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Andrews Diseases Of Skin > Chapter 3: Dermatoses Resulting from Physical Factors > Flashcards

Chapter 3: Dermatoses Resulting from Physical Factors Flashcards

1
Q

What are the classes of thermal burns

A

1st degree
2nd degree
3rd degree
4th degree

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2
Q

What is a 1st degree burn

A

An active congestion of the superficial blood vessels, causing erythema that may be followed by epidermal desquamation (peeling).

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3
Q

What is a 2nd degree burn

A

Two types of 2nd degree (Superficial and Deep)

Superficial: transudation of serum from the capillaries which causes edema of the superficial tissues

Deep: pale and anesthetic. Injury to the reticular dermis compromises blood flow and destroy appendages. Healing takes over 1 month and results in scarring.

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4
Q

What is a 3rd degree burn

A

Loss of tissue of the full thickness of the skin, and often some of the subcutaneous tissues.

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5
Q

what is a 4th degree burn

A

Involves the destruction of the entire skin and subcutaneous fat with any underlying tendons

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6
Q

What amount of burns is associated with a poor prognosis

A

Greater than 2/3rds of body surface area

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7
Q

What is an excellent dispersing agent for that facilitates the removal of hot tar from burns

A

Polyoxyetheylene sorbitan in Neosporin ointment or sunflower oil

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8
Q

What is miliaria

A

the retention of sweat as a result of occlusion of eccrine sweat ducts, produces an eruption that is communion hot, humid climates, such as in the topics and during the hot summer months in temperate climates

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9
Q

What effect does staphylococcus epidermadis play in miliaria

A

produces an extracellul polysaccharide substance that induces miliaira

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10
Q

What is miliaria crystallina

A

characterized by small, clear, superficial viesicles with no inflammatory reaction. It appears in bedridden patients in whom fever produces increases perspiration of heat and moisture.

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11
Q

What is miliaria rubra

A

Appear as discrete, extremely pruritic, erythematous papulovesicles accompanied by a sensation of prickling, turning, or tingling.

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12
Q

Where is the site of injury in miliaria rubra

A

the site of injury and sweat escape is in the prickle cell layer, where spongiosis is produced

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13
Q

What is miliaria pustulosa

A

preceded by another dermatitis that has produced injury, destruction, or blocking of the sweat duct.
- pustules are distinct, superficial and independent of the hair follicle

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14
Q

What is miliaria profunda

A

A non-pruritic, flesh colored, deep-seated, whitish papules.

  • Asymptomatic and last only 1 hour after overheating has ended
  • Concentrated on the trunk and extremities
  • Only seen in the tropics and often follows a severe bout of miliaria rubra
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15
Q

What is postmiliarial hypohydrosis

A

results from occlusion of sweat ducts and pores, and may be severe enough to impair an individuals ability to perform sustained work in a hot environment
- sweating may be depressed to half the normal amount for as long as 3 weeks

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16
Q

What is erythema ab igne

A

a persistent erythema - or the coarsely reticulated residual pigmentation resulting from it - that is usually produced by long exposure to excessive heat without the production of a burn
- pigmentation may become permanent, but tends to disappear gradually.

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17
Q

What is the treatment for erythema ab igne

A

emollients containing alpha-hydroxy acids or a cream containing fluocinolone acetone 0.01%, hydroquinone 4% and tretinoin 0.05% may help reduce the pigmentation

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18
Q

What is Acrocyanosis

A

a persistent blue discoloration of the entire hand or foot worsened by cold exposure

  • distinguished from raynauds syndrome by the persistent nature of acrocyanosis
  • May be a sign of malignancy
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19
Q

What is chilblains (pernio)

A

constitue a localized erythema and swelling caused by exposure to cold.

  • blistering and ulcerations may develop in severe cases
  • Occur chiefly on the hands, feet, ears, and face especially in children
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20
Q

What is the treatment for chilblains

A

affected parts should be protected against further exposure to cold or dampness.

  • Nifedipine 20mg TID
  • nicotinamide 500mg TID
  • Sildenafil 50mg BID
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21
Q

What is the treatment for frostbite

A

rewarming in a water bath between 37 and 43 degrees C.

