visible on X ray until 8 years after onset of disease – need MRI to investigate
Calcaneal spurs also, leading to plantar fasciitis
Alternating buttock pain, pain on sneezing
5 As:
 Anterior uveitis
 Achilles tendinopathy
 Apical lung fibrosis
 Aortic regurgitation
 Amyloidosis

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19
Q

Pathology of AS

A

Inflammation of intervertebral joints causes the formation of bony spurs (syndesmophytes) which outgrow into ligraments
In recurrent attacks, syndesmophytes bridge over intervertebral discs to fuse vertebrae together, preventing flexion of the spine

Death due to lung complications - intercostal muscles stop working -> recurrent chest infections, cardiac complications

Methotrexate/sulfasalazine ineffective - need anti-TNF adalimumab

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20
Q

Epidemiology of AS

A

More in men than women
Onset in 15-30
Takes 8 years to show on X ray

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21
Q

Reactive arthritis features

A

Secondary to infection - GI (salmonella, campylobacter) or STI (chlamydia, gonorrhoea) - but could be unknown/months ago
Urethritis
Uveitis/conjunctivitis
Joint arthritis, in knee/sacroiliac/lower limb joints
= can’t pee, can’t see, can’t climb a tree

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22
Q

Pathology of reactive arthritis

A

Abnormal immune response to infection, so body attacks one/a few of its own joints
Distinct from septic arthritis, where infection begins inside the join and inflammation is the appropriate response

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23
Q

Epidemiology of reactive arthritis

A

Men more than women

Young population 16-35 (often following STI)

24
Q

Treatment of reactive arthritis

A

Depends on aggression and whether progresses to a chronic condition
NSAIDs to reduce inflammation, and Abx if the causal organism can be identified (tetracyclines if chlamydia)
Usually self-limiting within 2-4 months (20 years on 10% will still have), if not then methotrexate/sulfasalazine

25
Q

Enteropathic/IBD associated arthritis

A

Typically affects large joints of lower limb and spine
Severity of arthritis reflects severity of IBD (flare-up together)
10% those with Crohn’s
20% those with UC
If UC/Crohn’s controlled, improvement of symptoms (In UC, total colectomy can cure arthritis also) - beware of NSAID use as may aggravate IBD

SULFASALAZINE

26
Q

Gout features and pathology

A

50% present with proximal interphalangeal joint of big toe first = podagra
Extreme pain!
Need to aspirate as could be septic arthritis
Sodium urate crystals form in synovial fluid, attract polymorphonuclear lymphocytes and launch acute inflammatory response
Serum urate levels usually kept soluble by serum proteins – if these systems fail or if urate levels rise too high then gout
Acute inflammation, so pain, redness, swelling, heat
In repeated attacks, chronic gout -> gouty tophi – tiny white lumps under the skin, often on ears, fingers or elbows

27
Q

Epidemiology of gout

A

Never in children or women before menopause
So much more common in men over 40
Age
Male
Alcohol
High purine diet (red meat, liver, kidneys, seafood)
Some diuretics – those that reduce urate excretion
Overweight
Smoking
Afro-caribbean race

Stress or illness may bring on acute attacks

28
Q

Treatment of gout

A

Diagnose by seeing urate crystals in synovial fluid – need to aspirate, as could be septic arthritis
Usually settles in 2-3 weeks if no treatment given
Long term treatment may be necessary to prevent recurrence – allopurinol or febuxostat to lower uric acid levels in body - STOP ALLOPURINOL IN ACUTE (use NSAIDs, paracetamol)

29
Q

Pseudogout (as opposed to gout)

A

More common in the knee, ankle, shoulder (gout is big toe, heel, fingertips) – larger joints!
Not uric acid, but calcium pyrophosphate deposition – aka CPD
Just as likely in women
No lifestyle features will affect
May be more insidious onset (gout is peak within 8-12 hours)
Usually resolves in 5-14 days
No tophi

