Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pediatric Primary Care Exam 2 > Dermatitis > Flashcards

Dermatitis Flashcards

1
Q

Dermatitis Presentation Overview (3)

A
  1. A broad term; talking about inflammation
  2. Acute phase: pattern of cutaneous inflammation that presents with erythema, vesiculation, and pruritus
  3. The chronic phase is characterized by dryness, scaling, lichenification, fissuring, and pruritus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Types of Dermatitis (4)

A
  1. Seborrheic
  2. Atopic
  3. Dyshidrotic
  4. Nummular
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Seborrheic Dermatitis (5)

A

DANDRUFF

  1. Under androgen control
  2. Common to see it around 11-13 as hormones start to kick in and androgens are being made (infancy and adolescence)
  3. Flakey scalp
  4. Unsusual to see it before puberty unless it is in neonatal period
  5. Responds to antifungal treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Seborrrheic Dermatitis in Pre-Pubertal Period (4)

A

Seborrhea after neonatal period and before puberty requires differential dx because there are no androgens present during this time:

  1. Is the child making excess androgens; growth curve would be increasing and crossing percentile ranks
  2. Seborrhea form of tinea capitis
    - May not have much hair loss
  3. Atopic dermatitis can appear as seborrhea in a child that is pre-pubertal
  4. Androgen excess
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where does seborrheic dermatitis present? (10)

A

Affect area where sebaceous blends in high frequency and are most active

  1. Scalp
  2. Eyebrows
  3. Eyelashes
  4. Forehead
  5. Nasolabial fold
  6. Very common to see it in children with cerebral palsy
  7. External ear canal
  8. Around the umbilicus
  9. Around inguinal groin area
  10. Underneath breast area
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Seborrheic Dermatitis Treatments (11)

A
  1. Frequent cleansing with soap removes oils
  2. Outdoor recreation improve seborrhea, but avoid sun damage
  3. Antidandruff shampoos (if one doesn’t work, try another)
  4. OTC with salicylic acid
  5. Pyrithione Zinc 1% (Head and shoulder, Zincon, Dandex)
  6. Pyrithione Zinc 2% (DHS zinc, Theraplex Z)
  7. Prescription medicine selenium sulfide
  8. Shampoos with coal tar
  9. Carmol HC
  10. Elidel
  11. Scalpazene with salicylic acid and has a very distinctive odor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Anti-dandruff shampoos for seborrheic dermatitis (4)

A
  1. 2.5% percent selenium sulfide
  2. 1-2% pyrithione zinc – Head and Shoulders
  3. Coal Tar – Available OTC
  4. Ketoconazole shampoo –Treats the fungal infection, May alternate between this and coal tar for someone with extensive seborrhea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

OTCs for salicylic acid for seborrheic dermatitis (2)

A
  1. X-Seb

2. Scalpicin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Prescription medicines for selenium sulfide for seborrheic dermatitis (5)

A
  1. Selsun
  2. Exsel
  3. pyrithione zinc
  4. DHS Zinc
  5. Head and Shoulders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Carmol HC (2)

A
  1. Contains urea; a smoothing agent that takes the top layers of the skin and smooths them down
  2. Works well for seborrheic dermatitis, but not aesthetic because it burns
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Elidel (2)

A
  1. Calceurine inhibitor; off label use for seborrhea

2. BBW of lymphoma so use as last line b/c it’s off label

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Special Considerations for African Americans with Seborrheic Dermatitis (5)

A
  1. Use of daily shampooing not applicable
    - Because washing hair daily dries their hair out
  2. Seborrhea responds well to topical steroids
  3. Weekly shampooing
  4. Fluocinolone acetonide in oil as pomade
  5. Moderate to mid potency topical Corticosteroid in ointment base
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Contact Dermatitis Presentation (3)

A
  1. Itch is severe
  2. Koebner’s phenomenon (papules in a line); Koebner’s phenomenon is the hallmark of contact dermatitis
  3. Contact dermatitis doesn’t follow a specific distribution

Koebner’s phenomenon and itchy rash = allergic contact dermatitis until proven otherwise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Allergic Contact Dermatitis Reaction (3)

