bones n joints

Question 1

altered bone consistency

2 dz

Answer 1

rickets

osteomylasia

Question 2

thyroidectomy result in

Answer 2

hypothyroidism causing

1. dry skin
2. alopecia
3. cataracts
4. tetany

Question 3

what causes primary hyperpyrathoidism

Answer 3

mostly adenomas→ increased pth→ osteoclastic bone resoption

Question 4

• 1° hyperparathyroidism lesions

Answer 4

hypercalcemia

» renal stones

» renal destruction and hypertension

» fibrous osteodystrophy

Question 5

2° hyperparathyroidism

1. how is the level of ca
2. what causes those levels of ca

Answer 5

1. low
2. chronic renal dz, nutritional imbalances eg. rickets, inadecuate vit d3, all bran diets, poor quality rouphages

Question 6

lesions of 2° hyperparathyroidism

Answer 6

hypocalcemia –> increased mobilization
from bone –> fibrous osteodystrophy

Question 7

fxns of calcitonin

Answer 7

think about ca abandance

decrease plasma calcium and phosphate levels

decrease the permeability of osteoblasts

decrease the activity of osteoclasts (think about ca abandanc

increases water and electrolyte secretion in the urine

Question 8

in state of high ca,which hormones helps secrete Ca

Answer 8

gastrin

» glucagon

» dopamine

» ß adrenergic agonists

_absence of calcitonin, or chronic excess produced
by tumours, do not disturb calcium levels_

Question 9

– Growth hormone effect on ca

Answer 9

increases urinary calcium excretion and intestinal
absorption, with a net gain

• increased rate of turnover assists in bone growth

Question 10

Glucocorticoids effect on ca

Answer 10

• ecreases plasma calcium and phosphate levels by
reducing absorption by an anti-vitamin D action
and increasing urinary excretion

• long term effect ⇒osteoporosis

Question 11

hyperthyroidism effect on ca

Answer 11

– hypercalcemia,

hypercalciuria (excess Ca excretion) and

osteoporosis

Question 12

estrogen effect on ca

Answer 12

• inhibit the action of PTH on bone

decreased estrogen levels –> senile osteoporosis

Question 13

osteopenia

Answer 13

loss of skeletal mass (too “little bone”)

Question 14

Intramembranous (appositional) ossification

Answer 14

flat bones

periosteal surfaces of long bone

Question 15

Endochondral ossification

Answer 15

bones with growth plates (long bones, etc.)

Question 16

what kind of lesion do u find in hypertrophic osteodystrophy

Answer 16

metaphyseal lesion

Question 17

Thickened and irregular epiphyseal cartilage is found in

Answer 17

rickets

Question 18

, hyperparathyroidism lesion on bones

Answer 18

• fibrous osteodystrophy

Question 19

chronic renal disease result in which endocrine abnormality

Answer 19

2° hyperparathyroidism and osseous lesions

Question 20

displacement of bone marrow tissue can be due to

Answer 20

• fibrous tissue
• malignant neoplasm
• myelophthisic anemia

Question 21

Disorders of bone resorption

Answer 21

ostreopetrosis

Question 22

Disorders of bone formation

Answer 22

• Osteogenesis imperfecta

Question 23

Disorders of bone modeling

Answer 23

Congenital cortical hyperostosis

• Craniomandibular osteopathy

Question 24

Disorders of endochondral ossification

Answer 24

Chondrodystrophies

• Osteochondrosis
• Osteochondrosis dissecans (OCD)
• Epiphysiolysis

Cervical vertebral myelopathies

Question 25

Osteopetrosis

Answer 25

– petros = rock – “marble bone disease

Question 26

**_Osteopetrosis (metaphyseal dysplasia)_** 1. inherited or acquired 2. mechanism 3. bone density

Answer 26

1. inherited 2. failure of the osteoclast to resorb the primary spongiosa →spicules of bone with central cores of calcified cartilage fill the medullary cavity 3. osteosclerosis (increased bone density/unit area)

Question 27

**osteopetrosis sequela**

Answer 27

defective osteoclasts fail to reabsorb and remodel the fetal bone (1° spongiosa) or 2° spongiosa – spongiosa persist into the diaphysis – failure in resorption results in ↑ bone density – concurrent reduction of medullary spaces » spicules of bone fill the medullary cavity » aplastic anemia

Question 28

**Osteopetrosis (petros = rock); “marble bone disease” Lesions**

Answer 28

bones are dense and thick (diffusely solid) – small or no medullary cavity marrow spaces increased bone mass – excess amounts of bone due to failure of normal osteoclastic activity

