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dematology Flashcards

1
Q

what are the advantages of clinical eye method of diagnosis

A
  • quick method
  • cheap
  • if effective generate confidence
    *
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2
Q

what are the disadvantages of ‘clinical eye” method

A
  • frequently fails
  • it cannot be repeated and it cannot be taught
  • it does not allow to progress
  • fastest way to reach a wrong dianosis
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3
Q

explain how the diagnosis is made with “performing successive diagnostic test’

A
  • different tests are performed until an abnormality is found
  • then a diagnosis is made on the basis of the alteration found.the clinical signs are therefore explained
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4
Q

how good is the diagnosis from performing successive diagnostic tests

A

apparently it is well founded

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5
Q

what are the disadvantages of successive diagnostic tests

A
  • slow and unpredictable
  • expensive.a lot of useless tests are performed, the ownrs get tired
  • it cannot be explained and systematized easily.
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6
Q

what is the advantage of performing successive diagnostic test

A

depending on the test chosen in the first place, a differential diagnosis can be reached

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7
Q

what is the advantage of problem orioented approach

A
  • it can be explained and taught
  • it mixes subjective decisions (problem definition) with science based actions
  • it is effective
  • minimum expenses to reach the dianosis
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8
Q

list all the primary cutaneous lesions

A
  1. macule/patch
  2. papule
  3. plague
  4. pustule
  5. vesicle or bulla
  6. wheal
  7. nodule
  8. tumer
  9. erythema
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9
Q

list all the secondary lesions

A
  1. epidermal collarette
  2. erosion
  3. ulceration
  4. excoriation
  5. lichenification
  6. scar
  7. fissure
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10
Q

list all the lesions which can be either primary or secondary

A
  1. alopecia
  2. scale
  3. follicular cast
  4. crust
  5. comedo
  6. pigmentary abnormalities/changes
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11
Q

circumscribed area up to 1 cm in diameter, characterised by change in the color of the skin i.e

  • hyperpigmented (melanotic)
  • erythematous
  • haemorrhagic
A

macule

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12
Q

circumscribed area greater than 1 cm in diameter characterised by change in color of the skin

A

patch

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13
Q

small elevation of the skin up to 1 cm in diameter

A

papule

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14
Q

what are the color characteristics of papule

A
  • normal color, erythematous,hyperpigmented
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15
Q

what is a plague

A

coalescing papules

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16
Q

small elevation of the epidermis which is filled with pus

A

pustules

  • it is fragile
  • follicular/non follicular
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17
Q

small elevation of the skin which is filled with clear fluid

A

vesicle

  • it is fragile and transient
    *
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18
Q

a vesicle with a diameter greater than 1 cm

A

bullae

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19
Q

sharply circumscribed,raised lesions consisting of dermal edema usually erythematous

A
  • wheal
  • variable shape and size
  • transient (appears and disappears in minutes or hrs)
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20
Q

solid elevation greater than 1 cm in diameter with a variable depth and attachment to the underlying tissue

A
  • nodule/tumer
  • it can be inflammatory or neoplastic
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21
Q

encircling rim of epidermal scalle with the free edges towards the central area.

A
  • epidermal collarette
  • represents the margins of an earlier pastule or visicle
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22
Q

breaks in the continuity of the skin with exposure of the dermis

A
  • erosions/ulcers
  • variable depth,shape,bleeding
  • erosion=more supeficial defect without damage of the basal membrane
  • excoriation= self produced erosion
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23
Q

thickening of the skin characterised by exagerated skin markings(wrinkles)

A
  • lichinification
  • usually due to chronic trauma(pruritis)
  • more frequent in the ventral skin
  • often accompanied by hyperpigmentation
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24
Q

areas of fibrious tissue that has replaced the damaged dermis or subq tissue

A
  • scar
  • most scars in cats and dogs are alopecic,atrophic, and depigmented
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25
Q

loose fragment of stratum cornum visible to the naked eye

A
  • scale
  • variable size,color,consistency
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26
Q

accumulation of keratin and sebaceous material that adheres to the hair shaft extending above the follicular ostia

A

follicular cast

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27
Q

accumulation of dried exudate,blood, cells,hairs, adhered to the skin

A

crust

  • the underlying skin is excoriated/eroded/ulcerated
  • variable color
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28
Q

dilated hair follicles which appears full of keratinaceous material

A
  • comedo
  • clinically appears as black points
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29
Q

cs of induced alopecia

A
  • appears in the areas of pruritus only.
  • commonly broad and symmetric
  • associated with arythema and other lesions such as lechinification
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30
Q

what are the cs of folliculitis alopecia

A

focal multifocal alopecia

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31
Q

what are the cs of allopecia due to disturbance of hair growth

A
  • symmetrical non pruritic alopecia
  • frequently on the trunk
  • slowly progressive
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32
Q

what are the cs of post scarring alopecia

A

localised,limited to areas of previous damage. pigment loss is permanent

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33
Q

discuss the pathogenesis of alopecia

A

Auto-induced:–Consequence of pruritus

Sequela of folliculitis:–Infectious/non-infectious

Disturbances of the hair growth:–Hair cycle abnormalities (telogenization)