Risk factors:
o	Age
o	Joint trauma
o	Family history 
o	Some underlying metabolic/endocrine disorders
30
Q

Sjogren’s

A

Connective tissue disease
Features - dry eyes, dry mouth, dry skin, tiredness, vaginal dryness, muscle and joint pain, photosensitive rash
More in women than men
Age of onset 40-60s
May be primary or secondary (ie associated with RA, SLE, scleroderma)
Usually following viral infection – genetic predisposition and then environmental trigger
Treatment only to help symptoms, hydroxychloroquine may be helpful
40x increased risk of lymphoid malignancy

31
Q

Systemic lupus erythematosus presentation

A 
Fatigue, fever, malaise, weight loss
Joint pain and swelling
Headaches
‘Butterfly rash’ on cheeks and nose
Hair loss – ‘scarring alopecia’
Anaemia 
Blood clotting symptoms
Raynaud’s phenomenon
Lung inflammation – pulmonary fibrosis a complication
Splenomegaly
Glomerulonephritis
Low platelets, low lymphocytes
High-risk pregnancies / difficulty conceiving

Multi-organ systemic disease with antinuclear antibodies
Flares and remission phases

32
Q

Treatment for SLE

A

Lifestyle – sun protection key
NSAIDs useful in joint pain, but be wary if renal disease
Hydroxychloroquine to suppress short term symptoms, but doesn’t stop long term organ damage
Corticosteroids in high dose in serious cases
Immunosuppressants – azathioprine, cyclophosphamide, and methotrexate
Thromboprophylaxis - aspirin

Ultimately will die from renal disease, cardiovascular disease or infection

33
Q

Epidemiology of SLE

A 
Common in young females (15-55 year olds, 9:1 females:males)
Genetic link
Smoking
African, Asian races higher risk
Sunlight exposure can precipitate flares
34
Q

Antiphospholipid Antibody (Hughes’) Syndrome

A

May be primary phenomenon or as a part of SLE

Venous and arterial thrombosis
Thrombocytopenia
Recurrent fetal loss (especially in 2nd trimester)
Cerebral disease (migrane, seizures)
Livedo reticularis rash 
- need lifelong anticoagulation

CLOT symptoms

  • Coagulation defects (eg DVT)
  • Livedo reticularis
  • Obstetric (recurrent miscarriage)
  • Thrombocytopenia
35
Q

Scleroderma = systemic sclerosis

A

‘CREST syndrome’ is one form:

  • Calcium deposits
  • Raynaud’s phenomenon
  • Esophageal dysmotility (dysphagia and heartburn)
  • Skin thickening and tethering
  • Talangectasia (areas of small dilated blood vessels)

3:1 female to male
Peak onset 30-50
Tends to present with Raynaud’s, and tightened thickened skin over the hands
Supportive management only – must stop smoking! Can try methotrexate/cyclophosphamide if interstitial lung disease

36
Q

Dermatomyositis/Polymyositis

A 
Inflammation of striated muscle – may be muscle pain, but usually presents as distal muscle weakness
Autoimmune, relapsing remitting course
Heliotrope rash with dermato
May be post-infectious
Treat with steroids
37
Q

Vasculitis

A

Consider in response to:

  • unexplained pyrexia with normal cultures
  • high inflammatory response
  • unexplained weight loss
  • unusual rashes (especially ulceration and “palpable purpura”)
  • new onset renal disease (especially microscopic haematuria)
  • widespread musculoskeletal symptoms
  • mouth ulcers, abdominal pain, bloody diarrhoea
  • dyspnoea, haemoptysis
  • sensory or motor loss

Steroids to treat, and disease will remiss in 48 hours
Large (eg GCA (scalp pain, unilateral headache) or Takayasu’s arteritis) or small vessels affected