A
  1. ACD occurs when contact with a particular substance elicits a delayed hypersensitivity reaction
  2. Naïve T-cell noticing something for the first time → develops T-cells against it that travel in blood stream → next time you are exposed it may cause a local reaction but b/c the T-cells have gone in the blood stream then the allergic reaction will spread as well
  3. The sensitization process requires 10-14 days
    - Upon re-exposure, dermatitis appears within 12-48 hrs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Most common cause of allergic contact dermatitis

A

Rhus dermatitis, from poison ivy, poison oak, or poison sumac (all contain the resin – urushiol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Other common causes of allergic contact dermatitis (9)

A
  1. Fragrances
  2. Formaldehyde
  3. Preservatives
  4. Neosporin
  5. Benzocaine
  6. Vitamin E
  7. Rubber compounds
  8. Nickel - Number 1 contact dermatitis
  9. Balsam of Peru → in all makeup products
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Clinical Manifestations of Allergic Contact Dermatitis (4)

A
  1. Main symptom of ACD is pruritis
    - Very itchy!
  2. Can be weeping
  3. Presents as eczematous, scaly edematous plaques with vesiculation distributed in areas of exposure
  4. ACD is bilateral if the exposure is bilateral (e.g., shoes, gloves, ingredients in creams, etc.) especially if due to creams, etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Poison Oak leaves (5)

A
  1. Are 3‐7cm in length
  2. Lobulated notched edges
  3. Groups of 3, 5, or 7
  4. Grows on bush‐like plants
  5. Turn colors in autumn
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Poison Ivy leaves (5)

A
  1. Are 3‐15cm in length
  2. Notched edges
  3. Grows in groups of 3s and up trees
  4. Grows on hairy‐stemmed vines or low shrubs
  5. Turn colors in autumn
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

When will first poison oak/ivy reaction occur?

A

Initial episode occurs after you have been exposed once due to the T-cell hypersensitivity reaction; difficult to turn it off quickly because of this (rash won’t disappear within a day)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Rhus Allergy (8)

A
  1. The initial episode occurs 7-10 days after exposure
  2. On subsequent outbreaks the rash may appear within hours of exposure and usually within 2 days
  3. It is not contagious!
  4. Individual sensitivity is variable so the eruption may be mild to severe
  5. Rhus dermatitis lasts from 10-21 days depending on the severity
  6. Initial episode is the longest (up to 6 weeks!)
  7. Lesions begin as erythematous macules that become papules or plaques
  8. Blisters often form over one to two days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Rhus Dermatitis: Mimics of Lesions (4 with descriptions of each)

A
  1. Bullous insect bites
    - Usually scattered
    - Not linear or grouped
    - No history of multiple bites
  2. Cellulitis
    - Spreading erythematous, non-fluctuant tender plaque
    - Can be associated with fever
  3. Herpes Zoster
    - Painful eruption of grouped vesicles in a dermatomal distribution
  4. Urticaria
    - MOVING edematous plaques, not vesicles
    - Early lesions of allergic contact dermatitis could be mistaken for urticaria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Minor/Supportive Rhus Dermatitis Treatment (4)

A
  1. Topical steroids for localized involvement
  2. Topical or oral antihistamines may improve pruritus
  3. Oatmeal soaks/calamine lotion may soothe weeping erosions
  4. Start patients at a 3-4 steroid
    - With contact dermatitis, prescribe nothing less than a 3 with an anti-itch medicine (ex: aveno anti-itch or ucerine calming cream; can also write for phenol and menthol lotion combined (which is in ucerine calming cream)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Severe Rhus Dermatitis Treatment (4)

A
  1. In cases of failing potent topical steroids, or widespread
  2. If given for less than 2-3 weeks, patients may relapse
  3. Do not give short bursts of steroids for this reason
  4. For severe poison ivy, do not use topical - go straight to oral (class I=most potent/strongest)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Rhus Allergy Prevention

A
  1. Avoid the plants
  2. Wash clothing, shoes, and objects after exposure (within 10 minutes if possible)
  3. Apply barrier: clothing, OTC products which bind resin more than skin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Eyelid Allergic Contact Dermatitis (3)

A
  1. Intensely pruritic
  2. Scaling red plaques on upper > lower eyelids
  3. Allergic contact dermatitis of the eyelid is often caused by transfer from the hands
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Eyelid Allergic Contact Dermatitis Common Causes (4)

