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DC 2 Flashcards

1
Q

What are some specific tests for coxofemoral luxation and hip dysplasia?

A

Coxofemoral luxation= thumb test, position of greater trochanter
Hip dysplasia= Ortolani test, Bardens hip lift (lift femur latrally)

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2
Q

In which situations may the cranial drawer test be negative?

A
  • if the craniomedial band is in tact
  • extensive medial buttress/ periarticular fibrosis preventing movement
  • stressed/anxious/ large patient with high muscle tone
  • if only tested in extension and the and one of the two bands is intact
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3
Q

When testing collateral stability of the hock by the application of valgus and varus stress, why test in flexion and extension?

A

In flexion, you test the short branches of the collaterals. In extension you test the long branches of the collaterals. Not the case in cats though because they don’t have long (only short).

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4
Q

What tests may be performed to assess cruciate disease?

A

Cranial drawer test
Cranial tibial thrust test
Sit test
May also be biceps atrophy and medial buttress (in chronic disease)

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5
Q

What is the biceps test?

A

Press on biceps tendon whilst simultaneously flexing shoulder and extending elbow. (to test for shoulder pain)

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6
Q

What is a normal shoulder abduction angle?

A

30 degrees

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7
Q

What is the best method for assessing cartilage and intra-articular ligaments?

A

Arthroscopy

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8
Q

What is osteochondrosis and what is its pathophysiology?

A

=a failure of endochondral ossification of growing cartilage
Pathophys:
1. Vessels from bone marrow anastamose with cartilage canal vessels
2. Microtrauma-> ischaemia-> necrosis
3. Cartilage infarct prevents endochondral ossification
4. thickening of cartilage adjacent to the region
5. Thickened cartilage degenerates susceptible to mechanical stress

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9
Q

What causes microclimate change in the external auditory ear canal?

A

Anything that:

  1. Causes inflammation of the ear canals
  2. Increases the moisture in the ear canals
  3. Interferes with “self cleaning”
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10
Q

What are the basic principles of treating otitis externa?

A
  1. Resolve the current infection
  2. Control “trigger” disease
  3. Control secondary predisposing factors
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11
Q

Ears will fail to get better despite treatment if what? (6)

A
  1. medication cannot get to site
  2. The wrong dose of med is applied
  3. The wrong type of med
  4. Poor owner compliance
  5. Failure to control infl.
  6. Maceration
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12
Q

What are secondary predisposing causes of otitis externa?

A
  1. Epidermal oedema
  2. Epidermal hyperplasia
  3. Glandular hyperplasia
  4. Stenosis due to fibrosis, calcification of fibrovascular occlusion
  5. Otitis media
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13
Q

What are some common reasons for treatment failure of otitis externa?

A
  1. Failing to adequately clean the ear (inhibits penetration of meds)
  2. Failing to control inflammation in the ear canal (GCs)
  3. Inadequate dose of med
  4. Poor owner compliance
  5. Wrong choice of medication
  6. Failure to address the trigger factors
  7. Failure to reassess, confirm cytological resolution and continue tx for 7 days past resolution
  8. Failure to address secondary changes
  9. Bacterial or fungal resistance
  10. Maceration
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14
Q

Rods are not normally found in healthy ears. True or False?

A

True. Staph and malassezia are though

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15
Q

What factors may trigger eosinophilic dermatoses?

A
  1. Hypersensitivities
  2. Ectoparasites
  3. Viral infection
  4. Neoplasia
  5. Tissue necrosis
  6. Infection
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16
Q

What are the different types of eosinophilic granuloma complex clinical patterns seen?

A
  1. Miliary dermatitis
  2. Oral granuloma
  3. Palatine ulcers
  4. Indolent lip ulceration
  5. Lower lip granuloma
  6. Eosinophilic plaque
  7. Eosinophilic granuloma
  8. Linear granuloma
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17
Q

For EGC miliary dermatitis pattern in cats, briefly identify:

a) what it is
b) Ddx
c) Historical clues
d) clinical clues
e) diagnostic approach

A

a) what: multiple crusted papules
b) Ddx: Hypersens., ectoparasites, folliculitis, immune-mediated dysfunction, neoplastic, nutritional
c) Hx clues: diet, seasonality, flea control, cattery
d) clinical clues: Breed (devon rex, persians), location
e) dx: wood’s lamp, fungassay, cytology, antimicrobial trial, biopsy, flea elimination trial, food trial, skin testing

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18
Q

For EGC indolent ulcer reaction pattern in cats, briefly identify:

a) what it is
b) Ddx
c) Historical clues
d) clinical clues
e) diagnostic approach

A

a) erosion/ ulceration of upper lip adjacent to the canines and philtrum
b) hypersens., neoplasia
c) hx: seasonality, inadequate flea control
d) clinical clues: lesion location
e) dx: cytology, antimicrobial trial, histopath (if severe), allergy investigation

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19
Q

For EGC eosinophilic plaque reaction pattern in cats, briefly identify:

a) what it is
b) Ddx
c) Historical clues
d) clinical clues
e) diagnostic approach

A

a) flat-topped plaques
b) Hypersens., Xanthoma, Infectious granulomas
c) hx: seasonality, flea control
d) clinical clues: lick accessible areas, very pruritic, erythematous, yellow foci
e) dx: cytology, antimicrobial trial, histopath (if severe), allergy investigation

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20
Q

For EGC oral granuloma/ platine ulceration in cats, briefly identify:

a) Ddx
b) Historical clues
c) clinical clues
d) diagnostic approach

A

a) Hypersens., Neoplasia, Infectious granulomas
b) Seasonality, inadequate flea control
c) Distinctive yellow foci
d) dx: cytology, histopath (if severe), allergy investigation

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21
Q

What are some options for the treatment/ management of eosinophilic granuloma complex in cats?`

A

Specific:
Flea control, dietary manipulation, allergen specific immunotherapy and avoidance strategies

Non-specific:
GCs, cyclosporin, apoquel

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22
Q

For feline cutaneous herpes, briefly identify:

a) what it is
b) Ddx
c) Historical clues
d) clinical clues
e) diagnostic approach
f) Tx

A

a) DNA virus associated with rhinotracheitis in a cat
b) ddx: other eosinophilic dermatoses
c) Hx: previous resp herpes, ocular herpes
d) ulcerative disease affecting face, dorsal nasal bridge or nasal planum
e) cytology, histopath, PCR, immunohistochem
f) L-Lysine, interferon, Famvir (famciclovir)

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23
Q

For feline mosquito hypersensitivity, briefly identify:

a) Ddx
b) Historical clues
c) clinical clues
d) diagnostic approach
e) Tx

A

a) ddx: PF, Feline herpes
b) seasonal history, access to outdoors at night
c) lateral aspects of pads affected, dorsal nasal bridge and pinna also
d) cytology, response to indoor housing
e) indoor housing

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24
Q

Compare lanolin and poloxamer as vehicles for A/b administration.

