1
Q
Function of the skin
A
- Temp and blood pressure regulation
- fluid regulation
- protection barrier to outside world
- sensation
- nutrient metabolism: Vit D
- Immune functions: SALT
2
Q
Layers of skin
A
- Epidermis
- surface of skin
- cell turnover ~ 10 days
- Dermis
- made of collagen and elastin
- Adnexa
- hair follicles
- apocrine glands (sweat glands)
- halocrine glands (sebaceous glands)
- mammary glands
- Panniculus
- subcutis
3
Q
Epidermis
A
- Stratum corneum (top)
- +/- stratum lucidum
- Stratum granulosum
- Stratum spinosum
- contains melanocytes
- Stratum basale (bottom)
4
Q
Diagnostic approach
A
- Signalment
- history: duration, pruritis, other animals
- Response/failure to tx
- overall health status
5
Q
Primary/secondary lesion
A
- Primary lesion
- best for bx
- Secondary lesion
- evolution of primary lesion over time
6
Q
epidermal response to injury
Acanthosis
A
- Acanthosis
- hyperplasia of cells in epidermis
- usually stratum spinosum
- regular: rare
- irregular: most common
- yeast infection
- Papillated
- papillomas or warts
- Psuedocarcinomatosis
- severe, chronic trauma
7
Q
epidermal response to injury
hyperkeratosis
A
- hyperkeratosis
- inc width of stratum corneum
- orthokeratotic
- buildup of excess keratin after normal cornification
- no nuclei
- perakeratotic
- thickening of stratum corneum with retention of nuclei
- Disease
- ichtyosis: congenital skin disorder, skin thickened with scales, hyperkeratosis crack into plates resembling fish scales
- superficial necrolytic dermatitis
- seborrhea
8
Q
epidermal response to injury
dyskeratosis
A
- dyskeratosis
- prematur keratinization of cells in epidermis
- often seen wtih parakeratosis
- cells rounded up, hypereosinophilic, nuclear degeneration
9
Q
epidermal response to injury
apoptosis
A
- apoptosis
- individual programmed cell death
- diseases
- SLE
- erythema multiforme
- UV light damage
10
Q
epidermal response to injury
necrosis
A
- necrosis
- can be partial/full thickness
- causes
- adverse drug rxns: toxic epidermal necrolysis
11
Q
epidermal response to injury
cutaneous atrophy
A
- cutaneous atrophy
- decreases in number and size of cells
- most common cause is endocrine dz
12
Q
epidermal response to injury
Edema
A
- Edema
- fluid in between cells of epidermis or within individual cells of epidermis
- Intercellular
- spongiosis: widening of spaces between keratinocytes
- Intracellular: fluid accumulation in the cells
- hydropic degeneration: at dermal-epidermal junction, causes separation of cells
- ballooning degeneration: at superficial layers of the epidermis.
- vesicle could form
- often associated with viral infections
13
Q
epidermal response to injury
Acantholysis
A
- acantholysis: loss of cohesion between keratinocytes due to breakdown of cell-to-cell attachments
- type II hypersensitivity: Pemphigus foleaceous
- enzymatic destruction: bacterial infection
*pemphigus foleaceous: primar lesion: pustule; secondary lesion: acantholysis
14
Q
epidermal response to injury
crusts
A
- crusts
- surface collection of plasma, leukocytes
- most vesicles, bullae and pustules for and then crust is secondary lesion
15
Q
epidermal response to injury
vesicles/bullae
A
- Vesicles/bullae
- fluid filled spaces at the epidermis or epidermal/dermal junction
- pathogenesis
- marked spongiosis, hydropic or ballooning degeneration
- enzymatic destruction
- immune destruction-acantholysis or other
- mechanical destruction-burn, friction
- genetic structural defects
16
Q
epidermal response to injury
Pustules
A
- pustule
- collection of fluid and inflammatory cells in epidermis or sub-epidermis region
- Neutrophilic:
- bacterial and some autoimmune dzs
- Eosinophils:
- parasitic dz, allergic, immune, microbial, some idiopathic
- Pautrier’s microabscesses:
- collection neoplastic lymphocytes in epidermis
- specific for mycoses, fungoides/epitheliotrophic cutaneous lymphoma
17
Q
epidermal response to injury
changes in pigmentation
A
- hyperpigmentation:
- chronic inflammation or idiopathic
- hyperpigmentation:
- damage to melanocytes or basement membrane zone
- defects in formation of melanin of lack of melanocytes
18
Q
Follicular changes
Hyperkeratosis
A
- Hyperkeratosis: similar to epidermal
- primary seborrhea
- vit A responsive dermatosis
- endocrine dermatosis
- others
19
Q
epidermal response to injury
atrophy
A
- atrophy: shrinking of hair follicles
- endocrinopathies
- ischemia
- traction
20
Q
epidermal response to injury
Folliculitis
A
- Folliculitis: inflammation of the hair follicle
- folliculocentric papules
- patchy alopecia
- Cause folliculitis in dogs
- Demodex
- dermatophytes
- bacteria
- Cause of folliculitis in cats
- dermatophytes
21
Q
epidermal response to injury
furunculosis
A
- furunculosis: wall of follicle is destroyed by infiltrate and contents of hair follicle are in dermis
- folliculocentric nodule
- can have ulcerative draining lesions
22
Q
epidermal response to injury
dysplasia
A
- dysplasia
- abnormal development of hair follicle that leads to alopecia
23
Q
Dermal response to injury
edema
A
- edema
- uticaria: hives
- angioedema: edema of dermis and subcutis
