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Papulosquamous Flashcards

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Dermatology Board Prep flashcards
1
Q

Pityriasis rotunda - types

A
  • Type 1: seen in 60s, associated with hepatocellular carcinoma or other malignancy
  • Type 2: seen in 40s, genetic - autosomal dominant
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2
Q

Pityriasis rotunda - histology

A

hyperkeratosis with loss of granular layer (looks like IV)

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3
Q

Pityriasis rotunda - clinical

A

asymptomatic thin finely scaling plaques, sharply demarcated that coalesce to form polycyclic plaques

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4
Q

Pityriasis rotunda - management

A
  • Topical retinoids
  • Topical lactic acid 10%
  • 5% salicylic acid ointment
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5
Q

Eczema food allergies

A

milk, egg, wheat, soy, peanut, fish

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6
Q

Four types of plant reactions

A
  1. Urticaria
  2. ICD
  3. ACD
  4. Phytophotodermatitis
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7
Q

Plants that cause ACD

A 
Garlic
Peruvian lily
Scourge of India
Poison ivy (toxicodendron radicans)
Poison oak
Tulips
Chrysanthemums
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8
Q

Plants that cause ICD

A 
Garlic
Daffodils
Poison ivy
Poison oak
Tulips
Prickly pear and others
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9
Q

Plants that cause phytophotodermatitis most commonly

A

Persian limes

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10
Q

Plant that most commonly causes urticaria

A

Stinging nettle

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11
Q

What is the epidemiology of immunologic contact urticaria

A
  • 95% long-time food handlers with underlying dermatitis
  • 1/2 of patients with protein contact dermatitis (Type 4 eczematous eruption arising from repeated Type 1 reaction) are not atopic
  • Reported urticants are common vegetables and fruits (celery, onions, potatoes, lettuce, tomatoes, bananas, lemons), herbs, nuts, shrubs, algaes, lichens, trees, grasses
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12
Q

What is the pathogenesis of immunologic contact urticaria

A
  • IgE mediated release of vasoactive mediators from mast cells leads to local urticaria
  • Rarely it can result in contact urticaria syndrome: local wheals plus systemic symptoms: nose, throat, lungs, GIT or CVS
  • Main cause is histamine release, but prostaglandins, kinins and leukotrienes also augment the response
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13
Q

What does immunologic contact urticaria look like

A
  • Contact with urticant –> within 30 minutes can experience pruritus, erythema, urticarial swelling, dyshidrotic like vesicles
  • Sometimes just develop symptoms: pruritis, burning, tingling
  • Oral allergy syndrome: oedema of lips, tongue, palate and pharynx, can get GIT and anaphylaxis
  • Any plant can cause urticaria, especially with repeated exposures on the wet, amcerated skin of food handlers
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14
Q

How can you reduce allergenicity of fruits

A

Cooking, deep-freezing, processing, crushing

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15
Q

Can you get cross-sensitization with immunologic contact urticaria

A

Yes - pollens and similar allergens. - For example: birch pollen with apples, pears, cherries, peaches, plums, apricots, almonds, celery, carrots, potatoes, kiwis, hazelnuts, mangoes
- Eating cross-reacted food: sudden, IgE mediated oral cavity itching, stinging and pain

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16
Q

What is protein contact dermatitis

A

chronic dermatitis with negative patch tests, but positive to prick tests to large protein allergens –> chronic dermatitis that acutely urticates within minutes of contact with the offending allergen

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17
Q

What are the common culprits in toxin-mediated contact urticaria in plants

A

Stinging nettle (Urtica dioica) - northern hemisphere, moist woods, roadsides, wasteland. We have it here in Australia.

