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Veterinary medicine year 2 > Derm > Flashcards

Derm Flashcards

1
Q

What is the main biting louse of the dog?

A

Trichodectes Canis

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2
Q

What is the main biting louse of the cat?

A

Felicola Subrostratus

Feel-ic- oh- la Sub-row-stratus

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3
Q

What is the main sucking louse of the dog?

A

Linognathus setosus

Pronounce:
Lino-(g)nathus setosus

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4
Q

What are the 3 long-legged mites of small animals?

A

Cheyletiella
Otodectes
Trombicula

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5
Q

What are the short legged mites of small animals?

A

Sarcoptes

Demodex

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6
Q

which mite has a ‘lemon’ shaped egg?

A

Demodex Canis

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7
Q

Which parasite may be found on a hair pluck?

A

Demodex

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8
Q

What are the 2 main derm conditions seen in dogs <1y old?

A

Parasites

Food induced atopy

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9
Q

Which derm condition is commonly seen in dogs 6m-3y old?

A

Environmental allergen induced atopy

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10
Q

What are the 2 main causes of dermatological dz in adult dogs?

A

Immune mediated

Endocrinopathy

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11
Q

What are 2 common signs of demodex overgrowth?

A

Greasy hair and pruritis on dorsum

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12
Q

Which mite leads to extreme pruritis, crusting and excoriation?

A

Sarcoptes

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13
Q

Which mite causes “walking dandruff” w/pruritis and erythema.

A

Cheyletiella

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14
Q

Which canine/feline mites are zoonotic?

A

Cheyletiella

Sarcoptes

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15
Q

Which mites cause a dark brown, waxy discharge?

A

Otodectes

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16
Q

Which flea/mite/lice treatment is best for small furry exotics?

A

Ivermectin/milbemycin

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17
Q

What can be used to treat otodectes in cats?

A

Imidacloprid + moxidectin
OR
Selamectin

IMID ACLO PRID

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18
Q

Which SA parasite is a possible vector of anaplasma and borrelia?

A

Neotrombicula

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19
Q

How is uncinaria treated?

A

Fenbendazole/milbemycin

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20
Q

What is the most common cause of bacterial pyoderma?

A

Staph pseudintermedius

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21
Q

What can be seen on cytology of superficial pyoderma?

A

Degenerative neutrophils

Phagocytosis of bacteria

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22
Q

What are the main clinical signs of superficial pyoderma?

A 
Macules
Papules/pustules
Collarettes
Hyperpigmentation
Erosion
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23
Q

What are the main clinical signs of deep pyoderma?

A 
systemically unwell
Furuncules, nodules, plaques
Crusts, ulcers, sinus tracts
Heat/erythema/swelling
Haemorrhagic bullae
Haemo-purulent exudate
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24
Q

Which breed of cat is predisposed to malassezia overgrowht?

A

Devon Rex

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25
Q

What are the signs of malassezia dermatitis?

A

Alopecia
Seborrhoea
Hyperpigmentation

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26
Q

How is malassezia dermatitis treated?

A

Chlorhexidine + miconazole shampoo

If unsuccessful: systemic anti-fungals

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27
Q

What are the key signs of atopic dermatitis?

A

Pruritis
Alopecia
Acral lick
Recurrent otitis externa

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28
Q

What are favrots criteria for cAD?

A

DOG PENN

Dog lives indoors
Onset <3yo
Glucocorticoid-responsive pruritus

Pruritus at onset
Ear pinnae +/- front feet
Nonaffected ear margins
Nonaffected dorso-lumbar area

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29
Q

How is canine food allergy diagnosed?

A

+ response to 6-8w diet trial w/novel or hydrolysed protein

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30
Q

What is the onset of improvement for allergen-specific immunotherapy?

A

3-9m

MUST DO FOR 12m

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31
Q

How can we control allergies medically?

A 
Glucocorticoids (low dose)
JAK inhibitor (oclacitinib)
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32
Q

What are the 2 contraindications for apoquel use?

A

<12m

<3kg

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33
Q

Name 3 glucocorticoids used to treat cAD.

A

Hydrocortisone
Ciclosporin
Tacrolimus

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34
Q

How would self-induced alopecia appear on a trichogram?

A

frayed/broken tips

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35
Q

What is the main cause of ringworm in dogs and cats?

