Skin I (a) Flashcards
Causes of Urticaria
Pollens, foods, drugs, and insect venom
Epi of Urticaria
20-40 yrs of age
Patho of Urticaria
Immediate (type 1) hypersensitivity reaction -> corss-linkage of IgE on mast cells which cause degranualtion
Microscopic Findings:
* Superficial perivenular infiltrate of mononuclear cells (Lymphatic vessel dilatation)
* Superficial dermal oedema, creating more widely spaced collagen bundles
* Degranulation of mast cells,
features of?
Urticaria
Degranulation of mast cells in Urticaria can highlighted using ——– stain
Giemsa stain
CP of Urticaria
Erythematous, oedematous, and Pruritic wheals(form after the degranulation of mast cells)
Tx of Urticaria
Antihistamines, systemic steroids
pressure Urticaria are lesions found only in areas exposed to ——–?
pressure
Heriditray Angioedema is caused by what type of deficiency?
C1 esterase inhibitor
Hereditary Angioedema affects?
1) lips,
2) throat,
3) eyelids,
4) genitals, and
5) distal extremities
CP of Acute Eczematous Dermatitis (Eczema)
Oozing/ crusted Red papules, often with overlying vesicles
Causes of Acute Eczematous Dermatitis (Eczema)
1. Allergic Contact Dermatitis (most common): Topical exposure to allergen
2. Atopic Dermatitis: Allergen exposure or defects in keratinocyte barrier function
3.Drug-related Eczematous Dermatitis: Hypersensitivity reaction to a drug
cause of Allergic Contact Dermatitis
Type IV hypersensitivity reaction secondary to contact allergens (e.g, poison ivy, nickel)
patho of Allergic Contact Dermatitis
Contact of allergen (poisin ivy) w/ skin –>
CP of allergic contact dermatitis
localized pruritic (itchy) skin lesions, blisters w/ clear fluid
* bullae: blisters w/ clear fluid
Microscopic Findings:
* Spongiosis (epidermal odema)
* Intercellular bridges are stretched
* Superficial perivascular lymphocytic infiltrate
* Oedema of dermal papillae
* Mast cell degranulation
features of?
Allergic Contact Dermatitis
*note very similar micro features of Urticaria
Cause of Erythema Multiforme
Hypersensitivity response to:
* Infections(Herpes Simplex Virus and Mycoplasma)
* Drugs (Sulfonamides, Penicillin, Salicylates, Hydantoins, Antimalarials)
*pathophysio
In Erythema Multiforme Skin-homing Cytotoxic T-cells attack the ———- of the skin and the ————, which may display antigens that cross-react with the inciting drug or microbe
Basal cells, mucosa
CP of Erythema Multiforme
Target- like papules
(consisting of red macules or papules with pale vesicular or eroded centers)
**
Macroscopic features:
* pathces have pale, vesicular, or eroded centers (Target-like papules)
Microscopic Findings:
* Dermal oedema
* lesions w/ degenerating (apoptotic) keratinocytes w/ lymphocytic infiltrates
Erythema Multiforme
*keratinocytes: the major cell type of the epidermis
2 severe forms of Erythema Multiforme
Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis
cause of Psoriasis
* chronic skin inflammatory disorder
Multifactorial immunologic disease, in which both genetic (e.g. Human Leukocyte Antigen [HLA] types) and environmental factors contribute to risk
Patho of Psoriasis
Sensitised populations of T cells secrete cytokines and growth factors that induce keratinocyte hyper- proliferation
CP of Psoriasis
pink to salmon-coloured palques w/ silvery scaling
Microscopic Findings:
* Epidermal thickening (acanthosis), w/ parakeratotic (nuclei still in stratum corneum)
* loss of the stratum granulosum and parakeratotic scale (due to lack of maturation)
* Regular elongation of the rete ridges
* Thinning of the epidermal cell layer overlying the tips of dermal papillae
Features of?
