Dog and Cat 8 Flashcards

1
Q

Carpus arthrodesis how common, indications and what need to identify beforehand

A
- Most frequently arthrodesed joint
• Indications:
- Carpal hyperextension injury - high-rise syndrome 
- Joint luxation
- Chronic, severe OA
• Identify the LEVEL of injury
- Palpation
- Stress Radiography
• Identify concurrent injury:
- Collateral ligaments
- Metacarpal fracture
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2
Q

Pancarpal arthrodesis what use

A
  • plate fixation
  • ESF
  • Cross pinning (small animals only)
  • THEN at least 8 weeks of a cast or splint
    • Evolution of implant design:
  • DCP (dynamic compression plate) -­> Hybrid -­> Castless PCA
  • Compression holes
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3
Q

Partial carpal arthrodesis what involved and why and the 2 main techniques used

A
  • 80% of carpal motion at antebrachiocarpal joint
  • Partial carpal arthrodesis – fusion of intercarpal and carpo-­ metacarpal joint
  • Ensure no involvement of the antebrachiocarpal joint (difficult)
  • Cats requirement for supination?
    • Techniques:
  • Plate Fixation - T plate
  • Pins (Very small animals only)
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4
Q

Stifle athrodesis indications and technique

A
• Indications:
- Severe degenerative joint disease:
- Intra-­articular fractures
- OCD
- Instability from collateral or multiple ligament injury
• Technique:
- Plate fixation (pin techniques in small animals)
- Maximise bone contact area by removal of intra-­articular structures:
○ Cranial & Caudal Cruciates
○ Menisci
- Long Lever arms – bone fracture
- Compression
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5
Q

Stifle arhrodesis complications

A
1) Implant failure:
○ Insufficient bone contact
○ Cycling
2) Fracture:
○ Long Lever Arms
○ Plate Span
3) Infection:
○ Strict asepsis
Consequences -­ implant removal
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6
Q

Hock arthrodesis how common, indications and what need to idetnfiy

A
• Indications:
- Severe degenerative joint disease:
- OCD
- Joint Instability
- Shearing Injury
- Calcanean Tendinopathy
- Hyperextension Injury
• Identify LEVEL of injury:
- Palpation
- Stress Radiography
• Identify concurrent injury
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7
Q

Hock arthrodesis technqiues and complications

A
Techniques:
- Plate fixation (Cranial vs Medial) -> medial 
- ESF
- Pin and Tension Band Wire
- Pantarsal vs Partial Tarsal Arthrodesis:
○ Calcaneoquartal
○ Tarso-­metatarsal
• Complications 
-  Plantar necrosis
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8
Q

Total hip replacement indications, outcome and complications

A

Indications:
- Severe degenerative joint disease (CHD) -> due to hip dysplasia
- Fractures of the femoral head/neck
- Salvage following acetabular fracture repair
- Avascular necrosis of the femoral head
- CONSIDERED - gold standard
Outcomes
- Good to excellent outcomes in 80-­98% cases
Complications:
- Coxo-­femoral Luxation - can revise the surgery and change the head size
- Sciatic neuropraxia
- Aseptic loosening
- Infection - require removal

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9
Q

Total hip replacement what are the 2 main techniques what provides stability

A
  1. Cemented:
    - Polymethylmethacrylate -­ cohesive interface btn implant and bone
    - Good early stability
    - Aseptic loosening:
    ○ Enzymatic osteolysis
    ○ Cytokine induction of osteoclasts - > Bone Resorption
  2. Uncemented:
    - Press-­fit or monocortical screws (early stability)
    - Meticulous preparation
    - Osseous integration with micro-­interlock (Late stability)
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10
Q

Elbow total replacement indications, 2 techniques and 4 complications

A
Indications:
- Severe bi-­compartmental disease:
- OCD
- Coronoid process disease
- Not luxation
• Techniques 
	- Lowa 
	- TATE 
• Complications: - may result in amputation or arthrodesis 
1. •Fracture
2. • Luxation
3. • Persistent lameness
4. • Infection
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11
Q

Stifle total replacement indications and complications

A
• Indications:
- End-­Stage OA:
○ OCD
○ Cruciate disease
- Combination System:
○ Press-­fit Femoral component
○ Cemented Tibial component
• Complications:
- Luxation
- Infection
- Aseptic loosening
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12
Q

Stifle total replacement outcomes

A
  • Improved ROM - RANGE OF MOTION
  • Improved objective functional data:
    ○ PVF 80% normal contralateral
    ○ Impulse 90% normal contralateral
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13
Q

Femoral head and neck excisional arthroplasty indications

A
  • Fractures of the femoral neck or head
  • Slipped capital physis (cats)
  • Avascular necrosis of the femoral head (dogs)
  • Chronic coxofemoral luxation
  • Failed total hip arthroplasty
  • Severe OA secondary to CHD & not palliated by medical management)
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14
Q

Femoral head and neck excisional arthroplasty technique and what equipment used and what done at the end

A
  • Craniolateral approach to the hip joint
  • Disarticulation if required
  • External rotation of the femur
  • Parallel to sagittal plane of neck:
    ○ Prevent caudal spur formation - limits the range of motion
    1. • Oscilating Saw (preferred)
    2. • Gigli Wire
    3. • Osteotome & Mallet
  • Check cut surface of proximal femur before you close -> need to ensure take whole neck out
    4. Rasp if spur present
    5. Post-­operative radiograph - to ensure you take enough
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15
Q

Femoral head and neck excisional arhtroplasty what are the 7 complications

A
  1. Infection
  2. Seroma
  3. Persistent lameness (leg shortening)
  4. Muscle atrophy
  5. Decreased ROM (extension and abduction)
  6. Patellar luxation
  7. Sciatic neuropathy
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16
Q