Question 29

Osteopetrosis (petros = rock); “marble bone disease” Lesions in affected Angus calves

Answer 29

stillborn – brachygnathia inferior (shortened mandible) – impacted molar teeth – deformed cranial vaults \>\> compress the brain • pathological fractures

Question 30

stillborn – brachygnathia inferior (shortened mandible) – impacted molar teeth – deformed cranial vaults \>\> compress the brain • pathological fractures are all lesions of

Answer 30

osteopetrosis in angus calves

Question 31

Osteopetrosis (metaphyseal dysplasia) lesions

Answer 31

1. bones are enlarged 2. no meulary cavity 3. susceptible to fracture

Question 32

**_Osteogenesis imperfecta_** 1. type of dz 2. animals affected 3. organs involved 4. cs

Answer 32

1. osteopenic disease – **reduced bone mass disease** 2. calves, lambs, puppies 3. involves bone, dentin, tendons, and sclera 4. **multiple fractures, joint laxity, and defective dentin**

Question 33

Osteogenesis imperfecta pathogenesis

Answer 33

defect in osteoblastic and/or odontoblastic production of type I collagen • decreased synthesis of osteonectin

Question 34

Osteogenesis imperfecta etiopathogenesis:

Answer 34

failure of normal osteoblastic activity and mineralization reduced bone production decrease concentrations of type I collagen and osteonectin (which is involved in mineralization of osteoid) extreme osteopenia with normal growth plates but no bone deposition

Question 35

Osteogenesis imperfecta 1. effect on growth plates 2. trabecular bone 3. fibrous tissue?

Answer 35

1. growth plates unsaffected 2. less trabecular bone than normal 3. no evidence of osteoclasis or proliferation of fibrous tissue

Question 36

teeth can be **_pink_** due to visibility of the dental pulp through the thin crown 1. name dz

Answer 36

Osteogenesis imperfecta

Question 37

Osteogenesis imperfecta histological lesions

Answer 37

dental tubules are short, tortuous, and sometimes absent • disorganization of the dentin is diagnostic of osteogenesis imperfecta because at birth, bones can be structurally normal

Question 38

**Congenital cortical hyperostosis** synonym: diaphyseal dysplasia 1. spp 2. lesion

Answer 38

1. inherited disease of newborn pigs autosomal recessive 2. **disorganization of the perichondrial ossification groove---\>chondrogenic membrane around the growth plate** * _new periosteal bone formation on major long bones of the limbs and edema (blocked lymphatic drainage?)_ * normal joints

Question 39

Congenital cortical hyperostosis 1. effect on growth plates 2. lesions

Answer 39

1. growth plates expand in diameter 2. very thick, swollen, hard, rigid bones 3. stillbirths or early neonatal death because of other defects 4. 5. starvation, cardiac insufficiency

Question 40

growth plates expand in diameter very thick,,swollen, hard rigid bones

Answer 40

Congenital cortical hyperostosis

Question 41

** Craniomandibular osteopathy (CMO)** 1. animal affected 2. cause

Answer 41

1. \* West Highland white or Scottish terrier dogs \* "westie jaw"; "scottie jaw"; "lion jaw 2. idiopathic, autosomal recessive

Question 42

**Craniomandibular osteopathy (CMO)** 1. pathogenesis

Answer 42

**_new periosteal bone formation and irregular resorption_** \>\> irregular thickening of bones  bilaterally symmetrical  mandibular, occipital and temporal bones  tympanic bullae (often severely affected)  limbs (less commonly)  4 to 7 months of age  painful mastication  atrophy of associated musculature  self-limiting

Question 43

**Chondrodystrophies (nutritional)** 1. location of the lesion 2. types n spp affected

Answer 43

1. 1° primary lesions in growth cartilage \* physis, articular epiphyseal [AE] complex and epiphyseal cartilage) **\*_epiphyseal dysplasias_** • spider lamb in Suffolk and Hampshire sheep ** \*_metaphyseal dysplasias_** • chondrodysplasia in the Alaskan malamute, Norwegian elkhound, and Great Pyrenees breeds

Question 44

clinicasl apperarance of Chondrodystrophies

Answer 44

disproportionate dwarfism – short-legged with normal-sized heads

Question 45

Chondrodystrophies – types described in cattle: **• Dexter type**

Answer 45

Dexter “bulldog”calves

Question 46

**Telemark type of Chondrodystrophies**

Answer 46

dome-shaped heads, brachygnathia, cleft palate, protruded tongue, short neck, and short limbs

