Brainscape's Knowledge GenomeTM

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


See full index

Locomotor core conditions > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

What is rheumatoid arthritis?

A

RA is a chronic systemic inflammatory disease, characterised by a symmetrical, deforming, peripheral polyarthritis.

RA = synovial disease characterised by synovitis

RA increases the risk of CVS disease 2-3 fold

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

Who does RA affect?

A

Women > men [3:1]

Higher risk in smokers

Peak onset : 5-6th decade

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

What is the aetiology (genetics, enviromental, autoantibodies) of rheumatoid arthritis?

A

Genetics:
=> Increased risk in 1st degree relative
=> HLA/DR4 assoc. with increased severity

Environment:
=> Smoking ± bronchial stress causes increased risk of RA with HLA-DR4 (acts synergistically)

Autoantibodies:

=> Rheumatoid factor - autoantibodies to the Fc portion of IgG in 80% of RA - specific but not sensitive

=> Anti-citrulinated peptide antibodies (ACPA) more sensitive and specific for RA

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

What is immunological basis of rheumatoid arthritis?

A

Synovitis in RA occurs due to overproduction of TNF-a => joint destruction

=> overproduction of TNF-a is driven by T & B lymphocytes
=> TNF-a stimulates IL-6

Dysfunction of cells => synovitis

  1. Synovial cells : produce pro-inflammatory cytokines
  2. Osteoclasts : bone & cartilage destruction
  3. Synovial B-cells : autoantibodies => IgM & IgG RF most common
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Is IgM RF diagnostic of RA and why?

A

No, RF is not diagnostic of rheumatoid arthritis - presence of RF does not confirm diagnosis of rheumatoid arthritis, nor does absence of RF exclude rheumatoid arthritis.

RF => useful in prognosis for rheumatoid arthritis

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

What is the significance of anti-citrulinated peptide antibodies (ACPA)?

A

ACPA present with RF in rheumatoid arthritis.

Better predictors of RA.

ACPA + RF => even more specific rheumatoid arthritis

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

What is the clinical presentation of RA?

A

~70% RA presents with:

=> progressive, symmetrical, peripheral polyarthritis

=> swollen, painful & stiff small joints of the hands and feet, eventually larger joints

=> worse in morning

=> evolves over weeks / months

=> between 30-50 years

~15% RA presents with:

=> sudden onset over few days

=> severe widespread, symmetrical, polyarticular involvement

=> in elderly

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

What are the signs & symptoms of early RA?

A

Inflammation but no joint damage

Pain & stiffness of small joints of hands & feet
=> swollen MCP, PIP, wrist or MTP joints
=> DIP is always spared in RA

Often symmetrical

Pain & stiffness worse in the morning

90% = polyarticular ; 10% = monoarticular

Tenosynovitis

Bursitis

Sleep disturbances + fatigue

Restricted movements + muscle wasting

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

What are the signs & symptoms of late RA?

A

Joint damage + deformity

Ulnar deviation

Subluxation of wrist & fingers

Boutoniere & swan neck deformities of fingers

Z-deformity of thumb

Rupture of hand extensor tendons

Larger joints involved i.e. hip / knee

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

What are the other 5 types of presentations of RA?

A
  1. Palindromic: monoarticular attacks lasting 24-48h => 50% progresses to other types of RA
  2. Transient: self-limiting, lasts <12months, no permanent joint damage. Seronegative for IgM RF and ACPA
  3. Remitting: several years of active RA but then remits, minimal damage
  4. Chronic persistent: typical form
    => may be sero+ve or -ve for RF
    => relapsing / remitting course over several years
    => sero+ve and ACPA patients develop greater joint damage & long term disability
    => need early, more aggressive treatment with DMARD
  5. Rapidly progressive: leads rapidly to severe joint damage + disability
    => sero+ve & ACPA = high incidence of systemic complications & difficult to treat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the factors predicting a poor prognosis for progression in early RA?

A

Older age

Female sex

Symmetrical small joint involvement

Morning stiffness >30mins

> 4 swollen joints

Smoking

Co-morbidity

High CRP

+ve RF and ACPA

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

What are the differential diagnosis of RA?

A

Postviral arthritis i.e. rubella, hepatitis B

Seronegative spondyloarthropathies

Polymyalgia rheumatica

Acute nodal osteoarthritis (PIP, DIP joints involved)

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

What are the complications of RA?

A

Septic arthritis

Amyloidosis - risk in uncontrolled RA but rare
*RA 2nd most common cause of amyloidosis

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

More than 6 points is the cut off for diagnosing RA.

What are the 4 main components of the diagnostic criteria for RA?