Femoral head and neck excisional biopsy outcome and how modified

A
  • Never return to normal function based on PVF (PEAK VERTICAL FORCE) and impulse.
  • Modified by:
    ○ Surgical technique (failure to remove all femoral neck)
    ○ Duration of clinical signs (muscle atrophy)
    ○ Age (immature vs mature)
    ○ Post-­operative care (physiotherapy)
    ○ Body weight/condition
    • Published outcomes:
  • Largely subjective
  • Acceptable function
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17
Q

Excision arthroplasty of the glenoid when used, indications and outcomes

A
  • Salvage for severe OA of the glenohumeral joint in small dogs
    • Indications:
  • Glenoid dysplasia
  • Chronic shoulder luxation
    • Acceptable outcomes in limited numbers of cases in small dogs
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18
Q

Intraoesseous transcutaneous amputation prosthesis what are they, used for and complications

A
  • Osseous and dermal integration of implants – robust prosthetic integration
  • Partial amputation
    • Complications:
  • Infection
  • Epidermal ingrowth
  • Marsupialisation
  • Peri-­prosthetic fracture
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19
Q

Oncologic limb sparing 2 main indications what is involved

A
•  Indications:
- Neoplasia of the extermities (OSA)
- Distal radius
• The affected bone is resected with appropriate margins (3cm)
• Antebrachiocarpal disarticulation
• Replacement of the missing segment:
- Cortical allograft (bone bank)
- Metal endoprosthesis
- Ulnar rollover
- Bone transport osteogenesis
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20
Q

Axial skeleton disease what commonly lead to and conditions involved

A
  • Diseases that affect the axial skeleton frequently cause dysfunction of the bone or nervous system (brain and spinal cord)
  • These conditions include congenital malformation, neoplasia, infection, and trauma resulting in fracture / luxation.
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21
Q

Congenital malformation and neoplasia of axial skeleton what involved

A
  1. Congenital malformation
    - Atlantoaxial luxation/subluxation
    - Cervical vertebral malformation (Wobbler) -
    stenosis
  2. Neoplasia
    - Oral and skull neoplasia (MLOs)
    - Primary and metastatic neoplasia of vertebral body
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22
Q

Infection of axial skeleton what called, common infection, how arrive, what leads to

A

Discospondylytis

  • Infection in vertebral endplates
  • Most commonly bacterial infection but can be fungal infection
  • Haematogenous spread -> from urinary tract infection
  • Lumbosacral disc space
  • Loss of structural stability of the vertebrae and impingement of the spinal cord causing pain and neurological dysfunction
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23
Q

Instability/degeneration/trauma of oxial skeleton what are the 3 main diseases and what result in

A

1) Vertebral fracture / luxation
○ Severe trauma results in unstable vertebral column and varying degrees of spinal cord compromise
○ Can result in complete core transection -> BAD
2) Lumbosacral disease / instability
○ Can lead to budging of the disc - putting pressure on nerve
§ Lumbosacral pain and ataxia can result
3) Intervertebral disc disease

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24
Q

Musculoskeletal neoplasia what is the most common form and some other causes

A
  • The most common form of primary bone cancer (85% of all cases) in dogs and cats is osteosarcoma (OSA).
  • Other types of primary bone cancer
    ○ Chondrosarcoma
    ○ Fibrosarcoma
    ○ Haemangiosarcoma
  • Metastatic (secondary) neoplasia of the bone is less common in companion animals than it is in people.
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25
Q

Osteosarcoma distribution - common signs and signalment

A

Distribution
- OSA most commonly affects the appendicular (75%) vs. axial skeleton (25%)
○ ‘Away from the elbow, towards the knee’ - mainly in forelimb
○ FL 2.5 x HL - more common in forelimb
§ Proximal humerus
§ Distal radius ** - MOST COMMON SITE
§ Distal femur
§ Proximal / Distal tibia - hindlimb
§ Axial skeleton (skull, spine, ribs)
Signalment
- Typically affects large to giant breed dogs
- Middle to older aged (7-9 yrs)
- ? Males > females, neutered > non neutered

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26
Q

Osteosarcoma character and prognosis with different treatmetn options

A
  • OSA is an aggressive tumour with local invasion and destruction and high metastatic potential - NOT GOOD
  • Expected median survival time (MST):
    ○ Amputation and chemotherapy - curative intent treatment -> CANNOT CURE but best option
    § MST 250-350 days (8-11months) - quality of life is good
    § 2 year survival time of 20%
    § 3 year survival time of 10%
    ○ Amputation alone
    § MST 4-5 months
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27
Q

Osteosarcoma risk factors and poorer prognosis

A
  • Negative prognostic factors for both mortality and metastasis
  • Tumor location
    ○ Proximal humerus, distal femur, proximal tibia -> higher muscle mass so less likely to detect mass earlier
    ○ MST for prox. humerus is 132 days < other locations
  • High ALP levels
    ○ Dogs with ↑ ALP lived 156 days less than dogs with normal ALP
  • Increasing body weight
  • Stage III disease (mets to lungs, bones, LNs)
    ○ Mets to bone (130d) longer MST than mets to lung (59d) or LN (59d)
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28
Q

Osteosarcoma diagnosis 6 options

A
  1. Signalment
  2. Clinical history - can present as lameness
  3. Clinical Pathology –ALP
  4. Radiographs
    ○ mixed lytic and proliferative pattern - sunburst affect
  5. Cytology (ALP staining)
    ○ Fine needle aspirates -> medullary sample
  6. Biopsy (Jamshidi needle core)
    Want to get the central part of lesion -> don’t want to go through the bone
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29
Q

