MSK pt 1 Flashcards
Label this image
A: epiphysis
B: Physis
C: metaphysics
D: Diaphysis
E: cortex/cortical bone/compact bone
F: medullary cavity
G: cancellous bone/spongy bone
During endochondral ossification, where are the primary and secondary centres of ossification?
primary: diaphysis (prenatal)
secondary: physis (post-natal)
Why are eunuchs tall with long fingers?
normal development:
maturity = increase in sex hormones –> growth plate thins and is replaced by bone
early castration:
maturity ≠ increase in sex hormones –> delayed growth plate closure –> tall, long fingers, etc.
What is the implication of castrating animals too young? (eunuchs)
they are taller with longer limbs/bones, so femoral head fxs in young happen lots, and overweight castrated male cats is a thing
What is Wolff’s law?
bone is remodelled in response to forces placed on them
what are the 2 responses to injury that bone has?
- resorption/lysis
- production of new bone (woven bone)
What is an exostosis?
projecting proliferation of bone from the periosteum, benign
AKA bony spurs
What is the arrow pointing to?
Exostosis
(bony spur)
Where is the weakest place in growing bones? why?
growth plate
cartilage is weaker than bone
How do we classify growth plate fractures?
Salter-Harris classification
What is the most common Salter Harris fracture? What is the consequence?
SH 2 (break along physics and into metaphysis)
growth still possible
What are the more serious Salter-Harris fractures? What is the consequence?
SH 3 & SH 4 (break across growth plate, going up or down, but either way going to the articular surface)
healing bone “closes” it –> no growth at site
What is the blue arrow pointing to? What type of fracture is the red arrow pointing to?
physis/growth plate (blue arrow)
Salter Harris fx (don’t have to know specific classification)
angular limb deformities are common in ____-____ animals. What are the 2 types?
fast-growing
1. valgus
2. varus
Describe the difference between valgus and varus.
Valgus: splay-legged. knees go together, feet go out laterally
varus: bow-legged. knees go out, feet go together medially
What angular limb deformity is this animal displaying?
valgus
What angular limb deformity is this animal displaying?
Varus
List 6 causes of angular limb deformities (you have to know the first one for sure!)
- asymmetric damage to growth plate –> one side closes while the other grows
- malposition in utero
- joint laxity due to weak supporting structures
- hypothyroidism
- malnutrition
- abnormalities in endochondral ossification
What is the definition of a fracture? when does this occur?
a break/rupture resulting in a physical discontinuity in a bone
occurs when there is a mechanical force that exceeds the bone’s strength
What are the 2 types of fractures? what do they mean?
- traumatic - excessive forces exerted on normal bone
- pathological - normal/minimal forces exerted on abnormal bone
What bone abnormalities can cause pathological fractures?
infection (osteomyelitis), neoplasia, metabolic bone disease
Tell me the main fracture descriptors (there are 5)
- closed/simple vs open/compound
- displaced vs non-displaced
- comminuted vs transverse/linear/oblique/spiral
- location (proximal/distal/midshaft)
- name the bone
What is an avulsion fracture?
ligament pulls bone at site of insertion
What is a greenstick fracture?
1 cortex is broken, the other bent
not displaced
usually young animals
List the steps of fracture healing and the timing. also note if it’s stable/unstable. (very general) (5 steps)
- hematoma - immediate - unstable
- fibrous tissue - 24-48 h - unstable
- woven bone & cartilage - 36 hr - unstable
- primary callus - 4-6 wks - stable
- secondary callus - months to years - stable
Hi Fred, We Prefer Salt
What is a non-union?
fracture doesn’t heal
List the reasons for non-unions to occur (6 things)
- inadequate blood supply
- instability
- infection
- fx result of bone pathology vs trauma
- malnutrition
- necrotic tissue (sequestrum) in fx site
What is osteodystrophy? can more than 1 type affect the same individual?
abnormal bone metabolism (metabolic bone disease)
yes
What are the causes of osteodystrophy?
nutritional/hormonal deficiencies/imbalances/toxicities
can be multifactorial
what is the possible result of osteodystrophy?
pathological fractures, pain (lameness)
Osteodystrophy is more common & severe in ____ animals. Why?
growing
rapid skeletal development vs slower remodelling of adults
What are the osteodystrophies/metabolic bone diseases that we have to know?
- malnutrition and starvation
- osteoporosis
- rickets
- osteomalacia
- fibrous osteodystrophy
MOROF
What are growth arrest lines?
slow longitudinal bone growth –> trabeculae in metaphysis are abnormally aligned
what are the 2 causes of growth arrest lines?
debilitating disease, malnutrition
Describe the pathogenesis of growth arrest lines?
- inciting cause (debilitating disease, malnutrition)
- long bone growth stops
- abnormal osteoclast activity
- lines are carried into metaphysis as growth resumes
What is the blue arrow pointing to?
growth arrest line
what is serous atrophy of fat?
normally dense fat becomes watery and gelatinous, in response to malnutrition/starvation
What is going on?!
serous atrophy of fat
What is osteoporosis?
reduced bone mass and density with associated pathological fractures
what is osteopenia?
reduced bone mass/density without pathological fractures
what is the difference between osteopenia and osteoporosis?
both are reduced bone mass and density, but osteopenia is without pathologic fx, and osteoporosis is with pathologic fx
What are the 3 causes of osteoporosis?
