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MSK2 > Small animal developmental disease > Flashcards

Small animal developmental disease Flashcards

1
Q

Outline the aetiopathogenesis of hip dysplasia

A
  • Inherited
  • Non-genetic factors play role in expression of disease including body size, growth rate, nutrition, exercise, muscle mass
  • Grossly normal at birth
  • Loss of congruency between articular surfaces of acetabulum and femoral head, leading to osteoarthritis and remodelling
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2
Q

What causes the pain evident in the initial stages of hip dysplasia?

A

Stretching of the joint capsule and microfractures in the dorsal acetabular rim

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3
Q

Explain why the pain experienced in hip dysplasia appears to subside with age

A
  • Gradual increase in stability to due intra- and peri-articular changes (mainly thickening of joint capsule)
  • Secondary changes later in life
  • As continues to progress, will get pain again as a result of osteoarthritis
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4
Q

Outline the diagnosis of hip dysplasia

A
  • Joint laxity (degree of subluxation)
  • Norberg-Olsson angle
  • Signs of osteoarthritis
  • NB poor correlation between the severity of radiographic changes and clinical signs
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5
Q

Explain how the Norberg-Olsson angle is used in the diagnosis of hip dysplasia

A
  • Angle between the centre of the femoral head and dorsal edge of the acetabular rim
  • Angles smaller than 105˚ are considered abnormal - indicate that femoral head has luxated to some degree out of the acetabulum
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6
Q

Describe the signs of osteoarthritis that are commonly seen in the hip as a result of hip dysplasia

A
  • Change in shape of dorsal acetabular edge
  • New bone formation in acetabular fossa, cranial and caudal acetabular edges, femoral head and neck
  • Degree of remodelling of the femoral head and neck
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7
Q

List some differentials for hip dysplasia in young dogs

A
  • Patellar luxation
  • Cranial cruciate ligament disease
  • hock adn stifle osteochondrosis
  • Legg-Calve-Perthes disease
  • Septic arthritis
  • Spinal disorders
  • Myasthenia gravis
  • Myopathies
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8
Q

List some differential diagnoses for hip dysplasia in mature dogs

A
  • Cranial cruciate ligament disease
  • Patellar luxation
  • Degenerative lumbosacral disease
  • Other spinal disorders
  • Achilles tendinopathy
  • Septic arthritis
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9
Q

What clinical signs would you expect to see in a young dog with hip dysplasia?

A
  • Variable pelvic limb lameness
  • Swaying of pelvis when walking
  • Bunny hopping at faster speeds
  • Weakness of pelvic limbs
  • Reluctance to exercise
  • Inability to jump
  • Inactivity stiffness
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10
Q

What clinical signs would you expect to see in an adult dog with hip dysplasia?

A
  • Difficulty rising
  • Pelvic limb inactivity stiffness
  • Exercise intolerance
  • Difficulty jumping
  • Behavioural changes e.g. aggression around HLs
  • Sudden onset lameness (uncommon)
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11
Q

What is the definition of elbow dysplasia in dogs?

A

Abnormal development of the cubital joint leading to incongruency

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12
Q

What are the 3 main diseases causing elbow dysplasia in dogs?

A
  • Ununited anconeal process (UAP)
  • Fragmentation of the medial coronoid process (FCP)
  • Osteochondritis dissecans (OCD) of the medial portion of the humeral condyle
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13
Q

Identify uncommon diseases that may be included within elbow dysplasia in dogs

A
  • Joint incongruity
  • Incomplete fusion of the medial epicondyle
  • Idiopathic osteoarthritis of the medial compartment of the elbow joint
  • Angular limb deformity
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14
Q

How may an un-united anconeal process occur?

A
  • Either due to development as a separate centre of ossification
  • Or separation secondary to non-traumatic premature closure of the distal ulnar growth plate
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15
Q

Which breed is predisposed to the development of an un-united anconeal process as a result of separate centres of ossification?

A

GSD

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16
Q

Which breed is predisposed to the development of an un-united anconeal process as a result of non-traumatic premature closure of the distal ulnar growth plate?

A

Bassett hound

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17
Q

Briefly explain how premature closure of the distal ulnar growth plate leads to an un-united anconeal process

A
  • Ulna does not grow at same rate as the radius, so radius forces heads of humerus caudally
  • Puts pressure on anconeal process, preventing fusion
  • Radius leads to joint incongruency
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18
Q

What are the consequences of an un-united anconeal process?

A
  • Irritation and instability following separation of the anconeal process causing osteoarthritis
  • Often seen in association with FCP
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19
Q

Which breeds are predisposed to elbow dysplasia as a result of an un-united anconeal process?

