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
Q

What is the primary objective of aseptic surgery?

A

Reducing infections

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26
Q

What host factors play a role in aseptic surgery efficacy?

A

Age
Physical condition
Nutritional status
Diagnostic procedures
Concurrent metabolic disorders
Current medication

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27
Q

What operating room practice needs to be carried out for success in aseptic surgical techniques?

A

Principles of aseptic technique
Sterilisation
Disinfection
Anaesthesia
Atraumatic technique

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28
Q

What are the 3 factors that reduce infection risk?

A

Patient prep (clipping, scrubbing, draping)
Surgeon prep (scrubbing, gowning, gloving, hats and masks)
Theatre behavior (etiquette, talking , flow etc)

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29
Q

What suggests a rational use of antibiotics in surgical treatments?

A

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

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30
Q

What are the characteristics of an ideal suture?

A

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

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31
Q

Natural suture

A

Raw materials from naturally occurring sources
Cat gut/ silk

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32
Q

Synthetic suture

A

Raw material produced in an industrial process
Nylon etc

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33
Q

absorbable suture

A

Materials that are fully degraded and absorbed by the body once placed

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34
Q

Non absorbable suture

A

Materials that stay in place for an indefinite period (60 days without changing in anyway

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35
Q

Monofilament vs multifilament suture

A

Monofilament suture - single filament
Multifilament - multiple strands that are braided to create a thicker thread of the desired diameter

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36
Q

Tensile strength

A

Breaking strength per unit area

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37
Q

Memory

A

Tendency to retain original configuration

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38
Q

“chatter” and tissue drag

A

Lack of smoothness or presence of friction whilst passing through tissue

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39
Q

Tissue reaction with suture material

A

Tissues respond to the implantation of sutures as they do to other foreign material and can provoke an inflammatory response

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40
Q

Advantages and disadvantages of absorbable suture material

A
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41
Q

Advantages and disadvantages of non absorbable suture material

A
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42
Q

What are the consequences of placing suture material and what are the factors

A

Suture material is foreign body
Tissue reaction
Amount of material
Presence of infection

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43
Q

What factors affect tissue reaction>

A

Absorption characteristics
Natural or synthetic
Phagocytosis vs hydrolysis

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44
Q

What is the diameter rating for suture materials?

A

2-0 is bigger than 3-0
0 is bigger then 00=2-0

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45
Q

What is a swaged needle?

A

Attached to the suture material

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46
Q

What are the issues with eye needles?

A

Threading the needle causes a double strand of suture material
Multiple uses causes bluntness
Increases tissue trauma

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47
Q

Benefits of swaged needle?

A

Minimal trauma
Single use
Optimal penetration properties
(more expensive)

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48
Q

What are the main parts of the needle?

A

The point
The body
The eye or the swage

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49
Q

What is the chord length of a needle?

A

The tip of the swage to the needle point

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50
Q

What are the different needle curvatures?

A

Curvature is measured in relation to a circle. Deeper the wound the more curved the needle

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51
Q

What are the different needle points?

A

Blunt - circular elliptic
Sharp (polygonal)
Compound (tapercut, short cutting point etc)

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52
Q

What is the composition of needles?

A

Made from stainless alloys
Sufficiently rigid to resist forces applied to them during handling
Sufficiently flexible to bend before breaking

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53
Q

What is meant by ductility?

A

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

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54
Q

What is the common composition of surgical instruments?

A

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

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55
Q

What implants may be placed in stainless steel instruments and why?

A

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

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56
Q

What is the role of scalpels and what are their properties?

A

Cutting skin
Baird parker no 3 is the most commonly used blade
Various blades can be used

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57
Q

What are the types of scalpel blades?

A

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)

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58
Q

What scalpel handle is used in large animal practice?

A

Number 4

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59
Q

When are different scalpel handling techniques used?

A

Power grip allows for thicker and tougher tissues to be cut
Pencil grip allows for delicate precise use

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60
Q

What are the different scissors used?

A
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61
Q

When are mayo scissors used

A
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62
Q

When are metzenbaum scissors used?

A
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63
Q

When are suture scissors used?

A
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64
Q

When are iris scissors used?

A
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65
Q

How should scissors be held?

A

Scissors held with the thumb in one ring and fourth finger in the other
Index finger is placed over the joint for increased stability

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66
Q

What is reverse grip for scissors?

A

Scissors held for cutting towards the dominant hand

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67
Q

What are needle holders?

A

Ringed instrument with a ratchet mechanism allowing the surgical needle to be held by the needle holder

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68
Q

What are the 3 designs of needle holders?

A

Mayo hegar
Olsen Hegar
Gillie

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69
Q

When are treves rat toothed forceps used?

A

Heavy duty with a single tooth interdigitating with two on the opposing tip
Can be traumatic to tissues

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70
Q

When are dressing forceps used?

A

Applying dressings
Have no rat teeth and are particularly traumatic to tissues as pressure is needed if used for this purpose

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71
Q

When are adson rat tooth forceps used?

A

Fine forceps with a small rat tooth grip

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72
Q

When are debakey forceps used?

A

LEAST TRAUMATIC These have longitudinal and transverse serrations
originally used for vascular use as they are the least traumatic

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73
Q

What are the grips for thumb forceps?

A

Penhold or chopstick grip

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74
Q

What are homeostatic forceps?

A

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

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75
Q

What are the main tissue holding forceps?

A
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76
Q

What is the role of retractors?

A

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

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77
Q

What can be seen in these images?

A

Left - abdominal retractor (balfour- 3 point retractor which prevents rotation)
Right - thoracic retractor with ratchet mechanism which can gradually retract ribs (2 point retractor)

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78
Q

What can be seen in these images?

A
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79
Q

What are the main handheld retractors?

A
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80
Q

What are the 2 main towel clamps?

A
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81
Q

What is the cascade of events through which wounds heal?

A

Haemostasis and inflammation (platelet aggregation and WBC)
Proliferation/ Fibroplasia (angiogenesis, granulation)
Maturation (remodelling of collagen 1->3) contraction of the wound

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82
Q

What occurs during haemostasis?

A

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

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83
Q

What occurs during the inflammatory phase?

A

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

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84
Q

What occurs during proliferation phase?

A

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

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85
Q

What occurs in the repair phase of proliferation?

A

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

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86
Q

What occurs during the maturation phase of wound healing?

A

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

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87
Q

What factors affect wound healing?

A

Patient factors - age and comorbidities
Wound factors - infection and location
Concurrent treatment - corticosteroids(delay healing)
Radiation (tissue fibrosis and vasc scarring)

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88
Q

What patient factors affect wound healing?

A

Age
Comorbidities (HAC and diabetes)
Nutrition status (hypoproteinaemia- will slow wound healing)

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89
Q

What wound factors affect wound healing?

A

Infection
Location (tension, movement, local blood supply)

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90
Q

How can concurrent treatment affect wound healing?

A

Corticosteroids- delay all stages of wound healing
Radiation - Tissue fibrosis and vascular scarring

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91
Q

How can wounds be classified?

A

Abrasion
Avulsion
Incision
laceration
Puncture

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92
Q

What wound can be seen below?

A

Abrasion Loss of epidermis and some dermis (blunt trauma/ shearing)

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93
Q

What wound can be seen how does it occur?

A

Avulsion - tearing of tissues from attachments
on limbs it’s a degloving injury

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94
Q

What wound can be seen and how does it occur?

A

Incision - created by a sharp object
Minimal trauma (neat)

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95
Q

What wound can be seen and how is it caused?

A

laceration - tearing type wound causes irregular defect Usually jagged

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96
Q

What wound can be seen and how is it caused?

A

Puncture
Penetrating wound
Superficial damage may be minimal
Deep damage may be substantial

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97
Q

Outline the skin vascular supply

A

Epidermis
Dermis
Hypodermis
Subdermal plexus
Terminal branched of direct cutaneous arteries
Within the panniculus and subcutis

protect subdermal plexus in mobilisation

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98
Q

What are the fundamentals of wound management?

A

Assessment of patient
other injuries
Life threatening complications
Stabilise
Examine with sedation

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99
Q

How to assess type of wound?

A

Degree of tissue damage
Depth of wound
VItal structures such as bones joints nerves and tendons
(especially important in puncture wounds)

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100
Q

How to assess wound age?

A

Golden period is 6-8hrs
Contaminated or infected
History from the owner
Has the bacteria started dividing

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101
Q

How to assess level of contamination of a wound?

A

Foreign material
devitalised tissue
Bacterial innoculum (bit vs clean glass etc)
Takes into account the age and nature of the wound

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102
Q

How does lavage occur for wound management>

A

Gross contamination- tap water
Copious lactated ringers or hartmanns
35-60 ml18G needle = higher pressure 7-8psi
Debridement - dressings, surgical etc

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103
Q

How can a management plan be created for a wound?

A

Primary intention closure
Secondary intention healing
Third intention closure

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104
Q

What is meant by golden period in wound healing?

A

6-12 hrs Bacteria divide
>12hr bacterial invasion

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105
Q

What factors influence bacterial contamination?

A

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

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106
Q

What are the goals of wound management?

A

Promote healing
Convert contaminated into clean
Control infection

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107
Q

What are the methods of wound debridement?

A

Surgical
Mechanical
Autolytic
Enzymatic - rare
Biological- rare

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108
Q

What is the role of wound debridement?

A

Remove dead necrotic contaminated particulate matter and bacteria from the wound
Ready for wound closure and healing

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109
Q

How is surgical debridement carried out?

A

debrided with sharp surgery to remove dead tissue
preserve vital structures
can carry out scraping to remove chronic granulation tissue
wound lavage and dressing

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110
Q

How is lavage used as a debridement agent?

A

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

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111
Q

What is a wet to dry dressing and how is it used?

A

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

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112
Q

What is the role of negative pressure wound therapy?

A

A mechanical pump attached to the wound reduces air pressure drawing off exudate and reducing oedema

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113
Q

How does negative air pressure therapy help with wound healing?

A

Reduces bacterial colonisation
Promotes granulation tissue development
Increases rate of mitosis
Spurs the migration of epithelial cells within the wound

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114
Q

what is shown in the image?

A

Topical negative pressure wound therapy

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115
Q

What issues arise with negative pressure wound therapy?

A

Creating an airtight water tight seal

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116
Q

What can be seen in the image?

A

Negative pressure wound therapy?

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117
Q

What effect does honey have on wound healing?

A

Antibacterial effect - reduction of bacteria
Healing stimulating properties
Debriding effect
Antiinflammatory effect
Odour reducing capacity
Reducing in wound pain

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118
Q

What is honeys role as a debriding agent?

A

Osmotic effect
Low pH
Both help to draw fluid from the wound area

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119
Q

How does honey have antimicrobial effects?

A

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)

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120
Q

What issues arise with using standard table honey?

A
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121
Q

What is biological debridement?

A

Medical grade maggots
Hard to keep in wound
Unable to identify healthy tissue from necrotic tissue

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122
Q

What is the ranked list of wound debridement?

A

Speed to effect and expense to cost
Scraping with scalpel often seen as the best
Wet to dry is second best

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123
Q

Why do we need bandages?

A

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

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124
Q

What types of wound dressing are available?

A

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)

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125
Q

What are the roles of topical wound gels and creams?

A

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

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126
Q

What are the layers of bandaging?

A

Primary layer - dressing (most important)
Secondary layer - padding material 2 components
Tertiary layer- vet wrap etc

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127
Q

What are the 2 components of the secondary layer of a bandage?

A

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

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128
Q

What are the properties of the tertiary layer of a bandage?

A

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)

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129
Q

Why are immobilised bandages used?

A

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-

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130
Q

How is an immobilised bandage applied?

A

Applied 1 joint above and 1 joint below to immobilise the bone to its maximum splinting stability

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131
Q

What are some complications with poorly applied or cared for bandages?

A

Swelling - distal limb not included
Tissue necrosis - bandage too tight
Decupital ulcers - over bony prominences
Patient interference due to uncomfortable bandage

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132
Q

How can decupital ulcers be avoided?

A

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)

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133
Q

What type of dressing is used for wounds that have chronic granulation and are struggling to heal?

A

Alginate based dressings - Seaweed stimulates the release of inflammatory factors for wound healign

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134
Q

What should be assessed with wounds in large animals?

A

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

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135
Q

How should a wound be assessed in large animals

A

History, clinical assessment and sedation considerations
Lameness level (suggests catastrophic injury through tendons etc)
Assess gait

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136
Q

What should be considered with sedation?

A

High blood loss is a contraindication
Regional anaesthesia might be required

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137
Q

What structures are affected

A

DDflexor tendon
Superficial digital flexor tendon

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138
Q

What structures could be affected?

A

Brachial plexus
Penetration of the thoracic cavity

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139
Q

What could have been damaged here

A

Synovial structure (calcaneal bursa) suggest a poor outcome
Would cause lameness
Synovial fluid samples and cellularity can assess inflammation etc

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140
Q

What can be used to assess joint wound damage?

A

Synovial fluid assessment
Sterile solution into calcaneal bursa allows for indication of bacteria presence in the wound
Imaging of wound for fractures

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141
Q

How can imaging be used in wound managment in large animals?

A

Bones (sequestrian - bone that acts as foreign body)
Acoustic shadow suggest foreign body
Soft tissue damage
Fractures

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142
Q

How do we determine wound management options?

A

Superficial or deep
Structures involved joints etc
Closing the wound options

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143
Q

What is meant by primary closure of wounds?

A

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.

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144
Q

What should be combatted in primary closure of wounds in large animals?

A

Tension
Matress suture patterns combats tension
Stents and quills distribute tension over the surface of the skin
Pressure on the skin is then reduced

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145
Q

How is secondary intention healing carried out in large animal wound healing?

A

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

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146
Q

What is delayed primary closure of wounds in large animals?

A

Allow natural debridement of the body
The primary closure after assessmetn for necrotic tissue

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147
Q

Why are drains used in wound healing?

A

Route for fluid and inflammatory exudate to exit the wound
Speeds up debridement of the wound

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148
Q

What are some drains that can be used in large animals?

A

Latex penrose drain in two separate incisions at wound bed
Active drains can be used sometimes

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149
Q

What has been used for healing here?

A

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

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150
Q

How can granulation tissue be fixed in large animal wounds?