A

Microsporum Canis

ALSO: M. gypseum & T. mentagrophytes

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36
Q

What is the gold standard test for ringworm in cats/dogs?

A

External lab fungal culture.

woods lamp and trichography have false +/-‘s.

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37
Q

Which antifungal treatment can be given to cats?

A

Itraconazole

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38
Q

Which antifungal treatment(s) can be given to dogs?

A

Itraconazole

Ketoconazole

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39
Q

What treatment is given for juvenile onset demodicosis?

A

None - most spontaneously resolve

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40
Q

What treatment is given for adult onset demodicosis?

A

Aggressive Tx:
Manage underlying Dz.
ABs as often 2e infection.

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41
Q

What are the two mites causing feline demodicosis and how do they differ?

A

D. Cati: non-pruritic, usually due to immunosuppresive drugs.
D. gatoi: pruritic and infectious.

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42
Q

How is feline demodicosis treated?

A

treat pyoderma

Imidacloprid 1st

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43
Q

When should demodicosis tx be stopped?

A

2-3 consecutive skin scrapes (4w apart)

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44
Q

What are the clinical signs of alopecia areata?

A

Focal to MF alopecia

Variable hyperpigmentation

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45
Q

Which breeds are predisposed to dermatomyositis?

A

Collies

Shetland sheepdogs

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46
Q

How does dermatomyositis present?

A 
6m old
patchy alopecia on face/extremities
erythema
scale
hyperpigmented
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47
Q

How is dermatomyositis treated?

A

Preds
Pentoxifylline
Vit E

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48
Q

What is sebaceous adenitis?

A

autoimmune attack on sebaceous glands

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49
Q

What are the derm signs of an endocrine Dz?

A

generalised alopecia
dull/dry/scaly
comedones
atrophic skin/poor healing

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50
Q

Which endocrine Dz presents with weight gain, tragic expression and truncal alopecia?

A

hypothyroidism

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51
Q

Which cancers cause feline paraneoplastic alopecia?

A

pancreatic/bile duct carcinoma

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52
Q

How does feline paraneoplastic alopecia present?

A

shiny, translucent skin.

Alopecia ventrum & legs.

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53
Q

How is alopecia X diagnosed?

A

Breed - plush coat

Exclude Ddx

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54
Q

Which 2 dog breeds are prone to pattern alopecia affecting the pinnae?

A

YRT

Daxie

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55
Q

Which 2 breeds are predisposed to sebaceous adenitis?

A

Akitas

Poodles

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56
Q

Clinical signs of sebaceous adenitis are…

A

Alopecia
Dry/Dull coat
Large adherent scales
Bacterial folliculitis

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57
Q

What is the treatment for sebaceous adenitis?

A

Skin care
Intense moisturisation
Manage 2e infection

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58
Q

What are the 5 main causes of head and neck pruritis in the cat?

A 
FBH
Otodectes
Neotrombicula
Bacteria
Malassezia
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59
Q

What are the 3 presentations of eosinophilic granuloma complex in the cat?

A

Eosinophilic plaque
Eosinophilic granuloma
Eosinophilic ulcer

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60
Q

What is a feline Eosinophilic plaque?

A

Raised, alopecic, erythematous, erosive to ulcerative plaque

HIGHLY PRURITIC

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61
Q

What is a feline Eosinophilic Granuloma?

A

Raised, alopecic, erythematous, erosive to ulcerative plaque.
Non-pruritic!!!

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62
Q

What is a feline Eosinophilic Ulcer?

A

Well circumscribed, red/brown ulcer with raised border on upper lip.
Non-pruritic, non-painful.

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63
Q

What is atopic dermatitis?

A

Genetically predisposed inflammatory & pruritic allergic skin disease - commonly environmental or food associated

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64
Q

Which type of hypersensitivity reaction is CAD?

A 
Type I (IgE)
Type IV Th2
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65
Q

What is an atopic flare?

A

Inc in staph and malassezia pyoderma due to defective skin barrier function

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66
Q

What are the 4 key features of cAD treatment?

A

Improve skin barrier
Allergen avoidance/AST
Control inflammation and pruritis
Control flare factors

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67
Q

How does Food-Induced Atopy differ for CAD?

A

Younger onset
Concurrent GI signs present
Not seasonal

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68
Q

What is the gold std Tx for FIA?

A

Home cooked diet trial with novel protein (min 6w)

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69
Q

What ways can we improve skin barrier function?

