Anatomy and physiology of the synovial joint Flashcards

1
Q

Anatomy of diarthrodial joint (out to in ish)

A

Soft tissue
Bone
Joint capsule - largely fibrous
Articular cartilage
Synovial membrane - usually very thin
Synovial cavity with synovial fluid - important for bathing articular cartilage (avascular)

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2
Q

Articular cartilage

A

Made of chondrocytes and extracellular matrix (largely collagen)

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3
Q

Breakdown of extracellular matrix of cartilage

A

Inflammatory insult
Pro-inflammatory cytokines

Net effect is cartilage destruction and changes to underlying subchondral bone

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4
Q

Synovial fluid

A

Fundamental role in boundary lubrication

Plasma dialysate supplemented with
- hyaluronan from synovial fibroblasts
- lubricin from chondrocytes

Provides glucose, other electrolytes, protein and CO2/O2 for cartilage metabolism

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5
Q

Non-inflammatory joint disease

A

DJD
Trauma
Neoplastic
Osteochondrosis

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6
Q

Inflammatory joint disease

A

Infectious and immunological joint disease

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7
Q

Osteochondral or full thickness defect

A

Right down to the cancellous bone

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8
Q

Chondral or partial thickness defect

A

Down to the subchondral bone

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9
Q

Degenerative joint disease (DJD), osteoarthritis, osteoarthrosis

A

Inherently non-inflammatory disease of synovial joints

CHaracterised by deterioration of articular cartilage and formation of new bone at joint margins

VERY COMMON

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10
Q

Clinical signs of Degenerative joint disease (DJD), osteoarthritis, osteoarthrosis

A

Usually a decreased range of motion
Pain (variable)
Joint swelling (fibrosis or effusive)
Crepitus

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11
Q

Pathology of DJD

A

Cartilaginous abnormalities:
- loss of matrix constituents and chondrocytes
- flaking
- fibrillation

Osteophytes develop at margin between joint capsule and articular cartilage

Synovial membrane changes:
- thickening
- mild inflammation
- joint capsule fibrosis

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12
Q

Radiographic changes indicative of DJD

A

Osteophytes formation
Soft tissue swelling
Joint effusion (often mild)
Subchondral sclerosis
Subchondral bone cysts - v rare in SA

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13
Q

Primary DJD

A

No identifiable cause
Rarely recognised in SAs (maybe aged beagles)

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14
Q

Secondary DJD

A

Secondary to:

  1. congenital problem e.g. dwarfism or achondroplasia
  2. Developmental disease e.g. hip dysplasia, osteochondrosis
  3. Acquired e.g. after articular fractures, luxations, cranial cruciate rupture etc.
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15
Q

Categories of inflammatory joint disease

A

Infectious

Non-infectious
- Immunological - erosive or non-erosive
- non-immnuological - crystal induced or chronic haemathrosis

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16
Q

Causes of infectious (septic) joint disease

A

External trauma and bite wounds

Iatrogenic

Endocarditis or remote infections

Immunodeficiency

Secondary to omphalophlebitis in puppies

Haematogenous spread in large breed dogs with estabilshed DJD

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17
Q

Clinical signs of infectious (septic) joint disease

A

Sudden onset
Pain
Swollen, effusive joint
Distal limb oedema
Lameness
More commonly a signle joint rather than multiple

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18
Q

Diagnosis of infectious (septic) joint disease

A

Radiographs to rule out other disease.
- soft tissue swelling and joint effusion
- later changes: periosteal bone reaction and discrete lucencies

Arthrocentesis
- turbid
- decreased viscosity
- increased volume
- high no. neutrophils, often degenerative

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19
Q

Techniques to increase success of culturing bacteria from joints

A

Incubation of synovial fluid in blood culture media for 24 hours

Submit a sample of synovial membrane for culture

Direct culture of synovial fluid - rarely successful

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20
Q

Treatment of infectious (septic) joint disease

A

Evacuate exudate

Treat with antibiotics - high dose IV

If no response consider lavaging with sterile saline

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21
Q

Prognosis of infectious (septic) joint disease

A

Acute infection: usually good
Chronic cases: much more guarded

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22
Q

Criteria to diagnose rheumatoid arthritis

A
  1. morning stiffness
  2. pain or tenderness on motion of at least one joint
  3. swelling of at least one joint
  4. swelling of one joint within a three month period
  5. symmetrical joint swelling
  6. subcutaneous nodules (not in dog)
  7. destructive radiological changes
  8. serological evidence of rheumatoid factor (IgG, IgM, IgA)
  9. abnomal synovial fluid
  10. characteristic histological changes in the synovial membrane
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23
Q

