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Systemic Pathology > Derm Path Vocab > Flashcards

Derm Path Vocab Flashcards

1
Q

Define acantholysis

A
  • loss of cohesion b/t keratinocytes due to the breakdown of intercellular bridges
  • can be due to immune destruction (i.e. pemphigus) or neutrophilic enzymatic destruction
  • usually assoc. w/ formation of pustules, vesicles, bullae, or clefts
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2
Q

Define acanthosis

A
  • hyperplasia, thickening of the spinous cell layer (stratum spinosum) of the epidermis
  • get rete ridge formation
    • regular (even rete ridge size)
    • irregular (uneven; more common)
    • papillated (surface projections)
    • pseudocarcinomatous (long, irregular, anastomosing rete ridges extending into dermis)
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3
Q

What is alopecia?

A

hair loss

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4
Q

What does anagen mean?

A

phase of hair cycle in which hair synthesis takes place

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5
Q

What is anaplasia?

A

lack of cellular differentiation and organization, a feature of neoplastic cells

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6
Q

Define angioedema

A
  • vascular reaction involving the deep dermis or subcutis and consisting of edema manifested as giant wheals and caused by dilation and incr permeability of capillaries (deeper version of urticaria)
  • often seen with Type I hypersensitivity reactions (insect bites, vax rxns, food allergy, atopy, drug reactions)
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7
Q

What is ballooning degeneration?

A
  • markedly swollen, eosinophilic keratinocytes usually in the more superficial layers of the epidermis
  • most freq assoc. w/ viral infections
  • can lead to vesicle formation
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8
Q

Define carcinoma in situ

A

a malignant neoplasm of epithelial origin that has not invaded through the basement membrane

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9
Q

Define catagen

A

transition phase of the hair cycle b/t growth and resting phases

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10
Q

Define dermatophytosis

A

infection of the stratum corneum of the epidermis, hair or claws with fungi of the genera Microsporum, Epidermophyton, or Trichophyton

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11
Q

What’s the difference b/t dermatitis and dermatosis?

A
  • dermatitis = inflammation of the dermis
  • dermatosis = noninflammatory lesion of the skin
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12
Q

Define dyskeratosis

A
  • premature keratinization of cells within the epidermis
  • dyskeratotic cells are rounded up, hypereosinophilic and have nuclear degeneration
  • common with parakeratosis and hyperplasia
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13
Q

Define elastosis

A

degeneration of dermal CT leading to accumulation of elastotic fibers; sometimes seen with solar dermatitis

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14
Q

Define epidermolysis

A

separation of the epidermis from the dermis

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15
Q

Define excoriation

A

superificial loss of epidermal layers due to physical trauma (scratching)

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16
Q

Define exogen

A

the stage of hair cycle where old hairs are shed

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17
Q

Define furuncle

A

circumscribed, painful nodule (accumulation of pus) in the dermis secondary to follicular rupture

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18
Q

Define furunculosis

A
  • rupture of follicles usually due to inflammation, distension, and/or trauma leading to entry of follicular contents into the dermis
  • seen most commonly with luminal folliculitis
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19
Q

Define genodermatosis

A

genetically determined disorder of skin

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20
Q

What is hydropic degeneration?

A
  • intracellular fluid accumulation in cells of the basal layer or outer follicular root sheath and can result in the separation of the epidermis and dermis
  • keratinocytes usually contain vacuoles
  • seen with SLE, drug eruptions, dermatomyositis
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21
Q

Define hyperkeratosis

A
  • histologic term for thickening of stratum corneum; can occur secondary to trauma or inflammation or as a specific characteristic of certain diseases
  • orthokeratotic or parakeratotic
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22
Q

Define ichthyosis

A

congenital skin disorder in which the skin is thickened by scales (hyperkeratosis) that can crack into plates resembling fish scales

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23
Q

Define impetigo

A

bacterial dermatitis characterized by pustules

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24
Q

Define indurated

A

hardening of skin due to inflammation or fibrosis

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25
Q

Define interface

A

inflammation arranged in a layer close to and often obscuring the epidermal-dermal junction (interface), and with vacuolated (hydropic degeneration) and sometimes apoptotic basal cells; can be mild (cell poor) or extensive (cell rich)

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26
Q

Define intertrigo

A

dermatitis that develops b/c of friction b/t apposing skin surfaces (e.g. adjacent folds)

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27
Q

Define keratinocytes

A

the epidermal cells that synthesize keratin and comprise more than 90% of epidermal cells

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28
Q

What are Langerhans’ cells?

