Brainscape's Knowledge GenomeTM

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


See full index

Yr2 Lily BRS MSK > intro to rheumatology > Flashcards

intro to rheumatology Flashcards

1
Q

what is rheumatology?

A

Rheumatology =
The medical specialty dealing with diseases of the musculoskeletal system including:

Joints = where 2 bone meets
Tendons = cords of strong fibrous collagen tissue attaching muscle to bone
Ligaments = flexible fibrous connective tissue which connect two bones
Muscles
Bones

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

what are the components of a synovial joint?

A

articular cartilage -
Type II collagen
Proteoglycan (aggrecan)

joint cavity

synovial  membrane (synovium) -
1-3 cell deep lining containing macrophage-like phagocytic cells (type A synoviocyte) and fibroblast-like cells that produce hyaluronic acid (type B synoviocyte)
Type I collagen

synovial fluid -
Hyaluronic acid-rich viscous fluid

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

what is arthritis and its types?

A

Arthritis = disease of the joints

There are many different types of arthritis, but there are 2 major divisions:

Osteoarthritis
(Degenerative arthritis)

Inflammatory arthritis
(main type is rheumatoid arthritis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is inflammation?

A

Inflammation = a physiological response to deal with injury or infection
However, excessive/inappropriate inflammatory reactions can damage the host tissues

Manifests clinically as:

  1. RED (rubor)
  2. PAIN (dolor)
  3. HOT (calor)
  4. SWELLING (tumor)
  5. LOSS OF FUNCTION

Physiological, cellular and molecular changes:

-Increased blood flow
-Migration of white blood cells (leucocytes) into the tissues
-Activation/differentiation of leucocytes
-Cytokine production
E.g. TNF-alpha, IL1, IL6, IL17

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

what are some condition that involve joint inflammation?

A

1)Crystal arthritis:
Gout – uric acid
Pseudogout – calcium pyrophospahate

2) Immune-mediated (“autoimmune”)
E.g.
Rheumatoid arthritis
Seronegative spondyloarthropathies
Connective tissue diseases

3) Infection
Septic arthritis
Tuberculosis

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

what is crystal arthritis and its types?

A

Gout:
a syndrome caused by deposition of urate (uric acid) crystals -> inflammation
High uric acid levels (hyperuricaemia) = risk factor for gout
Causes of hyperuricaemia:
Genetic tendency
Increased intake of purine rich foods (beer)
Reduced excretion (kidney failure)

Pseudogout:
a syndrome caused by deposition of calcium pyrophosphate dihydrate (CPPD) crystal deposition crystals -> inflammation
Risk factors: background osteoarthritis, elderly patients, intercurrent infection

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

what is gout?

A

Acute gout is a good example of arthritis

A disease in which tissue deposition of monosodium urate (MSU) crystals occurs as a result of hyperuricaemia and leads to one or more of the following:
Gouty arthritis
Tophi (aggregated deposits of MSU in tissue)

Gouty arthritis commonly affects the metatarsophalangeal joint of the big toe (‘1st MTP joint’)

symptoms:
podagra
Abrupt onset
Extremely painful
Joint red, warm, swollen and tender
Resolves spontaneously over 3-10 days
monoarthritis
rat bite erosions seen on x ray
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the investigations and management of gout?

A

Investigations:
Joint aspiration – synovial fluid analysis (usually don’t have to coz it Is so characteristic)

Management:
Acute attack – colcihcine, NSAIDs, Steroids
Chronic – allopurinol

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

what role does synovial fluid examination play in gout?

A

Synovial fluid samples are routinely examined for pathogens and crystals:
Rapid Gram stain followed by culture and antibiotic sensitivity assays
Polarising light microscopy to detect crystals which can be seen in arthritis due to gout or pseudogut

gout:
urate crystals
needle shaped
negative birefringence

pseudo gout:
calcium pyrophosphate dehydrate (CPPD) crystals
rhomboid shaped
positive birefringence

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

what is immune mediated inflammatory joint disease?

A

Most common form is rheumatoid arthritis (RA)

RA = chronic autoimmune disease characterised by pain, stiffness and symmetrical synovitis
(inflammation of the synovial membrane) of synovial (diarthrodial) joints

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

what is the pathogenesis of rheumatoid arthritis?

