Skin Pathology 3 Flashcards
-Explain, using appropriate terminology, the processes of inflammation and how they affect the skin. -List the cardinal signs of inflammation and the macroscopic and microscopic lesions of acute and chronic dermatitis. -Outline the pathogenesis of irritant contact dermatitis with reference to the cell types involved. -Discuss, using examples, the analysis of histological patterns in the diagnosis of skin disease. -Describe the effects of solar radiation on the skin -Explain the process
DERMATITIS
A non-specific cutaneous inflammatory reaction, with concomitant changes in the epidermis AND dermis.
Can be caused by a variety of agents.
Changes are not always visible.
KERATINOCYTES release PRIMARY CYTOKINES (including interleukins, TNFa etc.)
These activate DENDRITIC CELLS, MAST CELLS, Th2 CELLS, EOSINOPHILS, DERMAL FIBROBLASTS, which go on to produce further chemokines and “further reinforce proinflammatory circuits through their massive release of potent cytokines and chemokines”.
Downstream activation cascades are stimulated.
An ‘inflammatory soup’ is produced.
CARDINAL SIGNS OF INFLAMMATION
REDNESS HEAT SWELLING PAIN LOSS OF FUNCTION
NORMAL VS INFLAMED CAPILLARY
Normal- Central axial flow of cells (RBCs, WBCs), zone of plasma around edge. Tight junctions between endothelial cells.
Inflamed- CONGESTION/STASIS, LOSS OF AXIAL FLOW, MARGINATION, PAVEMENTING and EMIGRATION of POLYMORPHONUCLEAR LEUKOCYTES.
If inflammation is severe, RBCs can leak through gaps that form between endothelial cells.
ACUTE INFLAMMATION
eg. Urticaria.
Vasodilation leads to hyperaemia (increased blood flow).
Increased permeability leads to inflammatory oedema
Cell emigration of neutrophils, macrophages (scarce in urticaria).
DERMATITIS- ACUTE MACROSCOPIC LESIONS
Acute dermatitis not often seen in veterinary medicine- most clinical cases have chronic skin disease, and most lesions have been self-traumatised. VESICLES PAPULES ERYTHEMA OEDEMA EXUDATION
DERMATITIS- ACUTE MICROSCOPIC LESIONS
SPONGIOSIS LEUKOCYTE EXOCYTOSIS SUPERFICIAL DERMAL OEDEMA VASODILATION PERIVASCULAR INFLAMMATORY CELLS Not all changes will be present in every case.
DERMATITIS- CHRONIC MACROSCOPIC LESIONS
Chronic cases are most common. Most lesions have been traumatised. SCALE CRUST MILD ERYTHEMA LICHENIFICATION PIGMENT ALTERATION
DERMATITIS- CHRONIC MICROSCOPIC LESIONS
HYPERKERATOSIS EPIDERMAL HYPERPLASIA MILD-MODERATE DERMAL OEDEMA VASODILATION PERIVASCULAR INFLAMMATORY CELLS. Character of cell infiltrate varies with time- in chronic cases, neutrophils and plasma cells can be seen in follicles.
SPONGIOSIS/SPONGIOTIC VESICLES
Widened, fluid filled spaces between keratinocytes in the epidermis.
Intracellular space increases due to oedema.
Mechanism uncertain- increased hyaluron and altered E-cadherin adhesion suggested.
Fluid comes from the dermis, but the change is not explained by hydrostatic pressure alone (little/no spongiosis is seen in urticaria- hives)
SUPERFICIAL DERMAL OEDEMA
Mild reaction.
Minimal erpidermal change.
Some spongiosis and sparse cellular infiltrate seen.
eg. Reaction to folliculitis in adjacent field.
Acute.
CHRONIC DERMATITIS
Results in SCARRING.
Scar tissue is aligned parallel to skin surface.
Hyperplasia, compact hyperkeratosis, hypergranulosis can be seen.
Moderate cell infiltrate.
CONTACT DERMATITIS
An example of physicochemical trauma
eg. Reaction to Tradescantia (spiderworts- certain species).
This is via DIRECT ACTION of the plant chemical.
NOT an allergic reaction- most contacts will be affected.
IRRITANT CONTACT DERMATITIS vs. ALLERGIC CONTACT DERMATITIS
Irritant Contact Dermatitis (ICD) can become Allergic Contact Dermatitis (ACD).
If the animal has been exposed before, a much lower second exposure to the irritant can illicit and allergic response.
INNATE immunity must be activated- irritant contacts skin, which stimulates irritation/inflammation -> leukocyte recruitment, dendritic cell activation.
Activated dendritic cells take up cutaneous haptens (small molecules that can only elicit an allergic response when bound to a larger carrier), then migrate to the draining lymph nodes.
Here, specific T cells are activated and leave the lymph nodes for the circulation.
EFFECTOR T CELLS- CD8+
REGULATORY T CELLS- CD4+
Subsequent contact with the same hapten:
Hapten penetration induces cutaneous irritation, which permits recruitment of EFFECTOR T cells (CD8+).
Effector T cells are activated by presentation of haptenated peptides by MHC I, II on the surface of skin cells.
HISTOLOGICAL PATTERNS
Can be an aid to diagnosis. Consider lesions:
PERIVASCULAR, VESICULAR AND PUSTULAR, INTERFACE, VASCULAR, FOLLICULAR, NODULAR AND DIFFUSE, FIBROSING, PANNICULITIS, ATROPHIC (non-inflammatory dermatosis)
PERIVASCULAR
Perivascular reaction is common. In the abscence of other changes, it provides little clue as to definitive diagnosis.
It just tells us that there IS inflammation.
Subtypes are based on changes in the epidermis and what any cellular infiltrate is based on:
EPIDERMIS- Spongiotic or hyperplastic
CELL INFILTRATE- Neutrophilic, eosinophilic, mononuclear.
May be superficial, deep, or both.
Perivascular dermatitis eg. canine atopic dermatitis. Histologically we can see superficial perivascular dermatitis with epidermal hyperplasia and dermal oedema.
