Bone Edited (AH/LS) Flashcards
Edited in ref. to Muzzy's review and class notes. Reformatted to make more sense.
1
Q
Other names for Osteopetrosis
A
aka: Metaphyseal dyslasia, Marble bone dz.
2
Q
Spp. associated with Osteopetrosis?
A
Angus cattle = inherited
3
Q
Pathogenesis of Osteopetrosis?
A
Failure of osteoclasts to resorb the primary spongiosa –> accumulation of bony spicules in marrow spaces.**This can lead to Aplastic anemia ** TQ
4
Q
Other name for Congenital Cortical Hyperostosis?
A
Diaphyseal dysplasia
5
Q
Spp. associated with Congenital Cortical Hyperostosis?
A
Inherited in pigs
6
Q
Patho of Congenital Cortical Hyperostosis?
A
Periosteal bone formation on long bones. Deposition on radiating trebeculae –> increase in diameter.
7
Q
What other condition is associated with Congenital Cortical Hyperostosis?
A
Edema due to blockage of lymph
8
Q
Other names for Craniomandiblar Osteopathy?
A
Scottie jaw, lion jaw, westie jaw.
9
Q
Spp. associated with CMO?
A
Inheritied in west highland white terriers = dogs Usually appears @ 4-7 mo of age and regresses.
10
Q
Path of CMO?
A
Abnormal periosteal bone formation, irregular resorption –> irregular thickening of mandible/occipital/temporal bones. Tympanic bullae often severely affected.*
11
Q
Where is the primary lesion of Chondrodystrophy?
A
1* lesion in growth cartilage –> disproportionate dwarfism = short legs w/ normal-sized heads
12
Q
Types of Disproportionate Dwarfism?
A
Dexter type –> bulldog calves Telemark type.
Short headed type.
13
Q
Pathogenesis of Osteochondrosis?
A
Failure / delay of endochondral ossification of osteoid (bone matrix) = cartilage retention –> increase in cartilage width.
14
Q
Etiology of Osteochondrosis?
A
- Cu deficiencies induced by excess dietary Zn
- Increased Ca2+ intake
- Infarcts
- Idiopathic
(it can be 2* to anything that interferes with vascular invasion of cartilage. (infarct))
15
Q
Lesions of Osteochondrosis?
A
Multifocal and Focal
- Dyplasia = wedge shaped hyaline cartilage.
- Mineral debris and Hemorrhage at epiphysis
16
Q
Are lesions of Osteocondritis dessecans (OCD) focal or multifocal?
A
Non-Focal. Multifocal dysplasia only.
17
Q
Path of Osteochondritis Dessecans?
A
- Dysplasias at articular epiphyseal (AE) complex that form clefts in retained cartilage w/ subsequent fracture of overlying articular cartilage → cartilaginous or osteochondral flap
- If flap fractures off and floats free in joint → “joint mouse” → can interfere w/ mvmt of joint
18
Q
What is cervical verterbral myelopathy (CVM) also known as?
A
Wobbler syndrome
19
Q
What is cervical verterbral myelopathy (CVM) secondary to?
A
Compression/ irritation of the spinal chord.
20
Q
2 types of spinal chord compression?
A
Static or Dynamic (both lead to CVM)
21
Q
What animals are affected by static compression?
A
Horses 1-4yrs = Cervical static stenosis.
Dogs = cervical spondylomyelopathies.
22
Q
Where do horses get static compression? What does this cause?
A
C5-7. Hypertrophy of the ligamentum flavum
23
Q
What animals get Dynamic compression?
A
Horses 8-18mo = cervical vertebral instability
24
Q
Where do horses get Dynamic compression?
A
C3-5
25
With what is Dynamic compression associated?
Rapid growth. Genetic
26
what is another name for Hemivertebrae?
Butterfly vertebrae
27
Path of Hemivertebrae?
partial development of vertebrae --> compression of spinal chord.
28
In what spp. is Hemivertebrae desired?
Bulldogs, Pugs, Boston Terriers.
| corkscrew tail
29
Etiology of Growth Arrest Lines?
```
Viral (BVD, Canine distemper)
Lead Toxicit (lead line)
```
30
Pathogenesis of Osteoporosis?
Imbalance between absorption and formation.
| Increased resorption or decreased formation --> Atrophy.
31
Causes of Osteoporosis?
1. Deficiency of Ca → deficient Ca for mineralization
2. Malnutrition:
- Deficiency of protein, vitamin C, Cu → reduced bone formation.
- Lactational osteoporosis of young gilts → excess resorption.
3. Disuse: Physical inactivity and senility → excess resorption and decreased bone formation → disuse atrophy
4. Toxicity:
- Vitamin A toxicosis → decreased osteoblastic activity --> decreased bone formation.