Follicular dysplasia-Post-scarring

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34
Q

what are the ddx of focal-multifocal alopecia

A
  • demodicosis
  • dermatophytosis
  • bacterial folliculitis
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35
Q

discuss demodecosis

  • transmission to puppies
  • effect of bite
A
  • Mites are transmitted to nursing puppies by direct contact with bitch during the first 2-3 days of neonatal life
  • Innate immune system controls Demodex populations in the skin
  • Disease state: increased number of mites inside the hair
  • follicles folliculitis alopecia +/- bacterial infection =

demodicosis

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36
Q

name the 2 demodex identified in dogs

A
  • D. canis - commensal in hair follicles of all dogs
  • D. injai - found in sebaceous glands,

mostly terriers

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37
Q

name the parasite

A

D canis

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38
Q

name the parasite

A

D.injai

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39
Q

different presentation of demodecosis

A
  • localised
  • generalised
  • juvenile onset
  • adult onset
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40
Q

discuss localised democosis

A
  • transient and focal overpopulation of demodex mites
  • puppies 3-6 mnths of age
  • immature immune system
  • 1 to 4 areas of alopecia with variable erythema,scaling and hyperpigmentation
  • lesions no greater than 2.5 cm
  • no pruritus,no systemic signs
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41
Q

discuss generalised demodecosis

A
  • generalised overgrowth of demodex
  • +/-severe skin lesions
  • +/-systemic illness

fever,lethargy,inappetance

peripheral lympadenopathy

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42
Q

discuss juvenile onset of generalised demodecosis

A
  • likely a genetic defect leading to a dysfunctional control of demodex populations
  • affects dogs of 2 mnths to 2 yrs
  • there is breed predisposition
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43
Q

discuss adult onset of generalised demodecosis

A
  • dogs that are older than 2 yrs old
  • no sex or breed predisposition
  • immunocompromised
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44
Q

cs of demodecosis

A
  • multiple or regional alopecia(moth eaten appearance)
  • variable erythema
  • papules,crusts and comedones
  • pastules,collarretes, draining tracts=2ndary bacterial infection
  • non pruritic-mild to moderate when secondary infection is present
  • systemic signs (anorexea, fever) usually seen in advanced cases with secondary infection
  • lesions seen anywhere there are hair follicles
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45
Q

clinical presentation of pododemodecosis

A
  • erythema,swelling,draining tracts on haired skin
  • front paws or all four limbs affected
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46
Q

clinical presentation of otitis externa due to demodex

A
  • bilateral erythematous, ceruminatous otitis externa
  • mites found in ear cytology
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47
Q

diagnosis of demodex

A
  • skin scraping
  • trichinosis
  • cytology–bacterial infection
  • deep skin scraping
  • occassionally:biopsy and histological examinations
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48
Q

discuss D.injai

A
  • long episthosoma
  • live in the sebaceous glands
  • seen in terrier breeds
  • greasy seborrhea of dorsal stripe of trunk
  • mild to severe pruritis
  • diagnose thru deep scraping(sometimes difficult) or biopsy
  • histopath reveals a marked hyperplasia of the sebaceous glands
  • treatment is the same as for D.canis demodicosis
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49
Q

discuss treatment of localised demacosis

A
  • Benign neglect
  • Bathing with benzoyl peroxide 2.5% shampoo 1-2x/week

Demodicosis: treatment
Topical antibiotics

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50
Q

discuss treatment of genralised demodecosis

A
  • Amitraz deeps (0.03-0.05%) weekly
  • Macrocyclic lactones PO
            - ivermectin and moxidectin: 0.4-0.6 mg/kg PO daily
  • milbemycin: 2 mg/kg PO daily
  • Macrocyclic lactones topical
  • moxidectin (Advantage Multi®): q weekly

Don’t forget to treat the secondary pyoderma!

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51
Q

common sources of dermatophytosis

A
  • Microsporum canis (zoophilic)
  • M. gypseum (geophilic)
  • Trichophyton mentagrophytes (zoophilic)
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52
Q

clinical presentation of squamous form of dermatophytosis

A

alopecia,

erythema,

scales,
hyperpigmentation

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53
Q

clinical presentation of kerion form of dermatophytosis

A

alopecic,

erythematous and exudative,
papule or plaque

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54
Q

clinical presentation of pruritus form of dermatophytosis

A

variable, usually low

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55
Q

diagnosis of dermatophytosis

A
  • woodlamb examination
  • microscopic examination of hairs
  • fungual culture
  • biopsy
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56
Q

topical theraphy of dermatocosis

A
  • enilconazol 0.2%,clotrimazole
  • lime sulfur
  • clohexidine
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57
Q

systemic therapy of dermatophytosis

A
  • itraconazole
  • fluconazole
  • ketokenazole
  • terbinafine
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58
Q

where is D.injai found and in which breed is predispose

A
  • Live in the sebaceous glands
  • Seen in terrier breeds
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59
Q

histopath of sebaceous lnn reveals marked hyperplasia,which mites do u suspect

A

D.injai

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60
Q

treatment for localised demodex

A
  • Benign =neglect
  • Bathing with benzoyl peroxide 2.5% shampoo 1-2x/week
  • Topical antibiotics
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61
Q

treatment for Canine generalized demodicosis:

A
  • Amitraz deeps (0.03-0.05%) weekly
  • Macrocyclic lactones PO
           - **ivermectin and moxidectin:** 0.4-0.6 mg/kg PO daily
  • milbemycin: 2 mg/kg PO daily
  • Macrocyclic lactones topical
    - moxidectin (Advantage Multi®): q weekly
  • Don’t forget to treat the secondary pyoderma!
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62
Q

discuss the dosing of ivermectin

A

Ivermectin - start with 0.1 mg/kg/day and increase slowly in
0.1mg/kg increments daily until you reach 0.6mg/kg/day

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63
Q

in which breed should ivermectin be avoided

A
  • Do not use in collies and collie crosses!

“White feet, don’t treat

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64
Q

what are the side effects of ivermectin

A
  • neurologic toxicity

Miosis (u walk the dog in sunglight and the pupil is dilated instead of constricting), lethargy, ataxia, seizure, coma

  • Genetic testing for ABCB1-Δ1 (MDR-1) @ WSU esp. if its a mixed breed and u are nt sure if it has collie genes
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65
Q

when should you stop treatment for demodex

A
  • **Maintain therapy until two consecutive negative deep skin scrapings achieved
  • Negative skin scraping = zero mites, not dead mites
  • Avoid use of glucocorticoids
  • Correct possible underlying immunosuppressive factors (malnutrition, parasites, endocrinopathy, etc.)
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66
Q

whats the prognosis for demodex treatment

A

The cure rate in cases of good compliance is >90%.

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67
Q

what should be a plan in case the demodex is not cured after 4 months

A
  • Occasionally some patients need lifelong treatment

Pulse therapy with ivermectin
Advantage Multi q 2 weeks or monthly

  • If after 4 months of treatment lesions and/or parasites still persist, consider:
  • Check ivermectin dose is at 0.4 - 0.6 mg/kg/day
  • Change to different class of drug
  • Investigate hidden predisposing causes
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68
Q

which dematophyte is zoonotic

A

m.icrosporum canis

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69
Q

discuss the transmiossion of dermatophyte

A
  • Transmission by direct-indirect contact (contaminated environment)
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70
Q

discuss the effect of dermatophyte in dogs

A
  • Uncommon cause of canine focal-multifocal alopecia
  • Dogs of any age and breed can be affected,
  • however, more common in:
  • Young animals : < 1 year old, - Yorkshire terriers (and may be other terriers)
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71
Q

discuss the clinical picturre of dermatophyte

A
  • One or multiple alopecic areas on the trunk,head or limbs
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72
Q

discuss the clinical presentation of squamous dermatophyte

A
  • alopecia,
  • erythema,
  • scales,
  • hyperpigmentation
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73
Q

discuss the clinical presentation of kerion dermatophytosis

A
  • alopecic,
  • erythematous and exudative,
  • papule or plaque
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74
Q

dermatophytosis dx

A
  • woodlamp
  • microscopic examination of the hair
  • fungal culture
  • biopsy
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75
Q

list the drugs used to treat topical dermatocosis

A
  • enilconazole 0.2%, clotrimazole
  • lime sulfur 2% to 4%
  • chlorhexidine 3-4%
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76
Q

discuss drugs used systemically to treat dermatocosis

A
  • itraconazole (5-10 mg/kg/ 24h; PO with food)
  • fluconazole (10 mg/kg/ 24h; PO with food)
  • ketoconazole (10 mg/kg/ 24h, PO with food)
  • terbinafine (30-40 mg/kg/ 24h; PO)
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77
Q

discuss environmental treatment for dermatophytes

A

bleach diluted 1:10 in water

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78
Q

how long should treatment for dermatophyte be continued

A

Treatment has to be continued until 3 to 4 weeks beyond 2
consecutive negative follow-up fungal culture results
performed q 2-4 weeks

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79
Q

which bacteria causes more folliculitis

A
  • S. pseudintermedius is the etiologic agent in > 90% of cases;
  • the rest: S. aureus, S. schleiferi
  • Opportunistic pathogen
    Present in most dogs (perineum, perioral skin,
    nose)
    Usually a primary cause triggers the overgrowth of
    S. pseudintermedius
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80
Q

list the primary causes of bacterial folliculitis

A
  • atopic dermatitis
  • humidity,sarborrhea
  • corticotheraphy
  • hypotherodism
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81
Q

what are the cs of bactrial folliculitis

A
  • Multifocal areas of alopecia, follicular papules / pustules, crusts, scales, collarettes and hyperpigmentedmacules
  • Short-coated dogs present often a moth-eaten patchy alopecia
  • Long-coated dogs, typical signs include dull haircoat, scales and excessive shedding
  • All haired skin can be affected, but glabrous regions more commonly affected
  • Pruritus variable, from mild to moderate or severe
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82
Q

diagnosis for bacterial folliculitis

A
  • History, clinical signs
  • Cytological examination
                   (papules, pustules, epidermal collarettes)
  • Response to antibiotic therapy

