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Flashcards in Dermatology 2 Deck (62):
1

Phyto-Photo Dermatitis

Overview

 

  • Occurs after contact with photosensitizing compounds in plants and exposure to sunlight.
  • Mistaken for atopic dermatitis, type IV hypersensitivity reaction (contact dermatitis) or a chemical burn
  • Primary skin lesion of PhytoPD may range from delayed erythema (24-48 hours) to frank blisters
    • Go out into sun and get an erythema

2

Phyto-Photo Derm Triggers

  • Furocoumarins (e.g., 5- methoxypsoralen) found in limes, lemons, oranges, celery, fig, parsnip, parsley, carrots, dill, and perfumes, are commonly implicated
  • Citric fruits

3

Phyto-Photo Dermatitis

Clinical Findings

  • A post-inflammatory pigment alteration may follow the acute phase of this phototoxic reaction.
    • Melanin, which is normally found in the epidermis, "falls" into the dermis and is ingested by melanophages.
    • An increased number of functional melanocytes and melanosomes distributed in the epidermis following PPD also account for the hyperpigmentation
  • Greater number of melanocytes and have hypopigmentation
    • Some kids after varicella – some kids have a lot and some nothing; depends on skin
    • Post-inflammatory hyperpigmentation

4

Overview of Atopic Dermatitis

  • AD affects approximately 10% to 12% of the childhood population in the U.S. with higher incidence in other countries.
  • AD develops in 85% of children within the first 12 months of life, and in 95% of children before age 5 years.
  • Approximately 0.9% of adults have AD; some of whom had an adult onset but the majority had AD as a child.
  • AD is often the first manifestation of the “atopic march” with asthma and Allergic Rhinitis following.
  • Asthma also develops in approximately 30% and AR develops in 35% of those with AD. The incidence of AD is increasing in the U.S. (Schneider et al., 2013).

5

The Atopic Triad

Asthma

Atopic Derm

Allergic Rhinitis

6

Atopic Derm: The Basics

  • Chronic, pruritic, inflammatory skin disease with a wide range of severity
  • Diagnostic characteristics
    •  Pruritus
    •  Chronic or relapsing eczematous lesions with typical morphology and distribution

7

Primary Symptom of AD

  • Primary symptom is pruritus (itch)
    • AD is often called “the itch that rashes” chronic, relapsing
    • Scratching to relieve AD-associated itch gives rise to the ‘itch-scratch’ cycle and can exacerbate the disease
  • Patients experience periods of remission and exacerbation

8

Pathogenesis of AD

  • The cause of AD is multifactorial and not completely understood
  • The following factors are thought to play varying roles:
    • Genetics
    • Skin Barrier Dysfunction
    • Impaired Immune
    • Response
    • Environment
  • Prone to terrible secondary infection
  • Dry vs. Wet – more likely to have exacerbations in dry

9

Pathophysiology of AD

  • Increased serum IgE levels are common and correlate with disease severity
  • AD is in part initiated by skin barrier defects. These barrier defects can be acquired or genetic.
  • Inadequate innate immune response to epicutaneous microbes is partially responsible for
    • Increased susceptibility to infections
    • Colonization with Staphylococcus aureus and a number of viruses
  • Susceptibility to infection****

10

Clinical Findings AD

Infants and Toddlers

  • Lesions typically begin as erythematous papules, which then coalesce to form erythematous plaques that may display weeping, crusting, or scale
  • Distribution of involvement varies by age:
    • Infants and toddlers: eczematous plaques appear on the cheeks forehead, scalp and extensor surfaces
      • THINK ABOUT EXTENSOR SURFACES
  • Affects the cheeks, forehead, scalp, and extensor surfaces
  • Erythematous, ill-defined plaques on the cheeks with overlying scale and crusting
    • Not well demarcated

11

Clinical Findings AD

Older children (older than 2) and adolescents

Older children and adolescents: lichenified, eczematous plaques in flexural areas of the neck, elbows, wrists, and ankles

Flexed areas*

  • Lichenified, erythematous plaques behind the knees
  • Erythematous, excoriated papules with overlying crust in the antecubital fossa

12

Clinical Findings of AD

Adults

Adults: lichenification in flexural regions and involvement of the hands, wrists, ankles, feet, and face (particularly the forehead and around the eyes)

