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BOD 3 > Musculoskeletal System > Flashcards

Musculoskeletal System Flashcards

1
Q

supports regions for hematopoietic tissue

A

cancellous bone

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2
Q

Endoesteum is important for

A

maintenance and remodeling of bone

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3
Q

where your growth plate is

A

physis

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4
Q

metaphysis

A

area of active bone remodeling aiding in longitudinal growth

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5
Q

manufactures osteoid

A

osteoblasts

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6
Q

found along the periosteum
forms the bone-blood barrier and controls ions movement within matrices
can become active to form more bone

A

inactive osteoblasts

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7
Q

osteoblasts that become surrounded by matrix
the most numerous cell in bone
produces osteogenic compounds and functions in mechanosensation

A

osteocytes

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8
Q

most numerous cell in bone

A

osteocytes

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9
Q

derived from hematopoietic cell line (macrophage), resorb bone matrices, transient cells (undergoes apoptosis)

A

osteoclasts

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10
Q

where are osteoclasts derived from

A

derived from hematopoietic cell line (macrophage)

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11
Q

Components of bone

A

1) Organic: 90% osteoid which is type 1 collagen and 10% other proteins

2) Inorganic (mineralization) which is calcification of osteoid, hydroxyapatite, interplay of calcium, phosphrous and vitamin D

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12
Q

What kind of collagen is osteoid (organic component) made of

A

type I collagen: chain of repeating amino acids in tri-helix structure, which adds tensile strength

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13
Q

What is the organic component of bone

A

90% osteoid (type 1 collagen)
10% other proteins

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14
Q

What is the inorganic component of bone made of

A

the calcification of osteoid
hydroxyapatite
interplay of calcium, phosphorus, and vitamin D

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15
Q

Osteoblasts make ______ which is made of _________

A

osteoid which is type 1 collagen and then it becomes mineralized by an interplay of
-Calcium, phosphorus, and vitamin D (hydroxyapatite)

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16
Q

spongey bone
contains marrow
oriented parallel to the mechanical stress

A

trabecular bone (cancellous)

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17
Q

mature bone
most abundant bone in adult skeletal
fiber are oriented in parallel fashion

A

lamellar bone

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18
Q

osteon

A

a structure in lamellar bone (mature bone) where fibers are iroented in parallel fashion
lots of resistance to pressure

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19
Q

fetal bone, rapidly developing bone, injury repair
collagen fibers are haphazardly organized

A

woven bone - restructured/remodeled later to lamellar bone

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20
Q

In time, woven bone is remodeled to

A

lamellar bone

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21
Q

Where does the majority of intramembranous ossification occur

A

the cranial/facial bone formation

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22
Q

Describe the process of intramembranous ossification

A

1) Progenitor mesenchymal cells infiltrate the region
2) Differentiate into osteoblasts making osteoid and woven bone
3) Regions of ossification expand as additional peripheralized cells become osteoblasts
4) Bone is remodeled into mature bone

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23
Q

Does intramembranous ossification be a scaffolding to form?

A

No it does not
connective tissue is invaded by vascular supply

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24
Q

Intramembranous ossification is a key mechanism for all bone to undergo _________

A

appositional growth (increase in diameter)

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25
Q

In what bones does endochondral ossification occur in?

A

All bones of the axial and appendicular skeleton

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26
Q

Describe the process of endochondral ossification

A

1) There is an initial cartilaginous skeletal muscle
2) Central region of diaphysis hypertrophies and mineralizes
3) Vascular invasion and osteoblasts invade and form bone (primary centers of ossification)
4) Similar centers occur at the epiphyses (secondary center of ossification)

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27
Q

What separates the primary and secondary centers of ossification in endochondral ossification

A

growth plates

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28
Q

What is the most common form of bone formation embryologically

A

endochondral ossification (cartilage hypertrophies and ossified)

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29
Q

what drives longitudinal (interstitial) growth

A

the growth plate (physis)
-orderly zones leading to mineralized matrix for osteoid deposition and becomes lamellar bone

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30
Q

when does the growth plate close

A

with skeletal maturation

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31
Q

what drives width (appositional) growth

A

intramembranous ossification stemming from periosteum

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32
Q

What is Wolff’s law

A

explains the effect of decreased weight on the bone as the bone becomes less dense and weaker. Bone develops to withstand the most amount of mechanical pressure
-Application of force to curved bone increase compressive force on the side with the curvature. this produces electrical currents which stimulate osteoblasts
-Bone is deposited on inside of the curvature and taken away from the outside of the curvature
-Result is bone that is straighter and withstand more impact

*Interplay of osteoblasts (bone deposition) and osteoclasts (bone resorption)

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33
Q

what is a classic finding of a degenerative joint disease

A

Osteophytes- small nodules of bony formation

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34
Q

atrophy/thinning of the bone

A

osteoporosis- predisposition to fracture (can be caused by disuse or nutritional abnormalities)

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35
Q

What are the the most prone fracture points in young animals

A

the growth plates- growing cartilage point is weak, specifically Type II (just above the growth plate)

-good prognosis if proliferative zone is intact, blood supply is intact, no bony bridges between epiphysis and metaphysis are formed

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36
Q

Younger animals are more prone to fractures at their growth plates. What factors help you determine that there is a good prognosis with these fractures?

A

Good prognosis if:
1) Proliferative zone is intact
2) Blood supply is intact
3) No bony bridges between metaphysis and epiphysis are formed

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37
Q

an angular limb deformity that occurs due to growth plate injury where there is a lateral deviation of the limb distal

A

Valgus

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38
Q

What is valgus

A

an angular limb deformity that occurs due to growth plate injury where there is a lateral deviation of the limb distal (ballerina kinda looping “L”)
-Most common in horse and dog
88.4% of foals but most resolve with age
-Most common pathology in puppy is due to premature closure of distal ulna physis

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39
Q

What is the most common cause of valgus in dogs/cats?

A

*Premature closure of distal ulna physis. Radius keeps growing on the medial side and push the limb to a lateral deviation

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40
Q

Do most angular limb deformities in foals correct themselves?

A

Yes 88.4% have them and majority of them resolve with age

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41
Q

What might be the cause of limb deformities in large dog breeds

A

impaired endochondral ossification of the growth plates

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42
Q

Is Valgus or Vargus more common?

A

valgus

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43
Q

The medial deviation of the limb distally. occurs in puppies with only radial physis damage

A

Vargus

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44
Q

Puppies with radial physis damage would cause

A

Vargus- ulna keeps growing so their is a distal displacement medially (inward)

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45
Q

excessive mechanical force: compressive or transverse to a bone

A

physiological bone fracture

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46
Q

a fracture that occurs but there is normal mechanical force with weakened bone

A

Pathological Bone Fracture
Local/PrimaryLesion to bone : Osteosarcoma, Osteomyelitits

Systemic Lesion to bone: Fibrous osteodystrophy, osteoporosis (multiple sites of fracture)

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47
Q

Name 2 causes of systemic pathologic bone fractures

A

1) fibrous osteodystrophy
2) Osteoporosis

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48
Q

Describe the process of fracture repair

A

1) Hematoma formation (instant to a few days, acute inflammatory response, promotes fibroblast migration and neovascularization

2) Fibrocartilaginous callus- forms rapidly, serves as anchoring mechanism for bone ends, cartilage is deposited to connect the bone, osteoclasts clear the necrotic bone

3) Hard callus: bone replaces soft callus via endochondral ossification and osteooblast proliferation, forms matrix immature bone, allows return to function

4) Remodeling: months to years, replacement and organization of woven bone into mature bone, complete strength of bone is restored

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49
Q

occurs instant to a few days after bone fracture,
-acute inflammatory response, promotes fibroblast migration and neovascularization

A

hematoma formation

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50
Q

forms rapidly after bone fracture and subsequent hematoma, serves as anchoring mechanism for bone ends
-cartilage is deposited to connect the bone
-osteoclasts clear the necrotic bone

A

formation of fibrocartilaginous callus

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51
Q

forms after bone fracture where bone replaces soft callus (fibrocartilaginous callus) via endochondral ossification and osteoblast proliferation, forms matrix immature bone, allows return to function

A

hard callus formation

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52
Q

takes months to years, replacement and organization of woven bone into mature bone, complete strength of bone is restored

A

bone remodeling after fracture repair

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53
Q

What enables quick repair of a bone fracture back to original strength

A

close opposition of fragments

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54
Q

Displaced bone fractures require

A

formation of large repair callus and decreased healing ability

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55
Q

What are some complications to fracture repair?

