10 Patho Skin Pathology

PATHOLOGY
SKIN PATHOLOGY
P.B. CASUELA, M.D.
November 8, 2018
TABLE OF CONTENTS Skin cancer: most common cancer (epithelium of

•
I. Normal Skin and Common Skin Disorders breast and lungs)
A. Introduction 1 • Overt nature of skin disease may have profound
Layers of the skin impact on the quality of life (aesthetics)
-Epidermis
• Plenty of opportunities to improve a patient's physical
-Dermis
-Hypodermis and psychological well-being
B. Diagnostic approach in dermatosis 3 • Most superficial lesions are priority for treatment
C. Schematic Presentation of dermophologic patterns of skin Common Manifestations of Skin Disorders
disease 3 • Discomfort, depression, disfigurement, disablement,
D. Dermophologic patterns of skin disease 3
1. Dermatitis death
- Acute dermatitis 4 Major Functions of the Skin⌘
- Chronic dermatitis 7 1. Protection against physical factors –trauma,
2. Blistering Disease 12 temperature, UV light of the sun
3. Folliculitis 14
4. Vasculitis 15
2. Control of body temperature
5. FIbrosing Dermatitis 16 3. Hematopoetic organ, intrauterinely
6. Panniculitis 17 4. Endocrine function (synthesis of Vitamin D, which is
II. Common tumors of the Skin “powered” by sun exposure)
A. Primary tumors: Epithelial Tumors
1. Benign epithelial tumors 18
2. Precancerous Lesions and conditions 20 Layers of the Skin
3. Malignant lesions 21 The skin has three main layers from superficial to deep:
B. Primary tumors: Sweat glands and related tumors
• Epidermis
1. Benign 23
2. Malignant 23 • Dermis
C. Primary tumors: Tumors and lesions of the melanogenic system • Hypodermis
1. Common melanocyte nevi 23
2. Malignant melanoma 24
D. Migrant Tumor
1. Migrant Cells 26
2. Mycosis Fungoides 26
3. Lymphoma 26
E. Secondary/metastatic tumor 27
F. Most useful stains in dermatopathology 27
Textbook Must know Previous Trans/Notes

© ★ ⌘
I. NORMAL SKIN AND COMMON SKIN DISORDERS
A. Epidermis
A. INTRODUCTION
• Continuously proliferating stratified squamous
Rudolph Virchow epithelium which produces keratin
• Described the skin as a mere protective covering for • Thinnest layer (8-15 cell layer) ⌘
more delicate and functionally sophisticated internal • Most important part of the skin ⌘
viscera o Because the epithelium serves the major
Ferdinand Ritter Von Hebra function of the organ
• Considered as the Father of Modern Dermatology • Where majority of the skin disease is found ⌘
• First to classify skin diseases by structural alterations

(the foundation of present-day classification) 1. Layers of the Epidermis
Why study skin disorders? Stratum Corneum
• Largest organ; greatest number of diseases
[JKFC, ZYGA] ABELEDA, K., ABELON, K., ABILA, K., ABRENICA, C., ALER., N. 1 of 27
SKIN PATHOLOGY
• Flattened, horny plates of keratin (cytoplasm replaced *Basal Cell:Melanocyte Ratio

by keratin) – approximately 10:1
• Devoid of nuclei Dendritic • Immunologic
• Orthokeratosis – normal basket weave appearance of cells • Protective cells that work with the
this layer seen in normal skin (expect in thick skin) (Langerhans immune system to fight invaders
Stratum Lucidum cells in the (process and present antigen to
• Wavy, thin, light-staining clear zone interposed epidermis) activate the immune system)
between the stratum granulosum and the stratum • Found throughout the epidermis
corneum Merkel cells • Sensory receptors for touch
Stratum Granulosum • Found in the lowest levels of the
• Characteristic of the skin, not found in any other epidermis
epithelium of organs • Merkel cell carcinoma (only
• Keratinocyte acquired dense basophilic, keratohyaline known pathology, 4th most
granules common cancer) ★
Stratum Spinosum
• Majority of the epidermis B. Dermis
Stratum Basale • Composed of collagen and elastin fibers embedded in
• Single layer of cuboidal or low columnar cells bound scanty amounts of acellular ground substance
to the basal lamina • Contains skin appendages, the vascular supply of the
Basement membrane
skin and nerves, and sensory nerve endings
• Semipermeable membrane
• Attachment of the epidermis
• Underneath of the basement membrane are the superficial
1. Layers of the Dermis
plexus, blood vessels, and lymphatics Subdivided into:
o Site of the start of inflammation mechanism in the o Papillary Dermis
skin ▪ Thin, superficial layer immediately underneath
Cells of the Epidermis the epidermis
Basal cells • Immortal cells ▪ Composed of loose connective tissues and
elastic fibers, the latter are lost in aging resulting
• Turn-over time basal cells become
in wrinkling of skin in the aged
squamous epithelial cells is o Reticular Dermis
approximately 30 days ▪ Composed of collagen fibers
Keratinocytes • Mortal cells ▪ Deeper and relatively thick layer
(Squamous • Produce keratin, the protein that
epithelial endows skin with its protective 2. Other Structures in the Dermis
cells) properties Superficial/ Subpapillary plexus
• Most numerous cells in the • Blood vessels found at the junction between papillary
epidermis and reticular dermis
• Tightly adherent to each other • Where vasculitis occurs
through desmosomes
Deep Plexus/ Cutaneous plexus
• Produce cytokines, that regulate • Blood vessels found at the junction of dermis and
the cutaneous environment as subcutis
well as antimicrobial defensins Neurovascular Elements
• Undergoes maturation, Adnexa (Appendages)
senescence, atrophy, and • Mainly occupy the dermis and variably the superficial
subcutis
desquamation
• Arise as downgrowths from the epidermis into dermis
Melanocytes • Spider-shaped cells that produce
during embryological development
melanin, a (brown) pigment that
A. Hair follicle
gives skin its color and absorbs
B. Nails
and protects against potentially
C. Eccrine glands
injurious UV radiation in sunlight • Regulate body temperature
• Found in the lower level of the • Greatest number in palms and soles
epidermis • Separated by interstitial stroma
SKIN PATHOLOGY
• Very rare to have cancer of the gland > 2mm

• Fusion of gland = sign of malignancy Additional from Robbins
1. Sweat glands: Simple glands 10. Cyst Encapsulated cavity or sac lined with true
epithelium
2. Sebaceous glands: Absent in palms and soles
11. Scale Dry, horny, platelike excrescence; usually
• Majority are associated with hair follicles
the result of imperfect cornification
3. Apocrine gland: Gives odor
12. Wheal Itchy, transient, elevated lesion with variable
• Lecture: All glands are under eccrine glands blanching and erythema formed as the
• Wheaters: Only sweat glands result of dermal edema
13. Traumatic lesion breaking the epidermis
C. Hypodermis Excoriation and causing a raw linear area (i.e., deep
scratch); often self-induced
• Layer of loose connective tissue which varies from
14. Thickened, rough skin (similar to a lichen on
areolar to adipose in character Lichenification a rock); usually the result of repeated
• Composed of fat lobules rubbing
o a.k.a. subcutis or panniculus 15. Oncholysis Separation of nail plate from nail bed
B. DIAGNOSTIC APPROACH IN DERMATOSES C. SCHEMATIC PRESENTATION OF

