RA & OA & GOUT

Question 1

anatomy of synoviol joint

Answer 1

Question 2

what is the most common joint disease?

Answer 2

OA

Question 3

name some types of arthritis?

Answer 3

• OA
• Post-traumatic
• Inflammatory (RA)
• scondary to childhood hip disease

Question 4

Define Osteoarthritis, & what r the common areas in the body?

Answer 4

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

Question 5

pathogenesis of OA

Answer 5

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!

Question 6

Aeitology

Answer 6

Primary > dunno

secondary > trauma, infiltrative disease or connective tissue diseases

Question 7

risk factors (5)

Answer 7

1. obesity
2. female
3. manual labor work
4. FH
5. AGE

Question 8

DDx

Answer 8

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

Question 9

causes of secondary osteoarthritis!

(vitamen C)

Answer 9

Trauma
• Previous joint disorders;
• Developmental Dysplasia of the Hip (DDH)

• Infection: Septic arthritis, Brucella, Tb
• Inflammatory: RA, AS
• Metabolic: Gout
• Haematologic: Haemophilia
• Endocrine: DM

Question 10

Where does the patient complain in OA of the Hip joint?

Answer 10

-pain in the hip, gluteal, groin areas radiated to the knee

Question 11

Clinical Features & examination

Answer 11

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.

Question 12

Joint finding on xray

OA vs RA

Answer 12

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)

Question 13

Explain the reason behind the findin on Xray fro OA

Answer 13

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!

Question 14

what do u call osteoarthritis of the hip joint?

Answer 14

Coxarthrosis

Question 15

what is the age & speed of onset in RA vs OA

Answer 15

RA-happens at any age>>Rapid

OA-usually later in life>>Over year (Slow)

Question 16

Answer 16

Question 17

systemic symptoms for each? RA and OA

Answer 17

RA-fatigue-fever-night sweats

OA-none (doesn’t affect systemic remember?)

Question 18

what does the joint cartilage consist of?

how is that changed in osteoarthritis?

Answer 18

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!

Question 19

Management of OA

Answer 19

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

Question 20

how can we prevent OA?

Answer 20

• regular exercise
• weight control
• prevention of trauma

Question 21

name some risks of hip replacement

Answer 21

• dislocation
• leg length discrepancy
• infection!
• fracture
• loosening of components
• future surgery to revise components

Question 22

Explain the joint findings in OA and RA

Answer 22

Question 23

What is GOUT?

what crystals do u see?

Answer 23

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

Question 24

What is uric acid?

how does that lead to Gout?

Answer 24

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

1. ur kidneys r unable to get rid of it
2. or ur body is just making too much purines for some reason

Question 25

what could be the reason for increased Monosodium urate crystals?

Answer 25

Question 26

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?

Answer 26

Swollen, red, painful after a meal or alcohol consumption ( cuz alcohol metabolites compete for the same excretion sites in the kidney as uric acid!

Question 27

Causes?

Answer 27

* Heridietry * high dietry purine * alchohol excess * Dieuretics * tumor lysis (cytotoxins)

Question 28

Ix

Answer 28

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

Question 29

complications?

Answer 29

***long term urate crystal deposits*** * Gouty tophi (pinna, tendons, joints) * renal disease (interstitial nephritis, stones)

Question 30

1st line treatment of acute attack? What if attack has settled? what if u had previous gout?

Answer 30

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**

Question 31

Prevention | (avoid what?)

Answer 31

Lose weight avoid prolonged fasts avoid pruine rich foods avoid low dose aspirin (increases serum urate bc interfers with its excretion from kidneys)

Question 32

difference between osteoporosis and Osteomalacia?

Answer 32

Osteomalacia= defective mineralization of Osteoid due to VD deficiency (soft bones) Osteoposrosis= loss in bone mass (spongy bone)

Question 33

Question 34

what is osteoporosis? Types? risk factors?

Answer 34

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*

Question 35

what is perthes disease?

Answer 35

condition effecting the hip joint of chikdren blood to head of femur is disrupted

Question 36

explain osteomalacia

Answer 36

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*

Question 37

rickets?

Answer 37

is osteomalacia but in children. bc the epipheseal plate cannot caldify, long bone become abnormally long and widen