A

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

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151
Q

When might skin grafting be used in wound management of large animals?

A

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

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152
Q

What are the common bandages used in equine practice?

A

Simple bandage
A figure of 8 bandage
Robert jones bandage

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153
Q

What is the use of a figure of 8 bandage in equine practice?

A

Covers for carpus and tarsus to go around the hock
avoids pressure points

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154
Q

Properties of the robert jones bandage

A

Treatment modality
Support
At least 3 layers

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155
Q

What are the different equine bandaging materials?

A

Protective material
Padding
Conforming
Outer layer
Finishing

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156
Q

What is the role of the 3 conforming layers in a robert jones bandage?

A

Condense the padding to provide extra support

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157
Q

What is the role of splinting in equids?

A

Unstable fractures
Unstable tendon injuries

There is a variety of methods ranging from commercially available options and homemade materials

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158
Q

Where would the splint be placed for the 4 regions of damage in this image?

A

1- alignments of dorsal cortices, splint placed dorsally
2. Splint placed laterally and caudally
3- splint placed laterally and medially
4- forelimb - stabilise carpus

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159
Q

Where would splints be placed for the regions in the image?

A

1- alignments of dorsal cortices, splint placed dorsally
2. Splint placed laterally and caudally
3- splint placed laterally and medially

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160
Q

What are the 3 phases of bone healing?

A

Inflammatory
Restorative
Remodelling

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161
Q

What is the overall process for the inflammatory phase of bone healing?

A

Inflamatory response with fracture
Lysis of osteocytes liberates inflammatory mediators
IMs call in macrophages and inflammatory cells to clear wound and debris

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162
Q

What happens chronologically in the inflammatory phase of bone healing?

A

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

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163
Q

When is compartmental syndrome likely to occur in bone healing?

A

Inflammatory phase

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164
Q

What occurs in the restorative phase of bone healign

A

Soft callus formation
Hard callus formation

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164
Q

What occurs in soft callus formation of bone healing?

A

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

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165
Q

What occurs in hard callus formation of bone healing?

A

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

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166
Q

What occurs in the remodelling phase of bone healing?

A

Ends of the bones are enveloped by fusiform mass called a callus
Remodelling occurs involving osteoclasts
Slow process that can take years

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167
Q

Describe bone remodelling using the image

A
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168
Q

What are the two types of healing within the restorative phase of bone healing?

A

First intention (minimal bone callus formation)
Second intention (most common natural type of healing)

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169
Q

What occurs in first intention bone healing?

A

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

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170
Q

What is Roux law in first intention bone healing ?

A

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

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171
Q

What healing can be seen in the image?

A

First intention healing through the use of a dynamic bone plate
Bony formation with minimum formation of callus

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172
Q

How can vets ensure first intention healing of bones occurs?

A

ensure that the blood supply is not excessively damages (particularly the intraosseous supply)
Ossification by first intention takes place much faster the second intenteion

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173
Q

What are the issues with first intention bone healing?

A

At first, direct osteonal union is not as stable as primary healing with separation

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174
Q

When does second intention healing occur in fractures?

A

Late treatment
Deficient reduction of the fracture or loss of fragments
Poor blood supply
Infection
Absence of forces of compression

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175
Q

What bone healing has occured

A

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

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176
Q

What are the principles of fracture repair

A

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

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177
Q

What radiographs should be taken for fracture managment?

A

Orthogonal radiographs
Mediolateral view and craniocaudal view

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178
Q

How can fractures be assessed?

A

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

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179
Q

What is taken into account with fracture scores?

A

Patient factors
Fracture
Owner factors
Surgeon

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180
Q

What are the patient factors assessed in fracture scoring?

A

Weight of animal
Age
Boisterousness
Concurrent illnesses

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181
Q

What are fracture factors assessed in fracture scoring?

A

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

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182
Q

What owner factors are assessed in fracture scoring?

A

Will they comply with post op instructions
Finances

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183
Q

What surgeon factors are assessed in fracture scoring?

A

Are they able to manage the fracture
Is the equipment available

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184
Q

What mechanical factors are assessed in fracture scoring?

A

Degree of displacement/ comminution

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185
Q

What biological factors are assessed in fracture scoring?

A

Young dog vs old dog
Soft tissue components
Osteosarcoma = Pathological fracture = wont heal
Contamination if open fracture

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186
Q

What are the normal physiological forces that occur when weight bearing or from muscle contraction on a bone/ fractured bone?

A

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

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186
Q

What affects the fracture repair treatment?

A

determined by fracture type and forces that will be applied

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187
Q

What is the effect of axial compression on oblique fracture surfaces?

A

Shear force will be generated

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188
Q

What physiological forces can be seen in the image?

A
  1. axial compression
  2. tension
  3. bending
  4. torsion
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189
Q

What should be assessed with compression on tension aspects of long bones?

A

Diaphyseal bones are asymmetrically loaded when weight-bearing
mandible is asymmetrically loaded during mastication

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190
Q

Describe the forces that should be assessed and accounted for in fracture management of a long bone?

A

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

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191
Q

What are the tension aspects of the long bones?

A

Femur- lateral aspect
Tibia- medial aspect
Radius- craniomedial aspect
Humerus - laterocranial aspect
Mandible - dorsal aspect

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192
Q

What are the consequences of different forces acting on a fracture?

A

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

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193
Q

What does primary healing of the bone require?

A

Intimate contact of the bone ends under compression
Through application of bone plate and extensive dissection and manipulation of soft tissues

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194
Q

What does secondary healing of the bone require?

A

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)

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195
Q

What effects whether a fracture should be repaired at all?

A

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

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196
Q

What is the strain theory in fracture management?

A

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

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197
Q

What is the % elongation at rupture for fracture management?

A
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198
Q

How does the formation of a callus in bone healing affect strain?

A

Resorption of fragment ends increases the fracture gap and therefore creates greater stability and reduced movement at the fracture site and the strain decreases

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199
Q

What can be seen in the image

A

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

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200
Q

What treatment approach can be seen in the image and what will be the result?

A

External fixator with a LBDT approach
Results in secondary healing and callus formation

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201
Q

What is the importance of post operative assessments in fracture treatment?

A

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

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202
Q

When should post-operative radiographs be taken in fracture management?

A

Prior to the removal of implants
If the progression is not as anticipated
There is evidence of sepsis

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203
Q

What are the fracture treatment options for small animals?

A

Intramedullary pin and cercalge wire
Plating (w or wo compression
Intramedullary nail
External Fixator
Pin and tension band

Various combinations of these

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204
Q

What are the properties of the intramedullary pin?

A

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

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205
Q

What is the role of the cerclage wire in fracture management?

A

Cerclage wires draw fragments to their normal position and then fix them relying on the circular cross section of the bone to produce stability

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206
Q

Why might a plate be used with a transverse fracture?

A

if the fracture is transverse then rotation is possible
To prevent this rotation a plate can be used in addition to the pin

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207
Q

How is the IM pin placed normograde?

A

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

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208
Q

How is a retrograde IM pin placed?

A

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

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209
Q

What issues are there with retrograde placement of the IM pin?

A

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

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210
Q

What can be seen

A

Normograde placement of an IM pin

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211
Q

What treatment has been used in the image?

A

IM pin and cerclage wires

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212
Q

What treatment has been used and why?

A

IM pin and external fixator

The EF prevents rotation as well as offering resistance to axial compression both of which the IM achieves poorly

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213
Q

What are the properties and uses of the intramedullary interlocking nail?

A

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

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214
Q

What can be seen in the image?

A

Intramedullary interlocking nail

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215
Q

What are the properties of the external fixator?

A

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

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216
Q

What can be seen in the image? Wat are the placement options?

A

External fixator to radioulnar fracture

Placement can be uniplanar, biplanar, unilateral or bilateral

Bilateral are stronger
can be used to augment IM pin fixation

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217
Q

What complications arise with external fixators?

A

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)

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218
Q

What are the properties of plate fixation and when might they be used?

A

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

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219
Q

Plate fixation methods

A
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220
Q

What are the differences between locking and non locking plate fixations?

A

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

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221
Q

How can plates be classified by function?

A

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.

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222
Q

How does a compression plate work>

A

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

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223
Q

What plates are being used to treat each fracture?

A
  1. Simple transverse fracture repaired with compression plate
  2. Comminuted but reconstructable fracture repaired with neutralisation plate
  3. Comminuted fracture treated with buttress plate
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224
Q

How does cyclical loading lead to plate failure?

A

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

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225
Q

What are avulsion or tension fractures?

A

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

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226
Q

What is a lag screw and how are they used?

A

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

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227
Q

What is the role of the tension band?

A

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

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228
Q

What should be considered when dealing with avian fractures?

A

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

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229
Q

Describe the treatment

A

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

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230
Q

What factors in equine fractures should result in euthanasia?

A

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

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231
Q

What were Halsteds principles of surgery?

A
  • Gentle tissue handling
  • strict asepsis
    Haemostasis
    preservation of blood supply
    no tension on tissues
    Good approximation of tissues
    Obliteration of dead space
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232
Q

What might influence healing of tissues?

A

Age
Nutrition
Comorbidities
Medications

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233
Q

Define Exploratory laparotomy

A

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

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234
Q

How is an exploratory laparotomy performed?

A

Abdominal cavity is divided into 5 regions

  • Cranial abdomen
    GI tract
    Right paravertebral region
    Left paravertebral region
    Caudal abdomen
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235
Q

In an exploratory laparotomy what is being assessed in the greater peritoneal cavity?

A

Peritoneal fluid

to do this
Excision of the falciform ligament
Examination of the righ and paravertebral gutters

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236
Q

What is being assessed in the cranial abdomen for an Exp laparotomy?

A

Liver
Gall bladder and bile ducts
Hepatic hilus
Epiploic foramen
Spleen

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237
Q

What should be assessed of the GI tract in an Exp lap?

A

Stomach
Intestinal tract
Pancreas
Regional lymph nodes

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238
Q

What is assessed in the right paravertebral region of an Exp Lap?

A

Hepatic portal vein
Caudal vena cava
Coelic artery
Hepatic lymph nodes
Right adrenal gland
Right kidney and proximal ureter
Right ovary and uterine horn

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239
Q

What is being assessed in the left paravertebral region in an Explap?

A

Aorta
Left adrenal gland
Left kindey and proximal ureter
Left ovary and uterine horn

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240
Q

What is being assessed in the caudal abdomen during and Exp Lap?

A

Bladder and distal ureters
proximal urethra
Prostate gland and ductus deferens
Uterine body and proximal vagina
Regional lymph nodes

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241
Q

What is assessed of the abdominal wall, peritoneal surface and mesenteries in an Exp Lap?

A

Diaphragm
Oesophageal hiatus
Aortic and caval hiatus
Greater and lesser omentum
Internal inguinal rings

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242
Q

What are the fundamentals of tumour resection?

A

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

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243
Q

What are the roles of oncological surgery?

A

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

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244
Q

What is an example of prophylactic surgery?

A

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

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245
Q

What surgery may be classed as an oncological emergency?

A

Bleeding splenic haemangiosarcoma

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246
Q

How are diagnosis and grading of tumours carried out?

A

Cytology (FNA and impression smear)
Histology

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247
Q

What biopsies can be carried out for histology of a tumour?

A

core biopsy
Punch biopsy
Incisional biopsy
Excisional biopsy

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248
Q

What is the role of staging in tumour treatment?

A

Looking for metastatic tumours

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249
Q

What is meant by surgical dose in tumour treatment?

A

How much surgery

Debulking/cytoreduction
Marginal resection
Wide resection
Radical resection

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250
Q

Label the tumour below

A

Pseudocapsule
Reactive Zone
Tumour
Skip metastases
Satellite metastases

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251
Q

What is the role of cytoreductive excision?

A

Leaves macroscopic volumes of tumour. Will recur unless given adjuvant therapy (which is less effective if gross vs microscopic tumour remains)n

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252
Q

What is meant by marginal excision?

A

local excision
That is, tumour removal with minimal amount of surrounding normal tissue
Can result in microscopic or macroscopic presence of residual tumour

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253
Q

What is the role of wide excision?

A

Removal of the tumour with complete margins of normal tissue in all directions
Local recurrence is unlikeley

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254
Q

What should be taken into account with wide excision margins for a tumour?

A

Fascial planes are the best border to a margin (especially over fat)

Deep margins are much more difficult to achieve

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255
Q

What is meant by radical excision?

A

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

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256
Q

What are the layers of the bowel?

A

Suture holding is most important in the submucosal layer

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257
Q

What is the role of gastrotomy?

A

Making a hole in the stomach
For the removal of gastric foreign body

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258
Q

Procedure for gastrotomy?

A

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

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259
Q

What is the role of omentalisation?

A

Improved vascular supply
Improved lymphatic drainage
Rich source of inflammaotry and immunogenic cells (neut, t and b lymphs and macrophages)
Neovascularisation (angiogenic factors

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260
Q

Define omentalisation

A

Omentalization, the placement of omentum around organs or within cavities to improve vascularization or drainage,

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261
Q

What is intussusception ?

A

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.

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262
Q

Define intussuscipiens

A

invagination of a proximal portion of intestine (intussusceptum) into a more distal portion (intussuscipiens)

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263
Q

How long does healing of the intestine and bladder take?

A

14 days post suturing
Wound strength will have reached nearly normal levels
Urinary bladder takes 21-28 days post surgical repair

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264
Q

Whatis dehiscence?

A

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

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265
Q

What checks should be done at the end of an operation?

A

Integrity of the repair
Check for bleeding
lavage and suction
Count swabs
Change gloves
Change instruments

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266
Q

What are the signs of a post operative complication and how can they be checked?

A

Wound infection
peritonitis
Uroabdomen

check clinical signs
Radiography
Abd US
Abd Tap

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267
Q

What can be seen in the image?

A

Enterectomy dehiscence

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268
Q

What can be seen in the image?

A

Presence of peritoneal fluid

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269
Q

What can be seen in the slide produced via abdominocentesis?

A

Toxic neutrophils in high numbere
Bacterial presence

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270
Q

What can be seen in the image? Animal has had bladder surgery

A

Would expect the animal to be hyperkalaemic
Urethrogram is leaking from bladder repair into the peritoneal space
Peritonitis was also present on Exp Lap

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271
Q

How should the linea alba be closed?