A

1) Large necrotic bone fragments (bone sequestrum) inhibits healing
2) Continual movement of joints prevent healing (pseudoarthritis)
3) Bacterial osteomyelitis

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56
Q

inflammation of the periosteum (surface of the bone)

A

periostitis

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57
Q

inflammation across growth plate

A

physitis

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58
Q

inflammation of the bone tissue and marrow

A

osteomyelitis

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59
Q

what is the main cause of osteomyelitis

A

bacterial due to
1) trauma
2) local extension
3) hematogenous (most common cause)

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60
Q

Is hematogenous osteomyelitis more common in foals/ruminants or small animals

A

foals/ruminants
-if they are septic, assume that they have osteomyelitis

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61
Q

What is the most common bacterial isolate of hematogenous osteomyelitis

A

Staphylococcus

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62
Q

hematogenous osteomyelitis has a predilection for

A

the epiphysis and metaphysis region of bone
can occur on multiple bones/multiple sites in the same bone

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63
Q

How does osteomyelitis from local extension typically occur?

A

in the oral cavity
-extension of commensal oral bacteria into alveolar bone, mandible, and maxilla
-Common in older dogs and cats (periodontal disease)
-Lumpy jaw in cows (local invasion of actinomyces bovis) leading to granulomatous inflammation and boy reaction/proliferation

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64
Q

How might dogs and cats get osteomyelitis from local extension

A

if they have periodontal disease
-extension of commensal oral bacteria into alveolar bone, mandible, and maxilla

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65
Q

What is the cause of lumpy jaw (granulomatous inflammation and unilateral bony proliferation of the mandible in cattle)

A

Actinomyces bovis

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66
Q

Actinomyces bovis local extension into alveolar bone, mandible, and maxilla causes

A

Lumpy jaw

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67
Q

What are possible routes of traumatic osteomyelitis

A

1) open fractures
2) contamination during surgical repair of fracture
3) bite wound
4) gunshot
5) wound to claw or hoof

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68
Q

Potential sequela to osteomyelitis

A

1) Bone abscess: central cavitating purulent region
2) Sequestrum: large islands of necrotic bone
3) Involucrum: fluid filled/reaction tissue around region of infection

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69
Q

a potential result to osteomyelitis where there is fluid filled/reaction tissue around region of infection

A

Involucrum

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70
Q

a potential result to osteomyelitis where there is large islands of necrotic bone

A

Sequestrum

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71
Q

a potential reuslt to osteomyelitis where there is a central cavitating purulent region within the bone

A

bone abscess

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72
Q

Infectious osteomyelitis is typically bacterial origin but what are other differentials

A

1) Fungal: Coccidioides (disseminated), Blastomyces, Cryptococcus (cats)
2) Viral: BVDV, Adenovirus, Feline Herpes, FeLV

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73
Q

What are the two causes of non-infectious osteomyelitis

A

1) Panosteitis
2) Metaphyseal osteopathy

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74
Q

What is panosteitis

A

a non-infectious form of osteomyelitis
-typically 5-12month old large breed male dogs
-Clinical signs: shifting leg lameness, forelimb, 50% involve multiple bones, +/- fever, self-limiting

Radiographic lesion (leading diagnostic modality is medullary density in diaphysis
*proliferative, little to no inflammation

Due to fibroblast/osteoblast proliferation and medullary fibrosis and ossificaton

Idiopathic

excellent prognosis

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75
Q

What is the typical signalment for dogs with panosteitis

A

5-12 months old
large breed
male dog

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76
Q

How do you treat panosteitis in a dog

A

it is typically self-limiting
just treat for pain
*Excellent prognosis

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77
Q

How do you diagnose panosteitis

A

Radiography- dense medullary region in the diaphysis
“cotton-like densities with the medulalry space”
medullary fibrosis and osssification

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78
Q

Where does panosteitis typically occur in

A

diaphysis of long bones
due to fibroblasts/osteoblast proliferation
medullary fibrosis and ossification

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79
Q

What is the typical signalment for Metaphyseal Osteopathy

A

2-8 month old large and giant dog breeds
-Weimaraners, Great Danes, Boxers, German Shepherds

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80
Q

What breeds are predisposed to Metaphyseal Osteopathy

A

Weimaraners, Great Danes, Boxers, German Shepherds

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81
Q

Metaphyseal Osteopathy

A

also called Hypertrophic Osteodystrophy (HOD)
-2 to 8month old large and giant breed dogs (Weimaraners, Danes, Boxers, GSD)
-Present with severe lameness, swollen distal radius, ulna, tibia, pathological fractures, fever and anorexia
-Osteoblasts are destroyed, no new bone formation

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82
Q

Normally the primary spongiosa is lined by osteoblasts and osteoid but with metaphyseal osteopathy:

A

they lack osteoblasts and osteoid because neutrophils destroy them. Will see necrotic debris and neutrophils on histo

Predisposed to fractures

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83
Q

What are the acute lesions of Metaphyseal Osteopathy

A

suppurative osteomyelitis
Necrosis
lack of normal bone deposition (neutrophils destroy osteoblasts and osteoid)

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84
Q

What are the chronic lesions of metaphyseal ostopathy

A

periosteal reaction results in excessive bone production (swollen radius, ulna, tibia) and severe lameness

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85
Q

What is the cause of metaphyseal osteopathy

A

Idiopathic

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86
Q

What is prognosis of Metaphyseal osteopathy? What is the treatment

A

It can be self-limiting, recurrent bouts, will need to euthanize in severe cases

Clinically: treat with antibioitcs, NSAIDs/Steroids, and supportive treatment

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87
Q

What is the most common route of osteomyelitis *

A

Hematogenous spread
-typically large animals
-will die very quickly and will have osteomyelitis if survive

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88
Q

abnormalities primarily affecting bone formation or remodeling
-most considered lethal or semi-letha
primarily genetic in nature

A

Skeletal dysplasia

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89
Q

What are classical clinical findings of diseases causing skeletal dysplasia

A

-Short stature
-Abnormally shaped bones
-Increased bone fragility

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90
Q

a skeletal dysplasia resulting in shortening of mandible

A

brachygnathia inferior

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91
Q

a skeletal dysplasia resulting in shortening of mandible (breed standard for brachycephalic breeds)

A

brachygnathia superior (prognathism)

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92
Q

a localized skeletal dysplasia where there is concavity of sternum, most common in cats

A

pectus excavatum

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93
Q

What is pectus excavatum

A

a localized skeletal dysplasia where there is concavity of sternum, most common in cats

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94
Q

What species is pectus excavatum most common in

A

cats

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95
Q

What is a common finding of pectus excavatum in cats?

A

difficulty breathing- the concavity of the sternum prevents breathing

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96
Q

a localized skeletal dysplasia where there is increased number of limbs

A

polymelia

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97
Q

a localized skeletal dysplasia where there is partial absence of part of the distal limb

A

Hemimelia
-a rat Pox virus can cause rats limbs to slough off (wild)

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98
Q

a localized skeletal dysplasia where there is absence of one or more limbs

A

Amelia

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99
Q

a localized skeletal dysplasia where there is partial or complete fision of digit

A

Syndactyly
-some breeds of pigs

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100
Q

a localized skeletal dysplasia where there is increase in the number of digits

A

polydactyly
-common in cats

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101
Q

a defect in cartilage development
-abnormal endochondral ossification effects bones with growth plates (longitudinal growth) leading to uncontrolled growth or disproportionate dwarfism

A

Chondrodysplasia/Chondrodystrophy

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102
Q

What is the pathogenesis of Chondrodysplasia

A

a defect in cartilage development
-abnormal endochondral ossification effects bones with growth plates (longitudinal growth) leading to uncontrolled growth or disproportionate dwarfism
Lesions
-Disorganized chondrocytes/growth plate
-Failed endochondral ossification
-Deformed phyyses, joints, bones abnormal stature

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103
Q

FGFR4 is a gene that causes ___________ in Dachshunds, bassett hounds, and corgis

A

Chondrodysplasia - growth plate abnormality in appendicular skeleton (abnormal endochondral ossification effecting the longitudinal growth of limbs)

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104
Q

BMP3 is a gene that causes _______ of the skull in bulldogs and frenchies

A

chondrodystrophic leading to brachycephalic

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105
Q

T/F: Disproportionate dwarfism effects any breed

A

True- it is pathological

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106
Q

What causes Spider Lambs?

