Musculoskeletal System Flashcards
supports regions for hematopoietic tissue
cancellous bone
Endoesteum is important for
maintenance and remodeling of bone
where your growth plate is
physis
metaphysis
area of active bone remodeling aiding in longitudinal growth
manufactures osteoid
osteoblasts
found along the periosteum
forms the bone-blood barrier and controls ions movement within matrices
can become active to form more bone
inactive osteoblasts
osteoblasts that become surrounded by matrix
the most numerous cell in bone
produces osteogenic compounds and functions in mechanosensation
osteocytes
most numerous cell in bone
osteocytes
derived from hematopoietic cell line (macrophage), resorb bone matrices, transient cells (undergoes apoptosis)
osteoclasts
where are osteoclasts derived from
derived from hematopoietic cell line (macrophage)
Components of bone
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
What kind of collagen is osteoid (organic component) made of
type I collagen: chain of repeating amino acids in tri-helix structure, which adds tensile strength
What is the organic component of bone
90% osteoid (type 1 collagen)
10% other proteins
What is the inorganic component of bone made of
the calcification of osteoid
hydroxyapatite
interplay of calcium, phosphorus, and vitamin D
Osteoblasts make ______ which is made of _________
osteoid which is type 1 collagen and then it becomes mineralized by an interplay of
-Calcium, phosphorus, and vitamin D (hydroxyapatite)
spongey bone
contains marrow
oriented parallel to the mechanical stress
trabecular bone (cancellous)
mature bone
most abundant bone in adult skeletal
fiber are oriented in parallel fashion
lamellar bone
osteon
a structure in lamellar bone (mature bone) where fibers are iroented in parallel fashion
lots of resistance to pressure
fetal bone, rapidly developing bone, injury repair
collagen fibers are haphazardly organized
woven bone - restructured/remodeled later to lamellar bone
In time, woven bone is remodeled to
lamellar bone
Where does the majority of intramembranous ossification occur
the cranial/facial bone formation
Describe the process of intramembranous ossification
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
Does intramembranous ossification be a scaffolding to form?
No it does not
connective tissue is invaded by vascular supply
Intramembranous ossification is a key mechanism for all bone to undergo _________
appositional growth (increase in diameter)
In what bones does endochondral ossification occur in?
All bones of the axial and appendicular skeleton
Describe the process of endochondral ossification
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)
What separates the primary and secondary centers of ossification in endochondral ossification
growth plates
What is the most common form of bone formation embryologically
endochondral ossification (cartilage hypertrophies and ossified)
what drives longitudinal (interstitial) growth
the growth plate (physis)
-orderly zones leading to mineralized matrix for osteoid deposition and becomes lamellar bone
when does the growth plate close
with skeletal maturation
what drives width (appositional) growth
intramembranous ossification stemming from periosteum
What is Wolff’s law
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)
what is a classic finding of a degenerative joint disease
Osteophytes- small nodules of bony formation
atrophy/thinning of the bone
osteoporosis- predisposition to fracture (can be caused by disuse or nutritional abnormalities)
What are the the most prone fracture points in young animals
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
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?
Good prognosis if:
1) Proliferative zone is intact
2) Blood supply is intact
3) No bony bridges between metaphysis and epiphysis are formed
an angular limb deformity that occurs due to growth plate injury where there is a lateral deviation of the limb distal
Valgus
What is valgus
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
What is the most common cause of valgus in dogs/cats?
*Premature closure of distal ulna physis. Radius keeps growing on the medial side and push the limb to a lateral deviation
Do most angular limb deformities in foals correct themselves?
Yes 88.4% have them and majority of them resolve with age
What might be the cause of limb deformities in large dog breeds
impaired endochondral ossification of the growth plates
Is Valgus or Vargus more common?
valgus
The medial deviation of the limb distally. occurs in puppies with only radial physis damage
Vargus
Puppies with radial physis damage would cause
Vargus- ulna keeps growing so their is a distal displacement medially (inward)
excessive mechanical force: compressive or transverse to a bone
physiological bone fracture
a fracture that occurs but there is normal mechanical force with weakened bone
Pathological Bone Fracture
Local/PrimaryLesion to bone : Osteosarcoma, Osteomyelitits
Systemic Lesion to bone: Fibrous osteodystrophy, osteoporosis (multiple sites of fracture)
Name 2 causes of systemic pathologic bone fractures
1) fibrous osteodystrophy
2) Osteoporosis
Describe the process of fracture repair
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
occurs instant to a few days after bone fracture,
-acute inflammatory response, promotes fibroblast migration and neovascularization
hematoma formation
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
formation of fibrocartilaginous callus
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
hard callus formation
takes months to years, replacement and organization of woven bone into mature bone, complete strength of bone is restored
bone remodeling after fracture repair
What enables quick repair of a bone fracture back to original strength
close opposition of fragments
Displaced bone fractures require
formation of large repair callus and decreased healing ability
What are some complications to fracture repair?
1) Large necrotic bone fragments (bone sequestrum) inhibits healing
2) Continual movement of joints prevent healing (pseudoarthritis)
3) Bacterial osteomyelitis
inflammation of the periosteum (surface of the bone)
periostitis
inflammation across growth plate
physitis
inflammation of the bone tissue and marrow
osteomyelitis
what is the main cause of osteomyelitis
bacterial due to
1) trauma
2) local extension
3) hematogenous (most common cause)
Is hematogenous osteomyelitis more common in foals/ruminants or small animals
foals/ruminants
-if they are septic, assume that they have osteomyelitis
What is the most common bacterial isolate of hematogenous osteomyelitis
Staphylococcus
hematogenous osteomyelitis has a predilection for
the epiphysis and metaphysis region of bone
can occur on multiple bones/multiple sites in the same bone
How does osteomyelitis from local extension typically occur?
