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Patel Flashcards

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Dermatology Board Prep flashcards
1
Q

What is dermatitis? What are the 5 common types?

A
  • Aka, eczema: refers to heterogeneous group of disorders that share similarities in clinical appearance and histopathologic findings, but may have very different etiologies

—- Common types of dermatitis include:

—1. Allergic contact dermatitis

—2. Irritant contact dermatitis

  1. Atopic dermatitis
  2. Dyshidrotic dermatitis
  3. Lichen simplex chronicus
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2
Q

What do these 2 images show?

A

—- Acute dermatitis: vesicular or bullous (picture of allergic contact dermatitis from poison ivy)

—- Chronic dermatitis: may be red, scaly, and lichenified with fissures

—- Pruritus (itchy skin that makes you want to scratch) is a common symptom in all types of dermatitis

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3
Q

What is contact dermatitis? What are the 2 types?

A
  • Skin condition created by a rxn to an externally applied substance
  • There are two types of contact dermatitis:

—1. Irritant Contact Dermatitis (ICD)

  1. Allergic Contact Dermatitis (ACD)
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4
Q

What is the pathogenesis of allergic contact dermatitis?

A
  • Delayed-type (type IV) T-cell mediated hypersensitivity reaction
  • Two phases of the reaction: sensitization (induction) and elicitation (challenge)
  • The sensitization process requires 10-14 days
    1. Upon re-exposure, dermatitis appears within 12-48 hrs
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5
Q

What are the common causes of allergic contact dermatitis?

A
  • Most common cause: Rhus dermatitis, from poison ivy, oak, or sumac (urushiol resin)
  • Also: fragrances, formaldehyde, preservatives, topical antibiotics, Benzocaine, Vitamin E, rubber compounds, nickel
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6
Q

What are the clinical findings in ACD?

A
  • Main symptom is PRURITIS (itching)
  • Presents as eczematous, scaly edematous plaques with vesiculation distributed in areas of exposure
  • Bilateral if the exposure is bilateral (e.g., shoes, gloves, ingredients in creams, etc.)
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7
Q

What are these?

A
  • Poison oak (left): 3-7cm, lobulated notched edges, groups of 3, 5, or 7
    1. Grows on bush-like plants and turn colors in autumn
  • Poison ivy (right): 3-15 cm, notched edges, gps of 3
    1. Grows on hairy-stemmed vines or low shrubs, and turn colors in autumn
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8
Q

What is the typical timeline for Rhus allergy?

A
  • Initial episode occurs 7-10 days after exposure, and is the longest, lasting up to 6 weeks
  • On subsequent outbreaks, rash may appear w/in hours of exposure and usually w/in 2 days
    1. Individual sensitivity variable, so the eruption may be mild to severe -> lasts 10-21 days, depending on the severity
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9
Q

What is this showing?

A
  • Progression of Rhus dermatitis: lesions begin as erythematous macules that become papules or plaques
  • Blisters often form over one to two days
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10
Q

What do you see here?

A

Examples of severe Rhus allergy

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11
Q

What is this?

A
  • Linear streaks aid in diagnosis of Rhus dermatitis (from the linear contact of the plant)
  • NOTE: fomites can be contaminated by the plant oil and lead to recurrent eruptions
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12
Q

What is the treatment for Rhus dermatitis?

A
  • Most patients need minor supportive care:
    1. Topical steroids for localized involvement
    2. Topical or oral antihistamines may improve pruritus
    3. Oatmeal soaks/calamine lotion may soothe weeping erosions
  • Severe involvement may require oral steroids:
    1. Failing potent topical steroids, or widespread
    2. If given less than 2-3 wks, pts may relapse -> do NOT give short bursts of steroids
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13
Q

How can you prevent Rhus allergy?

A
  • Avoid the plants
  • Wash clothing, shoes, and objects after exposure (within 10 minutes if possible)
  • Apply barrier: clothing, OTC products which bind resin more than skin
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14
Q

What do you think happened here? Describe it. Common causes?

A
  • Eyelid allergic contact dermatitis: INTENSELY PRURITIC -> often via transfer from the hands
    1. Scaling red plaques on upper > lower eyelids
  • Common causes:
    1. Nail adhesive/polish
    2. Fragrances and preservatives in cosmetics
    3. Nickel
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15
Q

How should you evaluate dermatitis?

A
  • Comprehensive history
  • Complete dermatologic assessment of the patient
  • Shape, configuration, and location of dermatitis are useful clues in identifying the culprit allergen
  • Elimination of a suspected trigger may be both diagnostic and therapeutic
  • In chronic cases, patch testing is necessary to identify specific allergens
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16
Q

What additional questions might you ask a patient with suspected dermatitis?

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)
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17
Q

What is this? How is done?

A
  • Example of a pt with patches (allergens) on back
  • Patch testing: used to determine which allergens a pt with allergic contact dermatitis reacts against
  • A series of allergens are applied to the back, and they are removed after 2 days
    1. On day 4 or 5, the pt returns for the results
  • (+) reactions show erythema and papules or vesicles
  • Identification of specific allergens helps the patient find products free of those allergens
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18
Q

When do patients need to have patch testing? What does a (+) test mean?

A
  • NOT all patients with ACD need patch testing
    1. Refer patients when the allergen is unclear or the dermatitis is chronic
  • A positive reaction on patch testing does NOT mean the pt’s rash is due to that specific allergen
  • Elimination of the rash w/removal of the allergen confirms clinical relevance of the positive patch test
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19
Q

What do you see here?

A
  • Positive patch test reactions at 96 hour reading
  • This patient had three positive reactions:
    1. Nickel, Balsam of Peru, and Fragrance
  • Avoidance of these allergens should improve their rash
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20
Q

What is the treatment for ACD?

A
  • AVOID EXPOSURE to the offending substance
  • Tx of acute phase depends on the severity of the dermatitis:
    1. Mild 2 mod cases: topical steroids of med to strong potency for limited course is successful
    2. Short course of systemic steroids may be required for acute flares
  • Oatmeal baths or soothing lotions can provide further relief in mild cases
  • Wet dressings are helpful when there is extensive oozing and crusting
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21
Q

What is this?

A
  • Allergic contact dermatitis
  • Medication allergy to topical antibiotic cream
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22
Q

This 11-year-old girl presents with 3 months of an itchy rash on the sides of her nose and ears… What is going on?

A

She’s allergic to her nickel glasses (ACD)

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23
Q

What do you see here?

A
  • Nickel dermatitis (ACD): erythematous plaque with scattered papules above the umbilicus
  • 2nd most common allergic contact dermatitis next to Rhus dermatitis
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24
Q

This respiratory therapist has an intermittent rash that clears when she goes on vacation… What is going on? What are the 2 ways it can present?

A
  • Latex allergy: may present as delayed or immediate hypersensitivity
  • Delayed hypersensitivity (T4): pts develop an ACD
    1. Often presents on dorsal surface of hands
  • Immediate hypersensitivity (T1): may present with immediate sxs like burning, stinging, or itching with or w/o localized urticaria on contact w/latex proteins
    1. May include disseminated urticaria, allergic rhinitis, and/or anaphylaxis (rarely)
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25
Q

What do you see in these images?

A
  • Allergic contact dermatitis to:
    a: neoprene in keyboard pad
    b: paraphenylenediamene
    c: shoes
    d: bleached rubber
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26
Q

What do you see here?

A
  • Allergic contact dermatitis to:
    e: bacitracin
    f: neomycin in an otic suspension
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27
Q

What is going on here?

A

ACD

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28
Q

What happened here?

A

ACD

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29
Q

What are the key points for ACD?

A
  • One of two types of contact dermatitis
  • Occurs when contact with a particular substance elicits a delayed hypersensitivity reaction (T4)
    1. Most patients need minor supportive care, but some cases will require oral steroids
  • Patch testing used to determine which allergens a pt with allergic contact dermatitis reacts against
    1. Not all patients with ACD need patch testing
  • Latex allergy: may present as a delayed OR immediate hypersensitivity
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30
Q

What is ICD?

A
  • Irritant contact dermatitis: inflammatory rxn in the skin from exposure to substance that can cause an eruption in most people who come in contact with it
    1. Non-immunologic, so NO previous exposure is necessary
  • May occur from a single application with severely toxic substances, however, most commonly results from repeated application from mildly irritating substances (e.g., soaps, detergents)
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31
Q

What are the influencing factors in ICD?

A
  • Multifactorial disease where both exogenous (irritant and environmental) and endogenous (host) elements play a role
    1. Most important exogenous factor is the inherent toxicity of the chemical for human skin
  • Site differences in barrier function make face, neck, scrotum, and dorsal hands more susceptible
    1. Atopic dermatitis is a major risk factor for irritant hand dermatitis bc of impaired barrier function and lower threshold for skin irritation
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32
Q

What are the clinical findings in ICD?

A
  • Mild irritants produce erythema, chapped skin, dryness, fissuring after repeated exposures over time
  • Pruritus can range from mild to extreme
  • Pain is a common symptom when erosions and fissures are present
  • Severe cases present with edema, exudate, and tenderness
  • Potent irritants produce painful bullae within hours after the exposure
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33
Q

What do you see here?

A
  • Examples of ICD:
    1. Left -> accidental exposure to pepper spray
    2. Right -> exposure to liquid bleach
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34
Q

How do you evaluate and treat ICD?

A
  • Patch testing should be performed in occupational cases with suspected chronic irritant dermatitis to exclude an allergic contact dermatitis
  • Mainstay of treatment: identification and avoidance of the potential irritant
    1. Topical therapy w/steroids to reduce inflam and emollients to improve barrier repair are usually recommended
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35
Q

How do you prevent ICD?

A
  • Once irritant identified as causal factor, pts should be educated about irritant avoidance, incl everyday practices that may cause, contribute to ICD
  • Use personal protective equipment (e.g. protective gloves should be worn for any wet work)
  • Instead of soap, use less irritating substances, like emollients and soap substitutes when washing
  • Care should be taken for several months after the dermatitis has healed, as skin remains vulnerable to flares of dermatitis for a prolonged period
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36
Q

What are the key points for ICD?

A
  • Inflammatory rxn in skin resulting from exposure to a substance that can cause an eruption in most people who come in contact with it
  • Identification and avoidance of the potential irritant is the mainstay of treatment
  • Patch testing may be performed in cases with suspected chronic irritant dermatitis to exclude an allergic contact dermatitis
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37
Q

What is atopic dermatitis? Symptoms?

A
  • Chronic, pruritic, inflam skin disease w/wide range of severity -> primary symptom is PRURITIS
  • One of most common skin disorders in developed countries -> up to 20% of children and 1-3% of adults

—- Develops in most pts before the age of five, and typically clears by adolescense (“itch that rashes”)

—- “Itch-scratch” cycle can exacerbate the disease

—1. Lesions begin as erythematous papules, then coalesce to form erythematous plaques that may display weeping, crusting, or scale

  1. —Xerosis: common characteristic of all stages

—- Pts experience remission & exacerbations periods

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38
Q

How does distribution vary by age in atopic dermatitis?

A
  • Infants and toddlers: eczematous plaques appear on cheeks, forehead, scalp, and extensor surfaces

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

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

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39
Q

How is atopy related to AD?

A

—- AD is considered to be part of the inflammatory (type I) hypersensitivity triad that includes allergic rhinitis and bronchial asthma

—- There is a history of allergic rhinitis or asthma in up to 50% of patients with AD, and in 75%, there is a family history of atopy

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40
Q

What is going on in these folks?

A
  • Atopic dermatitis:
    a: flexural eczema
    b: flexural eczema
    c: flexural lichenification
    d: circumoral pallor
    e: Dennie Morgan folds (infraorbital line or fold caused by edema)
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41
Q

What do you see here?

A
  • Atopic dermatitis extending from the antecubital fossae to the wrists and hands
  • Note the excoriations and lichenification
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42
Q

What is this?

A

Atopic dermatitis

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43
Q

What is this?

A

Atopic dermatitis

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44
Q

What is this?

A

Atopic dermatitis

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45
Q

What is the pathogenesis of atopic dermatitis?

A
  • Cause of AD is multifactorial and not completely understood
  • Following factors are thought to play varying roles:
    1. Genetics
    2. Skin Barrier Dysfunction
    3. Impaired Immune Response
    4. Environment

—- —Inherited reduction or loss of the epidermal barrier protein filaggrin is a major predisposing factor

—- Favors Th2-mediated immunity

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46
Q

What are the treatment components for atopic dermatitis?

A
  • Avoidance of trigger factors, including irritants, relevant allergens and microbial agents
  • Skin care that aims to compensate for the genetically determined impaired epidermal barrier function
  • Anti-inflammatory therapy to control subclinical inflammation as well as overt flares
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47
Q

What agents are used to tx atopic dermatitis?

A
  • Emollients: Petrolatum
  • Topical corticosteroids: potency and structural class selection depend on clinical judgment
  • Immunomodulators: topical Tacrolimus or Pimecrolimus
  • Systemic corticosteroids: Prednisone in varied doses
  • Phototherapy (in refractory cases)
  • If infected, oral antibiotics
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48
Q

What are the (+)’s and (-)’s of phototherapy to tx atopic dermatitis?

A
  • Favorable side effect profile to systemic immuno-suppressive agents, w/potential risks of:
    1. Sunburn
    2. Photoaging (long-term tx)
    3. Possible induction of cutaneous malignancy (w/long-term tx)
  • Time and effort required to travel several times a wk to a phototherapy center may be problematic for some pts, and a home UV unit may be an option for those receiving chronic tx
  • Young children: may be difficult for practical reasons (e.g. lack of cooperation); some centers limit its routine use to patients ≥12 years of age
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49
Q

How often is atopic dermatitis complicated by infection? How can you tell?

A

—- 90% of atopic dermatitis skin lesions are colonized with microbes, usually Staphylococcus aureus

—- Presence of erosions, drainage w/yellow crusting may indicate an infection (see attached image)

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50
Q

What is going on here?

A
  • Atopic dermatitis and eczema herpeticum
  • Eczema herpeticum is a severe herpes simplex virus infection in an atopic patient
    1. Presents w/multiple widespread monomorphic, “punched-out” discrete erosions with hemorrhagic crusting

—- Severe cases may require hospitalization and IV anti-viral medications

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51
Q

What are the key points for atopic dermatitis?

A
  • Clinical manifestations: chronic, pruritic, inflam skin disease with a wide range of severity

—1. Distribution, morphology of skin lesions vary by age

  1. Large % of kids will devo asthma or allergic rhinitis
    - Pathogenesis: multifactorial -> genetics, skin barrier dysfunction, impaired immune response, environment

—- Treatment: includes long-term use of emollients and gentle skin care; short term tx for acute flares

—1. Acute inflammation is tx with topical steroids

—2. Secondary bacterial skin infections should be treated with systemic antibiotics

  1. Eczema herpeticum should be treated with systemic antivirals eg acyclovir
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52
Q

What is this? What is the clinical presentation of the disease?

A
  • Nummular dermatitis (discoid eczema): coin-shaped lesions of acute and subacute dermatitis

—- Clinical presentation: coin-shaped, well-demarcated plaques with scale and tiny vesicles

  1. —Legs, dorsal hands, extensor surfaces
  2. Intensely pruritic
  3. Worsens during the winter, due to less humidity in the air, increasing skin dryness
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53
Q

What is this? How would you treat it?

A
  • Nummular dermatitis (discoid eczema)
  • Treatment: like atopic dermatitis or any o/eczema
    1. Med to high-potency topical corticosteroid ointments, topical tacrolimus or pimecrolimus, and emollients
    2. # of pts will require phototherapy to clear the lesions
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54
Q

What are the key points for nummular dermatitis?

A

—- Pathogenesis unknown, but may be linked to impaired skin barrier function

—- More common in older individuals

  • —Often associated with dry skin

—- Presents with round, light pink, scaly, thin, 1 to 3 cm plaques on the extremities or trunk

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55
Q

What is this? What is the clinical presentation of the disease?

A

—- Dyshidrotic eczema/pompholyx: firm vesicles of palms, soles, lateral, medial aspects of fingers, toes

—- Presence of pruritus, burning, and prickling sensations

—- Association with atopic dermatitis and contact dermatitis (allergic and irritant): not an independent disease entity because it is often a manifestation of other types of eczema

—- No disturbance of sweat gland function

56
Q

What is this?

A
  • Dyshidrotic eczema/pompholyx: not-infrequent, chronic, relapsing palmoplantar eczematous dermatosis characterized by firm, pruritic vesicles and bullae
  • While the vesicles are due to spongiosis within the epidermis, their intact nature is explained by the thick tear-proof horny layer in these sites
57
Q

What is this?

A

Dyshidrotic eczema/pompholyx

58
Q

What is the pathogenesis of dyshidrotic eczema/pompholyx?

A

—- Unknown etiology

  • Higher relative risks are seen in association with stress, atopy, and ingested or topical allergens
59
Q

How do you treat dyshidrotic eczema/pompholyx?

A

—- Topical and systemic corticosteroids are the mainstay of treatment

  • Topical calcineurin inhibitors may be helpful
  • An underlying allergic or irritant contact dermatitis needs to be considered and addressed
60
Q

What are the key points for dyshidrotic eczema (pompholyx)?

A

—- Course is unknown and not related to dysfunction of sweat glands

  • Presents w/group 2 to 5 mm vesicles, sometimes likened to tapioca pudding

—- Commonly occurs on the lateral fingers, central palms, insteps, and lateral borders of the feet

61
Q

What is this?

A

—- Lichen simplex chronicus

  • Chronic, intensely pruritic skin condition triggered by repeated rubbing and scratching of the skin

—- Typically presents with a solitary, well-defined, pink to tan, thick, and lichenified plaque

—- Commonly on the lateral neck, scrotum/vulva, and dorsal foot

62
Q

What is the epi of psoriasis?

A

—- Approximately 2% of the population

—- Can present at any age, but most common in the third and sixth decades

—- Five main variants: plaque-type, guttate, pustular, inverse, and erythrodermic psoriasis

63
Q

What is this? Clinical presentation?

A
  • Plaque-type psoriasis: most common variant, 90%
  • Characterized by well-demarcated, erythematous plaques w/an adherent, silver to white-colored scale
  • Plaques most prevalent on scalp, extensor surfaces of extremities, periumbilical & sacral trunk
  • Rarely occur on the face, or on intertriginous areas of the body (inverse psoriasis)
  • Lesions may arise at sites of trauma (including bad sunburn), termed the Koebner phenomenon
64
Q

What do you see here?

A
  • Plaque-type psoriasis
  • Note how the popliteal fossa is spared, helping to differentiate this from atopic dermatitis
65
Q

What is this? What is Auspitz sign?

A
  • Plaque-type psoriasis
  • Auspitz sign: when you pick the scale off, it bleeds (characteristic of psoriasis)
66
Q

What is this? Clinical presentation?

A
  • Guttate psoriasis: 2nd most common variant
  • Occurs more commonly in young adults, and it presents with multiple small “drop-shaped” erythematous scaly plaques diffusely on the body, most frequently on the trunk
  • This variant of psoriasis is often preceded by streptococcal infections, especially pharyngitis (can treat with antibiotics)
67
Q

What is this? Clinical presentation?

A
  • Pustular psoriasis: characterized by superficial pustules
  • Pustules may be localized on palms and soles, as in palmoplantar pustulosis, or may be generalized
68
Q

What is this?

A
  • Erythrodermic psoriasis: characterized by diffuse erythroderma (full-body redness) with fine scaling
69
Q

What do you see in these images?

A
  • Psoriasis: c and d are pustular and e is penile
70
Q

What are these?

A
  • Psoriasis: f is guttate, g is generalized pustular, and h is erythrodermic
71
Q

What are some of the extra-dermal manifestations of psoriasis?

A
  • Mucosal and nail changes:
    1. Dorsal tongue may exhibit geographic, annular white patches (geographic tongue)
    2. Nail changes include “oil spots,” nail pitting, distal onycholysis (lifting up of the nail), and accumulation of subungual debris
  • Psoriatic arthritis is the major associated systemic manifestation; most comm presentation asymmetric oligoarthritis of small joints of the hands and feet
    1. May also present as isolated monoarthritis, sacroiliitis, arthritis mutilans (destructive, severe form), or enthesitis
  • Also at INC risk for obesity, diabetes, HTN, CV disease, and hyperlipidemia
72
Q

What is this?

A
  • Psoriasis:
    1. Distal onycholysis
    2. Sub-ungual debris
73
Q

What do you see?

A
  • Psoriasis: nail pitting
74
Q

What is this?

A
  • Psoriasis: geographic tongue
75
Q

What is this?

A
  • Psoriatic arthritis: asymmetric involvement of the DIP and proximal interphalangeal PIP joints
  • “Sausage” digit (third digit bilaterally) results from involvement of both the DIP and PIP joints
76
Q

What is the pathogenesis of psoriasis?

A

—- T-cell-mediated inflammatory disease; genetic factors involved

  • Flares may be associated with:
    1. Group A beta-hemolytic streptococcal infections (guttate)
    2. Meds: beta blockers, ACEI’s, NSAID’s, lithium, IFN, and anti-malarials
    3. Stress

—

—

—Psoriasis can be diminished by sunlight à phototherapy

77
Q

What is the treatment for psoriasis?

A

—- Topical txs: steroids, retinoids, vitamin D analogs, keratolytics, and topical tar products

  • Systemic treatments: phototherapy, oral retinoids (acitretin), methotrexate, and biologics

—- TNF-alpha inhibitors

—- IL12/23 blocker

—- IL-17 blocker

—

—Systemic steroids should NOT be used for the treatment of psoriasis because of the risk of disease flare upon discontinuation of the steroids

78
Q

What are the key points for psoriasis?

A
  • Chronic multisystem disease w/predominantly skin and joint manifestations (1/3 have a 1st-degree relative with psoriasis)

—1. Different morphological types: plaque (80-90%), guttate, inverse, pustular, erythrodermic

  • Need to take detailed history w/these pts

—1. Nail disease is common (look at their nails)

—2. May be associated with psoriatic arthritis (ask about joint pains/arthritis at visits)

—- Treatment: topical alone when localized

  1. Moderate to severe: often require systemic treatment in addition to topical therapy, which includes phototherapy, oral medications, and biologic agents
79
Q

What is seborrheic dermatitis?

A
  • Very comm inflam rxn to Malassezia (Pityrosporum ovale) yeast that thrives on seborrheic (oil-producing) skin -> face, nose, chest, behind the ears
  • Erythematous scaling patches on the scalp, hairline, eyebrows, eyelids, central face, nasolabial folds, external auditory canals, or central chest
  • Infants present with “cradle cap”, pink to yellow macules and patches with white greasy scales on the scalp, face, and diaper area
  • Can be hypopigmented, esp. in darker skin types
  • Chest: appears more central over the sternum
  • Often worse in patients with HIV
80
Q

What is this?

A
  • Seborrheic dermatitis
  • Very comm inflam rxn to Malassezia (Pityrosporum ovale) yeast that thrives on seborrheic (oil-producing) skin -> face, nose, chest, behind the ears
81
Q

What is this?

A
  • Seborrheic dermatitis
  • Erythematous scaling patches on the scalp, hairline, eyebrows, eyelids, central face, nasolabial folds, external auditory canals, or central chest
82
Q

What do you see?

A
  • Seborrheic dermatitis
  • Infants present with “cradle cap”, pink to yellow macules and patches with white greasy scales on the scalp, face, and diaper area
  • Often worse in patients with HIV
83
Q

What is this?

A

Seborrheic dermatitis: often hypopigmented in darker skin types

84
Q

What do you see?

A

Seborrheic dermatitis: favors central chest, and may be hypopigmented or erythematous

85
Q

What is the treatment for seborrheic dermatitis?

A
  • Low-potency topical steroids safe to use for flares on the face (don’t want to use steroids for too long)
    1. Twice daily for 1-2 weeks for flares
    2. Can also use topical ketoconazole, or topical pimecrolimus, in the same manner
  • Antidandruff shampoo for the scalp, chest
    1. Ketoconazole, selenium sulfide, zinc pyrithione shampoos
    2. Lather, leave on 10 minutes, rinse; repeat 3-5x/week
86
Q

What are the key points for seborrheic dermatitis?

A

—- Very common disorder associated with sebum production and Malassezia yeast

  • —In infants presents with “cradle cap”, pink to yellow macules and patches with white greasy scales on the scalp, face, and diaper area

—- In adults presents with erythematous plaques with white greasy scales on the scalp, forehead, eyebrows, eyelash line, nasolabial folds, ears, upper chest and intertriginous areas

—- Treatment with ketoconazole cream or dandruff shampoos or low-potency steroid for flares

87
Q

What is pityriasis rosea?

A

—- Acute, self-limiting, papulo-squamous eruption mainly occuring in young people (10-35 y/o)

  1. Peak incidence in late teens and early 20s

—- Some studies suggest a possible viral (HHV-6/7) etiology, but this has not been definitively proven

—- Usually asymptomatic, but patients may have associated flu-like symptoms -> malaise, nausea, loss of appetite, GI upset, upper resp symptoms

  1. Less commonly: fever, swollen lymph nodes, pain, or sore throat are noted
    - Attached image: characteristic “Xmas tree” pattern
88
Q

What are the clinical manifestations of pityriasis rosea?

A

—- Classically starts w/“herald patch” (see image), but pts often don’t remember or never have this

  • Annular erythematous 2-10 cm patch anywhere on the body, w/peripheral scaling and central clearing
  • 2o phase erupts in a “Christmas tree” pattern

—1. Similar oval patches and plaques erupt symmetrically over trunk, proximal extremities

  1. Follow relaxed skin tension lines, giving the appearance of a “Christmas tree” on the back
    - Classically described as salmon-colored, but in darker skin types, shades of purple, brown, or gray

—- Inverse pityriasis rosea is similar but localized to the groin and axilla (very rare)

89
Q

What is this?

A

Pityriasis rosea: peripheral, trailing scales

90
Q

What is the treatment for pityriasis rosea?

A
  • Self-limiting: mean duration about 5 weeks
    1. > 80% resolve by 8 weeks without treatment

—2. Most patients only need to be reassured

—- 25% request treatment for mild to severe pruritus

—1. OTC anti-itch lotions, topical steroids, oral anti-histamines

—2. Oral erythromycin has been reported to beneficial

91
Q

What are the key points for pityriasis rosea?

A

—- Common dermatosis that typically occurs in young adults -> acute onset, and lasts 6 to 8 weeks

—- May be associated with HHV-6 or -7 (herpes)

—- Presents initially with a single herald patch, a pink-salmon colored, oval, 2-to 10-cm plaque with central fine collarette scale

—- Followed by numerous smaller, similar lesions dispersed on the trunk in a “Christmas tree” pattern

92
Q

What is the clinical presentation of lichen planus?

A

—- Idiopathic inflammatory disease of the skin, hair, nails, mucous membranes (up to 60% of pts) -> seen most commonly in middle-aged adults

—- Pruritic (very itchy), purple, polygonal, flat-topped papules with a fine reticulated network of white lines (Wickham’s striae)

—- Lesions koebnerize (where they scratch) and are commonly found on flexor wrists, forearms, dorsal hands, lower legs, presacral area, neck, glans penis

93
Q

What are some clinical variants of lichen planus?

A

—- Lichen planopilaris (LPP): follicular variant of lichen planus that causes scarring alopecia

—- Clinical variants include: annular, bullous, inverse, hypertrophic, linear, ulcerative, vulvovaginal–gingival, and drug-induced

  1. Some lichenoid drug eruptions have a photodistribution; others clinically and histo indistinguishable from idiopathic lichen planus
  2. Most commonly incriminated drugs include ACEI’s, thiazides, antimalarials, quinidine, gold
94
Q

What do you see here?

A
  • Lichen planus: purple, polygonal papules
95
Q

What is this?

A
  • Lichen planus: oral and vulvar variants shown here
96
Q

What is this?

A
  • Lichen planus: pigmented, purple papules raised off of the skin, with a white scale
97
Q

What is this?

A

Oral lichen planus: look in these pts’ mouths

98
Q

What is this?

A

Hypertrophic lichen planus

99
Q

What are the pathogenesis and associations with lichen planus?

A
  • Pathogenesis: likely involves an autoimmune reaction against antigens on lesional keratinocytes

—- Associations: hepatitis C is more prevalent in patients with LP vs controls

  1. Atypical presentations are more likely to be associated with hepatitis C
  2. TEST THESE PTS FOR HEP C
100
Q

What is the treatment for lichen planus?

A
  • Initial: topical and intralesional corticosteroids

—- Hypertrophic lichen planus can be treated with high-potency corticosteroids under occlusion or intralesional corticosteroids

—- Tx of mucosal lichen planus especially challenging

—- Topical corticosteroids and topical calcineurin inhibitors

101
Q

What are the key points for lichen planus?

A

—- Uncommon disorder usually in ppl b/t 30 and 60

—- May be triggered by hep C infection or medication, including diuretics and anti-malarials

—- Violaceous, flat-topped papules on the flexor wrists, forearms, ankles, lower back, and genitals

—- Oral lesions present as net-like white streaks on the buccal mucosa

102
Q

Which papulosquamos disease does NOT require long-term treatment?

A

Pityriasis rosea

103
Q

What is the typical treatment for dermatitis and other papulosquamous diseases?

A

Usually respond well to topical steroids

104
Q

What is scabies?

A
  • Sarcoptes scabiei (scabies): affects pts of all ages and SES, but more common in women and children
  • Immunocompromised, ppl in congregated facilities (e.g., nursing homes) more prone to infestation
  • Most infections from direct contact with infected individual; however, fomites can transmit infection
105
Q

What is this?

A
  • Scabies mite: 0.35 x 0.3 mm in size and too small to be seen by the naked eye
  • Females lay about 3 eggs per day, which hatch in four days
  • Most pts have <20 mites on the skin at a time
106
Q

What are the clinical features of scabies?

A
  • Time from initial infestation to symptoms typically 3-4 weeks

—1. Once sensitized to the mite, re-infestation results in symptoms within 1-2 days

  • Papules may commonly involve axillae, breasts, umbilicus, penis, scrotum, finger webs and wrists
  • Scalp and head are more frequently involved in infants, elderly and immunosuppressed individuals
  • The hallmark feature is itching at night
107
Q

What do you see here?

A

Clinical findings of scabies

108
Q

What is this?

A
  • Burrows -> pathognomonic for SCABIES
  • Linear markings in the skin due to the movement of the mite
  • 1-10 mm in length and are most readily found in the interdigital spaces, wrists and elbows
109
Q

What is this?

A
  • Burrows -> pathognomonic for SCABIES
  • This is where you would scrape the patient
110
Q

What do you do in this patient with suspected scabies?

A
  • Skin scraping (MINERAL OIL PREPARATION)
  • Use a 15-blade scalpel and scrape a burrow on the skin; scraped material is placed on a slide and a drop of mineral oil is added
  • Cover slip is placed on top and you see the image below when you look through the microscope
111
Q

What is crusted scabies?

A
  • Immune suppressed or neurologically impaired ppl are at INC risk of crusted scabies (hyperkeratotic scabies, formerly called Norwegian scabies)
  • Thick, scaly, white-gray plaques w/minimal pruritus often localized to scalp, face, back, buttocks, feet
    1. These pts do NOT complain of itching
  • Fissures provide an entry for bacteria, leading to increased risk of sepsis and death
  • Immunocompetent persons who come into contact with crusted scabies develop typical scabies
112
Q

What is this?

A
  • Crusted scabies: far more difficult to treat
  • Incredibly high mite burden
113
Q

What is the patient treatment for scabies? How long can symptoms persist?

A
  • Two-pronged approach: patient and environment must both be treated
    1. Two topical treatments one week apart with prescription anti-scabietic medication
    2. Apply topical medication from neck down and leave on overnight; for infants and the elderly, include the face and scalp
  • Itch and lesions can persist for 2-4 weeks after successful treatment, referred to as “post-scabietic” pruritus or dermatitis
    1. This is not a treatment failure, but represents the body’s response to dead mites
114
Q

What is the environmental tx for scabies?

A
  • Environmental care includes washing all clothing and linens used within the last week in hot water and drying on high heat -> for items that cannot be washed, seal items in bags for at least 3 days
  • Isolation from other people is unnecessary as the causative organism cannot jump or fly, and can survive for only approximately 72 hours away from the skin.
115
Q

What are the first-line treatments for scabies (table)?

A
  • Ivermectin: reserved for really tough patients
116
Q

How do you treat crusted scabies?

A
  • Combo therapy typically used in crusted scabies
    1. Multiple doses of oral ivermectin (oral)
    2. Topical permethrin -> frequently more than two treatments are required
  • Given the high mite burden, patients with crusted scabies need to be isolated, and strict barrier nursing procedures instituted to avoid outbreaks in health care facilities
117
Q

What are the key points for scabies?

A
  • Affects all classes of patients, but those in group settings or in an immunocompromised state are at increased risk of infestation
  • Burrows w/a short, wavy line are pathognomonic
  • The primary diagnostic test for scabies is the skin scraping or mineral oil prep
  • 1st-line treatment for scabies in patients over two months of age who are not pregnant is permethrin 5% cream
118
Q

What is pediculosis? 3 types?

A
  • Three different varieties of lice may infest humans:
    1. Head louse: Pediculus humanus var. capitis
    2. Body louse: Pediculus humanus var. corporis
    3. Pubic or crab louse: Phthirus pubis
  • Spread by close physical contact and fomites (e.g., brushes, helmets, bedding)
  • Commonly affects school-age children
  • Affects all ethnic and socioeconomic groups, but is less common in African-Americans
119
Q

What is the pathogenesis of pediculosis?

A
  • Female adult lice live 30 days, and lay 5-10 eggs (nits) per day at base of hair where it meets scalp
    1. Eggs hatch in 8-12 days.
  • Live eggs remain close to scalp for warmth and moisture; as hair grows, nits move off scalp w/hair
    1. Hair grows at a rate of ~ 1 cm per month, so duration of infestation can be estimated by distance of the nit from the scalp
  • Adult head louse 2-3 mm in length; six legs
  • Presence of live adult lice, immature nymphs, and/or viable eggs indicate active infestation
  • Lice typically survive 1-2 days away from the scalp; eggs may survive up to 10 days away from scalp
120
Q

What are the clinical features of pediculosis?