  • Urticacea: wood nettle, Dendrocnide gigas/moroides/photinophylla - deadly stinging trees in eastern Australian rainforests
  • Euphorbiaceae: spurge nettles
  • Hydrophyllaceae: large leafed shrubs, seen in tropical America
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18
Q

What is the pathogenesis of toxin-mediated contact urticaria with plants

A
  • Have trichomes (sharp hairs) on the leaves and stems
  • Proximal silicaceous hair is attached to a distal calcified portion that possesses a terminal bulb. When rubbed against, the bulb dislodges to reveal a beveled, hypodermic needle-like, hollow hair
  • This releases an irritant chemical cocktail of histamine, acetylcholine and serotonin –> this is a defense mechanism against herbivores
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19
Q

Clinical toxin-mediated contact urticaria with plants

A
  • Wheals - achieve maximal size 3-5 minutes after contact
  • Erythema, burning and pruritis can last 1-2 hours, paraesthesias >12 hours. The chemical cocktail does not explain the paraesthesias.
  • The deadly stinging trees in Eastern Australia (Dendrocnide genus): young shoots are covered with stiff, stinging hairs –> severe urticaria can last for weeks, and contact with water or cold reactivates it. Severe intermittent stabbing pains may follow the course of lymphatics. It can cause death rarely.
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20
Q

How to diagnose toxin-mediated contact urticaria with plants

A
  • Can do pick and Scratch-chamber test: 5mm scratch made, test material is applied and occluded with a Finn chamber for 15 minutes, then reviewed every 15 minutes for an hour, then re-cover and check at 48 hours for delayed hypersensitivity
  • Open application test: most reliable test for toxin mediated: samples (0.1 mL) placed onto discrete 3X3 cm areas of skin and observed every 10-15 minutes for an hour –> maximal erythema and oedema typically occurs 30-40 minutes after application
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21
Q

Treatment of toxin-mediated contact urticaria with plants

A
  • Self-limited
  • Trichomes may be removed with glue and gauze
  • Topical pramoxine (topical anaesthetic) or oral analgesics may provide some relief
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22
Q

Plant mechanical irritant dermatitis pathogenesis

A
  • Cacti have large spines and small glochids: tufts of hundreds of short, barbed or hooked hairs - arise from areoles. The glochids often point outward and backward like a fishhook and produce considerable irritation and pruritis
  • Glochids occur on other plants too
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23
Q

What is Sabra dermatitis

A
  • Glochids from prickly pears (Opuntia) results in a pruritic, papular eruption in pickers.
  • The prickly pears contain the highest concentration of glochids, and the eruption results in a fibreglass dermatitis or scabies like picture.
  • Recommend them to only pick prickly pairs when wet, and cease when it is windy
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24
Q

What are some complications you can get from mechanical irritant dermatitis with plants

A
  • Spine and thorn - Clostridium tetani and staph aureus
  • Grasses, sphagnum moss and rose thorns - sporothix schenckii
  • Atypical mycobacteria: blackberries (kansasii), cactus spines (marinarum) and tropical (ulcerans)
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25
Q

What is the treatment of mechanical irritant dermatitis with plants

A
  • Remove glochids by detaching clumps with tweezers

- Then apply glue and gauze to the affected area, after the glue has dried peel off the gauze –> gets rid of about 95%

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26
Q

Tell me about calcium oxalate chemical irritant dermatitis

A
  • in Dieffenbachia picta - often a potplant in lots of places.
  • Upon exposure to water, releases water-insoluble calcium oxalate which is a chemical irritant
  • If swallowed: salivation, burning, mucosal oedema, blistering, hoarseness or aphonia
  • Rx: steroids, antacid mouthwash, analgesics, pain and oedema for 4-12 days
  • Enhances the irritancy of other chemicals such as bromelin which is in pineapples
27
Q

Tell me about pineapple irritant dermatitis

A
  • Pineapple workers: develop cracks, fissures, fingerprint loss, microhaemorrhages
  • Calcium oxalate microabrasions allow bromelin to have a proteolytic effect on blood vessels
  • Nitrile gloves can be worn for protection
28
Q

Tell me about daffodil itch

A
  • More common and less dramatic
  • Daffodil sap (in bulbs, stems, leaves) contains calcium oxlaate and causes daffodil itch
  • Dryness, scaling, fissures, erythema
  • Tulips and hyacinths can also cause this
29
Q

