MSK pathology Flashcards
vitamin D-deficient osteoporosis pathogenesis and presentation
pathogenesis: lack of oral vit D intake ± lack of sun exposure ± lack of 25α-hydroxylase in the liver ± lack of 1α-hydroxylase in the kidney ± increased PTH leads to osteomalacia (defective bone mineralisation) causing osteoporosis
presentation: osteopenia (pre-osteoporosis), frequent fractures
pathogenesis of osteoarthritis
multiple factors leading to degenerative, inflammatory and reparative activity involving articular cartilage and subarticular bone
- increased unit load on joint
- degradation of articular cartilage
- genetic abnormalities (mutation of type II collagen COL2A1)
- biochemical abnormalities (decreased proteoglycans/protein synthesis/chondrocyte replication)
- formation of osteophytes due to irregular bone outgrowth
- reactive thickening of synovium
- secondary changes to surrounding tissue
presentation and complications of osteoarthritis
presentation: pain upon movement (that doesn’t decrease after 30min in the morning), limitation of movement, swelling of joint, osteophytes
complications: cervical spondylosis, spinal nerve compression
variants of osteoarthritis
- primary generalized OA: post-menopausal women
- erosive inflammatory OA: severe destructive disease with rapid progression
- hypertrophic OA: florid osteophyte formation, bone sclerosis, slow progression
aetiology of degenerative intervertebral disc
- genetic predisposition
- age related wear and year
- mechanical factors resulting in cracks, fissures and tears to the disc annulus and nucleus pulposus
- nutrition/metabolism/infection
stages of disc herniation
- normal
- degeneration: nucleus pulposus bulges through annulus
- prolapse: nucleus pulposus continues bulging, but outer layer still intact
- extrusion: nucleus pulposus herniates out through a tear in the annulus
- sequestration: portions of the nucleus pulposus break free
rheumatoid arthritis classical presentation
- female
- 40-60yo
- symmetrical polyarthritis affecting the metacarpophalangeal joints
- morning stiffness subsiding after 30min
- synovial inflammation leading to swelling and villous formation of synovium
- pannus formation with granulation tissue destroying articular cartilage, causing ankylosis
- destruction of bone due to pannus causing joint deformity, formation of rheumatoid nodules, necrotising vasculitis of small vessels, amyloidosis
rheumatoid arthritis pathophysiology
- cytokine-mediated inflammation
- strongly associated with HLA-DR4
- autoantibodies against cyclic citrullinated peptides (CCP)
- indicated with seropositive autoantibodies: rheumatoid factor and anticitrullinated protein antibody
types of necrosis + cells found in rheumatoid arthritis
fibrinoid necrosis, increased macrophages and histiocytes
types of seronegative spondyloarthropathies
- ankylosing spondylitis: destruction and fusion of vertebral column and sacroiliac joints
- psoriatic arthropathy: asymmetric distal interphalangeal joints
- reactive arthritis (post infective): triad of conjunctivitis, polyarthritis, urethritis
types of autoimmune arthritis
- systemic lupus erythematous: increased ANA antibodies
- rheumatic fever (due to streptococcus pyogenes)
- systemic sclerosis
systemic sclerosis
septic arthritis pathogenesis and presentation
pathogenesis: infection caused by haematogenous dissemination / direct inoculation into skin / contiguous infective spread from adjacent soft tissue abscess
presentation: acute onset of severe joint pain, warm swollen joint, fever and systemic symptoms
diagnosis of crystal arthropathies
joint fluid aspiration and analysis under polarized microscopy: gout = strongly negatively birefringent needle shaped crystals, pseudogout = positively birefringent rhomboid shaped crystals
primary vs secondary gout pathogenesis
gout: increased serum uric acid and urate crystal deposition due to overproduction of purines + catabolism of nucleic acids + decreased uric acid excretion –> neutrophilic phagocytosis causing tissue inflammation
primary gout: idiopathic cause associated with obesity, alcohol, hypertension and fatty diet
secondary gout: caused by known conditions promoting hyperuricaemia (drugs, renal failure, familial juvenile hyperuricaemia nephropathy, congenital enzyme defects)
presentation of crystal arthropathies
deposition of crystals in joints and soft tissues, causing arthritis, acute pain, redness and swelling in the joints (particularly foot and big toe for gout)
complications of gout
deformities, joint erosion, gouty tophi, interstitial nephritis, kidney disease, renal failure
pathogenesis of pseudogout
deposition of calcium pyrophosphate crystals associated with trauma, hyperparathyroidism and haemochromatosis
how do infective agents enter the bone in osteomyelitis?
- direct implantation
- bloodborne spread
- extension from contiguous site
osteomyelitis common pathogens
Staphylococcus aureus, Escherichia coli, Group B Streptococcus, Haemophilus influenzae, Salmonella, anaerobes, Mycobacterium tuberculosis
common location of osteomyelitis in children vs adults
children: long bones (trauma), jaw (poor dental health)
adults: small bones of foot, femur and vertebral spine
types of osteomyelitis (and presentation)
suppurative: acute-on-chronic, pyogenic
non-suppurative: minimal pus, mainly chronic inflammation and fibrosis
histological findings of chronic osteomyelitis
- large amount of neutrophils
- langhans giant cells (for tuberculous OM)
- native necrotic bone (sequestrum) surrounded by reactive woven bone tissue (involucrum)
progression of osteomyelitis
- suppurative injury, causing tissue destruction
- elevation of periosteum: inflammation –> subperiosteal pus lifts up the periosteum –> impaired blood supply and bone necrosis
- rupture of periosteum: causes inflammation in surrounding skin and soft tissue
sequelae of osteomyelitis
- HEALED!! resolution (no scarring) or fibrosis (got some scarring)
or
- complications: pathological fracture, spread of infection, bone abscess (Brodie’s abscess), necrosis of bone, proliferative periostitis and involucrum, secondary amyloidosis, malignant transformation (rare)
complications of tuberculous osteomyelitis
- compression fractures
- severe deformities (scoliosis and kyphosis)
- neurological deficits due to cord and nerve compression
Garré’s sclerosing osteomyelitis pathogenesis and presentation
pathogenesis: chronic osteomyelitis with proliferative periostitis, usually in the jaw of children and adolescents after dental infection/trauma
presentation: growth in the jaw
common causes of soft tissue pain
systemic inflammatory rheumatic syndrome, rheumatic symptoms of endocrinopathy, toxic/drug reaction, generalized soft tissue pain syndromes
presentation of systemic inflammatory rheumatic syndromes
- significant morning stiffness that eases with movement
- insidious pain onset
- hallmarks of inflammation
- muscle weakness
- focal neurologic abnormalities
- e.g. polymyalgia rheumatica
drug reactions that can cause soft tissue pain
- HMG CoA reductase inhibitor
- zidovudine (used for HIV)
- ethanol
- clofibrate (used for hypercholesterolemia)
- ciclosporin A (immunosuppressant)
- penicillamine
generalized soft tissue pain syndromes
- fibromyalgia: diagnosis of exclusion
- major depressive disorder
- hypermobility syndrome
- somatoform pain disorder
- myofascial pain syndrome
lab tests for soft tissue pain
FBC!!
1. leukocytes + platelets high = systemic inflammatory process
2. anaemia = chronic disease
3. ESR high = inflammation (faster cell clumping)
4. ESR low = anaemia
5. CRP high = inflammation (binds to pathogens to encourage phagocytosis)
6. creatine kinase high = muscle injury
7. albumin low = inflammation