A

intraepidermal dendritic antigen-presenting cells

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29
Q

Define lichenification

A

thickening of skin with accentuation of skin creases due to marked acanthosis

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30
Q

Define macule

A

flat, circumscribed lesion of altered skin color

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31
Q

What is a Merkel cell?

A

a neuroendocrine cell found in the stratum basale

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32
Q

What is panniculitis?

A
  • inflammation of subcutaneous adipose tissue
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33
Q

What is parakeratosis/parakeratotic hyperkeratosis?

A
  • thickening of stratum corneum with retention of nuclei
  • indicates cornification process is abnormal
  • e.g. superficial necrolytic dermatitis, Zn responsive dermatosis
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34
Q

What are Pautrier’s microabscesses?

A

a localized intraepidermal collection of neoplastic lymphocytes characteristic of epitheliotrophic lymphoma (mycosis fungoides)

35
Q

What is pemphigus?

A

a group of cutaneous diseases associated with blistering

36
Q

Define pigmentary incontinence

A

melanin pigment within dermal macrophages or free in the dermis developing via injury to pigment containing basal layer cells

37
Q

What is seborrhea?

A

nonspecific term for clinical signs of scaling, crusting, and greasiness. Primary seborrhea is a more specific term applied to cornification disorders

38
Q

What is spongiosis?

A
  • intercellular edema which, by widening of the intercellular space and stretching of the intercellular bridges, creates a spongelike appearance of the epidermis
  • seen with inflammation, contact irritant dermatitis, feline eosinophilic plaques
  • severe spongiosis can lead to vesicle formation
39
Q

What is telogen?

A

resting phase of the hair cycle

40
Q

What is urticaria?

A

usually transient vascular reaction in the upper dermis consisting of edema manifested clinically as wheals (hives); a more superfical version of angioedema

41
Q

What is vitiligo?

A

direct damage to melanocytes due to immunogens on the surface of these cells

42
Q

What is orthokeratotic hyperkeratosis?

A
  • buildup of excess keratin after normal cornification has occurred (cells have lost their nuclei)
    • can be d/t excess production or lack of exfoliation of keratin
    • can be loosely arranged (endocrine dermatosis) or compact (chronic trauma)
43
Q

What is hypergranulosis?

A
  • increase in width of stratum granulosum, incr in cells with keratohyalin granules
  • lack of stratum granulosum in a hyperplastic epidermis may indicate incr epidermal turnover time w/ altered differentiation
44
Q

Define apoptosis

A
  • programmed cell death
  • usually seen in basal layer but can become transepidermal in some dz states
  • apoptotic keratinocytes resemble dyskeratotic keratinocytes and are shrunken and hypereosinophilic
  • often seen with immune mediated dz; e.g. systemic lupus erythematosus, erythema multiforme
45
Q

What are potential causes of epidermal necrosis?

A
  • physical injury, chemical exposure, ischemia, adverse drug reactions
  • injured cells release contents into extracellular space and incite inflammation
46
Q

Describe atrophy

A
  • thinning of the epidermis due to decr in # and size of cells of the epidermis
  • consequence of sublethal injury
  • most common cause: endocrine dermatoses, but can occur w/ partial ischemia, malnutrition
47
Q

What is intrakeratinocyte fluid accumulation typically seen with and what does the skin look like histologically?

A
  • superficial necrolytic dermatitis
  • cells appear enlarged and are pale staining
48
Q

What are clefts?

A

empty slit like spaces in the epidermis or at the epidermal/dermal junction; form from mechanisms similar to vesicles

49
Q

What is exocytosis?

A
  • migration of leukocytes or RBCs into the epidermis; if keratinocytes are damaged, they release cytokines that recruit inflamm cells
    • Neutrophils: nonspecific, common w/ bacterial dz
    • Eosinophils: allergic dz, ectoparasites
    • Lymphocytes: immune mediated, ectoparasites, atopy, seborrhea, mycosis fungoides
50
Q

What is hyperpigmentation?

