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LEC 03 - Dermatologic Inflammation
Terms in this set (61)
1. "Hives" (wheals)
2. Erythematous papules and plaques, pruritic.
3. Entire episode may last for days, but individual lesions are TRANSIENT (usually resolve in 24 hr),
4. Usually on trunk and extremities
Urticaria - Clinical
Antihistamines like Diphenhydramine (Benadryl) among others...
Urticaria - Treatment
1. Type I hypersensitivity
2. Antigen stimulated, IgE mediated release of mast cell granules (contain histamine & heparin)...
--> Microvascular permeability increased.
--> Interstitial edema
--> i.e. - leaky blood vessels in skin => swelling/wheals
3. Follows exposure to pollens, foods, drugs, pressure, temperature or other stimulus.
--> Often idiopathic
Urticaria - Pathophysiology
1. Severe urticaria-like swelling of face and airways.
2. Cause: C1 esterase inhibitor deficiency --> uncontrolled complement activation.
Urticaria - Hereditary Angioedema
1. Generally looks almost normal, BUT...
2. Sparse superficial perivascular infiltrate:
--> Scattered neutrophils, eosinophils, mast cells
3. Increased interstitial space between collagen bundles (edema).
1. Allergic contact dermatitis
--> Poison ivy, nickel dermatitis
2. Atopic dermatitis ("eczema")
3. Drug-related eczematous dermatitis
5. Irritant contact dermatitis
Spongiotic (Eczematous) Dermatitis - Clinical
1. Atopic/Eczema (babies): face, extensor surfaces
2. Atopic/Eczema (older): flexor surfaces
3. Contact dermatitis: at site of contact with allergen/irritant
4. Photodermatitis: sun-exposed sites
5. Drug: anywhere
***red, scaling, oozing, crusted lesions.
Spongiotic (Eczematous) Dermatitis - Anatomic Distribution
1. Topical corticosteroids
2. For atopic dermatitis - skin care techniques (avoid hot baths, use lots of lotion, etc...)
3. For contact dermatitis - avoid contactant substance (don't use poison ivy as toilet paper, etc)
Spongiotic (Eczematous) Dermatitis - Treatment
Controversial, but probably involves...
1. Decrease in skin barrier function (filaggrin defects)
2. Immune dysregulation with elevated IgE.
Eczema (Atopic dermatitis) - Pathophysiology
1. Mediated by sensitized T cells (type IV hypersensitivity)
2. At the time of initial exposure, the antigen is processed by Langerhans cells (antigen presenting cells) in the epidermis.
3. Langerhans cells present the antigen to naïve T cells (CD 4) in the lymph node.
4. Upon re-exposure, the MEMORY T cells release cytokines that mediate the inflammatory response...
--> Recruit inflammatory cells
--> Increased edema
Contact Dermatitis - Pathophysiology
- Associated with intracellular epidermal edema (spongiosis).
- White spaces seen between the keratinocytes.
(E.g., allergic contact dermatitis)
1. Hypersensitivity response to particular infections or drugs.
2. Self limited.
3. Characteristic TARGETOID lesions, but many different presentations...
Erythema Multiforme - Clinical
1. Herpes Simplex Virus (HSV)
--> MOST common.
2. Mycoplasma pneumoniae.
Associations of Erythema Multiforme - Infections
1. Antibiotics (penicillin),
2. Anticonvulsants (LAMOTRIGINE, phenytoin)
4. Sulfa-based drugs.
5. NUMEROUS others...
Associations of Erythema Multiforme - Specific Drugs
Associations of Erythema Multiforme - Malignancy
1. Lupus erythematosus
Associations of Erythema Multiforme - Collagen Vascular Diseases
1. Pattern: "Interface dermatitis" (many other diseases have similar histology)
2. "Fuzzy" dermal-epidermal junction (interface) b/c lymphocytes chewing up the basal layer.
***LESS than 10% of the body surface area is involved.
a. Related to erythema multiforme (EM), but...
1. Extensive and symptomatic
2. Erosion and crusting of mucosal surfaces
3. Usually caused by sulfonamide antibiotics...
b. Same histology & drug associations with Erythema Multiforme.
Stevens-Johnson Syndrome (SJS)
***MORE than 30% of the body surface area is involved.
a. Related to EM and SJS, but...
1. Extensive and symptomatic
--> 30% mortality
2. Diffuse necrosis and sloughing of cutaneous and mucosal surfaces.
3. Positive Nikolsky sign:
--> rubbing of skin produces blister
Toxic Epidermal Necrolysis (TEN)
Toxic Epidermal Necrolysis (TEN)
1. Most of epidermis is replaced by numerous dying keratinocytes (bright pink blobs at arrows) due to interface dermatitis.