- Ca2+ deficiency
- starvation
- physical disuse (atrophy)
basically anything that tips the balance so more bone is absorbed than replaced during remodelling
what is the pathogenesis of how calcium deficiency leads to osteoporosis?
low serum Ca2+ –> increase in parathyroid hormone –> stimulates osteoclasts to increase bone resorption
You treated a patient with a broken limb and put a cast on the limb. What metabolic bone disease is something that you should be wary of?
osteoporosis
What is this picture showing?
bone with osteoporosis
bones with osteoporosis are _____ mineralized. (extremely, normally, limitedly)
normally
How can bones be normally mineralized in osteoporosis if pathogenesis involves low calcium?
- bones were formed in a healthy individual = normal mineralization
- subsequent Ca2+ deficiency
- stimulates osteoclasts to resorb bone
- reduced bone density because removed bone isn’t replaced
- weak & brittle (but normal mineralization of trabeculae that remain)
The top bone is normal. What is wrong with the bottom one? (ignore the red lines)
osteoporosis (thin cortex, hardly any trabecular bone left)
Bone with osteoporosis is more _____ in radiographs (radiolucent/radiopaque)
radiolucent
What is rickets?
failure of bone mineralization in young, growing animals
thickened growth plates from lack of cartilage mineralization and abnormal endochondral ossification
what is the cause of rickets?
vitamin D & phosphorus deficiency
This is from the metatarsal of a young sheep. What is the lesion?
rickets
*note the thick cartilage still present
What are the white arrows pointing to?
retained cartilage deep in metaphysis of an animal with rickets
what are the gross lesions of rickets? where can you see these lesions best on necropsy?
- segmental growth plate thickening
- multifocal physis lesions (on multiple bones)
- tongues of un-resorbed cartilage extending into the metaphysis
most prominent at sites of rapid growth
What is rachitic rosary?
segmental growth plate thickening in the costochondral junctions, causing growths that looks like rosary beads
Even though this is a human, it has the same pathology as something we’ve talked about in class. What is the pathology? (hint: look at the white arrows)
rachitic rosary - rickets
What is osteomalacia?
softening of bones. similar cause and pathogenesis to rickets but occurring in adults
involves defective mineralization during bone remodelling
describe the difference between osteomalacia and rickets
Rickets is failure of bone mineralization in young growing animals and involves thickened growth plates.
osteomalacia involves defective mineralization during bone remodelling resulting in soft bones. It has the same/similar cause/pathogenesis as rickets but occurs in adults and does not have growth plate involvement
what is the consequence of osteomalacia?
bones have reduced resistance to pressure and tension - fractures occur
what are the gross lesions of osteomalacia?
expansion of the marrow cavity (bones often enlarged)
thin, spongy, soft cortex
pathologic fractures
what is fibrous osteodystrophy?
excessive bone resorption and replacement by fibrous connective tissue
what is the pathogenesis of fibrous osteodystrophy?
- hyperparathyroidism
- elevated parathyroid hormone (PTH)
- increase osteoclastic resorption and replacement by fibrous tissue
- soft, malleable bones
What are the two types of hyperparathyroidism and what is the difference between them?
- primary hyperparathyroidism: excessive PTH secreted from parathyroid glands. rare, often associated with parathyroid gland neoplasia. (usually excessive PTH secreted from functional parathyroid gland tumor)
- secondary hyperparathyroidism: stimulus to decrease serum Ca2+ leads to increase in PTH. Common, 2 subtypes
What are the 2 types of secondary hyperparathyroidism?
- nutritional
- renal
what is the overall cause of fibrous osteodystrophy? (very general)
hyperparathyroidism
Nutritional secondary hyperparathyroidism:
1. cause?
2. affects who?
2a. who is the exception?
3. who is resistant to this?
- diets low in calcium & high in phosphorus
- young growing animals
2a. horses - can occur in young and adult animals - cattle & sheep
Nutritional secondary hyperparathyroidism:
1. what are horses & sheep with this disease called?
2. what are the associated diets in horses & sheep?
3. gross lesions in horse?
4. what happens in severe cases?
- big heads
- cereal hay (oat straw), bran, grain
- bilateral enlargement of fascial bones = fascial swelling; can also lead to loose teeth
- develop lesions in other bones = lameness ± pathologic fxs
Tell me 1 lesion that you can see on the face of a horse with nutritional secondary hyperparathyroidism and 2 lesions you can see in the maxillary bone/nose area
- bilaterally symmetrical distorted facial contours
- maxillary bone is replaced with fibrous tissue including areas around teeth, fibrous tissues compress the nasal cavity towards the septum
what is the associated diet to nutritional secondary hyperparathyroidism in dogs/cats & pigs?
dogs/cats: all meat/offal
pigs: grain
what are the gross lesions of nutritional secondary hyperparathyroidism in dogs/cats/pigs?
facial swelling not always present, but skull affected: long bones predominantly affected (pathologic fxs common presenting signs)
Renal secondary hyperparathyroidism:
1. AKA?
2. lesions?
- renal osteodystrophy
- soft malleable bones (can cut bones with a knife); soft pliable mandible (rubber jaw); deformed mandible/maxilla & tooth loss
renal osteodystrohpy is a combination of _____ ____ and ______.
fibrous osteodystrophy & osteomalacia
renal osteodystrohpy is associated with severe, ___ (acute/chronic), _____ disease. Common in ____ (older/younger) ____ & ___.
severe, chronic renal disease
older dogs & cats
describe the pathogenesis of renal osteodystrophy
- renal disease
- reduced renal phosphate excretion
- hyperphosphatemia; phosphate reacts with Ca2+
- increase PTH
- increased bone resorption
AND
- renal disease
- reduced renal vitamin D metabolism
- reduced Ca2+ absorption from intestines
This is a maxilla from a dog. What caused this? (ignore the arrows/lines)
renal secondary hyperparathyroidism
What caused this poor horse to look like this?
nutritional secondary hyperparathyroidism