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
How might dogs and cats get osteomyelitis from local extension
if they have periodontal disease
-extension of commensal oral bacteria into alveolar bone, mandible, and maxilla
What is the cause of lumpy jaw (granulomatous inflammation and unilateral bony proliferation of the mandible in cattle)
Actinomyces bovis
Actinomyces bovis local extension into alveolar bone, mandible, and maxilla causes
Lumpy jaw
What are possible routes of traumatic osteomyelitis
1) open fractures
2) contamination during surgical repair of fracture
3) bite wound
4) gunshot
5) wound to claw or hoof
Potential sequela to osteomyelitis
1) Bone abscess: central cavitating purulent region
2) Sequestrum: large islands of necrotic bone
3) Involucrum: fluid filled/reaction tissue around region of infection
a potential result to osteomyelitis where there is fluid filled/reaction tissue around region of infection
Involucrum
a potential result to osteomyelitis where there is large islands of necrotic bone
Sequestrum
a potential reuslt to osteomyelitis where there is a central cavitating purulent region within the bone
bone abscess
Infectious osteomyelitis is typically bacterial origin but what are other differentials
1) Fungal: Coccidioides (disseminated), Blastomyces, Cryptococcus (cats)
2) Viral: BVDV, Adenovirus, Feline Herpes, FeLV
What are the two causes of non-infectious osteomyelitis
1) Panosteitis
2) Metaphyseal osteopathy
What is panosteitis
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
What is the typical signalment for dogs with panosteitis
5-12 months old
large breed
male dog
How do you treat panosteitis in a dog
it is typically self-limiting
just treat for pain
*Excellent prognosis
How do you diagnose panosteitis
Radiography- dense medullary region in the diaphysis
“cotton-like densities with the medulalry space”
medullary fibrosis and osssification
Where does panosteitis typically occur in
diaphysis of long bones
due to fibroblasts/osteoblast proliferation
medullary fibrosis and ossification
What is the typical signalment for Metaphyseal Osteopathy
2-8 month old large and giant dog breeds
-Weimaraners, Great Danes, Boxers, German Shepherds
What breeds are predisposed to Metaphyseal Osteopathy
Weimaraners, Great Danes, Boxers, German Shepherds
Metaphyseal Osteopathy
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
Normally the primary spongiosa is lined by osteoblasts and osteoid but with metaphyseal osteopathy:
they lack osteoblasts and osteoid because neutrophils destroy them. Will see necrotic debris and neutrophils on histo
Predisposed to fractures
What are the acute lesions of Metaphyseal Osteopathy
suppurative osteomyelitis
Necrosis
lack of normal bone deposition (neutrophils destroy osteoblasts and osteoid)
What are the chronic lesions of metaphyseal ostopathy
periosteal reaction results in excessive bone production (swollen radius, ulna, tibia) and severe lameness
What is the cause of metaphyseal osteopathy
Idiopathic
What is prognosis of Metaphyseal osteopathy? What is the treatment
It can be self-limiting, recurrent bouts, will need to euthanize in severe cases
Clinically: treat with antibioitcs, NSAIDs/Steroids, and supportive treatment
What is the most common route of osteomyelitis *
Hematogenous spread
-typically large animals
-will die very quickly and will have osteomyelitis if survive
abnormalities primarily affecting bone formation or remodeling
-most considered lethal or semi-letha
primarily genetic in nature
Skeletal dysplasia
What are classical clinical findings of diseases causing skeletal dysplasia
-Short stature
-Abnormally shaped bones
-Increased bone fragility
a skeletal dysplasia resulting in shortening of mandible
brachygnathia inferior
a skeletal dysplasia resulting in shortening of mandible (breed standard for brachycephalic breeds)
brachygnathia superior (prognathism)
a localized skeletal dysplasia where there is concavity of sternum, most common in cats
pectus excavatum
What is pectus excavatum
a localized skeletal dysplasia where there is concavity of sternum, most common in cats
What species is pectus excavatum most common in
cats
What is a common finding of pectus excavatum in cats?
difficulty breathing- the concavity of the sternum prevents breathing
a localized skeletal dysplasia where there is increased number of limbs
polymelia
a localized skeletal dysplasia where there is partial absence of part of the distal limb
Hemimelia
-a rat Pox virus can cause rats limbs to slough off (wild)
a localized skeletal dysplasia where there is absence of one or more limbs
Amelia
a localized skeletal dysplasia where there is partial or complete fision of digit
Syndactyly
-some breeds of pigs
a localized skeletal dysplasia where there is increase in the number of digits
polydactyly
-common in cats
a defect in cartilage development
-abnormal endochondral ossification effects bones with growth plates (longitudinal growth) leading to uncontrolled growth or disproportionate dwarfism
Chondrodysplasia/Chondrodystrophy
What is the pathogenesis of Chondrodysplasia
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
FGFR4 is a gene that causes ___________ in Dachshunds, bassett hounds, and corgis
Chondrodysplasia - growth plate abnormality in appendicular skeleton (abnormal endochondral ossification effecting the longitudinal growth of limbs)
BMP3 is a gene that causes _______ of the skull in bulldogs and frenchies
chondrodystrophic leading to brachycephalic
T/F: Disproportionate dwarfism effects any breed
True- it is pathological
What causes Spider Lambs?
