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COMMON DISEASES OF THE SKIN
ACUTE INFLAMMATORY DERMATOSES
• Acute dermatoses are often marked by
infiltrates consisting of mononuclear cells
rather than neutrophils
• Some acute lesions may persist, transitioning
to a chronic phase, while others are self-
limited.
Urticaria
• is a common disorder mediated by localized mast cell
degranulation, which leads to dermal microvascular
hyperpermeability.
• The resulting erythematous, edematous, and pruritic plaques are
termed wheals
• Pathogenesis - type 1 hypersensitivity reaction
• Sparse superficial perivenular infiltrate of mononuclear cells
• Superficial dermal edema causes splaying of collagen bundles
• Age- typically affects individuals between 20 and 40 years of age
• Individual lesions usually develop and fade within hours, but
episodes can persist for days or even months
Acute Eczematous Dermatitis
• New lesions take the form of erythematous papules, often with
overlying vesicles, which ooze and become crusted.
• Pruritus is characteristic.
• With persistence, these lesions coalesce into raised, scaling plaques
• “inside jobs” and “outside jobs”
• Allergic contact dermatitis, Atopic dermatitis, Drug-related
eczematous dermatitis, Photoeczematous dermatitis , Primary
irritant dermatitis
• Spongiosis characterizes all forms of acute eczematous dermatitis
Erythema Multiforme
• is characterized by epithelial injury mediated by skin-homing CD8+ cytotoxic T
lymphocytes.
• It is an uncommon, usually self-limited disorder that appears to be a
hypersensitivity response to certain infections and drugs
• The cytotoxic T cell attack is focused on the basal cells of cutaneous and mucosal
epithelia
• Present with a wide array of lesions, which may include macules, papules,
vesicles, and bullae
• Characteristic “targetoid” appearance
• Lymphocytes along the dermoepidermal junction
• With time confluent necrosis>>blister
Psoriasis
• is a common chronic inflammatory dermatosis
• is associated with an increased risk for heart attack and stroke
• Also associated in up to 10% of patients with arthritis
• Pathogenesis- T cell-mediated inflammatory disease, presumed to
be autoimmune in origin
– the antigens are not well described.
– Both genetic and environmental factors contribute to the risk.
– It is unclear whether the inciting antigens are self-antigens,
environmental antigens, or some combination of the two
– Sensitized populations of T cells home to the dermis, including CD4+
TH17 and TH1 cells and CD8+ T cells, and accumulate in the epidermis.
– These cells secrete cytokines and growth factors that induce
keratinocyte hyperproliferation
• Koebner phenomenon
• The typical lesion is a well-demarcated, pink to salmon–colored plaque
covered by loosely adherent silver-white scale.
• Acanthosis with regular downward elongation of the rete ridges(“test
tubes in a rack.”)
• loss of the stratum granulosum and extensive parakeratotic scale
• Thining of suprapapillary plates, and dilated and tortuous blood vessels
within the papillae >>Auspitz sign
• Neutrophils form small aggregates within both the spongiotic superficial
epidermis and the parakeratotic stratum corneum.
• Similar changes can be seen in superficial fungal infections
• most frequently affects the skin of the elbows,knees, scalp etc..
• In most cases psoriasis is limited in distribution
Lichen Planus
• The "6 Ps": purple, pruritic, planar , polygonal papules and plaques
• CD8+ T cell–mediated cytotoxic response against antigens in the
basal cell layer and the DEJ
• Sawtoothed rete ridges
• Interface dermatitis
• Wedge shaped hypergranulosis
• Civatte bodies (dyskeratotic keratinocytes)
• Wickham striae
• Lesions are multiple and are usually symmetrically distributed,
particularly on the extremities, and
• often occur around the wrists and elbows and on the vulva and
glans penis
Lichen simplex chronicus
• manifests as roughening of the skin
• It is a response to local repetitive trauma
Verrucae (Warts)
• are proliferative lesions of squamous
epithelial cells that are caused by HPV
• are most common in children and adolescents
• Different kinds on the basis of their gross
appearance and location
BLISTERING (BULLOUS) DISORDERS
Pemphigus (Vulgaris and Foliaceus)
Bullous Pemphigoid
TUMORS OF THE SKIN
Seborrheic Keratosis
• A common pigmented epidermal tumor
• occur most frequently in middle-age or older individuals.
• Arise spontaneously and are particularly numerous on the trunk
• are caused by acquired activating mutations in growth factor
signaling pathways
– FGFR3, PI3K/AKT pathway,RAS
• Are tan to dark brown round, exophytic, coinlike plaques that vary
in diameter
• Have a “stuck-on” appearance
• Leser-Trelat sign
Actinic keratosis
• Intraepidermal keratinocytic lesion secondary to solar
damage
• Most common precursor of cutaneous SCC
• Epidermal dysplasia that is not full thickness
• Parakeratosis, dermal solar elastosis and mild dermal
lymphocytic infiltrate
• Usually are less than 1 cm in diameter
• tan brown or red, and rough (sandpaper-like) to the touch
• rate of progression to SCC is small, varying from 0.1% to
2.6% per year
Squamous Cell Carcinoma
Basal Cell Carcinoma
• is a common slow-growing cancer
that rarely metastasizes.