A

Lanolin: lasts 7-10 d, less macerating, occasional irritant rxns known, longer shelf life (12w-6m)

Poloxamer: lasts 5-7 d, more macerating, easier application, middle ear safe

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25
Q

What are your first lines of defence in treating the following ear infections:

a) pseudomonas
b) coccal
c) yeast

A

a) enrofloxacin
b) as above unless MRSP (give Osurnia- florphenicol)
c) Osurnia (terbinafine)

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26
Q

What is PSOM? What clinical signs are associated with it? What breeds is it seen in?

A

Primary secretory otitis media= genetic fault in protein surfactant that lines the Eustachian tubes so that they can’t maintain a negative pressure and can’t drain through Eustachian tube-> middle ear canal fills up
Neurological signs, head and cervical pain.

CKCSs

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27
Q

What is the difference between osteochondrosis latens, manifesta and dissecans?

A

Latens: microscopic, no CSs
Manifesta: subclinical but macroscopic/ radiographic lesions
Dissecans: detached cartilage flap, clinical

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28
Q

What are the locations of OCD?

A

Shoulder, elbow, stifle, hock, lumbosacral

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29
Q

Persistent hypertrophic chondrocytes in the growth plate may lead to …?

A
  1. Incomplete ossification of humeral condyle
  2. Retained cartilaginous core
  3. Ununited anconeal process
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30
Q

What are the three fates of infarcted cartilage?

A
  1. Healed by replacement with granulation tissue
  2. Subchondral bone cyst
  3. Fissure formation (OCD lesion)
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31
Q

What are some predisposing factors to OCD?

A
  1. Hereditary- Polygenic trait
  2. Nutritional- overfeeding, vit D/ Ca supp
  3. Microtrauma and mechanical stress
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32
Q

What locations are predisposed to OCD?

A

Caudal humeral head, Medial humeral condyle, lateral femoral condyle, medial (or lateral) trochlear ridge of the talus, lumbosacral joint.

***bilateral involvement is common

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33
Q

What are the treatment options for OCD?

A

Conservative management: rest, weight loss, NSAIDs

Sx: Arthrotomy/ arthroscopy, removal of OCD mouse, curettage, fill with fibrocartilage, osteochondral grafting, platelet rich plasma (?), stem cell therapy (?)

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34
Q

In which breed of dog is there a predisposition to OCD of the hock?

A

Rottweiler

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35
Q

What is the prognosis of the following forms of OCD?

  • OCD of the humeral head
  • OCD of the medial humeral condyle
  • OCD of the femoral condyle
  • OCD of the hock
A
  • humeral head: excellent
  • medial humeral condyle: fair
  • femoral condyle: fair, more guarded than shoulder
  • hock: guarded
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36
Q

What are the four possible contributors to elbow dysplasia pathology?

A
  1. Ununited anconeal process
  2. Fragmented medial coronoid process (or more commonly medial coronoid disease)
  3. OCD of the medial humeral condyle
  4. Elbow incongruity
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37
Q

What is ununited anconeal process? By what age should we see the normal manifestation of this process?

A

Aetiology unknown. Anconeal process fails to unite and fuse with the ulna.

AP usually unites with ulna at 14-15 weeks of age in greyhounds, and 16-20 weeks in GSDs. Therefore cannot be diagnosed before 20 weeks

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38
Q

What are some clinical signs and tx options for ununited anconeal process?

A

CSs: lameness, pain on elbow manipulation, joint effusion
Tx: reattachment using screw and K-wire; surgical removal if fragment is too small, ulnar osteotomy

Good prognosis

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39
Q

What is medial compartment disease?

A

General term of the disease which affects the medial aspect of the elbow joint. = terminal disease involving medial coronoid disease, OCD, elbow incongruity and kissing lesions.

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40
Q

What is fragmented medial coronoid process and medial coronoid disease? What are some CSs?

A

=developmental defect of the medial coronoid processes-> develops a fissure or crack -> fragmentation.
Cartilage-> chondromalacia -> fibrillation-> fissures -> erosion

CSs: Lameness, muscle atrophy, joint effusion, elbow abduction when standing, pain on palpation, supination, pronation, decreased ROM

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41
Q

Describe the pathogenesis of incomplete ossification of humeral condyle? Which breeds are overrepresented for this condition?

A

Failure of ossification between the medial and lateral parts of the humeral condyle so that a fibrous band remains. Often bilateral

Spaniel breeds

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42
Q

Where are angular deformities most common and why? where else might they occur?

A

Most common in antebrachium bc distal ulnar physis is responsible for 100% of growth of ulna. For the radius, 60% of growth originates from the distal physis.

May also occur in crus, distal humerus or femur.

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43
Q

What is the aetiology of fragmented medial coronoid process?

What are some tx options?

A
  • Genetics, nutrition, environmental and trauma
  • incongruity: trochlear notch dysplasia, elliptical notch that is misplaced, proximodistal incongruence (due to short radius and short ulna)

Tx: Conservative (rest, NSAIDs, Chondroprotectants, nutraceuticals), Sx (arthroscopy/arthrotomy, fragment removal, subtotal coronoidectomy etc)

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44
Q

How would you treat the following:
Short ulnar syndrome
Short radius syndrome

A

Short ulnar syndrome: Proximal ulnar osteotomy

Short radius syndrome: Proximal ulnar ostectomy

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45
Q

What is the pathogenesis of angular limb deformities?

A

Asynchronous growth of paired bones due most commonly to trauma but can be heritable (in shitzhus and daschunds)

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46
Q

What is the aetiology of hip dysplasia?

A

Multifactorial!

