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Locomotor > Inflamatory Arthritis > Flashcards

Inflamatory Arthritis Flashcards

1
Q

What is often seen with inflammatory OA? ECHOOOO

A

PUO

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2
Q

How can immune mediated v. septic processes be differentiated?

A

> arthrocentesis
- neutrophils degenerate if septic
- poportion of nucleated/mononuclear/neutrophils different
changes on radiography with both
- subacute/chronic : eroision of cartilage and sunchondral bone

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3
Q

Causes of septic arthritis

A 
> haematogenous
- foal umbilicus 
- intestine 
> traumatic
- esp. horses
> Iatrogenic (often "aseptic") IA injections, surgery etc.
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4
Q

What bacteria is the most common cause of eptic arthritis iatrogenicaly?

A

Staph aureus

- forms a glycocalyx on implants especially. (titanium more resistant)

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5
Q

Tx SA inflammatory arthitis?

A
  • ABx (amoxy-clav 20mg/kg IV)
  • no differnece between medical and sx tx
  • 95% infections will resolve
  • may need to remove implants
  • 6 week Abx based on culture
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6
Q

Tx equine septic arthritis? Px?

A
  • acute infection = emergency
  • eliminate organisms from joint
  • eliminate enzymes and mediators causing cartilage destruction
  • Abx/through and thorugh lavage
  • Arthoscopy/arthrotomy
  • IA Abx, IV Abx (pen and gent)
  • resample joint fluid q48hrs
  • oral Abx
    > C+S but IV to start with amoxyclav
  • can deliver locally (gentamicin impregnated sponges, intrasynovial catheters)
    > early stages : rest
  • Px excellent if tx rpadily but only 50% return to racing
  • Physio/ hydrtherapy to reduce adhesions and pevent periarticular fibrosis
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7
Q

Aetiology of IMPA?

A
  • Ag/Ab complex -> formationi of inflammatory products
  • Host IgG and M bind to altered autlogous IgG
  • Ag/Ab complexes deposited on synovium -> neutrophil/macrophage chemotaxis
    [Erosive] - cellular or humoral immunopathogenic factors
  • release of chondrodestructive collagenases/proteases
  • failure of self-tolerance
  • production of immunogenic immunoglobulins
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8
Q

Outline path of Rheumatoid arthritis

A
  • Plasma cells/B lymphocytes -> RF factor
  • Synoviocytes in the synovium are activated
  • IL1, collagenases produced
  • Osteoclasts -> bone resorption and subchondral bone cyts
  • Pannus formation
  • > fibroblast proliferation leads to contracture and limb deformation
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9
Q

Outline autoimmune pathophysiolgy

A

> mistake 1
- immune systems fails to recognise self
- clones of potentially autoaggressive cells originally inactivated in thymus proliferate
mistake 2
- inappropriate reaction doesn’t know when to stop
= hypersensitivity

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10
Q

Risk factors for autoimmune dz?

A
  • hereditary (eg. beagles)
  • certain infections (GpA strep pharyngitis -> acute rheumatic factor)
  • bacterial endocarditis (full PE!!)
  • discospondylitis
  • immune mediated bowel disease
  • neoplsia
  • chronic hepatitis
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11
Q

What are the 4 types of hypersensitivity reactions? Which type causes IMPA?

A

> 1: immedite/anaphylactic
- IgE, mast cells and basophils
2: Ab dependent cytotoxic
- IgG, IgM against a cell surface component
3: immune complex mediated
- Large amonts of IgG or M + Ag -> microprecipitates
- cause of IMPA (precipitates lodge in joint or are created in joint)
4: cell-mediated, delayed type
- INtra-cellular organisms

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12
Q

Typical presentation of immune-mediated arthritis?

A
  • Polyarticular disease (>6 joints) usually
  • occasionally pauciarticular (2-5)
  • rarely mono-articular
    > if single joint affected but culure negative try empirical Abx tx
  • chronic dz
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13
Q

Outline immune-mediated arthritis process

A
  • continual or recurrent presence of inciting antigens
  • failure of normal down-regulation when incititing antigens gone
  • initial dmagae to host resulting in exposire of altered self Ag
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14
Q

Causes of a palmigrade stance?

A

> traumatic hyper-extension injuries
palmigade likley to be more severely afected (erosive dz)
systemic disease (eg. Addisons??) all 4 limbs
palmar fibrocartilage damage
autoimmune disease

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15
Q

What may be fond on clinicla exam with immune mediated joint disease?

A
  • multisystem pyrexia
  • depression
  • anorexia
  • ligament slackening
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16
Q

4 types of non-erosive polyarthritis? Most common? LOOK UP

A

> 1: uncomplicated idiopathic
- most common
- early RA?
- severe signs
2: reactive arthritis (assoc with remote infections)
- endocarditis/urogenital
- severe signs
3: reactive arthritis (assoc with GI/hepatic dz)
- less severe signs
4: reactive arthritis (assoc with remote neoplasia)
- less severe signs

17
Q

Invstigation of polyarthritis

A 
> polyarthropathy 
- arthrocentesis
- joint ads
- synovial biopsy
> underlying dz hunt 
- haem, biochem, urinalysis
- thoracic rads
- abdo ultrasound
- other tests (CSF? Serology? PCR?)
18
Q

Radiographic signs of immune mediated arthitis?

