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Year 4 > SA Dermatology and wounds > Flashcards

SA Dermatology and wounds Flashcards

1
Q

Where is the best place to test for sarcoptic mange?

A

Ear margin

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2
Q

Small orange-red colonies are likely to be which yeast?

A

Malassezia pachydermatitis

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3
Q

What is the most common cause of anal gland disease?

A

Impaction

May be associated with loose stools

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4
Q

What would you expect to see with anal gland carcinoma?

A

Hypercalcaemia

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5
Q

What is onychomadesis?

A

Sloughing of claws

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6
Q

What is paronychia?

A

Inflammation or infection of the claw folds

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7
Q

What is onychogryphosis?

A

Claws growing inwards

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8
Q

Where would you see scale associated with Cheyletiella?

A

Along back

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9
Q

What histological findings would you see with pemphigus foliaceus?

A

Subcorneal pustule with acanthocytes

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10
Q

What clinical sign in cats is a good indicator of pemphigus foliaceus?

A

Caseous paronychia

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11
Q

What do lots of follicular casts on a histological sample indicate?

A

Sebaceous adenitis

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12
Q

How long is the epidermal turnover?

A

21 days

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13
Q

What is pigmentary incontinence?

A

Loss of melanin from the epidermis, and accumulation in melanophages in the upper dermis.
Associated with immune-mediated and inflammatory diseases

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14
Q

What is CAD?

A

Genetically predisposed inflammatory and pruritic allergic skin disease, with characteristic features associated with IgE antibodies most commonly against environmental allergens

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15
Q

What is atopic-like dermatitis?

A

An inflammatory and pruritic skin disease with clinical features identical to those of CAD, but in response to non-environmental allergens

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16
Q

Describe the pathogenesis of CAD

A 
Complex, multi-factorial
Genetic predisposition:
-Skin barrier dysfunction
-Immune dysregulation
Environmental factors:
-Specific allergen sensitisation
-Enhanced microbial colonisation
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17
Q

How do you diagnose CAD?

A

Clinical signs: pruritus with skin lesions of characteristic distribution (ears, eyes, muzzle, feet, axilla, inguinal, perianal)
Ectoparasite/food trials

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18
Q

How do you manage CAD?

A

Improve skin barrier function (eg EFAs)
Anti-inflammatory drugs
Allergen avoidance and ASIT
Control microbial infection and other flare factors

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19
Q

How can we improve skin barrier function when treating CAD?

A

Non-irritating shampoos (eg emollients)
Oral EFAs
Topical formulations containing EFAs

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20
Q

How long does it take essential fatty acids to be incorporated into cell walls?

A

8-12 weeks

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21
Q

How are topical lipid formulations useful in treating CAD?

A

Help to normalise existing stratum corneum defects

However, likely to be of little benefit in addition to oral EFAs

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22
Q

Which anti-inflammatory drugs can you use to treat CAD?

A

Glucocorticoids (eg prednisolone,0.5mg/kg once to twice daily)
Calcineurin inhibitors (eg atopica)
Novel Janus Kinase inhibitor (eg aopquel)
Antihistamines
Recombinant interferons

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23
Q

Give some adverse effects of using systemic glucocorticoids (anti-inflammatories) to treat CAD

A

Polyphagia, PUPD, behaviour changes, panting, iatrogenic hyperadrenocorticism, increased risk of UTI

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24
Q

Which topical glucocorticoid could you use to treat CAD?
Where is it metabolised?
Give a side-effect

A

Hydrocortisone aceponate
Metabolised within the dermis so minimal systemic effects
Side effect: skin-thinning, so use intermittently

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25
Q

How do oral calcineurin inhibitors work in the treatment of CAD?
Give some adverse effects

A

Inhibit T lymphocyte function via blocking calcineurin

Adverse effects: GI signs, gingival hyperplasia, viral papillomas, hirsutism

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26
Q

When are janus kinase inhibitors contra-indicated when treating CAD?

A

<12 months old or <3kg BW

Breeding dogs or dogs with serious infections, underlying neoplasia or immune suppression

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27
Q

What dose of janus kinase inhibitor should you use when treating CAD?

