Exam 3: Lecture 27 - Developmental Done Diseases Flashcards

1
Q

What are the primarily inflammatory bone diseases

A
  1. panosteitis
  2. hypertrophic osteodystrophy (HOD)
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2
Q

when do the primarily inflammatory bone diseases appear?

A

characteristically during growth period of large and giant breed dogs

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3
Q

what is the definition of canine panosteitis

A

disease of young dogs causing lameness, bone pain (in long bones), endosteal bone production, and occasional periosteal bone production

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4
Q

what are some synonyms of canine panosteitis

A

enostosis, eosinophilic panosteitis, juvenile osteomyelitis and osteomyelitis of young GSDs

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5
Q

what is the etiology of canine panosteitis

A

unknown (maybe genetic, viral, or autoimmune??)

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6
Q

what is the pathophysiology of canine panosteitis

A

osseous compartment syndrome from protein rich high calorie diets

excessive protein leads to intraosseous edema and secondary increase medullary pressure and ischemia

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7
Q

T/F: Canine panosteitis is a disease of adipose bone marrow

A

true!

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8
Q

what is the usual signalment of canine panosteitis

A

male large breed dogs (~80%), young dogs under 2 years old, and SOMETIMES seen in older dogs

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9
Q

what is the usual history of canine panosteitis

A

shifting leg lameness, pain on deep bone palpation, may be acute lameness on one leg or chronic leg shifting

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10
Q

what do we usually see on gait analysis with canine panosteitis

A

single or multiple leg involvement, a varying severity of lameness (usually grade 1 or 2)

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11
Q

what do we usually see on PE with canine panosteitis

A

pain on direct palpation of affected bone(s) and generally weight bearing

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12
Q

T/F: you can diagnose canine panosteitis just by palpation of the long bones

A

FALSE!! Also need radiographs

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13
Q

T/F: With canine panosteitis clinical signs may preceed radiographic changes by up to 10 days and the radiograph sings are usually progressive

A

true!

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14
Q

What are the radiographic findings of canine panosteitis

A
  1. widening of the nutrient foramen
  2. intramedullary radiopacity (clouds)
  3. endosteal thickening
  4. perosteal new bone
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15
Q

What developmental bone disease are these rads showing

A

canine panosteitis

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16
Q

what is the medial treatment for canine panosteitis

A

self limiting disease, NSAIDs, exercise restriction when lame

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17
Q

T/F: You should surgically correct canine panosteitis

A

false!! Not indicated

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18
Q

is prognosis good or poor for canine panosteitis

A

good!

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19
Q

What is the definition of hypertrophic osteodystrophy (HOD)

A

disease causing disruption of metaphyseal trabeculae

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20
Q

what are some synonyms of HOD

A

skeletal scurvy, canine scurvy, Moeller-Barlow disease, osteodystrophy types 1 and 2, metaphyseal osteopathy and metaphyseal dysplasia

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21
Q

What is the etiology of HOD

A

unknown, maybe caused by diminished levels of vit C, and viral causes are suspected

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22
Q

why are viral causes suspected for HOD

A

usually have accompanying history of recent GI/respiratory problems

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23
Q

what is the pathophysiology of HOD

A

disturbance of metaphyseal blood supply, no bone formed on calcified cartilarge, and osteoclastic resorption

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24
Q

what do we see with disturbance of metaphyseal blood supply in HOD

A
  1. changes in physis and adjacent metaphyseal bone
  2. delayed ossification of physeal hypertrophic zone
  3. widening of physis (increased width of hypertrophied chondrocyte zone)
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25
Q

T/F: There is no bone formed in calcified cartilage with HOD and instead we see inflammatory infiltration of neutrophils and mononuclear cells

26
Q

What is the usual signalment seen with HOD

A
  1. young rapidly growing large breed dogs
  2. males more commonly than females
  3. clinical signs around 3-4 months old but can be seen as early as 2 months old
  4. Weimaraners are at increased risk
27
Q

what is the usual history we see with HOD

A
  1. acute onset of lameness
  2. may be severely affected (puppies may not walk)
  3. inappetence and lethargy
  4. history of recent diarrhea may precede lameness
28
Q

what do we usually see on PE with HOD

A
  1. mild to severe lameness of all 4 limbs (may be unable to stand or walk)
  2. long bone metastases swollen warm and painful on palpation
  3. swelling often present of all 4 limbs
  4. swelling in forelimbs may be more obvious
29
Q

what are some potential differential DDx’s when we see a patient with suspected HOD?