• Microscopical diagnosis of inflammatory skin conditions is DERMOPHOLOGIC PATTERNS OF SKIN
based partly on the: DISEASES
o Distribution type of the inflammation
Arranged from superficial to deep:
o Type of cells involved in the reaction: Keratinocytes,
granular cells, basal cells, melanocytes, Langerhans
cells & Merkel cells
• First step is to identify the primary lesion
• If complicated lesion (ex: with infection) treat infection
first before starting the dermapathologic treatment
D. DERMOPHOLOGIC PATTERNS OF SKIN DISEASES

• Acute Dermatitis
• Chronic Dermatitis
PRIMARY LESION (Termed MACROSCOPIC LESIONS • Blistering Diseases
in Robbins) • Folliculitis
• All Descriptions from Robbins
• Vasculitis
1. Macule Circumscribed, flat discoloration of the skin
<5mm • Fibrosing Dermatitis
2. Patch Circumscribed, flat discoloration of the skin • Panniculitis
>5mm
ACUTE DERMATITIS
3. Papule Elevated dome shaped or flat-topped
lesion, usually erythematous <5mm • In general, acute lesions last from days to weeks ©
4. Plaque Elevated flat topped lesion, usually • Characterized by infiltrates (usually composed of
erythematous >5mm lymphocytes and macrophages rather than
5. Nodule Deep elevated dome shaped or flat topped
neutrophils), edema, and variable degrees of
lesion reaching up to the subcutaneous
layer >5mm epidermal, vascular, or subcutaneous injury ©
6. Vesicle Elevated lesion containing fluid <5mm • Most common presentation: spongiosis (intercellular
(Blister) edema found in between epithelial cells)
7. Bullae Elevated lesion containing fluid >5mm
• Spongiotic Dermatitis
(Blister) • Flaccid if superficial; Tense if
subepidermal
Blister is the common term for either
Vesicle & Bullae
8. Pustule Elevated lesion, discrete pus filled lesion
9. Tumor Solid, well demarcated elevated lesion
SKIN PATHOLOGY
o Seen in most Acute Dermatitis

o Cells become separated from one another
▪ Separation is reflected by the clear
areas amongst them (green arrows)
▪ In normal: cohesive polyhedral
cells; closely attached to one
another through intercellular
bridges
o Can produce blisters if left untreated
ACUTE ECZEMA DERMATITIS

• Gk word eczema, meaning “to boil over,” vividly
describes the appearance of acute eczematous
CONTACT DERMATITIS
dermatitis – one of the most common skin disorders
• May be caused by:
• Can be subdivided, based on initiating factors:
o Allergens (plant, pollen, chemicals)
o Allergic contact dermatitis (will be
o Photoallergic drug reaction
elaborated later)
o Phototoxic drug reaction
o Atopic dermatitis
o Erythema multiforme – systemic
o Drug-related eczematous dermatitis
manifestation (will be discussed later)
o Photoeczematous dermatitis
• Clinical Presentation:
o Primary irritant dermatitis
o Pruritic MACULO-PAPULAR LESIONS
o Presence of blisters/vesicles
PATHOGENESIS:
o Point of maximal contact with infections will
• Eczematous dermatitis typically results from T
show the biggest and the most number of
cell-mediated inflammatory reactions (type IV
lesions. As it goes to the periphery, it
hypersensitivity). The subsequent pathogenesis is
decreases in size and number
attributed to cytokine release by recruited
memory cells and nonspecific accumulation of
additional inflammatory cells. UV exposures and
neuropeptides released near the epidermis can
affect Langerhans cell function.
HISTOLOGICAL PRESENTATION:
• Presence of blisters/vesicles intraepidermally
(orange)
• Prominent eosinophil with edema in the papillary
dermis (red)
SKIN PATHOLOGY
• Prominent loosening of the stratum corneum: basket

“weave” hyperkeratosis
ERYTHEMA MULTIFORME
• Uncommon self-limited hypersensitivity reaction to certain
infections and drugs
• Affects individuals of any age
• Associated with the following conditions:

o Infections (herples simplex, mycoplasmal
INSECT/ARTHROPOD BITE
infections, histoplasmosis, coccidiodomycosis,
typhoid, and leprosy, among others;
• Assumes a “wedged shaped” or triangular dermatitis
o Exposure to certain drugs (sulphonamides,
(blue arrow)
penicillin, barbiturates, salicylates, hydantoins,
o Base: at the superficial portion
and antimalarials)
o Apex: deeper, may show the sting of the
o Cancer (carcinomas and lymphomas);
insect
o Collagen vascular diseases (lupus erythematosus,
• Vesicle formation (green arrow)
dermatomyositis, and polyarteritis nodosa)
• Presence of eosinophils (yellow arrow)
PATHOGENESIS:
• Characterized by keratinocyte injury mediated by skin-
homing CD8+ cytotoxic T lymphocytes. The etiology
shares similarities to other immunologic cutaneous
disorders (e.g., graft-versus-host disease and skin
allograft rejection). Epithelial cells are injured by skin-
homing (CLA+) CD8+ cytotoxic T cells (CTLs)
responding to as yet uncharacterized antigens; these
cells are prominent in the central portion of lesions,
URTICARIA
whereas CD4+ T cells and Langerhans cells localize to
the raised erythematous periphery. • Hives
• Common disorder of the skin
• Characterized by localized mast cell degranulation and
resultant dermal microvascular hyperpemeability
• Combination of these effects produces pruritic
edematous plaques called wheals
• Most often occurs between ages 20 and 40 (all age
groups are susceptible
SKIN PATHOLOGY
• Individual lesions develop and fade within hours

(usually <24 hours), episodes may last for days or
persist for months
• Sites of predilection: any area exposed to pressure
PATHOGENESIS:
• Urticaria is most commonly the result of antigen-
induced release of vasoactive mediators from HISTOLOGICAL PRESENTATION:
mast cells but there are other less common • Malassezia furfur (An-an)
causes as well o Due to superficial infection in those who
sweat easily or have poor hygiene
o Branching hyphae with round budding
spores: spaghetti meatball morphology
(Yellow)
• Candidiasis: Non dermatophytes

o Can also produce superficial infection of
the dermis
o Pseudohyphae (bamboo appearance)
o Bud out spores: can be mistaken as RBC
FUNGAL INFECTIONS (DERMATOPHYTES)

• Fungal infection of the skin attributed to poor hygiene
• >90% fungal infection is confined in the stratum
corneum
• “Best imitator”
• Rule out “fungal infection” first before diagnosing
cancer SCABIES
• Periodic Acid Schiff (PSA) • “The burrow”
o Used to augment appearance of fungi • Vernacular: “Galis aso”
• Communicable: Infestation of Sarcopotes scabiei
CLINICAL PRESENTATION: mite under the skin
• Maculopapular lesions (“circinate lesion”) • Largest parasite demonstrable within stratum
corneum
• Common in people in the lower socio-economic
group
• Treat everyone in the family or else becomes a
“ping-pong disease”
• Will recur if everybody is not treated
SKIN PATHOLOGY
CLINICAL PRESENTATION:
• Maculopapular pruritic lesions of the webs of the
fingers, folds in the inguinal area or gluteal fold
• Confined to the stratum corneum
• Large parasite often calcified (blue arrow)
• Parakeratosis, hyperkeratosis, acanthosis

