NR 511 MIDTERM STUDY GUIDE
Dermatology
1. Actinic keratosis most common precancerous skin lesion in light skinned
patients, more common in patients 50 years or older (most common in Celtic, Irish,
and Scottish descent)
Found in sun exposed areas
Caused by skin cells that accumulate from repeated sun exposure
Pathophys: continued sun damage from UV radiation damages the DNA in
epithelial cells
Primary lesions: macules or plaques, poorly circumscribed
Secondary lesion: erythematous and scaly
(May feel like sandpaper when touched)
Not an aggressive form of cancer if/when it changes to squamous cell unless
on the lip
Patient complaints subjective: irritated, rough or scaly rash, pruritus, tenderness or
stinging sensation
Objective findings: reddened, scaly, rough, or uneven surfaces. Hard or spiny
lesion. Sandpaper like texture.
Diagnostic tests: fluorescence using photosensitizing drug (methyl ester of 5-
aminolevulinic acid) over area of concern will have a pink fluorescence with the
wood’s lamp
Treatment: no evidence to support removal of lesion as most will not turn
cancerous however it is standard to REMOVE the lesion(s)
Topical Therapy:
5-fluorouracil (5-FU) cream (Efudex, Carac) applied in a thin layer over the
lesion BID for 3 weeks, avoid eyelids, lips, and folds of the nose. This
, treatment causes red, raw, and painful skin in the areas applied which may
lead to noncompliance. Exposure to sunlight makes this worse
Imiquimod 5% cream used for face and scalp lesions. Applied 3x
weekly for 8 weeks.
Diclofenac 3% in 2.5% hyaluranon gell (Solaraza) applied BIF for 60
to 90 days
Adapalene 0.1%to 0.3% (topical retinoid)applied daily for 4 weeks and then
increased to BID
Side effects of these treatments include redness, itching, rash, and dry
skin
Topical chemotherapy combined with phototherapy with blue or red
wavelength have better cosmetic results than cryosurgery. 2 day course
Cryosurgery tissue is destroyed by freezing using liquid nitrogen.
Hypopigmentation may occur at site of previous lesion
Surgical curettage or shave excision are not considered first line treatments
for actinic keratosis
Surgical biopsy is the only way to obtain an intact sample to be analyzed as a way
to confirm diagnosis
If treatment does not work no matter the choice always refer to
dermatologist
Education is centered around prevention, avoidance of excessive sun exposure, use
of protective clothing, and use of sunscreen.
Should teach patients ABCDE mnemonic
A= asymmetry
B= border irregularity
C= color change
D= Diameter larger than a pencil eraser
,E= elevation from a flat lesion to a raised or evolving lesion
2. Dermatitis
DERMATITIS
ATOPIC DERMATITIS
• Atopic dermatitis (eczema) is not considered a distinct disease entity but is a
descriptive term for a group of skin disorders characterized by pruritus and
inflammation, whose distinct cause is unknown. • Eczemais a more general term
that is often used collectively to describe skin of an erythematous and inflamed
appearance, reflective of a superficial pathological process. Currently, the terms
eczema and dermatitisare often used synonymously in the clinical arena in a
nonspecific sense.
• The use of the term eczematous rash, although also indistinct, may be
helpful both diagnostically and therapeutically, because eczematous dermatitis
may be classified into two major etiological categories—contact dermatitis and
atopic dermatitis.
• Early in its presentation, atopic dermatitis is erythematous in appearance,
with papulovesicular lesions that ooze and crust. At its later stages, the rash
becomes a red-purple color, dries, and develops scaling and lichenification, which
is exacerbated by itching resulting from its highly pruritic nature.
Epidemiology and Causes
• Atopic dermatitis is a constitutional and inherited reaction, which usually
begins in infancy. • Children born to older women are more likely to develop
eczema than children born to younger women.
• Prevalence of atopic disease is now estimated at 1 in 18 or 5.5%, which
amounts to 15 million people in the United States. About 10% of the U.S.
population will have atopic dermatitis at some point in their lifetime.
• Atopic dermatitis presents more severely in childhood. Onset during the first
year of life occurs in up to 50% of all patients; in 85%, onset is before age 5 years.
Up to 5% of all children are affected by atopic dermatitis. Most cases (40%)
resolve by adulthood, however. The remainder of patients with atopic dermatitis
are affected with a chronic course of the disease that is characterized by acute
exacerbation
(often during times of stress) and intermittent remissions.
• No ethnic predisposition has been found for atopic dermatitis, and it occurs
equally in both sexes. • The cause of atopic dermatitis is unknown.