38
Q

Giant cell arteritis

A

Often occurs with Polymyalgia rheumatica
Severe headaches, scalp tenderness
Pain and intractable early morning stiffness around the shoulder and hip girdles
F:M 2:1
Onset age 70 usually (under 50 very rare)

39
Q

Osteoporosis features

A

Low bone mass, micro-architectural deterioration of bone tissue, leading to reduced bone strength and increased fracture risk
Fragility fractures especially in NOF, vertebrae, distal radius (Colles’)
On DEXA scan T score of -1 - -2.5 = osteopenia, >-2.5 = osteoporosis (number of standard deviations away the BMD is from the mean of young healthy adult, Z score is age/gender matched)

Most treatments target osteoclasts (reducing absorption), only one licensed (teriparathide) targets osteoblasts

40
Q

Risk factors for osteoporosis

A

Age – 60s more likely wrist fractures, older more likely hip and spine
Gender – female more likely, + age at menopause
Previous fractures
Parental fragility fractures – hip especially 2x risk
Race – Caucasian and Asian higher risk
Diet – should have 700mg calcium a day – dairy, leafy greens, tofu
Vitamin D deficiency
Alcohol – if 3 units/day average, worsened bone health
Smoking
Steroid use + antiepileptics, aromatase inhibitors (breast cancer), androgen deprivation therapy, heparin, thyroxine overtreatment
Rheumatoid arthritis/inflammatory diseases
BMI – if low, increased risk
Diabetes – type I and II
Falls

41
Q

Treatment of osteoporosis

A

Conservative - physiotherapy, patient education, walking aids

Bisphosphonates – eg zoledronic acid, alendronate

  • inhibit osteoclasts by working on RANKL receptors
  • need 2 years treatment, then 2 years off

Calcium and vitamin D supplementation

Surgery (joint replacements)

  • benefits – reduce pain, improve mobility and function
  • risks – before: bleeding, nerve damage, implant malpositioning, anaesthetic risk; early complications: bleeding, DVTs, wound problems, early infection; late complications: dislocation, late infection
42
Q

Osteoarthritis definition

A

Non-inflammatory, chronic, degenerative joint condition, characterized by progressive hyaline cartilage degeneration and capsular fibrosis, leading to pain and stiffness

43
Q

Features of osteoarthritis

A

Pain on exertion, improved by rest, worse at the end of the day – as bone on bone contact
- Also pain at night time, as when awake muscle spasm prevents bones contacting
Stiffness – as capsular fibrosis limits joint, and large osteophytes restrict (bony deformities ‘swellings’)
If hands, DIPs and PIPs mainly, bilateral and symmetrical-ish, dominant hand worse
- Heberden’s nodes at DIP, Bouchard’s nodes at PIP

44
Q

Osteoarthritis definition

A

Non-inflammatory, chronic, degenerative joint condition, characterized by progressive hyaline cartilage degeneration and capsular fibrosis, leading to pain and stiffness

More in women than men
Commonly knees, hips, CMCs, DIPs, PIPs, lumbar spine

45
Q

Primary and secondary OA

A

Primary

  • ageing
  • family history

Secondary (caused by another condition)

  • obesity – due to increased stress on weightbearing joints – knees, hips, spine
  • repeated trauma or surgery to the joint
  • congenital abnormalities
  • gout/RA
  • diabetes
  • joint overuse
  • Paget’s disease of bone
  • hypothyroidism
46
Q

Management of OA

A
  1. Education and pain relief (GP)
    What is OA, how to support, uncurable, lifestyle changes (weight loss if lower limb affected, activity changes, smoking cessation)
    WHO pain ladder (to a point)
  2. Physiotherapy (community)
    Working to increase ROM and improve stiffness, reduce joint reaction force (muscle strengthening around joint to reduce load off bone, to preserve bone and reduce pain)
    Mobility aids – walking sticks, crutches, splints
  3. Steroid injections – not sure why they work as OA is non-inflammatory
    May be useful in acute flares, and only temporary relief
  4. Surgery – the only curative measure.
    Arthroscopy and debridement – trim osteophytes, remove loose bone (rare now, not that effective)
    Osteotomy – cut bone and realign forces, so deformity correction (only useful if only part of joint is damaged – useful in medial OA of knee)
    Arthrodesis – joint fusion
    Arthroplasty – half or total or excisional (works well in hips and knees, may work in elbow/shoulder/ankle, doesn’t work anywhere else)
47
Q