A

Non-irritating shampoos
Supplementation of EFAs
Topical EFA containing formulations

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70
Q

Name 2 topical lipid formulations that can aid skin barrier function.

A

Alladerm Spot on

Dermoscent

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71
Q

Via which 2 route can glucocorticoids be given in CAD? Give examples of each.

A

Systemic: Preds, methypreds
Topical: Betamethasone, hydrocortisone

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72
Q

What systemic calcineurin inhibtors can be given in CAD?

A

Ciclosporin

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73
Q

What topical calcineurin inhibtors can be given in CAD?

A

Tacrolimus

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74
Q

How does oclacitinib work?

A

Janus Kinase Inhibitor

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75
Q

What is Lokivetmab?

A

Monoclonal Antibody against IL-31 (pruritic IL)

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76
Q

How should Glucocorticoids be used in CAD?

A

Crisis busting - relieve flares

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77
Q

Why is topical hydrocortisone a low-risk Tx for CAD flares?

A

MEtabolised in skin so very little drug reaches circulation

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78
Q

How do calcineurin inhibitors work?

A

Inhibit Tc function

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79
Q

How is oclacitinib (apoquel) given?

A

BID 2w then SID

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80
Q

What are the 2 contraindications of oclacitinib?

A

<12m

<3kg

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81
Q

What is the CI for lokivetmab?

A

<3kg

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82
Q

Which 2 anti-histamines show some effect at relieving CAD when combined?

A

Chlorpheniramine and hydroxyzine

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83
Q

What is the most important source of environmental allergen for CAD and how can we reduce this?

A

House Dust mites

Environmental Flea Sprays and cleaning!

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84
Q

What is ASIT?

A

Expose dog to gradually increasing allergen dose over 12m

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85
Q

What is the Tx for ear margin seborrhoea?

A

Emollient rinse
VAseline
Propylene Glycol

Backup: surgery

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86
Q

What are the 3 Ps of otitis?

A

Primary (pathogen/disorder)
Predisposing (hair, morphology)
Perpetuating Factors

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87
Q

What is the best Tx for localised otodectes cyanosis?

A

Selamectin/moxidectin spot on

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88
Q

What is the best Tx for secondary Dz to otodectes cyanosis?

A

Cleaner +/- steroids

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89
Q

What are the signs of otitis externa?

A

Malodour
Head Tilt
Aural pruritis
Deafness

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90
Q

What are the signs of otitis media?

A

Pain
Concurrent OE
Deafness
Pain Eating

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91
Q

What are 3 potential complications of Otitis Media?

A

Conductive Deafness
Horners
Vestibular Syndrome

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92
Q

What is the first diagnostic method used to asses OM?

A

Video otoscopy - assess drum

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93
Q

What Tx is indicted in cases of chonric OM or evidence of TM bulging/fluid behind it?

A

Myringotomy (w catheter)
+ swabs
+ saline flush

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94
Q

What is the best method for assessing internal damage caused by OM?

A

MRI

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95
Q

What are the clinical signs of Otitis Interna?

A

Ipsilateral head tilt
rotatory nystagmus
asymmetric ataxia/falling
Vomiting +/- anorexia

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96
Q

What is the underlying cause of “dry coffee ground” exudate from the ears?

A

Otodectes cyanotis

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97
Q

What is the underlying cause of “moist brown” exudate from the ears?

A

Staph spp/Malassezia

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98
Q

What is the underlying cause of “purlent yellow/green, malodorous” exudate from the ears?

A

Gram negative infection

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99
Q

What is the underlying cause of ceruminous discharge from the ears?

A

Allergy
Endocrinopathy
Bacteroides Spp

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100
Q

How should wax samples be stained?

A

Methylene blue only

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101
Q

How should purulent ear samples be stained?

A

Diffquick

102
Q

How should parasites from the ear be prepared for microscopic exam?

A

Mix in LP

103
Q

Which 3 flushing solutions are most commonly used in canine medicine?

A

Saline
Dilute Chlorhexidine
Povidone Iodine

104
Q

What 3 medications are sued to treat otitis?

A

AB + Anti-inflam + Anti-fungal

105
Q

Which drugs are ototoxic? (4 ABs, 2 cleaners)

A

Gentamicin
Polymixin B
Ticarcillin
Imipenem

Propylene Glycol
Chlorhexine (conc)

106
Q

What is the best method of identifying the pathogen responsible for otitis?

