Miscellaneous Lesions Flashcards

(35 cards)

1
Q

Angioedema description and forms

A
  • 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
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2
Q

Hereditary angioedema description, onset and triggers

A

• 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

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3
Q

Types of acquired angioedema

A

■ acute allergic angioedema (allergens include food, drugs, contrast media, insect venom, latex)

■ non-allergic drug reaction (drugs include ACEI)

■ acquired C1 inhibitor deficiency

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4
Q

Angioedema treatment

A

■ prophylaxis with danazol or stanozolol for hereditary angioedema

■ epinephrine pen to temporize until patient reaches hospital in acute attack

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5
Q

Urticaria description and pathophysiology

A
  • 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
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6
Q

DDx for urticaria

A

DAM HIVES

Drugs and foods
Allergic
Malignancy

Hereditary 
Infection 
Vasculitis 
Emotions 
Stings
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7
Q

Acute urticaria

A

> 2/3 of cases

Attacks last <6 wk

Individual lesions last <24 h

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8
Q

Acute urticaria etiology

A

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

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9
Q

Chronic urticaria

A

<1/3 of cases

Attacks last >6 wk

Individual lesion lasts <24 h

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10
Q

Chronic urticaria etiology

A

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

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11
Q

Approach to urticaria

A
  • 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
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12
Q

Wheal

A
  • 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
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13
Q

Mastocytosis (Urticaria Pigmentosa)

A

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

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14
Q

Urticarial vasculitis description and intervention

A

Individual lesions last >24 h

Often painful, less likely pruritic, heals with bruise type lesions

Requires biopsy

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15
Q

Urticarial vasculitis etiology

A
Idiopathic 
Infections 
Hepatitis 
Autoimmune diseases 
SLE 
Drug hypersensitivity 
Cimetidine and diltiazem
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16
Q

Erythema nodosum clinical presentation

A
  • 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
17
Q

Erythema nodosum etiology

A
  • 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
18
Q

Erythema nodosum epidemiology

A
  • 15-30 yr old, F:M = 3:1

* lesions last for days and spontaneously resolve in 6 wk

19
Q

Erythema nodosum investigations

A
  • chest x-ray (to rule out chest infection and sarcoidosis)

* throat culture, ASO titre, PPD skin test

20
Q

Erythema nodosum management

A
  • symptomatic: bed rest, compressive bandages, wet dressings
  • NSAIDs, intralesional steroids
  • treat underlying cause
21
Q

DDx of Erythema Nodosum

A
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
22
Q

Pruritus ddx

A
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

23
Q

Pruritus investigations

A

CBC, ESR, Cr/BUN, LFT, TSH, fasting blood sugar, stool culture and serology for parasites

24
Q

Pruritus management

A
  • 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
25
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
26
SPF meaning
burn time with cream/burn time without cream
27
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
28
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
29
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
30
UVC
UVC (200-290 nm) • Is filtered by ozone layer
31
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
32
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
33
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
34
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
35
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