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BRS Musculoskeletal System > Intro to Rheumatology > Flashcards

Intro to Rheumatology Flashcards

1
Q

Describe fibrous joints including their functional classification.

A

Synarthroses - Generally allow no movement OR
Amphiarthroses - Allow very limited movement
No space between the bones.
E.g. Sutures in skull, syndesmosis (sheet of connective tissue) in tibia and fibula joint (Ankle)

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2
Q

Describe cartilaginous joints including their functional classification.

A

Synarthroses - Generally allow no movement OR
Amphiarthroses - Allow very limited movement
Joints in which bones are connected by cartilage.
E.g. Joints between spinal vertebrae.

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3
Q

Describe synovial joints including their functional classification.

A

Diarthroses - Allow for free movement of the joint.
Have a space between adjoining bones (synovial cavity)
This space is filled with synovial fluid.

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4
Q

Describe the components of a synovial joint.

A

2 bone ends lined by articular cartilage. Joint cavity containing synovial fluid.

Articular cartilage - 1-3 cell deep lining containing macrophage-like phagocytic cells (type A synoviocyte) and fibroblast-like cells that produce hyaluronic acid (type B synovicocyte) + Type 1 Collagen

Synovial fluid - Hyaluronic acid-rich + viscous fluid

Synovium - Type II collagen + proteoglycan (mainly aggrecan) > Gives a smooth lining to the ends of the bones in the joint.

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5
Q

What is cartilage composed of and describe its blood supply?

A

Composed of specialised cells (chondrocytes) and ECM: water, collagen, proteoglycans (mainly aggrecan)

Cartilage is avascular (no blood supply)

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6
Q

What is aggrecan?

A

Proteoglycan that pocesses many chondroitin and keratin sulphate chains.
Characterised by its ability to interact with hyaluronan (HA) to form large proteoglycan aggregates.

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7
Q

What is arthritis?

A

Disease of the joints

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8
Q

What are the 2 major divisions of arthritis?

A

Osteoarthritis - Degenerative (Cartilage worn out)

Inflammatory arthritis - Primary problem is inflammation (main type is RA)

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9
Q

What are the pathological changes in OA?

A

Cartilage worn out, bony remodelling

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10
Q

What is the epidemiology of OA?

A

More prevalent as age increases.
Previous joint trauma (e.g. footballer’s knees)
Jobs involving heavy manual labour

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11
Q

Describe the onset of OA.

A

Gradual

Slowly progressive disorder

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12
Q

Which joints are typically affected in OA?

A

Joints of hand - Distal interphalangeal joints (DIP), proximal interphalangeal joints (PIP), 1st carpometacarpal (CMC)

Spine

Weight-bearing joints of lower limbs - esp. knees and hips, 1st metatarsophalangeal joint (MTP)

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13
Q

What is joint crepitus?

A

Creaking, cracking grinding sound on moving affected joint - often OA

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14
Q

What are the names of the nodes seen in OA?

A

Heberden’s Nodes - Osteophytes at the DIP joints are termed.
Bouchard’s Nodes - Osteophytes at the PIP joints are termed.

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15
Q

What are the symptoms and signs of OA?

A 
Joint Stiffness after immobility ('gelling') 
Joint Pain (worse with activity, better with rest) 
Joint Instability ('giving way') 
Joint Crepitus 
Joint Enlargement e.g. Heberden's Nodes 
Limitations of range of motion

Heberden’s Nodes (osteophytes at DIP)
Bouchard’s Nodes (osteophytes at PIP)

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16
Q

What features can be be seen on an X-ray (radiographic features) of an OA patient? (Classic findings)

A

Joint space narrowing (bone contacting bone) > Reflects wearing out of normal cartilage layer.
Subchondral bony sclerosis (increased white appearance on X-ray)
Osteophytes - bone spurs
Subchondral cysts

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17
Q

What is inflammation and what are its 5 cardinal features?

A

A physiological response to deal with injury or infection. Excessive/inappropriate inflammatory reactions can damage the host tissues.