Question 47

**Short-headed types of Chondrodystrophies**

Answer 47

– short-headed dwarf, long-headed dwarf, compact and/or compressed form

Question 48

Osteochondrosis

Answer 48

heterogenous group of lesions in growth cartilage of young animals

Question 49

1. lesion of Osteochondrosis 2. hallmark of the gross lesions

Answer 49

**focal or multifocal failure (or delay) of endochondral ****ossification** ``` – involves the metaphyseal growth plate (physis) and the AE (articular epiphyseal) complex ``` focal or multifocal retention of growth cartilage due to its failure to become mineralized and replaced by bone (failure of endochondral ossification)

Question 50

Osteochondrosis Etiology

Answer 50

idiopathic? • high incidence in species bred and fed to achieve maximal body weight at a young age – mechanical complication + defects of endochondral ossification • Cu deficiency induced by excess dietary Zn – lysis of the AE complex and formation of thin flaps of cartilage in thoroughbred suckling foals greater incidence in growing dogs fed highcalcium diets

Question 51

**Osteochondrosis lesions cont..**

Answer 51

## Footnote **dysplasia** – well demarcated wedge of white, firm hyaline cartilage at the AE complex or physis **• stages of resolution or 2° necrosis** • **bonehemorrhage and mineralized debris in the adjacent**

Question 52

well demarcated wedge of white, firm hyaline cartilage at the AE complex or physis

Answer 52

Osteochondrosis Lesion

Question 53

Osteochondrosis • common sites

Answer 53

distal femurs of pigs – distal femur, distal tibia, and vertebral articular facets of horses proximal humerus of dogs proximal tibia of rapidly growing birds

Question 54

Osteochondrosis sequelae

Answer 54

progression * resolution by endochondral ossification * necrosis and cystic cavitation

Question 55

Osteochondritis dissecans (OCD) 1. lesion 2. location of the lesion

Answer 55

## Footnote dysplasias at the AE complex formation of clefts in the retained cartilage + fracture of the overlying articular cartilage » cartilaginous or osteochondral flap

Question 56

WHATS THIS

Answer 56

cartilaginous flap in OCD

Question 57

“joint mouse”: free in the joint space

Answer 57

Osteochondritis dissecans (OCD) fracture of thes flap interfere with mechanical movement of thejoint

Question 58

Osteochondritis dissecans (OCD) – common sites of OCD 1. dogs 2. horses 3. pigs

Answer 58

humeral head (dog) ``` • anterior aspect of the intermediate ridge of the distal tibia (horses) ``` • distal humerus (pigs)

Question 59

Osteochondritis dissecans (OCD) Sequelae

Answer 59

degenerative joint disease * ulceration and exposure of subchondral bone * lameness

Question 60

Epiphysiolysis

Answer 60

separation of epiphysis from the metaphysis because of fissure formation horizontally through the physis – not associated with focal or multifocal dysplasia (as in osteochondroses) • other than that seen in foal with zinc toxicity

Question 61

Epiphysiolysis most common in

Answer 61

pigs (femoral head) • dogs (anconeal process of the ulna) – is the only form of osteochondrosis in cats

Question 62

the only form of osteochondrosis in cats

Answer 62

Epiphysiolysis

Question 63

Epiphysiolysis lesion

Answer 63

horizontal fissure/fracture through the physis + complete or partial separation of the epiphysis from the metaphysis

Question 64

Cervical vertebral myelopathy (CVM) 1. define 2. causes

Answer 64

2° to static or dynamic compression on the spinal cord by abnormal cervical vertebrae • compression constantly due to: – absolute stenosis of the canal (static compression) or – intermittently during movement [flexion] (dynamic compression)

Question 65

Cervical vertebral myelopathy (CVM) 1. other names 2. types

Answer 65

1. wobbler syndrone 2. **static** – malformation of vertebrae – osteochondrosis **• instability/laxity** – increased mobility of cervical vertebral joint » associated with rapid growth

Question 66

Specific examples 0f cervical vertebral myopathy 1. in dog 2. horse

Answer 66

Cervical vertebral stenotic myelopathy (horses) Cervical spondylomyelopathies (dogs)

Question 67

Cervical vertebral stenotic myelopathy (horses) 1. CS

Answer 67

**incoordination, abnormal locomotion** * compression of spinal cord, ataxia * narrowing of vertebral canal, myelomalacia

