RA & OA & GOUT Flashcards
anatomy of synoviol joint
what is the most common joint disease?
OA
name some types of arthritis?
- OA
- Post-traumatic
- Inflammatory (RA)
- scondary to childhood hip disease
Define Osteoarthritis, & what r the common areas in the body?
it is degenerative, chronic bone disease “wear & tear”>> progressive loss of articular cartilage and remodelling of the underlying bone.
it is a clinical syndrome of joint pain
- hips
- knees
- small joints of hands
pathogenesis of OA
the chondrocytes, which r important in mainting the articular cartilage has 2 activites which is kept in balance (see below).
The release of enzymes from these cells break down collagen and proteoglycans, destroying the articular cartilage.
The exposure of the underlying subchondral bone results in sclerosis, followed by reactive remodelling changes that lead to the formation of osteophytes and subchondral bone cysts. The joint space is progressively lostover time.
but in OA they mediate DEGREDATION more!
Aeitology
Primary > dunno
secondary > trauma, infiltrative disease or connective tissue diseases
risk factors (5)
- obesity
- female
- manual labor work
- FH
- AGE
DDx
inflammatory arthropathies ( rheumatoid arthritis)
crystal arthropathies (gout), septic arthritis, fractures, bursitis, or malignancy (primary or metastatic).
Joint specific differential diagnoses for osteoarthritis:
- Hand– De Quervain’s tenosynovitis, RA, and gout
- Hip – trochanteric bursitis, radiculopathy, spinal stenosis, or iliotibial band syndrome
- Knee– referred hip pain, meniscal or ligament tears, or chondromalacia patellae
causes of secondary osteoarthritis!
(vitamen C)
Trauma
• Previous joint disorders;
• Developmental Dysplasia of the Hip (DDH)
- Infection: Septic arthritis, Brucella, Tb
- Inflammatory: RA, AS
- Metabolic: Gout
- Haematologic: Haemophilia
- Endocrine: DM
Where does the patient complain in OA of the Hip joint?
-pain in the hip, gluteal, groin areas radiated to the knee
Clinical Features & examination
pain and stiffness in joints, worsened with activity* > relieved by rest.
Pain tends to worsen throughout the day
stiffness tends to improve.
EXAMINATION
INSPECT HANDS
Bouchard nodes (swelling of PIPJs)
Heberden nodes (swelling of DIPJs)
Fixed flexion deformity or varus malalignment in the knees.
Joint finding on xray
OA vs RA
OA
- *L** – loss of joint space
- O** – *osteophytes
- *S** – subchondral sclerosis
- *S** – subchondral cysts
RA
- *L** – loss of joint space
- *E** – erosions
- *S** – soft tissue swelling
- *S** – soft bones (osteopenia)
Explain the reason behind the findin on Xray fro OA
Loss of joint space> due to degredation of Articular cartilage
osteophytes> as bone gets damaged, new bones form around
subchondrial sclerosis> the function of the cartilage is to help transmit the forces of bone equally, when that is gone the exposure of the underlying bone compensates in thickening up causing sclerosis
subchondrial cysts (LATE) > as bone is being damaged w/ time, cavitation w/in the bone forms, and that fills us with cyst like fluid!
what do u call osteoarthritis of the hip joint?
Coxarthrosis
what is the age & speed of onset in RA vs OA
RA-happens at any age>>Rapid
OA-usually later in life>>Over year (Slow)
systemic symptoms for each? RA and OA
RA-fatigue-fever-night sweats
OA-none (doesn’t affect systemic remember?)
what does the joint cartilage consist of?
how is that changed in osteoarthritis?
The surface changes alter the distribution of the biochemical forces
u also get CHONDROCYTES CLONING! in ana attempt to restore articular cartilage
wtf? normal chondrocytes r fully differentiated and dont need to proliferate!
Management of OA
conservative, medical, surgical
- if fat> loose weight
- strengthening excersizes
- local heat or Ice
- joint supports and physio
Medical
simple analgesics and topical NSAIDS
intra-articular steroid injections
Surgical
- Osteotomy
- Arthrodesis (joint fusion)
- Arthroplasty
how can we prevent OA?
