DIFFERENTIAL DIAGNOSIS

1. Atopic Dermatitis
HISTORY TAKING
Gender? (more common in
female, with ratio of 1.3:1.0)
Small family size?
Increased income and education
both in whites and blacks
Migration from rural to urban
environment
Increased use of antibiotics?
FEATURES OF ATOPIC DERMATITIS
Major Features
1. Pruritus
2. Rash on face and/or extensors
in infants and young children
3. LIchenification in flexural
areas in older children
4. Tendency toward chronic or
chronically relapsing dermatitis
5. Personal or family history of
atopic disease: asthma, allergic
rhinitis, atopic dermatitis
Other Common Findings
1. Dryness
2. Dennie Morgan Folds
3. Allergic shiners
4. Facial pallor
5. Pityriasis Alba
6. Keratosis Pilaris
7. Ichthyosis vulgaris
8. Hyperlinearity of palms and
soles
9. White dermatographism
10. Conjunctivitis
11. Keratoconus
12. Anterior subcapsular catacts
13. Elevated IgE
14. Immediate Skin Test
reactivity

2. Seborrheic Dermatitis
CLUES SUGGESTING SEBORRHEIC DERMATITIS
History Taking
1. Age group? (there are two age
groups involve: infantile, first
three months of life, and adult
form)
(adult form fourth through the
seventh decade of life, peak at
40 years old)
2. Gender? (Male predominance)
3. Season (humidity and
temperature are noted to flare
this disease, especially winter
and early spring)
4. History of facial treatments or
facial trauma (triggers)
5. Medications? (Griseofulvin,
cimetidine, lithium, methyldopa,
arsenic, gold, chlorpromazine,
phenothiazines, haloperidol)
6. Presence of neurologic
disorder? Depression and
emotional stress?
7. Family history? (often
reported, mutation ZNF750
Cutaneous Findings
1. Gray-white or yellow-red skin
discoloration, prominent follicular
openings? (seborrheic stage)
2. If infant, concentrated on the
vertex of the scalp with adherent
yellow-brown, greasy scale,
which can sometimes spread to
the entire scalp, with oozing
crusts?
3. Adult form, seen on the face
with prominent symmetry
particularly medial eyebrows,
forehead, upper eyelids and
nasolabial folds and lateral nares

Microbial effects SD
- the pathogenic role of Malassezia furfur is controversial, number of
yeasts on the skin does not directly correlate with the severity of the
SD; however, clearance of SD with antifungals and recurrence following
cessation of therapy supports the premise that M. furfur is pathogenic
3. Irritant Contact Dermatitis
FEATURES OF IRRITANT CONTACT DERMATITIS
Major Features
Subjective
Onset of symptoms within
minutes to hours of exposure
Pain, burning, stinging or
discomfort exceeding itching
early in the clinical course
Objective
1. Macular erythema,
hyperkeratosis, or fissuring
predominating over vesiculation
2. Glazed, parched or scalded
appearance of the epidermis
3. Healing process begins
promptly on withdrawal of
exposure to the offending agent
4. Patch test is negative
Minor Features
Subjective
Onset of dermatitis within two
weeks of exposure
Many people in the environment
affected similarly
Objective
1. Sharp circumspection of the
dermatitis
2. Evidence of gravitational
influence, such as dripping effect
3. Lack of tendency of the
dermatitis to spread
4. Morphologic changes
suggesting small concentration
differences or contact time
produce large differences in skin
damage

Four interrelated mechanisms:

1. Removal of surface lipids and water holding substances
2. Damage to cell membranes
3. Epidermal keratin denaturation
4. Direct cytotoxic effects
4. Allergic Contact Dermatitis
CLUES SUGGESTING ALLERGIC CONTACT DERMATITIS
History Taking
1. Past history of skin disease?
Atopy?
2. Usage of personal care
products/change in use of
personal care products (soap,
shampoo, conditioner)?
3. Patients hobbies or activities
(school or work) that can be
related to patients current
dermatologic signs and
symptoms?
Cutaneous Findings
1. Localized presentation?
2. Pruritic?
3. Edema, erythema, vesicle
formation?
Oozing papules or plaques?
(Acute phase)
4. Erythema, scaly juicy papules
and weeping?
(Subacute)
5. Scaling, fissuring,
lichenification?
(Chronic)
5. Tinea Corporis
History Taking
Gender? Five times more
common in males
Age?
Wearing of occlusive clothing?
Climate is warm and humid?
Cutaneous Findings

1. Annular lesion with scale

across the entire erythematous
border?
2. is border vesicular? Advancing
centrifugally?
3. Center of the lesion with
clearing?
Dermatophytes can survive solely off of human stratum corneum
which provides a source of nutrition for the dermatophytes
Three main steps: 1. Adherence to keratinocytes; 2. Penetration
through and between cells; 3. Development of a host response
6. Dyshidrotic Eczema
7. Nummular eczema
History Taking
Gender? More common in men
Age? Peak incidence is at 50-65
years old, second peak for
women 15-25 years old;
nummular eczema is rare in
infancy and childhood, peaks at
5 years old
Infection in the upper and lower
respiratory tract (was found to
be associated at 68% of the
time)
Use of isotretinoin and gold? (has
been reported)
Hepatitis C infection, therapy
with interferon alpha and
ribavirin?
Cutaneous Findings
1. Well demarcated coin shaped
plaques form rom coalescing
papules and papulovesicles?
2. Central resolution? Annular?
3. Chronic plaques, dry, scaly,
lichenified?
4. Found in the extensor aspects
of the extremities?
8. Lichen simplex chronicus