Question 68

2 SYNDROMES OF– Cervical vertebral stenotic myelopathy (horses)

Answer 68

Cervical static stenosis • Cervical vertebral instability

Question 69

_Cervical static stenosis_ 1. SPP + AGE AFFECTECTED 2. LESIONS 3. WHICH AREA OF VETERBRAL CANAL IS AFFECTED

Answer 69

1. • older horses (1-4 years) 2. hypertrophy of ligamentum flavum • dorsal narrowing of vertebral canal @ C5 -C7 3. compressive myelomalacia 4. • fibrillation, eburnation, osteophytes • inherited, nutrition, environment, vertebral malformation, articular subluxation

Question 70

** Cervical vertebral instability** 1. spp+age 2. lesions

Answer 70

• young horses (8-18 months) • rapid growth, genetic • instability @ C3 -C5 • **fibrillation, eburnation, osteophytosis** • narrowed vertebral canal \> compression of spinal cord

Question 71

1. dz 2. lesions

Answer 71

Cervical vertebral stenotic myelopathy; horses; narrowed spinal canal, compression of spinal cord, myelomalacia

Question 72

Cervical spondylomyelopathies – Wobbler syndrome in dogs

Answer 72

cervical spondylopathy Dobermans, Great Danes, large breed dogs abnormality in cervical vertebrae C6 -C7 – compressive myelomalacia \>\> abnormal gait

Question 73

lordosis

Answer 73

ventral curvature or deviation of the spine

Question 74

kyphosis

Answer 74

dorsal curvature or deviation of the spine (hump-backed)

Question 75

**scoliosis**

Answer 75

a lateral deviation of the spine

Question 76

kyphoscoliosis

Answer 76

abnormal dorsolateral curvature of the spine

Question 77

absence of the dorsal portion of the vertebrae

Answer 77

Spina bifida various forms – based on the severity of the condition • seen most frequently in Manx cats

Question 78

Hemivertebrae • partial development of vertebrae; half vertebrae • clinically

Answer 78

silent or – compression of the spinal cord

Question 79

Duplicated limbs

Answer 79

» polymyelia

Question 80

sheep with long, thin, angular legs

Answer 80

"Spider lamb" chondrodysplasia abnormalities in many ossification centers » small heads, scoliosis, sternal deformity, kyphosis, etc.

Question 81

**cleft palate, harelip, brachygnathia, syndactyly**

Answer 81

Veratrum californicum (skunk cabbage) toxicosis

Question 82

virus that causes Growth arrest of long bones: growth retardation lattice

Answer 82

BVD, CANINE DISTEMPER also lead

Question 83

**Chondrodysplasias**

Answer 83

characterized by disproportionate body growth – usually involves abnormal endochondral bone growth • abnormal development of epiphyseal, articular and basocranial cartilages – intramembranous bone growth is normal – Angus, Hereford – Alaskan malamutes

Question 84

Chondrodysplasias lesions

Answer 84

## Footnote **• limbs** – short, abducted, very thick • **epiphyses** – enlarged and mushroom shaped due to arrested endochondral growth • cranial base and vertebral column extremely short

Question 85

cranium lesions in chondrodysplasias

Answer 85

enlarged and dome-shaped cranium – hydrocephalus

Question 86

Dexter 'bulldog' calf: homozygous (d/d) state lesions

Answer 86

retardation of chondral growth shortening of all endochondrally formed bones and the cranial base dome-shaped head brachygnathia protruded tongue short neck short limbs

Question 87

Chondrodysplasia of cattle – Telemark type (Telemark cattle) 1. breed

Answer 87

**• Norwegian breed** • autosomal recessive gene – heterozygous parents are phenotypically normal • affected calves – born alive but die shortly thereafter

Question 88

Telemark type (Telemark cattle) cs

Answer 88

• dwarf calves – dome-shaped heads – brachygnathia – cleft palate – protruded tongue – short neck – short limbs

Question 89

Chondrodysplasia of cattle Short-headed type 3 forms

Answer 89

brachycephalic dolichocephalic compact and/or compressed

Question 90

Chondrodysplasia of cattle – Short-headed type • **brachycephalic form (short-headed dwarf) lesions**

Answer 90

## Footnote -extremely short and broad head – forehead bulges – jaws are shortened » mandible is slightly longer than the maxilla – eyes are protruded and displaced laterally – vertebrae are compressed longitudinally

