Brainscape's Knowledge GenomeTM

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


See full index

Musculoskeletal > Introduction to Rheumatology > Flashcards

Introduction to Rheumatology Flashcards

1
Q

Define rheumatology

A

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 is the structural classification of joints?

A
  1. Fibrous Joints - No space between the bones
    Examples:
    -sutures in the skull
    -syndesmosis (sheet of connective tissue) in tibia and fibula joint (ankle)
  2. Cartilaginous Joints
    Joints in which the bones are connected by cartilage
    E.g. joints between spinal vertebrae
  3. Synovial Joints
    Have a space between the adjoining bones (synovial cavity). This space is filled with synovial fluid.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the functional classification of joints?

A 
1. Synarthroses
Generally allow no movement
2. Amphiarthroses
Allow very limited movement
3. Diarthroses
Allow for free movement of the joint
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How can structural classification of joints be functionally classified?

A

Synovial joints are diarthrosis joints while fibrous joints and cartilaginous joints are a mix of synarthrosis and amphiarthrosis.

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

What are the components of a synovial joint?

A

Bone is lined with articular cartilage and joint space surrounded by a joint capsule containing synovial fluid. Synovium is a 1-3 cell deep lining containing macrophage-like phagocytic cells (type A synoviocyte) and fibroblast-like cells that produce hyaluronic acid (type B synoviocyte). Contains type I collagen. The synovial fluid is a hyaluronic acid-rich viscous fluid. Articular cartilage is made of Type II collagen and the proteoglycan aggrecan.

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

What is cartilage composed of?

A

1) Specialized cells (chondrocytes)
2) Extracellular matrix: water, collagen and proteoglycans (mainly aggrecan)
Aggrecan is a proteoglycan that possesses many chondroitin sulfate and keratin sulfate chains. It is characterized by its ability to interact with hyaluronan (HA) to form large proteoglycan aggregates.

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

Why can’t cartilage repair easily?

A

Cartilage has no blood supply - it is avascular.

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

What is arthritis and what are the types?

A

Arthritis is a diseases of the joints. Two types: Osteoarthritis is degenerative arthritis. Main type of inflammatory arthritis is rheumatoid arthritis.

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

Describe pathological changes and epidemiology of osteoarthritis

A

Pathological changes: cartilage worn out, bony remodelling
Epidemiology:
-more prevalent as age increases,
-previous joint trauma (e.g. footballer’s knees)
-jobs involving heavy manual labour

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

Describe onset of osteoarthritis and state which joints are most commonly affected

A 
Gradual onset. Is a slowly progressive disorder. 
Joints of the hand:
Distal interphalangeal joints (DIP)
Proximal interphalangeal joints (PIP)
First carpometacarpal joint (CMC)
Spine
Weight-bearing joints of lower limbs:
esp. knees and hips
First metatarsophalangeal joint (MTP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are symptoms and signs of osteoarthritis?

A 
Joint pain - worse with activity, better with rest
Joint crepitus - creaking, cracking grinding sound on moving affected joint
Joint instability (‘giving way’)
Joint enlargement - e.g. Heberden’s nodes
Joint stiffness after immobility (‘gelling’)
Limitation of range of motion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are radiographic features of osteoarthritis?

A

Joint space narrowing
Subchondral bony sclerosis
Osteophytes
Subchondral cysts

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

What are the clinical features of and physiological, cellular and molecular changes during inflammation?

A

Features: Rubor, Dolor, Calor, Tumor, Loss of function
Changes:
1. Increased blood flow
2. Migration of white blood cells (leucocytes) into the tissues
3. Activation/differentiation of leucocytes
4. Cytokine production E.g. TNF-alpha, IL1, IL6, IL17

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

What are the causes of joint inflammation?

