Inflammatory Flashcards
1
Q
Inflammatory bone conditions
A
- Osteoarthritis (degenerative)
- Rheumatoid Arthritis (autoimmune)
- Gout & pseudogout (crystal deposition)
- Osteomyelitis & septic arthritis (infection)
2
Q
Features of osteoarthritis
A
- mot common degenerative joint disease
- involves chronic progressive erosion/destruction of articular cartilage
3
Q
Causes of osteoarthritis (2)
A
- Primary, idiopathic (95%)
2. Secondary - due to other joint disease, trauma, congenital abnormality, avascular necrosis, metabolic/endocrine
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
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
6
Q
Variants of osteoarthritis (3)
A
- Primary generalised OA - post menopausal women
- Erosive inflammatory OA - rapid progression
- Hypertrophic OA
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
8
Q
Morphology of osteoarthritis
A
- Destruction of articular cartilage - thinning, erosion, fibrillation - leading to narrowing of joint space
- Thickening of subchondral bone - due to constant friction bw 2 naked bone surfaces - eburnation (smooth polished surface)
- Subchondral cyst formation - cystic lesions representing intraosseus accumulation of synovial fluid, leak through gaps in exposed subchondral bone
- Osteophyte/bone spurs formation eg Heberden’s nodes - due to irregular outgrowths of bone
- Reactive thickening of synovium & other secondary changes to surrounding tissue eg muscle atrophy
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
10
Q
Clinical features of rheumatoid arthritis (4)
A
- Acute inflammation - pain, swelling, warmth, redness, loss of function/movement
- Commonly in joints of hand (PIP, MCP), wrist, elbows, knees
- Subcutaneous rheumatoid nodules (25%)
- Necrotising vasculitis, amyloidosis
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
12
Q
Morphology of rheumatoid arthritis (4)
A
- Synovial inflammation - synovitis w chronic inflammatory infiltrate, exudate & fibrin - swelling & villous formation
- Pannus formation - vascular granulation tissue that grows across cartilage surface + destruction of articular cartilage
- Destruction of adjacent bone (due to pannus) - joint deformity, erosions radiologically
- Formation of rheumatoid nodules
13
Q
Causes of gout (2)
A
- Primary gout - idiopathic, assoc w obesity, alcohol, HTN, fatty diet
- Secondary gout - conditions that promote hyperuricemia eg specific drugs, renal failure, familial juvenile hyperuricemic nephropathy, congenital enzyme defects
14
Q
Pathogenesis of gout (2)
A
- Problems of purine (precursor to uric acid) metab - increased uric acid (excreted by kidney) prod + decreased uric acid elimination
- 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)
15
Q
Complications of gout
A
- deformities
- erosion of joints
- gouty tophi
- interstitial nephritis, kidney disease (stones), renal failure