• Irregular elongation of the rete ridges
• Epidermis becomes irregularly capillary (hyperplastic
but irregular)
• Stratum corneum: Compact orthohyperkeratosis
(green arrow)
o NOT basket weave in comparison to Acute
Dermatitis
CHRONIC DERMATITIS
• Peculiar scar tissue/fibrosis: vertically arranged
• This category includes inflammatory skin disorders (orange arrow)
that persist for many months to years o Normally fibroblast are intermingled/
• Skin surface is roughened as a result of excessive or interlacing in papillary dermis
abnormal scale formation and shedding • No atypia of cells (do not be confused with squamous
• Presence of multinuclear cells and fibrosis cell carcinoma)
• Mononuclear cell infiltrates
• S. corneum becomes compact – orthohyperkeratosis
SEBORRHEIC DERMATITIS
LICHEN SIMPLEX CHRONICUS
• Vernacular: Balakubak
• Most common effect of chronic inflammation • More common than psoriasis (affecting up to 5% of
the general population)
• Common site: hairline (regions with a high density of
sebaceous glands)
• Associated with the inflammation of the epidermis
and is not a disease of the sebaceous glands per se
• Characterized by production of dandruff
• Risk factors: genetics, poor hygiene, and chronic
debilitating diseases such as diabetes mellitus
• Lichenification (yellow arrow) • From birth to elderly in the scalp to other parts of the
o Skin markings will be effaced body
o Instead of diamond shaped, these are
webbed like thicker markings that become PATHOGENESIS:
linear, indurated and darkened in color • Although the precise etiology is unknown,
o Result of chronic scratching
increased sebum production in response to
o Not good for protection. It is a complicated
androgens (or due to dopamine deficiency in the
skin lesion.
• Thickened plaques case of Parkinson patients) is likely contributory.
• Patients usually have a background of contact Nevertheless, sebum overproduction may be
dermatitis or atopic dermatitis necessary but not sufficient to cause the disorder.
HISTOLOGICAL PRESENTATION: Thus colonization of the skin by certain fungal
species of the genus Malassezia is also implicated.
A severe form of seborrheic dermatitis is also seen
in many human immunodeficiency virus (HIV)-
infected individuals with low CD4 counts.
SKIN PATHOLOGY
• Characterized by elongated epidermal hyperplasia

• Mild spongiotic dermatitis
• Parakeratosis
o Implies persistence of nuclei in the superficial layer
o Due to more rapid transit time of squamous cells
• Moderate acanthosis • Compact Hyperkeratosis (yellow arrow)
• Regular elongation of rete ridges • Regular finger-like/test-tube-like elongation of rete
ridges (orange arrow)
• Lymphocytic exocytosis
• Thinned-out epidermis overlying the papillary dermis
o WBC will exit and go up the epidermis, destroy the (red arrow)
basement membrane, penetrate the epidermis:
Epidermidization; you will see neutrophils in the BASIS OF THIS IMMUNE DISEASE:
epidermis • Phenomenon of exocytosis or epidermidization of
• Mild dermal mononuclear cell infiltrates lymphocytes
• Pathogenesis/ Journey of Lymphocytes
o Lymphocytes arise from the superficial plexus and travel
outward to invade the basement membrane, epidermis
up to the stratum corneum.
• Journey will cause:

1. Thinning out of epidermis
o Auspitz sign:
▪ Clinical test for this condition: Bleeding due
to pinching of the psoriatic lesion
▪ Historically, Auspitz is a place in Germany
wherein the Jews were murdered and
experimented on
2. Formation of abscess
Psoriasiform Dermatitis
• Common disease of the Caucasians (but there are also
many cases in the Philippines)
• Seen in Psoriasis
• Immune disease induced by excessive sun
exposure
• More common in Black people
• Erythematous maculopapular lesions on top (due to
orthokeratosis)
• Usually in extensor surfaces such as the elbow, knee,
inguinal area, gluteal area, and hairline
o Kogoj’s Microabscess (green arrow)

▪ In the Stratum spinosum/ prickle
cell layer
▪ (Spongiform pustules)
o Munro’s Microabscess (orange arrow)
▪ In the stratum corneum
• Differential diagnosis: Mycosis fungoides
SKIN PATHOLOGY
o Cancer of skin due to lymphocyte • Itchy, plateau like lesion (green arrow) with spider
o Also presents with Microabscess grayish/ silvery linear streaks called Wickham’s striae
(yellow arrow)
LICHEN PLANUS
• “Pruritic, purple, polygonal, planar, papules, and HISTOLOGICAL PRESENTATION:
plaques” are the tounge-twisting “six Ps” of lichen
planus, a disorder of skin and mucosa
• Vernacular: “Bakokang”
• Usually self-limited, most commonly resolving
spontaneously 1 to 2 years after onset leaving a residuum
of postinflammatory hyperpigmentation
• Koebner phenomenon
• Immune disorder characterized by prolonged exacerbation
and remission
PATHOGENESIS:
• The pathogenesis of lichen planus is not known. It is
Left Photo:
plausible that expression of altered antigens in basal
• Sawtooth squamous hyperplasia (orange arrow)
epidermal cells or the dermoepidermal junction elicit a
• Granular cell hyperplasia (green arrow)
cell-mediated cytotoxic (CD8+) T cell response. In
• Hyperkeratosis
support of this notion, T-lymphocyte infiltrates and
• Both squamous cells and stratum granulosum undergo
hyperplasia of Langerhans cells are characteristic
sawtooth hyperplasia
features of this disorder.
• Although the basement membrane is intact, the area
immediately underneath the epidermis form a belt of
inflammation (Lichenoid inflammation)
Right Photo:
• Interface Vacuolar Degeneration
• Lichenoid Inflammation
• Not completely well defined due to keratinocytes that
undergo necrosis – Apoptotic cells
• Seen in certain diseases such as: Lichen planus, drug
allergy, viral infection
• In extreme cases such as erythema multiforme (profound
systemic form of allergy)
• Characteristic lesion: Targetoid erythema of skin
• Usually in general parts of the body
HANSEN’S DISEASE (LEPROSY)
• Slowly progressive infection caused my M. leprae that