Manifest clinically as:
Redness (Rubor) 
Swelling (Tumor)
Pain (Dolor) 
Heat (Calor) 
Loss of function
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18
Q

What are the physiological, cellular and molecular changes that occur in inflammation?

A

Increased blood flow
Migration of WBCs (leucocytes) into tissues
Activation/differentiation of leucocytes
Cytokine production (E.g. TNF-alpha, IL-1,16 and 17 - Important ones for joint disease)

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19
Q

What are the causes of joint inflammation?

A

Infection - Septic arthritis, TB

Crystal arthritis - Gout and pseudo-gout

Immune-mediated (autoimmune) - Rheumatoid arthritis, psoriatic arthritis, reactive arthritis, SLE

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20
Q

What causes septic arthritis?

A

Bacterial infection (usually caused by haematogenous spread)

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21
Q

What are the risk factors of SA?

A

Immunosuppressed, pre-existing joint damage, intravenous drug use (IVDU)

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22
Q

Why is septic arthritis classified as a medical emergency?

A

Untreated, septic arthritis can rapidly destroy a joint.

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23
Q

How many joints are usually affected in septic arthritis?

What is the main exception?

A

1 (mono-arthritis)

Gonococcal septic arthritis - often affects multiple joints (polyarthritis); it is less likely to cause joint destruction.

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24
Q

When should you consider septic arthritis for a patient?

A

Any patient with an ACUTE painful, red, hot swelling of a joint, especially if there is a fever.

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25
Q

What technique can you use to diagnose septic arthritis?

A

Joint aspiration (then send sample for urgent gram stain and culture)

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26
Q

What bacteria are commonly responsible for septic arthritis?

A

Staphylococcus aureus, Streptococci, Gonococcus

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27
Q

How can you treat septic arthritis?

A

Surgical wash out (lavage) and IV antibiotics

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28
Q

When does crystal arthritis occur?

A

Results when crystals deposit in the joint triggering an inflammatory reaction.

(2 main types → Gout and pseudogout)

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29
Q

What is gout caused by?

A

Deposition of urate (uric acid) crystals → Inflammation

30
Q

What is hyperuricaemia?

A

High uric acid levels in blood → Risk factor for gout (not everyone who has high levels will have develop attacks of gout)

31
Q

What are the causes of hyperuricaemia?

A

Genetic tendency

Increased uptake of purine rich foods (Purine gets broken down into uric acid → Beer drinkers particularly vulnerable).

Reduced excretion (kidney failure) of uric acid

32
Q

What is pseudo-gout?

A

Syndrome caused by deposition of calcium pyrophosphate dihydrate (CPPD) crystals → Crystals lead to inflammation.

33
Q

What are the risk factors of pseudo-gout?

A

Background osteoarthritis, elderly patients, intercurrent infection.

34
Q

What are the clinical features of gout?

A

Typically presents with an acute mono-arthritis. First MTP joint is the most commonly affected joint (Podagra)

Other joints affected → joints in foot, ankle, knee, wrist, finger and elbow are most frequently affected.

Crystal deposits (tophi) developing around hands, feet, elbows and ears. → Yellowish appearance

35
Q

The diagnosis of crystal arthritis is made by aspirating fluid from affected joint and examining under a microscope using polarised light. What would you see for gout and pseudo-gout?

A

Gout - needle-shaped crystals with -ive birefringence.

Pseudo-gout - rhomboid shaped crystals with +ive birefringence.

36
Q

What is the most common immune-mediated inflammatory disease and explain what this condition is?

A

Rheumatoid arthritis (RA) - chronic autoimmune disease characterised by pain, stiffness and symmetrical synovitis of synovial (diarthroidal) joints.

37
Q

What are the 3 key features of rheumatoid arthritis?

A

Chronic arthritis: Polyarthritis - swelling of small joints of hand and wrists.
Symmetrical
Early-morning stiffness in and around joints (gradually eases up as patient starts moving); Lasts more than 30 minutes. May lead to joint damage and destruction - ‘joint erosions’ on radiographs.