, • Family history is positive for atopy in two-thirds of all cases. Genetic
predisposition may be the most important etiological factor in all-atopic
conditions. A personal or family history of all or part of the
“atopic triad”—asthma, allergic rhinitis, and eczema—is often present.
• It has been proposed that individuals with any of these three conditions have
preferential production of allergen-specific immunoglobulin E (IgE) and that the
presence of such antibodies should be a mandatory criterion for the diagnosis of
atopic dermatitis. Such a diagnostic test, however, only establishes the diagnosis of
atopic syndrome, not atopic dermatitis. Any patient with a history of hives
(urticaria), hay fever, or rashes should be considered to have an atopic
history.
• All atopic individuals seem to have itchier skin, yet what seems to be unique
about the atopic patient's skin is its hypersensitivity.
• Many factors that do not make non-atopic individuals itch will make the
atopic person feel itchy. Atopic patients are known to itch seconds after
experiencing a stressful event. This type of reaction is thought to be caused by
neuropeptide-induced vasodilation, which produces a rise in skin temperature and
erythema.
• Symptoms are triggered or exacerbated through the interaction between
genetic predisposition and environmental factors. Environmental factors that
trigger atopic dermatitis include dust mites, animal dander, pollen, microbes,
pollutants, climate, and emotional stress.
• Excessively hot or cold climates or excessively dry or moist environments
are particularly suitable for setting the stage for the atopic process. Anything that
dries the skin can aggravate symptoms: • Common triggers include excessive
bathing, hand washing, lip licking, sweating, or swimming. • Contact with
irritants such as solvents, detergents, deodorants, tobacco, cosmetics, soap, and
woolen and synthetic fabrics can precipitate an exacerbation of atopic dermatitis.
Heat and sweat may also be aggravating factors for atopic dermatitis.
• Factors that generate an increase in body temperature include hot showers or
baths, overdressing, use of heating pads, and electric blankets.
• Patients with atopy are intolerant of heat, have difficulty with thermal
sweating, and are more likely to develop heat exhaustion. It is thought that
perspiration retention might be a complicating factor in atopic patients.
• Excessive humidity is, therefore, a problem, because it interferes with
normal evaporation of sweat from the body. Improperly fitting clothes can create
Dermatology
1. Actinic keratosis most common precancerous skin lesion in light skinned
patients, more common in patients 50 years or older (most common in Celtic, Irish,
and Scottish descent)
Found in sun exposed areas
Caused by skin cells that accumulate from repeated sun exposure
Pathophys: continued sun damage from UV radiation damages the DNA in
epithelial cells
Primary lesions: macules or plaques, poorly circumscribed
Secondary lesion: erythematous and scaly
(May feel like sandpaper when touched)
Not an aggressive form of cancer if/when it changes to squamous cell unless
on the lip
Patient complaints subjective: irritated, rough or scaly rash, pruritus, tenderness or
stinging sensation
Objective findings: reddened, scaly, rough, or uneven surfaces. Hard or spiny
lesion. Sandpaper like texture.
Diagnostic tests: fluorescence using photosensitizing drug (methyl ester of 5-
aminolevulinic acid) over area of concern will have a pink fluorescence with the
wood’s lamp
Treatment: no evidence to support removal of lesion as most will not turn
cancerous however it is standard to REMOVE the lesion(s)
Topical Therapy:
5-fluorouracil (5-FU) cream (Efudex, Carac) applied in a thin layer over the
lesion BID for 3 weeks, avoid eyelids, lips, and folds of the nose. This
, treatment causes red, raw, and painful skin in the areas applied which may
lead to noncompliance. Exposure to sunlight makes this worse
Imiquimod 5% cream used for face and scalp lesions. Applied 3x
weekly for 8 weeks.
Diclofenac 3% in 2.5% hyaluranon gell (Solaraza) applied BIF for 60
to 90 days
Adapalene 0.1%to 0.3% (topical retinoid)applied daily for 4 weeks and then
increased to BID
Side effects of these treatments include redness, itching, rash, and dry
skin
Topical chemotherapy combined with phototherapy with blue or red
wavelength have better cosmetic results than cryosurgery. 2 day course
Cryosurgery tissue is destroyed by freezing using liquid nitrogen.
Hypopigmentation may occur at site of previous lesion
Surgical curettage or shave excision are not considered first line treatments
for actinic keratosis
Surgical biopsy is the only way to obtain an intact sample to be analyzed as a way
to confirm diagnosis
If treatment does not work no matter the choice always refer to
dermatologist
Education is centered around prevention, avoidance of excessive sun exposure, use
of protective clothing, and use of sunscreen.