A

Synovial membrane is abnormal in rheumatoid arthritis:
The synovium becomes a proliferated mass of tissue (pannus) due to:

Neovascularisation
Lymphangiogenesis
inflammatory cells:
activated B and T cells
plasma cells
mast cells
activated macrophages

Recruitment, activation and effector functions of these cells is controlled by a cytokine network
There is an excess of pro-inflammatory vs. anti-inflammatory cytokines (‘cytokine imbalance’)

Sterile – not associated with infection

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

what is a key cytokine involved in rheumatoid arthritis?

A

Dominant detrimental role of TNFα in rheumatoid arthritis validated by the therapeutic success of TNFα inhibition in this condition

TNFα inhibition is achieved through parenteral administration (most commonly sub-cutaneous injection) of antibodies or fusion proteins

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

what are the key features of rheumatoid arthritis?

A

Chronic arthritis:
Polyarthritis - swelling of the small joints of the hand and wrists is common
Symmetrical
Early morning stiffness in and around joints
May lead to joint damage and destruction - ‘joint erosions’ on radiographs

Extra-articular disease can occur:
Rheumatoid nodules – under skin on ulnar border of elbow
Others rare e.g. vasculitis, episcleritis

Rheumatoid ‘factor’ may be detected in blood:
Autoantibody against IgG - should really call this rheumatoid ‘antibody’ not ‘factor’

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

what is the pattern of joint involvement in rheumatoid arthritis?

A

Symmetrical

Affects multiple joints (polyarthritis)

Affects small and large joints, but particularly hands and feet

Commonest affected joints:
Metacarpophalangeal joints (MCP)
Proximal interphalangeal joints (PIP)
Wrists 
Knees
Ankles
Metatarsophalangeal joints (MTP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the primary site of pathology in rheumatoid arthritis?

A

the synovium, which includes:
synovial joints
tenosynovium surrounding tendons
bursa

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

what are the extra-articular features of rheumatoid arthritis?

A

Common:
Fever, weight loss
Subcutaneous nodules

Uncommon:
vasculitis
Ocular inflammation e.g. episcleritis
Neuropathies
Amyloidosis
Lung disease – nodules, fibrosis, pleuritis
Felty’s syndrome – triad of splenomegaly, leukopenia and rheumatoid arthritis

17
Q

what are subcutaneous nodules?

A

Central area of fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissue

Occur in ~30% of patients

Associated with:
Severe disease
Extra-articular manifestations
Rheumatoid factor

18
Q

what is rheumatoid factor?

A

Rheumatoid factor:
Antibodies that recognize the Fc portion of IgG as their target antigen
typically IgM antibodies i.e. IgM anti-IgG antibody !

(IgM, the autoantibody is pentameric)
(IgG, the one we all have is a single antibody)

Positive in 70% at disease onset and further 10-15% become positive over the first 2 years of diagnosis

19
Q

what are anti-CCP antibodies?

A

Antibodies to citrullinated protein antigens (ACPA):

Antibodies to citrullinated peptides are highly specific for rheumatoid arthritis
Anti-cyclic citrullinated peptide antibody ‘anti-CCP antibody’

Citrullination of peptides is mediated by enzymes termed:
Peptidyl arginine deiminases (PADs)

20
Q

how is rheumatoid arthritis treated?

A

Treatment goal: prevent joint damage

Requires:
Early recognition of symptoms, referral and diagnosis
Prompt initiation of treatment: joint destruction = inflammation x time
Aggressive treatment to suppress inflammation

Drug treatment:
Disease-modifying anti-rheumatic drugs (‘DMARDs’) = drugs that control the disease process

1st line treatment:
methotrexate in combination with hydroxychloroquine or sulfasalazine

2nd line:
Biological therapies offer potent and targeted treatment strategies
New therapies include Janus Kinase inhibitors : Tofacitinib & Baricitinib

Important roles for glucocorticoid therapy (prednisolone) but avoid long-term use because of side-effects.

Multidisciplinary approach also important e.g. physiotherapy, occupational therapy, hydrotherapy, surgery

21
Q

what are the biological therapies used in rheumatoid arthritis?

