Osteo-Arthritis and Rheumatoid Arthritis Flashcards
Roughly compare OA and RA
Both are disorders of joints (chronic inflam) but differ in their pathogenesis, presentation and complcations
. OA: result in subchondral cysts/sclerosis
. RA: result in panus and have ankylosis
What is OA?
. AKA ‘Wear and tear’ disease
. Degenerative joint disease
. Erosion and disordered repair of articular cartilage that result in subchondral bone damage
. affect LARGE joints
Etiology (causes) of OA?
. physical stress - affects weight bearing joints
. wear and tear disease (age)
. genetic predispose to chondrocyte injury
What altered chondrocytes homeostasis (making it proliferate)?
. decrease proteoglycan conc
. decrease collagen type II fibres
=> result in hyperplasia of chondrocytes
List the main pathological changes of OA
- Fibrillation of cartilage
- Eburnation
- Sclerosis
- Subchondral cysts
- Osteophytes
Pathological changes of OA (1)
Fibrillation of cartilage
. loose cartilage
. cartilage break down and become dehydrated until it’s completely lost
Pathological changes of OA (2)
Eburnation
. Bone grinding bone - ‘shiny’ due to devoid of cartilage
Pathological changes of OA (3)
Sclerosis
. Hardening of bone
. may contribute to the weight distribution
Pathological changes of OA (4)
Subchondral Cysts
. Joint’s fluid (synovial) creep into the eburnated articulating bone forming cysts surrounded by fibrosis
Difference between cyst and abscess
Cyst = cavity filled with fluid (synovial) Abscess = cavity filled with pus
Pathological changes of OA (5)
Osteophytes
. Narrowing of joint space due to mushroom-shaped bony outgrowths
note: osteophytes of the distal interphalangeal joints in women called ‘Herberden nodes’
What’s special about OA?
NO ankylosis
NO inflam at synovial
NO swollen joints
NO treatment or prevention yet
What is RA?
. Systemic autoimmune disease chracterized by inflam polyarthritis
. have RF and ACPAs
RF= rheumatoid factor which is aB against IgG
APACs = anti-citrullinated peptide aB
. affects SMALL joints (hand and feet)
In RA, what makes T and B cells response to self antigens, including antigens in joint tissue?
- Susceptibility genes (HLA) leads to failure of tolerance and unregulated lymphocyte activation
- Environmental factors (infection, smoking) leads to enzymatic modification of self protein (citrullination)
In RA, what cytokines create joint inflammation, triggering activation and proliferation of synovial cells, chondrocytes and fibroblasts?
IFN-g : Th1 cells
IL-17 : Th17 cells
TNF : Mø (main)
What are clinical features of RA?
Female bias
Pain in hand joints, morning stiffness
Swelling wrist, metacarpal phalangral and proximal of interphalangeal (not distal)
What diseases associated with RA?
Diabetes Type 1
SLE (Systemic lupus erythematosis)
Graves Disease
Hashimoto Thyroiditis
What does joint changes in RA? What is the name of change?
. Proliferated synovial lining cells, inflammatory cells, granulation tissue and fibrous tissue
. they release proteases to damage cartilage
. called PANNUS
What can we see in synovial histology in RA patients?
. synovial cell thickening with formation of villi + multiple layers of synovium –> HYPERPLASIA
. Lots infiltration of synovium by inflammatory cells (p/m B cell and lymphocyte)
What are local complication of RA?
Joint instability
Eroding cartilage
Bony and fibrous ankylosis
What are systemic complications of RA?
Hallmarks of chronic disease:
- anaemia
- fatigue
- loss of appetite
- high CRP and acute phase proteins
- intermittent fever, weight loss
Subcutaneous rheumatoid nodules develop along extensor of skin and may involve viscera
4 features of hand deformities in RA
- Radius deviation = wrist
- Ulnar deviation = finger (metacarps)
- Boutonnière = flexion of proximal interphalangeal + hyperextension of distal
- Swanneck = opposite
Aim of treatment for RA
. Control pain
. Early treatment to prevent joint destruction and consequent deformity and disability
. Active monitoring
. Improving patient’s quality of life
Treatment available for RA
. pain relief
. physiotherapy
. immunosuppression (steroids, Disease-modifying Anti-Rheumatic drugs) like TNF antagonists
. methotrexate
What is osteomyelitis?
Inflammation of Bone MARROW caused by infection of bacteria (S.aureus)
In osteomyelitis, how does bacteria gain entry into the bone?
Haematogenous dissemination, spread of infection from adjacent side, trauma, iatrogenic
What happens if not treating osteomyelitis?
. becomes CHRONIC:
- increase P leads to dead medullary bone which forced pus to arrive to under periosteum
- Lifting periosteum stops supply of blood to cortical bone, lead to necrotic bone - sequestrum
- Periosteum lays down new bone on surface that entraps the sequestrum - involucrum
- Pus ooze out into soft tissues - sinuses
note: sequestrum may extrude through a sinuse
Treatment of osteomyelitis
. Antibiotics
. Surgical debridement (if no clinical improvement in 24-48h)