Extra-articular disease - Rheumatoid nodules. Other rare e.g. vasculitis, episcleritis (type of inflammation of eye)

Rheumatoid ‘factor’ may be detected in blood of patients - Autoantibody against IgG

38
Q

What is the pattern of joint involvement in rheumatoid arthritis and what are the most commonly affected joints?

A

Symmetrical

Polyarthritis

Affects small and large joints, but particularly hands and feet.

39
Q

What joints are most commonly affected in RA?

A 
MCP 
PIP
Wrists 
Knees 
MTP
40
Q

The primary site of pathology for rheumatoid arthritis is the synovium (inflammation occurs here). What 3 things does this include?

A

Synovial joints

Tenosynovium surrounding tendons

Bursa (fluid-filled sacs that provide lubrication to allow easy movement)

41
Q

What are the common and uncommon extra-articular features of rheumatoid arthritis?

A

Common - Fever, weight loss, Subcutaneous nodules

Uncommon - Vasculitis, Ocular inflammation - episcleritis, Neuropathies, Amyloidosis, Lung disease - nodules, fibrosis, pleuritis (inflammation of pleura which are the lining of the lungs)
Felty’s Syndrome - triad of splenomegaly, leukopenia and RA

42
Q

What is Felty’s Syndrome a triad of?

A

splenomegaly, leukopenia and RA

43
Q

What is a typical position for detection of a rheumatoid nodule?

A

Ulnar border → Presence confirms diagnosis of rheumatoid arthritis as it is invariably associated with rheumatoid factor.

44
Q

Describe a healthy synovial membrane?

A

1-3 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.

45
Q

In the rheumatoid arthritis the synovium becomes a proliferated mass of tissue (pannus) due to what?

A

Neovascularisation

Lymphangiogenesis

Inflammatory cells → activated B and T cells, plasma cells, mast cells and 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)

46
Q

What cytokine is the dominant pro-inflammatory cytokine in the rheumatoid synovium?

A

TNF-alpha

47
Q

What does TNF-alpha do for a person to develop rheumatoid arthritis?

A

TNF-alpha has an affect on multiple process contributing to inflammatory response and destruction of the joint in the long term.

48
Q

What are the actions of TNF-alpha that develop RA in a person?

A

Osteoclast activation (excessive bone erosion)

Pro-inflammatory cytokine release

Hepcidin induction

PGE2 production

Chondrocyte activation - Cartilage degradation > Joint narrowing

Angiogenesis

Chemokine release (RANTES, MCP-1, IL-8, SDF-1)

Endothelial cell activation (up regulation of E-selectin and VCAM-1 + leukocyte activation)

Leukocyte accumulation

49
Q

How is inhibition of this cytokine achieved?

A

Through parenteral administration of either antibodies or fusion proteins.

50
Q

What are the 2 types of autoantibodies that are found in blood of patients with rheumatoid arthritis and explain their mechanisms?

A

Rheumatoid factor - Abs that recognise the Fc portion of IgG as their target antigen. Typically IgM antibodies i.e. IgM anti-IgG antibody.

Antibodies to citrullinated protein antigens (ACPA) - highly specific for rheumatoid arthritis (Anti-cyclic citrullinated peptide antibody - anti-CCP Ab)
Citrullination is mediated by enzymes termed peptidyl arginine deaminase (PADs). Convert arginine to citrulline.

51
Q

What is citrullination mediated by?

A

Enzymes termed peptidyl arginine deaminase (PADs). Convert arginine to citrulline

52
Q

What is the overall treatment goal for rheumatoid arthritis and what does this goal therefore require?

A

Treatment goal - Prevent joint damage.

This requires early recognition of symptoms and referral from GP to a rheumatologist, prompt initiation of treatment (joint destruction gets worse with time) and AGGRESSIVE treatment to suppress inflammation.

53
Q

What drugs are used for treatment of rheumatoid arthritis and what are the 1st and 2nd line treatments?

A

Disease-modifying anti-rheumatic drugs (DMARDs)

1st Line treatment - Methotrexate in combination with with hydroxychloroquine or sulfasalzine.

