Inflammatory Dermatoses Flashcards
6 Ps of Lichen Planus
Planar, Purple, Polygonal, Pruritic, Papular, Plaques
Acute Inflammatory Dermatoses
Urticaria*** (Dermis)
Erythema Multiforme (Ep/Dermis)*
Stevens Johnson Syndrome/Toxic Epidermal Necrolysis* (Epi/Dermis)
Fixed Drug Eruption (Epidermis)
Panniculitis (Subcutaneous) - Erythema Nodosum, Erythema Induratum
Pruritic, Transient raised wheals
Urticaria
Common places for angioedema
Lip, eye, groin, palms, soles
Acute vs. Chronic Urticaria/Angioedema
Acute (⅔) → duration 6wks, cause often idiopathic, requires long term tx for suppression
Causes (U/A)
Immune -Type 1 IgE mediated - Autoimmune -Infection Nonimmune - Physical urticarias - Direct Mast Cell Degranulation - Foods w/ high histamine
Triggers of Type 1 IgE mediated U/A
Foods, latex, stinging insects, meds, aeroallergens
Types of physical urticarias
Solar, cholinergic, cold, dermographism, aquagenic, vibratory angioedema, pressure urticaria
Types of Autoimmune diseases –> U/A
Hashimoto’s immune thyroiditis, SLE, vasculitis
Direct mast cell degranulation triggers
Narcotics, aspirin, NSAIDs, radio-contract media, dextran, ACE inhibitor, vancomycin
Foods w/ high levels of histamine
Strawberries, tomatoes, shrimp, lobster, cheese, spinach eggplant
Basic lab eval for U/A
CBC, ESR, TSH, and basic chemistry panel
How to check for Lupus if seeing U/A
Anti-thyroid antibody and ANA
Therapy U/A
Avoid Allergen/triggers/alcohol
Antihistamines
Preferences of Antihistamines for Acute Urticaria
First - second generation non-sedating H1 blockers (i.e. Cetirizine = Zyrtec, Allegra, Clarinex…)
Then 1st gen sedating H1 blockers (Benadryl) –> H2 blocker (Zantac, Tagamet) –> H1/H2 combo blocker (Sinequan = treats anxiety too) –> Leukotriene modifier (Singular = montelukast)
Last resort = oral corticosteroid (prednisone)
Then immunosuppressives, immunology, etc
Target area, multiple involving extremities and mucous membranes
Erythema Multiforme
Etiology of Erythema Multiforme
Cutaneous rexn to variety of antigenic stimula
Drugs - sulfa, phenytoin, allopurinol
Infection - HERPES SIMPLEX VIRUS, mycoplasma
Idiopathic (common)
EM Minor vs Major
Minor - involving
Therapy for EM Minor, Major
Control underlying (i.e. herpes), for severe: glucocorticoids (prednisone)
EM vs. Hives
EM fixed and usually doesn’t itch
Stevens Johnson Syndrome
drug induced or idiopathic
skin tenderness/erythema –> extensive cutaneous and mucosa epidermal necrosis and sloughing
Differentiation of EM, SJS, TEN
Erythema Multiforme (1 mucosal membrane)
Stevens-Johnson Syndrome (SJS): Considered a Maximal Variant of EM Major (2+ mucosal membrane and
Risk factors for SJS/TEN
SEL, HLA-B12, HIV
SJS/TEN Etiology
Drugs (80% TEN, 50% SJS)
Cytotoxic immune rxn aimed at destroying keratinocytes expressing foreign drug-related antigens
Hallmark: Swelling/pain lips (burning)
Angioedema, considered emergency
Hallmark: 2> mucus membranes, 10% of skin, sloughing of skin, sulfa drugs
SJS
Hallmark: Target lesions, palms/soles, 1+ rash
Erythema mulitforma
Hallmark: 30% body covered in rashes, sloughing
TENS
Hallmark: One red spot, hyperpigmentation, sharp demarcation
Fixed drug eruption
Hallmark: Anterior shin nodule
Erythema nodosmi (septal)
Hallmark: Posterior leg, associated with TB
Erythema induratum (lobular)
Trigger: Erythema nodosum
Infection, meds, autoimmune
Trigger: Erythema induratum
TB
Hallmark: Scaling, auspitz sign, koebner
Psoriasis
Hallmark: Butterfly rash
SLE
Hallmark: 6Ps
Lichen Planus
Genetics of Psoriasis
Autosomal dominance, modifying features + environmental triggers
Clinical features psoriasis
Sharply demarcated erythema, usually with thick micaceous scale (i.e. silvery)
Auspitz sign = bleeding after removal of scale