  • genetics
  • environmental (maternal milk, exogenous oestrogen, exercise and temperament)
  • nutritional (XS feeding)
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47
Q

What is the pathogenesis of hip dysplasia?

What are some clinical signs?

A

Repeated subluxation ->cartilage wear and remodelling of femoral head, neck and acetabulum-> synovitis,-> OA

Periarticular fibrosis can then make the joint more stable.

Progression of OA leads to lameness and poor pelvic limb function

CSs: bunny hopping, spinal sway, reluctant to run, jump or climb stairs, muscle atrophy. Usually bilateral.

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48
Q

How might you diagnose hip dysplasia?

A

CSs, Lordosis test, Ortolani maneuver, Barden’s test

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49
Q

What is juvenile pubic symphysiodesis?

A

Procedure done in young dogs to manage hip dysplasia where growth of the pubic symphysis is arrested to allow gradual increase in ventral rotation of the acetabulum during growth. Can’t do after 16 weeks old.

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50
Q

What is avascular necrosis of the femoral head caused by?

A

Cause unknown. Vascular infarction of epiphyseal and metaphyseal bone leading to bone necrosis and collapse of subchondral bone plate.-> deformation of femoral head and thickening of articular cartilage

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51
Q

What is the pathogenesis of medial patellar luxation?

A
  1. coxa vara (decreased angle of inclination of the femoral neck)
  2. genu varum (medial bowing of the distal femur)
  3. external rotation of the distal femur
  4. poorly developed medial ridge of the tibia
  5. internal rotation of the tibial tuberosity
  6. Internal torsion of the proximal tibia, external torsion of the distal tibia
  7. internal rotaion of the foot
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52
Q

How is medial patellar luxation graded?

A

Grade 1: patella in groove. luxates intermittently, spontaneoulsy returns to groove
Grade 2: Patella normally in groove; luxates intermittently, stays luxated
Grade 3: Permanently luxated, Can be reduced to groove by manipulation
Grade 4: Perm. luxated. Can’t be manipulated back

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53
Q

What are some treatment options for medial patellar luxation?

A

Tibial tuberosity transposition
Trochleoplasty (wedge, rectangular block)
Corrective osteotomy of the femur +/- tibia
Exercise, NSAIDs, physiotherapy
Desmotomy
Imbrtication

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54
Q

What is panosteitis?

A

Sclerosis of long bones. Pain on long bone palpation. Causes shifting lameness, waxing and waning severity. Self-limiting

Giant breeds (5-12 months) and males are more predisposed

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55
Q

What supplies blood to the medullary circulation of bone?

A

Nutrient artery

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56
Q

What is the difference between primary and secondary osteonal reconstruction?

A 
Primary= contact healing. No callus formation (gap <1mm)
Secondary= too much strain. Lamellar bone laid down perpendicular to long axis. Resorption and callus formation reduce strain.
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57
Q

What is indirect bone healing? What are it’s stages?

A

Occurs with larger fracture gap. Get a lot of bony callus
Inflammation -> soft callus -> hard callus-> remodelling.

Relies on periosteal tissues (blood supply)

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58
Q

What does viscoelasticity mean?

A

Ability of substance to react to different speeds of loading. The stiffness and strength of bone vary depending on the rate at which load is applied.

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59
Q

Bone is anisotropic. This means it is stronger when loaded ?longitudinally/transversely? and in ?compression/tension?

85-90% of internal stress in bone is due to what force?

A

Longitudinally
Compression

Bending

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60
Q

As a general rule, on which surface of bones do we want to place metal implants?

A 
On the tension side (metal is strongest against this force)
Examples: 
Radius= cranial
Ulna= caudal
Femur, tibia, humerus= craniolateral
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61
Q

What are common bone sites of tension?

A

Tibial tuberosity, olecranon, calcaneous, greater trochanter

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62
Q

Granulation tissue needs an interfragmentary strain of how much?

A

Less than 2%

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63
Q

What is a fracture assessment score?

A

Involves:

  • Mechanical factors
  • Biological factors
  • Patient/ owner factors

Scored 1-10 for each factor. Better score-> better fracture outcome

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64
Q

How might you classify fractures on radiographs?

A
  1. Nature (traumatic, stress, pathological)
  2. Energy level of trauma
  3. Completeness
  4. Number of fracture lines
  5. Direction of fracture lines/ morphology
  6. Location of fracture
  7. Relationship of fracture fragments
  8. Soft tissue injury (open/closed)
  9. Associated joint injury
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65
Q

What are the AO principles?

A
  1. Fracture reduction to restore anatomical relationships
  2. Stability by fixation or splintage as required
  3. Preservation of the blood supply to soft tissues and bone by careful handling and gentle reduction techniques
  4. Early/ safe mobilisation of patient and limb
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66
Q

External coaptation is only good at preventing what force? What are the situations in which it can be used?

A

Bending (may reduce rotational forces but only if joint above and below the fracture are immobilised).

Used as primary method of immobilisation, temporary immobilisation, adjunctive support, or to prevent weight bearing

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67
Q

What are some advantages and disadvantages of external coaptation?

A

Adv:

  • cheap (initially)
  • no disruption of extraosseous blood supply
  • reduced risk of infection/ osteomyelitis

Disadv:

  • aftercare is intensive nad expensive
  • Doesn’t protect against tension or compression
  • Relies on owner compliance and revisits
  • Ischaemic necrosis of skin and other bandage related skin problems
  • Can’t use above elbow or knee
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68
Q

What is fracture reduction? What are the two types?

A

The restoration of normal or near normal bone alignment and apposition. Required prior to fixation.

Direct (open approach) and indirect (closed or minimally invasive. Traction remote from fracture site)

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69
Q

What are some adv and disadvantages of internal fracture fixation?

A

Adv:

  • May allow complete anatomical reconstruction/ load sharing
  • Creates rigid stability allowing rapid weight bearing and minimising fracture disease.
  • Comfortable for patient

Disadv:
-Cost and invasiveness

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70
Q

Intramedullary pins resist what forces?

A

Bending forces

Won’t prevent axial compression, rotation or shear forces

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71
Q

What are K wires?

A

= Kirschner wires
Small diameter pins(<1.6mm) used for:
-primary stabilisation for very stable fractures in young/ small patients
-achieving temp stabilisation
-adjunctively (2 points fixation required to prevent rotation)

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72
Q

What is cerclage wire?