Osteosarcoma what are the 5 steps in staging

A
  1. 3 view thoracic radiographs - 2 laterals and ventrodorsal
    ○ 10% dogs have macroscopic mets at Dx
  2. Thorough orthopaedic exam - can they tolerate an amputation
    ○ Bone is 2nd most common site of metastasis
  3. Nuclear Scintigraphy –Tc99-m - screen whole body for metastasis to other bones
  4. Evaluate regional lymph nodes
    ○ Axially and prescapular lymph nodes if forelimb
  5. Whole body CT or MRI or radiographic survey
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30
Q

Osteosarcoma treatment goal and the 2 main types of treatment

A
  • Effective treatment requires careful diagnostic workup and communication with the patient owner about expected outcome of treatment
  • Goal of therapy is best QOL for patient
    a. Curative Intent
    b. Palliative therapy
    1. Curative Intent
    2. pallitative therapy
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31
Q

Curative intent treatment for osteosarcoma what is the goal, how achieve and the 2 main options and complications with this

A
  • Goal is to provide best quality of life AND extend life for as long as possible
  • Local tumour control can be achieved with either amputation or limb salvage
  • Control of metastatic spread requires the use of adjuvant chemotherapy
    ○ Carboplatin
    1. Amputation -> steps on previous lecture
    2. Limb salvage - forelimb
  • Resect OSA affected bone
  • Replace bone defect with metal endoprosthesis or cortical allograft
  • Distal radius most successful
  • Complications
    ○ Implant failure
    ○ Infection -↑ survival time
    ○ Local recurrence - 30% of cases
  • Equivalent MST with chemotherapy to amputation + chemotherapy
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32
Q

Osteosarcoma palliative therapy what is the goal and 5 options

A
  • Goal is to provide best quality of life but not necessarily extend duration of life
    1. Amputation –pain control
    2. NSAIDs, Analgesics
    3. Bisphosphonates –pamidronate, zoledronicacid -> inhibit osteolysis -> used for osteoporosis in people
    ○ Inhibits osteoblasts -> inhibits ongoing bone destruction
    4. Radiation therapy
    ○ 75% good to excellent analgesic response for 3-4 months
    ○ Radiopharmaceuticals –Samarium-153
    5. Combination therapy
    ○ XRT + Chemo + bisphosphonates
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33
Q

Palliative therapy osteosarcoma disease progression within

A
  • Disease Progression
    ○ Development of metastatic disease
    ○ Pathologic fracture - generally leads to euthanasia decision -> cannot heal
    ○ MST > amputation alone but < curative intent
    § XRT + Chemo longest MST
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34
Q

Chondrosarcoma how common, common sites, character and median survival

A

○ Second most common primary bone
○ Nasal cavity = most common site
○ Flat bones (ribs, pelvis, scapula)
○ Slower progression, slower metastasis - chemotherapy not needed
○ *Grade may influence
○ Median survival = 979 days (2.7 yrs) surgery alone

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35
Q

Metastatic bone neoplasia how common in dogs, commonly from what cancers

A
  • Rare in dogs compared to people
  • Commonly from carcinomas
    ○ bladder, prostate, mammary
    ○ squamous cell carcinoma
    ○ diaphysis (nutrient foramen)
  • Sarcomas
    ○ especially following chemotherapy
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36
Q

Skull neoplasia what is the most common one, location, breed, radiographic findings, character, histological grade prognosis, prognosis and adjuvant therapy

A

MLO - Multilobular Osteochondrosarcoma (MLO)
- Affects flat bones of the skull
○ Maxilla, mandible, calvarium
- Older, medium-to large-breed dogs
- On radiographs, mass with nodular or stippled mineralized densities and lysis of bone
○ “Popcorn ball” appearance
- Slow-growing, locally invasive tumor with moderate metastatic potential
- Histological grade prognostic
○ Higher grade more aggressive biological behaviour
- Good Px if complete excision
- Adjuvant therapy no proven benefit

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37
Q

Oral neoplasia what are the 6 general appraoch to the diagnosis and management of oral massess

A
1. Biopsy the lesion THROUGH THE MOUTH (inside out) -malignant or benign
○ Bx from oral side not from skin side
○ Tumour type, grade
2. Radiology / CT of mouth / head / neck
○ Sx planning, staging, osteolysis
3. Assess regional lymph nodes
○ Palpation, FNA Cytology +/-biopsy
4. Tumour Staging
○ Thoracic radiographs or CT
○ Regional LN evaluation
5. Radical surgical excision
○ Maxillectomy or mandibulectomy
6. Adjunct therapy
○ Radiation (XRT), Cryotherapy, tumour vaccine
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38
Q

Oral neoplasia clinical signs and most common ones in dogs and cats

A
Clinical Signs 
- Mass in mouth
- Halitosis
- Dysphagia
- Bloody discharge
- Loose teeth (esp. SCC)
- Drooling*
- Poor grooming* -> * esp. cats
Dogs - melanoma, then SCC, then fibrosarcoma 
Cats - SCC - can look like resorptive lesions
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39
Q

Malignant oral tumours list the 3 main ones and the 2 main benign ones

A

1) malignant melanoma
2) squamous cell carcinoma
3) fibrosarcoma
Benign
1) papillomas
2) fibromas
3) odontogenic tumours
4) epulides

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40
Q

Malignant melanoma what age generally occur in, location, character, types, treatment and prognosis

A
  • Older animals
  • Gingiva, mucosa, palate and tongue
  • Locally invasive
  • Met rapidly to the lungsand regional LNs
  • Melanotic or amelanotic form - doesn’t have to have pigment
  • Treatment: Wide excision, cryotherapy, immunotherapy (Oncoceptvaccine) - quite effective
  • Prognosis: Guarded MST 8-9 months
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41
Q

