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Locomotor > General > Flashcards

General Flashcards

1
Q

What info can allow you to gain a subjective assessment of the current lameness?

A

Hx of trauma, duration, deterioration/ improvement, circumstances, effects of exercise, management changes

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2
Q

What factors do you assess by distance examination?

A

Symmetry, posture, conformation

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3
Q

What factors does an objective assessment of lameness include?

A

Distance exam, observation of gait, palpation and hoof testers, manipulation of joints

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4
Q

What does manipulation of joints assess?

A

Determine ROM/ abnormal movement, pain related to movement, load/ unload specific structures in the limb

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5
Q

What is a varus/ valgus deformity?

A

A deformity involving oblique displacement of part of a limb away from the midline.

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6
Q

What is the safety factor?

A

Max stress a structure withstands until breakage divided by stress mostly to undergo in its lifetime

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7
Q

How do you calculate stress?

A

Force/ CSA

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8
Q

What are the different types of force and which structures undergo them?

A

Tension- tendons, bones
Compression- joints, bones
Bending- bones
Shear- joints

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9
Q

What is the cause secondary nutritional hyperparathyroidism?

A

Low dietary Ca–>incr PTH–> incr Ca release from bone. Kidney releases vit D increases Ca release from bone and Ca absorption from intestine.

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10
Q

What is secondary renal hyperparathyroidism?

A

CRF (normally adult). Decr activation of D. Lowered PO4 excretion (PO4 binds to Ca, serum Ca lowered)
Incr PTH drive and effects on bonees

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11
Q

What is MBD of reptiles and chelonians?

A

Low diet Ca. Decr activation/ availability of vit D. Lethargy, lameness- joint/ limb swelling, muscular tone and atrophy.

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12
Q

How is MBD of reptiles and chelonians diagnosed?

A

Radiography- joints, limbs and spine, egg binding, spontaneous fractures.
Blood sample- low Ca.
Confirmation- swollen bones, poor density, misshapen, pliant mandibles, lethargy, unable to lift body off ground, path fractures and low serum Ca (tail vein

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13
Q

How is MBD of reptiles and chelonians treated?

A

Ca gluconate, dietary adjustment (2% Ca diet), UV light and or direct sunlight (not through glass), monitor blood Ca

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14
Q

What are the components of hyaline cartilage and where is it found?

A

Provides interface between bones at a synovial joint.

Cartilage, PGs, water. To resist compressive forces. Chondrocytes responsible for turnover of matrix

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15
Q

What is osteochondrosis?

A

Group of conditions of developing cartilage and its supporting bone. Initiated by a vascular problem in the epiphysis, failure of normal cartilage to bone succession.

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16
Q

What is osteochondritis dissecans?

A

Detachment of a chondral or osteochondral fragment from the articular surface.

17
Q

What conditions occur in fast growing high performance patients?

A

Dogs- OCD, FCP (fragmented coronoid process), UAP (united anconeal process)
Horses- OCD, SBC (subchondral cystic lesions)
Pigs- OCD esp hip
Broiler chickens- OCD stifle

18
Q

What is the classical presentation of osteochondrosis?

A

Young, fast growing, large, pure bred. Joint effusion- inconsistent. Often bilateral. Lameness variable. Sub clinical dz possible.

19
Q

What is canine elbow dysplasia?

A

Osteochondrosis is 1ry dz in this syndrome. Incl- humeral osteochondritis dessecans (OCD), FCP, UAP, 2ry OA. Combo of some or all

20
Q

How does osteochondrosis cause osteoarthritis?

A

Direct irritation, direct cartilage damage, incongruency, mechanical incompetence. Cycle of reaction to these factors. The 2 are intimately linked together. Often temp stabilises in young adult as osteochondrosis gone away- left w/ degree of diability e.g. loss of ROM but not a great problem w/ OA.

21
Q

What is the most common medication for orthopaedic problems?

A

NSAIDS- inexpensive and efficient

22
Q

How do NSAIDs work and what are some common side effects of their use?

A

Inhibit COX therefore PG synthesis- this decreases synovitis, reduces cartilage degradation and prevents sensitisation of pain receptors
GI ulceration, nephritis, PLE, -ve influence on cartilage and bone metabolism

23
Q

What is the mechanism of corticosteroids?

A

Inhibit PG synthesis (block PL A and COX pathways). Inhibit synthesis of cartilage degrading cytokines (IL1 and TNF-a). Inhibit cartialge-degrading enzymes (matrix metallowproteinases, aggrecanase-1)

24
Q

What are the side effects of intra-articular steroids?

A

-ve effects on cartilage metabolism and healing. Incr risk of iatrogenic joint infections. Laminitis (although extremely rare)

25
Q

What are the functions of cartilage?

A

Template for bone growth, resists compression, resilience, support, flexibility, lubrication and movement at diarthrodial joints

26
Q

Where do you find hyaline cartilage (type II coll)?

A

Articular cartilage, nasal septum, trachea and bronchi, ventral end of ribs, embryonic skeleton, epiphyseal growth plate

27
Q

Where do you find fibrocartilage (type II and type I coll)?

A

IV disc, meniscus

28
Q

Where do you find elastic cartilage (type II coll w/ elastin and also some type I coll)?

A

Epiglottis

Ear

29
Q

What are the general characteristics of cartilage?

A

Chondrocytes- synthesis all the ECM
Avascular- no new supply of cells, poor capacity to repair
Aneural
ECM- major component coll II and often type I present, PGs

30
Q

How does cartilage get its blood supply?

A

Via vascularised subchondral bone and the synovial surface

31
Q

What are the physical properties of the components of cartilage?

A

Aggrecan- resilience and compressive resistance

Collagen- tensile strength

32
Q

How does the thickness of cartilage differ between congruent and incongruent joints?

A

Congruent: thin cartilage deforms only a small amount, yet the area is sufficiently large to distribute low and maintain low stress
Incongruent: deformation of the thick cartilage incr SA under compression sufficiently to decr the stress appropriately

33
Q

Which 3 components of collagen determine its mechanical behaviour?

A

Water
Collagen- increases stiffness- disruption in OA decreases strength
Proteoglycans

34
Q

What are the risk factors of osteoarthritis?

A

Age- thinning of cartilage
Genetic factors incl M/F bias
Environmental
Mechanical Trauma

35
Q

Why is age a contributing risk factor for osteoarthritis?

A

Thinning of cartilage
Junk accumulation- loss of PGs, accumulation of junk degraded products, altered activity of cells in response
Reduce GF response

36
Q

How do cell alterations with age in cartilage contribute to risk factors of OA?

A

Cellularity decr w/ advanced age- fewer to maintain ECM, fewer stem cells
Calcification of ECM incr
Proliferation of chondrocytes reduced

37
Q

What are enthesocytes and osteophytes?

A

Enthesocytes- abnormal projections at attachment of tendons and ligaments
Osteophytes- abnormal projections in joint spaces

Locomotor (4 decks)

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