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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
Q

How is immune-mediated joint disease managed and treated?

A

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

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26
Q

What causes infective arthritis?

What are common causes?

A

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
Q

Describe the pathophysiology of infective arthritis?

A

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
Q

How is infective arthritis diagnosed?

What are the DDXs?

A

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
Q

How does normal and septic fluid appear from synoviocentesis?

How does it appear on smear?

A

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
Q

What are the aims for oesteoarthritis?

A

Provide analgesia

Control articular inflammation

Limit damage to articular tissues

Promote healing- holy grail

31
Q

What considerations are the for the efficacy of treatments?

A

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
Q

How can osteoarthritis be conservatively and medically managed?

A

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
Q

What is hyaluronic acid?

What are its actions?

A

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
Q

What is pentosan polysulphate?

What is its action?

A

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
Q

What are bisphosphates?

A

Potent inhibitors of bone resorption

Inhibit osteoclasts

May inhibit collagenase release in chondrocytes/synovial cells

Clodronate and tiludronate- licensed in horses

36
Q

What are biologics?

What surgical treatments can be done for osteoarthritis?

A

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
Q
A
38
Q

What are the principles for treatment of infectious arthritis?

A

Treat underlying cause/infective agent

Systemic and local antimicrobials

Remove inflammatory mediators- joint lavage

39
Q

What is the carrier of Lyme disease?

What does Lyme disease cause?

How is it diagnosed and treated?

A

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
Q

What do tendons and ligaments do?

A

Tendons-
passively transfer force generated by muscle to bony attachments
support joints
store energy

Ligaments-
attach/stabilise joints and bones
Protect tendons
Proprioception

41
Q

What is the ultrastructure of tendons and ligaments and how are they different?

What is responsible for synthesis, maintenance and degradation?

A

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
Q

What are the types of injuries of tendons/ligaments?

A

Extrinsic- external trauma

Intrinsic- overload/degenerative

43
Q

How are tendon/ligament injuries diagnosed?

A

History-
age, type, previous injury, recent excercise, wound/laceration

Clinical exam- stance/gait, palpation

Diagnostic imaging- ultrasound, radiography

44
Q

How can ultrasound be used for tendon/ligament disorders?

A

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
Q

What are the repair phases of tendon/ligaments?

A

Inflammatory response- chemokines, cytokines

Proliferative phase-
Cell migration, macrophages, monocytes
Angiogenesis

Tissue remodelling phase-
ECM and collagen deposition

46
Q

What are the clinical signs, pathology and treatment principles of the acute inflammatory phase of tendon/ligament injuries?

A

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
Q

What are the clinical signs, pathology and treatment principles of the proliferative phase of tendon/ligament injuries?

A

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
Q

What are the clinical signs, pathology and treatment principles of the tissue modelling phase after ligament/tendon injury?

A

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
Q

With the following injuries to tendons/ligaments

What are options for surgery?

Laceratoin

Avulsion fracture

Intra-synovial tendon/ligament tear

Joint instability

A

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
Q

How are skeletal muscles diagnosed?

A

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
Q
A
52
Q

How can muscles react to myopathies?

A

Atrophy

Hypertrophy

Degeneration

Regeneration

Calcification and ossification

Pigmentation

Circulatory disturbances

53
Q
A
54
Q

What is atrophy and what can cause it?

A

Reduction in size of muscle

Disure- reversible

Denervation-
irreversible- when cells degenerate or de-differentiate
trauma
myasthenia gravis

Cachexia-
1-5% muscle protein

55
Q

What are the types of degeneration of muscle?

A

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
Q

What is the regeneration and repair of muscle?

What commonly causes it?

A

Reconstruction of normal function to the fibre without complication

Calcification and ossification-
calcification due to irreversibly damages tissue

57
Q

What circulatory disturbances can happen in muscles?

A

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
Q

What causes white muscle disease?

What are the clinical signs and treatment?

A

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
Q

What causes stiff lamb disease?

How is it treated?

A

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
Q

What are the clinical signs of acute exercise that induces exertional rhabdomyolysis in the horse?

How is it diagnosed?

What is the treatment?

A

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
Q

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?

A

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
Q

What are the clinical signs of inflammatory eosinophilic myositis?

How does histology appear?

What is the treatment?

A

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
Q

What are the parasitic and bacterial infectious conditions that affect muscles?

A

Bacterial-
blackles- Clostridium chauveoid
Malignant oedmema- Cl septicum, perfringens

Patasitic-
Trcihonellosis
Cysticercosis
Toxoplasmal myostisis
Sarcocysts

64
Q

What are the clinical signs of toxic myoglobunlinuria?

What is the TXs?

A

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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