A

Chondrodysplasia due to genetic mutation (FGFR3) leading to uncontrolled gorwth
-Suffolk and Hampshire sheep

Lesions: aberrant ossification centers, endochondral ossification failure
long twisted neck, limbs, scoliosis, kyphosis

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107
Q

What are reasons you may get Chondrodysplasia leading to uncontrolled longitudinal bone growth

A

Spider lambs (FGFR3 point mutation)
Lesions: aberrant ossification centers, endochondral ossification failure
long twisted neck, limbs, scoliosis, kyphosis

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108
Q

Snorter cows

A

Cows that have mild chondrodysplasia
Disproportionate dwarfism
have:
1) Board head
2) Bugling eyes
3) Short legs
*look brachycephalic
Diagnose on ration of limb length to body

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109
Q

Bull dog calfs

A

most severe form of chondrodysplasia in cows
-Extremely short limbs
-Domed head with protruding tongue
-Cleft palate
-Abdominal hernia

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110
Q

You see a cow with board head, bugling eyes, and short legs. What likely occured

A

Mild Chondrodysplasia
-Look brachycephalic

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111
Q

You have a calf with extremely short limbs, domed head with protruding tongue, cleft palate, and abdominal hernia. What likely occured

A

Severe Chondrodysplasia
-failure of most cartilage to form

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112
Q

a condition where there is excessive bone fragility due to a genetic mutation (COL1A1/2) leading to abnormal type I collagen
occurs in calves, lambs, puppies, kittens

A

osteogenesis imperfecta (not just occurs in bone)

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113
Q

T/F: Osteogenesis imperfecta only affects bone

A

False: it is due to a mutation of COL1A1/2 leading to abnormal type 1 collagen. there is type I collagen in tendon, teeth, and the eye
Signs: Joint hyper-motility, thin cortical bone, thinned ocular slcera, intrauterine fractures of ribs, loss of tooth dentin

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114
Q

An animal presents with multiple fractures with no known traumatic cause. Upon physical exam you see thinned ocular sclera, joint hypermotility, and loss of tooth dentin. What likely occured

A

Osteogenesis imperfecta- mutation leading to abnormal type 1 collagen

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115
Q

What are the clinical signs of osteogenesis imperfecta

A

Joint hyper-motility, thin cortical bone, thinned ocular slcera, intrauterine fractures of ribs, loss of tooth dentin, bone fractures

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116
Q

What is the prognosis for osteopetrosis

A

it is lethal (fetus is typically stillborn)

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117
Q

What are the two forms of osteopetrosis

A

1) Congenital/heritable (cats, dogs, sheep, horses, cattle, rats, mice, poultry)
2) Acquired: BVDV, FeLV, canine distemper

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118
Q

What viruses can cause osteopetrosis

A

BVDV, FeLV, canine distemper

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119
Q

What is the pathogenesis of osteopetrosis

A

osteoclastic dysfunction leading to failure of bone resportion/remodeling -> dense metaphysis and diaphysis with thinned cortical bone and increased bone fragility
clinical signs:
-Brachygnathism inferior and protruding tongue
-Long bones and vertebra are short
-Increased bone fragility

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120
Q

What are the clinical signs of osteopetrosis

A

-Brachygnathism inferior and protruding tongue
-Long bones and vertebra are short
-Increased bone fragility

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121
Q

Process of forming compact cortical bone
1) Growth plate
2)
3)
4)
5)
6)

A

Growth plate
Primary spongiosa
Osteoclastic remodeling
Secondary spongiosa
Osteoclastic remodeling
Compact cortical bone

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122
Q

T/F: in osteopetrosis the growth plate abnormally grows leading dense metaphysis and diaphysis

A

False-> the growth plate is normal. This condition actually is due to osteoclastic dysfunction leading to failure of bone resorption and a dense metaphysis and diaphysis

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123
Q

causes overly dense bone (dense metaphysis and diaphysis with thinned cortical bone and increased bone fragility)
clinical signs:
-Brachygnathism inferior and protruding tongue
-Long bones and vertebra are short
-Increased bone fragility

A

osteopetrosis

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124
Q

Congenital Hyperostosis affects _______ (species)

A

swine (young piglets)

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125
Q

What part of the bone does congenital hyperostosis typically affect in swine?

A

predominately the forelimbs
-marked periosteal reaction with edema
-very large forelimbs

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126
Q

What is Congenital Hyperostosis

A

a rare skeletal dysplasia that typically affects young piglets, born either stillborn or die shortly after birth
there is a marked periosteal reaction with edema (typically the forelimbs)
Pathogenesis is unknown.

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127
Q

What causes crooked-calf disease

A

lupine toxicity (quinolizidine alkaloid- Anagyrine) ingested during 40-80 days of gestation
causes fetal immobilization and uterine contraction
Arthrogryposis, troticolis, scoliosis, and cleft palate

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128
Q

congenital angular deformity of the joints with articular rigidity, cleft palate also accompanies

A

Arthrogryposis

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129
Q

What are the causes of arthrogyposis

A

-Spontaneous congenital anomaly
-Hereditary: Angus, Holstein
-Viral: BVDV, Bluetongue virus, Cache Valley virus
-Toxicity: Lupine-Quinolizidine alkaloid

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130
Q

What is “loin jaw”

A

Craniomandibular Osteopathy
-a hyperostotic disease that typically presents at 4-7months and is self-limiting
Usually confined to the skull
Symmetric but irregular proliferation
Breed: West Highland White Terrier
*Might affect eating
unknown pathogenesis
-Pooching of mandibular bone and tympanic bulla are severely affected

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131
Q

a hyperostotic disease that typically presents at 4-7months and is self-limiting
Usually confined to the skull
Symmetric but irregular proliferation
Breed: West Highland White Terrier

A

Craniomandibular Osteopathy

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132
Q

What breed is predisposed to Craniomandibular Osteopathy

A

West Highland White Terrier

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133
Q

What is the prognosis of Craniomandibular osteopathy

A

it is usually self-limiting

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134
Q

T/F: Craniomandibular osteopathy presents with unilateral bony proliferation of the skull

A

False- it is usually symmetric

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135
Q

Diffuse periosteal bone formation along the diaphysis and metaphysis
mostly reported in dogs but can be seen in many species
*Typically due to thoracic mass effect (neoplasia vs infectious)
bone reaction is limited to distal limbs

A

Hypertrophic osteopathy

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136
Q

What are causes of hypertrophic osteopathy (bone reaction of the distal limbs)

A

Thoracic mass effect (ie. pulomary neoplasm, granulomatous pleuritis, bronchitis, bacterial endocarditis, heartworm, spirocerca lupi)

abdominal masses (rhabomyosarcoma of bladder and ovarian tumors of horse)

unknown pathogenesis but thought to be bloodflow vs vagal stimulation

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137
Q

How do you fix the lesions of the distal limbs caused by hypertrophic osteopathy

A

remove the primary cause (the mass)

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138
Q

What is Legg-Calve-Perthes Disease

A

Ischemic necrosis of the femoral head
rarefaction of femoral head with collapse

typically young small dog breeds (minature poodles), present with pain and lameness

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139
Q

How do you diagnose Legg-Calve-Perthes Disease

A

Destruction of the femoral head- flattening and decreased radiodensities due to avascular necrosis of the femoral head

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140
Q

What are the causes of Legg-Calve-Perthes Disease

A

Traumatic: vessels are normally encased in bone around femoral head but in small dogs with genetic component, they arent encased and with walking and force it leads to rupture of vessels and ischemic necrosis of the femoral head

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141
Q

What disease do dachshund and corgis have?

A

Chondrodysplasia
-defective cartilage development affecting endochondral ossification effecting bones with longitudinal growth

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142
Q

diffuse periostal reaction on ventral aspect of skull and tympanic bullae, self limiting

A
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143
Q

what cell type is abnormal in osteopetrosis

A

osteoclast

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144
Q

Ratio of calcium stored in bone vs ionized calcium

A

Bone: 99%
Ionized: 1% (biologically active)

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145
Q

The 1% of calcium in the ionized form functions for

A

1) Bone mineralization (hydroxyapatite)
2) Muscle contraction
3) Coagulation
4) Neuronal function

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146
Q

What is phosphorus needed for

A

1) Bone mineralization
2) Biological products (DNA/RNA, cell membrane, ATP)
3) Tissue repair

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147
Q

Two sites of PTH to increase ionized calcium

A

Bone: increase osteoclast activity (increase iCa and iP)

Kidney: increased iCa retention and iP excretion

Net effect: increased iCa and iP

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148
Q

What is the net affect of parathyroid hormone

A

Increased iCa
Decreased iP

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149
Q

What is secreted in result to increase calcium

A

calcitonin: increases osteoblast activity to decrease iCa and iP

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150
Q

What hormones:
Increase osteoclast activity?
Increase osteoblast activity?

