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Z Dermatology Clin Med > Eczema and Glandular Disease > Flashcards

Eczema and Glandular Disease Flashcards

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1
Q

Two types of contact dermatitis?

A

irritant and allergic

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2
Q

Which is more common - Irritant or allergic contact dermatitis?

A

Irritant - 80%

Allergic - 20%

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3
Q

Definition of Irritant Contact Dermatitis?

A

Direct contact of the skin when an irritant directly damages the skin

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4
Q

Etiology of Irritant contact dermatitis?

A
  • disruption of normal skin barrier triggers inflammation.
  • almost any material may be a cutaneous irritant with sufficient exposure in time and/or concentration .
  • most common irritants are dry air, water, soap, solvents.
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5
Q

Epidemiology of irritant contact dermatitis?

A
  • Those with light-colored/fair skin are at greatest risk.
  • Occurs at any age, more frequent in elderly who have thinner skin.
  • More common in women due to environmental factors.
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6
Q

Pertinent history of Irritant contact dermatitis?

A
  • sufficient exposure to a cutaneous irritant
  • itching and pain caused by fissuring of skin
  • symptoms occurs within minutes to hours of exposure in acute ICD; symptoms may be delayed by weeks in cumulative ICD
  • common in occupations that involve repeated hand washing or exposure of the skin to water, food materials, and other irritants.
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7
Q

Exam findings for Irritant contact dermatitis?

A
  • erythematous patches, hyperkeratosis (thickening of skin), or fissuring
  • may be well-demarcated (well-defined)
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8
Q

Tx options for irritant contact dermatitis?

A
  • withdrawal of offending agent
  • moisturizers
  • use of bland cleansers instead of soap
  • topical steroids
  • avoid abrasive cleansers that traumatize the skin
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9
Q

Definition of allergic contact dermatitis?

A

Direct contact of the skin with an allergen provokes an immune reaction

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10
Q

Pathophys of allergic contact dermatitis?

A
  • delayed sensitivity reaction to an allergen
  • once an individual is sensitized to an allergen, ACD develops within hours to days of exposure.
  • memory T cells persist in the dermis after ACD clinically resolves.
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11
Q

Epidemiology and common allergens of allergic contact dermatitis?

A

no racial, age, or gender predilection

ACD is 1 of the 10 leading occupational illnesses.

Common allergens: poison ivy/oak/sumac, nickel,dyes, fragrances, cosmetics, rubber, preservatives, formaldehyde (common in clothing), neomycin (antibiotic in neosporin), leather, topical steroids, benzocaine, thimerosol (mercury based preservative)

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12
Q

Pertinent hx for allergic contact dermatitis?

A

intensely itching

rash occurs within 12-48hrs of exposure

ask about profession/hobbies

sx may improve on weekends and holidays

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13
Q

Diagnosis technique for allergic contact dermatisis?

A

patch testing for chronic cases non-responsive to traditional treatment

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14
Q

Treatment options for allergic contact dermatitis?

A

avoidance: sx resolve 2-4wks after exposure stops

topical steroids; oral steroids for severe cases

topical immunomodulators (can be used on more sensitive areas where you wouldn’t want to use steroids-face, eyelids, etc.)

oral antihistamines (avoid topical antihistamines)

wet compresses

phototherapy

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15
Q

What is the most common type of non-scarring hair loss?

A

androgenic alopecia

(male/female pattern baldness)

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16
Q

Male/female exam findings for androgenic alopecia

A

M: bitemporal recession, frontal or vertex thinning, or total hair loss sparing occipital and temporal regions

F: diffuse thinning around the crown

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17
Q

Treatment options for androgenic alopecia

A
  • topical minoxidil solution (Rogaine)
  • finasteride (males only)
  • antiandrogens (females only)
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18
Q

Description of androgenic alopecia cause

A

Combined effect of a genetic predisposition and the action of androgren on the hair follicles of the scalp

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19
Q

Exam findings for alopecia areata

A
  • one or multiple focal areas of smooth hair loss
  • typically involves the scalp, but can affect any area of the body
  • no scarring or atrophy
  • nail pitting may occur in 30% of cases
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20
Q

Ways to treat alopecia areata

A

There is no cure so treatments are aimed at management. Hair is likely to grow back on its’ own, but intralesional steroid injections, corticosteroids, or minoxidil can be used.

