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BRS Bioregulatory Systems > Intro To Rheumataology > Flashcards

Intro To Rheumataology Flashcards

1
Q

2 main divisions of arthritis

A

Osteoarthritis (Degenerative arthritis)

Inflammatory arthritis (main type is rheumatoid arthritis)

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2
Q

What are the pathological changes of osteoarthritis?

A

Cartilage worn out and bony remodeling

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3
Q

Outline the epidemiology and onset of osteoarthritis.

A

Epidemiology - more prevalent as age increases, more likely if you’ve had previous joint trauma and people who have jobs involving heavy manual labour are more prone to it.

Onset - Gradual, slowly progressive disorder.

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4
Q

Which joints are affected typically in osteoarthritis?

A

Joints of hand - DIP, PIP, first CMC

Spine

Weight-bearing joints of lower limbs - especially knees and hips, first MTP (metatarsophalangeal joint)

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5
Q
  • What signs and symptoms are associated with 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 and Bouchard’s Nodes)

Joint stiffness after immobility

Limitations of range of motion

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6
Q

List the radiographic features of osteoarthritis.

A

Joint space narrowing

Subchondral bony sclerosis

Osteophytes

Subchondral cysts

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7
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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8
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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9
Q

What causes septic arthritis?

A

Bacterial infection of a joint (usually caused by haematogenous spread)

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10
Q

What are the risk factors of septic arthritis?

A

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

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11
Q

Why is septic arthritis classified as a medical emergency?

A

Untreated, septic arthritis can rapidly destroy a joint.

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12
Q

How many joints are usually affected in septic arthritis?

A

1 monoarthritis
Exception of gonoccocal septic as it affects multiple joints and can cause joint destruction

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13
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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14
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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15
Q

What bacteria are commonly responsible for septic arthritis?

A

Staphylococcus aureus, Streptococci, Gonococcus

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16
Q

How can you treat septic arthritis?

A

Surgical wash-out (lavage) and IV antibiotics

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17
Q

When does crystal arthritis occur?

A

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

(2 main types → Gout and pseudogout)

18
Q

What is gout caused by?

A

Deposition of urate (uric acid) crystals → Inflammation

19
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)

20
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

21
Q

What is pseudo-gout?

A

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

22
Q

What are the risk factors of pseudo-gout?

A

Background osteoarthritis, elderly patients, intercurrent infection.

23
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:

24
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.

25
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

-

26
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.

Commonest affected joints

MCP

PIP

Wrists

Knees

MTP

27
Q

The primary site of pathology for rheumatoid arthritis is in 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)

28
Q

Describe a healthy synovial membrane?

A

Has 1-3 cel layers which line synovial joints containing macrophages like (type A) fribroblast like (type b) and type 1 collagen

29
Q

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 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

Pro inflammatory cytokines in rheumatoid synovial

A

TNF alpha

31
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

Antibodies 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)

ACPAs are 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.

-

32
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 treatmentMethotrexate in combination with with hydroxychloroquine or sulfasalzine.
  • 2nd Line treatmentBiological therapies.New therapies include Janus Kinase inhibitors: Tofacitinib and Baricitinib

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

33
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)

Fusion proteins (etanercept)

B-cell depletion

Rituximab - Ab agains 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) - Antibody against IL-6 receptor

Sarilumab (Kevzara) - Ab against IL-6 receptor.

-

34
Q

RA VS OA

A

RA- age of onset 30-50,rapid onset,symmetrical pain,movement improves symptoms,am stiffness, PIP &MCP affected,warm red swelling,ESR &CRP elevated and positive for RF

OA-older than 50,sow onset,asymmetrical!movement worsens pain,am stiffness uncommon,DIP thumb cmc affected,bony swelling,ESR CRP normal and negative RF

35
Q

Are rheumatoid factors present in patients with psoriatic arthritis?

A

No seronegative

36
Q

What is the classical clinical presentation of psoriatic arthritis?

A

Classically asymmetrical arthritis affecting IPJs

37
Q

What is septic arthritis?

A

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

38
Q

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

A

Enthesitis (another form of tendon inflammation)

Skin inflammation

Eye inflammation

39
Q

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

A

HIV hep c

40
Q

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.

41
Q

What are the clinical tests for SLE?

A

Antinuclear antibodies (ANA) - high sensitivity for SLE but not specific. Negative test rules out SLE, but positive doesn’t mean patient has SLE.

Anti-double stranded DNA antibodies (anti-dsDNA Abs) - High specificity for SLE in context of appropriate clinical signs.

42
Q

Epidemiology

A

F:M is 9:1

15-40 yrs

Increased prevalence in African and Asian ancestry populations.

Prevalence varies.

BRS Bioregulatory Systems (54 decks)

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