Lecture 3 11/27/25 Flashcards

1
Q

What are the responses of the epidermis to injury?

A

-changes in growth or differentiation
-changes in fluid balance or cell adhesion
-inflammation
-alterations in epidermal pigment

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2
Q

What are the potential alterations in epidermal growth/differentiation?

A

-hyperkeratosis
-epidermal hyperplasia
-dysplasia
-atrophy
-dyskeratosis/apoptosis/necrosis

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3
Q

What are the characteristics of hyperkeratosis?

A

-increased thickness of stratum corneum/keratin layer
-can be a non-specific reaction to chronic stimuli

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4
Q

What are the conditions that cause orthokeratotic (lacking nuclei) hyperkeratosis?

A

-seborrhea
-ichthyosis
-vitamin A deficiency

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5
Q

What are the conditions that cause parakeratotic (retaining nuclei) hyperkeratosis?

A

-zinc-responsive dermatosis
-superficial necrolytic dermatitis

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6
Q

What are the characteristics of epidermal hyperplasia?

A

-increased thickness of epidermis due to increased number of cells
-typically in stratum spinosum; termed acanthosis
-non-specific response to chronic stimuli

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7
Q

What are the characteristics of rete pegs?

A

-down-growths of epidermis into dermis
-normal in areas of high friction
-seen in areas with chronic irritation (abnormal)

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8
Q

What are the characteristics of epidermal hysplasia?

A

-abnormal development of the epidermis
-disorganization of any of the epidermal layers
-typically occurs in basal cells
-often a pre-neoplastic lesion

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9
Q

What is epidermal atrophy?

A

decrease in the number and size of cells within the epidermis

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10
Q

What are the possible causes of epidermal atrophy?

A

-hyperadrenocorticism
-partial ischemia
-severe malnutrition

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11
Q

What are the characteristics of dyskeratosis, apoptosis, and necrosis?

A

-distinct pathogenesis that are histologically identical
-cells become shrunken and hyper

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12
Q

Which diseases have dyskeratosis/apoptosis/necrosis confined to the basal layer?

A

-discoid lupus
-mucocutaneous pyoderma

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13
Q

Which disease has dyskeratosis/apoptosis/necrosis in multifocal spots throughout all layers?

A

erythema multiforme

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14
Q

Which diseases have dyskeratosis/apoptosis/necrosis in a diffuse pattern/full thickness?

A

-toxic epidermal necrolysis
-thermal injury

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15
Q

What are the potential consequences of alterations in the epidermal adhesion molecules?

A

-edema/fluid buildup
-acantholysis/loss of cell adhesion

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16
Q

What are the mechanisms of vesicle formation?

A

-widening of intercellular spaces due to worsening edema; causes spongiosis
-loss of cells due to worsening edema; causes ballooning degeneration/intra-cellular edema
-loss of intercellular junctions resulting in separation of cells; causes acantholysis

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17
Q

Which disease processes can lead to acantholytic cells?

A

-immune-mediated processes
-neutrophilic enzyme destruction

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18
Q

How do acantholytic cells differ from apoptotic cells on cytology?

A

-acantholytic cells are typically disassociated from other cells
-apoptotic cells are not disassociated from other cells

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19
Q

How does vesicle location and appearance within the epidermis differ with different pemphigus types?

A

-pemphigus folicaceous: vesicle develops “between” epidermis and stratum corneum and contains acantholytic cells
-pemphigus vulgaris: vesicle develops “between” epidermis and dermis and contains acantholytic cells
-bullous pemphigoid/thermal burns: vesicle develops “between” epidermis and dermis with no acantholytic cells

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20
Q

What is exocytosis?

A

inflammatory cells “walking” through the epidermis

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21
Q

What is a pustule?

A

accumulation of cells in the epidermis that have moved via exocytosis

22
Q

Which cells accumulate in a pustule and when?

A

-neutrophils: bacterial infection, pemphigus
-eosinophils: ectoparasites, pemphigus

23
Q

When do crusts form?

A

as pustules dry up and are pushed off by the hyperplastic epidermis

24
Q

What are the potential alterations in epidermal pigmentation?