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
What are reasons you may get Chondrodysplasia leading to uncontrolled longitudinal bone growth
Spider lambs (FGFR3 point mutation)
Lesions: aberrant ossification centers, endochondral ossification failure
long twisted neck, limbs, scoliosis, kyphosis
Snorter cows
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
Bull dog calfs
most severe form of chondrodysplasia in cows
-Extremely short limbs
-Domed head with protruding tongue
-Cleft palate
-Abdominal hernia
You see a cow with board head, bugling eyes, and short legs. What likely occured
Mild Chondrodysplasia
-Look brachycephalic
You have a calf with extremely short limbs, domed head with protruding tongue, cleft palate, and abdominal hernia. What likely occured
Severe Chondrodysplasia
-failure of most cartilage to form
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
osteogenesis imperfecta (not just occurs in bone)
T/F: Osteogenesis imperfecta only affects bone
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
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
Osteogenesis imperfecta- mutation leading to abnormal type 1 collagen
What are the clinical signs of osteogenesis imperfecta
Joint hyper-motility, thin cortical bone, thinned ocular slcera, intrauterine fractures of ribs, loss of tooth dentin, bone fractures
What is the prognosis for osteopetrosis
it is lethal (fetus is typically stillborn)
What are the two forms of osteopetrosis
1) Congenital/heritable (cats, dogs, sheep, horses, cattle, rats, mice, poultry)
2) Acquired: BVDV, FeLV, canine distemper
What viruses can cause osteopetrosis
BVDV, FeLV, canine distemper
What is the pathogenesis of osteopetrosis
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
What are the clinical signs of osteopetrosis
-Brachygnathism inferior and protruding tongue
-Long bones and vertebra are short
-Increased bone fragility
Process of forming compact cortical bone
1) Growth plate
2)
3)
4)
5)
6)
Growth plate
Primary spongiosa
Osteoclastic remodeling
Secondary spongiosa
Osteoclastic remodeling
Compact cortical bone
T/F: in osteopetrosis the growth plate abnormally grows leading dense metaphysis and diaphysis
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
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
osteopetrosis
Congenital Hyperostosis affects _______ (species)
swine (young piglets)
What part of the bone does congenital hyperostosis typically affect in swine?
predominately the forelimbs
-marked periosteal reaction with edema
-very large forelimbs
What is Congenital Hyperostosis
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.
What causes crooked-calf disease
lupine toxicity (quinolizidine alkaloid- Anagyrine) ingested during 40-80 days of gestation
causes fetal immobilization and uterine contraction
Arthrogryposis, troticolis, scoliosis, and cleft palate
congenital angular deformity of the joints with articular rigidity, cleft palate also accompanies
Arthrogryposis
What are the causes of arthrogyposis
-Spontaneous congenital anomaly
-Hereditary: Angus, Holstein
-Viral: BVDV, Bluetongue virus, Cache Valley virus
-Toxicity: Lupine-Quinolizidine alkaloid
What is “loin jaw”
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
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
Craniomandibular Osteopathy
What breed is predisposed to Craniomandibular Osteopathy
West Highland White Terrier
What is the prognosis of Craniomandibular osteopathy
it is usually self-limiting
T/F: Craniomandibular osteopathy presents with unilateral bony proliferation of the skull
False- it is usually symmetric
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
Hypertrophic osteopathy
What are causes of hypertrophic osteopathy (bone reaction of the distal limbs)
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
How do you fix the lesions of the distal limbs caused by hypertrophic osteopathy
remove the primary cause (the mass)
What is Legg-Calve-Perthes Disease
Ischemic necrosis of the femoral head
rarefaction of femoral head with collapse
typically young small dog breeds (minature poodles), present with pain and lameness
How do you diagnose Legg-Calve-Perthes Disease
Destruction of the femoral head- flattening and decreased radiodensities due to avascular necrosis of the femoral head
What are the causes of Legg-Calve-Perthes Disease
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
What disease do dachshund and corgis have?
Chondrodysplasia
-defective cartilage development affecting endochondral ossification effecting bones with longitudinal growth
diffuse periostal reaction on ventral aspect of skull and tympanic bullae, self limiting
what cell type is abnormal in osteopetrosis
osteoclast
Ratio of calcium stored in bone vs ionized calcium
Bone: 99%
Ionized: 1% (biologically active)
The 1% of calcium in the ionized form functions for
1) Bone mineralization (hydroxyapatite)
2) Muscle contraction
3) Coagulation
4) Neuronal function
What is phosphorus needed for
1) Bone mineralization
2) Biological products (DNA/RNA, cell membrane, ATP)
3) Tissue repair
Two sites of PTH to increase ionized calcium
Bone: increase osteoclast activity (increase iCa and iP)
Kidney: increased iCa retention and iP excretion
Net effect: increased iCa and iP
What is the net affect of parathyroid hormone
Increased iCa
Decreased iP
What is secreted in result to increase calcium
calcitonin: increases osteoblast activity to decrease iCa and iP
What hormones:
Increase osteoclast activity?
