Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Rheumatology > Rheumatoid arthritis > Flashcards

Rheumatoid arthritis Flashcards

1
Q

How is Rheumatoid arthritis diagnosed?

A

Chronic (at least x6/52: insidious onset) inflammatory joint disease causing bilateral symmetrical polyarthritis in proximal joints of hands or feet
- Note: joint involvement may be less symmetrical in atypical presentation, early RA, early initiation of DMARDs

Presence of Rheumatoid nodules (fingers, behind elbow)/ peri-articular erosions on XR

Biological Markers:

1) RhF
- Not Required for Dx!
- Only +ve in 70% of RA Pt!
- Not Specific!
2) Anti-CCP
- Much more reliable
- Diagnostic & Prognostic marker
- As sensitive (70%) and more specific

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

What is the risk factors for RA?

A

F>M, commonly 40-60 years

Genetic assoc HLA DR4/DR1 (a/w poor prog)

***SMOKING IS IMPT RF –> promotes citrullination of proteins

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

What are the markers of poor prog for progression in early RA?

A

Clinical picture

  • Insidious rather than explosive onset of RA
  • Level of disability at onset of RA
  • Female sex, old
  • Increasing no. of peripheral joints involved

Blood tests

  • High CRP/ESR
  • Anaemia
  • High titres of ACPA and RF

Imaging

  • XR w early erosive damage
  • (U/S and MRI show cartilage and bone damage earlier than XR)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the progression of RA joint manifestations?

A

Stage 1: Preclinical

  • Not clinically apparent
  • May have raised ESR, CRP RF

Stage 2: Synovitis

  • Joint painful, swollen and tender
  • Vascular congestion w angiogenesis, infiltration of immune cells into synovial membrane, proliferation of synoviocytes, cell rich effusion into joint and tendon sheaths

Stage 3: Destruction
- Erosion of bone (by osteoclastic resorption and granulation tissue invasion) and cartilage (by proteolytic enzymes, granulation tissue), disruption and rupture of tendons

Stage 4: Deformity
- Instability and deformity of joints

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

What is the clinical presentation of chronic progressive RA (70%)?

A
  • Chronic (wks-mths) insidious onset, symmetrical, peripheral polyarthritis
  • Relapsing, remitting course over several yrs
  • Sero + pts higher risk of jt damage and LT disability -> Earlier DMARDs Tx!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the clinical presentation of rapidly progressive RA (15%)?

A
  • Rapid onset (days or overnight), symmetrical, peripheral polyarthritis, progresses rapidly over a few years to severe joint damage and disability
  • Esp in elderly
  • Difficult to treat
  • Usually sero +, w high incidence of systemic complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the clinical presentation + course of rapidly Palindromic RA (5%)?

A

Features:

  • Recurring short-lived episodes of acute mono/polyarthritis lasting 1-2 days
  • Joints are acutely inflamed (pain, redness, swelling, disability)
  • Symptom-free periods for days-mths, w NO PERMANENT DAMAGE

Course:

  • 50% progress to other types of RA –> after delay of mths-yrs
  • 50% remit or continue to have acute episodic arthritis
  • Detection of RF/ACPA predicts progression to chronic, destructive synovitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the clinical presentation + course of seronegative RA?

A

Seronegative are LESS AGGRESSIVE and LESS EROSION with Better long-term prognosis!

Opposite for Seropositive! Consider earlier aggressive DMARDs

Initially affects wrist more than fingers, and has less symmetrical joint involvement

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

What are the early articular symptoms & signs of RA?

A

Inflammation arthritis of proximal joints of hand (MCPJ and PIPJ [vs always DIPJ in OA]) and feet (MTPJ) spreading to other synovial joints eg shoulders and knees

Pain: worse in morning, ↓ by movement, a/w swelling, +/- redness, heat

Stiffness: early morning stiffness of >1hr, ↓ by movement, ↑ after resting

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

What are the late articular symptoms & signs of RA?

A

Rheumatoid deformities and limited ROM

Hand and wrists
• Ulnar deviation of MCP joints w MCP palmar subluxation
• Swan neck and boutonniere of fingers, Z thumb
• Radial and dorsal subluxation of ulnar styloid-> ‘piano key sign’; causes wrist pain +/- rupture of finger extensor tendons (req urgent Sx repair!)

Feet and legs
• Valgus knees, valgus feet and hammer toes

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

What are the C spine symptoms & signs of RA?

A

Atlanto-axial instability

AA instability –> subluxation –> SC compression (rare but NEUROSX EMERGENCY – do MRI C spine OR XR Lateral C Spine in Flexed & Extended positions)

Signs of subluxation
• Limited global ROM of C spine
• Neck pain radiating to bilateral occipital and parietal areas
• A/w paraspinal muscle spasm
• A/w audible ‘clunk’ on flexion – instability is accentuated on flexion!