A

1) Infection - Septic arthritis, Tuberculosis
2) Crystal arthritis - Gout, Pseudogout
3) Immune-mediated (“autoimmune”) - E.g. Rheumatoid arthritis, Psoriatic arthritis, Reactive arthritis, Systemic lupus erythematosus (SLE)

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

What causes septic arthritis and what are risk factors?

A

Bacterial infection of a joint (usually caused by spread from the blood). Risk factors are being immunosuppressed, pre-existing joint damage, intravenous drug use (IVDU).

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

What are considerations regarding septic arthritis?

A

Septic arthritis is a medical emergency - Untreated, septic arthritis can rapidly destroy a joint. Usually only 1 joint is affected* (monoarthritis). Consider septic arthritis in any patient with an acute painful, red, hot, swelling of a joint, especially if there is fever.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is septic arthritis diagnosed and what commonly causes it? How is it treated?

A

Diagnosis is by joint aspiration. Send sample for urgent Gram stain and culture. Common organisms:
Staphylococcus aureus, Streptococci, Gonococcus. Gonococcal septic arthritis is an exception:
It often affects multiple joints (polyarthritis) and it is less likely to cause joint destruction. Treatment is with surgical wash-out (‘lavage’) and intravenous antibiotics.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is gout and what is it caused by?

A

Gout is a syndrome caused by deposition of urate (uric acid) crystals which leads to inflammation. High uric acid levels (hyperuricaemia) is a risk factor for gout. Causes of hyperuricaemia include genetic tendency, increased intake of purine rich foods and reduced excretion (kidney failure).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is pseudogout and what is it caused by?

A

Pseudogout is a syndrome caused by deposition of calcium pyrophosphate dihydrate (CPPD) which causes inflammation. Risk factors: background osteoarthritis, elderly patients, intercurrent infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are clinical features of gout?

A

Gout typically presents as an acute monoarthritis of rapid onset. The first metatarsophalangeal joint is the most commonly affected joint (podagra). Gout also affects other joints: joints in the foot, ankle, knee, wrist, finger, and elbow are the most frequently affected. Crystal deposits (tophi) may develop around hands, feet, elbows, and ears.

21
Q

What are features of crystal arthritis seen radiologically and through synovial fluid analysis?

A

X-rays show juxta-articular ‘rat bite’ erosions at the MTPJ of the great toe if gout present. The diagnosis of crystal arthritis is made by aspirating fluid from the affected joint and examining it under a microscope using polarized light. If gout, needle shaped crystals with negative birefringence seen. If pseudogout, rhomboid shaped crystals with positive birefringence seen.

22
Q

What is rheumatoid arthritis characterised by?

A

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

23
Q

What are key features of rheumatoid arthritis?

A
  1. 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
  2. Extra-articular disease can occur
    Rheumatoid nodules
    Others rare e.g. vasculitis, episcleritis
  3. Rheumatoid ‘factor’ may be detected in blood
    Autoantibody against IgG - should really call this rheumatoid ‘antibody’ not ‘factor’
24
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)
25
Q

What is the primary pathology in rheumatoid arthritis?

A

Primary site of pathology is in the synovium which includes synovial joints, tenosynovium and bursa.

26
Q

What are 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.

27
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.

28
Q

What are 2 areas that should be checked for subcutaneous nodules?

A

Rheumatoid nodule found in ulnar border of forearm. If they are present it confirms the diagnosis of rheumatoid arthritis and is invariably associated with rheumatoid factor. May also be present in the hands around the PIP joint of the right index and left index, middle and ring fingers.

29
Q

What is abnormal about synovial membrane in rheumatoid arthritis?

A

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’).

30
Q

What are the features of a healthy synovial membrane?

A

1 to 3 cell layer that lines synovial joints. Contains macrophage-like (type A synoviocyte) and fibroblast-like (type B synoviocyte) cells and type I collagen. Functions include the maintenance of synovial fluid, the hyaluronate-rich viscous fluid within joint space.

31
Q

What is the characteristic pathological feature (cytokine) of rheumatoid arthritis?

