SA Joint Dx and OA Flashcards

1
Q

What is the difference between primary and secondary arthritis?

A

Primary arthritis has no underlying aetiology - it is more rare

Secondary arthritis is much more common and occurs usually due to some form of damage to the joint

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2
Q

Is primary or secondary arthritis more common?

A

Secondary more common

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3
Q

What are you likely to see in the animals history when they ahve arthritis?

A

Stiffness particularly on rising - watch the dog as they come into the consult room

Worse after exercise

Waxes and wanes

Shifting lameness? Could suggest autoimmune dx

Worse in colder weather?

Exposure to ticks - lyme dx can potentially cause lameness

Bleeding tendency? Blood in the joint is very painful

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4
Q

What are you likely to see on a physical exam in an animal with arthritis?

A
  • Lame
  • Pain on manipulation
  • Swelling to joints
  • Associate muscle atrophy
  • Neurological deficits?
  • Systemic signs?
  • Always compre with opposite limb
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5
Q

How can you make a provisional diagnosis for arthritis?

A
  • If lameness mild - not unreasonable to trial therapy e.g. rest and analgesia
  • If failts to respond after 1 - 2 weeks, a definitive dagnosis should be sought after
  • Always try to get the owner to come back/make contact with the owner to find out if its worked or not
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6
Q

How can you confirm the diagnosis of arthritis?

A

Confirming the diagnosis

  • further manipulation of joints ± sedation or GA: standard and joint specific (e.g. cranial draw, Ortolani)
  • diagnostic imaging: radiography ( ± contrast), ultrasound, EMG, CT, MRI, scintigraphy
  • arthrocentesis
  • intra-articular or regional blocks (rarely performed in small animals)
  • arthroscopy
  • exploratory arthrotomy
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7
Q

What is ortolani a sign of?

A

Hip dysplasia

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8
Q

How should you perform radiography when trying to diagnose arthritis?

A
  • Good quality: positioning, exposure and development
  • Standard orthogonal views +/- stress views
  • Radiograph opposite side for comparison if unsure
  • Read filsm methodically
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9
Q

WHat is one of the first things you will see with an unhappy joint?

A

Joint effusion

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10
Q

Comment on these 2 radiographs

A

Left - normal

Arthritis joint on the right - can see new bone on distal end of patellar and some sclerosis

Area of whiteness within joint on right - joint effusions

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11
Q

What is demonstrated in these radiographs? What is it used for?

Which joint is it often used in?

A

Contrast arthrogram - a series of images of a joint after injection of a contrast medium

The canine shoulder is the only joint routinely assessed with positive contrast arthrography

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12
Q

What is ultrasound useful for with regards to arthritis?

A

Good for peri-articular soft tissue structures e.g. bicipital tendon

Can be used for detection of meniscal tears but requires a very skilled operator

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13
Q

What is arthrocentesis?

A

Arthrocentesis is a diagnostic test that is performed to determine the cause of joint swelling or arthritis, including septic bursitis, gout, or rheumatoid arthritis. Also known as joint aspiration, the procedure uses a sterile needle and syringe to drain fluid from a joint for further examination.

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14
Q

With arthrocentesis, when are you likely to just look at a single joint and when are you most likely to look at multiple joints?

A

Single joint likely to be septic or traumatic

Multiple joints (at least 3) for detection of polyarthritis

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15
Q

Where do you collect the artocentesis sample into?

A

Done by aseptic technique

Collection into plain, EDTA and blood culture medium if likely to be infected

Smears for cytology as well as count from EDTA sample

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16
Q

When doing a synovial fluid analysis, what should you look for?

A

Gross appearance

Viscosity (string test)

Protein content and mucin test

Cytology

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17
Q

What is normal synovial fluid like?

A

Honey coloured

Like syrup

Relatively clear

Good viscosity

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18
Q

With synovial fluid cytology, what is likely with small numbers of foamy macrophages?

A

Suggestive of degeneratiev disease

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19
Q

With synovial fluid cytology, what is likely with large numbers of neutrophils?

A

Large numbers of neutrophils in both sepsis and polyarthritis

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20
Q

Have a look at this table about synovial fluid analysis with regards to normal joint, degenerative joint disease, immune mediated arthritis and bacterial infective arthritis

A
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21
Q

What is a fragmented coronoid process most common in?

A

Most common in elbow dysplasia

22
Q

What is arthroscopy?

What are some pros and cons?

A

Diadvantages:

  • Difficult to do

Advantages:

  • Joint morbidity reduced
  • Magnification
  • Therapeutic as well as diagnosti
23
Q

What is this arthroscopy of?

A

Fragmented coronoid process - damaged articular cartilage

24
Q

How can arthrotomy be useful for diagnostic?

