Dermatology

Dr. Okon, MD, MRCS

 HISTOLOGY AND PHYSIOLOGY

Divided into the dermis and the overlying
epidermis.

Cellular component of the dermis consists of
fibroblasts, adipocytes, and macrophages.

Acellular connective tissue composed primarily
of type 1 collagen (for strength), elastin (for
flexibility), and glycosaminoglycans.

Dermis is mechanically responsible for
cushioning the body and is also the site of the
skin’s adnexal structures (such as hair follicles),
lymphatics, nerve fibers, and blood vessels.

Epidermis
 Most superficial layer of skin and consists primarily
of keratinocytes arranged as stratified squamous
epithelium.
 Melanocytes, Langerhans cells, and Merkel cells
can also be found in the epidermis.

Layers of epidermis:

Stratum corneum

Stratum granulosum

Stratum spinosum

Stratum basale

Stratum basale
 Deepest layer
 Contains keratinocyte stem cells resting on a
basement membrane. These cells divide and
migrate upward to populate the stratum spinosum,
where keratinization begins.

The skin has two major functions:
 thermoregulation and protection.

Melanocytes
 Epidermal cells that produce melanin
 Also responsible for the color of an individual’s skin.
 Melanocyte activation is under neurohormonal
control of melanocyte-stimulating hormone (MSH)
 Melanin is synthesized from the amino acid
tyrosine.


Langerhans Cells: Dendritic antigen-presenting
cells that populate the dermis and epidermis
 Langerhans cells in the mucosa of the vagina and
foreskin are thought to be the initial target of human
immunodeficiency virus (HIV).

Merkel Cells: Sensory neuroendocrine cells
found in the stratum basale of the epidermis
that communicate with large, myelinated
sensory afferents. They are responsible for fine
touch
 Adnexal Structures

Eccrine Glands: Sweat glands that cover the majority of
the human body and participate in thermoregulation by
secreting hypotonic NaCl for evaporation.
 They are stimulated by cholinergic fibers in the
sympathetic nervous system.

Apocrine Glands: Sweat glands that are found only in the
axillae, genitoanal region, and areolae.
 Activated at puberty and produce a viscous, protein-rich
fluid that takes on its characteristic odor when
metabolized by local bacteria.
 These are vestigial remnants of the mammalian sexual
scent gland and serve no apparent function.

Pilosebaceous Unit: The hair fiber is composed
of keratin that grows directly from the hair
matrix.
 The arrector pili muscle is responsible for
piloerection (“goose bumps,” a vestigial response to
cold).

The sebaceous glands produce sebum, which
oils the skin and hair, preventing them from
drying.

 PATHOLOGY

Primary Lesions

Macule
 Flat lesion < 0.5 cm
 Ephelides (freckles)

Patch
 Flat lesion > 0.5 cm
 Vitiligo
 Melasma

Papule
 Raised lesion < 0.5 cm
 Acne vulgaris
 Rosacea

 
Primary Lesions

Plaque
 Raised lesion > 0.5 cm
 Psoriasis

Vesicle
 Fluid-filled blister < 0.5 cm
 Herpes simplex

Bulla
 Fluid-filled blister > 0.5 cm
 Bullous pemphigoid
 Pemphigus vulgaris

Pustule
 Pus-filled lesion
 Acne vulgaris
 Rosacea

Nodule
 Firm or indurated lesion usually located in the
dermis or subcutaneous fat. May or may not be
raised
 Erythema nodosum

Wheal
 Dermal edema leading to a raised, erythematous,
pruritic lesion lasting < 24 hr
 Urticaria (hives)
 Secondary Lesions

Excoriation
 Trauma to skin caused by scratching. Characterized
by linear breaks in the epidermis
 Scabies

Lichenification
 Thick, rough area with accentuated skin lines;
usually the result of repeated trauma or scratching
 Eczema

Crust
 Dried collection of serum, blood, pus, epithelial
cells, and/or bacteria
 Impetigo (honey-colored crust)

