Bones II Flashcards

1
Q

In situations of bone loss, ex: ostopenia, osteoporosis, bone lysis, what takes up the newly created space?

A
  • existing tissue expands or loosens
  • may include fluid ex: serous atrophy of fat
  • replaced by fibrous tissue
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2
Q

Two concepts Allen likes:

A
  1. in order to diagnose a specific disease, you have to know that the specific disease exists
  2. the diagnosis of a bone disease requires the recognition of a pattern of bone loss, bone production, or both
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3
Q

Bone is susceptible to the same pathologic processes as ither tissues & organs, what are these?

A
  • alterations of growth (aplasia, hypoplasia, atrophy, hyperplasia, neoplasia)
  • circulatory disorders (hemorrhage & ischemia)
  • inflammation & repair
  • degeneration & necrosis
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4
Q

Sometimes in bone the pathologic processes like other tissues are overshadowed by underlying & more intuitive concepts concerning the pathogenesis of a lesion or disease: examples of this?

A
  • trauma leading to a fracture
  • nutritional or metabolic disorders leading to so-called metabolic bone disease
  • like other organs, bone has a limited range of reactions to injury & mechanisms of repair
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5
Q

Which two processes that usually occur together are involved in the reaction of bone to injury?

A
  • removal of damaged bone (resorption or lysis)
  • production of new bone
  • the proportion of these two reactions will vary
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6
Q

Injury to the periosteum (& endosteum) will usually be followed by?

A

formation of periosteal (& endosteal) new bone

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7
Q

Bone density will change in response to?

A

change in use

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8
Q

How is bone related to calcium & phosphorus?

A
  • bone is a body’s main reservoir of calcium (~99%) & phosphorus (~85%) & is involved in plasma calcium & phosphorus homeostasis
  • therefore, bone is affected by any disease involving abnormal calcium & phosphorus metabolism, including disorders of nutritional origin
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9
Q

What is a fracture?

A
  • a break or rupture in a bone
  • a common occurrence
  • represents a physical discontinuity in a bone which results in instability & pain
  • which may manifest as impaired movement (lameness, immobility, or recumbency)
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10
Q

What kind of fracture is this?

A

Greenstick

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11
Q

What kind of fracture is this?

A

spiral

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12
Q

What kind of fracture is this?

A

Comminuted

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13
Q

What kind of fracture is this?

A

Transverse

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14
Q

What kind of fracture is this?

A

compound

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15
Q

What is happening here?

A

vertebral compression

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16
Q
  • What is the pathogenesis of fractures?
A

fractures occur under one of two circumstances:
1. either a normal bone fractures under excessive force - TRAUMATIC FRACTURE
2. or an abnormal bone fractures under normal force - PATHOLOGIC FRACTURE

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17
Q

What is fracture repair?

A

the healing of a fractured bone

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18
Q

What is the process of fracture repair?

A
  • can be conveniently divided into 5 phases
  • but important to appreciate that the divisions are arbitrary, they overlap & are concurrent, they may occur at different rates in different areas of a fracture, & they represent a summary of a complex & incompletely understood process
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19
Q

What are the 5 phases of fracture repair?

A

Phase I - Injury & Inflammation
Phase II - Organization of the Hematoma
Phase III - Callus formation: External & internal callus
Phase IV: Callus remodeling
Phase V: Callus modeling

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20
Q

What is phase I of fracture repair?

A

Injury & Inflammation
- when bone is fractured there is tearing of the periosteum & endosteum, rupture of blood vessels of the bone, & injury to surrounding soft tissue
- these events result in ischemic necrosis of bone at the fracture lines & associated marrow, formation of a hematoma, & inflammation
- these changes promote the immediate activation & recruitment of platelets, macrophages, & other leukocytes, all of which release growth factors

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21
Q

What is phase II of fracture repair?

A

Organization of the hematoma
- w/in 24-48 hrs, the hematoma btwn bone fragments begins to organize
- undifferentiated mesenchymal cells of the periosteum, endosteum, & bone marrow are activated, proliferate, & invade the hematoma
- similarly, endothelial cells proliferate to form new blood vessels, aka, neovascularization

22
Q

What is phase III of fracture repair?

A

Callus formation: internal & external callus
- mass of exudate & CT that forms around a fracture during repair is called a callus or primary callus
- there is an external callus & an internal callus
- the external callus is usually more substantial (& easily noticed) w/ the periosteum making an important contribution
- where the blood supply is adequate & the oxygen tension is high (away from the fracture gap), undifferentiated mesenchymal cells become osteoblasts that produce (de novo) woven bone
- where the blood supply is poor & the oxygen tension is low (at or near the fracture gap), undifferentiated mesenchymal cells become fibroblasts & chondroblasts
- the cartilage produced by the chondroblasts is later REPLACED by woven bone via endochondral ossification
- the internal callus is produced by the endosteum & is formed in the same manner as the external callus
- it is usually smaller than the external callus & may temporarily occlude the medullary space

23
Q

How quickly does callus formation occur?