A
  • GSD primarily

- Large breed dogs e.g. Wolfhound, Rottweiler, St Bernard, Great Dane

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20
Q

Outline the clinical signs of an un-united anconeal process

A
  • Progressive thoracic limb lameness 4-5months of age
  • Strange gait with elbow abducted +/- outward rotation of foot
  • Palpation/manipulation reveals joint thickening and varying amounts of joint effusion
  • Reduced joint movement, pain, maybe crepitus
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21
Q

How is an un-united anconeal process diagnosed?

A
  • Fully flexed lateral radiograph of joint

- Arthroscopy possible for evaluation of remainder of joint for FCP and OCD

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22
Q

What should be avoided when taking a radiograph in a case with a suspected un-united anconeal process?

A

Superimposition of medial epicondyle on the olecranon

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23
Q

What is the most common cause of elbow lameness in young, rapidly growing dogs of large and giant breeds?

A

Fragmentation of the medial coronoid process

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24
Q

Which breeds are predisposed to a fragmented medial coronoid process?

A
  • Rottweilers
  • Labrador retrievers
  • Bernese mountain dog
  • GSD
  • Golden retriever
  • St. Bernard
  • Chow chow
  • Rhodesian ridgeback
  • Newfoundland
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25
Q

What is the main difference between an FCP and a UAP?

A

There is no separate centre of ossification for the coronoid process - is a result of fracture of this fragment

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26
Q

List the potential causes of a fragmented coronoid process

A
  • Osteochondrosis
  • Microfracture/fracture
  • Radioulnar incongruity
  • Humeroulnar incongruity
  • Abnormal pressure on medial coronoid process
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27
Q

Outline the consequences of a fragmented coronoid process

A
  • Fragment may have fractured from inner aspect of medial coronoid process immediately adjacent to the radial head, or from apex of the process
  • Fragment may project causing irritation of medial humeral condyle (aka kissing lesion)
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28
Q

Outline the clinical signs of a fragmented coronoid process

A
  • Outward rotation of foot
  • Reduced range of flexion and extension
  • Painful response to external rotation and hyperextension
  • Crepitus in advanced cases
  • Pressure on medial coronoid process elicits strong pain response
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29
Q

Outline the diagnosis of a fragmented coronoid process

A
  • Conventional radiography: difficult to see lesion unless large fragment on craniocaudal or craniolateral-caudomedial oblique projections
  • CT images better
  • Arthroscopy, also for assessment of severity
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30
Q

Outline the development of osteochondrosis of the medial condyle

A
  • Lesion initiates within articular epiphyseal cartilage complex in developing joint
  • necrosis of vascular channels leads to development of cartilage flap
  • Separates from underlying bone, leading to discomfort
  • Usually bilateral, on and on outer edge of central weight bearing region of the articular surface of medial portion of humeral condyle
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31
Q

Which breeds are predisposed to elbow dysplasia due to osteochondrosis of the medial condyle?

A

Labrador and golden retrievers

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32
Q

Outline the clinical signs of osteochondrosis of the medial condyle

A
  • Similar to FCP
  • Outward rotation of foot
  • Reduced range of flexion and extension
  • Pain on external rotation and hyperextension
  • Crepitus in advanced cases
  • Pressure on medial coronoid process elicits strong pain response
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33
Q

Outline the diagnosis of osteochondrosis of the medial condyle

A
  • Radiography: flexed lateral radiographs (anconeal process osteoarthritis), craniocaudal or craniolaterla-caudomedial oblique,(defect of subchoondral bone of medial part of humeral condyle)
  • CT scans
  • Arthroscopy
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34
Q

Outline the appearance of osteochondrosis of the medial condyle on radiography

A
  • Surface not smooth

- Some increased radiodensity where the flap is gone

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35
Q

What is a varus limb deformity?

A

Medial deviation of distal limb

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36
Q

What is a valgus limb deformity?

A

Lateral deviation of the distal limb

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37
Q

What is the underlying abnormality that leads to angular limb deformities?

A

Differing growth rates of the 2 bones of the antebrachium (radius and ulna)

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38
Q

List the potential causes of an angular limb deformity in the dog

A
  • Unilateral: trauma to all or part of an active growth plate in immature dogs
  • Abnormal endochondral ossification e.g retained cartilaginous core
  • Metaphyseal osteopathy
  • Bilateral more likley to be systemic problem e.g. nutrition, growth rate
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39
Q

If the growth plate of the radius is damaged on the medial aspect, in what direction will the limb be deformed?