A

Charcoal Swab and Culture

107
Q

Why does pseudomonas otitis cause ear drum rupture?

A

Bacteria produces collagenase

108
Q

What 2 Tx cane be used for a multi-resistant otitis?

A

Flamazine 1:9 in sterile water

Ticarcillin solution

109
Q

What are the 4 Tx for stenosis?

A

Potent topical steroids
Oral steroids
Tacrolimus ointment BID
Intralesional steroids

110
Q

What is the Tx of choice for an end-stage ear?

A

TECA

111
Q

What are the 3 signs of surface bacterial pyoderma?

A

Hotspots
Intertrigo
Bacterial Overgrowth

112
Q

How should Malassezia be sampled?

A

If dry: acetate tape

If greasy: indirect smear w/cotton bud

113
Q

What can be seen on cytology with superficial pyoderma?

A

Degen neutrophils and phagocytosis of bacteria

114
Q

What are the signs of superficial bacterial pyoderma?

A 
Papule/Pustules/Colarettes
ALopecia
Erythema
Hyperpigmentation
Lichenification
115
Q

What are the signs of DEEP pyoderma?

A 
Inflammation
furuncules/nodules/bullae
plaques
sinus tracts
ulcers/exudation/crusts

Sytemically unwell!!

116
Q

How should a direct impression smear be performed on a pustule?

A

Pop it/lift crust - then apply slide SEVERAL times

117
Q

How should acetate strips be stained?

A

Eosin and Basophil stains ONLY - no fixative

118
Q

What size needle and syringe should be used for an FNA?

A

21G

2-5ml

119
Q

What is the 1st line Tx for malassezia dermatits?

A

Chlorhexidine + miconazole shampoo

120
Q

What is the Tx for chronic malassezia dermatits?

A

systemic antifungals

121
Q

How longs should ABs be prescribed for a superficial pyoderma?

A

2-3w past clinical cure

122
Q

How longs should ABs be prescribed for a deep pyoderma?

A

3m past clinical cure

123
Q

How is the skin a protective barrier?

A

Strength of the skin is provided by factors including epithelial and dermal structures

124
Q

How is the skin a chemical barrier?

A

Lipid barrier

125
Q

How does the skin inhibit infectious agents?

A

Normal flora
Lipids-> fatty acids for the flora
Microbial proteins for epithelial cells and commensal bacteria support the microbiome

126
Q

How does the skin regulate temperature?

A

Altered blood flow in the superficial plexus allows regulation of the temperature of the skin
Sweating in horses and other
Hair is insulation

127
Q

How does the skin provide photoprotection?

A

Melanin in skin protects epidermal cells
Nuclear capping prevents damage of the basal cell nuclei

128
Q

How does the skin carry out immunosurveillance?

A

Langerhans cells are crucial antigen presenting cells in cutaneous diseases

129
Q

How is vitamin D produced in the skin?

A

Vit D conversion with UV light

130
Q

What is the mechanism for Type I hypersensitivity reactions?

A

Mediator release from mast cells following cross linkage of IgE by allergen causing swelling, itching and inflammation

131
Q

What is the mechanism for Type II hypersensitivity?

A

Complement or cellular damage to target bound by IgG

132
Q

What is the mechanism for type III hypersensitivity?

A

Immune complexes of IgG or IgM and antigen are deposited and then complement or cellular damage follows

133
Q

What is the mechanism for type IV hypersensitivity?

A

T cells orchestrate specific immune responses through production of cytokines (Th1 and Th2)
or through direct cell contact

134
Q

Type I hypersensitivity time until onset

A

<30 minutes

135
Q

Type II hypersensitivity time until onset

A

5-10 hours

136
Q

Type III hypersensitivity time until onset

A

4-8 hours

137
Q

Type IV hypersensitivity time until onset

A

24-72 hours

138
Q

What type of hypersensitivity is Hives?

A

I

139
Q

What type of hypersensitivity is insect bite reactions?

A

I

140
Q

What type of hypersensitivity is pemphigus foliaceus

A

II

141
Q

What type of hypersensitivity is drug reactions in the skin due to sulphonamides?

A

ii

142
Q

What type of hypersensitivity is vasculitis?

A

III

143
Q

What type of hypersensitivity is tuberculin response?