A

osteoclast = PTH
osteoblast = calcitonin

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151
Q

What is the net effect of vitamin D

A

to increase iCa and iP absorption/retention in the intestine/kidney

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152
Q

where is vitamin D produced

A

the kidney in response to decrease iCa/iP

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153
Q

where is calcitonin produced in response to increased iCa

A

C cells in the thyroid

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154
Q

a metabolic bone disease where there is reduction in bone quantity with normal bone quality

A

osteoporosis

clinical findings: occurence of fracture without excessive trauma or in herds-increased fractures

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155
Q

why are osteoporosis cases typically undiagnosed or subclinical

A

because you would need to know the bone density for that species at that specific age for the individual
animals typically lose bone density naturally when they age
hard to tell if natural or pathological

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156
Q

what are the causes of osteoporosis

A

1) Nutritional (+/- starvation)- decreased rates of bone formation **
2) Uncomplicated calcium deficiency-leading to PTH bone resportion
3) Disuse osteoporosis
4) Senile osteoporosis
5) Chronic steroid adminitration
6) Enteritis/malabsorption

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157
Q

what is the first bone to be reabsorbed in osteoporosis

A

loss of metaphyseal trabecular bone

in severe cases the cortical bone loss results in porous appearance

*vertebrae, flat bones, and ribs have increased trabecular bone so they are prone

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158
Q

what bones are prone to be reabsorbed in osteoporosis

A

trabecular bone
vertebrae, flat bones, and ribs are all predisposed

159
Q

what bony changes do you see with an animal that suffered starvation

A

loss of trabecular bone with serous atrophy of fat

160
Q

2 defects in mineralization due to nutritional abnormalities (Ca, P, of Vit D) leading to decrease quantity and quality of bone

A

metabolic bone diseases
1) rickets
2) osteomalacia

161
Q

Rickets occurs in ______ while osteomalacia occurs in ______

A

Rickets= young animals (growth plate open)
Osteomalacia = adult animals (closed epiphyseal line)

162
Q

How is the pathogenesis of rickets different from osteomalacia

A

rickets occurs in younger animals where the growth plates are open so due to nutritional abnormalities there are defect in endochondral ossification at the growth plates and bone abnormalities

osteomalacia is in younger animals so there are defects only in the bone that is being remodeled due to nutritional abnormalities

163
Q

T/F: rickets and osteomalacia are defects in mineralization due to nutritional abnormalities with calcium being the most common primary deficiency

A

False- calcium deficiency is rare as it is controlled by PTH

you are likely to always have enough calcium to mineralize however the PTH can lead to osteoporosis/fibrous osteodystrophy

164
Q

Rickets and Osteomalacia is typically due to a deficiency in

A

Phosphorus
Vitamin D
(Calcium is unlikely due to PTH regulation)

165
Q

why might result in a vitamin D deficiency

A

Decreased bone quantity and quality of bone (Rickets/Osteomalacia)
also there can be increase in PTH leading to fibrous osteodystrophy

166
Q

How might you get Vitamin D deficiency leading to rickets or osteomalacia

A

Nutritional
1) Vitamin D deficiency in winter or high latitude locations, sheep are predisposed (needs UV contact to skin and wool inhibits this)
2) Phosphorus deficiency- grazing animals with low phosphorus
Hereditary
1) Vitamin D dependent rickets type I (pigs)
2) Vitamin D-resistant rickets (common marmoset monkey)
3) Hypophosphatemic rickets

167
Q

What lesions will you see in rickets

A

-failed mineralization of physes (thick and irregular, esp ribs)
-fragile bone with microfractures
-metaphyseal flate
-bone deformities (bowed forelimbs, pathologic fractures)

Clinical signs: lameness
histo: thick cartilaginous growth plate (retained)

168
Q

what histo lesions will you see in an animal in rickets

A

-hypertrophic cartilage
-thick growth plate that is retained
-unmineralized bone when stained

169
Q

a condition where you have increased bone resorption with fibrous placement, driven by PTH and therefore excess osteoclastic activity and bone resorption

A

Fibrous Osteodystrophy

170
Q

decreased quantity and quality matrix and increased poor quality of connective tissue in the bone

A

Fibrous osteodystrophy

171
Q

What drives Fibrous osteodystrophy

A

PTH leading to excess osteoclastic activity and bone resorption
replacement of bone with non-mineralized fibrous tissue
-Primary hyperPTH
-Secondary hyperPTH (Renal or Nutritional)

172
Q

Primary hyperparathyroidism leads to

A

fibrous dystrophy
Adenoma pumps out high amounts of PTH leading to osteoclastic activity (increased iCa and decreased iP)

173
Q

How does secondary hyperparathyroidism occur

A

1) Renal Hyperparathyroidism
with liver disease leads to increased PTH because Ca is lost and P is retained

2) Nutritional hyperparathyroidism
a) Diets with decreased Ca or increased P
b) Vitamin D def (decreased Ca and P) leads to rickets

both of these lead to fibrous osteodystrophy

174
Q

What kinds of diets lead to fibrous osteodystrophy

A

Those that are low Ca/high P diets
Horse: grain, bran diets
PigL cereal grain diets
Carnivores: all meat diets
lead to high amounts of PTH that cause excess osteoclastic activity and bone resorption- replacing bone with non-mineralized fibrous tissue
a secondary hyperPTH

175
Q

renal osteodystrophy

A

fibrous osteodystrophy from renal disease (loss of Ca and retention of P leading to PTH secretion)

175
Q

all meat diets in carnivores can cause

A

lots of things but in this case but know that it can cause fibrous osteodystrophy

176
Q

what lesions are seen with fibrous osteodystrophy

A

-bone loss and fibrous replacement (prominent in skull)
-brittle to rubbery bones (osteopenia)
-pathological fracture
-marked bone deformity
-physes are normal
-“rubber jaw”
Histo: abundant connective tissue in bone

177
Q

a nutritional deficiency that leads to a defet with collagen synthesis, deposition, and strength

A

Vitamin C deficiency (Scurvy)

178
Q

Vitamin C (ascorbic acid) functions to

A

-Essential cofactor to collagen synthesis and cross-linking
-Needed for proper wound healing
-Serves as an antioxidant

179
Q

Process of Vitamin C synthesis

A

Glucose -> Gulonolactone -> ascorbic acid (vit C) via L-gulonolactone oxidase

Humans, primates, guinea pigs, and bats do not have L-gulonolactone oxidase and therefore require Vit C in their diet

180
Q

Why do humans, primates, guinea pigs, and bats require Vitamin C in their diet

A

because they do not have gulonolactone oxidase

181
Q

What species do not have gulonolactone oxidase and therefore require Vitamin C in their diet

A

Humans, Primates, Guinea Pigs, Bats

182
Q

What lesions are seen with scurvy

A

1) Hemorrhage along periosteum and joints (weak collagen under mechanical stress)
2) osteopenic bone and increased fragility
3) bony spicules with no osteoid (histo)
4) Oral hemorrhage

183
Q

What species typically get fluoride toxicity

A

herbivores grazing in high fluoride pasture

184
Q

Fluoride toxicity

A

fluoride is rapidly incorporated into bone matrix (like calcium)- deposited in region of new bone formation

effects young and adult animals
<3 years- dental and bone lesions
>3 years only bone lesions

lesions: chalky to opaque bone and teeth (black discoloration), periosteal hyperostosis, brittle bones, enamel hypoplasia

*can get it in fetus

185
Q

Vitamin A toxicity affects

A

osteoblast functionality
leading to osteoporosis and periosteal hyperostosis

186
Q

How might periosteal hyperostosis or osteoporosis from vitamin A toxicity occur

A

continual ingestion of livers or iatrogenic administration

187
Q

Lesions seen in Vitamin A toxicity

A

-Osteoporosis
-Periosteal hyperostosis
*affects osteoblast functionality

188
Q

How might vitamin D toxicity occur

A

ingestion of plants/supplements or iatrogenic administration

189
Q

What lesions will you see with vitamin D toxicity

A

1) Diffuse visceral mineralization (metastatic mineralization)
2) Marked osteopetrosis

190
Q

benign tumor of osteoblasts/osteocytes forming mature bone
typically in flat bones of head, rostal mandible (young cattle and horses)
disruptive in oral cavity
poor prognosis because difficult to remove and the location

A

Osteoma

191
Q

what is the most common malignant primary bone neoplasm in the dog and cat

A

Osteosarcoma

192
Q

What is the median survival time for dogs and cats with osteosarcoma

A

Dogs: 14-19 weeks
Cats: 49 months
six subtypes but all can carry grave prognosis

193
Q

what sites do osteosarcoma in dogs and cats

A

-3x-4x more likely appendicular skeleton (sometimes ribs)
-forelimb little more likely
-Proximal humerus/distal scapula (Shoulder)
-Carpal joint
-Around stifle joint

*Doesnt cross the joint

194
Q

Does osteosarcoma cross the joint?