Osteomalacia/rickets

A

Normal amount of bone but low mineral content – excess uncalcified osteoid and cartilage
Rickets if before epiphyses have fused, osteomalacia if after

Causes

  • Vitamin D deficiency – malabsorption, poor diet, lack of sunlight
  • Renal osteodystrophy
  • Drug-induced (inducing liver enzymes)
  • Vitamin D resistance – often inherited conditions
  • Liver disease
  • Tumour-induced osteomalacia

Treat by giving vit D in appropriate form (eg if hepatic/renal disease must be later stage modified). Need close monitoring of plasma calcium.

48
Q

Features of rickets

A

Growth retardation, atonia, apathy in infants
Once walking – knock-kneed, bow-legged
Will be ill seeming
Maybe mild symptoms of hypocalcaemia

49
Q

Features of osteomalacia

A

Bone pain and tenderness
Fractures, especially at femoral neck
Proximal myopathy (waddling gait)
Reduced phosphate and vitamin D deficiency

See Looser’s zones on XR (partial fractures failed to heal)

50
Q

Paget’s disease of bone presentation

A

Increased bone turnover, increased numbers of osteoblasts and osteoclasts -> remodelling, bone enlargement, deformity, weakness

Increased incidence with age, M>F
Commoner in temperate climates, Anglo-Saxons
Asymptomatic in >70%
Maybe:
⁃ Deep boring pain
⁃ Bony deformity and enlargement
⁃ Typically in pelvis, lumbar spine, skull, femur, tibia
Pathological fractures, osteoarthritis, hypercalcaemia, nerve compression, high-output CCF, osteosarcoma are possible complications
Raised ALP

51
Q

DMARDs

A

Methotrexate (folate inhibitor, need folic acid alongside)
Sulfasalazine
Leflunomide
Hydroxycholoroquine (fewer side effects but can’t take in PA)

Side effects:
Common - nausea, fatigue, hypertension, infection risk
Serious - liver toxicity, bone marrow toxicity, lung toxicity

Need close monitoring every 2 weeks until at stable dose, then 6 monthly for life

52
Q

Biologics

A

A type of DMARD
Some are anti-TNF (TNF increases inflammation in excess)
eg Rituximab, infliximab

Only given when conventional DMARDs ineffective
By infusion, every 8 weeks ish

53
Q

Fibromyalgia symptoms

A

FIBRO

  • Fatigue
  • Insomnia, Irritability, Irritable bowel, Irritable bladder
  • Blues (anxiety + depression)
  • Rigidity (morning muscle and joint stiffness)
  • Ow (widespread pain in 11/18 tender joints, for more than 3 months)

Diagnosis of exclusion - bloods and imaging normal

54
Q

Fibromyalgia epidemiology + treatment

A

F>M (10:1)
Age 20-50
May follow physical trauma / psychological trauma / post-viral infection

Treat with exercise, CBT, pain relief:
- paracetamol -> tramadol/codeine -> amitriptyline

55
Q

Polymyalgia rheumatica presentation

A 
Age > 50, F>M 3:1
Muscle pain
Acute onset bilateral shoulder/hip pain
Morning stiffness > 1 hour
Duration > 2 weeks
Weight loss
GCA association
Depression
HLA DR4 genetics

Rapid response to steroid treatment
Bisphosphonates/PPIs if need long term steroids
Monitor for GCA

3rd year MDEMO (6 decks)

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