Sys Path - Musculoskeletal System

Front 1

Contractional Units of Muscle

Back 1

-Sarcomeres

Front 2

2 Main fiber types of muscle

Back 2

-type 1 myofibers
-type 2 myofibers

Front 3

Type 1 Myofibers
-what are they
-describe

Back 3

-slow and steady muscles

-"Red Muscle" due to high myoglobin content
-undergo oxidative metabolism
-capable of sustained activity (diaphragm)

Front 4

Type 2 Myofibers
-what are they
-describe

Back 4

-fast and short muscles

-Pale due to high glycogen content
-undergo glucose metabolism
-capable of rapid, short term activity (limb muscles)

Front 5

Muscle type more susceptible to exertional damage

Back 5

-Type 2

Front 6

Describe the process of myocyte function

Back 6

-Ca2+ is sequeserd in the sarcoplasmic reticulum
-Depolarization occurs and the Ca2+ is released from the sarcoplasmic reticulum
-ATP is used, and the duration and depth of the muscle contraction is determined
-More ATP is used to allow Ca2+ to re-enter the Sarcoplasmic Reticulum for muscle relaxation

Front 7

Describe the process of myocyte degeneration

Back 7

-Myocyte membrane damage and depletion of cellular energy stores (ATP) --> leads to excessive cytoplasm calcium
-mitochondria become overloaded with calcium
-calcium overload leads to mitochondrial degeneration
-mitochondria can no longer provide energy to the myocyte and cytoplasmic calcium can no longer be adequately sequestered

-excess cytoplasm causes hypercontration of myofibrils
-myofilament proteins coagulate and myofibers degenerate

Front 8

Ion disorder myopathies
-what are they
-examples

Back 8

-inherited disorders with significant myotonia and spastic paresis
-examples) scotty cramp, hyperkalemic Periodic Paresis (HYPP)

Front 9

Hyperkalemic Periodic Paresis
-pathogenesis

Back 9

-inherited disorder of the sodium channels in muscle
-delayed functional closure of sodium channels
-excess influx of sodium into sarcocplasm with compensatory efflux of potassium
-decreased depolarization threshold
-horse becomes weak and develops respiratory problems

Front 10

HYPP
-common sign

Back 10

-muscle hypertrophy from continuous muscle stimulation

Front 11

HYPP
-sequelae

Back 11

-respiratory problems

Front 12

Muscular dystrophy in dogs and cats
-pathogenesis

Back 12

-inherited deficiency of dystrophin in males
-myofibers are predisposed to degeneration and fibrosis
-affects skeletal muscles and heart

Front 13

Muscular dystrophy
-clinical signs

Back 13

-progressive weakness
-difficulty in eating/swallowing
-respiratory difficulty

Front 14

Muscular atrophy
-common causes

Back 14

-denervation (laryngeal hemiplegia, sweeny, trauma, immune-mediated)
-disuse
-malnutrition (protein deficiency)
-endocrine disorders (hypothyroidism, hypoadrenocorticism)

Front 15

Laryngeal hemiplagia
-define

Back 15

-degeneration of the left recurrent laryngeal nerve in horses

Front 16

Sweeny
-define

Back 16

-compression of the supraspinatous nerve in horses

Front 17

Nutritional myopathy
-pathogenesis

Back 17

-Vitamin E/Selenium deficiency
-failure to remove free radicals
-cell membrane damage
-decreased ATP levels in myofibers
-calcium accumulates causing myofiber degeneration

Front 18

Nutritional Myopathy in Cattle
-Presentation
-Lesions

Back 18

-Presentation: 4-6 wk old calves

-Lesions: pale cardiac and skeletal muscles; degeneration, fragmentation, hyalinization, calcification of myofibers

Front 19

Nutritional Mopathy in Cattle
-Presentation
-Lesions

Back 19

-Presentation: 6-20 wk old calves

-Lesions: Hepatosis dietetica, Mulberry heart disease; pale cardiac and skeletal muscles

