Inflammatory arthritis

Question 1

Clinical presentation - inflammatory arthritis

Answer 1

• can be stilted/ crouched
• arthralgia (subtle to severe)
• may present as ataxia

Question 2

What is the first investigation of arthralgia?

Answer 2

Cytological evaluation of joint flud to determine if purulent or sterile.

• If purulent, run C+S, suggests septic arthritis
• If sterile, C+S negative, run other tests (CBC, biochem, ultrasound, thoracic rads, echocardiography, further blood work)

Question 3

Methods to investigate arthralgia

Answer 3

• rads.
• arthrocentesis
• synovial investigation
• systemic investigation (thorough PE, hx, CBC/ biochem)

Question 4

Why might arthrocentesis be useful?

Answer 4

• to determine if septic vs. immune-mediated
• look for increased neutrophils (+/- lymphocytes)
• degenerate neutrophils = septic
• non-degenerate = immune-mediated

Question 5

Why might rads. be useful for inflammatory arthritis dx?

Answer 5

• to determine if septic/ immune-mediated
• acute: normal (may be primary dz)
• sub-acute/ chronic: erosion of cartilage/ sub-chondral bone

Question 6

Describe normal synovial fluid

Answer 6

• clear
• pale
• yellow
• high viscosity

Question 7

Causes - septic arthritis

Answer 7

• haematogenous: from focus elsewhere
• traumatic (esp horses): lacerations, punctures
• Iatrogenic (often ‘aseptic’ procedures): intra-articular injections of PSGAG - rare, sx

Question 8

Tx - septic arthritis - SA

Answer 8

• AB (amox/clav acid)
• no difference b/w sx and medical tx
• 94% infxn will resolve
• may need to remove implants d/t infxn
• 6wk course AB, based on culture results

Question 9

Tx - septic arthritis - EQ

Answer 9

• acute infxn = emergency
• eliminate organisms from joint
• eliminate enzymes and mediators that cause cartilage destruction
• AB/ Through and through lavage/ arthrocopy and artrotomy
• intra-articular ABs, IV ABs (penicillin and gentamicin)
• resample joitn fluid every 48 hr
• oral AB
• AB on C+S, IV to start (amox/clav acid), possible local delivery (gentamicin, impregnated sponges), intrasynovial catheters. Tx even if negative C+S result if there is a response to empirical ABs.
• daily changed dressings for wounds
• early stages rest
• Px excellent if tx rapidly
• physio/hydro to reduce adhesions and prevent periarticular fibrosis

Question 10

Px - septic arthritis - EQ

Answer 10

• increased with prompt recognition, aggressive tx and local AB
• other factors: intended use, structures involved, concurrent bone involvement

Question 11

Define IMPA

Answer 11

Immune-mediated polyarthritis

Question 12

Aetiology -IMPA

Answer 12

• Ab/Ag complex –> formation of inflammatory products
• Host IgG and M bind to altered autologous IgG
• Ag/Ab complex deposited on synovium –> neutrophil/ macrophage chemotaxis

Question 13

Aetilogy - erosive IMPA

Answer 13

• cellular or humoral immunopathogenic factors
• release of chondrodesctuctive collagenases/ proteases
• failure of self-tolerance or production of immunogenic immunoglobulins
• plasma cells/ BCs –> RF –> synovium –> activated synoviocytes –> IL1, collagenases etc –> osteoclasts cause bone resorption and subchondral bone cysts –> pannus formation (i.e. GT formation) –> fibroblast proliferation leads to contracture and limb deformation

Question 14

What are the autoimmune aspects of IMPA - 2

Answer 14

• clones of potentially autoaggressive cells originally inactivated in the thymus proliferate
• hypersensitivity reaction

Question 15

Risk factors - autoimmune dz - 7

Answer 15

• hereditary component - beagles
• certain ifxn (GpA strep pharyngitis –> acute rheumatic fever)
• bacterial endocarditis
• discospondylitis
• IMBD
• neoplasia (various)
• chronic hepatitis

Question 16

What is a type 1 hypersensitivity reaction?

Answer 16

• immediate/ anaphylactic reaction

- IgE –> mast cells, basophils

Question 17

What is type 2 hypersensitivity?

Answer 17

• Ab-dependent cytotoxic reaction

- IgG or IgM against a cell-surface component

Question 18

What is type 3 hypersensitivity?

Answer 18

• Immune-complex mediated reaction
• Large amounts of IgG or IgM plus Ag –> microprecipitates
• clinical manifestations depend on where complexes form/ lodge
• immune-mediated arthritis: immune-complexes generated locally (joint) or systemically or both

Question 19

What is type 4 hypersensitivity?

Answer 19

• cell-mediated/ delayed-type reaction

- intra-cellular organism

Question 20

Outline features of immune-mediated arthritis

Answer 20

• polyarticular dx (6+ joints), occasionally pauciarticular (2-5), rarely monoarticular (this is more likely septic arthritis)
• Chronic dz, d/t:
• continual or recurrent presence of inciting Ag
• failure of normal down-regulation when inciting Ags gone
• initial damage to host tissues resulting in exposure of altered self-antigens

Question 21

Ddx - palmigrade stance (carpus sinking)

Answer 21

• carpal hyperextension injury
• IMPA
• endocrine dz (Cushings, both usually causes palmi- and planti- grade stance)

Question 22

How to examine patient with suspect IMPA

Answer 22

• observe walking, stiffness, difficulty rising
• general PE - pyrexia, depression, anorexia
• palpation and manipulation +/- sedation
• ROM, pain, heat, swelling, crepitus, assess ligament laxity

Question 23

With IMPA, how many animals tend to be lame vs. joint effusion?