Biopsy / bacterial culture –
not first line tests

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83
Q

discuss topical treatment of bacterial folliculitis

A
  • Chlorhexidine 2-4%
  • Benzoyl peroxide 2.5%
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84
Q

discuss antibiotic therapy for bacterial folliculitis

A
  • Cephalexin (25-30mg/Kg/ 12h; PO)
  • Amoxicillin-clavulanate (25mg/kg/ 12h; PO)
  • Clindamycin (11mg/kg/12h; PO)
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85
Q

discuss the length of treatment for deep and superficial bacterial folliculitis

A
  • **Superficial pyoderma – 4-6 weeks
  • **Deep pyoderma – 8-12 weeks
86
Q

what type of alopecia is seen in short coated dogs due to bacterial folliculitis

A

Short-coated dogs present often a moth-eaten
patchy alopecia

87
Q

what type of alopecia is seen in long coated dogs due to bacterial folliculitis

A

Long-coated dogs, typical signs include dull haircoat, scales and excessive shedding

88
Q

list 2 topical medication for bacterial folliculitis

A
  • chlohexidine
  • benzol peroxide
89
Q

list the antibacterials used to treat bacterial folliculitis

A
  • cephalexine
  • amoxiciline
  • clindamycin
90
Q

how long does it take to treat superficial pyodema

A

4-6 weeks

91
Q

how long does it take to treat deep pyodema

A

8-12 weeks

92
Q

which ares are normally affected by demodecosis

A

head,trunk and legs

93
Q

which areas are normally affected by dematophytosis

A

head and legs

94
Q

which areas are normally affected by bacterial folliculitis

A
  • Trunk,
  • abdomen,
  • glabrous skin,
  • head is typically spared
95
Q

Lesions/Clinical manifestations of acute pruritus

A
  • erythema
  • partial alopecia
  • scaling
  • escoriation
  • pyotraumatic dermatitis
  • crusting
96
Q

Lesions/Clinical manifestations of chronic pruritus

A
  • same as with acute( list them)
  • hyperpigmentation,
  • lichenification (dog),
  • acral lick dermatitis
97
Q

discuss pruritus due to malassazia

A
  • M. pachydermatis is a commensal of the skin
  • Overgrowth = marked pruritus (hypersensitivity)
  • Usually secondary to allergic dermatitis
  • Primary Malassezia dermatitis due to abnormalities in

the cutaneous ecosystem

  • Normal to find large numbers in Bassett hounds
98
Q

clinical signs of mallassazia dermatitis

A
  • Alopecia, erythema, scaling, hyperpigmentation,

lichenification
Greasy to the touch
Malodourous (esp. ears)

99
Q

discuss distribution of Malassezia dermatitis

A
  • Skin
  • , claw folds
  • , mucocutaneous junctions,

ear canals

100
Q

mallassazia diagnosed

A

skin cytology

101
Q

list the topical medication for malassazia

A
  • chlohexidine
  • enilconazol
  • miconazole
102
Q

list the systemic treatment of malassazia

A
  • ketaconazole
  • itraconazole
  • fluconazole
  • \terbinafine
103
Q

list the drugs that can be used to prevent malassazia infection

A
  • chlohexedine
  • enilconazole
    *
104
Q

discuss transmission of sarcoptic mange

A
  • direct transmission from infected host or environment
105
Q

severity of sarcoptic mange depends on

A
  • hypersensitivity 1
  • n.b.zoonotic:the owner may complain about rash
106
Q

cs of sarcoptic mange

A
  • **Severe pruritus (9-10/10)
  • Usually non-/poorly responsive to glucocorticoids
  • Signs may worsen with glucocorticoids
  • Erythema, papules, alopecia, excoriations, scaling,
  • crusts, lichenification (chronicity) and self-induced alopecia
107
Q

distribution of sarcoptic mange

A
  • ear margins
  • legs
  • elbows
  • hocks
  • ventrum
  • In chronic cases: lesions are generalized +/-
    lethargy, lymphadenopathy, weight loss
108
Q

discuss diagnosis of sarcoptic mange

A
  • History
  • Clinical signs (PRURITUS)
  • Pinnal-pedal reflex (~80%)
  • Broad, superficial to deep skin scrapings

*Mites are found only 25-50% of the time

  • Therapeutic trial (selamectin, ivermectin
109
Q

which topical is used to treat topical sarcoptic mange

A

amitraz

110
Q

discuss systemic treatment of sarcoptic mange

A
  • ivermectin
  • moxidictine
    *
111
Q

which ectoparasites is ivermectine used for

A
  • sarcoptic mange
  • demodicosis
112
Q

ddx of ectoparasites which causes prutitis in dogs

A
  • sarcoptic mange
  • cheylectiellosis
  • fleas
113
Q

ddx for allergic dermatitis

A
  • Flea allergy dermatitis
  • Atopic dermatitis
  • Food intolerance/allergy
114
Q

which hypersensitivity reactions are due to flea bite

A

hypersensitivity type 1 and 4

115
Q

discuss the distrbution of pruritis in dogs as a result of flea allergy dermatitis (FAD)