Squamous cell carcinoma in oral cavity location, character, how common and treatment

A
  • Tonsillar crypts or on the gingiva.
  • Locally invasive
    ○ Except for the tonsillar form, which are highly malignant, only 10% metastasise
  • Most common oral tumour in cats
  • Treatment: Wide excision can be curative
    ○ Radiosensitive, cryosurgery
42
Q

Fibrosarcoma of oral cavity location character, recurrence, treatment and type within goldern Ret

A
  • Maxillary gingiva and hard palate and
  • Aggressively locally invasive
  • Recurrence following excision is common
  • Treatment: Wide surgical incision, cryosurgery
    ○ They are not radiosensitive
  • Hi-Lo FSA in Golden Ret. Histologically benign appearance but biologically aggressive
43
Q

Papillomas and fibromas of oral cavity character and common age

A

Papillomas
- Younger dogs and may be solitary or multiple
- These tumours will normally regress with age
Fibromas
- These are rare benign tumors of the oral cavity

44
Q

Odontogenic tumours and epulides of the oral cavity, how common, main types and treatment

A

Odontogenic tumours
- Rare tumours which arise from the dental laminar epithelium
- Ameloblastomas being the most common
- They require radical excision or cryotherapy
Epulides
- The most common type of benign tumours
- 3 types described:
○ Fibromatous, ossifying, acanthomatous
- All arise from the periodontal ligament
- Treatment: excision, curetage, radation.
- Acanthomatous epulides, whilst benign, are regarded as very invasive and require wide excision with maxillectomyor mandibulectomy

45
Q

What are the 5 main respiratory mechanisms

A
  1. Sneeze/ Reverse Sneeze
  2. Cough
  3. Nasal discharge
  4. Dyspnoea
  5. Stridor/Stertor
46
Q

Sneezing what is it, why occurs, accompanied by and differential fr sneezing with and without discharge

A
  • An explosive release of air from the lungs through the nose and mouth
  • A protective mechanism to rapidly remove chemical and physical irritants from the nasal epithelial surface
  • Often accompanied by nasal discharge
  • Need to look at environment pollutants, stress (stocking density) etc.
    Sneezing without discharge
    1. Acute Foreign Body
    2. Acute Allergic Process
    Sneezing with discharge
  • Did it start serous and then become purulent?
  • Cats- FHV,FCV
  • Dogs -> rare to be just bacterial infection -> don’t just give antibacterial
47
Q

Reverse sneezing why occurs, purpose and cause

A
  • Usually nasopharyngeal irritation - generally quite benign
  • Purpose is to move secretions and foreign material into the orophranyx so it can be swallowed
  • Causes– excitement, epiglottic entrapment of the soft palate, nasal mite, viral infections, foreign bodies
48
Q

Snuffling cause and when an issue

A
  • Usually because the nasal passages are congested
  • Not too much of a problem EXCEPT in nasal obligate breathers
    ○ Cats– respiratory viruses
    ○ Rabbits – bacterial infection often secondary to teeth problems
    ○ Obligate nose breathers such as horses and especially, rabbits and rodents can be greatly affected by nasal discharge that block the nasal passages
49
Q

Cough define, stimulatedand types of cough

A
  • Sudden noisy expulsion of air from the lungs against a closed glottis
  • Stimulated by mechanical or chemical irritation of the pharynx, larynx, trachea, bronchi and smaller airways
  • Categorise
    ○ Dry C⁺⁺– cough without expectoration
    ○ Productive C⁺⁺– material expectorated(maybe swallowed)
    ○ Goose honk C⁺⁺ -chronic , harsh dry cough characteristic of collapsed trachea
    ○ Nocturnal C⁺⁺- associated with the initial phase of cardiac disease, psychogenic coughing or collapsed trachea
50
Q

Causes of cough

A
  • Less common causes– pleural, pericardial, diaphragm, nasal, nasal sinuses and mediastinal disease
  • If infection is it contagious?
    ○ Dogs- Kennel cough - give anti-inflammatories
    ○ Cats - Respiratory viruses FCV/FHV
    ○ Equine- influenza, strangles, herpes virus
  • Or opportunistic– eg. Pasteurella in rabbits - not contagious
51
Q

Dyspnoea prolonged inspiratiory phase with and without noise what location is the problem most likely and same with prolonged expiratory phase

A

-Prolonged inspiratory phase with noise is likely to be an upper airway problem - stridor
-Prolonged inspiratory phase with no noise— think pleural space problem
§ Think pleural fluid, mass, abdominal organ through a hernia of the diaphragm
§ The respiratory rate is usually increased
-Prolonged expiratory phase why is it hard to get the air out?
§ Think small airway disease such as COPD (chronic obstructive pulmonary disease) in horses, asthma in cats

52
Q

pleural space problem what is important with the examination

A

□ Auscultate the chest to see if chest sounds are increased, normal or decreased
□ Check ventrally and dorsally
® Loud/normal dorsally dull ventrally–pleural fluid highly likely
® Loud ventrally, dull dorsally – pneumothorax highly likely
® Loud all over lungs- harsh or crackles – diffuse disease often mixed respiratory pattern (insp and exp)
® Oedema – cardiogenic or non-cardiogenic
◊ Listen for murmurs, gallop rhythms
◊ Non cardiogenic – strangulation, head trauma, seizures, electrocution
® Dull in parts- aspiration pneumonia?, pulmonary contusions

53
Q

Stridor define, what need to determine, what may need and common cause in old dogs

