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Year 3 MOD > Orthopaedics: Cattle Lameness, Arthritides, Tendons, Ligaments and Muscle > Flashcards

Orthopaedics: Cattle Lameness, Arthritides, Tendons, Ligaments and Muscle Flashcards

1
Q

What is lameness commonly mistaken for?

A

Disease

Lameness is a sign not a disease

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2
Q

Why is lameness on farms important to monitor and aim to reduce?

A

Animal welfare- painful

High yielding animals more susceptible and reduced lactation yield

Cows have delayed cyclicity

Increased ovarian cycts

Lower oestrus intensity

Prolonged calving intervals

Increased culling

Reduced eating/DMI

Low BCS

Costs- treatment, labour, reduced yields, culling

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3
Q

How can lameness be monitored?

A

Mobility scoring and lesion recording

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4
Q

How is mobility scored?

A

Different ways- fortnightly

Video analytics

Scale 0-3

0- even weight baring, rhythm, long strides, flat back
action- none needed, routine trimming

1- steps uneven, strides shortened, affected limb not identifiable
action- could benefit from routine foot trimming, further observation

2- Uneven weight baring on an identifiable limb, shortened stride usually with an arch
action- lame, likely to benefit from treatment, identify the cause, attend ASAP

3- unable to walk as fast as brisk human pace, signs of score 2
actions- very lame, treatm urgent attention, don’t make walk, cull?

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5
Q

What are the different foot lesions?

A

Sole bruising
Sole ulcer
White line disease
Digital dermatitis
Heel erosion
Interdigital growths
Heel ulcer
Foul
Axial wall fissure
Toe necrosis
Foreign body
Toe ulcer

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6
Q

How are hocks assessed?

A

Score 1- no swelling, no hair missing

Score 2- not swelling, bald area

Score 3- swelling, lesion through the hide

Score the rear hock

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7
Q

Define the following terms:

Foot
Claw
Claw capsule
Cannon bone
Axial Surface
Abaxial surface
Dorsal surface
Flexor surface
Solear surface
Dewclaw
Wall
Exostosis

A

foot- the region from hock to apex of claw
Claw- end of the digit
Claw capsule- structure composed of horn- pedal bone fit
Cannon bone- bone between the hock and fetlock (metatarsal)
Axial surface- the surface of the claw facing the space between the claws
Abaxial surface- the surface of the claw facing away from the claws
Flexor surface- back of the limb
Dorsal flexure- transition from axial to abaxial
Solear- sole
Dewclaw- miniature editions of claw
Wall- coronary segment of claw
Exostosis- bony growth protruding the surface

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8
Q

Label the following bones

Hind limb

A
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9
Q

What are the different labels?

A
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10
Q

What are lamellae and laminae?

A

Lamellae- these are leaflets of horn lining the inside of the wall

Laminae- leaflets of connective tissue, collagen fibres blood vessels and nerves that fit between lamellae

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11
Q

What attaches the pedal bone to the dermal lamellae?

A

Collagen fibres

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12
Q

What are the biomechanics of the cows foot?

A

Continuous growth

Continuous wear

Forelimbs attached to the body by more elastic componsnet

Lateral claws outgrow mdeial

Solar dermis is under pressure between the pedal bone and the sole

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13
Q

How should a foot be ideally trimmed?

What angle?

A
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14
Q

What is the dutch method to functional claw trimming?

A
  • Start with medial hind claw
  • Trim dorsal wall length to 7, 5-8cm
  • Reduce sole depth at the toe to approx 5 to 7 mm
  • Spare the heel
  • Correct wall length
  • Model- dish out
  • Deeper and wider modelling of the lateral hind/medial foreclaw
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15
Q

What are the infectious and non-infectious lesions that cause lameness?

A

Infectious- digital dermatitis, foul, interdigital dermatitis, heel horn erosion

Non- infectious- sole haemorrhages/bruising, sole ulcers, white line lesions

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16
Q

What are arthritides?

What is arthritis?

A

Conditions causing pain and dysfunction related to joints

Arthritis- inflammation/degeneration of the joint including osteoarthritis, inflammation, infective

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17
Q

What is a diarthrodial joint?

A

A specialised joint consisting of a synovial cavity allowing articulation between two or more bones

Common examples- bone and socket

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18
Q

What is osteoarthritis?

Why is it important?

A

the degenerative condition ultimately leading to cartilage breakdown and loss of function

Importance-

Cause of pain and suffering- welfare

Cost to clients- drugs, milk loss

Loss of function- joint diseases most common cause of euthanasia with horses

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19
Q

What is synovial fluid?