A
  • may begin w/in 24 hrs
  • woven bone may be visible MICROSCOPICALLY as quickly as 36 hrs after fracture, but may not be visible RADIOGRAPHICALLY for 2 weeks
  • under favourable conditions, it takes 4-6 wks for the primary callus to be replaced by a so-called bony callus
24
Q

What causes the time for callus formation & remodeling to vary?

A
  • animal’s age & health (including nutrition), the fracture type & location, associated injuries & infection, & the method & quality of fixation, if any
24
Q

What is fixation?

A
  • refers to fastening something firmly in position (holding something in a fixed position)
  • in orthopedic surgery, fixation refers to the immobilization of the parts of a fractured bone
  • fixation can be external (splint or cast), internal (various metal devices, or both
24
Q

What is phase IV of fracture repair?

A

Callus remodeling
- w/ time, woven bone is replaced w/ lamellar bone, compact bone is formed in the cortex, & cancellous bone is formed in the metaphysis & diaphysis
- since resorption & formation are about equal, this represents remodeling

25
Q

What is this and what does it do?

A
  • cutting cones perform osteoclastic tunneling
  • series of osteoclasts at the front of the cone & behind it are osteoblasts that lay down new bone
26
Q

What is phase V of fracture repair?

A

Callus modeling
- final phase of fracture repair results in restoration of the fractured bone to its original form (size & shape) & function (or as close as possible)
- specifically, callus modelling involves the reduction in size of the callus & sculpting of the bone in response to the stresses of weight bearing & muscle pull
- this phase make take months to years

27
Q

What does the end result of fracture repair look like?

A
28
Q
A
29
Q

What is the tissue & stability at the repair site at each of these times?

A
30
Q

What are the complications of fracture repair?

A

nonunion, delayed union, malunion

31
Q

What is nonunion?

A

failure of the fragments of a fractured bone to heal - to become fused bone

32
Q

What causes nonunion?

A
  • inadequate blood supply
  • instability (movement)
  • infection
  • presence of necrotic fragments of bone or soft tissue w/in the fracture gap
  • pathologic fractures rarely heal w/o intervention
33
Q

What is a delayed union?

A
  • describes a fracture that takes longer than normal to heal
  • since the time required for fracture healing can be highly variable, the criteria for the diagnosis of a delayed union are also variable
34
Q

When does a delayed union become a non-union?

A
  • it is often difficult to differentiate btwn a nonunion & a delayed union
  • some authorities define a nonunion as a fracture that fails to display any progressive changes - usually using radiography - for @ least 3 months after the time when normal fracture healing would have occurred
  • others believe that a fracture that has not healed w/in 6 months of the injury will likely remain unhealed (w/o intervention) & is, therefore, defined as a nonunion
35
Q

What is malunion?

A
  • (mal is a prefix meaning ill or bad)
  • refers to a fracture that has healed, but in an abnormal alignment (ex: results in a deformed limb or other structure)
  • malunions can result in a shorter limb due to the fusion of overriding fragments; axial deformities (or crooked/bent limbs); & rotational deformities (or twisted limbs)
36
Q

What is the physis?

A
  • site of longitudinal growth (& sometimes growth in other directions) in endochondral bones
  • it’s a temporary structure composed of hyaline cartilage
  • it’s widest when growth is most rapid & becomes narrow as growth slows
  • growth stops when the physis is entirely replaced by bone
  • this is referred to as closure of the growth plate & marks skeletal maturity
37
Q

What are 5 disorders associated w/ the physis?

A
  1. physeal/growth plate fractures (Salter-Harris fractures)
  2. growth retardation lattices
  3. growth arrest lines
  4. premature closure
  5. osteochondrosis/ osteochondritis
38
Q

What are growth plate or physeal fractures?

A
  • b/c the physis is composed of cartilage, it is physically weak compared to bone & can be more easily injured
  • since the physis is the site of longitudinal growth, injury to the physis can affect longitudinal bone growth
39
Q

what is the Salter-Harris classification?

A
  • classifies growth plate injuries, including fractures, was 1st described for humans in 1963 & has been widely accepted & applied in both human & vet med
  • classification groups physeal injuries into 1 of the original 5 types (or 4 additional types that are rare & have been added since)
  • this classification system is useful in communicating the nature of an injury & predicting prognosis
  • as the number associated with the type of injury increases, the prognosis for a return to a functional, straight, pain-free limb decreases
40
Q
A

I - (S) - straight across (separated or slipped)
II - (A) - above (or away from joint)
III - (L) - lower (into joint)
IV - (TE) - through everything (both/all)
V - (R) - rammed (crushed)

41
Q

What are capital femoral physeal fractures of Fe?