Definite rheumatoid arthritis- diagnosis

A

Can be diagnosed if 5 criteria are met - including at least the presence of two criteria 7, 8, or 10

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24
Q

Classical rheumatoid arthritis - diagnosis

A

can be diagnosed if 7 criteria are met - including at least the presence of two criteria 7, 8, or 10

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25
Q

Signalment of rheumatoid arthritis

A

Small breeds, female, middle aged

26
Q

Clinical signs of rheumatoid arthritis

A

Most commonly affects the carpus and tarsus and distal joints

Present with collapse and deformity

May be palmigrade or plantigrade

Laxity, subluxation, and crepitus

May be pyrexic with lymphadenopathy

27
Q

Radiography of rheumatoid arthritis

A

Subchrondral erosions, soft tissue swelling, subluxations, disuse osteoporosis

28
Q

Laboratory features of rheumatoid arthritis

A

Rheumatoid factor test: RF is an autoantibody of the IgM (IgG) class against IgG.

Not specific

Titre greater than 1 in 40 may be significant, but negative result doesn’t exclude

29
Q

Treatment of rheumatoid arthritis

A

Waxes and wanes so in quiescent stages treatment may not be necessary

Acute exacerbations can be treated with NSAIDs, steroids, or immunosuppression

SUrgical therapy such as cranial crutiate ligament rupture repair or arthrodesis

30
Q

Prognosis of rheumatoid arthritis

A

Guarded

Rarely is a cure obtained
May be managed successfully for variable lengths of time

31
Q

Rare erosivejoint conditions

A

Periosteal porliferative polyarthritis - in young male cats

Mycoplasmal polyarthritis - greyhounds, seen in Australia

Feltys syndrome - Rheumatoid arthritis, splenomegaly, and neutropenia

32
Q

Idiopathic immune mediated polyarthritis

A

Most common inflammatory joint disease

Non-erosive polyarthritis

33
Q

Pathophysiology of idiopathic mediated polyarthritis

A

Thought to involve the deposition of immune complexes - or a type III hypersensitivity

4 types:
1. uncomplicated
2. associated with a remote infection e.g. pyometra
3. associated with GIT disease
4. associated with neoplasia e.g. lymphoma in cats

34
Q

Signalment of idiopathic mediated polyarthritis

A

Often large breeds, spaniels, shelties, young adults

35
Q

Clinical signs of idiopathic mediated polyarthritis

A

Waxing and waning

Lameness, distal joints such as carpus and tarsus most commonly affected, joint effusions, pain on flexion/extension of joints, migratory problem, lethargy, and pyrexia

36
Q

Radiology of idiopathic mediated polyarthritis

A

Soft tissue swelling, effusion, no erosions, no DJD

Image thorax and abdomen to rule out GI disease (type III) and neoplasia

37
Q

Laboratory investigations of idiopathic mediated polyarthritis

A

Mild anaemia, leucocystosis

Negative for ANA and RF

Synovial fluid: low viscosity, increased volume, cell count increased neutrophils

38
Q

Treatment of idiopathic mediated polyarthritis

A

Treat underlying cause e.g. pyometra

Immunosuppressive therapy using corticosteroids in a gradually decreasing dosing regime

DO NOT taper dose too quickly and continue treatment for several months past remission

39
Q

Prognosis of idiopathic mediated polyarthritis

A

Type I - in 50% of cases a cure should be obtained, in the other 50% continual therapy may be needed

In a few cases medication may be ineffective and euthanasia may be requested

40
Q

Systemic lupus erythematosus

A

Very rare

An inflammatory non-erosive joint disease associated with involvement of other body systems

41
Q

Diagnostic criteria of systemic lupis erythematosus

A
  1. a significant titre of serum anti nuclear antibody (ANA)
  2. involvement of more than one body system - e.g. dermatological lesions, AIHA, IMT, IML, glomerulonephritis, NM disease, GIT disease
  3. Immunopathological features consistent with clinical involvement should be demonstrable e.g. IMT should be matched by presence of antibodies to platelets
42
Q