A

IV - uses Th1

144
Q

What type of hypersensitivity is late phase allergic reactions?

A

IV uses Th2

145
Q

What is the pathophysiology of atopic contact dermatitis?

A

Allegen -> skin
allergen penetrates the stratum corneum and is taken up by langerhans cells
Langerhans-> lymph nodes
Antigens taken up are incontact with T lymphocytes
Clonal expansionn and cytokine induced proliferation = antigen specific T lymphocytes
T cells-> blood-> epidermis
This is the sensitisation phase

146
Q

What follows the sensitisation phase of allergic contact dermatitis?

A

Provocation phase = after rexposure
Langerhans cells containing antigen interacts with the specific T cells for that antigen
Initiaites cytokine induced proliferation
Causes a localised inflammatory response

147
Q

In Atopic contact dermatitis how does the T cell proliferation affect the outcome?

A

Clonal expansion -> Th2 cell = allergic response = IL4-IL5- IL31-> IgE
Clonal expansion -> Th1 = non allergic response = IL2, IFNy = IgG

148
Q

What promotes Th2 response in allergic contact dermatitis?

A

Thymic stroma lymphopoeitin (TSLP)
Works via the langerhans cells

149
Q

What factors affect the response influenced by the APC in allergic dermatitis?

A

the amount and type of antigen
Via toll like receptors
Via lipid content of antigens
Cytokine environment
Microbiome

Antigens are presented to T cells in the local lymph node after migration from the epidermis

150
Q

What does tissue inflammation result in, in cAD?

A

Skin thickening through hyperplasia
Increase in numbers of langerhans cells
Reduced cutaneous barrier function
INcreased bacterial numbers on or in the skin

151
Q

Define dermatophyte

A

apathogenicfungusthat grows on skin,mucousmembranes, hair, nails, feathers, and other body surfaces, causingringwormand related diseases.

152
Q

What samples could be used to investigate demodicosis in a lively puppy with periocular lesions?

A

Hair plucj

153
Q

What samples would be the most appt to detect demodicosis on the thick of a well behaved dog?

A

Deep skin scraping

154
Q

What is demodicosus?

A

deep follicular mites

155
Q

What is not suitable for detection of dermatophytosis?

A

Unstained acetate tape strip

156
Q

WHat is cheyletiellosis?

A

Surface mites

157
Q

What is the best staining technique for cytological examination of an acetate strip sample?

A

Eosin and methylene blue

158
Q

Which cells increase with chronicity of skin inflammation?

A

Macrophages

159
Q

Lowest magnification for viewing demodex canis

A

X4

160
Q

Lowest magnification for malassezia

A

x40

161
Q

Lowest magnification for rod bacteria

A

x100

162
Q

What is the Mckenzie coat brushing used for?

A

Sampling dermatophyte culture

163
Q

What does a woods lamp detect?

A

Some but not all strains of microsporum canis

164
Q

Best area to sample for skin scraping

A

Primary lesion

165
Q

What is a DTM plate?

A

Dermatophyte test medium

based on sabourauds dextrose agar with added cycloheximide to inhibit saprotrophic growth. Has an antibiotic to inhibit antibiotic growth

Phenol red pH indicator= sacrophytic fungus present

166
Q

What causes colour dilution alopecia?

A

Macromelanosomes

167
Q

How will hair appear when there is self trauma?

A

Broken off hair tips

168
Q

How will hair appear when there is endocrine disorders or inflammation involving the follicle?

A

Tapered hair tips
Hair loss is caused by events within the follicle

169
Q

How will hair appear when in anagen phase?

A

roots of anagen hairs are rounded, curled, bent
Often smooth and pigmented

170
Q

How will hair appear when in the telogen phase?

A

Lancet shaped and lack pigmentation
Base of the hair may show a roughened brush like edge

171
Q

How will hair appear when there is dermatophysis?

A

Covered with spores and penetrated with hyphae?

172
Q

How will hair appear when there is colour dilution alopecia?

A

Melanin clumped in the hair shaft

173
Q

Appearance of demodex canis

A

lives in the hair follicles of dogs. Under the microscope, this mite is shaped like a cigar with eight legs. Demodectic mange, sometimes just called ‘Demodex’ or ‘red mange’, is the most common form of mange in dogs.

174
Q

When should unstained acetate tape tests be used?

