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Pre malignant and malignant
epidermal tumours
Actinic Keratosis (Solar keratosis)
• Premalignant skin lesion induced by ultraviolet light
damage
– Sun exposed areas (face, hands, forearms)
– Excess production of keratin to produce cutaneous horns
– May progress to squamous carcinoma in situ (Bowen’s disease)
or invasive cancer
– Lesion measures <1cm, tan brown, with rough sand paper like
consistency
– HISTOLOGY:
– - Parakeratosis and atypia (dysplasia) of the keratinocytes
– Solar damage to underlying elastic and collagen tissue (solar
elastosis)
Actinic keratosis – note scaling appearance
ACTINIC KERATOSIS
• Note the epidermal atypia and the parakeratosis
Squamous Cell Carcinoma
• Occur secondary to:
– Ultraviolet light damage
– Industrial carcinogens
– Chronic ulcers or sinus tracts (particularly chronic
osteomyelitis), Burn scars (Marjolin’s ulcer)
– Chewing tobacco (inside mouth) -Leukoplakia
– Radiation
– Patients who are immunocompromised
– Xeroderma pigmentosum
– Viral infections –HPV type36
Squamous Cell Carcinoma
• Gross: Shallow ulcer with a raised edge
• Microscopic: Usually well-differentiated tumor
with invasion of the dermis
• They exhibit variable differentiation ranging from
polygonal cells with keratinization and
intercellular bridges to highly anaplastic round
cells with scant keratinization
• Unlike BCCs, SCCs may develop on both sun-
exposed and non exposed areas of the body (the
latter are more likely to metastasize)
Squamous Cell Carcinoma of Lip in
Pipe Smoker
SCC
SCC – Keratin pearl
Basal Cell Carcinoma (BCC)
• Most common malignant tumor of the skin
• Occurs on sun-exposed, hair-bearing surfaces
• BCC’s are locally aggressive, infiltrating
cancers arising from the basal cell layer of the
epidermis
• Infiltrate the underlying superficial dermis
• DO NOT METASTASIZE
• Commonly located on the face on the inner aspect of
the nose, around the orbit and the upper lip
Basal Cell Carcinoma
• Appear as raised nodules containing a central crater
with a pearly-colored skin surface and vascular
channels (“pearly-white lesion”)
• Histology: Proliferation of basaloid cells arising from
the epidermis and extending into the dermis in lobules
or strands. Tumour cells also exhibit peripheral
pallisading. Clefts separating tumor cell nests from the
dermis are typical.
• Basal cell nevus syndrome: AD inheritance with
multiple BCC of skin & many other tumours in bone,
CNS, reproductive organs
Basal Cell Carcinoma
• Note the rolled pearly border & Prominent blood
vessel
Basal Cell Carcinoma
• Locally aggressive – Rodent ulcer
Basal Cell Carcinoma
• Typical clefting is noted
Basal Cell Carcinoma
• At higher power note the peripheral
pallisading of cells
Acute inflammatory dermatoses
• Urticaria
• Eczema
• Erythema multiforme
Urticaria
• Urticaria (hives) refers to the presence of
edema within the dermis and itchy
elevations of the skin
• Angioedema refers to edema in the
subcutaneous tissue
URTICARIA - pathophysiology
• Type I hypersensitivity
• Antigen stimulated, IgE mediated release of mast cell
granules
• Follows exposure to pollens, foods, drugs, pressure,
temperature or other stimulus
• C1 esterase inhibitor deficiency causes uncontrolled
complement activation (hereditary angioneurotic
edema)
Urticaria
Histology: Dermal edema and a minimal perivascular infiltrate of lymphocytes,
eosinophils and neutrophils. These changes may be relatively inconspicuous
and often very little is seen in the biopsy
Acute Eczematous dermatitis
• It is a clinical term embracing many
pathologically different lesions
• Eczema means “to boil over”.
• These lesions initially are characterized by red,
papulovesicular (Vesicles and bullae), oozing
crusted lesions (Bacterial superinfection) and
later with persistance forms raised scaling
plaques (Hyperkeratosis and acanthosis).
Stages of Eczema Development
A: Initial dermal edema and perivascular infiltration by inflammatory cells is followed
within 24 to 48 hours by epidermal spongiosis and microvesicle formation (B).
C: Abnormal scale, including parakeratosis, follows, along with progressive epidermal
hyperplasia (D) and hyperkeratosis (E) as the lesion enters into a more chronic stage.