  • Slow thawing results in more extensive tissue damage
  • Analgesics should be administered
  • TPA to lyse thrombi decrease the need for amputation if given within 24 hours of injury.
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22
Q

What are the divisions of the solar spectrum

A

The parts of the solar spectrum important in photo medicine:

  • UV radiation (below 400nm)
  • Visible light (400-760nm)
  • infrared radiation (beyond 760nm)
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23
Q

What are the bands of UV radiation

A 
UVA - 320-400nm
     UVA I - 340-400nm
     UVA II - 320-340nm
UVB - 280-320nm
UVC - 200-280nm
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24
Q

What is MED

A

minimal erythema dose
- the minimal amount of a particular wavelength of light capable of inducing erythema on an individuals skins

  • UVB is up to 1000 times more erythrogenic than UVA, essentially all solar erythema is caused by UVB
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25
Q

How does water, snow, and sand effect UVB

A

Sand and snow reflect as much as 85% of the UVB

80% of UVB is able to penetrate up to 3 feet of water

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26
Q

When is UVB greatest

A

the middle 4-6 hours of the day UVB is 2-4 times greater

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27
Q

What is sunburn

A

Normal cutaneous reaction to sunlight in excess of an erythema dose

  • UVB erythema becomes evident at around 6 hours after exposure and peaks at 12-24. Onset is sooner with greater severity
  • Desquamation is common about 1 week after sunburn even in areas that have not blistered.
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28
Q

How is skin pigmentation effected after sun exposure

A
  1. IPD (immediate pigment darkening)
    - Maximal within hours after sun exposure and results from metabolic changes and redistribution of the melanin already in the skin.
    - IPD is not photoprotective
  2. Delayed melanogenesis
    - Occurs 2-3 days after exposure and lasts for 10-14 days
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29
Q

How is epidermal thickness effected by sun exposure

A

Exposure to UVB and UVA causes an increase in the thickness of the epidermis, especially the stratum corneum.

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30
Q

What is the time period of the highest UVB intensity

A

between 0900 and 1600

- accounts for the vast majority of potentially hazardous UV exposure

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31
Q

What is UPF

A

UV Protection Factor

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32
Q

What is SPF

A

Sun protection factor

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33
Q

What are the key ingredients in sunscreen

A

Chemical Sunscreens

  • p-aminonezoic acid [PABA]
  • PABA esters
  • cinnamates
  • salicylates
  • anthranilates
  • benzophenones
  • benzylidene camphors
  • dibenzoylmethanes
  • tinosorb

Physical Sunscreens

  • zinc oxide
  • titanium dioxide
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34
Q

What type of sun screen is recommended for skin types I-III

A

Daily application of a sunscreen with an SPF of 30 in a facial moisturizer, foundation, or aftershave is recommended

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35
Q

What are the skin types

A

I - [white] Always burns never tans
II - [white] Always burns, tans minimally
III - [white] Burns moderately, tans gradually
IV - [olive] Minimally burns, tans well
V - [brown] Rarely burns, tans darkly
VI - [dark brown] Never burns, tans early black

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36
Q

When should you apply sunscreen

A

20 minutes before sun exposure and again 30 minutes after sun exposure has begun

Sunscreen should be reapplied after swimming and after toweling vigorously

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37
Q

What are ephelides

A

Freckles

  • become prominent during the summer when exposed to sunlight and subside, sometime completely during the winter
  • Usually appear around age 5
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38
Q

What is the difference between ephelides and lentigos

A

Ephelis shows increased production of melanin pigment by a normal number of melanocytes.

The lentigo has elongated rete ridges that appear to be club shaped.

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39
Q

What are dermatoheliosis

A

Characteristic changes induced by chronic sun exposure ; also called photo aging.

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40
Q

What is Favre-Racouchot syndrome

A

Nodular elastoidosis with cysts and comedones occurs the inferior periorbital and malar skin on the forearms or the helix of the ear

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41
Q

What is milian citrine skin

A

The skin becomes atrophic, scaly, wrinkled, inelastic, or leathery with a yellow hue.

The result of chronic sun exposure

42
Q

What is poikiloderma of civatte

A

Associated with chronic sun exposure and refers to reticulate hyper pigmentation with telangiectasia, and slight atrophy of the sides of the neck, and V of the chest
- Men and women in their 30s-40s

43
Q

What is cutis rhomboidalis nuchae

A

[Sailors neck or Farmers neck] Characteristic of long-term, chronic sun exposure.
- The skin on the back becomes thickened, tough, and leathery, and the normal skin markings are exaggerated.