--> Blister Roof: note all keratinocytes are necrotic.
2. Full thickness necrosis/death of epidermis is classic buzzword for TEN on exam.
3. In real life, erythema multiforme, SJS, & TEN can all look identical to each other on biopsy.
1. Relatively common, 1 - 2% of US population.
2. Generally on elbows, knee, scalp, lumbosacral area, intergluteal cleft (koebner phenomenon).
3. Well-demarcated, pink plaque covered with loosely adherent silvery scales.
--> Picking off these scales results in pinpoint hemorrhage (Auspitz sign).
4. "Oil-slick" nail discoloration.
5. Nail pitting.
Psoriasis - Clinical
1. "Oil-slick" nail discoloration
2. Nail pitting
Psoriasis - Nail Changes
5. Cardiovascular disease
Psoriasis - Associations
1. Multifactorial pathogenesis: genetic and immune
2. Sensitized T-cells infiltrate the skin and secrete cytokines and growth factors...
--> INCREASED EPIDERMAL KERATINOCYTE TURNOVER (Keratinocytes proliferate too quickly).
--> Vascular proliferation
--> Inflammatory infiltrate
Psoriasis - Pathophysiology
--> Hyperkeratosis and parakeratosis.
--> Capillary loop dilation.
1. Diffuse parakeratosis (thick corneal layer w/ nuclei).
2. Diminished/absent granular layer
3. Regular elongation of the rete ridges...
4. Tortuous capillaries in papillary dermis.
5. Neutrophil microabscess (of Munro) in stratum corneum of epidermis
Psoriasis - Characteristics of Histology
The THREE P's...
3. Polygonal Papules & Plaques on skin and mucosa.
Lichen Planus (LP) - Mnemonic
1. Flat-topped papules may coalesce to plaques.
2. Usually self-limited, 1-2 yrs
3. Symmetric on extremities, esp. wrists, elbows...
4. Mucosal involvement can be extensive and morbid:
--> gingival, buccal, vulvar
5. Sometimes associated with Hepatitis C, but actual etiology of LP is unknown...
Lichen Planus (LP) - Clinical
--> Whitish lines visible in the papules of lichen planus and other dermatoses, typically in the oral mucosa.
3. Dense band-like lymphocytic infiltrate along the dermoepidermal (DE) junction - "sawtoothing" jagged/zigzag rete ridge...
4. Apoptotic dying keratinocytes (Civatte body).
1. "Lichen" shows up in name of lots of different unrelated diseases in derm.
2. Histologically "lichenoid" means band of lymphocytes at dermal epidermal junction with interface change (vacuoles, dying kertinocytes)
***Not all "lichen" diseases have this band of lymphocytes....argh! So confusing!!!
Leukoplakia with thick, leathery vulvar skin associated with chronic irritation and scratching.
--> hyperplasia of the vulvar squamous epithelium.
--> seen in older/elderly individuals and there is NO increased risk for cancer.
Lichen Simplex Chronicus
1. Thin papery itchy skin, often genital area.
2. Risk of squamous cell carcinoma
Lichen sclerosus (et atrophicus)
1. Discoid lupus erythematosus (DLE)
--> Localized cutaneous form of lupus.
--> Usually, does NOT develop systemic disease (SLE).
2. But converse is NOT true:
--> More than 1/3 of patients with SLE develop cutaneous lesions identical to discoid LE.
3. Other forms: acute/bullous lupus, subacute cutaneous lupus (SCLE), hypertrophic lupus.
Lupus Erythematosus - Clinical
1. Malar erythema
--> Usually with systemic lupus erythematosus (SLE)
--> Needs rheumatology workup to exclude internal organ involvement, etc.
2. Large, well-circumscribed erythematous, scaling plaques (discoid lesions).
3. Typically, this is worse in sun-exposed skin.
Lupus Erythematosus - Presentation
1. Superficial and deep perivascular lymphocytic infiltrate, often w/ PLASMA cells.
2. Also (not shown):
--> inflammation around hair follicles & sweat glands.
--> Dermal mucin (hyaluronic acid/glycosaminoglycans)
1. Uncommon, usually seen in adults.
2. Large, necrotic ulcers; rolled, undermined red-purple borders.
3. May persist for years, may resolve and recur repeatedly.
4. Associated with inflammatory bowel disease (Crohn's disease and ulcerative colitis) and rheumatoid arthritis...
--> 1-2 % of IBD patients get PG
--> ~25% of PG patients also have IBD
Pyoderma gangrenosum - General
1. Clinically (and microscopically) often mistaken for infectious abscess or necrotizing fasciitis...
2. Histology: Ulcer with rolled border and numerous dermal neutrophils
3. Infection must be excluded clinically and by microbial cultures.
4. TOTALLY DIFFERENT TREATMENT
--> PG: systemic corticosteroids or other immunosuppressive drugs.