A

Varus deformity

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40
Q

If the growth plate of the radius is damaged on the lateral aspect, in which direction will the limb be deformed?

A

Valgus deformity

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41
Q

If the distal ulna fuses prematurely, what limb deformity will occur and how?

A

Ulna stops growing, leg forced out laterally leading to a valgus deformity as radius continues to grow
- Also get external rotation of food and cranial bowing of the radius

42
Q

Outline the clinical signs of an angular limb deformity of the dog

A
  • Bent leg
  • Variable degree of lameness depending on severity
  • May be a painful and mechanical lameness
43
Q

In which region will an angular limb deformity be most painful and why

A
  • Elbow
  • Carpal joint impacts on elbow joint
  • If ulnar growth plate fuses, radius grows, radial head pushes against condyles of humerus
  • Leads to incongruency of elbow joint leading to elbow dysplasia and pain
44
Q

Outline the diagnosis of an angular limb deformity

A
  • Radiography, orthogonal views of both legs, including antebracium with elbow and carpal joints, and at least proximal 1/2 of metacarpals/tarsals
  • Straighten elbow
  • Measure and record degree of valgus/varus, length of radius and ulna
  • Up to 15˚ of valgus angulation is usually clinically insignificant
45
Q

What are the potential consequences of premature closure of the distal ulna growth plate

A
  • Elbow incongruity
  • Antebrachiocarpal joint incongruity (less common)
  • Carpal pain, pad sores etc. due to valgus deformity
46
Q

List the potential surgical treatment options for premature closure of the distal ulnar growth plate in a young dog with considerable growth potential

A
  • Proximal ulnar osteotomy
  • Distal ulnar ostectomy to remove bow-string effect and preserve elbow joint
  • Stapling medial side of radius
  • Proximal (“dynamic”) ulnar osteotomy
47
Q

Explain how a proximal ulnar osteotomy works to treat premature closure of the distal ulnar growth plate

A
  • Cut the ulnar proximally

- Allows the radius to continue growing, as the ulna will separate to facilitate this

48
Q

Explain how an ulnar ostectomy and radial stapling works to treat premature closure of the distal ulnar growth plate

A
  • Ulna has section removed to reduce restriction of growth
  • Radius stapled at growth plate to limit radial growth and prevent movement
  • Prevents incongruency developing
49
Q

List the treatment options for premature ulnar distal growth plate closure in animals near skeletal maturity

A
  • Proximal ulnar osteotomy
  • Distal ulnar ostectomy
  • Radial osteotomy with either one stage correction and stabilisation using linear ex-fix/bone plate OR staged correction using illizarov fixator
50
Q

What is the main aim of treatment of premature ulnar distal growth plate closure in animals near skeletal maturity

A
  • Elbow and carpal joints parallel to each other and to the ground
  • Aim for straight line
  • Correction of elbow incongruity is top priority
51
Q

Outline the process of normal bone development

A

1: Chondrocytes at centre of growing cartilage enlarge then die as matrix calcifies
2: Newly derived osteoblasts cover shaft of cartilage in thin layer of bone
3: Blood vessels penetrate cartilage, new osteoblasts form primary ossification centre
4: Bone of shaft thickens, cartilage near each epiphysis is replaced by shafts of bone
5: Blood vessels invade epiphyses and osteobalsts form secondary centres of ossification

52
Q

Outline the signalment for panosteitis

A
  • Young dogs 5-12months usually (reported 2mo-7yrs)
  • Large breed dogs (23kg or more, incl. Bassetts)
  • M>F
53
Q

Outline the aetiology of panosteitis

A
  • Unknown
  • May have some genetic influence
  • Some seasonal and geographical variation in incidence
54
Q

Outline the presenting signs of panosteitis

A
  • Shift leg lameness
  • Pain on deep palpation of long bones, may be multifocal
  • Lameness, vocalisation, loss of appetite
  • Waxing and waning signs
  • Humerus and radius most commonly affected
55
Q

Outline the diagnosis of panosteitis

A
  • Radiography of multiple long bones
  • Signalment
  • Clinical history
  • Physical examination (lack of joint effusion, no enlarged LNs)
56
Q

Discuss the use of radiography in the diagnosis of panosteitis

A
  • Normal in early stages (lag for radiographic signs)
  • May need to repeat after 2-3 weeks
  • Radiograph other limbs, may show signs if affected 2 weeks ago
  • No link between severity of radiographic signs and clinical signs
57
Q

