Fundamentals of clinical practice Flashcards

1
Q

Sepsis

A

Presence of pathogens

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2
Q

Asepsis

A

Free from pathogens

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3
Q

What is the preoperative preparation plan for a patient?

A

Food and water - some kind of starvation
Clipping before surgical day
prior to induction
Once induction has been done
Specific surgical prep
Catheters and cannulas

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4
Q

How can skin be prepped aseptically?

A

Surgical scrub solution
Different concentrations for different areas of sensitivity

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5
Q

What are the different surgical scrub solutions that can be used?

A

Chlorhexidine
Povidone iodine
Isopropyl alcohol

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6
Q

What is the concentration required for surgical spirit when used orally for dogs?

A

Oral 0.1% chlorhexidine dogs

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7
Q

What is the concentration of surgical spirit when in ocular use?

A

0.2-2% or 1:50 dilution of ocular povidone iodine

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8
Q

What are the different styles for draping a patient?

A

Plain 4 corner draping
Draping a limb
Fenestrated drapes
Adhesive barrier drapes

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9
Q

Bacterial infection

A

More than 10^5 bacteria per gram of tissue

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10
Q

What are SSI?

A

Surgical site infections are infections of the tissues, organs or spaces exposed by surgeons during performance of an invasive procedure

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11
Q

How can SSIs be classified?

A

Incisional infections
1. superficial (skin and subcut tissue)
2. deep incisional
Organ/space infections

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12
Q

What are the risks with SSIs?

A

Result in an increased morbidity and mortality in surgical patients

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13
Q

How are surgical wounds classified?

A

classified by the degree of contamination to help predict the likelihood that infection will develop
- clean
- clean contaminated
- contaminated
- dirty

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14
Q

What are the properties of clean wounds?

A

Non traumatic, non inflamed operative wounds in which the resp, G, genitourinary and oropharyngeal tracts are not entered

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15
Q

What are the published infection rates for clean wounds?

A

0-4.4%

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16
Q

What are examples of clean wounds?

A

Exploratory coeliotomy
Elective neuter
Total hip replacement

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17
Q

What are the properties of clean contaminated wounds?

A

Operative wounds in which the resp GI urogen tract are entered, but inder controlled conditions without unusual contamination. An otherwise clean wound in which a drain is placed

cleanwound with GI repro or resp involved (drain often used)

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18
Q

What are the examples of clean contaminated wounds?

A

Bronchoscopy
Cholecystectomy
Enterotomy

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19
Q

What are the published infection rates for clean contaminated wounds?

A

4.5-9.3%

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20
Q

What are the properties of contaminated wounds?

A

Open, fresh, accidental wounds
Procedures in which GI contents or infected urine is spilled or a major break in aseptic technique occurs

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21
Q

What are the examples for contaminated wounds?

A

Cystotomy with spillage of infected urine
Open cardiac massage for CPR

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22
Q

What are the published infection rates for contaminated wounds?

A

5.8-28.6%

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23
Q

What are the properties of dirty wounds?

A

Old traumatic wounds with purulent discharge, devitalised tissue or foreign bodies. Procedures in which a viscus is perforated or faecal contamination occurs

Gross infection is present

old, purulent, devitalised, fb, faeces

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24
Q

What are examples of dirty wounds?

A

Excision or drainage of abscess
Bulla osteotomy for otitis media
Perforated intestinal tract