Scale
 Fragment of stratum corneum (keratin) atop or
peeling from the rest of the epidermis. Often
secondary to rapid epidermal turnover
 Psoriasis (silvery scale)

Erosion
 Incomplete loss of epidermis causing shallow,
moist, and well-circumscribed lesion
 Pemphigus vulgaris (secondary to ruptured bullae)

Ulceration
 Complete loss of epidermis with or without
destruction of subcutaneous tissue and fat
 Basal cell carcinoma (may have central ulceration)
 Histologic Terms

Hyperkeratosis
 Thickening of the stratum corneum
 Callus

Parakeratosis
 Thickening of the stratum corneum with persistence of
nuclei (normally absent at this layer)
 Psoriasis

Acanthosis
 Thickening of stratum spinosum
 Acanthosis nigricans

Acantholysis
 Separation of keratinocytes caused by loss of
intercellular cohesion
 Pemphigus vulgaris
 Common Dermatologic Conditions

Acne Vulgaris:
 The formation of a comedone occurs in a four-step
process:

1. Hyperproduction of sebum within a
sebaceous gland.

2. Formation of a plug blocking the
pilosebaceous unit.

3. Inflammatory reaction to Propionibacterium
acnes, an anaerobic bacterium and a
component of skin flora.

4. Follicular wall rupture and spread of
perifollicular inflammation.

Sebum’s exposure to air causes oxygenation of sebum and an
open comedone (blackhead).

Persistent occlusion leads to accumulation of sebum and a
closed comedone (whitehead).

Treatment
 Topical retinoids and/or topical antibiotics, including benzoyl
peroxide.
 Oral doxycycline or tetracycline may be used for moderate
acne.
 Isotretinoin (Accutane) is reserved for nodulocystic acne.

Treatments for hormonal acne (which is characterized by flares
related to menstrual cycles and a jawline distribution)
 oral contraceptive pills and spironolactone.

Rosacea: Clinically distinguish this condition from acne vulgaris.
 Rosacea may cause red papules and pustules on the face
 Age – older than 30 years
 Distinguishing features also include telangiectasias (which blanch),
rhinophyma (a bulbous erythematous nose), and a lack of comedones.

Triggers include extreme temperatures or winds, strenuous exercise, severe
sunburn, and certain foods such as alcohol, caffeinated beverages, and
spicy foods.

Treatment
 Topical antibiotics such as metronidazole or oral antibiotics such as
tetracyclines.
 In a patient older than 30 years with newonset papules and pustules with
strong environmental triggers, think rosacea before acne vulgaris.
 Etiology of rosacea is unclear, but it is thought to be from a pathologic
interaction between the innate immune system and skin microbes.

Lichen Planus: Inflammatory lesions of the skin
of unknown etiology

Sometimes associated with hepatitis C
infection.

6 Ps mnemonic: purple, polygonal, pruritic,
planar, plaques, and papules.

Treatment – high-potency topical steroids.
 May be associated with Wickham’s striae (whitish
lines visible in the papules commonly seen on the
oral mucosa) and Koebner phenomenon (new
lesions that appear along lines of trauma, usually in
linear patterns after scratching)

Pityriasis Rosea: Secondary to a virus, this
dermatologic condition may begin with a virus-
like prodrome and a herald patch—a raised
oval, pink patch with central clearing.
 Appears on the trunk and may be confused with
tinea corporis.
 Herald patch is followed 7 to 14days later by
multiple lesions similar in appearance but smaller.
 They form on the back and follow skin cleavage
lines in a “Christmas tree” pattern.
 No treatment is necessary because the condition is
usually

Keloid: Firm, shiny nodule of scar tissue (type 1
collagen) as a result of granulation tissue (type
3 collagen) overgrowing the boundaries of a
wound.

Overgrow the boundaries of the initial injury,
unlike hypertrophic scars, which are raised
scars that respect wound margins.

Keloids are common in African American
individuals.

Arise over scars but can also develop at sites of
piercings or tattoos

Contact Dermatitis:
 Delayed (type IV) hypersensitivity reaction in which
contact with an antigen recruits previously
sensitized T cells to initiate local inflammation.
 The sensitization can occur at any time after the
initial exposure, even years later.
 Lesions are well-circumscribed, erythematous
plaques that may have vesicles or bullae over the
area of exposure

.