A
  • Shrill harsh sound especially the respiratory sound heard during inspiration in laryngeal obstruction
  • Does it only occur with exercise or at rest - rest brachycephalic
  • May need tracheostomy or other form of oxygen delivery before diagnostics are performed
  • Old dogs– laryngeal paralysis – usually chronic, worse in summer as unable to thermoregulate as efficiently, often there is a history of voice change (may be chronic -> history within the past year)
  • May be at rest but often early in course of disease clinical signs seen with exercise or stress
54
Q

Stertor what is it and due to

A
  • Snoring, sonorous respiration
  • Usually due to partial obstruction of the upper airway eg laryngeal stenosis, nasal obstruction, pharyngeal obstruction
55
Q

what are the steps in normal inspiration

A

• contraction of diaphragm

• expansion of thorax

• drop in pressure in pleural cavity (754 mm Hg)

• expansion of lungs and drop in intra-alveolar pressure

• airflow down pressure gradient into lungs (until pressure equal to atmospheric pressure)

56
Q

Paradoxical abdominal movement what occurs and causes

A
  • The diaphragm is pulled inwards because the lungs are not expanding as they should
  • Diffuse parenchymal lung disease causing poor lung compliance eg fibrosis, neoplasia
  • Upper airway obstruction
  • Diaphragm dysfunction
  • Pleural space disease
57
Q

Assessment of normal breathing what is the normal RR, respiratory pattern and effort

A
  • Respiratory rate - 15-25bpm
  • Normal respiratory pattern
    ○ Diaphragmatic contraction accounts for 70-80% of a resting inspiration
    ○ Diaphragmatic contraction results in passive abdominal movement
    ○ On inspiration, chest and abdomen move out
  • Normal respiratory effort
    ○ Inspiration is active, but effortless
    ○ Expiration is passive
58
Q

Pulmonary auscultation what do harsh, crackles, wheezes indicate as well as absent lung sounds, what sounds hear of trachea, bronchoal tree and alveolar tree

A
  • Harsh, crackles, wheezes
    ○ Crackles caused by fluid or alveoli opening and closing
    ○ Wheezes caused by narrow airways
    Absent lung sounds = pleural space disease; no flow
    Tracheal sounds -> soft no crackles
    Bronchoal tree -> hear heart on background, increased sound due to turbulence
    Alveolar sounds -> becoming softer again
59
Q

What are some common clinical signs of dyspnoic patients

A
  • Tachypnoea -> Increased abdominal movement
    ○ Paradoxical abdominal movement
    ○ Extended neck and abducted elbows (orthoponea) - indicated very severe dyspnoea
    ○ Open mouth breathing -> less resistance through mouth than nares
    ○ Cyanosis
    ○ Lateral recumbency
    BEWARE -> of rapidly changing body position and pupillary dilation in cats
60
Q

What are 6 anatomic origin of dysponea and location generally for increased inspiratory, expiratory and inspiratory and expiratory effort

A
  1. Upper airway
  2. Small airway
  3. Pulmonary parenchyma
  4. Pleural space
  5. Chest wall and diaphragm
  6. Look-alikes
    Increased inspiratory effort
    - Upper airway obstruction (stretor or stridor)
    - Severe pleuritis (chronic pleural effusion)
    Increased expiratory effort
    - Small ariway disease
    Increased inspiratory and expiratory effort
    - Pulmonary parenchymal disease
61
Q

List 4 main dog and 3 main cat upper airway diseases/conditions

A
- Dogs 
○ Laryngeal paralysis 
○ Brachycephalic airway disease 
○ Tracheal collapse 
○ Upper airway inflammatory polyps or neoplasia 
- Cats 
○ Laryngeal neoplasia - LSA v SCC
○ Nasopharyngeal polyps 
○ Laryngeal paralysis
62
Q

What are the 3 main clinical signs of upper airway disease

A
  1. Dynamic v fixed obstruction
    ○ Dynamic = inspiratory dyspnoea -> due to pressure change inspiratory will be worse
    ○ Fixed = inspiratory AND expiratory dyspnoea
  2. Long inspiratory phase - stretor or stridor
    ○ Stretor = nasopharyngeal - snoring sound
    ○ Stridor = laryngeal
  3. Paradoxical abdominal movement - SEVERE DISEASE
63
Q

small airway what are the 2 main diseases and clinical signs

A
  • Lower airway disease (Asthma) in cats
  • Chronic bronchitis in dogs
  • Clinical signs
    ○ Increased airway resistance
    ○ Air trapping
    ○ Expiratory push
    ○ Cough
64
Q

Pulmonary parenchyma disease what are the 6 main causes and clinical signs

A

Causes
1. Pulmonary oedema - cardiogenic vs non-cardiogenic
2. Pneumonia
○ Puppies with complicated bordatella infection
○ Old dogs with aspiration pneumonia
3. Pulmonary haemorrhage
○ Pulmonary contusions, rodenticide, ITP
4. Pulmonary thromboembolism
5. Severe, diffuse, metastatic disease (neoplasia)
6. Interstitial disease
○ Interstitial fibrosis in west highland white terriers
Clinical signs
- Short, shallow breaths = can be subtle
- May hear crackles

65
Q

Pleural space disease what are the 5 main causes and clinical signs

A
Cause 
1. Pneumothorax
○ Traumatic v spontaneous v iatrogenic 
2. Hydrothorax 
○ Congestive heart failure 
3. Pyothorax 
4. Haemothorax 
○ Trauma vs coagulopathy v neoplasia 
5. Solid tissue 
Diaphragmatic hernia (organs), neoplasia 
Clinical signs 
- Paradoxical (asynchronous) abdominal movement during inspiration 
- Dull lung sounds 
○ Ventrally dull - fluid 
○ Dorsally dull - air 
○ All over for severe fluid and air accumulations 
- Inspiratory dyspnoea with chronic pleural effusions/pleuritis
66
Q