Increase osteoblast activity?
osteoclast = PTH
osteoblast = calcitonin
What is the net effect of vitamin D
to increase iCa and iP absorption/retention in the intestine/kidney
where is vitamin D produced
the kidney in response to decrease iCa/iP
where is calcitonin produced in response to increased iCa
C cells in the thyroid
a metabolic bone disease where there is reduction in bone quantity with normal bone quality
osteoporosis
clinical findings: occurence of fracture without excessive trauma or in herds-increased fractures
why are osteoporosis cases typically undiagnosed or subclinical
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
what are the causes of osteoporosis
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
what is the first bone to be reabsorbed in osteoporosis
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
what bones are prone to be reabsorbed in osteoporosis
trabecular bone
vertebrae, flat bones, and ribs are all predisposed
what bony changes do you see with an animal that suffered starvation
loss of trabecular bone with serous atrophy of fat
2 defects in mineralization due to nutritional abnormalities (Ca, P, of Vit D) leading to decrease quantity and quality of bone
metabolic bone diseases
1) rickets
2) osteomalacia
Rickets occurs in ______ while osteomalacia occurs in ______
Rickets= young animals (growth plate open)
Osteomalacia = adult animals (closed epiphyseal line)
How is the pathogenesis of rickets different from osteomalacia
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
T/F: rickets and osteomalacia are defects in mineralization due to nutritional abnormalities with calcium being the most common primary deficiency
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
Rickets and Osteomalacia is typically due to a deficiency in
Phosphorus
Vitamin D
(Calcium is unlikely due to PTH regulation)
why might result in a vitamin D deficiency
Decreased bone quantity and quality of bone (Rickets/Osteomalacia)
also there can be increase in PTH leading to fibrous osteodystrophy
How might you get Vitamin D deficiency leading to rickets or osteomalacia
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
What lesions will you see in rickets
-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)
what histo lesions will you see in an animal in rickets
-hypertrophic cartilage
-thick growth plate that is retained
-unmineralized bone when stained
a condition where you have increased bone resorption with fibrous placement, driven by PTH and therefore excess osteoclastic activity and bone resorption
Fibrous Osteodystrophy
decreased quantity and quality matrix and increased poor quality of connective tissue in the bone
Fibrous osteodystrophy
What drives Fibrous osteodystrophy
PTH leading to excess osteoclastic activity and bone resorption
replacement of bone with non-mineralized fibrous tissue
-Primary hyperPTH
-Secondary hyperPTH (Renal or Nutritional)
Primary hyperparathyroidism leads to
fibrous dystrophy
Adenoma pumps out high amounts of PTH leading to osteoclastic activity (increased iCa and decreased iP)
How does secondary hyperparathyroidism occur
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
What kinds of diets lead to fibrous osteodystrophy
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
renal osteodystrophy
fibrous osteodystrophy from renal disease (loss of Ca and retention of P leading to PTH secretion)
all meat diets in carnivores can cause
lots of things but in this case but know that it can cause fibrous osteodystrophy
what lesions are seen with fibrous osteodystrophy
-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
a nutritional deficiency that leads to a defet with collagen synthesis, deposition, and strength
Vitamin C deficiency (Scurvy)
Vitamin C (ascorbic acid) functions to
-Essential cofactor to collagen synthesis and cross-linking
-Needed for proper wound healing
-Serves as an antioxidant
Process of Vitamin C synthesis
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
Why do humans, primates, guinea pigs, and bats require Vitamin C in their diet
because they do not have gulonolactone oxidase
What species do not have gulonolactone oxidase and therefore require Vitamin C in their diet
Humans, Primates, Guinea Pigs, Bats
What lesions are seen with scurvy
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
What species typically get fluoride toxicity
herbivores grazing in high fluoride pasture
Fluoride toxicity
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
Vitamin A toxicity affects
osteoblast functionality
leading to osteoporosis and periosteal hyperostosis
How might periosteal hyperostosis or osteoporosis from vitamin A toxicity occur
continual ingestion of livers or iatrogenic administration
Lesions seen in Vitamin A toxicity
-Osteoporosis
-Periosteal hyperostosis
*affects osteoblast functionality
How might vitamin D toxicity occur
ingestion of plants/supplements or iatrogenic administration
What lesions will you see with vitamin D toxicity
1) Diffuse visceral mineralization (metastatic mineralization)
2) Marked osteopetrosis
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
Osteoma
what is the most common malignant primary bone neoplasm in the dog and cat
Osteosarcoma
What is the median survival time for dogs and cats with osteosarcoma
Dogs: 14-19 weeks
Cats: 49 months
six subtypes but all can carry grave prognosis
what sites do osteosarcoma in dogs and cats
-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
Does osteosarcoma cross the joint?
no
malignant tumor of cartilage that affects all species
typically in flat bones, appendicular skeleton, joints, soft tissue
slow development, metastasizes late in disease course
Chondrosarcoma
what is the typical signalment of osteosarcoma
large breed dogs about 7.5 years (small population of 18-24 months)
older cats
does chondrosarcoma cross the joint
no
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
Multilobular Tumor of Bone (ML)
Where does Multilobular Tumor of Bone (ML) typically occur
the flat bones of the skull
Rank the neoplasms by prognosis
Chondrosarcoma
Osteosarcoma
Fibrosarcoma
Fibrosarcoma
Chondrosarcoma
Osteosarcoma
malignant tumors of fibroblasts
affects all species
sites: periosteal/medulla of all bones
significantly better prognosis than osteosarcoma
fibrosarcoma
Fibrosarcomas typically arent that aggressive unless they are at the ________ **
mandibular and maxillary region
histologically benign but biologically aggressive
rate of reoccurrence is high!