History Taking
Age? 30-50 years old
Gender? Females are more
affected
Constant rubbing and scratching
because of an itch?
History of anxiety? Stress?
Depression?
Cutaneous Findings
1. Lichenified, scaly plaque with
excoriations?
2. Hyper or hypopigmentation?
(seen with chronicity)
3. Found in the scalp, the nape of
the neck, the ankeles, the
extensor aspects of the majora,
scrotum?
9. Adenoma Sebaceum
- sebaceous adenomas are rare benign tumors that typically
present on the head and neck of elderly individuals. These tumors
serve as marker for Muir-Torre syndrome
- clinical findings sebaceous adenoma usually presents as a smooth,
well circumscribed slow growing pink, flesh-colored or yellow papule
or nodule measuring less than 0.5cm. the most common location is
the head followed by the neck, trunk and legs
-histopathology: reveal multiple well-circumscribed sebaceous
lobules. Each lobule has two cell populations: peripheral basaloid
germinative cells and mature lipid-filled vacuolated sebocytes in the
center of the lobule
10.

Seborrheic keratosis

History Taking
Family history? ( many
individuals with SKs have a
positive family history of the
condition, expression of the
apoptosis markers p53 and BCL2)
History of viral infection?
Sun exposure?
Age? (common in middle aged

individuals but can arise as early

as adolescence)
Cutaneous Findings
1. Well circumscribed, dull, flat,
tan or brown patches?
2. popular, taking on a waxy,
verrucous or stuck on
appearance?
Seborrheic keratosis is the most common benign epidermal tumor,
usually beginning as a well-circumscribed dull flat, tan or brown
patches with pseudohorn cyts
Histopathologic hallmarks: acanthosis, papillomatosis, pseudohorn
cysts and hyperkeratosis
11.
Melanocytic Nevi
12.
Verrucae
13.
Acrochordons
Acrochordons are pedunculated papules or tumors that are most
commonly located on the eyelids, neck, axillae and groin. There is
familial disposition. Seen mostly in obese individuals, sometimes with
overlying acanthosis nigricans. Usually asymptomatic but can be
irritated or necrotic.
14.
15.

Follicular Hamartomas
Solar Lentigo

History Taking
Age? (prevalence is directly
correlated with increasing age,
over 60 years old)
Sunburns easily and do not tan?
Use of tanning bed?
Great sun exposure?
Fair skinned?
Cutaneous Findings
1. Pigmented macule on skin
exposed to natural sunlight or
artificial sources of UVR?
2. Size: may be tiny (<1mm) or
large with a tendency to
confluence in severely sun
damaged skin and with smooth
or irregular outlines

Solar lentigines are thought to represent a marker of intermittent high

intensity UVR, cumulative UVR, and or unique susceptibility to the
proliferative, stimulatory and or mutagenic effects of UVR. Pronounced
link between UVR exposure and the development of lentigines
16.

Lichen Planus

History Taking
Age? (usually between 30-60
years old)
History of infection? Amoebiasis,
chronic bladder infection,
Hepatitis c, HPV? (not supported
by clinical evidence but
mentioned in Fitzpatrick)
Low grade chronic exposure to
gold or other chemicals?
Common inducers (Gold salts,
beta blockers, antimalarials,
diueretics, penicillamine)
LP by contact (color film
developers, nickel, gold)
Cutaneous Findings
1. Erythematous to violaceous,
flat topped, polygonal papule?
2. Fine, whitish puncta or
reticulated networks (Wick-ham
striae)?
3. Spread from onset is within 14 months?
4. Symmetric distribution?
5. Involved are flexural areas of
the wrists, arms and legs?
6. Face is spared? (usually
spared)
7. Pruritic (usually yes)

NOTES
Biology of the Sebaceous Glands
- Sebaceous glands are unilobular or multilobular structures that
consist of acini connected to a common excretory duct, which is
composed of stratified squamous epithelium
-Sebaceous glands are composed of lipid producing sebocytes and
keratinocytes that line the sebaceous ducts and are usually
associated with a hair follicle
Cells progress toward the middle of the gland and accumulate lipid
droplets as they terminally differentiate
SG are associated with hair follicles all over the body
A sebaceous gland associated with a hair follicle is termed a
pilosebaceous unit

