types Epidemiology clinical picture description differential diagnosis treatment
-Race: Most often found in fair-skinned individuals, but can
beseen in all races.
-Occuption : Worked outdoors . Edge : irregular. • Seborrhoeic keratosis
Actinic keratosis Definition: Actinic= sun. hence Sun- induced
Keratosis -Sun damaged skin Flat or elevated ,hard, keratitic lesions on sun exposed Size :less than 1cm in diameter. • Bowen’s disease
areas, with adherent often yellowish- or brown crust Site: e.g. Scalp , face, neck ,ear , lip, dorsal hand • Discoid lupus erythematosus.
(AKs) Synonum: Solar keratoses Age : Elderly people
. • Psoriasis
Sex: Men
In individualswith history of Aks
Preventive:
• Avoid sun exposure
Age: Elderly • Protective cloths
Sex: Males > females -Actinic keratosis • Sun screens
- Tinea corporis Therapeutic :
Risk factors : clinical picture: Border: Well- defined, irregular border. -Patch of eczema
• Imiquimod (aldara)
Bowen’s disease Squamous cell carcinoma in situ - Solar radiation
- radiotherapy,
-Erythematous , scales plaque with slight crusting Size: up to 3cm in diameter. -Psoriasis
-SCC
• 5- Fluorouracil (5-FU)
resembling psoriasis ,solitry or multiple. Site: head, neck, trunk and limbs. • Cryotherapy
- human Papilloma virus warts (HPV 16) -Superficial basal cell carcinoma(BCC). • Electro cautery
-tar, chronic heat exposure -amelanotic melanoma, and Paget disease
• Surgical excision
-ingestion of arsenic and exposure to chemicals. • Photodynamic therapy (PDT)
• CO2 laser
Sex : Men
Oral leukoplakia Age: 50-70 years -Hairy leukoplakia
premalignant (OL)
Term reserved for white patches or plaques of
oral mucosa .
Risk factors :
C/P: Present as white non-removable plaquenon-
homogenous OL is more risky than homogenous
-Candidiasis
-Lichen planus
Tobacco, alcohol ,HPV
in Children Histopathlogy:
junctional nevi Site: Flat brown to tan macules. -Melanocytes proliferating into nests that sit
Palm, soles, genitalia and mucosa. along dermoepidermal junction .
-Raised & pigmented papules. Histopathlogy:
-Thickness and pigmentation increase with age. nests of nevus cells are found both
Compound nevi
-The surface may be smooth or papillomatous. dermoepidermal junction, and within the
-Symmetric. dermis.
skin findings :
Melanocytic nevi size: Variable - Flesh colored or pale-brown papules.
Histopathlogy:
Intradermal nevi Nests of nevus cells are found within
age: After adolescence -Terminal hairs may grow.
dermis only.
-most commonly on the face
c/p:
Defintion :
Atypical nevi
Moles that look atypical DD
Large,indistinct,color variable (pink,tan, brown black) Histopathlogy:
Types :Familial, sporadic Melanocytic nevus Treatment
Dysplastic nevi largerthan 5 mm with an irregular border ,surface Nestcell variable in size and form bridges
Race :White-skinned people Basal cell carcinoma Follow up
irregular,and a degree of inflammation. between adjacent rete ridges
Sex: Equally Melanoma
Skin tumors Age: Continue after age 30
Solitry or multiple
site: Commonly on trunk, and upperextremities.