A

External rectal sheath is most important?
reconstruct the original anatomy
Rectus muscle has no wound holding strength

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272
Q

What is the rectus sheath made up of?

A

External and internal leaf

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273
Q

What is clinical reasoning?

A

The process by which veterinary surgeons integrate clinical and contextual factors to make decisions about the diagnoses, treatment options and prognoses of their patients

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274
Q

What are the methods of clinical reasoning?

A

Pattern recognition, illness scripts
Problem based clinical reasoning
Often dual process reasoning used

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275
Q

What are the properties of pattern recognition reasoning?

A

Pattern - No memory reliance
Fast unconscious and intuitive
Pattern recognition mode or heuristics (experience)
Cognitive biases and emotional influences are sources of error

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276
Q

What are the properties of inductive reasoning?

A

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

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277
Q

What questions should be answered in inductive reasoning?

A

What is the problem
Which body system is involved and how
Where in the body system is the problem located
What is the lesion

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278
Q

How is a clinical problem defined and refined?

A

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)

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279
Q

How can we differentiate between primary or secondary clinical problems?

A

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

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280
Q

How is the location of a clinical lesion located?

A

History and clinical exam
Further testing such as imaging
Endoscopy etc

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281
Q

What is DAMNIT-V?

A

Degenerative, Anomalous, Metabolic, Neoplastic, Nutritional, Inflammatory, Idiopathic, Toxic, Traumatic, Vascular

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282
Q

What is a sign time graph?

A

Graphical representation of changes in pathology over time

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283
Q

What are the 2 components of pharmacology?

A

Pharmacodynamics
Pharmacokinetics

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284
Q

What is pharmacodynamics

A

The action of the dryg
What does it target and what is the responseW

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285
Q

What is pharmacokinetics

A

Movement of the drug in the body
Where does it go
Consider therapeutic plasma concentration

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286
Q

What are the aims of pharmacology?

A

Right drug
Right dose
RIght onset and duration of action
Supervision and surveillance
Modification and refinement

Do no harm

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287
Q

What are the interacting considerations for drug use?

A

Underlying disease factors
Drug data
Owner needs
Patient factors
Practice
Compliance

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288
Q

What are the different targets for drugs?

A

Receptors
Ion channels
Structural proteins
Enzymes
Carrier molecules
DNA

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289
Q

What type of drug is shown in this dose curve?

A

Agonistic drug

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290
Q

What are the 2 types of agonists?

A

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

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291
Q

What is meant by potency of agonistic drugs?

A

The amount of drug req to produce a 50% of its maximal effects ED50

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292
Q

What is meant by efficacy of an agonistic drug?

A

The maximum therapeutic response that a drug can produce

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293
Q

What is meant by specificity of a drug?

A

Capacity of a drug to cause a particular action in an population

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294
Q

What is meant by selectivity of a drug>

A

Relates to the drugs ability to target only a selective population ie cell/tissue/signalling pathway
In preference to others

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295
Q

What is meant by therapeutic index?

A
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296
Q

What is the action of a non competitive antagonist?

A

Either bind to a different receptor site or block “post binding” chain of events
Ie act downstream of the receptor

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297
Q

What is the action of a competitive antagonist?

A

Shifts the agonist dose-response curve to the right in parallel

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298
Q

What is the action of an antagonist on enzymes?

A

Bind to catalytic site
Inhibits normal reaction therefore decreased production of undesired product

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299
Q

What is the tachyphylaxis?

A

The effect of a drug can decrease when given continuously or repeatedly

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300
Q

What are the causes of tachyphylaxis?

A

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)

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301
Q

Unit conversion for calculating drug doses

A
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302
Q

What is meant by dose of a drug?

A

Amount/volume of medication taken at one time

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303
Q

How can we calculate the volume of a drug needed?

A
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304
Q

What is a 1%w/v solution

A

1g of powder dissolved in 100ml
Or equivalent

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305
Q
A
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306
Q

How are dilution factors used?

A
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307
Q

What is the C1V1 = C2V2 equation?

A
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308
Q

How are drip rates calculated?

A
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309
Q

What are the two options of allometric scaling in drug dosing?

A

Surface area
Metabolic rate

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310
Q

What is the prescribing cascade?

A

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

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311
Q

What is step 2 in drug cascade?

A

A suitable vet med authorised in NI with import certificate

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312
Q

What is step 3 in drug cascade use?

A

Veterinary medicine with marketing authorisation valid in GB or NI wide for a diff species or condition
Import certificate required

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313
Q

What is step 4 in the drug cascade use?

A

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

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314
Q

What is step 5 in the drug cascade?

A

Extemporaneous preparation
create a product to use for animals - purity and concentration needs be controlled
bought in
This could include mixing drugs

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315
Q

What is step 6 in the drug cascade?

A

Human medicines authorised outside of the UK

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316
Q

What is the northern Ireland drug cascade?

A
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317
Q

Dx

A

Diagnosis

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318
Q

Px

A

prescription

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319
Q

Tx

A

Treatment

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320
Q

AE

A

Adverse event

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321
Q

AR

A

Adverse reaction

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322
Q

SAR

A

Suspected adverse reaction

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323
Q

SQP

A

Suitably qualified problem

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324
Q

RQP

A

Registered Qualified person

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325
Q

VMD

A

Veterinary medicines directorate

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326
Q

NOAH

A

National office of animal health

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327
Q

COPC

A

RCVS code of professional conduct

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328
Q

CD

A

Controlled drugs

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329
Q

POM-V

A

Prescription only medicine veterinary

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330
Q

POM-VPS

A

Prescription only medicine veterinarian/pharmacist/SQP

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331
Q

NFA-VPS

A

Non food animals VPS

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332
Q

AVM-GSL

A

Authorised veterinary medicine general sale list

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333
Q

Define veterinary prescription

A
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334
Q

What are the 2 classifications of medicines available on veterinary prescription?

A

POM-V
POM-VPS

POM-V medicines must have a prescription from a veterinary surgeon

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335
Q

Who can prescribe POM-VPS medicine?

A

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

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336
Q

How should a prescription be written?

A
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337
Q

What added points should there be on a prescription?

A
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338
Q

What are the five schedules of controlled drugs under the misuse of drugs regulations 2001?

A
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339
Q

What is the validity of CD prescriptions?

A

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

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340
Q

Single prescriptions with multiple dispenses are not allowed for CDs in Schedules _________ however an instalment prescription can be used if required

A

Schedules 2 and 3

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341
Q

How are instalment prescriptions written?

A

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

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342
Q

When do further instalments need to dispensed in CDs?

A

for schedule 2,3 and 4 CDs the instalments do not need to be dispensed in the first 28 days

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343
Q

What is the under care guidance for RCVS?

A

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

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344
Q

When must a physical examination be carried out before prescribing POM-Vs?

A
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345
Q

Define clinical assessment

A

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

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346
Q

How should prescriptions be noted in clinical records?

A

Name and amount
dosage
Admin instructions
Any accessory warnings

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347
Q

What are the health and safety aspects of prescribing?

A
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348
Q

How should Px misuse be reported?

A

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

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349
Q

What is an adverse event?

A

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

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350
Q

What are the types of AE?

A

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

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351
Q

SLEE

A

Suspected lack of expected efficacy

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352
Q

Define adverse reaction

A

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

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353
Q

When to report an AE?

A

After using an authorised VM
Following off label use
Using a human product in animals
After using a compounded preparation
Using an imported product

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354
Q

How should AEs be reported?

A

Record what happened in as much detail as possible
Report the event electronically to the VMD within 15 calendar days

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355
Q

PSUR

A

Periodic safety update report

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356
Q

What is the Misuse of drugs act 1971

A

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.

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357
Q

What is the misuse of drugs regulations 2001?

A

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

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358
Q

What are the 5 schedules of CDs?

A

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

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359
Q

Drug Schedule examples

A
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360
Q

How are controlled drugs procured?

A

Details of drugs requested and supplier
RCVS number

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361
Q

How are schedule 2 drugs kept?

A

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

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362
Q

Who can a prescribe a CD?

A
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363
Q

How should controlled drugs be disposed of?

A

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

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364
Q

Who regulates prescribing veterinary drugs and why?

A
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365
Q

How is regulation of veterinary drugs achieved?

A

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

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366
Q

What are the drug distribution classifications?

A
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367
Q

What is a suitably qualified person?

A
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368
Q

What is POM-V drugs?

A

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

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369
Q

What medicines are classed as POM-V

A

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

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370
Q

What is a POM-VPS

A

clinical exam is not required

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371
Q

What is NFA- VPS

A

only for non food animals
limits the effect of endemic diseases

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372
Q

SEAS

A

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

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373
Q

Controlled drugs

A
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374
Q

Specified feed additives

A
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375
Q

Define prescribing

A

Any prescription for a veterinary medicinal product issued by a professional person qualified to do so in accordance with applicable national law

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376
Q

How is the supply process of medications checked and ensured?

A
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377
Q

How are records, storage and disposal of drugs regulated?

A
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378
Q

What are the determinants of a dosage regimen?

A

Activity and toxicity
Pharmacokinetics
Clinical factors
Other factors - dosage form, route of administration

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379
Q

What factors of pharmacokinetics should be considered?

A

Dose - potency and efficacy
Onset - absorption and distribution
Loading dose - Vd
Maintenance dose - clearance
Time to steady state- Half life

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380
Q

What influences dosage?

A

The potency of the drug - partial agonist vs full agonist
Bioavailability and first-pass metabolism
Absorption- drug needs to cross the membrane
Distribution

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381
Q

Most drugs are lipo_____ to pass the plasma membrane

A

Lipophilic

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382
Q

What are the factors that affect onset of activity of a drug?

A

Time to reach the maximum (Tmax)

Route of administration
Chemical structure and formulation - pH of location
Clinical situations

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383
Q

How can orally adminstrated drugs affect the onset of action?

A

Polypharmacy
Gut content
Splanchnic blood flow

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384
Q

How can clinical situations affect onset of action of a drug?

A

Pathology
Tissue blood perfusion
Changes in pH
States of shock

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385
Q

What is meant by life of a drug?

A

Administration
Absorption and distribution
Elimination

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386
Q

What is loading dose?

A

Enables therapeutic concentrations to be reached sooner
Principally determined by Vd

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387
Q

What is maintenance dose?

A

Principally determined by clearance

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388
Q

When is steady state achieved?

A

Within 5 half lives

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388
Q

What is the calculation for loading dose?

A
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389
Q

How can steady state be maintained?

A

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

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390
Q

What are the 2 types of saturation with multiple dosing?

A

1, Normal kinetics
2, saturation kinetics

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391
Q

What are normal kinetics of multiple dosing drugs?

A

Plasma concentration increase proportionally with dose

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392
Q

What is saturation kinetics of multiple doseing drugs?

A

If dose is increased then disproportionate increase in steady-state concentrations
Necessitates smaller dose increments

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393
Q

What is plasma protein binding and how does it afffect drug action?

A

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

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394
Q

What factors affect drug absorption?

A

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

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395
Q

What factors affect drug distribution?

A

Inc adipose tissue increases Vd for lipid soluble drugs
High water body content increases vd for water soluble drugs

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396
Q

What factors affect drug metabolism?

A
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397
Q

What are polymorphisms in relation to drugs and pharmacology?

A

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.

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398
Q

What factors affect the excretion of drugs?

A
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399
Q

How does the neonate and paedriatric patient alter pharmacokinetics?

A

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

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400
Q

What alterations need to be made to neonate drugs?

A

Absorption is variable
Plasma level affected therefore alterations to dose and dose frequency
Possible lower metabolic clearance
Possible lower excretion clearance

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401
Q

How does the geriatric patient alter pharmacokinetics?

A

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)

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402
Q

How should drugs be altered for geriatric patients?

A

Reduced bioavailability lowers Cmax Later Tmax
Affects plasma level- dose and dosing frequency
Little change in metabolic clearance
Lower excretion clearance

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403
Q

How do pharmacokinetics change for chronic cardiovascular disease?

A

decreased metnation- inc effects of sedatives
Decreased blood flow = lower clearance for highly cleared drugs eg anaesthetics

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404
Q

How do pharmacokinetics change for renal disease?

A

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

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405
Q

How do PK change for liver disease?

A

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

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406
Q

How does PK change for respiratory disease?

A

Altered serum pH and protein binding

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407
Q

How does disease affect dosing regimen of drugs?

A
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408
Q

What is the therapeutic index of drugs?

A
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409
Q

What drugs have a high therapeutic index?

A
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410
Q

What drugs have a low therapeutic index?

A
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411
Q

Drugs with a ____ therapeutic index used in chronic therapy may require therapeutic monitoring for altered physiological states

A

Low

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412
Q

How is therapeutic monitoring of drugs carried out?

A
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413
Q

What are the routes at which drugs can be eliminated? PK

A

Urine
feaces
Milk and sweat
Expired air

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414
Q

Pharmacokinetics of a drug

A

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

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415
Q

What is the onset of action of a drug?

A

The time taken for the drug to become effective

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416
Q

What is the Cmax?

A

The concentration max which is the peak concentration
This needs to be below the toxic levels

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417
Q

What affects drug absorption?

A

IV bolus = instant
Infusion= zero order
Oral or IM= inc slowly and then decline

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418
Q

What is the termination of action?

A

When elimination of drug brings concentration below the minimal effective concentration

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419
Q

What is the elimination rate?

A

The amount of parent drug eliminated from the body per unit of time

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420
Q

How does elimination of a drug occur?

A

Metabolites then excreted
Direct excretion via the kidneys
Hepatobiliary system

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421
Q

What are the principles of drug metabolism?

A

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

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422
Q

What is the role of CYP450?

A

Cytochrome P450 (CYP) is a hemeprotein that plays a key role in the metabolism of drugs and other xenobiotics

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423
Q

Explain drug renal excretion

A

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

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424
Q

What transporters are found in the proximal tubule?

A

OATs and OCTs

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425
Q

If a drug is lipophilic what will be the action in the distal tubule of the kindey?

A

Lipophilic drugs will be reabsorbed

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426
Q

Drug clearance

A

Measure the efficiency of drug elimination

The volume of blood/plasma cleared of a parent drug per unit time

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427
Q

How is drug clearance calculated?

A
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428
Q

Bioavailability?