Koebner phenomenon = lesions induced by trauma (if develop psoriatic lesion after trauma, have psoriasis)
Nail disease up to 50% prevalence
Rarely pustular
Auspitz sign
bleeding after removing scale (psoriasis)
Koebner phenomenon
Lesions induced by trauma (psoriasis)
Histopathology of Psoriasis
Extensive hyperkeratosis w/ parakeratosis (retained flat nuclei in keratinocytes)
Uniform elongation of rete ridges
Dermal papillae are edematous w/ suprapapillary thinning and dilated capillaries
Neutrophils in epidermis
Pustular Psoriasis composed of intraepidermal neutrophilic pustules- spongiform pustule
Pathogenesis of Psoriasis
Environmental Factors (ie. virus) → T cell produce cytokines → stimulate keratinocyte proliferation and production of antigenic adhesion molecules in dermal blood vessels → adhesion molecules further stimulate T cells to make cytokines…
Diagnosis of Psoriasis (differential)
Differential: Lichen simplex chronicus (neurodermatitis), nummular eczema (coin-shaped lesions), seborrheic dermatitis, tinea corporis Punch biopsy (if in doubt, usually use pattern recognition) Remember: chronic - if antifungal/antibiotic don’t help....
Types of Psoriasis
Chronic
Inverse - skin folds
Guttate - post-strep
Pustular
Treatment Psoriasis
Topicals → steroid, anthralin, tar, calcipotriol (Vit D), retinoids, tacrolimus
System → retinoids, ciclosporin, PUVA/UVB/Narrow Band UVB, Methotrexate, Etanercept/Efalizumab/Alefacept (tumor necrosis factor block for AI diseases)
Combination topical steroid and PUVA if >20% body
Usually topical med to soften thick skin, systemic to control T cell response
Wickham’s Stria
white lines visible in stria of papula of lichen planus
IgM mediated chronic
Lichen Planus
T cell mediated chronic
Psoriasis
Cutaneous LP Forms
Linear, Annular, Atrophic, Hypertrophic, Vesicobullous, Erosive/ulcerative, scalp
Oral LP forms
Reticular, atrophic, bullous, erosive
Treatment of LP
Cutaneous may resolve on own in 1-2 years, relapse
Topical steroids, oral steroids
Phototherapy
Stop aggravating drug
IgG mediated chronic
Systemic Lupus Erythematosus
Acute, Subacute, Chronic SLE
Acute: Pauci-inflammatory (few, little) interface dermatitis; prominent dermal edema and dermal mucin
Subacute: Prominent suprabasilar exocytosis of lymphocytes, prominent epidermal atrophy; lymphocytic infiltrate
Chronic Cutaneous/Discoid: Very thick basement membrane, follicular plugging; Dense perivascular and peri-adenxal infiltrate
Lab Tests for SLE
CBC, ESR, Kidney/Liver tests, UA, ANA - antinuclear antibody (don’t forget urine when ruling out SLE)
Treatment of SLE
NSAIDs, Antimalarials (plaquenil), Corticosteroids, immunosuppressants - cyclophosphamids (Cytoxan), azathaprine (imuran)
Herpes Simples 1 vs. 2
HSV 1: Primary infection usually occurs in childhood with lesions on the lips or face - more common
HSV 2: STD of adults involving the genital area, primary infection extensive, painful vesiculations and necrosis
Tx HS1
Oral acyclovir (recurrent tx with acyclovir, famciclovir and valacylclovir)
Tx HS2
Recurrent w/ no cure
Rx: Acyclovir, famciclovir, valacyclovir
Varicella
Chickenpox
Herpes Varicella Zoster virus
dew drop on rose petal
Incubation of VZ
14 days average, prodrome 2-3 days of fever/chills/malaise before rash
Immunization for Chickenpox
Children who have never had chickenpox should receive 2 doses:
1st dose at 12-15 months, 2nd dose at 4-6 years
People over 13 years of age who have never had chickenpox should receive 2 doses at least 28 days apart
Herpes Zoster (shingles)
Recurrence of varicella
Following nerve root
Tx shingles
Acyclovir, Prednisone, IV Acyclovir
Immunization shingles
Immunization: Zostavax-live, attenuated vaccine for prevention of herpes zoster in patients aged 50 and over
Why worry about tip of nose in shingles?