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
Osteochondroma
what neoplasia of bone has lesions that appear soon after birth but cease at skeletal maturity
osteochondroma
what is the signifcance of osteochondroma
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
in regard to bone neoplasia _________ metastasis is far more common than _________ metastasis
carcinoma metastasis is far more common than sarcoma metastasis
why is bone biopsy hard to make diagnosis off of
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
severe hypovitaminosis D in a puppy can lead to
-Fibrous osteodystrophy
-Rickets
What are the predilection sites of the appendicular skeleton for osteosarcomas
Proximal humerus
Distal Ulna/Radius
Stifle: distal femur/proximal tibia
What is the point of disease and type of herniation for the corgi breed
Nucleus pulposis, Hansen type 1
what are the 3 different types of joints in the body
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
What are examples of fibrous joints
teeth/periodontal ligament
skull sutures
what are some examples of cartilaginous joints
growth plates
intervertebral joints
specialized cartilage to handle compressive forces
avascular with liited repair properties
articular cartilage
highly vascular layer of joint capsule
has synviocytes (type A- macrophage like and type b-fibroblast like)
Synovial membrane
type A synoviocytes are
macrophage like
type B synoviocytes are
fibroblast like
modified plasma in the synovial joint that provides nutrients to cartilage and lubricant for movement
synovial fluid
why does articular cartilage have limited reparative ability
it is avascular
-surface defects typically persist but dont progress to degenerative joint disease
Defects to articular cartilage that _______________________ does progress to degenenerative joint disease
extends into subchondral bone often filled with fibrovascular tissue and metaplastic fibrocartilage (scar tissue breaks down with other structures over time)
What lesions will you see to articular cartilage and subchondral bone on histo
Fibrillation, Erosion and Clefting
Eburnation (sclerosis of underlying exposed bone)
Periarticular osteophytes, enthesiophytes
What changes the fluid viscosity of synovial fluid
inflammation changes fluid viscosity and alters content
watery=decreased hyaluronic acid pyogenic bacteria enzymatic activity
thickened=fibrin
How does the synovium change in response to damage
synovial cell hypertrophy and synovial villous hyperplasia
how does the joint capsule change in response to injury
capsular thickening- can lead to fibrous ankylosis
umbrella term for degeneration of articular cartilage and the associated structures
Degenerative joint disease (Osteoarthritis, osteoarthrosis)
multifactorial: trauma, infection, conformation abnormality, age
primary cause: no cause (age related)
secondary: underlying disease or trauma
How do the lesions change from early DJD to more advance DJD
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)
eburnation
happens in advanced DJD where there is exposure of subchondral bone from complete loss of articular cartilage
What kind of horses get DJD
horses related to trauma/high performance
joints with high weight bear stress are predisposed
what kinds of dogs get DJD
common in medium to large breed dogs
primary: considered due to aging
secondary: common in chondrodystrophic or hip/elbow dysplasia
What breed of cat is predisposed to DJD
Siamese cats
(DJD is typically much less common in cats)
How do dogs typically get DJD
Primary: aging
Secondary: chondrodystrophy or hip/elbow dysplasia
a focal failure of blood supply to the growing epiphyseal cartialge leading to failure of the cartilage to ossify and degenerative joint disease
osteochondrosis dissecans
What species typically get osteochondrosis dissecans
typically: young dogs and horses
pigs, poultry, and cattle also get it (not as much)
clinical signs of osteochondrosis dissecans
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
what is the pathogenesis of osteochondrosis dissecans
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
what are the site predilection for osteochondrosis dissecans
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
Where do dogs typically get osteochondrosis dissecans
the humeral head/shoulder joint
where do horses typically get osteochondrosis dissecans
Hind limbs, specifically
a) stifle area; medial condyle of femur, patella, lateral trochlear ridge, distal tibia
b) also the hock
where do pigs typically osteochondrosis dissecans
a) Shoulder- humeral condyle, humeral head,
b) Hip- dorsal acetabulum
c) Stifle
Osteochondrosis typically affects _____ dogs while OCD affects _____
young; older
lack of conformity of the femoral head and acetabulum leading to joint laxity and degenerative joint disease
hip dysplasia
what is the inciting lesion of hip dysplasia
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
what is the most common skeletal disease of large/giant breed dogs
hip dysplasia
what species get hip genetic due to hereditary polygenetic coxofemoral joint laxity
GSD, rottweiler, Labradors
GSD, rottweiler, Labradors get hip dysplasia due to
hereditary polygenetic coxofemoral joint laxity
What are factors that influence hip dysplasia development
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
whatm ight you see on radiograph with a patient with hip dysplasia
shallow acetabulum
flattened femoral head
inflammation of any joint component
arthritis
acute inflammation of the joint
that returns to normal
articular cartilae is not affected and DJD wont develop
fibrinous arthritis
T/F: suppurative arthritis is only seen in infectous arthritis
false- it can be non-infectious too
septic arthritis typically occurs in
neonatal large animals
polyarthritis often with concurrent osteomyelitis
What might be a viral cause of infectious arthritis
caprine arthritis-encephalitis virus
causes unilateral or bilateral carpal hygroma
What is a major bacterial etiology of infectious arthritis in sheep/goats, swine, and cattle
Mycoplasma species
causes unilateral or bilateral carpal hygroma in goats