A

Plain tape strips can be used to collect hair and skin debris to detect ectoparasites

175
Q

Define pruritis

A

Unpleasant sensation that elicits the desire or reflex to scratch (rub, lick, chew)

may be acute or chronic

176
Q

What is the role of pruritis?

A

Pruritis is a physiological self protective mechanism that is designed to remove the agent causing the sensation from the skin

177
Q

What is pruriceptive pruritis?

A

due to stimulation of peripheral receptors in skin (in presence of healthy nervous system

usually due to skin disease

178
Q

What is neuropathic pruritis?

A

Generated in the CNS in response to

Circulating pruritogens

pharmacological mediators

anatomical lesion of PNS or CNS

179
Q

What receptors are involved in the somatosensory activity of the skin?

A

Mechanoreceptors
Thermoreceptors
Nociceptors

180
Q

What is pruritis mediated by?

A

Unmyelinated slow conduction C fibres
A-delta fibres

181
Q

What are the chemical mediators of the cutaneous itch?

A
  • various proteases/leukotrienes and neurotropins
  • peptides
  • prostaglandins
  • cytokines - such as IL4, IL13, IL31 and IL33
  • histamine
182
Q

Where do chemical mediators of the skin originate?

A
  • Keratinocytes
    • leukotriene B4
    • endogenous cannabinoids
    • thymic stromal lymphopoietin
  • mast cells
    • Histamine
    • LTB-4
    • IL2
    • nerve growth factor
  • skin leucocytes
    • T cells - IL 31
    • eosinophils - NGF
183
Q

What are the 3 different ways that mediators can act?

A
  1. Direct stimulation of intraepidermal nerve fibres
  2. stimulate mast cells
  3. stimulate other mediators/transduction cascades
184
Q

What produces IL31 and what is its role?

A

produced by activated T cells in allergic skin disease

bnds to recepotrs on surface of neurons in skin leading to the activation of JAK enzymes which stimulated the pruritic impulse to the brain

185
Q

What are the neural pathways for itch

A
  1. Sensory afferent from skin
    1. mainly C neurones - slow conducting
  2. Dorsal nerve root to spinal cord
  3. Dorsal horn- synapse with spinal interneurones
  4. Cross and ascend in lateral spinothalamic tract
  5. Thalamus to the internal capsule
  6. To the sensory cortex (left hemisphere dominance, cf pain)
186
Q

Which cranial nerves carry the sensory fibres in from the head?

A

Trigeminal
Facial
Glossopharyngeal
Vagus

187
Q

How does scratching suppress pruritis?

A

Scratch -> fast conducting A beta neurones-> activation of inhibitory neuronal circuits -> widespread surround inhibition

188
Q

How does distraction suppress pruritis?

A

Distraction-> increased activity in descending pathways from reticular formation -> activation of inhibitory circuits in dorsal horns of spinal cord-> close gated mechanisms-> diminishes afferent itch messages

189
Q

Outline peripheral sensitisation of chronic pruritis

A

Scratching → increase local inflammation → production of pruritogens by inflammatory cells → INCREASE C FIBRE RESPONSIVENESS

190
Q

Outline the central sensitisation of chronic pruritis

A

chronic inflammation of skin→ altered perception of gentle mechanical/ other stimuli→ percieved as pruritis (allokinesis)

191
Q

What are the 3 responses to skin damage?

A

Epidermal responses
Dermal responses
Alopecia

192
Q

What is hyperkeratosis?

A

Increase depth of cornified layer

Scaling = production of abnormal or excessive scale

193
Q

What is ichthyosis?

A

Primary keratinisation defects

194
Q

What might non specific signs of secondary defects be indicative of?

A

Increased turnover of epidermis
Imbalance between turnover and desquamation

195
Q

Follicular hyperkeratosis

A
    • keritinaceous plugs in hair follicle infundibula= comdefo/ comedones (blackheads)
196
Q

What is a keratinaceous collar around hair emerging called?

A

Follicular cast

197
Q

What is acanthosis?

A

Increased depth of the whole epidermis

198
Q

What causes acanthosis?

A
  1. repeated lowgrade blunt trauma
  2. release of cytokines from keratinocytes
  3. increased division of basal epidermal cells occurs
  4. increases the depth of the epidermis
199
Q

Which cytokines stimulate the epidermal growth that leads to acanthosis?