A

Wire used for long oblique fractures or spiral fractures to create compression. Need to have perfect anatomical reconstruction and need a minimum of 2. They have very little bending strength

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73
Q

What is interfragmentary wiring useful for?

A

Skull fractures

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74
Q

What is the difference between a positional screw and lag screw?

A

“Lag” refers to how it is placed.
-> overdrill the near cortex so threads don’t engage the near cortex so that when we tighten it, it applies interfragmentary compression

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75
Q

What are advantages of bone plates?

A 
Can apply minimally invasively
Resist all fracture forces 
Take all the load
Can allow a load sharing repair
Minimal post op pain/ rapid return to function

(Disadv: extensive dissection required, plate is peripheral to mechanical axis)

How well did you know this?
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2
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76
Q

What is the tension band principle?

A

Counters tension associated with muscle contraction sites. Two parallel pins inserted across fracture site and orthopaedic wire placed in figure 8 pattern opposing pull of muscle. This converts the tensile forces into compressive forces.

77
Q

What is the focus of the gardener’s approach to fracture repair?

A

Anatomical repair is not attempted. Focus is on preserving the axial and rotational alignment of the diaphysis of the long bones and the orientation of the joints above and below fracture site

78
Q

What is the difference between the Velpeau and Ehmer sling?

A

Velpeau sling is used to prevent weight bearing in thoracic limbs and can immobilise the shoulder and elbow joints. The Ehmer sling in used for the pelvic limbs. It results in internal rotation of the femur which may be beneficial after open or closed reduction of cranio-dorsal coxofemoral luxation.

79
Q

What is the area moment of inertia?

A

Property of a material to resist bending forces.
For a rod, it’s proportional to the radius4
For a plate, it’s proportional to the height3

80
Q

In which direction should IM pins be placed in bones?

A

In the humerus, ulna and femur, they can be placed normograde or retrograde.
In the tibia, they can only be placed normograde.

Cant be placed in radius

81
Q

What is the difference between cortical and cancellous bone screws?

A

Designed accordingly to the bone type. Cortical bone screws have increased pitch and less thread depth.

82
Q

What are the 4 A’s to remember when assessing fractures radiographically?

A

Alignment (angulation and rotation)
Apposition (size of fracture gap)
Apparatus
Activity (healing of bone)

83
Q

Stability of conventional bone plates are reliant on what?

A

Friction between the plate, bone and screw. They require a minimum of 5 cortices above and below the fracture

84
Q

What are the 4 different types of plate (when describing methods of application)?

A
  1. Compression plate (achieves compression at fracture site)
  2. Neutralisation plate
  3. Bridging plate (fractures aren’t reduced)
  4. Buttress plate (supports an area of collapsed epiphysis)
85
Q

What are the advantages of interlocking nails?

A

Good at resisting bending
Prevent axial compression or rotation
Can be placed minimally invasively

86
Q

What are some advantages and disadvantages of external skeletal fixation?

A

Adv:

  • versatile/adaptable
  • rapid return to function
  • components can be reused

Disadv:

  • decreased limb use
  • draining pin tracts
  • increased patient care
87
Q

How might open fractures be classified?

A

Type 1: wound <1cm
Type 2: wound >1cm ut without extensive soft tissue damage
Type 3: Extensive ST damage
Type 4: Near amputation/ noon viable

88
Q

What are the two different types of bone grafts (and where are they from)? What are the advantageous properties of bone grafts?

A
  1. Autogenous cancellous bone graft: prox humerus, ilial wing or proximal tibia
  2. Cortical grafts (osteoconductive and osteoinductive)
    Properties:
    Osteogenesis (Produce new bone)
    Osteoinduction (recruitment and differentiation)
    Osteoconduction (microstructural support/ scaffold) Osteopromotion (structural support)
89
Q

How might you classify ligament sprain or tendon strain?

A

Grade 1= infl., pain, swelling or myositis but FIBRES INTACT
Grade 2= tearing of some fibres but still functional
Grade 3= complete tear (NON-FUNCTIONAL)

90
Q

How can infective arthritis occur?

A

Haematogenously
Bite wounds
Penetrating wound
Iatrogenic

91
Q

How might you tell the difference between osteoarthritis, septic arthritis and immune-mediated arthritis?

A

Arthrocentesis:

  • OA should have mildly increased cell count, predominantly mononuclear cells (synoviocytes and macs)
  • Septic should have a high cell count (>50), predominantly degenerate neutrophils and intracellular bacteria, monoarthropathy
  • IMA should have a markedly increased cell count (350), predominantly non-degen neutrophils and polyarthropathy. Also has pyrexia
92
Q

What are some radiographic findings of medial coronoid process disease?

A

Abnormal contour or poor definition of MCP
Subchondral sclerosis of medial portion of numeral trochlea
Secondary osteoarthritis
Separate fragment arising from medial coronoid process

93
Q

The anconeal process arises from a separate centre of ossification and fuses to the olecranon at ……of age.

A

3-5 months

94
Q

What are some radiographic signs of hip dysplasia and coxofemoral osteoarthritis?

A
  • rounding of acetabular margin/ shallow acetabulum
  • increased width of CF joint space
  • incongruity between femoral head and acetabulum
  • centre of femoral head sits lateral relative to dorsal acetabular rim
  • osteophytes/ enthesophtes
  • subchondral sclerosis
  • modelling of femoral head and thickening of neck
  • thickening of dorsocranial acetabular margin
95
Q

In what conditions should a stabilisation cast be avoided?

A
  1. In radius/ulna fractures of toy breeds due to poor blood supply-> nonunion
  2. Avoid in slow healing scenarios
  3. Avoid when patient or owner compliance is expected to be low
  4. Avoid if low cost is primary motivation (bc they can become costly over time)
96
Q

In order for an alteration in bone mass to be seen on radiography, what percentage of change is needed?

A

30-50%

97
Q

When assessing soft tissues structures with ultrasound, superficial structures are best imaged using …………… transducers whereas deeper structures are best imaged using……… transducers

A

High freq, linear transducers

Low freq, curvilinear transducers

98
Q

How would you expect the appearance of a tendinous lesion to appear on US as it moves through different stages of healing?