• It tends to occur at sites subject to chronic sun exposure and in
lightly pigmented individuals
• The molecular hallmark is loss-of function mutations in PTCH1
• Manifest as pearly papules, often with prominent, dilated
subepidermal blood vessels
• multifocal superficial growths or nodular lesions
• Are not encountered on mucosal surfaces
Melanocytic Nevi
• refers to any benign congenital or acquired neoplasm of
melanocytes
• caused by somatic gain-of-function mutations in BRAF or RAS
• Are tan-to-brown, uniformly pigmented, small papules (5 mm or
less across) with well-defined, rounded borders
• Nuclei are uniform and round, and contain inconspicuous nucleoli
with little or no mitotic activity
• junctional nevi , compound nevi, intradermal nevi
Melanoma
• As with other cutaneous malignancies, melanoma is mainly
caused by UV light–induced DNA damage that leads to the
stepwise acquisition of driver mutations
• Intense intermittent exposure at an early age is particularly
harmful.
• Hereditary predisposition also plays a role in an estimated 5% to
10% of cases
• Often exhibit striking variations in pigmentation
• The borders are irregular and often “notched.”
• Microscopically, malignant cells grow as poorly formed nests or as
individual cells at all levels of the epidermis (pagetoid spread) and
in expansile dermal nodules
• Increasing thickness strongly correlates with
worse biologic behavior of melanomas (termed
Breslow thickness)
• Individual melanoma cells usually are
considerably larger than nevus cells.
• They have large nuclei with irregular contours,
chromatin that is characteristically clumped at
the periphery of the nuclear membrane, and
prominent “cherry red” eosinophilic nucleoli
The main clinical warning signs are as follows:
1. Rapid enlargement of a preexisting nevus
2. Itching or pain in a lesion
3. Development of a new pigmented lesion during
adult
life
4. Irregularity of the borders of a pigmented lesion
5. Variegation of color within a pigmented lesion
“ABCs” of melanoma: asymmetry, border, color,
diameter, and evolution (change of an existing nevus)
END

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COMMON DISEASES OF THE SKIN.pptx

  • 2. ACUTE INFLAMMATORY DERMATOSES • Acute dermatoses are often marked by infiltrates consisting of mononuclear cells rather than neutrophils • Some acute lesions may persist, transitioning to a chronic phase, while others are self- limited.
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  • 5. Urticaria • is a common disorder mediated by localized mast cell degranulation, which leads to dermal microvascular hyperpermeability. • The resulting erythematous, edematous, and pruritic plaques are termed wheals • Pathogenesis - type 1 hypersensitivity reaction • Sparse superficial perivenular infiltrate of mononuclear cells • Superficial dermal edema causes splaying of collagen bundles • Age- typically affects individuals between 20 and 40 years of age • Individual lesions usually develop and fade within hours, but episodes can persist for days or even months
  • 6. Acute Eczematous Dermatitis • New lesions take the form of erythematous papules, often with overlying vesicles, which ooze and become crusted. • Pruritus is characteristic. • With persistence, these lesions coalesce into raised, scaling plaques • “inside jobs” and “outside jobs” • Allergic contact dermatitis, Atopic dermatitis, Drug-related eczematous dermatitis, Photoeczematous dermatitis , Primary irritant dermatitis • Spongiosis characterizes all forms of acute eczematous dermatitis
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  • 8. Erythema Multiforme • is characterized by epithelial injury mediated by skin-homing CD8+ cytotoxic T lymphocytes. • It is an uncommon, usually self-limited disorder that appears to be a hypersensitivity response to certain infections and drugs • The cytotoxic T cell attack is focused on the basal cells of cutaneous and mucosal epithelia • Present with a wide array of lesions, which may include macules, papules, vesicles, and bullae • Characteristic “targetoid” appearance • Lymphocytes along the dermoepidermal junction • With time confluent necrosis>>blister
  • 9.