A

0.4-.0.6 mg/kg twice a day for 2 weeks

Then once a day for maintenance

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28
Q

What is primary wound closure?

A

Direct suture closure

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29
Q

What is delayed primary wound closure/tertiary closure?

A

Leave part/all of wound, then close 1-5 days later before full granulation has occurred

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30
Q

What is secondary wound closure?

A

Wound edges cannot be apposed, so wound is left open. Involves repeated bandaging and debridement. Before granulation tissue develops, use wet-to-dry dressings. Once granulation tissue develops, use dry non-stick dressings so as not to disrupt granulation.
May be closed over 5 days later; granulation will have occurred so excise granulated edges

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31
Q

What are the aims of skin reconstruction?

A
  • Square skin edges
  • Accurate apposition
  • No overlapping
  • Slight eversion of wound edges (ensure base of epidermis is touching on both sides)
  • Follow Halsted’s principles (follow the tension lines-want wound to run parallel to tension lines to make it easier to close)
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32
Q

When would you undermine and advance the skin when closing a wound?

A

Indicated when wound is too large for closure using tension-relieving sutures, but too small for a flap

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33
Q

What are the 2 ways of undermining and advancing skin to close a wound?

A
  • Blunt (scalpel handle, scissors)

- Sharp (scalpel blade, scissors)

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34
Q

Why might we undermine and advance skin to close a wound?

A

Frees skin from its subcutaneous attachments to allow us to stretch it over the wound

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35
Q

What must we remember to do when we undermine and advance skin to close a wound?

A
  • Maintain vascular supply (direct cutaneous arteries/veins)
  • Undermine deep to the panniculus muscle layer where present (ie neck, thorax, abdomen). If not, undermine in loose areolar fascia deep to dermis
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36
Q

What are walking sutures?

A

Tension-type sutures that can be used to close large skin defects in areas where sufficient skin surrounds the wound that can be moved or stretched to close the wound
Used to eliminate dead space

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37
Q

Why do we not want walking sutures to go through the skin?

A

Possible route of infection

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38
Q

Give some possible disadvantages of using multiple punctate relaxing sutures to close a wound (making multiple stab incisions in skin to allow it to stretch)

A
  • Damages subdermal plexus (blood supply to edge of wound)
  • Holes would heal by 2nd intention -> patches of hairless skin -> fragile, prone to damage
  • Too many (or too closely-placed) stab incisionsmay damage the circulation to the wound edges -> ischaemic necrosis
  • Hence this technique not used much now
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39
Q

Which suture material should you use when doing walking sutures?
Where should they be placed?

A
  • Absorbable 2/0 or 3/0 sutures between the dermis and the subcutaneous fascia in rows no closer than 2-3cm apart
  • Place as few as possible
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40
Q

What is the ‘Z-plasty’ method of wound closure?

A

-Incisions are marked at 60 degrees to the original wound
-Creation of 2 triangular skin flaps
-Transposition of the skin flaps
-Wound is closed, giving a length gain
of approximately 75%

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41
Q

What is the ‘V-Y plasty’ method of wound closure?

A

A V-shaped incision is created perpendicular to the wound and closed in the shape of a Y
This technique will only relieve tension over a relatively limited area

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42
Q

How can you close crescent-shaped wounds where the 2 sides are of unequal length?

A

By spacing sutures further apart on the longer side of the crescent shape
(Or by excising dog ears that form at the corners)

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43
Q

How would you close triangular/square/rectangular-shaped wounds?

A

Begin suturing at the corners and proceed to the centre

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44
Q

What is a skin graft (pedicle graft)?

A

Portions of skin with a vascular attachment moved from one area of the body to another, that survive after transfer because of their intact circulation

45
Q

Pedicle (skin) grafts work best when done on which parts of the body?

A

Head, neck and trunk

46
Q

What should you consider when planning a skin (pedicle) graft?

A

•Use donor sites with ample skin and without excessive tension or mobility
•Use an appropriate flap for the shape of the wound
•Avoid narrowing the pedicle of the flap/creating flaps that are too long
•Undermine below the panniculus
•Develop a flap that is initially larger than the defect you wish to cover
•Use fine suture material, with initial tacking sutures to
ensure that flap conforms well to recipient bed with minimal, even tension
•Ensure the recipient bed is free of infection, contamination and necrotic tissue
•Do not exceed a length-width ratio of 3:1 for unipedicle flaps and 4:1 for bipedicle flaps

47
Q

How long after transfer of a skin graft does collateral blood supply develop?

A

7-10 days

48
Q

What are subdermal plexus flaps?

A

Flaps which are nourished by the subdermal plexus and attenuated branches of distant direct cutaneous arteries

49
Q

What are axial pattern flaps?

A

Pedicle grafts which incorporat a direct cutaneous artery and vein

50
Q

Why might it be beneficial to divide skin flaps?

When would you do this?

A 
To stimulate revascularisation 
-Direct flaps 10-14d post-transfer 
-Tubed pedicles ≥ 1 month postop 
-Can partially divide tubed pedicles 2 weeks 
post-op
51
Q

Why may a skin flap fail?

A
  • Arterial and/or venous occlusion by thrombi, torsion or stretching of direct cutaneous vessels
  • Excessive tension -> elevation of interstitial pressure -> reduced circulation and necrosis
  • Underlying haematomas/seromas/over-tight dressings -> pressure on flap -> reduce circulation
  • Infection (esp if blood supply is compromised)
52
Q

How can you subjectively assess the health of a skin flap?

A
  • Colour (unreliable)
  • Temperature
  • Sensation (unreliable)
  • Hair growth is associated with circulatory adequacy but is of little use immediately post-op
53
Q

How can you objectively assess the health of a skin flap?

A
  • Various laboratory measurements- no clinical use.

- Fluorescein dye fluorescence- non-fluorescent areas often dehisce, although not too reliable

54
Q

How can you salvage a failing skin flap?

A
  • Apply ointments to prevent desiccation
  • Debride non-viable tissue
  • Hyperbaric oxygen, hypothermia- less clinical use in veterinary surgery
  • Open wound management +/- secondary closure or development of a second flap to deal with areas of dehiscence
55
Q

What is a free skin graft?

A

Segments of dermis and epidermis completely detached from their donor site and transferred to a distant recipient site, usually one where a lack of skin mobility prevents local closure or flap construction e.g. extremities

56
Q

What are the different types of free skin grafts?

A 
Full thickness 
Split thickness 
Pinch 
Punch 
Strip 
Mesh
57
Q

How do free skin grafts survive?

A

By absorbing tissue fluid from the recipient bed during the initial 48hrs after transplantation, then by developing a new blood supply from the recipient bed

58
Q

Why are split-thickness grafts not indicated in cats?

A

As their skin is so thin

59
Q

Which type of skin graft is most commonly used in small animals?

A

Full-thickness mesh graft

60
Q

How does graft revascularisation occur?

A

3 steps:

  • Plasmatic imbibition (intake of fibrinogen-free, serum-like fluid into capillaries in the grafted skin by capillary action; days 1-3)
  • Inosculation (growth of new capillaries from the graft bed into the remnants of capillaries in the graft; day 3 onwards)
  • Vessel ingrowth (up to 1-2 weeks)
61
Q

Give some important factors in the survival of a skin graft

A

-Good contact between graft and recipient bed
-Recipient bed must be a fresh surgical wound or
healthy granulation bed
-Immobilisation of the graft on the bed is essential to allow revascularisation. Initially the graft adheres to the bed with fibrin (weak). The fibrin gradually changes to fibrous tissue over the first 10 days after graft placement
-Prevention of seromas or haematomas by gentle bandaging/meshing
-Body movement
-Host factors e.g. age, intercurrent disease, medication

62
Q

Why are surgical drains placed?

A

To remove unwanted fluid from a wound and eliminate dead space

63
Q

Give a possible complication of placing a surgical drain

A

Ascending infection
Can maintain asepsis by covering drain exit with a
dressing

64
Q

What are the 2 basic types of surgical drains?

A

Active

Passive (eg Penrose drain)

65
Q

How do passive drains work?