Tell me about garlic irritant dermatitis

A
  • High concentrations can lead to second and third degree burns
  • Can also cause subungual hyperkeratosis and haemorrhage that can look like nail psoriasis
30
Q

Tell me about buttercup irritant dermatitis

A
  • Contain glycoside ranunculinthat is converted to protoanemonin after plant injury
  • This causes linear vesiculation which can look like early phytophotodermatitis, but no hyperpigmentation
  • Only freshly damaged plants cause this reaction
31
Q

Tell me about capsaicin irritant dermatitis

A
  • In Chili peppers
  • Capsaicin depolarizes nerves causing vasodilation, smooth muscle stimulation, glandular secretion and sensory nerve activation
  • Only nerves are affected, so there is erythema but no vesicles
  • Symptoms may be delayed, and last hours to days
  • Rx: wash with soap and water, then immerse in vegetable oil for an hour to remove the fat soluble capsaicin
32
Q

Tell me about century plant irritant dermatitis

A
  • In tropical climates
  • Has rosettes of tough, sword-shaped leaves with spiny margins
  • Marked pruritis and stinging when come into contact –> latex derived calcium oxalate crystals and saponins, and purpura
  • Soldiers used to induce sick leave with these, as you can get systemic sx
33
Q

What two plant groups cause phytophotodermatitis

A

Apiaceae and Rutaceae

Mulberry and pea as well, and St John’s wort and wild spinach

34
Q

What is under the Apiaceae group

A
  • Apiacea family: False Bishop’s weed, Angelica, wild Angelica, cow parsley, celery, fig, fennel, tromso palm, cow parsnip, wild rhubarb, hogweed, blister bush, parsnip, parsley
  • Distinctive floral umbel: numerous small flowers are held in a simple umbel, can be umbrella like or compounded
  • Common hogweed are major causes, and grow invasively in Europe and North America. Biggest threat in Autumn, when weather spreads the seeds
  • Fruits contain the highest concentrations of psolarens, followed by leaves and stems
35
Q

What is under the Rutaceae group

A
  • Citrus family: lime, oranges, lemons, grapefruits, berry rue, burning bush, coast spice bush, mokihana (makes leis in Hawaii), blister bush (WA), rue
  • Grow as shrubs or trees and produce fleshy fruit
  • Persian lime contain 10X more 5-MOP in the rind than the pulp, and outdoor bartenders commonly develop
  • Sweet orange can cause phototoxic cheilitis
  • Garden rue: bitter tasting and smelling sub-shrub native to the Mediterranean –> used in folk medicine and as insect repellant. Contains 5-MOP, 8-MOP and angelicins
  • Gas plant or burning bush (dictamnus albus) has an aromatic oil that can be ignited briefly without harming the plant. Common yard plant
36
Q

What is the pathogenesis of phytophotodermatitis

A
  • Foucoumarins have psoralens or angelicins: psoralens are linear tricyclic structures, and angelicins are angular tricyclic structures
  • 5-MOP and 8-MOP cause the most severe reactions
  • UVA (320 - 340): psoralens react with oxygen –> produces reactive oxygen species –> cytoplasmic vacuolization and keratinocyte membrane rupture
  • Within 2 hours: desmosomal plaques detach and degenerate leading to blister formation
  • UVA also causes psoralens to form covalent inter-strand DNA cross-links by binding to pyrimidines:
    • Keratinocyte cell death
    • Increased melanocyte mitosis and dendricity–> hyperpigmentation
    • Melanocyte hypertrophy
    • Increased tryosinase activity
    • Larger melanosomal size
    • Enhanced distribution of melanosomes throughout the epidermis
  • Foucoumarins help plants from fungi –> celery produces more psolarens when infected with pink rot fungus, or less likely to get fungal infection with higher psoralen release
37
Q

Clinical presentation of phytophotodermatitis

A
  • Sensitivity peaks 30-12 minutes post exposure
  • Morphology: bizarre configurations of erythema, oedema and bullae appear ~24 hours after exposure, and peak 72 hours after exposure
  • Distribution: sun exposed sites (different to poison ivy dermatitis)
  • Longer term:
    • Hyperpigmentation 1-2 weeks later, which can last months-years. Sometimes you can go straight to the pigment change without the blistering
    • Sometimes the involved areas may remain hypersensitive to UV radiation for years
  • Exacerbating factors: wet skin, sweating and heat
38
Q

What are all the environments you should ask about when diagnosing phytophotodermatitis?