Front 20

Toxic myopathy
-pathogenesis

Back 20

-initial event is calcium accumulation causing myofiber degeneration

Front 21

Toxic Myopathy
-Causes

Back 21

-Copper, Iron, Cobalt
-Gossypol (Pigs)
-Monensin (horses)
-Cassia (cattle)

Front 22

Monensin
-what is it
-effects of toxicity

Back 22

-ionophore that predisposes to intracellular calcium accumulation

-stiffness, muscle weakness, heart failure

Front 23

Toxic Myopathy
-cause of death

Back 23

-heart failure

Front 24

Exertional Rhabdomyolysis
-pathogenesis

Back 24

-Glycogen stored in muscle during rest (normal)
-Predisposed horses have polysaccharide storage disease
-Polysaccharide accumulates in myofibers
-Exhaustive exercise utilizes glycogen
-Heat and lactic acid are produced by muscle metabolism
-Membrane damage and cytoplasmic calcium accumulation cause myfiber degeneration with decreased ATP playing a minor role

Front 25

Exertional Rhabdomyolysis
-clinical signs

Back 25

-acute onset hind limb weakness
-muscle swelling & rigidity
-pain
-myoglobinuria
-lactic acidosis
-electrolyte imbalance

Front 26

Exertional Rhabdomyolysis
-lesions

Back 26

-muscle is dark red and edematous
-kidney with tubular nephrosis and necrosis

Front 27

How is Exertional Rhabdomyolysis related to capture myopathy?

Back 27

-capture myopathy occurs in wild animals due to chase, stress, transport
-can have myoglobinuria or renal failure
-dyspnea, muscle weakness and rigidity

Front 28

Malignant hyperthermia
-pathogenesis

Back 28

-Homozygous mutation of the RYR-1 gene causes increased susceptibility to stress
-Ryanodine receptors mediate the release of calcium from the sarcoplasmic reticulum
-stimulated to transport Ca2+ into the cytosol by recognizing Ca2+ on its cytosolic side
-small amount of Ca on the cyosolic side causes the release of more Calcium (calcium induced calcium feedback)
-sarcoplasmic calcium accumulates causing uncontrolled muscle contraction
-lactic acid, heat, CO2 produced
-granular and hyaline myofiber degeneration

Front 29

Malignant hyperthermia
-clinical signs

Back 29

-high temperature
-severe acidosis
-tachycardia and dyspnea
-muscle rigidity
-high mortality
-Inc. myoglobin and potassium in plasma

Front 30

Malignant hyperthermia
-lesions

Back 30

-muscles are pale, soft, exudative (PSE)
-possible tubular nephrosis in kidney

Front 31

Ischemic myopathy
-pathogenesis

Back 31

-membranolysis leading to an accumulation in metabolites and a decrease in ATP
-reperfusion injury ---> oxidative damage

Front 32

Ischemic myopathy
-types

Back 32

-compartment syndrome
-downer syndrome
-muscle crush syndrome
-vascular occlusion

Front 33

Ischemic myopathy
-compartment syndrome pathogenesis

Back 33

-muscles are surrounded by bone or dense connective tissue
-exercise causes swelling of enclosed muscle
-swelling causes compression and subsequent ischemia

Front 34

Ischemic myopathy
-Downer syndrome pathogenesis

Back 34

-large animal in recumbency
-body weight compresses vessels supplying musculature --> muscle ischemia
-weight removed ---> blood returns ---> edema (edema prolongs ischemia)

Front 35

Ischemic myopathy
-lesions

Back 35

-transient ischemia (1-3 hrs): regeneration
-prolonged ischemia (18-24 hrs): fibrosis
-edema

Front 36

Bacteria that use muscles for latency

Back 36

-Clostridium chauvoei (spores activated when anaerobic)
-Clostridium perfringens
-Clostridium septicum

Front 37

Protozoa that use muscles for latency

Back 37

-Trichinosis (ingest infected meat; zoonotic)
-Cysticercosis (cyst formation in tongue, heart, masticatory muscles)
Sarcocystis