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21
Q

Diagnosis of alopecia areata

A

Hx and PE

(a gentle hair pull with reveal 10+ anagen or telogen hairs per pull)

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22
Q

Define Atopic Dermatitis

A

An inflammatory, chronic, pruritic skin disorder

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23
Q

Discuss the pathophysiology of Atopic Dermatitis.

A

Defective barrier of the skin leads to the entry of antigens.

Various antigen react with antibodies to produce increased levels of IgE.

Pts may have genetic predisposition to react to various antigens.

Pts may have defective lipid production.

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24
Q

Discuss the etiology of Atopic Dermatitis.

A

The skin of pts is colonized by Staphylococcus Aureus bacteria.

Sxs may flare in extreme climates, with the interaction of wool, or various food such as soy, eggs, meat, milk or fish.

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25
Q

What is hyperhidrosis and what causes it?

A
  • Sweating in excess of that required for normal thermoregulation (glandular disease)
  • Common, chronic idiopathic condition (no known cause)
  • Could be result of metabolic or neurologic disorder, febrile illness, malignancy, drug side effects​
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26
Q

What pt population is most suseptible to Atopic Dermatitis?

A

8-25% of people worldwide have atopic dermatitis.

The disease is equal among races and genders.

It is more common in children than adults.

Personal or family history of asthma, allergic rhinitis or hayfever.

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27
Q

Common characteristics of hyperhidrosis, including age of onset and location on the body?

A
  • Excessive sweating that impairs daily activities
  • At least 1 episode/wk for 6 months
  • Onset before age 25 (later onset should prompt search for secondary cause, like malignancy or neurological issue)
  • Focal sweating (localized to one area) that stops during sleep
  • Bilateral and relatively symmetric; usually affects axillae, palms, and/or soles
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28
Q

Clinical presentation of Atopic Dermatitis?

A

Xerotic, erythematous, scaly, lichenified, ill-defined plaques and patches.

Incessant pruritis.

More common in fexure folds or creases, but can be present anywhere.

May be associated with Dennie-Morgan folds (see pic), allergic conjunctivitis, or hyperlinear palms.

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29
Q

How is Atopic Dermatitis dx?

A

Clinical presentation, Hx, PE

Can check IgE levels

Allergy testing is not extremely helpful.

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30
Q

Hyperhidrosis dx, tx, prognosis

A
  • Dx based on Hx and PE
  • Tx
    • Topical aluminum chloride (drysol or Xerac)
    • iontonphoresis
    • botulinum toxin
    • anticholineragic or sympathectomy for severe
  • Prognosis: difficult to treat but newer therapies are beginning to offer better prognosis
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31
Q

Atopic Dermatitis Tx?

A

Emollients

Topical Steroids/Immunomodulators

ABx for S. aureus

Oral antihistamines

Humidifier, cotton clothing, avoid bleach or fabric softners, eliminate exacerbating factors, phototherapy.

32
Q

Name this skin condition.

A

Atopic Dermatitis

33
Q

What condition is this?

A

Hyperhidrosis

34
Q

Name the skin characteristic and the disease it is often associated with?

A

Hyperlinear creases of the palms is associated with Atopic Dermatitis.

35
Q

How would you differentiate hyperhidrosis from the other glandular diseases discussed?

A

The other two glandular diseases discussed (hidradenitis suppurativa and miliaria) are related to blockage/occlusion of glands and resulting inflammation, while hyperhidrosis is overproduction/sweating excessively.

Also it appears on palms and soles in addition to axillae

36
Q

Identifiy this skin condition.

A

Atopic Dermatitis.

37
Q

What is the definition of Rosacea?