44
Q

What effect does the sun have on connective tissue

A

Sun damages the connective tissue of the dermis, skin fragility is prominent, and patients note skin tearing from trivial injury which leads to an echymosis –> actinic purpura

45
Q

What treatment is available for sun damaged skin

A

Alpha hydroxy acid may improve skin texture when used in lower, nonirritating concentrations.
Topical Tretinoin, adapalene, and tazarotene can improve the changes of photo aging

46
Q

What is chemically induced photosensitivity

A

substances that may induce an abnormal reaction in skin exposed to sunlight or its equivalent

47
Q

What is phototoxicity

A

Increased sunburn response without allergic sensitization

  • occurs on initial exposure
  • onset of less than 48h
  • histologically similar to sunburn
48
Q

What are photoallergic reactions

A

photoallergic reactions are true allergic sensitizations triggered by sunlight, produced either by internal administration (photoallergic drug reaction) or by external contact (photoallergic contact dermatitis)

  • occurs only in sensitized persons
  • may have a delayed onset (up to 14 days)
  • histologically similar to ACD
49
Q

What findings are typically associated with chemicals that induce photosensitivity.

A

Usually resonating compounds with a molecular weight of less than 500.

50
Q

What is phytophotodermatitis

A

Furocoumarins in many plants may cause a phototoxic reaction when they come in contact with skin that is exposed to UVA light.

  • limited to sun exposed areas
  • burning pain begins in 48 hours and marked hyperpigmentation results
  • ie lime juice

Tx–> avoidance of the sun and use of topical steroids immediately after may reduce pigmentation.

51
Q

What is bergapten

A

a component of oil of bergamot that was previously a product found in fragrances, now a rare condition as laws limit its use.

52
Q

What is a polymorphous light eruption

A

Most common form of photosensitivity.
- Clinically: papular (or erythematopapular) variant is the most common, but papulovesicular, eczematous, erythematous ,and plaque-like lesions also occur

  • Scarring and atrophy do not occur
  • A change in the amount of sun exposure appears to be more critical than the absolute amount of radiation.
53
Q

When do lesions appear with PLE

A

1-4 days after sun exposure

54
Q

What is the treatment for PLE

A

avoiding the sun.
Sunblocks should contain specific absorber of long-wave UVA (Parsol 1789, mexoryl, zinc oxide, and titanium dioxide)

  • topical tacrolimus can be used at night, or BID combined with sun protection
  • Antihistamines for pruritus
55
Q

What is actinic prurigo

A

A variant of PLE;

  • typically occur before the age of 10
  • Lesions begin as small papules or papulovesicles that crust and become impetiginized. They are intensely pruritic and frequently excoriated.
  • The Cheeks, distal nose, ears and lower lip are typically involved.
56
Q

Brachioradial pruritus

A

Currently believed to represent a form of neuropathic pruritus, related to cervical spine disease.

PLE may present initially and only on the brachioradial area.

57
Q

How can you identify patients with photosensitivity induced brachioradial pruritus?

A

Apply a high SPF sunscreen to one arm only for several weeks. PLE will improve on the one arm.

Primary neuropathic pain will have minimal to no improvement.

58
Q

How can you identify patients with photosensitivity induced brachioradial pruritus?

A

Apply a high SPF sunscreen to one arm only for several weeks. PLE will improve on the one arm.

Primary neuropathic pain will have minimal to no improvement.

59
Q

What is Solar Urticaria

A

Most common in females aged 20-40

Within seconds to minutes after light exposure, typical urticarial lesions appear and resolve in 1-2 hour, rarely lasting more than 24 hours.

Severe attacks, syncope, bronchospasm, and anaphylaxis may occur.

UVA sensitivity is the most common, but visible light sensitivity

Virtually always idiopathic

60
Q

What testing is available for diagnosis of solar urticaria

A

Phototesting to determine the wavelengths of sensitivity, and to ascertain the minimal urticarial dose (MUD) if UVA desensitization is being considered.