A

Acute phase: damaged region fills with blood, matrix debris and oedema fluid. Loss of fibre alignment will be evident in longitudinal plane.
After a few days, an organised haematoma forms and early granulation tissue forms. Appears as a discrete hypoechoic region= core lesion

99
Q

How is synovial effusion identified on US? What does septic effusion normally look like?

A

Increased volume of fluid within the joint or tendon sheath where it creates a halo around the tendon.

Septic= echogenic and particulate

100
Q

How is nuclear scintigraphy used in imaging MKS disorders?

A

IV injection of radiopharmaceutical (technetium methylene diphosphonate) which localises to areas of increased bone turnover by binding to surface of exposed hydroxyapatite crystals. Gamma radiation emitted detected by gamma camera

101
Q

How are scintigraphy images acquired?

A

Acquired in 3 phases:

  1. Vascular phase. Very rapid (1-2mins post injection). Distribution within intravasc space
  2. Soft Tissue phase. 5-10 mins. Equilibration with EC fluid
  3. Bone phase. 2-3 hours later. Radiopharmaceutical binds to bone
102
Q

Where are some common sites of stress fractures?

A

Scapula, humerus, tibia, mid-metacarpus and pelvis

103
Q

What are some primary indications for scintigraphy use in dogs?

A

Lameness that is difficult to localise (incl. medial coronoid disease and sesamoid fragmentation)
Primary bone neoplasia

104
Q

How do bones, tendons, IM fat, art. cartilage and muscle appear on T1W and T2W sequences (MRI)?

A

Bone/ tendons= hypointense
IM fat= hyperintense
Art. cartilage and muscle= intermediate signal

105
Q

Why are physeal fractures more common in younger patients? Include discussion of the hypertrophic zone in your answer.

A

Bc the physis is weaker than surrounding bone/ligaments. Cells in the hypertrophic zone are larger than those in the surrounding matrix and there is less matrix around them.

106
Q

What might happen if cells in the proliferative zone of bones is damaged?

A

Growth arrest may occur bc the physis becomes bridged by bone

107
Q

In dogs, when does most longitudinal bone growth take place? When do growth plates usually mineralise?

A

Bw 12-26 weeks of age

Between 4-12 months

108
Q

What is the Salter-Harris Scheme?

A

Classification system of physeal fractures.
Salter Harris 1= fracture involves physis only (Single)
SH 2= Physis and portion of metaphyseal bone (Above)- most common
SH3= Physis and epiphysis (articular) (Lower)
SH4= physis, epiphysis and metaphysis (Through)
SH5= crushing or compressive injuries of physis

109
Q

What are some advantages and disadvantages of physeal fracture and repair in young patients? What are some do’s and don’ts of fracture repair?

A

Adv: good blood supply and rapid healing
Disadv: ltd bone stock, soft bone, juxta-articular, potential for ongoing distraction forces on repair

DO:
-early, appropriate rigid internal fixation
-remove implants early for growth
-watch for angular limb deformities
-inform clients of potential consequences
DON'T:
-cast, bandage or splint
-use implants that bridge the physis
-cause compression across growth plate
-handle the epiphyseal side of physis
110
Q

What are the two common presentations of femoral capital physeal separations? How would they each be repaired?

A
  1. Immature, growth plate fractures in young patients with major displacement. Usually associated with major trauma. Repair with K wire
  2. Mature, minimally displaced separations= Capital physeal dysplasia= separation after physeal closure. Repair with lag screws +/- k wire. May get apple coring 3-6 weeks post sx.
    - in cats= feline physeal dysplasia syndrome. Overweight castrated males >1yo
    - in dogs=canine epiphysiolysis
111
Q

What are some indications for femoral capital physeal fracture salvage sx?

A
  • metaphyseal osteopathy in cats
  • cases where primary sx repair is impossible/ difficult
  • chronic presentation with established OA
  • client financial concerns
  • failed primary repair

Involves femoral head and neck excision (FHNE) and total hip replacement

112
Q

Describe distal femoral physeal fractures.

A

Seen in young dogs/ cats. Most often a SH2. Simple fractures are best treated with cross pins driven retrograde.
SH3-4 fractures require more complex internal fixation

113
Q

How might a simple tibial tuberosity avulsion fracture be treated? How about a proximal tibial physeal fracture?

A

Two K wires +/- tension band wire

Cross pinning

114
Q

What are the two common populations in which humeral condylar fractures are seen? Are there any breed dispositions with this? What is the difference between a unicondylar and dicondylar humeral fracture?

A
  1. Young, after trauma. Commonly SH3-4
  2. Mature adults, often secondary ti incomplete ossification of humeral condyle. Common in spaniels

Unicondylar: lateral side more commonly affected
Dicondylar: Y or T fractures with an intra-articular component and both lateral and medial epicondylar crests affected.

115
Q

What methods are available to surgically repair a humeral condylar fracture?

A

Transcondylar lag screw. If on epicondylar crest, K wires, lagscrews or a plate and screws.
Y and T fractures are more difficult

116
Q

What are the two main presentations of radial carpal bone fractures?
How are they treated?

A
  1. Chronic insidious mild lameness with no antecedent history of trauma. Often bilateral with established OA. Have male/breed predilections (boxers, english springer spaniel)
  2. Trauma associated with right radial carpal bone in racing greyhounds (often oblique and difficult to dx)

Conservative tx: NSAID’s for OA + external coaptation
Sx: lag screws, arthrodesis?

117
Q

There are 5 classifications of accessory carpal bone fractures. What is the px for each of these?

A

For types 1-4, px is good- 91% of dogs can return to racing

118
Q

What are some tx options for metacarpal/ metatarsal fractures?

A

Conservative: Cast or palmar splint to mid antebrachium/ tibia
Sx:
-miniplates for MC/MT 3 and 4
-IM pins (normograde distal, retrograde dowel pins)
-IM pins + ESF (tie in pins)

119
Q

What are some guidelines for when to treat metacarpal/tarsal fractures surgically?

A
  1. > 2 bones affected
  2. MC/MT 3 + 4 affected
  3. If articular
  4. If fragments are displaced >50%
  5. Large breed/ athletic dogs
  6. Fractures affecting base of MC 2 + 5
120
Q

When a pelvic fracture case comes in, what should you always assess? What is required for pelvic displacement?
What are some indications for sx?