A

Measure of extent of absorption from administration site to measurement site

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429
Q

How is the bioavailability of a drug calculated?

A
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430
Q

Volume of distribution of a drug?

A

The volume into which a drug appears to be distrubted with a concentration equal to that in the plasma

Vd is a reversible process

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431
Q

What affects Vd of a drug?

A

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

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432
Q

What is meant by a half life of a drug?

A

The time taken for the plasma concentration of the drug to halve

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433
Q

what are the potential drug-drug interactions?

A

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

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434
Q

Drug - drug interactions

A

Altered pharmacological response to one drug caused by the presence of a second drug

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435
Q

What are the potential outcomes of drug to drug interactions?

A

Enhanced, inhibited or has new effects or no change at all
Summation
Potentiation
Synergism

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436
Q

Summation Pk

A

The combined effect of two drugs produced a result that equals the sum of the individual effects of each agent

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437
Q

Potentiation pK

A

When a drug on its own does not have an effect but may affect/be affected in combination with another drug

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438
Q

Synergism

A

Drug combinations produce a therapeutic or toxic effect greater than the sum of each drug’s action

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439
Q

What are the mechanisms of drug interactions? Pharmaceutical?

A

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

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440
Q

What pharmokinetic drug interactions can occur?

A
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441
Q

How can pharmacodynamic interactions of drugs occur?

A

Additive
Synergistic
Negation

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442
Q

Define ADE

A

Unintended or noxious response to a drug that occurs within a reasonable time frame following administration

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443
Q

What are the types of adverse events?

A
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444
Q

How is pain caused?

A

Results form the interplay of facilitatory and inhibitory pathways throughout the peripheral and central nervous systems

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445
Q

What is the role of maladaptive pain?

A

Represents malfunction of neurological transmission and serves no physiological purposehat

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446
Q

What is the role of Adaptive pain?

A

Altering behaviour to avoid damage or minimise further damage

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447
Q

How can pain be assessed?

A

TPR & pain assessment
Treat pain and reassess

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448
Q

What are the 3 different signs of pain?

A

Clinical
Biochemical
Behavioural

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449
Q

What are the different pain assessment tools?

A

Physiological measurements
SDS, NRS, VAS
DIVAS
Composite scales
Pain faces
Acute vs Chronic pain
QoL scales
Analgesiometry and accelerometers
Gait analysis
Pressure sensitive walkways

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450
Q

What are the challenges of pain scoring?

A

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

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451
Q

What are the steps to creating a pay scale?

A

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

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452
Q

What is being assessed in grimace scales?

A

. Ear Changes : fold, curl and angle forwards or outwards, pointed shape
2. Orbital Tightening: narrowing of the orbital area,partial or complete eye closure orsqueezing
3. Nose/Cheek Flattening: with eventual absence of thecrease between the cheek and whisker pads
4. Whisker Change:move forward away from face

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453
Q

Ear positions

A
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454
Q

Orbital tightening

A
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455
Q

Muzzle tension

A
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456
Q

What is evaluated in cattle for pain?

A
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457
Q

Head position

A
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458
Q

How can pain be assessed in pigs?

A

Ear position (held backwards= pain )

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459
Q

How can pain be assessed in horses ears?

A

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
Q

How can pain be assessed in the eyes of horses?

A

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
Q

What can be assessed with equine nostrils when in pain?

A

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
Q

What can be assessed in equine face muscles to determine pain?

A

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
Q

What can be assessed in the equine muzzle for pain?

A

Increased tonus of the lips and tension of the chin during pain stimuli results in a more edges shape of the muzzle

464
Q

Equine pain scale

A
465
Q

What are the most common signs of pain in horses?

A

Asymmetrical/low ears or ears held stiffly backwards
Angled eye/tension above the eye area and orbital tightening
Withdrawn and tense stareNostrils – square-like/strainedTension of the muzzle/strained mouth and pronounced chin
Tension of the mimic muscles/chewing muscles

466
Q

How can acute pain be prevented from becoming chronic?

A

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
Q

What is the pathway of NSAIDs

A

The COX enzymes are the targets for NSAIDs.
NSAIDs also target descending pain pathways PAG+ NRM

468
Q

What are the common NSAIDs for equids?

A

Phenylbutazone
Flunixin meglumine
Meloxicam

469
Q

What are the common NSAIDS used in cattle?

A

Meloxicam
Ketoprofen

Cattle and small ruminants should receive NSAIDs for castration, disbudding and assisted calving

470
Q

When is the use of NSAIDs contraindicated?

A

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
Q

Suggested protocol for monitoring dogs on long term NSAIDs

A
472
Q

What is Grapiprant?

A

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
Q

Properties of paracetamol

A

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
Q

Properties of opiods?

A

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
Q

What are the properties of local anaesthetics?

A

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
Q

When are local anaesthetics used?

A

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
Q

What are the properties of alpha 2 agonists?

A

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
Q

What are the effects of alpha 2 agonists?

A

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
Q

What are the properties of ketamine and NMDA antagonists?

A

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
Q

How does ketamine work?

A

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
Q

How is chronic pain different to acute pain?

A

is multifactorial (posture, mood, movement - scales reflect this)

482
Q

What pain scales can be used to determine chronic pain?

A

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
Q

What are the treatment options for dogs and cats with chronic pain?

A
484
Q

What adjunctive therapies can be used to manage chronic pain?

A

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
Q

What are the effects of Mesenchymal Stem cells?

A

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
Q

What are the uses for cannabidiol in chronic pain?

A

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
Q

What does each category of HHHHHMM mean for a dog approaching its EoL?

A

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
Q

What is the mechanism of action for local anaesthetics?

A

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
Q

Where are LAs broken down and why?

A

LAs are amides or esters
Amide versions will be broken down by liver
Esters will be broken down by plasma cholinesterases

490
Q

What are the rapid onset LAs

A

Procaine- cattle
Lidocaine - all species
Proparacaine - eyedrops

491
Q

What are the slow onset LAs?

A

Bupivacaine- SA
Mepivacaine- Equine

492
Q

How do slow onset and rapid onset LAs compare?

A

Slow onset LAs are often more potent and more toxic

493
Q

What is shown?

A

Preinscional block

494
Q

What is shown

A

Intra testicular block

495
Q

What is shown?

A

Direct infilitration of the mesovarium ligament (splash block on ovaries also works)

496
Q

What is shown?

A

Retro bulbar anaesthesia

497
Q

What is shown?

A

Infiltration of LA following enucleation and suture closure

498
Q

What is shown?

A

Lumbosacral and sacrococcygeal epidurals

499
Q

What are the indications for lumbosacral and sacrococcygeal epidurals?

A

: 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
Q

What is shown

A

Rostral maxillary dental block
Infraorbital
Provides analgesia to soft tissue of rostral maxillaru

501
Q

What nerves can be seen?

A
502
Q

What is shown?

A

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
Q

What can be seen?

A

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
Q

What is shown?

A

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
Q
A

Bier block in cattle

506
Q

What is shown and what are the properties?

A

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
Q

What block is shown?

A

Femoral and sciatic nerve block
PNBs offer and alternative to epidural with reduced risk of urine retentiona and reduced postoperative opoid consumption

508
Q

What nerves can be seen?

A

Femoral artery (arrow) and femoral nerve (solid arrow).

509
Q

What are the uses other than nerve blocks do LAs have?

A

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
Q

What is LA toxicity and how is it prevented and treated?

A

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
Q

How can anaesthesia be administered?

A

Intramuscular
Intravenous
Subcutaneous
Inhalation
Across the mucous membrane

512
Q

How do anaesthetics work?

A

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
Q

What are the properties of propofol?

A

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
Q

What are the pharmokinetic properties of propofol?

A

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
Q

What are the properties of alfaxalone?

A

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
Q

What are the pharmokinetics of alfaxalone?

A

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
Q

What are the properties of ketamine?

A

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
Q

What are the uses of volatile agents in anaesthesia?

A

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
Q

How do volatile agents work in anaesthesia?

A

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
Q

What are the less commonly used induction agents?

A

Zoletil’ (zolazepam & tiletamine)
MS-222
Thiopentone
‘Ketofol’ (ketamine + propofol)
Etomidate

521
Q

CEPSAF

A

Confidential enquiry into perioperative small animal facilities

522
Q

What has been shown through CEPSAF?

A

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
Q

What are the risk factors associated with recovery from anaesthesia?

A

ASA category
Breed
Age
Weight
Length of anaesthesia
Type of surgery
Drugs given
Temperature
Species
Vigilance/ experience of staff
Available equipment

524
Q

What should be the properties of a recovery area for post anaesthesia?

A

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
Q

What emergency equipment may be required post anaesthesia?

A

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
Q

How should recovery monitoring charts be used post op?

A

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
Q

What is the end procedure sequence of events for anaesthesia surgery?

A

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
Q

How is disconnection from anaesthesia achieved post op?

A

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
Q

When are dogs extubated?

A

gag-reflex returns; indicated by swallowing, tongue flicking (same in most species i.e. horses, ruminants, pigs etc.)

530
Q

When are cats extubated?

A

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
Q

When are brachycephalic breeds extubated?

A

BOAS
Extubate on inspiration

532
Q

How should patients be kept post extubation?

A

patients head and neck should be extended ant the tongue gently pulled forward to maintain patent airway

533
Q

What should be monitored post extubation?

A

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
Q

How long post op should patients be monitored?

A

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
Q

What are the common causes of upper airway obstruction?

A

Loss of pharyngeal muscle tone
Regurgitation or vomiting
Laryngospasm or laryngeal oedema

536
Q

What are the signs of airway obstruction post op?

A

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
Q

How should airway obstruction be treated?

A

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
Q

What is being assessed of circulation post op?

A

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
Q

What is being assessed of temperature post op?

A

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
Q

When is analgesia given post op?

A

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
Q

What is the role of discharge instructions?

A

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
Q

What are the anaesthetic mortality rates for equines?

A

1% in elective cases
2% in non colic emergency cases
5.4% in emergency colic surgery cases

543
Q

Why do horses die during or after anaesthesia?

A

Fractures in recovery (highest mortality)
Post anaesthetic myopathy
Neuropathies and spinal cord malacia
Intraoperative cardiac arrest
Respiratory obstruction

544
Q

What are the risk factors for equine anaesthesia?

A

Increasing ASA grade
Increasing age and foals
Surgery type and position
Duration
Time of day, OOH provision
Agents used (premed/TIVA)
Recovery quality

545
Q

What is standing sedation and how is it used in horses?

A

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
Q

What is the night before preparation for equine GA?

A

Admit the night before
Complete physical exam - murmurs?
Blood samle
Starve
Remove shoes
Ensure horse is clean

547
Q

What is the morning or preparation for equine GA

A

IV cannula always
Flush out mouth
Tail bandage/plait
Clip if possible
Weigh
Make anaesthetic plan
Pre medicate the horse

548
Q

How should we prep for equine Anaesthesia?

A

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
Q

What are the types of breathing circuit for equines?

A

Rebreathing circuit- CIRCLE
Fresh gas flow rate?
Start 6-8L/min
After 15min reduce to 3-4L/min

550
Q

What premedication is given to horses pre op?

A

Acepromazine

551
Q

What is the role of the equine premed acepromazine?

A

Anxiolytic
Reduces catecholamines (dec cardiac arrest)
Reduced anaesthetic gase requirement
Improves recoveries
Improved tissue perfusion through vasodilation

552
Q

What are the risks with Acepromazine?

A

Penile prolapse
Hypovalaemia

553
Q

When should acepromazine be given to horses?

A

IM 40 mins before sedation
IV 20 mins before sedation

554
Q

What are the premedication options for horses?

A

Alpha 2 agonists
Opiods

555
Q

What is the role of alpha 2 agonists in horses premedication?

A

Sedation for induction
Analgesia
Vasoconstriction and bradycardia

556
Q

What is the role of opioids as a premed in horses?

A

Analgesia
Improved sedation quality
Respiratory depression?

557
Q

What are the typical equine premeds?

A

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
Q

What are the signs that a horse is ready for induction?

A

Head down, wide based stance
Horses are insensible to surroundings

559
Q

What is the induction agent for equines?

A

IV ketamine
A benzodiazepene (midazolam can be combined with the ketamine)
Occasionally guaifenesin IV can be used instead of an alpha 2 agonist

560
Q

Example anaesthesia protocol for equine

A
561
Q

What are the steps following premed for anaesthesia of horses?

A

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
Q

What can anaesthesia be substituted for in equines?

A

Can supplement anaesthesia with injectables for maintaining plane of anaesthesia (PIVA) e.g. lidocaine

563
Q

What is the role of volatile anaesthetic agent in horses?

A

Maintenance of anaesthesia

564
Q

What is the normal volatile anaesthetic agent used in horses?

A

Isoflurane or sevoflurane (only iso is licensed)

565
Q

What are the issues with volatile anaesthetic agent in horses?

A

Hypotension
Need lowest dose that ensures anaesthesia

566
Q

What is the starting concentration for volatile anaesthetic agent in horses?

A
567
Q

What can be assessed to monitor anaesthetic agent of horses?

A

Palpating pulses
Reflexes and eye signs
Muscle tone

Machine
Multiparameter
Pulse oximeter
Blood gases

568
Q

TIVA

A

Total intravenous anaesthesia (alternative to volatile agent)

569
Q

How can TIVA be achieved?

A

Top up bolus injections( ketamine 0.5mg/kg)
Continuous rate infusions (triple drip in equine anaesthesia - useful for field work)

570
Q

What are the benefits of TIVA?

A

Produces a lower anaesthesia stress response compared with inhalation agents and is therefore physiologically superior method

571
Q

What is triple drip anaesthesia?

A
572
Q

PIVA

A

Partial intravenous anaesthesia

573
Q

What is used for PIVA?

A

Reduces amount of inhalant gas required

574
Q

What problems are seen with equines and anaesthesia?

A

Problems we see
Hypotension
Hypoxaemia
Hypercapnia
Bradycardia
Tachycardia
Neuropathy
Eye problems

575
Q

How can anaesthesia induced hypotension in horses be mitigated?

A

Use positive inotrope
Reduce isoflurane
Use PIVA
Increase fluids

<70mmHg using invasive arterial monitoring

576
Q

Hypotension of equines on anaesthesia can lead to ________ on recovery

A

myopathy

577
Q

What are the properties of spinal cord malacia in anaesthesia? Equine

A

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
Q

What is spinal cord malacia?