caprine arthritis- encephalitis virus (lentivirus)
What type of hypersensitivity is immune-mediated polyarthritis (IMPA)
type III hypersensitivity- antibody complex deposited
immune-mediated polyarthritis (IMPA) typically occurs in
dogs and cats
What disease cause immune-mediated polyarthritis (IMPA) in dogs and cats
1) Systemic lupus erythematosus- sterile, nonerosive, lymphoplasmacytic proliferative synovitis
2) Rheumatoid arthritis- idiopathic, sterile, chronic
destrictive, rhematoid factor IgG or IgM
erosive arthritis
What form of immune-mediated polyarthritis (IMPA) is erosive
Rhematoid arthritis via rhematoid factor (IgG or IgM)
tumors that typically infect the joint capsule and tendon sheath in larger joints (stifle, elbow, shoulder)
synovial tumors
1) synovial sarcoma (soft tissue sarcoma)
2) periarticular histiocytic sarcoma
synovial sarcomas resemble
soft tissue sarcomas
might just be soft tissue sarcomas that just encompass the joint
-look the same on histo
a neoplasm of synovial dendritic cells
most common joint tumor of dog
-on the appendicular skeleton
poor prognosis
periarticular histiocytic sarcoma
most common joint tumor of dog
periarticular histiocytic sarcoma
What are the different componnts of the vertebral colum and what is their function
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
Where are the intercapital ligaments present
exist T2-T1-
absent: cervical and lumbar
congential lateral deviation of the spinal column
scoliosis
congenital dorsal curvature of the spinal column
kyphosis
congenital ventral curvature of the spinal column
lordosis
congenital anomaly where part of the vertebrae is missing
hemivertebrae
what is the nucleus pulposus made of
water and proteoglycans
function for shock and flexibility
what is the most common cause of paresis or paralysis in the dog
intervertebral disk degeneration (IVDD)
vertebral joint collapse with dorsal herniation of joint material into spinal
intervertebral disk degeneration (IVDD)
types:
Hansen type 1 (chondrodystrophic breeds)
Hansen type 2 (non-chondrodystrophic breeds)
vertebral joint collapse with dorsal herniation of joint material into spinal in chondrodystrophic breeds
intervertebral disk degeneration (IVDD)- Hansen type 1
vertebral joint collapse with dorsal herniation of joint material into spinal in non-chondrodystrophic breeds
intervertebral disk degeneration (IVDD)- Hansen type 2
What are the most common sites for IVDD
Lumbar spine (>70%)T12-L2
cervical spine (15%)
intervertebral disk degeneration (IVDD)- Hansen type 1
pathogenesis
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
what is the signalment for intervertebral disk degeneration (IVDD)
Hansen type 1: chondrodystrophic breeds 3-7 years of age
Hansen type 2: animal breed; 6-8 years of age
intervertebral disk degeneration (IVDD)- Hansen type 2
pathogenesis
genetical
1) trauma
2) disruption of annulus fibers
3) degeneration of annulus
4) slow bulging of annulus into the spinal cord
5) paresis
bony bridging (ankylosis) of the vertebral bodies caused by chronic instability/trauma, ventral DJD of the vertebral joints
spondylosis
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
spondylosis
sepsis of vertebral end-plate and disk typically in the lumbosacral suppurative osteomyelitis lesions
commonly caused by Staph. pseudointermedius, Brucella, Ecoli, and rarely fungal
Diskospondylitis
what are the etiologies of diskospondylitis in a dog
Staph. pseudointermedius, Brucella, Ecoli, and rarely fungal
see suppurative osteomyelitis +/- meningitis/myelitis with cord compression at the lumbosacral region of large breeds
wobbler’s syndrome- cervical instability and cord compression due to static stenosis of the vertebral canal
Cervicospinal arthropathy (spondylomyelopathy)
What lesions do you see with Cervicospinal arthropathy (spondylomyelopathy)
typically in quarterhorses and dogs (dobermann)
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
What is typically the pathogenesis of Cervicospinal arthropathy (spondylomyelopathy)
genetic/congenital/trauma causes stenosis of the vertebral canal and subsequent cord compression, myelomalacia and myelodegeneration
what are the clinical signs of Cervicospinal arthropathy (spondylomyelopathy)
paresis/tetraparesis
stiff painful neck
what kind of animals typically get Cervicospinal arthropathy (spondylomyelopathy)
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
why does IVDD typically happen at the lumbar sites (>70%) T12-L2 and cervical spine (15%)
because those regions do not have have intercapital ligaments there
the outer most connective tissue sheath of muscle
epimysium
connective tissue that surrounds the myofiber bundles
perimysium
the connective tissue that surrounds individual myofibers
endomysium
mature cell that performs contraction, multinucleated
myocyte (myofiber)
immature muscle cells capable of regeneration
satellite cells (myoblasts)
the functional contractile unit of muscle
composed of thin (actin) and thick (myosin) filament
contraction via ATP and calcium
sarcomere
myocytes that are:
slow twitch (endurance)
oxidative aerobic
Type I myocyte
myocytes that are:
fast twitch (speed, fatigue)
glycolytic (anaerobic)
Type II myocyte
decrease in sarcoplasmic diameter due to denervation, disuse, endocrine disorders, malnutrition/cachexia
muscle atrophy
increase in sarcoplasmic diameter due to physiologic (more contraction) and pathology
muscle hypertrophy
deneration injury to the left recurrent laryngeal nerve in horses causes
laryngeal hemiplegia
causing muscle atrophy to the left cricoarytenoideus dorsalis
laryngeal hemiplegia
denervation injury to the left recurrent laryngeal nerve causing muscle atrophy to the left cricoarytenoideus dorsalis
‘response to long standing and recurrent muscle injury- polyphasic injury
muscle fibrosis
T/F: muscle tissue has an amazing capacity for regeneration
can regenerate to completely normal and mature myocytes
True
one time muscle injury in response to trauma or a toxin
monophasic muscle necrosis
-called polyphasic if there is a recurrent insult (nutritional, myopathies, genetic)