Acute Eczema
Contact (Spongiotic) Dermatitis
• Histology: Acute phase - spongiosis, migration of
lymphocytes into the epidermis;
Eczematous (Spongiotic) Dermatitis
Note numerous spaces in the epidermis. This corresponds to vesicles seen clinically
and is typical for spongiotic dermatitis. Contact dermatitis is the major sub-category
of Eczematous dermatitis
Classification of Eczematous
Dermatitis
• Atopic Dermatitis
• Allergic Contact Dermatitis
• Drug-related eczematous dermatitis
• Photoeczematous eruption
• Primary Irritant dermatitis
Allergic Contact Dermatitis
Irritant Contact Dermatitis
• Due to the local toxic effect of the chemical on
the skin (e.g. detergents present in soaps,
shampoos, household cleaners)
Photodermatitis in patient taking
tetracycline
• Similar to allergic
contact dermatitis
except the reaction is
dependent on
ultraviolet light
• Drugs that are
photosensitizing
include:
– Tetracycline
– Sulfonamides
– Thiazides
Erythema Multiforme
• Hypersensitivity reaction to an infection, drugs,
various autoimmune diseases, or pregnancy
– Probable immunologic disease
– Infection associations include:
• Mycoplasma
• HSV I and II (MOST COMMON Herpes simplex)
– Drug associations include:
• Sulfonamides
• Anticonvulsants - Phenytoin
• Penicillins
• NSAIDS
Erythema multiforme
• EM Minor - Erythematous macules, papules, or
vesicles
– Papular lesions frequently look like a target with a
pale central area
– Commonly located on the palms and soles
• EM major – (Stevens-Johnson syndrome)-Extensive
skin and mucous membrane involvement with fever
and respiratory symptoms
• Histology – Cytotoxic reaction where there is
degenerating keratinocytes. Early lesions have
lymphocytic infiltrate in the dermo-epidermal
junction but later zones of epidermal necrosis occurs
forming blisters
Erythema Multiforme
Erythema Multiforme
Note ‘target-like’ papules
Target Lesions in Erythema Multiforme
Erythema Multiforme
• Note the interface change, necrosis of skin, and
lifting of necrotic epidermis. This corresponds to
the center of the target lesion.
Erythema Multiforme
• Early lesion or periphery of target lesion. Note
milder changes, basal layer focally obscured by
inflammation

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Premalignant and Malignant Skin Tumors and Inflammatory Dermatoses

  • 1. Pre malignant and malignant epidermal tumours
  • 2. Actinic Keratosis (Solar keratosis) • Premalignant skin lesion induced by ultraviolet light damage – Sun exposed areas (face, hands, forearms) – Excess production of keratin to produce cutaneous horns – May progress to squamous carcinoma in situ (Bowen’s disease) or invasive cancer – Lesion measures <1cm, tan brown, with rough sand paper like consistency – HISTOLOGY: – - Parakeratosis and atypia (dysplasia) of the keratinocytes – Solar damage to underlying elastic and collagen tissue (solar elastosis)
  • 3. Actinic keratosis – note scaling appearance
  • 4. ACTINIC KERATOSIS • Note the epidermal atypia and the parakeratosis
  • 5. Squamous Cell Carcinoma • Occur secondary to: – Ultraviolet light damage – Industrial carcinogens – Chronic ulcers or sinus tracts (particularly chronic osteomyelitis), Burn scars (Marjolin’s ulcer) – Chewing tobacco (inside mouth) -Leukoplakia – Radiation – Patients who are immunocompromised – Xeroderma pigmentosum – Viral infections –HPV type36
  • 6. Squamous Cell Carcinoma • Gross: Shallow ulcer with a raised edge • Microscopic: Usually well-differentiated tumor with invasion of the dermis • They exhibit variable differentiation ranging from polygonal cells with keratinization and intercellular bridges to highly anaplastic round cells with scant keratinization • Unlike BCCs, SCCs may develop on both sun- exposed and non exposed areas of the body (the latter are more likely to metastasize)
  • 7. Squamous Cell Carcinoma of Lip in Pipe Smoker
  • 8. SCC
  • 10. Basal Cell Carcinoma (BCC) • Most common malignant tumor of the skin • Occurs on sun-exposed, hair-bearing surfaces • BCC’s are locally aggressive, infiltrating cancers arising from the basal cell layer of the epidermis • Infiltrate the underlying superficial dermis • DO NOT METASTASIZE • Commonly located on the face on the inner aspect of the nose, around the orbit and the upper lip