A
  1. Nail adhesive/polish (scratching eyes with the polish on)
  2. Fragrances and preservatives in cosmetics
  3. Nickel
  4. Balsam of Peru
28
Q

History Taking for Dermatitis (6)

A

In addition to the dermatitis-specific history (e.g., onset, location, temporal associations, treatment), be sure to ask about:

  1. Daily skin care routine
  2. All topical products
  3. Occupation/hobbies
  4. Regular and occasional exposures (e.g. lawn care products, animal shampoos)
  5. Ask about anything that they could be exposed to
  6. In chronic cases, patch testing is necessary to identify specific allergens
29
Q

Steroid Potency/Options for Dermatitis (5)

A
  1. Regular use of Class 1, 2, or 3 steroids on thin skin will lead to steroid atrophy (thinning and easy bruising/purpura)
    - Also hypopigmentation in darker skin types
  2. For the face: Class 6, 7 steroids (e.g., desonide) can safely be used intermittently during flares
    - Never use anything above a 6 on the face
  3. Hydrocortisone cream 1%
  4. Elidel and protopic (Black Box Warnings)
    - Works well on contact dermatitis but go with a steroid first because of the BBW
  5. If topical steroids are to be used on the eyelid for a period of more than one month, refer to an ophthalmologist for monitoring of intraocular pressure and the development of cataracts
30
Q

Patch Test Overview (7)

A
  1. Patch testing is used to determine which allergens a patient with allergic contact dermatitis reacts against
  2. A series of allergens are applied to the back, and they are removed after 2 days
  3. On day 4 or 5, the patient returns for the results
  4. May be red for 2-4 days
  5. Positive reactions show erythema and papules or vesicles
  6. Identification of specific allergens helps the patient find products free of those allergens
  7. Best test for allergic contact dermatitis
31
Q

Positive Patch Test Results

A

Positive patch test reactions at 96 hour reading

32
Q

Identifying Allergens (5)

A
  1. Not all patients with ACD need patch testing
  2. Refer patients when the allergen is unclear or the dermatitis is chronic
  3. A positive reaction on patch testing does not mean that the patient’s rash is due to that specific allergen
  4. CLINICAL TEST IS NOT THE CONFIRMATION! It is the avoidant of the allergen and the dermatitis disappearing
  5. Elimination of the rash with removal of the allergen confirms the clinical relevance of the positive patch test
33
Q

ACD Treatment (6)

A
  1. Avoid exposure to offending substance
  2. In mild to moderate cases, topical steroids of medium to strong potency for a limited course is
  3. A short course of systemic steroids may be required for acute flares
  4. Oatmeal baths or soothing lotions can provide further relief in mild cases
  5. Wet dressings are helpful when there is extensive oozing and crusting
  6. Chronic cases or patients with dermatitis involving over 10% of the BSA should be referred to a dermatologist
34
Q

Latex Allergy Delayed Hypersensitivity

A

Often presents on the dorsal surface of the hands

35
Q

Latex Allergy Immediate Hypersensitivity (2)

A
  1. May present with immediate symptoms such as burning, stinging, or itching with or without localized urticaria on contact with latex proteins
  2. May include disseminated urticaria, allergic rhinitis, and/or anaphylaxis
36
Q

Latex Allergy Overview (3)

A
  1. Can be delayed or immedaite
  2. Biggest risk of latex allergy among pediatric population = patient with spina bifida
    - 100% develop latex allergy due to manipulation
  3. Latex allergy is the number 1 and only allergen that will go from having a localized reaction to a systemic reaction
    - Can get an anaphylactic type 1 reaction after years of having a type 4 t-cell mediated allergic reaction
37
Q

Insect Bite SCRATCH Acronym

A
  1. S from SCRATCH stands for symmetrical.
    - Commonly affected areas include exposed surfaces such as the face, neck, arms, and legs
    - Covered areas such as the abdomen, palms, soles, diaper area, etc. are spared
  2. C stands for cluster.
    - Lesions usually appear in a “meal cluster,” that is often described as “breakfast, lunch, and dinner.” This grouping of lesions are characteristic of bedbug bites, but also are seen in flea bites and with IBIH.
    - Usually symmetrical, appear in meal cluster
    - 3 in a row at breakfast, lunch, dinner
    - Flea bites, bed bugs, and other bugs
  3. R stands for Rover
    - Is there is a family pet where the child could come into contact with fleas?
  4. A stands for age.
    - IBIH is rarely seen in babies, and these reactions peak after the age of 2.
  5. T stands for target and time.
    - Target lesions are characteristic for IBIH, particularly in dark‐pigmented patients. Time refers to the chronic nature of this condition.
  6. C stands for confused.
    - Patients and their parents are often confused/surprised that these reactions are due to bugs.
  7. H stands for history.
    - IBIH is not often associated with family history, unlike with scabies and atopic dermatitis where we see a strong family history correlation.
38
Q