What is in the fibrous joint capsule of synovial joints?

A

Synovial fluid- ultra filtrate of the plasma plus protein- hyaluronic acid

Fibrous joint capsule- synovial membrane, nerves and blood vessels- proprioception, supportive ligaments/tendons- collateral

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20
Q

What is articular cartilage?

A

Highly specialised- predominantly extracellular matrix with a low density of articular chondrocytes

Chondrocytes are responsible for the maintenance of the matrix
Matrix mainly- collagens, proteoglycans and water-
collagens confer shear resistance, hydrates proteoglycans provide compression

Limited repair

Dynamic loading/unloading- loading important for health of joint

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21
Q

What is osteoarthritis?

What are predisposing factors?

A

Classically thought of as articular cartilage disease
Number of tissues- contributing to progression- articular cartilage, subchondral bone, synovial membrane, joint capsule, ligaments, fat pad

Predisposing factors-
Excercise, trauma, biomechanics- normal joint, abnormal forces
sclerosis, intra-articular fracture, soft-tissue surgery
DOD- normal forces, abnormal joints-
hip and elbow dysplasia, osteochondrosis
Obesity- weight stress
Sepsis
Repeat medication- corticosteroids
Ageing- wear and tear

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22
Q

What history needs to be taken for osteoarthritis?

Describe the clinical exam for a dog with potential osteoarthritis?

A

History-
age, signalment, use
level of excercise
determine onset and progression of disease
response to medication

Clinical examination-
general physical examination
TPR, thoracic auscultation
Assessment of body condition, confirmation, muscling
Lamenss examination- observation, palpation, manipulation, movement
Diagnostic imaging

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23
Q

What are the radiographic signs of osteoarthritis?

A
  • Soft tissue swelling
  • Oestoephysis- new bone formation around the joint- extensions along margins- painful and restrictive
  • Enthesiophytosis- new bone formation in soft tissues
  • Subchondral bone sclerosis- increased bone density
  • Intra-articular mineralisation- meniscus
  • Fragmentation/joint mice
  • Collapsed joint space
  • Subchondral bone cysts
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24
Q

How does immune-mediated joint disease often present?

What is the cause?

Describe the pathophysiology

How is it diagnosed?

A

Usually, polyarthritis and can be erosive or non-erosive

Predominantly idiopathic- may be related to extra-articular disease- genetic
Most relate to abnormal activity of immune cells and antigen presentation

Path- early changes occur in the synovium
Chronic antigenic stimulation
Antibodies to infective agents or macromolecule modification leading to inappropriate immune response
Development of immune complexes

Diagnosis-
Multiple limb joint pain/swelling, generalised stiffness, shifting lameness, neck pain
Variable and intermittent, secondary to OA and fibrosis