Describe the radiographic signs seen in panosteitis

A

Thumbprint lesions typical - areas of increased opacity, which resolve to coarse trabecular pattern +/- smooth periosteal reaction (but often do not)

58
Q

List differentials for panosteitis

A
  • Elbow dysplasia
  • Metaphyseal osteopathy
  • IMPA (NB usually older, joint pain rather than bone pain)
  • Septic arthritis (NB usually older, joint pain in single joint)
  • Bone metastasis
59
Q

Discuss bone metastases as a differential for panosteitis

A
  • Rare
  • Signalment different- mets usually older dogs
  • May identify primary neoplastic process elsewhere
  • Usually presented for problems caused by primary tumour
60
Q

Outline the treatment for panosteitis

A
  • Self limiting disease
  • Supportive treatment only: rest, analgesia (NSAIDs, opioids if needed, some may need nutritional/fluid support)
  • Relapse possible, but excellent prognosis
61
Q

Outline the signalment for metaphyseal osteopathy

A
  • Usually young dogs, 2-7mo
  • Giant breeds
  • Weimeraners (inherited)
  • M>F
62
Q

Outline the aetiology of metaphyseal osteopathy

A
  • Aetiology unknown
  • Some geographical and seasonal distribution reported
  • Considered to a systemic disease, possible causes under investigation (viral, bacterial, nutritional)
63
Q

Outline the presenting signs of metaphyseal osteopathy

A
  • Severe lameness
  • Pyrexia
  • Inappetance, GI signs
  • Bilaterally symmetrical, painful metaphyseal swellings affecting long bones
  • Often affects distal radius, ulna, tibia, but can affect ribs, digits, metacarpal/tarsal bones
64
Q

Outline the diagnosis of metaphyseal osteopathy

A

Radiography of both limbs, +/- back limbs, ensure inclusion of joints above and below

65
Q

Describe the radiographic signs seen with metaphyseal osteopathy

A
  • Can be subtle to severe

- Metaphyseal lucent lines parallel to the physis (double physis appearance), adjacent sclerotic line

66
Q

What causes the sclerotic line seen adjacent to the radiolucent line in metaphyseal osteopathy?

A

Collapsed necrotic trabeculae

67
Q

List the differentials for metaphyseal osteopathy

A
  • Septic physitis
  • Septic arthritis
  • Inflammatory joint disease
  • Hypertrophic osteopathy
68
Q

Compare hypertrophic osteopathy an metaphyseal osteodystrophy

A
  • Hypertrophic osteopathy usually older animals, underlying cause is mass lesion in chest/abdomen
  • Often neoplastic
69
Q

Outline the treatment of metaphyseal osteopathy

A
  • Self limiting, usually weeks but can be months
  • Supportive treatment only: rest, analgesia (NSAIDs, opioids), extreme cases may need fluids/nutritional support
  • Relapse possible, long term prognosis more guarded vs panosteitis but usually good
70
Q

Outline the signalment for craniomandibular osteopathy

A
  • WHWT, but also other breeds and cross breeds

- Young pups 3-8mo

71
Q

Outline the clinical signs of craniomandibular osteopathy

A
  • Pain (pup miserable)
  • Reluctance to eat, dysphagia
  • Weight loss
  • Salivation
  • Signs can wax and wane with periods of growth
72
Q

Explain the pathology underlying craniomandibular osteopathy

A
  • Excessive and abnormal bone growth affecting mandibles, tympanic bullae, temporomandibular joints, +/- other bones of skull or rarely, long bones
  • Pain noted before changes on radiography
73
Q

Outline the radiographic appearance of craniomandibular osteopathy

A
  • Increased density of mandible

- May look like pillars of bone along ventral aspect of mandible

74
Q

Discuss the risks associated with radiography in a cases of suspected craniomandibular osteopathy

A
  • May be difficult to intubate as difficult to open jaw
  • Increased risks of aspiration under GA due to hypersalivation
  • Consider placement of oesophageal feeding tube as same time as puppy may not want to eat
75
Q

Discuss the prognosis for craniomandibular osteopathy

A
  • Depends on involvement of TMJ
  • Episodes of pain resolve by ~12mo
  • Some bone remodelling can occur
  • Usually left with thick smooth jaws, tongue sticks out a little
76
Q

What condition may craniomandibular osteopathy be related to?

A

Calvarian hyperostosis seen in Bull Mastiffs

77
Q

When does secondary renal hyperparathyroidism occur?