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25
What is the primary objective of aseptic surgery?
Reducing infections
26
What host factors play a role in aseptic surgery efficacy?
Age Physical condition Nutritional status Diagnostic procedures Concurrent metabolic disorders Current medication
27
What operating room practice needs to be carried out for success in aseptic surgical techniques?
Principles of aseptic technique Sterilisation Disinfection Anaesthesia Atraumatic technique
28
What are the 3 factors that reduce infection risk?
Patient prep (clipping, scrubbing, draping) Surgeon prep (scrubbing, gowning, gloving, hats and masks) Theatre behavior (etiquette, talking , flow etc)
29
What suggests a rational use of antibiotics in surgical treatments?
Surgery exceeding 90 mins Prosthesis implantation Patients with existing prostheses undergoing certain surgical procedures Severly infected or traumatised wounds Rational selection of antibiotics for prophylactic use | Traumatic surg, long surg, prothesis prescence
30
What are the characteristics of an ideal suture?
high tensile strength Easy to use and tie Uniform tensile strength = finer suture material can be used Inhibit tissue reactions and wicking Non toxic Non carcinogenic Non allergic Easily sterilised Minimal bacterial adhesion Standardisable characteeristics Sufficient length of properties Inexpensive | uniform tensile strength, easy, non toxic or carginogenic, sterilised
31
Natural suture
Raw materials from naturally occurring sources Cat gut/ silk
32
Synthetic suture
Raw material produced in an industrial process Nylon etc
33
absorbable suture
Materials that are fully degraded and absorbed by the body once placed
34
Non absorbable suture
Materials that stay in place for an indefinite period (60 days without changing in anyway
35
Monofilament vs multifilament suture
Monofilament suture - single filament Multifilament - multiple strands that are braided to create a thicker thread of the desired diameter
36
Tensile strength
Breaking strength per unit area
37
Memory
Tendency to retain original configuration
38
"chatter" and tissue drag
Lack of smoothness or presence of friction whilst passing through tissue
39
Tissue reaction with suture material
Tissues respond to the implantation of sutures as they do to other foreign material and can provoke an inflammatory response
40
Advantages and disadvantages of absorbable suture material
41
Advantages and disadvantages of non absorbable suture material
42
What are the consequences of placing suture material and what are the factors
Suture material is foreign body Tissue reaction Amount of material Presence of infection
43
What factors affect tissue reaction>
Absorption characteristics Natural or synthetic Phagocytosis vs hydrolysis
44
What is the diameter rating for suture materials?
2-0 is bigger than 3-0 0 is bigger then 00=2-0
45
What is a swaged needle?
Attached to the suture material
46
What are the issues with eye needles?
Threading the needle causes a double strand of suture material Multiple uses causes bluntness Increases tissue trauma
47
Benefits of swaged needle?
Minimal trauma Single use Optimal penetration properties (more expensive)
48
What are the main parts of the needle?
The point The body The eye or the swage
49
What is the chord length of a needle?
The tip of the swage to the needle point
50
What are the different needle curvatures?
Curvature is measured in relation to a circle. Deeper the wound the more curved the needle
51
What are the different needle points?
Blunt - circular elliptic Sharp (polygonal) Compound (tapercut, short cutting point etc)
52
What is the composition of needles?
Made from stainless alloys Sufficiently rigid to resist forces applied to them during handling Sufficiently flexible to bend before breaking
53
What is meant by ductility?
Needles are flexible and therefore bend before breaking This is important as it warns the surgeon that the forces placed on the needle are too great
54
What is the common composition of surgical instruments?
Stainless steel- strong and resistant to corrosion Chromium plated carbon steel- cheaper but prone to corrosion and pitting Titanium - light weight and used to handle delicate tissues. Reduced glare from operating light | stainless steel, chromium plated, titanium
55
What implants may be placed in stainless steel instruments and why?
Tungsten carbide implants which are particularly strong and used as blades or for gripping Generally have gold handles for identification | tungston carbide makes stronger- identified by gold handle
56
What is the role of scalpels and what are their properties?
Cutting skin Baird parker no 3 is the most commonly used blade Various blades can be used
57
What are the types of scalpel blades?
No 10 is most commonly used - large convex surface No 11 = stab incisions into hollow viscera such as bladder or stomach no 15 = more delicate with smaller convex cutting edge (precise cuts such as urethrostomies)
58
What scalpel handle is used in large animal practice?
Number 4
59
When are different scalpel handling techniques used?
Power grip allows for thicker and tougher tissues to be cut Pencil grip allows for delicate precise use
60
What are the different scissors used?
61
When are mayo scissors used
62
When are metzenbaum scissors used?
63
When are suture scissors used?
64
When are iris scissors used?
65
How should scissors be held?
Scissors held with the thumb in one ring and fourth finger in the other Index finger is placed over the joint for increased stability
66
What is reverse grip for scissors?
Scissors held for cutting towards the dominant hand
67
What are needle holders?
Ringed instrument with a ratchet mechanism allowing the surgical needle to be held by the needle holder
68
What are the 3 designs of needle holders?
Mayo hegar Olsen Hegar Gillie
69
When are treves rat toothed forceps used?
Heavy duty with a single tooth interdigitating with two on the opposing tip Can be traumatic to tissues
70
When are dressing forceps used?
Applying dressings Have no rat teeth and are particularly traumatic to tissues as pressure is needed if used for this purpose
71
When are adson rat tooth forceps used?
Fine forceps with a small rat tooth grip
72
When are debakey forceps used?
LEAST TRAUMATIC These have longitudinal and transverse serrations originally used for vascular use as they are the least traumatic
73
What are the grips for thumb forceps?
Penhold or chopstick grip
74
What are homeostatic forceps?
Designed to occlude blood vessels and prevent haemorrhage Wide variety all have rings with a ratched mechanism Straight ot curved and come in variety of sizes with different interdigitations commonly used = Halsted mosquito, Spencer wells and Carmalt
75
What are the main tissue holding forceps?
76
What is the role of retractors?
Varied in their form but can be divided into self retaining and handheld Improve visibility or exposure for easier and more accurate surgery placing tissue under tension reduces bleeding and allows easier cutting and dissection
77
What can be seen in these images?
Left - abdominal retractor (balfour- 3 point retractor which prevents rotation) Right - thoracic retractor with ratchet mechanism which can gradually retract ribs (2 point retractor)
78
What can be seen in these images?
79
What are the main handheld retractors?
80
What are the 2 main towel clamps?
81
What is the cascade of events through which wounds heal?
Haemostasis and inflammation (platelet aggregation and WBC) Proliferation/ Fibroplasia (angiogenesis, granulation) Maturation (remodelling of collagen 1->3) contraction of the wound
82
What occurs during haemostasis?
Tissue damage Blood leakage from vessels Activation of clotting cascade by damage to endothelium ( intrinsic and extrinsic) Platelet aggregation and release of cytokines Stabilisation of platelet plug by fibrin formation
83
What occurs during the inflammatory phase?
Overlaps with haemostasis First 72 hours of injury Vasodilation following transient vasoconstriction Cytokines in fibrin clot will attract WBCs (neutrophils then macrophages) Destruction of cells by phagocytosis cleans up bacteria and devitalised tissue
84
What occurs during proliferation phase?
Overlaps inflammatory phase Formation of granulation tissue - formed of macrophages, firboblasts and new blood vessels Fibroblasts proliferate and produce new extracellular matrix, elastin and collagen = strength More resistant to infection
85
What occurs in the repair phase of proliferation?
Formation of new epithelial tissue (pale pink tissue) Shrinking grows across wound Myofibroblasts cause wound contraction Contact inhibition- contact of epithelial cells stops growth = smoothness which is normal Measure wound regularly for deficit shrinking
86
What occurs during the maturation phase of wound healing?
Remodelling Type 3 collagen is replaced by type 1 collagen Cross-linking of collagen Components of extra cellular matrix change Increase in tensile strength Can take weeks to months
87
What factors affect wound healing?
Patient factors - age and comorbidities Wound factors - infection and location Concurrent treatment - corticosteroids(delay healing) Radiation (tissue fibrosis and vasc scarring)
88
What patient factors affect wound healing?
Age Comorbidities (HAC and diabetes) Nutrition status (hypoproteinaemia- will slow wound healing)
89
What wound factors affect wound healing?
Infection Location (tension, movement, local blood supply)
90
How can concurrent treatment affect wound healing?
Corticosteroids- delay all stages of wound healing Radiation - Tissue fibrosis and vascular scarring
91
How can wounds be classified?
Abrasion Avulsion Incision laceration Puncture
92
What wound can be seen below?
Abrasion Loss of epidermis and some dermis (blunt trauma/ shearing)
93
What wound can be seen how does it occur?
Avulsion - tearing of tissues from attachments on limbs it's a degloving injury
94
What wound can be seen and how does it occur?
Incision - created by a sharp object Minimal trauma (neat)
95
What wound can be seen and how is it caused?
laceration - tearing type wound causes irregular defect Usually jagged
96
What wound can be seen and how is it caused?
Puncture Penetrating wound Superficial damage may be minimal Deep damage may be substantial
97
Outline the skin vascular supply
Epidermis Dermis Hypodermis Subdermal plexus Terminal branched of direct cutaneous arteries Within the panniculus and subcutis protect subdermal plexus in mobilisation
98
What are the fundamentals of wound management?
Assessment of patient other injuries Life threatening complications Stabilise Examine with sedation
99
How to assess type of wound?
Degree of tissue damage Depth of wound VItal structures such as bones joints nerves and tendons (especially important in puncture wounds)
100
How to assess wound age?
Golden period is 6-8hrs Contaminated or infected History from the owner Has the bacteria started dividing
101
How to assess level of contamination of a wound?
Foreign material devitalised tissue Bacterial innoculum (bit vs clean glass etc) Takes into account the age and nature of the wound
102
How does lavage occur for wound management>
Gross contamination- tap water Copious lactated ringers or hartmanns 35-60 ml18G needle = higher pressure 7-8psi Debridement - dressings, surgical etc
103
How can a management plan be created for a wound?
Primary intention closure Secondary intention healing Third intention closure
104
What is meant by golden period in wound healing?
6-12 hrs Bacteria divide >12hr bacterial invasion
105
What factors influence bacterial contamination?
Blood supply reduced ability to fight infection Divitalised tissue ()inc bac growth) FB (red ability to fight infection) Type of contamination (soil better than organic debris, clean glass vs bite wound) Type of bacteria
106
What are the goals of wound management?
Promote healing Convert contaminated into clean Control infection
107
What are the methods of wound debridement?
Surgical Mechanical Autolytic Enzymatic - rare Biological- rare
108
What is the role of wound debridement?
Remove dead necrotic contaminated particulate matter and bacteria from the wound Ready for wound closure and healing
109
How is surgical debridement carried out?
debrided with sharp surgery to remove dead tissue preserve vital structures can carry out scraping to remove chronic granulation tissue wound lavage and dressing
110
How is lavage used as a debridement agent?
Lactated ringers solution due to pH and its compatability with tissue 0.9% saline is often used Fluid at body temp 35ml with syringe and 18G needle = 7-8psi high vol on newly presented wounds
111
What is a wet to dry dressing and how is it used?
Chronic granulation bed to healthy granulation bed Sterile swabs soaked in isotonic crystalloids such as Hartmanns Placed on chronic granulation bed Dry swabs on top of the bed to bandage Changed every 24 hrs
112
What is the role of negative pressure wound therapy?
A mechanical pump attached to the wound reduces air pressure drawing off exudate and reducing oedema
113
How does negative air pressure therapy help with wound healing?
Reduces bacterial colonisation Promotes granulation tissue development Increases rate of mitosis Spurs the migration of epithelial cells within the wound
114
what is shown in the image?
Topical negative pressure wound therapy
115
What issues arise with negative pressure wound therapy?
Creating an airtight water tight seal
116
What can be seen in the image?
Negative pressure wound therapy?
117
What effect does honey have on wound healing?
Antibacterial effect - reduction of bacteria Healing stimulating properties Debriding effect Antiinflammatory effect Odour reducing capacity Reducing in wound pain
118
What is honeys role as a debriding agent?
Osmotic effect Low pH Both help to draw fluid from the wound area
119
How does honey have antimicrobial effects?
Hydrogen peroxide (glucose oxidase) Antioxidant (flavinoids) High sugar content (osmotic effect) Acidic (pH 3.2-4.5) Methylglyoxal found in manuka honey (nectar from manuka plant 15+ at least)
120
What issues arise with using standard table honey?
121
What is biological debridement?
Medical grade maggots Hard to keep in wound Unable to identify healthy tissue from necrotic tissue
122
What is the ranked list of wound debridement?
Speed to effect and expense to cost Scraping with scalpel often seen as the best Wet to dry is second best
123
Why do we need bandages?
Aid to healing of wound, surgical site Stabilise wound and prevent disruption to healing process Prevent self trauma and trauma to wound Prevent debris entering wound Migrating bacteria Helps with local pain relief Aid clotting and prevent further contamination
124
What types of wound dressing are available?
Dry sterile swab dressing - normally for wet-dry or dry-dry debridement Impregnated dressings - coated with petroleum jelly or antibiotics Semi occlusive dressing- central absorptive core with non stick layer to absorb exudate (post op) Absorbent dressings - for large exudating wounds Alginates - naturally occuring fibres from seaweeds- moistened and packed into to encourage wound inflammatory factors (dry out eventually and need to be changed)
125
What are the roles of topical wound gels and creams?
Alginate gels - encourage new tissue growth on stalled wound Contact cream- flamazine (siver sulfadine) for burns Dermasol- antibioitc for small wounds Aluminium liquid spray- large animals covers wounds for protection
126
What are the layers of bandaging?
Primary layer - dressing (most important) Secondary layer - padding material 2 components Tertiary layer- vet wrap etc
127
What are the 2 components of the secondary layer of a bandage?
Supportive padding dressing - cotton roll (placed for comfort and absorbs exudate that makes it through the dressing, holds away from clean wound) thick enough to prevent strikethrough Open weave conforming gauze- allows light pressure to be applied can be absorbent (can cause restriction and compression= discomfort and can cause tissue death)W
128
What are the properties of the tertiary layer of a bandage?
Protection from the outside environment More important for limb and paw Usually cohesive layer so sticks to itself Adhesive layer can be used - stronger and thicker but don't stick directly to patient (paws normally)
129
Why are immobilised bandages used?
Robert jones bandage- multiple species in long bone fractures post op protection Gutter splints - fractures below the carpus (small dogs and cats) Plaster of paris on a roll - needs to be wetted and applied over the secondary layer Fibreglass impregnated with resin-
130
How is an immobilised bandage applied?
Applied 1 joint above and 1 joint below to immobilise the bone to its maximum splinting stability
131
What are some complications with poorly applied or cared for bandages?
Swelling - distal limb not included Tissue necrosis - bandage too tight Decupital ulcers - over bony prominences Patient interference due to uncomfortable bandage
132
How can decupital ulcers be avoided?
Ring dressings over the elbows and hock etc to prevent rubbing of the bandage It comes with its own issue( removes pressure from bony prominence but can apply pressure to the sides of the wound)
133
What type of dressing is used for wounds that have chronic granulation and are struggling to heal?
Alginate based dressings - Seaweed stimulates the release of inflammatory factors for wound healign
134
What should be assessed with wounds in large animals?
Classify the wound How and why it occurred What structures are involved How much contamination of the wound is there? Clean -> contaminated Location is key for determining wound healing
135
How should a wound be assessed in large animals
History, clinical assessment and sedation considerations Lameness level (suggests catastrophic injury through tendons etc) Assess gait
136
What should be considered with sedation?
High blood loss is a contraindication Regional anaesthesia might be required
137
What structures are affected
DDflexor tendon Superficial digital flexor tendon
138
What structures could be affected?
Brachial plexus Penetration of the thoracic cavity
139
What could have been damaged here
Synovial structure (calcaneal bursa) suggest a poor outcome Would cause lameness Synovial fluid samples and cellularity can assess inflammation etc
140
What can be used to assess joint wound damage?
Synovial fluid assessment Sterile solution into calcaneal bursa allows for indication of bacteria presence in the wound Imaging of wound for fractures
141
How can imaging be used in wound managment in large animals?
Bones (sequestrian - bone that acts as foreign body) Acoustic shadow suggest foreign body Soft tissue damage Fractures
142
How do we determine wound management options?
Superficial or deep Structures involved joints etc Closing the wound options
143
What is meant by primary closure of wounds?
Primary intention healing is when the wound edges are brought and kept together by sutures or staples. The healing occurs with wound epithelisation and connective tissue deposition.
144
What should be combatted in primary closure of wounds in large animals?
Tension Matress suture patterns combats tension Stents and quills distribute tension over the surface of the skin Pressure on the skin is then reduced
145
How is secondary intention healing carried out in large animal wound healing?
WBCs are encouraged to be attracted to the wounds - Several days/ weeks To speed this up debridement can be carried out (surgically or wet-dry swabs) Speeds up route to proliferation
146
What is delayed primary closure of wounds in large animals?
Allow natural debridement of the body The primary closure after assessmetn for necrotic tissue
147
Why are drains used in wound healing?
Route for fluid and inflammatory exudate to exit the wound Speeds up debridement of the wound
148
What are some drains that can be used in large animals?
Latex penrose drain in two separate incisions at wound bed Active drains can be used sometimes
149
What has been used for healing here?
Primary closure The deep pocket suggested use of Penrose drain to allow exudate to exit Quils and stents reduce skin tension Mattress sutures also decrease skin tension Wound can heal faster due to primary intention wound healing
150
How can granulation tissue be fixed in large animal wounds?
Granulation tissue and fibroblasts stops epithelial migration Has little nerve supply but very good blood supply This tissue can be trimmed back using a scalpel blade below the skin surface for epithelial migration to occur
151
When might skin grafting be used in wound management of large animals?
Punch grafting - cores of skin are applied Pinch grafting - small sections of skin can be embedded into granulation tissue Apply epithelial cells into the centre of the wound so that epithelial granulation can occur
152
What are the common bandages used in equine practice?
Simple bandage A figure of 8 bandage Robert jones bandage
153
What is the use of a figure of 8 bandage in equine practice?
Covers for carpus and tarsus to go around the hock avoids pressure points
154
Properties of the robert jones bandage
Treatment modality Support At least 3 layers
155
What are the different equine bandaging materials?
Protective material Padding Conforming Outer layer Finishing
156
What is the role of the 3 conforming layers in a robert jones bandage?
Condense the padding to provide extra support
157
What is the role of splinting in equids?
Unstable fractures Unstable tendon injuries There is a variety of methods ranging from commercially available options and homemade materials
158
Where would the splint be placed for the 4 regions of damage in this image?
1- alignments of dorsal cortices, splint placed dorsally 2. Splint placed laterally and caudally 3- splint placed laterally and medially 4- forelimb - stabilise carpus
159
Where would splints be placed for the regions in the image?
1- alignments of dorsal cortices, splint placed dorsally 2. Splint placed laterally and caudally 3- splint placed laterally and medially
160
What are the 3 phases of bone healing?
Inflammatory Restorative Remodelling
161
What is the overall process for the inflammatory phase of bone healing?
Inflamatory response with fracture Lysis of osteocytes liberates inflammatory mediators IMs call in macrophages and inflammatory cells to clear wound and debris
162
What happens chronologically in the inflammatory phase of bone healing?
The blood clot is formed at the fracture site w/in 2 hrs (blood clot plays a role in neovascularisation) Phagocytes called to the location
163
When is compartmental syndrome likely to occur in bone healing?
Inflammatory phase
164
What occurs in the restorative phase of bone healign
Soft callus formation Hard callus formation
164
What occurs in soft callus formation of bone healing?
The first callus is similar to hypercellular fibrocartilaginous tissue Callus plays a role in stabilisation of the fracture site Process takes 4 days to 3 weeks
165
What occurs in hard callus formation of bone healing?
Blood supply is restored by soft callus support This means cartilage formed can be substituted by bone tissue (endochondral ossification) this results in the formation of a hard callus begins 2 weeks after fracture and ends between 6th and 12th week
166
What occurs in the remodelling phase of bone healing?
Ends of the bones are enveloped by fusiform mass called a callus Remodelling occurs involving osteoclasts Slow process that can take years
167
Describe bone remodelling using the image
168
What are the two types of healing within the restorative phase of bone healing?
First intention (minimal bone callus formation) Second intention (most common natural type of healing)
169
What occurs in first intention bone healing?
Characterised by direct bone formation on the fracture line Occurs when the fracture is stabilised with a good blood supply and reducible fracture compression on fracture site
170
What is Roux law in first intention bone healing ?
Interfragmentary compression This can be caused by: - Patients' weight - application of osteosynthesis systems that compress the fracture lines - placement of osteosynthesis systems that redistribute the weight
171
What healing can be seen in the image?
First intention healing through the use of a dynamic bone plate Bony formation with minimum formation of callus
172
How can vets ensure first intention healing of bones occurs?
ensure that the blood supply is not excessively damages (particularly the intraosseous supply) Ossification by first intention takes place much faster the second intenteion
173
What are the issues with first intention bone healing?
At first, direct osteonal union is not as stable as primary healing with separation
174
When does second intention healing occur in fractures?
Late treatment Deficient reduction of the fracture or loss of fragments Poor blood supply Infection Absence of forces of compression
175
What bone healing has occured
Within the restorative phase there is poor blood supply, anatomical reduction hasn't occurred and there are few compressive forces This means that second intention healing (soft callus formation followed by excessive hard callus formation) Right xray shows remodelling of hard callus bone
176
What are the principles of fracture repair
Stabilise animal Orthogonal radiographs Fracture score and assess what forces are applied to the fracture and how these can be managed Make sure expertise and equipment is available
177
What radiographs should be taken for fracture managment?
Orthogonal radiographs Mediolateral view and craniocaudal view
178
How can fractures be assessed?
Fracture scoring gives an indication of severity and biological nature of the fracture as well as non biological factors such as financing and surgeons abilities Higher score= more demanding to repair and therefore greater chance of complications
179
What is taken into account with fracture scores?
Patient factors Fracture Owner factors Surgeon
180
What are the patient factors assessed in fracture scoring?
Weight of animal Age Boisterousness Concurrent illnesses
181
What are fracture factors assessed in fracture scoring?
Type of fracture - does it allow compression plating or req external fixator Open or closed Associated soft tissue injuries Single or one of several fractures
182
What owner factors are assessed in fracture scoring?
Will they comply with post op instructions Finances
183
What surgeon factors are assessed in fracture scoring?
Are they able to manage the fracture Is the equipment available
184
What mechanical factors are assessed in fracture scoring?
Degree of displacement/ comminution
185
What biological factors are assessed in fracture scoring?
Young dog vs old dog Soft tissue components Osteosarcoma = Pathological fracture = wont heal Contamination if open fracture
186
What are the normal physiological forces that occur when weight bearing or from muscle contraction on a bone/ fractured bone?
Bending- when leg placed at angle to ground or asymmetrical muscle contraction Torsion - when body changes direction with leg planted on ground Tension Axial compression
186
What affects the fracture repair treatment?
determined by fracture type and forces that will be applied
187
What is the effect of axial compression on oblique fracture surfaces?
Shear force will be generated
188
What physiological forces can be seen in the image?
1. axial compression 2. tension 3. bending 4. torsion
189
What should be assessed with compression on tension aspects of long bones?
Diaphyseal bones are asymmetrically loaded when weight-bearing mandible is asymmetrically loaded during mastication
190
Describe the forces that should be assessed and accounted for in fracture management of a long bone?
Asymmetrical forces are applied to the bone and result in internally generated forces This produces tension or compression a plate should be applied to the tension side as it will not be broken by tensile forces but would be by successive compressions