A

septic arthritis, septic physitis, and panosteitis

30
Q

what are the radiographic findings of HOD

A
  1. irregular radiolucent line metaphyseal side of physis (a “double physis”)
  2. widening of physis
  3. usually evidence in multiple limbs
31
Q

What is this radiograph showing

A

osteolysis on metaphyseal side of active physis…. AKA the “second growth plate”

32
Q

what is A

A

active physis

33
Q

what is B

A

osteolysis

34
Q

What disease are these progressive rads showing

35
Q

what is the treatment for HOD in animals that are NOT severely affected

A

HOD is self limiting so we focus on supportive care like analgesics to control pain

36
Q

how do we treat severely affected animals with HOD

A
  1. corticosteroids
  2. antibiotics
  3. vit c
  4. IV fluids
37
Q

What must we rule out prior to using corticosteroids for HOD treatment

A

MUST RULE OUT bacteremia!!!

38
Q

what is the prognosis for HOD

A

most recovery fully in 7-10 days but relapses may occur

39
Q

when should we consider euth for HOD

A

if there is severe debilitation or multiple severe relapses

40
Q

What are retained ulnar cartilaginous cores

A

cones of growth plate cartilage that project from distal ulnar growth plate into distal metaphysis

41
Q

what is retained ulnar cartilaginous cores also known as

A

Retained endochondral cartilage core

42
Q

what is the usual clinical presentation of retained ulnar cartilaginous core

A
  1. large to giant immature canines
  2. growth plate manifestation of osteochrondrosis
  3. +/- carpal valgus
  4. forelimb deformities may be identical to premature closure of distal ulnar and radial growth plates
43
Q

How do we definitively diagnose retained ulnar cartilaginous core

A

radiographs

44
Q

What is this rad showing

A

retained ulnar cartilaginous core

45
Q

What is the treatment for retained ulnar cartilaginous core with no forelimb deformities

A

no treatment needed

46
Q

What is the treatment for retained ulnar cartilaginous core with forelimb deformities

A
  1. surgical correction of deformity may be required
  2. all patients should be prescribed well balanced diet
  3. cores may disappear spontaneously
47
Q

What is legg-calve-perthes disease

A

non-inflammatory aseptic necrosis of femoral head in young patient prior to capital femoral physis closure

48
Q

what is the pathophysiology of Legg-calve-perthes disease

A

collapse of femoral epiphysis caused by interruption of blood flow (a hypoxic event leads to necrosis and collapse of femoral epiphysis)

49
Q

what is the etiology of legg-calve-perthes disease

A

unknown but proposed theories of hereditary factors, hormonal influence, anatomic conformation, intracapsular pressure, and infarction of femoral head

50
Q

T/F: Synovitis or sustained abnormal limb position may increase intra-articular pressure and collapse fragile veins which inhibits blood flow

51
Q

T/F: vascular supply to the femoral head in young animals comes from the epiphyseal vessels

52
Q

T/F: metaphyseal vessels cross the physis to help contribute to femoral head vascularity

A

false, they do NOT cross physis

53
Q

T/F: epiphyseal vessels course along femoral neck surface, cross growth plate, penetrate bone, and supplies nourishment to the femoral epiphysis

54
Q

What is the usual signalment of legg-calve-perthes disease

A
  1. young small breed dogs
  2. peak incidence 6-7 months old but ranges from 3-13 months
  3. males and females affected equally
  4. occurs bilaterally 10-17% of affected animals
55
Q

what is the usual history for legg-calve-perthes disease

A
  1. slow onset with weight bearing lameness that worsens over 6 to 8 weeks
  2. lameness may progress to NWB
  3. may present as acute onset due to sudden collapse of epiphysis
  4. other clinical signs such as irritability, reduced appetite, and chewing at skin over hip
56
Q

what is the PE we usually see with legg-calve-perthes disease

A

hip joint pain and with advanced disease can have limited range of motion, muscle atrophy, and cepitus

57
Q

What disease is the radiograph showing

A

legg-calve-perthes disease

58
Q

how do we medically manage legg-calve-perthes disease

A

can in early stages of disease and if it is not painful

can use NSAIDs, limited leash walking or NWB exercises like swimming

59
Q

How do we surgically treat legg-calve-perthes disease

A

Excision of femoral head and neck (FHO)

60
Q

what is the post op care for legg-calve-perthes disease

A
  1. limb should be used immediately after sx
  2. NSAIDs to reduce pain and encourage early fcn
  3. passive flexion-extension exercises
  4. physical therapy
61
Q

when is the prognosis good for legg-calve-perthes disease

A

after FHO and when there is slight intermittently lameness

62
Q

when is prognosis poor for legg-calve-perthes disease

A

NWB prior to surgery, severe preoperative muscle atrophy, incorrect surgical techniques