--> Infection/Nec Fasc: antibiotics and surgical debridement.
Pyoderma Gangrenosum - Medical Importance
--> Ulcer with rolled border and numerous dermal neutrophils.
1. Pathergy effect: ulcerations in PG can develop secondary to trauma, including surgical trauma from debridement attempts
--> Surgery will only make it worse!
2. Dermatologists often recognize PG but many other specialties are not familiar with it...
--> before debriding a big ulcer on a patient, consider a derm consult!
--> Could save your patient from serious harm!!!
Pyoderma Gangrenosum - Surgical Complications
***Level where blister splits the skin is very important for diagnosis
Keratinocyte Junctions - Desmosome
--> attach keratinocytes to neighbor keratinocytes.
--> attach epithelial cells to the basement membrane.
Blistering Diseases - Traumatic
1. Pemphigus vulgaris
2. Bullous pemphigoid
3. Dermatitis herpetiformis
Blistering Diseases - Autoimmune
1. Middle age and elderly
2. FLACCID blisters that rupture easily resulting in shallow erosions with crust...
--> Blisters may be hard to appreciate or absent.
3. Affects SKIN and MUCOSA.
--> P. vulgaris almost always has oral involvement.
4. Before systemic corticosteroids (prednisone) it was often fatal...
Pemphigus vulgaris - Clinical
1. P. vulgaris - most common
2. P. foliaceus - more indolent; no oral lesions.
3. P. vegetans - rare, presents with wart-like plaques...
4. P. erythematosus - lupus/pemphigus overlap...
5. Paraneoplastic pemphigus - occurs in patients with internal malignancy
Pemphigus - Variants
1. Autoimmune blistering disorder
2. Loss of normal intercellular attachments within the epidermis...
--> IgG autoantibodies against desmosomal proteins (desmogleins; member of cadherin family)
--> Cause loss of integrity of the intercellular attachments between keratinocytes.
***Type II hypersensitivity reaction
Pemphigus vulgaris - Pathophysiology
1. Suprabasilar blister.
2. Epidermis separates from basal layer leaving "tombstone row" of basal keratinocytes attached to floor of blisters.
1. Deposition of auto-antibodies (IgG) & complement (C3) along keratinocyte membranes giving a "fish net" appearance on direct immunofluorescence staining.
***"Fish net" stockings are Vulgar (p. vulgaris).
2. Much more common than pemphigus...
3. TENSE BULLAE filled with clear fluid...
4. Involves thighs, flexor surface of forearms, axillae, groin and lower abdomen.
5. Oral involvement in 30%
Bullous pemphigoid - Clinical
1. systemic corticosteroids
2. rituximab (monoclonal antibody against B lymphocytes)
3. other immunosuppressive drugs
Bullous pemphigoid - Treatment
1. Antibodies develop against bullous pemphigoid antigen (BPAg1, BPAg2).
--> They are proteins in lamina lucida layer and HEMIDESMOSOMES of basement membrane zone.
2. Hemidesmosomes lose integrity causing subepidermal split.
--> Epidermis detaches from dermis
***Type II hypersensitivity reaction
Bullous pemphigoid - Pathophysiology
1. Total separation of epidermis from dermis.
--> With pemphigus vulgaris, one would still see epidermis left behind.
Bullous pemphigoid - Direct Immunofluorescence
--> Deposition of IgG antibody & complement C3 along basement membrane zone.
1. M>F, 3rd - 4th decade
2. Itchy grouped vesicles; often excoriated.
--> May present as erosions without obvious blisters.
3. Extensor surfaces, elbows, knees, upper back and buttocks.
4. May be associated with intestinal celiac disease (autoimmune gluten intolerance)...
5. Associated with HLA-DQ2
Dermatitis herpetiformis - Clinical
2. Gluten avoidance.
Dermatitis herpetiformis - Treatment
1. Develop antibodies to gluten by B cells in the intestine...
2. These antibodies circulate systemically and cross-react with transglutaminase in papillary dermis of skin (anti-tissue transglutaminase antibodies in serum).
Dermatitis herpetiformis - Pathophysiology
--> Subepidermal blisters filled with neutrophils that form at tips of dermal papillae.
Dermatitis herpetiformis - direct immunofluorescence
--> Granular deposits of IgA at the tips of the dermal papillae.
1. EB: group of CONGENITAL blistering diseases due to genetic mutations in structural proteins in skin like keratin or collagen VII.
2. EBA: ACQUIRED autoimmune blistering disease due to antibody against collagen VII.
Epidermolysis bullosa (EB) vs. Epidermolysis bullosa aquisita (EBA)
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