191
What are the tension aspects of the long bones?
Femur- lateral aspect Tibia- medial aspect Radius- craniomedial aspect Humerus - laterocranial aspect Mandible - dorsal aspect
192
What are the consequences of different forces acting on a fracture?
Axial compression is good when transverse if not then this will cause the fracture to collapse or shear Tension causes the fracture to be distracted (lag screwing or tension bands) Torsion results in rotation of the fracture ( plates or external fixator) Bending due to asymmetrical nature can be corrected with pin in the medullary cavity
193
What does primary healing of the bone require?
Intimate contact of the bone ends under compression Through application of bone plate and extensive dissection and manipulation of soft tissues
194
What does secondary healing of the bone require?
Doesn't require reduction of fracture Adopting look but do not touch approach or minimally invasive plate os (MIPO when a plate is placed through the subcut tunnels)
195
What effects whether a fracture should be repaired at all?
Strain that tissues will tolerate as the fracture heals Some fractures naturally have movement Younger the animal the fracture may only require that the animal be cage rested Cage rest can cause pressure sores and joint stiffness
196
What is the strain theory in fracture management?
Strain is the change in length over the original length of the fracture Small gap and much movement then the strain is high ad the fracture fails to heal as the tissue rupture
197
What is the % elongation at rupture for fracture management?
198
How does the formation of a callus in bone healing affect strain?
Resorption of fragment ends increases the fracture gap and therefore creates greater stability and reduced movement at the fracture site and the strain decreases
199
What can be seen in the image
Plating of a tibial fracture Accurate reduction of the fracture Not under compression as the fracture is oblique No callus should form and there will be bone to bone union
200
What treatment approach can be seen in the image and what will be the result?
External fixator with a LBDT approach Results in secondary healing and callus formation
201
What is the importance of post operative assessments in fracture treatment?
Radiographs are used to assess - alignment of the fracture - Positioning of implants - encroachment of implants into joints or soft tissues or the bridging of growth plates in young animals
202
When should post-operative radiographs be taken in fracture management?
Prior to the removal of implants If the progression is not as anticipated There is evidence of sepsis
203
What are the fracture treatment options for small animals?
Intramedullary pin and cercalge wire Plating (w or wo compression Intramedullary nail External Fixator Pin and tension band Various combinations of these
204
What are the properties of the intramedullary pin?
Counteracts bending forces as it lies in the centre of the bone Poor at axial compression using this pin means that the bone column is reformed with the aid of cerclage wire
205
What is the role of the cerclage wire in fracture management?
Cerclage wires draw fragments to their normal position and then fix them relying on the circular cross section of the bone to produce stability
206
Why might a plate be used with a transverse fracture?
if the fracture is transverse then rotation is possible To prevent this rotation a plate can be used in addition to the pin
207
How is the IM pin placed normograde?
Normograde This is when the pin is placed from proximal end of the proximal fragment Small skin incision is made and pin is seated into the bone. This pin is advanced proximal to the fracture site The pin is then pushed into the distal fragment More difficult that retrograde pinning but allows accurate placement of the pin proximally avoiding the sciatic nerve
208
How is a retrograde IM pin placed?
The pin enters the proximal fragment distally Leaves the proximal bone fragment and a small wound is made in the skin for the pin to be pushed through The pin is grasped by the Jacobs chick pulled proximally until it is positioned proximal to the fracture site Fracture is reduced and pin driven into the distal fragment
209
What issues are there with retrograde placement of the IM pin?
Pinning in retrograde suffers from loss of control to where the proximal part of the pin lies In cat this could lead to damage of the sciatic nerve
210
What can be seen
Normograde placement of an IM pin
211
What treatment has been used in the image?
IM pin and cerclage wires
212
What treatment has been used and why?
IM pin and external fixator The EF prevents rotation as well as offering resistance to axial compression both of which the IM achieves poorly
213
What are the properties and uses of the intramedullary interlocking nail?
Requires special jigs to ensure the screws enters the nail Strong and excellent at preventing rotation and bending Only be used in straight bones (tibia and femur) Infrequently used in vet med
214
What can be seen in the image?
Intramedullary interlocking nail
215
What are the properties of the external fixator?
Series of pins placed through the skin connected to a connecting bar Pins are attached to the bar with clamps or epoxyresin Pins may be threaded or the triagulation of pins prevents them pulling out Very versatile and counteracts all the forces applied to a fracture (esp with IM pin) Good for open fractures
216
What can be seen in the image? Wat are the placement options?
External fixator to radioulnar fracture Placement can be uniplanar, biplanar, unilateral or bilateral Bilateral are stronger can be used to augment IM pin fixation
217
What complications arise with external fixators?
pins prone to infection Prone to discharge where pins pass through muscle masses Req freq exams and reap of loose pins req staging down (removal of pins to change load bearing from fixator to the bone)
218
What are the properties of plate fixation and when might they be used?
Lots of diff types Allow for reconstruction of comminuted fractures Protect against axial and rotational forces Not as good at preventing bending as they are not positioned along the central axis of the bone- worse when plate is exposed to cyclical loading
219
Plate fixation methods
220
What are the differences between locking and non locking plate fixations?
Non locking are older and req plate to adhere to screws by friction - applies to plate and bone Locking plate there is a thread where the screw engages as well as in the bone - diameters of the screw that engages in the plate is greater than that which engages in bone Special guides needed for locking Can be considered a internal external fixator Locking means limited ability to angle screws
221
How can plates be classified by function?
Buttress plate = strong central section that bridges comminuted section of fracture Neutralisation plate allows reconstruction of fracture by taking some of the load Compression plate compresses the fracture by making use of eccentrically placed screws in an oval screw hole.
222
How does a compression plate work>
Screw starts its flight at the top of the slope and when tightened it moves down the slop and shifts one fragment towards the fracture therefore compressing it Using this way means the bone takes all of the load
223
What plates are being used to treat each fracture?
1. Simple transverse fracture repaired with compression plate 2. Comminuted but reconstructable fracture repaired with neutralisation plate 3. Comminuted fracture treated with buttress plate
224
How does cyclical loading lead to plate failure?
the trans cortex is incomplete in this image and radius is compounded by the force strain section of the ulna This results in the plate being exposed to cyclical loading and failure In the humerus, femur and tibi this bending tendency can be managed with an IM in, a rod plate
225
What are avulsion or tension fractures?
Special set of fractures that are produced by distractive forces generated internally As a result they are exposed to distractive forces during healing larger fragments can be repaired by screw placement and compression by lagging technique Distractive forces can be converted into compressive using a tension band
226
What is a lag screw and how are they used?
Allow for compression to be applied to the fracture The near hole is over drilled to have the same diameter as the thread so it doesnt grip When the screw is tightened it pulls the far fragment against the near Used to produce rigid fixation and will counteract the distractive forces
227
What is the role of the tension band?
Fracture is reduced and then 2 pins are used to fix it in position A figure 8 of wire is applied opposite to the distractive foce and the two arms are tightened With the wire tightened and pulling in the opp direction the end result is compressive force applied to the fracture
228
What should be considered when dealing with avian fractures?
Pneumatised bone with periosteal blood supply needs to be preserved Avian bone is brittle and prone to splintering Avian bone heals primarily from the endosteum Rapid healing Anatomical abnormalities due to flight adaptation Fractures involving joint or w/in 10cm = poor prog IM pins and external fixators used for thin and brittle bones
229
Describe the treatment
Humeral fracture in a kestrel repaired with an IM pin tied to a uniplanar external fixatory Clamps are replaced with epoxyresin to reduce the weight of the device
230
What factors in equine fractures should result in euthanasia?
Comminuted fractures - esp of pastern region compound fractures of long bone complete fractures of long bone and proximal long bone fracture of pelvis where the animal is recumbent PONY UNDER 300KG - potentially fixable issues
231
What were Halsteds principles of surgery?
- Gentle tissue handling - strict asepsis Haemostasis preservation of blood supply no tension on tissues Good approximation of tissues Obliteration of dead space
232
What might influence healing of tissues?
Age Nutrition Comorbidities Medications
233
Define Exploratory laparotomy
coeliotomy Performed with the objective of obtaining information that is not available via clinical diagnostic methods once underlying pathology has been determined the procedure can continue as a therapeutic procedure
234
How is an exploratory laparotomy performed?
Abdominal cavity is divided into 5 regions - Cranial abdomen GI tract Right paravertebral region Left paravertebral region Caudal abdomen
235
In an exploratory laparotomy what is being assessed in the greater peritoneal cavity?
Peritoneal fluid to do this Excision of the falciform ligament Examination of the righ and paravertebral gutters
236
What is being assessed in the cranial abdomen for an Exp laparotomy?
Liver Gall bladder and bile ducts Hepatic hilus Epiploic foramen Spleen
237
What should be assessed of the GI tract in an Exp lap?
Stomach Intestinal tract Pancreas Regional lymph nodes
238
What is assessed in the right paravertebral region of an Exp Lap?
Hepatic portal vein Caudal vena cava Coelic artery Hepatic lymph nodes Right adrenal gland Right kidney and proximal ureter Right ovary and uterine horn
239
What is being assessed in the left paravertebral region in an Explap?
Aorta Left adrenal gland Left kindey and proximal ureter Left ovary and uterine horn
240
What is being assessed in the caudal abdomen during and Exp Lap?
Bladder and distal ureters proximal urethra Prostate gland and ductus deferens Uterine body and proximal vagina Regional lymph nodes
241
What is assessed of the abdominal wall, peritoneal surface and mesenteries in an Exp Lap?
Diaphragm Oesophageal hiatus Aortic and caval hiatus Greater and lesser omentum Internal inguinal rings
242
What are the fundamentals of tumour resection?
Make a diagnosis Grading and staging the condition - histologic degree of malignancy - metastatic spread - paraneoplastic syndrome Use this to determine how the tumour will behave
243
What are the roles of oncological surgery?
Prophylactic surgery Diagnosis and staging Definitive excision palliative surgery Cytoreduction - follow up w chemo Management of oncological emergencies Surgery for supportive therapy Treatment of metastatic disease
244
What is an example of prophylactic surgery?
Ovariectomy/ ovariohysteractomy and mammary neoplasia Reduces the risk of mammary neoplasia with and incidence of 0.5% if before neutered before the first oestrus 8% before second and 26% after 2 cycles No effect after 2.5 years
245
What surgery may be classed as an oncological emergency?
Bleeding splenic haemangiosarcoma
246
How are diagnosis and grading of tumours carried out?
Cytology (FNA and impression smear) Histology
247
What biopsies can be carried out for histology of a tumour?
core biopsy Punch biopsy Incisional biopsy Excisional biopsy
248
What is the role of staging in tumour treatment?
Looking for metastatic tumours
249
What is meant by surgical dose in tumour treatment?
How much surgery Debulking/cytoreduction Marginal resection Wide resection Radical resection
250
Label the tumour below
Pseudocapsule Reactive Zone Tumour Skip metastases Satellite metastases
251
What is the role of cytoreductive excision?
Leaves macroscopic volumes of tumour. Will recur unless given adjuvant therapy (which is less effective if gross vs microscopic tumour remains)n
252
What is meant by marginal excision?
local excision That is, tumour removal with minimal amount of surrounding normal tissue Can result in microscopic or macroscopic presence of residual tumour
253
What is the role of wide excision?
Removal of the tumour with complete margins of normal tissue in all directions Local recurrence is unlikeley
254
What should be taken into account with wide excision margins for a tumour?
Fascial planes are the best border to a margin (especially over fat) Deep margins are much more difficult to achieve
255
What is meant by radical excision?
Removal of an entire anatomical structure or compartment containing the tumour Local recurrence unlikely This often applies for sarcomas which can extend along fascial planes rather than through them
256
What are the layers of the bowel?
Suture holding is most important in the submucosal layer
257
What is the role of gastrotomy?
Making a hole in the stomach For the removal of gastric foreign body
258
Procedure for gastrotomy?
Stay sutures Sterile swabs Operate outside of the peritoneal cavity Closure Absorbable monofilament and atraumatic needle 3/0 cats 3/0 or 2/0 in dogs Pattern Continuous - simple cont- contin invertinfg Two layer - sub mucosal / mucosal and then seromuscular layer Omentalise
259
What is the role of omentalisation?
Improved vascular supply Improved lymphatic drainage Rich source of inflammaotry and immunogenic cells (neut, t and b lymphs and macrophages) Neovascularisation (angiogenic factors
260
Define omentalisation
Omentalization, the placement of omentum around organs or within cavities to improve vascularization or drainage,
261
What is intussusception ?
Intussusception (in-tuh-suh-SEP-shun) is a serious condition in which part of the intestine slides into an adjacent part of the intestine. This telescoping action often blocks food or fluid from passing through. Intussusception also cuts off the blood supply to the part of the intestine that's affected.
262
Define intussuscipiens
invagination of a proximal portion of intestine (intussusceptum) into a more distal portion (intussuscipiens)
263
How long does healing of the intestine and bladder take?
14 days post suturing Wound strength will have reached nearly normal levels Urinary bladder takes 21-28 days post surgical repair
264
Whatis dehiscence?
Breakdown of the intestine and the urinary bladder usually occurs within 72-96 hrs post op Occurs during the lag phase of healign during this time all support and strength of the wound comes from the sutures
265
What checks should be done at the end of an operation?
Integrity of the repair Check for bleeding lavage and suction Count swabs Change gloves Change instruments
266
What are the signs of a post operative complication and how can they be checked?
Wound infection peritonitis Uroabdomen check clinical signs Radiography Abd US Abd Tap
267
What can be seen in the image?
Enterectomy dehiscence
268
What can be seen in the image?
Presence of peritoneal fluid
269
What can be seen in the slide produced via abdominocentesis?
Toxic neutrophils in high numbere Bacterial presence
270
What can be seen in the image? Animal has had bladder surgery
Would expect the animal to be hyperkalaemic Urethrogram is leaking from bladder repair into the peritoneal space Peritonitis was also present on Exp Lap
271
How should the linea alba be closed?
External rectal sheath is most important? reconstruct the original anatomy Rectus muscle has no wound holding strength
272
What is the rectus sheath made up of?
External and internal leaf
273
What is clinical reasoning?
The process by which veterinary surgeons integrate clinical and contextual factors to make decisions about the diagnoses, treatment options and prognoses of their patients
274
What are the methods of clinical reasoning?
Pattern recognition, illness scripts Problem based clinical reasoning Often dual process reasoning used
275
What are the properties of pattern recognition reasoning?
Pattern - No memory reliance Fast unconscious and intuitive Pattern recognition mode or heuristics (experience) Cognitive biases and emotional influences are sources of error
276
What are the properties of inductive reasoning?
Relies on working memory Slow analytical and abstract Modes are inductive and hypothetico-deductive reasoning working cognitive overload and knowledge base can be a source of error
277
What questions should be answered in inductive reasoning?
What is the problem Which body system is involved and how Where in the body system is the problem located What is the lesion
278
How is a clinical problem defined and refined?
Identify and clarify problems vomiting vs regurgitation Prioritise the most specific problems Jaundice vs lethargy Focus diagnostic or therapeutic plans on these Don't forget the other problems Body system responsible and how is it involved? primary (structural) or secondary (functional)
279
How can we differentiate between primary or secondary clinical problems?
History and clinical exam Further testing Vomiting animal- mass in abdomen or haemotology may show secondary Knowing between the two saves clients time and money
280
How is the location of a clinical lesion located?
History and clinical exam Further testing such as imaging Endoscopy etc
281
What is DAMNIT-V?
Degenerative, Anomalous, Metabolic, Neoplastic, Nutritional, Inflammatory, Idiopathic, Toxic, Traumatic, Vascular
282
What is a sign time graph?
Graphical representation of changes in pathology over time
283
What are the 2 components of pharmacology?
Pharmacodynamics Pharmacokinetics
284
What is pharmacodynamics
The action of the dryg What does it target and what is the responseW
285
What is pharmacokinetics
Movement of the drug in the body Where does it go Consider therapeutic plasma concentration
286
What are the aims of pharmacology?
Right drug Right dose RIght onset and duration of action Supervision and surveillance Modification and refinement Do no harm
287
What are the interacting considerations for drug use?
Underlying disease factors Drug data Owner needs Patient factors Practice Compliance
288
What are the different targets for drugs?
Receptors Ion channels Structural proteins Enzymes Carrier molecules DNA
289
What type of drug is shown in this dose curve?
Agonistic drug
290
What are the 2 types of agonists?
Partial - acts on a receptor and elicits a 50% response or a smaller response Full agonist- acts on a receptor and elicits a full response
291
What is meant by potency of agonistic drugs?
The amount of drug req to produce a 50% of its maximal effects ED50
292
What is meant by efficacy of an agonistic drug?
The maximum therapeutic response that a drug can produce
293
What is meant by specificity of a drug?
Capacity of a drug to cause a particular action in an population
294
What is meant by selectivity of a drug>
Relates to the drugs ability to target only a selective population ie cell/tissue/signalling pathway In preference to others
295
What is meant by therapeutic index?
296
What is the action of a non competitive antagonist?
Either bind to a different receptor site or block "post binding" chain of events Ie act downstream of the receptor
297
What is the action of a competitive antagonist?
Shifts the agonist dose-response curve to the right in parallel
298
What is the action of an antagonist on enzymes?
Bind to catalytic site Inhibits normal reaction therefore decreased production of undesired product
299
What is the tachyphylaxis?
The effect of a drug can decrease when given continuously or repeatedly
300
What are the causes of tachyphylaxis?
Change in receptors Loss of receptor number Exhaustion of mediators Increased metabolic degradation of the drug Physiological adaptation (crosstalk between body systems, one takes over) Drug transporters (active extrusion of the drug)
301
Unit conversion for calculating drug doses
302
What is meant by dose of a drug?
Amount/volume of medication taken at one time
303
How can we calculate the volume of a drug needed?
304
What is a 1%w/v solution
1g of powder dissolved in 100ml Or equivalent
305
306
How are dilution factors used?
307
What is the C1V1 = C2V2 equation?
308
How are drip rates calculated?
309
What are the two options of allometric scaling in drug dosing?
Surface area Metabolic rate
310
What is the prescribing cascade?
Risk based decision tree Legal and professional req Suitable and authorised medicine for the condition and species you are treating Where there is no suitable drug we are required to move through the drugs that may work to avoid suffering
311
What is step 2 in drug cascade?
A suitable vet med authorised in NI with import certificate
312
What is step 3 in drug cascade use?
Veterinary medicine with marketing authorisation valid in GB or NI wide for a diff species or condition Import certificate required
313
What is step 4 in the drug cascade use?
Human medicine UK with marketing authorisation or authorised medicine from outside the UK Medicine for livestock must be approved for food production in the country it is coming from
314
What is step 5 in the drug cascade?
Extemporaneous preparation create a product to use for animals - purity and concentration needs be controlled bought in This could include mixing drugs
315
What is step 6 in the drug cascade?
Human medicines authorised outside of the UK
316
What is the northern Ireland drug cascade?
317
Dx
Diagnosis
318
Px
prescription
319
Tx
Treatment
320
AE
Adverse event
321
AR
Adverse reaction
322
SAR
Suspected adverse reaction
323
SQP
Suitably qualified problem
324
RQP
Registered Qualified person
325
VMD
Veterinary medicines directorate
326
NOAH
National office of animal health
327
COPC
RCVS code of professional conduct
328
CD
Controlled drugs
329
POM-V
Prescription only medicine veterinary
330
POM-VPS
Prescription only medicine veterinarian/pharmacist/SQP
331
NFA-VPS
Non food animals VPS
332
AVM-GSL
Authorised veterinary medicine general sale list
333
Define veterinary prescription
334
What are the 2 classifications of medicines available on veterinary prescription?
POM-V POM-VPS POM-V medicines must have a prescription from a veterinary surgeon
335
Who can prescribe POM-VPS medicine?
RQP Clinical assessment of the animals does not have to be carried out when prescribing POM-VPS medicines and the animal does not have to be under the RQPs care but the RQP requires sufficient info
336
How should a prescription be written?
337
What added points should there be on a prescription?
338
What are the five schedules of controlled drugs under the misuse of drugs regulations 2001?
339
What is the validity of CD prescriptions?
CD in schedules 1-4 have a pres validity of up to 28 days Prescriptions for schedule 5 CDs have a validity of up to 6 months
340
Single prescriptions with multiple dispenses are not allowed for CDs in Schedules _________ however an instalment prescription can be used if required
Schedules 2 and 3
341
How are instalment prescriptions written?
When the total quantity of the prescription is to be dispensed in instalments, the written prescription needs to state the dates for the instalments and the amount or quantity to be dispensed First instalment must be dispensed within the 28 day validity period
342
When do further instalments need to dispensed in CDs?
for schedule 2,3 and 4 CDs the instalments do not need to be dispensed in the first 28 days
343
What is the under care guidance for RCVS?
A VS cannot usually have an animal under their care if there has been no physical examination, therfore a VS should not treat an animal or prescribe POM-V medicines via the internet alone
344
When must a physical examination be carried out before prescribing POM-Vs?
345
Define clinical assessment
A clinical assessment is any assessment which provides the VS with enough information to diagnose and prescribe safely and effectively May include a physical examination byt not always
346
How should prescriptions be noted in clinical records?
Name and amount dosage Admin instructions Any accessory warnings
347
What are the health and safety aspects of prescribing?
348
How should Px misuse be reported?
Alteration to an existing prescription or prescription fraud can be reported to the veterinary medicines directorate via The RCVS considers reporting Px misuse in public interest and in most cases a report to the VMD will be a justified breach of client confidentiality
349
What is an adverse event?
Any observation in animals whether or not considered to be product-related that is unfavourable and unintended and that occurs after any use of a veterinary medicine Included are events related to a suspected lack of expected efficacy or noxious reactions in humans after being exposed to a Vet medicien
350
What are the types of AE?
Lack of expected efficacy Unexpected AE (event that is not described in SPC) Serious AE= death or life threatening clinical signs, disability or incapacity, birth defects Non serious = AE all other adverse reactions of lack of efficacy following treatment w VM are non serious
351
SLEE
Suspected lack of expected efficacy
352
Define adverse reaction
A reaction to veterinary medicine which is harmful and unintended and which occurs at doses normally used in animals for the prophylaxis, diagnosis or treatment of disease or to restore, correct or modify a physiological function
353
When to report an AE?
After using an authorised VM Following off label use Using a human product in animals After using a compounded preparation Using an imported product
354
How should AEs be reported?
Record what happened in as much detail as possible Report the event electronically to the VMD within 15 calendar days
355
PSUR
Periodic safety update report
356
What is the Misuse of drugs act 1971
imposing a complete ban on the possession, supply, manufacture, import and export of controlled drugs except as allowed by regulations or by licence from the Secretary of State.
357
What is the misuse of drugs regulations 2001?
The Misuse of Drugs Regulations 2001 allow for the lawful possession and supply of controlled (illegal) drugs for legitimate purposes. They cover prescribing, administering, safe custody, dispensing, record keeping, destruction and disposal of controlled drugs to prevent diversion for misuse
358
What are the 5 schedules of CDs?
1 - no current therapeutic use 2- have therapeutic use but are highly addictive (highly restricted) 3- therapeutic use but misuse may lead to moderate or low physical dependence or high psychological dependence (subject to restrictions and Px 4- Therapeutic use but misuse may lead to limited physical dependence or psychological dependence 5- contain small quantities of substances that might cause dependence but potential for abuse is very low