A
  • Weed-whackers and strimmers –> strimmer dermatitis, sprays phototoxic plants
  • Cosmetics: Berlock dermatitis - applications of colognes (means trinket or charm)
  • Ruit and vegetable processing
  • Gardening
  • Hiking
  • Ingestion (celery before tanning)
  • Medications - psolaren for PUVA, application of rue as an insect repellant
  • Play - weapons, wearing a lei (Pelea anisata), peashooters
  • Parents can put it on children accidentally and it can mimic abuse
39
Q

Phytophotodermatitis

A
  • Prevention

- Prompt washing with soap and water to prevent a reaction

40
Q

How do you identify poison ivy?

A
  • Compound leaves with three leaflets
    • Flowers or fruit that arise from axillary position between leaf and twig
    • Black dots of urushiol often present on leaves and fruit: this with the enzyme lassaze is oxidised to form a black, plastic like polymer with great tensile strength
    • Common poison ivy climbs as a vine with hairy aerial roots
  • Black spot test: helps identify toxic: stone crushes plant contents and then fold in white paper, the urushiol turns dark brown within 10 minutes and black by 24 hours
41
Q

What is in the anacardiaceae family?

A 
Poison ivy
Poison oak
Cashew nut tree
Mango
Florida holly
Japanese lacquer tree
42
Q

Tell me about cashew nut tree ACD

A

Anacardium occidentale: nut have oily, brown juice, its also in the bark and can cause a dermatitis

43
Q

Tell me about mango ACD

A

leaves, barks, stems and fruit skin have resorcinols - peeling before eating prevents an ACD, although you can be allergic to mango pulp. Those in Hawaii rarely develop given young exposure and subsequent tolerance

44
Q

Tell me about florida holly

A

sensitizing catchols and resorcinols

45
Q

What are cross-reactors with the anacardiaece family?

A
  • Gingko tree: the seed had catechol ginkgolic acid –> contact with the pulp of the seed causes the vast majority of allergic reactions.
    • Unique fan shaped leaf makes it easy to recognise
  • Proteaceae (Grevillea) from Australia: contains pentadecylresorcinol, has no side chain double bonds, and is less allergenic
  • Grevillea banksii - Hawaiian kahili tere -> causes ACD
46
Q

What is the pathogenesis of Anacardiaceae ACD

A
  • Urushiol - mixture of catechols and resorcinols that bind to the skin
  • Catechols and alkyl side chains are immunologically inert, but combining them results in potent sensitizers
  • Longer side chains increase irritancy and allergenicity
  • Location of the catechol ring at position 3 increases antigenicity, placement at position 6 induces tolerance
  • Pentadecylcatechol is inappropriate for patch testing, because some people don’t react to it and the diolefin is the major component in poison ivy and poison oak uroshiols (and it doesn’t have a diolefin)
47
Q

What are the clinical features of Anacardiaceae ACD

A
  • Exposure: in the late fall, plants spontaneously release urushiol and you can get it that way, however you can get it from indirect contact with something else
  • Urushiol is partially water soluble, and must be washed off quickly
  • Time period: after exposure, a sensitized person develops and erythematous, pruritic eruption within 2 days, that peaks 1-14 days
  • The dermatitis can occur up to 3 weeks after primary contact, or within hours of a secondary contact
  • Morphology: sstreaks of erythema and oedematous papules typically precede vesicles and bullae, if the antigen load is lower you may only see erythematous, oedematous reactions. May be polymorphic due to different levels of antigen load in exposure
  • Sequelae:
    • Rarely can develop erythema multiforme ~ 2 weeks after dermatitis onset (can also get with tea tree oil and wild feverfew)
    • Uncommonly: nephritis, eruptions resembling measles, scarlatina or urticaria develop
    • Without treatment, lasts 2-3 weeks
    • Long-term: PIH
  • Ddx include phytophotoderamtitis and chemical irritant dermatitis
  • If you patch test: ~70% are allergic, ~ 50% react to plants in nature, only 15% are atopic
  • Studies suggest may be hereditary
  • Black spot poison ivy dermatitis: irritant and allergen, oxidised resin creates a black discolouration on the skin
  • If you get urushiol on clothes, it cannot be washed off and will retain its allergenicity indefinitely
48
Q

What are in the asteraceae family?