A
  • Severe pruritus predominantly in the lumbosacral area and caudal half of the body (“pants”)
116
Q

what is the primary lesion due to flea allergy dermatitis

A

papules

117
Q

secondary lesions due to Flea allergy ermatitis(FAD)

A
  • alopecia,
  • erythema
  • , scaling
  • , crusts,
  • lichenification,
  • pyotraumatic dermatitis
118
Q

discuss dx of flea allergic dermatits (FAD)

A

In most cases the diagnosis is based on history and clinical signs
Confirmation can be obtained:
Evidence of fleas or flea faeces (flea dirt)
Good response to flea control program (8 weeks)
Flea allergy test (serology/intradermal

119
Q

discuss ways of treating fleas

A
  • flea control
  • Anti-pruritic drugs (ex. Prednisone; short term)
120
Q

ch topical drugs are used to treat fleas

A
  • Imidacloprid,
  • fipronil,
  • indoxicarb,
  • dinotefuranq 3 weeks
121
Q

systemic drugs used to treat fleas

A
  • Spinosadq 3 weeks to monthly
  • Nitenpyramas needed
122
Q

Food allergy vs. intolerance

A
  • food intolerance
  • No involvement of the immune system
  • Reactions are dose dependant
  • Gradual onset of clinical signs; never life-threatening

Food allergy

  • Type I, III, and IV hypersensitivity reactions
  • Any amount of offending food will cause reaction
  • Can be life threatening
123
Q

clinical signs and distribution of of Cutaneous adverse food reactions (CAFR)

A
  • Non-seasonal pruritus
  • Only partially responsive to steroids
  • Erythema, signs of self-trauma
  • 2ndary infections
  • Face, neck, abdomen, perianal and perioral regions, paws
  • Otitis externa
  • Concurrent GI signs in 20% cases
124
Q

offending allerges in Cutaneous adverse food reactions (CAFR

A
  • In humans -glycoproteins MW > 12 kD
  • In dogs –typically meat proteins
  • Beef, chicken, soy, dairy, corn, wheat
  • Cross-reactive proteins:
  • Duck, turkey, venison, buffalo
125
Q

define Canine atopic dermatitis (CAD)

A

Inflammatory and pruritic skin disease associated with a genetic predisposition to produce IgEagainst environmental allergens

126
Q

most common allergens for Canineatopic dermatitis (CAD)

A
  • House dust mites, storage mites
  • Pollens, molds, feline and human dander, insects
127
Q

discuss the pathogenesis Canineatopic dermatitis (CAD)

A
  • Type I hypersensitivity reaction (IgE)
  • Epidermal barrier abnormalities
  • Increased adherence of bacteria / yeast = infection
128
Q

discuss age of onset of CAD

A

6 mnths to 3 yrs

129
Q

cuss seasonality of CAD

A
  • Variable
  • Many dogs start with season signs that progress to non-seasonal after 2-3 years
  • **MAIN CLINICAL SIGN IS PRURITUS
130
Q

what are the cs of CAD

A

none or erythema

131
Q

secondary cs of CAD

A

red-brown salivary staining, excoriations, self-induced alopecia, papules, collarettes, crusts (2o pyoderma), lichenification(2o Malasseziadermatitis)

132
Q

discuss the distribution of CAD

A

face, ears, extremities, paws and abdomen

133
Q

CAD Diagnosis

A
  • history, clinical signs and ruling out other pruritic diseases

Sarcopticmange(scabies)
Fleasandfleaallergy
Bacterial folliculitis
Malasseziadermatitis
Cutaneousadversefoodreaction

  • Atopicdermatitis is a diagnosis madebyexclusion
134
Q

Atopicdermatitis: Treatmentof acuteflare-ups

A
  • Control secondary infection: topical treatment (chlorhexidine) or systemic antibiotics
  • Increase hygiene: frequent baths
  • Use topical or systemic steroids (prednisone, 0.5-1 mg/kg/24 h)
135
Q

Atopicdermatitis: Long-termtreatment

A
  • Allergen-specific immunotherapy
                       Custom-formulated based on intradermal and/or serum allergy test results
  • Cyclosporine A
  • Oclacitinib

Improve skin barrier functionw topical tx
Atopicdermatitis: Long-termtreatment

136
Q

discuss disadvantages of allegy testng

A
  • Identification of the main allergens causing clinicalsigns
  • **Cannot use allergy testing to makea diagnosis of atopicdermatitis
  • Clinicallynormal dogs can have false positivere sultson IDAT and SAT
  • Only test if owners want to pursue allergen specifici mmunotherapy Allergy testing
137
Q

advantages of Allergen specific immunotherapy (ASIT)

