Joint Pathology Flashcards

1
Q

What should the bones at synovial joints be like?

A

Fit nicely together with even distribution of pressure

Not touch - separated by cartilage

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2
Q

What type of cartilage is articular cartilage?

A

Hyaline

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3
Q

What attracts water in cartilage?

A

Glycosaminoglycans

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4
Q

How is the collagen arranged in articular cartilage?

A

To hold glycosaminoglycans compressed together

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5
Q

Are there any blood vessels in articular cartilage?

A

No

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6
Q

How is articular cartilage perfused?

A

Compression/decompression of cartilage > pushes water in and out

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7
Q

What do the capsule, tendons, and ligaments at the joint do?

A

Hold everything together

Crucial to joint stability and movement

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8
Q

Where is the synovium?

A

Lines joint space

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9
Q

Where is the synovium attached?

A

Firmly anchored to capsule and bone at edges of cartilage

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10
Q

What is the synovium?

A

Vascular connective tissue with synovial membrane

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11
Q

What are the cell types of the synovium?

A

25% type A “macrophage-like” synoviocytes

75% type B “fibroblast-like” synoviocytes

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12
Q

Why is the synovial membrane not an epithelium?

A

No basement membrane

No junctional complexes

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13
Q

What makes up synovial fluid?

A

Plasma filtrate - easily crosses in and out of joint space
Hyaluronic acid - makes viscous
Lubricin - makes slippery
Etc

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14
Q

How thick is the synovial membrane?

A

1-4 cell layers

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15
Q

Why is osteoarthritis classified as a degenerative disease?

A

Cartilage wears away

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16
Q

Does osteoarthritis present symmetrically?

A

No

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17
Q

When is pain worst in osteoarthritis?

A

At end of day

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18
Q

What is released by the cartilage matrix and synovial cells in osteoarthritis?

A
Enzymes
- Collagenases
- MMPs
Cytokines
- IL-1
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19
Q

What parts of the joint does osteoarthritis affect?

A

Capsule
Synovium
Bone

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20
Q

What is the pathophysiology of osteoarthritis?

A
Damage stimulates chondrocyte
- Hypertrophy
- Proliferation
- Enzyme/cytokine secretion
Unravelling of cartilage matrix, release of enzymes, loss of frictionless mechanical function
Changes in bone
- Thickening
- Microfractures
Shedding of cartilage
- Fibrillation
- Erosions
Bone-on-bone
- Eburnation
- Cysts
- Osteophytes
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21
Q

What is the morphology of osteoarthritis?

A
Remaining cartilage looks rough
Eburnation of bone
Fibrillation of articular cartilage
Subchondral cysts
Non-uniform loss of cartilage
Subchondral thickening
Osteophytes
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22
Q

What is eburnation?

A

Bone looks like ivory

23
Q

What are osteophytes?

A

Cartilage growths which become bone through endochondral ossification

24
Q

How can osteophytes affect the joint?

A

Can impinge on range of movement/nearby structures; eg: in spine, impinge on nerves
Can improve joint stability

25
Q

What are the symptoms of osteoarthritis?

A
Pain
- Deep, achy
- Worse after activity
Onset over years
Non systemic symptoms
26
Q

What are the signs of osteoarthritis?

A

Reduced range of movement
Crepitus
Osteophytes

27
Q

What are Bouchard’s nodes?

A

Osteophytes in proximal interphalangeal joints

28
Q

What are Heberden’s nodes?

A

Osteophytes in distal interphalangeal joints

29
Q

What is the relationship between x-ray and clinical findings in osteoarthritis?

A

Severity of x-ray findings don’t always correlate with severity of clinical findings

30
Q

What is subchondral sclerosis?

A

Bone thicker under damaged cartilage

31
Q

What are the risk factors for osteoarthritis?

A

Increasing age
Obesity
Previous injury/abnormality of joint
Repeated heavy use of joint

32
Q

What is the disease classification of rheumatoid arthritis?

A

Systemic inflammatory disease

33
Q

What is rheumatoid arthritis?