Xerosis is a common characteristic of all stages = DRY SKIN

13

Allergens and Atopic Dermatitis

  • The role of allergy in AD remains controversial
  • Many patients with AD have sensitization to food and environmental allergens
    • However, evidence of allergen sensitization is not proof of a clinically relevant allergy
  • Food allergy as a cause of, or exacerbating factor for, AD is uncommon
    •  Identification of true food allergies should be reserved for refractory AD in children in whom the suspicion for a food allergy is high
    • Infants with AD and food allergy may have additional findings that suggest the presence of food allergy, such as vomiting, diarrhea, and failure to thrive
  • Elimination of food allergens in patients with AD and confirmed food allergy can lead to clinical improvement

14

Understanding the Clinical Presentation

Acute/subacute skin lesions vs. Chronic AD

  • Acute and subacute skin lesions
    • Characterized by intensely pruritic, erythematous papulovesicular lesions with excoriation and serous exudate in young children
  • Chronic AD
    • Characterized by lichenification, papules, and excoriations

15

Treatment for AD

Clinical Guidelines

  • Clinical Guidelines
    • Clinicians should use a systematic, multipronged approach that includes skin hydration, topical anti-inflammatory medications, antipruritic therapy, antibacterial measures, and elimination of exacerbating factors.
    • Clinicians should evaluate the success of the approach and modify the treatment plan, if needed. (A)
    • HYDRATION HYDRATION HYDRATION
    • Hydroxyzine
      • 10mg per 5mL

16

  • Intensity of Atopic dermatitis treatment depends on

  • Severity of illness
  • Effect on the quality of life The clinician should establish treatment

 

  • The clinician should establish treatment
    • Establish goals with the patient

17

What is a characteristic of AD?

  • Reduced skin barrier is characteristic of AD
    • Leads to enhanced water loss and dry skin;
    • Hydration of the skin with warm soaking baths for at least 10 minutes followed by the application of a moisturizer

18

  • SOAK AND SEAL

  • Shower
  • Rub with cream and ointment

19

First Line for AD?

Exacerbated in what months?

  • MOISTURIZER IS FIRST LINE!
    • Xerosis contributes to the development of epithelial microfissures and cracks, which allow entry of microbes and allergens.
    • Exacerbated during the dry winter months and aggravated in certain work environments.
    • Addition of oatmeal or baking soda to the bath water can have a soothing antipruritic effect for certain patients but does not increase water absorption.

20

Moisturizers in AD

  • Help control pruritus
  • Maintaining a soft texture to the skin.
  • When applied to dry skin and after bathing to maintain hydration of the epidermis.
  • Consistent use has a corticosteroid-sparing effect
    • HELPS TO SPARE USE OF STEROIDS

21

Other anecdotes for AD

  • Baking soda
  • ½ cup of regular oatmeal, use ¼ Crisco, add a cup of water
    • Mix in clean jar and then you put a tablespoon or 2 in every bath – hydrates and soothes skin

22

  • TYPES OF MOISTURIZERS for AD

  • Emolliate with a moisturizer.
  • Lubricants maintain the skin’s hydration
  • An ointment-based emollient
  • Eucerin cream, Crisco (plain, not butter flavored), Aveeno, Moisturel,
  • Neutrogena, Dermasil, Curel, or petroleum jelly (an occlusive agent).
  • If a child is sensitive to fragrances, scented creams, such as Nivea and Vaseline
  • Intensive Care, should be avoided.
  • TriCeram is a moisturizer that repairs the stratum corneum barrier function.
    • Prescription
  • Like Cereve, it is a ceramide-dominant, lipid-based emollient.
    • For DRY skin
  • Urea-containing products, such as Aquacare cream or lotion and Ureacin Crème,
  • Soften and moisturize dry skin.
    • Stinging is a side effect when using urea containing product on fissured or flaring skin.
  • Comes back if you stop using creams

23

AD: 

  • An ointment-based emollient

  • e.g., Vaseline, petrolatum jelly, Crisco, vegetable oil, whipped petrolatum, Aquaphor) can be applied just before getting out of the bath water or just after getting out of the bath while still damp.
  • If patients do not like the greasy feel of an ointment, other topical creams (e.g., Vanicream, Cereve, Cetaphil) can be used.
    • Vanicream – contains no chemicals and its great that way
  • This is also a good time to apply TCPs because absorption of the agent is more effective if the skin is hydrated.

