Miscellaneous Lesions Flashcards
Angioedema description and forms
- deeper swelling of the skin involving subcutaneous tissues; often involves the eyes, lips, and tongue
- may or may not accompany urticaria
- hereditary or acquired forms
Hereditary angioedema description, onset and triggers
• hereditary angioedema (does not occur with urticaria)
■ onset in childhood; 80% have positive family history
■ recurrent attacks; 25% die from laryngeal edema
■ triggers minor trauma, emotional upset, temperature changes
Types of acquired angioedema
■ acute allergic angioedema (allergens include food, drugs, contrast media, insect venom, latex)
■ non-allergic drug reaction (drugs include ACEI)
■ acquired C1 inhibitor deficiency
Angioedema treatment
■ prophylaxis with danazol or stanozolol for hereditary angioedema
■ epinephrine pen to temporize until patient reaches hospital in acute attack
Urticaria description and pathophysiology
- also known as “hives”
- transient, red, pruritic well-demarcated wheals
- each individual lesion lasts less than 24 h
- second most common type of drug reaction
- results from release of histamine from mast cells in dermis
- can also result after physical contact with allergen
DDx for urticaria
DAM HIVES
Drugs and foods
Allergic
Malignancy
Hereditary Infection Vasculitis Emotions Stings
Acute urticaria
> 2/3 of cases
Attacks last <6 wk
Individual lesions last <24 h
Acute urticaria etiology
Drugs; especially ASA, NSAIDs
Foods: nuts, shellfish, eggs, fruit
Idiopathic (vast majority)
Infection
Insect stings (bees, wasps, hornets)
Percutaneous absorption: cosmetics, work exposures
Stress
Systemic diseases: SLE, endocrinopathy, neoplasm
Chronic urticaria
<1/3 of cases
Attacks last >6 wk
Individual lesion lasts <24 h
Chronic urticaria etiology
IgE-dependent: trigger associated
- Idiopathic (90% of chronic urticaria patients)
- Aeroallergens
- Drugs (antibiotics, hormones, local anesthetics)
- Foods and additives
- Insect stings
- Parasitic infections
- Physical contact (animal saliva, plant resins, latex, metals, lotions, soap)
Direct mast cell release
- Opiates, muscle relaxants, radio-contrast agents
Complement-mediated
- Serum sickness, transfusion reactions
- Infections, viral/bacterial (>80% of urticaria in pediatric patients)
- Urticarial vasculitis
Arachidonic acid metabolism
- ASA, NSAIDs
Physical
- Dermatographism (friction, rubbing skin), cold (ice cube, cold water), cholinergic (hot shower, exercise), solar, pressure (shoulder strap, buttocks), aquagenic (exposure to water) adrenergic (stress), heat
Other
- Mastocytosis, urticaria pigmentosa
Approach to urticaria
- Thorough Hx and P/E
- Acute: no immediate investigations needed; consider referral for allergy testing
- Chronic: further investigations required: CBC and differential, urinalysis, ESR, TSH, LFTs to help identify underlying cause
- Vasculitic: biopsy of lesion and referral to dermatology
Wheal
- Typically erythematous flat-topped, palpable lesions varying in size with circumscribed dermal edema
- Individual lesion lasts <24 h
- Associated with mast cell release of histamine
- May be pruritic
Mastocytosis (Urticaria Pigmentosa)
Rare disease due to excessive infiltration of the skin by mast cells. It manifests as many reddish-brown elevated plaques and macules. Friction to a lesion produces a wheal surrounded by intense erythema (Darier’s sign), due to mast cell degranulation; this occurs within minutes
Urticarial vasculitis description and intervention
Individual lesions last >24 h
Often painful, less likely pruritic, heals with bruise type lesions
Requires biopsy
Urticarial vasculitis etiology
Idiopathic Infections Hepatitis Autoimmune diseases SLE Drug hypersensitivity Cimetidine and diltiazem
Erythema nodosum clinical presentation
- acute or chronic inflammation of subcutaneous fat (panniculitis)
- round, red, tender, poorly demarcated nodules sites: asymmetrically arranged on extensor lower legs (typically shins), knees, arms
- associated with arthralgia, fever, malaise
Erythema nodosum etiology
- 40% are idiopathic
- drugs: sulfonamides, OCPs (also pregnancy), analgesics, trans retinoic acid
- infections: GAS, TB, histoplasmosis, Yersinia
- inflammation: sarcoidosis, Crohn’s > UC
- malignancy: acute leukemia, Hodgkin’s lymphoma
Erythema nodosum epidemiology
- 15-30 yr old, F:M = 3:1
* lesions last for days and spontaneously resolve in 6 wk
Erythema nodosum investigations
- chest x-ray (to rule out chest infection and sarcoidosis)
* throat culture, ASO titre, PPD skin test
Erythema nodosum management
- symptomatic: bed rest, compressive bandages, wet dressings
- NSAIDs, intralesional steroids
- treat underlying cause
DDx of Erythema Nodosum
NODOSUMM NO cause (idiopathic) in 40% Drugs (sulfonamides, OCP, etc.) Other infections (GAS+) Sarcoidosis UC and Crohn’s Malignancy (leukemia, Hodgkin’s lymphoma) Many Inections
Pruritus ddx
SCRATCHED Scabies Cholestasis Renal Autoimmune Tumours Crazies (psychiatric) Hematology (polycythemia, lymphoma) Endocrine (thyroid, parathyroid, Fe) Drugs, Dry skin
• dermatologic – generalized
■ asteatotic dermatitis (“winter itch” due to dry skin)
■ pruritus of senescent skin (may not have dry skin, any time of year)
■ infestations: scabies, lice