Front 38

Clostridium sp. muscle disease
-Bacterial species
-name
-pathogenesis

Back 38

-Clostridium chauvoei
-Black Leg

-latent spores in muscle get activated in anaerobic environment from tissue damage and decreased vascular supply
-sporulation from bacterial reproduction
cytolytic toxins released --> gangrenous myositis
-toxins have systemic effect --> death

Front 39

Idiopathic myosities

Back 39

-Eosinophilic myositis
-Atrophic masticatory myositis

Front 40

Eosinophilic mysitis
-describe

Back 40

-immobiliy and pain of the jaw with swelling of masticatory muscles due to immune response to antigenically distinct myosin in masticatory muscles
-results in muscle fibrosis

Front 41

Atrophic masticatory myositis
-describe

Back 41

-chronic variant of eosinophilic myositis

Front 42

Myasthenia gravis
-pathogenesis

Back 42

-Inherited: abnormal development of the neuromuscular endplate ---> congenital deficiency in acetylcholine receptors

-Acquired: autoimmune destruction of neuromuscular end plates from antibody production against acetylcholine receptors

Front 43

Myasthenia gravis
-clinical signs

Back 43

-weakness
-fatigue
-episodic collapse
-weight loss

Front 44

Myasthenia gravis
-predisposing lesion

Back 44

-thymoma

Front 45

Myasthenia gravis
-sequelae

Back 45

-megaesophagus
-aspiration pneumonia

Front 46

Bone cells
-types
-function

Back 46

-osteoprogenitor cells (differentiate into chondroblasts, fibroblasts, osteoblasts)
-Osteoblasts (form osteoid and initiate bone matrix mineralization)
-Osteocytes (osteoblasts embedded in mineralized bone matrix; can possibly cause osteolysis but not osteoplasia)
-Osteoclasts (reabsorb bone to maintain Ca2+ levels)

Front 47

Bone matrix
-components

Back 47

-organic matrix (osteoid): Type I collagen & ground substance
-inorganic matrix (mineral): hydroxyapatite, Ca, P, Na, K, ...

Front 48

Osteogenesis
-mechanisms

Back 48

-Intramembranous ossification
-Endochondral ossification

Front 49

Intramembranous ossification
-describe
-where found

Back 49

-blood vessels invade mesenchyme
-mesenchymal cells --> osteoblasts
-osteoblasts produce osteoid
-osteoid mineralized to bone

-flat bones, diaphysis of long bones

Front 50

Endochondral ossification
-describe
-where found

Back 50

-cartilage model forms from mesenchyme
-vascular invasion and cartilage degeneration
-diaphyseal and epiphyseal ossification centers form
-bone length increases due to continued growth at physeal plate


-long bones

Front 51

Physeal zones

Back 51

-zone of resting cartilage
-zone of cell proliferation (columnar)
-zone of cell maturity and hypertrophy
-zone of cartilage calcification
-zone of ossification

Front 52

Processes that determine bone shape and structure

Back 52

-genetics establish limits of size and shape
-gravity and mechanical forces influence modeling and remodeling
-nutrition
-hormones (GH, cortical steroids)

Front 53

What always occurs concurrently with developmental joint diseases?

Back 53

-joint anomalies

Front 54

Chondrodysplasia
-what is it

Back 54

-primary disorder of bone cartilage differentiation manifested as premature cessation of bone growth

Front 55

Chondrodysplasia
-typically characterized by...

Back 55

Dwarfism
-proportionate dwarfism: interstitial and appositional bone growths are coordinated
-disproportionate dwarfism: interstitial and appositional bone growths are not coordinated

Front 56

Chondrodysplasia
-manifestatione

Back 56

-Bulldog dwarfs (dexter type): seen in cattle
-Snorter dwarfs (Telemark type): herefords, angus
-Alaskan malamute dwarfism
-Pseudochondrodysplasia: poodles with short limbs predisposed to DJD
-Spider lamb syndrome