Prevention of insect bite hypersensitivity

A

Wearing protective clothing for outdoor play with use of insect repellents.

39
Q

Pruritis control of insect bite hypersensitivity

A
  1. Topical steroids may help
    - Due to depth of inflammatory, topical agents can ineffective.
  2. Use of antihistamine
    - Little evidence to support due to the predominance of T‐cell–mediated response and a lack of histamine‐mediated lesions.
40
Q

Irritant Contact Dermatitis (4)

A
  1. Inflammatory reaction in the skin resulting from exposure to a substance that can cause an eruption in most people who come in contact with it
  2. No previous exposure is necessary
  3. May occur from a single application with severely toxic substances
  4. Most commonly results from repeated application from mildly irritating substances (e.g., soaps, detergents)
41
Q

Irritant Contact Dermatitis as Multifactorial Disease (4)

A
  1. Multifactorial disease where both exogenous (irritant and environmental) and endogenous (host) elements play a role.
  2. Most important exogenous factor for ICD is the inherent toxicity of the chemical for human skin
  3. Site differences in barrier function, making the face, neck, scrotum, and dorsal hands more susceptible
  4. Atopic dermatitis is a major risk factor for irritant hand dermatitis because of impaired barrier function and lower threshold for skin irritation
42
Q

Irritant Contact Dermatitis Clinical Findings (5)

A
  1. Mild irritants produce erythema, chapped skin, dryness and fissuring after repeated exposures over time
  2. Pruritus can range from mild to extreme
  3. Pain is a common symptom when erosions and fissures are present
  4. Severe cases present with edema, exudate, and tenderness
  5. Potent irritants produce painful bullae within hours after the exposure
43
Q

What to use for itch (5)

A
  1. Topical steroids
  2. Antihistamines
    - Only provide relief when pruritus is mediated by antihistamine as in case of urticaria
    - Eczema—anti histamine does not work
  3. Pramoxine topical anesthetic
    - Aveeno anti itch
    - Pramasone
    - Ucerine calming cream
    - Menthol and phenol lotion (gets covered under insurance)
  4. Capsaicin
    - Capzasin cream activate the TRP-V1 channel to produce mildly painful sensation and interferes with itch
    - Very good for pruritic bug bite
  5. Menthol
    - Topical ant-itch product—Sarna, and aveeno
    - Activates TRP channels to create a competitive sensation to itch
    - Example of menthol is vix vapor rub
44
Q

Phyto-photo dermatitis (3)

A
  1. Occurs after contact with photosensitizing compounds in plants and exposure to sunlight.
  2. Mistaken for atopic dermatitis, type IV hypersensitivity reaction (contact dermatitis) or a chemical burn
  3. Hint if it is on one side and only one side was exposed to the sun at that time
45
Q

Phyto-photo dermatitis triggers

A

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

46
Q

Phyto-photo dermatitis overview

A
  1. Occurs after contact with photosensitizing compounds in plants and exposure to sunlight.
  2. Mistaken for atopic dermatitis, type IV hypersensitivity reaction (contact dermatitis) or a chemical burn
  3. Primary skin lesion of PhytoPD may range from delayed erythema (24-48 hours) to frank blisters
  4. Sometimes occurs immediately, sometimes occurs later
47
Q

Phyto-photo dermatitis clinical manifestations (3)

A
  1. A postinflammatory 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.
  2. An increased number of functional melanocytes and melanosomes distributed in the epidermis following PPD also account for the hyperpigmentation
  3. Tendency to become postinflammatory hyperpigmented is mainly dictated by genetics
    - Itch a lot and then afterwards there will be a dark spot there
48
Q

Irritant Contact Dermatitis Evaluation and Treatment (4)

