Inflammatory arthritis Flashcards
1
Q
Clinical presentation - inflammatory arthritis
A
- can be stilted/ crouched
- arthralgia (subtle to severe)
- may present as ataxia
2
Q
What is the first investigation of arthralgia?
A
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)
3
Q
Methods to investigate arthralgia
A
- rads.
- arthrocentesis
- synovial investigation
- systemic investigation (thorough PE, hx, CBC/ biochem)
4
Q
Why might arthrocentesis be useful?
A
- to determine if septic vs. immune-mediated
- look for increased neutrophils (+/- lymphocytes)
- degenerate neutrophils = septic
- non-degenerate = immune-mediated
5
Q
Why might rads. be useful for inflammatory arthritis dx?
A
- to determine if septic/ immune-mediated
- acute: normal (may be primary dz)
- sub-acute/ chronic: erosion of cartilage/ sub-chondral bone
6
Q
Describe normal synovial fluid
A
- clear
- pale
- yellow
- high viscosity
7
Q
Causes - septic arthritis
A
- haematogenous: from focus elsewhere
- traumatic (esp horses): lacerations, punctures
- Iatrogenic (often ‘aseptic’ procedures): intra-articular injections of PSGAG - rare, sx
8
Q
Tx - septic arthritis - SA
A
- 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
9
Q
Tx - septic arthritis - EQ
A
- 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
10
Q
Px - septic arthritis - EQ
A
- increased with prompt recognition, aggressive tx and local AB
- other factors: intended use, structures involved, concurrent bone involvement
11
Q
Define IMPA
A
Immune-mediated polyarthritis
12
Q
Aetiology -IMPA
A
- 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
13
Q
Aetilogy - erosive IMPA
A
- 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
14
Q
What are the autoimmune aspects of IMPA - 2
A
- clones of potentially autoaggressive cells originally inactivated in the thymus proliferate
- hypersensitivity reaction
15
Q
Risk factors - autoimmune dz - 7
A
- hereditary component - beagles
- certain ifxn (GpA strep pharyngitis –> acute rheumatic fever)
- bacterial endocarditis
- discospondylitis
- IMBD
- neoplasia (various)
- chronic hepatitis
16
Q
What is a type 1 hypersensitivity reaction?
A
- immediate/ anaphylactic reaction
- IgE –> mast cells, basophils
17
Q
What is type 2 hypersensitivity?
A
- Ab-dependent cytotoxic reaction
- IgG or IgM against a cell-surface component
18
Q
What is type 3 hypersensitivity?
A
- 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
19
Q
What is type 4 hypersensitivity?
A
- cell-mediated/ delayed-type reaction
- intra-cellular organism
20
Q
Outline features of immune-mediated arthritis
A
- 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
21
Q
Ddx - palmigrade stance (carpus sinking)
A
- carpal hyperextension injury
- IMPA
- endocrine dz (Cushings, both usually causes palmi- and planti- grade stance)
22
Q
How to examine patient with suspect IMPA
A
- observe walking, stiffness, difficulty rising
- general PE - pyrexia, depression, anorexia
- palpation and manipulation +/- sedation
- ROM, pain, heat, swelling, crepitus, assess ligament laxity
23
Q
With IMPA, how many animals tend to be lame vs. joint effusion?
A
- 35% lame
- 40% joint effusions
24
Q
Causes non-erosive PA
A
- 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),
25
Q
How to investigate non-erosive PA
A
- 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
26
Q
List some other examples of non-erosive PA
A
- 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)
27
Q
What can joint rads help you distinguish?
A
erosive vs. non-erosive arthritis
28
Q
Describe erosive dz
A
- 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
29
Q
Examples - erosive joint dz
A
- rheumatoid arthritis
- periosteal proliferative PA in cats
- PA of greyhounds (Felty’ syndrome)
- Felty’s syndrome - RA, splenomegaly, neutropaenia
30
Q
How to diagnose RA
A
- 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 (
31
Q
Describe radiographic changes in erosive forms
A
- 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
32
Q
Describe serology of erosive joint diseases
A
- 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
33
Q
Principles of erosive joint disease tx
A
- 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
34
Q
What is the main drug tx for erosive joint dz?
A
- prednisolone
- immunosuppressive doses initially
- then taper dose
35
Q
What tx can be given for erosive joint dz?
A
- 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
36
Q
How to monitor tx for erosive joint dz
A
- response often within 7d
- substantial decrease in WBCs and neutrophils are good prognostic indicators
- Type 1 56% cured, 13% relapsed, 18% lifelong tx
37
Q
Outline sx options for joint dz
A
= 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
38
Q
What is crystal-based arthritis?
Cause?
Tx?
A
= 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
39
Q
What is one of the main ddx for lethargy in an inguana?
A
- crystal based arthritis