A
  • Wild flowers and seeds: ragweeds, yarrow, mugwort, sneezeweed, marsh elder, scourge of India, pyrethrym, tansy, feverfewm dandelion
  • Ornamental: dahlia, chrysanthenum, sunflower, black-eyed Susan
  • Herbal medicine: marigold, roman chamomile, elecampe
  • Vegetables: lettuce, artichoke, chicory, endive
49
Q

What are cross-reactors with asteraceae

A
  • Tulip poplar bark
  • Magnolia trees
  • Liverworts
  • Bay laurel tree
50
Q

What is the pathogenesis of asteraceae ACD

A
  • Sesquiterpene lactones: composed of sesquiterpene and a lactone ring - cyclic ester
  • Patch testing relies on mixing 3 together: Compositae mix - false negative of 15-65%
  • SQL mix has false negative in 65-70%
  • New formula SQL2 has been made to take advantage of the 3D variability in SQLs
51
Q

Clinical - Ateraceae dermatitis

A
  • Caused by SQL
  • Chrysanthemums probably cause it the most in gardeners, contact is common when removing dead flowers to encourage further blooming
  • Middle aged men with a history of outdoor exposure may develop Asteraceae allergy that resembles airborn contact dermatitis
  • SQLs are bound to airbone trichomes and dried leaves
  • Typically, a single region of the body is involved for several years, flaring in the summer and going in the winter, then later it becomes chronic, pruritic and lichenified
  • Generally the eyelids, melolabial folds, retroauricular sulci and antecubital fossae are involved unlike in a photosensitive dermatitis
  • Ragweed: can cause an immediate hypersensitivty ocular and airway reaction, and rarely causes an ACD. Can rarely cause dyshidrotic eczema and ABCD
  • Type 1 allergic reactions are caused by HMW, water-soluble antigens found in pollen
  • Pollen can rapidly penetrate the skin, but don’t have SQLs
  • Parthenium hysterophorus: accounts for 40% of contact dermatitis clinic visits in India, presenting as ABCD, 14% erythroderma, 10% chronic actinic dermatits
52
Q

What is the deal with photosensitivity and Asteraceae allergy

A
  • SQLs don’t have phototoxic or photoallergic properties, however patients often develop abnormally low minimal erythema and minimal phototocic doses to 300-350 nm, and up to 85% of patients with chronic photosensitivity dermatoses react to Asteraceae
  • Chronic actinic dermatitis that develops in some patients who are allergic to SQLs is thoguht to be an autoimmune photodermatosis mediated sunlight-induced antigens in the skin
53
Q

Treatment for plant ACD

A
  • If known that there has been exposure urushiol- thoroughly wash with copious amounts of water:
    • 10 mins after exposure 50% can be removed
    • 15 minutes 25%
    • 30 minutes only 10%
    • after an hour none can be removed
  • Don’t use soap or alcohol initially as it can enhance resin permeability since these are better solvents for urushiol than water
  • GSCM:
    • Weepy lesions - tepid baths
    • Wet/dry soaks
    • Bland shake lotions: calamine
    • Astringent (aluminium acetate) can cool and dry lesions
    • Topical antihistamines, topical anaesthetics: benzocaine and antibiotics should be avoided –> can cause sensitisation
  • Topical steroids only help in the earliest of stages, and abrupt discontinuation can cause rebound inflammation
  • Calcineurin inhibitors are ineffective
  • Zanfel wash (surfactant) has been reported to relieve itch and erythema
  • Steroids are effective when indicated
    • 1-2 mg/kg and tapered over 2-3 weeks
    • Six day tapering may be too short, and too low dose to be effective
    • IM Kenacort (1mg/kg) with fast-acting betamethasone –> patients experience rapid relief and fewer side effects
  • Sedating antihistamine may help with sleep
  • Hyposensitization programs generally fail –> ‘treatment worse than the disease’
  • Ivy-Block can help prevent - 5% quaternium-18 bentonite lotion
  • Poison ivy passes through rubber gloves, but not heavy-duty vinyl gloves
  • Chronic actinic dermatitis: steroids aren’t helpful
    • ?Very low dose PUVA + oral steroid, azathioprine or MMF may be necessary
54
Q