Common allergens include poison ivy, rubber, and nickel. Nickel
can be found in jewelry and buttons, and the distribution of rash
matches the area of contact.

Treatment involves avoidance of the culprit allergen and topical
steroids applied to any affected area.

Systemic steroids may be needed in severe cases. After an
exposure, contact dermatitis often takes days to develop.
Consider a type 1 immunoglobulin E (IgE)–mediated reaction if
development of rash (often urticaria) immediately follows an
exposure (e.g., latex).

Atopic Dermatitis (Eczema): Known as “the itch that rashes” because
symptoms begin as itching that erupts into an erythematous, scaling
lesion.
 Vesicles may be present early, and lichenification occurs if the
area is aggressively scratched. In adults, the distribution is in
flexural areas (antecubital and popliteal fossae) and on the hands.
 The face and body may be affected in children.
 Etiology involves an overlap among genetics, environment, and
the immune system.
 Terms atopic march and atopic triad describe the other
hypersensitivity comorbidities that patients may later develop:
 Eczema → asthma → allergic rhinitis. Treatment of eczema
involves protecting the skin from excessive drying, avoiding
irritants, and applying topical steroids and moisturizers
(emollients).

Urticaria (Hives):
 Pruritic wheals caused by mast cell degranulation spilling histamines
and other inflammatory mediators into the surrounding tissue.
 Acute urticaria (<6 weeks) is often secondary to an environmental
allergy
 Chronic urticaria is thought to be an autoimmune condition.
 Treatment - second-generation H1-antagonists (antihistamines).

Psoriasis:
 Interaction between the environment and genetics (HLA-B27) that
causes a local inflammatory reaction and hastens the growth cycle of the
epidermis, leading to thickened skin from keratinocyte accumulation in
the stratum corneum at affected sites.
 Histologic examination reveals hyperkeratosis and parakeratosis.
Clinically, psoriasis presents as red papules with silvery scales that
coalesce

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into well-defined plaques, often on extensor surfaces (elbows
and knees)

Lesions may develop on sites of previous trauma (Koebner
phenomenon). Removal of the scale will reveal pinpoint
bleeding (Auspitz sign).

Psoriasis can also affect nail beds (pitting) and joints (psoriatic
arthritis).

Treatment - skin lesions involves topical steroids.

Systemic steroids should be avoided because initial
improvement is often followed by a rebound phenomenon upon
tapering.

Severe psoriasis may necessitate stronger agents such as
methotrexate or tumor necrosis factor α inhibitors, including
etanercept and infliximab.

The rash of psoriasis is usually improved with sunlight

Langerhans Cell Histiocytosis (Histiocytosis X): Abnormal
proliferation of histiocytes.

Presents as red papules on the scalp or trunk that may display
crusting or scaling. Painful osteolytic bone lesions of the skull
are also characteristic. Lung nodules may also occur
accompanied by cough.

Skin biopsy will reveal Langerhans cells, which are very large
(about four times larger than a lymphocyte).

Key diagnostic feature is often the presence of Birbeck granules
on electron microscopy—tennis racket–shaped organelles
within the cell
 Autoimmune Diseases

Pemphigus Vulgaris:
 Autoimmune bullous condition caused by IgG antibodies within
the epidermis that attack desmosomes and lead to a loss of
adhesion between keratinocytes (acantholysis).
 Clinical result is the formation of painful, superficial, flaccid,
intraepidermal bullae.
 Bullae may expand on gentle stroking of normal-appearing
adjacent skin (Nikolsky sign) and may rupture, leading to painful
erosions
 Mucous membrane involvement
 Immunofluorescence reveals IgG deposits between keratinocytes.
 Treatment includes use of systemic steroids and supportive
measures to maintain homeostasis (often treated like severe burn
patients).

Bullous Pemphigoid (BP):

Less severe autoimmune condition in which antibodies
attack hemidesmosomes, which connect epidermal basal
cells to the basement membrane.