■ drug eruptions: ASA, antidepressants, opiates
■ psychogenic states
• dermatologic – local ■ atopic and contact dermatitis, lichen planus, urticaria, insect bites, dermatitis herpetiformis ■ infection: varicella, candidiasis ■ lichen simplex chronicus ■ prurigo nodularis
• systemic disease – usually generalized
■ hepatic: obstructive biliary disease, cholestatic liver disease of pregnancy
■ renal: chronic renal failure, uremia secondary to hemodialysis
■ hematologic: Hodgkin’s lymphoma, multiple myeloma, leukemia, polycythemia vera, hemochromatosis, Fe deficiency anemia, cutaneous T-cell lymphoma
■ neoplastic: lung, breast, gastric (internal solid tumours), non-Hodgkin’s lymphoma
■ endocrine: carcinoid, DM, hypothyroid/thyrotoxicosis
■ infectious: HIV, trichinosis, echinococcosis, hepatitis C
■ psychiatric: depression, psychosis
■ neurologic: post-herpetic neuralgia, multiple sclerosis
Pruritus investigations
CBC, ESR, Cr/BUN, LFT, TSH, fasting blood sugar, stool culture and serology for parasites
Pruritus management
- treat underlying cause
- cool water compresses to relieve pruritus
- bath oil and emollient ointment (especially if xerosis is present)
- topical corticosteroid and antipruritics (e.g. menthol, camphor, phenol, mirtazapine, capsaicin)
- systemic antihistamines: H1 blockers are most effective, most useful for urticaria
- phototherapy with UVB or PUVA
- doxepin, amitriptyline
- immunosuppressive agents if severe: steroids and steroid-sparing
Sunburn description, consequences, prevention
- erythema 2-6 h post UV exposure often associated with edema, pain and blistering with subsequent desquamation of the dermis, and hyperpigmentation
- chronic UVA and UVB exposure leads to photoaging, immunosuppression, photocarcinogenesis
- prevention: avoid peak UVR (10 am-4 pm), wear appropriate clothing, wide-brimmed hat, sunglasses, and broad-spectrum sunscreen
- clothing with UV protection expressed as UV protection factor (UPF) is analogous to SPF of sunscreen
SPF meaning
burn time with cream/burn time without cream
Sunscreens
• under ideal conditions an SPF of 10 means that a person who normally burns in 20 min will burn in 200 min following the application of the sunscreen
• topical chemical: absorbs UV light
■ requires application at least 15-30 min prior to exposure, should be reapplied every 2 h (more often if sweating, swimming)
■ UVB absorbers: PABA, salicylates, cinnamates, benzylidene camphor derivatives
■ UVA absorbers: benzophenones, anthranilates, dibenzoylmethanes, benzylidene camphor derivatives
• topical physical: reflects and scatters UV light
■ titanium dioxide, zinc oxide, kaolin, talc, ferric chloride, and melanin
■ all are effective against the UVA and UVB spectrum
■ less risk of sensitization than chemical sunscreens and waterproof, but may cause folliculitis or miliaria
• some sunscreen ingredients may cause contact or photocontact allergic reactions, but are uncommon
UVA effect
UVA (320-400 nm): Aging
- Penetrates skin more effectively than UVB or UVC
- Responsible for tanning, burning, wrinkling, photoallergy and premature skin aging
- Penetrates clouds, glass and is reflected off water, snow and cement
UVB effect
UVB (290-320 nm): Burning
- Absorbed by the outer dermis
- Is mainly responsible for burning and premature skin aging
- Primarily responsible for BCC, SCC
- Does not penetrate glass and is substantially absorbed by ozone
UVC
UVC (200-290 nm)
• Is filtered by ozone layer
Sunburn management
- sunburn: if significant blistering present, consider treatment in hospital; otherwise, symptomatic treatment (cool wet compresses, oral anti-inflammatory, topical corticosteroids)
- antioxidants, both oral and topical are being studied for their abilities to protect the skin; topical agents are limited by their ability to penetrate the skin
Relative percutaneous absorption per body site for steroids
Forearm 1.0 Plantar foot 0.14 Palm 0.83 Back 1.7 Scalp 3.7 Forehead 6.0 Cheeks 13.0 Scrotum 42.0
Calculation of strength of steroid compared to hydrocortisone on forearm relative strength of steroid x relative percutaneous absorption
Steroid amount required to cover body surface area
30 g covers full adult body once. Children have a greater surface area/volume ratio and there are consequently greater side effects
Side effects of topical steroids
- Local: atrophy, perioral dermatitis, steroid acne, rosacea, contact dermatitis, tachyphylaxis (tolerance), telangectasis, striae, hypertrichosis, hypopigmentation
- Systemic: suppression of HPA axis
Potency ranking of topical steroids
Weak x1 - hydrocortisone
(2.5%, 1% available OTC)
EmoCort
Usage on intertriginous areas, children, face, thin skin
Moderate x3 - Hydrocortisone 17-calerate-0.2%, desonide, mometasone furoate
Westcort, Tridesilon, Elocom
Usage on arm, leg, trunk
Potent x6 - betamethasone 0.1%, 17-valerate 0.1%, amcinonide
Betnovate, Celestoderm - V, Cyclocort
Usage on body
Very potent 9x - betamethasone, dipropionate 0.05%, fluocinonide 0.05%, halcinonide
Diprosone, Lidex, Topsyn gel, Lyderm, Halog
Use on palms and soles
Extremely potent 12x - clobetasol propionate 0.05% (most potent), betamethasone, dipropionate ointment, halobetasol propionate 0.05%
Dermovate, Diprolene, Ultravate
Use on palms and soles