A

common condition characterized by symptoms of facial flushing and a spectrum of clinical signs including erythema, telangiectasias, and an inflammatory papulopustular eruption resembling acne

38
Q

What skin condition is this?

A

Rosacea

39
Q

What is the etiology and predisposing conditinos of rosacea?

A

Etiology: Unknown, Demodex species may play a role

Predisposing Conditions: harsh climactic exposures; spicy foods, alcohol, hot drinks and emotions; indiscriminate use of steroids

40
Q

What are the clinical features of rosacea?

A

increased vasculature, facial flushing, gritty quality of eyes, facial edema

Erythematotelangiectatic: central facial flushing often accompanied by burning or stinging

Papulopustular: central facial flushing and small erythematous papules and pustules

Phymatous: marked skin thickenings and irregular surface nodularities of teh nose, chin, forehead, ears, and eyelids

Ocular: eye stinging, burning, dryness, irritation with light or grittiness

41
Q

How can you distinguish between acne and rosacea?

A

Rosacea is differentiated from acne by the presence of telangiectasias and lack of comedones.

42
Q

How do you treat rosacea?

A

identify and avoid triggers; suncreen with both UVA/UVB protection; topical or oral antibiotics; NO topical steroids

43
Q

A chronic, suppurative, cutaneous process that results from occlusion of follicles and secondary inflammation of apocrine glands.

A

Hydradenitis Suppurativa

44
Q

What is the typical progression of

A

Dyshidrotic Eczema

Itching at the site and then sudden eruption of small uniform clear fluid filled vesicles on the lateral fingers, palms and/or plantar feet. This lasts about 1-3 weeks. Then they diminsh and the skin desquamates (part of the normal healing process). Frequently relapses.

45
Q

What are some contributing factors for Dyshidrotic Eczema?

A

Atopic personal or family history. Hyperhidrosis. Distal fungal infection causing autoeczematizaiton (Id reaction). Warm sweaty environments. Summer months.

46
Q

How do you treat

A

Dyshidrotic Eczema

Cool wet dressings. Topical steroids. Oral steriods for severe cases. Antihistamines for itching. Phototherapy for refractory cases.

47
Q

The cause of hidradenitis suppurativa is…?

A

Unknown, however, there is increased incidence among obese persons and is thought to start with occluded hair folicles leading to bacterial growth.

48
Q

This is a heat rash of the eccrine sweat glands

A

Miliaria

49
Q

Perioral Dermatitis Definition, Etiology, and Predisposing Factors

A

Def: a papulaopustular facial dermatosis occuring mainly in women.

Etiology: unknown; indiscriminate use of topical steroids can cause symptoms

Predisposing Factors: may be related to topical steroid use, heavy makeup, drooling

50
Q

Communicating, open comedones, papules or abcesses, within intertriginous & inframamillary areas, accompanied by contracted scarring.

This describes…

A

Hidradenitis Suppurativa

51
Q

Pathophysiology of Miliaria

A

blockage of the sweat ducts results in leakage of eccrine sweat into the skin

resident bacteria are thought to play a role

common in tropical environments

52
Q

This is a common condition in neonates, asymptomatic and self limiting, results w/o complications in days

ductal obstruction is most superficial occuring in the stratum corneum

PE would show tiny fragile clear vesicles that occur in crops

A

Miliaria crystallina

53
Q

Perioral dermatitis treatment/patient education

A

*use topical or systemic antibiotics

*explain to patients importance of avoiding topical steroids and to avoid all cosmetics until symptoms clear

54
Q

Initial Tx of hidradenitis suppurativa includes…

A

Generally removing the cause. …weight loss, smoking cessation, cleaning the affected area (antibacterial soaps), and warm compresses.

55
Q

Clinical features of Miliaria Profunda

A

Obstruction occurs at dermal epidermal junction

Occurs from repeated episodes of Miliaria rubra

asympotomatic flesh colored papules

May report increased sweating in unaffected skin

widespread inability to sweat results in symptoms of heat exhaustion

56
Q

what is this skin disorder

A

Miliaria rubra

57
Q

Treatment for Miliaria

A

Remove occlusive clothing, limit activity, provide air conditioning, moving to a cooler climate

topical tx: lotions containing calamine, boric acid, or menthol, cool compress, topical corticosteroids; topical abx

58
Q

Common predispositions for hidradenitis suppurativa include…

A

obesity, smoking, poor hygiene, acne & other bacterial skin infections, immune & hormonal defects.