- Adriamycin toxicity → depressed osteoblastic activity
- Fluoride toxicity → abnormal osteocytes
5. Hypercortisolism, prolonged steroid therapy
6. post-menopausal women
7. Sterility --> decreased activity, hormones and vit D metabolites.
32
3 Lesions of Osteoporosis?
Decreased bone mass + Increased bone spaces:
- Cortical bone → decreased thickness, high porosity
- Trabecular bone → decreased thickness with perforations
- Medullary cavity → ENLARGED
33
Pathogenesis of Rickets (Rachitic Rosary)
Failure of calcification of osteoid and cartilaginous matrices → bones become soft and swollen.
34
Causes of Rickets?
- Low vitamin D (most common) → Hypocalcemia --> deficient osteoid mineralization and 2* fibrous osteodystrophy
- Also low Ca and P
35
Pathogenesis of Osteomalacia?
- MATURE softening of bones after growth plate closure.
| - Unmineralized osteoid resistant to osteoclastic activity -->accumulates in bones fractures
36
3 Causes of Osteomalacia?
- Low Vit D → low Ca & P → high intestinal P absorption →lower Ca
- Chronic Renal Dz → low calcitriol → altered vit D metabolism → decreased vit D activity → decreased Ca absorption → decreased response to PTH → 2ry hyperparathyroidism
- Chronic Fluorosis
37
3 Lesions of Osteomalacia?
- Soft bones → limb deformities
- Accumulation of excess unmineralized osteoid and thin cortices
- Fractures
38
Fibrous Osteodystrophy is a form of _______.
Osteopenia
39
Other names for Fibrous Osteodystrophy?
```
Recklinghausen's Dz
Renal Rickets
Big Head
Bran Dz
Rubber jaw
Osteogenesis imperfecta
```
40
Pathogenesis of Fibrous Osteodystrophy?
- Abnormal bone quality
- Decrease in Ca2+ --> Excess resorption by osteoclasts --> replacement with fibrous connective tissue = secondary fibrosis.
41
Causes of Fibrous Osteodystrophy (Osteopenia)?
1. 2° Hyperparathyroidism (most common)
2. Nutrional:
- Ingestion of high Oxalate plants,
- HIGH P diets
- LOW Vit D3 diets
3. Renal → failure to eliminate P-Drug Induced (Adriamycin)--> osteoblastic activity
42
Pathogenesis of Vit A. Deficiency?
low A → abnormal intramembranous ossification w/ defective remodeling and reduced resorption of endosteal bone --> bone is laid down when resorption should be taking place
43
3 lesions of Vit. A Deficiency?
1. Small brain case
2. Increased ICP
3. Blindness (compression of optic canals)
44
Pathogenesis of Hypertrophic Osteodystrophy (HOD)? Who gets it?
METAPHYSEAL osteopathy
-Excess Ca / Vit D or Vit C def. -->Bilateral, Symmetrical inflammation of growth plates in long bones (Physitis) --> spontaneous recovery.
Common in: Young, growing large/giant breed DOGS
45
Pathogenesis of Hypertrophic (Pulmonary) Osteopathy (HOP/HPO)?
Not clear but...Incr. blood flow → Incr. arterial pressure & pulmonary lesions → periosteal growth in the dyaphyseal regions of the distal limbs --> Bilateral, symmetrical new bone formation
Megakaryocyte involvement?
46
Causes of HOP/HPO
- Rhabdomyosarcomas of Urinary Bladder → Dogs
| - Ovarian Neoplasms → Horses
47
CS of Acute Osteofluorosis?
- GI signs
| - CNS signs
48
2 CS of Chronic Osteofluorosis?
- Dental abnormalities
| - Osteodystrophy
49
Pathogenesis of Osteofluorosis?
F- BINDS Ca2+ → Ricket-like lesions
F- REPLACES hydroxl radical in Hydroxyapatite → abnormal osteoid
F- ACCUMULATES in periosteum --> thickened periosteum
50
Pathogenesis of Vit. A Toxicity?
Cats!
Excess Vit. A from liver consumption -->:
1. --> Decreased chondrocyte proliferations --> DESTRUCTION OF GROWTH PLATES.
2. -->Decreased osteoblasts --> OSTEOPEROSIS
3. --> Stimulation of periosteal osteoblasts --> osteophytes--> Cervical SPONDYLOSIS from periarticular osteophytes.
51
Excesses of which 2 vitamins cause an INCREASED activity of both Osteoblasts and Osteoclasts?
Vit. A & D
52
Pathogenesis of Vit. D. Toxicosis?
Acute: Massive Vit. D exposure --> excessive intestinal Ca2+ absorption→ widespread mineralization.
Chronic: Persistant vit D exposure -->
1. Decreased PTH, increased Calcitonin --> stops bone resportion --> Osteosclerosis (hard/stiffening)
2. Direct stimulation of osteoblasts --> increased formation
53
What affect does Calcitonin have on osteoclasts?