A
  • incr in melanin in the epidermis and possibly in dermal melanophages; non specific change that occurs in any chronic dermatitis
51
Q

What are lentigines?

A

focal areas of hyperpigmentation that correspond to melanocyte hyperplasia; common in cream, orange, tricolored cats, rare in dogs

52
Q

What is hypopigmentation?

A
  • most often acquired d/t damage to melanocytes and adjacent keratinocytes or basal layer –> leads to pigmentary incontinence
  • seen with SLE, drug eruptions, pemphigus, mycosis fungoides, vitiligo
  • very characteristic of uveodermatologic syndrome
53
Q

What are the definitions of leukoderma and leukotrichia?

A
  • decr pigmentation of skin and hair, respectively
54
Q

What is follicular hyperkeratosis seen with?

A
  • primary seborrhea, vitamin A responsive dermatosis, and endocrine dermatoses
55
Q

What is follicular atrophy?

A
  • shrinking of hair follicles typically seen in endocrinopathies, ischemia, traction (tight bows on Yorkies); may also occur as a physiologic process related to normal cyclic changes
56
Q

What is follicular dysplasia?

A
  • abnormal development of hair follicle that leads to alopecia
  • most associated with uncommon coat colors (blue, fawn) –> Color Mutant Alopecia
57
Q

Define folliculitis

A
  • hair follicles are the primary focus of the inflammatory infiltrate
    • luminal: inflamm within lumen of follicle; e.g. bacterial (Staph), fungal (dermatophytosis), or parasitic dz (demodicosis)
    • mural: leukocytes target the wall; e.g. feline mosquito bite hypersensitivity
    • bulbar: e.g. alopecia areata
58
Q

What are the various layers of the epidermis and what are specific characteristics of each?

A
  • Stratum corneum - mostly dead, fully keratinized cells, flattened, most superficial
  • Stratum lucidum - only present in non-haired skin - composed of compact fully keratinized cells
  • Stratum granulosum - dying cells, contain keratohyalin granules
  • Stratum spinosum - polyhedral shape, prominent intercelluar bridges, growing/synthesizing keratin
  • Stratum basale - germinal layer - gives rise to the above layers
  • Basement membrane - barrier b/t epidermis and dermis, anchors cells
59
Q

What are considered adnexa?

A
  • hair follicles
  • sweat glands (apocrine, eccrine on footpads)
  • sebaceous glands (holocrine)
  • mammary glands
60
Q

What is the difference between a primary and secondary lesion?

A
  • Primary - the initial lesion, most representative of the underlying etiology and are most useful for evaluation
  • Secondary - evolutionary lesions
61
Q

What are causes of sebaceous gland hyperplasia?

A

chronic inflammation, seborrhea, aging change

62
Q

What are causes of sebaceous gland atrophy?

A
  • endocrine dermatoses, aging, end result of severe chronic inflammation of glands (i.e. sebaceous adentitis)
63
Q

Define sebaceous adenitis

A
  • inflammation that targets sebaceous glands and can lead to their complete destruction resulting in severe hyperkeratosis
  • often seen with folliculitis, demodicosis
64
Q

Describe fibrosis

A
  • increase in collagen and fibroblasts (spec. in dermis), the end result of tissue repair that may be preceded by formation of granulation tissue, essentially a scar
  • may be secondary to chronic trauma, inflammation
65
Q

Define collagen degeneration or collagenolysis

A
  • collagen can become granular and fragmented and have altered staining qualities such as incr eosinophilia/basophilia
  • “flame figures” - granular eosinophilic debris on and around collagen seen w/ dz w/ eosinophilic infiltrates (mast cell tumors, arthropod bites)
66
Q

What causes collagen mineralization?

A
  • most often a form of dystrophic mineralization seen in Cushing’s dz; can be metastatic as in Vit D/Ca/Phos imbalance, some idiopathic cases
67
Q

What occurs with collagen atrophy?

A
  • decr in size of collagen bundles most commonly seen in a Cushingoid cat
  • entire dermis is thinner than normal, very fragile, and easily torn
68
Q

What happens with collagen dysplasia?