59
Q

Identify this skin disorder

A

Lichen Simplex Chronicus

60
Q

Lichen Simplex Chronicus Definition

A

LSC: a localized form of lichenification – usually occurring in circumscribed plaques – due to repeated rubbing and scratching.

61
Q

Lichen Simplex Chronicus Pathophysiology

A

Pruritus provokes rubbing that produces clinical lesions, but the underlying pathophysiology is unknown.

62
Q

Lichen Simplex Chronicus Predispositions

A
  • Atopic dermatitis, insect bites, scars, and xerosis (dry skin), are common factors.
  • Anxiety or obsession has been suggested as part of the pathological process of developing lesions.
  • Epidemiology: LSC occurs mostly in mid-to-late adulthood, more common in females.
63
Q

Common Clinical Features of Lichen Simplex Chronicus

A

History:

•pruritus is intermittent; usually more noticeable at rest

  • usually there is a past history of an acute or chronic skin condition
  • scratching is usually an automatic, reflexive habit

Exam:
•common sites include scalp, nape of neck, extensor forearms and elbows, vulva and scrotum, upper medial thighs, knees, lower legs, and ankles
•plaques are slightly erythematous, scaly, well-demarcated, lichenified, firm, and rough with exaggerated skin lines
•hyperpigmentation common

64
Q

Treatment for Lichen Simplex Chronicus

A
  • difficult!! Behavior modification.
  • topical or intralesional steroids
  • doxepin cream or capsaicin cream
  • oral antihistamines
  • occlusive dressings
  • consultation with a psychiatrist may be necessary for patients with severe stress or compulsive scratching.
65
Q

Lichen Simplex Chronicus Prognosis

A

Prognosis: lesions may clear completely. Pruritus may resolve, but some mild scarring and pigmentary changes remain after successful treatment. In patients who do not comply with the treatment regimen and scratching cessation, lesions will not improve and may last for decades.

66
Q

Identify this skin disorder

A

Lichen Simplex Chronicus

67
Q
A
68
Q

What is this?

What is a common name for this?

(I couldn’t get the image from the lecture into this card, so I found a similar picture on the internet… sorry :P ).

A

Seborrheic Dermatitis

or

Dandruff or Cradle Cap in infants

69
Q

What causes Seborrheic Dermatitis?

A

Increased sebum and abnormal immune response to the yeast Pityosporum

70
Q

What are the commonon clinical findings for Seborrheic Dermatitis?

A

Yellowish-red or gray-white, crusty, greasy or dry, scaly patches, usually sharply marginated.

Commonly found in sebum-rich areas: scalp, eyebrows, lashes, pre/post auricular skin, nasolabial folds, chest.

71
Q

Seborrheic Dermatitis has different levels of severity on the scalp; describe these.

A

Mild

Patchy scaling

Widespread, thick adherant crusts

72
Q

Diagnosis for Seborrheic Dermatitis

A

Exam, fungal culture to rule out tinea capitis

73
Q

What is the treatment for Seborrheic Dermatitis?

A

More/frequent shampooing with longer lathering, using shampoos with salicylic acid, tar, selenium sulfide or zinc - use more than one in an alternating schedule.

Treat seborrheic blepharitis with bably shampoo.

Use anti-yeast creams

Topical steroids for acute flare-ups.

74
Q
A
75
Q

perioral dermatitis history and exam findings

A

a papulopustular facial dermatosis occurring mainly in women

History:

•usually asymptomatic
•may have history of topical steroid use, heavy makeup, drooling
Exam:
•erythematous papulopustules that often become confluent
•most often seen on the perioral, perinasal, and periorbital skin

76
Q
A

Z Dermatology Clin Med (18 decks)

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