359
Drug Schedule examples
360
How are controlled drugs procured?
Details of drugs requested and supplier RCVS number
361
How are schedule 2 drugs kept?
Locked cabinet Recorded register lock box in the car - secured to vehicle and not left unattended Some schedule 3 drugs should also be kept in locked cabinet
362
Who can a prescribe a CD?
363
How should controlled drugs be disposed of?
Made irretrievable before disposal Denaturing kits Soap for tablets Cat litter Destruction of schedule 2 drugs should be witnessed by VMR inspector CDLO Independence MRCVS Recorded in CDR
364
Who regulates prescribing veterinary drugs and why?
365
How is regulation of veterinary drugs achieved?
Data assessment and authorisation in GB via the VMD or centralised application to the European medicine agency (EMA) Prescribing dispensing and supply of veterinary medicines Testing, inspection and investigation Post-marketing authorisation
366
What are the drug distribution classifications?
367
What is a suitably qualified person?
368
What is POM-V drugs?
Prescription-only medication - vet Medicined must only be prescribed by a VS following a clinical assessment of the animal or group of animals which must be under their care
369
What medicines are classed as POM-V
Stict limitation on its use specifice safety reasons Specialised knowledge for use and application Narrow safety margin Government policy to demand control at a high level
370
What is a POM-VPS
clinical exam is not required
371
What is NFA- VPS
only for non food animals limits the effect of endemic diseases
372
SEAS
medicines for pet species the active ingredient of which has been declared by the secretary of stat as not req veterinary control Exempt from the requirement for marketing authorisation These are over the counter medications
373
Controlled drugs
374
Specified feed additives
375
Define prescribing
Any prescription for a veterinary medicinal product issued by a professional person qualified to do so in accordance with applicable national law
376
How is the supply process of medications checked and ensured?
377
How are records, storage and disposal of drugs regulated?
378
What are the determinants of a dosage regimen?
Activity and toxicity Pharmacokinetics Clinical factors Other factors - dosage form, route of administration
379
What factors of pharmacokinetics should be considered?
Dose - potency and efficacy Onset - absorption and distribution Loading dose - Vd Maintenance dose - clearance Time to steady state- Half life
380
What influences dosage?
The potency of the drug - partial agonist vs full agonist Bioavailability and first-pass metabolism Absorption- drug needs to cross the membrane Distribution
381
Most drugs are lipo_____ to pass the plasma membrane
Lipophilic
382
What are the factors that affect onset of activity of a drug?
Time to reach the maximum (Tmax) Route of administration Chemical structure and formulation - pH of location Clinical situations
383
How can orally adminstrated drugs affect the onset of action?
Polypharmacy Gut content Splanchnic blood flow
384
How can clinical situations affect onset of action of a drug?
Pathology Tissue blood perfusion Changes in pH States of shock
385
What is meant by life of a drug?
Administration Absorption and distribution Elimination
386
What is loading dose?
Enables therapeutic concentrations to be reached sooner Principally determined by Vd
387
What is maintenance dose?
Principally determined by clearance
388
When is steady state achieved?
Within 5 half lives
388
What is the calculation for loading dose?
389
How can steady state be maintained?
Ideal situation is constant IV infusion Increasing dose frequency minimises the peaks and troughs so the drug will approach Css Owner and patient compliance is reduced with multiple daily dosign Need for balanced approach and considerations if dose is missed
390
What are the 2 types of saturation with multiple dosing?
1, Normal kinetics 2, saturation kinetics
391
What are normal kinetics of multiple dosing drugs?
Plasma concentration increase proportionally with dose
392
What is saturation kinetics of multiple doseing drugs?
If dose is increased then disproportionate increase in steady-state concentrations Necessitates smaller dose increments
393
What is plasma protein binding and how does it afffect drug action?
Bound and free fractions in equilibrium Only the free drug is active Free drug can be distributed, metabolised or excreted saturable binding could lead to non linear relation between dose and free concentration by the effective concentration range is below that at which this would be important in most scenarios Extensive protein binding slows drug elimination
394
What factors affect drug absorption?
Related to the drug - High for lipid-soluble drug -Low for molecular size -Decreases for high degree of ionisation - Formulation can improve absorption Related to the body - increases with SA and absorptive surface pH will affect the extent of ionisation GI motility (slow =inc fast = dec) The integrity of absorptive surfaces Diseases
395
What factors affect drug distribution?
Inc adipose tissue increases Vd for lipid soluble drugs High water body content increases vd for water soluble drugs
396
What factors affect drug metabolism?
397
What are polymorphisms in relation to drugs and pharmacology?
polymorphic forms of a drug differ in the physicochemical properties like dissolution and solubility, chemical and physical stability, flowability and hygroscopicity. These forms also differ in various important drug outcomes like drug efficacy, bioavailability, and even toxicity.
398
What factors affect the excretion of drugs?
399
How does the neonate and paedriatric patient alter pharmacokinetics?
Absorption is variable as there is altered gastric emptying and rapid topic absorption Distribution inc for non lipid Distribution dec for lipid drugs Metabolism is dec as there is dec hepatic function Excretion - GFR is normal but drug tubular secretion in the nephron is longer for weak acid or basic drugs
400
What alterations need to be made to neonate drugs?
Absorption is variable Plasma level affected therefore alterations to dose and dose frequency Possible lower metabolic clearance Possible lower excretion clearance
401
How does the geriatric patient alter pharmacokinetics?
Absorption reduced Body mass inc so lower water inc fat content Metabolism changes are minimal so decreased plasma albumin Excretion has decreases renal elimination as decreased renal mass and GFR (similar to animals with chronic renal disease)
402
How should drugs be altered for geriatric patients?
Reduced bioavailability lowers Cmax Later Tmax Affects plasma level- dose and dosing frequency Little change in metabolic clearance Lower excretion clearance
403
How do pharmacokinetics change for chronic cardiovascular disease?
decreased metnation- inc effects of sedatives Decreased blood flow = lower clearance for highly cleared drugs eg anaesthetics
404
How do pharmacokinetics change for renal disease?
Associated with most profound changes in PK A gradual loss of urine concentrated ability and ability to acidify Also altered drug distribution patterns Change in acid base balance Uraemia - chronic acidosis, red albumin binding of drug and less hepatic metabolism
405
How do PK change for liver disease?
Content and activity of phase 1/II reactions is decreased Little effect on drug metabolism untile 80% functional loss no adequate functional tests Most antimicrobials are well tolerated
406
How does PK change for respiratory disease?
Altered serum pH and protein binding
407
How does disease affect dosing regimen of drugs?
408
What is the therapeutic index of drugs?
409
What drugs have a high therapeutic index?
410
What drugs have a low therapeutic index?
411
Drugs with a ____ therapeutic index used in chronic therapy may require therapeutic monitoring for altered physiological states
Low
412
How is therapeutic monitoring of drugs carried out?
413
What are the routes at which drugs can be eliminated? PK
Urine feaces Milk and sweat Expired air
414
Pharmacokinetics of a drug
we want drugs to be above the minimal effect concentration but below toxic levels This window is the therapeutic window a we want this to stay in the therapeutic window until the issue is resolved
415
What is the onset of action of a drug?
The time taken for the drug to become effective
416
What is the Cmax?
The concentration max which is the peak concentration This needs to be below the toxic levels
417
What affects drug absorption?
IV bolus = instant Infusion= zero order Oral or IM= inc slowly and then decline
418
What is the termination of action?
When elimination of drug brings concentration below the minimal effective concentration
419
What is the elimination rate?
The amount of parent drug eliminated from the body per unit of time
420
How does elimination of a drug occur?
Metabolites then excreted Direct excretion via the kidneys Hepatobiliary system
421
What are the principles of drug metabolism?
Enzymatic conversion of drug to a metabolite Lipid soluble to water soluble is the aim Lipid soluble -> catabolic phase-> drug derivative -> Anabolic phase -> Water soluble drug
422
What is the role of CYP450?
Cytochrome P450 (CYP) is a hemeprotein that plays a key role in the metabolism of drugs and other xenobiotics
423
Explain drug renal excretion
Passive filtration of small drugs (effected by GFR and plasma protein binding) Secretion (affinity for transporters, lipophilicity and polarity effect) Reabsorption (effected by lipophilicity, polarity and urine pH) If remain in the nephron then excretion via the urine
424
What transporters are found in the proximal tubule?
OATs and OCTs
425
If a drug is lipophilic what will be the action in the distal tubule of the kindey?
Lipophilic drugs will be reabsorbed
426
Drug clearance
Measure the efficiency of drug elimination The volume of blood/plasma cleared of a parent drug per unit time
427
How is drug clearance calculated?
428
Bioavailability?
Measure of extent of absorption from administration site to measurement site
429
How is the bioavailability of a drug calculated?
430
Volume of distribution of a drug?
The volume into which a drug appears to be distrubted with a concentration equal to that in the plasma Vd is a reversible process
431
What affects Vd of a drug?
The magnitude of Vd for a drug is influenced by its reversible affinity for tissue proteins vs plasma proteins. It is expressed in units of volume per Kg body weight
432
What is meant by a half life of a drug?
The time taken for the plasma concentration of the drug to halve
433
what are the potential drug-drug interactions?
Pharmaceutical - interaction prior to administration Pharmacokinetic - tissue/plasma levels of one drug altered by another one Pharmacodynamic- action of one drug is altered by another one
434
Drug - drug interactions
Altered pharmacological response to one drug caused by the presence of a second drug
435
What are the potential outcomes of drug to drug interactions?
Enhanced, inhibited or has new effects or no change at all Summation Potentiation Synergism
436
Summation Pk
The combined effect of two drugs produced a result that equals the sum of the individual effects of each agent
437
Potentiation pK
When a drug on its own does not have an effect but may affect/be affected in combination with another drug
438
Synergism
Drug combinations produce a therapeutic or toxic effect greater than the sum of each drug's action
439
What are the mechanisms of drug interactions? Pharmaceutical?
Physical - incompatibility interaction (binding to plastic or insolubility in some solutions) Chemical - Stability of drugs is often pH dependent, oxidation and reduction reactions, complex formation , inactivated by certain vehicles
440
What pharmokinetic drug interactions can occur?
441
How can pharmacodynamic interactions of drugs occur?
Additive Synergistic Negation
442
Define ADE
Unintended or noxious response to a drug that occurs within a reasonable time frame following administration
443
What are the types of adverse events?
444
How is pain caused?
Results form the interplay of facilitatory and inhibitory pathways throughout the peripheral and central nervous systems
445
What is the role of maladaptive pain?
Represents malfunction of neurological transmission and serves no physiological purposehat
446
What is the role of Adaptive pain?
Altering behaviour to avoid damage or minimise further damage
447
How can pain be assessed?
TPR & pain assessment Treat pain and reassess
448
What are the 3 different signs of pain?
Clinical Biochemical Behavioural
449
What are the different pain assessment tools?
Physiological measurements SDS, NRS, VAS DIVAS Composite scales Pain faces Acute vs Chronic pain QoL scales Analgesiometry and accelerometers Gait analysis Pressure sensitive walkways
450
What are the challenges of pain scoring?
Difficult, subjective and other drugs can affect evaluation Environment and owner can affect the animal Species variation Interspecies variation Domestication, hierarchy, feeding, aggression The pain scale must reflect or accomodate these differences
451
What are the steps to creating a pay scale?
Follow an established psychometric approach Validity is the most fundamental attribute of the questionnaire Validity in the criteria, content and construct Utiity - quick and easy to us
452
What is being assessed in grimace scales?
. Ear Changes : fold, curl and angle forwards or outwards, pointed shape 2. Orbital Tightening: narrowing of the orbital area, partial or complete eye closure or squeezing 3. Nose/Cheek Flattening: with eventual absence of the crease between the cheek and whisker pads 4. Whisker Change: move forward away from face
453
Ear positions
454
Orbital tightening
455
Muzzle tension
456
What is evaluated in cattle for pain?
457
Head position
458
How can pain be assessed in pigs?
Ear position (held backwards= pain )
459
How can pain be assessed in horses ears?
The distance between the ear canal becomes larger and the ears fall down to the side and turn outwards. move in diff directions or positioned asymmetrically
460
How can pain be assessed in the eyes of horses?
Muscles around eye are stretched gives upper eyelide a distinctive angled appearance Sclera is more evident in the medial canthus Stare is withdrawn and intense during the induction of pain
461
What can be assessed with equine nostrils when in pain?
Nostrils are dilated laterally and change from a normal elongated shape to a square with more marked edges noticeable in the medial part of the nostrils, where they are drawn more sharply towards the medial plane
462
What can be assessed in equine face muscles to determine pain?
Jaw muscles on the side of the horses face become mroe stressed and marked Especially m. Zyomaticus and m. Caninus, but also m.Masseter may be tense
463
What can be assessed in the equine muzzle for pain?
Increased tonus of the lips and tension of the chin during pain stimuli results in a more edges shape of the muzzle
464
Equine pain scale
465
What are the most common signs of pain in horses?
Asymmetrical/low ears or ears held stiffly backwards Angled eye/tension above the eye area and orbital tightening Withdrawn and tense stare Nostrils – square-like/strained Tension of the muzzle/strained mouth and pronounced chin Tension of the mimic muscles/chewing muscles
466
How can acute pain be prevented from becoming chronic?
Opioids, NSAIDs, local anaesthetics Ketamine and alpha 2 agonists Cold therapy Tissue handling Nursing care (bandages, massage, IV lines, monitoring, ROM, ensuring sleep) Other therapies (limited evidence) e.g. Laser, TRPV1 agonists, pulsed EMF
467
What is the pathway of NSAIDs
The COX enzymes are the targets for NSAIDs. NSAIDs also target descending pain pathways PAG+ NRM
468
What are the common NSAIDs for equids?
Phenylbutazone Flunixin meglumine Meloxicam
469
What are the common NSAIDS used in cattle?
Meloxicam Ketoprofen Cattle and small ruminants should receive NSAIDs for castration, disbudding and assisted calving
470
When is the use of NSAIDs contraindicated?
Renal or hepatic insufficiency (how bad?) Hypovolaemia Congestive heart failure & pulmonary disease Coagulopathies, active haemorrhage Spinal injuries Gastric ulceration Concurrent use of steroids Shock, trauma Pregnancy
471
Suggested protocol for monitoring dogs on long term NSAIDs
472
What is Grapiprant?
An new class of piprant NSAID that doesn't block COX It works lower down the inflammatory pathway by blocking some activity of specific prostaglandin
473
Properties of paracetamol
Used to be classified as a NSAID (blocks central & peripheral COX) CB1 & TRPV1 actions & antipyretic Used IV in dogs & horses (no licence) Pardale-V (paracetamol & codeine) has licence in dogs Licensed in pigs NEVER USE IN CATS
474
Properties of opiods?
Use in pre-emptive, multimodal and preventive analgesia Controlled drugs Full agonist, partial agonists and agonist-antagonists and antagonist exist 4 key receptors mu, delta, kappa & orphanin Morphine, methadone, pethidine, fentanyl, buprenorphine, butorphanol, tramadol
475
What are the properties of local anaesthetics?
Local anaesthetics are amides or esters Esters hydrolysed by plasma cholinesterases, amides by the liver Narrow therapeutic index (easy to overdose, care with dosing) Overdose? Use 20% intralipid IV Lidocaine can also be given IV as CRI for analgesia (dogs & horses) Mechanism of action – ionized charged form interacts with Rc
476
When are local anaesthetics used?
one spray delivers 2-4mg of lidocaine. Lidocaine jelly (2% 20mg/ml) for catheterising the urethra Somatic tissue can be infiltrated, reliable & safe Lidocaine is most often used (0.5-2.0%) Anaesthesia is produced by multiple intradermal (or subcut) injections The local is slowly injected as needle is advanced along the proposed surgical site Best performed in sedated/anaesthetised animals Place the needle in the 1st desensitized area & make injections at the periphery of advancing wheal Don’t use xylocaine spray (reactions)
477
What are the properties of alpha 2 agonists?
Bind to alpha 2 receptors Analgesic & other actions (sedation, ↓HR) Sedation for all spp Premedication, rescue analgesia Short lived approx. 1 hr analgesia Can antagonise with atipamezole
478
What are the effects of alpha 2 agonists?
Sedation (A) Decrease MAC Analgesia (somatic & visceral) (A & B) Hyper (B) then hypotension (A) Decreased CO & HR, increased SVR Respiratory depression Increased urine production Decreased GI motility Decreased surgical stress response Hyperglycaemia, GH enhanced, Thermoregulation affected Sweating
479
What are the properties of ketamine and NMDA antagonists?
Uses of ketamine: induction agent (dissociative anaesthesia), perioperative analgesic, restraint of fractious cats (sprayed in mouth) Combined with other drugs for sedation (IM or IV) Very versatile, useful for zoo and exotic animals NMDA receptor antagonism (but also interacts at many other Rc) Memantine
480
How does ketamine work?
Triggers glutamate release in the brain through blocking NMDA receptors on inhibitory neurones Neurones release NT that keep other neurones from firing and releasing glutamate stores when glutamate gets released it triggers synaptic formation and strengthening in the brain
481
How is chronic pain different to acute pain?
is multifactorial (posture, mood, movement - scales reflect this)
482
What pain scales can be used to determine chronic pain?
Helsinki Chronic Pain Index GuvQuest Canine Brief Pain Inventory (CBPI) (OA & bone cancer pain) Liverpool osteoarthritis in Dogs (LOAD e) CSOM (client specific outcome measures)
483
What are the treatment options for dogs and cats with chronic pain?
484
What adjunctive therapies can be used to manage chronic pain?
Hydrotherapy & physiotherapy Chondroprotectives Exercise management Weight control & diet Joint replacement/salvage Anti NGF Ab (Librela, Solensia) Irap Accupuncture Other drugs: garlic & fenugreek, sodium hyaluronate (Hyonate), prednoleucotropin (PLT), steroids, paracetamol (not cats) Stem cell therapies (MCS)
485
What are the effects of Mesenchymal Stem cells?
The effects of MSCs are exerted primarily through their secreted factors, including extracellular vesicles and bioactive molecules such as chemokines, cytokines and growth factors These paracrine factors have a range of immunomodulatory, anti-inflammatory, angiogenic and anti-apoptotic properties - rename “Medicinal Signalling Cells” Adipose tissue-derived MSCs (ADSCs)
486
What are the uses for cannabidiol in chronic pain?
Potential efficacy as analgesics in patients with chronic pain Cannabinoids act on peripheral, spinal & supra-spinal sites to exert antinociceptive and antihyperalgesic effects Clinical trials investigating the use of CBD oil in dogs with OA have had mixed results No licence in the UK, and vets must be aware of the legal position regarding prescribing
487
What does each category of HHHHHMM mean for a dog approaching its EoL?
Hurt Hunger  Hydration Hygiene  Happiness Mobility More good days than bad Each category score out of 10. 0 = unacceptable, 10=excellent, >35 acceptable QoL
488
What is the mechanism of action for local anaesthetics?
Have a narrow therapeutic index Ionised charge form interacts with the receptors The receptor for LAs are located within the port of the Na channel close to the cytoplasm and on the ionised charged form the LA can interact with the receptor
489
Where are LAs broken down and why?
LAs are amides or esters Amide versions will be broken down by liver Esters will be broken down by plasma cholinesterases
490
What are the rapid onset LAs
Procaine- cattle Lidocaine - all species Proparacaine - eyedrops
491
What are the slow onset LAs?
Bupivacaine- SA Mepivacaine- Equine
492
How do slow onset and rapid onset LAs compare?
Slow onset LAs are often more potent and more toxic
493
What is shown?
Preinscional block
494
What is shown
Intra testicular block
495
What is shown?
Direct infilitration of the mesovarium ligament (splash block on ovaries also works)
496
What is shown?
Retro bulbar anaesthesia
497
What is shown?
Infiltration of LA following enucleation and suture closure
498
What is shown?
Lumbosacral and sacrococcygeal epidurals
499
What are the indications for lumbosacral and sacrococcygeal epidurals?
: Canine and feline tail amputations, perineal urethrostomies, anal sacculectomies, catheterisation for relief of urethral obstruction, perineal relaxation for delivery of puppies/kittens, and other surgeries of the penis or perineal region.
500
What is shown
Rostral maxillary dental block Infraorbital Provides analgesia to soft tissue of rostral maxillaru
501
What nerves can be seen?
502
What is shown?
Caudal maxillary Extra oral Needle inserted below the cranioventral border of the zygomatic arch, between caudal border of maxilla and cranial border of mandibular ramus Needle advanced parallel to the plane of the hard palate and 1cm caudal to the lateral canthus of the eye The needle is advanced until bone is felt, aspirate! ++ risk of venepuncture
503
What can be seen?
Mandibular block The (green) inferior alveolar nerve (IAN) is a branch of the mandibular nerve Individual alveolar nerves branch dorsally through short section of bone to each individual tooth to innervate the tooth structures and adjacent bone Nerves exit mental foramina to innervate soft tissue of rostral lower lip
504
What is shown?
Rostral mandibular block The (green) inferior alveolar nerve (IAN) is a branch of the mandibular nerve Individual alveolar nerves branch dorsally through short section of bone to each individual tooth to innervate the tooth structures and adjacent bone Nerves exit mental foramina to innervate soft tissue of rostral lower lip
505
Bier block in cattle
506
What is shown and what are the properties?
This technique provides safe, short-term anaesthesia of the extremity. To perform IVRA or a Bier block, place a catheter distally in an appropriate vein (cephalic or saphenous) in the limb requiring analgesia. De-sanguinate the limb by placing an Esmarch bandage, and then place a tourniquet proximally and tighten it. Remove the Esmarch bandage and inject lidocaine into the cannula, remove cannula and prep leg for surgery. Bier block used in cattle.
507
What block is shown?
Femoral and sciatic nerve block PNBs offer and alternative to epidural with reduced risk of urine retentiona and reduced postoperative opoid consumption
508
What nerves can be seen?
Femoral artery (arrow) and femoral nerve (solid arrow).
509
What are the uses other than nerve blocks do LAs have?
The intravenous route - CRI Only use pure lidocaine IV (no adrenaline!) More benefit in soft tissue pain?? Can be used in both dogs and equines (colics) as an infusion (is it prokinetic?) Decreases MAC, reduces opioid dose Contributes to balanced anaesthesia Post op can be useful Best avoided in cats
510
What is LA toxicity and how is it prevented and treated?
Overdose with local anaesthetic can occur occasionally Support patient (airway, seizures, arrhythmias, can also administer intralipid) Prevent by carefully calculating dose and always aspirate before injecting The risk of toxicity is small if care is taken
511
How can anaesthesia be administered?
Intramuscular Intravenous Subcutaneous Inhalation Across the mucous membrane
512
How do anaesthetics work?
Anaesthetics are pharmacological agents that target specific central nervous system receptors. Once they bind to their brain receptors, anaesthetics modulate remote brain areas and end up interfering with global neuronal networks, leading to a controlled and reversible loss of consciousness.
513
What are the properties of propofol?
Rapid onset of action, rapid uptake by CNS, 5-8 mins unconsciousness Milky alkyl phenol Respiratory and cardiovascular depression Rapid and smooth recovery Suitable for ‘top ups’ or TIVA, only given IV, licensed for dogs and cats No analgesia Works at GABA
514
What are the pharmokinetic properties of propofol?
Pharmacokinetics of propofol: Absorption (minimal oral bioavailability) Solubility (minimally soluble in water) Distribution (98% protein bound) Metabolism (liver, glucuronidation) Elimination (renal) GABAA beta subunit (inward directed Cl current hyperpolarizes the postsynaptic membrane and inhibits neuronal depolarization)
515
What are the properties of alfaxalone?
Rapid onset of action, rapid uptake by CNS Respiratory and cardiovascular depression Rapid and smooth recovery (if premedicated) Clear, colourless neuroactive steroid Suitable for ‘top ups’ or TIVA, and can be give IM for sedation No analgesia Works at GABA Licensed for dogs, cats, rabbits
516
What are the pharmokinetics of alfaxalone?
Pharmacokinetics Absorption (good bioavailability) Solubility (soluble in water) Distribution (30-50% protein bound) Metabolism (liver, rapid, also lungs, kidney) Elimination (renal, and small % bile) GABAA allosteric modulator
517
What are the properties of ketamine?
Dissociative anaesthesia’ & analgesia Clear colourless solution, IV or IM (can sting) Licensed for cats, dogs, ruminants, rodents, rabbits, primates, horses Poor muscle relaxation, therefore combined with other drugs (BZD, alpha 2) Schedule 2 drug Component of the feline ‘triple’ or ‘’quad’ IM protocols Mechanism of action is primarily due to antagonism at NMDA receptor
518
What are the uses of volatile agents in anaesthesia?
Occasionally these drugs can be used for induction (their main use is maintenance) A mask/induction chamber is used Often used in birds, rodents, & very compromised animals But stress is involved with restraint/breathing the agent (isoflurane > sevoflurane) Deliver via precision vaporiser, in oxygen, slowly increase % until animal unconscious Mechanism of action (GABA, 2PK)
519