A
  • Can induce a change in the immune response and “cure” the disease
  • Veryfew side effects (itch in some patients)
  • Can combined with other therapies
138
Q

disadvantages of Allergen specific immunotherapy (ASIT)

A
  • Lowefficacy (especially in very severe cases of CAD)
  • Requires allergy testing with clear results
  • Long time before improvementin clinical signs is noted(resultsshould not be evaluated prior to 9 months)
  • No predictabilityof results
  • Lackof standardized, validated protocols
  • Needs high compliance and time dedication of the owners
139
Q

drug is use to treat CAD

A

Inhibits synthesis of several interleukins (IL-2) and cytokines (considered immunomodulatingagent at low doses)
5 mg/Kg PO QD; 1 month, then reduce the dose
(5mg/kg/48h, then 5 mg/kg/72 h)
High effectiveness in the control of CAD 85% cases.
Slow acting (14-28 days)
Side effects common [but mild]: vomiting, diarrhea, anorexia; 10-15% of cases

140
Q

what are the advantages of cyclosporine

A
  • High effectiveness, almost as effective as steroids
  • Can be used safely for long term treatment
  • Very easy to use, previous allergy testing not needed
  • Can be combined with other therapies
141
Q

disadvantages of cyclosporin

A
  • Side effects (15% dogs vomit)
    Long term side effects not completely assessed
  • Slight delay in response time
  • Cost can be a limitation in some big dogs
142
Q

discuss the pharmacokinetics of Oclacitinib [Apoquel]

A

Inhibits Janus Kinase 1 (JAK 1) and 3 (JAK 3) blocking the action of many pro-inflammatory/allergic cytokines (stops the signal transmission and gene transcription)

143
Q

in which ways does the cat manifest pruritus

A
  • Scratching
  • Licking, chewing
  • Overgrooming
  • Rubbing
  • Seizure-like activity
  • Often secretive
  • Many different clinical presentations for the same diseases
144
Q

what are the clinical presentations of pruritic cats

A
  • 1 Facial pruritus with facial lesions: excoriations, crusts
    1. Miliary dermatitis: crusted papules over

dorsum

    1. Symmetric truncal/flank/inguinal alopecia
    1. Eosinophilic plaques, ulcers, granulomas
145
Q

what are the ddx for pruritus in cats

A
  • ectoparasites
  • allergic dermatits
  • infectious dz
146
Q

list the ectoparasites that causes prutitus in cats

A
  • notoedris cati
  • demodex cati/gatoi
  • fleas
  • otodectes cynotis
147
Q

which allergies causes pruritus in cats

A
  • flea allergy dermatitis
  • atopic dermatitis
  • food intolerance/allergy
148
Q

which infectious dz causes pruritus in cats

A
  • dermatophytosis
  • malassezia dermatitis (rare)
  • superficial pyoderma
149
Q

what are the cs of notoedric mange

A
  • intense pruritus (9-10/10)
  • typically affects head and pinnae–occassionally entire body and feet
  • crusting,scalling, erythema, alopecia, 2dary self trauma, “suizures”
  • in severe cases,peripheral lymphadenopathy, anorexia, emanciation,death
150
Q

discuss the pathogenesis for notoedric mange

A
  • Transmission through direct contact with infected cat (obligate parasite)
  • ı Female mite burrows into skin, then lays eggs
  • ı Complex hypersensitivity reaction
  • ı Rarely zoonotic
  • ı Can transiently infest dogs
151
Q

diagnosis for notoedric mange

A
  • superficial skin scraping
  • response to treatment i.e if history is suspecious, do emperical acaricidal therapy
152
Q

treatment for demodicosis in cats

A
  • selamectin–q 2 weeks ,3 times
  • ivermectin
  • 2% lime sulfur
  • amitraz
  • treat all in contact animals
153
Q

discuss D,gatoi

A
  • contagious
  • normal habitat unknown
  • found in stratum corneum
  • in the US most frequently encounted in the south
  • rare to common (depends on geometry
154
Q

discusss D.cati

A
  • normal comensal of the skin
  • usually only seen in very sick cats–metabolic dz,immunosuppressive dz
  • non pruritic condition
  • patchy,regional multifocal alopecia
  • can be localised or generalised very rare
155
Q

what are the cs of feline demodicosis

A
  • variable pruritus;non -moderate
  • alopecia- focal,patchy,generalised,symetrical
  • +/-erythema,crusts,scales
  • +/-secondary pyoderma
  • +/-ceruminous otitis externa
    *
156
Q

dx for feline dermodecosis

A
  • superficial skin scraping -non affected cats
  • acetate tape
  • fecal floats
  • emperical treatment and response to lime sulfur dips
157
Q

treatment for feline dermodicosis

A
  • lime sulfur dips- 1-2 times per week
  • amitraz dips-anorexia,lethargy,diarrhoea
  • D. cati
    can resolve spontaneously if
    underlying disease is addressed
158
Q

walking dundraft

A
  • Cheyletiellosis
  • C. blakei, C. yasguri, C. parasitovorax
159
Q

discuss the characteritics for Cheyletiellosis

  • where it lives
  • feeding habits
  • transmission
A
  • Live on hair, feed on skin

–

  • Very superficial!