A
  • abnormally formed collagen found in certain inherited metabolic conditions
  • has decr tensile strength and incr distensibility leading to freq tears and non-healing wounds
69
Q

Define solar elastosis

A
  • incr in production of elastin by fibroblasts that are not functioning normally as a result of chronic actinic damage; often seen along with sun-induced SCC
  • most common in the horse
70
Q

What is mucinosis?

A
  • incr in glycosaminoglycans that trap water leading to myxedema and separation of collagen bundles, leads to a puffy look of the skin
    • can form vesicles if severe
  • normal in Shar Peis
  • often seen in hypothyroidism and lupus erythematosus
71
Q

What is fat necrosis?

A
  • may occur anytime there is inflammation, necrotic fat often seen in cases of atypical mycobacteriosis of cats
  • damaged adipocytes release lipid into areas of inflammation
  • can also see in lupus and rabies vax rxns, trauma to panniculus, or pancreatitis
72
Q

Describe vasculitis

A
  • dermal vessels targeted by inflammation - mural infiltrates of neutrophils, fragmentation of PMNs, fibrinoid necrosis of vessel wall
  • may see ulceration or sloughing of extremities
  • usually a feature of Type III hypersensitivity rxns (immune complex dz)
    • e.g. SLE, septicemia, DIC, toxins, frostbite, cold agglutinin dz
73
Q

When should you biopsy?

A
  • in the face of devastating dz
  • when a neoplastic process is possible
  • when the condition is longstanding and tx have failed
  • when you have little to no idea what the dz process is
74
Q

What do you biopsy?

A
  • select multiple cutaneous sites representative of the range of lesions present
  • look for fully developed primary lesions (e.g. vesicles, pustules, papules)
    • if not evident, select secondary lesions and be sure to include crusts, leading margins, and edges of ulcerated lesions
75
Q

What disease pattern might you expect to see with a particular cellular infiltrate?

A
  • Neutrophils - active inflammation, e.g. folliculitis due to parasites, dermatophytes, or bacteria
  • Eosinophils - ectoparasitism or allergic dz, furunculosis
  • Mononuclear phagocytes - ticks, viruses, cell-mediated immune response, persistent antigen in tissues stimulating cell-mediated immunity
  • Lymphocytes and plasma cells - (present in normal skin), local or systemic antigenic stimulation
  • Mast cells - (present in normal skin), IgE mediated hypersensitivity, cell mediated type IV hypersensitivity
76
Q

Describe perivascular dermatitis. What are some conditions suggested by this disease pattern?

A
  • Pathogenesis - most common pattern, not specifc for any one dz, but most often suggestive of hypersensitivity rxn
  • Conditions suggested:
    • w/ irregular epidermal hyperplasia
      • acral lick dermatitis, flea bite hypersens, sarcoptic mange, atopic dermatitis
    • w/ orthokeratotic hyperkeratosis
      • seborrhea, ichthyosis
    • w/ parakeratotic hyperkeratotis
      • Zn responsive dermatitis, malassezia dermatitis
    • w/ marked epidermal spongiosis
      • feline eosinophilic plaque, miliary dermatitis
    • w/ severe ulceration
      • physicochemical injury: photosensitization, hot spots
77
Q

Describe interface dermatitis. What are some conditions suggested by this disease pattern?

A
  • hydropic degeneration and apoptosis in basal layer of epidermis accompanied by bands of lymphocytes, plasma cells, +/- macrophages at dermal/epidermal junction; pigmentary incontinence
  • may see depigmentation, thickening of epidermis, erosions, or ulcerations
  • Pathogenesis: damage to basal cell layer of epidermis, often involves T-cell attack
  • Conditions suggested:
    • Cell poor: familial canine dermatomyositis, toxic epidermal necrolysis
    • Lymphoplasmacytic - erythema multiforme, SLE
    • Lymphohistiocytic - uveodermatologic (VHK) syndrome
78
Q

Describe vasculitis. What are some conditions suggested by this disease pattern?

A
  • leukocytes within walls of arterioles or venules, possible fibrinoid necrosis
  • Gross lesions = edema, cutaneous hemorrhage, infarction, sloughing of extremities, ulcers, atrophic dermatitis
  • Pathogenesis:
    1. immune mediated Type II hypersensitivity (ab/ag complex deposition)
    2. primary bacterial dz
    3. bacterial septicemia/systemic infxn
  • Conditions suggested: SLE (1), eriselothrix rhusiopathiae septicemia (3), rickettsia rickettsi (3), idiopathic
79
Q

Describe nodular to diffuse dermatitis. What are some conditions suggested by this disease pattern?