SUPPRESSES osteoclasts
54
Pathogenesis of Lead Posioning?
DECREASED OSTEOCLASTS
| → decr. trabecular remodeling →retention of primary trabeculae (spicules)--> increased bone density.
55
Histologic Lesion of Lead Posioning?
- Acid-fast inclusion bodies in osteoclasts & renal epithelial cells
- "Lead line"
- Increased tissue Pb
56
Lesions of Necrosis (Osteosis)?
Gross: soft, discolored bones Histo: Empty lacunae with resorption occuring
57
Sequelea of Osteosis?
Resportion → inflammation → Exostosis or scar
| No resorption → Sequestrum and involucrum (collar of reactive bone around sequestrum)
58
Legg-Calve-Perthes Dz refers to what?
ASEPTIC necrosis of the femoral head --> DJD
59
Pathogenesis of Ischemic Necrosis
Decreased VENOUS outflow from bone --> increased BM pressure --> Empty lacunae
60
3 Routes of Infection for Osteitis/Osteomyelitis?
1. Hematogenous → omphalophlebitis (navel ill, joint ill), and swine spondylitis
2. Local Extension
3. Penetration
61
Term for Destruction Inflammation of Bone?
Osteolytic
62
Term for Productive Inflammation of Bone?
Sclerotic
63
Causes of Osteitis/Osteomyelitis in order of prevalance?
BacT > mycotic > viral > parasitic
64
Osteitis is inflammation of _______.
Bone
65
Osteomyelitis is inflammation of _______ & _____ _______.
bone and medullary cavity
66
Spondylitis is inflammation of the _____ ______.
Vertebral body
67
3 List the causes of Suppurative Inflammation?
Brucella → Swine spondylitis
A. pyogens → vertebral abscesses
R. equi → foals
68
2 Causes of Granulomatous Inflammation?
1. A. bovis → lumpy jaw, mandibular osteomyelitis
| 2. Mycotic osteomyelitis
69
3 Lesions of Osteomyelitis?
1. Purulent exudate → medullary cavity
2. Thrombosis/infarct
3. Bone resorption
70
Sequelae of Osteomyelitis?(8)
- Exudate
- Extension to adjacent bone
- Hematogenous spread
- Pathological FX
- Sequestration
- Fistulae
- Vertebral osteomyelitis
- Lysis of articular cartilage
71
Most common primary neoplasm of bone in Dogs & Cats?
Osteosarcoma AKA Osteogenic sarcoma
72
Where is the common site for Osteosarcoma to occur?
Metaphysis
73
3 Classifications of Osteosarcoma & location affected?
1. Simple → bone
2. Compound → bone & cartilage
3. Pleomorphic → anaplastic w/ only small islands of osteoid
74
Classification of Osteosarcoma?
- Cell type & activity
- Radiographic appearance
- Origin
75
Lesions of Osteosarcoma?
- Grey-white masses →
- hemorrhage & necrosis
- Reactive bone
- Pleomorphism
- Agressive w/ Pulmonary metastasis
76
8 responses of Joints to injury?
- Fibrillation
- Eburnation
- Joint mice
- Osteophytosis
- Villous hyperplasia of synovial membrane
- Pannus
- Capsular fibrosis
- Ankylosis
77
5 responses of Bone to Injury?
- Disruption of endochondrial ossification
- Bone modeling
- Altered mass
- Rapidily deposited bone
- Injured periosteum
78
What DZ is associated with pink teeth & disorganization of d
Osteogenesis imperfecta
79
Term for Chondrodysplasia in Suffolk/Hampshire lambs?
"Spider lamb"
80
Pathogenesis of Osteochondrosis dissecans (OCD/OD)?
DYSPLASIA @ AE complex → weak, retained cartilage → FX →cartilaginous or osteochondral flap
81
Lesions of OCD?
- Joint mouse/mice
| - Interference w/ joint movement
82
Sequelae of OCD?
- DJD
- Ulcercation/exopsure of subchondrial bone
- Lameness
83
Common locations of OCD (by animal)?
- Dog → humeral head
| - Horse → ant. aspect of intermediate ridge of distal tibia -Pigs → distal humerus
84
What is the only form of Osteochondrosis that Cats get?
Epiphysiolysis
85
Which animal can get Osteoporosis during lactation?
Gilts(young pigs)
86
Osteoporosis is abnormal ______ of normal bone.
QUANTITY
87
Rickets is due to abnormal ______ of bone.
QUALITY
88
Dogs & Cats get Fibrous Osteodystrophy most commonly due to
Renal dz.
89
Which 3 animals get Fibrous Osteodystrophy from improper nut
* Horses
* Reptiles
* Captive primates
90
Tell me about K9 Eosinophilic Panosteosteitis!
* young Male GSD