clinical term for myonecrosis- can be used in any situation where nyonecrosis results in clinical signs
rhabdomyolysis
With muscle necrosis (rhabdomyolysis) you typically get
mineralization (white tissue) due to high concentration of calcium
inherited X-linked disorder in dystrophin, progressive myopathy characterized by ongoing necrosis and degeneration (polyphasic)
Muscular Dystrophy (Duchenne’s)
Muscular Dystrophy (Duchenne’s)
inherited X-linked in dystrophin, progressive myopathy characterized by ongoing necrosis and degeneration (polyphasic)
mostly dogs (also cats, mice +/- sheep)
only in males
What protein is affected by Muscular Dystrophy (Duchenne’s)
Dystrophin- X linked mutation
(only males)
T/F: Muscular Dystrophy (Duchenne’s) affects males and females equally
False: only males
inherited X-linked in dystrophin
what is the signalment of muscular dystrophy
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
what will you see clinically in a male puppy with muscular dystrophy
marked necrosis- most severe in diaphragm, muscle moss and progressive weakness, markedly elevated CK and AST
what will you see clinically in a kitten with muscular dystrophy
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
What is unique about cats with muscular dystrophy, in comparison to dogs *
cats get marked hypertrophy* (dogs get marked necrosis)
cats also can develop malignant hyperthermia
what species do you typically think of with malignant hyperthermia
pigs (can also occur in dogs and horses)
hypercontraction of all striated muscle due to ryanodine receptor mutation (unregulated Ca2+ channels) leading to hyperthermia and lactic acidosis
malignant hyperthermia (porcine stress syndrome)
what is typically the stressor for malignant hyperthermia (uncontrolled muscle contraction leading to hyperthermia and lactic acidosis)
general anesthesia or stress
muscular dystrophy (not mutation but causes Ca++ release)
what causes malignant hyperthermia
ryanodine receptor mutation (unregulated Ca2+ channels) leading to hyperthermia and lactic acidosis
what lesions are seen with malignant hyperthermia
myonecrosis
tachycardia
respiratory distress
heart failure leading to death
sodium channel defect leading to changed action potential
typically in quarter horses
hyperkalemic periodic paralysis (HYPP)
what is the pathogenesis of hyperkalemic periodic paralysis (HYPP)
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)
How do you manage horses with hyperkalemic periodic paralysis (HYPP)
genetic testing
Low potassium diet (no alfalfa or molasses)
do not ride them (sudden recumbency)
glycogen accumulation leading to muscle dysfunction and necrosis (rhabdomyolysis)
common in draft breeds
caused by genetic mutation in GSYI
equine polysaccharide storage myopathy (EPSSM)
what is the pathogenesis of equine polysaccharide storage myopathy (EPSSM)
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
breakdown of neuromuscular joint communication leading to decreased muscle contraction
myasthenia gravis
what are the clinical signs of myasthenia gravis
1) megaesophagus
2) weakness in appendicular muscular (exercise induced collapse)
Dog breeds:
___________ typically get acquired myasthenia gravis while _________ have congenital myasthenia gravis
German shephard (acquired- typically thymoma or thymic hyperplasia)
Jack Russell (congenital- decreased receptor density)
inherited defect in acetylcholine receptors
congenital myasthenia gravis
-typically more rare but common among jack russell terriers
how is myasthenia gravis typically acquired
thymoma or thymic hyperplasia
*Paraneoplastic
*Antibodies attack the acetylcholine receptors
how do you test for myastenia gravis
Tensilon Test
-Administer Anticholinesterase
-Overcome receptor deficiency = normal
3 ways you can get ischemic myopathy
1) Recumbency (compression)
2) Compartmental syndrome
3) Loss of circulation
immobile/recumbent animals leading to increased intramuscular pressure -> collagenous of venous system -> red infarct/ischemic necrosis
Downer Syndrome
vigorous muscular contraction leading to increased intramuscular pressure -> collagenous of venous system -> red infarct/ischemic necrosis
compartment syndrome
-typical of broiler chickens
what is the typical route cause of suppurative myositis
inoculation or extension route (unlike bone where hematogenous is the star of the show)
what causes pigeon fever or pigeon breast
corynebacterium pseudotuberculosis
pigeon breast pathogenesis
corynebacterium pseudotuberculosis living in soil contaminates a woind or inoculation from insects -> spreads to pectoral muscles and causes abscesses
what causes malignant edema, marked myonecrosis through contamination and toxin production
Clostridium septicum
what causes gas gangrene, marked necrosis through contamination and toxin production
Clostridium perfringens
what causes black leg
Clostridium chauvoei
what is needed for malignaant edema/gas gangrene forms of infectious myositis (caused by clostridium septicum and perfringens)
wounds for spores contamination and then proliferate under anaerobic conditions
What is the pathogenesis of black leg
-Clostridium chauvoei spores ingested*
-deposited dormant in muscle
-muscle trauma
-activation (vegative)
-myonecrosis
-toxemia
rapid death and myonecrosis of any striated muscle resulting in marked crepitus/ emphysema due to clostridial spores being ingested
Black Leg (Clostridium chauvoei)
T/F: black leg is more localized than malignant edema and gas gangrene
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
what causes wooden tongue (granulomatous myositis)
actinobacilus lignieresii
what is the pathogenesis of wooden tongue
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
you have a cow with anorexia, weight loss, decreased milk production, unilateral mandibular swelling (radiographic opaque mass). What is your diagnosis
lumpy jaw- actinomyces bovis
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
Hypertrophic osteopathy
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
Osteopetrosis- caused by genetic defect or acquired (BLDV)
if dog (distemper) or cat (FeLV)
Legg Calve Perthes disease, what is the primary cause?