Glands may be found in some nonhairy sites such as the eyelids

(Meibomian), the nipples (Montgomery), and around the genitals
(Tyson glands)
Only palms and soles are devoid of sebaceous glands
The largest glands and greatest density of the glands are located on
the face and scalp
Embrogenesis and Morphogenesis
SG develop in the 13-16th week of gestation from bulges (epithelial
placodes) on the developing hair follicles
Physiology
Holocrine secretion the SG exude lipids by disintegration of entire
cells, a process known as holocrine secretion. The life span of a
sebocyte from cell division to holocrine secretion is approximately
21-25 dys
Human sebum, as it leaves the sebaceous gland, contains squalene,
cholesterol, cholesterol esters, wax esters, and triglycerides
During passage of sebum through the hair canal, bacterial enzymes
hydrolyze some of the triglycerides so that lipid micture reaching
the skin surface contains free fatty acid and small proportions of
mono and diglycerides
(sa internal organs, no wax and little squalene)
Sapienic acid is the major fatty acid of adult human sebum
Precise function of sebum in humans is unknown
It has been suggested that sebum reduces water loss from the skin
surface and functions to keep skin soft and smooth
SG require androgenic stimulation to produce significant quantities
of sebum
Isotretinoin is the most potent pharmacologic inhibitor of sebum
production
Significant reduction in sebum production can be observed as early
as 2 weeks
Acne vulgaris
Acne is a self limited disorder of the pilosebaceous unit that is seen
primarily in adolescents
Mild degrees of acne are frequently seen at birth, probably resulting
from follicular stimulation by adrena androgens, and may continue
into the neonatal period
Acne often herals the onset of puberty
Etiology and Pathogenesis
1. Follicular epidermal hyperproliferation
a. Results in the formation of a microcomedo

b. Epithelium of the upper hair follicle, the infundibulum,

becomes hyperkeratotic with increased cohesion of
keratinocytes
c. Excess cells and their tackiness results in a plug in the
follicular ostium
d. This plug then causes downstream concretions of keratin,
sebum and bacteria to accumulate in the follicle
e. These packed concretions cause dilation of the upper hair
follicles producing a microcomedo
f. Stimulus is unknown but proposed are androgen
stimulation, decreased linoleic acid, increased interleukin
1 activity and effects of P. acnes
2. Excess Sebum production
a. Patients with acne produce more sebum than those without
acne, although the quality of the sebum is the SAME
b. Components of sebum triglycerides and lipoperoxides
may play a role in acne pathogenesis
c. Triglycerides are broken down into free fatty acids by P.
acnes
d. These free fatty acids promote further bacterial clumping
and colonization, incite inflammation and may be
comedogenic
3. Inflammation
a. Extrusion of the keratin, sebum and bacteria into dermis
results in a brisk inflammatory response, the predominant
cell type within 24 hours of comedo rupture is the
lymphocyte
b. CD4 lymphocytes are found around the pilosebaceous unit
c. CD8 are found perivascularly
d. One to two days after comedo ruptre, the neutrophil
becomes the predominant ell type
e. Dermal inflammation may precede comedo formation (?)
4. Presence and activity of P. acnes
a. P. acnes is a gram positive, anaerobic and microaerobic
bacterium found in the sebaceous follicle
b. Cell wall of P. acnes contains a carbohydrate antigen that
stimulates antibody development
c. P.acnes also facilitates inflammation by eliciting a delayed
type hypersensitivity response and by producing lipases,
proteases, hyaluronidases and chemotactic factors
d. It also has been shown to stimulate expression of cytokines
by binding to TLR-2 on monocytes -> after binding, pro
inflammatory cytokines such as IL-1, IL-8, IL-12 and TNF-a
are released.
Four types of Acne Scars

1. Ice pick narrow deeps scars that are widest at the surface of e
sin and taper to a point in the dermis
2. Rolling shallow, wide sars that have an undulating appearance
3. Boxcar wide sharply dermarcated scars
4. Hypertrophic
Cutaneous lesions
- primary site of acne is the face and to a lesser degree the back, chest
and shoulders
- lesions may either be noninflammatory on inflammatory
- non inflammatory lesions are comedo which may either be closed or
open
- inflammatory lesions vary from small papules with a red border to
pustules and large, tender, fluctuant nodules
Treatment for acne vulgaris
Mild - with topical retionoid
Moderate TR plus topical antimicrobial
Severe- oral antibiotic + TR
Conglobata/Fulminans oral isotretinoin and or oral corticosteroids
Pressure Ulcers
-common in the elderly, especially those over the age of 70, in patients
who have had surgery for hip fracture and in patients with spinal cord
injury
- majority of pressure ulcers occur on the lower parts of the body, 65%
in the pelvic area and 30% on the lower limbs
etiology and pathogenesis
- main etiologic factors pressure, shearing forces, friction and
moisture
- normal tissue pressure is 12-32 mmHg, pressures higher than this
upper limit can compromise tissue circulation and oxygenation
- when a patient lies immobile on a hospital bed, pressures as high as
150 mmHg can be generated specially on bony prominences
- at pressures of 70 mmHg, there is an inverse time-pressure curve
with rapid ulcer formation
- duration as well as degree of pressure is important
- shear force results from the motion of bone and subcutaneous tissues
relative to the skin when the skin is fixed
- friction is the force that resists the relative motion between two
surfaces that are in contact; this cause damage to the superficial
layers of the skin

- a moist environment from urinary or fecal incontinence, perspiration,

or excessive wound drainage can cause maceration of the skin, which
increases the risk of pressure ulcer formation