A
  • dermis and possibly panniculus have nodules, sheets or diffuse infiltrates of inflamm cells (typically granulomatous to pyogranulomatous)
  • Gross lesions: multiple papules and nodules that may coalesce, ulcerate, and drain
  • Pathogenesis: persistent Ag stim inciting a CMI response, may be infectious or noninfectious
  • Conditions suggested:
    • Infectious: pathogenic/opportunistic fungi, bacterial granulomas, Leishmania, Pythium (oomycetes), algae
    • Non-infectious: FBs
    • Idiopathic: cutaneous reactive histiocytosis, idiopathic sterile nodular dermatosis
    • Eosinophilis = linear granulomas in cats
    • Neutrophilic = deep pyodermas, abscesses
80
Q

Describe vesicular or pustular patterns. What are some conditions suggested by this disease pattern?

A
  • gross lesions: primary lesions = vesicles, pustules, or bullae, secondary lesions = erosions, ulcers, crusts
  • Intraepidermal- suggested conditions
    • ​subcorneal vesicle/pustule: superficial pyodermas (PMNs), pemphigus foliaceus (PMS, EOS), SLE - feline (PMNs), ectoparasites/allergies (EOS)
    • suprabasilar acantholysis: pemphigus vulgaris (separation just above basal layer, “tombstones”)
  • Subepidermal - entire epidermis is separated from the dermis
  • Pathogenesis: immune mediated and enzymatic destruction of basement membrane; genetic defects in structural components of BM, physical damage of BM
  • Suggested conditions: severe lichenoid dermatosis (SLE), mechanobullous dz, thermal burns, TEN, bullous pemphigoid
81
Q

Describe the patterns of folliculitis and furunculosis. What are some conditions suggested by this disease pattern?

A
  • inflammation targets some part of follicles or sebaceous glands; furunculosis occurs once follicular wall is destroyed by infiltrate, releasing contents into the dermis
  • grossly: follicular papules or nodules and patchy alopecia, ulcerated/draining lesions if severe
  • Pathogenesis: colonization/infestation of hair follicles by bacteria, parasites, or fungi; could be immune mediated or idiopathic
  • Suggested conditions:
    • demodicosis (PMNs or lymphs)
    • bacterial (staph) infxs (PMNs)
    • dermatophyte infections
    • feline acne (PMNs)
    • pelodera infxns
    • arthropod bites
    • alopecia areata (lymphocytic bulbar folliculitis)
    • eosinophilic mural folliculitis
82
Q

Describe panniculitis. What are some conditions suggested by this disease pattern?

A
  • inflammation targets the subcutaneous tissues
  • grossly: variably sized papules and nodules that may ulcerate and drain an oily substance
  • pathogenesis: infectious agents, may be traumatic implantation or part of systemic disease, many sterile or idiopathic
  • suggested conditions:
    • atypical mycobacteriosis (cats)
    • nocardia
    • FBs
    • idiopathic
    • vaccine induced - lymphocytic
    • feline nutritional pansteatitis
    • feline dermatophytic mycetomas (Persians)
83
Q

Describe atrophic dermatoses. What are some conditions suggested by this disease pattern?

A
  • epidermal and follicular atrophy w/ orthokeratotic hyperkeratosis; follicles in telogen or catagen, sebaceous gland and dermal atrophy, hyperpigmentation of the epidermis
  • grossly: lesions are bilateral and symmetrical hypotrichosis, thin, often translucent skin with comedones and possible telangiectasia and hyperpigmentation (if d/t systemic condition)
  • pathogenesis: most common is a hormonal imbalance leading to altered microenvironment and failure of appropriate stimulus for maintenance of skin components, genetic defects
  • Suggested conditions:
    • Hyperadrenocorticism
    • Hypothyroidism
    • Sex hormone related dermatoses
    • Dermatospraxis
    • Ischemia
    • Feline psychogenic alopecia
    • Color mutant alopecia
    • Feline paraneoplastic alopecia

Systemic Pathology (8 decks)

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