61
Q

What is the treatment for solar urticaria

A

Broad spectrum sunscreens

nonsedating H1 agents (loratadine, cetirizine, fexofenadine) may increase the MUD 10-fold or more.

62
Q

What is the treatment for solar urticaria

A

Broad spectrum sunscreens

nonsedating H1 agents (loratadine, cetirizine, fexofenadine) may increase the MUD 10-fold or more.

63
Q

What is hydroa vacciniforme

A

Within 6 h of exposure stinging begins. At 24 h or sooner erythema and edema appear, followed by the characteristic 2-4 mm vesicles.

Over the next few days the lesions rupture and become centrally necrotic and heal with a smallpox-like scar.

Ears, nose, cheeks, extensor arms, and hands are affected.

64
Q

What is the epidemiology of hydroa vacciniforme

A

A rare chronic photodermatosis with onset in childhood.

Boys = Girls; bimodal (1-7 and 12-16). Typically remits by age 20.

65
Q

What is associated with hydroa vacciniforme-like lesions

A

Lymphoma. Hydroa vacciniforme-like skin lesions may precede the diagnosis of the lymphoma by up to a decade and initially the patient may appear to have hydroa vacciniforme of the self limiting type.

66
Q

What is chronic actinic dermatitis

A

Represents the end stage of progressive photosensitivity in some patients.

Skin lesions consist of edematous, scaling, thickened patches and plaques that tend to be confluent.

67
Q

What can be used for chronic actinic dermatitis

A

maximum sun avoidance.

Tacrolimus may be beneficial in some patients

68
Q

Who is affected by HIV and photosensitivity

A

African American.

Photosensitivity may be initial presentation of HIV

Photosensitivity may be associated with ingestion of a photosensitizing medication, especially NSAIDs or TMP-SMX

69
Q

When do HIV patients experience greater photosensitivity

A

When the CD4 count is below 50, especially in black patients, chronic actinic dermatitis with features of actinic prurigo is typical.

70
Q

What is acute radiodermatitis

A

When an “erythema dose” of ionizing radiation is even to the skin there is a latent period of up to 24 hours before visible erythema appears.

Initial erythema last 2-3 days. May be followed by a second phase that lasts 1 month.

Vesiculation, edema, and erosion or ulceration may occur, accompanied by pain. The skin may develop a dark color that may be mistaken for hyperpigmentation, but that desquamates.

71
Q

Chronic radiodermatitis

A

Telangiectasia, atrophy, and hypo pigmentation with residual focal increased pigment (freckling) may appear.

The skin becomes dry, thin, smooth, and shiny. The nails may become striated, brittle, and fragmented. The capacity to repair injury is substantially reduced, resulting in ulceration from minor trauma.

72
Q

What type of cancers are associated with radiation

A

After a latent period averaging 20-40 years, various malignancies may develop. Most frequent are basal cell carcinoma (BCC) followed by squamous cell carcinoma (SCC).

SCC arising in sites of radiation therapy are more likely metastasize than sun induced SCC.

SCC is common to arms and hands

BCC is common to head, neck and lumbosacral region.

73
Q

What is the treatment of acute radiodermatitis

A

Acute radiodermatitis may be reduced with a topical corticosteroid ointment combined with an emollient cream applied twice a day and instituted at the onset of therapeutic radiotherapy.

74
Q

What is a callus

A

a non-penetrating, circumscribed hyperkeratosis produced by pressure

75
Q

What is a clavus

A

Corn

Corns are circumscribed, horny, conical thickenings with the base on the surface and the apex pointing inward and pressing on subjacent structures.

76
Q

What is the difference between a callus and a clavus?

A

The callus differs from the clavus in that it has no penetrating central core and it is a more diffuse thickening

77
Q

What is the treatment for a callus

A

Padding to relieve the pressure, paring of the thickened callus, and the use of keratolytics such as 40% salicylic acid plasters.

12% ammonium lactate lotion or a urea containing cream is often helpful

78
Q

What are the two varieties of corns?

A
  1. The hard corn: occur on the dorsum of the toes or on the soles
  2. The soft corn: occur between the toes and are softened by the macerating action of sweat.
79
Q

What causes the pain associated with corns

A

It is the core that causes a dull/boring or sharp/lancinating pain by pressing on the underlying sensory nerves.