A

The cytokine tumour necrosis factor-alpha (TNFα) is the dominant pro-inflammatory cytokine in the rheumatoid synovium. Produced mainly by activated macrophages in rheumatoid synovium. Actions include:

  1. Pro-inflammatory cytokine release - IL-1, IL-6, IL-8, IL-23, GM-CSF
  2. Chemokine release - leukocyte accumulation
  3. Endothelial cell activation
  4. Chondrocyte activation - metalloproteinase production, cartilage degradation
  5. Osteoclast activation - bone resorption
32
Q

How is TNFα inhibited?

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.

33
Q

What antibodies are found in patients with RA?

A
  1. Rheumatoid factor
    Antibodies that recognize the Fc portion of IgG as their target antigen - typically IgM antibodies i.e. IgM anti-IgG antibody
    Positive in 70% at disease onset and further 10-15% become positive over the first 2 years of diagnosis
  2. Antibodies to citrullinated protein antigens (ACPA)
    Antibodies to citrullinated peptides are highly specific for rheumatoid arthritis e.g. Anti-cyclic citrullinated peptide antibody ‘anti-CCP antibody’
    Citrullination of peptides is mediated by enzymes termed Peptidyl arginine deiminases (PADs)
34
Q

What is the treatment goal of RA and what does this require?

A

Treatment goal is to 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.

35
Q

What drug treatment is used against RA?

A

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

36
Q

What is biological therapy?

A

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

37
Q

What biological therapies are used against RA?

A
  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.
38
Q

Rheumatoid vs OA: age of onset, speed of onset, joint pattern, movement, AM stiffness

A

RA: 30-50, rapid, bilateral/symmetrical, often better movement
OA: Over 50, slow onset, asymmetric, often worse movement

39
Q

Rheumatoid vs OA: Affected hand joints, wrist/ankle/elbow, systemic symptoms, joint swelling, ESR/CRP, Serology

A

RA: PIP/MCP, common, common, effusion red warm, elevated ESR/CRP, positive for RF.
OA: DIP, thumb CMC, uncommon, not present, bony, normal, negative

40
Q

What are radiographic changes observed in RA and OA?

A

Joint space narrowing seen with RA and OA. Subchondral sclerosis seen in OA but not in RA. Osteophytes seen in OA but not RA. Osteopenia seen in RA but not OA (juxta-articular osteopenia is common early radiographic sign in inflammatory arthritis of any cause). Bony erosions seen in RA but not OA.

41
Q

What is psoriatic arthritis and how does it classically present?

A

Psoriasis is an autoimmune disease affecting the skin (scaly red plaques on extensor surfaces eg elbows and knees). Unlike RA, rheumatoid factors are not present (“seronegative”) and there is a varied clinical presentation but classically asymmetrical arthritis affecting IPJs (interphalangeal joints).

42
Q

How can psoriatic arthritis also present?

A

But also can manifest as:

  • Symmetrical involvement of small joints (rheumatoid pattern)
  • Spinal and sacroiliac joint inflammation
  • Oligoarthritis of large joints
  • Arthritis mutilans
43
Q

What is reactive arthritis and what are extra-articular features of it?

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

44
Q

What are key points about reactive arthritis?

A
  • 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
  • Reactive arthritis is distinct from infection in joints (septic arthritis)
45
Q

What are key differences between septic arthritis and reactive arthritis?

A

Synovial fluid culture is positive for septic arthritis and negative for reactive arthritis. Antibiotics used to treat septic arthritis but not reactive arthritis, similarly for joint lavage.

46
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).

47
Q

Why are autoantibodies useful in SLE?

A

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.

48
Q

Describe epidemiology of SLE

A

F:M ratio 9:1
Presentation 15 - 40 yrs
Increased prevalence in African and Asian ancestry populations
Prevalence varies 4-280/100,000

Musculoskeletal (5 decks)

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