Type II hypersensitivity
-MOA, mediated by, examples
Cytotoxic allergy
MOA: IgM and IgG bind to the antigen, causing lysis by complement or phagocytosis
Mediated by antibodies and complement -> MAC
Examples: autoimmune hemolytic anemia, erythroblastosis fetalis, Goodpasture’s syndrome, rheumatic fever
Type I hypersensitivity
-MOA, mediated by, examples
Anaphylactic and atopic hypersensitivity
MOA: Specific IgE antibodies against an antigen are bound to mast cells and basophils; when triggered, they cause release of vasoactive amines (histamine)
Rapid reaction (first and fast) Antibody mediated
Examples: anaphylaxis, asthma, urticarial drug reactions, local wheal and flare
Type III hypersensitivity subgroups
Serum sickness, immune complex, arthus reaction
Immune complex
-MOA, examples
Antigen-antibody complex activates complement which attracts PMNs; these PMNs release lysosomal enzymes
Includes many glomerulonephritides and vasculitides ie PAN, immune complex glomerulonepritis, SLE, rheumatoid arthritis
Serum sickness
-MOA, types and symptoms
Antibodies to foreign proteins are formed in around 5 days
Immune complexes then form and are deposited in membranes and lead to tissue damage 2/2 complement activation
Types: most serum sickness is now caused by drugs and not serum
-fever, urticaria, arthralgieas, proteinuria, LAD 5-10 days after antigen exposure
Arthus reactions
-MOA and types
MOA: local reaction to antigen by preformed antibodies leading to vascular necrosis and thrombosis
This occurs rarely 4-12 hours after a vaccination
Causes hypersensitivity pneumonitis
Type IV hypersensitivity
-MOA, types
MOA: this is a delayed hypersensitivity mediated by sensitized T lymphocytes; they encounter antigens and release lymphokines which activate macrophages
-cell mediated, THE ONLY ONE THAT IS
Examples: Tb skin test, transplant rejection, contact dermatitis
Symptoms of atopic dermatitis
Pruritis leading to lichenification. Differs by age groups
Increases risk of bacterial (S aureus) and viral (HSV and molluscum) superinfection
Atopic dermatitis in infants
-what kind of rash, where on body
Erythematous, edematous, weeping, pruritic papules and plaques present on the face, scalp, and extensor surfaces
Diaper area is usually spared
Atopic dermatitis in children
-rash description and where
Dry, scaly, pruritic, excoriated papules and plaques in the flexural areas and neck
Atopic dermatitis in adults
-presentation and where
Lichenification and dry, fissured skin
Flexural distribution
Often has hand or eyelid involvement
Assocations with atopic dermatitis
Asthma and allergic rhinitis
First line therapy for eczema
Aka atopic dermatitis Topical corticosteroids = 1st line. DO NOT USE LONGER THAN 2-3 WEEKS Topical immunomodulators (tacrolimus, pimecrolimus) for moderate to severe asthma in patients > 2 y/o
Atopic dermatitis vs contact dermatitis
Eczema vs. type IV hypersensitivity (poison oak)
Eczema can be present in many places, usually as excoriations
Poison oak usually is present on contact surfaces and is weeping with erythematous papules and vesicles
Erythema toxicum neonatorum
A rash that resembles eczema, present in neonates about 1-3 days after delivery
Red papules, pustules, and/or vesicles with surrounding erythematous halos
Eosinophilia in the pustules/vesicles
Benign rash that resolves in 1-2 weeks with no treatment
Infant w/ hx of eczema treated w/ corticosteroids has new-onset rash and fever, showing grouped vesicles involving eczematous areas of the extremities and face. What is it and how to treat?
Eczema herpeticum
Superinfection of HSV on eczema
Medical emergency because HSV has a propensity to spread systemically
Tx w/ IV acyclovir
Common contact dermatitis allergens
Poison oak, poison ivy, nickel, soaps/detergents/cosmetics, rubber products containing latex
Treatment of contact dermatitis
Topical or systemic corticosteroids
Cool, wet compresses to soothe crusted lesion
Types of dermatitis
Atopic dermatitis (eczema) vs. contact dermatitis (type IV hypersensitivity) vs. seborrheic dermatitis (Pityrosproum ovale (fungal) infection)
Cause of seborrheic dermatitis
Pityrosporum ovale, usually in oily skin
What diseases are associated with seborrheic dermatitis?
HIV and Parkinsons disease
Appearance of seborrheic dermatitis in infants and children/adults
Infants: severe, red diaper rash. yellow scaling, erosions, and blisters. thick crust develops on scalp (cradle cap)
Children/adults: red, scaly patches around ears, eyebrows, nasolabial folds, midchest, scalp; less severe than in infants
Treatment of seborrheic dermatitis
Selenium sulfide
Zinc pyrithion shamppos for the scalp
Topical antifungals
Topical corticosteroids for other areas in adults
Psoriasis: what causes it and describe the rash
Cause: T cell mediated inflammatory dermatosis
Rash: erythematous plaques with silvery scales 2/2 dermal infalmmation and epidermal hyperplasia
Nails: pitting, oil spots, and onycholysis (lifting of the nail plate)
Location of rash in psoriasis
Extensor surfaces (elbow, knee, scalp, lumbosacral regions)
Rash that affects extensor surfaces is….?