mainly affects the skin and peripheral nerves
• Fite-Faraco’s stain
o Stain used for AFB
• Three major types of Leprosy
o Tuberculoid Leprosy
o Borderline Leprosy
o Lepromatous Leprosy
CLINICAL PRESENTATION: Lichen
Pathogenesis: Inhaled M. leprae are phagocytized by pulmonary
macrophages and disseminated hematogenously; however,
they replicate only in cooler tissues of the periphery. • M.
leprae secretes no toxins, and its virulence is based on the
properties of its cell wall.
SKIN PATHOLOGY
TUBERCULOID LEPROSY
• Less severe
• Dry, scaly skin lesions that lack sensations
• Asymmetric involvement of large peripheral nerves
• TH1 response associated with production of IL-2 and
IFN- γ
• Presence of Non-Caseating Granuloma
o Good prognosis since granuloma is a delayed
type hypersensitivity reaction (patient will have
certain amount of protection)
• Lepromin Test: similar to Tuberculin with the same
principle
o (+): Tuberculoid
o (-): Lepromatous leprosy
• In History: Ask for numbness/hypoesthesia
o Loss of sense of touch
o Most important and most prominent
characteristic
o Since neuritis is the single important pathology of
leprosy
BORDERLINE LEPROSY
• Intermediate form of the disease
• Combination of tuberculoid and lepromatous leprosy
• Presence of lymphocytes and clear cells
• Solitary/ singular (macule) lesion (at point of chronic LEPROMATOUS LEPROSY
contact), it is protected
• Poorest prognosis
o Ears, arms, extremities
o Skin to skin contact: Children/babies of mothers • More severe form
with leprosy or adults in close proximity • Lepromin test (-)
• May resemble Tinea because of its papule or macule • Symmetric skin thickening and nodules
• Widespread invasion of the mycobacteria into Schwann
HISTOLOGICAL PRESENTATION: cells and into the endoneural and perineural macrophages
damages the peripheral nervous system
• Associated with weak TH1 response and, in some cases, a
relative increase in the TH2 response
• Most often in this form, antibodies are produced against
M. leprae antigens but these are not protective but they
may form immune complexes with free antigens that can
lead to erythema nodosum, vasculitis, and
glomerulonephritis
• Presence of Non-Caseating Granuloma CLINICAL PRESENTATION:
• Granuloma does not touch the epidermis
• Grenz Zone: Free space between epidermis and
granuloma
• Lymphocytes (red arrow)
o Most important mediator of inflammation
• Langhans type Giant Cells (yellow arrow)
• Epithelioid histiocytes (green arrow)
• Fibroblast
• Neuritis (nerve inflammation)
SKIN PATHOLOGY
• Multiple lesions creating leonine facies (Due to absence of

protection)
• No granuloma
• Clear cells
o Lipid laden macrophages
o Within macrophages are plenty AFB of M. leprosy
Lupus Vulgaris (TB of the Skin)
• Diffuse lesion confined to dermis
o There is also Grenz zone • Rarer than leprosy
REMEMBER:
• Represented with draining sinus and ulceration of

the skin
Inverse proportion
• Lymphocytes (most important)
o More lymphocytes = less # of Lepra cells
• Example:
o Towards Tuberculoid/Nodular
▪ More lymphocytes, Epitheloid & Langhan’s
o Towards Lepromatous leprosy
▪ Less lymphocytes, Epitheloid, & Langhan’s
• Current classification • Produces caseating granulomatous inflammation
o Tuberculoid, Bimorphic, Lepromatous o Granuloma
• Conventional classification o Caseous Necrosis (green arrow)
o Tuberculoid, Borderline Tuberculoid, True borderline, • Hyperkeratosis/ Acanthosis of epidermis
Lepromatous • Ziehl Neelsen stain
• In practice, clinicians biopsy skin for baseline o Staining AFB (orange arrow)
o Lesion from Borderline becomes Lepromatous o Similar in appearance with leprosy in terms
▪ Treatment is inadequate of AFB staining and needs to be cultured to
o Lesion from Lepromatous becomes Tuberculoid differentiate
▪ Correct treatment
• Follow-up is important in correlation with clinical
presentation
SKIN PATHOLOGY
SYPHILIS o Cardiovascular syphilis (>80% of tertiary syphilis)

• Chronic STD with varied clinical and pathologic results in aortitis (due to endarteritis of the aortic
manifestations vasa vasorum) with aortic root and arch aneurysms
• T. pallidum subsp. Pallidum and aortic valve insufficiency.
• Resurgence due to paucity of present society o Neurosyphilis can be symptomatic
• History of the patient: sexual contact, blood transfusion (meningovascular disease, tabes dorsalis, or diffuse
brain parenchymal disease, so-called general paresis)
CLINICAL PRESENTATION: or asymptomatic (cerebrospinal fluid [CSF]
Can be local or systemic abnormalities only, with pleocytosis, increased
• Primary stage: painless ulcer of genitalia (localized) protein, and decreased glucose).
o Occurring approximately 3 weeks after infection o “Benign” tertiary syphilis is associated with
o Features a single firm, nontender, raised, red lesion necrotic, rubbery masses (gummas due to delayed-
(chancre) located at the site of treponemal invasion type hypersensitivity to the organisms), which form
o Spirochetes are plentiful within the chancre and in various sites (bone, skin, oral mucosa)
spread from there throughout the body by
hematologic and lymphatic dissemination HISTOLOGICAL PRESENTATION:
o Ulcerations and irregular hyperplasia of the epidermis, • Common denominator among the three is the presence
confused with squamous cell carcinoma of plasma cells (purple arrow) and obliterative
• Secondary stage: presence of maculopapular lesion endarteritis
• Granuloma or Gumma (3rd Stage)
o Marked by painless, superficial lesions of the skin

and mucosal surfaces
o Occurs 2-10 weeks after the primary chancre in
approx. 75% untreated people
o Lesions frequently occur in the palms/soles of the feet
o Lesions may be maculopapular, scaly, or pustular
BLISTERING DISEASE
o Moist areas of the skin may have condylomata lata
Familiarize with Onset, Distribution, Size, and Layer of skin
(broad-based, elevated plaques) 1. VARICELLA-HERPES-ZOSTER INFECTION
o Silvery-gray superficial erosions may form on the oral, 2. PEMPHIGUS VULGARIS
pharyngeal and genital mucous membranes. 3. BULLOUS PEMPHIGOID
o Lymphadenopathy, mild fever, malaise, and weight Varicella-Herpes-Zoster Infection
loss are also common in secondary syphilis.
• Intraepidermal blister
o Develop with or without treatment of primary syphilis
• Sexually transmitted disease
o Usually lesions are systemic but sometimes appear
only in buccal cavity
1. Varicella
o Secondary syphilis lasts several weeks and then the
• Acquired during childhood
person enters the latent stage of the disease.
• Characteristic exanthematous infection of
o Spontaneous healing (false hope) → may develop
children
after several weeks or months → spontaneous healing
• Presents with widespread vesicles on the body as
(again, false hope) → third stage
well as high grade fever (after lysis of fever,
• Third Stage: has three main manifestations:
rashes will occur)
cardiovascular, neurosyphilis, and benign tertian syphilis
• Most important complication: Pneumonia
(may occur alone or in combination)
o Occurs in one third of untreated patients, after a long
latent period (>5 years).
SKIN PATHOLOGY
o Primary Herpes (acute case)