A

Biological therapies are proteins (usually antibodies) that specifically target a protein such as an inflammatory cytokine

  1. Inhibition of tumour necrosis factor-alpha (‘anti-TNF’)
    antibodies (infliximab, and others)
    fusion proteins (etanercept)
  2. B cell depletion
    Rituximab – antibody against the B cell antigen, CD20
  3. Modulation of T cell co-stimulation
    Abatacept - fusion protein - extracellular domain of human cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) linked to modified Fc (hinge, CH2, and CH3 domains) of human immunoglobulin G1
  4. Inhibition of interleukin-6 signalling
    Tocilizumab (RoActemra) – antibody against interleukin-6 receptor.
    Sarilumab (Kevzara) – antibody against interleukin-6 receptor.
22
Q

what is ankylosing spondylitis?

A

Seronegative spondyloarthropathy – no positive autoantibodies

Chronic sacroillitis – inflammation of sacroiliac joints

Results in spinal fusion – ankylosis

Common demographic: 20-30yrs, M

Associated with HLA B27

23
Q

what is the clinical presentation of ankylosing spondylitis?

A

Lower back pain + stiffness
Early morning
Improves with exercise

Reduced spinal movements

Peripheral arthritis

Plantar Fasciitis, Achilles Tendonitis

Fatigue

Back pain >3 months, <45 years is suggestive of possible Ank Spond

24
Q

what investigations are done for ankylosing spondylitis?

A

Bloods:
Normocytic anaemia
Raised CRP, ESR
HLA-B27

Imaging:
X-Ray
MRI
Squaring Vertebral bodies, Romanus lesion
Erosion, sclerosis, narrowing SIJ
Bamboo Spine 
Bone Marrow Oedema
25
Q

what is the management of ankylosing spondylitis?

A 
Management:
Physiotherapy
Exercise regimes
NSAIDs
Peripheral joint disease - DMARDs
26
Q

what is psoriatic arthritis?

A

Psoriasis is an autoimmune disease affecting the skin (scaly red plaques on extensor surfaces eg elbows and knees)

~10% of psoriasis patients also have joint inflammation

Unlike RA, rheumatoid factors are not present (“seronegative”)

Varied clinical presentations:
-Classically asymmetrical arthritis affecting IPJs

But also can manifest as:

  • Symmetrical involvement of small joints (rheumatoid pattern)
  • Spinal and sacroiliac joint inflammation
  • Oligoarthritis of large joints
  • Arthritis mutilans
27
Q

what are the investigations for psoriatic arthritis?

A

X-rays of affected joints – pencil in cup abnormality
MRI – sacroiliitis and enthesitis

Bloods – no antibodies as seronegative

28
Q

how is psoriatic arthritis managed?

A

DMARDs – methotrexate

Avoid oral steroids – risk of pustular psoriasis due to skin lesions

29
Q

what is reactive arthritis?

A

Sterile inflammation in joints following infection especially urogenital (e.g. Chlamydia trachomatis) and gastrointestinal (e.g. Salmonella, Shigella, Campylobacter infections) infections

Important extra-articular manifestations include:
Enthesitis (tendon inflammation)
Skin inflammation
Eye inflammation

Reactive arthritis may be first manifestation of HIV or hepatitis C infection
Commonly young adults with genetic predisposition (e.g. HLA-B27) and environmental trigger (e.g. Salmonella infection)
Symptoms follow 1-4 weeks after infection and this infection may be mild
Condition is usually self-limiting – can be managed with NSAIDS or DMARDs if required
Reactive arthritis is distinct from infection in joints (septic arthritis)

30
Q

what is systemic lupus erythematous?

A

Lupus = a multi-system autoimmune disease

Multi-site inflammation: can affect any almost any organ.
Often joints, skin, kidneys, haematology. Also: lungs, CNS involvement

Associated with antibodies to self antigens (‘autoantibodies’)
Autoantibodies are directed against components of the cell nucleus (nucleic acids and proteins)

Autoantibodies can be useful diagnostically. Clinical tests include:

  1. Antinuclear antibodies (ANA):
    High sensitivity for SLE but not specific.
    A negative test rules out SLE, but a positive test does not mean SLE.
  2. Anti-double stranded DNA antibodies (anti-dsDNA Abs):
    High specificity for SLE in the context of the appropriate clinical signs.
Epidemiology:
F:M ratio 9:1   
Presentation 15 - 40 yrs 
Increased prevalence in African and Asian ancestry populations
Prevalence varies  4-280/100,000

may come with a malar or ‘butterfly’ rash

31
Q

what are some other connective tissue diseases?

A

Systemic Sclerosis
Myositis
Sjogrens syndrome
Mixed connective tissue disease

Yr2 Lily BRS MSK (5 decks)

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