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25
How is immune-mediated joint disease managed and treated?
Managment- Synoviocentesis- cell count, protein smear, differentiate from sepsis Full clinical exam- characterise the involvement of other body systems, haematology Diagnostic imaging- early non-specific effusion Treatment- corticosteroids
26
What causes infective arthritis? What are common causes?
Inflammatory arthropathy is due to an infective organism- usually bacteria arthropathy but occasionally fungi, mycoplasma, protozoa Haematogenous- often the separate focus of infection More common in neonates- failure of passive transfer Trauma/wound- often seen in horses, cat bites- Pasteurella multicoda adjacent infection Iatrogenic- Post joint/fracture surgery or following intra-articular injection
27
Describe the pathophysiology of infective arthritis?
Marked inflammatory response- vasodilation and influx of neutrophils, the release of inflammatory cytokines/enzymes Fibrin clots trap bacteria- protects bacteria, reduced synovial nutrient exchange Cartilage destruction and extension of subchondral bone
28
How is infective arthritis diagnosed? What are the DDXs?
History- a wound, FPT, recent injection clinical signs- acute onset, severe lameness- stiffness wound near/over joint pain on palpation Ultrasound/radiography- check for concurrent injury of bone infection systemic disease- resp, umbilical Synoviocentesis DDXs- Traumatic joint injury- ligament/fracture Osteochondrosis Bursitis, hygroma, cellulitis
29
How does normal and septic fluid appear from synoviocentesis? How does it appear on smear?
Normal- pale yellow, high viscosity WBC \<1x10^9 \<10% neutrophils Septic- serosanguinous/turbid/reduced viscosity WBV \>1x10^9 and total protein \>30-40g/l \>90% neutrophils Smear- PMNs Free or intracellular bacteria Distended joint with sterile saline
30
What are the aims for oesteoarthritis?
Provide analgesia Control articular inflammation Limit damage to articular tissues Promote healing- holy grail
31
What considerations are the for the efficacy of treatments?
Heterogenicity of the disease Poor correlation between imaging and disease process In vivo versus in vitro Inter-animal variation High expectations/demands of owners Shotgun approach- several drugs
32
How can osteoarthritis be conservatively and medically managed?
Conservative- rest/restricted activity- acute flare-ups, cold therapy, support Weight loss- reduce strain and adipokines Excercise- beneficial effects of exercise on cartilage/bone Medical management- most common- anti-inflam, anti-pyretic, analgesic Cox inhibition- Small animal- carprofen, firocoxib, meloxicam, paracetamol/codeine Equine- phenylbutazone, flunixin, firocoxib, carprofen
33
What is hyaluronic acid? What are its actions?
Hyaluronic acid- large unbranched nonsulphated glycosaminoglycan- important component of synovial fluid and articular cartilage Action- Chondroprotection anti-inflam stimulate proteoglycan synthesis mechanical effect- improves viscosity Analgesia- binds to stretch receptors Often used with corticosteroids
34
What is pentosan polysulphate? What is its action?
Marked as DMOAD Action- enhances proteoglycan synthesis reduction in articular cartilage fibrillation fibrinolytic- improves joint Improves SF viscosity Increase release of free radical scavengers Licensed in dogs
35
What are bisphosphates?
Potent inhibitors of bone resorption Inhibit osteoclasts May inhibit collagenase release in chondrocytes/synovial cells Clodronate and tiludronate- licensed in horses
36
What are biologics? What surgical treatments can be done for osteoarthritis?
Biologics- autologous conditioned serum Autologous- AKA IRAP or orthokine Mesenchymal stem cells- bind to fibrillated cartilage, reduced progression of OA Nutraceuticals- highly popular with owners Surgical Arthroscopy- assess damage, debride cartilage defects, flushing inflam mediators Joints replacement Arthrodesis- destruction of cartilage, bone-bone primary healing (horse pastern, DIPJ, carpus, tarsus)
37
38
What are the principles for treatment of infectious arthritis?
Treat underlying cause/infective agent Systemic and local antimicrobials Remove inflammatory mediators- joint lavage
39
What is the carrier of Lyme disease? What does Lyme disease cause? How is it diagnosed and treated?
Tick borne spirochaete borrelia burgdorferi Multisystemic inflammatory disorder- dogs present with inflammatory, non-errosive arthropathy with shifting lameness and swollen joints Diagnosis- Synoviocentesis- increased cell counts- PMNs Treat with doxycycline for 30 days
40
What do tendons and ligaments do?
Tendons- passively transfer force generated by muscle to bony attachments support joints store energy Ligaments- attach/stabilise joints and bones Protect tendons Proprioception
41
What is the ultrastructure of tendons and ligaments and how are they different? What is responsible for synthesis, maintenance and degradation?
Hierarchical structure which is adapted based on function Differences in content and organisation of ECM Tenocytes/ligamentocytes responsible for synthesis maintenance and degradation of ECM
42
What are the types of injuries of tendons/ligaments?
Extrinsic- external trauma Intrinsic- overload/degenerative
43
How are tendon/ligament injuries diagnosed?
History- age, type, previous injury, recent excercise, wound/laceration Clinical exam- stance/gait, palpation Diagnostic imaging- ultrasound, radiography
44
How can ultrasound be used for tendon/ligament disorders?
Change in cross sectional area Fibre echogenicity- anechoic/hypoechoic/hyperechoic/mineralised Margination Position- rupture Focal lesion versus generalised changes Acute versus chronic changes Blood flow- assess neovascularisation
