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Vet Derm Review > SAD - Chapter 16 - Environmental Skin Dz > Flashcards

SAD - Chapter 16 - Environmental Skin Dz Flashcards

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Dermatology Board Prep flashcards
1
Q

Which is more erythemogenic: UVA or UVB?

A

UVB – known as the sunburn or erythema spectrum

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2
Q

Which penetrates deeper into the skin: UVA or UVB?

A

UVA – spectrum associated with photosensitivity reactions

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3
Q

What are natural barriers to UV light damage?

A

stratum corneum, melanin, blood, carotenes

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4
Q

_____ is the classic sunburn reaction and is a dose-related response to light exposure.

A

Phototoxicity

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5
Q

_____ occurs when the skin has increased susceptibility to the damaging effects of UV light because of the production, ingestion, injection of, or contact with a photodynamic agent.

A

Photosensitivity

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6
Q

T/F: Solar dermatitis is purely a phototoxic reaction.

A

True - sunburn type reaction

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7
Q

Histopathological features of solar dermatitis

A

clusters of vacuolated keratinocytes in the superficial epidermis (sun-burn cells), apoptotic keratinocytes, vascular dilatation and leakage

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8
Q

How quickly do apoptotic keratinocytes occur after UVA exposure? By what mechanism is apoptosis induced?

A

biphasic apoptosis – seen within 4 hours due to UVA’s direct damaging effect on the cell membrane; seen 24 hours after exposure – due to DNA alteration

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9
Q

What are the key features of nasal solar dermatitis?

A

restriction of lesions to sun-exposed, nonpigmented, sparsely haired skin; onset of signs after solar exposure; absence of skin lesions in the affected area before the condition began; complete resolution with removal from sunlight

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10
Q

What are some of the long-term consequences of nasal solar dermatitis?

A

scarring, squamous cell carcinoma

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11
Q

DDX for nasal solar dermatitis

A

DLE, SLE, dermatomyositis, epidermolysis bullosa, pemphigus foliaceus, pemphigus erythematosus, drug reaction, infectious folliculitis, neoplasia, vasculitis, granulomatous diseases

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12
Q

Histopathological features of nasal solar dermatitis

A

early depigmented areas of nose – fewer melanocytes and less melanin pigment; after exposure to solar radiation –> epidermal hyperplasia with intraepidermal edema; vacuolated (sunburn cells) and apoptotic keratinocytes; superficial perivascular dermatitis, vascular dilatation; solar elastosis (basophilic degeneration of elastin); bandlike superficial dermal fibrosis

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13
Q

What stain can help to highlight solar elastosis (basophilic degeneration of elastin)?

A

Verhoeff stain

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14
Q

Feline solar dermatitis is most common in what color of cats? What areas are most affected?

A

white cats – ears&raquo_space; eyelids, nose, lips

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15
Q

DDX for feline solar dermatitis affecting the pinna

A

dermatophytosis, notoedric mange, fight wounds, vasculitis, frostbite, cryoglobulinemia, DLE, SLE, PE, PF

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16
Q

Histopathological features of feline solar dermatitis

A

superficial perivascular dermatitis (spongiotic, hyperplastic changes); vacuolated (sunburn cells) or apoptotic keratinocytes; solar elastosis in the superfical dermal connective tissue; with SCC –> epidermal surface becomes ulcerated and the dermis is invaded by nests of polyhedral epithelial tumor cells

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17
Q

Treatments for feline solar dermatitis

A

avoidance of sun; sunscreen; Beta-carotene, canthaxanthin; retinoic acids; superficial irradiation with strontium probe; imiquimod; surgical removal

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18
Q

What breeds are predisposed to truncal solar dermatitis?

A

dalmatian, American Staffordshire terrier, German shorthaired pointers, white boxers, whippets, beagles, and white bull terriers

19
Q

Describe the progression of lesions of truncal solar dermatitis

A

sunburn (erythema, scale) –> actinic folliculitis, actinic follicular cyst formation, dermal fibrosis –> erosions, ulceration, crusting, comedones –> necrosis, fistulae, scarring –> squamous cell carcinoma

20
Q

What is different in the areas of the body that are affected by solar dermatitis vs. photosensitivity?