A
  • joint effusion with cranial displacement of the fat pad

- not very excited

19
Q

Egs. of other Non-Erosive polyarthritis?

A
  • SLE
  • Lyme dz
  • Drug-associated (eg. Dobies, sulphonamides, penicillin, phenobarb)
  • Vax induced (seen within 30d of vax)
  • Calicivirus kittens
  • Steroid-responsive meningitis-arteritis in adolescent dogs
  • IBD
20
Q

Why are rads important when they are rarely exctiing for immne mediated arthritis?

A
  • r/o erosive disease

> much poorer prognosis (but rare!)

21
Q

Outline pathophysiology of erosive disease. How common is erosive dz?

A
  • chronic synovitis -> production proliferative granulation tissue (PANNUS)
  • pannus invades articular cartilage and can erode subchondral bone
  • pannus and inflamed synovium produce enzymes (proteases, collagenases) -> destruction
  • similar changes in septic arthritis
    > 1% of PA
22
Q

Types of erosive joint disease?

A
  • rheumatoid arthritis
  • periosteal proliferative polyarthritis in cats
  • polyarthritis of greyhounds (Felty’s syndrome in humans: RA
23
Q

Is classic RA diagnosis applicable to animals? What shold be looked for?

A 
> rarely applicable to animals (dont have nodules, rarely abnormal synovial fluid) 
- stiffness after rest
- pain
- swelling of one joint + another within 3mo
- symmetrical joint swelling 
- subcut nodules
- rad signs of eroision
- RF + serology
- abnormal synovial fluid  
- synovial histology 
- nodule histology 
> theoretically should have 7 of these inclusing 2/3 of erosion, RF+ and synovial histology
24
Q

Radiogrpahic changes seen with erosive joint disease?

A
  • subchondral bone erosion
  • destructive symmetric multi-joint arthropathy
  • early may be only soft tissue changes
  • chronic: collapse of joint spaces, joint deformity or sub-luxation, peri-articular new bone formation, calcification of peri-articular soft tissues
25
Q

Dx of RA?

A
  • R/O SLE with ANA test (though SLE generally non-eroisive, RA erosive)
  • 75% cases have high levels circlating R fator
  • some dogs can have both SLE and RA
26
Q

General principles of Tx of RA?

A

> NB. septic arthritis can -> 2* immune mediated arthritis , in these cases DO NOT IMMUNOSUPPRESS

  • identify inciting factor and remove/tx
  • modify lifestyle to decrease joint stress
  • control inflame/suppress immune response
  • analgesia
  • NB. RA and multisystemic dz (SLE) often need more aggressive and prolonged tx than uncomplicated PA
  • may be able to stop tx, may not
27
Q

What must be remembered if tx animal that has been on NSAIDS?

A

Need wash out period before immunosupressive drugs started

28
Q

What is the key drug for tx of IMPA? Other tx?

A

PREDNISOLONE
+- cytotoxic drugs (BM suppressino)
- cyclophosphamide (haemmorhagic cystitis, use for

29
Q

What may happen with high dose steroids?

A
  • induces palmigrade stance!! Iatrogenic Cushings
30
Q

Tx rickettsial dz?

A

Doxycycline

31
Q

Does azathrioprene need tapered dosing schedule?

A

NO

32
Q

If combination protocol for IMPA used, which drug should be tapered first?

A
  • one with greatest side effects
33
Q

Monitoring tx of immune-mediated arthrits?

A
  • response within 7d
  • suubstancial decrease in WBCs and neutroophils is a good prognostic indicator
  • type 1 :56% cured 13% relapsed 18% lifelong tx
    > if clinically well, potentially no need to retap? Sometimes ta will still be +, dillemmaaaa!
34
Q

Aspect to consider wrt surgical tx of inflammatory joint disease?

A

> manage pain in chronic dz
- persistnet inflam can -> joint subluxation
- synovectomy
- arthrodesis/excision arthroplasty/total joint replacement
cost, morbidity and surgical failure
- d/t ongoing dz in other joints
- effects of therapeutic agents on healing and infection

35
Q

What is crystal-bsed arthritis?

A

= True gout

  • in species that dont have the enzyme uricase (huans, birds, reptiles)
  • reptils asscoaited with renal failure -> v urate excretion
  • white periarticular deposits (urate crystals)
  • > inflammatory reaction
  • Lethargic iguana = suspect gout!*
36
Q

Clinical signs with inflammatory arthritis

A
  • stilted/crouched
  • neurological gait (ataxia)
  • arthralgia (subtle -> severe)
37
Q

Tx of crystal-based arthritis in reptiles?

A
  • fluid tx

- avoid meds that ^ renal excretion

38
Q

5 main key points when thinking about inflammatory arthritis?

A
  1. multi-system involvmenet (pyrexia, stiffness +- joint pan and lameness)
  2. Type 3 hypersesntivity Ag-Ab complexes
  3. Commonest is type 1 immune-mediated polyarthritis (idiopathic)
  4. Differentiate between erosive and non-erosive dz for PROGNOSIS
  5. Immunosuppressive drugs (prednisolone) poss for life

Locomotor (29 decks)

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