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Musculoskeletal > Rheumatology Intro > Flashcards

Rheumatology Intro Flashcards

1
Q

What is 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

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2
Q

How can joints be classified?

A

classified on the basis of structure or function

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3
Q

What are the characteristics of fibrous joints?

A

Structural classification:

No space between the bones
Examples:
-sutures in the skull
-syndesmosis (sheet of connective tissue) in tibia and fibula joint (ankle

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4
Q

What are the characteristics of Cartilaginous Joints?

A

Joints in which the bones are connected by cartilage
E.g. joints between spinal vertebrae

Amphiarthroses
Allow very limited movement

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5
Q

What are the characteristics of Synovial Joints

A

Have a space between adjoining bones - synovial cavity

Filled by synovial fluid

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6
Q

What is Synarthroses?

A

Functional classification:

Generally allow no movement

( fibrous/some cartilaginous )

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7
Q

What is Amphiarthroses?

A

Functional classification

Allow for very limited movement

( Cartilaginous / some fibrous )

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8
Q

What is Diarthroses?

A

Functional classification

Allow for free movement of the joint

Synovial

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9
Q

What is the synovium? ( component of a synovial joint )

A

1-3 cell deep lining containing:

  • macrophage-like phagocytic cells (type A synoviocyte)
  • fibroblast-like cells that produce hyaluronic acid (type B synoviocyte)
  • Type I collagen
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10
Q

What is the synovial fluid? ( component of a synovial joint )

A

Hyaluronic acid-rich viscous fluid

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11
Q

What is the Articular cartilage? ( component of a synovial joint )

A

Type II collagen

Proteoglycan (aggrecan)

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12
Q

What is cartilage composed of?

A

Cartilage is composed of:
1) specialized cells (chondrocytes)
2) extracellular matrix: water, collagen and proteoglycans
(mainly aggrecan)

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13
Q

Why does cartilage heal poorly after injury?

A

Cartilage is avascular

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14
Q

What is aggrecan?

A

Aggrecan is:
-a proteoglycan that possesses many chondroitin sulfate and keratin sulfate chains

  • characterized by its ability to interact with hyaluronan (HA) to form large proteoglycan aggregates
  • diagram on ppt
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15
Q

What is arthiritis?

A

diseases of the joint

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16
Q

What are the 2 types of arthiritis?

A

Osteoarthritis
(Degenerative arthritis)

Inflammatory arthritis
(main type is rheumatoid arthritis)
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17
Q

What are the characteristics of Osteoarthritis?

A

cartilage worn out, bony remodelling

Epidemiology:

  • more prevalent as age increases,
  • previous joint trauma (e.g. footballer’s knees)
  • jobs involving heavy manual labour

Onset: gradual. Slowly progressive disorder

Joints affected typically are:
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)
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18
Q

What are the 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

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19
Q

How to diagnose Osteoarthritis?

A

X-rays

Find:
Narrowing of joint space

subchondral bony sclerosis - white

osteophytes - bone spurs
…

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20
Q

What are the causes of joint inflammation? (3)

A

Infection:
Septic arthritis
Tuberculosis

Crystal arthritis:
Gout
Pseudogout

Immune-mediated (“autoimmune”):
Rheumatoid arthritis
Psoriatic arthritis
Reactive arthritis
Systemic lupus erythematosus (SLE)
21
Q

What causes septic arthritis?

A

Bacterial infection of a joint spread by blood:
Staphylococcus aureus, Streptococci, Gonococcus*

Risk factors: immunosuppressed, pre-existing joint damage, intravenous drug use (IVDU)

22
Q

Why is septic arthritis known as monoarthitritis?

A

Usually only 1 joint is affected* (monoarthritis)

  • gonococcal septic arthritis is an exception:
  • It often affects multiple joints (polyarthritis)
  • It is less likely to cause joint destruction
23
Q

What are the signs, symptoms of septic arthritis?

How to diagnose it?

A

Consider septic arthritis in any patient with an acute painful, red, hot, swelling of a joint, especially if there is fever

Diagnosis is by joint aspiration. Send sample for urgent Gram stain and culture

Treatment is with surgical wash-out (‘lavage’) and intravenous antibiotics

24
Q

What are the characteristics of gout?

physiology, causes

A

( crystal arthritis )

Gout is 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
Reduced excretion (kidney failure)

25
Q

What are the characteristics of Pseudogout?

pathophysiology and risk factors

A

Pseudogout is a syndrome caused by deposition of calcium pyrophosphate dihydrate (CPPD) crystal deposition crystals -> inflammation

Risk factors: background osteoarthritis, elderly patients, intercurrent infection
* ppl with osteoarthritis gets uti and develops pseudogout

26
Q

What are the clinical features of gout?

A

( similar presentation as septic arthritis so should consider )

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.

27
Q

How to diagnose crystal arthritis with synovial fluid analysis?

A

The diagnosis of crystal arthritis is made by aspirating fluid from the affected joint and examining it under a microscope using polarized light

Gout: needle shaped crystals with negative birefringence

Pseudogout: rhomboid shaped crystals with positive birefringence

  • picture on slide
28
Q

What is the most common form of 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

29
Q

What are the characteristics of RA?