▪ Presence of inclusion bodies, rarely
seen
• Differentiated from Langhan cells
o Langhan cells: nuclei are peripherally seen,
nuclei overlap
• Presence of balloon cells – due to cytopathic effect of
virus on the nucleus
2. Herpes Simplex
a. Herpes I (Peri-oral)
PEMPHIGUS GROUP
b. Herpes II (Genital area) – associated with
• Uncommon chronic blistering diseases
STDs
• Acantholysis with consequent intraepidermal blister
• Implicate in cervical carcinogenesis but less commonly
formation
than HPV
• Largest blisters
• Prior to modern antibiotic era – cause of most
mortalities among blister diseases
Pemphigus Vulgaris
• Affect middle-aged
• Begins in the mouth with painful erosions or bullae &
3. Herpes Zoster
after a period of weeks or months, spread to involve
• Elderly and immunosuppressed are commonly
the skin
infected
• Predilection to scalp, face, axilla, buccal, palatine &
• Affects the dermatomes: very painful
gingival mucosae, or generalized
• Causes of mortality:
o Can induce hypovolemic shock thru fluid and
plasma loss (blister rupture) especially in
children
o Sites of local infection or septicemia (large
bare areas)
CLINICAL PRESENTATION;
HISTOLOGICAL PRESENTATION
• Tzanck’s Smear: for Herpes
o PAP Smear: found at the same year herpes
was screened
• Manifests as large blisters within epidermis which

easily ruptures
• Often multiple; can be systemic and can affect mucus
membrane
• Size: 1-20cm in diameter
• Nikolosky’s sign (+)
Multinucleated giant cells o When you press the blister -> spreads out to
• Moulding phenomenon the adjacent parts of the body
o Nuclei push and mold on another but do not
overlap
o Usually seen in recurrent cases
SKIN PATHOLOGY
HISTOLOGICAL PRESENTATION: • Often contains clear or blood-stained fluid

• Predilects lower abdomen, inner aspect of thigh, and
the flexural surfaces
• Remission often occurs
Immune disorders which leads to damage of intercellular

bridges (attachment of individual stratified squamous cells)
• Happens above the basal layer (basal layer is
preserved) - RED
• Epidermis and keratinocytes are separated
• Characteristic cell: Acantholytic cells - GREEN
o Nucleus is surround by halo
• Prominent cells: Eosinophils
• Few inflammatory cells
• Subepidermal unilocular vesicle
• Overlying epithelium attenuated
IMMUNOFLOURESENCE (IFAT):
• Retention of dermal papillary outline (festooning)
IMMUNOFLOURESCENCE (IFAT):
Characteristic Fishnet appearance
Bullous Pemphigoid
• Generalized Cutaneous Pemphigoid
IgG reaction seen in the basement membrane
• Usually of unknown etiology
FOLLICULITIS
• Common in the elderly (7th decade)
• Resembles Pemphigus Vulgaris – but less severe
Suppurative Folliculitis
• Caused by Acne Vulgaris or Staphylococcus or
Streptococcus (bacterial)
o hair follicle and sebaceous glands are
affected
• Blister is immediately underneath the epidermis

o Epidermis is stiff
o Lesion is intact and rigid; not easily ruptured
SKIN PATHOLOGY
• Infection may produce pustule/nodule formation -

YELLOW
• May develop into skin depression if left untreated
• May be caused by hormonal background
(adolescents)
Leukocytoclastic Vasculitis
• Commonly due to allergy
• Induces rupture of hair follicle (BLUE) and

granulomatous inflammation
• Presence of neutrophils (GREEN) around the hair shaft
(ORANGE) and interstitium
• Infundibulum (RED)
VASCULITIS • Presence of papules/petechiae, ecchymosis, purpura
HISTOLOGICAL PRESENTATION: • In normal blood vessels: when pressure is applied and
removed -> color returns (blanching)
o In this condition -> color does not return
(Palpable purpura)
• Histological Criteria: Fibrinoid necrosis of the wall of

small blood vessels
• Inflammatory cells seen in the superficial plexus
• Mononuclear cells
o In allergic reactions: Eosinophils
• Fibrinoid necrosis of the wall -YELLOW
• Small basophilic bodies: nuclear dust - GREEN
o Part or entire thickness
o Fragments of nuclei of WBC
• Prominent nuclear dust - GREEN
o Differentiate with larger nucleus
• Presence of eosinophils
o Seen in Leukocytoclastic Vasculitis
Polyartritis Nodosa
• May be from contact dermatitis or manifestation of
• Multisystemic, multifocal medium sized arterial blood
septicemia
vessel involvement
Septic Vasculitis
• Affectation of small arterioles and capillaries
• Disseminated Intravascular Coagulopathy
• Threatening due to septicemia
• Aside from necrosis there is presence of thrombus -
GREEN
• Bacteria and its toxic product induce DIC which can
kill the patient by blocking arteries and organs
SKIN PATHOLOGY
• Depends on the blood vessel affected • Broader extent, often producing deformities especially
o Coronary artery (MI), Renal artery (renal in the face
infarct) HISTOLOGICAL PRESENTATION:
o Diagnosis is by occlusion
• Fibrinoid necrosis of blood vessel wall, WBC
3 Phases
1. Acute Phase – Characterized by fibrinoid necrosis
and neutrophils
2. Healing Phase – Diminution of necrosis, WBC is
replaced by mononuclear cells
3. Healed Phase
• Thick bands of collagen which are anucleated
• Period between 2nd & 3rd Phase: stage where
thrombus may occur -> produce infarct in organ
Lichen Sclerosus Et Atrophicus
supplied -> ulcer formation
• Skin atrophy among post-menopausal females ->
HISTOLOGICAL PRESENTATION;
mucosa is easily injured
o Affects the anterior lower abdomen, vulva &
vagina
• Atrophicus – pertain to the epidermis (inflammation of
epidermis -> prone to injury)
• Sclerotic – basal structure (eg. Hair follicles)
• Fibrinoid necrosis in lateral extremities of the vascular

segment – BLUE
FIBROSING DERMATITIS
Hypertrophic Scar/Fibrosis
• Collagen deposited is confined in the original area of
the wound
HISTOLOGICAL PRESENTATON:
• Loss of skin markings: they become shiny - YELLOW
o More prone to trauma; especially to sexually
active menopausal women
HISTOLOGICAL PRESENTATION;
• Spindle cells with nuclei, vertically oriented - GREEN

• Blood vessels are also vertically oriented
Keloid
• Collagen deposition goes beyond the wound area
• Atrophy of epidermis - PURPLE

o Decreased number of layers
o Loss of rete ridges and adnexal structures
• Edema - RED
• Lichenoid Dermatitis - ORANGE
SKIN PATHOLOGY
Scleroderma VI. PANNICULITIS

• Collagen disease
• Generalized/localized fibrosis of the skin Septal Panniculitis
o Morphea – localized scleroderma • Inflammation of hypodermis
o Systemic disease – may affect the respiratory • Inflammation around the fat lobule - ORANGE
tract and the GIT especially the esophagus
ERYTHEMA NODOSUM
• Lesions usually found in the anterior thigh,
characterized by brownish discoloration - GREEN
• Morphea (localized lesion)
HISTOLOLOGICAL PRESENTATION:
• Fibrosis and collagenization of the dermis - YELLOW
Discoid Lupus Erythematosus