types definition description
-Oncogenes: Act in a dominant fashion and
gain-of-function results inincreased
proliferation. Epidemiology:
- Tumor suppressor genes :Act in a recessive treatment
fashion and loss of normalfunction resultsin age of onset : Vary in race surgical options:
uncontrolled growth. differential diagnosis
Sex:Males > females, but SCC can occur more -Excision (including Mohs'micrographic Surgery)
features:
-second most common ca
frequently on the legs of female clinical picture -Excision and grafting
Squamous cell carcinoma develops in previously normal skin or pre-existing -Arise trom keratinocytes of the skin or mucus
Race: Persons witn white skin and poor tanning
capacity (skin phototypes T and N)
firm nodule with surface changes
including:crusting,
-Keratoacanthoma
-Bowen's disease
-Curettage and cautery
Medica options:
lesions such as actinic keratoses or Bowen’sdisease. membrane surtaces
The major risk factor:
(SCC) -Invasive in character
Risk factors
-As BCC in addition to chronic wound or scar, or
ulceration in center
- verrucous or horn like
-Actinic keratosis
-Warts
-Systemic chemotherapy
-Imiquimod 5%
-UV light exposure -Metastases to lymph nodes -Basal cell carcinoma
chronic infections or HPV infection -Radiotherapy
1. Non-melanoma skin - Exposure to ionizing radiation site -Melanome -Cryotherapy
cancer -Arsenic or organic chemicals -head (lips,pinna),neck -Immunotherapy & PDT
- Human papillomavirus infection -arms, hands and legs
(NMSC) - Immunosuppression
-Genetic predisp
The nodular type
-the most common cutaneous malignancy. -is the most common type of BCC (rodent ulcer, Morphea form basal cell carcinoma
phagedenic ulcer) -least common variant Differential diagnosis of
BCC is 3-6 times > SCC this ratio is reversed in Several clinical variants: Fibroepithelial basal cell carcinoma
immunesuppressd patients • Nodular • character : Shiny, translucent, pearly white or pink Supericial basa cell carcinoma -clinicaly scar like, plaque of morphea.
BCC
pigmented basal cell carcinoma -Uncommon
Basal cell carcinoma -arise without precursors, and showno sign of • Pigmented basal cell carcinoma ,dome -shapedpapule or nodule.
• Surface: Smooth and the presence of arborizing
Nodular or hyperpigmented plaque
-Flat red scaling plaques
-Border less distinctive
-Pink to white incolor, -Pedunculated plaque
-Eczema
-Tinea
progression • Superficial basal cell carcinoma
( BCCs) • Locally invasive • Morpheaform telangiectasia's, multilobular in character.
Well defined Irregular in outline
May resemble MM
-Trunk and extremities -Wypically smooth suface ildefined, -Variable incolor brown, pink yllow, skincolor
-Affect individuals between 40and 60yeas of
-Seborrheic (Pigmented)
indistinct. -Pigmented naevi
malignant • Fair skin
• After 40
• Fibroepithelial ( fibroepithelioma of Pinkus) • Edge: Rolled edge.• Sites: face, especially the cheeks,
nasolabial folds, forehead andeyelids , and ears.
-Less aggressive
-Agressive,recur
age -Melanoma
• Metastasis: is rare -Difficult to eradicate
• Perinural invasion : is poor prognostic sign
Diagnosis
Risk Factors
The American ABCD (E) role of 3)Lentigo Maligna Melanoma
genetic and phenotypic: melanoma
- incidence :5-10percent
-red or fair colored hair -A(Asymmetry)
-light colored eyes Differential diagnosis -B (Border irregularity) - c/p: 4)Acral Lentiginous Melanoma:
1)superficial Spreading Melanoma -uncommon type 5%
-Tendency to burn , inability to tan -Pyogenic granuloma (nodular) -C(Color variegation) Treatment -most common type 60-70% of all melanomas
2)Nodular Melanoma Slowly growing -Blacks >Asians
-congenital defect of DNA repair -Pigmented basal cell carcinoma (nodular) -Diameter greater than 5 mm) 1. Early-stage melanomas are often curable by incidence:15%to30% of all melanomas Sixth
-personal or family history of melanoma -Blue nevi(nodular) Investigations: -Age: Asymmetric ,brown to black macule with -Age:Mostfrequently in the seventh decade
types of primary melanomas: -E( enlargement) surgical excision( Mohs micrographic surgery) 40 and 60 years. decade oflife.
-melanocytic nevi and solar lentigines -Biopsy oflife.
-Atypical melanocytic nevi. 1)Superficial spreading melanoma(SSM)60-70%
-Plantar warts (acraL)
-Black heel -Sentineal node biopsy
2. Systemic Therapy such as cytotoxic
types of primary -Site: sex: color variation -Sex: Males than females
2. Melanoma: 2)Nodular melanoma( NM)15% to 30 -Mole (superficial melanoma) lasgowseven-pointcheck-list -Human Melanoma Black-45 (HMB-45, Melan-A
chemotherapy, Most frequently seen on the trunk of men and More frequently in men than in women
iregular,indented outline C/P
environmental factors:
-intense intermittent sun exposure
3)Lentigo maligna melanoma (LMM)5-10% -Bowen's disease (superficial) Major&minor criteria Tyrosinase , S100, MART-1)
-Immunostains and HMW
3. Radiotherapy
4. Interferon 2a melanomas: the legs of women.
-C/P:
site:
Frequently seen on the trunk ,head and neck.
-Age: seventh decade of life
-Asymmetricflat,brown to black macule,with
color variation and irregular borders.
4)Acral lentiginous melanoma (ALM) 5% -Dysplastic navus Major signs(Change in size, shape and 5. Immunotherapy It begins as an asymptomaticbrown to black c/P:
-chronic sun exposure -Seborrheic keratosis (superficial melanoma ,LMM) -Serum lactate dehydrogenase Site:
color) - Interleukin 2 macule with color variations and irregular, A blue to black,but some times pink to -site: Palms and soles orin and around the nail
-PUVA -Solar keratosis (LMM) -Target therapy red,nodule which maybe ulcerated or bleeding.
-tanning bed -Black heel (acral) Minor signs (infammation,crusting notched borders. Face with a preference for the nose and apparatus.
-residence in equatorial latitudes bleeding,sensory change,diameter27) Longitudinal melanonychia or Hutchinson sign)
chcek
- immunosuppression
- 3-Phophotography Extra facial (arm,hand or leg)
-
4-Dermoscopy Occasionally, periocular lentigo maligna
5-Wood's lamp
by fatema okoff
-Race: Most often found in fair-skinned individuals, but can
beseen in all races.
-Occuption : Worked outdoors . Edge : irregular. • Seborrhoeic keratosis
Actinic keratosis Definition: Actinic= sun. hence Sun- induced
Keratosis -Sun damaged skin Flat or elevated ,hard, keratitic lesions on sun exposed Size :less than 1cm in diameter. • Bowen’s disease
areas, with adherent often yellowish- or brown crust Site: e.g. Scalp , face, neck ,ear , lip, dorsal hand • Discoid lupus erythematosus.
(AKs) Synonum: Solar keratoses Age : Elderly people
. • Psoriasis
Sex: Men
In individualswith history of Aks
Preventive:
• Avoid sun exposure
Age: Elderly • Protective cloths
Sex: Males > females -Actinic keratosis • Sun screens
- Tinea corporis Therapeutic :
Risk factors : clinical picture: Border: Well- defined, irregular border. -Patch of eczema
• Imiquimod (aldara)
Bowen’s disease Squamous cell carcinoma in situ - Solar radiation
- radiotherapy,
-Erythematous , scales plaque with slight crusting Size: up to 3cm in diameter. -Psoriasis
-SCC
• 5- Fluorouracil (5-FU)
resembling psoriasis ,solitry or multiple. Site: head, neck, trunk and limbs. • Cryotherapy
- human Papilloma virus warts (HPV 16) -Superficial basal cell carcinoma(BCC). • Electro cautery
-tar, chronic heat exposure -amelanotic melanoma, and Paget disease
• Surgical excision
-ingestion of arsenic and exposure to chemicals. • Photodynamic therapy (PDT)
• CO2 laser
Sex : Men
Oral leukoplakia Age: 50-70 years -Hairy leukoplakia
premalignant (OL)
Term reserved for white patches or plaques of
oral mucosa .
Risk factors :
C/P: Present as white non-removable plaquenon-
homogenous OL is more risky than homogenous
-Candidiasis
-Lichen planus
Tobacco, alcohol ,HPV
in Children Histopathlogy:
junctional nevi Site: Flat brown to tan macules. -Melanocytes proliferating into nests that sit
Palm, soles, genitalia and mucosa. along dermoepidermal junction .
-Raised & pigmented papules. Histopathlogy:
-Thickness and pigmentation increase with age. nests of nevus cells are found both
Compound nevi
-The surface may be smooth or papillomatous. dermoepidermal junction, and within the
-Symmetric. dermis.
skin findings :
Melanocytic nevi size: Variable - Flesh colored or pale-brown papules.
Histopathlogy:
Intradermal nevi Nests of nevus cells are found within
age: After adolescence -Terminal hairs may grow.
dermis only.
-most commonly on the face
c/p:
Defintion :
Atypical nevi
Moles that look atypical DD
Large,indistinct,color variable (pink,tan, brown black) Histopathlogy:
Types :Familial, sporadic Melanocytic nevus Treatment
Dysplastic nevi largerthan 5 mm with an irregular border ,surface Nestcell variable in size and form bridges
Race :White-skinned people Basal cell carcinoma Follow up
irregular,and a degree of inflammation. between adjacent rete ridges
Sex: Equally Melanoma
Skin tumors Age: Continue after age 30
Solitry or multiple
site: Commonly on trunk, and upperextremities.
types definition description
-Oncogenes: Act in a dominant fashion and
gain-of-function results inincreased
proliferation. Epidemiology:
- Tumor suppressor genes :Act in a recessive treatment
fashion and loss of normalfunction resultsin age of onset : Vary in race surgical options:
uncontrolled growth. differential diagnosis
Sex:Males > females, but SCC can occur more -Excision (including Mohs'micrographic Surgery)
features:
-second most common ca
frequently on the legs of female clinical picture -Excision and grafting
Squamous cell carcinoma develops in previously normal skin or pre-existing -Arise trom keratinocytes of the skin or mucus
Race: Persons witn white skin and poor tanning
capacity (skin phototypes T and N)
firm nodule with surface changes
including:crusting,
-Keratoacanthoma
-Bowen's disease
-Curettage and cautery
Medica options:
lesions such as actinic keratoses or Bowen’sdisease. membrane surtaces
The major risk factor:
(SCC) -Invasive in character
Risk factors
-As BCC in addition to chronic wound or scar, or
ulceration in center
- verrucous or horn like
-Actinic keratosis
-Warts
-Systemic chemotherapy
-Imiquimod 5%
-UV light exposure -Metastases to lymph nodes -Basal cell carcinoma
chronic infections or HPV infection -Radiotherapy
1. Non-melanoma skin - Exposure to ionizing radiation site -Melanome -Cryotherapy
cancer -Arsenic or organic chemicals -head (lips,pinna),neck -Immunotherapy & PDT
- Human papillomavirus infection -arms, hands and legs
(NMSC) - Immunosuppression
-Genetic predisp
The nodular type
-the most common cutaneous malignancy. -is the most common type of BCC (rodent ulcer, Morphea form basal cell carcinoma
phagedenic ulcer) -least common variant Differential diagnosis of
BCC is 3-6 times > SCC this ratio is reversed in Several clinical variants: Fibroepithelial basal cell carcinoma
immunesuppressd patients • Nodular • character : Shiny, translucent, pearly white or pink Supericial basa cell carcinoma -clinicaly scar like, plaque of morphea.
BCC
pigmented basal cell carcinoma -Uncommon
Basal cell carcinoma -arise without precursors, and showno sign of • Pigmented basal cell carcinoma ,dome -shapedpapule or nodule.
• Surface: Smooth and the presence of arborizing
Nodular or hyperpigmented plaque
-Flat red scaling plaques
-Border less distinctive
-Pink to white incolor, -Pedunculated plaque
-Eczema
-Tinea
progression • Superficial basal cell carcinoma
( BCCs) • Locally invasive • Morpheaform telangiectasia's, multilobular in character.
Well defined Irregular in outline
May resemble MM
-Trunk and extremities -Wypically smooth suface ildefined, -Variable incolor brown, pink yllow, skincolor
-Affect individuals between 40and 60yeas of
-Seborrheic (Pigmented)
indistinct. -Pigmented naevi
malignant • Fair skin
• After 40
• Fibroepithelial ( fibroepithelioma of Pinkus) • Edge: Rolled edge.• Sites: face, especially the cheeks,
nasolabial folds, forehead andeyelids , and ears.
-Less aggressive
-Agressive,recur
age -Melanoma
• Metastasis: is rare -Difficult to eradicate
• Perinural invasion : is poor prognostic sign
Diagnosis
Risk Factors
The American ABCD (E) role of 3)Lentigo Maligna Melanoma
genetic and phenotypic: melanoma
- incidence :5-10percent
-red or fair colored hair -A(Asymmetry)
-light colored eyes Differential diagnosis -B (Border irregularity) - c/p: 4)Acral Lentiginous Melanoma:
1)superficial Spreading Melanoma -uncommon type 5%
-Tendency to burn , inability to tan -Pyogenic granuloma (nodular) -C(Color variegation) Treatment -most common type 60-70% of all melanomas
2)Nodular Melanoma Slowly growing -Blacks >Asians
-congenital defect of DNA repair -Pigmented basal cell carcinoma (nodular) -Diameter greater than 5 mm) 1. Early-stage melanomas are often curable by incidence:15%to30% of all melanomas Sixth
-personal or family history of melanoma -Blue nevi(nodular) Investigations: -Age: Asymmetric ,brown to black macule with -Age:Mostfrequently in the seventh decade
types of primary melanomas: -E( enlargement) surgical excision( Mohs micrographic surgery) 40 and 60 years. decade oflife.
-melanocytic nevi and solar lentigines -Biopsy oflife.
-Atypical melanocytic nevi. 1)Superficial spreading melanoma(SSM)60-70%
-Plantar warts (acraL)
-Black heel -Sentineal node biopsy
2. Systemic Therapy such as cytotoxic
types of primary -Site: sex: color variation -Sex: Males than females
2. Melanoma: 2)Nodular melanoma( NM)15% to 30 -Mole (superficial melanoma) lasgowseven-pointcheck-list -Human Melanoma Black-45 (HMB-45, Melan-A
chemotherapy, Most frequently seen on the trunk of men and More frequently in men than in women
iregular,indented outline C/P
environmental factors:
-intense intermittent sun exposure
3)Lentigo maligna melanoma (LMM)5-10% -Bowen's disease (superficial) Major&minor criteria Tyrosinase , S100, MART-1)
-Immunostains and HMW
3. Radiotherapy
4. Interferon 2a melanomas: the legs of women.
-C/P:
site:
Frequently seen on the trunk ,head and neck.
-Age: seventh decade of life
-Asymmetricflat,brown to black macule,with
color variation and irregular borders.
4)Acral lentiginous melanoma (ALM) 5% -Dysplastic navus Major signs(Change in size, shape and 5. Immunotherapy It begins as an asymptomaticbrown to black c/P:
-chronic sun exposure -Seborrheic keratosis (superficial melanoma ,LMM) -Serum lactate dehydrogenase Site:
color) - Interleukin 2 macule with color variations and irregular, A blue to black,but some times pink to -site: Palms and soles orin and around the nail
-PUVA -Solar keratosis (LMM) -Target therapy red,nodule which maybe ulcerated or bleeding.
-tanning bed -Black heel (acral) Minor signs (infammation,crusting notched borders. Face with a preference for the nose and apparatus.
-residence in equatorial latitudes bleeding,sensory change,diameter27) Longitudinal melanonychia or Hutchinson sign)
chcek
- immunosuppression
- 3-Phophotography Extra facial (arm,hand or leg)
-
4-Dermoscopy Occasionally, periocular lentigo maligna
5-Wood's lamp
by fatema okoff