A

no

195
Q

malignant tumor of cartilage that affects all species
typically in flat bones, appendicular skeleton, joints, soft tissue
slow development, metastasizes late in disease course

A

Chondrosarcoma

196
Q

what is the typical signalment of osteosarcoma

A

large breed dogs about 7.5 years (small population of 18-24 months)

older cats

197
Q

does chondrosarcoma cross the joint

A

no

198
Q

tumor that consists of lobular arrangement of fibrous tissue, cartilage, and bone
typically dog, horse, cat
site: flat bones of skull
can be malignant but local disease typically more important than metastasis

A

Multilobular Tumor of Bone (ML)

199
Q

Where does Multilobular Tumor of Bone (ML) typically occur

A

the flat bones of the skull

200
Q

Rank the neoplasms by prognosis
Chondrosarcoma
Osteosarcoma
Fibrosarcoma

A

Fibrosarcoma
Chondrosarcoma
Osteosarcoma

201
Q

malignant tumors of fibroblasts
affects all species
sites: periosteal/medulla of all bones
significantly better prognosis than osteosarcoma

A

fibrosarcoma

202
Q

Fibrosarcomas typically arent that aggressive unless they are at the ________ **

A

mandibular and maxillary region
histologically benign but biologically aggressive

rate of reoccurrence is high!

203
Q

masses consisting of cartilage cap adjacent to physes
benign
possibly hereditary
lesions appear soon after birth, growth ceases as skeletal maturity
While benign, these lesions can undergo malignant transformation to chondrosarcoma or osteosarcoma

A

Osteochondroma

204
Q

what neoplasia of bone has lesions that appear soon after birth but cease at skeletal maturity

A

osteochondroma

205
Q

what is the signifcance of osteochondroma

A

1) Physical interference with the tendons and ligaments
2) may protrude into vertebral canal
3) While benign, these lesions can undergo malignant transformation to chondrosarcoma or osteosarcoma

206
Q

in regard to bone neoplasia _________ metastasis is far more common than _________ metastasis

A

carcinoma metastasis is far more common than sarcoma metastasis

207
Q

why is bone biopsy hard to make diagnosis off of

A

might look like different etiologies
ex:
fracture (good prognosis), chondrosarcoma (ok prognosis) and osteosarcoma (bad prognosis) may all resemble each other

take radiograph info- might rule out fracture

additional section can help you look at histo to make a different diagnosis

*give pathologist multiple samples

208
Q

severe hypovitaminosis D in a puppy can lead to

A

-Fibrous osteodystrophy
-Rickets

209
Q

What are the predilection sites of the appendicular skeleton for osteosarcomas

A

Proximal humerus
Distal Ulna/Radius
Stifle: distal femur/proximal tibia

210
Q

What is the point of disease and type of herniation for the corgi breed

A

Nucleus pulposis, Hansen type 1

211
Q

what are the 3 different types of joints in the body

A

1) fibrous joints (fibrous union of bones, very limited movement) -skull sutures and teeth with periodontal ligament

2) cartilaginous joints (cartilaginous union of bones, relatively limited movement) -growth plates

3) Synovial joints- bone union via fibrous (synovial capsule) and cartilage capped bone) - lots of diverse movement - appendicular skeleton

212
Q

What are examples of fibrous joints

A

teeth/periodontal ligament
skull sutures

213
Q

what are some examples of cartilaginous joints

A

growth plates
intervertebral joints

214
Q

specialized cartilage to handle compressive forces
avascular with liited repair properties

A

articular cartilage

215
Q

highly vascular layer of joint capsule
has synviocytes (type A- macrophage like and type b-fibroblast like)

A

Synovial membrane

216
Q

type A synoviocytes are

A

macrophage like

217
Q

type B synoviocytes are

A

fibroblast like

218
Q

modified plasma in the synovial joint that provides nutrients to cartilage and lubricant for movement

A

synovial fluid

219
Q

why does articular cartilage have limited reparative ability

A

it is avascular
-surface defects typically persist but dont progress to degenerative joint disease

220
Q

Defects to articular cartilage that _______________________ does progress to degenenerative joint disease

A

extends into subchondral bone often filled with fibrovascular tissue and metaplastic fibrocartilage (scar tissue breaks down with other structures over time)

221
Q

What lesions will you see to articular cartilage and subchondral bone on histo

A

Fibrillation, Erosion and Clefting

Eburnation (sclerosis of underlying exposed bone)

Periarticular osteophytes, enthesiophytes

222
Q

What changes the fluid viscosity of synovial fluid

A

inflammation changes fluid viscosity and alters content

watery=decreased hyaluronic acid pyogenic bacteria enzymatic activity

thickened=fibrin

223
Q

How does the synovium change in response to damage

A

synovial cell hypertrophy and synovial villous hyperplasia

224
Q

how does the joint capsule change in response to injury

A

capsular thickening- can lead to fibrous ankylosis

225
Q

umbrella term for degeneration of articular cartilage and the associated structures

A

Degenerative joint disease (Osteoarthritis, osteoarthrosis)
multifactorial: trauma, infection, conformation abnormality, age

primary cause: no cause (age related)
secondary: underlying disease or trauma

226
Q

How do the lesions change from early DJD to more advance DJD

A

1) Cartilage roughening (fibrillation)
2) Osteophyte formation (periosteal reaction), Subchondral sclerosis, synovial hyperplasia restricts movement and painful
3) complete loss of articular cartilage and exposure of subchondral bone (eburnation)

227
Q

eburnation

A

happens in advanced DJD where there is exposure of subchondral bone from complete loss of articular cartilage

228
Q

What kind of horses get DJD

A

horses related to trauma/high performance
joints with high weight bear stress are predisposed

229
Q

what kinds of dogs get DJD

A

common in medium to large breed dogs
primary: considered due to aging
secondary: common in chondrodystrophic or hip/elbow dysplasia

230
Q

What breed of cat is predisposed to DJD

A

Siamese cats
(DJD is typically much less common in cats)

231
Q

How do dogs typically get DJD

A

Primary: aging
Secondary: chondrodystrophy or hip/elbow dysplasia

232
Q

a focal failure of blood supply to the growing epiphyseal cartialge leading to failure of the cartilage to ossify and degenerative joint disease

A

osteochondrosis dissecans

233
Q

What species typically get osteochondrosis dissecans

A

typically: young dogs and horses

pigs, poultry, and cattle also get it (not as much)

234
Q

clinical signs of osteochondrosis dissecans

A

lameness
degenerative osteoarthritis
subchondral bone cyst/fracture

due to:
vascular insult and necrotic cartilage
necrotic cartilage gets resorbed and resolved
but cartilage fails to ossify, continues into articular cartilage (defect/flap) OCD
leading to degenerative joint disease

235
Q

what is the pathogenesis of osteochondrosis dissecans

A

vascular insult and necrotic cartilage
necrotic cartilage gets resorbed and resolved
but cartilage fails to ossify, continues into articular cartilage (defect/flap) OCD
leading to degenerative joint disease

236
Q

what are the site predilection for osteochondrosis dissecans

A

Horse: Hind limb
a) stifle area; medial condyle of femur, patella, lateral trochlear ridge, distal tibia
b) also the hock

Dog: the humeral head

Pig:
a) Shoulder- humeral condyle, humeral head,
b) Hip- dorsal acetabulum
c) Stifle

237
Q

Where do dogs typically get osteochondrosis dissecans

A

the humeral head/shoulder joint

238
Q

where do horses typically get osteochondrosis dissecans

A

Hind limbs, specifically
a) stifle area; medial condyle of femur, patella, lateral trochlear ridge, distal tibia
b) also the hock

239
Q

where do pigs typically osteochondrosis dissecans

A

a) Shoulder- humeral condyle, humeral head,
b) Hip- dorsal acetabulum
c) Stifle

240
Q

Osteochondrosis typically affects _____ dogs while OCD affects _____

A

young; older

241
Q

lack of conformity of the femoral head and acetabulum leading to joint laxity and degenerative joint disease

A

hip dysplasia

242
Q

what is the inciting lesion of hip dysplasia

A

shallow acetablum and joint laxity leading to degenerative joint disease
1) cartilage erosion/ulceration
2) Joint capsule and synovial acetabulum
3) capital ligament tears
4) Subchondral bone sclerosis
5) Osteophytes

243
Q

what is the most common skeletal disease of large/giant breed dogs

A

hip dysplasia

244
Q

what species get hip genetic due to hereditary polygenetic coxofemoral joint laxity