24

Bathing with AD

  • Frequent bathing may exacerbate their pruritus and thus aggravate their skin problems.
  • Bathing must be limited in these patients and emollients used.
  • If a child experiences stinging when bathing during acute exacerbations, adding 1 cup of table salt into the bath may reduce the stinging sensation.

25

When moisturizers fail AD...

  • Low-potency corticosteroids are recommended for maintenance therapy, whereas intermediate and high-potency corticosteroids should be used for the treatment of clinical exacerbation over short periods of time.
    • Low dose and then bump up

26

No potent fluorinated corticosteroids for...

use on the face, eyelids, genitalia, and intertriginous areas or in young infants

27

  • Topical corticosteroids (TCPs) are a mainstay of therapy
    • AD

  • TCPs reduce inflammation and pruritus.
  •  The classification of the TCP should be known because potent and very potent TCPs are associated with more side effects such as thinning of the skin or adrenal axis suppression than milder preparations (Wollenberg and Schnopp, 2010).
  • A proactive approach to the treatment of AD includes twice weekly application of a low dose TCP for up to 4 months once the lesions are quiet (Eichenfield et al., 2014).
  • The rationale for this approach is that the skin is actually not normal and has a defect in hydration, which can be treated using an intermittent approach (Wollenberg and Schnopp, 2010: Eichenfield et al, 2014).

28

Application of TCP

  • Finger tip method: The amount of steroid should be from the distal interphalangeal joint to the top of the adult finger for an area equaling two adult palms. Apply a thin layer of TCP to affected areas marked with acute exacerbations twice a day or once a day if using a newer formulation (Eichenfield et al.,2014) .
  • When applied over large areas of dermatitis or if occlusion (covering with plastic wrap) is used, the possibility of significant systemic absorption is greatly increased, especially in infants and young children.

29

Topical Steroids AD -- Overview

  • 7 levels of steroid with class 1 being very high potency to class 7 being the lowest potency (Eichenfield et al., 2014).
  • Greater caution is needed when applying the steroids to the face, neck and skin folds as the skin is thinner and there is higher risk of systemic absorption (Eichenfield et al., 2014; Schneider et al., 2013)
  • Tapering of the strength of the steroids should occur only once the outbreak is fully controlled and then the child is switched to once a twice weekly application of a low dose
    • TCS at areas of outbreak to reduce the relapse.
  • The baseline moisturizing skin care should continue with a low strength TCS once to twice a week to reduce inflammation (Eichenfield et al., 2014).

30

  • TOPICAL STEROID STRENGTH

  • Remember to look at the class not the percentage
    • Note that clobetasol 0.05% is stronger than hydrocortisone 1%
  • When several are listed, they are listed in order of strength
    • Note that triamcinolone ointment is stronger than triamcinolone cream or lotion because of the nature of the vehicle
  • Low potency topical corticosteroids are safe when used for short intervals
    • Can cause side effects when used for extended durations
  • High potency steroids must be used with caution and vigilant clinical monitoring for side effects in children
  • Potent steroids should be avoided in high risk areas such as the face, folds, or occluded areas such as under the diaper

31

  • Know difference between classes of topical steroids

  • Mild outbreak = use class 4
  • Exacerbation = use the 3 over the 6
  • Baseline =

32

Topical Steroids - Super High - Class 1

Clobetasol 0.05%

33

TCS - High - Class II

Fluocinonide 0.05%

34

TCS - Medium - III-IV

Triamcinolone ointment

Cream

Lotion

All 0.1%

35

TCS-- Low Potency-- VI-VII

Fluocinolone 0.01%

Desonide 0.05%

Hydrocortisone 1%

36

  • Topical calcineurin inhibitors
    • Overview

  • TCI are second line therapy that is useful in both acute and chronic AD.
  • The two agents are available—topical tacrolimus (Protopic) ointment 0.03% and 0.1% strengths and pimecrolimus (Elidel) 1% cream—have been shown to be as effective as mid-strength TCS.
  • They can be combined with TCS in the treatment of patient’s whose AD has not responded to TCS. They are considered a steroid sparing agent (Eichenfield et al., 2014; Schneider et al., 2013).