Psoriasis
patho of Linchen PLanus
* chronic inflammatory skin disorder
CD8+ T cell-mediated cytotoxic immune response against antigens in the basal cell layer and the dermo-epidermal junction
Epi of Lichen Planus
Uncommon disorder; Middle-aged adults
**
CP of Lichen Planus
6 P’s
1) Pruritic, purple, polygonal, planar papules, and plaques of skin and squamous mucosa
2) Mucosal involvement –> Wickham striae
**
Microscopic Findings:
* The lymphocytes are intimately associated with basal keratinocytes, which often atrophy or become necrotic
* “zig-zag” contour/”saw-tooth” infiltrate of lymphocytes at Dermo-epidermal interface (junction)
* Presence of anucleate, necrotic basal cells (colloid bodies or Civatte bodies)
features of?
Lichen Planus
cause of Lichen simplex Chronicus
Response to local repetitive trauma, such as continual rubbing or scratching
CP of Lichen Simplex Chronicus
Raised, erythematous, and scaly lesions
Microscopic Findings:
* Acanthosis (epi thickening)
* Hyperkeratosis
* Hypergranulosis ( ↑ thickness of the stratum granulosum)
* Solar elastosis
* Elongation of the rete ridges
* Fibrosis of the papillary dermis
* Dermal chronic inflammatory infiltrate
features of?
Linchen Simplex Chronicus
cause of Impetigo
* superficial bacterial infection
Staphylococcus aureus, Streptococcus pyogenes
Epi of Impetigo
- Most common bacterial infections of the skin
- Primarily in children
CP of Impetigo
lesions w/ Honey-coloured crusting
Microscopic Findings:
* Accumulation of neutrophils beneath the stratum corneum that often produces a sub-corneal pustule
* Superficial dermal inflammation accompany these findings
* Bacterial cocci in the superficial epidermis (demonstrated by Gram stain)
features of?
impetigo
obv+ skin condition
Skin condition: Superficial dermal fungal infection caused by Candida albicans
Obv: Satelite lesions
Microscopic Findings:
*Neutrophilic infiltrate in the epidermis
*Psoriasiform hyperplasia
Candidiasis of the Skin
Psoriasiform hyperplasia-> Candida
Stain used for Candida causing superfical Dermal fungal infection
PAS
Obv+ skin disorder
Condition: Deep dermal fungal infection caused by Apergillus
Obv: A- Erythematous subcutaneous nodule
B- Focally haemorrhagic lesion
Deep Dermal fungal infection caused by Aspergillus is due to Tissue damage and often —————– Response
granulomatous
Histochemistry for Deep Dermal fungal infection caused by Aspergillus
1) PAS- Periodic Acid-Schiff
2) Gomori methenamine silver stains
*identify fungal organisms
cause of Verrucae (Warts)
* viral infection
Human Papilloma Virus (HPV)
patho of Verrucae (Wrats)
Viral E6 and E7 onco-proteins lead to dysregulated epidermal cell growth and increased survival
Microscopic Findings:
* Epidermal hyperplasia
* Cytoplasmic vacuolisation [koilocytosis] (preferentially of the more superficial epidermal layers) –> Halos of pallor surrounding infected nuclei
* Infected cells with prominent kerato-hyalin granules and jagged eosinophilic intracytoplasmic protein aggregates (result of impaired maturation)
features of?
Verrucae (Warts)
the 4 types of Verrucae (Wrats)
- Verruca Vulgaris
- Verruca Plana (Flat Wart)
- Verruca Plantaris/Palmaris
- Condyloma Acuminatum (Venereal Wart)
most common type of Verrucae (Wrats)
Verruca Vulgaris
loc of Verruca Vulgaris
dorsum of the hand
CP of Verruca Vulgaris
Gray-white to tan, flat to convex, 0.1-1 cm papule with a rough, pebble-like surface
Loc of Verruca Plana (Flat Wart)
face
CP of Verruca Plana (Flat Wart)
Flat, smooth, tan macules
Verucca Vulgaris presents w/ Rough, ————–to ————— skin coloured papule/plaque Macroscopically
hyperkeratotic to papillomatous
Hyperkeratotic –> thickening of the outer layer of the skin
Macroscopic features:
- Rough, hyperkeratotic to papillomatous skin coloured papule/plaque
microscopic features :
- Papillomatous hyperplasia
- Prominent granular layer
- Inward bending of rete
- Koilocytosis
features of ?