A

GSD, rottweiler, Labradors

245
Q

GSD, rottweiler, Labradors get hip dysplasia due to

A

hereditary polygenetic coxofemoral joint laxity

246
Q

What are factors that influence hip dysplasia development

A

1) hereditary polygenetic coxofemoral joint laxity
2) Mechanical: abnormal forces on acetabulum leading to slow endochondral ossification of pelvis and femoral head -> DJD
3) Environmental: rapid weight gain, increased stress-load

247
Q

whatm ight you see on radiograph with a patient with hip dysplasia

A

shallow acetabulum
flattened femoral head

248
Q

inflammation of any joint component

A

arthritis

249
Q

acute inflammation of the joint
that returns to normal
articular cartilae is not affected and DJD wont develop

A

fibrinous arthritis

250
Q

T/F: suppurative arthritis is only seen in infectous arthritis

A

false- it can be non-infectious too

251
Q

septic arthritis typically occurs in

A

neonatal large animals
polyarthritis often with concurrent osteomyelitis

252
Q

What might be a viral cause of infectious arthritis

A

caprine arthritis-encephalitis virus
causes unilateral or bilateral carpal hygroma

253
Q

What is a major bacterial etiology of infectious arthritis in sheep/goats, swine, and cattle

A

Mycoplasma species

254
Q

causes unilateral or bilateral carpal hygroma in goats

A

caprine arthritis- encephalitis virus (lentivirus)

255
Q

What type of hypersensitivity is immune-mediated polyarthritis (IMPA)

A

type III hypersensitivity- antibody complex deposited

256
Q

immune-mediated polyarthritis (IMPA) typically occurs in

A

dogs and cats

257
Q

What disease cause immune-mediated polyarthritis (IMPA) in dogs and cats

A

1) Systemic lupus erythematosus- sterile, nonerosive, lymphoplasmacytic proliferative synovitis

2) Rheumatoid arthritis- idiopathic, sterile, chronic
destrictive, rhematoid factor IgG or IgM
erosive arthritis

258
Q

What form of immune-mediated polyarthritis (IMPA) is erosive

A

Rhematoid arthritis via rhematoid factor (IgG or IgM)

259
Q

tumors that typically infect the joint capsule and tendon sheath in larger joints (stifle, elbow, shoulder)

A

synovial tumors
1) synovial sarcoma (soft tissue sarcoma)
2) periarticular histiocytic sarcoma

260
Q

synovial sarcomas resemble

A

soft tissue sarcomas
might just be soft tissue sarcomas that just encompass the joint
-look the same on histo

261
Q

a neoplasm of synovial dendritic cells
most common joint tumor of dog
-on the appendicular skeleton
poor prognosis

A

periarticular histiocytic sarcoma

262
Q

most common joint tumor of dog

A

periarticular histiocytic sarcoma

263
Q

What are the different componnts of the vertebral colum and what is their function

A

Intervertebral disks: distribute mechanical forces

Nucelus pulposus: shock and flexibility

Annulus fibrosus: compression and equalize load

Intercapital ligaments: stabilize vertebrae and prevent herniation
only T2-T10 (ribs)
absent in cervical and lumbar

264
Q

Where are the intercapital ligaments present

A

exist T2-T1-
absent: cervical and lumbar

265
Q

congential lateral deviation of the spinal column

A

scoliosis

266
Q

congenital dorsal curvature of the spinal column

A

kyphosis

267
Q

congenital ventral curvature of the spinal column

A

lordosis

268
Q

congenital anomaly where part of the vertebrae is missing

A

hemivertebrae

269
Q

what is the nucleus pulposus made of

A

water and proteoglycans
function for shock and flexibility

270
Q

what is the most common cause of paresis or paralysis in the dog

A

intervertebral disk degeneration (IVDD)

271
Q

vertebral joint collapse with dorsal herniation of joint material into spinal

A

intervertebral disk degeneration (IVDD)
types:
Hansen type 1 (chondrodystrophic breeds)
Hansen type 2 (non-chondrodystrophic breeds)

272
Q

vertebral joint collapse with dorsal herniation of joint material into spinal in chondrodystrophic breeds

A

intervertebral disk degeneration (IVDD)- Hansen type 1

273
Q

vertebral joint collapse with dorsal herniation of joint material into spinal in non-chondrodystrophic breeds

A

intervertebral disk degeneration (IVDD)- Hansen type 2

274
Q

What are the most common sites for IVDD

A

Lumbar spine (>70%)T12-L2
cervical spine (15%)

275
Q

intervertebral disk degeneration (IVDD)- Hansen type 1
pathogenesis

A

1) congenital chondrodystrophy
2) increased collagen in nucleus puloposus
3) chondroid metaplasia
4) mineralization (less flexibility)
5)degeneration/mineralization of the annulus fibrosus
6) spontaneous and traumatic rupture
7) paresis/paralysis

276
Q

what is the signalment for intervertebral disk degeneration (IVDD)

A

Hansen type 1: chondrodystrophic breeds 3-7 years of age

Hansen type 2: animal breed; 6-8 years of age

277
Q

intervertebral disk degeneration (IVDD)- Hansen type 2
pathogenesis

A

genetical
1) trauma
2) disruption of annulus fibers
3) degeneration of annulus
4) slow bulging of annulus into the spinal cord
5) paresis

278
Q

bony bridging (ankylosis) of the vertebral bodies caused by chronic instability/trauma, ventral DJD of the vertebral joints

A

spondylosis

279
Q

you have a dog with backpain and hindlimb weakness. upon radiograph you see some osteophyte formation on the vertebrae and fusion of the vertebral bodies. what is diagnosis

A

spondylosis

280
Q

sepsis of vertebral end-plate and disk typically in the lumbosacral suppurative osteomyelitis lesions
commonly caused by Staph. pseudointermedius, Brucella, Ecoli, and rarely fungal

A

Diskospondylitis

281
Q

what are the etiologies of diskospondylitis in a dog

A

Staph. pseudointermedius, Brucella, Ecoli, and rarely fungal
see suppurative osteomyelitis +/- meningitis/myelitis with cord compression at the lumbosacral region of large breeds

282
Q

wobbler’s syndrome- cervical instability and cord compression due to static stenosis of the vertebral canal

A

Cervicospinal arthropathy (spondylomyelopathy)

283
Q

What lesions do you see with Cervicospinal arthropathy (spondylomyelopathy)
typically in quarterhorses and dogs (dobermann)

A

Wobbler’s syndrome
1) Static stenosis- narrowing of canal due to congenital vertebral body defect
2) Dynamic stenosis (cervical vertebral instability) congenital defect vertebrae/osteochondrosis facets

284
Q

What is typically the pathogenesis of Cervicospinal arthropathy (spondylomyelopathy)

A

genetic/congenital/trauma causes stenosis of the vertebral canal and subsequent cord compression, myelomalacia and myelodegeneration

285
Q

what are the clinical signs of Cervicospinal arthropathy (spondylomyelopathy)

A

paresis/tetraparesis
stiff painful neck

286
Q

what kind of animals typically get Cervicospinal arthropathy (spondylomyelopathy)

A

1) Horses- males are 3x more likely;
a) dynamic lesions (C3-C5) are 8-18 months and often with osteochondrosis of articular facets
b) static lesions (C5-C7) are 1-4 years

2) Dogs
a) Doberman (4-8 years) stenotic malformation and IVDD: C5-C6-C7
b) Great dane (<2 years): stenotic malformation: C4-C6

287
Q

why does IVDD typically happen at the lumbar sites (>70%) T12-L2 and cervical spine (15%)

A

because those regions do not have have intercapital ligaments there

288
Q

the outer most connective tissue sheath of muscle

A

epimysium

289
Q

connective tissue that surrounds the myofiber bundles

A

perimysium

290
Q

the connective tissue that surrounds individual myofibers

A

endomysium

291
Q

mature cell that performs contraction, multinucleated

A

myocyte (myofiber)

292
Q

immature muscle cells capable of regeneration

A

satellite cells (myoblasts)

293
Q

the functional contractile unit of muscle
composed of thin (actin) and thick (myosin) filament
contraction via ATP and calcium

A

sarcomere

294
Q

myocytes that are:
slow twitch (endurance)
oxidative aerobic

A

Type I myocyte

295
Q

myocytes that are:
fast twitch (speed, fatigue)
glycolytic (anaerobic)

A

Type II myocyte

296
Q

decrease in sarcoplasmic diameter due to denervation, disuse, endocrine disorders, malnutrition/cachexia

A

muscle atrophy

297
Q

increase in sarcoplasmic diameter due to physiologic (more contraction) and pathology

A

muscle hypertrophy

298
Q

deneration injury to the left recurrent laryngeal nerve in horses causes

A

laryngeal hemiplegia
causing muscle atrophy to the left cricoarytenoideus dorsalis