A

Chronic

Symmetrical

Polyarthritis

early morning stiffness

joint erosions on x-rays

  • Extra-articular disease can occur.
    Rheumatoid nodules, fever, weight loss
    Others rare e.g. vasculitis, episcleritis
30
Q

What can be detected in the blood of a person with RA?

A

Rheumatoid factor = antibody against IgG

31
Q

Which joints are most Commonly affected in RA?

A 
Metacarpophalangeal joints (MCP)
Proximal interphalangeal joints (PIP)
Wrists 
Knees
Ankles
Metatarsophalangeal joints (MTP)
  • in contrast to osteoarthritis which has issues in finger joints
32
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

  • typically seen in ulna of forearm, hands
33
Q

Describe the pathophysiology of RA?

A

Abnormal synovial membrane

Synovium becomes a proliferated mass of tissue due to:

neovascularisation
lymphangiogenesis
inflammatory cells : 
-active B T cells
-plasma cells
-mast cells
-active 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’)

34
Q

Where is the primary site of pathology of RA?

A

Is in the Synovium:

synovial joints
Tenosynovium
Bursa

  • Px with tenosynovium damage to extensor tendon in hands cannot extend little, ring finger
35
Q

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

How to treat this?

A

Cytokine tumour necrosis factor alpha ( TNF-alpha )

Its pleotropic actions are detrimental in this setting

TNFα inhibition in this condition by paranteral administration of antibodies/fusion proteins

36
Q

What autoantibodies are found in the blood of RA patients?

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

  1. Anti-cyclic citrullinated peptide antibody
37
Q

What is the citrullination of peptides mediated by?

A

Peptidyl arginine deiminases ( PADs )

38
Q

What is the first line treatment for RA?

A

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

methotrexate in combination with hydroxychloroquine or sulfasalazine

  • treatment of goal is to prevent joint damage. early on
39
Q

What is the second line treatment for RA?

A

Biological therapies are potent and targeted.

Janus Kinase inhibitors : Tofacitinib & Baricitinib

Important for glucocorticoid therapy (prednisolone)

*avoid long-term use = side-effects.

40
Q

Give four examples of biological therapies for RA?

A

Inhibition of tumour necrosis factor-alpha (‘anti-TNF’)

B cell depletion

Modulation of T cell co-stimulation

Inhibition of interleukin-6 signalling

  • check slide 40 for medication names
41
Q

What are the differences between RA and OA

  • onset age
  • onset speed
  • joints
  • movement
  • hand joints
  • systemic
  • joint swelling
  • ESR/CRP
  • Serology
A

RA:

  • onset age 30-5-
  • onset speed fast
  • symmetric
  • better movement
  • PIP, MCP
  • systemic common
  • effusion ,red ,warm
  • ESR/CRP elevated
  • Serology positive RF

OA:

  • onset age before 50
  • onset speed slow
  • asymmetric
  • bad movement
  • DIP, thumb, CMC
  • not systemic
  • bony swelling
  • ESR/CRP normal
  • Serology negative
42
Q

What is CRP?

A

C-reactive protein

43
Q

What is ESR?

A

erythrocyte sedimentation rate

44
Q

How may OA and RA be differentiated from radiographs?

A

OA : Osteophytes - as Heberden’s nodes or Bouchard’s nodes

OA : Subchondral sclerosis seen

RA : Osteopenia is a sign of inflammatory arthritis

RA: Bony erosions

  • joint space narrowing observed in both ( occur in osteoarthritis (primary abnormality) and in Rheumatoid Arthritis (secondary damage due to synovitis)
45
Q

What are the characteristics of Psoriatic arthritis?

A

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

No RFs

classically asymmetrical

But also can manifest as:

  • Symmetrical involvement of small joints (rheumatoid pattern)
  • Spinal and sacroiliac joint inflammation
  • Oligoarthritis of large joints
  • Arthritis mutilans
46
Q

What is reactive arthritis?

A

first manifestation of HIV or hepatitis C infection ( viral )

  • Reactive arthritis is distinct from infection in joints (septic arthritis)
47
Q

What is sterile infection?

A

joint inflammation following infection especially urogenital

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

48
Q

What are the differences between sterile and reactive arthritis?

A

Synovial fluid culture is + in septic and - in reactive

Antibiotic therapy is used for septic not for reactive ( which is immune caused by virus )

Joint lavage used for large septic joints, not for reactive.

49
Q

What is Systemic Lupus Erythematous (SLE)?

How can it be diagnosed?

A

Lupus is any multi-system autoimmune disease

Can affect multiple organs

Autoantibodies against nucleic acids and proteins

Diagnosis :

Antinuclear antibodies (ANA):
High sensitivity for SLE but not specific.
A negative test rules out SLE, but a positive test does not mean SLE.
  1. Anti-double stranded DNA antibodies (anti-dsDNA Abs):
    High specificity for SLE in the context of the appropriate clinical signs.

Increased in africans, asians, females, 15- 40

Musculoskeletal (4 decks)

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