2nd Line treatment - Biological therapies.
New therapies include Janus Kinase inhibitors: Tofacitinib and Baricitinib

(Can also use glucocorticoid therapy (prednisolone) → Avoid long term use due to side effects)

54
Q

What MDT approaches are important in the management of rheumatoid arthritis?

A

Physiotherapy, OT, hydrotherapy, (surgery → barely needed)

55
Q

What can biological therapies do to help in the treatment of rheumatoid arthritis and give examples of each?

A

Inhibition of TNF (anti-TNF) - Antibodies (infliximab and others) and Fusion proteins (etanercept)

B-cell depletion - Rituximab - Ab against the B-cell antigen CD20.

Modulation of T cell co-stimualtion - Abatacept - fusion protein - extracellular domain of human CTL associated antigen 4 (CTLA-4) linked to modified Fc (hinge, CH2, CH3 domains) of human IgG1

Inhibition of IL-6 signalling - Tocilizumab (RoActemra) and Sarilumab (Kevzara) antibody against IL-6 receptor.

56
Q

What is anakinra?

A

IL-1 receptor antagonist → not currently recommended for rheumatoid arthritis treatment in UK

57
Q

Why might treatment with infliximab and rituximab be rejected by a patient?

A

Both have Fab regions which have a mouse sequence hence they are chimeric (human/mouse) antibodies.

Patient likely to develop antibodies to this mouse component → Effect of drugs on TNF and CD20 respectively will wear off.

58
Q

What are the differences between rheumatoid arthritis and osteoarthritis (excluding radiographic)?

A

RA: 30-50 yrs; rapid onset; bilateral + symmetric joint pattern; movement often better; >1hr of AM stiffness, hand joints - PIP, MCP; wrist, ankle, elbow is common; systemic symptoms common; joint swelling: effusion, red, warm; elevated ESR, CRP; serology (sero+ RF)

OA: >50 yrs; slow onset; asymmetric joint pattern; movement often worse; uncommon AM stiffness, hand joints - 1st CMC, DIP; wrist, ankle, elbow is uncommon; systemic symptoms not present; joint swelling:bony; normal ESR, CRP; serology (sero-)

59
Q

What are the differences and similarities in the radiographic features (X-rays) of rheumatoid and osteoarthritis?

A

Similarities - Joint space narrowing

Differences - OA has subchondral sclerosis and osteophytes RA doesn’t. RA has osteopenia and bone erosion OA doesn’t.

60
Q

What is psoriatic arthritis?

A

Autoimmune disease affecting skin (scaly red plaques on extensor surfaces)

61
Q

Are rheumatoid factors present in patients with psoriatic arthritis?

A

No; they are seronegative

62
Q

What is the classical clinical presentation of psoriatic arthritis?

A

Classically asymmetrical arthritis affecting IPJs

63
Q

What else can psoriatic arthritis manifest as other than the classical presentation?

A

Symmetrical involvement of small joints (rheumatoid pattern)
Spine and sacroiliac joint inflammation
Oligoarthritis of large joints
Arthritis mutilans

64
Q

What is septic arthritis?

A

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

65
Q

What are the important extra-articular manifestations of reactive arthritis?

A

Enthesitis (another form of tendon inflammation)
Skin inflammation
Eye inflammation

66
Q

Reactive arthritis may be the first manifestation of what 2 infections?

A

HIV and Hep-C infection

67
Q

How long do symptoms follow for reactive arthritis after infection?

A

1-4 weeks after infection

68
Q

What is SLE?

A

Multi-system autoimmune disease. Autoantibodies are directed against components of the cell nucleus (nucleic acids and proteins).

Can affect almost any organ - often joints (get pain), skin, kidneys, haematology, lungs and CNS.

69
Q

What are the key differences between septic and psoriatic arthritis?

A

SA - Synovial fluid culture positive; AB therapy - YES; Joint Lavage? - Yes for large joints

PA - Synovial fluid culture negative; AB therapy - NO; Joint Lavage? - No

70
Q

What is the epidemiology for SLE?

A

F:M is 9:1
15-40 yrs
Increased prevalence in African and Asian ancestry populations.
Prevalence varies.

BRS Musculoskeletal System (6 decks)

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