Inflammatory Flashcards

1
Q

Inflammatory bone conditions

A
  1. Osteoarthritis (degenerative)
  2. Rheumatoid Arthritis (autoimmune)
  3. Gout & pseudogout (crystal deposition)
  4. Osteomyelitis & septic arthritis (infection)
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2
Q

Features of osteoarthritis

A
  • mot common degenerative joint disease

- involves chronic progressive erosion/destruction of articular cartilage

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3
Q

Causes of osteoarthritis (2)

A
  1. Primary, idiopathic (95%)

2. Secondary - due to other joint disease, trauma, congenital abnormality, avascular necrosis, metabolic/endocrine

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4
Q

Clinical presentations of osteoarthritis

A
  • deep achy pain, worsens with use, swelling, limited ROM, morning stiffness
  • OA of intervertebral joints - impingement of osteophytes on spinal foramina - nerve root compression - pain, spasms, muscle atrophy
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5
Q

Radiology of osteoarthritis (4)

A
  • XR
    1. narrowing of joint space
    2. sclerosis - increased thickness of subchondral bone
    3. subchondral cyst formation
    4. osteophyte formation - peripheral growths of bone & cartilage
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6
Q

Variants of osteoarthritis (3)

A
  1. Primary generalised OA - post menopausal women
  2. Erosive inflammatory OA - rapid progression
  3. Hypertrophic OA
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7
Q

Pathogenesis of osteoarthritis

A
  • Multiple factors eg increased unit load on joint, degradation of articular cartilage, biochemical abnormalities, genetic abnormalities
  • Degenerative, inflammatory & reparative activity involving articular cartilage & subarticular bone, with secondary effects on synovium, muscle & nerves
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8
Q

Morphology of osteoarthritis

A
  1. Destruction of articular cartilage - thinning, erosion, fibrillation - leading to narrowing of joint space
  2. Thickening of subchondral bone - due to constant friction bw 2 naked bone surfaces - eburnation (smooth polished surface)
  3. Subchondral cyst formation - cystic lesions representing intraosseus accumulation of synovial fluid, leak through gaps in exposed subchondral bone
  4. Osteophyte/bone spurs formation eg Heberden’s nodes - due to irregular outgrowths of bone
  5. Reactive thickening of synovium & other secondary changes to surrounding tissue eg muscle atrophy
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9
Q

Features of rheumatoid arthritis

A
  • multi-systemic chronic inflammatory disease
  • involves joints symmetrically & bilaterally
  • more common in women (3:1), 4th-6th decades
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10
Q

Clinical features of rheumatoid arthritis (4)

A
  1. Acute inflammation - pain, swelling, warmth, redness, loss of function/movement
  2. Commonly in joints of hand (PIP, MCP), wrist, elbows, knees
  3. Subcutaneous rheumatoid nodules (25%)
  4. Necrotising vasculitis, amyloidosis
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11
Q

Pathogenesis of rheumatoid arthritis

A
  • strong association w HLA-DR4
  • several autoantibodies produced eg rheumatoid factor RF, anticitrullinated protein antibody (ACPA)
  • inappropriate activation of CD4 T helper cells - activation of inflam pathways
    (A) B cell activation - RF formation - immune complex formation & deposition - injury
    (B) macrophage activation - releases cytokines - promotes fibroblast, chondrocyte & synovial cell prolif + release of enzymes eg collagenase, PGE2
    (C) endothelial activation - expression of adhesion molecules - accumulation of inflamm cells
  • pathways converge - pannus formation, destruction of bone, cartilage, fibrosis, ankylosis
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12
Q

Morphology of rheumatoid arthritis (4)

A
  1. Synovial inflammation - synovitis w chronic inflammatory infiltrate, exudate & fibrin - swelling & villous formation
  2. Pannus formation - vascular granulation tissue that grows across cartilage surface + destruction of articular cartilage
  3. Destruction of adjacent bone (due to pannus) - joint deformity, erosions radiologically
  4. Formation of rheumatoid nodules
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13
Q

Causes of gout (2)

A
  1. Primary gout - idiopathic, assoc w obesity, alcohol, HTN, fatty diet
  2. Secondary gout - conditions that promote hyperuricemia eg specific drugs, renal failure, familial juvenile hyperuricemic nephropathy, congenital enzyme defects
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14
Q

Pathogenesis of gout (2)

A
  1. Problems of purine (precursor to uric acid) metab - increased uric acid (excreted by kidney) prod + decreased uric acid elimination
  2. Overproduction of purines (high purine diet eg meat or increased de novo synthesis), increased catabolism of nucleic acids due to high cell turnover (eg infection, cancer, decreased excretion by kidneys)
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15
Q

Complications of gout

A
  • deformities
  • erosion of joints
  • gouty tophi
  • interstitial nephritis, kidney disease (stones), renal failure
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16
Q

Features of gout

A
  • characterised by increased serum uric acid & urate crystals deposition
  • strongly birefringent needle shaped crystals under polarised microscopy
17
Q

Features of pseudogout

A
  • or calcium pyrophosphate crystal arthritis
  • idiopathic, assoc w trauma, hyperparathy, hemochromatosis
  • asymptomatic/presents as acute arthritis
  • weakly birefringent rhomboid shaped crystals under polarised light
18
Q

Causes of osteomyelitis

A
  • S. aureus, E. coli, strep, H. influenzae, salmonella, M. tb
    may enter via
    1. direct implantation (trauma w open fracture, wound, surgery)
    2. blood borne spread (eg lung TB to bone)
    3. extension from contiguous site (eg middle ear infection with mastoiditis)
19
Q

Clinical presentation of osteomyelitis

A
  • pyogenic - acute or chronic, tuberculous

- pain, fever, swelling, constitutional symptoms

20
Q

Sites of osteomyelitis

A
  • involves bone cortex, medulla, periosteum
  • children: long bones - upper & lower limbs
  • adults: feet, vertebral spine, femur
21
Q

Progression of osteomyelitis

A
  • bacterial proliferation in bone - acute inflam + cell death (bone necrosis)
  • bacteria & inflamm spread within shaft of bone, haversian system & periosteum
  • if infection extends to joint/synovium - septic arthritis