  • 11. Basal Cell Carcinoma • Appear as raised nodules containing a central crater with a pearly-colored skin surface and vascular channels (“pearly-white lesion”) • Histology: Proliferation of basaloid cells arising from the epidermis and extending into the dermis in lobules or strands. Tumour cells also exhibit peripheral pallisading. Clefts separating tumor cell nests from the dermis are typical. • Basal cell nevus syndrome: AD inheritance with multiple BCC of skin & many other tumours in bone, CNS, reproductive organs
  • 12. Basal Cell Carcinoma • Note the rolled pearly border & Prominent blood vessel
  • 13. Basal Cell Carcinoma • Locally aggressive – Rodent ulcer
  • 14. Basal Cell Carcinoma • Typical clefting is noted
  • 15. Basal Cell Carcinoma • At higher power note the peripheral pallisading of cells
  • 16. Acute inflammatory dermatoses • Urticaria • Eczema • Erythema multiforme
  • 17. Urticaria • Urticaria (hives) refers to the presence of edema within the dermis and itchy elevations of the skin • Angioedema refers to edema in the subcutaneous tissue
  • 18. URTICARIA - pathophysiology • Type I hypersensitivity • Antigen stimulated, IgE mediated release of mast cell granules • Follows exposure to pollens, foods, drugs, pressure, temperature or other stimulus • C1 esterase inhibitor deficiency causes uncontrolled complement activation (hereditary angioneurotic edema)
  • 19.
  • 20. Urticaria Histology: Dermal edema and a minimal perivascular infiltrate of lymphocytes, eosinophils and neutrophils. These changes may be relatively inconspicuous and often very little is seen in the biopsy
  • 21. Acute Eczematous dermatitis • It is a clinical term embracing many pathologically different lesions • Eczema means “to boil over”. • These lesions initially are characterized by red, papulovesicular (Vesicles and bullae), oozing crusted lesions (Bacterial superinfection) and later with persistance forms raised scaling plaques (Hyperkeratosis and acanthosis).
  • 22. Stages of Eczema Development A: Initial dermal edema and perivascular infiltration by inflammatory cells is followed within 24 to 48 hours by epidermal spongiosis and microvesicle formation (B). C: Abnormal scale, including parakeratosis, follows, along with progressive epidermal hyperplasia (D) and hyperkeratosis (E) as the lesion enters into a more chronic stage.
  • 24. Contact (Spongiotic) Dermatitis • Histology: Acute phase - spongiosis, migration of lymphocytes into the epidermis;
  • 25. Eczematous (Spongiotic) Dermatitis Note numerous spaces in the epidermis. This corresponds to vesicles seen clinically and is typical for spongiotic dermatitis. Contact dermatitis is the major sub-category of Eczematous dermatitis
  • 26. Classification of Eczematous Dermatitis • Atopic Dermatitis • Allergic Contact Dermatitis • Drug-related eczematous dermatitis • Photoeczematous eruption • Primary Irritant dermatitis
  • 28. Irritant Contact Dermatitis • Due to the local toxic effect of the chemical on the skin (e.g. detergents present in soaps, shampoos, household cleaners)
  • 29. Photodermatitis in patient taking tetracycline • Similar to allergic contact dermatitis except the reaction is dependent on ultraviolet light • Drugs that are photosensitizing include: – Tetracycline – Sulfonamides – Thiazides
  • 30. Erythema Multiforme • Hypersensitivity reaction to an infection, drugs, various autoimmune diseases, or pregnancy – Probable immunologic disease – Infection associations include: • Mycoplasma • HSV I and II (MOST COMMON Herpes simplex) – Drug associations include: • Sulfonamides • Anticonvulsants - Phenytoin • Penicillins • NSAIDS
  • 31. Erythema multiforme • EM Minor - Erythematous macules, papules, or vesicles – Papular lesions frequently look like a target with a pale central area – Commonly located on the palms and soles • EM major – (Stevens-Johnson syndrome)-Extensive skin and mucous membrane involvement with fever and respiratory symptoms • Histology – Cytotoxic reaction where there is degenerating keratinocytes. Early lesions have lymphocytic infiltrate in the dermo-epidermal junction but later zones of epidermal necrosis occurs forming blisters
  • 34. Target Lesions in Erythema Multiforme
  • 35. Erythema Multiforme • Note the interface change, necrosis of skin, and lifting of necrotic epidermis. This corresponds to the center of the target lesion.
  • 36. Erythema Multiforme • Early lesion or periphery of target lesion. Note milder changes, basal layer focally obscured by inflammation