80
Q

What is porokeratosis planters discreta

A

a sharply marginated, cone-shaped, rubbery lesion that commonly occurs beneath the metatarsal heads. Painful.

Multiple lesions may occur.

3:1 female predominance

81
Q

What are pseudoverrucous papules and nodules

A

These striking 2-8mm, shiny, smooth, red, moist, flat-topped, round lesions in the perianal area of children are considered to be a result of encopresis or urinary incontinence.

Protection of the skin eliminates lesions.

82
Q

What infection is associated with coral cuts

A

Mycobacterium marinum

be concerned for infection in prolonged healing after a coral cut

83
Q

What is a pressure ulcer

A

The pressure sore is caused by ischemia of the underlying structures of the skin, fat, and muscles as a result of sustained and constant pressure

Bony prominence are the most commonly affected site.

95 occur in the lower body: 65% in the pelvic region; 30% in the legs

84
Q

How will a pressure ulcer evolve.

A

The ulcer usually begins with erythema at the pressure point; in a short time a “punched-out” ulcer develops.

85
Q

How are pressure ulcers graded

A

4 stages:

Stage I: Changes in one or more of the following - skin temperature, tissue consistency, and / or sensation

Stage II: superficial ulcer involving the epidermis and / or dermis,

Stage III: damage to the subcutaneous fat

Stage IV: damage to the muscle, bone, tendon, or joint capsule.

86
Q

How are pressure ulcers prevented

A

redistributing pressure at minimum interval of 2 hours.

87
Q

What is the cause of and treatment for the putrid odor of a decubitus ulcer

A

anaerobic organisms.

Topical application of metronidazole eliminates the odor within 36 hours.

88
Q

What is the treatment for friction blisters

A

if the skin is tense and uncomfortable, the blister should be drained, but the roof should not be completely removed as it may act as its own dressing.

89
Q

What is the best way to prevent friction blisters of the feet

A

acrylic fiber socks with drying action have been found to be effective

90
Q

What are fracture blisters

A

Blisters that overlie the sites of closed fractures, especially the ankle and lower leg.

Appear a few days to 3 weeks after injury and are thought to be related to vascular compromise.

Generally heal spontaneously in 5-14 days.

91
Q

What is Mondor’s disease

A

Sclerosing lymphangitis

Lesion is a cordlike structure encircling the coronal sulcus of the penis, or running the length of the shaft, that has been attributed to trauma during vigorous sexual play

92
Q

What is Mondor’s disease

A

Sclerosing lymphangitis

Lesion is a cordlike structure encircling the coronal sulcus of the penis, or running the length of the shaft, that has been attributed to trauma during vigorous sexual play

Results from a superficial thrombophlebitis

No treatment necessary; benign, self limiting course.

93
Q

What is black heel

A

A sudden shower of minute, black, punctate merciless occurs most often on the posterior edge of the plantar surface of one or both heels (sometimes distally on one or more toes).

94
Q

What is the most common cause of subcutaneous emphysema

A

Gas producing organisms, particularly clostridia, and leakage of free air from the lung or GI tract are the most common causes

95
Q

What are painful piezogenic pedal papules

A

Painful fat herniation

A rare cause of painful feet represents fat herniations through thin fascial layers of the weight bearing parts of the heel

96
Q

What is narcotic dermopathy associated with heroin?

A

The result of IV administration is a thrombosed, cordlike, thickened veins at the injection site.

97
Q

What is skin popping

A

subcutaneous injection can result in multiple, scatter ulcerations, which heal with discrete atrophic scars.

98
Q

What is the most common cause of delayed reactions with tattoos

A

Red Tattoos, with the histologic findings typically showing a lichenoid process

99
Q

What elements are associated with tattoo color that can induce a dermatitis?

A

Red: Mercury
Green: Chromium
Blue: Cobalt

100
Q

How is a mercury granuloma identifiable

A

egg-shaped, extracellular, dark grey to black irregular globules. The gold lysis test is positive in tissues

101
Q

What is one of the most common causes of a zirconium granuloma

A

Patient shaving under the arms and using a deodorant containing zirconium

A papular eruption that have lessons that are brownish-red, dome-shaped with shiny papules

102
Q

What is a silica granuloma

A

tattooing of dirt (silica dioxide) during an accident

Andrews Diseases Of Skin (5 decks)

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