A 
a) Joint involvement 
1 large joint = 0 points
2-10 large joints = 1 point
1-3 small joints = 2 points 
4-10 small joints = 3 points 
>10 joints (at least 1 small joint) = 5 points

b) Serology
-ve RF and anti-CCP = 0 points
Low +ve RF or low +ve anti-CCP = 2 points
High +ve RF or high +ve anti-CCP = 3 points

c) Acute phase reactants
Normal CRP / ESR = 0 points
Abnormal CRP or ESR = 1 point

d) Duration of symptoms
>6 weeks = 1 point

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

What investigations are carried out if RA is suspected?

A

Bloods: Raised platelets, ESR, CRP
=> Anaemia of chronic disease

Serology:
=> RF +ve in 70% - high titre assoc. with severe disease, erosions & extra-articular disease
=> Anti-CCP - highly specific (98%) for RA + sensitive (70-80%) ; also predicts disease progression

X-rays:
=> Soft tissue rheumatoid nodules, juxta-articular osteopenia and reduced joint space
=> Later, bony erosion, subluxation, complete carpal tunnel destruction

MRI / Ultrasound:
=> Synovitis
=> Bone erosions

Aspiration of the joints

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

ANTI-CCP (Anti-cyclic citrullinated peptides) = ACPA (anti-citrullinated protein antibodies)

A

Both anti CCP and ACPA are the same/interchangeable

17
Q

~40% of patients with RA experience non-articular features.

What are the non-articular features of RA?

A
  1. Subcutaneous Nodules:
    => Firm , intradermal nodules occuring over pressure points i.e. elbows, finger joints, achilles tendon
    => Lungs, cardiac, CNS, lymphadenopathy, vasculitis
  2. Tenosynovitis of flexor tendons in the hand - stiffness
    => Bursitis
3. Lungs:
=> Pleural effusion
=> Interstitial lung disease
=> Small airway disease 
=> Nodules
  1. CVS
    => Pericarditis / pericardial effusion
    => Endocarditis
    => Myocardial disease i.e. MI, IHD
  2. CNS
    => Carpal tunnel syndrome
    => Peripheral neuropathy
6. Eye
=> Scleritis / episcleritis 
=> Scleromalacia 
=> Keratoconjunctivitis sicca
=> Sjögren's syndrome (dry eyes/mouth)
  1. Osteopororis
  2. Amyloidosis
  3. Splenomegaly (Felty syndrome)
  4. Anaemia
  5. Atlantoaxial subluxation may cause cervical cord compression
18
Q

How do you manage RA?

A
  1. Early diagnosis & referral to rheumatologist
  2. Early use of DMARDs + biological agents => improves long term outcomes
  3. Steroids => rapidly reduce symptoms & inflammation
    => used in acute exacerbation
    => intra-articular steroids for rapid but short term effect
    => oral steroids for difficult symptoms
  4. NSAIDs good for symptom relief but no effect on disease progression
  5. Surgery may help relieve pain, improve function and prevent deformity.
    * paracetamol & weak opiates not effective
19
Q

RA increases risk of cardiovascular/cerebrovascular disease

=> RA accelerates atherosclerosis

=> Manage risk factors of atherosclerosis

A

Smoking increases symptoms of RA

20
Q

What are disease-modifying anti-rheumatic drugs (DMARDs)?

What are some side effects?

A

DMARDs = 1st line in RA and started within 3 months of persistent symptoms

=> 6-12 weeks for symptomatic relief

=> Combination of methotrexate, sulfasalazine and hydroxychloriquine (all types of DMARD) = best results

Side effects:
=> Immunosuppression - can be fatal with pancytopenia, increased risk of infection with atypical organisms, neutropenic sepsis

=> Methotrexate: pneumonitis, oral ulcers, teratogenic, hepatotoxicity

=> Sulfasalazine: rash, reduced sperm count, oral ulcers, GI upset

=> Hydroxychloroquine: retinopathy

21
Q

Biologics are initiated by specialists when at least 2 DMARD trial has failed.

What are biological agents and when is it used in RA?

A
  1. TNF-a inhibitor i.e. infliximab => 1st line
  2. B-cell depletion i.e. rituximab
    => used in combination with methotrexate for active RA
    => when DMARD and TNF-a inhibitor failed
  3. IL-1 & IL-6 inhibitor i.e. tocilizumab
    => used in combination with methotrexate
    => when TNF-a inhibitor has failed
  4. Inhibitor of T-cell co-stimulation i.e. abatacept
    => active RA when DMARDs / TNF-a blocker failed
22
Q

What are some side effects of biologics used in RA?

A

Severe infection

Reactivation of TB

Hepatitis B

Worsening HF

Hypersensitivity

Skin cancers

23
Q

What is the mechanism of action of methotrexate?

A

Methotrexate is an antimetabolite, which inhibits enzyme dihydrofolate reductase, thus inhibiting the synthesis of the purines and pyrimidines necessary for nucleic acid synthesis.

=> Anti-inflammatory effects

Adenosine signalling in RA - increases adenosine levels and adenosine interaction with its extracellular receptors => an intracellular cascade is activated promoting an overall anti-inflammatory state

Locomotor core conditions (16 decks)

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