A
  • PDGF released by keratinocytes
  • TGF- alpha released by keritanocytes
  • TGF- beta released by fibroblasts
  • EGF released by platelets and macrophages
200
Q

What is lichenification?

A

thickening and hardening of the skin characterised by exaggeration of the superficial skin markings

201
Q

When do vesicles usually occur?

A
  • with viruses
    • foot and mouth disease
  • Autoimmune diseases - autoantibodes attach intercellular proteins → this leads to separation of the keratinocytes
202
Q

What is a pustule

A
  • small circumscribed elevation of the epidermis that is filled with pus
  • usually associated with infection but some are sterile
  • such as bacterial pyoderma caused by staphylococcus pseudintermedius infection
203
Q

What causes hyper or hypopigmentation?

A

Feature of diseases affecting the basal epidermis and dermoepidermal junction in the dog

204
Q

What is crusting?

A

formed when dried exudate, serum, pus, blood, cells, scales or modifications adhere to skin surface

Caused by multiple exudate and ulcerative diseases

205
Q

How is erythema caused?

A

Damage leads to release of proinflammatory mediators including histamine

this causes vasodilation of dermal vessels

causing erythema

206
Q

What causes oedema?

A

Mediated by histamine and other cytokines which increases vascular permeability leading to leakage of tissue fluid

this leads to urticarial lesions

Type I hypersensitivity

207
Q

What is dermal thickening associated with?

A

Longer standign allergic reactions
Chronic inflammatory conditions

208
Q

What is alopecia a result of?

A

Failure to grow hair properly
Damage to hair follicles or shafts

209
Q

How may a testicular tumour lead to alopecia?

A

Sertoli cell tumour produces oestrogens causing alopecia

210
Q

Diplococci

A

bacteria- of various spherical Gram-positive bacteria that occur in pairs

211
Q

Escherichia coli

A

acteria Gram-negative andits envelope has three layers: cytoplasmic membrane, peptidoglycan, and outer membrane
. The peptidoglycan is rigid determining the rod shape

212
Q

Actinomyces

A

Gram postive bacteria
Filamentous
Rod

213
Q

Clostridium spp

A

anaerobic, Gram-positive, spore-forming bacteria belonging to the family Clostridiaceae- vibrion

214
Q

What cells are involved in the defence against parasites?

A

Basophils and mast cells - surface recetors for IgE, contain histamine, prostaglandins, leukotrienes and proteases

215
Q

What cels are involved in phagocytosing pathogens?

A

monocytes, macrophages, neutrophils, dendritic cells, osteoclasts, and eosinophils

216
Q

What term is used to describe a solid elevation of the skin greater than 1cm in diameter associated with cellular infiltration and or proliferation?

A

Nodule

217
Q

Is a papule a primary or secondary lesion?

A

primaru

218
Q

what is the name of a lesion that results from self trauma?

A

Excoriations

219
Q

What lesion results from loss of the epidermis and the basement membrane (ie. exposing the dermis)

A

ulcer

220
Q

What name is given to an elevated oedematous area of skin often caused by an urticarial reaction?

A

Wheal

221
Q

What name is given to a flat, solid elevated lesion of >1cm often considered to be an accumulation of papules?

A

plaque

222
Q

What lesion is composed of an enclosed cavity with a solid membranous linign that contains a liquid or semi solid material?

A

cyst

223
Q

Which term is used to describe the thickening of the skin and exaggerated skin markings?

A

lichenification

224
Q

Is crusting a primary or secondary lesion>

A

Secondary

225
Q

What makes the physical protection of the skin?

A

Poor conditions
Low pH
Competition by normal flora
Physical barrier and desquamation

226
Q

What secretions protect the skin>

A
  • Antimicrobial peptides
  • Protective substances such as mucus
  • soluble proteins such as complement
  • secretory immunoglobulins
227
Q

What makes up cell mediated immunity of the skin

A
  • Phagocytic cells
  • Intraepithelial lymphocytes and natural killer cells
  • Mast cells
  • cytokines and chemokines
  • the development of inflammation
228
Q

What makes up the adaptive immunity of the skin?

A

Immunoglobulins

229
Q

How does bacteria adapt to evade immune response on the skin?