A

Autoimmune attack on connective tissue

34
Q

What other organs can rheumatoid arthritis affect?

A

Skin
Blood vessels
Heart
Lungs

35
Q

What is the primary stimulus in rheumatoid arthritis?

A

Unknown

Triggered in genetically susceptible individuals

36
Q

What is the pathophysiology of rheumatoid arthritis?

A
Self reactive Th1 and Th17 cells activate
Secrete cytokines
- IL-1
- IL-6
- IL-17
- TNF-alpha
Induce
- Fibroblasts
- Macrophages
- Osteoclasts
- B cells
- T cells
- DCs
- Mast cells
Exuberant granulation tissue-like synovium
Collagenases and MMPs
Breakdown of cartilage and bone
37
Q

What is the morphology of the inflammatory changes in the joints in rheumatoid arthritis?

A

Neutrophils and fibrin may be found in joint space
Mononuclear infiltrate in synovium
- Germinal centres
Hyperplasia of synovium with villus formation
- Pannus
Pannus invades and erodes cartilage and bone
Weakening and destruction of ligaments

38
Q

What is pannus?

A

Inflammatory granulation-like tissue in synovium

39
Q

What are the symptoms of rheumatoid arthritis?

A
Symmetrical polyarthritis
- Usually starts in hands and feet
- Distal interphalangeal joints often spared
Morning stiffness
- Eases with activity
Systemic symptoms
- Fever
- Weight loss
- Anaemia
40
Q

What are the signs of rheumatoid arthritis?

A

Warm, swollen joints
Rheumatoid nodules
- Common under skin but can get elsewhere
- 30-40% of patients
- Predicts severe disease
Evential destruction and deformity of joints

41
Q

What does a rheumatoid nodule look like histologically?

A

Evidence of granulomatous inflammation
Epithelioid macrophages
Lymphocytes and fibrosis
Central necrosis

42
Q

What do general inflammatory tests show in rheumatoid arthritis?

A

CRP, ESR, and FBE all show changes of inflammation

43
Q

What are more specific tests that can be done to diagnose rheumatoid arthritis?

A

Rheumatoid factor
- Not high specificity and sensitivity
Anti-cyclic citrullinated peptide (anti-CCP) Abs (ACPAs)
- More specific

44
Q

What is the role of x-rays in diagnosing rheumatoid arthritis?

A

Little role

45
Q

What are the risk factors for rheumatoid arthritis?

A

Genetic
Female
Smoking
Increasing age from 25-55

46
Q

What is the pathophysiology of gout?

A

Too much uric acid in body
- Asymptomatic at first
- Eventually precipitates in cool areas with low pH and nucleating agents
- Especially after alcohol/dehydration/dietary indiscretion
Crystals can activate inflammatory cells, synovial cells, and complement
- Acute inflammatory cascade
- IL-1, complement, and chemotaxis > crystals lyse neutrophils

47
Q

What happens if gout remains untreated?

A

Progresses into chronic, disabling, tophaceous gout

48
Q

What is tophaceous gout?

A
Involvement of multiple joints
Recurrent joint inflammation causes damage
- Can form pannus
Urate deposition in other soft tissue
- Forms tophi
Gouty neuropathy and kidney stones
49
Q

What type of inflammation is a gouty tophus?

A

Granulomatous inflammation (foreign body type)

50
Q

What are the signs of gout?

A

Acutely inflamed joint
Seldom systemically unwell
Tophi if chronic

51
Q

What are the symptoms of gout?

A
Spontaneous onset of
- Excruciating pain
- Swelling
-  Heat
- Redness
Classically in big toe in early morning
52
Q

What is the gold standard for diagnosing gout?

A

Joint/tophus aspiration

- Negatively birefringent crystals with neutrophils

53
Q

Why is measuring serum urate confusing?

A

Acute gout attack can lower serum urate
Urate-lowering therapy can precipitate gout
Most people with high urate don’t have gout

54
Q

What are the risk factors for gout?

A
Male
Increasing age
Menopaus
Abnormal uric acid metabolism
Genetics and ethnicity
Obesity
Hypertension
Metabolic syndrome