Chapter 16 - Environmental Flashcards

1
Q

Is UVA or UVB associated with photo-sensitivity reactions?

A

UVA

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2
Q

Which UVA wavelengths are most damaging?

A

320-340nm

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3
Q

Is solar dermatitis a photo-toxic or -sensitive reaction?

A

Phototoxic

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4
Q

Why do you get a second, late-phase keratinocyte apoptosis 24hrs after UVA exposure?

A

DNA alteration

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5
Q

When does immediate apoptosis occur after UVA exposure?

A

Within four hours of UVA exposure

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6
Q

Solar dermatitis can progress to which neoplasm?

A

SCC

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7
Q

What are the first signs of feline solar dermatitis?

A

Erythema and fine scaling of the pinnal margins

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8
Q

Which colour skin is most affected by photosensitivity?

A

White/light colour

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9
Q

What are the primary lesions of irritant contact dermatitis?

A

Erythema and papules

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10
Q

Do heat pad burns cause hard, dry skin or erosive/necrotic lesions?

A

Hard, dry skin

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11
Q

Do chemical, electrical, solar and microwave burns cause hard, dry skin or erosive/necrotic lesions?

A

Erosive/necrotic

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12
Q

Gram negative bacterial infections occur how many days after burn wounds appear?

A

Three to five days

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13
Q

Which histopathological finding is typical of a thermal/chemical burn?

A

Gradually tapering coagulation necrosis of the epidermis and deeper tissues

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14
Q

Which type of burn causes full thickness coagulation necrosis?

A

Microwave

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15
Q

Which type of burn causes a fringe of elongated cytoplasmic process from detached basal cells?

A

Electric

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16
Q

Which type of burn causes epidermal necrosis with subepidermal vesicle formation?

A

Superficial

17
Q

Which type of burn has a drip formation?

A

Radiant heat burns

18
Q

What is the pathogenic mechanism of radiation burns?

A

Mitotic activity of the epidermis, melanocytes, hair follicles and sebaceous glands stops. There is a two to three week lag before clinical signs are apparent.

19
Q

Which cells line the cystic spaces formed with hygromas?

A

Flattened fibroblasts

20
Q

How do decubital ulcers form?

A

Pressure concentrated over a bony prominence compresses capillary circulation causing tissue damage +/- necrosis.

21
Q

What depth do grades 1, 2, 3 and 4 decubital ulcers reach?

A
1 = epidermis and superficial dermis
2 = stops at subcutis
3 = deep fascia
4 = bone
22
Q

How can you differentiate canine nasal solar dermatitis from DLE/PF/PE?

A

Nasal architecture is unaffected

Restricted to non-pigmented, sparsely haired areas, typically junction of haired skin and nasal planum affected

23
Q

Dorsal thermal necrosis has been reported in which species?

A

Dogs, sheep and a pot-bellied pig

24
Q

What are the reported risk factors for dorsal thermal necrosis?

A

Short, dark hair, recent shearing in sheep, high sunlight intensity and temperatures, obesity (sheep)

25
Q

The exact cytokine profile of irritant contact dermatitis is unknown and likely varies between patients and chemicals; which cytokines appear to play central roles in the pathogenesis of ICD in people?

A

IL-1a, IL-1b and TNF-a

26
Q

In irritant contact dermatitis, in addition to their action in the epidermis, cytokines released by keratinocytes also affect dermal cells leading to fibroblasts producing what?

A

Fibroblasts start producing collagenases and prostaglandin E, further worsening cell injury and local inflammation.

27
Q

What is myospherulosis?

A

Very rare, granulomatous reaction (solitary dermal or SC nodule +/- draining tract)
Interaction of ointments, antibiotics or endogenous fat with erythrocytes
Small, saclike structures (parent bodies) filled with endobodies (spherules)
Commonly reported after injection of or topical application to wounds of oil-based products

28
Q

What are the histopathological changes seen with erythema ab igne?

A
  • Cell poor interface dermatitis
  • Epidermal acanthosis
  • Keratinocyte nuclear atypia
  • Karyomegaly
  • Occasional keratinocyte apoptosis
  • Follicular atrophy
  • Increased superficial dermal mucinosis, collagen fiber attenuation and thick, wavy eosinophilic elastic fibers