- type I hypersensitivity rxn
- insect bites
- vax rxns
- food allergy
- atopy
- drug rxns
24
Q
dermal response to injury
mucinosis
A
- mucinosis: stringy characteristic to dermis
- inc amount leads to puffy looking skin
- sharpeis have inc mucin
25
dermal response to injury
collagen
* collagen
* fibrosis
* degeneration/collagenolysis
* mineralization
* often dystrophic mineralization in hyperadrenocorticism (calcinosis cutis)
26
subcutis response to injury
panniculitis
* panniculitis
* inflammation of the panniculus
27
subcutis response to injury
fat necrosis
* fat necrosis
* may occur anytime there is inflammation
28
Vessel response to injury
vasodilation
* vasodilation
* may lead to erythema, edema
29
Vessel response to injury
vasculitis
* vasculitis
* thrombosis
* ischemia
* edema
* hemorrhage
* atrophy
30
BX
* devastating dz
* neoplasm
* unsuccessful treatments
* no clue about the dz
* quick answer
* primary lesions: leading margins, edges of ulcers, crusts
* multiple sites
31
Cellular infiltrates
* neutrophils: active inflammation
* Eosinophils: allergic or ectoparasites
* Mononuclear phagocytes: persisten antigen in tissue
* macrophages
* epitheliod macs
* multinucleated giant cells
* Lymphocytes/plasma cells: indicates local/systemic antigen stim
* type IV hypersensitivity
* Mast cells: some normal, too many = IgE mediated hypersensitivity
32
Perivascular dermatitis
* Most common type dermatitis
* aggregates of inflammatory cells around hair follicles
* generic inflammatory response
33
Types of perivascular dermatitis and assoc dz
* Eosinophils
* Irregular epidermal hyperplasia
* acral lick dermatitis
* flea bite hypersensitivity
* sarcoptic mange
* atopic dermatitis
* orthokeratotic hyperkeratosis
* seborrhea
* icthyosis
* parakeratotic hyperkeratosis
* Zn responseive dermatitis
* malassezia dermatitis
* severe ulceration
* hot spot
* photosensitization
34
Interface dermatitis
about
* inflammation at interface between epidermis and dermis
* target: anything in basal layer, epidermal junction
* hydropic degeneration/apoptosis in basal layer
* bands of lymphs, plasma cells, macs at epidermal/dermal juncton
* pigmentary incontinence
* +/- vesicles at interface
35
Interface dermatitis
Pathogenesis
* cytotoxic T cll attack on keratinocytes, melanocytes or basement membrane components
* non-immune mediated damage
* unknown
36
Interface dermatitis
Diseases
* Toxid Epidermal Necrosis (TEN)
* Erythema multiforme (EM)
* Systemic lupus erythematosus (SLE)
* Uveodermatologic syndrome (VKE)
37
Vasculitis
about
* leukocytes within the walls of capillaries and venules
* will see evidence of vessel damage
* edema, necrosis/thrombosis, leukoclasis
* mild damage
* atrophy and alopecia
* severe damage
* cutaneous infarction and ulceration
* if multicentric
* lesions at extremities (places with little collateral blood flow)
* tail, footpads, ears
38
Vasculitis
pathogenesis
* Type III hypersensitivity: immune complex deposition in vessels
* primary bacterial skin disease
* bacterial septicemia
* systemic infection with endotheliotropic organisms such as rickettsia
* rabies vax assoc vasculitis
39
Nodular to diffuse dermatitis
about
* Dermis +/- panniculus infiltrates of leukocytes
* types of leukocytes present help point to a cause
40
Nodular to diffuse dermatitis
pathogenesis
* persistence of antigen in tissue stimulates cell mediated immune response
* Gross lesions: multiple papules, nodues
* Fungi: zygomycetes , deep pyoderma, higher bacteria
* Parasites, protozoans
* Oomycetes: pythum, lageridium
* Algae
* Idiopathic: sterile
* foreign material
* neoplasms
* Histiocytic disorders
* eosinophilic granulomas
41
Vesicular or pustular dermatitis
about
* Intradermal
* subcorneal: pemphigus folliaceous, superficial pyoderma
* suprabasilar: pemphigus vulgaris (row of tombstones)
* Subepidermial
* burns, SLE, TEN, Bullous pemphigoid
42
Vesicular or pustular dermatitis
pathogenesis
* Marked spongiosis, hydropic or ballooning degeneration
* Enzymatic destruction
* Immune destruction
* Mechanical destruction: burn, friction
* Genetic: structural defects
\***Level of vesicle formation, degree and type of cellular infiltrate, signalment and distribution of lesions all are needed to determine the disease present**
43
Folliculitis
* inflammation of the hair follicle
* folliculocentric papules, patchy alopecia
* cause of folliculitis in dogs:
* demodex
* dermatophytes
* bacterial infection
* cause of folliculitis in cats
* dermatophytes
44
Furunculosis
* wall of follicle is destroyed by infiltrate and contents of hair follicle are in dermis
* folliculocentric nodule
* can have draining lesions
45
Atrophic dermatoses
about
* symmetric hypotricosis, think skin
* comedones (black heads)
* Telangiectasia (vessels in skin are very torturous)
* Hyperpigmentation (inc pigment)
46
Atrophic dermatoses
pathogenesis
* hormonal imbalance (hyperadrenocorticism, hypothyroidism, sex hormone imbalance)
* ischemia: if focal
* need additional clinical and biochem info for definitive diagnosis
2nd path test
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