A

-hyperpigmentation
-pigmentary incontinence

25
Q

What are the characteristics of hyperpigmentation?

A

-most commonly due to increased production of melanin by existing melanocytes
-pigment may be in all layers of epidermis
-can occur with chronic inflammatory disease and endocrine dermatoses

26
Q

What is the less common cause of hyperpigmentation?

A

proliferation of melanocytes

27
Q

What are the characteristics of pigmentary incontinence?

A

-loss of melanin from the pigmented cells in the basal layer
-non-specific change associated with inflammation
-seen with discoid lupus, mucocutaneous pyoderma, and uveodermatologic syndrome

28
Q

What are the responses of the dermis to injury?

A

-alterations in growth
-collagen degradation
-dermal deposits
-inflammation in the dermis

29
Q

What are the characteristics of dermal atrophy?

A

-decrease in the quantity of collagen fibrils and fibroblasts in the dermis
-seen in hyperadrenocorticism

30
Q

What are the characteristics of collagen degradation?

A

-hyper-eosinophilic “flame figures”
-degradation is surrounded by eosinophils and major basic protein
-seen with eosinophilic diseases

31
Q

Which eosinophilic diseases can lead to collagen degradation?

A

-feline eosinophilic granuloma complex
-canine eosinophilic granulomas
-equine nodular necrobiosis
-habronemiasis
-mast cell tumors

32
Q

What are dermal deposits?

A

deposits within the dermis that lead to expanding and separating of normal skin

33
Q

When are dermal deposits seen?

A

-shar peis (normal for breed)
-hypothyroidism

34
Q

What is calcinosis cutis?

A

-mineralization of collagen that occurs with no pattern
-seen with hyperadrenocorticism

35
Q

What is calcinosis circumscripta?

A

mineralization of collagen that is deposited in nodules

36
Q

What are the different patterns of dermatitis?

A

-perivascular
-vasculitis
-interface
-nodular/diffuse

37
Q

What are the characteristics of perivascular dermatitis?

A

-inflammatory cells are centered around blood vessels
-usually superficial
-not specific

38
Q

What are the characteristics of vasculitis dermatitis?

A

-inflammation targets walls of blood vessels
-consists of damage to vessel wall, fibrin deposition, thrombosis, and hemorrhage
-results in ischemia
-seen in immune-mediated disease and sepsis

39
Q

What are the characteristics of interface dermatitis?

A

-superficial dermal inflammation
-inflammatory cells surround dermo-epidermal junction
-damage to basal cells occurs
-obscuring of dermo-epidermal junction
-pigmentary incontinence

40
Q

What is lichenoid?

A

interface dermatitis in which there is just a band beneath the dermis with no obscuring

41
Q

What are the characteristics of nodular to diffuse dermatitis?

A

-usually infectious
-pathogenesis varies with type of inflammatory cell present
-can be sterile

42
Q

How do the different inflammatory cells indicate the pathogenesis of nodular to diffuse dermatitis?

A

-neutrophils: bacterial
-granulomatous: fungi or foreign body
eosinophils: parasites
-lymphocytes and plasma cells: non-specific

43
Q

What are the responses of the adnexa to injury?

A

-alterations in growth
-inflammation of the adnexa

44
Q

What can lead to atrophy of the adnexa?

A

-endocrine disease
-ischemia

45
Q

What can lead to hypertrophy of the adnexa?

A

chronic irritation

46
Q

What are the characteristics of folliculitis?

A

-usually infectious
-can be immune-mediated
-progresses to furunculosis

47
Q

What are the characteristics of furunculosis?

A

-inflammation associated with follicular rupture
-free keratin/hairs act as foreign bodies in dermis
-leads to granulomatous inflammation

48
Q

What is sebaceous adenitis?

A

immune-mediated reaction targeting the sebaceous glands that can result in a total loss of the glands

49
Q

What are the changes in growth seen in the panniculus?

A

-atrophy due to chronic negative energy balance
-hypertrophy due to obesity

50
Q

What are the potential causes of panniculitis?

A

-infectious
-immune-mediated
-nutritional
-pancreatic disease
-idiopathic
-vaccine/injection site reaction
-trauma