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*MSK-Rheum > OA and RA > Flashcards

OA and RA Flashcards

1
Q

What is the conservative management of OA?

A

Conservative:

  1. RICE, hot water bottle
  2. lifestyle changes e.g. quitting smoking and weight loss
    • physio (muscle strengthening) & walking aids may help to achieve these!
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2
Q

What is the medical management of OA?

A

Medical

Pain management

  • paracetamol +/- anti-inflammatory (with PPI) +/- codeine (pain ladder);
    • Beware of GI bleeding & worsening asthma with NSAIDs
  • topical analgesic - Topical capsaicin (derived from chillies) may help

Injections:

  1. Steroid & Local Anaesthetic (mixed) injections,
  2. Hyaluronic acid injections
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3
Q

What is the surgical managament of OA?

A

Surgical:

replace joint! = Arthroplasty - replacement of all or part of joint surface by an artificial material

Other surgical options include:

  • Osteotomy -
    • realignment of joint to unload an arthritic area
  • Arthrodesis
    • permanent stiffening of a joint by excision & fusion to stop pain
  • Excision
    • removal of joint without fusion
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4
Q

What are the 4 signs of OA on radiograph?

A

LOSS

  • Loss of joint space
  • osteophytes
  • subchondral cysts (within bone)
  • subchondral sclerosis/thickening (white line)
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5
Q

What are the investigations for OA?

A

OA Ix:

Bedside

  • Hx
  • Exam

Bloods

  • Raised CRP

Imaging

  • X-ray (2 views e.g. AP & lateral)
  • Arthroscopy
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6
Q

What are the common joints affected in OA?

A

Commonly affected joints are:

Weight bearing joints:

(1) Hips, (2) Knees, (3) Lumbar, (4) Cervical spine

Hands:

  • 1st CMC (base of thumb)
  • Hebardens nodes = DIPs ==> really common in OA (not RA)
  • Sometimes Bouchard nodes on PIP (but more RA)
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7
Q

What are the symptoms patients may report in OA?

A

Patients may complain of pain:

  • Site: in the joints
  • Onset: insidious (dont know when it started)
  • Character: rubbing, achy
  • Radiation: none, Localised disease (hip; knee)
  • Assoc syx: crepitis, joint gelling (stiffness up to 30mins after exercise), Bony tenderness ,Mild swelling
  • Timing: worse @ end of day)
  • (Exac/reliving factors)
  • Severity: background / achy
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8
Q

What will you see O/E of someone with OA?

A

Look/inspect:

  • Swelling/deformity

Feel:

  • Pain on palpation
  • Mild synovitis (warmth, tenderness to the touch, swelling, or thickening of the joint that feels “spongy.”)

Move:

  • Active motion is limited and pain limits passive movement (flexion & internal rotation of hip too)
  • Resisted movement fine but can be weakness if not used
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9
Q

What are the primary causes of OA?

A

Primary causes

  • Idiopathic
  • Wear & tear/ trauma/ high impact sports
  • age
  • Obesity
  • Occupation
  • Poor nutrition
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10
Q

What are the secondary causes of OA?

A

Secondary causes

  • Pre-existing joint damage
    • (gout, joint damage)
  • Metabolic disease
    • (haemochromatosis - increased Fe absorption from gut = deposits in joints, liver, heart, pancreas, pituitary, adrenals, skin)
  • Systemic
    • (haemophilia- bleeding into joint space - pressure pain and chronic swelling)

Genetics

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11
Q

What is OA?

A

OA is where there is:

  1. Age-related (joint) degeneration of
  2. Articular cartilage -
  3. Progressive, degenerative joint disease;
  • Commonest joint condition
  • 3x more common in men
  • Typically >50s,
    • risk increases with age,
    • >80% over 75s have radiological evidence of OA
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12
Q

Which of OA or RA is more likely to be symmetrical?

A

RA is more likely to be symmetrical

OA can be a polyarthritis but also a monoarthritis or oligo arthritis (basically anything)

Whereas RA is more likely to be a symmetrical polyarthritis (>5 joints)

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13
Q

What is RA?

A
  1. Systemic
  2. autoimmune
  3. inflammatory disorder
  4. characterised by symmetrical polyarthritis

Peak incidence:

  • female
  • aged 20-40yrs

Can affect Heart, Lung & Blood Vessels

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14
Q

What is the pathophysiology of RA?

A
  • In the joint:
    • Synovial vascularity and hypertrophy –>
  • Immune problems:
    • T&B cells and macrophages invade and excessive cytokines are released - TNFa, IL6 and IL17..
  • Bone problems: IL6 and IL17 –> OC activation –> resorption/Destruction of cartilage & bone
    • –> ‘Pannus’ - abnormal layer of fibrovascular or granulomatous tissue (dead macrophages) on due to chronic inflammation (in joint = RA)

[TNFa is by macrophages in aute inflam = necrosis and apoptosis]

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15
Q

What are the symptoms of RA as SOCRATES?

TF what is the sign triad of RA?

