Day 5 - Lameness 2 (Diseases) Flashcards

1
Q

Osteoarthritis - pathogenesis

A

Pathogen.: degradation and destruction of articular cartilage causing progressive loss of hyaline cartilage
- Subchondral sclerosis
- Decreased range of motion
- Subchondral cysts
- Osteophytes
- Synovitis, capsulitis (fibrosis)

Angular limb deformities

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2
Q

Osteoarthritis - CS

A
  • Joint effusion increased
  • Lameness
  • Joint range of motion decreased
  • Changes in the synovia
  • Cartilage damage (Osteoarthritis)
  • New bone formation (Osteophytes)
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3
Q

Osteoarthritis - Dx

A
  • Lameness Examination
  • Visualisation, Palpation
  • Examination during motion
  • Provocating tests (flexion is painful)
  • Perineural and intrasynovial anesthesia
  • Diagnostic imaging: X-rays, Ultrasound
  • Diagnostic arthroscopy
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4
Q

Osteoarthritis - joint cartilage

A
  • Chondrocytes: Matrix degeneration
  • PSGAG: loss? –> decr water binding capasity
  • Hyaluronic acid: Lubricant
  • Stratum fibrosum: Stability, motion
  • Stratum synoviae: HA, and Collagen production
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5
Q

OA: DITJ - TMTJ Bone spavin
dist. intertarsal joint (DITJ)
tarsomtatarsal joint (TMTJ)

A
  • adults
  • recurrance of compression and rotation
  • Conformational abnormalities
  • Metabolic causes protein and mineral imbalances endocrine disorders
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6
Q

OA: DITJ - TMTJ Bone spavin
CS

A
  • Acute onset of lameness
  • Shortened cranial phase of the strait
  • low arc of foot flight
  • In chronic cases: palpable bony swelling
  • Positive hock flexion test
  • Mild case: improves in training
  • Severe case: worsening during work
  • Outside of the hoof (shoe) is wearing off
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7
Q

OA: DITJ - TMTJ Bone spavin
Dx

A

Diagnostic anesthesia
- Intraarticular anaesthesia
- TibFib (N. tibialis and peroneus)

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8
Q

OA: DITJ - TMTJ Bone spavin
Tx

A
  • I.A. injection into the tarsometatarsal joint:
  • Na-hyaluronat + Glycocorticoids
  • Cunean tenectomy
  • Chemical / surgical arthrodesis
  • Osteosynthesis with LCP..
  • Kerf-cut cylinder
  • Orthopedic shoeing:
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9
Q

Synovial analysis - causes of synovial damage

A
  1. Congenital cartilage developmental disturbance
  2. Subchondral sclerosis
  3. Damage of healthy cartilage
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10
Q

Synovial analysis - Tx
Corticosteroids - Short acting, Long acting

A

Short acting
* Dexamethason,
* Flumethason,
* Hydrocortison,
* Triamcinolon acetat

Long acting
* Methylprednisolon acetat
* Triamcinolon hexacteonid
* Bethametason acetat

Methylprednisolon acetat, Triamcinolon acetate

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11
Q

Synovial analysis - Tx
NSAIDS

A

Fenilbutazone, Flunixin meglumin, Firocox, Carprofen

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12
Q

Synovial analysis - Tx
Na-hyaluronate

A

Na-hyaluronate
Hyaluronic acid

Decreases joint effusion

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13
Q

Synovial analysis - Tx
PSGAG’s

A

Glycosaminoglycans - Adequan
* Effect: anabolic on synovial fibroblasts and chrondrociytes (Hyaluronic acid and collagen
production)
* Inhibition of cytokines and PGE synthesis
* Increases Synovia viscosity
* Antiinflammatory effect

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14
Q

Synovial analysis - Tx
Tildren

A

Biphosphonate
Goal: inhibition of subchondral bone production
* Inhibition of osteoclast activity (bone resorption)
* Anti-inflammatory effect
* No direct effect on cartilage
* Side effects: nephrotoxicity especially if given too fast

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15
Q

Synovial analysis - Tx
Rest

A

Rest
* After treatment: few days generally accepted
* Reason:
Decrease clearance
Increase time of effect
* No EBM support to date

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16
Q

Synovial injury - surgical (4)

A
  • Arthrotomy
  • Synovectomy
  • Chondroplasty
  • Arthrodesis
17
Q

Synovial injury - surgical
Chondroplasty

A
  • Debridement (shaver)
  • Microfracture
  • Fixation
  • BMAC
  • Autograft
  • Allograft.
18
Q