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.
you see a lamb with long, lanky and poorly formed limbs. what is your diagnosis
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.
upon necropsy of a horse you see a fluid filled pocket around the necrotic bone. what is this
involucrum
upon necropsy of a guinea pig you notice abnormal collagen cross linking, weakened collagen and finally hemorrhage at the joints. what is diagnosis
scurvy (vitamin C) deficiency
what are causes of parasitic myositis
1) Neospora caninum
2) Toxoplasma gondii
3) Sarcocystis
4) Hepatozoon
*Require two host
-Intermediate herbivore
-Predator definitive host (enteric)
How can dogs get Neospora caninum
1) trans-placental infection
2) eating intermediate host
neospora caninum causes
infection of ventral spinal rootlets and muscle leading to progressive deneveration atrophy, esp of hindlimbs
mid-gestation abortion
causes degenerative protozoal cysts leading to eosinophilic inflammation
Sarcocystis sp.
what the definitive host of hepatozoon americanum
brown tick via ingestion
what lesions does Hepatozoon Americanum cause *
1) Pyogranulomatous myositis **
2) Periosteal reaction **
3) Onion cysts in tissues
4) marked leukocytosis
5) fever, anorexia, weight loss
Why is trichonella called a true parasite
because they never leave the host
-no external aspect of lifecycle
how is trichonella spread
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
How do you prevent Trichonella infection
cook meat
What causes “Beef Measles”
Taenia- parasitic cyst in muscle
causes pyogranulomatous inflammation with fibrosis
an exertional myopathy in horses where myofiber damage occurs as a result of exercise stress as the primary cause
Equine Rhabdomyolysis
what are the clinical signs of Equine Rhabdomyolysis
Often draft horses (also QH and thoroughbreds)
-Stiff weakened muscles, inability to move, recumbency
-High CK, AST, myoglobinuric nephrosis
Three causes of equine rhabdomyolysis
1) intense activity
2) high carb diet
3) equine polysaccharide storage myopathy
non-infectious myopathy that is caused by exertion or hyperthermia of many wildlife species causes lactic acidosis with myonecrosis
myoglobinuria and CK elevation
Capture Myopathy
what kind of hypersensitivity is purpura hemorrhagica
Type III- immmue complex formation against Strep. M protein
What is the pathogensis of equine purpura hemorrhagica
post-streptococcal infection there is immune complex formation against the M protein
this causes necrotizing vasculitis, skeletal muscle infarction and limited inflammation
What kind of hypersensitivity is seen in young quarter horses after they are infected with streptococcus equi
Type II- autoantibodies targets against the muscle
rapid atrophy
Two immune hypersensitivty reactions seen after horses get streptococcus equi
1) Purpura hemorrhagica (Type III)- immune complex against strep m protein
2) young quarter horses (type II)- autoantibodies against muscle
What kind of hypersensitivty is canine masticatory myositis
type II- autoantibody against type 2M myosin
In canine masticatory myositis, it is type II hypersensitivity. what do the autoantibodies target
type 2M myosin
What is the pathogensis of canine masticatory myositis
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
How do you diagnose canine masticatory myositis
Signs: swelling, difficulty in opening, painful, may lead to atrophy with “locked jaw”
very painful
Serology for 2M myosin Antibodies
Many muscle biopsies
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
Canine polymoyositis
What is the mechanism of canine polymyositis
lymphocytic myositis often with lupus or neoplasia
Vitamin E/Selenium deficiencies are most commonly seen in
Fetal to Young (2-4months)
Herbivores
Reptiles
Birds
(rarely carnivores)
Vitamin E/Selenium deficiencies cause ___________
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
How might an animal have nutritional myopathies Vitamin E/Selenium deficiencies
1) poor quality feed
2) increased/unusual physical activity (more oxidative stress)
What is unique about Vitamin E/Selenium deficiencies in Pigs
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
mullberry heart disease
epicardial hemorrhage and necrosis seen in pigs with Vitamin E/Selenium deficiencies
hepatosis dietetica
diffuse/excessive hepatocellular necrosis seen in pigs with Vitamin E/Selenium deficiencies
how might reptiles/birds with Vitamin E/Selenium deficiencies present
degenerative encephalopathy
“Crazy Chick Disease”
What animals have high susceptibility to ionophores
monogastric animals (horses, dogs, and pigs)
ruminants can get them if there is a dosing miscalculation
is ionophore toxicity monophasic or polyphasic
Monophasic
Ionophores like Monensin & Laslocid alter ______
Ca2+ flux
toxicity causes monophasic myopathy
myocyte and myocardial necrosis
mineralization
fibrosis
What species do you typically see monophasic necrosis from gossypol toxicity in?
Pigs
Goosypol toxicity causes monophasic or polyphasic myopathy
monophasic necrosis
-mineralization and fibrosis
-central lobular hepatic necrosis and pulmonary congestion
-muscle pain
-recumbency dyspnea
-Heart failure
T/F: Ingestion of Cassia, Eupatorium, Karwinski plants causes necrosis of skeletal and cardiac tissue
Falso- cardiac tissue is not usually involved
a rare benign neoplasm of skeletal muscle
typically young pigs and dogs
dog-larynx
pig-heart
clinical signs are dyspnea and stridor
Rhabdomyoma
the most common skeletal tumor but still very rare
Rhabdomyosarcoma
Bladder botryoid rhabdomyosarcoma
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
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
Bladder botryoid rhabdomyosarcoma
T/F: neoplasm metastasis to muscle is generally rare
True- there is some extension but muscle tissue typically isnt a normal secondary site despite high blood flow