Veruuca Vulgaris
**
what type of Verruca (Wrats) has the following microscopic features:
- Multiple “bird’s eye” nuclei in the granular cell layer
Verruca Plana
loc of Verruca Plantaris/Palmaris
Soles and palms
CP of Verucca PLantaris/ Palmaris
Rough, scaly lesions
Loc of Condyloma Acumuinatum (Venereal Wrat)
Penis, female genitalia, and perianal areas
Macroscopic features:
- Warty cauliflower-like lesion w/ papillary or polypoid fronds
Microscopic features :
- Papillomatous mammillated epithelial hyperplasia
- Koilocytic changes
- Hyperkeratosis
features of?
Condyloma Acuminatum (Venereal Wart)
cause of Pemphigus
Autoimmune disorder
patho of Pemphigus
- Antibody-mediated (type II) hypersensitivity reactions
- IgG auto-antibodies that bind to intercellular desmosomal proteins (Desmoglein types 1 and 3) of skin and mucous membranes
Epi of Pemphigus
Rare; Elderly women
Clinical presentation of Pemphigus
Superficial flaccid vesicles and bullae that rupture easily
Microscopic Findings:
* Acantholysis: Lysis of the intercellular adhesive junctions between neighbouring squamous epithelial cells that results in the rounding up of detached cells
* Superficial dermal infiltrates comprised of lymphocytes, macrophages, and eosinophils
features of?
Pemphigus
Direct Immuno-Fluorescence of Pemphigus
Fishnet-like pattern of intercellular IgG deposits
- Acantholysis selectively involves the layer of cells immediately above the basal cell layer, giving rise to a supra-basal acantholytic blister
what type of Pemphigus is this?
Pemphigus Vulgaris
**
microscopic features;
- Acantholysis in the granular cell layer with “missing” stratum corneum
- Neutrophils in the granular cell layer
- Separation of the corneum from the rest of the epidermis
features of?
Pemphigus Foliaceus
Cause of Bullous Pemphigoid
Autoimmune disorder
Patho of Bullous Pemphigoid
- Antibody mediated (type II) hypersensitivity reactions
- Linear deposition of IgG antibodies and complement in the epidermal basement membrane
CP of Bullous Pemphigoid
Multiple fluid filled blisters
Microscopic Findings:
* Perivascular infiltrate of lymphocytes and variable numbers of eosinophils, occasional neutrophils
* Superficial dermal oedema
* Associated basal cell layer vacuolisation; The vacuolated basal cell layer eventually gives rise to a fluid-filled sub-epidermal non-acantholytic blister
features of?
Bullous Pemphigoid
Direct Immuno-Fluorescence of Bullous Pemphigoid
Linear deposition of IgG antibodies and complement in the epidermal basement membrane
cause of Dermatitis Herpetiformis
Autoimmune disorder
Epi of Dermatitis Herpetiformis
- Males
- 80% occurs is ass. w/ Coeliac disease
patho of Dermatiis Herpetiformis
Genetically predisposed persons develop:
* IgA antibodies to dietary Gluten (derived from the wheat protein Gliadin) and
*IgA auto-antibodies that cross-react with epidermal transglutaminase , expressed by keratinocytes
**
CP of Dermatitis Herpetiformis
Pruritic urticaria and grouped vesicles
**
Microscopic Findings:
* Neutrophils accumulate selectively at the tips of dermal papillae, forming small micro-abscesses- “Papillary Abscess”
* The basal cells overlying these micro-abscesses show vacuolisation and focal dermo-epidermal separation that ultimately coalesce to form subepidermal blisters
features of?
Dermatitis Herpetiformis
**
Direct immunofluorescence of Dermatitis Herpetiformis
Discontinuous, granular deposits of IgA localised in the tips of dermal papillae