RA, OA, etc

Question 1

Stage 1 RA

Answer 1

Preclinical
Well before signs arise, immune pathology begins
Raised erythrocytes, C-reactive proteins + rheumatoid factors may be detectable years before diagnosis

Question 2

Stage 2 RA

Answer 2

Synovitis
Synovial membrane becomes inflamed + thickened
Although painful + swollen Jt + tendon still intact, disorder potentially reversible

Question 3

Stage 3 RA

Answer 3

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

Question 4

Stage 4 RA

Answer 4

Deformity
Combination of articulate destruction, capsular stretching + tendon rupture leads to progressive instability + deformity

Question 5

RA presentation

Answer 5

Insidious emergence of symmetrical poly arthritis affecting hands/feet
Morning stiffness
Women affected 3x more

Question 6

Early stage RA presentation

Answer 6

Swelling, stiffness, increased warmth + tenderness of proximal inter-pharyngeal Jt

Question 7

Progressive symptoms of RA

Answer 7

Increase restriction
Deformity
Constant ache

Question 8

RA deformities

Answer 8

Ulnar deviation of fingers
Valgus knees/feet
Clawed toes

Question 9

Epidemiology of RA

Answer 9

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

Question 10

Risk factors of RA

Answer 10

High frequency of HLA-DR4
Being female
Multiple Jt involvement
Younger age
Prescience of erosion at diagnosis

Question 11

RA age groups

Answer 11

40-60

Question 12

Treatment of RA

Answer 12

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

Question 13

Ankylosing spondylitis pathology

Answer 13

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

Question 14

Inflammation process of ank spon

Answer 14

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

Question 15

Presentation of ank spon

Answer 15

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

Question 16

Causes of ank spon

Answer 16

Genetics- specifically HLA-B27
Potentially triggered by recent event- often genitourinary or bowel induced

Question 17

Risk factors of ank spon

Answer 17

HLA-B27 gene
Male

Question 18

Ge groups of ank spon

Answer 18

Young men
15-25
M:F 2:1

Question 19

Treatment for ank spon

Answer 19

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

Question 20

Initial process of OA

Answer 20

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

Question 21

OA presentation

Answer 21

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

Question 22

Epidemiology of OA

Answer 22

increased age- takes years to develop
Relationship between stress on articulate cartilage + ability of cartilage to withstand stress

Question 23

Risk factors of OA

Answer 23

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

Question 24

Age groups affected y OA

Answer 24

Usually after middle age
Cartilage changes start 10-20 years before this
In younger Pt, almost always Hx of Jt disorder

Question 25

Treatment of OA

Answer 25

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

Question 26

Gout pathology

Answer 26

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

Question 27

Gout presentation

Answer 27

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

Question 28

DDX of gout

Answer 28

Pseudo-gout
Infection
RA

Question 29

Epidemiology of gout

Answer 29

Obesity
Kidney disease
Drinking too much alcohol

Question 30

Risk factors of gout

Answer 30

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