• Localized to the skin
o If affecting the kidney and skin = SLE
Lobular Panniculitis
• Inflammation of hypodermis
• Inflammation inside the fat lobule
• Presence of Malar rash
ERYTHEMA INDURATUM
• Affects the posterior portion of the leg
CLINICAL & HISTOLOGICAL PRESENTATION
• Characterized by liquefactive degeneration of basal

cells
• Atrophy of the epidermis; absence of rete ridges
• Fibrinoid necrosis of the dermis
• In chronic LE: thickening of the basement membrane -
BLUE
• Differential Diagnosis: Dermatomyositis
o Involvement of skin (similar to DLE) & muscle
SKIN PATHOLOGY
• Inflamed necrotic fat in the buttocks. You may also transfer it to another
• Many xanthoma cells person)
• There can be granulomatous inflammation. May affect • Gray-white to tan, flat to convex, 0.1cm to 1cm
the epidermis, dermis, hair follicle, subcutaneous papules with a rough, pebble- like surface
o If there is Caseous necrosis: TB is 1st
consideration HISTOLOGICAL PRESENTATION
CUTANEOUS MANIFESTATIONS OF SYSTEMIC DISEASES • Verrucous or Papillomatous Epidermal hyperplasia
o Squamous Hyperplasia is in Filiform/
Papillary form
o Rete ridges are delineated and converge
towards the imaginary center
• Papillary or cuneiform with outward and inward
growth with inclusion body and convergence of ridges
• Cytoplasmic vacuolization (koilocytosis) and
Inclusion bodies in more superficial epidermal layers
II. COMMON TUMORS OF THE SKIN
(important vital signs)
Differential Diagnosis:
A. PRIMARY TUMORS: EPITHELIAL TUMORS
• Condyloma acuminatum: Broad Rete Ridges
BENIGN EPITHELIAL TUMORS
o In Verruca vulgaris: Filiform Rete Ridges
• Callous especially with Veruca plantaris: No inclusion
1. Squamous Papilloma bodies, no converging rete ridges and simply
• Can be viral, the gross and microscopic histology orthokeratosis.
might confuse you with squamous cell
carcinoma.
• Finger-like or papillary projections on the surface
lined by stratified squamous epithelium
• Benign because:
o Basement membrane is intact
o Normal stratification and maturation
3. Condyloma Acuminatum
2. Verruca Vulgaris • Venereal Wart: Occurs in on the penis, female
• Common wart genitalia, urethra, perianal areas and rectum
• Warty nodule very common to the skin • Sexually transmitted disease
• They can be solitary or multiple • Due to a variant of HPV
• Most common type of Wart • Can be single or multiple
• “Verruca”: Squamoproliferative disorders caused by • Trogoocytosis (for HPV type 16) is more prominent
HPV than in Verruca vulgaris
• General term: verruca vulgaris • Soft, tan, cauliflower-like masses that occasionally
o Head- verucca capitis reach many cm
o Sole of the feet- verruca plantaris
Palm of Hand: Verruca palmaris HISTOLOGICAL PRESENTATION:
o Dorsal of Hand: Verruca plana • Hyperkeratosis, acanthosis, Squamous hyperplasia
• Communicable and autoinoculable (if you scratch with broad rete ridges
your kulugo in your finger, and you scratch your • Koilocytes also present in superficial epidermis
buttocks, you may transfer /induce another formation • Cervix- may predispose to squamous cell carcinoma
SKIN PATHOLOGY
• Grayish/ Blackish Unicolor: Within this color there are

white spot
o Grayish/ Blackish, alternating with white spot
▪ Clinically not seen in basal cell
carcinoma and malignant
melanoma
o Pressing on the lesion will cause exudation of
4. Keratinous Cyst: Pillar/Epidermal Cyst whitish lesion (likened to pimple)
• Most common cyst o Grayish: due to basal cell Hyperplasia
• Invagination of the epidermis into the dermis o Secretion: due to keratin plaque
o The neck is fibrosed and isolated as a mass
with stratum corneum which produce laminar MORPHOLOGY:
proliferation • Appear as round, flat, coin like, waxy plaque that vary
o Causes trapping and oxidation producing in diameter
lamellated keratin plaques • Uniformly tan to dark brown with velvety to granular
• Rupture can impart foul odor surface
• Remove the entire lesion; otherwise will recur • Inspection with hand lens: small, round, pore-like ostia
impacted with keratin
• Histological exam: neoplasms are exophytic and
sharply demarcated from adjacent epidermis
• Variable melanin pigmentation present
• Characteristic features:
o Exuberant keratin production
(hyperkeratosis)
o small keratin-filled cysts (horn cysts)
5. Tumors of Hair Follicle: Trichoepithelioma
o invagination of keratin into main mass
• May resemble cancer (basal cell carcinoma because of
(invagination cysts)
basaloid lesions)
• Keratin: a feature helpful in differentiating it from
• Basaloid cells are within the dermis
Melanomas
PATHOGENESIS:
• Mutation in the fibroblast growth factor receptor-3
(FGFR3): drive growth of tumor
• May suddenly appear as large numbers as part of
paraneoplastic syndrome (Leser-Trelat sign) due to
6. Tumor-Like Lesions: Seborrheic Keratosis stimulation of keratinocytes by transforming growth

factor-alpha produced by tumor cells
• Pigmented lesion of the elderly
• No malignant potential
• May resemble basal cell carcinoma
• Treatment: razorgrain excision
• Arise spontaneously and are particularly numerous on

the trunk, although the extremities, head, and neck
may also be involved
• Rarely associated with cancer of GI tract
• Seborrheic – due to keratosis
• Keratosis – due to basal cell hyperplasia
• Uniform hyperplasia at the basal cells
• Flat or elevated lesions
o Must be differentiated from common
melanocytic nevus, basal cell carcinoma,
malignant melanoma
SKIN PATHOLOGY
2. Dysplastic Nevi
PRECANCEROUS LESIONS & CONDITIONS
• Premalignant lesion of the nevus
• Atypical cells involving the junction of epidermis and
1. Actinic Keratosis dermis
• Dysplasia of the skin • Rete ridges hyperplastic and anastomose
• Premalignant lesion that can give rise to squamous • Usually greater than 0.6 cm
cell carcinoma (SCC) in situ, which can evolve into an
invasive squamous carcinoma
• Usually occur in sun exposed part of the body even
the scalp
o Common in Farmers
• Analogous to the Squamous carcinoma of uterine
cervix
3. Radiation dermatosis
• Most important premalignant lesion
• Plaque like Lesion with Sand-paper like consistency
• In history taking, it is important to extract exposure of
• “Cutaneous Horn” in some lesions that produce so
radiation
much keratin
o Helpful to rule out differential diagnosis
o Stratum corneum form a hornlike extension
• Squamous hyperplasia may be atypical
o Can be confused with Squamous cell
• Simply Squamous dysplasia
carcinoma
• Intact basement membrane
• Stromal cells (fibroblast) may also be atypical
• Cytologic Atypia
o Can be confused with Fibrosarcoma
• Disorganized cells (basal or middle or full thickness)
SKIN PATHOLOGY
MALIGNANT LESIONS
1. Basal Cell Carcinoma

• Most common invasive cancer of the 3 primary cancer
of the skin that arises in the basalis
• Locally invasive but do not metastasize
• Predisposing factors: immunosuppression and
disorder of DNA repair as in xenoderma pigmentosum
• Associated with mutations that activate the Hedgehog
pathway signaling
o Nevoid basal C CA syndrome (NBCCS) --
PTCH tumor suppressor -- SMO -GL11--
genes support tumor growth and survival
o Loss of PTCH function-- activates SMO
&GL11-- Development of BCCA
• Found on exposed part of the skin especially in the
face and upper extremity
• Rodent type of Ulcer

• Present as pearly papules containing prominent
dilated subepidermal blood vessels (telangiectasias)
• Pigmented because melanocytes are admixed with
basal cell
o May resemble melanocytic nevi or
melanomas
2. Squamous Cell Carcinoma