A
  • S -Symmetrical, small joints of hands and feet
  • O - worse in morning
  • C - swollen, stiff, painful
  • R - N/A
  • A- can affect, heart, lungs and BV’s
  • T - worse in morning
  • E- better on movement
  • S - N/A

(1) JOINT PAIN (2) INFLAMM (red,swollen) (3) STIFFNESS (morning >30mins)

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16
Q

What are the risk factors for RA?

A

Risk factors of RA

Environmental:

  • higher prevalence in smokers

Genetics:

  • HLA DR4/DRB1 linked variations
    • –> associated with increased severity
    • [HLA is human MHC which recognises SA of certain immune cells to trgger immune responses]
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17
Q

What are the early signs of RA?

A

Early:

  1. warm joints
  2. inflammation
  3. but no joint damage
    • As joint damage = late sign

e.g. early = fluctuating symptoms/joints

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18
Q

What are the late signs of RA?

A

Late signs of RA = joint damage

  • Foot changes
  • Larger joints can be involved
  • Hands:
    • Dorsal wrist subluxation
    • Boutonniere, swan fingers
    • Z deformity of thumb
  • MCPS:
    • Ulnar deviation (MCP)
    • Guttering between MCPs –> synovitis
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19
Q

What are the extra-articular signs of RA in the bones/tendons?

A

RA Bones/tendons signs:

  • rheumatoid nodules (posterior border of ulnar),
  • osteoporosis,
  • recurrent soft tissue problems e.g.
    • frozen shoulder (thickened, hard to move capsule)
    • carpal tunnel syndrome,
    • de Quervain’s tenosynovitis (CMCJ tendon swelling).
20
Q

What are the extra articular signs of RA in the skin?

A

Skin:

  • Raynaud’s,
  • palmar erythema,
  • livedo reticularis,
    • Mottled, purpleish discolouration from capillary obstruction by small clots –> venule swelling
  • pyoderma gangrenosum
    • skin ulcers develop - seen in IBD as well as arthritis
21
Q

What are the extra articular signs of RA in the abdomen?

A

RA Abdo impact:

  • Splenomegaly
    • Felty’s syndrome
      • RA,
      • splenomegaly,
      • neutropenia
22
Q

What are the extra articular signs of RA in the lungs?

A

Resp signs of RA:

  • pulmonary fibrosis ( e.g. thickened, stiff, lung tissue)
    • NB: RA drugs also cause pulmonary fibrosis
  • pleural effusion
    • e.g. inflamm causing exudate
  • fibrosing alveolitis
    • affecting gas exhange part of lungs
  • obliterative bronchiolitis
    • obstruction of smallest lung airways
23
Q

What are the extra-articular signs of RA in the heart?

A

Cardiac RA signs:

  • pericardial effusion,
  • coronary artery disease
24
Q

What are the extra-articular signs of RA in the eyes?

A

RA effect on Eyes:

  • Episcleritis
    • inflammation of the superficial, episcleral layer of the eye - relatively common, benign and self-limiting.
  • Scleritis
    • inflammation involving the sclera (eye white)
    • is severe ocular inflammation- often with ocular complications!
      • nearly always requires systemic treatment!
  • keratoconjunctivitis sicca
    • dryness of the conjunctiva
      • (the membrane that lines the eyelids and covers the white of the eye)
    • and cornea
      • (the clear layer in front of the iris and pupil).
    • Too few tears may be produced, or tears may evaporate too quickly.
25
Q

What are the “other” extra articular signs of RA?

A

Other:

  • Lymphadenopathy
  • Vasculitis
  • Amyloidosis (amyloid fibrils from misfolded proteins by clonal plasma cells)
26
Q

What bedside tests would you do for RA and what could you see?

A

Ix:

  • Hx
  • Exam
    • Commonly affected joints: WARM + SWOLLEN, OFTEN SYMMETRICAL
    • MCP
    • PIP - Bouchard’s nodes (more common in RA)
    • Wrist joint

28-joint disease activity score:

  1. assesses tenderness & swelling at 28 joints
    • (PIPS, MCPS, wrist, elbows, shoulders, knees),
  2. ESR
  3. patient’s self-reported symptom severity

*score >6 is significant

27
Q

What blood tests would you do for RA?

A

Bloods:

  1. Anti-CCP (gold standard)
  2. RhF
  3. raised ESR/CRP
    1. (proportional to degree of inflammation)
  4. FBC
    1. (anaemia of chronic disease),
  5. U&E
  6. LFTs
28
Q

What imaging do you do for RA?

A

Imaging:

  • X-ray
    • loss of joint space,
    • osteopenia,
    • soft tissue swelling,
    • erosions
  • MRI
    • synovitis
  • US
    • synovial hypertrophy,
    • increased blood flow
  • can aspirate joint
    • neutrophils
  • Arthroscopy
29
Q

What is the difference between the American collegs or rheum (ACR) and the ACR & european league against rheumatism (EULAR) guidelines?

A

ACR alone needs 4/7 of the criteria for RA Dx however, this method doesnt catch early inflam RA in patients whereas the ACR and EULAR use 4 different areas (A-D) to show if the score is 6 or over then it is significant.

30
Q

What are the criteria for ACR dx of rheum?

A

Arthritis of:

  1. >/= 3 joints
  2. hand joint
  3. symmetrical

and

  1. morning stiffness
  2. rheumatoid nodules
  3. +ve RF
  4. Radiological changes (LOJ space, osteopenis, ST swelling, bone erosions)

need 4/7

31
Q

What are the criteria for ACR and EULAR classification of RA?

A

A = joint involvement ( > 10small joints get the biggest score)

B = serology –> e.g. if RF or anti CCP are high positive

C = acute phase reactants = +ve ESR and / or CRP

D = duration of syx lasting for over 6 weeks

need a scorre of >/= 6/10

32
Q

What are the differences on radiograph between OA and RA

A

The joint in RA is not as damaged cartilage as in OA (sever cartilage damage)

but the joint is inflammed, swelling and cell infiltration - the growth of the synovial membrane can invage bone and cause loss of space in the synovial cavity

  • loss of joint space –> erosions

in OA you can see loose cartilage particles and bone spurs (osteophytes)

33
Q

What are the poor prognostic markers of RA at presentation?

A
  • Large number of involved joint
  • RF strong +ve / CCP strong +ve
  • Smoking
  • High disability scores
  • Early erosions
    • *URGENCY to refer - risk of erosions to occur within a year - once got damage can’t go back!!
    • *psychosocial impact
    • *die early of atheroma - MI or stroke - NOT SUPPRESSED INFLAMMATION (including obese state - raised CRP)
34
Q

What is the management of RA?

A

MDT:

  • Refer early to a rheumatologist (before irreversible destruction)
  • Physio & OT (aids & splints)
  • Manage cardio & cerebro-vascular risk factors

Medical:

  • Early use of DMARDs (within 3 months) & biological agents
  • Steroids for flares (rapidly reduce symptoms & inflam - useful for treating flares)
  • IM depot methylprednisolone 80-120mg
    • Intra-articular steroids have rapid but ST effects
    • Oral prednisolone 7.5mg/d may control difficult symptoms but SE’s
  • NSAIDs (good for symptom relief, no effect on disease progression)

Surgical

  • Surgery
    • relieve pain, improve function & prevent deformity
  • Replacement
  • Fusion
  • Synovectomy (dc pain and ic ROM)
35
Q

What is the management of RA flares?

A
  1. analgesia,
  2. splinting,
  3. corticosteroids –> (oral or intra-articular [rapid but ST effect])
36
Q

What are DMARDs?

A

1st line for treating RA;

should be started within 3 months of persistent symptoms; delayed benefit (6-12wks)
-best results often achieved with combo of

  1. methotrexate,
  2. sulfalazine &
  3. hydroxychloroquine
37
Q

What are the side effects of DMARDs?

A

SE’s of DMARDS:

  • Immunosuppression –> pancytopenia, ↑susceptibility to infection & neutropenic sepsis
  • Methotrexate - risk pneumonitis, oral ulcers, hepatotoxicity
  • Sulfalazine - risk rash, low sperm count, oral ulcers
  • Hydroxychloroquine - risk irreversible retinopathy, need annual ophthalmology review
38
Q

What does the guidance say for treatment of RA?

A

Guidance:

1st Line = Methotrexate OW + one of (sulfasalazine, hydroxychloroquine or leflunomide)

2nd Line= Add Anti-TNF (e.g. infliximab) or Anti-IL6 (Toclizumab) -

if no impact by 6 months re-review

3rd line - rituximab (b-cell depletion if DMARDs and TNF-a has failed)

Last line- abatacept e.g. causes t cell function disrutption, although rare

39
Q

What are TNF-a inhibitors?

A

TNF-a inhibitors: e.g. Infliximab

1st line biological agent for active RA after failure to respond to 2x DMARDs

& with a DAS28 >5.1

(disease activity score of 28 joints)

40
Q

What are B cell depletors?

A

B cell depletion: e.g. Rituximab,

Use in combination when methotrexate for severe RA where DMARDs & TNFa blocker have failed (alt: can use IL-1 or IL-6)

41
Q

What are IL1/IL6 inhibitors?

A

IL-1 & IL-6 inhibition e.g. Tocilizumab

Use in combination with methotrexate, pts where TNFa blocker & rutuximab have failed or are CI’d

42
Q

When is disruption of T cell function used in RA?

A

Disruption of T cell function e.g. Abatacept

Use infrequently for severe active RA in pts not responded to TNFa blocker or rituximab (e.g. the one used after TNF/il-1,6)

43
Q

What are the SE’s of biological agents?

A

SE’s of biological agents:

  • From immunosupression:
    • serious infection,
      • including reactivation of TB,
    • hepatitis B,
    • hypersensitivity,
    • injection-site reactions
  • & blood disorders (LT safety unknown)
  • worsening heart failure,
44
Q

What is a key to know side effects of methotrexate?

A

LFT derrangement and lung fibrosis

45
Q

what is a key to know side effect of Sulfasalazine?

A

azoospermia (so non motile sperm)

myelosupression

46
Q

What is a key to know side effect of Hydroxychloroquine?

A

retinopathy - need opthalm input

47
Q
A

*MSK-Rheum (6 decks)

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