A

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
Q

What is hypoxaemia and how does it occur in equines on anaesthesia?

A

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
Q

How is hypoxaemia recognised and treated in horses on anaesthesia?

A

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
Q

What is hypercapnia and how does it occur in horses on anaesthesia?

A

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
Q

How is hypocapnia treated for horses on anaesthesia?

A

Reduce the volatile agent (isoflurane)
Instigate ventilation

583
Q

What are the considerations for horses with bradycardia induced by anaesthesia?

A

Breed/fitness of horse and their HR prior to anaesthesia
If blood pressure or oxygen delivery is compromised too - you need to act

584
Q

How is anaesthesia induced bradycardia treated in horses?

A

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
Q

What are the potential causes for anaesthesia induced hypotension in horses?

A

Volatile agednt
Vagal tone
Opiod
Alpha 2 agonist
Toxaemia
Hypoxia

586
Q

What are the considerations for horses with tachycardia induced by anaesthesia?

A

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
Q

How is anaesthesia induced tachycardia treated in horses?

A

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
Q

What are the causes of anaesthesia induced tachycardia in horses?

A

Sympathetic stimulation (nociception is likely)
CO2 acid base disturbance
Drug reaction
Cardiac issue
Hypotension

589
Q

What are the causes of equine anaesthesia induced neuropathy and what will be the outcome?

A

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
Q

What are the causes of equine anaesthesia induced eye problems and how can they be prevented?

A

Usually when a horse has been in lateral recumbency
Must protect lowermost eye with padding
Lubrication for eye

591
Q

How is recovery of a horse carried out following anaesthesia?

A

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
Q

What is the optimum recovery environment for an equine post anaesthesia?

A

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
Q

How is sedation given in anaesthesia recovery of a horse?

A

Sedation  low dose alpha 2 agonists. Given once in recovery and breathing spontaneously (romifidine) or once signs of reduced anaesthestic depth occur (xylazine)

594
Q

What are the complications in recovery for equines post anaesthesia?

A

Upper airway obstruction
Laryngeal obstruction
Nasal oedema

595
Q

What are the signs of upper airway obstruction in equines post op?

A

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
Q

How can laryngela obstruction in equines post op be treated?

A

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
Q

What is the treatment for nasal oedema in equines post op?

A

Common usually resolves as horse stands
Use nasopharyngeal tubes, or phenylephrine or both
Can recover horse to standing with ET tube in place

598
Q

Tree of life

A
599
Q

What can cause bradycardia in surgery and how can this be detected?

A

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
Q

How can bradycardia be treated?

A

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
Q

What can cause tachycardia in surgery and how is this detected?

A

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
Q

How is tachycardia during surgery approached?

A

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
Q

What are the causes of ventricular ectopic beats in surgery and how can they be detected?

A

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
Q

How are ventricular ectopic beats in surgery approached?

A

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
Q

How is hypotension detected and treated in surgery?

A

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
Q

feline hypotension treatment

A
607
Q

What are the causes of hypercapnia in surgery?

A

Increased CO2
depth of anaesthesia
hypoventilation
pyrexia
rebreathing
fresh gas flow rates too low
exhaustion of soda lime
changes in dead space

608
Q

What are the causes of hypocapnia in surgery?

A

Low CO2
Disconnection (check breathing system)
Mis-intubation ??

609
Q

Which species has lower CO2 readings and why?

A

Cats on non-rebreathing systems (T piece or mini Lack)
Often lower ET CO2 readings

610
Q

What are the causes of decreasing CO2?

A

Obstruction
Hyperventilation
Circulatory failure
Hypotension
Cardiac arrest

611
Q

What can be seen in the image?

A

Failing ET CO2 values
In this case due to partial airway obstruction but could be Circ failure, hypervent, hypotens. CA

612
Q

Troubleshooting ventilation with Failing CO2 readings

A
613
Q

What can be seen in the image?

A

Cardiogenic oscillations

614
Q

What is the treatment path for hypoxaemia?

A

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
Q

What are the common recovery issues?

A

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
Q

Troubleshooting dysphoria

A
617
Q

Trouble shooting prolonged recovery?

A
618
Q

What are the properties of propofol?

A

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
Q

What are the pharmokinetics of propofol?

A

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
Q

What are the pharmacodynamics of propofol?

A

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
Q

What are the properties of alfaxalone?

A

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
Q

What are the pharmacodynamics of alfaxalone?

A

Pharmacodynamics of alfaxalone:
Anaesthesia, decreased CMRO2,
Haemodynamic effects minimal
- Stable cardiac output- Stable heart rate- Stable MAP, SVR, CVP

623
Q

What are the pharmacokinetics of alfaxalone?

A

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
Q

How is alfaxalone or propofol used?

A

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
Q

What is the role of volatile agents?

A

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
Q

What is the determinant of patient safety during anaesthesia?

A

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
Q

What are the ASA statuses?

A

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
Q

ASA status chart

A
629
Q

How should anaesthesia be approached in sick patients ASA III-IV?

A

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
Q

What should be carried out in preoperative patient evaluation of sick patients?

A

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
Q

What should be taken into account for the perioperative preparation for ASA III-IV

A

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
Q

What premedication should be given to ASA III-IV patients? Anaesthesia

A

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
Q

How should induction of ASA III-IV dogs and cats be carried out?

A

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
Q

What are the monitoring protocols post op for ASA III-IV?

A

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
Q

What is the approach to Anaesthesia of sick horses EG with colic?

A

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
Q

What is meant by antibiotic stewardship?

A

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
Q

Critically important antibiotics

A
638
Q

Decision making

A
639
Q

How can misuse of antibiotics be avoided?

A

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
Q

How can we avoid the need for antimicrobials?

A

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
Q

How can we avoid inappropriate use of antimicrobials?

A

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
Q

When are antibacterials indicated?

A

Where cytology and or culture is positive

643
Q

How can we ensure that we chose the correct antimicrobial

A

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
Q

How can we monitor antimicrobial sensitivity?

A

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
Q

Antimicrobial sensitivity flow chart

A
646
Q

How can we minimise use of antibiotics?

A

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
Q

What is the importance of recording and justifying deviations from antimicrobial protocols?

A

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
Q

How is the suspected failure of antimicrobial treatments reported?

A

Report through the suspected adverse reaction surveillance scheme (SARSS)

This may be the first indication of resistance

649
Q

SARSS

A

Suspected adverse reaction Surveillance Scheme

650
Q

What is the In practice Protect scheme plan

A

Practice policy based on what is expected and then what is sensible to use and what the practice will use

651
Q

Overview for antimicrobial selection

A
652
Q

What is the mechanism of action of antibiotics?

A

Narrow spectrum or Broad spectrum

653
Q

What is a narrow spectrum AB?

A

Targets a narrow group of bacteria (either gram pos or neg

654
Q

What are Broad spectrum ABs?

A

Targets the Gram pos and gram neg bacteria

655
Q

What are bacteriocidal ABs?

A

Kills the organism
Penecillins Cepahlosporins

656
Q

What are bacteriostatic ABs?

A

Drugs that temporarily inhibit the growth of an organism (reversible if removed)
Examples are tetracyclines and chloramphenicol

657
Q

How should we determine concentration of ABs?

A
658
Q

AB concentrations

A
659
Q

What are the target of actions of antibiotics on bacteria?

A
660
Q

How do ABs target the cell wall?

A

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
Q

What are the Beta lactams?

A

Penicillins
Cephalosporins

662
Q

How do ABs inhibit protein synthesis?

A

Target the ribosome so that proteins cannot be formed

663
Q

Summary of ribosome binding antibiotics

A
664
Q

Other groups of AB targets?

A
665
Q

What are the properties and applications of cationic antimicrobial peptides

A

Topical application
interact with membranes and disrupt
Product licensed for dermatology
Lipids/charge properties of host vs bacterial membrane allow for distinction

666
Q

On top of spectrum of ABs what are the other categories

A

Aerobic or anaerobic drugs

667
Q

What are the considerations for effect of ABs?

A
668
Q

Groups of antibiotics and relative activities

A
669
Q

What are the reasons for antibiotic therapy failure?

A

Unjustified therapy
poor selection
Wrong dose
Suppressed host response
Resistance

670
Q

What is C&AST

A

Culture and antibiotic sensitivity testing

671
Q

What are the 2 main approaches for looking at AMR?

A

Disc diffusion - antibiotic gradient from disc (inhibition zone)
MIC determination using liquid cultures in wells

672
Q

MIC

A

Minimum inhibitory concentration

673
Q

What is resistance of AB defined by?

A

Clinical breakpoint values
There are interpretive criteria with clinical breakpoints for MIC values for diff bacteria

674
Q

How are the clinical break points interpreted?

A

Break point is determined and then anything above is resistant and everything below is sensitive

675
Q

What is being shown about resistance in the image? AB

A

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
Q

What is meant by intrinsic resistance to AB?

A

An innate ability to resist activity of a particular antimicrobial agent through inherent structural or functional characteristics which allow tolerance of the drug

677
Q

What is an example of intrinsic resistance to AB?

A

Lacks the target or altered target

678
Q

What is acquired resistance to ABs?

A

When a microorganism obtains the ability to resist the activity of a drug. Can be a mutation or new gene acquisition

679
Q

How might a bacteria have acquired resistance to a drug?

A

Alteration drug
Alteration of target
bypass mechanism
Efflux systems

680
Q

What bacteria have intrinsic resistance to Vancomycin?

A

Gram negative bacteria as the AB cannot penetrate the outer membrane of the bacteria

681
Q

Which genera of bacteria are resistant to cephalosporins and why?

A

Enterococci as the AB has a low affinity for penicillin binding proteins

682
Q

Which antibiotics cannot be used to treat mycoplasmas and why?

A

Mycoplasmas lack a cell wall so a cell wall targeting AB will not work

683
Q

What are the mechanisms for acquired AB resistance?

A

Gene mutations - change binding site
Gene acquistiion
Coresistance

684
Q

How does Gene acquisition lead to acquired AB resistance?

A

Mechanism transfer, Conjugations of plasmids or other routes
Risks transfer between potential pathogens and commensals

685
Q

How does co resistance lead to acquired resistance?

A

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
Q

Acquired resistances

A
687
Q

What is an efflux system in acquired AB resistance?

A

The drug is pumped out of the bacteria maintaining very low concentrations reducing the efficacy

688
Q

Mutation and modification of targets for ABs

A
689
Q

What is degradation and how does this lead to acquired resistance?

A

Degrades the AB
most common with B-lactamases

690
Q

Which drug is efflux most common for AB?

A

Tetracyclines

691
Q

Which AB is modification in acquired resistance most likely to occur with?

A

acetylation of aminoglycosides

691
Q

How does resistance occur to Beta lactams?

A

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
Q

Common resistance mechanisms to ABs

A
692
Q

What factors increase the risk of selection of ABs>

A

Underdosing
Length of selective level
Presence of resistant bacteria to select

693
Q

MSC

A

Minimum selective concentration

694
Q

MIC

A

Minimum inhibitory concentration

695
Q

MDR?

A

Multi drug resistance strains

Non susceptible to > agent in >3 clinical antimicrobial categories

696
Q

XDR?

A

Extensive drug resistance
Non susceptible to >1 agent in all but >2 clinical Ab categories

697
Q

PDR?

A

Pandrug resistance
Non susceptible to all antimicrobial agents listed

698
Q

What is meant by good antibiotic stewardship?

A
699
Q

Biosecurity?

A

Stopping infectious agents coming onto site
Management movement of animals and materials into hospitals, farms, clinics

700
Q

What is the role of disinfection?

A

Reduce infection
Spread on surfaces and fomites
Effective management of infective material
Effective cleaning

701
Q

Relative resistance to disinfection

A
702
Q

What are the risks with disinfectants?

A

Generalised action
Therefore damaging so self harm or patient harm
Some toxic so tainting a risk
Hypersensitivity

703
Q

What are the groups of disinfectants?

A

Alcohols
Alkalis
Aldehydes
Oxidising agents
Phenols
QACs

704
Q

What considerations should be taken with an animal with parvoviris to prevent spread?

A
  • 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
Q

Example infection control strategy - faecal oral route

A
706
Q

Example infection control strategy- contacts?

A
707
Q

Examples of interventions strategies- fomites

A
708
Q

Examples of interventiosn strategies - farm facilities

A
709
Q

How would we plan an intervention strategy for streptococcus equi?

A
710
Q

How would a disinfection strategy be carried out for salmonella?

A
711
Q

What is parvovirus?

A

Highly contagious - acute GI disease
Persistent as non enveloped virus
Expelled contaminated material (organic matter

712
Q

What is the management and biosecurity for parvovirus?

A
713
Q

Summary of disinfectants

A
714
Q

What is pasteurisation?

A

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
Q

What is sterilisation?

A

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
Q

What are the 3 types of autoclave?

A

gravity displacement autoclave and the high-speed prevacuum sterilizer.

717
Q

What autoclave can be seen?

A

Vacuum assisted sterilisation system

718
Q

What is chemical sterilisation and what are its properties?

A
719
Q

What is gas sterilisation and what are its properties?

A

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
Q

How are surgical instruments prepared ?

A

Clean and check
Pack
Sterilise
Monitor sterilisation
Check out of date supplies

721
Q

Why chose combinations of antibiotics?

A

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
Q

What is meant by synergy in ABs?

A

Where the activity is greater than either of the 2 individually

723
Q

What is meant by additive effect with ABs?

A

Where there is a benefit for treatment but there is no increase of individual acitivity

724
Q

Generally ________ antibiotics act in an additive fashion

A

Bacteriostatic

725
Q

Generally ________ antibiotics act in an synergistic pattern when combined

A

Bacteriocidal

726
Q

Several __________ antibiotics are substantially impaired by simultaneous use of drugs the are _______

A

Several bactericidal antibiotics are substantially impaired by simultaneous use of bacteriostatic drugs (most are ribosomal inhibitors)

This is an example of antagonism

727
Q

What antibiotic is used with Trimethorprim?

A

Sulphonamide
Act on different targets making them more effective - synergistic result

728
Q

Which antibiotic is used with Clavulanic acid?

A

Amoxycillin
Amoxycalv

Breaks down penicillins by breaking fown Beta lactamase inhibitors

729
Q

What should Beta lactams not be combined with?

A

Bacteriostatic drugs

730
Q

What should procaine not be used with?

A

Procain is metabolised to paraaminobenzoic acid which can reduce effectiveness of SULPHONAMIDE treatment

731
Q

What is the issue with using lots of drugs that bind to the same AB target?

A

Reduces efficacy as they compete for the target site

732
Q

What is pleuropneumonia?

A

Mixed infection

733
Q

How is pleuropneumonia used?

A

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
Q

What should be the AB treatment of mastitis?

A

Sometimes there may be combination treatment but cultures will confirm the need

735
Q

What are the potential pathogens for mastitis?

A

Staph aureus- beta lactam R
Strep uberis - beta lactam sen
E coli - gram neg

736
Q

What is a chemotherapeutic agents?

A

A drug used to treat cancer by causing cell death and stopping cells from dividing

737
Q

What are the routes of administration for chemotherapeutic drugs?

A

Oral
By injection
IV infusion
Topical

738
Q

How are chemotherapeutic agents used?

A

Chemo drugs only
Chemotherapeutic drugs as part of a treatment plan eg with radiotherapy

739
Q

What chemotherapeutic drugs do vets use?

A

Cytotoxic drugs such as Vincristine
Doxorubicin
Chlroambucil
Cylophosphamide

740
Q

What are the properties of cytotoxic drugs?

A

Inhibit mitosis and /or damage DNA
Kill rapidly dividing cells
Neoplastic cells
GI tract epithelium
Bone marrow cells

741
Q

What are the targeted approaches that can be used as chemotherapeutic agents?

A

Tyrosine kinase inhibitors
Monoclonal antibodies

742
Q

What are the targets for newer therapies against cancer?

A

Receptors
Signalling pathways
Antigens

743
Q

How can tyrosine kinase inhibitors be used in cancer therapies?

A

For mast cell tumours in dogs

Masitinib
Toceranib

744
Q

How can monoclonal antibodies be used in cancer therapies?

A

Monoclonal antibodies against specific tumour antigens

745
Q

What are the limitations for cytotoxic drug treatments against cancer?

A

Palliative not curavtive
Toxicity limits dose or freq of dose

746
Q

What is the maximum tolerated dose of cytotoxic drugs for cancer treatment?

A

Highest dose with the acceptable side effects

747
Q

What is metronomic chemotherapy?

A

Aims: delay or slow disease progression/ not kill cancer cells
Inhibits angiogenesis
Modulates immune response to cancer cells

748
Q

How do cytotoxic drugs affect the cell cycle?

A

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
Q

What are the common cell cycle phase specific cytotoxic drugs?

A

Vincristine
Vinblasine
Cytrabine

750
Q

What are the common non cell cycle specific cytotoxic drugs?

A

Doxorubicin
Cyclophosphamide
Lomustine
Chlorambucil

751
Q

Class of chemotherapeutic drugs

A
752
Q

What is the mode of action of alkylating agents (Chemo)?

A

Alkyl group binds to and cross links DNA

753
Q

What is the mode of action of plant alkaloids (chemo)

A

Bind to tubulin in cells and disrupt mitotic spindle

754
Q

What is the role of anti metabolite cytotoxic drugs?

A

Inhibit use of cell metabolites used in growth and cell division

755
Q

What is the role of antitumour antibiotics ?

A

Inhibit topoisomerase -II causing the breakage of DNA and cell death

Forms free radicals

756
Q

What is the mode of action of Platinum analog cytotoxic drugs?

A

Bind platinum to DNA causing cross linkage and cell death

757
Q

What is the mode of action of Tyrosine kinase inhibitor chemo drugs?

A

Inhibit various TK receptors eg KIT or VEGFR

758
Q

How do vets choose chemotherapeutic agents?

A

Maximising the benefits
Minimising harm

759
Q

How can the benefit of chemo drugs be maximised?

A
760
Q

How can the harm of chemo drugs be minimised?

A
761
Q

What is meant by anaesthesia?

A

Without sensation
General anaesthesia is total lack of sensations
Local anaesthesia relates to lack of sensation in a localised part of the body

762
Q

How does anaesthesia affect nociception?

A

Lack of awareness of painful inputs is caused

763
Q

What is meant by balanced anaesthesia?

A

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
Q

What is required for anaesthesia?

A

Unconsciousness
Narcosis
Tranquilisation
Hypnosis
Analgesia
Muscle relaxation
Immobilisation
Amnesia
Sedation

765
Q

What are the aneasthetic events?

A

Induction
Maintenance
Emergence/ recovery

766
Q

CEPSAF?

A

Confidential enquiry into perioperative small animal fatalities

767
Q

What is the aim of anaesthesia?

A

Normal physiology
Minimal loss of temperature
Minimal pain
GOod organ function
BP maintained
Less cardiovascular depression
Less cerebral hypoxia
Less dysrhythmias

768
Q

What affects the risk of anaesthesia drugs?

A

Patient
Drug pose minimal risk
Procedure
Staff
Emergency or planned
Facilities and equipment

769
Q

What are the important guidelines for anaesthesia use?

A

AVA and RECOVER

770
Q

What are the objectives of clinical audits?

A

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
Q

How long do adult dogs need to fast for?

A

4-6 hrs

772
Q

How long do adult cats need to fast for?

A

3-4 hours

773
Q

How long do kittens and puppies need to fast for?

A

1-2 hours

774
Q

How long do rabbits need to fast for pre op?

A

NO FASTING

775
Q

What is the challenge with treating endo parasites?

A

Different body systems can be affected by helminths, protozoa and maggots of some flies
Control of these endoparasites is difficult

776
Q

Ectoparasitacides

A

kill External parasites

777
Q

Endoparasitacides

A

Kill internal parasites

778
Q

endectocides

A

Kill internal and external parasits

779
Q

Anthelmintics

A

Used to treat infections of animals with parasitic worms

Flat worms eg Fluke (trematodes)
Tapeworms (cestodes)
Round worms (nematodes)

780
Q

What are the common classes of anthelminthic drugs?

A

Organophosphates
Benzimidazoles
Salicylanilides
Pyrazinoisoquinolones
Sulphonamides
Tetrahydropyrimidines
Imidazothiazoles
Hexahydropyrazine
Macrocyclic lactones

781
Q

What are the targets for anthelmintics?

A

Betatubulin
Nicotinergic
acetylcholine receptor
GABA receptor and glutamate gated chloride channel

782
Q
A
783
Q

What is the action of Benzimidazoles?

A

Bind to Beta tubulin
Inhibit/blockage of polymerisation causing abnormal microtubule formation and disruption intracellular homeostasis and energy metabolism

784
Q

What is the most important pair of antagonistic neurones of locomotion?

A

Excitatory ACh containing neurones
Inhibitory GABA containing neurones

785
Q

What is the mechanism of action of piperazine and macrocyclic lactones?

A

Flaccid paralysis of the worms through increasing GABA and therefore increasing the relaxation

Pip acts on GABA
Macro acts on glutamate

786
Q

What is the mechanism of tetrahydropyrimidines or imidazothiazoles

A

Act on ACh to increase contraction and therefore cause spastic paralysis of the worms

787
Q

What are the classes of anthelmintic drugs for treating nematodes, trematodes and cestodes?

A

Cyclic octadepsinpeptide
Aminoacetonitrile derivatives
Spiroindole

788
Q

What do cyclic octadepdsipeptide act on?

A

Acts on specific classes of transmembrane G protein couples receptors latrophilin receptor class

This causes flaccid paralysis of the pharynx

789
Q

What is the mechanism of action for Aminoacetonitrile derivatives?

A

MPTL -1 receptors , a unique kind of Ach receptor that causes spastic paralysis

790
Q

What is the mechanism of action of spiroindole?

A

Acetylcholine antagonist causing flaccid paralysis and expulsion of parasites

791
Q

Rapid development of resistance to the major anthelmintic classes ?

A
792
Q

Current state of anthelminthic resistance

A
793
Q

Why is ectoparasitic control important?

A

Animal welfare
Economic loss
Vectors of disease
Source of zoonotic infection

794
Q

How can ectoparasites be controlled 2?

A

Chemical and non chemical
Work in conjunction with each other

795
Q

What are the non chemical control related factors of ectoparasite control?

A

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
Q

How can environmental or physical methods of endoparasite control be used?

A

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
Q

Which parasite transmits lyme disease?

A

Ticks
Babesiosis

798
Q

What are the chemical control related factors?

A

Drug action required
Spectrum of activity
Speed of onset required
Duration of action/frequency of reapplication
Contraindications
Safety
Development of resistance

799
Q

What are the actions fo anti ectoparasiticides?

A

Neurotoxins
Insect growth factors
Others (repellants, desiccants and mechanical agents)

800
Q

What are the host factors that affect control of ectoparasites?

A

Species
Age restrictions (lower age for many products)
Suitable mode of application
Meat/milk withdrawal periods

801
Q

Ectoparasite treatment take-home messages

A
802
Q

What are the steps for diagnosis of common ectoparasites?

A

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
Q

Which parasite diagnostic test to select?

A
804
Q

How can we carry out physical identification of the parasite?

A
805
Q

What are the properties of antibody serology?

A

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
Q

What are the properties of sarcoptes IgG serology?

A

Canine
NB potential for Fals pos - takes 1 months to seroconvert
False negatives- occasional cross reaction with antihousedust mite antibodies in environmental atopics

807
Q

What are the properties of flea IgE serology?

A

Detects flea allergy or hypersensitivity not infestation
Detects Type I hypersensitivity but not Type IV

808
Q

Sampling and microscopy for parasites?

A
809
Q

How should you take samples for sheep scab?

A

Psoroptes
Take superficial at leading edge of the lesions

809
Q

How can we use skin scrapings to monitor treatment for demodicosis?

A
810
Q

What is the skin scraping sensitivity to sarcoptes?

A

50% Treatment trial oftern req to thoroughly rule out fleas sarcoptes and cheyletiella

811
Q

Parasite ID?

A
812
Q

Chewing lice?

A
813
Q

Sucking lice

A
814
Q

Surface mites

A
815
Q

What can be seen in the image?

A

Top = psoroptes jpinted pedicel and funnel shaped sucker

Other surface mites= unjointed pedical and cup shape sucker

816
Q

Burrowing mites?

A
817
Q

Define general pathology?

A

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
Q

Define systemic pathology

A

Pathology of organ systems
The study of alterations in specialised organs and tissues

819
Q

Define anatomic pathology

A

Examination of tissues taken during life (biopsy) or after death (necropsy)
Examines nature and extent of disease process

820
Q

Define clinical pathology

A

Examination of blood and other body fluids as well as cells (cytology) during life

821
Q

Define pathology

A

The study of the structural, biochemical and functional changes in cells, tissues and organs that underlie disease

→ An understanding of pathology is fundamental to understandinghow disease occurs and, consequently, how disease can be diagnosed, treated, and prevented

822
Q

Aetiology

A

Cause

823
Q

Pathogenesis

A

mechanisms of disease development

824
Q

Clinical manifestation

A

Functional consequences of molecular and morphologic changes

825
Q

What are internal aetiologies?

A

Aging
Immunologic defects
Genetic defects

826
Q

What are external aetiologies?

A

Agents- physical, chemical or biological
Deficiencies - nutritional, environmental deficits

827
Q

Molecular changes

A

Biochemical alterations in cells or tissues that alter the function

828
Q

Morphologic changes

A

Structural alterations in cells or tissues

829
Q

Inflammation

A

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
Q

What is involved in healing?

A
831
Q

Thrombosis

A

INteraction of the blood coagulation system and platelets to form within a vascular lumen an aggregate of fibrin and platelets

832
Q

Neoplasia

A

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
Q

Metabolic dysfunction

A

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
Q

necrosis

A

Death of cells and tissues in the living aniaml

835
Q

biopsu

A

Removal and examination of a tissue dample from a living animla body for diagnostic purposes

836
Q

Necropsy

A

Methodical examination of the dead animal

837
Q

DiagnosiS

A

Conclusion concerning the nature, cause of name of a disease

838
Q

Lesions

A

Abnormal structural and functional changes that occur in the body

839
Q

Clinical diagnosis

A

Based on data obtained from the case history, clinical signs and physical examination

840
Q

Clinical pathologic diagnosis

A

Based on changes observed in the chemistry of fluids and the haemotology, structure and function of cells collected from the living patient

841
Q

Morphologic diagnosis

A

Also known as lesion diagnosis
Based on the predominant macroscopic and microscopic lesions

842
Q

Aetiologic diagnosis

A

Names the specific cause of the disease

843
Q

Disease diagnosis

A

Stated the common name of the disease

844
Q

What methods are used to reach a diagnosis?

A

Morphology, molecular biology, microbiology, immunology, genetics, informatics…

Morphology is cornerstone of pathology

845
Q

What methods are there to detect morphologic changes>

A

Macroscopic examination
Microscopic examination

Observation by the unaided eye
LIght microscopy and electron microscopu

846
Q

What molecular techniques can be used to reach a diagnosis?

A

Polymerase chain reaction (PCR)
In situ hybridization (ISH)
Genomics (DNA sequencing, DNA microarrays)
Transcriptomics (RNA sequencing)
Proteomics
Metabolomics….
Immunological approaches

847
Q

Putrefaction

A

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
Q

What postmortem changes may there be?

A

Rigor mortis
Algor mortis
Livor mortis (hypostatic congestion)
Post-mortem clotting
Haemoglobin imbibition, bile imbibition
Pseudomelanosis
Bloating
Softening
Lens opacity

849
Q

Rigor mortis

A

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
Q

Algor mortis

A

GRadual cooling of the cadaver

851
Q

Livor mortis

A

Gravitational pooling of blood down the side of the animal

852
Q

Post mortem clotting

A

Occurs mainly in the heart and blood vessels

853
Q

Haemoglobin inhibition

A

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
Q

Bile imbition

A

Bile imbibition:Bile in the gallbladder penetrates its wall and stains adjacent tissue yellowish/greenish/brown

855
Q

Pseudomelanosis

A

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
Q

Bloating

A

Result of post-mortem bacterial gas formation in the lumen of the gastrointestinal tract

857
Q

Post mortem softening

A

Softening of tissue results from autolysis of cells and connective tissue often aided by putrefactive bacteria

858
Q

Lens opacity post mortem

A

Occurs when the carcass is very old or frozen
Reversible on warming

859
Q

How can lesions be recognised and described?

A

Need to distinguish the normal from the abnormal
Need to distinguish lesions from post mortem change

860
Q

What criteria is used to describe a lesion?

A

Location
Number/extent
Demarcation
Distribution
Colour
Size
Shape
Consistency and texture

861
Q

What is the morphologic diagnosis of a lesion?

A

Severity, duration, distribution, location and the disease process

Macroscopic

862
Q

Describe the lesion seen

A

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
Q

Describe the lesion

A

The 1. stomach was 4. diffusely distended, 8. gas-filled and 5. diffusely dark red

864
Q

Describe the lesion

A

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
Q

Describe the lesion

A

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
Q

Describe the lesion

A

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
Q

Describe the lesion

A

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
Q

Describe the lesion

A

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
Q

What are the causes of cell injury?

A

Causes
Oxygen deprivation
Physical agents
Chemical agents and drugs
Infectious agents
Immunologic reactions
Genetic derangements
Nutritional imbalances

870
Q

What causes of oxygen deprivation lead to cell injury?

A

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
Q

What physical agents lead to cell injury?

A

Mechanical trauma
Extremes of temperature
Radiation
Electric shock

872
Q

What chemical agents and drugs lead to cell injury?

A

Hypertonic concentrations (glucose, salt…)
Poisons (arsenic, cyanide…)
Environmental pollutants
Insecticides, herbicides
Therapeutic drugs

873
Q

What infectious agents lead to cell injury?

A

Viruses (and prions)
Bacteria
Fungi
Parasites

874
Q

What immunologic reactions lead to cell injury?

A

Immune reactions to external agents (microbes) and environmental substances
Immune reactions to endogenous self-antigens(autoimmune diseases)

875
Q

What genetic derangements lead to cell injury?

A

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
Q

What nutritional imbalances lead to cell injury?

A

Nutritional excess
Nutritional deficiency

877
Q

What causes reversible degeneration that leads to cell injury?

A

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
Q

What are the properties of necrosis?

A

Always pathologic
Cell membranes are damaged
Often with inflammation

879
Q

What are the properties of apoptosis?

A

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
Q

What are the properties of irreversible necrosis?

A

Morphologic changes
Increase eosinophilia
Cytoplasmic vacuolation

881
Q

What can be seen in the images?

A
882
Q

What are the patterns of irreversible necrosis?

A

Patterns of tissue necrosis:

Coagulative necrosis
Liquefactive necrosis
Gangrenous necrosis
Caseous necrosis
Fat necrosis

883
Q

Infarct

A

Localised area of coagulative necrosis caused by ischaemia due to vascular obstructio

884
Q

What can be seen?

A

Pus collection of necrotic neutrophils and tissue debris (encapsulated pus= abscess)

885
Q

What is gangrenous necrosis?

A

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
Q

what is caseous necrosis?

A
887
Q

What can be seen and why?

A

Fat necrosis
Focal areas of fat destruction
Fat appears white, firm chalky resembling flecks of soap
Typically resulting from release of pancreatic lipases

888
Q

What are the morphologic alterations that lead to irreversible apoptosis?

A

Cell shrinkage
Chromatic condensation
Cytoplasmic blebs and apoptotic bodies
phagocytosis of apoptotic cells or cell bodies

889
Q

What are cell/tissue adaptations?

A

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
Q

What are the types of cell/tissue adaptations and what are there causes?

A
891
Q

What is the ability of cells to adapt?

A
892
Q

What are the properties of hypertrophy of tissues?

A

Increase in the size of cells (by producing more organelles), resulting in an increase in the size of the organPhysiologic 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
Q

What are the properties of hyperplasia?

A

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
Q

What are the different types of atrophy?

A

Physiologic, pathologic

895
Q

What is physiologic atrophy, when does it occur?

A

During embryonal, fetal development, uterus atrophy after parturition

896
Q

What is pathologic atrophy and when does it occur?

A

Decreased workload
Loss of innervation
Diminished blood supply
INadequate nutrition
Loss of endocrine stimulation
Pressure

897
Q

What are the properties of metaplasia?

A

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
Q

What are the different types of growth disorders?

A

Agenesis – never developed
Aplasia – started development but stopped early
Atresia – absence of an orifice
Hypoplasia – incomplete development
Dysplasia – disordered growth
Neoplasia

899
Q

What are the signs of acute inflammation?

A

Heat
Redness
Swelling
Pain
Loss of function

900
Q

Define acute inflammation

A

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
Q

What are the causes of acute inflammation?

A

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
Q

What are the morphologic hallmarks of acute inflammation?

A

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
Q

What are the steps of acute inflammation?

A

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
Q

What are the mediators of acute inflammation?

A

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
Q

What is the role of mediators in acute inflammation?

A

Vasodilation
Increased vascular permeablility
Leukocyte recruitment and activation
Pain
Tissue damage

906
Q

What are the outcomes of acute inflammation?

A

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
Q

What is the acute phase response in acute inflammation>

A

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
Q

How does pyrexia occur in acute inflammation?

A
909
Q

What are the biomarkers of acute inflammation?

A

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
Q

Define transudate in acute inflammation

A

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
Q

How does transudate occur in acute inflammation?

A
912
Q

Define exudates in acute inflammation

A

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
Q

How does exudate form in acute inflammation?

A
914
Q

What are the types of exudates in acute inflammation>

A

Serous
FIbrinous
Purulent
Haemorrhagic

915
Q

What is serous inflammation?

A

Inflammation with exudation of fluid with a low concentration of plasma protein and no to low numbers of leukocytes.

916
Q

What is fibrinous inflammation?

A

Inflammation with exudation of fibrinogen and fluid, and formation of thick friable, loosely adherent fibrin

917
Q

What is purulent inflammation?

A

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
Q

What is haemorrhagic inflammation?

A

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
Q

When does inflammation become chronic?

A

Normally 24-72 hours after acute inflammation
Persists for weeks months or years

920
Q

What cell types are involved in chronic inflammation?

A

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
Q

What are the proinflammatory cytokines involved in chronic inflammation?

A

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
Q

How do granulomas form in chronic inflammation?

A

Persistent Stimulus
Inert irritant (suture material?)
Granuloma formation:
Necrotic Centre
Foreign material + Neutrophils
Macrophages (Giant cells)

Infectious granuloma?
Lymphocytes

923
Q

How does chronic inflammation lead to tissue repair?

A

Wound Healing (See Surgery week)
Inflammation
Proliferation
Maturation
M2 Macrophages
Proline
TGF – B
Promotes collagen deposition

924
Q

What are the types of chronic inflammation without a clear pathogen?

A

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
Q

What are the types of chronic inflammation with a clear pathogen?

A

Parasitic
Fungal
Neoplastic

926
Q

What pyogranulomatous lesions occur with chronic inflammation?

A

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
Q

What can be seen in the image?

A

Johnes disease
Granulomatous lesions in the lymph node of a johnes cow

928
Q

What can be seen in the image?

A

H&E image shows a circular mass of cells caused by a granulomatous lesion
Johnes disease

929
Q

What are the types of granulomas in chronic inflammation

A

Caseous granuloma
Chronic granulomatous disease

930
Q

What are the properties of caseous granulomas in chronic inflamation?

A

Affects organ function
Breakdown could lead to excessive bacterial dissemination throughout the body

931
Q

What are the properties of chronic granulomatous disease?

A

Inherited disorder
Phagocytes dont work properly
Increased susceptibility to repeated bacterial or fungal infections

932
Q

What can be seen in the image?

A

Chronic pyelonephritis in a dog’s kidney
Pyogenic granulomas are small raised red bumps
Hydronephrosis
Kidneys have become swollen and stretched

933
Q

What can be seen in the image?

A

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
Q

What can be seen in the image?

A

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
Q

What can be seen in the image?

A

Chronic inflammation (mastitis) caused by tuberculosis

Biosecurity
Economic implications
Zoonotic risk

936
Q

What can be seen in the image?

A

Immune mediated arteritis
Inflammation occurs in the blood vessels
Swelling of the heart muscle
not often any main clinical signs until severe stage

937
Q

What can be seen in the image?

A

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
Q

What can be seen in the image?

A

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
Q

What can be seen in the image?

A

Granulomatous inflammatory lesion
Activated and giant multinucleate cells
Internal intracellular organisms within the giant macrophage cells
Lymphocytes and plasma cells

940
Q

What can be seen in the image?

A

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
Q

What can be seen in the image?

A

Chronic nephritis in the cat
Granulomatous vasculitis

Development of renal interstitial pyogranuloma.

Multiple, large, irregular, and pale grey subcapsular cortical foci

942
Q

What can be seen in the image?

A

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
Q

What can be seen in the image?

A
944
Q

What can be seen in the image?

A

Healing bone

945
Q

Neoplasm

A

Abnormal mass of tissue occuring due to abnormal cell proliferation

946
Q

What are the different types of neoplasm

A

Benign
Premalignanat
Malignant

947
Q

Oncogenesis

A

Process of gradual steps toward tumour development

948
Q

How can we determine if a lesion is neoplasia?

A

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
Q

What is the invasive scales for different tumours?

A

Benign= non invasive
Malignant= invades surrounding tissue

950
Q

What are the characteristics of benign tumours?

A

Slow growing masses
Good demarcation from surrounding tussue
Minimal necrosis

951
Q

What kind of tumour is lipoma?

A

Benign

952
Q

What are the characteristics of malignant tumours?

A

Can grow rapidly
Invasiveness to surrounding tissue
Can spread to other sites in the body (metastasis)
Increased necrosis

953
Q

What kind of tumour is squamous cell carcinoma?

A

Malignant tumour

954
Q

Features of benign vs malignant tumours

A
955
Q

Cytological features of benign vs malignant tumours

A
956
Q

What is the criteria for malignancy of a tumour?

A

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
Q

Benign tumour nomenclature

A
958
Q

Malignant tumour nomenclature

A
959
Q

Role of oncogenes

A

Promote proliferation

960
Q

Role of tumour suppressor genes

A

Suppress proliferation in induce cell death

961
Q

What do oncogenes code for?

A

Oncoproteins

962
Q

What are oncoproteins?

A

Proteins that promote cell growth in the absence fo normal growth promotion signals and despite normal check point controls

963
Q

Where does neoplasia come from?

A

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
Q

What causes cells to become neoplastic?

A

Sustaining proliferative signalling
Evading growth suppressors
Resisting cell death
Inducing angiogenesis
Activation invasion and metastasis
Enabling replicative immortality

965
Q

How does oncogenesis occur?

A

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
Q

mutagen

A

An agent that damages DNA

967
Q

Carcingogen

A

A mutagen that causes neoplasia

968
Q

What are the intrinsic and extrinsic factors of mutagenesis?

A

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
Q

What are the types of chemical factors of mutagenesis?

A

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
Q

How do physical extrinsic factors lead to mutagenesis?

A

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
Q

What are the actions of direct oncogenic viruses on mutagenesis?

A

Dominant oncogene mechanismMutation in viral gene causes host cells to produce oncoprotein => neoplasia
e.g. Feline leukaemia virus, canine papilloma virus

Insertional mechanismNo oncogene in virusInsertion of viral DNA into host cells activates proto-oncogenes > oncogenes => neoplasia
e.g. Avian leukosis virus

972
Q

What are the actions of indirect oncogenic viruses on mutagenesis?

A

Suppress host immune system
DIrectly stimulate host cell proliferation

973
Q

Neoplasia summary

A

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
Q

What are the common presenting signs of neoplasia?

A

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
Q

What causes the presenting signs of neoplasia?

A

Can be direct or indirect
Direct being compression, obstruction, pain, bleeding

Indirect= paraneoplastic syndromes

976
Q

What are paraneoplastic syndromes?

A

Caused by products of the tumour cells not the tumour mass

977
Q

Why is it important to identify paraneoplastic syndromes?

A

Can be life threatening
May help diagnose the primary tumour
Can affect response to treatment
Affect the QoL

978
Q

What are the indirect effects causing the neoplasia presenting signs?

A

Effusions
infection Paraneoplastic syndromes

979
Q

What are the different paraneoplastic syndromes?

A

Endocrine
Haematological
Gastrointestinal
Dermatological
Neuromuscular
Other

980
Q

What are the common paraneoplastic endocrine syndromes?

A

Hypercalcaemia
Hypoglycaemia

981
Q

When is hypercalcaemia seen as a paraneoplastic syndrome?

A

Associated with lymphoma and anal sac carcinoma
Commonly presents as inappetence, polydipsia, vomiting

982
Q

When is hypoglycaemia seen as a paraneoplastic syndrome?

A

Associated with insulinoma
Commonly presents as weakness, ataxia and seizures

983
Q

What are the properties of hypercalcaemia of malignancy?

A

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
Q

What are the common Paraneoplastic haematological syndromes?

A

Anaemia
Thromocytopenia
Coagulopathies

985
Q

When is aneamia seen as a paraneoplastic syndrome?

A

Can be common across cancer types
Associated with Lymphoma
GI tumours
Mast cell tumours

986
Q

When is thrombocytopenia seen as a paraneoplastic sydrome?

A

Can be common across all cancer types
Mechanisms include
Increased consumption
Increased sequestration
Immune mediated distruction

987
Q

When can coagulopathies be seen as paraneoplastic syndromes?

A

Common across all cancer types
Hypercoagulability
Disseminated intravascular coagulation

988
Q

What are the common GI paraneoplastic syndromes?

A

Ulceration
Associated with mast cell tumours
Commonly presents as Melaena
Haematemesis

989
Q

How do mast cell tumours cause ulceration

A

Increase histamine relaease
Increased gastric acid secretion
Ulceration

990
Q

What are the common Dermatological paraneoplastic syndromes?

A

Epidermal necrosis
Alopecia
Nodular deramtofibrosis
Exfoliative dermatitis

991
Q

When is epidermal necrosis seen as a paraneoplastic syndrome?

A

Associated with Pancreatic and hepatic tumours

992
Q

When is alopecia seen as a paraneoplastic syndrome?