A

Photosensitivity can occur in well-haired regions of the body; solar dermatitis affects lightly haired areas

21
Q

UV light may induce or exacerbate the lesions of what underlying skin conditions?

A

DLE, SLE, pemphigus foliaceous/erythematosus, pemphigoid

22
Q

What layers of the skin are affected with superficial burns?

A

epidermis

23
Q

What layers of the skin are affected with partial-thickness burns?

A

epidermis and superficial dermis

24
Q

What layers of the skin are affected with full-thickness burns?

A

epidermis, dermis, adnexa

25
Q

What organisms colonize burn wounds?

A

initially – gram positive, 3-5 days later –> gram-negative flora (P. aeruginosa)

26
Q

What is a diagnostic histopathological feature of electric burns?

A

fringe of elongated degenerated cytoplasmic processes that protrudes from the lower end of the detached basal cells into the space separating the epidermis and the dermis; nuclei of the basal cells appear stretched in the same direction as the fringe of cytoplasmic processes (keratinocytes “standing at attention”)

27
Q

T/F: Systemic antibiotics are useful to prevent burn wound infection.

A

False - not effective and may allow invasion by resistant organisms

28
Q

Histopathological features of radiant burns

A

nonulcerated lesions – hyperplastic with surface and infundibular hyperkeratosis; keratinocyte atypia, karyomegaly, basaloid dysplasia; focal hydropic degeneration of basal cells and pigmentary incontinence; occasional apoptotic cells in suprabasilar layers; superficial dermal mucinosis; wavy eosinophilic elastin fibers in the superficial dermis

29
Q

How long after radiation therapy do skin changes appear? Why?

A

2-3 weeks later; treatment stops the mitotic activity of the epidermis, melanocytes, hair follicles, sebaceous glands

30
Q

What is the pattern of progression with radiation burns?

A

scaly/alopecic –> exudation and ulceration

31
Q

Why should an animal have skin testing before administration of antivenin?

A

contains horse serum –> can lead to anaphylaxis

32
Q

T/F: Antibiotics should be administered after a snake bite.

A

True – snake bites are contaminated with oral flora, which often includes Pseudomonas spp. And Clostridium tetani

33
Q

What analgesics should be avoided after a snake bite? Why?

A

morphine and NSAIDs –> might result in histamine release or predispose to clotting disorders

34
Q

T/F: Pit viper bites always inject venom.

A

False - 20-25% of pit viper bites can be dry; if no pain or swelling at the bite site occurs within 1.5 hours of the bite, no venoma was injected

35
Q

Cutaneous lesions of snake bites with venom

A

rapid progression of edema (obliterates the fang marks), pain, hemorrhage –> ecchymosis and discoloration –> necrosis and sloughing

36
Q

T/F: Antivenin should be given to all animals with a snake bite.

A

False – for maximum efficacy, needs to be administered within 4 hours of the bite, given 8 hours after a bite –> little value

37
Q

What is Hordeum jubatum?

A

foxtail

38
Q

What is Arctium spp.?

A

burdock

39
Q

Myospherulosis

A

rare granulomatous reaction thought to be due to the interactioin of ointments, antibiotics, endogenous fat, oily contents of cysts with erythrocytes

40
Q

T/F: Skin lesions are not seen in acute thallium intoxication.

A

TRUE

41
Q

Clinical signs of chronic thallium poisoning

A

hyperemic mucous membranes, mild to moderate GI signs, skin lesions of erythema & alopecia, hyperkeratosis and ulceration of footpads

42
Q

Hygroma

A

false or acquired bursa that develops subcutaneously over bony prominences

43
Q

Histopathological features of hygromas

A

cystic spaces surrounded by dense walls of granulation tissue, inner layer of which is a flattened layer of fibroblasts

Vet Derm Review (44 decks)

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