Question 91

Chondrodysplasia of cattle – Short-headed type • **brachycephalic form (short-headed dwarf)**

Answer 91

premature synostosis (fusion of bones) of the basocranial synchondrosis (where the connecting medium is hyaline) – cerebellum is compressed – rounded heart

Question 92

Chondrodysplasia of cattle – Short-headed type **• dolichocephalic form (long-headed dwarf)** size n shape of head

Answer 92

extreme elongation of the head in proportion to the whole body » elongated head tapers to a fine muzzle – unthrifty – slow growth – slightly larger than the brachycephalic form

Question 93

Chondrodysplasia of cattle – Short-headed type • compact and/or compressed forms

Answer 93

phenotypically normal individuals – proportionately reduced body size (primordial dwarfism) – selection for this type of dwarfism is responsible for the wide dissemination of the genes for chondrodysplasia

Question 94

Chondrodysplasias of dogs types:

Answer 94

Chondrodysplasias of dogs – inherited – several types: pseudoachondroplastic dysplasia in poodles * multiple epiphyseal dysplasia in beagles * chondrodysplasia in Alaskan malamutes * chondrodysplasia in Norwegian elkhounds

Question 95

Dyschondroplasia Pathogenesis

Answer 95

abnormal direction of cartilage growth ↓ • cartilage mass covering osseous stalk

Question 96

Dyschondroplasia Types

Answer 96

\*Ecchondroses * Enchondroses * Tibial dyschondroplasia

Question 97

Dyschondroplasia – Types **• Ecchondroses**

Answer 97

Syn.: osteochondromatosis, osteochondromas, multiple cartilaginous exostoses • dog, horse • multiple bony/cartilaginous nodules on periosteal surface over physes • tumor or dysplasia ?

Question 98

Multiple cartilaginous exostoses

Answer 98

eccentric masses projecting from bony surfaces (long bones, ribs, vertebrae, scapula, pelvic bones) • **cartilaginous cap covering the proliferative bone**

Question 99

Multiple cartilaginous exostoses clinical importance

Answer 99

mechanical interference with action of tendons/ligaments space-occupying masses \>\> spinal compression malignant transformation to chondrosarcomas

Question 100

Dyschondroplasia – Types **• Enchondroses**

Answer 100

cartilaginous masses on endosteal surface

Question 101

Dyschondroplasia – Types **• Tibial dyschondroplasia**

Answer 101

**chickens** – physeal cartilage retained into metaphysis and diaphysis – a form of osteochondritis dissecans (OCD)

Question 102

Osteoporosis etiopathogenesis:

Answer 102

reduced production of bone • failure of normal osteoblastic activity • increased removal of previously formed bone • due to excess stimulation of osteoclasts by excess parathyroid hormone production (1° or 2° hyperparathyroidism)

Question 103

Osteoporosis – etiology:

Answer 103

* calcium deficiency * malnutrition * disuse * toxicity

Question 104

Osteoporosis – etiology: **• calcium deficiency --\>process**

Answer 104

hypocalcemia ---\>increased output of PTH ---\> increased bone resorption

Question 105

Osteoporosis – etiology: • **physical inactivity (disuse osteoporosis)**

Answer 105

increased bone resorption decreased bone formation » mediated through changes in piezoelectrical activity and stretch receptors

Question 106

Osteoporosis – etiology: **• toxicity**

Answer 106

**vitamin A** » ↓ osteoblastic activity \> ↓ bone formation **– adriamycin** » ↓ osteoblastic activity **– Fluoride** » abnormal osteocytes

Question 107

vit.A toxicity on bones

Answer 107

decreased osteoblastic activity--\>decreased bone formation

Question 108

adriamycin toxicity

Answer 108

causes reduced osteoblastic activity hence osteoporosis

Question 109

fluoride toxicity

Answer 109

abnormal osteocytes

Question 110

lesions of postmenopausal osteoporosis in women

Answer 110

vertebral deformity or collapse –pathologic fractures of the femoral neck

Question 111

• administration of glucocorticoids 1. bone dz 2. lesions 3. mechanism

Answer 111

**Osteoporosis** decrease rate at which bone is formed decreases amount of bone produced interfere with differentiation to osteoblasts

Question 112

Osteoporosis – etiology: **• senility**

Answer 112

– decreased activity – decreased sex steroid hormones decreased formation of vitamin D metabolites – ecreased responsiveness to vitamin D metabolites