A

Associated with sertoli cell tumours in dogs
Pancreatic carcinomas in cats

993
Q

When is nodular dermatofibrosis seen as a paraneoplastic syndrome?

A

Associated with renal adenocarcinoma (usually in GSDsP

994
Q

When is exfoliative dermatitis seen as a paraneoplastic syndrom?

A

Associated with thyoma in cats

995
Q

What are the common neuromusclar paraneoplastic syndromes?

A

Myasthenia gravis
Peripheral neuropathy

996
Q

When is myasthenia gravis seen as a paraneoplastic syndrome?

A

Associated with thymoma, osteosarcoma, bile duct carcinoma

Commonly presents as muscle weakness and dysphagia

997
Q

When is peripheral neuropathy seen as a paraneoplastic syndrome?

A

Associated wth multiple cancer types
Commonly presents as Weakness
-Progressive paraparesis/tetraparesis

998
Q

What are the non system related paraneoplastic syndromes?

A

Cachexia
Pyrexia
Hypertrophic osteopathy

999
Q

When is cachexia seen as a paraneoplastic syndrome?

A

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
Q

When is pyrexia seen as a paraneoplastic syndrome?

A

Pyrexia
Associated with:
-Multiple cancer types

Commonly presents as:
-Fever

1001
Q

When is hypertrophic osteopathy seen as a paraneoplastic syndrome?

A

Hypertrophic osteopathy
Associated with:
-Lung tumours (primary and metastatic)
-Less commonly liver, kidney, bladder tumours

Commonly presents as:
-Swollen/painful distal limbs
-Lameness

1002
Q

What is hypertrophic pulmonary osteopathy?

A

rapid periosteal new bone growth affecting distal limbs. Most commonly associated with lung tumours (primary or metastatic)

1003
Q

Why is cancer spread important?

A

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
Q

Define metastasis

A

Movement of cancer cells from one tissue or organ to another

1005
Q

What are the characteristics and mechanisms of metastasis?

A

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
Q

what are the pathways of metastases of tumours?

A

Haematogenous
Lymphatic
Transcoelomic

1007
Q

What are the properties of haematogenous metastases?

A

Most common route for sarcomas
Tend to invade thinner-walled veins rather than arteries
Ultimately enter lungs and liver

1008
Q

What are the properties of Lymphatic metastases?

A

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
Q

What are the properties of transcoelomic metastases?

A

Transcoelomic
Cancer cells spread across the surface of abdominal and thoracic structures
E.g. Mesotheliomas, ovarian adenocarcinomas

1010
Q

What are the fundamentals for cancer spread?

A

Intravasation
Extravasation
Colonisation

1011
Q

What affects the metastatic sites?

A

Dependent on the ability of tumour cells to adapt to the microenvironment of distant tissues
And the layout of the circulation

1012
Q

How does metastases of cancer cells reach the bone and what is the effect?

A

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
Q

What are the common lung metastatic tropisms?

A

Osteosarcoma
Haemangiosarcoma
Melanoma
Mammary tumours
Others (thyroid, tonsillar, pancreatic)

1014
Q

What are the common liver spleen and kidney metastatic tropisms?

A

Mast cell tumours
Haemangiosarcoma

1015
Q

What are the common bone metastatic tropisms?

A

Mammary tumours
Prostatic adenocarcinoma
Urinary bladder tumours

1016
Q

What are the different types of biopsy?

A

Fine needle aspirate and surgical biopsy?

1017
Q

Fine needle aspirate (FNA)

A

For cytology
Examination of cells that have exfoliated from mass

1018
Q

Surgical biopsy

A

For histopathology
Examination of tissue architecture of mass

1019
Q

When are incisional and excisional biopsies carried out

A

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
Q

What are the pros of FNA?

A

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
Q

What are the cons of FNA

A

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
Q

What are the pros of surgical biopsy?

A

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
Q

What are the cons of surgical biopsy?

A
1024
Q

What is the role of grades in tumours?

A

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
Q

What is the role of grades in cancer?

A
1026
Q

How do we follow a definite diagnosis for cancer?

A
1027
Q

When should tumour biopsy not be carried otu?

A
1028
Q

What are the different lesion distributions?

A
1029
Q

What is the distribution of the lesion in this image?

A

Cranioventral

1030
Q

What is the distribution of the lesion?

A

Segmental

1031
Q

What is the distribution of the lesion?What

A

Fibrino suppurative inflammation

1032
Q

What is the morphologic diagnosis of the lesion?

A

Liver, severe chronic multifocal to coalescing granulomatous hepatitis

1033
Q

What is the morphologic diagnosis of the lesions?

A

Haired skin, severe, subacute multifocal to coalescing dermal infarctions

1034
Q

What is the morphologic diagnosis of the image?

A

Brain, sever diffuse acute to subacute suppurative meningitis

1035
Q

What is the morphologic diagnosis of the image?

A

Heart, severe diffuse subacute fibrino- suppurative pericarditis

1036
Q

What is the morphologic diagnosis of the image?

A

Lung, cranioventral peracute mild agonal blood inhalation

1037
Q

What is the morphologic diagnosis of the image?

A

Haired skin, papillomas

1038
Q

What are the causes of cardiopulmonary arrest?

A

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
Q

What are the causes of acute failure of cardio respiratory systems?

A

Lack of oxygen delivery to tissues (DO2)
Unconsciousness and systemic cellular death
Cerebral hypoxia
brain death within 4 to 6 minutes

1040
Q

What are the signs of cardiopulmonary arrest?

A

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
Q

Outline the CPR algorithm

A

BLS = chest compressions and ventilation

1042
Q
A
1043
Q

How to act as the cardiac pump?

A
1044
Q

How to act as the thoracic pump?

A
1045
Q

How to carry out internal cardiac compressions?

A
1046
Q

How should CPR be carried out on large animals?

A

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
Q

How should the airway be treated in CPR?

A

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
Q

How is ventilation supplied during CPR?

A

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
Q

What are the principles of advanced life support?

A

Monitoring
Obtain vascular access
Administer reversals

1050
Q

How can monitoring be carried out for ALS?

A

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
Q

What clinical changes are being monitored in advanced life support?

A

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
Q

How can we gain vascular access in advanced life support?

A

Cephalic, sephaenous or jugular IV
Intraosseous route IO
Intratracheal IT

1053
Q

What are the properties of IV vascular access?

A

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
Q

What are the properties of IO vascular access?

A

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
Q

What are the properties of IT vascular access?

A

Dilute and use urinary catheter inserted beyond carina
Chest inflations will distribute the drugs
Higher doses are needed

1056
Q

What are the common ALS reversals?

A

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
Q

What is the treatment if an animal is in asystole?

A

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
Q

What drugs can be used if an animal is in asystole

A

Adrenaline
Vasopressin
Atropine

1059
Q

What are the properties of vasopressin when used for an animal in asystole?

A

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
Q

What are the properties of atropine when used for an animal in asystole?

A

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
Q

What are the properties of adrenaline when used for animals in asystole?

A

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
Q

What are the properties of high dose adrenaline when used for ALS?

A

Increased myocardial oxygen demand
Increased rate of ROSC
No increase in survival rates
Can be considered in prolonged arrest - >10 minutes

1063
Q
A
1064
Q

What are the properties of fluid therapy when used for an animal in asystole?

A

Administration to euvolaemic patients is associated with reduced coronary perfusion.
Only considered in patients with known hypovolaemia

1065
Q

What are the properties of bicarbonate when used for an animal in asystole?

A

Metabolic acidosis is a common occurrence in CPA
Mixed results in experimental studies so considered only in prolonged CPA

1066
Q

What are the properties of open chested CPR when used for an animal in asystole

A

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
Q

ROSC

A

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
Q

What are the principles of postROSC care?

A

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
Q

Outline the post ROSC care algorithm

A
1070
Q

What is meant by clinical pathology?

A

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
Q

What makes up anatomic pathology?

A

Surgical pathology (biopsy)
Necropsy

1072
Q

What are the common anticoagulants?

A

Haematology
Clinical chemistry
Glucose
Haemostasis/ coagulation

1073
Q

What is the effect of haemolysis?

A

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
Q

What is the effect of lipaemia?

A

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
Q

What are the sources of variation and errors in lab results

A

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
Q

How can we control analytical variation?

A

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
Q

How do we ensure an analytical technique is valid?

A

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
Q

Precision and accuracy

A
1079
Q

What are the common quality control systems

A

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
Q

Why should blood smears be carried out in practice regularly?

A

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
Q

How is a low power evaluation of a blood smear carried out?

A

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
Q

How is a high power examination of a blood smear carried out?

A

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
Q

What can be seen in the blood smear?

A
1084
Q

What may be seen on the feathered edge of a blood smear?

A

Platelet clumps
Big cells
Heart worm

1085
Q

What can we see at x40 with oil in red cell morphology?

A

Closer look at:
Anisocytosis
Polychromasia
Poikilocytosis
Inclusions

1086
Q

What does X40 allow view of with WBCs?

A

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
Q

How can we carry out a systemic approach to evaluating blood smears?

A

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
Q

This tissue is from a puppy. What is the morphologic diagnosis?

A

Small intestine: Enteritis, necrohaemorrhagic, segmental, acute, severe

1089
Q

Is this a lesion? Explain your answer

A

No this is livor mortis

1090
Q

This tissue is from a dog. What is the morphologic diagnosis?

A

t is a hemangiosarcoma.

1091
Q

What is an appropriate description for this lesion?

A

There are multifocal, round, red hairless massess on haired skin.

1092
Q

This is tissue from a cat. What is your morphologic diagnosis?

A

Left ventricular hypertrophy, diffuse, severes and chronic

1093
Q

This is tissue from a dog. What is your morphologic diagnosis?

A

Lungs , haemorrhage multifocal to coalescing sever and acute

1094
Q

This is tissue from a Ferret. What is your appropriate lesion description?

A

severe mucopurulent discharge coming from the eyes and nares.

1095
Q

This is tissue from a cat. What is your morphologic diagnosis?

A

Cerebrum meningioma

1096
Q

What can be seen in the image?

A

Pseudomelanosis

1097
Q

This is tissue from a dog. What is your morphologic diagnosis?

A

mandible and a melanoma.

1098
Q

Can a lesion be seen in the image?

A

it is not a lesion. What we see is oedema.

1099
Q

What is the morphologic diagnosis of the image?

A

This is bone, with physis. We see a fracture which is focally extensive, severe and acute.

1100
Q

What is your morphologic diagnosis?

A

Haired skin, sarcoma

1101
Q

What is the diagnosis for this image?

A

urinary bladder, there are multiple white gritty crystals.

1102
Q

What is the morphologic diagnosis of this image?

A

diaphragm. We see a hernia, focal, severe, acute, with visceral displacement.

1103
Q

What is the diagnosis for this image?

A

duodenum is a focal perforating ulcer with a 1.5cm diameter.

1104
Q

This is tissue from a cat, what is your morphological diagnosis?

A

haired skin, on the chin of the cat. We see folliculitis which is multifocal, moderate and chronic.

1105
Q

What is the morpholigcal diagnosis of the pathology in the image?

A

Thryoid, §Adenomatous hyperplasia, bilateral, sever and chroni

1106
Q

This is tissue from a dog, what is your morphological diagnosis?

A

perianal gland. Here we see an adenoma.

1107
Q

What are the common cytological diagnosis?

A

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
Q

Define cytology

A

The study of cell numebr and type in a tissue mass or fluid accumulation to investigate its cause §

1109
Q

What are the common cytological specimens

A

Common cytological specimens include:
Fine needle samples
Capillary action sample
Aspirate
Touch imprints
Body fluids
Lavages

1110
Q

What can cytology detect?

A

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
Q

What are the advantages of cytology?

A

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
Q
A
1113
Q

What are the limitations of cytology?

A

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
Q

FNS vs Biopsy

A

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
Q

What are the different lesion types?

A

Inflammation- neutrophilic, eosinophilic, granulomatous
Cystic- epidermal, sialcoele, seroma, haematoma
Neoplastic- epithelial, round, mesenchymal

1116
Q
A

Epithelial cells
High yield, cells associated with one another, rafts, sheets, acini, cuboidal or culmnar

1117
Q
A

Spindle/ mesenchymal
Low yield, spindle shaped cells, usually single but may be in association/sheets, may be matrix

1118
Q
A

Round cells
High yield, discrete round cells that are non adherent

1119
Q

What cytology can tell us

A
1120
Q

Process for masses

A
1121
Q

What types of inflammation may be seen in cytology?

A

Neutrophilic inflammation (suppurative acute)
- This includes abscesses
Pyogranulomatous inflammation
Granulomatous (macrophagic, chronic) inflammation
Eosinophilic inflammation

1122
Q

What are the most common canine tumours?

A

histiocytoma
Lipoma
Adenoma

1123
Q

What are some different kinds of epithelial skin tumours?

A

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
Q

What are the properties of mesenchymal skin tumours?

A

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
Q

What can be seen

A

Mesenchymal skin tumour

1126
Q

What can be seen?

A

Lipoma

1127
Q

What are the properties of lipoma?

A

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
Q

What are the different types fo round cell tumours?

A
1129
Q

What can be seen?

A

Plasmacytoma

1130
Q

What are the properties of plasmacytoma?

A

Discrete cells
Eccentric nuclei
Chromatin clumping
Perinuclear clear zones
Golgi, Ig production

1131
Q

Cytology summary?

A

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
Q

Describe and diagnose (dog lymph node)

A

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
Q

Describe and diagnose Canine lymph node

A

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
Q

Describe and diagnose Dog subcutaneous mass

A

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
Q

Describe and diagnose Dog eyelid mass

A

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
Q

Describe and diagnose dog flank skin mass

A

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
Q

Describe and diagnose dog flandk skin mass

A

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
Q

Descrbe and diagnose dog flank skin mass

A

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
Q

Describe and diagnose dog lymph node

A

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
Q

Describe and diagnose dog flank skin mass

A

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
Q

Describe and diagnose dog flank skin mass

A

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
Q

Describe and diagnose puppy flank skin mass

A

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
Q

Describe and diagnose dog flank skin mass

A

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
Q

Describe and diagnose prostate FNA

A

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
Q

Describe and diagnose Ventral skin mass

A

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
Q

Describe and diagnose dog skin mass

A

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

1147
Q
A