  • 10. Psoriasis • is a common chronic inflammatory dermatosis • is associated with an increased risk for heart attack and stroke • Also associated in up to 10% of patients with arthritis • Pathogenesis- T cell-mediated inflammatory disease, presumed to be autoimmune in origin – the antigens are not well described. – Both genetic and environmental factors contribute to the risk. – It is unclear whether the inciting antigens are self-antigens, environmental antigens, or some combination of the two – Sensitized populations of T cells home to the dermis, including CD4+ TH17 and TH1 cells and CD8+ T cells, and accumulate in the epidermis. – These cells secrete cytokines and growth factors that induce keratinocyte hyperproliferation • Koebner phenomenon
  • 11. • The typical lesion is a well-demarcated, pink to salmon–colored plaque covered by loosely adherent silver-white scale. • Acanthosis with regular downward elongation of the rete ridges(“test tubes in a rack.”) • loss of the stratum granulosum and extensive parakeratotic scale • Thining of suprapapillary plates, and dilated and tortuous blood vessels within the papillae >>Auspitz sign • Neutrophils form small aggregates within both the spongiotic superficial epidermis and the parakeratotic stratum corneum. • Similar changes can be seen in superficial fungal infections • most frequently affects the skin of the elbows,knees, scalp etc.. • In most cases psoriasis is limited in distribution
  • 12.
  • 13. Lichen Planus • The "6 Ps": purple, pruritic, planar , polygonal papules and plaques • CD8+ T cell–mediated cytotoxic response against antigens in the basal cell layer and the DEJ • Sawtoothed rete ridges • Interface dermatitis • Wedge shaped hypergranulosis • Civatte bodies (dyskeratotic keratinocytes) • Wickham striae • Lesions are multiple and are usually symmetrically distributed, particularly on the extremities, and • often occur around the wrists and elbows and on the vulva and glans penis
  • 14.
  • 15. Lichen simplex chronicus • manifests as roughening of the skin • It is a response to local repetitive trauma
  • 16. Verrucae (Warts) • are proliferative lesions of squamous epithelial cells that are caused by HPV • are most common in children and adolescents • Different kinds on the basis of their gross appearance and location
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  • 18. BLISTERING (BULLOUS) DISORDERS Pemphigus (Vulgaris and Foliaceus) Bullous Pemphigoid
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  • 23. Seborrheic Keratosis • A common pigmented epidermal tumor • occur most frequently in middle-age or older individuals. • Arise spontaneously and are particularly numerous on the trunk • are caused by acquired activating mutations in growth factor signaling pathways – FGFR3, PI3K/AKT pathway,RAS • Are tan to dark brown round, exophytic, coinlike plaques that vary in diameter • Have a “stuck-on” appearance • Leser-Trelat sign
  • 24.
  • 25. Actinic keratosis • Intraepidermal keratinocytic lesion secondary to solar damage • Most common precursor of cutaneous SCC • Epidermal dysplasia that is not full thickness • Parakeratosis, dermal solar elastosis and mild dermal lymphocytic infiltrate • Usually are less than 1 cm in diameter • tan brown or red, and rough (sandpaper-like) to the touch • rate of progression to SCC is small, varying from 0.1% to 2.6% per year
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  • 29. Basal Cell Carcinoma • is a common slow-growing cancer that rarely metastasizes. • It tends to occur at sites subject to chronic sun exposure and in lightly pigmented individuals • The molecular hallmark is loss-of function mutations in PTCH1 • Manifest as pearly papules, often with prominent, dilated subepidermal blood vessels • multifocal superficial growths or nodular lesions • Are not encountered on mucosal surfaces
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  • 31. Melanocytic Nevi • refers to any benign congenital or acquired neoplasm of melanocytes • caused by somatic gain-of-function mutations in BRAF or RAS • Are tan-to-brown, uniformly pigmented, small papules (5 mm or less across) with well-defined, rounded borders • Nuclei are uniform and round, and contain inconspicuous nucleoli with little or no mitotic activity • junctional nevi , compound nevi, intradermal nevi
  • 32.
  • 33. Melanoma • As with other cutaneous malignancies, melanoma is mainly caused by UV light–induced DNA damage that leads to the stepwise acquisition of driver mutations • Intense intermittent exposure at an early age is particularly harmful. • Hereditary predisposition also plays a role in an estimated 5% to 10% of cases • Often exhibit striking variations in pigmentation • The borders are irregular and often “notched.” • Microscopically, malignant cells grow as poorly formed nests or as individual cells at all levels of the epidermis (pagetoid spread) and in expansile dermal nodules
  • 34. • Increasing thickness strongly correlates with worse biologic behavior of melanomas (termed Breslow thickness) • Individual melanoma cells usually are considerably larger than nevus cells. • They have large nuclei with irregular contours, chromatin that is characteristically clumped at the periphery of the nuclear membrane, and prominent “cherry red” eosinophilic nucleoli
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  • 36.
  • 37. The main clinical warning signs are as follows: 1. Rapid enlargement of a preexisting nevus 2. Itching or pain in a lesion 3. Development of a new pigmented lesion during adult life 4. Irregularity of the borders of a pigmented lesion 5. Variegation of color within a pigmented lesion “ABCs” of melanoma: asymmetry, border, color, diameter, and evolution (change of an existing nevus)
  • 38. END