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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 - 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 - 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 - 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 - Benign Cutaneous Lumps
This summarizes common benign cutaneous lumps, focusing on their clinical presentation and key histological features for effective study and understanding.
I. Epithelial Tumors
A. Fibroepithelial Polyps:
A. Melanocytic Naevi (Moles):
A. Lipoma:
This summarizes common benign cutaneous lumps, focusing on their clinical presentation and key histological features for effective study and understanding.
I. Epithelial Tumors
A. Fibroepithelial Polyps:
- Clinical: Multiple small, pedunculated papules around neck, axillae, and groin. Often removed for cosmetic reasons.
- Histology: Core of fibrovascular tissue covered by normal or hyperplastic epidermis.
- Clinical: Common cysts on face, neck, upper trunk, vulva, or scrotum.
- Histology: Cyst filled with laminated keratin; lined by squamous epithelium with a granular layer.
- Clinical: Common cysts, almost always on the scalp.
- Histology: Lined by pale squamous epithelial cells; abrupt keratinization without a granular layer (key differentiating feature from epidermoid cysts).
- Clinical: Very common in middle-aged/elderly; brown-black, greasy, warty nodules; often multiple; occur anywhere except palms and soles.
- Histology: Proliferation of basaloid keratinocytes with variable squamous differentiation; hyperkeratosis and horn cyst formation.
- Clinical: Brown to black, well-circumscribed macules; can occur anywhere.
- Histology: Elongated epidermal rete ridges; increased basal melanocytes; increased pigmentation in epidermis and papillary dermis.
A. Melanocytic Naevi (Moles):
- Clinical: Extremely common; virtually universal in white individuals; found anywhere on the body; evolve temporally (junctional → compound → intradermal).
- Histology:
- Junctional: Melanocyte nests at rete ridge tips.
- Compound: Dermal melanocytes in addition to junctional nests.
- Intradermal: Dermal melanocytes only.
- Clinical: Relatively common dermal naevus; dark blue papule; wide age range; more common on hands, feet, buttocks, scalp, and face.
- Histology: Heavily pigmented spindled and dendritic dermal melanocytes.
- Clinical: Benign; typically in children/young adults; pink or red/brown papule or nodule; usually on head, neck, and extremities.
- Histology: Compound melanocytic lesion; large epithelioid and/or spindled cells with abundant eosinophilic cytoplasm and conspicuous nucleolus. (Important: Large melanocytes can mimic melanoma – crucial for differential diagnosis).
A. Lipoma:
- Clinical: Very common benign fatty tumor; slow-growing, mobile, painless subcutaneous lump.
- Histology: Lobules of mature adipocytes.
- Clinical: Common benign fibrous tumor; reddish-brown papule on trunk or lower legs.
- Histology: Ill-defined dermal lesion; short interlacing spindle cells; variable collagen, foamy macrophages, blood vessels, and inflammatory cells.
- Clinical: Benign vascular tumor; red papules or nodules; often ulcerate and bleed; mostly on head/neck or extremities.
- Histology: Polypoid dermal lesion; lobules of small capillaries.
- Clinical: Common benign nerve sheath tumor; mostly sporadic, but multiple neurofibromas and café-au-lait spots are associated with neurofibromatosis type 1; soft, flesh-colored papule or nodule.
- Histology: Dermal or subcutaneous lesion; Schwann cells and fibroblasts in a fibrillar background.
- Clinical: Common benign skin tumor; hair matrix differentiation; firm papule or nodule in children/young adults; often on the cheek.
- Histology: Nodules of basaloid cells transforming into anucleate eosinophilic ("ghost") cells; calcification is common.
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Pathology - Erythema nodosum
A syndrome clinically defined by an acute, painful, erythematous nodular skin eruption and histologically characterized by septal panniculitis. Epidemiology • Primarily impacts young adults, with a significant inclination towards women.
Aetiology • Various aetiologies have been identified. • The most prevalent associations include sarcoidosis, infections, inflammatory bowel disease and pharmaceuticals. Pathogenesis • Etiology is unclear, but likely constitutes a type of hypersensitive reaction to infection, medication, or an underlying systemic disorder.
Presentation • Abrupt emergence of erythematous, warm, and sensitive cutaneous nodules. • Typically affects the shins, though other areas may be involved. • Systemic manifestations, including fever and malaise, may also occur. Histopathology • Biopsies reveal septal panniculitis marked by an inflammatory infiltrate localized to the septa of the subcutaneous adipose tissue. • The inflammatory infiltrate primarily consists of lymphocytes and macrophages. • Aggregates of histiocytes encircled by cleft-like spaces are well-documented (Mieschner’s radial granuloma).
Prognosis: The ailment typically resolves spontaneously within weeks, with the skin nodules ultimately diminishing and discoloring similarly to a bruise.
A syndrome clinically defined by an acute, painful, erythematous nodular skin eruption and histologically characterized by septal panniculitis. Epidemiology • Primarily impacts young adults, with a significant inclination towards women.
Aetiology • Various aetiologies have been identified. • The most prevalent associations include sarcoidosis, infections, inflammatory bowel disease and pharmaceuticals. Pathogenesis • Etiology is unclear, but likely constitutes a type of hypersensitive reaction to infection, medication, or an underlying systemic disorder.
Presentation • Abrupt emergence of erythematous, warm, and sensitive cutaneous nodules. • Typically affects the shins, though other areas may be involved. • Systemic manifestations, including fever and malaise, may also occur. Histopathology • Biopsies reveal septal panniculitis marked by an inflammatory infiltrate localized to the septa of the subcutaneous adipose tissue. • The inflammatory infiltrate primarily consists of lymphocytes and macrophages. • Aggregates of histiocytes encircled by cleft-like spaces are well-documented (Mieschner’s radial granuloma).
Prognosis: The ailment typically resolves spontaneously within weeks, with the skin nodules ultimately diminishing and discoloring similarly to a bruise.
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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