Question 113

what hapens to the medullary cavity in osteoperosis

Answer 113

enlarged due to endosteal resorption and removal of metaphyseal cancellous bone

Question 114

disease of immature bone  characterized by failure of mineralization, with subsequent bone deformities and fractures  disease of bone and cartilage undergoing endochondral ossification

Answer 114

rickets

Question 115

main causes of rickets

Answer 115

**hypovitaminosis d**  also, deficiency of calcium and phosphorus  dietary  malabsorption  renal disease

Question 116

growth plates: thickened and irregular  “rachitic rosary”

Answer 116

**rickets due to failure of epiphyseal cartilage to mineraluse** as a consequence chondrocytes in the growth plates fail to degenerate \> **retention of cartilage matrix** capillaries from the metaphysis are unable to penetrate the cartilage

Question 117

Rickets basic lesions on bones

Answer 117

## Footnote excessive production of osteoid which fails to mineralise  resistant to normal remodelling via osteoclasts  soft and deformed

Question 118

 Rickets lesions:

Answer 118

failure of endochondral ossification  thickened physes  flared metaphyses due to excess unmineralized osteoid  wide seams of osteoid on bone-forming surfaces  hypocalcemia --\> 2° fibrous osteodystrophy  bones: soft, deformed, fracture easily

Question 119

Osteomalacia (softening of bones) 1. old or new bone 2. characteristic

Answer 119

disease of **mature skeleton**  characterized by **failure of mineralizatio**n with subsequent bone deformities and fractures  accumulation of **excess unmineralized osteoid**  disease only of bone in adults after endochondral bone growth has ceased

Question 120

Osteomalacia (softening of bones) etiology

Answer 120

 deficiency of vitamin D or phosphorus (most commonly)  chronic renal disease  chronic fluorosis

Question 121

Osteomalacia (softening of bones) hypophosphatemia

Answer 121

 stimulates renal production of calcitriol (active D3)  which increases intestinal absorption of phosphorus by a PTH-independent mechanism and  **provokes osteoclastic resorption of bone**  both bone resorption and hypophosphatemia tend to **increase plasma ionized Ca2**+ thus  suppressing PTH release and decreasing renal excretion of phosphorus

Question 122

Osteomalacia (softening of bones)  chronic renal disease

Answer 122

decreased renal mass or phosphate retention causes:  altered vitamin D metabolism  decreased synthesis of 1,25 (OH)2 D3  diminished intestinal absorption of calcium  decreased calcemic response of the skeleton to PTH  impaired suppression of PTH secretion for any increase in serum calcium level  altered collagen synthesis

Question 123

Osteomalacia (softening of bones) in chronic fluorosis

Answer 123

fluoride ions replace hydroxyl radicals in the apatite crystal resulting in abnormal osteoid  defective and irregularly mineralized

Question 124

Osteomalacia lesions

Answer 124

similar to rickets except that physeal cartilage and associated lesions are not present in the adult skeleton  wide seams of unmineralized osteoid  marrow cavity enlarged with extension into epiphysis  cortex is thin, spongy, and soft  bone pain  pathologic fractures  deformities:  kyphosis, scoliosis, or both

Question 125

Fibrous osteodystrophy

Answer 125

 widespread increased osteoclastic resorption of bone and replacement by fibrous tissue eg rubber jaw

Question 126

examples of Fibrous osteodystrophy dz

Answer 126

1. rubber jaw 2. osteogenesis impefecta 3. big head dz 4. ostitis fibrosa cystica 5. von Recklinghausen‟s disease 6. bran dz 7. renal rickets 8. ”, Simian bone disease

Question 127

Fibrous osteodystrophy Etiology:

Answer 127

** deficiency of Ca and vitamin D**  high dietary Ca:P ratio  severe renal disease  ingestion of high oxalate plants (bind Ca) \>\> excess osteoclastic resorption of bone in response to PTH due to low blood [Ca] \>\> deposition of fibrous connective tissue

Question 128

Fibrous osteodystrophy due to hyperparathyroidism

Answer 128

**primary**  parathyroid adenoma, carcinoma, or hyperplasia  rare in domestic animals ** secondary**  more common  nutritional  renal (renal osteodystrophy)

Question 129

nutritional hyperparathyroidism  **factors that tend to decrease the concentration of serum ionized calcium and to increase the output of PTH**

Answer 129

 diets deficient in calcium  diets high in phosphorus (interfere with the intestinal absorption of calcium)  unsupplemented cereal grain rations fed to swine  all-meat diets fed to dogs and cats  horses on high-grain/poor quality roughage or all-bran diets