A

Neurological function and urinary tract function
Fracture in 3 places req’d for displacement
-if on weightbearing axis (eg. SI joint, ilium, acetabulum)
-If acetabular involvement
-if sig pelvic canal narrowing (>50%)
-if hernia has occurred.

121
Q

What does conservative management of pelvic fractures entail? In which cases is this an option?

A
  • Cage rest for 4-12 weeks, analgesia, bladder care, padded bedding/ turning, monitor for pressure sores, physio
  • non-articular, non weightbearing, minimally painful, no canal narrowing
122
Q

What landmarks can be used to assess pelvic symmetry from lateral aspect?

A

Ileum, greater trochanter and ischium (make a triangle)

123
Q

When assessing pelvic fractures, it is important to assess neuro function so it is not confused as post op complications. What nerves are primarily assessed and how?

A

Sciatic nerve- withdrawal reflex (knuckling with conscious proprioceptive deficit= peroneal component; plantigrade stance= tibial component)
Pudendal nerve- anal tone/reflex
Cauda equina- tail tone/sensation

124
Q

What are some tx options for sacroiliac luxation?

A 
Conservative as long as contralateral hemipelvis is intact and no neuro deficits/ other orthopaedic injuries
Sx:
-lag screws 
-transilial pin/ bolt
-Pin/ tension band
125
Q

In which orientation are ilial fractures most common? What are some tx options?

A 
Long oblique (CV to CD)
Note: minimal bone stock available makes sx more difficult
-Lateral plating is most common
-ESF
-interragentary screws
-Ventral tension plating
-Dorsal plating in cats
126
Q

What are some treatment options for acetabular fractures?

A

-Acetabular/ reconstruction plates
-Dynamic compression plates
-Locking plates (esp string of pearls)
-Composites
-conservative tx in small patients-> salvage later?
Note: it is an articular fracture so early intervention is needed and perfect reduction is required

127
Q

Sacral fractures are classified in relation to sacral foramina. ______= medial to foramina, ________=lateral to foramina. ________ fractures are more likely to have neurological defects

A

Axial
Abaxial
Axial

128
Q

What surgical procedures are commonly done to correct pelvic floor fractures?

A

Surgery is not commonly done as it is not part of the weight bearing axis. Exceptions to this are with:

  1. Ischial tuberosity avulsion (origin of hamstrings)
  2. Pubic fractures associated with abdominal rupture (site of insertion of cranial pubic ligament)
129
Q

Why are depression fractures more common cf. displaced in maxilla?

A

Due to its inherent stability provided by medial, lateral and caudal buttresses which attach it to skull

130
Q

What is the main force acting on the mandible?

A

Bending (applied by masticatory muscles). Max tensile stress at alveolar margin, max compression on ventral surface

131
Q

How might you repair mandibular body fractures or caudal mandibular fractures?

A

Mand. body:

  • Tape muzzles (not in cats or brachycephalic dogs though)
  • intraosseous wires
  • intraoral splints
  • ESF
  • miniplates, bridging plates

Caudal:
-miniplates or interfragmentary wire

132
Q

What are some ddx for swellings between the toes?

A
  • pododermatitis
  • grass seed
  • tumour (SCC)
133
Q

Describe the treatment for acral lick granulomas in dogs?

A
  1. identify primary trigger and treat
  2. Treat infection
  3. Break the cycle (+/- behaviour modifying drugs/ environmental mod)
134
Q

What is plasmacytic pododeratitis?

A

Cause of foot pad swelling and ulceration in cats. Eventually causes lameness and pain. Tx with doxy

135
Q

What are some common types of fracture complications?

A
  1. Delayed, non-union (delayed= healing is progressing more slowly than expected; non-union= healing ceased and fracture healing not possible w/o intervention)
  2. Malunion
  3. Osteomyelitis
  4. Implant failure
  5. Refracture
  6. Late complications- neoplasia
136
Q

Non-union of fractures may be classified as viable or non-viable. Explain this is more detail.

What are some causes of non-union?

A

Viable= tissue present at fracture ends. May be hypertrophic or oligotrophic

Non-viable= no viable cells at fracture ends. May be:

  • dystrophic (radiographic appearance is similar to an oligotrophic non-union)
  • necrotic (presence of a sequestrum surrounded by an involucrum)
  • defect (fracture gap is too large)
  • atrophic (resorption of fracture ends -> pseudarthrosis)

Causes:

  • Instability-> hypertrophic
  • Stress protection (contstruct too rigid-> atrophic)
  • Too much gap -> defect n-u
  • Poor blood supply -> delayed, malunion, defect, necrotic, atrophic
  • Infection -> necrotic
137
Q

How might you tx viable non-unions/ delayed unions?

A
  • remove loose implants
  • improve stability
  • treat infection
  • destabilisation if due to stress protection
  • remove fibrous tissue
  • apply autogenous cancellous bone graft (or similar)
138
Q

define the following terms in reference to bone grafts:
Osteogenesis
Osteoinduction
Osteoconduction

A 
Osteogen= surviving graft osteoblasts produce new bone
Osteoind= chemical sign from growth factors to recruit pluripotent mesenchymal cells and induce them to differentiate into osteoblastic/ chondroblastic lineage
Osteocond= microstructural scaffold support for deposition of new bone
139
Q

From which areas can you collect autogenous cancellous bone for grafts? How about corticocancellous grafts?

A

Proximal humerus*, proximal tibia, iliac crest

Rib or iliac crest

140
Q

What is demineralised bone matrix?

A

osteoinductive, freeze dried cortical bone

141
Q

How might stress protection be prevented?

A
  • Staged destabilization
  • Circular or hybrid ESF
  • Use of titanium implants instead of stainless steel
  • Locking system and minimally invasive plate osteosynthesis to preserve surrounding soft tissue and vascularity
142
Q

What are the four types of malunion?

A
  1. Frontal-> varus, valgus
  2. Axial-> rotational
  3. Sagittal -> cavatus
  4. Shortening
143
Q

15% difference on length between R and L limbs are well tolerated. True or False?

A

False. ~10% is tolerated

144
Q

What is the most common organism responsible for post op osteomyelitis?
What are some common clinical signs and radiographic signs of osteomyelitis?