299
Q

laryngeal hemiplegia

A

denervation injury to the left recurrent laryngeal nerve causing muscle atrophy to the left cricoarytenoideus dorsalis

300
Q

‘response to long standing and recurrent muscle injury- polyphasic injury

A

muscle fibrosis

301
Q

T/F: muscle tissue has an amazing capacity for regeneration
can regenerate to completely normal and mature myocytes

A

True

302
Q

one time muscle injury in response to trauma or a toxin

A

monophasic muscle necrosis

-called polyphasic if there is a recurrent insult (nutritional, myopathies, genetic)

303
Q

clinical term for myonecrosis- can be used in any situation where nyonecrosis results in clinical signs

A

rhabdomyolysis

304
Q

With muscle necrosis (rhabdomyolysis) you typically get

A

mineralization (white tissue) due to high concentration of calcium

305
Q

inherited X-linked disorder in dystrophin, progressive myopathy characterized by ongoing necrosis and degeneration (polyphasic)

A

Muscular Dystrophy (Duchenne’s)

306
Q

Muscular Dystrophy (Duchenne’s)

A

inherited X-linked in dystrophin, progressive myopathy characterized by ongoing necrosis and degeneration (polyphasic)
mostly dogs (also cats, mice +/- sheep)
only in males

307
Q

What protein is affected by Muscular Dystrophy (Duchenne’s)

A

Dystrophin- X linked mutation
(only males)

308
Q

T/F: Muscular Dystrophy (Duchenne’s) affects males and females equally

A

False: only males
inherited X-linked in dystrophin

309
Q

what is the signalment of muscular dystrophy

A

1) male puppies (golden retrievers are overrepresented), born normally but the disease progressively gets worse from 8-12 months. stabilizes after a year
marked necrosis- most severe in diaphragm, muscle moss and progressive weakness, markedly elevated CK and AST

2) Male kittens (5-2 years)
marked hypertrophy, stiff gait (bunny hopping on rear limbs), difficulty jumping, enlarged tongue causing prehension troubles, can develop malignant hyperthermia

310
Q

what will you see clinically in a male puppy with muscular dystrophy

A

marked necrosis- most severe in diaphragm, muscle moss and progressive weakness, markedly elevated CK and AST

311
Q

what will you see clinically in a kitten with muscular dystrophy

A

Male kittens (5-2 years)
marked hypertrophy, stiff gait (bunny hopping on rear limbs), difficulty jumping, enlarged tongue causing prehension troubles, can develop malignant hyperthermia

312
Q

What is unique about cats with muscular dystrophy, in comparison to dogs *

A

cats get marked hypertrophy* (dogs get marked necrosis)

cats also can develop malignant hyperthermia

313
Q

what species do you typically think of with malignant hyperthermia

A

pigs (can also occur in dogs and horses)

314
Q

hypercontraction of all striated muscle due to ryanodine receptor mutation (unregulated Ca2+ channels) leading to hyperthermia and lactic acidosis

A

malignant hyperthermia (porcine stress syndrome)

315
Q

what is typically the stressor for malignant hyperthermia (uncontrolled muscle contraction leading to hyperthermia and lactic acidosis)

A

general anesthesia or stress
muscular dystrophy (not mutation but causes Ca++ release)

316
Q

what causes malignant hyperthermia

A

ryanodine receptor mutation (unregulated Ca2+ channels) leading to hyperthermia and lactic acidosis

317
Q

what lesions are seen with malignant hyperthermia

A

myonecrosis
tachycardia
respiratory distress
heart failure leading to death

318
Q

sodium channel defect leading to changed action potential
typically in quarter horses

A

hyperkalemic periodic paralysis (HYPP)

319
Q

what is the pathogenesis of hyperkalemic periodic paralysis (HYPP)

A

1) delayed Na+ channel inactivation
2) excess intracellular Na+
3) K+ released to extracellular/bloodstream leading to hyperkalemia
4) myocyte membrane instability
5) myotonia

leading to muscle fasciculation ranging form hypercontraction to flaccidity (collapse/recumbency)

320
Q

How do you manage horses with hyperkalemic periodic paralysis (HYPP)

A

genetic testing
Low potassium diet (no alfalfa or molasses)
do not ride them (sudden recumbency)

321
Q

glycogen accumulation leading to muscle dysfunction and necrosis (rhabdomyolysis)
common in draft breeds
caused by genetic mutation in GSYI

A

equine polysaccharide storage myopathy (EPSSM)

322
Q

what is the pathogenesis of equine polysaccharide storage myopathy (EPSSM)

A

1) mutation in GSY1
2) polysaccharide accumulation in type 2 muscle
3) unknown pathogenesis of muscle degeneration and necrosis

*exertional rhabdomyolysis-muscle pallor and streaking (severe in diaphragm)
*progressive weakness, stiffness, muscle atrophy

323
Q

breakdown of neuromuscular joint communication leading to decreased muscle contraction

A

myasthenia gravis

324
Q

what are the clinical signs of myasthenia gravis

A

1) megaesophagus
2) weakness in appendicular muscular (exercise induced collapse)

325
Q

Dog breeds:
___________ typically get acquired myasthenia gravis while _________ have congenital myasthenia gravis

A

German shephard (acquired- typically thymoma or thymic hyperplasia)

Jack Russell (congenital- decreased receptor density)

326
Q

inherited defect in acetylcholine receptors

A

congenital myasthenia gravis
-typically more rare but common among jack russell terriers

327
Q

how is myasthenia gravis typically acquired

A

thymoma or thymic hyperplasia
*Paraneoplastic
*Antibodies attack the acetylcholine receptors

328
Q

how do you test for myastenia gravis

A

Tensilon Test
-Administer Anticholinesterase
-Overcome receptor deficiency = normal

329
Q

3 ways you can get ischemic myopathy

A

1) Recumbency (compression)
2) Compartmental syndrome
3) Loss of circulation

330
Q

immobile/recumbent animals leading to increased intramuscular pressure -> collagenous of venous system -> red infarct/ischemic necrosis

A

Downer Syndrome

331
Q

vigorous muscular contraction leading to increased intramuscular pressure -> collagenous of venous system -> red infarct/ischemic necrosis

A

compartment syndrome
-typical of broiler chickens

332
Q

what is the typical route cause of suppurative myositis

A

inoculation or extension route (unlike bone where hematogenous is the star of the show)

333
Q

what causes pigeon fever or pigeon breast

A

corynebacterium pseudotuberculosis

334
Q

pigeon breast pathogenesis

A

corynebacterium pseudotuberculosis living in soil contaminates a woind or inoculation from insects -> spreads to pectoral muscles and causes abscesses

335
Q

what causes malignant edema, marked myonecrosis through contamination and toxin production

A

Clostridium septicum

336
Q

what causes gas gangrene, marked necrosis through contamination and toxin production

A

Clostridium perfringens

337
Q

what causes black leg

A

Clostridium chauvoei

338
Q

what is needed for malignaant edema/gas gangrene forms of infectious myositis (caused by clostridium septicum and perfringens)

A

wounds for spores contamination and then proliferate under anaerobic conditions

339
Q

What is the pathogenesis of black leg

A

-Clostridium chauvoei spores ingested*
-deposited dormant in muscle
-muscle trauma
-activation (vegative)
-myonecrosis
-toxemia

340
Q

rapid death and myonecrosis of any striated muscle resulting in marked crepitus/ emphysema due to clostridial spores being ingested

A

Black Leg (Clostridium chauvoei)

341
Q

T/F: black leg is more localized than malignant edema and gas gangrene

A

False- it is more distributed bc Clostridium chauvoei spores are ingested and go go throughout body- even cause myocardial necrosis

however septicum and perfringens spores contaminate wounds to cause malignant edema and gas gangrene

342
Q

what causes wooden tongue (granulomatous myositis)

A

actinobacilus lignieresii

343
Q

what is the pathogenesis of wooden tongue

A

1) focal trauma to the tongue
2) infiltration of actinobacilllus
3) granulomatous inflammation
4) region lymphadenitis

leads to very hard, diffusely swollen tongue
excessive salivation
poor prehension

344
Q

you have a cow with anorexia, weight loss, decreased milk production, unilateral mandibular swelling (radiographic opaque mass). What is your diagnosis

A

lumpy jaw- actinomyces bovis

345
Q

you have a dog with forelimb lamness and swelling, lethargy, harsh respiratory sounds, with weight loss and muscle wasting. Upon imaging you notice dense nodules in the lung fields and in necropsy you have multiple variable cavitated masses partially effacing all lung lobes and ulna with diffuse periosteal proliferation leading to bony defomity. What is the diagnosis

A

Hypertrophic osteopathy

346
Q

you have a new born calf with domed skulls, brachygnathism inferior, protruding tongue, and distorted contorted limbs. open necropsy you see dense cone of metaphyseal trabecular bone extending from epiphysis into the mid diahphysis. What is the diagnosis

A

Osteopetrosis- caused by genetic defect or acquired (BLDV)

if dog (distemper) or cat (FeLV)

347
Q

Legg Calve Perthes disease, what is the primary cause?

