Patel 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
What do you see in these images?
- Allergic contact dermatitis to: a: neoprene in keyboard pad b: paraphenylenediamene c: shoes d: bleached rubber
26
What do you see here?
- Allergic contact dermatitis to: e: bacitracin f: neomycin in an otic suspension
27
What is going on here?
ACD
28
What happened here?
ACD
29
What are the key points for ACD?
- 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
30
What is ICD?
- **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)
31
What are the influencing factors in ICD?
- _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
32
What are the clinical findings in ICD?
- 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
33
What do you see here?
- Examples of ICD: 1. Left -\> accidental exposure to pepper spray 2. Right -\> exposure to liquid bleach
34
How do you evaluate and treat ICD?
- _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
35
How do you prevent ICD?
- 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
36
What are the key points for ICD?
- **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
37
What is atopic dermatitis? Symptoms?
- 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 2. —Xerosis: common characteristic of all stages —- Pts experience _remission & exacerbations_ periods
38
How does distribution vary by age in atopic dermatitis?
- _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)
39
How is atopy related to AD?
—- 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_
40
What is going on in these folks?
- 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)
41
What do you see here?
- Atopic dermatitis extending from the antecubital fossae to the wrists and hands - Note the excoriations and lichenification
42
What is this?
Atopic dermatitis
43
What is this?
Atopic dermatitis
44
What is this?
Atopic dermatitis
45
What is the pathogenesis of atopic dermatitis?
- 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_
46
What are the treatment components for atopic dermatitis?
- _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
47
What agents are used to tx atopic dermatitis?
- _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_
48
What are the (+)'s and (-)'s of phototherapy to tx atopic dermatitis?
- _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
49
How often is atopic dermatitis complicated by infection? How can you tell?
—- **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)
50
What is going on here?
- 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_
51
What are the key points for atopic dermatitis?
- _Clinical manifestations_: chronic, pruritic, inflam skin disease with a wide range of severity —1. Distribution, morphology of skin lesions vary by age 2. 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 3. Eczema herpeticum should be treated with systemic antivirals eg acyclovir
52
What is this? What is the clinical presentation of the disease?
- **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
53
What is this? How would you treat it?
- **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
54
What are the key points for nummular dermatitis?
—- _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
55
What is this? What is the clinical presentation of the disease?
—- **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
What is this?
- **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
What is this?
Dyshidrotic eczema/pompholyx
58
What is the pathogenesis of dyshidrotic eczema/pompholyx?
—- Unknown etiology - Higher relative risks are seen in association with stress, atopy, and ingested or topical allergens
59
How do you treat dyshidrotic eczema/pompholyx?
—- 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
What are the key points for dyshidrotic eczema (pompholyx)?
—- 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
What is this?
—- **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
What is the epi of psoriasis?
—- 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
What is this? Clinical presentation?
- **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
What do you see here?
- _Plaque-type psoriasis_ - Note how the popliteal fossa is spared, helping to differentiate this from atopic dermatitis
65
What is this? What is Auspitz sign?
- _Plaque-type psoriasis_ - _Auspitz sign_: when you pick the scale off, it bleeds (characteristic of psoriasis)
66
What is this? Clinical presentation?
- **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
What is this? Clinical presentation?
- **Pustular psoriasis**: characterized by superficial pustules - Pustules may be localized on palms and soles, as in palmoplantar pustulosis, or may be generalized
68
What is this?
- **Erythrodermic psoriasis**: characterized by diffuse erythroderma (full-body redness) with fine scaling
69
What do you see in these images?
- _Psoriasis_: c and d are pustular and e is penile
70
What are these?
- _Psoriasis_: f is guttate, g is generalized pustular, and h is erythrodermic
71
What are some of the extra-dermal manifestations of psoriasis?
- _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
What is this?
- _Psoriasis_: 1. Distal onycholysis 2. Sub-ungual debris
73
What do you see?
- _Psoriasis_: nail pitting
74
What is this?
- _Psoriasis_: geographic tongue
75
What is this?
- **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
What is the pathogenesis of psoriasis?
—- _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
What is the treatment for psoriasis?
—- _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
What are the key points for psoriasis?
- _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
What is seborrheic dermatitis?
- 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
What is this?
- **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
What is this?
- **Seborrheic dermatitis** - Erythematous scaling patches on the scalp, hairline, eyebrows, eyelids, central face, nasolabial folds, external auditory canals, or central chest
82
What do you see?
- **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
What is this?
Seborrheic dermatitis: often hypopigmented in darker skin types
84
What do you see?
Seborrheic dermatitis: favors _central chest_, and may be hypopigmented or erythematous
85
What is the treatment for seborrheic dermatitis?
- _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
What are the key points for seborrheic dermatitis?
—- 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
What is pityriasis rosea?
—- _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
What are the clinical manifestations of pityriasis rosea?
—- 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 2. 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
What is this?
Pityriasis rosea: peripheral, trailing scales
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What is the treatment for pityriasis rosea?
- _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
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What are the key points for pityriasis rosea?
—- 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
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What is the clinical presentation of lichen planus?
—- 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
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What are some clinical variants of lichen planus?
—- _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_
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What do you see here?
- Lichen planus: purple, polygonal papules
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What is this?
- Lichen planus: oral and vulvar variants shown here
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What is this?
- _Lichen planus_: pigmented, purple papules raised off of the skin, with a white scale
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What is this?
Oral lichen planus: look in these pts' mouths
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What is this?
Hypertrophic lichen planus
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What are the pathogenesis and associations with lichen planus?
- _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
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What is the treatment for lichen planus?
- _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
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What are the key points for lichen planus?
—- 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
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Which papulosquamos disease does NOT require long-term treatment?
Pityriasis rosea
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What is the typical treatment for dermatitis and other papulosquamous diseases?
Usually respond well to topical steroids
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What is scabies?
- **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
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What is this?
- **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
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What are the clinical features of scabies?
- 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**
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What do you see here?
Clinical findings of scabies
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What is this?
- 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
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What is this?
- Burrows -\> pathognomonic for SCABIES - This is where you would scrape the patient
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What do you do in this patient with suspected scabies?
- 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
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What is crusted scabies?
- _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
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What is this?
- **Crusted scabies**: far more difficult to treat - Incredibly high mite burden
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What is the patient treatment for scabies? How long can symptoms persist?
- _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
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What is the environmental tx for scabies?
- 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.
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What are the first-line treatments for scabies (table)?
- Ivermectin: reserved for really tough patients
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How do you treat crusted scabies?
- **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
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What are the key points for scabies?
- 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_
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What is pediculosis? 3 types?
- 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
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What is the pathogenesis of pediculosis?
- 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
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What are the clinical features of pediculosis?
- 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
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What is going on here?
Pediculosis: numerous nits (oval egg capsules) firmly fixed to the hair shaft
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What is this?
- 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
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What is the treatment for pediculosis?
- 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
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How should pediculosis patients be educated?
- _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
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Where do body and crab lice infest?
—- **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
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What are the key points for pediculosis?
- 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
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What is lyme disease?
—- 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
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What is this? How do you treat it?
- **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
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What are the key points for lyme disease?
—- 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
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What are bed bugs?
- **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_”
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What is this?
- **Bed bugs**: edematous papules scattered over the body, some are excoriated
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What is this?
- **Cimex lecularius** (bed bugs): red-brown in color with a segmented abdomen and vestigial wings (really wingless)
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What is the clinical presentation of bed bugs?
- 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
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What is the treatment for bed bugs?
- 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
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What are the key points for bed bugs?
- 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