A

Staph aureus

CSs:

  • May be acute or chronic
  • Excessive/ cloudy/ purulent discharge
  • pyrexia
  • systemic signs, swelling, sudden deterioration in limb use

Radiographic:

  • soft tissue swelling/ emphysema
  • irregular diffuse periosteal rxn and lysis
  • osteoporosis
145
Q

What is the difference between fatigue failure, overload failure and biological failure of an implant?

A 
Fatigue= repetitive lower loads
Overload= single large load
Biological= tissue trauma and ischaemia
146
Q

What are some indications for amputation?

A
  1. Severe fracture comminution
  2. Neoplasia
  3. Severe soft tissue injury, loss or ischaemic necrosis
  4. Sever contamination
  5. Post-op complications
  6. Severe joint disease poorly responsive to appropraite medical mngt
  7. Peripheral nerve problems
  8. Financial concerns
147
Q

What are the two amputation techniques of the thoracic limb? Which is preferred method?
What techniques are available for the hindlimb?

A
  1. Scapulohumeral disarticulation
  2. Forequarter amputation**
  3. Mid femoral
  4. coxofemoral disarticulation
148
Q

What are some indications of arthrodesis? (7) What are some complications? (5)

A
  1. Collateral lig injury
  2. Hyperextension injury with or without luxation
  3. Shearing injury
  4. Irreparable articular fracture
  5. Severe DJD
  6. Immune mediated arthritis
  7. Neurogenic injury affecting the distal limb

Complications:

  1. Increased stress on surrounding joints
  2. Non-union
  3. Infection
  4. Implant failure
  5. Plantar necrosis
149
Q

80% of carpal motion occurs at which joint?

A

antebrachiocarpal joint

150
Q

What are some indications for a total hip replacement?

What are some complications of a total hip replacement?

A

Severe DJD
Fractures of femoral head/ neck
Salvage following acetabular fracture repair
Avascular necrosis of femoral head

Complications:
1) luxation, 2) sciatic neuropaxia, 3) aseptic loosening, 4) infection

151
Q

What is the difference between a cemented and non cemented total joint replacement?

A

Cemented= PMMA between implant and bone -> good early stabilty

Uncemented= Press fit or monocortical screws (early stability), osseous integration with microinterlock (late stability)

152
Q

What is arthroplasty and in which cases is it indicated?

A

=replacement, remodelling or realignment of joint bu osteotomy or some other procedure. Aims to relieve pain and restore function

  • Severe joint instability
  • irrepairable articular fracture
  • chronic lux
  • severe OA
153
Q

What are indications for excisional arthroplasty of glenoid?

A

glenoid dysplasia and chronic shoulder luxation

154
Q

What is ITAP?

A

Intraosseous transcutaneous Amputation prosthesis-> osseous and dermal integration of implants

155
Q

What is caudal cervical spondylomyelopathy?

A

= wobblers syndrome

->cervical spinal cord and nerve root compression

156
Q

What is discospondylitis? Where is it most common?

A

=infection in vertebral endplates (most commonly bacterial but can also be fungal) -> loss of structural stability of the vertebrae and impingement of the spinal cord causing pain and neurological dysfunction
Most common in lumbosacral space

157
Q

The most common form of primary bone cancer in dogs and cats is ________. Other forms of primary bone cancer include _______, _________, and _________.

A

Osteosarcoma (away from the elbow, towards the knee)

Chondrosarcoma (2nd most common, often in nasal cavity)
Haemangiosarcoma
Fibrosarcoma

158
Q

What is the typical signalment for OSA?

A

Large to giant breed dogs
Middle to older age (7-9)
males> females ??
neutered >non neutered

(**median survival time is 8-11 months with amputation and chemo)

159
Q

What is the median survival time for a chondrosarcoma? Where do they usually occur?

A

2.7 years with surgery

Nasal cavity but also occur on other flat bones (ribs, pelvis, scapula)

160
Q

Cf. people, metastatic bone cancer in dogs is quite common. T or F?

A

F. It’s actually quite rare. If it occurs it is more commonly from carcinomas (of the bladder, prostate, mammary glands)

161
Q

What neoplasia affects bones of the skull?

A

Multilobular osteochondrosarcoma (has “popcorn ball” appearance on radiographs)- Maxilla, mandible, calvarium

Has good Px if complete excision (has moderare metastatic potential)

162
Q

What are some clinical signs of oral neoplasia? What would be your general approach to the diagnosis and management of oral masses?

A

CSs: mass in mouth, halitosis, dysphagia, bloody discharge, loose teeth, drooling, poor grooming

Dx: Stage tumour, surgical excision (maxillectomy, mandibulectomy), adjunct therapy

163
Q

What are some Ddx for oral neoplasias in dogs and cats?

A

Dogs: melanoma, SCC, Fibrosarcoma
Cats: SCC, fibrosarcoma

Other less common: OSA, MCT, plasmacytoma, MLO, Epulidies

164
Q

Malignant melanomas in dogs are locally invasive and met rapidly to ______ and _______. They can be melanotic or amelanotic. Tx involves ______. Px is guarded (_______)

A

Lungs and regional LNs
Wide excision, cryotherapy and immunotherapy (oncocept vaccine)
8-9m

165
Q

SCC are the most common oral tumour in _____. They can occur _______ or _______. They’re locally invasive and, except for the _________ form which is highly malignant, only 10% metastasize. They are radiosensitive.

A

Cats
In tonsillar crypts or on the gingiva
Tonsillar form

166
Q

Oral fibrosarcomas are most commonly seen on _________ and _______. They are aggressively locally invasive. Are they radiosensitive? What is a Hi-Lo?

A

Maxillary gingiva and hard palate
Not radiosensitive
Hi-Lo FSA in golden retrievers= histologically benign appearance but biologically aggressive

167
Q

Papillomas are benign oral tumours in ____(younger or older?) dogs. Do they need tx?
Fibromas are rare benign oral tumours.
Odontogenic tumours arise from _____. The most common type are ______.

A

younger dogs. They regress with age

Dental laminar epithelium
Ameloblastomas

168
Q

The most common type of benign oral tumour is _________. The three types described are _____, ______, _____. They arise from the _________.

A

An Epulides.
Fibromatous, ossifying, acanthomatous (these ones are very invasive)
Periodontal ligament

169
Q

What are some signs of the dyspnoeic patient?