A

primary lesion here is a vascular insult and ischemic necrosis to the femoral head. This necrosis leads to bony change and degeneration as observed in the radiographs.

348
Q

you see a lamb with long, lanky and poorly formed limbs. what is your diagnosis

A

Spiderlamb. Chondrodysplasia- defect in cartilage and commonly leads to growth plate abnormalities. on necropsy youll see a growth plate defect, with multiple growth plates within the epiphysis.

349
Q

upon necropsy of a horse you see a fluid filled pocket around the necrotic bone. what is this

A

involucrum

350
Q

upon necropsy of a guinea pig you notice abnormal collagen cross linking, weakened collagen and finally hemorrhage at the joints. what is diagnosis

A

scurvy (vitamin C) deficiency

351
Q

what are causes of parasitic myositis

A

1) Neospora caninum
2) Toxoplasma gondii
3) Sarcocystis
4) Hepatozoon

*Require two host
-Intermediate herbivore
-Predator definitive host (enteric)

352
Q

How can dogs get Neospora caninum

A

1) trans-placental infection
2) eating intermediate host

353
Q

neospora caninum causes

A

infection of ventral spinal rootlets and muscle leading to progressive deneveration atrophy, esp of hindlimbs

mid-gestation abortion

354
Q

causes degenerative protozoal cysts leading to eosinophilic inflammation

A

Sarcocystis sp.

355
Q

what the definitive host of hepatozoon americanum

A

brown tick via ingestion

356
Q

what lesions does Hepatozoon Americanum cause *

A

1) Pyogranulomatous myositis **
2) Periosteal reaction **
3) Onion cysts in tissues
4) marked leukocytosis
5) fever, anorexia, weight loss

357
Q

Why is trichonella called a true parasite

A

because they never leave the host
-no external aspect of lifecycle

358
Q

how is trichonella spread

A

Animal to animal transmission via infected muscle consumption (no external aspect of lifecycle)
commonly pig meat
resistant to freezing
cysts can survive for 20 years
very wide host range

359
Q

How do you prevent Trichonella infection

A

cook meat

360
Q

What causes “Beef Measles”

A

Taenia- parasitic cyst in muscle
causes pyogranulomatous inflammation with fibrosis

361
Q

an exertional myopathy in horses where myofiber damage occurs as a result of exercise stress as the primary cause

A

Equine Rhabdomyolysis

362
Q

what are the clinical signs of Equine Rhabdomyolysis

A

Often draft horses (also QH and thoroughbreds)
-Stiff weakened muscles, inability to move, recumbency
-High CK, AST, myoglobinuric nephrosis

363
Q

Three causes of equine rhabdomyolysis

A

1) intense activity
2) high carb diet
3) equine polysaccharide storage myopathy

364
Q

non-infectious myopathy that is caused by exertion or hyperthermia of many wildlife species causes lactic acidosis with myonecrosis
myoglobinuria and CK elevation

A

Capture Myopathy

365
Q

what kind of hypersensitivity is purpura hemorrhagica

A

Type III- immmue complex formation against Strep. M protein

366
Q

What is the pathogensis of equine purpura hemorrhagica

A

post-streptococcal infection there is immune complex formation against the M protein
this causes necrotizing vasculitis, skeletal muscle infarction and limited inflammation

367
Q

What kind of hypersensitivity is seen in young quarter horses after they are infected with streptococcus equi

A

Type II- autoantibodies targets against the muscle
rapid atrophy

368
Q

Two immune hypersensitivty reactions seen after horses get streptococcus equi

A

1) Purpura hemorrhagica (Type III)- immune complex against strep m protein

2) young quarter horses (type II)- autoantibodies against muscle

369
Q

What kind of hypersensitivty is canine masticatory myositis

A

type II- autoantibody against type 2M myosin

370
Q

In canine masticatory myositis, it is type II hypersensitivity. what do the autoantibodies target

A

type 2M myosin

371
Q

What is the pathogensis of canine masticatory myositis

A

1) Eosinophilic-plasmacytic myositis (Type II) against type 2M myosin (only in masticatory muscles)
2) Compartmental syndrome and fibrosis (ischemic necrosis)
3) Chronic atrophy and fibrosis

*causes swelling, difficulty in opening, painful, may lead to atrophy with “locked jaw”
very painful

372
Q

How do you diagnose canine masticatory myositis

A

Signs: swelling, difficulty in opening, painful, may lead to atrophy with “locked jaw”
very painful

Serology for 2M myosin Antibodies

Many muscle biopsies

373
Q

lymphocytic myositis that typically comes with lupus or neoplasia.
causes muscle atrophy on the facial muscles, can also cause megaesophagus
often large breeds, vizsla, and 6mo newfoundlands

A

Canine polymoyositis

374
Q

What is the mechanism of canine polymyositis

A

lymphocytic myositis often with lupus or neoplasia

375
Q

Vitamin E/Selenium deficiencies are most commonly seen in

A

Fetal to Young (2-4months)
Herbivores
Reptiles
Birds
(rarely carnivores)

376
Q

Vitamin E/Selenium deficiencies cause ___________

A

polyphasic muscular damage (continual damge due to lack of nutrients)

deficiency in these antioxidants cause formation of free radicals at high rate leading to membrane damge, loss of homeostasis and release of calcium, necrosis and mineralization

377
Q

How might an animal have nutritional myopathies Vitamin E/Selenium deficiencies

A

1) poor quality feed
2) increased/unusual physical activity (more oxidative stress)

378
Q

What is unique about Vitamin E/Selenium deficiencies in Pigs

A

They can present with 3 forms
1) Hepatosis dietetica (diffuse/excessive hepatocellular necrosis)
2) White muscle disease
3) Mullberry heart disease- epicardial hemorrhage and necrosis

379
Q

mullberry heart disease

A

epicardial hemorrhage and necrosis seen in pigs with Vitamin E/Selenium deficiencies

380
Q

hepatosis dietetica

A

diffuse/excessive hepatocellular necrosis seen in pigs with Vitamin E/Selenium deficiencies

381
Q

how might reptiles/birds with Vitamin E/Selenium deficiencies present

A

degenerative encephalopathy
“Crazy Chick Disease”

382
Q

What animals have high susceptibility to ionophores

A

monogastric animals (horses, dogs, and pigs)

ruminants can get them if there is a dosing miscalculation

383
Q

is ionophore toxicity monophasic or polyphasic

A

Monophasic

384
Q

Ionophores like Monensin & Laslocid alter ______

A

Ca2+ flux

toxicity causes monophasic myopathy
myocyte and myocardial necrosis
mineralization
fibrosis

385
Q

What species do you typically see monophasic necrosis from gossypol toxicity in?

A

Pigs

386
Q

Goosypol toxicity causes monophasic or polyphasic myopathy

A

monophasic necrosis
-mineralization and fibrosis
-central lobular hepatic necrosis and pulmonary congestion
-muscle pain
-recumbency dyspnea
-Heart failure

387
Q

T/F: Ingestion of Cassia, Eupatorium, Karwinski plants causes necrosis of skeletal and cardiac tissue

A

Falso- cardiac tissue is not usually involved

388
Q

a rare benign neoplasm of skeletal muscle
typically young pigs and dogs
dog-larynx
pig-heart
clinical signs are dyspnea and stridor

A

Rhabdomyoma

389
Q

the most common skeletal tumor but still very rare

A

Rhabdomyosarcoma

390
Q

Bladder botryoid rhabdomyosarcoma

A

skeletal muscle tumors of the trigone of the bladder that leads to urinary obstruction
occur in young large breed dogs

low rare of metastasis
poor prognosis because difficult to remove and maintain integrity of bladder

391
Q

skeletal muscle tumors of the trigone of the bladder that leads to urinary obstruction
occur in young large breed dogs

low rare of metastasis
poor prognosis because difficult to remove and maintain integrity of bladder

A

Bladder botryoid rhabdomyosarcoma

392
Q

T/F: neoplasm metastasis to muscle is generally rare

A

True- there is some extension but muscle tissue typically isnt a normal secondary site despite high blood flow

393
Q
A

BOD 3 (5 decks)

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