A
  1. Identification and avoidance of the potential irritant is the mainstay of treatment
  2. Topical therapy with steroids to reduce inflammation and emollients to improve barrier repair are usually recommended
  3. Referral to a dermatologist should be made for patients who are not improving with removal of the irritant or in severe cases
  4. Patch testing should be performed in occupational cases with suspected chronic irritant dermatitis to exclude an allergic contact dermatitis
49
Q

Irritant Contact Dermatitis Prevention (5)

A
  1. Patient Education about things the irritant is included in
  2. Use personal protective equipment (e.g. protective gloves should be worn for any wet work)
  3. Instead of soap, use less irritating substances, such as emollients and soap substitutes when washing
    - Only recommended soap is white dove, all the others are very alkaline and not well tolerated
  4. Care should be taken for several months after the dermatitis has healed, as the skin remains vulnerable to flares of dermatitis for a prolonged period
  5. Have tendency to get it back again when they get it, so prevention is important
50
Q

Contact Dermatitis Take Home Points (12)

A
  1. Allergic contact dermatitis (ACD) and Irritant contact dermatitis (ICD) are the two types of contact dermatitis.
  2. ACD occurs when contact with a particular substance elicits a delayed hypersensitivity reaction.
  3. Most patients need minor supportive care, but some cases will require oral steroids.
  4. Patch testing is used to determine which allergens a patient with allergic contact dermatitis reacts against.
  5. Not all patients with ACD need patch testing.
  6. Latex allergy may present as a delayed or immediate hypersensitivity.
  7. ICD is an inflammatory reaction in the skin resulting from exposure to a substance that can cause an eruption in most people who come in contact with it.
  8. Identification and avoidance of the potential irritant is the mainstay of treatment.
  9. Patch testing may be performed in cases with suspected chronic irritant dermatitis to exclude an allergic contact dermatitis.
  10. If a rash is due to an exposure at work, the medical evaluation may be covered by worker’s compensation.
  11. Important to ask about the patient’s occupation/school related activity
  12. Referral to a dermatologist should be made for patients with contact dermatitis who are not improving with the removal of the allergen/irritant or severe cases.
51
Q

AD Overview (5)

A
  1. AD develops in 85% of children within the first 12 months of life, and in 95% of children before age 5 years.
    - So most get it by 1-5 years old
  2. Some of them outgrow it
  3. AD is often the first manifestation of the “atopic march” with asthma and Allergic Rhinitis following.
  4. Asthma also develops in approximately 30% and allergic rhinitis develops in 35% of those with AD
  5. Incidence of AD is increasing in the US
52
Q

Atopic Triad (6)

A
  1. Atopic is the tendency for allergy
  2. Whether you get any of these depends on environmental factors and whether there is a trigger
  3. Children with atopic dermatitis are at higher risk for getting asthma (30%) or allergic rhinitis (35)
  4. The three A’s go together (asthma, atopic dermatitis, allergic rhinitis)
  5. Characterized by the itch that rashes; if you rub enough it gets worse
  6. Continued scratching causes thickened lichenified skin
53
Q

Basics of Atopic Dermatitis (5)

A
  1. Chronic, pruritic, inflammatory skin disease with a wide range of severity
  2. Diagnostic characteristics are pruritus and chronic or relapsing eczematous lesions with typical morphology and distribution
  3. Primary symptom is pruritus (itch)
    - AD is often called “the itch that rashes”
  4. Scratching to relieve AD-associated itch gives rise to the ‘itch-scratch’ cycle and can exacerbate the disease
  5. Patients experience periods of remission and exacerbation
54
Q

Pathogenesis of Atopic Dermatitis (8)

A

The cause of AD is multifactorial and not completely understood, the following factors are thought to play varying roles:

  1. Genetics
  2. Skin Barrier Dysfunction
  3. Impaired Immune Response (T-cell impairment)
  4. Prone to terrible secondary infections
  5. Environment
  6. Dry environments increase exacerbations
  7. A little moisture is good
  8. Diaper area will be clear due to chronic moisture
55
Q

Pathophysiology of AD (3)

A
  1. Increased serum IgE levels are common and correlate with disease severity
  2. AD is in part initiated by skin barrier defects. These barrier defects can be acquired or genetic.
  3. Inadequate innate immune response to epicutaneous microbes is partially responsible for
    - Increased susceptibility to infections
    - Colonization with Staphylococcus aureus and a number of viruses
56
Q