Alliaceae ACD

A
  • Onions, garlic, chives
  • Fingertip dermatitis –> thumb, infex and middle fingertips of non-dominant hand with hyperkeratosis, desquamation and fissuring
  • Don’t patch test to garlic (irritant). Irritant and allergen is diallyl disulfide
  • Onion dermatitis is rare
  • Wear gloves
55
Q

Alstroemeriaceae and Liliaceae ACD

A
  • Tulip fingers: ACD and ICD
    • first and second fingers of dominant hand: erythematous, scaly plaques –> diffuse xerotic hand with prolonged exposure
    • can get id, paronychia, pulpitis
  • Tuliposide A is in the white epidermis of bulbs, and acidic hydrolysis convers it to Tulipalin A (allergen)
  • Tuliposide B is found in tulips, but its hydrolytic product, Tulapalin B, is a much weaker sensitizer
  • For Peruvian lillies, presentation is often non-inflamed distal finger fissuring and hyperkeratosis –> the allergen can pass through vinyl gloves, so need nitrile gloves (synthetic rubber). Flowers have more allergens than the stems.
56
Q

Tea tree oil ACD

A

Myrtaceae

  • Australian tea tree
  • At least 2/3 of Australians have been exposed to it, and 2-7% are allergic
  • It is a weak sensitizer
57
Q

Botanic ACD

A
  • most common culprit is tea tree oil, followedby feverfew, lichen acid mix (in deodorants)
  • Screens: Balsam of peru, fragrance mix, compositae, SQL mix
  • Repeat open application test performed by applying the suspected allergenic product to the antecubital fossa twice daily for 7 days may help diagnose an alelrgy to botanical extracts
58
Q

So what should I look for in terms of plant reactions in Australia?

A
  • Lyngbya majuscula: seaweed dermatitis can cause an ICD
  • Melaleuca - tea tree oil –> ACD
  • Dendrocnide tree –> toxin mediated urticaria
59
Q

What will we see in bakers?

A

High rates of immunologic contact urticaria
Flours, grains and feeds ranked third for these causes (after cow dander and latex)
Omalizumab may be way to treat protein contact dermatitis

60
Q

What will we see in florists?

A

ICD more common
Most common sensitizers: SQL, tulipalin A, primin
Most common ICD: Daffodil itch
Atopic history increases risk of developing urticaria

61
Q

What will we see in food handlers

A

Increased risk for immunologic contact urticaria and protein contact dermatitis
PCD –> 60% need to change jobs
Grocery store workers: touching celery then indoor tanning –> phytophotodermatitis

62
Q

What will we see in outdoor workers?

A

Poison ivy dermatitis
Up to 25% of firefighters need to leave the fire line due to this dermatitis
Woodcutter’s eczema: ACD to airborne or rainwater dispersed SQLs from liverworts growing on rocks and trees. Worse in winter, pseudo-photodistribution, involves upper eyelids but spares submental area

63
Q

MTX dose for paediatric psoriasis

A

Start at 0.3 mg/kg, can titrate up
To 0.7 mg/kg
This is from
Up to date

64
Q

Dosage of ustekinumab for paediatric psoriasis

A

If <60 kg then 0.75 mg/kg
If between 60-100 kg then 45 mg
If Over 100 then 90 mg

Derm (57 decks)

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