A
  • fracture through the physis of the head (caput) of the femur (ex of Salter-Harris type I fracture) is a surprisingly common lesion in Fe
  • some believe this condition is a traumatic fracture
  • most affected Fe are young (4-24 months), overweight, neutered males
  • histologically, the fractured physis is thickened w/ irregularly arranged chondrocytes, which gives rise to the term physeal dysplasia
  • pathogenesis of this condition is uncertain
  • however, there is some evidence that certain physes of Fe that are neutered before 6 months of age - males more common than females - remain open longer than sexually intact Fe
  • (the normal age at the time of closure of the proximal physis in Fe has reported to be about 9 months (or 270 days), w/ a range of 210 to 290 days)
  • this has led some to believe that early neutering delays the closure of the proximal femoral physis, may lead to physeal dysplasia &, as these Fe become stronger & heavier, predisposes these Fe to a “slipped” capital femoral physis
  • btwn 24% & 38% of affected Fe will develop bilateral fractures
42
Q

What are growth retardation lattices (GRLs)?

A
  • typically detected in aborted, stillborn, or neonatal animals
  • thin lines to wide bands of increased bone density (osteosclerosis) in the metaphyses, parallel to the physes (but can also be seen w/in epiphyses)
  • represent areas of impaired osteoclastic activity leading to the retention of LONGITUDINAL trabeculae of primary spongiosa
  • GRLs is a poor term b/c growth need not be retarded for the lattices to appear
  • THE LESION IS A FAILURE OF REMODELING
  • GRLs are a nonspecific change (are lesions that can be caused by a variety of insults)
  • a few known causes of GRLs include in utero infection of fetal calves w/ Bovine Viral Diarrhea (BVD) virus; canine distemper virus infection in growing puppies; & exposure to lead in any developing or growing animal
43
Q

What are growth arrest lines (GALs)?

A
  • are typically detected in young, growing animals
  • GALs are also linear lesions in the metaphysis parallel to the physis
  • however, they represent TRANSVERSE (vs. longitudinal) trabeculae of bone & are a result of a period of retarded or arrested longitudinal growth
  • layer or layers of transverse trabeculae are carried into the metaphysis if growth resumes
  • any debilitating disease of general malnutrition can retard growth & produce GALs
44
Q

What is the importance of recognizing GRLs & GALs?

A
  • these lesions are the consequence of a chronic, underlying disease condition, not an acute or spontaneous change
  • need to go looking for underlying cause (pneumonia, starvation, parasitism)
45
Q

What is premature closure of the physis?

A
  • closure may be partial (focal) or complete (diffuse)
  • if the closure is focal, it results in an altered shape of a growing bone
  • if the closure is complete, it results in abnormally short bones
  • trauma, vitamin A toxicity, manganese deficiency, & radiation injury known causes
  • there may be others
  • damage to epiphyseal vessels nourishing the proliferative zone of the physis can also cause localized physeal closure
  • feeding moldy cereal straw to pregnant cows has produced this lesion & a disease known as congenital spinal stenosis in western Canada
46
Q
  • What is osteochondrosis or osteochondritis?
A
  • THE FOCAL OR MULTIFOCAL FAILURE (OR DELAY) OF ENDOCHONDRAL OSSIFICATION RESULTING IN LOCALIZED THICKENING OF HYALINE CARTILAGE
  • may occur at the physeal or articular areas of endochondral ossification
  • pain & lameness may result b/c the retained cartilage is not as stable as bone & subject to injury
  • clinically, osteochondrosis or osteochondritis are terms used to ID a variety of manifestations & sequelae of the presence of the thickened cartilage
47
Q

What is the etiology of osteochondrosis?

A
  • there appears to be multiple & interrelated factors which are associated w/ osteochondrosis & the factors at play may depend on the sp & location of the lesion
  • genetic, hormonal, nutritional, metabolic, & mechanical factors are all thought to be involved
47
Q

What are some examples of osteochondrosis that are treated like specific diseases?

A

Some forms of osteochondrosis, in certain spp, & at certain locations, are treated like specific diseases:
- ununited anconeal process of Ca - is the failure of the anconeal process (a secondary center of ossification) to fuse w/ the ulna
- epiphysitis or physitis (more accurate) in Eq - is a clinical term, but an inaccurate pathologic diagnosis, for a generalized disease of young horses characterized by thickening & dysplasia of physes of certain long bones
- osteochondrosis of swine - was relatively common at one time but is now rare. when used in relation to Sw, osteochondrosis is a generalized condition that is most common & easily diagnosed around joints