A 
tachypnoea
Increased abdominal movement
Paradoxical abdominal movement
Extended neck + abducted elbows (=orthopnea)
Open mouth breathing 
Cyanosis
Lateral recumbency
170
Q

What may be the general cause of the following respiratory problems:

  1. Increased inspiratory effort
  2. Increased expiratory effort
  3. Increased inspiratory AND expiratory effort
A
  1. Upper airway obstruction, severe pleuritis
  2. Small airway disease
  3. Pulmonary parenchymal disease
    (eg. pulm oedema, pneumonia, pulm. haemorrhage, pulm. thromboembolism, diffuse neoplasia, interstitial disease)
171
Q

What are some examples of upper airway obstructions in dogs and cats?

A

DOGS:

  • Laryngeal paralysis
  • Brachycephalic airway disease
  • Tracheal collapse
  • Upper airway inflammatory polyps or neoplasia

CATS:

  • Laryngeal paralysis
  • Laryngeal neoplasia
  • Nasopharyngeal polyps
172
Q

What is stertor and stridor?

A

Stertor= nasopharyngeal obstruction

Stridor=laryngeal obst.

173
Q

With what conditions might you see paradoxical abdominal movement?

A
  • Upper airway obstruction
  • stiff lungs
  • Pleural effusion
  • Diaphragm dysfunction
174
Q

Most dyspnoeic cats will have one of what three things?

A
  1. Cardiogenic pulmonary oedema (skinny old cats and young cats, hypothermia, gallop rhythm or heart murmur)
  2. Pleural effusion
  3. Lower airway disease (hx of cough, younger and hyperthermic)
175
Q

Which respiratory disorders are common in the following patients:

  1. Old toy and small-breed dogs
  2. Brachycephalic breeds
  3. Old large-breed dogs
A
  1. Cardiogenic pulm. oedema, collapsing trachea, PTE
  2. Upper airway obstruction, aspiration pneumonia
  3. Laryngeal paralysis, Cardiogenic pulmonary oedema (arrhythmia in dobermans and other large breeds)
176
Q

In puppies with neurogenic oedema, which lung fields typically have harsh sounds?

A

dorsocaudal distribution in puppies with neurogenic oedema

177
Q

What are the 5 points for thoracic ultrasound?

A

2x chest tube site (between 8th and 9th intercostal space dorsally)
2x pericardial sites (3rd, 4th and 5th intercostal spaces)
1x diaphragmatico-hepatic

178
Q

A normal PaO2 is _____. A normal PvO2 is ______. A normal O2 sat Hb is _______.

A

80-100 mmHg (<75, treat with O2 supp; <55=life threatening)
40 mmHg
60-70 mmHg

179
Q

When sampling an arterial blood gas, from which sites can you sample? What are some rules about sampling an arterial blood gas?

A

Percutaneous: femoral, dorsal metatarsal, brachial or auricular arteries

Catheter: dorsal metatarsal artery

  • remove all air bubbles (air changes pO2/pCO2)
  • cap with an airtight seal
  • place on ice
  • analyse within 2 hours
  • adjust for body temp?
180
Q

A normal pulse ox reading should be between _____. An acceptable reading is _______.

A

95-99%

93-99% (93= PaO2 of 80mmHg)

181
Q

What are some methods of oxygen supplementation (include their FiO2)?

A
  1. Flow by O2 (0.25-0.4)
  2. Oxygen mask (up to 0.6)
  3. Nasal oxygen (~0.4)
  4. Oxygen hood (0.3-0.4)
  5. Oxygen cage (high)
182
Q

What are three mechanisms of hypoxaemia?

A
  1. Low inspired oxygen partial pressure (low FiO2 or low barometric pressure)
  2. Hypoventilation (CO2 accumulation)
  3. Pulmonary gas exchange abnormalities: venous admixture (anatomic shunt, perfusion of poorly ventilated lung areas and oxygen diffusion impairment)
183
Q

What are example causes of hypoventilation?

A
  • airway obstruction
  • neuromuscular disease
  • anaesthesia
  • spinal cord dysfunction cranial to C4-C5
  • phrenic nerve dysfunction
  • chest wall injury
  • resp fatigue
  • malignant hyperthermia
184
Q

Decreasing tissue metabolism for the management of UA obstruction can be achieved with sedation. What drugs are useful for such causes and what are some pros and precautions associated with their use?

A

Ace, butorphanol, midazolam

Pros: reduced O2 consumption, reduced metabolic heat production (-> decr hyperthermia and decr CO2 prod), less resp drive (less risk of dynamic airway collapse)

Precautions: CV collapse, relaxation of pharyngeal dilator muscles (airway collapse), less resp drive (resp arrest)

185
Q

What are some causes of venous admixture?

A
  • Pulmonary oedema
  • Pneumonia
  • Pulmonary contusions
  • Atelectasis
  • Lung collapse
  • Pulmonary TE
186
Q

What is the difference between pressure-controlled ventilation and volume-controlled ventilation?

A

Pressure-controlled= preset inspiratory pressure delivered, pressure constant, volume variable

Volume controlled= preset tidal volume delivered (8-10ml/kg), volume constant, pressure variable

187
Q

What are some major ddx for:

a) sneezing?
b) serous discharge?
c) mucopurulent discharge?
d) epistaxis?

A

a) Nasal FB, Feline URTI, exposure to irritant aerosols, canine nasal mites
b) normal, virus, irritants, early stages of…..
c) viral, bacterial or fungal infections, nasal parasites, FB, neoplasia, polyps, allergic rhinitis etc
d) acute trauma/ FB, neoplasia, fungus, coagulopathy, systemic hypertension, polycythaemia, hyperviscosity syndrome, vasculitis, infection.

188
Q

Which cats are most prone to feline URTI? How may it present ? Which organisms are responsible most of the time?

A

young, stressed and/or immunosuppressed cats in stressful or crowded environments with poor husbandry

Acute sneezing, serous to MP ocular and nasal discharge, conjunctivitis, hypersalivation, fever, anorexia, dehydration

Feline calcivirus and feline herpesvirus 1 (others include chlamydia felis and bordetella bronchiseptica)

Self-limiting

189
Q

What is Pneumonyssoides caninum?

A

=canine nasal mites
directly transmitted and occurin frontal sinuses and caudal nose. Cause acute rhinitis signs. Tx with ivermectin, milbemycin or selamectin

DVM3 (13 decks)

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