How do volatile agents work in anaesthesia?
At the spinal cord level, inhalation anaesthetics decrease transmission of noxious afferent information ascending from the spinal cord to the cerebral cortex via the thalamus, thereby decreasing supraspinal arousal. There is also inhibition of spinal efferent neuronal activity reducing movement response to pain. Hypnosis and amnesia, on the other hand, are mediated at the supraspinal level. Inhalation agents globally depress cerebral blood flow and glucose metabolism. Tomographic assessment of regional uptake of glucose in anaesthetized volunteers indicates that the thalamus and midbrain reticular formations are more depressed than other regions. Electroencephalographic changes including generalized slowing, increased amplitude, and uncoupling of coherent anteroposterior and interhemispherical activity occur during anaesthetic-induced unconsciousness.
520
What are the less commonly used induction agents?
Zoletil’ (zolazepam & tiletamine) MS-222 Thiopentone ‘Ketofol’ (ketamine + propofol) Etomidate
521
CEPSAF
Confidential enquiry into perioperative small animal facilities
522
What has been shown through CEPSAF?
60% of the fatalities occurred within the recovery period with half of these dying within 3 hours of disconnection Greater vigilance is required regarding monitoring the recovering patient
523
What are the risk factors associated with recovery from anaesthesia?
ASA category Breed Age Weight Length of anaesthesia Type of surgery Drugs given Temperature Species Vigilance/ experience of staff Available equipment
524
What should be the properties of a recovery area for post anaesthesia?
Staff always present consider the logistics Separate species to red stress Good ventilation to eliminate exhaled gases Open fronted kennels and cages Warming equipment Protective clothing and gloves should be worn Emergency equipment
525
What emergency equipment may be required post anaesthesia?
Anaesthetic machine Breathing systems Anaesthetic induction drugs and anagesics Equipment for IVFT Endotracheal tubes and laryngoscope Suction apparatus Monitoring equipment Emergency drugs (crash box) Defibrillator (if poss)
526
How should recovery monitoring charts be used post op?
Separate to anaesthetic monitoring sheet Need all information from the anaesthetic (hand-over) TPR every 5 mins initially, reduce to every 10 as recovery progresses Remember ABC on recovery
527
What is the end procedure sequence of events for anaesthesia surgery?
Surgery/procedure ends Vaporiser is switched off (do NOT turn down early) If using nitrous oxide, switch off and increase oxygen to deliver adequate FGF and minimise diffusion hypoxia (leave on 100% O2 for 10 mins if N2O was used) ‘Dump’ the reservoir bag on the breathing system (with valve open) and fill with fresh gas- oxygen by increasing the flowmeter
528
How is disconnection from anaesthesia achieved post op?
Disconnect the patient from the breathing system Switch off oxygen Move patient to recovery area Do not deflate cuffs until apt Cuff may not be fully deflated following dental or oral procedures to prevent inhalation of blood and debris Check oropharynx with laryngoscope in these cases
529
When are dogs extubated?
gag-reflex returns; indicated by swallowing, tongue flicking (same in most species i.e. horses, ruminants, pigs etc.)
530
When are cats extubated?
approximately 15 seconds before swallowing, try checking for palpebral reflexes, provoked ear twitches, but it’s hard to judge. Don’t delay as can cause laryngospasm
531
When are brachycephalic breeds extubated?
BOAS Extubate on inspiration
532
How should patients be kept post extubation?
patients head and neck should be extended ant the tongue gently pulled forward to maintain patent airway
533
What should be monitored post extubation?
Level of consciousness, activity and recovery of physiological reflexes Body temp Oxygenation Ventilation and airway patency Circulation (HR, pulse quality, MM colour, CRT) Postoperative analgesia
534
How long post op should patients be monitored?
They are alert, lifting head and swallowing Showing normal ocular reflexes. Jaw tone indicates good muscle strength They are not shivering, and body temp is above shivering threshold (>35°C) MM are pink while breathing room air (if in doubt, use pulse oximeter) They are breathing well without ETT in place. No signs of upper airway obstruction present Effective analgesia has been provided and is likely to last until the next assessment is due.
535
What are the common causes of upper airway obstruction?
Loss of pharyngeal muscle tone Regurgitation or vomiting Laryngospasm or laryngeal oedema
536
What are the signs of airway obstruction post op?
Increase resp noise or effort Abdominal effort, nares flaring Air hunger posture (head and neck extended) Cyanosis (late sign)n Agitation and restlessness Agonal breathing (terminal sign)
537
How should airway obstruction be treated?
Call for help Open mount use laryngoscope Pull tongue forward and suction blood/mucous Reintubate if possible Always have induction agent ready just in case
538
What is being assessed of circulation post op?
Monitor pulse rate & quality every 5 minutes in first stage of recovery Where will you palpate the pulse? Can also monitor blood pressure, mucous membrane colour & CRT, ECG & temp ICU cases will have further monitoring
539
What is being assessed of temperature post op?
Very important to keep animal normothermic during anaesthesia and continue in recovery Ambient temp Breathing system (circle vs non re-breathing) & HME Prep solution/alcohol kept to min Bubble wrap/socks/space blankets Warm IV fluids and flushing solution Hot air blankets
540
When is analgesia given post op?
Is the patient comfortable? Is the animal restless/vocalising because it is… In pain Dysphoric Emerging from the anaesthesia Uncomfortable (bladder full/ needs to defecate) If in doubt , give an analgesic & re-assess Pain scales
541
What is the role of discharge instructions?
Don’t underestimate the importance Utilise the nurses, they are experts in this Talk to owners before reuniting with pet Home with sufficient analgesia Owners aware of how to spot problems Owners aware of what to do/who to call? Instruction sheets/specific surgery/condition Buster collars Cage rest/sufficient advice given? Post op/check-up appointment booked?
542
What are the anaesthetic mortality rates for equines?
1% in elective cases 2% in non colic emergency cases 5.4% in emergency colic surgery cases
543
Why do horses die during or after anaesthesia?
Fractures in recovery (highest mortality) Post anaesthetic myopathy Neuropathies and spinal cord malacia Intraoperative cardiac arrest Respiratory obstruction
544
What are the risk factors for equine anaesthesia?
Increasing ASA grade Increasing age and foals Surgery type and position Duration Time of day, OOH provision Agents used (premed/TIVA) Recovery quality
545
What is standing sedation and how is it used in horses?
Some surgical procedures can be performed with the horse standing e.g. castration, sarcoid removal Sedatives and analgesics and local anaesthetic combinations can be used Cases where used: sedated with romifidine and butorphanol IV, and then had two intratesticular injections of lidocaine, and IV NSAID received an infusion of detomidine, and increments of butorphanol IV, and local anaesthetic infiltration at the surgical site, plus a NSAID. ODSP (kissing spine) surgery
546
What is the night before preparation for equine GA?
Admit the night before Complete physical exam - murmurs? Blood samle Starve Remove shoes Ensure horse is clean
547
What is the morning or preparation for equine GA
IV cannula always Flush out mouth Tail bandage/plait Clip if possible Weigh Make anaesthetic plan Pre medicate the horse
548
How should we prep for equine Anaesthesia?
Prepare monitoring equipment Prime anaesthetic circuit with isoflurane Select ET tube Change soda lime Label and prepare drugs Leak test anaesthetic machine and ventialor nad set Tidal volume Prepare fluids and dobutamine Prep tabel
549
What are the types of breathing circuit for equines?
Rebreathing circuit- CIRCLE Fresh gas flow rate? Start 6-8L/min After 15min reduce to 3-4L/min
550
What premedication is given to horses pre op?
Acepromazine
551
What is the role of the equine premed acepromazine?
Anxiolytic Reduces catecholamines (dec cardiac arrest) Reduced anaesthetic gase requirement Improves recoveries Improved tissue perfusion through vasodilation
552
What are the risks with Acepromazine?
Penile prolapse Hypovalaemia
553
When should acepromazine be given to horses?
IM 40 mins before sedation IV 20 mins before sedation
554
What are the premedication options for horses?
Alpha 2 agonists Opiods
555
What is the role of alpha 2 agonists in horses premedication?
Sedation for induction Analgesia Vasoconstriction and bradycardia
556
What is the role of opioids as a premed in horses?
Analgesia Improved sedation quality Respiratory depression?
557
What are the typical equine premeds?
ASA 1 & 2 With or without Acepromazine Wait 20-40 mins Add alpha 2 agonist with or without opioid Remember with NSAID and then potentially antibiotic
558
What are the signs that a horse is ready for induction?
Head down, wide based stance Horses are insensible to surroundings
559
What is the induction agent for equines?
IV ketamine A benzodiazepene (midazolam can be combined with the ketamine) Occasionally guaifenesin IV can be used instead of an alpha 2 agonist
560
Example anaesthesia protocol for equine
561
What are the steps following premed for anaesthesia of horses?
Intubate (ET tubes, cuffs checked, gag, lubricant) Attach hobbles and move horse Place on table and connect to anaesthetic machine Maintain horse in dorsal or lateral recumbency on oxygen in isoflurane Monitor as usual, place arterial line for ABP, ECG, Et CO2 Catheterise Connect IV fluids
562
What can anaesthesia be substituted for in equines?
Can supplement anaesthesia with injectables for maintaining plane of anaesthesia (PIVA) e.g. lidocaine
563
What is the role of volatile anaesthetic agent in horses?
Maintenance of anaesthesia
564
What is the normal volatile anaesthetic agent used in horses?
Isoflurane or sevoflurane (only iso is licensed)
565
What are the issues with volatile anaesthetic agent in horses?
Hypotension Need lowest dose that ensures anaesthesia
566
What is the starting concentration for volatile anaesthetic agent in horses?
567
What can be assessed to monitor anaesthetic agent of horses?
Palpating pulses Reflexes and eye signs Muscle tone Machine Multiparameter Pulse oximeter Blood gases
568
TIVA
Total intravenous anaesthesia (alternative to volatile agent)
569
How can TIVA be achieved?
Top up bolus injections( ketamine 0.5mg/kg) Continuous rate infusions (triple drip in equine anaesthesia - useful for field work)
570
What are the benefits of TIVA?
Produces a lower anaesthesia stress response compared with inhalation agents and is therefore physiologically superior method
571
What is triple drip anaesthesia?
572
PIVA
Partial intravenous anaesthesia
573
What is used for PIVA?
Reduces amount of inhalant gas required
574
What problems are seen with equines and anaesthesia?
Problems we see Hypotension Hypoxaemia Hypercapnia Bradycardia Tachycardia Neuropathy Eye problems
575
How can anaesthesia induced hypotension in horses be mitigated?
Use positive inotrope Reduce isoflurane Use PIVA Increase fluids <70mmHg using invasive arterial monitoring
576
Hypotension of equines on anaesthesia can lead to ________ on recovery
myopathy
577
What are the properties of spinal cord malacia in anaesthesia? Equine
Becomes apparent in recovery period Fatal Cause is potentially hypotension Usually heavy bred horses and yound More common in dorsal recumbency Not related to duration of anaesthesia
578
What is spinal cord malacia?
Myelomalacia, or “soft cord,” is characterized by an absence of confluent spinal cord cysts. Histologically, myelomalacia is characterized by microcysts, reactive astrocytosis, and thickening of the pia arachnoid.
579
What is hypoxaemia and how does it occur in equines on anaesthesia?
Low O2 tension in blood - Shown by low stats on SPO2% and low SaO2 on blood gases PaO2 <60mmHg Occurs due to O2 failure or V/Q mismatch The animal is turned on its back, RR is reduced (by drugs), CO is reduced (by drugs) = low O2 delivery
580
How is hypoxaemia recognised and treated in horses on anaesthesia?
Check the SPO2% reading - some pulse oximeter probes don’t work well on horse tongues, so check it first Take blood gas - if PaO2 is much lower than it should be (remember is should be 4-5 x FIO2%) – act Switch down the isoflurane/sevoflurane Ventilate/IPPV… increase resp/tidal volume Ensure adequate circulating blood volume (IVFT) Tilt table (head up) slightly if possible Give beta agonist (down the ETT) eg salbutamol
581
What is hypercapnia and how does it occur in horses on anaesthesia?
High CO2 – seen on capnograph and blood gas Why does it happen? The animal is turned on its back, RR is reduced (by drugs and position), so CO2 rises in the body We tolerate a bit of hypercapnia Spontaneous breathing in recovery Increased oxygen dissociation in tissues
582
How is hypocapnia treated for horses on anaesthesia?
Reduce the volatile agent (isoflurane) Instigate ventilation
583
What are the considerations for horses with bradycardia induced by anaesthesia?
Breed/fitness of horse and their HR prior to anaesthesia If blood pressure or oxygen delivery is compromised too - you need to act
584
How is anaesthesia induced bradycardia treated in horses?
Consider the cause and address those Then if HR is still low use drug - Hyoschine N butykbromide (buscopan) Other drugs include atropine or glycopyrrolate
585
What are the potential causes for anaesthesia induced hypotension in horses?
Volatile agednt Vagal tone Opiod Alpha 2 agonist Toxaemia Hypoxia
586
What are the considerations for horses with tachycardia induced by anaesthesia?
Breed/fitness of horse and their HR prior to anaesthesia Evaluate ABP and reflexes too, especially nystagmus and palpebral reflex, may need to act fast if horse moves
587
How is anaesthesia induced tachycardia treated in horses?
Consider the causes… sympathetic stimulation (nociception is most likely), but can be CO2, acid base disturbance, drug reaction, cardiac issue, hypotension… Depth not adequate… Administer ketamine bolus IV and consider the % volatile agent – may need to increase too (increase FGF too to speed this rate of change up) More analgesia? Check arterial blood gas… hypercapnia? BP Low…. Treat as for hypotension
588
What are the causes of anaesthesia induced tachycardia in horses?
Sympathetic stimulation (nociception is likely) CO2 acid base disturbance Drug reaction Cardiac issue Hypotension
589
What are the causes of equine anaesthesia induced neuropathy and what will be the outcome?
Evident when horse wakes up, may cause poor recovery Can resemble myopathy Not usually as painful as myopathy Radial nerve, facial nerve (headcollar left on during sx)
590
What are the causes of equine anaesthesia induced eye problems and how can they be prevented?
Usually when a horse has been in lateral recumbency Must protect lowermost eye with padding Lubrication for eye
591
How is recovery of a horse carried out following anaesthesia?
Volatile agent switched off Reconnected to hoist Head supported Positioned in RLR in recovery box (if dorsal or RLR on table), LLR if LLR on table Pull dependent limb forwards (why?) Demand valve can be used to stimulate breathing Nasal tubes (obligate nasal breather) Extubate when swallowing or just before Exit recovery box, watch, can recover with ropes outside
592
What is the optimum recovery environment for an equine post anaesthesia?
Quiet Dark Empty bladder Analgesia Allow time for anaesthetic drug elimination Sedation Lateral: 30 minutes Sternal: 10-15minutes Standing: 15 minutes then taken back to stable
593
How is sedation given in anaesthesia recovery of a horse?
Sedation  low dose alpha 2 agonists. Given once in recovery and breathing spontaneously (romifidine) or once signs of reduced anaesthestic depth occur (xylazine)
594
What are the complications in recovery for equines post anaesthesia?
Upper airway obstruction Laryngeal obstruction Nasal oedema
595
What are the signs of upper airway obstruction in equines post op?
Stridor or stertor following tracheal extubation Nostril flaring on inspiration Abdominal respiratory effort Exaggerated thoracic excursion Absence of airflow at the nostrils Obstruction tends to occur within the nasal passages or at the level of the larynx
596
How can laryngela obstruction in equines post op be treated?
Select appropriate ET tube size and insert gently Dorsal displacement of soft palate Epiglottic retroversion Following laryngeal surgery may leave ET tube in place for recovery (secured) If obstruction occurs be prepared to reintubate (may need more drugs) Emergency tracheostomy
597
What is the treatment for nasal oedema in equines post op?
Common usually resolves as horse stands Use nasopharyngeal tubes, or phenylephrine or both Can recover horse to standing with ET tube in place
598
Tree of life
599
What can cause bradycardia in surgery and how can this be detected?
Consider what is the normal for that animal first (do you have pre-op results?) Next – ask yourself if it is actually causing a problem with perfusion & oxygen delivery Check SPO2% and the ABP to decide Consider what might be causing it Drugs (volatile, alpha 2 agonist, induction agent, opioid) Toxaemia (endogenous/exogenous) Vagus Heart problem (e.g. sick sinus) Hypoxia Hypothermia
600
How can bradycardia be treated?
Approach to treatment: Is output being compromised? (ABP & SPO2%) – if yes – need to intervene Why is it happening? Check depth of anaesthesia, vagal tone causes, hypoxia, toxaemia Treat cause first if possible, for alpha 2 induced bradycardia – use atipamezole (alpha 2 antagonist) Otherwise consider anticholinergics 2 options: atropine or glycopyrrolate
601
What can cause tachycardia in surgery and how is this detected?
Consider what is the normal for that animal first (do you have pre-op results?) Next – ask yourself if it is actually causing a problem with perfusion & oxygen delivery Check SPO2% and the ABP to decide Consider what might be causing it Sympathetic stimulation, too ’light’ PaCO2, PaO2, pH abnormalities CNS disturbances Low ABP, or cardiac disease Drugs e.g. anticholinergics
602
How is tachycardia during surgery approached?
Approach to treatment: Is output being compromised? (ABP & SPO2%) Why is it happening? Check depth of anaesthesia, CO2 etc, then consider an IV opioid, or lidocaine or propranolol/esmolol Vaporiser setting can be increased in addition to opioid
603
What are the causes of ventricular ectopic beats in surgery and how can they be detected?
Ask yourself if it is actually causing a problem with perfusion & oxygen delivery Commonest causes of ectopic beats Circulating catecholamines (stress) Hypoxia or hypercapnia Hypovolaemia or hypotension Anaesthetic drugs Myocardial inflammation or stimulation Trauma CHF or HCM Major organ dz e.g. intracranial dz Detected via ECG
604
How are ventricular ectopic beats in surgery approached?
Is output being compromised? (ABP & SPO2%) Is there a danger of ventricular fibrillation? Are the VPCs multiform, in sequence or paroxysms? Why is it happening? Check depth of anaesthesia, CO2 etc, then consider an IV opioid, lidocaine or propranolol/esmolol Vaporiser setting can be increased in addition to opioid
605
How is hypotension detected and treated in surgery?
Check equipment (cuff size, cuff position, transducer, patency of cannula, fluid line) Urine production?? i.e. other crude indicators of output Commonest causes of hypotension: Anaesthetic drugs Hypovolaemia and haemorrhage Cardiac insufficiency Check patient and attempt to determine cause Reduce volatile/inhalant agent (TIVA/PIVA) Increase IVFT (intravenous fluid therapy) Check urine output if possible Re-check ABP Consider use of inotrope (dobutamine) Consider use of vasopressor (norepinephrine)
606
feline hypotension treatment
607
What are the causes of hypercapnia in surgery?
Increased CO2 depth of anaesthesia hypoventilation pyrexia rebreathing fresh gas flow rates too low exhaustion of soda lime changes in dead space
608
What are the causes of hypocapnia in surgery?
Low CO2 Disconnection (check breathing system) Mis-intubation ??
609
Which species has lower CO2 readings and why?
Cats on non-rebreathing systems (T piece or mini Lack) Often lower ET CO2 readings
610
What are the causes of decreasing CO2?
Obstruction Hyperventilation Circulatory failure Hypotension Cardiac arrest
611
What can be seen in the image?
Failing ET CO2 values In this case due to partial airway obstruction but could be Circ failure, hypervent, hypotens. CA
612
Troubleshooting ventilation with Failing CO2 readings
613
What can be seen in the image?
Cardiogenic oscillations
614
What is the treatment path for hypoxaemia?
Palpate a pulse Check O2 is connected/ animal is not disconnected Check the pulse ox to verify the SPO2% Reconnect breathing system if disconnected Re-intubate if extubated or tube is blocked Replace the pulse oximeter probe Reduce the volatile agent Improve perfusion (IVFT) & inotropes (e.g. dobutamine in equine) Ventilate the animal if there is hypoventilation/obesity (tilt table) In equine GA s verify with arterial blood gas (other interventions will then be tried) e.g. beta agonist, recruitment (> D1C) Investigate other causes (haemorrhage, pneumothorax)
615
What are the common recovery issues?
Dysphoria and prolonged recovery are common Discern if dysphoria is pain or hypoxia or emergence/confusion Provide analgesia IV, oxygen or sedation (microdoses) as necessary Delayed recovery is often hypothermia, can antagonize other drugs and also check glucose
616
Troubleshooting dysphoria
617
Trouble shooting prolonged recovery?
618
What are the properties of propofol?
Rapid onset of action, rapid uptake by CNS, 5-8 mins unconsciousness Milky alkyl phenol Respiratory and cardiovascular depression Rapid and smooth recovery Suitable for ‘top ups’ or TIVA, only given IV, licensed for dogs and cats No analgesia Works at GABA
619
What are the pharmokinetics of propofol?
Pharmacokinetics of propofol: Absorption (minimal oral bioavailability) Solubility (minimally soluble in water) Distribution (98% protein bound) Metabolism (liver, glucuronidation) Elimination (renal) GABAA beta subunit (inward directed Cl current hyperpolarizes the postsynaptic membrane and inhibits neuronal depolarization)
620
What are the pharmacodynamics of propofol?
Pharmacodynamics Anaesthesia, respiratory depression, decreased CMRO2, depressed cardiovascular reflexes Haemodynamic effects are largely result of sympathetic depression  - Stable cardiac output - Decreased heart rate (blunted baroreceptor reflex) - Decreased MAP, SVR, CVP
621
What are the properties of alfaxalone?
Rapid onset of action, rapid uptake by CNS Respiratory and cardiovascular depression Rapid and smooth recovery (if premedicated) Clear, colourless neuroactive steroid Suitable for ‘top ups’ or TIVA, and can be give IM for sedation No analgesia Works at GABA Licensed for dogs, cats, rabbits
622
What are the pharmacodynamics of alfaxalone?
Pharmacodynamics of alfaxalone: Anaesthesia, decreased CMRO2, Haemodynamic effects minimal - Stable cardiac output - Stable heart rate - Stable MAP, SVR, CVP
623
What are the pharmacokinetics of alfaxalone?
Absorption (good bioavailability) Solubility (soluble in water) Distribution (30-50% protein bound) Metabolism (liver, rapid, also lungs, kidney) Elimination (renal, and small % bile) GABAA allosteric modulator
624
How is alfaxalone or propofol used?
Choose the drug (how?) Calculate the dose Look at the data sheet dose suggestions Dose is reduced is animals that have been premedicated Dose is reduced in unhealthy animals (ASA II-V) Draw up slightly more drug than you anticipate using Inject either drug slowly to effect over 60 seconds (you might not need all the drug) Animal will become sedated and then unconscious
625
What is the role of volatile agents?
Volatile anesthetics (VA) are gases that are used to induce and maintain general anesthesia, with benefits of relatively rapid onset and recovery with acceptable effects on peripheral organs in most patients.
626
What is the determinant of patient safety during anaesthesia?
The presence of an appropriately trained and experienced anaesthetist is the main determinant of patient safety during anaesthesia The associated of anaesthetists of GB and Ireland 2007
627
What are the ASA statuses?
I - healthy pet no disease II- mild systemic disease of localised disease III- moderate systemic disease limiting activity but not life-threatening IV- Severe systemic disease incapacitating and life-threatening not expected to live without surgery V- Moribund, not expected to liver >24 hours with or without surgery
628
ASA status chart
629
How should anaesthesia be approached in sick patients ASA III-IV?
Efforts must be directed towards thorough preoperative patient evaluation and improvement of the patients clinical state if possible The identification of risk factors before anaesthesia should lead to increased levels of anaesthetic surveillance performed ideally by well trained staff | use benzodiazapiense not Acepromazine maleate
630
What should be carried out in preoperative patient evaluation of sick patients?
Clinical evaluation & recent history Previous GA history Current medications Current comorbidities Temperament/anxiety Pain Hydration status Oxygenation Plan (know the surgery/diagnostics and position and possible complications), use a checklist
631
What should be taken into account for the perioperative preparation for ASA III-IV
Pre-operative blood tests & diagnostics are indicated! IVFT resuscitation Anti anxiety medication may be indicated Continue medications during peri-op period Pre-place IV access Pre-oxygenate (mask, flow by, cage, nasal prongs) Drain chest/abdomen or decompress
632
What premedication should be given to ASA III-IV patients? Anaesthesia
ASA III-V Avoid the alpha 2 agonists in compromised animals V low doses of alpha 2 agonist may be used if animal very distressed Opioid alone may be sufficient to sedate patient (but patients are often quiet/compromised) e.g. methadone or butorphanol Fentanyl and midazolam (IV) useful Ketamine and midazolam (IM or IV) cats (not in HCM) Alfaxalone and opioid is an option (NB volume of injectate is disadvantage), can add BZD too if necessary
633
How should induction of ASA III-IV dogs and cats be carried out?
Dont leave unsupervised after premed Continue to provide oxygen IV admin of premed often followed soon by induction drugs Titrate induction drugs slowly to effect in small animals Palpate pulse during induction Observe MM Be ready to intubate and secure airway swiftly to provide O2 Consider attaching monitoring equipment before induction
634
What are the monitoring protocols post op for ASA III-IV?
Comprehensive and continual monitoring Avoid a deep plane of anaesthesia PIVA & TIVA can reduce reliance on volatile agents IVFT – goal directed Analgesia, local blocks Have emergency drugs ready/calculated Encourage efficiency and discourage slow/time wasting Keep patient warm from the outset
635
What is the approach to Anaesthesia of sick horses EG with colic?
IVFT before induction (?hypertonic saline) PCV, TP, lactate, glucose (minimum), belly tap, NG tube Often omit acepromazine Still use standard dose of alpha 2 agonist followed by ketamine & NSAIDs Often have had additional alpha 2 during work up Careful positioning Comprehensive monitoring, often are ventilated (IPPV) IVFT during GA v important PIVA is recommended to reduce volatile agent Regular blood gases recommended
636
What is meant by antibiotic stewardship?