More likely to get to eye
Impetigo types
Non-bullous (Group A strep pyogenes, coagulase positive staph aureus and mixed) - more common
Bullous - phage group II staph aureus, epidermolytic toxin mediated
Etiology Nonbullous impetigo
Nonbullous impetigo begins as single red macule/papule → quickly becomes vesicle → vesicle ruptures easily to form erosion → contents dry to form characteristic honey-colored crusts (HALLMARK) that may be pruritic
Etiology Bullous impetigo
Superficial vesicles progress to rapidly enlarging, flaccid bullae with sharp margins and no surrounding erythema → bullae rupture, yellow crusts with oozing result
More on axillary, groin, fold areas
Tx Impetigo
Tx: Hygienic Measures, Topical Antibiotics, Oral Antibiotics
Bullous Diseases
Bullous pemphigoid
Pemphis vulgaris
Dermatitis herpetiformis
Bullous pemphigoid
IgG at basement membrane, AI, prednisone
Pemphigus vulgaris
intracellular IgG pattern, AI, skin/muccous, flaccid blisters (Nikolsky sign = blister sliding)
Dermatitis herpetiformis
IgA clumps basement membrane
Gluten sensitivity
Porphyria Cutanea Tarda
Deficiency in heme-synthesizing enzyme
Blistering of skin, sun-exposed
Hypertrichosis of forehead/cheeks, skin hyperpigmentation and urine discoloration
RF: Hep c, hemochromatosis and alcoholism
Hallmark: mouth lesions/vesicles, less recurrance
Herpes simplex 1
Hallmark: STD, recurrent, viral
HS2
Hallmark: “Dew drops on a rose petal”
Varicella
Hallmark: Dermatomes and unilateral
Zoster
Hallmark: Honey-colored crusting
Impetigo
Hallmark: Tense blisters
bullous pemphigoid
Hallmark: Celiac disease associated
dermatitis H
Hallmark: Flaccid blisters
Pemphigus vulgaris
Hallmark: Hyperpigmentation
Prophyria cutanea tarda
Vancomycin “Red Man” Syndrome is an example of ______
Urticaria/Angioedema
d/t direct mast cell degranulation
What should patient’s with type I IgE mediated hypersensitivities have (med)?
EpiPen
Rash along with Herpes Simplex Virus? - but not the blisters (Hallmark)
Erythema Multiforme
Major cause of EM minor
Herpes Simplex Virus
Time from first drug exposure to SJS/TEN sxs
1-3 weeks
Beginning of SJS/TENS
Fever, malaise, arthralgias (days to weeks after exposure) –> painful morbilliform rash –> confluent/bullous/exfoliative
How to diagnose panniculitis?
skin biopsy (in subcutaneous)
Nail pitting/onycholysis associated with ______
Psoriasis in 50%
LP happens where in skin?
epidermis-dermis junction
Hallmark of linear lichen planus
Wickham’s striae (white lines or grooves that cover surface of LP lesions)
pinna
visible ear
Hutchinson’s Sign
Shingles on tip of nose –> worry about eye involvement
Nonbullous impetigo causative agent
Group A strep pyogenes, Coagulase positive staph or mixed
Bullous impetigo causative agent
Phage group II Staph aureus (epidermolytic toxic)
Nikolsky sign
top layers of skin slip away from lower layers when slightly rubbed - maybe make blister
Pemphigus vulgaris