•

  • Highly contagious

–

  • Often more than one pet affected

•

  • Uncommon, but can be common in areas

where flea preventatives not used

160
Q

discuss the pathogenesis of Cheyletiellosis

A
  • Transmission via direct contact with infested animals, through fomites

•

  • Hypersensitivity reaction likely

•

  • Occasionally zoonotic
161
Q

cs of Cheyletiellosis

A

Scaling/crusting*
•
Miliary dermatitis
•
Walking dandruff
•
Primarily a disease that causes dorsal lesions*
•
Pruritus is absent to severe

162
Q

treatment for Cheyletiellosis

A

Acaricidal therapy

Selamectin q 2 weeks, 3 times
•

  • Ivermectin
  • 2% lime sulfur
  • •

Amitraz
•
Milbemycin oxime
•
Treat all in-contact mammals!

163
Q

Superficial fungal infection of hair shafts
and stratum corneum

A
  • Dermatophytosis

•

  • Microsporum canis

(zoophilic)
•

  • Microsporum canis
  • Microsporum gypseum (geophilic )

•

  • Trichophyton mentagrophytes

(zoophilic)
•
Transmission by direct-indirect contact

164
Q

which dermatophytosis is common in cats

A
  • M. canis

* in 98% of cases
•

  • Zoonotic

•

  • Common in Long haired cats, shelters, multi haired cats, shelters, multi

-
cat homes cat homes
•

  • Asymptomatic carriers

–
Long-haired cats, Persians
•

  • Young, immunocompromised more

susceptible

165
Q

what are the cs of dermatophytosis

A
  • Highly variable
  • Circular areas of alopecia with erythematous border
  • Transient follicular pustules
  • Miliary dermatitis
  • Scale/crusts absent to severe
  • Rarely, dermal nodules

(pseudomycetoma)
•

  • Pruritus variable
166
Q

Dx forDermatophytosis (cats)

A
  • Wood’s lamp examination

–
Only 50% of M.canis will fluoresce

  • Trichogram
  • Fungal culture and ID
  • Biopsy + special stains (PAS)
167
Q

discuss treatment of dermatophytosis in cats

A

Treatment of individuals:
•
Identify all affected animals/carriers
•
Everyone receives treatment
•
Quarantine
•
Clipping hair (controversial)
•
Treat until 2 consecutive negative fungal
cultures

168
Q

discuss topical treatment of dematophytosis in cats

A

Lime sulfur dips

169
Q

disadvantages of treating dermatophytosis in cats with sulfur dips

A
  • Will stain white cats

–

  • Smells awful

–

  • Remove silver jewelry
170
Q

discuss systemic therapy of dermatophytosis

A
  • Itraconazole/fluconazole 7-10mg/kg PO q 24h

–

  • Cats do not tolerate ketoconazole

–

  • Terbinafine ~40mg/kg PO q 24h
171
Q

treatment of environment for dermatophytosis

A
  • Dilute bleach 1:10 for all hard surfaces
  • Change air filters
  • Throw away anything that may harbour spores

•

  • Steam clean carpets, drapes, wash bedding
  • Enilconazole
172
Q

cs of food allergy dermatitis in cats

A

Pruritus

  1. Self-induced alopecia

Typically neck, back, lumbar skin

  1. Papules, miliary dermatitis
  2. Eosinophilic skin disease
173
Q

what iis the most common allergen in cats

A

fish

174
Q

cs of Food allergy/intolerance

(cutaneous cutaneous adverse food reaction)

A
  • Pruritus

**Face/neck in 40-50% of cases

  • Self-induced alopecia

Focal, generalized, bilaterally symmetrical,
regional

  • Papules, miliary dermatitis
  • Eosinophilic skin disease
175
Q

other cs of Cutaneous adverse food reaction

A
  • Vomiting, diarrhea concurrent in 10% of
  • If GI signs and pruritus = food allergy
  • Lymphocytic-plasmacytic colitis
176
Q

what causes feline topical dermatitis

A
  • Type I hypersensitivity reaction
  • similiar to dogs
  • Signalment is not well characterized
  • Barrier dysfunction not characterized in cats
177
Q

what are the cs of Feline atopic dermatitis (syndrome)

A
  • Pruritus
  • Self-induced alopecia

Focal (facial), generalized, bilaterally
symmetrical, regional

  • Papules, miliary dermatitis
  • Eosinophilic skin disease
  • Sneezing, respiratory signs
178
Q

Diagnostic approach to the pruritic cat

A
  • Rule out ectoparasites
  • . Implement strict flea preventative program

–Selamectin, spinetoram

  • If skin lesions present,–cyt/bx
  • . Treat secondary infections if present
  • . Begin elimination diet trial 8-12 weeks
  • . Diagnosis of atopic dermatitis
179
Q