Signs of Cervical Myelo: as above +
• Difficulty walking (unexplained by arthritis), LL weakness, and loss of bowel output + passing urine control, cannot feel toilet paper when wiping
• Clumsiness of hands, non-specific loss of sensation of UL

Note: Lateral flexed and extended C spine XR before Sx or endoscope to check for instability and↓ risk of cord injury during intubation

Note: AA instability not as common now due to intro of DMARDs

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

What are the MSK (non joint) features of RA?

A
  • Tenosynovitis: dropped fingers (tendon rupture), trigger finger (trapped tendon in a thickened synovium)
  • Carpal tunnel syndrome: due to tenosynovitis, wrist deformity
  • Peri-articular muscle wasting
  • Drug-induced myopathy (eg glucocorticoids)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the CVS features of RA?

A
  • ↑ risk of CAD, possibly heart failure and atrial fibrillation (poorly controlled RA w persistently high CRP and high cholesterol is CVRF)
  • Pericarditis, endocarditis (usually subclinical) -> 10% Carditis detected clinically, 30% on echo
  • MR, AR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the respi features of RA?

A
  • Cricoarytenitis (RA of Cricoarytenoid joint) -> hoarse voice
  • ILD eg cryptogenic organising pneumonia
  • Pleural effusion (from serositis)
  • Bronchiectasis
  • Reactivation of TB 2° to DMARD use
  • Rheumatoid nodules in lungs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the neuro features of RA?

A

Peripheral sensory neuropathies 2’ vasculitis of vaso vasorum eg mononeuritis multiplex, symmetrical peripheral polyneuropathy

Mononeuritis Multiplex is a class of peripheral neuropathy

  • Occurs when there is damage to nerves in separate areas of the body!
  • Neuropathy of 1 nerve = mononeuropathy
  • Neuropathy of >1 nerve in 1 location = polyneuropathy
  • Neuropathy of nerves in multiple non-contiguous locations = mononeuritis multiplex (or also called polyneuritis multiplex)
  • Results in loss of sensation / loss of motor function / pain
  • Asymmetric involvement
  • But as the disease progresses, deficit(s) becomes more confluent and symmetrical, making it difficult to differentiate from polyneuropathy.
  • Therefore, attention to the pattern of early symptoms is important

Entrapment neuropathy –> CTS or TTS (tarsal tunnel syndrome)

C myelopathy 2’ cord compression from atlanto-axial sublux

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

What are the haem features of RA?

A

Anaemia

  • NCNC usually (ACD, haemolysis from hypersplenism in Felty’s),
  • microcytic (IDA due to BGIT from NSAID/steroids)
  • megaloblastic (pernicious anaemia, MTX-induced folate def, AIHA)

Thrombocytosis in active disease

Sometimes mild leucocytosis

Felty syndrome: RA + neutropenia + splenomeg

17
Q

What are the eye features of RA?

A

Sclera: episcleritis/scleritis

Conjunctiva: keratoconjunctivitis sicca (Sjogren’s)

  • keratoconjunctivitis sicca = dryness of conjunctiva and cornea
  • Secondary Sjogren’s can occur in pt w pre-existing Rh Dz (RA, SLE etc)

Lens/vitreous: cataracts/ glaucoma from prolonged steroids

Fundus: vasculitis, chloroquine-induced maculopathy

18
Q

What are the cutaneous features of RA?

A

**Rheumatoid nodules (pathognomonic) –> firm, intradermal, over pressure points (elbows, finger joints, Achilles tendon)

Vasculitis (small vessel) –> palpable purpura, nailfold and digital infarcts (splinter haemorrhage)

Vasculitis (large vessel) –> ulcers, digital gangrene (vasculitis is not significant compared to other CTDz)

Palmar erythema

19
Q

What are the investigations to be performed for RA?

A

Basic bloods

  • FBC: often NCNC anaemia 2’ ACD
  • ESR, CRP: a/w disease activity
  • RP LFT: for Mx

Autoantibodies
- RF: +ve in 40% of pts w early RA, but in 60-80% during course of disease
- Anti-CCP: higher specificity (90-98%) than RF
- ANA: +ve in 40% of pts
RF and CCP is somewhat prognostic and determines aggressiveness of Dz

Imaging
- XR
o Early (synovitis): juxta-articular osteopenia, soft tissue swelling
o Late (destruction): uniform narrowing of joint space, juxta-articular bony erosions, NO osteophytes
o Advanced (deformity): articular destruction and joint deformity
- MRI: synovitis, early erosions, useful in cervical spine disease

Evaluate disease activity - DAS28 can be used to evaluate disease activity, and help monitor effectiveness of therapy

  • Range from 2.0-10.0 (higher number = higher Dz activity)
  • 28 = 28 different joints included in the measurement
  • DAS = Disease Activity Score
20
Q

How do you manage a patient with RA?