A
  • Antigenic variation
  • inhibiton of antigen processing
  • Inhibition of complement activation
  • Resistance to phagocytosis
  • Inactivation of reactive oxygen species
  • Escape from the phagolysosome
  • Production of cytokine receptor homologues
230
Q

Why do commensals proliferate and cause pathogenic disease?

A

Usually due to a primary cause such as

  • Hypersensitivity
  • Systemic disease
  • Damage of compromise of defences
231
Q

Define (in relation to microbiology) resident

A

Can replicate on the skin and persist

232
Q

Define (in relation to microbiology) nomad

A

Nomad organisms can colonise and reproduce on the skin for short times

233
Q

Define (in relation to microbiology) transient

A

can not replicate so stay for a short time on the skin

234
Q

Define (in relation to microbiology) pathogens

A

Organisms that become established and can proliferate in the skin surface and deeper that are deleterious to normal physiology of the skin

235
Q

What do bacterial niches colonise based on?

A

Local secretions
pH
Contamination from local structures
Moisture

236
Q

What transient bacteria can be found on dog skin?

A
  • Staphylococcys psuedintermedius
  • S. aureus
  • E coli
  • Proteus mirabilis
  • Corynebacterium spp
  • Bacillus spp
  • Pseudomonas spp
237
Q

What are the most common microbes on canine skin?

A

Staphylococcus
malassezia

238
Q

What are the most common microbes in canine ears?

A

staphylococcus

malassezia

but can also get

pseudomonas sp

proteus sp

239
Q

What bacteria is high risk around the anus?

A

Enteric bacteria

240
Q

What is would you expect to find on canine skin>

A

Malassezia and gram positive cocci

241
Q

What should not be on canine skin?

A

Gram negative or rod bacteria

242
Q

Properties of the staphylococcus species

A
  • Gram positive, facultative anaerobes that occur in pairs, tetrads or clusters
  • Non motile opportunistic pathogens
  • There are at least 30 different species on skin of mucous membranes as commensals

Use baird parker selective indicator agar

243
Q

Which virulence factors are expressed by staphylococcus sp?

A

coagulase
Lipases and elastase
Protein A inhibits opsonisation
Range of toxins

244
Q

How do staphylococcal super antigens lead to hypersensitivity?

A
  1. Stimulation by super antigens (staphylococcus sp)
  2. Super antifens over activate T lymphocytes by bypassing the normal processes
  3. Activation by binding MHC and lymphocytes by not through the peptide binding cleft
  4. This can lead to cytokine production and an inflammatory response
  5. Uncontrolled immune response contributes to pathology
245
Q

What is an abscess?

A
  • A collection of pus formed by tissue destruction in an inflamed area of localised infection
  • A defensive reaction of the tissue to prevent the spread of infectious material
    Attract WBC - inc regional blood flow
246
Q

Example of surface infection

A

Secondary bacterial colonisation of lesions on the skin surface

  • Acute moist dermatitis
  • Eczemas
  • intertrigo
247
Q

Example of superficial infection

A

Infection involves skin and hair follicle epithelium

  • Impetigo
  • superficial bacterial folliculitis
  • dermatophilosis
  • pyotraumatic folliculitis
  • mucocutaneaous pyoderm
248
Q

Example of deep infection

A

Infection involves the dermis and subcutaneous tissue

  • furnculosis
  • cellulitits
  • furunculosis
  • acral lick furnculosis
  • subcutaneous abscess
249
Q

Pathogenesis of dermatophilosis?

A
  1. Zoospres attracted to sites on the skin due to respiratory low levels of carbon dioxide
  2. Germinate to produce hyphae which penentrate into the living epidermis and subsequently spread in all directions from the initial focus
  3. Penetration causes an acute inflammatory reaction
  4. In most acute infections the filamaentous invasion of the epidermis ceases in 2-3 weeks and the lesions heal spontaneously
  5. in chronic infections the affected hair follicles and scabs are sites from which intermittent invasions of non infected hair follicles and epidermis occur
250
Q

What is coagulase?

A

Enzyme produced by staphylococcus aureas that converts fibrinogen to fibrin
Reacts with prothrombin
Staphylothrombin complex is formed which causes blood to clot by converting fibrinogen to fibrin

251
Q

What is the coagulase test?

A

Rabbit plasma is inoculated with a staphylococcal colony

incubated at 37 degrees celsius for 60-90 mins

positive serum will coagulate while the negative plasma remains liquid

Veterinary medicine year 2 (23 decks)

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