RA & OA & GOUT Flashcards

1
Q

anatomy of synoviol joint

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the most common joint disease?

A

OA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

name some types of arthritis?

A
  • OA
  • Post-traumatic
  • Inflammatory (RA)
  • scondary to childhood hip disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

pathogenesis of OA

A

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!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Aeitology

A

Primary > dunno

secondary > trauma, infiltrative disease or connective tissue diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

risk factors (5)

A
  1. obesity
  2. female
  3. manual labor work
  4. FH
  5. AGE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

DDx

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

causes of secondary osteoarthritis!

(vitamen C)

A

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

  • Infection: Septic arthritis, Brucella, Tb
  • Inflammatory: RA, AS
  • Metabolic: Gout
  • Haematologic: Haemophilia
  • Endocrine: DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Clinical Features & examination

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Joint finding on xray

OA vs RA

A

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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Explain the reason behind the findin on Xray fro OA

A

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!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what do u call osteoarthritis of the hip joint?

A

Coxarthrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

RA-happens at any age>>Rapid

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
A
17
Q

systemic symptoms for each? RA and OA

A

RA-fatigue-fever-night sweats

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

18
Q

what does the joint cartilage consist of?

how is that changed in osteoarthritis?

A

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!

19
Q

Management of OA

A

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
20
Q

how can we prevent OA?

A
  • regular exercise
  • weight control
  • prevention of trauma
21
Q

name some risks of hip replacement

A
  • dislocation
  • leg length discrepancy
  • infection!
  • fracture
  • loosening of components
  • future surgery to revise components
22
Q

Explain the joint findings in OA and RA

A
23
Q

What is GOUT?

what crystals do u see?

A

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
24
Q

What is uric acid?

how does that lead to Gout?

A

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
25
Q

what could be the reason for increased Monosodium urate crystals?

A
26
Q

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?

A

Swollen, red, painful

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

27
Q

Causes?

A
  • Heridietry
  • high dietry purine
  • alchohol excess
  • Dieuretics
  • tumor lysis (cytotoxins)
28
Q

Ix

A

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

29
Q

complications?

A

long term urate crystal deposits

  • Gouty tophi (pinna, tendons, joints)
  • renal disease (interstitial nephritis, stones)
30
Q

1st line treatment of acute attack?

What if attack has settled?

what if u had previous gout?

A

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

31
Q

Prevention

(avoid what?)

A

Lose weight

avoid prolonged fasts

avoid pruine rich foods

avoid low dose aspirin (increases serum urate bc interfers with its excretion from kidneys)

32
Q

difference between osteoporosis and Osteomalacia?

A

Osteomalacia= defective mineralization of Osteoid due to VD deficiency (soft bones)

Osteoposrosis= loss in bone mass (spongy bone)

33
Q
A
34
Q

what is osteoporosis?

Types?

risk factors?

A

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*
35
Q

what is perthes disease?

A

condition effecting the hip joint of chikdren

blood to head of femur is disrupted

36
Q

explain osteomalacia

A

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*
37
Q

rickets?

A

is osteomalacia but in children.

bc the epipheseal plate cannot caldify, long bone become abnormally long and widen