Angle of regular hoof

A
  • 45-50 ° front hoof
  • 50-55 ° hind hoof
19
Q

Trush

A

Degenerative infective condition of the frog
- Wet, unhygienic
- Predisposing factor: long contracted heels, deep sulci
- Fusobacterium necrophorum
* Clinical signs: Black necrotic exudate, odor
(cellulitis, phlegmon)
* Treatment: Cleaning, Debridement
- Dry clean bedding
- Cooper sulphate; phenol : iodine 7%; 10% formalin

20
Q

Canker

A

Chronic hypertrophic moist pododermatitis of the epidermal tissue starting mainly at the frog region
(Moist pasture, unhygenic conditions
Fusobacterium necrophorum, Bacteroides

No lameness

Topical AB
- Superficial or radical debridement??
- AB therapy (procain penicillin, tetracyclin

21
Q

OCD - pathogen

A
  • Disturbance of cellular differentiantion in the growing cartilage
  • Damage to vessels in cartilage canals: Improper vascular supply of the young cartilage
  • Loading: mechanical insult, fragmentation on weak points

Result: resorption

22
Q

OCD - growth rate

A

Large foals
Hyperinsulinaemia -> rapid removal of T3, T4 from the circulation
* T3 T4 responsible for chondrocyte differentiation + invasion of blood vessels

23
Q

OCD - predeliction sites (5)

A
  • Neck facet joints
  • Shoulder
  • Fetlock
  • Hock
  • Femoropatellar-joint
24
Q

OCD/OC - shortenings

Clinical forms (5)

A

OCD/OC – Clinic
* Osteochondrosis (OC)
* Osteochondritis dissecans (OCD)
* Subchondral Bone Cysts

Clinical forms
* Flattening of the joint surface
* Cartilage flaps
* Cartilage with subchondral bone changes
* OCD fragments free in joint

25
OCD/OC - Diagnosis
- 2-4 months, joint effusion, lameness, normal synnovial fluid. Improve with ana
26
OCD/OC - Tx surgical and conservative
Arthroscopy conservative have bad prognosis
27
Subchondral Bone Cysts Predil sites and Dx
* Medial Femoral Condyle * Distal MCIII/MTIII * Medial proximal Radius epiphysis * Distal phalanx * Scapula cavum glenoidale * Intraarticular block is not always positive * X-rays * Scintigraphy
28
Subchondral Bone Cysts - CS
Lameness after work Sometimes acutely lame - Medial Femur Condylus - Distal MCIII Joint effusion not always
29
Subchondral Bone Cysts - Treatment
* Steroid inj. into the cyst * Extra-articular approach and Parathormon * Enucleation of the cyst inside lining * Position screw through the cyst * Bone Morphogenic Protein-2 into the debrided cyst * Autologous Osteochondral Transplantation
30
With regard to strength (transport) Compression, shear, tension
* Bone is strongest in compression * Weakest in shear * Intermediate in tension
31
A- translation B- angulation C- Shortening
32
33
Laminitis - pathophysiology
* Hyperinsulinaemia- lamellar lamellar attachment apparatus defomation * Injury of basement membrane- lysis
34
Laminitis theories (13)
* Enzymatic theory * Ischemia/reperfusion injury * Decreases digital blood flow, lamellar perfusion * Gram negative – endotoxin * Hyperinsulinemia, insulin resistance * Lamellar separation * Equine Metabolic Syndrome * Cresty neck * Increased adipose tissue * Cushing disease * Pituitary enlargement * Corticosteroids * Supporting limb laminitis
35
Laminitis - Dx
* Most often both front feet are affected * Lameness is worse on hard ground * Digital pulse amplitude occurs * Radiographic examination
36
Laminitis - Tx
* Cryotherapy – all four limbs * Aggressive treatment of primary disease * Fluids and electrolyte therapy * Antibiotics and NSAIDs * Uterine lavage – retained placenta * Cushing’s disease Generally to lift heal to get less tension of DDFT
37
Septic arthritis - general
Foals *Haematogen – joint/bone *Gram-negative *Bacteremia, septicemia
38
Septic arthritis - Types of infections (3)
S-type: Synovial fluid and synovial membran E-type: Articular epiphyseal complex P-type: Majority. Long bones physis and joints. Enerobacteriacae( E. Coli, Salm.) Streptococcus, Rhodococcus
39
OA - Tx
Conservative: - Rest - PSGAGs, Hyaluronic acid - NSAIDs, Corticosteroids - Stem cells Surgical: - Synovectomy and arthroscopy