37

Age approvals for

Tacro 0.03%

Pimecrolimus

Tacro -.1%

  • Tacrolimus 0.03% and pimecrolimus 1% is approved for use at age 2 and over where as tacrolimus 0.1% is approved in children over 15 years of age (Eichenfield et al., 2014)
  • TCI do have black box warnings due to the higher rate of lymphoma in rats given high dosages of these drugs.

38

TCI Physiology

  • These drugs block calcineurin, which is a protein phosphatase that causes T-cell activation.

39

TCI Side Effects

Most common side effect is itching, stinging, or burning, which starts 5 minutes after the application and can last for an hour but usually decreases after 1 week (Schneider at al., 2013), usually during the first several days of administration and in severe cases of AD.

40

TCI additional info (4)

  • Safe steroid-sparing agents and work well on thinner skin of the face, neck, groin, and axillae.
  • Sun protection is needed with their use (Atkins and Leung, 2011).
  • Patients need to be informed of the black box warning and the pros and cons of their use discussed.
  • There is an increased theoretical risk of cutaneous viral infections with the use of TCI (Eichenfield et al., 2014

41

TCI is great for...

AD around the eye

42

Prescription Emollient Devices

  • Skin barrier repair and treatment: Drugs (EpiCeram and Eletone) that improve the skin hydration barrier are available by prescription.
    • Hydration barriers
    • One bottle = $100
  • Used twice a day.
  • Unique ratios of lipids that resemble endogenous compositions (Schneider et al, 2013).
  • Expensive and not covered by all insurance plans.

43

Treatment for AD Continued

  • Tar preparations

  • No randomized controlled studies have demonstrated their efficacy
  • Newer coal tar products are more cosmetically acceptable, with respect to odor and staining

44

  • Treatment for AD continued
    • Antihistamine

  • May relieve pruritus associated with AD
  • Topical antihistamines not recommended due to potential cutaneous sensitization

45

Patients with AD

Supplementation

  • Supplementation with vitamin D, particularly if they have a documented low level or low vitamin D intake
  • 400 units if not 600 units
  • Atopic dermatitis is worse in kids with low vitamin D

46

  • Dilute bleach baths
    • AD

  • Addition of dilute bleach baths twice weekly
  • Reduction in the severity of AD, especially in patients with recurrent skin infections

47

  • Wet Wrap Therapy (WWT)

  • WWT can be used in significant flares with recalcitrant disease.
  • The usual topicals are applied and then a wet layer of tubular gauze or cotton pajama is applied with a dry outside layer.
  • The child sleeps overnight with the WWT (Eichenfield et al., 2014; Schneider et al., 2013)
    • Dry clothes not fully
    • Lots of moisture with Vanicream

48

AD -- 

  • Topical Antimicrobials and Antiseptics

  • Immune dysregulation in AD causes a tendency to colonize with S. aureus as well as viral infection including herpes simplex.
  • Reduction of colonization with staphylococcus as well as treatment of infection may be equally as important.
  • Presence of staphylococcus aureus is a frequent colonizer of the skin in AD.
  • Use of bleach baths with intranasal topical mupirocin for 3 months may be helpful (Eichenfield et al., 2014).
  •  Schneider et al., (2013) recommends dilute bleach baths twice a week in patients with recurrent infection.

49

AD -- phototherapy

  •  Ultraviolet narrow band UVB light treatment may benefit and should only be done by center where phototherapy is available, however, it is rarely used because of the risk of skin cancer.