Binding of complement leads to destruction of the
basement membrane, separation of the dermoepidermal
junction, and the formation of subepidermal blisters.

Creates the appearance of tense bullae and subsequent
erosions at the site of ruptured bullae.

Presents in older adults (>60 years old), and mucous
membranes are rarely involved and

Nikolsky sign is negative.

Often responds to topical steroids alone.
 Conditions of Pigmentation

Vitiligo:
 Autoimmune condition in which antibodies target melanocytes within the
epidermis.
 May occur in any race but is more noticeable in dark-skinned individuals.
 Depigmented areas fluoresce under a Wood lamp (ultraviolet light),
which can help detect depigmentation in light-skinned individuals.
 Vitiligo should not be confused with tinea versicolor, which causes
hypopigmentation, not depigmentation. Key feature: absent
melanocytes.

Albinism:
 Autosomal recessive inability to convert tyrosine into melanin (usually
because of an inherited mutation in or deficiency of the tyrosinase
enzyme).
 Patients have pale skin, white hair, and blue eyes. The risk for skin
cancer is extremely high in these individuals. Key feature: decreased
melanin.

Solar Lentigo:
 Hyperpigmented patches seen in sun-exposed areas such as the face,
chest, and arms, often seen in older patients who have had years of UV-
light exposure.
 Also known as lentigo senilis and “old-age spots.” Although these
lesions are benign, they can develop into a type of melanoma known as
lentigo maligna. Key feature: increased melanocytes.



Melasma:

Estrogen and progesterone stimulate melanocytes during pregnancy or oral
contraceptive use to increase production of melanin. Hyperproduction of
melanin causes formation of hyperpigmented macules and patches on sun-
exposed areas.

Also known as the “mask of pregnancy,”

Treatment is with either makeup to darken surrounding skin, or topical
hydroquinone to lighten the affected areas. Key feature: increased melanin.

Melanocytic Nevus (Common Mole):
 Benign neoplasms of melanocytes that need no
intervention.
 Several different types including junctional,
intradermal, and compound nevi.
 Key feature: increased melanocytes.

Ephelis (Common Freckle):
 Contain normal numbers of melanocytes but
increased concentrations of melanin. Key feature:
increased melanin.
 Freckles have similar histology to the café au lait
spots of neurofibromatosis type 1.
 Neoplasms, Dysplasias, and
Malignancies

Basal Cell Carcinoma (BCC):
 Most common human malignancy.
 BCCs develop in the stratum basale, often as a result of UV-
induced DNA damage.
 Patients present with lesions on sun-exposed areas that are
characteristically pearly nodules with rolled edges.
 Central ulceration and overlying telangiectasias also may be
present.
 Diagnosis can be confirmed with biopsy, which reveals nests
of basal cells demonstrating peripheral palisading.
 BCCs are treated with excision. The prognosis is extremely
good because the risk of metastasis is vanishingly small.
They are locally invasive.

Actinic Keratosis (AK):
 Precancerous, dysplastic lesion characterized by
excessive keratin buildup forming crusty, scaly,
rough papules and plaques.
 Occur in sun-exposed areas such as the face and
scalp and may progress to squamous cell
carcinoma (SCC).
 Diagnosis is based on physical examination,
although lesions suspicious for SCC should be
biopsied. AKs are usually treated with cryotherapy
or topical 5-fluorouracil.

Squamous Cell Carcinoma (SCC):

Patients present with scaling plaques in sun-exposed
areas.

Histologic examination reveals keratin pearls. Lesions are
locally invasive and are more likely to metastasize than
BCCs.

Risk factors include sun exposure, immunosuppression,
arsenic exposure, and chronic draining sinus tracts (e.g.,
from osteomyelitis).

SCCs also have a tendency to grow on areas of scarring;
an aggressive, ulcerative SCC that grows in an area of
previous scarring or trauma is called a Marjolin ulcer.
Erythroplasia of Queyrat is a specific term for SCC in situ
on the glans penis, usually