Front 57

Collagen disorders of bone

Back 57

-osteogenesis imperfecta
-hereditary collagen dysplasia
-mucopolysaccharidoses

Front 58

Osteogenesis imperfecta
-pathogenesis
-lesions
-manifestations

Back 58

-pathogenesis: failure to convert fetal to adult collagen

-lesions: skeletal, ocular, aural, articular, and tooth lesions

-manifestation: bones are thin and brittle

Front 59

Hereditary collagen dysplasia
-pathogenesis
-manifestations

Back 59

-pathogenesis: defect in collagen fibrillogenesis

manifestations:
-dermatosparaxis: loose, fragile skin (bovine)
-rubber puppy syndrome: loose, hypermobile joints

Front 60

Mucopolysaccharidoses
-pathogenesis
-lesions
-manifestations

Back 60

-pathogenesis: lysosomal storage disease

-lesions: flat face, short thoracic vertebrae, fused lumbar and cervical vertebrae

-manifestations: dwarfism, cardiovascular, neurologic, ocular abnormalities in cats

Front 61

-fetal monster lacking a lower jaw and having ears united below the face

Back 61

-otocephalus

Front 62

-skull deformity caused by premature fusion of the cranial sutures

Back 62

-craniostenosis

Front 63

-a congenital fissure of the cranium

Back 63

-cranioschisis

Front 64

-a double fetal monster united by the heads

Back 64

-craniopagus

Front 65

a short, wide head

Back 65

-brachycephalic

Front 66

a short lower jaw

Back 66

-brachygnathia

Front 67

potrusion of the jaw

Back 67

-prognathia

Front 68

lack of jaw

Back 68

-agnathia

Front 69

-incomplete development of one side of a vertebra

Back 69

-hemivertebra

Front 70

-a defective closure of the bony encasement of the spinal cord

Back 70

-dysraphism
-spina bifida

Front 71

-lateral deviation of the spine

Back 71

-scoliosis

Front 72

anterior-posterior deviation of the spine

Back 72

-kyphosis

Front 73

fetus with a greatly deformed body or trunk

Back 73

-perosomus

Front 74

gross aplasia or hypoplasia of a long bone

Back 74

-ectromelia

Front 75

the absence of all or part of a distal limb

Back 75

-hemimelia

Front 76

the absence of the proximal part of the limb

Back 76

-phocomelia

Front 77

fusion of the digits

Back 77

-syndactyly

Front 78

deviation of the distal portion of a limb

Back 78

-angular limb deformity (valgus, varus)

Front 79

Osteoporosis
-define

Back 79

-reduction in the amount of bone (osteopenia) with clinical disease (fracture)
-imbalance between formation and resorption of bone which favors resorption causing accelerated bone loss with normal formation

Front 80

Osteoporosis
-causes

Back 80

-calcium deficiency
-Vitamin D or A deficiency
-disuse due to fracture or paralysis
-senility
-nutrition deficiency
-hormonal imbalance (dec. sex hormones, inc. adrenal, thyroid, pituitary)

Front 81

Osteoporosis
-lesions

Back 81

Widening of the marrow cavity with thinning of compact and cancellous bone
-bones become porous
-cone deformity and fractures
-maintenance of normal plasma calcium and phosphorus

Front 82

Osteomalacia
-define

Back 82

-metabolic condition characterized by the softening of bones due to inadequate mineralization of osteoid
-osteoid deposition is normal but there is inadequate and incomplete mineralization

Front 83

Osteomalacia
-causes

Back 83

-Phosphorus or Vit D deficiency (dietary or lack of sunlight)

-more common in older animals
-lactation and gestation predispose cattle

Front 84

Osteomalacia
-lesions

Back 84

mineralized centers and outer layers of un-mineralized osteoid in the trabecular and cortical bones
-thick cortex that may be deformed, compressed, fractured
-bones are soft and can't bear weight
-concurrent reduction in amount of normal bone (osteoporosis)

Front 85

Rickets
-define

Back 85

-osteomalacia of young, growing animals that occurs during active bone growth
-failure of mineralization of both osteoid and the growth plate of growing bones
-changes in growth plate due to failure of the chondrocytes in the physeal cartilage to degenerate and mineralize