Chest wall and diaphragm what are the 4 main conditions within that lead to dyspoea

A
1. Thoracic muscle paralysis 
○ Lower motor neuron disease 
○ Cervical spinal disease 
○ Fish mouth breathing 
2. Diaphragmatic hernia 
○ Congenial vs traumatic 
3. Phrenic nerve transection
4. Flail chest 
○ Flail segment in the chest - generally ribs fractured in multiple areas 
§ Section of chest moves in opposite direction of what the chest should do
67
Q

List 6 conditions that look like respiratory disease by leading to dyspnoea

A
  1. Metabolic acidosis
  2. Sepsis - cytokines can react with respiratory centre
  3. Hyperthermia
  4. Pain
  5. Anxiety/fear
  6. Drugs (opioids, steroids)
68
Q

What are the 3 most common things dyspnoeic animals will have after trauma and others

A
○ Pulmonary contusions 
○ Pneumothorax 
○ Haemothorax 
3 MOST COMMON
○ Diaphragmatic rupture 
○ Flail segment 
○ Upper airway rupture 
○ Neurogenic pulmonary oedema 
○ Spinal cord injury
69
Q

What are the 3 main things that cause dyspnoeic cats, what most common in and general clinical signs

A
1) Cardiogenic pulmonary oedema 
§ Skinny old cats, young cats 
§ Gallop rhythm or heart murmur +/- thyroid slip 
§ Hypothermic
2) Pleural effusion 
§ CHF, Pyothorax in young cats 
§ Muffles heart and lung sounds, hypothermic 
3) Lower airway disease 
§ Younger cats 
§ History of COUGH 
§ Hyperthermia
70
Q

What are the 3 main things that causes dyspnoea in small breeds and 2 in brachycephalic breeds

A
- Old toy and small breed dogs 
○ Cardiogenic pulmonary oedema 
○ Collapsing trachea 
○ Mitral valve disease 
- Brachycephalic breeds 
○ Upper airway obstruction 
○ Aspiration pneumonia
71
Q

what are the 2 main causes of dyspnoea in large breeds and 3 in puppies

A
- Old large-breed dogs 
○ Laryngeal paralysis 
○ Cardiogenic pulmonary oedema 
§ Dobies and giant breeds 
§ Typically have an arrhythmia 
- Puppies 
○ Neurogenic pulmonary oedema 
○ Pulmonary haemorrhage - rodenticide toxicity 
○ Pneumonia 
§ Bacterial or viral
72
Q

What are the 7 main diagnostics to run on dyspnoeic patient and when don’t perform

A
  1. Upper airway exam
  2. Thoracic ultrasound (TFAST)
  3. Thoracic radiographs
  4. Arterial blood gas analysis
  5. CT scan
  6. Tracheoscopy/bronchoscopy
  7. Airway cytology
    Unstable patient -> DO NOT PERFORM ARTERIAL BLOOD GAS/RADIOGRPAHS
    - No stress, supplemental oxygen needed
73
Q

Quantifying hypoxaemia what are the 2 ways, when do and what is cyanosis

A
  • No immediate need if dyspnoeic!
  • If signs are subtle, or you are unsure
    1. Pulse oximetry
    2. Arterial blood gas
  • Cyanosis
    ○ Life-threatening hypoxaemia
    ○ PaO2 20-40mmHg, >5g/dL deoxyhaemoglobin
    ○ Difficult to see with severe anaemia
74
Q

Arterial blood gas what are the 3 ways to get information and which are the best with normal ranges and what ranges have clinical significance

A
1. Arterial blood gas - GOOD 
○ PaO2 normal = 80-100mmHg 
2. Venous blood gas - NOT SO GOOD 
○ PvO2 normal = 40mmHg 
3. O2 saturation of Hb
○ SaO2/SpO2 > 90% at PaO2 of 60-70mmHg 
Sig
- PaO2 values <75mmHg 
○ Treated with oxygen supplementation 
- PaO2 values <55mmHg 
○ Life-threatening and required immediate action
75
Q

Pulse oximetry how done, location, normal and acceptable levels

A
  • Optical transcutaneous non-invasive method
  • Continuous measurement
  • Sensory on
    ○ Pinna, lip, skin fold, toe, tongue
    Normal = 95-99% Acceptable = 93-99%
    SpO2 95% = PaO2 90mmHg
    SpO2 93% = PaO2 80mmHg
    SpO2 90% = PaO2 60mmHg
  • Curve starts to get step at this point
76
Q

What are the 5 ways to supplement oxygen in dyspnoeic patient and how to assess if working

A

1) flow by oxygen
2) oxygen mask
3) nasal oxygen catheters
4) oxygen hood
5) oxygen cage
Assess
1. Assess for improvement of respiratory distress
2. Pulse oximetry: SpO2

77
Q

Flow-by oxygen and oxygen mask what makes them good and bad, flow rate and when used

A
  1. Flow-by oxygen
    ○ Easy and well tolerated
    ○ Tubing help closely to animals nostril/mouth
    ○ 2-3 litres per minute of oxygen
    ○ FiO2 achieved: 0.25 to 0.4 (25-40% inspired oxygen)
    ○ Useful when performing initial evaluation, not for long-term
    ○ Able to analyse the head - mucous membranes etc.
  2. Oxygen mask
    ○ Easy and cheap
    ○ Stressful for some patients, OK when sedated
    ○ May require restraint
    ○ Useful when performing initial evaluation
    ○ Relatively low inspired oxygen concentration
    ○ Flow depends on size of animal and of mask
    ○ Avoid risk of rebreathing (CO2 accumulation) - respiratory acidosis
78
Q