Clinical Findings of AD (3)

A
  1. Lesions typically begin as erythematous papules, which then coalesce to form erythematous plaques that may display weeping, crusting, or scale
  2. Distribution of involvement varies by age
  3. Xerosis (dry skin) is a common characteristic of all stages
57
Q

Distribution of AD by age (3)

A
  1. Infants and toddlers: eczematous plaques appear on the cheeks forehead, scalp and extensor surfaces
  2. Older children and adolescents: lichenified, eczematous plaques in flexural areas of the neck, elbows, wrists, and ankles
    - Flexed areas
  3. Adults: lichenification in flexural regions and involvement of the hands, wrists, ankles, feet, and face (particularly the forehead and around the eyes)
58
Q

Clinical Manifestations of AD in infants and toddlers (6)

A
  1. Affects the cheeks, forehead, scalp, and extensor surfaces
  2. Erythematous, illdefined plaques on the cheeks with overlying scale and crusting
  3. Erythematous, ill‐defined plaques on the lateral lower leg with overlying scale
  4. On nasolabial folds, extensor surfaces
  5. Ill definied and not well demarcated
  6. 2 and under is when it’s common to get it on the face
59
Q

Clinical Manifestations of AD in children (4)

A
  1. Affects flexural areas of neck, elbows, knees, wrists, and ankles
  2. Lichenified, erythematous plaques behind the knees
  3. Erythematous, excoriated papules with overlying crust in the antecubital fossa
  4. These are classic for older children (2 and above)
60
Q

Allergens and atopic dermatitis (6)

A
  1. Many patients with AD have sensitization to food and environmental allergens
  2. However, evidence of allergen sensitization is not proof of a clinically relevant allergy
  3. Food allergy as a cause of, or exacerbating factor for, AD is uncommon
  4. Identification of true food allergies should be reserved for refractory AD in children in whom the suspicion for a food allergy is high
  5. 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
  6. Elimination of food allergens in patients with AD and confirmed food allergy can lead to clinical improvement
61
Q

Acute vs Chronic AD Presentation

A

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

62
Q

Education on Complications of AD (7)

A
  1. Identification and elimination of triggering factors
  2. Avoidance of common irritants (eg, soaps, toiletries, wool, and chemicals)
  3. Control of temperature and humidity to avoid increased pruritus
  4. Patch tests, which can produce immediate or delayed reactions to protein allergens
  5. Testing should only be done for relevant allergens because testing, especially for foods, has low specificity
    - Food allergens as triggers of AD is more commonly in young infants and children.
  6. 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.
  7. No extensive elimination diets based only on positive skin or specific IgE test results because potential nutritional deficiency can occur
63
Q

Complications of AD (6)

A
  1. Skin bacterial culture should be considered during hyperacute, weepy flares of AD and when pustules or extensive yellow crust are present
  2. Patients with AD are susceptible to a variety of secondary cutaneous infections such as Staphylococcus aureus and Group A Streptococcal infections
    - These infections are a common cause of AD exacerbations
  3. Systemic antibiotics should be used to treat these infections
  4. Recurrent viral skin infections, such as herpes simplex, warts, and molluscum contagiosum. The clinician should diagnose and promptly
  5. Treat disseminated herpes simplex or eczema herpeticum with systemic antiviral agents. (B)
  6. 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
64
Q

Fungal infections that can complicate AD (3)

A
  1. Using KOH preparation or culture can diagnose for certain
  2. 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.
  3. Specific IgE to Malassezia species might also be obtained
65
Q

Treatment of AD due to complications from staphylococcus aureus (3)

A

For Skin infections with Staphylococcus aureus

  1. Recurrent problem in patients with AD, and patients with moderate-to-severe
  2. Pt. makes IgE antibodies against staphylococcal toxins present in their skin.
  3. Short course of an appropriate systemic antibiotic in patients infected with S aureus.
66
Q

Treatment of AD due to complications from MRSA (2)

A

If high levels of methicillin-resistant S aureus

  1. Use clindamycin, doxycycline, or trimethoprimsulfamethoxazole while awaiting culture results
  2. Nasal spray with alcohol base
67
Q

AD Patient Treatment (4)

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

Pediatric Primary Care Exam 2 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions