Derm Flashcards

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1
Q

What are the common types of dermatitis (eczema)?

A

—Allergic contact dermatitis

—Irritant contact dermatitis

—Atopic dermatitis

—Dyshidrotic dermatitis

—Lichen simplex chronicus

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2
Q

What is this? How does it present?

A

Allergic contact dermatitis

Presentations: pruritis (common to all dermatites), vesicular/bullous formation, and commonly lichenification

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3
Q

What mediates allergic contact dermatitis? Timeline?

A

type IV hypersensitivity that presents in two phases

1) sensitization (induction)- 10-14 days or 12-48 hrs upon re-exposure
2) elicitation (challenge)

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4
Q

Common causes of ACD?

A
  • Rhus dermatitis (poison ivy, poison oak- all contain urushiol)
  • fragrances
  • Nickel
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5
Q

How does a Rhus allergy present?

A

initial episode occurs 7-10 days after exposure and within hours upon re-exposure and lastly 10-21 days depending on the severity with the initial exposure being the most severe and presents as:

linear erythema that can blister

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6
Q

How is Rheu dermatitis treated?

A

Minor supportive care with topical steroids and anti-histamines

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7
Q

What causes latex allergy?

A

Latex allergy may present as a delayed (on the dorsum of the hand) or immediate hypersensitivity

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8
Q

Key points about acute dermatitis

A

-1 of 2 types of contact dermatitis that occurs primarily due to a type IV hypersensivity (except latex- I or IV) that can be diagnosed using a Patch test and generally requires supportive care, topical steroids, and antihistamines

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9
Q

What is Irritant contact Dermatitis?

A

A non-immuologic, inflammatory rxn resulting from exposure to a toxic substance like bleach that can occur due to single exposure but is most commonly due to repeated exposure and is strongly associated with major risk factors that impair the barrier function of the skin like atopic dermatitis

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10
Q

What are the most sensitive areas of the body for an ICD?

A

face, neck, scrotum, and dorsal hands

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11
Q

How is ICD treated?

A

removal of the irritant, topical steroid therapy to reduce inflammation, emollients to improve barrier function, and prolonged caution is advice because the skin remains vulnerable to flares of dermatitis for prolonged periods

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12
Q

What is Atopic Dermatits?

A

a very common chronic, pruritic, inflammatory disease that is characterized by periods of remission and exacerbations and xerosis BUT that can present differently based on the age group affected

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13
Q

How does atopic dermatitis typically present in infants? What areas of the body?

A

erythematous plaques common on the face (cheeks, forehead, scalp), and extensor surfaces

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14
Q

How does atopic dermatitis typically present in older children? What areas of the body?

A

—lichenified, eczematous plaques in flexural areas of the neck, elbows, wrists, and ankles

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15
Q

How and where does atopic dermatitis tend to present in adults?

A

—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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16
Q

What mediates AD?

A

—AD is considered to be multifoactorial (skin function, genetics, etc.) and part of the inflammatory (type I) hypersensitivity triad that includes allergic rhinitis and bronchial asthma (a Hx of these illnesses is often present)

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17
Q

What is a major pre-disposing factor for developing AD?

A

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

—Favors Th2-mediated immunity

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18
Q

How is AD treated?

A
  • avoidance of trigger factors
  • anti-inflammatory therapy to control subclinical inflammation as well as overt flares (prednisone)
  • in selected cases, adjunctive or complementary modalities such as —Topical tacrolimus or pimecrolimus
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19
Q

—90% of atopic dermatitis skin lesions are colonized with microbes, usually _______

A

Staphylococcus aureus (—Presence of erosions, drainage with yellow crusting may indicate an infection)

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20
Q

What is Eczema Herpeticum?

A

—A severe herpes simplex virus infection in an atopic patient that presents with multiple wide spread monomorphic, “punched-out” discrete erosions with hemorrhagic crusting

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

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21
Q

What is this? Describe them. When do you see them?

A

Nummular Dermatitis/Discoid eczema- presents as —Coin-shaped, well-demarcated plaques with scale and possibly tiny vesicles, cracking or crusting that are very pruritic, —show, spongiotic dermatitis, and are more common in winter

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22
Q

Describe Dyshidrotic Eczema/Pompholyx?

A

a 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. Dyshidrotic eczema is not an independent disease entity because it is often a manifestation of other types of eczema, especially atopic dermatitis and irritant or allergic contact dermatitis.

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23
Q

T or F. Dyshidrotic eczema causes —disturbance of sweat gland function

A

F.

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24
Q

What is this?

A

Lichen Simplex Chronicus- Chronic, intensely pruritic skin condition triggered by repeated rubbing and scratching of the skin that typically presents with a solitary, well-defined, pink to tan, thick, and lichenified plaque

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

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25
Q

What are the papulosquamous skin diseases?

A

—-Psoriasis

—-Seborrheic dermatitis

—-Pityriasis rosea

—-Lichen planus

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26
Q

What is Psoriasis?

A

A chronic immune-mediated disease with predominantly skin and joint manifestations that can present at any age, but occurs most commonly in two peaks: ages 20-30 and ages 50-60 and has a strong genetic component

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27
Q

What are the five main variants of psoriasis?

A

—plaque-type,

guttate,

pustular,

inverse

erythrodermic psoriasis

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28
Q

What is this? Describe it. Where is it common?

A

Plaque psoriasis, the most common variant (90%) of psoriasis that is most prevalent on the scalp, extensor surfaces of the extremities, and the periumbilical and sacral trunk; they rarely occur on the face, or on intertriginous areas of the body (inverse psoriasis).

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29
Q

What is the the Koebner phenomenon

A

Plaque psoriasis arising at sites of trauma

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30
Q

What is this?

A

Ausptiz Sign

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31
Q

How does the second most common variant of psoriasis, Guttate psoriasis, present?

A

It 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 and is often preceded by streptococcal infections, especially pharyngitis.

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32
Q

What is this?

A

Inverse/Flexural psoriasis- Erythematous plaques in the axilla, groin, inframammary region and skin folds that may lack scale due to moistness of area and are often symmetric

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33
Q

Describe pustular psoriasis

A

Disease characterized by superficial pustules that may be localized on the plams and soles or they may be generalized and are often triggered by corticosteroid withdrawal

34
Q
A
35
Q

What are some other common manifestations of psoriasis?

A
  • mucosal and nail changes.
  • The dorsal tongue may exhibit geographic, annular white patches.

•Psoriatic nail changes include “oil spots,” nail pitting, distal onycholysis, and accumulation of subungual debris.

-arthritis

36
Q

How does psoriatic arthritis present?

A

The most common presentation is asymmetric oligoarthritis of the small joints of the hands (sausage hands- below) and feet

  • Psoriatic arthritis may also present as isolated monoarthritis, sacroiliitis, arthritis mutilans, or enthesitis.
  • In addition, psoriatic patients appear to be at an increased risk for developing obesity, diabetes mellitus, hyperlipidemia, hypertension, and cardiovascular disease
37
Q

What mediates psoriasis?

A

A T-cell-mediated inflammatory disease that may be influenced by genetic factors and that can be diminished by sunlight

38
Q

—Flares of psoriasis may be associated with ______

A

group A beta-hemolytic streptococcal infections,

medications (eg, beta blockers, ACE – inhibitors, nonsteroidal anti-inflammatory drugs, lithium, interferon and antimalarials), and

stress

39
Q

How is psoriasis treated?

A

-When localized, topical treatments including topical steroids, topical retinoids, topical vitamin D analogs, topical keratolytics, and topical tar products

—-—Systemic treatments including phototherapy, oral retinoids (acitretin), methotrexate, and biologics (—TNF-alpha inhibitors, —IL12/23 blockers, and —IL-17 blockers)

—

40
Q

T or F. —Systemic steroids should not be used for the treatment of psoriasis

A

T. because of the risk of disease flare upon discontinuation of the steroids

41
Q

Describe Seborrheic dermatitis

A

An inflammatory reaction to the Malassezia (Pityrosporum ovale) yeast that thrives on seborrheic (oil-producing) skin and presents as erythematous scaling patches

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

42
Q
A
43
Q
A

On the chest, it appears more central over the sternum

44
Q

Seborrheic dermatitis is often worse in patients with ____

A

HIV

45
Q

How is Seborrheic dermatitis treated?

A
  • Low-potency topical steroids for flares on face
  • Antidandruff shampoo for scalp and chest
46
Q

What is Pityriasis Rosea?

A

—An acute papulosquamous eruption that mainly occurs in young people (most patients are between the ages of 10 and 35) with a suggested possible viral (HHV-6/7) etiology,

47
Q

How does Pityriasis Rosea present?

A

Usually an asymptomatic disease, but flu-like symptoms including malaise, nausea, loss of appetite, etc. and even fever and LAD can be seen AND

classically starts with a ‘herald’ patch and then a secondary phase with a symmetric, salmon-colored ‘Christmas tree” pattern rash

48
Q

Pityriasis rosea

A
49
Q

How is Pityriasis Rosea treated?

A

Self-limiting (takes about 5-8 weeks) but OTC anti-lotions and oral erythromycin can help with pruritis

50
Q

Describe Lichen Planus

A

Adult diopathic inflammatory disease of the skin, hair, nails, and mucous membranes characterized by pruritic, purple, flat-topped papules with reticulated networks of white lines (Wickham’s striae)

51
Q

—Some lichenoid drug eruptions have a photodistribution, while others are clinically and histologically indistinguishable from idiopathic lichen planus. What drugs commonly cause this?

—

A

angiotensin-converting enzyme (ACE) inhibitors, thiazide diuretics, antimalarials, quinidine and gold

52
Q
A
53
Q

Lichen planus

A

Lichen planus

54
Q

What mediates Lichen Planus?