50

AD -- 

  • Systemic immunomodulating agents

  • Immunomodulating agents such as cyclosporine, azathioprine, mycophenolate mofetil and systemic corticosteroids can provide help to patients with severe, refractory AD but due to side effect profiles should only be used by specialist after all other options have failed.
  • 99% of kids will not come to this

51

Atopic Dermatitis Alternative Treatments

Evening primrose oil or borage oil for atopic dermatitis

  • Evening primrose oil or borage oil for atopic dermatitis
    • Oral preparations of evening primrose oil and borage oil, which are rich in the essential fatty acid gamma-linoleic acid, have been promoted as complementary and alternative medicine treatments for atopic dermatitis.
    • Meta-analysis of 19 randomized trials of evening primrose oil and eight trials of borage oil
      • No significant difference in global eczema symptoms (assessed by both participants and clinicians) between the active treatment and the placebo group
      • There were some adverse gastrointestinal effects with use of these oils, and because long-term safety data are not available, we suggest that patients not take these oils for management of eczema symptoms.
    • No good data to show this works*

52

Treatment of AD: Education

  • Avoidance of common irritating substances including toiletries, wool, harsh chemicals
  • Keep fingernails short to decrease additional skin trauma from scratching
  • Consider stopping the use of fabric softeners and using a sensitive skin detergent (e.g., All Free Clear)
    • JUST COTTON
    • No polyester/wool

53

AD Education (3)

  • Educate patients and family members
    • Chronic nature of the disease
    • Exacerbating factors
    •  Safety/side effects of the medications.
    •  Skin-care techniques, written treatment plans
    • Patient support organizations
  • Quality of life and emotional stress
    • Significant effect on patient and family quality of life
    • Patients have an increased risk for psychological distress.
    • Stress and emotional factors
      • Can cause exacerbations
      • Found to induce immune activation, as well as to trigger pruritus and scratching.
  • Assess for sleep disturbances.
    • Improves with treatment of inflammation
    • Referral if not better

54

Complications of AD - Education

  • Identification and elimination of triggering factors
    • Avoidance of common irritants (eg, soaps, toiletries, wool, and chemicals)
    • Control of temperature and humidity to avoid increased pruritus
  • Possible triggers of AD confirmation
    • Skin tests
    • In vitro tests for specific IgE antibodies
    • Patch tests, which can produce immediate or delayed reactions to protein allergens
  • Testing should only be done for relevant allergens because testing, especially for foods, has low specificity

55

Food Allergens as triggers for AD

  • Food allergens as triggers of AD is more commonly in young infants and children.
    •  For children less than 5 years of age with moderate-to-severe AD limited food allergy testing if the child has persistent AD in spite of optimized management and topical therapy, the child has a reliable history of an immediate allergic reaction after ingestion of the food, or both.
  • No extensive elimination diets based only on positive skin or specific IgE test results because potential nutritional deficiency can occur

56

AD - Complications - Infections

  • Skin bacterial culture should be considered during hyperacute, weepy flares of AD and when pustules or extensive yellow crust are present
  • Patients with AD are susceptible to a variety of secondary cutaneous infections such as Staphylococcus aureus and Group A Streptococcal infections

57

AD Complications - Viral

  • Recurrent viral skin infections, such as herpes simplex, warts, and molluscum contagiosum. The clinician should diagnose and promptly
  • Treat disseminated herpes simplex or eczema herpeticum with systemic antiviral agents. (B)
  • No smallpox vaccination for patient or household contacts since they develop a severe, widespread, potentially fatal cutaneous infection called eczema vaccinatum, similar in appearance to eczema herpeticum

58

  • Fungal infections that can complicate AD

  • Using KOH preparation or culture can diagnose for certain
  • Malassezia species, which is a particular problem in young adults with refractory head and neck eczema, can be diagnosed clinically or with a KOH preparation.
    • Specific IgE to Malassezia species might also be obtained

59

Treatment for AD due to complications

  • Skin infections with Staphylococcus aureus

  • Recurrent problem in patients with AD, and patients with moderate-to-severe
  • Pt. makes IgE antibodies against staphylococcal toxins present in their skin.
  • Short course of an appropriate systemic antibiotic in patients infected with S aureus.

60

  • If high levels of methicillin-resistant S aureus
    • Treatment for AD w/ Complications

 

  •  Use clindamycin, doxycycline, or trimethoprimsulfamethoxazole while awaiting culture results
  • Nasal spray with alcohol base
  • Drops that you place on a Q-tip
  • Bactroban, Bactrim

61

Eczema infected w/ Herpes

IV acyclovir

  • Exact distribution where the eczema could be
  • Staph in there
  • May have a fever
  • Herpes can go systemic à encephalitis and die

62