Front 86

Rickets
-causes

Back 86

-phosphorus or Vit. D deficiency

Front 87

Rickets
-bone lesions

Back 87

Same as osteomalacia:

mineralized centers and outer layers of un-mineralized osteoid in the trabecular and cortical bones
-thick cortex that may be deformed, compressed, fractured
-bones are soft and can't bear weight
-concurrent reduction in amount of normal bone (osteoporosis)

Front 88

Rickets
-physeal lesions

Back 88

-physes become thick and irregular from retention of cartilage and deposition of osteoid on retained cartilage
-metaphysis contains strips of un-mineralized cartilage covered by osteoid with large amounts of fibrous tissue

Front 89

Osteopetrosis
-define

Back 89

-metabolic condition characterized by excessive bone accumulation

Front 90

Osteopetrosis
-causes

Back 90

Defective osteoclast activity and failure to resorb bone

Congenital disease: inherited or due to inutero viral infection
-BVDV
-FLV
-Avian leukosis virus

Acquired disease: caused by fluoride toxicity
-fluorine replaces hydroxyl radicals in bone when low levels are ingested over long periods

Front 91

Osteopetrosis
-lesions

Back 91

-bones are thick and brittle
-spondylosis between vertebrae
-depressed hematopoeisis due to lack of space for effective hematopoeisis

Front 92

Vitamin A deficiency musculoskeletal diseases

Back 92

Excessive proliferation of bone due to a low rate of bone resorption because osteoclasts need Vitamin A

-vitamin A upregulates Vitamin D receptors

-results in optic nerve compression due to thickened cranial bones and narrow optic foramina

Front 93

Vitamin C deficiency musculoskeletal diseases

Back 93

Inadequate cross-linking of collagen
-only a problem in species that lack L-glucolactone oxidase which is needed for the synthesis of ascorbic acid

-similar features to rickets
-osteoid formation is abnormal and physes become thick and disorganized
-epiphyseal and periarticular capillaries are weak and rupture

Front 94

Manganese deficiency musculoskeletal diseases

Back 94

Perosis
-failure of ossification of the epiphyseal cartilage of the tarsometatarsus due to suppressed physeal cartilage proliferation and reduced osteoblast activity --> medial displacement of the gastrocnemius tendon

-important in Chickens and turkeys

-short, thick legs and wings, and globular heads

Front 95

How to classify fractures

Back 95

-intrinsic (muscle or tendon) vs. extrinsic (trauma)
-incomplete vs. complete
-closed vs. compound vs. comminuted

Front 96

Ways fractures heal

Back 96

Depends on stabilization, reestablishment of blood supply, and formation of callus
-callus formation (proliferation of endosteal and periosteal osteoblasts)
-cartilage forms first due to low initial oxygen tension
-bone replaces cartilage as the blood supply is reestablished

Front 97

Fracture complications

Back 97

-nonunion
-infection/sequestrum
-premature epiphyseal closure
-soft tissue injury
-fat emboli from bone marrow that lodge in brain, lung, others

Front 98

Osteomyelitis
-define

Back 98

-inflammation of the medullary cavity
-commonly occurs in septicemic animals from bacteria lodging in metaphyseal vessels

Front 99

Bacterial Osteomyelitis
-etiologies

Back 99

-Arcanobacterium pyogenes (cattle, pigs, lambs; vertebral abscesses)
-Brucella (cattle, pigs; bones and joints)
-Actinomyces bovis (cattle; lumpy jaw)
-Salmonella spp. (foals; supperative)
-Mycobacterium spp. (discrete granulomatous foci)
-Staphylococcus intermedius (dogs)

Front 100

Fungal Osteomyelitis
-etiologies

Back 100

Pyogranulomatous osteomyelitis
-Coccidioides immitis (dogs)
-Blastomyces dermatitidis (dogs)
-Cryptococcus neoformas (cats)