Coordinated interventions designed to improve and measure the appropriate use of antimicrobials by promoting the selection of the optimal antimicrobial drug regimen, dose, duration of therapy and route of administration Suitable selection of antibiotics
637
Critically important antibiotics
638
Decision making
639
How can misuse of antibiotics be avoided?
Work with clients to avoid the need for antimicrobials Avoid inappropriate use Choose the right drug Monitor antimicrobial sensitivity Minimise use Record and justify deviations from the protocol Report suspected treatment failure to the VMD
640
How can we avoid the need for antimicrobials?
Inform owners about the benefits of regular pet health checks Use symptomatic relief or topical preparations where appt Integrated disease control programmes Animal health and welfare planning Isolate infected animals wherever possible
641
How can we avoid inappropriate use of antimicrobials?
For uncomplicated viral infectiosn Restrict use to ill or at risk animals Advise clients on correct administrates and storage of products and completion of course Avoid underdosing
642
When are antibacterials indicated?
Where cytology and or culture is positive
643
How can we ensure that we chose the correct antimicrobial
Identify likely target organisms and predict their susceptibility Create practice based protocols for common infections based on clinical judgement and up to date knowledge Know how antimicrobials woerk and their pharmacodynamic properties Use narrow spectrum anitmicrobials where possible
644
How can we monitor antimicrobial sensitivity?
While clinical diagnosis is often the initial basis for treatment, bacterial culture and sensitivity must be determined whenever possible so that a change of treatment can be implemented if necessary Monitor bacterial culture and sensitivity trends
645
Antimicrobial sensitivity flow chart
646
How can we minimise use of antibiotics?
Use only when necessaru and evidence that usage reduces morbidity and or mortality Regularly assess antimicrobial use and develop written protocols Use alongise strict aseptic techniques
647
What is the importance of recording and justifying deviations from antimicrobial protocols?
Be able to justify your choice of antimicrobial and dose Keep an accurate record of treatement and the outcome to help evaluate therapeutic regimens
648
How is the suspected failure of antimicrobial treatments reported?
Report through the suspected adverse reaction surveillance scheme (SARSS) This may be the first indication of resistance
649
SARSS
Suspected adverse reaction Surveillance Scheme
650
What is the In practice Protect scheme plan
Practice policy based on what is expected and then what is sensible to use and what the practice will use
651
Overview for antimicrobial selection
652
What is the mechanism of action of antibiotics?
Narrow spectrum or Broad spectrum
653
What is a narrow spectrum AB?
Targets a narrow group of bacteria (either gram pos or neg
654
What are Broad spectrum ABs?
Targets the Gram pos and gram neg bacteria
655
What are bacteriocidal ABs?
Kills the organism Penecillins Cepahlosporins
656
What are bacteriostatic ABs?
Drugs that temporarily inhibit the growth of an organism (reversible if removed) Examples are tetracyclines and chloramphenicol
657
How should we determine concentration of ABs?
658
AB concentrations
659
What are the target of actions of antibiotics on bacteria?
660
How do ABs target the cell wall?
Peptidoglycan wall is unique to bacteria ABs target the wall Lysozyme produced by host breaks the bonds in polysacs Beta-Lactam ABs inhibit transpeptidase PBP so peptide cross-links cannot be formed Glycopeptides - bind to peptide chains so peptide cross-links cannot form
661
What are the Beta lactams?
Penicillins Cephalosporins
662
How do ABs inhibit protein synthesis?
Target the ribosome so that proteins cannot be formed
663
Summary of ribosome binding antibiotics
664
Other groups of AB targets?
665
What are the properties and applications of cationic antimicrobial peptides
Topical application interact with membranes and disrupt Product licensed for dermatology Lipids/charge properties of host vs bacterial membrane allow for distinction
666
On top of spectrum of ABs what are the other categories
Aerobic or anaerobic drugs
667
What are the considerations for effect of ABs?
668
Groups of antibiotics and relative activities
669
What are the reasons for antibiotic therapy failure?
Unjustified therapy poor selection Wrong dose Suppressed host response Resistance
670
What is C&AST
Culture and antibiotic sensitivity testing
671
What are the 2 main approaches for looking at AMR?
Disc diffusion - antibiotic gradient from disc (inhibition zone) MIC determination using liquid cultures in wells
672
MIC
Minimum inhibitory concentration
673
What is resistance of AB defined by?
Clinical breakpoint values There are interpretive criteria with clinical breakpoints for MIC values for diff bacteria
674
How are the clinical break points interpreted?
Break point is determined and then anything above is resistant and everything below is sensitive
675
What is being shown about resistance in the image? AB
Above MIC the resistant bacteria will be left and Below the MIC the sensitive bacteria will survive but grow slowly while resistant bacteria will proliferate quickly and overgrow
676
What is meant by intrinsic resistance to AB?
An innate ability to resist activity of a particular antimicrobial agent through inherent structural or functional characteristics which allow tolerance of the drug
677
What is an example of intrinsic resistance to AB?
Lacks the target or altered target
678
What is acquired resistance to ABs?
When a microorganism obtains the ability to resist the activity of a drug. Can be a mutation or new gene acquisition
679
How might a bacteria have acquired resistance to a drug?
Alteration drug Alteration of target bypass mechanism Efflux systems
680
What bacteria have intrinsic resistance to Vancomycin?
Gram negative bacteria as the AB cannot penetrate the outer membrane of the bacteria
681
Which genera of bacteria are resistant to cephalosporins and why?
Enterococci as the AB has a low affinity for penicillin binding proteins
682
Which antibiotics cannot be used to treat mycoplasmas and why?
Mycoplasmas lack a cell wall so a cell wall targeting AB will not work
683
What are the mechanisms for acquired AB resistance?
Gene mutations - change binding site Gene acquistiion Coresistance
684
How does Gene acquisition lead to acquired AB resistance?
Mechanism transfer, Conjugations of plasmids or other routes Risks transfer between potential pathogens and commensals
685
How does co resistance lead to acquired resistance?
Where genes physically linked on the same mobile elements. The are found together once established BInd the same or very close sites One change effects binding of multiples or modification of site
686
Acquired resistances
687
What is an efflux system in acquired AB resistance?
The drug is pumped out of the bacteria maintaining very low concentrations reducing the efficacy
688
Mutation and modification of targets for ABs
689
What is degradation and how does this lead to acquired resistance?
Degrades the AB most common with B-lactamases
690
Which drug is efflux most common for AB?
Tetracyclines
691
Which AB is modification in acquired resistance most likely to occur with?
acetylation of aminoglycosides
691
How does resistance occur to Beta lactams?
AB works by bingin to PBP affecting the peptide cell wall cross linking = weakened cell wall Beta lactamase (enz) breaks down the Beta lactam Methicillin then has resistance Alternate PBPs called MecA now increase resistance to Beta lactams
691
Common resistance mechanisms to ABs
692
What factors increase the risk of selection of ABs>
Underdosing Length of selective level Presence of resistant bacteria to select
693
MSC
Minimum selective concentration
694
MIC
Minimum inhibitory concentration
695
MDR?
Multi drug resistance strains Non susceptible to > agent in >3 clinical antimicrobial categories
696
XDR?
Extensive drug resistance Non susceptible to >1 agent in all but >2 clinical Ab categories
697
PDR?
Pandrug resistance Non susceptible to all antimicrobial agents listed
698
What is meant by good antibiotic stewardship?
699
Biosecurity?
Stopping infectious agents coming onto site Management movement of animals and materials into hospitals, farms, clinics
700
What is the role of disinfection?
Reduce infection Spread on surfaces and fomites Effective management of infective material Effective cleaning
701
Relative resistance to disinfection
702
What are the risks with disinfectants?
Generalised action Therefore damaging so self harm or patient harm Some toxic so tainting a risk Hypersensitivity
703
What are the groups of disinfectants?
Alcohols Alkalis Aldehydes Oxidising agents Phenols QACs
704
What considerations should be taken with an animal with parvoviris to prevent spread?
- door closed - white coats removed - Full-body apron - Gloves Masks and visor - Double bag waste -Dispose of bedding - cleaning using Trigene advance high level disinfectant
705
Example infection control strategy - faecal oral route
706
Example infection control strategy- contacts?
707
Examples of interventions strategies- fomites
708
Examples of interventiosn strategies - farm facilities
709
How would we plan an intervention strategy for streptococcus equi?
710
How would a disinfection strategy be carried out for salmonella?
711
What is parvovirus?
Highly contagious - acute GI disease Persistent as non enveloped virus Expelled contaminated material (organic matter
712
What is the management and biosecurity for parvovirus?
713
Summary of disinfectants
714
What is pasteurisation?
Passing of heat over a contaminated item - sterilisation via hot air oven 150degrees over 30 minutes to kill microorganisms Not effective against spore creating bacteria Takes a long time Certain items can go in (metal and glass) Risk of fire
715
What is sterilisation?
Effective against spores Heat form Chemical form It is best to use heat steam and pressure (autoclave) Boils water to produce steam = pressure pushes steam into packaging some forms do not remove air which can inhibit sterilisation
716
What are the 3 types of autoclave?
gravity displacement autoclave and the high-speed prevacuum sterilizer.
717
What autoclave can be seen?
Vacuum assisted sterilisation system
718
What is chemical sterilisation and what are its properties?
719
What is gas sterilisation and what are its properties?
Ethylene oxide in large scale practice (endoscopes etc) Inactivates DNA cells - strict COSHH controls Req specialist training and takes a relatively long time without interruption
720
How are surgical instruments prepared ?
Clean and check Pack Sterilise Monitor sterilisation Check out of date supplies
721
Why chose combinations of antibiotics?
Treatment of mixed bacterial infections in which one drug is not effective To achieve synergistic antimicrobial activity against particularly resistant strains To reduce the risk of or overcome AB resistance
722
What is meant by synergy in ABs?
Where the activity is greater than either of the 2 individually
723
What is meant by additive effect with ABs?
Where there is a benefit for treatment but there is no increase of individual acitivity
724
Generally ________ antibiotics act in an additive fashion
Bacteriostatic
725
Generally ________ antibiotics act in an synergistic pattern when combined
Bacteriocidal
726
Several __________ antibiotics are substantially impaired by simultaneous use of drugs the are _______
Several bactericidal antibiotics are substantially impaired by simultaneous use of bacteriostatic drugs (most are ribosomal inhibitors) This is an example of antagonism
727
What antibiotic is used with Trimethorprim?
Sulphonamide Act on different targets making them more effective - synergistic result
728
Which antibiotic is used with Clavulanic acid?
Amoxycillin Amoxycalv Breaks down penicillins by breaking fown Beta lactamase inhibitors
729
What should Beta lactams not be combined with?
Bacteriostatic drugs
730
What should procaine not be used with?
Procain is metabolised to paraaminobenzoic acid which can reduce effectiveness of SULPHONAMIDE treatment
731
What is the issue with using lots of drugs that bind to the same AB target?
Reduces efficacy as they compete for the target site
732
What is pleuropneumonia?
Mixed infection
733
How is pleuropneumonia used?
Combination therapy Mixed infection where the use of 1 antibiotic will not be effective The empirical selection must be made. Penicillins kill the anaerobic bacteria Aminoglycosides treat gram-negative bacteria Presentation of a strict anaerobe means that metronidazole is added
734
What should be the AB treatment of mastitis?
Sometimes there may be combination treatment but cultures will confirm the need
735
What are the potential pathogens for mastitis?
Staph aureus- beta lactam R Strep uberis - beta lactam sen E coli - gram neg
736
What is a chemotherapeutic agents?
A drug used to treat cancer by causing cell death and stopping cells from dividing
737
What are the routes of administration for chemotherapeutic drugs?
Oral By injection IV infusion Topical
738
How are chemotherapeutic agents used?
Chemo drugs only Chemotherapeutic drugs as part of a treatment plan eg with radiotherapy
739
What chemotherapeutic drugs do vets use?
Cytotoxic drugs such as Vincristine Doxorubicin Chlroambucil Cylophosphamide
740
What are the properties of cytotoxic drugs?
Inhibit mitosis and /or damage DNA Kill rapidly dividing cells Neoplastic cells GI tract epithelium Bone marrow cells
741
What are the targeted approaches that can be used as chemotherapeutic agents?
Tyrosine kinase inhibitors Monoclonal antibodies
742
What are the targets for newer therapies against cancer?
Receptors Signalling pathways Antigens
743
How can tyrosine kinase inhibitors be used in cancer therapies?
For mast cell tumours in dogs Masitinib Toceranib
744
How can monoclonal antibodies be used in cancer therapies?
Monoclonal antibodies against specific tumour antigens
745
What are the limitations for cytotoxic drug treatments against cancer?
Palliative not curavtive Toxicity limits dose or freq of dose
746
What is the maximum tolerated dose of cytotoxic drugs for cancer treatment?
Highest dose with the acceptable side effects
747
What is metronomic chemotherapy?
Aims: delay or slow disease progression/ not kill cancer cells Inhibits angiogenesis Modulates immune response to cancer cells
748
How do cytotoxic drugs affect the cell cycle?
Cell cycle non specific drugs act through all phases of the cell cycle Cell cycle phase specific drugs kill a limited number of cells with any single dose
749
What are the common cell cycle phase specific cytotoxic drugs?
Vincristine Vinblasine Cytrabine
750
What are the common non cell cycle specific cytotoxic drugs?
Doxorubicin Cyclophosphamide Lomustine Chlorambucil
751
Class of chemotherapeutic drugs
752
What is the mode of action of alkylating agents (Chemo)?
Alkyl group binds to and cross links DNA
753
What is the mode of action of plant alkaloids (chemo)
Bind to tubulin in cells and disrupt mitotic spindle
754
What is the role of anti metabolite cytotoxic drugs?
Inhibit use of cell metabolites used in growth and cell division
755
What is the role of antitumour antibiotics ?
Inhibit topoisomerase -II causing the breakage of DNA and cell death Forms free radicals
756
What is the mode of action of Platinum analog cytotoxic drugs?
Bind platinum to DNA causing cross linkage and cell death
757
What is the mode of action of Tyrosine kinase inhibitor chemo drugs?
Inhibit various TK receptors eg KIT or VEGFR
758
How do vets choose chemotherapeutic agents?
Maximising the benefits Minimising harm
759
How can the benefit of chemo drugs be maximised?
760
How can the harm of chemo drugs be minimised?
761
What is meant by anaesthesia?
Without sensation General anaesthesia is total lack of sensations Local anaesthesia relates to lack of sensation in a localised part of the body
762
How does anaesthesia affect nociception?
Lack of awareness of painful inputs is caused
763
What is meant by balanced anaesthesia?
Achieving the desired effects of an anaesthetic by using multiple drugs, allowing a more conservative dose for each drug thereby reducing the side effects An additional factor involved in reduced drug dose is reducing patient stress
764
What is required for anaesthesia?
Unconsciousness Narcosis Tranquilisation Hypnosis Analgesia Muscle relaxation Immobilisation Amnesia Sedation
765
What are the aneasthetic events?
Induction Maintenance Emergence/ recovery
766
CEPSAF?
Confidential enquiry into perioperative small animal fatalities
767
What is the aim of anaesthesia?
Normal physiology Minimal loss of temperature Minimal pain GOod organ function BP maintained Less cardiovascular depression Less cerebral hypoxia Less dysrhythmias
768
What affects the risk of anaesthesia drugs?
Patient Drug pose minimal risk Procedure Staff Emergency or planned Facilities and equipment
769
What are the important guidelines for anaesthesia use?
AVA and RECOVER
770
What are the objectives of clinical audits?
quality improvement process that seeks to improve patient care and outcomes through systematic review of care against expicit criteria and the implementation of change
771
How long do adult dogs need to fast for?
4-6 hrs
772
How long do adult cats need to fast for?
3-4 hours
773
How long do kittens and puppies need to fast for?
1-2 hours
774
How long do rabbits need to fast for pre op?
NO FASTING
775
What is the challenge with treating endo parasites?
Different body systems can be affected by helminths, protozoa and maggots of some flies Control of these endoparasites is difficult
776
Ectoparasitacides
kill External parasites
777
Endoparasitacides
Kill internal parasites
778
endectocides
Kill internal and external parasits
779
Anthelmintics
Used to treat infections of animals with parasitic worms Flat worms eg Fluke (trematodes) Tapeworms (cestodes) Round worms (nematodes)
780
What are the common classes of anthelminthic drugs?
Organophosphates Benzimidazoles Salicylanilides Pyrazinoisoquinolones Sulphonamides Tetrahydropyrimidines Imidazothiazoles Hexahydropyrazine Macrocyclic lactones
781
What are the targets for anthelmintics?
Betatubulin Nicotinergic acetylcholine receptor GABA receptor and glutamate gated chloride channel
782
783
What is the action of Benzimidazoles?
Bind to Beta tubulin Inhibit/blockage of polymerisation causing abnormal microtubule formation and disruption intracellular homeostasis and energy metabolism
784
What is the most important pair of antagonistic neurones of locomotion?
Excitatory ACh containing neurones Inhibitory GABA containing neurones
785
What is the mechanism of action of piperazine and macrocyclic lactones?
Flaccid paralysis of the worms through increasing GABA and therefore increasing the relaxation Pip acts on GABA Macro acts on glutamate
786
What is the mechanism of tetrahydropyrimidines or imidazothiazoles
Act on ACh to increase contraction and therefore cause spastic paralysis of the worms
787
What are the classes of anthelmintic drugs for treating nematodes, trematodes and cestodes?
Cyclic octadepsinpeptide Aminoacetonitrile derivatives Spiroindole
788
What do cyclic octadepdsipeptide act on?
Acts on specific classes of transmembrane G protein couples receptors latrophilin receptor class This causes flaccid paralysis of the pharynx
789
What is the mechanism of action for Aminoacetonitrile derivatives?
MPTL -1 receptors , a unique kind of Ach receptor that causes spastic paralysis
790
What is the mechanism of action of spiroindole?
Acetylcholine antagonist causing flaccid paralysis and expulsion of parasites
791
Rapid development of resistance to the major anthelmintic classes ?
792
Current state of anthelminthic resistance
793
Why is ectoparasitic control important?
Animal welfare Economic loss Vectors of disease Source of zoonotic infection
794
How can ectoparasites be controlled 2?
Chemical and non chemical Work in conjunction with each other
795
What are the non chemical control related factors of ectoparasite control?
Depends on life stage (normally adlt) Sometimes ineffective in killing the adult so target another stage May intervene at multiple stages Which animals require treatment (contagious or species specific)
796
How can environmental or physical methods of endoparasite control be used?
Avoid contact with parasite (barriers, most useful where only part of the lifecycle is on the host) Create conditions that are unsuitable for the parasite to live Change host env (dagging tails) Change off host env (dung management)
797
Which parasite transmits lyme disease?
Ticks Babesiosis
798
What are the chemical control related factors?
Drug action required Spectrum of activity Speed of onset required Duration of action/frequency of reapplication Contraindications Safety Development of resistance
799
What are the actions fo anti ectoparasiticides?
Neurotoxins Insect growth factors Others (repellants, desiccants and mechanical agents)
800
What are the host factors that affect control of ectoparasites?
Species Age restrictions (lower age for many products) Suitable mode of application Meat/milk withdrawal periods
801
Ectoparasite treatment take-home messages
802
What are the steps for diagnosis of common ectoparasites?
Know which parasites you are looking for based on host species, history and clinical signs Select apt test Carry out test correctly and take adequate samples from representative areas Examine the sample systematically to find the parasite Identify the parasite
803
Which parasite diagnostic test to select?
804
How can we carry out physical identification of the parasite?
805
What are the properties of antibody serology?
Sheep scab Detects host antibodies to recombinant mite antigen Can detect sheep scab infestation within 2 weeks of contact- potentially prior to the appearance of clinical signs Potential for false positives from previous resolved infection
806
What are the properties of sarcoptes IgG serology?
Canine NB potential for Fals pos - takes 1 months to seroconvert False negatives- occasional cross reaction with antihousedust mite antibodies in environmental atopics
807
What are the properties of flea IgE serology?
Detects flea allergy or hypersensitivity not infestation Detects Type I hypersensitivity but not Type IV
808
Sampling and microscopy for parasites?
809
How should you take samples for sheep scab?
Psoroptes Take superficial at leading edge of the lesions
809
How can we use skin scrapings to monitor treatment for demodicosis?
810
What is the skin scraping sensitivity to sarcoptes?
50% Treatment trial oftern req to thoroughly rule out fleas sarcoptes and cheyletiella
811
Parasite ID?
812
Chewing lice?
813
Sucking lice
814
Surface mites
815
What can be seen in the image?
Top = psoroptes jpinted pedicel and funnel shaped sucker Other surface mites= unjointed pedical and cup shape sucker
816
Burrowing mites?
817
Define general pathology?
Th e study of basic responses of cells and tissues to insults and injuries irrespective of the organs, systems or species of animal involved
818
Define systemic pathology
Pathology of organ systems The study of alterations in specialised organs and tissues
819
Define anatomic pathology
Examination of tissues taken during life (biopsy) or after death (necropsy) Examines nature and extent of disease process
820
Define clinical pathology
Examination of blood and other body fluids as well as cells (cytology) during life
821
Define pathology
The study of the structural, biochemical and functional changes in cells, tissues and organs that underlie disease → An understanding of pathology is fundamental to understanding how disease occurs and, consequently, how disease can be diagnosed, treated, and prevented
822
Aetiology
Cause
823
Pathogenesis
mechanisms of disease development
824
Clinical manifestation
Functional consequences of molecular and morphologic changes
825
What are internal aetiologies?
Aging Immunologic defects Genetic defects
826
What are external aetiologies?
Agents- physical, chemical or biological Deficiencies - nutritional, environmental deficits
827
Molecular changes
Biochemical alterations in cells or tissues that alter the function
828
Morphologic changes
Structural alterations in cells or tissues
829
Inflammation
Vascular and interstitial tissue changes that develop in response to tissue injury and that are designed to sequester, dilute and destroy the causal agent
830
What is involved in healing?
831
Thrombosis
INteraction of the blood coagulation system and platelets to form within a vascular lumen an aggregate of fibrin and platelets
832
Neoplasia
Intrinsic mutations in somatic cells that underlie abnormal mechanisms for control of mitosis, differentiation and cell to cell interactions Lead to uncontrolled replication of cells that impinges on adjacent normal tissue
833
Metabolic dysfunction
Abnormalitied or imbalances of carbohydrate, fat and protein metabolism in the cell lead to accumulation of glycogen, lipid or protein as well as complexes of abnormally folded protein derivateves
834
necrosis
Death of cells and tissues in the living aniaml
835
biopsu
Removal and examination of a tissue dample from a living animla body for diagnostic purposes
836
Necropsy
Methodical examination of the dead animal
837
DiagnosiS
Conclusion concerning the nature, cause of name of a disease
838
Lesions
Abnormal structural and functional changes that occur in the body
839
Clinical diagnosis
Based on data obtained from the case history, clinical signs and physical examination
840
Clinical pathologic diagnosis
Based on changes observed in the chemistry of fluids and the haemotology, structure and function of cells collected from the living patient
841
Morphologic diagnosis
Also known as lesion diagnosis Based on the predominant macroscopic and microscopic lesions
842
Aetiologic diagnosis
Names the specific cause of the disease
843
Disease diagnosis
Stated the common name of the disease
844
What methods are used to reach a diagnosis?
Morphology, molecular biology, microbiology, immunology, genetics, informatics… Morphology is cornerstone of pathology
845
What methods are there to detect morphologic changes>
Macroscopic examination Microscopic examination Observation by the unaided eye LIght microscopy and electron microscopu
846
What molecular techniques can be used to reach a diagnosis?
Polymerase chain reaction (PCR) In situ hybridization (ISH) Genomics (DNA sequencing, DNA microarrays) Transcriptomics (RNA sequencing) Proteomics Metabolomics…. Immunological approaches
847
Putrefaction
Colour and texture changes, gas production, and odours that are caused by post-mortem bacterial metabolism and dissolution of host tissues (post-mortem decomposition)
848
What postmortem changes may there be?
Rigor mortis Algor mortis Livor mortis (hypostatic congestion) Post-mortem clotting Haemoglobin imbibition, bile imbibition Pseudomelanosis Bloating Softening Lens opacity
849
Rigor mortis
Contraction of muscles occuring after death Due to depletion of ATP and glycogen, commences 1-6 hours after death and persists for 1-2 days
850
Algor mortis
GRadual cooling of the cadaver
851
Livor mortis
Gravitational pooling of blood down the side of the animal
852
Post mortem clotting
Occurs mainly in the heart and blood vessels
853
Haemoglobin inhibition
Haemoglobin imbibition: Red staining of tissue (Once the integrity of blood vessel walls is lost, haemoglobin released by lysed erythrocytes penetrates the vessel wall)
854
Bile imbition
Bile imbibition: Bile in the gallbladder penetrates its wall and stains adjacent tissue yellowish/greenish/brown
855
Pseudomelanosis
Blue-green discoloration of the tissue by iron sulphide (FeS) (formed by the reaction of hydrogen sulphide (H2S) generated by putrefactive bacteria and the iron from haemoglobin released from lysed erythrocytes)
856