A
  • Late stages of CKD

- May occur in juveniles with congenital renal disease

78
Q

Outline the clinical signs of secondary renal hyperparathyroidism

A
  • Signs of CKD usually predominate

- Increased risk of pathological fracture e.g. in dentals, manual restraint of cats

79
Q

Explain the elevation in PTH in secondary renal hyperparathyroidism

A
  • Relative hyperphosphataemia (from decreased GFR)

- Relative calcitriol deficiency (decreased production by kidneys)

80
Q

Describe the radiographic appearance of secondary renal hyperparathyroidism

A
  • May see “floating teeth/rubber jaw”

- Demineralisation of bone more likely in younger animals with congenital renal disease, but possible in older

81
Q

Discuss the development of secondary nutritional hyperparathyroidism in dogs and cats

A
  • Young dogs and kittens due to increased demand for Ca and minimal reserves
  • Related to an inappropriate diet (chronic calcium deficiency, calcium/phosphate imbalance)
  • Increased PTH upregulates osteoclasts compared to osteoblasts, leading to Ca resorption
82
Q

Describe the presenting signs of secondary nutritional hyperparathyroidism

A
  • Bone pain
  • Pathological fractures (lameness, spinal cord damage if vertebrae involved, pelvic damage)
  • Seizures reported in cats/kittens with severe hypocalcaemia
  • Poor radiographic contrast between bone and soft tissues
83
Q

Outline the treatment of secondary nutritional hyperparathyroidism

A
  • Dietary correction leads to normal mineralisation in 6-8 weeks
  • Cats may require O tube feeding
  • Rest important
84
Q

Discuss the prognosis for secondary nutritional hyperparathyroidism

A
  • Good unless fractures have caused long term issues e.g. neurological signs, joint problems, pelvic narrowing leading to constipation
  • May look misshapen
85
Q

What is Legg-Calve-Perthes disease also known as?

A

Avascular necrosis of the femoral head/ischaemic or aseptic necrosis of the femoral head

86
Q

Outline the signalment of Legg-Calve-Perthes disease

A
  • Young

- Miniature and small breed dogs

87
Q

Outline the aetiology of Legg-Calve-Perthes disease

A

Unknown, likely multifactorial (genetic, trauma)

88
Q

Outline the cinical signs of Legg-Calve-Perthes disease

A
  • HL lameness (often bilateral)
  • Atrophy og quadriceps
  • Pain on hip manipulation
89
Q

Outline the pathophysiology of Legg-Calve-Perthes disease

A
  • Bone infarction leads to collapse of femoral head and neck
  • Revascularisation, resorption and remodelling occur
  • Chronic osteoarthritis is the end result
90
Q

Outline the radiographic signs of Legg-Calve-Perthes disease

A
  • Depends on stage of disease
  • Irregular bone opacity in femoral head and neck
  • Collapse of the femoral neck, rather than abnormal acetabulum
  • Fragmentation of bone
  • Distortion of femoral head
91
Q

Compare the diagnosis of LCP vs hip dysplasia

A
  • Breed predisposition should help
  • Also less distortion of femoral head and neck in HD
  • End stages appears similar
92
Q

Compare the development of rickets in dogs and cats

A
  • Cats linked to genetic issues, rare

- Dogs: deficiency of vit D, hereditary defect, lack of exposure to sunlight

93
Q

Describe the appearance of rickets in dogs

A
  • Young
  • Stunted
  • Bow-legged
  • Plantigrade
94
Q

Describe the radiographic appearance of rickets in dogs

A
  • Bone osteopaenic
  • Epiphyseal lines very wide
  • Failure to ossify
95
Q

Outline the treatment and prognosis for rickets in dogs

A
  • Correct diet
  • Expose to sunlight
  • May be permanent damage to growth plates
  • Prognosis guarded for hereditary causes
96
Q

What is a key differential for rickets in cats?

A

Nutritional secondary hyperparathyroidism

97
Q

Outline the clinical signs of rickets in cats

A
  • From 3 mo of age
  • Stiffness, reluctance to move, pain
  • Signs of hypocalcaemia (tremors, seizures, GI disturbance)
98
Q

Outline the common findings on physical exam of a cat with rickets

A
  • Stiff joints
  • Epiphyseal swelling
  • Small stature
  • Spinal abnormalities e.g. lordosis, kyphosis
99
Q

Outline the diagnosis of rickets in cats

A
  • Radiography shows wide physes

- Diagnosis based on blood tests for calcium, phosphate, PTH, vit D

100
Q

Outline the treatment and prognosis for rickets in cats

A
  • Treatment is supplementation of calcium and vit D

- Prognosis variable

MSK2 (29 decks)

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