45
What are the repair phases of tendon/ligaments?
Inflammatory response- chemokines, cytokines Proliferative phase- Cell migration, macrophages, monocytes Angiogenesis Tissue remodelling phase- ECM and collagen deposition
46
What are the clinical signs, pathology and treatment principles of the acute inflammatory phase of tendon/ligament injuries?
CS- lameness, pain, heat, swelling Pathology- haemorrhage, inflammation- neutrophils, macrophages, increased blood flow, oedema Treatment principles- limit inflammation- cold therapy Protect limb- supportive bandage
47
What are the clinical signs, pathology and treatment principles of the proliferative phase of tendon/ligament injuries?
CS- reduction or absence of lameness resolution of signs or inflammation tendon enlarged and soft signs of re-injury if exercised too early Pathology- angiogenesis fibroplasia Treatment principles- promote angiogenesis minimise formation of excessive scar tissue early exercise
48
What are the clinical signs, pathology and treatment principles of the tissue modelling phase after ligament/tendon injury?
CS- stiffer, thicker Pathology- fibrosis, gradual change from collagen III to I Treatment- increased loading and exercise programme improve fitness monitor progress by repeat ultrasound exam
49
With the following injuries to tendons/ligaments What are options for surgery? Laceratoin Avulsion fracture Intra-synovial tendon/ligament tear Joint instability
Laceration- repair ends, cast if feasible Avulsion fracture- re-attach avulsed bone fragment Intrasynovial tendon/ligament tear- debire torn tendon/ligament Joint instability- TPLO
50
How are skeletal muscles diagnosed?
History- injury/trauma breed, feeding management frequency/severity Clinical examination acute: swelling/pain chronic: stiffness, cramping, pain, fasciculations, weakness Biochemistry- serum muscle enzymes, urine samples Ultrasound- acute- haematoma, chronic- fibrosis/calcification Muscle biopsy
51
52
How can muscles react to myopathies?
Atrophy Hypertrophy Degeneration Regeneration Calcification and ossification Pigmentation Circulatory disturbances
53
54
What is atrophy and what can cause it?
Reduction in size of muscle Disure- reversible Denervation- irreversible- when cells degenerate or de-differentiate trauma myasthenia gravis Cachexia- 1-5% muscle protein
55
What are the types of degeneration of muscle?
Cellular swelling- minor chemical imbalances within the muscle, exhaustion leading to Ca2+ overload in mitochondria, moderate swelling but nuclei remain normal Hyaline degeneration- affects the sarcoplasm but spares the sarcolemma often seen with nutritional myopathies Granular degeneration- severe damage with large basophilic granules of coagulated protein stain positive for calcium fibrosis or fat replacement
56
What is the regeneration and repair of muscle? What commonly causes it?
Reconstruction of normal function to the fibre without complication Calcification and ossification- calcification due to irreversibly damages tissue
57
What circulatory disturbances can happen in muscles?
Collateral circulatory- compensates in local injury Blockage of main arteries- Arterial- partial blockage of distal aorta/iliacs can cause an ischaemic paralysis Venous- blockage of large veins leading to congetsion with leakage of blood to muscles with eventual muscle necrosis and fibrosis
58
What causes white muscle disease? What are the clinical signs and treatment?
Selenium/Vitamin E deficiency most commonly in calves less than 6mo degeneration of muscle Clinical signs- Muscle weakness/stiffness, recumbency, dyspnoea Arrhythmias/murmurs when the myocardium is affected Myoglobinuria Serum- selenium Treatment- parenteral administration of selenium/vitamin E
59
What causes stiff lamb disease? How is it treated?
2-4 week old Similar aetiologies to white muscle- poor ewe rations Neck and tongue muscles or shoulder, thigh, back and intercostal muscles Similar appearance to calves but calcification Treatment- vit E/Se supplementation
60
What are the clinical signs of acute exercise that induces exertional rhabdomyolysis in the horse? How is it diagnosed? What is the treatment?
Unfit horses- tying up, colic signs Stiffness to severe pain Commonly gluteals, semitendinosus, semimembranosus Diagnosis- clinical exam, muscle enzymes- myoglobulinaemia Treatment- pain relief, fluid therapy, acepromazine
61
What are the clinical signs of chronic exercise induced exertional rhabdomyolysis in the horse? How is it diagnosed and treated? What is polysaccharide storage myopathy?
Chronic- stress/nervous, poor performance/stiffness/cramps Diagnosis- history, muscle enzymes, biopsy Treatment- warm up, avoid stress and high energy feeds PSSM- accumulation of glycogen Dx- semimembranous muscle biopsy Tx- diet
62
What are the clinical signs of inflammatory eosinophilic myositis? How does histology appear? What is the treatment?
Large breed dogs Acute recurrent pain and mandibular immobility Bilateral enlarged temporal/masticatory muscles High percentage of eosinophils in the blood Histology- central necrotic area with dead eosinophils and sarcoplasmic clumping, numerous eosinophils in periphery Tx- corticosteroids
63
What are the parasitic and bacterial infectious conditions that affect muscles?
Bacterial- blackles- Clostridium chauveoid Malignant oedmema- Cl septicum, perfringens Patasitic- Trcihonellosis Cysticercosis Toxoplasmal myostisis Sarcocysts
64
What are the clinical signs of toxic myoglobunlinuria? What is the TXs?
CS- acure onset, rapid and frequently fatal muscle weakness/recumbancy increased CK/AST TXs- supportive therapy if survive

Year 3 MOD (42 decks)

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