Bloating
Result of post-mortem bacterial gas formation in the lumen of the gastrointestinal tract
857
Post mortem softening
Softening of tissue results from autolysis of cells and connective tissue often aided by putrefactive bacteria
858
Lens opacity post mortem
Occurs when the carcass is very old or frozen Reversible on warming
859
How can lesions be recognised and described?
Need to distinguish the normal from the abnormal Need to distinguish lesions from post mortem change
860
What criteria is used to describe a lesion?
Location Number/extent Demarcation Distribution Colour Size Shape Consistency and texture
861
What is the morphologic diagnosis of a lesion?
Severity, duration, distribution, location and the disease process Macroscopic
862
Describe the lesion seen
On the 1. forelimb, there was a clipped area measuring 10 x 5 cm. Within the clipped area is 2. a 3.well-demarcated, 4. focal, 5. pink to dark red, 6. 3 cm in diameter x 2 cm height 7. round, raised, 8. firm, hairless mass.
863
Describe the lesion
The 1. stomach was 4. diffusely distended, 8. gas-filled and 5. diffusely dark red
864
Describe the lesion
Affecting 20% of the right kidney, within the renal cortex and extending into the medulla, was a focal, well-demarcated, 3 x 2 cm, light tan to dark red, wedge-shaped lesion.
865
Describe the lesion
Affecting 30% of the tongue, on the left underside and extending to the lingual surface, there was a focal, moderately well demarcated, pink to red, 5 x 2 x 1 cm, oval, multinodular, firm mass
866
Describe the lesion
Focally extensively, effacing the perineum and base of the tail, was a well-demarcated, black to red, approximately 1 meter by 50 cm x 10 cm, ulcerated, multinodular mass.
867
Describe the lesion
Adhered to the viscera and mesentery of the ileum and paired caeca, were numerous, well demarcated, multifocal, up to 2 cm in diameter, pink to tan, round firm masses.
868
Describe the lesion
Affecting up to 90% of the mammary gland, there was multifocal to coalescing, poorly demarcated areas of grey to light pink, friable tissue, admixed with haemorrhage and abundant light pink purulent exudate (pus).
869
What are the causes of cell injury?
Causes Oxygen deprivation Physical agents Chemical agents and drugs Infectious agents Immunologic reactions Genetic derangements Nutritional imbalances
870
What causes of oxygen deprivation lead to cell injury?
Causes of hypoxia (= oxygen deficiency): Reduced blood flow (= ischaemia) Inadequate oxygenation of the blood (cardiorespiratory failure) Decreased oxygen-carrying capacity of the blood (anaemia, carbon monoxide poisoning, blood loss)
871
What physical agents lead to cell injury?
Mechanical trauma Extremes of temperature Radiation Electric shock
872
What chemical agents and drugs lead to cell injury?
Hypertonic concentrations (glucose, salt…) Poisons (arsenic, cyanide…) Environmental pollutants Insecticides, herbicides Therapeutic drugs
873
What infectious agents lead to cell injury?
Viruses (and prions) Bacteria Fungi Parasites
874
What immunologic reactions lead to cell injury?
Immune reactions to external agents (microbes) and environmental substances Immune reactions to endogenous self-antigens (autoimmune diseases)
875
What genetic derangements lead to cell injury?
Deficiency of functional (e.g. enzymes) or structural proteins → errors of metabolism, accumulation of damaged DNA or misfolded proteins Influence the susceptibility of cells to injury by chemicals and other environmental insults
876
What nutritional imbalances lead to cell injury?
Nutritional excess Nutritional deficiency
877
What causes reversible degeneration that leads to cell injury?
Key points: Depletion of cellular energy stores (adenosine triphosphate ATP) Cellular swelling / fatty change Alterations of intracellular organelles → In early stages or mild forms of cell injury, the functional and morphologic changes are reversible if the damaging stimulus is removed
878
What are the properties of necrosis?
Always pathologic Cell membranes are damaged Often with inflammation
879
What are the properties of apoptosis?
May be physiologic or pathologic Cell membranes are intact No inflammation Cell suicide or programmed death Once the cells DNA or proteins are damaged beyond repair
880
What are the properties of irreversible necrosis?
Morphologic changes Increase eosinophilia Cytoplasmic vacuolation
881
What can be seen in the images?
882
What are the patterns of irreversible necrosis?
Patterns of tissue necrosis: Coagulative necrosis Liquefactive necrosis Gangrenous necrosis Caseous necrosis Fat necrosis
883
Infarct
Localised area of coagulative necrosis caused by ischaemia due to vascular obstructio
884
What can be seen?
Pus collection of necrotic neutrophils and tissue debris (encapsulated pus= abscess)
885
What is gangrenous necrosis?
Variant of coagulative necrosis Usually applied to a limb that has lost its blood supply (also tail, ears, udder) 3 types of gangrene: dry, moist or gas
886
what is caseous necrosis?
887
What can be seen and why?
Fat necrosis Focal areas of fat destruction Fat appears white, firm chalky resembling flecks of soap Typically resulting from release of pancreatic lipases
888
What are the morphologic alterations that lead to irreversible apoptosis?
Cell shrinkage Chromatic condensation Cytoplasmic blebs and apoptotic bodies phagocytosis of apoptotic cells or cell bodies
889
What are cell/tissue adaptations?
Reversible functional and structural responses to more severe physiologic stresses and some pathologic stimuli, allowing the cell to survive and continue to function → changes in size, number, phenotype, metabolic activity or function of cells → cell injury once the limits of adaptive responses are exceeded
890
What are the types of cell/tissue adaptations and what are there causes?
891
What is the ability of cells to adapt?
892
What are the properties of hypertrophy of tissues?
Increase in the size of cells (by producing more organelles), resulting in an increase in the size of the organ Physiologic compared with pathologic Stimuli: Increased functional demand (e.g. muscle) or by stimulation by hormones (e.g. uterus during pregnancy) or growth factors (or even some viruses)
893
What are the properties of hyperplasia?
Increase in the number of cells in an organ or tissue = inc mass and size Physiologic compared with pathologic Stimuli = same as hypertrophy Hypertrophy and hyperplasia often occur together and have the same gross appearance
894
What are the different types of atrophy?
Physiologic, pathologic
895
What is physiologic atrophy, when does it occur?
During embryonal, fetal development, uterus atrophy after parturition
896
What is pathologic atrophy and when does it occur?
Decreased workload Loss of innervation Diminished blood supply INadequate nutrition Loss of endocrine stimulation Pressure
897
What are the properties of metaplasia?
Potentially reversible change in which one differentiated cell type is replaced by another Most common - columnar to squamous epithelial Causes are chronic irritation, deficiencies, result of cell/tissue injury, oestrogen toxicity
898
What are the different types of growth disorders?
Agenesis – never developed Aplasia – started development but stopped early Atresia – absence of an orifice Hypoplasia – incomplete development Dysplasia – disordered growth Neoplasia
899
What are the signs of acute inflammation?
Heat Redness Swelling Pain Loss of function
900
Define acute inflammation
Acute Inflammation is a redundant, complex, adaptative and protective response of vessels, resident cells and leucocytes to noxious stimuli. Inflammation brings cells and molecules of host defense from the circulation to the sites where they are needed, in order to eliminate the offending agents and repair the tissues. It lasts hours to days
901
What are the causes of acute inflammation?
Infections (bacterial, viral, fungal, parasitic) and microbial toxins Tissue necrosis; ischemia; trauma, physical and chemical injury; irradiation Foreign bodies (splinters, dirt, sutures); endogenous substances urate crystals (in gout), cholesterol crystals (in atherosclerosis), and lipids Immune reactions (hypersensitivity)
902
What are the morphologic hallmarks of acute inflammation?
The morphologic hallmarks of acute inflammatory reactions are: dilation of blood vessels, activation and recruitment of leukocytes and active exudation of fluid in the extravascular tissues.
903
What are the steps of acute inflammation?
Recognition of the injurious agent Reaction of blood vessels Recruitment of leukocytes Removal/clearance of the agent Regulation (control) of the response Repair (resolution)
904
What are the mediators of acute inflammation?
Vasoactive Amines (Histamine, Serotonine) Released/Produced by mast cells, basophils, platelets Inflammatory Lipids (Prostaglandins, Leukotrienes) Produced by mast cells, leukocytes Complement (C5a, C3a) Plasma (produced in liver) Cytokines (IL-1, TNF, IL-6) Produced by macrophages, endothelial cells, mast cells Others: Kinins, Chemokines, Nitric Oxide, Coagulation Cascade, PAF,….
905
What is the role of mediators in acute inflammation?
Vasodilation Increased vascular permeablility Leukocyte recruitment and activation Pain Tissue damage
906
What are the outcomes of acute inflammation?
1- Complete resolution Clearance of the offending agent and regeneration. 2-Scarring, or fibrosis Connective tissue growth into the area of damage or exudate, this occurs after substantial tissue destruction. 2-Progression to chronic inflammation Unresolved inflammatory process due to either the persistence of the injurious agent or some interference with the normal process of healing.
907
What is the acute phase response in acute inflammation>
The acute phase response is characterized by different systemic effects of acute inflammation (and other conditions) including pyrexia, leucocytosis, metabolic changes. The response also includes changes in the concentrations of plasma proteins, called acute phase proteins (APPs).
908
How does pyrexia occur in acute inflammation?
909
What are the biomarkers of acute inflammation?
Biomarker: a biological molecule that is objectively measured and is an indicator of a normal or abnormal process, or of a condition or disease.
910
Define transudate in acute inflammation
Transudate: Extravascular filtrate of protein and cell poor fluid. It is due to increased hydrostatic pressure or to decreased colloido-osmotic pressure, or combination of both. It is accumulated in body cavities and extracellular compartments. The fluid appears grossly clear and watery.
911
How does transudate occur in acute inflammation?
912
Define exudates in acute inflammation
Exudate: extravascular fluid that has a high protein concentration and can contain leucocytes. Its presence implies the existence of an inflammatory process that has increased the permeability of blood vessels.
913
How does exudate form in acute inflammation?
914
What are the types of exudates in acute inflammation>
Serous FIbrinous Purulent Haemorrhagic
915
What is serous inflammation?
Inflammation with exudation of fluid with a low concentration of plasma protein and no to low numbers of leukocytes.
916
What is fibrinous inflammation?
Inflammation with exudation of fibrinogen and fluid, and formation of thick friable, loosely adherent fibrin
917
What is purulent inflammation?
Inflammation with the production of pus, viscous to creamy liquid, an exudate consisting of degenerated and necrotic neutrophils, debris and fluid. It is typically associated to bacterial infections
918
What is haemorrhagic inflammation?
Haemorrhagic inflammation Inflammation with vascular damage, loss of integrity of endothelium and/or extensive tissue necrosis, with leakage of red blood cells. This type of acute inflammation reflects a severe inciting stimulus.
919
When does inflammation become chronic?
Normally 24-72 hours after acute inflammation Persists for weeks months or years
920
What cell types are involved in chronic inflammation?
Macrophages M1 cells or M2 cells M1 Arginine to nitric oxide Highly toxic to phagocytosed organisms M2 Non-inflammatory Arginine to Orthinine Orthinine = proline in Extra-cellular fluid Proline = precursor for collagen synthesis.
921
What are the proinflammatory cytokines involved in chronic inflammation?
Systemic illness comes with tissue inflammation Pro-inflammatory cytokines E.g Interleukin 1, Interleukin 6 Pyrexia Lethargy Weight loss? Stimulate Acute phase proteins E.g C reactive proteins = immunosuppressive? Indicators of chronic inflammation in blood
922
How do granulomas form in chronic inflammation?
Persistent Stimulus Inert irritant (suture material?) Granuloma formation: Necrotic Centre Foreign material + Neutrophils Macrophages (Giant cells) Infectious granuloma? Lymphocytes
923
How does chronic inflammation lead to tissue repair?
Wound Healing (See Surgery week) Inflammation Proliferation Maturation M2 Macrophages Proline TGF – B Promotes collagen deposition
924
What are the types of chronic inflammation without a clear pathogen?
Atopic Dermatitis Inflammatory bowel disease Toxic agent Inflammatory Bowel disease Year 2 (GI) - allergic response, a chronic inflammatory state remains due to cytokines and immune cells
925
What are the types of chronic inflammation with a clear pathogen?
Parasitic Fungal Neoplastic
926
What pyogranulomatous lesions occur with chronic inflammation?
Chronic inflammatory lesion Characterised by predominance of macrophages and neutrophils Large Granuloma Examples: Feline Infectious Peritonitis Johnes Disease in cattle Slow growth despite aggressive clinical signs T cell : Macrophage interactions important
927
What can be seen in the image?
Johnes disease Granulomatous lesions in the lymph node of a johnes cow
928
What can be seen in the image?
H&E image shows a circular mass of cells caused by a granulomatous lesion Johnes disease
929
What are the types of granulomas in chronic inflammation
Caseous granuloma Chronic granulomatous disease
930
What are the properties of caseous granulomas in chronic inflamation?
Affects organ function Breakdown could lead to excessive bacterial dissemination throughout the body
931
What are the properties of chronic granulomatous disease?
Inherited disorder Phagocytes dont work properly Increased susceptibility to repeated bacterial or fungal infections
932
What can be seen in the image?
Chronic pyelonephritis in a dog’s kidney Pyogenic granulomas are small raised red bumps Hydronephrosis Kidneys have become swollen and stretched
933
What can be seen in the image?
Actinobacillosis Bacterial cause. Rarely be an outbreak of this (an individual cow condition) Present with increased salivation and difficulty chewing? Typically acute in its presentation Proliferative and ulcerative chronic-active inflammatory lesions Contains neutrophils mixed with mononuclear inflammatory cells (lymphocytes, macrophages, plasma cells). Fibrous tissue present in the tongue.
934
What can be seen in the image?
Cross section Chronic inflammation= loss of muscle of the tongue Replaced by fibrous tissue during healing White interwoven bands of fibrous tissue called arrowheads Granulomatous inflammation in the centre of the image
935
What can be seen in the image?
Chronic inflammation (mastitis) caused by tuberculosis Biosecurity Economic implications Zoonotic risk
936
What can be seen in the image?
Immune mediated arteritis Inflammation occurs in the blood vessels Swelling of the heart muscle not often any main clinical signs until severe stage
937
What can be seen in the image?
Chronic hepatitis Acute hepatitis = infectious, toxic or idiopathic Etiology of chronic hepatitis is not known Acute hepatic failure can progress to chronic active hepatitis. Clinically, this might be seen as weight loss, lethargy and depression within the animal. Think about liver disease and impact on protein breakdown (with liver disease, branched chain amino acids are not catbolised correctly)
938
What can be seen in the image?
Lung pyogranuloma Granulomas and pyogranulomas in the lung of a dog. Grey nodules which vary in size throughout the lung parachyma. nodules would be composed of granulomatous inflammatory lung lobes would fail to collapse.
939
What can be seen in the image?
Granulomatous inflammatory lesion Activated and giant multinucleate cells Internal intracellular organisms within the giant macrophage cells Lymphocytes and plasma cells
940
What can be seen in the image?
Chronic interstitial nephritis Kidney disorder and inflammation of the kidney. Acute interstitial nephritis = uncommon in cats Chronic progressive interstitial nephritis = common and more commonly referred to as chronic kidney disease. Cause = infectious agents? infectious disease?
941
What can be seen in the image?
Chronic nephritis in the cat Granulomatous vasculitis Development of renal interstitial pyogranuloma. Multiple, large, irregular, and pale grey subcapsular cortical foci
942
What can be seen in the image?
chronic interstitial nephritis Diffuse interstitial fibrosis Fine pitting of the capsular cortical surface Stippled red Bands of greay fibrous tissue surrounding islands of renal cortex
943
What can be seen in the image?
944
What can be seen in the image?
Healing bone
945
Neoplasm
Abnormal mass of tissue occuring due to abnormal cell proliferation
946
What are the different types of neoplasm
Benign Premalignanat Malignant
947
Oncogenesis
Process of gradual steps toward tumour development
948
How can we determine if a lesion is neoplasia?
Through histology Organisation of tissue structure Degree of cellularity Nuclear to cytoplasmic ratio Nuclear morphology Necrosis Mitotic index Individualisation of cells Invasiveness of cells
949
What is the invasive scales for different tumours?
Benign= non invasive Malignant= invades surrounding tissue
950
What are the characteristics of benign tumours?
Slow growing masses Good demarcation from surrounding tussue Minimal necrosis
951
What kind of tumour is lipoma?
Benign
952
What are the characteristics of malignant tumours?
Can grow rapidly Invasiveness to surrounding tissue Can spread to other sites in the body (metastasis) Increased necrosis
953
What kind of tumour is squamous cell carcinoma?
Malignant tumour
954
Features of benign vs malignant tumours
955
Cytological features of benign vs malignant tumours
956
What is the criteria for malignancy of a tumour?
pleomorphism anisokaryosis- variation in nuclear size Prominent nucleoli Macrocytosis Macrokaryosis Macronuclei Asinonucleoliosis - varied nucleolar size Multiple nuclei Increased N:C ratio Coarse chromatin nuclear molding Abnormal mitotixc figures
957
Benign tumour nomenclature
958
Malignant tumour nomenclature
959
Role of oncogenes
Promote proliferation
960
Role of tumour suppressor genes
Suppress proliferation in induce cell death
961
What do oncogenes code for?
Oncoproteins
962
What are oncoproteins?
Proteins that promote cell growth in the absence fo normal growth promotion signals and despite normal check point controls
963
Where does neoplasia come from?
Neoplasia is a multi-factorial process (not a single cause) Genetic factors Epigenetic factors Environmental factors Multiple hit hypothesis One mutation (genetic or epigenetic) usually not enough to cause neoplasia on its own
964
What causes cells to become neoplastic?
Sustaining proliferative signalling Evading growth suppressors Resisting cell death Inducing angiogenesis Activation invasion and metastasis Enabling replicative immortality
965
How does oncogenesis occur?
Starts with mutagenesis or carcinogenesis These are the initiating factors that cause genetic change This change makes cells more likely to divide in an uncontrolled way in the right conditions
966
mutagen
An agent that damages DNA
967
Carcingogen
A mutagen that causes neoplasia
968
What are the intrinsic and extrinsic factors of mutagenesis?
Intrinsic factors Normal by-products of cell metabolism that cause DNA damage e.g. reactive oxygen species (ROS) AKA free radicals Extrinsic factors Environmental agents Chemical Physical Oncogenic viruses
969
What are the types of chemical factors of mutagenesis?
Direct acting= effective in the form in which they enter the body Indirect acting = require activation by enzymes in the body in order to act as carcinogens (Cytochrome P450)
970
How do physical extrinsic factors lead to mutagenesis?
All types of radiation are complete carcinogens Initiators of oncogenesis Also promoters of oncogenesis through continued exposure Ionising radiation => Direct DNA damage => ROS generation Can result in G to T transversion UV radiation (sunlight) => Pyrimidine dimer formation (can cause cause misreading during transcription or replication) => ROS generation
971
What are the actions of direct oncogenic viruses on mutagenesis?
Dominant oncogene mechanism Mutation in viral gene causes host cells to produce oncoprotein => neoplasia e.g. Feline leukaemia virus, canine papilloma virus Insertional mechanism No oncogene in virus Insertion of viral DNA into host cells activates proto-oncogenes > oncogenes => neoplasia e.g. Avian leukosis virus
972
What are the actions of indirect oncogenic viruses on mutagenesis?
Suppress host immune system DIrectly stimulate host cell proliferation
973
Neoplasia summary
Neoplasia is a disease characterised by abnormal cell growth It is the result of an imbalance in the mechanisms that regulate cell proliferation Both genetic and epigenetic alterations of somatic cell DNA contribute to neoplastic growth Cancer grows progressively from normal tissue and multiple alterations are required for the onset of malignancy Gain of function in genes that promote cell proliferation (oncogenes) promote cancer Loss of function in genes that oppose cell proliferation (tumour suppressor genes) promote cancer
974
What are the common presenting signs of neoplasia?
Pain Visible lump(s) Reduced appetite Vomiting Weight loss Increased drinking Change in toileting Change in breathing/cough Off legs/reluctance to walk Seizures/neurological changes
975
What causes the presenting signs of neoplasia?
Can be direct or indirect Direct being compression, obstruction, pain, bleeding Indirect= paraneoplastic syndromes
976
What are paraneoplastic syndromes?
Caused by products of the tumour cells not the tumour mass
977
Why is it important to identify paraneoplastic syndromes?
Can be life threatening May help diagnose the primary tumour Can affect response to treatment Affect the QoL
978
What are the indirect effects causing the neoplasia presenting signs?
Effusions infection Paraneoplastic syndromes
979
What are the different paraneoplastic syndromes?
Endocrine Haematological Gastrointestinal Dermatological Neuromuscular Other
980
What are the common paraneoplastic endocrine syndromes?
Hypercalcaemia Hypoglycaemia
981
When is hypercalcaemia seen as a paraneoplastic syndrome?
Associated with lymphoma and anal sac carcinoma Commonly presents as inappetence, polydipsia, vomiting
982
When is hypoglycaemia seen as a paraneoplastic syndrome?
Associated with insulinoma Commonly presents as weakness, ataxia and seizures
983
What are the properties of hypercalcaemia of malignancy?
Cancer is the most common cause of hypercalcaemia in dogs and top 3 in cats Caused by parathyroid hormone related protein produced directly from the tumour cells Acts on bones and kidneys to stimulate calcium release into blood
984
What are the common Paraneoplastic haematological syndromes?
Anaemia Thromocytopenia Coagulopathies
985
When is aneamia seen as a paraneoplastic syndrome?
Can be common across cancer types Associated with Lymphoma GI tumours Mast cell tumours
986
When is thrombocytopenia seen as a paraneoplastic sydrome?
Can be common across all cancer types Mechanisms include Increased consumption Increased sequestration Immune mediated distruction
987
When can coagulopathies be seen as paraneoplastic syndromes?
Common across all cancer types Hypercoagulability Disseminated intravascular coagulation
988
What are the common GI paraneoplastic syndromes?
Ulceration Associated with mast cell tumours Commonly presents as Melaena Haematemesis
989
How do mast cell tumours cause ulceration
Increase histamine relaease Increased gastric acid secretion Ulceration
990
What are the common Dermatological paraneoplastic syndromes?
Epidermal necrosis Alopecia Nodular deramtofibrosis Exfoliative dermatitis
991
When is epidermal necrosis seen as a paraneoplastic syndrome?
Associated with Pancreatic and hepatic tumours
992
When is alopecia seen as a paraneoplastic syndrome?
Associated with sertoli cell tumours in dogs Pancreatic carcinomas in cats
993
When is nodular dermatofibrosis seen as a paraneoplastic syndrome?
Associated with renal adenocarcinoma (usually in GSDsP
994
When is exfoliative dermatitis seen as a paraneoplastic syndrom?
Associated with thyoma in cats
995
What are the common neuromusclar paraneoplastic syndromes?
Myasthenia gravis Peripheral neuropathy
996
When is myasthenia gravis seen as a paraneoplastic syndrome?
Associated with thymoma, osteosarcoma, bile duct carcinoma Commonly presents as muscle weakness and dysphagia
997
When is peripheral neuropathy seen as a paraneoplastic syndrome?
Associated wth multiple cancer types Commonly presents as Weakness -Progressive paraparesis/ tetraparesis
998
What are the non system related paraneoplastic syndromes?
Cachexia Pyrexia Hypertrophic osteopathy
999
When is cachexia seen as a paraneoplastic syndrome?
Associated with: -Multiple cancer types (Complex mix of cytokines and prostaglandins alter protein, carbohydrate and lipid metabolism) Commonly presents as: -Loss of muscle mass and fat despite adequate nutrition
1000
When is pyrexia seen as a paraneoplastic syndrome?
Pyrexia Associated with: -Multiple cancer types Commonly presents as: -Fever
1001
When is hypertrophic osteopathy seen as a paraneoplastic syndrome?
Hypertrophic osteopathy Associated with: -Lung tumours (primary and metastatic) -Less commonly liver, kidney, bladder tumours Commonly presents as: -Swollen/painful distal limbs -Lameness
1002
What is hypertrophic pulmonary osteopathy?
rapid periosteal new bone growth affecting distal limbs. Most commonly associated with lung tumours (primary or metastatic)
1003
Why is cancer spread important?
Only malignant neoplasms (cancer) spread to other parts of body Once cancer has spread, it affects treatment options and prognosis Primary tumours only account for 10% of cancer deaths 90% of cancer deaths are due to cancerous growths at sites in the body distant from the primary tumour
1004
Define metastasis
Movement of cancer cells from one tissue or organ to another
1005
What are the characteristics and mechanisms of metastasis?
Metastases aka ‘mets’ –new cancerous growths at distant body sites Cancer cells break away from primary tumour and usually travel through blood and lymphatic vessels to new tissues/organs Can take years for metastasis to become apparent
1006
what are the pathways of metastases of tumours?
Haematogenous Lymphatic Transcoelomic
1007
What are the properties of haematogenous metastases?
Most common route for sarcomas Tend to invade thinner-walled veins rather than arteries Ultimately enter lungs and liver
1008
What are the properties of Lymphatic metastases?
Lymph node(s) closest to the tumour are colonised first These first lymph nodes develop the largest tumour masses E.g. Intestinal adenocarcinoma metastasises first to the mesenteric lymph nodes
1009
What are the properties of transcoelomic metastases?
Transcoelomic Cancer cells spread across the surface of abdominal and thoracic structures E.g. Mesotheliomas, ovarian adenocarcinomas
1010
What are the fundamentals for cancer spread?
Intravasation Extravasation Colonisation
1011
What affects the metastatic sites?
Dependent on the ability of tumour cells to adapt to the microenvironment of distant tissues And the layout of the circulation
1012