• 2nd most common tumor
• Metastasize to regional lymph nodes.
o More deeply invasive and involves the
HISTOLOGICAL PRESENTATION: subcutis
• Resemble basal cell of epidermis • Important cause: DNA damage due to UV light
• More bluish since nuclei are larger and therefore • Predisposing factors:
basophilic o Acquired defects and sun exposure-
• Assume a nest or island wherein the nuclei at the Dysfunction in p53 as in Actinic keratosis
periphery of tumor nest stand in a picket fence o Immunosuppression – chemotherapy or
pattern organ transplant
• Peripheral palisading of the nuclei usually o Susceptibility of keratinocytes to infection
accompanied clear space around them and transformation by oncogenic viruses –
• Believed to be: simply retraction or mucin-bearing HPV 5 & 8
• Since the basal cells are in the same plane with the ▪ implicated in tumors arising in
melanocytes, it is common that there’s melanin patients with a rare autosomal
pigment in the tumor (but they don’t produce the recessive condition,
melanin); commonly confused with malignant epidermodysplasia verruciformis,
melanoma which is marked by a high
susceptibility to cutaneous
squamous cell carcinomas
SKIN PATHOLOGY
o Industrial carcinogens (tars, oil), chronic Erythroplasia of Queyrat

ulcers, draining osteomyelitis, old burn • In males: Squamous cell carcinoma in situ of the penis
scars, arsenicals, ionizing radiation (IR) ,
tobacco and betel nut, xeroderma
pigmentosum.
2 groups:
• Sun exposed - less aggressive
• Membrane (lips)- more aggressive
• Destruction of Basement membrane
3. Merkel cell carcinoma
o No Destruction: Squamous cell carcinoma in
•May present as nodules
situ
•Least common among 4 major types of malignant
• Presence of keratin pearl, keratohyaline, and cancer: (Other 3: Basal cell CA, Squamous Cell CA,
intercellular bridges Melanoma)
• Limited within the epithelium or epidermis HISTOLOGICAL PRESENTATION:
• Rare; seen as small cell tumors
• Can be confused with Lymphomas and Carcinoid
tumors
4. Paget’s Disease
• Mammary / Extra -mammary
• Intraepithelial adenocarcinoma
• Occurs in the breast, nipple areola and vulva
• More commonly seen in the breast (90% of cases
associated with invasive ductal CA)
• Vulva - 30% associated with eccrine CA
• Management on breast/ vulva: mastectomy/
vulvectomy
• Clusters of tumor cells surrounded by halo, usually
confined to lower portion of the epidermis, the upper
portion is normal
• Must be differentiated from Squamous cell carcinoma
in situ
Two Intraepidermal Squamous Cell Carcinoma
Bowen’s Disease
• In females: Squamous cell carcinoma in situ of the vulva
with intra-abdominal Carcinoma
SKIN PATHOLOGY
B. PRIMARY TUMORS: SWEAT GLANDS AND RELATED 1. Junctional Nevus

TUMORS • Mole in the junction
• This may be flat or elevated and may be less than 0.5
BENIGN cm (benign nevi)
1. Sebaceous Adenoma • Melanocytes normally in the basalis but in this case,
they aggregate in the junction, assuming a teardrop
appearance
• Highest malignant potential Nevus
• Most ominous: usually the Mucocutaneous junction
o 2 steps towards malignancy
MALIGNANT
1. Sebaceous Gland Carcinoma
• Carcinoma of sebaceous glands
• Carcinoma of ceruminous glands
2. Intradermal Nevus
• Mole in the dermis (smallest malignant potential)
• Flat or elevated
• Completely benign
• Does not become dysplastic nevus
2. Sweat Gland Carcinoma
C. PRIMARY TUMORS: TUMORS AND LESIONS OF THE 2. Compound Nevus

MELANOGENIC SYSTEM • Junctional + Intradermal nevi
• Intermediary potential to becoming cancer
COMMON MELANOCYTIC NEVI • Elevated lesions
• Journey: From intraepidermal nevus (modified
melanocytes within the epidermis especially in the
basal layer)
o May go down to the junction: Junctional
Nevus
o May go down to the dermis: Intradermal
nevus
o Compound nevus- combination of junctional
and intradermal
• By age 16: 16 nevi in the body
SKIN PATHOLOGY
3. Dysplastic Nevus MALIGNANT MELANOMA

• It can be junctional, intraepidermal and compound • 10-15 % inherited as autosomal dominant
nevus but the cells become atypical and the rete • Generally sporadic
ridges anastomose • Major predisposing factor – UVR damage
• Usually >0.6 cm • Usually metastatic when discovered
• Initial term: D-K • Most deadly skin cancer, most difficult or recalcitrant
o Corresponding to the initials of family names to therapy primary to the skin
of the 2 families where this condition is • When it is clinically manifested: It is metastatic to
isolated in 1970s lymph nodes or other important organs of the body
• 1 step towards malignant carcinoma in situ • Melanomas of the skin is usually asymptomatic
• have acquired activating mutations in the NRAS and (although itching, pain may be early manifestations)
BRAF genes; inherited loss of function mutations in • Majority of lesion: >10mm in diameter
CDKN2A • Pigmented lesions >6 mm, change in appearance,
o RAS or BRAF activation and increased CDK4 onset of itching or pain should raise concern
activity contributes to the development of • There is acquired mutation due to exposure to UV,
dysplastic nevi. inherited autosomal dominant trait
• Management: Chemotherapy
PATHOGENESIS:
• Up to 15% autosomal dominant trait
• Most important single predisposing factor – UV
radiation damage from sun exposure
• Most frequent driver mutations
o Mutations that disrupt cell cycle control
genes
▪ Cdkn2a is mutated in 40%
▪ It encodes p16/ink4a, p15 ,p14 loss
of which is implicated in
melanoma.
o Mutations that activate pro-growth signaling
pathways - ras & p13k / akt signaling –
promote cell growth and survival
o Mutation that activate telomerase
▪ Telomerase –preserves telomeres
and protects cells from senescence
and have a key role in the
development of melanoma
PROGRESSION OF MELANOMA & CLINICAL FEATURE:

1. Radial and vertical growth phases
Malignant melanoma (Radial Growth M.M.)
• Superficial Spreading
• “Satellite lesions”
• Horizontal spread of melanoma within the epidermis
and superficial dermis
• Tumor cells lack the capacity to metastasize.
• Tumors fall into several clinicopathologic classes:
o Lentigo maligna: indolent lesion on the face
of older men that may remain in the radial
growth phase for several decades
SKIN PATHOLOGY
o Superficial spreading: most common type of 2. Nodular Melanoma

melanoma, usually involving sun-exposed • Nodule with ulceration at the top
skin
o Acral/ mucosal lentiginous melanoma:
unrelated to sun exposure.
Microstaging of Melanoma
2. Malignant melanoma (Vertical Growth M.S.) A. Clark’s Microstaging
• Shift to Vertical growth: tumor cells invade downward • Based on whether the cancer is confined in the
into the deeper dermal layers as an expansile mass epidermis, papillary dermis, reticular dermis, or
• Characterized by appearance of a NODULE and subcutaneous layer
correlates with the emergence of a tumor subclone • Clark 1- confined to epidermis
• with metastatic potential.
• Clark 2- extending to papillary dermis or portion of
• Probability of metastasis correlates with the depth of
reticular dermis
invasion
• Warning signs: • Clark 3- full dermis
o A: Asymmetry • Clark 4- up to subcutaneous tissue
o B: Border irregularity B. Breslow
o C: Color change • Based on thickness of the tumor (granular layer up to
o Multicolor/variable in color: because there is base of tumor)
necrosis hemorrhage, edema and congestion
• Tumor thickness (0.75, 1.5, 3, 4mm, 2cm) from stratum
o Benign: Unicolor
granulosum to deepest layer
o D: Diameter >6mm
o E: Elevation C. TNM (WHO)
• Tumor size, Nodal involvement, Metastasis
• Vacuolated cells are found in the full thickness of the
skin
• More likely confused with Paget’s disease which is
found in lower epidermis, here it is full thickness of
pigmented atypical melanocytes
1. Acral Lentiginous melanoma