- regular exercise
- weight control
- prevention of trauma
name some risks of hip replacement
- dislocation
- leg length discrepancy
- infection!
- fracture
- loosening of components
- future surgery to revise components
Explain the joint findings in OA and RA
What is GOUT?
what crystals do u see?
accumalation of Monosodium Urate crystals in joints
due to Hyperurecima
Negatively Birefringent crystals
- due to underexcretion of uric acid
- due to overproduction of uric acid
What is uric acid?
how does that lead to Gout?
the break down product of purines contain in DNA
Urate is created every day when our bodies break down purines.
Purines are chemicals that are naturally created in our body, but they are also present in certain foods.
It’s normal and healthy to have some urate in your bloodstream.
some ppl think its caused mainly from what we eat, but 3/4 of the urate comes from the breakdown of purines already exsisting our bodies.
so the main cause can be either
- ur kidneys r unable to get rid of it
- or ur body is just making too much purines for some reason
what could be the reason for increased Monosodium urate crystals?
Which areas does Gout mostly effect?
describe the symptoms?
when does the attack mostly occur?
what do u call pain in the MTP joint in GOUT?
Swollen, red, painful
after a meal or alcohol consumption ( cuz alcohol metabolites compete for the same excretion sites in the kidney as uric acid!
Causes?
- Heridietry
- high dietry purine
- alchohol excess
- Dieuretics
- tumor lysis (cytotoxins)
Ix
Labs (do all bloods to check for kidney function)
- hyperuricemia (> 6.8 mg/dL)
(not sufficient for the diagnosis)
- the level may be lower during an attack?
Synovial fluid analysis
- joint fluid aspiration
crystal analysis is gold-standard negatively birefringent needle-shaped crystals under polarized light
yellow under parallel light and blue under perpendicular light
complications?
long term urate crystal deposits
- Gouty tophi (pinna, tendons, joints)
- renal disease (interstitial nephritis, stones)
1st line treatment of acute attack?
What if attack has settled?
what if u had previous gout?
Rest & elevate legs/ ice packs
In acute attacks
high dose NSAID or Coxib > etoricoxib 120mg/24hrs
If Ci (peptic ulcer, anticoagul, HF) > Colichine 0.5mg/6-12hr
After attack has settled, pt is given ULT to prevent further gouts from occuring.REMEMBER that dont give ULT in acute attacks!! CAN HAVE MORE ATTACKS within the first 6 mnths of starting them.
Don’t stop taking your ULTs if this happens to you, as this is actually a sign that the drugs are working. As the drugs start dissolving the crystals, they become smaller and are more likely to get into the joint cavity, triggering an attack.
ALLOPURINOL> Xanthine oxidase inhibitor
Prevention
(avoid what?)
Lose weight
avoid prolonged fasts
avoid pruine rich foods
avoid low dose aspirin (increases serum urate bc interfers with its excretion from kidneys)
difference between osteoporosis and Osteomalacia?
Osteomalacia= defective mineralization of Osteoid due to VD deficiency (soft bones)
Osteoposrosis= loss in bone mass (spongy bone)
what is osteoporosis?
Types?
risk factors?
Bones become “porous”
decrease in bone mass!
- enhanced bone resorption relative to formation!*
- Type 1> occurs in postmenopausal women, & is due to INCREASE IN OSTEOCLAST #! as a result of estrogen withdrawl!*
- Type 2> occurs in elderly, due to attenuated osteoblast function.*
RISK FACTORS:
- -genetic*
- -low ca+ intake*
- -insufficient Ca+ absorption*
- -Excersize*
- -cigarette smoking*
what is perthes disease?
condition effecting the hip joint of chikdren
blood to head of femur is disrupted
explain osteomalacia
defective bone mineralization due to lack of VD (which is needed to absorb Ca from the gut)
- The osteoid is produced, BUT, Ca+ salts r not adequetly deposited>> bones r soft and weak*
- osteoid is the ground matrix which consists of ground substance*
rickets?
is osteomalacia but in children.
bc the epipheseal plate cannot caldify, long bone become abnormally long and widen