Rash that affects flexor surfaces is….?
Psoriasis
Eczema (atopic dermatitis)
Koebner’s phenomenon
Psoriatic lesions that are provoked by local irritation or by trauma
Medications that can induce psoriasis
B-blockers, ACEi, lithium
Dx of psoriasis
Clinical: Auspitz sign ie bleeding when scale is scraped
Biopsy: thickened epidermis elongated in rete ridges, absent granular cell layer, preservation of nuclei in the stratum corneum (parakeratosis), and a sterile neutrophilic infiltrate in the stratum corneum
Munro’s microabscess
Biopsy finding in psoriasis: sterile neutrophilic infiltrate in the stratum corneum
Tx of psoriasis
Topical steroids + keratolytic agents, tar OR
anthralin + UV therapy
MTX for severe cases
Vitamin A (retinoids) and Vitamin D3 analogs can be helpful
What condition is associated with psoriasis?
Seronegative arthritis (psoriatic arthritis)
What are urticara?
Hives: superficial, intense erythema and edema in a localized area
Type I hypersensitivity response: histamine and prostaglandin release
Urticaria rash description
Elevated papule or plaque that is reddish or white and variable in size. These lesions are widespread and last a few hours
Extracutaneous manifestation of hives
i.e. in severe allergic reactions Tongue swelling and angioedema Asthma GI symptoms Joint swelling Fever
Tx of urticaria
Systemic antihistamines
Anaphylaxis: IM epinephrine, IVF, antihistamines, airway maintenance
Hospitalized patient who develops a cutaneous rash?
Likely a drug reaction. They can take many forms (all 4 types of hypersensitivities)
Time-course of drug eruption
Reaction occurs 7-14 days after exposure
If a patient reacts within 1-2 days, that drug is probably not the causative agent
Relatively short-lived, disappears within 1-2 weeks after removal of the offending agent
Description of typical drug eruption
Widespread, symmetrical, pruritic
More widespread form of Stevens Johnson disease?
Toxic epidermal necrolysis
SJS < 10% of body surface area
TEN > 30% of body surface area
Targetoid lesions are caused by?
Erythema multiforme
Erythematous macuels that become centrally clear and develop a blister
Usually affects palms and soles
a/w fever, myalgias, headaches, arthralgias
Complication of erythema multiforme?
Stevens Johnson or toxic epidermal necrolysis
Erythema nodosum description
Painful, erythematous nodules (paniculitis ie inflammation of subcutaneous adipose tissue) that appear on lower legs and slowly spread. They turn brown or gray, and p/w fever and joint pain
May have false VDRL
Erythema nodosum triggers
Infection: Streptococcus, Cocci, Yersinia, Tb
Drug reactions: sulfonamides, various antibiotics, and OCPs
Chronic inflammatory diseases: sarcoid, Crohn’s disease, UC, Behcet disease
Workup for erythema nodosum
ASO, PPD, CXR, small bowel series
Strep, Tb, Sarcoid, IBD
Tense vs. flaccid blisters
Bullous pemphigoid vs. pemphigus vulgaris
Nikolky’s sign
Sloughing off of skin with light rubbing
Present in Stevens Johnson, toxic epidermal necrolysis, pemphigus vulgaris
Scalded skin syndrome vs. Stevens Johnson/TEN
Scalded skin: caused by Staph, usually affects children
SJ/TEN: caused by drugs, usually affects adults
History of Stevens Johnson and TEN
Preceded by EM, flulike prodrome, skin tenderness, maculopapular drug rash, painful mouth lesions
Exam: severe mucosal erosions with widespread erythema, dusky red/purpuric macules or atypical targeoid lesions
Biopsy results of Stevens Johnson vs. TEN
Stevens Johnson: degeneration of basal layer of epidermis
TEN: full-thickness eosinophilic epidermal necrosis
Treatment of SJ and TEN
Treat like burn victims
Skin coverage, maintenance of fluid and electrolyte balance
Systemic corticosteroids in early disease
Blistering skin conditions
Bullous pemphigoid vs. pemphigus vulgaris
Bullous pemphigoid
-location of blisters, what antibodies, blister appearance, Nikolsky’s sign, mucosal involvement, patient age, associated medication triggers, mortality, diagnosis, treatment
Location: basement membrane zones Abs: anti-bullous pemphigoid antigen Blister appearance: firm, tense, stable blisters; preceded by urticaria Nikolsky sign is negative Mucosal involvement is rare Age is usually > 60 Medication triggers: idiopathic Mortality: rare and milder course Diagnosis: clinical features, skin biopsy w/ immunofluorescence and/or ELISA Treatment: prednisone
Pemphigus vulgaris
-location of blisters, what antibodies, blister appearance, Nikolsky’s sign, mucosal involvement, patient age, associated medication triggers, mortality, diagnosis, treatment
Location: intraepidermal
Abs: anti-desmogelin (desmoglein is responsible for keratinocyte adhesion)
Appearance: erosions are more common (ie popped blisters) due to the lack of keratinocyte adherence; flaccid blisters
Nikolsky sign positive
Mucosal involvement is common
Age: 40-60
Medication triggers: ACEIs, penicillamine, phenobarbital, PCN
Mortality is possible
Dx: clinical features, skin biopsy w/ IF, and ELISA
Tx: high dose prednisone + IVIG/MMF/rituximab