A
  • Frequently has associated scalp pruritus
  • May also have posterior cervical lymphadenopathy
  • Dermatitis may be present on the posterior neck
  • Nits are noted more commonly than lice on exam (live lice scurry away from light) -> most common sites to find them are retroauricular & occipital scalp
  • Nits within 1 cm of the scalp are typically viable, but distance may be greater in warm environments
  • Nits must be distinguished from hair casts (normal variants of hair)
    1. Hair casts encircle hair shaft and move freely in contrast to nit, which is cemented to the hair
121
Q

What is going on here?

A

Pediculosis: numerous nits (oval egg capsules) firmly fixed to the hair shaft

122
Q

What is this?

A
  • Pediculosis hair mount
  • This image shows a nit without an intact cap (operculum), and is not viable (no larva inside)
    1. Viable eggs are usually tan to brown in color
    2. Hatched eggs are clear to white
  • Empty egg casings are often easier to see b/c they appear white against darker hair
123
Q

What is the treatment for pediculosis?

A
  • Individual pt factors should be assessed prior to choosing a topical therapy (age, allergy history, prior treatment, etc.)
  • Prudent to re-treat with topical therapies 7-9 days after initial therapy to kill the newly hatched lice
  • First-line over-the-counter and prescription topical therapies are listed on the attached table
    1. Use OTC permethrin 1% or pyrethrins when resistance is not suspected
    2. Use malathion 0.5% when resistance to permethrin or pyrethrins is documented, or when treatment with these products fails
  • Adjunctive nit combing can be performed
  • Occlusive methods have also been used to suffocate head lice (petroleum jelly, mayonnaise) but study results have been variable
124
Q

How should pediculosis patients be educated?

A
  • All persons living in the home should be examined to avoid re-infestation
    1. Those with live lice or nits within 1 cm of the scalp should be treated
    2. Prudent to treat family members who share a bed with the person with infestation, even if no lice are found
    3. If it is not possible to examine household members, treat without an exam if the treatment is not contraindicated
  • Clothing and bedding should be washed and dried on the hot cycle of the dryer
  • Brushes, combs and other hair care items can be placed in hot (> 60°C) water for 10 minutes
  • Non-washable items may be placed in the dryer or stored in a sealed plastic bag for 3 days
  • Children should NOT be restricted from attending school because of lice
125
Q

Where do body and crab lice infest?

A

—- Body lice: infest back, neck, shoulders, and waist

—1. Nits and live lice may be seen on clothing

—- Crab lice: infest lower abdomen, pubic area, and thighs

  • NOTE: pyoderma and regional lymphadenopathy may be present with any form of pediculosis
126
Q

What are the key points for pediculosis?

A
  • Pediculosis capitis commonly affects school-aged children
  • Adult lice and/or nits within 1 cm of the scalp are diagnostic of pediculosis capitis
  • Pyoderma and regional LAD may be present with any form of pediculosis
127
Q

What is lyme disease?

A

—- Caused by Borrelia, a spirochete transmitted by Ixodes ticks (deer tick)

—- 90% of cases occur in the NE United States, and in Minnesota and Wisconsin

—- Presents with erythema migrans, a 3- to 15-cm or larger annular plaque about a week after bite

128
Q

What is this? How do you treat it?

A
  • Erythema migrans: represents initial cutaneous manifestation of Lyme disease
  • Seen in 60-90% of pts diagnosed with the disease

—- Early treatment of Lyme Disease with doxycycline, amoxicillin or cefuroximine is highly successful

129
Q

What are the key points for lyme disease?

A

—- Caused by Borrelia, a spirochete transmitted by Ixodes ticks (deer tick)

—- Erythema migrans represents the cutaneous expression of Lyme Disease

—- Early treatment with antibiotics is successful

130
Q

What are bed bugs?

A
  • Cimex lectularius (most common type) affect people from all racial and socioeconomic groups
  • May be spread during travel on clothing, bedding, mattresses, and laundry, etc
  • Stay hidden during the day and feed at night
  • Bites may be multiple in a linear array; referred to as “breakfast, lunch and dinner”
131
Q

What is this?

A
  • Bed bugs: edematous papules scattered over the body, some are excoriated
132
Q

What is this?

A
  • Cimex lecularius (bed bugs): red-brown in color with a segmented abdomen and vestigial wings (really wingless)
133
Q

What is the clinical presentation of bed bugs?

A
  • Pruritic, erythematous and edematous papules
  • Appearance and duration of lesions vary depending on the patient’s degree of sensitization
  • Some individuals have little or no reaction to bedbug bites
    1. Common for only one or a few family members (even among those sleeping in the same bed) to report lesions
134
Q

What is the treatment for bed bugs?

A
  • Bites will typically resolve within 1-2 weeks
  • For symptomatic relief, treat with potent topical steroids and antihistamines
  • Ultimate treatment requires detection and eradication of the household infestation
    1. Bed linens need to be laundered and furniture vacuumed
    2. A professional exterminator may be needed to treat the home
135
Q

What are the key points for bed bugs?

A
  • Bedbugs typically feed at night and infest all populations
  • Bedbug bites cause edematous papules which may be arranged in a “breakfast, lunch and dinner” pattern

MSK, Rheum, Derm (21 decks)

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