A

1) Symptom control: reduce pain/swelling/inflammation
- SMOKING CESSATION
- NSAIDs for pain: TRO PUD, Allergy, Renal Impairment
- Short course low dose Prednisolone for flares

2) Disease modification: reduce synovitis and joint damage, increase function
- DMARDs ASAP (DMARDs take 2-3months to be effective)
- KIV escalation to biologic agents (1st line TNFα-inhibitors, 2nd line Rituximab, 3rd line tocilizumab & abatacept) – is expensive but may be more effective, consider if severe

3) Optimizing function:
- PT: rest during flares, exercise to maintain ROM and muscle power
- OT: manage ADLs
- Surgery: prophylactic (joint stabilisation), reconstructive (e.g. tendon repair, arthroplasty), urgent synovectomy (in uncontrolled RA synovitis causing massive soft tissue swelling)

Aim to reduce DAS28 to <2.6
- if <2.6, considered REMISSION 😊

21
Q

What if a patient requires DMARDs but want to get pregnant?

A

If planning to conceive, give pred + SSZ (but slow onset), monitor FBC and LFT

  • MTA and LEF are teratogenic!
  • SSZ & HCQ are not, but SSZ is more effective 😊
  • All DMARDs are Myelosuppressive & hepatotoxic -> hence monitor FBC & LFTs
22
Q

What do you need to monitor for when starting DMARDs?

A

1) Screen for Latent Infections (HSV, EMV, CMV, Tb, HBV, VCZ)
2) Monitor FBC and LFTs (all are myelotoxic and hepatotoxic)
3) Assess G6PD Def (for SSZ and HCQ)
4) Ophthalmology Assessment (for HCQ)

23
Q

What are the C/Is of Methotrexate?

A

C/I in pregnancy – delay conception 3-6/12 off the drug for either partner

C/I in renal impairment, liver cirrhosis, HBV/HCV carrier

24
Q

What are the S/Es of Methotrexate?

A
  • TB reactivation: CXR, IGRA in high risk pts to exclude TB
  • Pneumococcal and yearly influenza vacc
  • N&V & poor absorption might reduce efficacy: change to SC
  • Myelosuppression due to anti-Folate activity: monitor FBC, give adjunct folic acid 5mg once a week: Folic acid does not antagonist MTX effects
  • Hepatotoxicity causing transaminitis: monitor LFTs
  • GI S/E: mouth ulcers, dyspepsia
25
Q

What are the S/Es of Hydroxychloroquine?

A

Bull’s Eye maculopathy: Irreversible retinopathy 2’ retinal toxicity (1/2000): baseline macular fx using Amsler chart w annual reviews + Humphrey visual field testing

Caution in G6PD def, may cause haemolysis

26
Q

What are the side effects of Leflunomide?

A

Avoid in pregnancy (due to long half-life of 4-28 days)

Diarrhoea (diminishes w time)

27
Q

What are the side effects of TNFa blockers e.g. Infliximab, Adalimumab?

A

TB reactivation: CXR, IGRA in high risk pts to exclude TB. Treat if active, prophy if latent before starting TNF-a

Infections: hep screen

Heart failure: C/I in severe heart failure

28
Q

What is the American College of Rheumatology (ACR) criteria for disease remission (≥5 criteria below for at least 2/12)?

A
  • Morning stiffness <15min
  • No fatigue
  • No joint pain, joint tenderness
  • No soft tissue swelling or tendon sheaths
  • ESR <30 in women, <20 in men
29
Q

What hx do you need to take in a patient with RA?

A

Ask about the joint pain, characterise it

Assess risk factors

Functional assessment

Extra articular manifestations

Assess RF for treatment

  • Methotrexate: Macrocytic Anaemia
  • NSAIDs: BGIT and NCNC Anaemia
  • DMARDs: Myelosuppression (anaemia, easy bruising, infection)

Assess complications of treatment

30
Q

What does the RHEUMATOIDS mnemonic for extra-auricular features of RA stand for?

A
  • Respiratory
  • Hematological
  • Eyes – Episcleritis / Scleritis; Ant Uveitis, Sicca
  • Ulcers and other skin manifestations
  • Mononeuritis multiplex
  • Atlanto-axial subluxation
  • Tendon rupture / Tenosynovitis (trigger finger, CTS, TTS)
  • Osteoporosis
  • Incompetent valves (mitral/aortic regurgitation)
  • Dry eye and mouth – Sjogren’s
  • Serositis eg pleural effusion and pericarditis (pericarditis can lead to pericardial effusion)

Rheumatology (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions