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Pathology - Bullous pemphigoid
It is an immunobullous dermatological condition characterized by the presence of autoantibodies targeting epidermal hemidesmosomal proteins.
Epidemiology • The most prevalent immunobullous skin disorder, however still an uncommon condition with an annual incidence of 7 per million individuals. • The majority of cases occur in older adults over the age of 70. Aetiology • Generation of autoantibodies targeting epidermal hemidesmosomal proteins. • The principal antigens are identified as BPAg1 and BPAg2.
Pathogenesis • Antibody binding results in complement fixation and the influx of inflammatory cells, notably eosinophils. • Direct cytotoxic effects disrupt the hemidesmosomes that anchor the epidermis to the dermis, causing complete separation of the epidermis from the dermis.
Presentation • Characteristic skin lesions consist of substantial, tight, intact blisters that arise on either normal or erythematous skin. • Preferred locations include the lower trunk, inner thighs, forearms, axillae, and groin regions.
Histopathology • Biopsies reveal a subepidermal blister populated by numerous eosinophils. • The underlying dermis exhibits edema and is infiltrated by a significant inflammatory response rich in eosinophils. Direct immunofluorescence on perilesional skin demonstrates linear deposition of IgG and C3 along the basement membrane zone.
Prognosis • Mortality rates remain low with suitable immunosuppressive protocols. • The majority of problems are associated with therapy.
It is an immunobullous dermatological condition characterized by the presence of autoantibodies targeting epidermal hemidesmosomal proteins.
Epidemiology • The most prevalent immunobullous skin disorder, however still an uncommon condition with an annual incidence of 7 per million individuals. • The majority of cases occur in older adults over the age of 70. Aetiology • Generation of autoantibodies targeting epidermal hemidesmosomal proteins. • The principal antigens are identified as BPAg1 and BPAg2.
Pathogenesis • Antibody binding results in complement fixation and the influx of inflammatory cells, notably eosinophils. • Direct cytotoxic effects disrupt the hemidesmosomes that anchor the epidermis to the dermis, causing complete separation of the epidermis from the dermis.
Presentation • Characteristic skin lesions consist of substantial, tight, intact blisters that arise on either normal or erythematous skin. • Preferred locations include the lower trunk, inner thighs, forearms, axillae, and groin regions.
Histopathology • Biopsies reveal a subepidermal blister populated by numerous eosinophils. • The underlying dermis exhibits edema and is infiltrated by a significant inflammatory response rich in eosinophils. Direct immunofluorescence on perilesional skin demonstrates linear deposition of IgG and C3 along the basement membrane zone.
Prognosis • Mortality rates remain low with suitable immunosuppressive protocols. • The majority of problems are associated with therapy.
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Pathology - Dermatitis herpetiformis
Definition: An immunobullous skin disorder marked by severe pruritus, papules, and vesicles, granular IgA deposition in the papillary dermis, and a significant correlation with celiac disease.
Epidemiology • Uncommon. The condition can afflict individuals of any age, while the highest frequency occurs in young people aged 20 to 40 years. Males are impacted twice as frequently as females. This illness is very prevalent in Northern Europe and Ireland. Up to 90% of individuals exhibit indications of celiac disease, although this may be asymptomatic.
Aetiology mediator. • IgA transglutaminase antibodies generated in the gastrointestinal tract seem to be pivotal.
Pathogenesis • IgA transglutaminase antibodies interact with transglutaminase enzymes present in the skin. The fixation of complement induces chemotaxis of neutrophils into the papillary dermis. • Enzymes secreted by neutrophils induce blister development.
Presentation • The rash consists of clusters of papules and vesicles that are highly pruritic. • Preferred locations are the shoulders, back, buttocks, elbows, and knees.
Histopathology Biopsies from first lesions reveal aggregates of neutrophils within the papillary dermis (papillary dermal microabscesses). Biopsies from established lesions reveal a subepidermal blister abundant in neutrophils. Immunofluorescence Direct immunofluorescence of perilesional skin demonstrates granular deposition of IgA in the papillary dermis.
Prognosis: The condition is typically chronic and persistent; nevertheless, it exhibits a significant response to the medication dapsone.
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Pathology - Granuloma annulare
Definition: An inflammatory dermatosis often characterized by annular lesions clinically and necrobiotic granulomatous inflammation histologically.
Epidemiology: Prevalent. Aetiology • Predominantly unknown in most instances. • Borrelia infection has been associated with a limited number of instances.
Pathogenesis • Current information indicates it constitutes a cutaneous reaction pattern to undefined antigens.
Presentation • Localized lesions of granuloma annulare manifest as flesh-colored or red papules that coalesce to form an annular lesion of 1–5 cm. • Acral regions are typically involved, particularly the knuckles and fingers.
Histopathology • The dermis exhibits a palisading granuloma, defined by a core region of degraded (necrobiotic) collagen encircled by radially oriented histiocytes, lymphocytes, and fibroblasts. • Mucin is frequently observed within the necrobiotic focal area. • Sometimes, the process results in a more nuanced ill-defined lesion in the dermis instead of a conventional well-formed palisaded granuloma (interstitial granuloma annulare).
Prognosis: Approximately 50% of cases resolve after two years of commencement, however recurrences are rather frequent.
Definition: An inflammatory dermatosis often characterized by annular lesions clinically and necrobiotic granulomatous inflammation histologically.
Epidemiology: Prevalent. Aetiology • Predominantly unknown in most instances. • Borrelia infection has been associated with a limited number of instances.
Pathogenesis • Current information indicates it constitutes a cutaneous reaction pattern to undefined antigens.
Presentation • Localized lesions of granuloma annulare manifest as flesh-colored or red papules that coalesce to form an annular lesion of 1–5 cm. • Acral regions are typically involved, particularly the knuckles and fingers.
Histopathology • The dermis exhibits a palisading granuloma, defined by a core region of degraded (necrobiotic) collagen encircled by radially oriented histiocytes, lymphocytes, and fibroblasts. • Mucin is frequently observed within the necrobiotic focal area. • Sometimes, the process results in a more nuanced ill-defined lesion in the dermis instead of a conventional well-formed palisaded granuloma (interstitial granuloma annulare).
Prognosis: Approximately 50% of cases resolve after two years of commencement, however recurrences are rather frequent.
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Pathology - Pemphigus vulgaris
Definition: An immunobullous dermatosis resulting from autoantibodies targeting epidermal desmosomal proteins.
Epidemiology • Infrequent, occurring at a rate of 0.1–1 per 100,000 individuals annually. • Typically impacts middle-aged persons aged 40–60 years.
Aetiology: Production of autoantibodies targeting the epidermal desmosomal cadherin, desmoglein-3.
Pathogenesis • The autoantibody attaches to the extracellular domain of desmoglein-3, resulting in desmosomal impairment and acantholysis. • The conventional perspective posited that complement fixation resulted in acantholysis; however, other researchers have proposed that acantholysis may arise via cytoskeletal collapse independent of complement activity.
Exposition • The majority of cases commence with oral erosions and blisters, then followed weeks or months later by the emergence of cutaneous lesions. The cutaneous lesions are delicate vesicles arising on unremarkable or erythematous skin. The blisters readily burst, resulting in a painful eroded region. • The skin lesions generally manifest on the face, scalp, axillae, and groin.
Histopathology • Biopsies reveal a blister cavity within the epidermis populated by acantholytic keratinocytes. • Generally, the cleavage occurs at a suprabasal level, resulting in the blister floor being lined by a solitary layer of intact basal keratinocytes. • Acantholysis may also affect the epidermis of adnexal structures. • Typically, there exists a fundamental dermal inflammatory infiltrate characterized by a significant presence of eosinophils.
Immunofluorescence
Direct immunofluorescence on perilesional skin demonstrates the deposition of IgG and C3 in the intercellular space of the epidermis.
Prognosis: Mortality rates are minimal with suitable immunosuppressive therapies. • The majority of problems are associated with therapy.
Definition: An immunobullous dermatosis resulting from autoantibodies targeting epidermal desmosomal proteins.
Epidemiology • Infrequent, occurring at a rate of 0.1–1 per 100,000 individuals annually. • Typically impacts middle-aged persons aged 40–60 years.
Aetiology: Production of autoantibodies targeting the epidermal desmosomal cadherin, desmoglein-3.
Pathogenesis • The autoantibody attaches to the extracellular domain of desmoglein-3, resulting in desmosomal impairment and acantholysis. • The conventional perspective posited that complement fixation resulted in acantholysis; however, other researchers have proposed that acantholysis may arise via cytoskeletal collapse independent of complement activity.
Exposition • The majority of cases commence with oral erosions and blisters, then followed weeks or months later by the emergence of cutaneous lesions. The cutaneous lesions are delicate vesicles arising on unremarkable or erythematous skin. The blisters readily burst, resulting in a painful eroded region. • The skin lesions generally manifest on the face, scalp, axillae, and groin.
Histopathology • Biopsies reveal a blister cavity within the epidermis populated by acantholytic keratinocytes. • Generally, the cleavage occurs at a suprabasal level, resulting in the blister floor being lined by a solitary layer of intact basal keratinocytes. • Acantholysis may also affect the epidermis of adnexal structures. • Typically, there exists a fundamental dermal inflammatory infiltrate characterized by a significant presence of eosinophils.
Immunofluorescence
Direct immunofluorescence on perilesional skin demonstrates the deposition of IgG and C3 in the intercellular space of the epidermis.
Prognosis: Mortality rates are minimal with suitable immunosuppressive therapies. • The majority of problems are associated with therapy.
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Pathology - Erythema multiforme
Definition: An inflammatory dermatosis characterized by unique targetoid lesions clinically and an interface reaction pattern histologically.
Epidemiology: • Fairly prevalent. • Primarily impacts the youth, encompassing youngsters.
Etiology • The majority of cases are associated with current or prior infections of the herpes simplex virus (HSV), which may not always be clinically evident. • Additional infectious organisms, such as Mycoplasma, have been implicated. • Pharmaceuticals are also acknowledged as a causative factor. Pathogenesis • Believed to signify a delayed-type hypersensitivity response to HSV antigens conveyed to the skin via circulating lymphocytes.
Presentation: Discrete circular erythematous patches, measuring 1–2 cm, with central darkening that may form blisters, referred to as 'target' lesions. • The majority of instances pertain to the extremities. • Mild oral involvement is prevalent.
Histopathology • Biopsies reveal interface dermatitis typified by a superficial lymphohistiocytic inflammatory infiltrate, substantial basal cell vacuolar degeneration, and keratinocyte death. • Instances of significant basal cell destruction may lead to subepidermal clefting and blister formation.
Prognosis: Most instances are self-limiting; however, recurring episodes are prevalent.
Definition: An inflammatory dermatosis characterized by unique targetoid lesions clinically and an interface reaction pattern histologically.
Epidemiology: • Fairly prevalent. • Primarily impacts the youth, encompassing youngsters.
Etiology • The majority of cases are associated with current or prior infections of the herpes simplex virus (HSV), which may not always be clinically evident. • Additional infectious organisms, such as Mycoplasma, have been implicated. • Pharmaceuticals are also acknowledged as a causative factor. Pathogenesis • Believed to signify a delayed-type hypersensitivity response to HSV antigens conveyed to the skin via circulating lymphocytes.
Presentation: Discrete circular erythematous patches, measuring 1–2 cm, with central darkening that may form blisters, referred to as 'target' lesions. • The majority of instances pertain to the extremities. • Mild oral involvement is prevalent.
Histopathology • Biopsies reveal interface dermatitis typified by a superficial lymphohistiocytic inflammatory infiltrate, substantial basal cell vacuolar degeneration, and keratinocyte death. • Instances of significant basal cell destruction may lead to subepidermal clefting and blister formation.
Prognosis: Most instances are self-limiting; however, recurring episodes are prevalent.
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Pathology - Mycosis fungoides
A low-grade T-cell lymphoma characterized by variably epidermotropic skin-homing T-lymphocytes.
Epidemiology: The most prevalent type of primary cutaneous lymphoma, however it remains a rare condition, impacting 0.3 individuals per 100,000 yearly. • Typically an affliction of maturity, however it may sporadically impact children.
Aetiology: Unknown. Genetics • The course of the disease correlates with chromosomal abnormalities, especially those involving chromosomes 8 and 17.
Presentation • Defined by the progressive emergence of patches, plaques, and tumors on non-sun-exposed skin, mainly in the regions of the buttocks and trunk.
Patches are several extensive (> 10mm) flat erythematous scaly sores.
• Plaques are raised lesions that may arise inside existing patches or develop independently.
• Tumour nodules and, at times, erythroderma may subsequently arise. • Advanced illness may affect the bone marrow, lymph nodes, and visceral organs.
Histopathology The patch stage has a modest upper dermal T-cell infiltrate accompanied by variable epidermotropism. The early stages of the disease are frequently challenging to detect due to overlapping characteristics with many inflammatory disorders. • The plaque stage has a more pronounced, band-like infiltration of T-cells with increased epidermotropism. Aggregates of neoplastic cells within the epidermis are commonly observed (Pautrier microabscesses). The nuclear atypia of the lymphocytes is more pronounced. The tumor stage indicates a more widespread skin infiltrate that may migrate into the subcutaneous fat. Epidermotropism may be diminished. Immunophenotype: Most instances exhibit a T-helper cell phenotype, specifically CD3 + CD4 + CD8–.
Prognosis: The likelihood of progression and mortality is associated with the illness stage at presentation. • The 10-year survival rates are elevated (85–95%) in patch and plaque stage disease, decreasing to 40% in tumor stage, and to 20% with nodal involvement.
A low-grade T-cell lymphoma characterized by variably epidermotropic skin-homing T-lymphocytes.
Epidemiology: The most prevalent type of primary cutaneous lymphoma, however it remains a rare condition, impacting 0.3 individuals per 100,000 yearly. • Typically an affliction of maturity, however it may sporadically impact children.
Aetiology: Unknown. Genetics • The course of the disease correlates with chromosomal abnormalities, especially those involving chromosomes 8 and 17.
Presentation • Defined by the progressive emergence of patches, plaques, and tumors on non-sun-exposed skin, mainly in the regions of the buttocks and trunk.
Patches are several extensive (> 10mm) flat erythematous scaly sores.
• Plaques are raised lesions that may arise inside existing patches or develop independently.
• Tumour nodules and, at times, erythroderma may subsequently arise. • Advanced illness may affect the bone marrow, lymph nodes, and visceral organs.
Histopathology The patch stage has a modest upper dermal T-cell infiltrate accompanied by variable epidermotropism. The early stages of the disease are frequently challenging to detect due to overlapping characteristics with many inflammatory disorders. • The plaque stage has a more pronounced, band-like infiltration of T-cells with increased epidermotropism. Aggregates of neoplastic cells within the epidermis are commonly observed (Pautrier microabscesses). The nuclear atypia of the lymphocytes is more pronounced. The tumor stage indicates a more widespread skin infiltrate that may migrate into the subcutaneous fat. Epidermotropism may be diminished. Immunophenotype: Most instances exhibit a T-helper cell phenotype, specifically CD3 + CD4 + CD8–.
Prognosis: The likelihood of progression and mortality is associated with the illness stage at presentation. • The 10-year survival rates are elevated (85–95%) in patch and plaque stage disease, decreasing to 40% in tumor stage, and to 20% with nodal involvement.
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Pathology - Malignant melanoma
A malignant melanocytic tumor.
Epidemiology • Less prevalent than basal or squamous cell carcinomas of the skin, however far more lethal. • Primarily observed in those with pale skin who have been exposed to sunlight.
Aetiology • Intermittent exposure to high doses of UV radiation constitutes the primary risk factor. • A component of genetic predisposition may also be pertinent. Genetics • Melanomas that develop in areas intermittently exposed to sunlight generally exhibit mutations in BRAF as an initial genetic occurrence. • Progression correlates with the accumulation of mutations in genes such as KIT, MITF, CDKN2A, TP53, and PTEN. • The majority also have chromosomal abnormalities characterized by gains and/or losses of chromosomal segments.
Presentation • The majority of melanomas manifest as pigmented cutaneous lesions exhibiting A symmetry, irregular B ordering, heterogeneous C olour, and D iameter exceeding 6mm (the ‘ABCD’ abbreviation).
Histopathology • A characteristic feature of all types of malignant melanoma is the existence of a neoplastic proliferation of markedly abnormal melanocytes. If the process is restricted to the epidermis, the term melanoma in situ may be utilized. • The term invasive melanoma may be utilized once penetration into the dermis has transpired.
Evolution • The majority of melanomas initially develop as a flat lesion in a radial manner, referred to as the radial growth phase. In this phase, there is either an absence of dermal invasion or the cells within the dermis are incapable of surviving and proliferating. • As advancement occurs, the growth transitions, enabling cells inside the dermis to proliferate. This phase is referred to as the vertical growth phase and is linked to the development of metastatic potential
Prognosis: Survival correlates with the disease stage at the time of diagnosis. • The primary factors determining the stage are the Breslow thickness of the melanoma and the presence of ulceration. • The mitotic rate is also acknowledged as a significant prognostic predictor in vertical growth phase melanomas.
A malignant melanocytic tumor.
Epidemiology • Less prevalent than basal or squamous cell carcinomas of the skin, however far more lethal. • Primarily observed in those with pale skin who have been exposed to sunlight.
Aetiology • Intermittent exposure to high doses of UV radiation constitutes the primary risk factor. • A component of genetic predisposition may also be pertinent. Genetics • Melanomas that develop in areas intermittently exposed to sunlight generally exhibit mutations in BRAF as an initial genetic occurrence. • Progression correlates with the accumulation of mutations in genes such as KIT, MITF, CDKN2A, TP53, and PTEN. • The majority also have chromosomal abnormalities characterized by gains and/or losses of chromosomal segments.
Presentation • The majority of melanomas manifest as pigmented cutaneous lesions exhibiting A symmetry, irregular B ordering, heterogeneous C olour, and D iameter exceeding 6mm (the ‘ABCD’ abbreviation).
Histopathology • A characteristic feature of all types of malignant melanoma is the existence of a neoplastic proliferation of markedly abnormal melanocytes. If the process is restricted to the epidermis, the term melanoma in situ may be utilized. • The term invasive melanoma may be utilized once penetration into the dermis has transpired.
Evolution • The majority of melanomas initially develop as a flat lesion in a radial manner, referred to as the radial growth phase. In this phase, there is either an absence of dermal invasion or the cells within the dermis are incapable of surviving and proliferating. • As advancement occurs, the growth transitions, enabling cells inside the dermis to proliferate. This phase is referred to as the vertical growth phase and is linked to the development of metastatic potential
Prognosis: Survival correlates with the disease stage at the time of diagnosis. • The primary factors determining the stage are the Breslow thickness of the melanoma and the presence of ulceration. • The mitotic rate is also acknowledged as a significant prognostic predictor in vertical growth phase melanomas.
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Pathology - Squamous cell carcinoma
Definition: A malignant epidermal tumor with squamous differentiation.
Epidemiology: Common tumors constitute around 15% of all skin cancers. • The majority occur on sun-exposed skin of older individuals with fair complexions.
Aetiology • The majority are associated with cumulative exposure to UV radiation. • Immunosuppression elevates the risk. Transplant recipients are especially susceptible to the development of numerous tumors. Carcinogenesis • The majority originate from actinic keratoses, which are dysplastic epidermal lesions that develop on sun-damaged skin. UV light, especially UVB, causes DNA damage in genes that regulate development, such as KRAS and CDK4.
Presentation • Dermal plaques or nodules, frequently exhibiting a keratinized surface crust. • Ulceration may occur.
Histopathology • Atypical squamous epithelial cells are observed in nests, sheets, and cords, originating from the epidermis and infiltrating the underlying dermis. • Tumors are classified as well, moderately, or poorly differentiated based on the degree of keratinization.
Prognosis: • The majority are primarily locally infiltrative upon diagnosis and can be effectively treated with surgical excision. Factors contributing to recurrence or metastasis encompass invasion depth, poor differentiation, perineural invasion, restricted excision, and immunosuppression.
Pathological classification of cutaneous carcinomas Primary tumor (T) pT1: tumor is 2 cm or smaller in diameter. pT2: tumor exceeds 2 cm in size. pT3: tumor infiltrates muscle, bone, cartilage, jaws, and orbit. pT4: tumor infiltrates the skull base and axial skeleton. Regional lymphatic nodes (N) pN1: solitary nodal metastasis measuring less than 3 cm in size. pN2: solitary nodal metastasis ranging from 3 to 6 cm in size or several nodal metastases, with none exceeding 6 cm. pN3: any nodal metastasis over 6 cm
Definition: A malignant epidermal tumor with squamous differentiation.
Epidemiology: Common tumors constitute around 15% of all skin cancers. • The majority occur on sun-exposed skin of older individuals with fair complexions.
Aetiology • The majority are associated with cumulative exposure to UV radiation. • Immunosuppression elevates the risk. Transplant recipients are especially susceptible to the development of numerous tumors. Carcinogenesis • The majority originate from actinic keratoses, which are dysplastic epidermal lesions that develop on sun-damaged skin. UV light, especially UVB, causes DNA damage in genes that regulate development, such as KRAS and CDK4.
Presentation • Dermal plaques or nodules, frequently exhibiting a keratinized surface crust. • Ulceration may occur.
Histopathology • Atypical squamous epithelial cells are observed in nests, sheets, and cords, originating from the epidermis and infiltrating the underlying dermis. • Tumors are classified as well, moderately, or poorly differentiated based on the degree of keratinization.
Prognosis: • The majority are primarily locally infiltrative upon diagnosis and can be effectively treated with surgical excision. Factors contributing to recurrence or metastasis encompass invasion depth, poor differentiation, perineural invasion, restricted excision, and immunosuppression.
Pathological classification of cutaneous carcinomas Primary tumor (T) pT1: tumor is 2 cm or smaller in diameter. pT2: tumor exceeds 2 cm in size. pT3: tumor infiltrates muscle, bone, cartilage, jaws, and orbit. pT4: tumor infiltrates the skull base and axial skeleton. Regional lymphatic nodes (N) pN1: solitary nodal metastasis measuring less than 3 cm in size. pN2: solitary nodal metastasis ranging from 3 to 6 cm in size or several nodal metastases, with none exceeding 6 cm. pN3: any nodal metastasis over 6 cm
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Pathology - Basal cell carcinoma
Definition: A collection of malignant epidermal tumors consisting of basaloid cells.
Epidemiology • Extremely prevalent neoplasms constituting 70% of all cutaneous cancers. • Primarily observed in fair-skinned people exhibiting sun damage.
Aetiology Cumulative exposure to ultraviolet (UV) radiation is the primary risk factor. Carcinogenesis • Nearly all exhibit mutations in genes that encode proteins associated with the sonic hedgehog pathway, predominantly PTCH1. A lesser percentage exhibit mutations in SMOOTHENED, which encodes the protein typically suppressed by the PATCHED1 protein.
Presentation: • Predominantly manifest as pearly papules or nodules in sun-exposed dermal regions. • Ulceration may transpire. Superficial variants manifest as erythematous patches that may be misidentified as eczematous lesions.
Histopathology: The tumor consists of clusters of tiny basaloid cells with little cytoplasm, exhibiting diverse growth patterns. The cells at the periphery of the clusters generally align in a palisade formation (peripheral palisading). The tumor stroma is generally loose and mucinous. Artefactual retraction gaps between tumor cells and stroma are frequently observed and may serve as a valuable diagnostic characteristic. A variety of morphological subtypes are identified, including nodular, superficial, infiltrative, morphoeic, and micronodular.
Prognosis: Exhibits locally invasive behavior; nonetheless, metastasis is exceedingly uncommon. Complete excision is typically curative. Recurrences are more prevalent at high-risk locations (head and neck) and with specific morphological subtypes (infiltrative, morphoeic, micronodular).
Pathological staging of skin carcinomas
Primary tumour (T)
pT1: tumour measures 2cm or less in size.
pT2: tumour measures > 2cm in size.
pT3: tumour invades muscle, bone, cartilage, jaws, and orbit.
pT4: tumour invades skull base, axial skeleton.
Regional lymph nodes (N)
pN1: single nodal metastasis measuring <3cm in size.< />pan>
pN2: single nodal metastasis measuring 3–6cm in size or multiple
nodal metastases, none measuring > 6cm.
pN3: any nodal metastasis measuring > 6cm
Definition: A collection of malignant epidermal tumors consisting of basaloid cells.
Epidemiology • Extremely prevalent neoplasms constituting 70% of all cutaneous cancers. • Primarily observed in fair-skinned people exhibiting sun damage.
Aetiology Cumulative exposure to ultraviolet (UV) radiation is the primary risk factor. Carcinogenesis • Nearly all exhibit mutations in genes that encode proteins associated with the sonic hedgehog pathway, predominantly PTCH1. A lesser percentage exhibit mutations in SMOOTHENED, which encodes the protein typically suppressed by the PATCHED1 protein.
Presentation: • Predominantly manifest as pearly papules or nodules in sun-exposed dermal regions. • Ulceration may transpire. Superficial variants manifest as erythematous patches that may be misidentified as eczematous lesions.
Histopathology: The tumor consists of clusters of tiny basaloid cells with little cytoplasm, exhibiting diverse growth patterns. The cells at the periphery of the clusters generally align in a palisade formation (peripheral palisading). The tumor stroma is generally loose and mucinous. Artefactual retraction gaps between tumor cells and stroma are frequently observed and may serve as a valuable diagnostic characteristic. A variety of morphological subtypes are identified, including nodular, superficial, infiltrative, morphoeic, and micronodular.
Prognosis: Exhibits locally invasive behavior; nonetheless, metastasis is exceedingly uncommon. Complete excision is typically curative. Recurrences are more prevalent at high-risk locations (head and neck) and with specific morphological subtypes (infiltrative, morphoeic, micronodular).
Pathological staging of skin carcinomas
Primary tumour (T)
pT1: tumour measures 2cm or less in size.
pT2: tumour measures > 2cm in size.
pT3: tumour invades muscle, bone, cartilage, jaws, and orbit.
pT4: tumour invades skull base, axial skeleton.
Regional lymph nodes (N)
pN1: single nodal metastasis measuring <3cm in size.< />pan>
pN2: single nodal metastasis measuring 3–6cm in size or multiple
nodal metastases, none measuring > 6cm.
pN3: any nodal metastasis measuring > 6cm
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Pyoderma gangrenosum
Definition: An inflammatory dermatosis marked by the formation of one or more extensive necrotic ulcers featuring irregular, undermined, violaceous margins.
Epidemiology: Rare occurrence. • Generally impacts individuals in middle age.
Aetiology • Unknown; however, over fifty percent of cases are linked to a systemic condition, notably inflammatory bowel disease and arthritis.
Pathogenesis • The etiology remains unidentified, but numerous immunological anomalies have been documented. • The classification as a type of vasculitis is contentious.
Presentation • The lesion initially manifests as an erythematous pustule or nodule, usually located on the lower extremity. • There is frequently a history of antecedent mild trauma (pathergy). • Subsequently, there is swift progression to a necrotic ulcer characterized by weakened red-purple margins.
Histopathology • Histological findings are heterogeneous and non-specific. Epidermal ulceration is seen, accompanied by significant underlying dermal inflammation and abscess development.
Prognosis • Recurrence is prevalent, and over fifty percent of patients necessitate prolonged treatment to manage the disease.
Definition: An inflammatory dermatosis marked by the formation of one or more extensive necrotic ulcers featuring irregular, undermined, violaceous margins.
Epidemiology: Rare occurrence. • Generally impacts individuals in middle age.
Aetiology • Unknown; however, over fifty percent of cases are linked to a systemic condition, notably inflammatory bowel disease and arthritis.
Pathogenesis • The etiology remains unidentified, but numerous immunological anomalies have been documented. • The classification as a type of vasculitis is contentious.
Presentation • The lesion initially manifests as an erythematous pustule or nodule, usually located on the lower extremity. • There is frequently a history of antecedent mild trauma (pathergy). • Subsequently, there is swift progression to a necrotic ulcer characterized by weakened red-purple margins.
Histopathology • Histological findings are heterogeneous and non-specific. Epidermal ulceration is seen, accompanied by significant underlying dermal inflammation and abscess development.
Prognosis • Recurrence is prevalent, and over fifty percent of patients necessitate prolonged treatment to manage the disease.