• Usually found in distal extremities
• Better prognosis by incision
• Elongated rete ridges
• Supposed to be less aggressive because of location
(distal) and can be easily amputated
SKIN PATHOLOGY
• Sezary syndrome- seeding of the blood by malignant

T cells is accompanied by diffuse erythema and
scaling of the entire body surface (erythroedema)
MORPHOLOGY:
Sezary-Lutzner cells – histologic hallmark of CTCL of mycosis
fungoides (bandlike aggregates within superficial dermis
invading the epidermis as single cells and small clusters called
D. MIGRANT TUMOR Pautrier microabscess)
MIGRANT CELLLS
1. Reactive Lymphoid hyperplasia
2. Benign Lymphocytoma Cutis
Pautrier Microabscess
• Microabscess in in the epidermis
• Well-defined collections of mycosis cells located
within the epidermis in T-cell lymphoma and mycosis
fungoides.
• Can be demonstrated using CD3 therefore a T-
lymphocyte malignant cutaneous lesion
• Differentiate with the Munro’s Microabscess seen in
Psoriasis
MYCOSIS FUNGOIDES
• Most common form of Cutaneous T-cell lymphoma
• Affects all ages but most commonly persons over 40
yrs old
• Usually localized but can evolve to systemic
lymphoma
• Cutaneous T-cell Lymphoma (CTCL) that spans
spectrum of lymphoproliferative disorders affecting
skin
• Homing CD4+ T Helper cells
LYMPHOMA
• Usually seen in truncal areas
• Starting from superficial plexus attacking epidermis
will produce microabscess called Pautrier’s
Microabscess
• Culprit: lymphocytes, emanating from the superficial
plexus travelling within the epidermis
• The same phenomena of exocytosis or
epidermidization (as in the case of Psoriasis) however
the lymphocytes are malignant (T cells)
• Description: Scaly, red-brown patches; raised, scaling
plaques and fungating nodules • Monoclonal
SKIN PATHOLOGY
E. SECONDARY/METASTATIC TUMOR
• Diagnosed via Exclusion
• If it is Adenocarcinoma of skin (based on biopsy), first
rule out that it is metastasis from the breast, lung, GIT,
and kidney
F. MOST USEFUL STAINS IN DERMATOPATHOLOGY

• PAS - for Basement membrane thickening and Fungi
• Gram stain - for Bacteria
• Ziehl-Neelsen stain - for AFB
• Cytokeratin - Carcinomas
• HMB & S100 - Melanomas
• CD3 – for T Cell
• CD20 – for B cells
• Vimentin – Mesenchymal elements
• Other procedures:
o Tzanck’s prep. Cutaneous cytology
o Indirect fluorescent antibody technique
(IFAT)
REFERENCES
1. Dr. Casuela’s PowerPoint and Lecture
2. Potato notes for Pathology
3. SecD 2020 Trans
4. Robbins and Cotran Pathologic Basis of Disease (9th ed.)

10 Patho Skin Pathology

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PATHOLOGY

TABLE OF CONTENTS Skin cancer: most common cancer (epithelium of

Textbook Must know Previous Trans/Notes

I. NORMAL SKIN AND COMMON SKIN DISORDERS

Rudolph Virchow epithelium which produces keratin

viscera o Because the epithelium serves the major

Ferdinand Ritter Von Hebra function of the organ

• First to classify skin diseases by structural alterations

• Flattened, horny plates of keratin (cytoplasm replaced *Basal Cell:Melanocyte Ratio

• Very rare to have cancer of the gland > 2mm

B. DIAGNOSTIC APPROACH IN DERMATOSES C. SCHEMATIC PRESENTATION OF

D. DERMOPHOLOGIC PATTERNS OF SKIN DISEASES

o Seen in most Acute Dermatitis

ACUTE ECZEMA DERMATITIS

• Prominent loosening of the stratum corneum: basket

• Associated with the following conditions:

• Individual lesions develop and fade within hours

• Candidiasis: Non dermatophytes

o Bud out spores: can be mistaken as RBC

FUNGAL INFECTIONS (DERMATOPHYTES)

• Parakeratosis, hyperkeratosis, acanthosis

• Characterized by elongated epidermal hyperplasia

• Journey will cause:

o Kogoj’s Microabscess (green arrow)

• Differential diagnosis: Mycosis fungoides

HANSEN’S DISEASE (LEPROSY)

• Slowly progressive infection caused my M. leprae that

• Multiple lesions creating leonine facies (Due to absence of

• Represented with draining sinus and ulceration of

SYPHILIS o Cardiovascular syphilis (>80% of tertiary syphilis)

o Marked by painless, superficial lesions of the skin

o Primary Herpes (acute case)

• Manifests as large blisters within epidermis which

HISTOLOGICAL PRESENTATION: • Often contains clear or blood-stained fluid

Immune disorders which leads to damage of intercellular

Characteristic Fishnet appearance

• Blister is immediately underneath the epidermis

• Infection may produce pustule/nodule formation -

• Induces rupture of hair follicle (BLUE) and

• Histological Criteria: Fibrinoid necrosis of the wall of

• Fibrinoid necrosis in lateral extremities of the vascular

• Spindle cells with nuclei, vertically oriented - GREEN

• Atrophy of epidermis - PURPLE

Scleroderma VI. PANNICULITIS

Discoid Lupus Erythematosus

• Presence of Malar rash

• Characterized by liquefactive degeneration of basal

• Grayish/ Blackish Unicolor: Within this color there are

6. Tumor-Like Lesions: Seborrheic Keratosis stimulation of keratinocytes by transforming growth

• Arise spontaneously and are particularly numerous on

1. Basal Cell Carcinoma

• Rodent type of Ulcer

2. Squamous Cell Carcinoma

o Industrial carcinogens (tars, oil), chronic Erythroplasia of Queyrat

B. PRIMARY TUMORS: SWEAT GLANDS AND RELATED 1. Junctional Nevus

2. Sweat Gland Carcinoma

C. PRIMARY TUMORS: TUMORS AND LESIONS OF THE 2. Compound Nevus

3. Dysplastic Nevus MALIGNANT MELANOMA

PROGRESSION OF MELANOMA & CLINICAL FEATURE:

o Superficial spreading: most common type of 2. Nodular Melanoma

1. Acral Lentiginous melanoma

• Sezary syndrome- seeding of the blood by malignant

2. Benign Lymphocytoma Cutis