Signalment of systemic lupis erythematosus

A

GSDs, Afghans, Irish setters, OES may be represented

Female

Any age

43
Q

Clinical signsof systemic lupis erythematosus

A

Involvement of symmetrical joints, pyrexia, lethargy, inappetant, lymphadenopathy

Disease often phasic

44
Q

Labratory findings of systemic lupis erythematosus

A

Anti nuclear antibody test positive (titre >1:64 - use fluorescent antibody test)

Coombs positive if AIHA

RF negative

Anaemia, leucopenia, thrombocytopaenia, hyperglobulinaemia

45
Q

Treatment of systemic lupis erythematosus

A

Corticosteroids
Cytotoxic drugs

46
Q

Prognosis of systemic lupis erythematosus

A

Guarded

47
Q

Other very rare inflammatory non-erosive diseases

A

Canine polyarthritis/polymyositis

Canine polyarthritis/meningitis

Canine sjorgrens syndrome - KCS, dry mouth (xerostomia) and polyarthritis

Polyarteritis nodosa - vasculitis, beagles

Plasmacytic lymphocytic gonitis - recognised with cranial cruciate rupture in small breeds

Vaccination reaction - calicivirus in cats

Drug reactions - potentiated sulphonamides in Dobermanns and Weimaraners

Shar-pei fever (familial renal amyloidosis) - sharpei, swollen hocks and pyrexia

Heritable polyarthritis in Akitas - young Akitas. Guarded prognosis

48
Q

Management of DJD

A

Usually multi-modal appraoch needed

Surgery critical for end-stage disease

Regenerative medicine for the future

49
Q

Most frequently encountered joint disease in general practice

A

DJD A.K.A oestoarthritis/osteoarthrosis

50
Q

Treatment considerations for DJD

A

Exercise modulation

Weight loss

Physical therapy and hydrotherapy

Drugs (e.g. NSAIDs, anti-NGF)

Surgical options (e.g. osteotomy, arthrodesis, total joint replacement)

51
Q

What causes damage in DJD?

A

Abnormal wear on normal cartilage

Normal wear on abnormal cartilage

Age-related ‘wear and tear’

52
Q

Exercise for DJD

A

Eliminate long periods of inactivity

Short and frequent periods of gentle controlled exercise

53
Q

Physical therapy for DJD

A

Massage - stimulates circulation and disperses oedema, relaxes muscles in spasm and prevents or breaks down adhesions

Passive range of motion (PROM) exercises - aim to maintain or restore a normal range of motion in affected limbs and may help prevent tendon contractures

54
Q

Hydrotherapy for DJD

A

Allows joint movement in a non-weight bearing mode - improves joint range of motion, improves muscle strength and general fitness

55
Q

NSAIDs for DJD

A

Analgesic due to inhibition of prostaglandin synthesis

Some studies show that it actually abolishes cartilage synthesis

Possible side effects: vomiting, diarrhoea, gastrointestinal ulceration, nephropathy

56
Q

Corticoid steroids for DJD

A

Potent anti-inflammatort effects

Should be reserved for cases that are unresponsive to NSAIDs

Repeat injections can cause cartilage degeneration

57
Q

Surgical options for DJD

A

Correct inciting cause

Joint stabilisation

Ensure normal joint loading

Salvage procedures for chronic arthritis: joint fusion, arthrodesis, joint replacement

58
Q

Chondroprotectants for DJD

A

Better defined as disease-modifying OA drugs

Hyaluronic acid
- IV or IA
- used in synovitis and early DJD

PSGAGs
- SC or IM (horse)
- Reduces PG degredation and MMP synthesis

59
Q

Regenerative medicine for OA

A

Platelet rich plasma (PRP)
- autologous concentrated platelets
- increased PDGF, VEGF, FGF-2, TGF-B
- Widely used in management of soft tissue injuries, esp. ligament and tendon

60
Q

Librela and solensia for DJD

A

Monoclonal antibodies to Nerve Growth Factor (NGF) - implicated in pain in OA

Administered by SC injection once monthly

Simple, long-lasting, safe

Cost reasonable (about £70 pm)

Efficacy (in long term) remains unproven