RA, OA, etc Flashcards
Stage 1 RA
Preclinical
Well before signs arise, immune pathology begins
Raised erythrocytes, C-reactive proteins + rheumatoid factors may be detectable years before diagnosis
Stage 2 RA
Synovitis
Synovial membrane becomes inflamed + thickened
Although painful + swollen Jt + tendon still intact, disorder potentially reversible
Stage 3 RA
Destruction
Persistent inflammation cause Jt + tendon destruction
Articulate cartilage eroded, partly by prolific enzymes, vascular tissue, direct invasion of cartilage by granulated tissue
Can occur in tendons, causing partial or complete destruction
Stage 4 RA
Deformity
Combination of articulate destruction, capsular stretching + tendon rupture leads to progressive instability + deformity
RA presentation
Insidious emergence of symmetrical poly arthritis affecting hands/feet
Morning stiffness
Women affected 3x more
Early stage RA presentation
Swelling, stiffness, increased warmth + tenderness of proximal inter-pharyngeal Jt
Progressive symptoms of RA
Increase restriction
Deformity
Constant ache
RA deformities
Ulnar deviation of fingers
Valgus knees/feet
Clawed toes
Epidemiology of RA
Cause unknown
Believed that foreign antigen- possibly virus- sets off chain of events —> chronic inflammatory disorder in which abnormal immunological reactions are prominent (e.g., production of antibodies)
Immune response may be genetically predetermined. High levels of HLA-DR4
Risk factors of RA
High frequency of HLA-DR4
Being female
Multiple Jt involvement
Younger age
Prescience of erosion at diagnosis
RA age groups
40-60
Treatment of RA
Runs variable course, difficult to predict
No cure, multi-disciplinary approach needed from beginning
Corticosteroid used for rapid action, NSAIDs to control P + stiffness
Exercise programmes for strength/flexibility
Preventative splint-age
Encourage activity
Operation if conservative doesn’t work
Ankylosing spondylitis pathology
Synovitis of diarthrodial Jt
Inflammation at fibro-Seoul’s junction of syndesmotic Jt, tendon + lig
Ossification across periphery of intervertebral disc
Starts as inflammation of sacroiliac + vertebral Jt + lig
Inflammation process of ank spon
Inflammation- granulation tissue formation- erosion of articulate cartilage or bone- replacement b fibrous tissue- ossification of fibrous tissue- ankylosing
If many vertebrae are involved, spine may become rigid
Presentation of ank spon
Persistent backache + stiffness
Often worse in morning or after periods for rest
Reduced ROM, specifically ext
Occasionally peripheral Jt swollen + tender
Complaints of painful heels + tenderness at Achilles
Causes of ank spon
Genetics- specifically HLA-B27
Potentially triggered by recent event- often genitourinary or bowel induced
Risk factors of ank spon
HLA-B27 gene
Male
Ge groups of ank spon
Young men
15-25
M:F 2:1
Treatment for ank spon
Not as crippling as RA
General measures to maintain satisfactory posture + preserve movement
Anti-inflammation drugs to counteract P + stiffness
TNF inhibitors for severe diseases
Operations to correct deformity or restore movement
Initial process of OA
Softening of cartilaginous surface
Becomes frayed
Eventually worn away to expose underlying bone
In areas of great stress, bone can develop cysts, surrounding trabecular can become thickened
Vascular congestion
Ossification producing bony growths
Destruction + repair
OA presentation
May be confined to 1/2 Jt
Women tend to have multiple Jt affected
P starts insidiously + increase slowly over few months
Aggravated by exertion + relieved by rest
Stiffness usually worse after rest
Swelling, crepitus, deformity, tenderness, muscle wasting, reduced ROM
Epidemiology of OA
increased age- takes years to develop
Relationship between stress on articulate cartilage + ability of cartilage to withstand stress
Risk factors of OA
Ageing
Weakening of cartilage could be due to genetic defects
Increased stress on articulate surface- sport
Conditions causing Jt incongruent- inevitably develop OA
Trauma- fractures of articulate surface, injuries resulting in Jt instability
Occupation- receptive stress (constant knee bending)
Family history
Age groups affected y OA
Usually after middle age
Cartilage changes start 10-20 years before this
In younger Pt, almost always Hx of Jt disorder
Treatment of OA
Principles of early treatment- relive P, increase movements, reduce load
NSAIDs, rest, activity, modification
JT mobility can be improved by physio
Walking stick, wearing soft-soled shoes, avoidance of prolonged stressful activity
Intermediate- operative treatment may be needed if conservative doesnt work (e.g, removal of osteopahytes)
Late- Jt replacement
Gout pathology
Forms conditions characterised by presence of crystals in Jt, bursa, tendons
Disorders- gout, pseudogout, basic calcium phosphate
Consequences of these- deposit may be inert + asymptomatic, may include acute inflammatory reaction, may result in slow destruction of affected tissue
Gout presentation
Acute attack- 1-2 weeks
Spontaneous, may be precipitated by minor trauma, operation, excessive alcohol
Most common site- metatarsopharyngeal Jt of big toe, ankle, olecranon bursa + finger Jt
Skin looks red, shiny, swollen, hot + tender
DDX of gout
Pseudo-gout
Infection
RA
Epidemiology of gout
Obesity
Kidney disease
Drinking too much alcohol
Risk factors of gout
More common in Caucasian people
M:W 20:1- higher uric acid levels
Menopause (rarely seen before)
Increasing levels of serum uric acid
Family HX