Treatment for feline atopic dermatitis

A
  • Chlorpheniramine 2/kg/12 hours

–

  • PreniSOlone 1 – 1.5mg/kg/day
  • Methylprednisolone 0.8mg/kg/day

–

  • Cyclosporine A 7mg/kg/day
  • Allergy testing + allergen-specific
    immunotherapy
180
Q

discuss Feline allergy testing

A
  • Some dermatologists do NOT recommend doing IDAT (intradermal allergy testing) because cats do not make “nice” wheal-flare reactions
  • Serum allergy testing
    • Allergy testing is only recommended if owners want to follow through with hyposensitization with allergen-specific immunotherapy (ASIT)
  • *
181
Q

what are the most common allergens ASAIT( cats(

A
  • House dust mites,
  • house dust,
  • weeds,

grass

, tree pollens

182
Q

feline allergy dermatitis treatment

A
  • Antihistamines:
              Pretty safe
  • Glucocorticoids:
               PU/PD/PP not as common in cat --\>Skin                                fragility,  Curling of pinnae
  • Cyclosporine A
                 GI upset, weight loss, possible renal toxicity
183
Q
A
184
Q

what predispose the cats toEosinophilic granuloma complex (EGC) / Eosinophilic skin disease

A
  • Genetic predisposition to aeosinophilic response
  • persensitivity reaction (fleas, food, environmental allergens…)
185
Q

list the 3 main clinical presentation of Eosinophilic granuloma complex (EGC) / Eosinophilic skin disease

A
  • Eosinophilic plaque
    :
  • Eosinophilic granuloma
  • Indolent ulcer
186
Q

describe eosinophilic plaque in Eosinophilic granuloma complex (EGC) /Eosinophilic skin disease

A
  • erythematous pruritic coalescing papules and plaques (groin, abdomen)
    *
187
Q

describe eosinophilic granuloma in Eosinophilic granuloma complex (EGC) /Eosinophilic skin disease

A

: nodules, nodules, plaques with
variable pruritus (rear thighs, footpad, lower
lip, oral cavity)

188
Q

describe indolesent ulcer in Eosinophilic granuloma complex (EGC) /Eosinophilic skin disease

A

non-pruritic, non-painful
unilateral or bilateral non-bleeding ulcers
(upper lip

189
Q

what are the clinical presentation of cutaneous and mucocutaneous erossive-ulcerative disease

A

Erythema,

depigmentation,

erosions,

ulcerations

and crusts

  • Occasionally, vesicles / pustules are seen
    •
    Pruritus is minimal, not the main complaint
190
Q

what are the specific areas affected by cutaneous and muco-cutaneous erosive-ulcerative disease

A
  • nose(planum nasale)
  • fooodpads
  • mucosal membranes( oral,urogenital)
191
Q

Clinical diagnostic criteria for cutaneous n mucocutaneous erosive -ulcerative disease

A
  • Uncommon diseases
  • Adult dogs
  • Chronic/progressive diseases
  • Non-pruritic
  • Non-antibiotic or corticosteroid responsive
  • Symmetrical lesions (erosions, ulcers, pustules,crusts)
  • Presence of lesions in non-haired skin and MM
  • Possible concurrent systemic signs
192
Q

list the cutaneous and mucocutaneous erosive-ulcerative diseases which are autoimmune

A
  • Discoid lupus erythematous (DLE),
  • Pemphigus foliaceus,

Uveo-dermatologic syndrome (VKH)

193
Q

list the cutaneous and mucocutaneous erosive-ulcerative diseases which are immune mediated

A
  • Erythema multiforme (EM) / Toxic epidermal necrolysis (TEN),
  • Adverse drug reactions
194
Q

list the cutaneous and mucocutaneous erosive-ulcerative diseases which are metabolic

A

Superficial necrolytic dermatitis

(NME / hepatocutaneous syndrome)

195
Q

list the cutaneous and mucocutaneous erosive-ulcerative diseases which is neoplasia

A

Epitheliotrophic T-cell lymphoma

196
Q

Autoimmune skin disease characterized by formation
of subcorneal pustules due to
acantholysis

A

Pemphigus folicaeus

197
Q

discuss pampificus folicaeus

A
  • breaking of intercellular bridges-desmosomes resulting in intrathelial blister formation
  • Vesicles contain acantholytic cells and variable numbers of polymorphonuclear (PMN) cells
198
Q

what causes Pemphigus folicaeus

A

IgG autoantibodies against desmosomal
proteins (autoimmune mechanism)

  • Humans–target is desmoglein I
  • Dogs–desmocollin I
199
Q

list the Three main clinical presentations (lesions): of pampifigus foliaceous

A
  1. Papules, pustules,collarettes, crusts (yellowish);generalized
  2. 2Depigmentation, erosions, ulcers, crusts on planum nasale, dorsal muzzle, pinnae, periocular skin
  3. Footpad hyperkeratosis

Single patient can present with 1, 2 or 3

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small animal medicine (1 decks)

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