Eq2 - mid1 - Osteoarthritis Flashcards
1
Q
Definition
A
Degenerative, inflammaotry process, causing progressive loss of hyaline cartilage
2
Q
Pathogenesis
A
- Cartilage loss (on weight-bearing surfaces)
- Subchondral sclerosis
- Subchondral cysts
- Osteophytes
- Synovitis, capsulitis (fibrosis)
- Decreased range of motion
3
Q
OA pathogenesis
- abnormal forces on the joint surface, due to?
A
angular limb deformities
4
Q
OA pathogenesis
- Disturbance in cartilage development, due to?
A
- OCD
- Genetic predisposition
- feeding, management
5
Q
Composition of hyaline cartilage
A
- Cells: Chondrocytes
- Extracellular matrix:
- water
- collagen type 2 (chondrocytes)
- GAGs
- Chondroitinsulphate
- Keratansulphate
- Hyaluronic acid chains
6
Q
Composition of Joint Cartilage
A
Chondrocytes
- ECM synthesis
- Matrix degradation:
- Matric metalloproteinase (MMPS)
- Agrecanase
- Cathepsine
- IL-1, TNF
- Normal ECM: balance between production - reparation and degradation
7
Q
Joint cartilage
- PSGAG role in OA
A
- Negative charge –> binding water
- chondrontil sulphate, keratan sulphate
- OA: PSGAG loss –> water-binding capacity decreases
8
Q
Joint cartilage
- role of Hyaluronic acid
A
- produced by Typ B synoviocytes and chondrocytes
- basic element of cartilage
- water-binding capacity
- works agains tearing forces
- lubricant function together with water
9
Q
Joint capsule
- role of Stratum fibrosum and Sratum synoviale
A
- Stratum fibrosum:
- Stability + serves for motion of the joint
- Stratum synoviale:
- Synovia production (filtrated plasma)
- HA, and collagen production
- Type A (phagocytosis), Type B (syntesis) cells
10
Q
What are found in the joint capsule
A
- Stratum fibrosum
- Stratum synoviale
- Vessels and nerve fibers
- Nociceptors (even in subchondral level)
11
Q
Clinical signs of OA
A
- Increased joint effusion
- lameness
- joint range of motion decrease
- changes in the synovia
- cartilage damage (osteoarthritis)
- newborn formaton (osteophytes)
12
Q
Diagnosis of OA
A
- Lameness examination
- visualisation, palpation
- examination during motion
- provocating tests (flexion is painfull)
- perineural and intrasynovial anesthesia
- arthrocentesis, analysis of the synovia
- Diagnostic imaging
- X-rays
- UL
- Scintigraphy
- MRI
- Diagnostic arthroscopy
13
Q
Diagnosis
- what can be seen on X-ray
A
- Periarticular osteophytes (pathognomic sign)
- Subchondral sclerosis
- Subchondral cystic lesions
- Narrowing joint space
14
Q
OA
- Bone spavin
A
Bone spavin is osteoarthritis, or the final phase of degenerative joint disease (DJD), in the lower three hock joints. It usually affects the two lowest joints of the hock (the tarsometatarsal and the distal intertarsal joints), with the third joint, the proximal intertarsal, being the least likely to develop bone spavin. The condition is most commonly seen in teenage to elderly horses.
- DITJ: dist. intertarsal joint
- TMTJ: tarsometatarsal joint
15
Q
OA: DITJ - TMTJ - Bone spavin
- pathogenesis
A
- Occurence: more often in adults
- recurance of compression and rotation
- conformational abnormalities:
- cow hocks
- too straight behind
- Metabolic causes:
- protein and mineral imbalance
- endocrine disorders
16
Q
OA: DITJ - TMTJ - Bone spavin
- clinical symptoms
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
17
Q
OA: DITJ - TMTJ - Bone spavin
- diagnosis
A
- Clinical signs: Knee pain
- Diagnostic anesthesia
- intraarticular anaesthesia
- “TibFib”: N. tibialis and peroneus
18
Q
OA: DITJ - TMTJ - Bone spavin
- radiological examination findings
A
- Periostal reaction
- Osteophyte formation
- development of cyst like lesions
- bone sclerosis
- narrowing of the joint space
- anyclosis
19
Q
OA: DITJ - TMTJ - Bone spavin
- treatment
A
- Injection into the tarsometatarsal joint:
- Na- hyaluronat
- Glucocorticoids
- Cunean tenectomy
- chemical advancement of arthrodesis
* 70% alcohol: DIT, TMT? - surgical arthrodesis
- surgical treatment
- Osteosynthesis with LCP
- Kerf-cut cylinder
- Orthopedic shoeing:
* Rolling inside in craniomedial direction
20
Q
OA: DITJ - TMTJ - Bone spavin
- pathogenesis
A
Hypothesis (stick/auer)
- congenital cartilage developmental disturbance
- subchondral sclerosis
- repetitive trauma
- overuse –> cartilage damage
- Damage of healthy cartilage
- due to trauma
- i.a fracture
- OCD
- septic arthritis
- Autoimmune reaction (repetitive i.a HA treatment)
21
Q
OA
- treatment
A
- Medication:
- NSAIDs
- Steroids
- PSGAG
- HA
- IRAP
- Tilrden
- Stemcell therpay
- Polyacrylamide hydrogel
- Surgery:
- Arthrotomy
- Arthroscopy
- Synoviectomy
- chondroplasty
- Arthrodesis
- Alternatives:
- supplements
22
Q
OA treatment
- NSAIDs to be used
A
- Fenilbutazone (IV, PO 2.2mg/kg SID)
- Side effects: gastric ulcers, RD colitis, papillary kidney necrosis
- Cheap, PO
- Flunixin meglumin (IV, PO 1.1 mg/kg SID)
- analgetic effect mainly for soft tissues, post-op
- Fibrocoxib (IV, PO, 0.1mg/kg, max 14 days)
- selective COX2 inhibitor
- similary effectivity but elongated effect
- Carprofen (IV, 0.7 mg/kg, PO 1.4mg/kg. 12 hr effect)
- Ketoprofen (IV, IM 2.2 mg/kg, 3-5 days)
23
Q
OA treatment
- corticosteroids
A
- intraarticular application
- phospholipase inhibition
- antiinflammatory and analgetic effect
- Side effects: cartilage damage, decreased PG synthesis
- Short acting:
- Dexamethason, flumethason, hydrocortison, triamcinolon acetat
- Long acting:
- Methylprednisolon acetat, triamcinolon hexacteonid, bethametason acetat