A

Rely on gravity and capillary action to draw fluid from the wound
Don’t fenestrate!

66
Q

How should a passive drain be placed?

A
  • Should exit through a separate stab incision at the most dependent/distal part of the wound and be secured to the skin with a single suture
  • Can exit the proximal end of the drain through a second incision to avoid air being suctioned into the wound and trapped in the subcutaneous tissues
67
Q

How do active drains work?

A
  • Are typically closed suction drains, created by applying negative pressure to a tube drain
  • They efficiently evacuate fluid and collapse dead space
  • Suction may be continuous or intermittent (at least every 6 hours)
68
Q

Why should you not exit a drain through, or place it directly underneath, a suture line?

A

Promotes dehiscence

69
Q

When should a drain be removed?

A

When a consistently small volume of serosanguineous fluid is produced

70
Q

Give some underlying causes of pyoderma

A 
Allergens (most common)
Ectoparasites
Self-trauma (pain)
Other infections (Leishmaniasis, Dermatophytosis)
Immune deficiency (endocrinopathy, chemotherapy, drug-induced)
Keratinisation defects
Follicular dysplasia
Environment/hygiene issues
Anatomical defects (eg skin folds)
Metabolic disease
Iatrogenic
Neoplasia
71
Q

Which bacteria most commonly causes pyoderma?

A

Staphylococcus pseudintermedius

72
Q

Besides S. psuedintermedius, which other bacteria may cause pyoderma?

A

S aureus, S hyicus

Gram -ve or atypical bacteria: E.coli, Proteus spp, Psuedomonas

73
Q

How can we classify pyoderma?

A

On the depth of infection:

1) Surface (bacterial overgrowth rather than infection)
2) Superficial (epidermis and hair follicles)
3) Deep (epidermis, hair follicles, dermis +/- subcutaneous fat)

74
Q

What is intertrigo?

A

Surface pyoderma of the skin folds eg around nose

75
Q

What are ‘hotspots’?

A

Form of surface pyoderma; pyotraumatic dermatitis
Lesions develop due to self-trauma
Underlying allergy or pruritic/painful trigger
Cheek/rump/neck

76
Q

How do you treat ‘hotspots’?

A

Clip, clean, topical antiseptic/antimicrobial and systemic/topical anti-inflammatory

77
Q

How does intertrigo (skin fold pyoderma) develop?

A

Compromised barrier (friction, altered microclimate, loss of ventilation)
Microbes proliferate -> toxins -> inflammation
May have concurrent skin disorder eg CAD
May progress to superficial or deep infection

78
Q

How do you treat intertrigo (skin fold pyoderma)?

A

Topical anti-septics/antimicrobials, topical/systemic anti-inflammatories
Weight loss may also help (eg vulval folds)

79
Q

Bacterial overgrowth syndrome affects which parts of the body?

A

Ventral trunk and interdigital spaces

80
Q

How do you treat bacterial overgrowth syndrome?

A

Topical anti-septics/anti-inflammatories

Identify and treat underlying disease

81
Q

Which primary lesions are seen with superficial folliculitis?

A

Follicular papules and pustules -> folliculitis

82
Q

What is meant by a ‘denegerate’ neutrophil?

A

Swollen nucleus, stains lighter and looks smudged
Nuclear border may be difficult to see
Often intracellular bacteria

83
Q

How would you identify a pyoderma on a microscope slide?

A

Degenerate neutrophils with intracellular (phagocytosis) bacteria

84
Q

What are epidermal collarettes?

A

Rims of scale

85
Q

What may you see on the skin with a deep pyoderma?

A

Heat, swelling, erythema, furuncles (boils), nodules, bullae, plaques, sinus tracts, ulcers, exudate, crusts
Lesions usually haemorrhagic
Less pruritic, more painful
Pain, systemic illness, fever, lymphadenopathy

86
Q

How can you diagnose pyoderma?

A

Cytology:

  • Direct impression smear (moist erosion)
  • Cotton tip/swab smear (ears, moist skin folds)
  • Adhesive tape strip (dry lesions)
  • FNA (21G needle +/- 2-5ml syringe)
87
Q

When should you perform culture and sensitivity when treating pyoderma?

A

Recurrent/chronic infection
Poor response to empirical treatment
Rod-shaped or unusual organisms on cytology
Degenerate neutrophils but absence of bacteria on cytology
Deep infections
Non-healing wounds
Post-op infections
Life-threatening infections
Risk factors for antimicrobial resistance (eg history of multiple courses of ABs)

88
Q

How can you sample deep pyoderma infections?

A

Fresh tissue biopsy
Rupture intact lesion if possible
Deep in sinus tract (last resort)

89
Q

Which skin antiseptic should you use when treating pyoderma?

A

Chlorhexidine

90
Q

Staphylococcus psuedintermedius is susceptible to which antibiotics?

A

Beta lactams

91
Q

MRSP are resistant to which bacteria?

A

All beta-lactams and fluoroquinalones

92
Q

Give some risk factors for MRSP

A

Hospital admission
Multiple vet visits
Previous, particularly broad-spectrum, systemic antimicrobials

93
Q

What is an appropriate duration for treating superficial and deep pyoderma?

A

Superficial: 1 week past clinical and cytological cure (2-3 weeks)

Deep: 2 weeks past clinical, cytological and palpable cure (4-12 weeks) (If progress stops, repeat culture)

94
Q

What are the stages of wound healing?

A

Inflammatory (day 0-5)
Proliferative (day 3-4 weeks)
Remodelling (day 20- years)

95
Q

What happens during the inflammatory phase of wound healing?

A 
Initiates inflammation of tissues
Haemorrhage followed by haemostasis 
Heat, redness, pain, swelling
Localised vasodilation, oedema, serous-type ooze
Migration of WBCs
Phagocytosis of bacteria
Cellular debris is removed
96
Q

What happens during the proliferative phase of wound healing?

A

Repair of damaged tissues
Formation of a fibrin framework and granulation tissue
Wound contraction and epithelialisation

97
Q

What happens during the remodelling phase of wound healing?

A

Repaired tissue is replaced by collagen
Wound continues to contract
Tissue regains some elasticity and protective barrier function

98
Q

When would you use wet-to-dry or dry-to-dry dressings?

How often should you change them?

A

Wound debridement (adherent dressings)
When dressing is removed, necrotic tissue/debris is removed with it
Change at least every 24 hours
Can be painful to remove

99
Q

What kind of dressing is Melolin?

A

Non-adherent
Used eg on post-op incision sites
Should not be used on granulating wounds as may disrupt healing when removed

100
Q

What kind of dressing is Allevyn?

A

Absorbent foam
Used for wounds that produce high volumes of exudate
Provides a moist environment suitable for granulation and epithelialisation
No debriding properties

101
Q

What kind of dressing is a hydrogel?

A

Active dressing
Gentle debriding action at the wound’s surface (less traumatic and painful than wet-to-dry dressings)
Can use on infected wounds

102
Q

What kind of dressing is a silver dressing?

A

Broad-spectrum antimicrobial dressing

Indicated in chronic infection and delayed healing

103
Q

What kind of dressing is manuka honey?

A

Topical, broad-spectrum antimicrobial
Some debriding action
Contra-indicated in arterial or actively bleeding wounds as may encourage further haemorrhage

104
Q

Which suture patterns can you use to relieve tension and provide skin eversion?

A

Horizontal and vertical mattress

105
Q

What are Favrot’s criteria for cAD?

A

1) Onset of signs <3 years old
2) Dogs living mostly indoors
3) Glucocorticoid-responsive pruritus
4) Alesional pruritus at onset
5) Affected front feet and/or ear pinnae
6) Non-affected ear margins
7) Non-affected dorso-lumbar area

106
Q

Where on the body is the usual distribution of sarcoptic mange?

A

Ear margins, around eyes, ventrum

107
Q

Where on the body is the usual distribution of cheyletiella?

A

Dorsum

108
Q

Where on the body is the usual distribution of fleas?

A

Rump/tail base, back, inguinal area

109
Q

How long should a food trial be carried out for?

A

6-8 weeks (home-cooked= gold standard)

Year 4 (51 decks)

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