Question 130

nutritional hyperparathyroidism in young cats and dogs

Answer 130

meat diets high in phosphorus and low in calcium

Question 131

 in horses ("bran disease"; "Miller's disease")

Answer 131

hypertparahyroidism  diets with excessive phosphorus in proportion to calcium

Question 132

fibrous osteopathy in monkeys

Answer 132

 deficiency of vitamin D3  lack of exposure to UV radiation or sunshine

Question 133

Renal osteodystrophy

Answer 133

skeletal lesions 2° to chronic, severe renal disease; **common in dogs** ** pathogenesis:**  renal disease  loss of glomerular function  inability to excrete phosphate  inadequate production of 1,25- dihydroxyvitamin D3 by the kidneys  uremic acidosis  phosphate retention due to decreased secretion → hyperphosphatemia

Question 134

Renal osteodystrophy pathogenesis ** calcium and phosphorus product exceeds solubility**

Answer 134

 precipitation of calcium in soft tissue  hypocalcemia → increased PTH output  increased bone resorption → fibrous osteodystrophy

Question 135

 Renal osteodystrophy pathogenesis ## Footnote **acidosis of uremia**

Answer 135

reduced production of 1,25-dihydroxyvitamin D3 by the kidneys  impaired mineralization → osteomalacia

Question 136

bone pain--\>lameness loss of teeth deformity of the maxilla or mandible due to loss of bone and replacement by fibrous tissue

Answer 136

renal osteodystrophy lesions

Question 137

fxn of vitamin C in bone formation

Answer 137

required for the hydroxylation of proline and lysine  promotes cell differentiation  facilitates the production of osteoblasts from progenitors  facilitates hypertrophy of chondrocytes | (essential to the formation of collagen)

Question 138

which animals lack the absobic enzyme

Answer 138

primates and guinea pigs lack the hepatic enzyme

Question 139

Hypovitaminosis C  pathogenesis:

Answer 139

reduction or failure in the secretion and deposition of collagen →production of faulty fragile collagen  faulty osteoblast function  production of unstable bone matrix

Question 140

CS of Hypovitaminosis C in pigs

Answer 140

 normal at birth  2-3 weeks post weaning loss of condition reluctant to stand or move develop swellings around the joints

Question 141

 Fracture repair stages

Answer 141

 **inflammatory phase** hematoma  **repair phase** temporary callus granulation tissue bony callus ** remodelling phase** resorption and replacement

Question 142

Fracture repair  Factors affecting healing

Answer 142

 age  nutritional, metabolic hormonal influences  infection  stability  vascular supply

Question 143

Osteosis (necrosis of bone) lesions

Answer 143

cortical bone: **dry, chalky appearance** – periosteum can be easily removed – **_yellow-white or pale_** areas of infarction surrounded by a zone of hemorrhage – cell death and loss of osteocytes from their lacunae – softening, discoloration – empty lacunae, resorption

Question 144

sequestrum

Answer 144

a piece of necrotic bone isolated from the remaining viable bone **• pale, chalky**

Question 145

Osteosis  pathogenesis of sequestration:

Answer 145

infection into a comminuted fracture directly or hematogenously  pathologic fracture with fragmentation in a focus of established osteitis  separation of portions of necrotic bone from adjacent viable tissue following osteomyelitis

Question 146

Osteosis (necrosis of bone)  significance of sequestration

Answer 146

cannot be resorbed by osteoclasts dissolution and/or discharge in exudate large ones require surgical removal  formation of involucrum sequestrum surrounded by reactive bone  fistulation of the involucrum  reversal of the process if infection is eliminated  persistence --\> interference with repair

Question 147

Osteosis (necrosis of bone)  definitions: – 

Answer 147

a dense collar of reactive bone surrounding a sequestrum involucrum

Question 148

Osteosis (necrosis of bone)  definitions: – exostosis (osteophyte)

Answer 148

nodular, benign, bony growth ± cartilage • projects outward from the surface of a bone

Question 149

bony growth within the medullary cavity

Answer 149

Osteosis (necrosis of bone) : **– enostosis** origin: cortical-endosteal surface (usually) • obliteration of the marrow cavity

Question 150

increased dimension of bone

Answer 150

**hyperostosis** uniform growth on the periosteal surface

Question 151

osteophyte at the insertionof a ligamentor tendon

Answer 151

enthesophyte

Question 152

new (reactive), excessive bone formation also occurs in

Answer 152

– fracture repair – chronic osteomyelitis – degenerative joint disease (DJD) as periarticular osteophytes