How does metastases of cancer cells reach the bone and what is the effect?
Cancer cells reach the bone thrugh the vessels of the marrow They adhere to the specialised stromal cells coating the bone facing the marrow They are attracted by growth factors contained in the ECM Cancer cells activated osteoclasts and osteoblasts at different extents resulting in osteolytic and osteoblastic metastasis
1013
What are the common lung metastatic tropisms?
Osteosarcoma Haemangiosarcoma Melanoma Mammary tumours Others (thyroid, tonsillar, pancreatic)
1014
What are the common liver spleen and kidney metastatic tropisms?
Mast cell tumours Haemangiosarcoma
1015
What are the common bone metastatic tropisms?
Mammary tumours Prostatic adenocarcinoma Urinary bladder tumours
1016
What are the different types of biopsy?
Fine needle aspirate and surgical biopsy?
1017
Fine needle aspirate (FNA)
For cytology Examination of cells that have exfoliated from mass
1018
Surgical biopsy
For histopathology Examination of tissue architecture of mass
1019
When are incisional and excisional biopsies carried out
Incisional best for planning surgery afterwards so can determine margins etc. Excisional best when tumour type is highly suspected and pre-op biopsy will not affect outcome e.g. bleeding splenic mass
1020
What are the pros of FNA?
Pros Gives an idea of cell type involved and presence of any malignant features Good for external masses where the suspected cell type exfoliates easily (e.g. MCTs) Easy, quick, cheap (usually) Often a good starter to rule ddx in or out
1021
What are the cons of FNA
Cons Unlikely to obtain any results for poorly exfoliative tumours (e.g. fibrosarcoma) Cannot grade disease Does not give a prediction of how the tumour will behave biologically or a prognosis Does not allow formulation of a targeted treatment plan
1022
What are the pros of surgical biopsy?
Pros Allows definitive diagnosis Allows grading of disease Contributes to formulation of a targeted treatment plan Gives detail as to margins required at surgical removal Contributes to a prognosis
1023
What are the cons of surgical biopsy?
1024
What is the role of grades in tumours?
Grade describes the appearance of the cancer cells and the surrounding tissue Low grade tumours contain organised cells and look more like relatively normal tissue High grade tumour tissue is disorganised and cells look very abnormal
1025
What is the role of grades in cancer?
1026
How do we follow a definite diagnosis for cancer?
1027
When should tumour biopsy not be carried otu?
1028
What are the different lesion distributions?
1029
What is the distribution of the lesion in this image?
Cranioventral
1030
What is the distribution of the lesion?
Segmental
1031
What is the distribution of the lesion?What
Fibrino suppurative inflammation
1032
What is the morphologic diagnosis of the lesion?
Liver, severe chronic multifocal to coalescing granulomatous hepatitis
1033
What is the morphologic diagnosis of the lesions?
Haired skin, severe, subacute multifocal to coalescing dermal infarctions
1034
What is the morphologic diagnosis of the image?
Brain, sever diffuse acute to subacute suppurative meningitis
1035
What is the morphologic diagnosis of the image?
Heart, severe diffuse subacute fibrino- suppurative pericarditis
1036
What is the morphologic diagnosis of the image?
Lung, cranioventral peracute mild agonal blood inhalation
1037
What is the morphologic diagnosis of the image?
Haired skin, papillomas
1038
What are the causes of cardiopulmonary arrest?
anaesthetic complications severe trauma severe electrolyte disturbances hypovolemia vagal stimulation cardiac arrhythmias cardiorespiratory disorders debilitating or end-stage diseases Myocardial hypoxia Drugs and toxins pH abnormalities Electrolyte disturbances Temperature problems
1039
What are the causes of acute failure of cardio respiratory systems?
Lack of oxygen delivery to tissues (DO2) Unconsciousness and systemic cellular death Cerebral hypoxia brain death within 4 to 6 minutes
1040
What are the signs of cardiopulmonary arrest?
Loss of consciousness Apnoea or agonal gasping No corneal reflex or palpebral reflex No heart sounds No palpable pulse Central eye position Pupils fixed and dilated Bleeding stops at surgical site Mucous membrane grey/blue/white CRT altered (can be normal!) Dry cornea General muscle flaccidity ECG arrhythmias (VF, VT, Asystole, PEA/EMD)
1041
Outline the CPR algorithm
BLS = chest compressions and ventilation
1042
1043
How to act as the cardiac pump?
1044
How to act as the thoracic pump?
1045
How to carry out internal cardiac compressions?
1046
How should CPR be carried out on large animals?
Need LOTS of people EXHAUSTING Need to swop in every 2 minutes AIM highest compression rate you can Throw whole body onto caudo-dorsal lung field Horse needs to be in lateral recumbency on solid surface Success reported in the literature limited
1047
How should the airway be treated in CPR?
Airway: May need to clear this manually or with suction. Orotracheal intubation with ET tube. Or Emergency Tracheostomy 3-5cm midline incision and blunt dissection. Trachea entered 2-4cm caudal to larynx, ET tube placed between rings. Takes time…. Large Guage Needle with a syringe and ET tube connector for instant access.
1048
How is ventilation supplied during CPR?
Positive Pressure Ventilation (PPV) is required: ET tube connected to AMBU Bag, Anaesthetic machine or a demand valve (Large Animal). Or Mouth-to-snout/nose/mask ventilation. Be careful – you are in full control of the lungs! Tidal volume – approx. 10ml/kg Iatrogenic barotrauma, pulmonary haemorrhage or pneumothorax is easy to do. Ventilation rate – 10 breaths per minute or less Potential for oxygen toxicity considering low cardiac output
1049
What are the principles of advanced life support?
Monitoring Obtain vascular access Administer reversals
1050
How can monitoring be carried out for ALS?
Capnography – ETCO2 Measures perfusion; movement of carbon dioxide from the tissues to the lungs >15-20mmHg = Good compressions. ECG Allows rhythm assessment – is it a shockable rhythm or not – VF/pulselessVT Does NOT tell you about perfusion/cardiac output Other methods include SPO2% - not very reliable (movement error) Blood gas analysis Venous blood gas samples preferred Blood pressure – not very reliable (movement error) Doppler monitoring of arterial blood flow or direct monitoring
1051
What clinical changes are being monitored in advanced life support?
Clinical changes: Pulses – difficult to palpate! Mucous membrane colour Eye position changes (central  ventromedial) Pupil changes size Palpebral, corneal, gag reflex may be noticed Breathing or chest movements (twitches) resume Lacrimation Animal regains consciousness
1052
How can we gain vascular access in advanced life support?
Cephalic, sephaenous or jugular IV Intraosseous route IO Intratracheal IT
1053
What are the properties of IV vascular access?
Route of choice for drugs & fluids Tricky during CPCR because of the movement Jugular venous canula is ideal for administration but risk of thrombophlebitis, other veins not as effective but you can ‘flush’ the drug centrally
1054
What are the properties of IO vascular access?
As rapid as peripheral veins Useful in small animals, very collapsed animals and birds Sites used include the greater tubercle of the humerus, tibial crest or trochanteric fossa of the femur In neonates can be achieved with a needle, however, in older patients with a mature cortex, a drill is often needed.
1055
What are the properties of IT vascular access?
Dilute and use urinary catheter inserted beyond carina Chest inflations will distribute the drugs Higher doses are needed
1056
What are the common ALS reversals?
Antagonists: Atipamezole – Alpha-2’s e.g. medetomidine Naloxone – Opiods e.g. methadone Flumazenil – Benzodiazepines e.g. midazolam These are primarily drugs used in sedation/premedication or analgesia.
1057
What is the treatment if an animal is in asystole?
Asystole = flat line. Pulseless Electrical Activity = can look normal – don’t get caught out. More responsive to CPR -> drug therapy to augment this. Adrenaline/Epinephrine Adrenergic agonist – α and β receptors. Positive inotrope and chrono trope. Increases myocardial oxygen demand. α adrenergic effects include peripheral vasoconstriction ‘Shunts’ blood from the periphery to the heart, brain and lungs. Low dose adrenaline is recommended.
1058
What drugs can be used if an animal is in asystole
Adrenaline Vasopressin Atropine
1059
What are the properties of vasopressin when used for an animal in asystole?
Causes peripheral vasoconstriction without deleterious effects on myocardial oxygen demand Similar efficacy to adrenaline in dogs (small studies) Meta-analyses in humans have failed to demonstrate an advantage Expensive
1060
What are the properties of atropine when used for an animal in asystole?
Parasympatholytic Evidence does not show a clear benefit Theoretically good for patients with high vagal tone – common in veterinary patients Rabbits can have atropinase as a naturally occurring enzyme so not recommended.
1061
What are the properties of adrenaline when used for animals in asystole?
Adrenergic agonist – α and β receptors. Positive inotrope and chrono trope. Increases myocardial oxygen demand. α adrenergic effects include peripheral vasoconstriction ‘Shunts’ blood from the periphery to the heart, brain and lungs. Low dose adrenaline is recommended.
1062
What are the properties of high dose adrenaline when used for ALS?
Increased myocardial oxygen demand Increased rate of ROSC No increase in survival rates Can be considered in prolonged arrest - >10 minutes
1063
1064
What are the properties of fluid therapy when used for an animal in asystole?
Administration to euvolaemic patients is associated with reduced coronary perfusion. Only considered in patients with known hypovolaemia
1065
What are the properties of bicarbonate when used for an animal in asystole?
Metabolic acidosis is a common occurrence in CPA Mixed results in experimental studies so considered only in prolonged CPA
1066
What are the properties of open chested CPR when used for an animal in asystole
More effective than external compressions Requires significant resources both during and especially in recovery Can be considered for intra-thoracic pathology e.g. tension pneumothorax, or if already in surgery
1067
ROSC
Return of Spontaneous Circulation (ROSC) Capnography – sudden increases in ETCO2 are associated with ROSC ECG – Return of a normal rhythm is not necessarily supportive – PEA Return of consciousness/movement/reflexes
1068
What are the principles of postROSC care?
Many patients re-arrest Respiratory optimisation Supportive oxygen +/- ventilation if required Target PaO2 80-100mmHg or SpO2 94-98% Beware hyperoxia and oxidative damage with reperfusion Cardiovascular optimisation If hypotensive – beware fluid overload, so use of vasopressor therapy is sensible Hypothermia Can be beneficial to cardiac and neurologic outcomes – re-warm slowly 0.5oC/h
1069
Outline the post ROSC care algorithm
1070
What is meant by clinical pathology?
The practice of pathology as it pertains to the care of patients The subspeciality in pathology concerned with the theoretical and technical aspects of lab tech that pertain to the diagnosis and prevention of disease
1071
What makes up anatomic pathology?
Surgical pathology (biopsy) Necropsy
1072
What are the common anticoagulants?
Haematology Clinical chemistry Glucose Haemostasis/ coagulation
1073
What is the effect of haemolysis?
Choos ept gauge needle Never dispense blood sample through needle Increases in plasma/serum values of some compounds/ enzymes due to their higher concentration in the RBC Interferes determinations by colorimetry or interference in chemical interactions
1074
What is the effect of lipaemia?
Increases or decreases values of some compounds due presence of extra lipid fractions Turbidity caused by the lipids interfering in light detection methods Main changes are Incr in total lipid triglycerides and cholesterol Many determinations either cannot be carried out or results are sig affected
1075
What are the sources of variation and errors in lab results
Pre analytical - patient prep, sample prep, shipping Analytical - apt equ and reagents, still working Post analytical- results match patient, apt intervention, diagnostic sensitivity and specificity
1076
How can we control analytical variation?
Validation of the techniques used Quality control performed before and/or during analysis Only know the equipment was working when the last QC was checked
1077
How do we ensure an analytical technique is valid?
Precision Repeatability/reproducibility Accuracy Measuring the right thing correctly Specificity (analytical) Different from « diagnostic specificity » Sensitivity (analytical) and range (linearity) When do we need to dilute a sample Others
1078
Precision and accuracy
1079
What are the common quality control systems
A control material (known composition) which is treated/ measured as a specimen to check the analytical process is still working correctly. Quality control is performed before or during the analysis to ensure the validity of the result. Should be performed regularly Your analysis is only as good as the last passed QC How many cases do you want to recall/reavaluate? Internal QC: with patient samples External QC (EQA): not contemporaneous
1080
Why should blood smears be carried out in practice regularly?
Spot equipment errors Find things the machines cant Bands, metamyelocytes, toxic change nRBC’s, inclusions, parasites Red cell morphology (spherocytes, acanthocytes) Early red cell regeneration (polychromatophils)
1081
How is a low power evaluation of a blood smear carried out?
Low/Medium power (x10, x20 obj) Orientation, identify 3 zones Feathered edge Platelet clumps, big cells, big parasites Body Rouleaux, agglutination Monolayer RBC density, WBC numbers, Estimated differential
1082
How is a high power examination of a blood smear carried out?
Medium/High power (x40 and x100 (oil) obj) - monolayer Platelet numbers and morphology RBC morphology (small parasites) WBC morphology WBC differential count 3 cell series (RBC, WBC and Platelets) Up to 3 magnifications (x10, x40, x100)
1083
What can be seen in the blood smear?
1084
What may be seen on the feathered edge of a blood smear?
Platelet clumps Big cells Heart worm
1085
What can we see at x40 with oil in red cell morphology?
Closer look at: Anisocytosis Polychromasia Poikilocytosis Inclusions
1086
What does X40 allow view of with WBCs?
Neutrophils Left-shift (bands) Young cells inflammation Distinguish from high neutrophils due to stress Right shift Hypermature Toxic change Vacuolation Blue cytoplasm “Dohle” bodies High demand/septicaemias etc
1087
How can we carry out a systemic approach to evaluating blood smears?
Remember all 3 series (e.g. do platelets first so don’t forget) Once found monolayer, use battlement approach to ensue aren’t going over the same area again and again Try to stay within monolayer (if dog, should be able to see central pallor)
1088
This tissue is from a puppy. What is the morphologic diagnosis?
Small intestine: Enteritis, necrohaemorrhagic, segmental, acute, severe
1089
Is this a lesion? Explain your answer
No this is livor mortis
1090
This tissue is from a dog. What is the morphologic diagnosis?
t is a hemangiosarcoma.
1091
What is an appropriate description for this lesion?
There are multifocal, round, red hairless massess on haired skin.
1092
This is tissue from a cat. What is your morphologic diagnosis?
Left ventricular hypertrophy, diffuse, severes and chronic
1093
This is tissue from a dog. What is your morphologic diagnosis?
Lungs , haemorrhage multifocal to coalescing sever and acute
1094
This is tissue from a Ferret. What is your appropriate lesion description?
severe mucopurulent discharge coming from the eyes and nares.
1095
This is tissue from a cat. What is your morphologic diagnosis?
Cerebrum meningioma
1096
What can be seen in the image?
Pseudomelanosis
1097
This is tissue from a dog. What is your morphologic diagnosis?
mandible and a melanoma.
1098
Can a lesion be seen in the image?
it is not a lesion. What we see is oedema.
1099
What is the morphologic diagnosis of the image?
This is bone, with physis. We see a fracture which is focally extensive, severe and acute.
1100
What is your morphologic diagnosis?
Haired skin, sarcoma
1101
What is the diagnosis for this image?
urinary bladder, there are multiple white gritty crystals.
1102
What is the morphologic diagnosis of this image?
diaphragm. We see a hernia, focal, severe, acute, with visceral displacement.
1103
What is the diagnosis for this image?
duodenum is a focal perforating ulcer with a 1.5cm diameter.
1104
This is tissue from a cat, what is your morphological diagnosis?
haired skin, on the chin of the cat. We see folliculitis which is multifocal, moderate and chronic.
1105
What is the morpholigcal diagnosis of the pathology in the image?
Thryoid, §Adenomatous hyperplasia, bilateral, sever and chroni
1106
This is tissue from a dog, what is your morphological diagnosis?
perianal gland. Here we see an adenoma.
1107
What are the common cytological diagnosis?
Carcinoma Cutaneous histiocytoma Follicular cyst Lipoma or subcut adipose Lymphoma Mast cell tumour Mixed inflammation Neutrophilic inflammation with sepsis Lymph node reactive hyperplasia Sebaceous adenoma Sarcome
1108
Define cytology
The study of cell numebr and type in a tissue mass or fluid accumulation to investigate its cause §
1109
What are the common cytological specimens
Common cytological specimens include: Fine needle samples Capillary action sample Aspirate Touch imprints Body fluids Lavages
1110
What can cytology detect?
Cytological examination may allow: Differentiation of inflammation from tissue growth (hyperplasia/neoplasia) Differentiation of types of inflammation Detect neoplasia [Malignant vs benign] [Should indicate general type of neoplasm e.g., sarcoma vs carcinoma] [May identify the specific neoplasm] Differentiation of different fluids (exudates, transudates etc)
1111
What are the advantages of cytology?
Sampling is quick, safe and inexpensive: Cells can often be safely retrieved from lesions near vulnerable structures in conscious animals, making anaesthesia & surgical biopsy unnecessary. Sampling demands little equipment or skill(?)* Results can be quickly available
1112
1113
What are the limitations of cytology?
In the detection of neoplasia there are: False negatives: Poor exfoliation of a neoplasm Failure to sample tumour tissue Extensive necrosis/inflammation present (also, a neoplasm may not be well-differentiated enough to allow an accurate diagnosis) False positives: Dysplasia (which can mimic neoplasia) may occur in inflammatory diseases Histopathology provides information on tissue architecture, adequacy of excision, invasion etc and is often the next diagnostic procedure.
1114
FNS vs Biopsy
FNS Minimal patient prep and restraint Dry, stain, dry in minutes Microscopic review <5mins “bricks” rather than buildings Architecture seldom preserved – cells come through a hypodermic needle Not always conclusive Biopsy More patient prep, restraint anaesthesia as more invasive (Tru-cut, incisional, excisional) Fix in formalin (overnight?) Trim, process (dehydrate) embed in wax, slice, stain, coverslip (minimum 1 day) Architecture preserved (even if obtained by biopsy needle (e.g. Tru-cut) More often conclusive
1115
What are the different lesion types?
Inflammation- neutrophilic, eosinophilic, granulomatous Cystic- epidermal, sialcoele, seroma, haematoma Neoplastic- epithelial, round, mesenchymal
1116
Epithelial cells High yield, cells associated with one another, rafts, sheets, acini, cuboidal or culmnar
1117
Spindle/ mesenchymal Low yield, spindle shaped cells, usually single but may be in association/sheets, may be matrix
1118
Round cells High yield, discrete round cells that are non adherent
1119
What cytology can tell us
1120
Process for masses
1121
What types of inflammation may be seen in cytology?
Neutrophilic inflammation (suppurative acute) - This includes abscesses Pyogranulomatous inflammation Granulomatous (macrophagic, chronic) inflammation Eosinophilic inflammation
1122
What are the most common canine tumours?
histiocytoma Lipoma Adenoma
1123
What are some different kinds of epithelial skin tumours?
Trichoblastoma (basal cell tumour) Trichoepithelioma (hair follicle tumour) Squamous cell carcinoma Sebaceous cell tumours (adenoma, carcinoma, epithelioma) Anal sac apocrine adenocarcinoma Perianal gland (hepatoid) adenoma
1124
What are the properties of mesenchymal skin tumours?
Arise from connective tissue, muscle, bone & cartilage, nerve, endothelial cells Cells in non-cohesive aggregates or individually Cell borders are variably defined and often indistinct Embedded in matrix Spindle shaped cells with cytoplasmic tails common Cells can be oval or plump
1125
What can be seen
Mesenchymal skin tumour
1126
What can be seen?
Lipoma
1127
What are the properties of lipoma?
Adipocytes with small nucleus and abundant (single vacuole/globule) cytoplasm Free fatty droplets NB cells may fall off slides during staining / fixation Avoid methanol fixation (Soln. A) – use soln’s B & C only Consider drop rather than dip Subcutaneous fat appears identical!
1128
What are the different types fo round cell tumours?
1129
What can be seen?
Plasmacytoma
1130
What are the properties of plasmacytoma?
Discrete cells Eccentric nuclei Chromatin clumping Perinuclear clear zones Golgi, Ig production
1131
Cytology summary?
Cytology very useful in evaluation of skin tumours Don’t make assumptions – aspirate all masses Be prepared to take biopsies where results are inconclusive Always interpret in context of clinical history Take lots of smears to increase likelihood of diagnostic smear Don’t be tempted to make a diagnosis from poorly cellular samples
1132
Describe and diagnose (dog lymph node)
Lymphoma x. The smear has poor stain penetration and colour differentiation. The sample is highly cellular consisting of round cells on a pale basophilic background including RBC's, disrupted cell nuclei and cytoplasmic blebs (lymphoglandular bodies). The rounds cells are lymphoid in appearance (round nuclei with thin rim of cytoplasm). Small lymphocytes are in the minority. Most cells (>50%) are relatively monomorphic large lymphocytes (>2 cell diameters). Poor stain penetration makes nuclear morphology difficult to discern but there may be irregular nuclear borders and conspicuous nucleoli. A disorderly mitotic figure is observed. Rare neutrophils and eosinophils are present.
1133
Describe and diagnose Canine lymph node
Lymph node reactive hyperplasia The smear has low cellularity on a clear background of occasional RBC's, disrupted cell nuclei and cytoplasmic blebs (lymphoglandular bodies). The cells are lymphoid in appearance (round nuclei with little or no discernible cytoplasm). There is variation in lymphocyte size but the large majority (>75%) are small lymphocytes with the remainder being intermediate and large lymphocytes.
1134
Describe and diagnose Dog subcutaneous mass
Follicular (epidermal inclusion) cyst There sample is almost acellular on a background of RBC's and non-degenerate neutrophils (?iatrogenic sampling haemorrhage). There are ill defined basophilic patches reminiscent of keratin content but not intact squames. A large cholesterol crystal is observed.
1135
Describe and diagnose Dog eyelid mass
Sebaceous adenoma viii. The smear contains clusters of adherent cells on a clear background with RBC's. The cells have a roundish monomorphic appearance, eccentric nuclei and abundant foamy cytoplasm. No nuclear atypia nor evidence of inflammation is observed.
1136
Describe and diagnose dog flank skin mass
Follicular (epidermal inclusion) cyst The smear contains few if any nucleated cells but does have an abundance of anuclear blue staining structures with irregular variably defined angular borders. The morphology is most consistent with keratin/squames. No evidence of inflammation is observed.
1137
Describe and diagnose dog flandk skin mass
Mixed pyogranulomatous inflammation xii. The smear has low cellularity on a lightly proteinaceous background including RBC's. The observed cells are a mixture of mostly degenerate neutrophils, non-degenerate neutrophils and vacuolated foamy macrophages with occasional keratin squames. Infectious agents are not observed.
1138
Descrbe and diagnose dog flank skin mass
Mast cell tumour A moderately cellular sample on a background of RBC's and scattered metachromatic granules. Nuclear staining is poor. Cells are all of the same round type, in seemingly non-adherent clusters. Pale staining eccentric nuclei are surrounded by intensely metachromatic granular cytoplasm. The nuclear staining quality prevents further evaluation of nuclear characteristics.
1139
Describe and diagnose dog lymph node
Lymphoma The smear has low cellularity on a lightly staining background with numerous RBC's, cytoplasmic blebs (lymphoglandular bodies) and disrupted cell nuclei. Occasional neutrophils are observed consistent with the degree of background haemorrhage. The cells are morphologically lymphoid, (round with small amount of cytoplasm). Of the intact cells, the majority are intermediate or large in size. Small lymphocytes are in the minority. Irregular nuclear borders and variably conspicuous nucleoli are observed.
1140
Describe and diagnose dog flank skin mass
Lipoma or subcutaneous adipose iii. Clusters of swollen, rounded cells with abundant pale/colourless cytoplasm; nuclei are compressed to one edge of the swollen cells
1141
Describe and diagnose dog flank skin mass
Mixed pyogranulomatous inflammation v. The smear is moderately cellular with a pale staining background including debris, erythrocytes and occasional disrupted cells. Cells include degenerate neutrophils and macrophages with foamy/vacuolated cytoplasm.
1142
Describe and diagnose puppy flank skin mass
cutaneous histiocytoma The smear contains scattered small groups of medium-sized, round cells with variably small amounts of pale basophilic cytoplasm. Nuclei are round or oval and either centrally or slightly eccentrically placed. There is moderate anisokaryosis (variation in nuclear size). Rare examples of binucleation and nuclear moulding are observed.
1143
Describe and diagnose dog flank skin mass
Sarcoma vii. The smear is moderately cellular on a haemorrhagic background. There scattered small groups of individual and loosely associated medium-sized, elongated polyhedral or 'spindle shaped' cells with indistinct cytoplasmic borders. Nuclei are round or oval; contain single nucleoli and there is moderate anisocytosis (2-3x).
1144
Describe and diagnose prostate FNA
Carcinoma The sample is highly cellular with a moderately staining background of debris. Inflammatory cells are not a feature. The cellular population is pleomorphic marked anisocytosis, anisokaryosis, and highly variable N:C ratio. There are occasional examples of cellular adherence but in the main, cells are loosely associated. Bi- and multi-nucleate cells are observed
1145
Describe and diagnose Ventral skin mass
Carcinoma A moderately cellular sample on a variably staining proteinaceous background including debris and occasional RBC's. Cells are tightly adherent in clusters with often take the form of attempts to create ducts and acini. There is moderately anisocytosis and anisokaryosis and variable but often high N:C ratio. Multinucleation may be present. Inflammatory cells are not a feature.
1146
Describe and diagnose dog skin mass
Neutrophilic inflammation with sepsis The sample is moderately cellular on a background of variably staining debris and some nuclear disruption and nuclear streaming. The cells are exclusively degenerate neutrophils. Coccoid bacteria are observed commonly in pairs or quartets
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