Nasal oxygen catheters what need to give, how to apply and flow rate

A

○ Local analgesia (and wait)
○ Measure to medial canthus
○ Anchor as close to nose as possible - otherwise will shake off
○ Tape butterflies and suture or super glue
○ Variable inspired oxygen concentration
○ 100mL/kg/min will achieve FiO2 = 0.4
§ If use two can get up to 80%
○ Humidification of gas -> need to occur as otherwise dry and will result in dry airways

79
Q

Oxygen hood and cage which preferred, what need to do, why good and bad

A
Oxygen hood - not preferred 
○ Elizabethan collar (cone) 
○ Clear plastic wrap over the top with a hole 
○ No access to the patient - especially around the head 
○ Moisture accumulation 
○ Carbon dioxide accumulation 
○ FiO2 = 0.3 to 0.4 
Oxygen cage 
○ HIGH inspired oxygen concentrations 
○ LOW STRESS environment 
○ Relatively EXPENSIVE 
○ Limited ACCESS to patients 
○ Temperature/humidity 
○ Accumulation of CO2
80
Q

What are the 3 main mechanisms of hypoxaemia and causes within

A
  1. Low inspired oxygen partial pressure
    ○ Low FiO2
    ○ Low barometric pressure (high altitude)
  2. Hypoventilation
    ○ CO2 production > CO2 elimination
    ○ Higher PACO2 - respiratory acidosis
    § Normal PaCO2 = 35-45 mmHg
    ○ This increase results in a decrease in pressure of other gases including PaO2 in the alveoli
  3. Pulmonary gas exchange abnormalities: venous admixture
    ○ Anatomic shunt (right to left)
    ○ Perfusion of poorly ventilated lung areas
    ○ Oxygen diffusion impairment
81
Q

What are the 8 main causes of hypoventilation

A
  1. Airway obstruction
  2. Neuromuscular disease
  3. Anaesthesia
  4. Spinal cord dysfunction cranial to C4-C5
  5. Phrenic nerve dysfunction
  6. Chest wall injury
  7. Respiratory fatigue
  8. Excessive CO2 production (malignant hyperthermia)
82
Q

Management of upper airway obstructive what are the 3 things that need to occur

A
  1. Oxygen supplementation
  2. Reduce Tissue metabolism to reduce CO2 production
    And only if dyspnoea continues despite maximum oxygen supplementation
  3. Increase Alveolar ventilation
83
Q

Reduced CO2 production in tissues what are the 2 ways to do it

A

1) sedation - acepromazine, butorphanol, midazolam

2) reduction of body temperature - body surface wetting, ice packs, radiation, cool intravenous fluids NOT NSAIDS

84
Q

In terms of sedation when trying to reduce CO2 production in dysponeic patient what are pros and precautions

A

○ Pros
§ Anxiolysis - reduced of oxygen consumption
§ Reduced metabolic heat production -> hyperthermia decrease
§ Less respiratory drive -> dynamic airway collapse decrease
○ Precautions
§ Cardiovascular collapse
§ Relaxation of pharyngeal dilator muscles -> airway collapse increase
§ Less respiratory drive -> respiratory arrest

85
Q

What is the main way to increase alveolar ventilation for dyspnoeic patients when would you do it and goal

A
- Intubation - make airway patent again 
○ Severe respiratory distress alone! 
§ High grade upper airway obstruction or acute with high PvCO2
§ Chronic upper airway obstruction with worsening pH 
§ No improvement upon O2 and sedation 
○ Goal 
§ Preserve the patient's life 
§ Safe diagnostics 
§ Etiological treatment
86
Q

Pulmonary gas exchange abnormalities leading to hypoxaemia what results from 3 main mechanisms and pathogenesis

A
  • Degree of admixture of venous (non-oxygenated) blood with pulmonary end-capillary (oxygenated) blood
  • Mechanisms
    ○ Anatomic shunt (right to left)
    ○ Diffusion impairment
    ○ V/Q mismatch: perfusion of poorly ventilated lung areas
    Pathogenesis
    ○ Normal
    § Venous blood moves alongside alveoli where gas exchange occurs then moves into arterial blood system
    ○ Venous admixture
    § Flooded or collapsed alveolus without O2 HOWEVER venous blood still perfuse this area -> no arterialised blood from this section resulting in mixture of arterial and venous blood leaving the lungs -> low oxygen content
87
Q

Wha are the main causes of pulmonary gas exchange abnormalities leading to hypoxaemia

A
○ Pulmonary parenchymal disease 
§ Pulmonary oedema 
□ Cardiogenic or non-cardiogenic 
§ Pneumonia 
§ Pulmonary contusions 
§ Atelectasis 
§ Lung collapse: pneumothorax, pleural effusions 
§ Pulmonary thromboembolism
88
Q

What are the 5 steps in emergency management of dyspnoeic patient

A
  1. Oxygen supplementation and no stress
  2. Rule out or treat pleural effusion/pneumothorax
    - Auscultation, US, thoracocentesis (Diagnostic and therapeutic)
  3. Treat for the treatable in severely dyspnoeic cats
    ○ Empirical furosemide, terbutaline, corticosteroids
  4. Give furosemide (diuretic), if CHF (cardiogenic heart failure) is likely
    ○ 2-4mg/kg, then 2mh/kg every hour until more comfortable
    ○ Not useful for cardiogenic pleural effusion
  5. Sedation can be beneficial and humane
89
Q

What to do if the 5 step emergency management of dyspnoea doesn’t work

A

INTUBATION/VENTILATION

  1. mechanical ventilation
  2. prssure-controlled ventilation
  3. volume controlled ventilation
90
Q