A

—Likely involves an autoimmune reaction against antigens on lesional keratinocytes

55
Q

Associations of Lichen planus?

A

—Hepatitis C

—

—

56
Q

Tx of Lichen Planus?

A

-topical steroids and topical calcineurin inhibitors

57
Q

How does scabies infection occur? Patient population?

A

Can affect anyone but more common in women, children, immunocompromised individuals, and close groups of people and occurs from direct contact with an infected individual or fomites (below)

58
Q

How does scabies present?

A

There is typically a 3-4 week incubation period from infection initially (or as fast as 1-2 days with re-infestation) that results in papule formation throughout the body that are characteristically more itchy at night and may show pathognomonic BURROWS

59
Q

While most scabies papules occur on the body, the scalp and head are more frequently involved in _______

A

infants, elderly and immunosuppressed individuals.

60
Q

What are these?

A

Burrows - linear markings in the skin due to the movement of the mite. They are 1-10 mm in length and are most readily found in the interdigital spaces, wrists and elbows

61
Q

How should suspected scabies be addressed?

A

perform a mineral oil preparation on the patient.

•You use a 15-blade scalpel and scrape a burrow on the skin. The scraped material is placed on a slide and a drop of mineral oil is added. A cover slip is placed on top and you see the image below when you look through the microscope.

62
Q

What are hyperkeratotic scabies, formerly called Norwegian scabies?

A

Immune suppressed or neurologically impaired individuals are at increased risk of developing crusted scabies that are far more difficult to treat

63
Q

How is scabies treated?

A

Scabies treatment includes a two-pronged approach. The patient and the environment must both be treated.

•Two topical treatments separated one week apart with a prescription 5% permerthin cream (if not pregnant). Apply topical medication from the 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.This is not a treatment failure, rather it represents the body’s response to dead mites.

64
Q

What is the ‘environmental’ treatment of scabies?

A

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.

65
Q

T or F. Isolation from other people is necessary

A

F. As the causative organism cannot jump or fly, and can survive for only approximately 72 hours away from the skin.

66
Q

How are crusted scabies treated?

A

Combination therapy is typically used including multiple doses of PO Ivermectin and Topical permethrin (if not pregnant).

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.

67
Q

What are the types of Pediculosis (lice) that can infest humans?

A
  • Head louse – Pediculus humanus var. capitis
  • Body louse – Pediculus humanus var. corporis
  • Pubic or crab louse – Phthirus pubis
68
Q

Lice affects all ethnic and socioeconomic groups, but is less common in ____

A

African-Americans

69
Q

Describe the pathogenesis of pediculosis

A

Female adult lice live 30 days and lay 5-10 eggs (nits) per day at the base of the hair where it meets the scalp.

Live eggs remain close to the scalp to maintain warmth and moisture but as the hair grows, the nits move off the scalp with the hair.

Because hair grows at a rate of ~ 1 cm per month, the duration of infestation can be estimated by the distance of the nit from the scalp.

70
Q

How does head lice present?

A

Frequently pruritic, associated with posterior cervical LAD, and dermatitis on the posterior neck

71
Q

What is the most common sites to find nits?

A

On the retroauricular and occipital scalp.

72
Q

How can nits be distinguished from hair casts?

A

Hair casts encircle the hair shaft and move freely in contrast to the nit which is cemented to the hair.

73
Q

How is Pediculosis treated?

A

It is prudent to re-treat with topical therapies 7-9 days after initial therapy to kill the newly hatched lice

  • Use OTC permethrin 1% or pyrethrins when resistance is not suspected.
  • 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 using substances such as petroleum jelly and mayonnaise, but study results have been variable.

74
Q

Other parts of pediculosis treatment?

A

All persons living in the home should be examined to avoid re-infestation.

  • Those with live lice or nits within 1 cm of the scalp should be treated.
  • It is prudent to treat family members who share a bed with the person with infestation, even if no lice are found.
  • If it is not possible to examine household members, treat without an exam if the treatment is not contraindicated.
75
Q

Pediculosis: Patient Education

A
  • 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.
76
Q

T or F. Children should not be restricted from attending school because of lice.

A

T.

77
Q

What causes Bed Bugs?

A

Cimex lectularius (most common type) affect people from all racial and socioeconomic groups

78
Q

Describe the transmission of bed bugs

A

Bed bugs may be spread during travel on clothing, bedding, mattresses, and laundry, etc and tend to stay hidden during the day and feed at night

Bites may be multiple in a linear array; referred to as “breakfast, lunch and dinner”

79
Q
A
80
Q

How does a bed bug infestation present?

A

Usually presents as pruritic, erythematous and edematous papules with the appearance and duration of lesions vary depending on the patient’s degree of sensitization (Some individuals have little or no reaction to bedbug bites)

•Common for only one or a few family members (even among those sleeping in the same bed) to report lesions

81
Q

How are bed bugs treated?

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. Bed linens need to be laundered and furniture vacuumed

82
Q

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