Front 101

Viral Osteomyelitis
-etiologies

Back 101

-FeLV
-CDV
-CHV

Rare

Front 102

Canine Hypertrophic Osteodystrophy
-define

Back 102

-inflammatory condition of young, rapidly growing, large and giant breed dogs

Front 103

Canine Hypertrophic Osteodystrophy
-likely causes

Back 103

-genetic predisposition
-Vit. C deficiency
-Hypervitaminosis D

Front 104

Canine Hypertrophic Osteodystrophy
-lesions

Back 104

Metaphyseal regions of long bones become swollen and hot
-disruption with occasional necrosis and supperative inflammation of metaphyseal trabecuale adjacent to the growth plate
-metaphyseal thickening from fibrous thickening and periosteal new bone formation

Front 105

Canine Hypertrophic Osteodystrophy
-outcome

Back 105

-episodic signs: lameness, fever, anorexia, weight loss
-lesions can resolve spntaneously with residual deformities or completely return to normal

Front 106

Canine Panosteitis
-clinical features

Back 106

-young, male, large and giant breed dogs
-mild to severe shifting leg lameness and painful long bones

Front 107

Canine Panosteitis
-causes

Back 107

-genetic predisposition suspected
-viral infections and autoimmune responses possible

Front 108

Canine Panosteitis
-lesions

Back 108

Primary degeneration of medullary cavity adipose tissue
-endosteal and periosteal new bone formation

Front 109

Craniomandibular Osteopathy
-clinical features

Back 109

-5-8 mo. old terriers
-difficulty chewing
-inability to open mouth
-tenderness of jaw bones
-can be fatal from not eating

Front 110

Craniomandibular Osteopathy
-causes

Back 110

-genetic
-infectious

Front 111

Craniomandibular Osteopathy
-lesions

Back 111

-production of woven bone on the endosteal and periosteal surfaces of the jaw and facial bones
-bones become thickened, coarse, crumbly
-lymphocytes, plasma cells, neutrophils in newly formed bone

Front 112

Hypertrophic Osteopathy
-pathoenesis possibilities

Back 112

-effect of toxic substances produced by pulmonary lesion
-alteration in peripheral blood flow (periosteal congestion and low O2 concentration stimulating bone formation)
-Neurogenic changes associated with vagus nerve involvement
-excessive growth hormone production

Front 113

Hypertrophic Osteopathy
-causes

Back 113

Space occupying lesions of the thoracic cavity:
-Pulmonary tumors
-Megaesophagus
-Spirocerca lupi granulomas
-Cardiac disease

Urinary Bladder neoplasm

Hepatozoon americanum (dogs)

Front 114

Hypertrophic Osteopathy
-lesions

Back 114

-proliferation of periosteal new bone on long bones of the appendicular skeleton

Front 115

Hypertrophic Osteopathy
-outcome

Back 115

-bone returns to normal if inciting lesion is removed

Front 116

Neoplasms that arise in the bone

Back 116

-osteosarcoma
-osteoma
-chondrosarcoma
-chondroma
-osteochondroma
-feline osteochondromatosis
-multilobular chondrosarcoma

Front 117

Osteosarcoma
-cell of origin

Back 117

-osteoblasts
-osteoprogenitor cells

Front 118

Osteosarcoma
-most likely location

Back 118

Appendicular skeleton (front limbs primarily)
-distal radius
-doesn't cross joint space (differentiate from fungal osteomyelitis)

Front 119

Osteosarcoma
-gross morphology

Back 119

-local swelling of the limb
-doesn't cross joint space

Front 120

Osteosarcoma
-microscopic morphology

Back 120

-production of osteoid/bone
-chondrocytic or fibrocytic differentiation

Front 121

Osteosarcoma
-outcome/prognosis

Back 121

-rapidly growing
-aggressive
-metastasize rapidly

-Poor prognosis (9 wk survival time)

Front 122

Chondrosarcoma
-cell of origin

Back 122

-chondroblasts
-chondrocytes

Front 123

Chondrosarcoma
-incidence

Back 123

-10% of primary bone tumors in dogs

Front 124

Chondrosarcoma
-most likely location

Back 124

-flat bones
-physeal cartilage

Front 125

Chondrosarcoma
-microscopic morphology

Back 125

-sheets of neoplastic chondroblasts

Front 126

Chondrosarcoma
-outcome/prognosis

Back 126

-prognosis better than osteosarcoma but still poor (18 wk survival time)

-slower to metastasize

Front 127

Osteochondroma
-cell of origin

Back 127

-considered a developmental disturbance associated with physeal cartilage that cease growth at skeletal maturity
-considered non-neoplastic

Front 128

Osteochondroma
-incidence

Back 128

-cartilage capped exostoses in dogs and horses

Front 129

Osteochondroma
-location

Back 129

-adjacent to growth cartilage

Front 130

Osteochondroma
-outcome

Back 130

-may progress to chondrosarcoma

Front 131

Metastatic neoplasm that occurs in bones

Back 131

-prostatic adenocarcinoma

Front 132

Synarthroses

Back 132

-joints composed of fibrous tissue

Front 133

Amphiarthroses

Back 133

-joints comprised of cartilage

Front 134

Diarthroses

Back 134

-joints that contain synovial fluid

Front 135

Infectious arthritis
-occurs most commonly in

Back 135

-farm animals
-young animals via umbilical infection

Front 136

Infectious arthritis
-route of infection

Back 136

-hematogenous

Front 137

Infectious arthritis
-morphological appearance

Back 137

-fibrinous due to hyperemia and increased permeability of synovial vessels resulting in the leakage of fibrin into the joint
-synovial hyperplasia and pannus in severe cases

Front 138

Infectious arthritis
-bacterial causes

Back 138

-Streptococcus sp. (young large animals; bacteremia secondary to naval infection; purulent polyarthritis)
-Erysipelothrix rhusiopathiae (young pigs; wound infection, fibrinopurulent polyarthritis)
-Haemophilus suis & parasuis (5-12 wk old pigs; polyserositis)
-Brucella suis (diskospondylitis)
-Mycoplasma sp. (young or old animals)
-E. coli
-Salmonella sp.
-Klebsiella
-Actinobacillus equuli
-Staphylococcus sp.

Front 139

Infectious arthritis
-viral causes

Back 139

-Retroviral induced (goats, Caprine arthritis-encephalitis)

Front 140

Non-infectious arthritis
-forms

Back 140

-erosive
-non-erosive

Front 141

Erosive form of non-infectious arthritis
-pathogenesis

Back 141

Primary immunologic disease located at joint
-rhematoid or rheumatoid-like factor produced
-IgG or IgM bind to antigens that get deposited into joints
-factors activate complement
-attraction of neutrophils
-complement and neutrophils cause cartilage erosion and exposure of subchondral bone

Front 142

Erosive form of non-infectious arthritis
-Morphology

Back 142

-cartilage erosion
-proliferative synovitis
-pannus formation

Front 143

Erosive form of non-infectious arthritis
-manifestations

Back 143

-fusion and deformation of the joint if the joint space collapses (fibrous ankylosis)

Front 144

Erosive form of non-infectious arthritis
-clinical signs

Back 144

-shifting leg lameness
-anorexia
-depression
-progressive deforming arthritis

Front 145

Non-erosive form of non-infectious arthritis
-pathogenesis

Back 145

Primary immunologic disease located elsewhere in the body
-products of the immune process are transported to the capillary bed and synovium
-deposition of immune complexes in synovial vessels

Front 146

Non-erosive form of non-infectious arthritis
-associated with

Back 146

-systemic lupus erythematosus
-endocarditis
-pyometra
-dirofilariasis

Front 147

Non-erosive form of non-infectious arthritis
-morphology

Back 147

-synovitis (inflammation restricted to synovium)
-NO synovial hyperplasia or pannus formation
-normal articular cartilage

Front 148

Non-erosive form of non-infectious arthritis
-clinical signs

Back 148

-lesions involving 1 or more joints
-widespread synovitis
-recurrent lameness

Front 149

Hip dysplasia
-define

Back 149

-multifactorial disease resulting in the progressive degeneration of the coxo-femoral joint

Front 150

Hip dysplasia
-multifactorial causes in large breed dogs

Back 150

-genetic predisposition
-intrinsic developmental joint defect (osteochondrosis)
-abnormal joint conformation and resultant stresses
-rapid growth & large body size
-inadequate muscles and soft tissues to hold the joint in place properly

Front 151

Hip dysplasia
-step-wise pathogenesis

Back 151

-loose thendons and muscles
-subluxation of the femoral head
-elongation of the teres ligament and stretching of the joint capsule
-subluxations become more frequent and severe
-delayed ossification of the acetabular rim
-acetabulum becomes shallow and the femoral head no longer fits deeply in
-roughening of the femoral head cartilage due to traumatic contact with the acetabular rim

Front 152

Hip dysplasia
-progressive lesions

Back 152

-acetabular rim breaks down (rounder, shallower, wider)
-articular cartilage fibrillates, ulcerates, and eburnation of exposed subchondral bone
-extensive synovial hyperplasia
-joint capsule becomes thickened (restricts joint movement)
-periarticular ossification in an attempt to stabilize the joint

Front 153

Osteochondrosis
-define

Back 153

disturbance in the normal differentiation of cartilage in physeal plate and subarticular cartilage
-manifested as joint disease
-most cases are transient and subclinical

Front 154

Osteochondrosis
-predisposing cuases

Back 154

-genetics
-rapid growth rate
-high levels of nutrition
-intensive management

Front 155

Osteochondrosis
-lesions

Back 155

In actively growing cartilage
-cartilage becomes thickened and is retained (doesn't mineralize)
--blood vessels cannot penetrate the metaphyseal/epiphyseal region to supply nutrients for mineralization

Front 156

Osteochondrosis
-sequelae

Back 156

-necrosis

Front 157

Osteochondrosis
-manifestations

Back 157

-osteochondrosis dissecans
-epiphysiolysis
-physeal fusion defects
-abnormalities leading to hip dysplasia and cervical vertebral instability

Front 158

Osteocondrosis dissecans
-pathogenesis

Back 158

-caused by thickened osteochondrotic subarticular cartilage
-mechanical stress and movement cause cartilage fissures to form
-flaps and erosions occur in the articular cartilage
-damage to opposing articular cartilage
-dissection of synovial fluid into underlying bone causes necrosis and subchondral cyst formation

Front 159

Osteocondrosis dissecans
-sequela

Back 159

-DJD

Front 160

Cervical Vertebral Stenosis
-pathogenesis

Back 160

-lesions of articular facets (cartilage erosion, cartilage eburnation, asymmetry of articular facets)
-narrowing of the spinal canal and compression and stretching of the spinal cord
-degeneration and malacia occur in the spinal cord

Front 161

Epiphysiolysis
-define

Back 161

-separation of the physis from the diaphysis of a bone

Front 162

Epiphysiolysis
-pathogenesis

Back 162

-thickened osteochondrotic physeal cartilage
-weakening of the physes
-separation of the epiphysis from the metaphysis from trauma or stress

Front 163

Epiphysiolysis
-sequela

Back 163

-bone deformity
-joint abnormalities

Front 164

Epiphysiolitis
-manifestations

Back 164

-ununited bony processes
-epiphysel fractures

Front 165

DJD
-inciting cause

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-improper alignment of the joint leading to progressive cartilage degeneration

Front 166

DJD
-morphology

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-degeneration and thinning of articular cartilage
-eburnation and sclerosis of underlying bone
-synovial hyperplasia
-thickened joint capsule and osteophyte formation

Front 167

DJD
-examples

Back 167

-Ringbone (interphalangeal joint of horses)
-Spavin (tarsol joint in horses)
-Shoulder arthropathy (old dogs)
-Legg-Calve-Perthes Disease (ischemic necrosis of femoral head in horses)

Front 168

Navicular Disease
-define

Back 168

-Ischemia, stress, or poor conformation causes degeneration and erosion of fibrocartilage of the navicular bone

Front 169

Navicular disease
-appearance

Back 169

-rarefaction
-fibrosis

Front 170

Navicular disease
-sequelae

Back 170

-fraying and tearing of the flexor tendon
-navicular bursitis
-necrosis and stress fracture of the navicular bone

Front 171

Malignant neoplasm that arises in the joint

Back 171

-synoviosarcoma (maliganant, metastatic)