Question 153

Legg-Calvé-Perthe’s disease is wat type of bone dz 1. which animals are affecte 2. lesions

Answer 153

Osteosis (necrosis of bone) young, small, and miniature breed dogs • necrosis of femoral head

Question 154

– Legg-Calvé-Perthe’s disease pathogenesis

Answer 154

**: trauma, inflammation, swelling** – venous compression ↓ – ischemia \>\> infarction ↓ – resorption of necrostic subchondral bone ↓ – collapse of the articular cartilage

Question 155

 bone inflamation

Answer 155

osteitis

Question 156

periosteum inflamation

Answer 156

periostitis

Question 157

bone and medullary cavity (marrow) inflamation

Answer 157

osteomyelitis

Question 158

vertebral body inflamation

Answer 158

\> spondylitis

Question 159

physis/epiphysis inflamation

Answer 159

epiphysitis

Question 160

suppurative Inflammation of bone causes

Answer 160

Hematogenous osteomyelitis

Question 161

\*Mandibular osteomyelitis and periostitis (cattle) and \*Mycotic osteomyelitis are both ......

Answer 161

granulomatous Inflammation of bone

Question 162

Hematogenous osteomyelitis pathogenesis:

Answer 162

localization where capillaries make sharp bends obstruction of vessels and local tissue necrosis predispose to bacterial osteomyelitis omphalophlebitis in neonates e,.g., navel ill \>\> joint-ill (foals) spondylitis in pigs tail biting \>\> infection \>\> abscessation

Question 163

Osteomyelitis lesions

Answer 163

 accumulation and spread of purulent exudate in the medullary cavity  thrombosis and infarction of intramedullary fat, bone marrow, and bone  osteoclastic bone resorption:  stimulated by PGs and cytokines  promoted by reduced blood flow through large vessels

Question 164

Osteomyelitis  sequelae

Answer 164

 **exudation** and irregular new bone formation  **extension** to adjacent bone  **hematogenous spread** to other bones and soft tissues pathologic fractures  fistulae that penetrate cortical bone and drain to the exterior  sequestration  vertebral osteomyelitis → necrosis and cavitation  lysis of articular cartilage

Question 165

Granulomatous osteomyelitis

Answer 165

Actinomyces bovis ** "lumpy jaw"**  chronic pyogranulomatous osteomyelitis with bone lysis and irregular new bone formation

Question 166

pathogenesis of lumpy jaw

Answer 166

**Actinomyces bovis** (soil-borne; gram +ve)  oral mucosal ulceration and eruption of teeth → entrance of the organism to the osseous tissues of the mandible → pyogranulomatous inflammation  necrosis and loss of bone  new bone formation, scarring  abscessessation and fistulation  mandible is irregularly enlarged  teeth loosen up and fall out

Question 167

Granulomatous osteomyelitis agents

Answer 167

**mycotic agents**  Blastomyces dermatitidis  Coccidioides immitis  Cryptococcus neoformans  hematogenous spread to bone  granulomatous or pyogranulomatous osteomyelitis  + osteolysis and exostoses

Question 168

name virus that causes Viral osteomyelitis

Answer 168

HC (hepatitis c) ICH: FLV in cats BVD virus

Question 169

**HC, ICH** 1. dz caused 2. lesions

Answer 169

endothelial damage resulting in **metaphyseal** **hemorrhage and necrosis, and acute inflammation** osseous localization of canine distemper virus:  **injures osteoclasts, causing metaphyseal bone to accumulate (growth retardation lattice)** N.B growth arrest of long bones

Question 170

virus causing myelosclerosis (increased density of medullary bone)

Answer 170

FLV in cats

Question 171

virus that causes growth retardation in bovine fetuses

Answer 171

BVD virus

Question 172

what happens to pth n vit. d after injesting meal with high when P

Answer 172

pth is elevated vit d3 also elevated increased P excretion

Question 173

in low P what happens to pth and vit 3 levels

Answer 173

pth is decresed vit 3 increased to reabsorb P in the kidney

Question 174

effects of increased pth on P

Answer 174

increases P loss on kidneys

Question 175

disorganisation of the perichondrial ossification growth around the growth plates

Answer 175

congenital cortical hyperostosis

Question 176

new bone formation on long bones of the limbs and edema

Answer 176

congenital cortical hyperstosis