Should teach patients ABCDE mnemonic
A= asymmetry
B= border irregularity
C= color change
D= Diameter larger than a pencil eraser
,E= elevation from a flat lesion to a raised or evolving lesion
2. Dermatitis
DERMATITIS
ATOPIC DERMATITIS
• Atopic dermatitis (eczema) is not considered a distinct disease entity but is a
descriptive term for a group of skin disorders characterized by pruritus and
inflammation, whose distinct cause is unknown. • Eczemais a more general term
that is often used collectively to describe skin of an erythematous and inflamed
appearance, reflective of a superficial pathological process. Currently, the terms
eczema and dermatitisare often used synonymously in the clinical arena in a
nonspecific sense.
• The use of the term eczematous rash, although also indistinct, may be
helpful both diagnostically and therapeutically, because eczematous dermatitis
may be classified into two major etiological categories—contact dermatitis and
atopic dermatitis.
• Early in its presentation, atopic dermatitis is erythematous in appearance,
with papulovesicular lesions that ooze and crust. At its later stages, the rash
becomes a red-purple color, dries, and develops scaling and lichenification, which
is exacerbated by itching resulting from its highly pruritic nature.
Epidemiology and Causes
• Atopic dermatitis is a constitutional and inherited reaction, which usually
begins in infancy. • Children born to older women are more likely to develop
eczema than children born to younger women.
• Prevalence of atopic disease is now estimated at 1 in 18 or 5.5%, which
amounts to 15 million people in the United States. About 10% of the U.S.
population will have atopic dermatitis at some point in their lifetime.
• Atopic dermatitis presents more severely in childhood. Onset during the first
year of life occurs in up to 50% of all patients; in 85%, onset is before age 5 years.
Up to 5% of all children are affected by atopic dermatitis. Most cases (40%)
resolve by adulthood, however. The remainder of patients with atopic dermatitis
are affected with a chronic course of the disease that is characterized by acute
exacerbation
(often during times of stress) and intermittent remissions.
• No ethnic predisposition has been found for atopic dermatitis, and it occurs
equally in both sexes. • The cause of atopic dermatitis is unknown.
, • Family history is positive for atopy in two-thirds of all cases. Genetic
predisposition may be the most important etiological factor in all-atopic
conditions. A personal or family history of all or part of the
“atopic triad”—asthma, allergic rhinitis, and eczema—is often present.
• It has been proposed that individuals with any of these three conditions have
preferential production of allergen-specific immunoglobulin E (IgE) and that the
presence of such antibodies should be a mandatory criterion for the diagnosis of
atopic dermatitis. Such a diagnostic test, however, only establishes the diagnosis of
atopic syndrome, not atopic dermatitis. Any patient with a history of hives
(urticaria), hay fever, or rashes should be considered to have an atopic
history.
• All atopic individuals seem to have itchier skin, yet what seems to be unique
about the atopic patient's skin is its hypersensitivity.
• Many factors that do not make non-atopic individuals itch will make the
atopic person feel itchy. Atopic patients are known to itch seconds after
experiencing a stressful event. This type of reaction is thought to be caused by
neuropeptide-induced vasodilation, which produces a rise in skin temperature and
erythema.
• Symptoms are triggered or exacerbated through the interaction between
genetic predisposition and environmental factors. Environmental factors that
trigger atopic dermatitis include dust mites, animal dander, pollen, microbes,
pollutants, climate, and emotional stress.
• Excessively hot or cold climates or excessively dry or moist environments
are particularly suitable for setting the stage for the atopic process. Anything that
dries the skin can aggravate symptoms: • Common triggers include excessive
bathing, hand washing, lip licking, sweating, or swimming. • Contact with
irritants such as solvents, detergents, deodorants, tobacco, cosmetics, soap, and
woolen and synthetic fabrics can precipitate an exacerbation of atopic dermatitis.
Heat and sweat may also be aggravating factors for atopic dermatitis.
• Factors that generate an increase in body temperature include hot showers or
baths, overdressing, use of heating pads, and electric blankets.
• Patients with atopy are intolerant of heat, have difficulty with thermal
sweating, and are more likely to develop heat exhaustion. It is thought that
perspiration retention might be a complicating factor in atopic patients.
• Excessive humidity is, therefore, a problem, because it interferes with
normal evaporation of sweat from the body. Improperly fitting clothes can create