Mechanical ventilation what for, what is good and bad about it

A

§ For ventilatory failure (hypoventilation)
§ For severe gas exchange abnormalities
Good
§ Allows 100% inspired oxygen concentrations
§ Full control of ventilation and oxygenation
□ Rate, pressure, volume, inspiratory time § Positive pressure and PEEP (positive end-expiratory pressure) - to open up the alveoli for perfusion
BAD
§ Expensive and very labour intensive
§ Long term <24 hours: intensive care unit

91
Q

Pressure-controled ventilation and volume control ventilation which is preferred and what is controlled and variable

A

Pressure-controlled ventilation -> preferable to protect against too high pressure
§ Present inspiratory pressure is delivered to patient - once pressure delivered then expiration
§ Pressure constant, volume variable
Volume-controlled ventilation
§ Present tidal volume is delivered to patient - once volume delivered then expiration
§ Volume constant, pressure variable

92
Q

how to set up pressure and volume controlled ventilation

A

Start setting for volume controlled
§ Tidal volume = 8-10mL/kg
§ Respiratory rate = 15-20 breaths per minute
§ Inspiratory: expiratory ratio = 1:2 (or I=50% of E) (inspiratory phase shorter than expiratory phase)
§ 100% oxygen
§ PEEP (positive end-expiratory pressure) = 5cm H20
- Follow by adjusting volume and respiratory rate to patient needs
§ Oxygenation: PaO2 and/or SpO2
§ Ventilation: PaCO2 or PvCO2 or PetCO2
Start setting for pressure controlled
§ Inspiratory pressure = 10cm H2O above PEEP
§ REST AS ABOVE

93
Q

List some common, less common and uncommon signs of nasal disease

A

Common
- Sneezing
- Stertor (snoring or snorting sounds)
- Nasal discharge
Less common
- Facial pain or deformity, epiphora
- Depigmentation or ulceration of the nasal planum(fungal)
Uncommon
- Systemic signs (lethargy, inappetence, weight loss) - generally stay localised to the nose
- Central nervous system signs -> through cribriform plate into brain
- Open-mouth breathing (with severe nasal obstruction)

94
Q

What are the 3 main clinical signs of nasopharyngeal disease and possible causes

A

1) Stertor (also oropharyngeal)
2) Reverse sneezing - forceful inspiration -> clear nasopharyngeal area
○ Small breed terrier dogs more common -> acute don’t worry about
§ Trickle of water or syringe of water will stop the tickle in the throat
○ Nasal mites, irritation or more significant diseases
3) Gagging/retching
○ Also with post-nasal drip

95
Q

What are the most common causes of uni and bilateral nasal discharge

A
- Unilateral
○ FB
○ Tooth root abscess/ oronasal fistula
- Bilateral
○ Infectious disorders
○ Idiopathic inflammation
○ Systemic conditions
- Either (may progress)
○ Neoplasia
○ Fungal
○ Polyps
○ Bilateral processes
96
Q

what are the 7 main things need to do for a physical exam of nasal discharge

A
  1. Body condition
  2. Nasal or lacrimal discharge
  3. Facial symmetry and pain, oral cavity
  4. Gently retropulse eye -> should have some give and be symmetrical
  5. Palpate LNs
  6. Check nasal patency - if blocked and no air generally something solid
  7. Listen and watch breathing -> exaggerated or noise associated with breathing -> stridor or sterdor -> upper respiratory tract issues
97
Q

When to investigate nasal discharge

A
- Acute paroxysmal sneezing in dogs 
○ Dog -> foreign body generally easier to assess when early 
○ Cat -> generally viral infection 
- Reverse sneezing if
○ Severe or progressive
○ Other respiratory signs
○ Atypical breed (nasal mites?)
○ Cats without URTI!
- Facial pain or deformity - indicates destructive process 
- Nasal planum ulceration
- Nasal obstruction
- Epistaxis
- Chronic nasal discharge and/or sneezing
- Neurologic or systemic signs
98
Q

sneezing what are the 4 main differentials and causes of serous and mucopurulent discharge

A
Sneezing
- Nasal foreign body (esp. dogs)
- Feline upper respiratory tract infection (URTI)
- Canine nasal mites
- Exposure to irritant aerosols
Discharge 
- Serous 
○ Normal (small amounts) 
○ Viral infections
○ Irritants 
○ Early stage of mucopurulent causes  
- Mucopurulent - not very specific -> don't learn them all 
○ Viral, Bacterial, Fungal
○ Nasal parasites
○ Foreign body
○ Neoplasia
○ Nasopharyngeal polyps
○ Canine chronic L-P rhinitis
○ Feline chronic rhinosinusitis
○ Allergic rhinitis
○ Extension of oral disease
99
Q

Epistaxis what are the 5 main nasal cause and some systemic causes

A
Nasal causes
- Acute trauma
- Acute foreign body
- Neoplasia - common
- Fungal infection - common
- Other causes of MP discharge (uncommon)
Systemic causes - less common -> want to rule out before biopsy 
- Coagulopathy
- Systemic hypertension
- Polycythaemia
- Hyperviscosity syndrome
- Vasculitis
100
Q

Destructive lesions what are the clinical signs and differential diagnosis

A
signs
- Stertor/obstruction
- Facial pain
- Epistaxis
- Exopthalmos
- Facial deformity
- Naris/nasal planum depigmentation/ulceration
Differential diagnosis 
- Tooth root abscess 
- Neoplasia 
- Fungal infection - most don't cause destruction but some can
101
Q

What are the 5 things to diagnose epistaxis

A
1. Haematology, chemistry - is the patient anaemic 
○ HCT, platelet count
○ TP, globulins
2. PT and aPTT - specific coagulopathy before do biopsy 
3. Buccal mucosal bleeding time
4. vWF assay
○ affected pure breeds
5. Blood pressure