A

Visualisation of pathology

Synovial biopsy

25
What is this, from arthrotomy?
Bucket handle tear assocaited with cruciate disease
26
What is a bucket handle tear associated with?
Associated with cruciate disease
27
What are some high return, relatively low cost tests when investigating joint disease?
Radiographs Synovial fluid analysis
28
What are some predispositions to OA?
Genetics Age Systemic factors e.g. obesity
29
What are some joint biomechanics that can cause OA?
Injury Developmental abnormality Instability Overload
30
What is pathophysiology of OA?
Fibrillation of articular cartilage of WEIGHT BEARING areas leads to fissuring leads to ulceration There are microfractures that lead to stiffening of subchondral bone which leads to abnormal loading Joint remodelling due to osteophyte development
31
What causes pain during OA?
Synovitis Exposure of subchondral bone
32
What are some radiographic signs of OA?
* Joint effusion * Osteophyte formation and bone remodelling e.g. patella * Joint sclerosis * Muscle atrophy
33
What is the cycle of presentation of OA in young animals?
Primary disease --\> pain, instability OA initiated --\> pain, lameness, restriction of movement Muscular growth provides support --\> stabilisation and limitations of signs
34
What is the cycle of presentation of OA in adult animals?
Signs can be intermittent and vary in severity Chronic atate +/- acute flare ups Stiffness Restriction of movement Pain and lameness
35
Which muscles are important in preventing hip dysplasia if the animal is predisposed to HD?
Gluteal muscles
36
What are clinical signs of OA?
Clinical effects depend to some extent on the affected joint * Worse in small 'tight' joints such as tarsus or elbow, comapred to large padded joints such as stifle or hip * Worse in high motion joints such as antebracheocarpal joint vs low motion joints e.g. carpometacarpal
37
Which joints is OA worse in?
Worse in small 'tight' joints such as tarsus or elbow, comapred to large padded joints such as stifle or hip. Tarsus and elbow worst - particularly tarsus as small joint and surface area and same weight on it as the hip! So tend to get greater changes on the smaller joints
38
How can you investigate OA?
Radiography (plain +/- contrast) Arthrocentesis Advanced imaging - CT or MRI Arthroscopy Synovial biopsy Serology
39
What radiographic features do you see with OA?
* Soft tissue swelling * Joint effusion * Osteophytes * Enthesiophytes * Sub-chondral sclerosis * Sub-chondral cyst * Intra-articular mineralisation
40
What is the objectives of treatment of OA?
Control pain Achieve an acceptable level of exercise Limite the progression of the disease
41
What is the multi-modla approach to the treatment of OA?
Weight control Exercise modification +/- physio Analgesia Neutraceuticals/ structure-modifying drugs Treatments in development Salvage procedures
42
What is the genreal therapeutic strategy for the treatment of OA?
* Weight control * maintenance * stick to appropriate exercise regime and bodyweight * (strategic analgesia?) * control ‘ flare-ups ’ * initial analgesia (7-10 days) * rest e.g. 5 min. walks 3x day on lead * gradual re-introduction of exercise * ± physiotherapy / hydrotherapy
43
How can you control acute flare ups of OA with NSAIDs?
7-10 days of NSAID for acute flare up
44
What are some drug treatments for OA?
* Non-steroidal anti-inflammatories –mainstay * Usually reserve corticosteroids for severe, non-responsive or end-stage cases * NEVER combine CCS with NSAID ’ s * Remember that all NSAIDs may have side-effects * Switch from high to low dose rates * Switch drugs if response is poor * Pentasonpolysulphate(Cartrophen). Disease modifying compound. Studies inconclusive * Try ‘ nutraceuticals ’ if response is poor
45
What are neutraceuticals and how can they be useful for OA?
* This is an area where evidence for use in small animals is lacking * Off the shelf preparations may vary in their bioavailability when compared to veterinary designated products * Chondroitin sulphate and glucosamine have been used in man to some benefit * Glucosamine has mild anti-inflammatory action as well as an effect on chondrocyte metabolism * Essential fatty acids maybe beneficial * Also consider turmeric and green lip mussel
46
What are some research developments with regards to the treatment of OA?
Research developments * Micropicking * perforation of sub-chondral bone plate * Joint resurfacing * full thickness defects * fibrin plugs and other biodegradable scaffolds * Platelet rich plasma * variable results * Stem cell therapy * harvest adipocytes and remove stem cells, grow on and inject into joint * Gene therapy
47
48
When would you use micropicking?
If there is perforation of sub-chondral bone plate
49
When would you use joint resurfacing?
Full thickness defects Fibrin plugs and other biodegradable scaffolds
50
What would you see with feline OA?
More difficult to detect Discuss reduced activity levels and the ability to jump with the owners General demeanour Ability to groom Over lamness is a rare sign
51
Give 2 examples of salvage procedures
Hip replacement with cemented stem Fuse joint