Answer 23

• 35% lame

- 40% joint effusions

Question 24

Causes non-erosive PA

Answer 24

• Type 1 (uncomplicated idiopathis) commonest = 50%
• Type 2 (associated with remote infections, reactive arthritis), 25%
• Type 3 (associated with GIT dz/ hepatic 15%)
• Type 4 (associated with remote neoplasia),

Question 25

How to investigate non-erosive PA

Answer 25

• POLYARTHTOPATHY: arthrocentesis, joint rads., synovial biopsy
• UNDERLYING DZ HUNT: haematology, biochemistry, urinalysis, thoracic rads., abdominal ultrasound, other tests (CSF, serology, PCR)
• Joint radiography = usually not v interesting

Question 26

List some other examples of non-erosive PA

Answer 26

• SLE
• Lyme disease (Borrelia burgdorferi)
• Drug associated (e.g. Dobies + sulphonamides)
• Caliciviral in kittens
• associated with SRMA = steroid-responsive meningitis-arteritis in adolescent dogs
• IBD
• vaccine induced (within 30d vaccine)

Question 27

What can joint rads help you distinguish?

Answer 27

erosive vs. non-erosive arthritis

Question 28

Describe erosive dz

Answer 28

• chronic synovitis –> production of proliferative GT (pannus)
• pannus invades articular cartilage and can erode subchondral bone
• pannus + inflamed synovium produce enzymes including proteases and collagenases –> further joitn destruction
• similar changes in septic arthritis
• accounts for 1% PA

Question 29

Examples - erosive joint dz

Answer 29

• rheumatoid arthritis
• periosteal proliferative PA in cats
• PA of greyhounds (Felty’ syndrome)
• Felty’s syndrome - RA, splenomegaly, neutropaenia

Question 30

How to diagnose RA

Answer 30

• system in humans, but is rarely applicable in animals
• must have seven of the below present, including two of 7, 8 and 10
  1 stiffness after rest
  2 pain
  3 swelling of one joint
  4 swelling of another joint (

Question 31

Describe radiographic changes in erosive forms

Answer 31

• subchondral bone erosions
• destructive symmetric multi-joint arthropathy
• EARLY: may be only soft tissue change
• CHRONIC: collapse of joint spaces, joint deformity or subluxation, peri-articular new bone formation, calcification of peri-articular soft tissues

Question 32

Describe serology of erosive joint diseases

Answer 32

• about 75% dogs with RA have high levels of circulating RF, but not specific for RA
• differentiate from SLE by ANA test
• some dogs with RA can be positive for both

Question 33

Principles of erosive joint disease tx

Answer 33

• ID inciting factor (remove/tx)
• modify life-style to decrease joint stress (controlled exercise, weight loss, physio/hydro
• suppress immune response/ control inflammation
• pain relief
• (RA and mutlisystemic diseases e.g. SLE often need more aggressive and prolonged tx than uncomplicated PA)
• may be able to withdraw tx, may not

Question 34

What is the main drug tx for erosive joint dz?

Answer 34

• prednisolone
• immunosuppressive doses initially
• then taper dose

Question 35

What tx can be given for erosive joint dz?

Answer 35

• prednisolone - mainstay
  +/- cytotoxic drugs (cause BM suppression) e.g. cyclophosphamide (causes haemorrhagic cystitis, use for resp. depression)
• disease modifying antirheumatic drugs (DMARDs) such as leflunomide, methotrexate, gold therapy)
• biologic agents (anti-TNFa, IL-1 blockers)
• tick-borne or lyme disease areas: empirical tx with doxycycline
• cyclphosphamide
• sulfasalazine (a DMARD)
• duration of tx tapered by 25-30% every 2-3 wks
• dose tapered based on repeat arthrocentesis and CS
• risk of relapse, if this occurs, remission not attained or side effects encountered other drugs can be used
• with combination prototcols, taper drug causing greatest side effects 1st

Question 36

How to monitor tx for erosive joint dz

Answer 36

• response often within 7d
• substantial decrease in WBCs and neutrophils are good prognostic indicators
• Type 1 56% cured, 13% relapsed, 18% lifelong tx

Question 37

Outline sx options for joint dz

Answer 37

= for management of pain in chronic dz

• persistent inflammation may cause joint subluxation
• synovectomy
• arthrodesis/ excision arthrplasty/ total joint replacement?
• cost, morbidity and sx failure rates: ongoing dz in other joints, effects of therapeutic agents on healing and infxn, welfare, complications

Question 38

What is crystal-based arthritis?
Cause?
Tx?

Answer 38

= true gout

• in spp without enzyme uricase (humans, birds, reptiles)
• reptiles: renal damage –> decreased excretion of urate
• white, peri-articular deposits (urate crystals) –> inflammatory reaction.
• renal failure most common cause in reptiles
• failure to excrete uric acid
• tx: fluids, avoid meds that increse renal excretion

Question 39

What is one of the main ddx for lethargy in an inguana?

Answer 39

• crystal based arthritis