Dermatopathology PDF

Summary

This presentation provides an overview of dermatopathology, covering various skin conditions such as inflammatory diseases, blistering disorders, pigmentation disorders, and neoplastic conditions. It details normal skin structure and function, and examines specific diseases like psoriasis, vitiligo, and melanoma. The presentation also includes diagnostic features, risk factors, and histological details of the conditions discussed.

Full Transcript

Dermatopathology Dr Mbayah J Etabale Anatomical Pathologist and Lecturer of Pathology Outline Normal structure and function Inflammatory diseases Blistering disorders Disorders of skin pigmentation Neoplastic conditions 2 Objectives To...

Dermatopathology Dr Mbayah J Etabale Anatomical Pathologist and Lecturer of Pathology Outline Normal structure and function Inflammatory diseases Blistering disorders Disorders of skin pigmentation Neoplastic conditions 2 Objectives To describe the normal structure and function of the skin To write short notes on conditions under the term acute eczematous dermatitis To describe the pathogenesis and morphological features of psoriasis To highlight the distinguishing pathogenetic features of pemphigus vulgaris, bullous pemphigoid and dermatitis herpetiformis To classify naevi To describe the aetiology, pathogenesis, morphological and clinical features of melanoma 3 Normal Structure and Function 4 Normal Structure and Function Junqueira’s Basic Histology, Text and Atlas, 14 e 5 Normal Structure and Function Protection Temperature UV light Thermoregulation Chemical stimuli Metabolic Functions Thermal stimuli Synthesis of vitamin D3 Mechanical insults Adipose stores triglycerides Immunity Cosmesis Sensory Touch Pressure Pain 6 Inflammatory Diseases 1. Acute Eczematous Dermatitis: Atopic Dermatitis, Contact Dermatitis 2. Chronic Inflammatory Dermatosis: Psoriasis 7 Atopic Dermatitis Pruritic, erythematous, oozing rash with vesicles Type I hypersensitivity reaction sciencephotolibrary 8 Contact Dermatitis Pruritic, erythematous, oozing rash with vesicles Arises from contact with inducing agent Poison ivy, certain metals (allergic contact dermatitis) Irritants e.g. detergent (irritant contact dermatitis) Type IV hypersensitivity reaction The Australasia College of Dermatologists 9 Psoriasis 1 – 2% of population Immunological basis Interplay between host genetic susceptibility and environmental factors Unknown antigen Pathogenesis Sensitized T cells (CD4 & CD8) accumulate in the epidermis and secrete cytokines and GF that induce keratinocyte hyperproliferation IL-12, γIFN, TNF, IL-17 Condition characterized by exacerbations and remissions Gross Preference for extensor surfaces (elbows, knees), groin, scalp, lumbar region, umbilical region Red plaque covered with silvery-white scales Removal of the scale causes petechial bleeding (Auspitz sign) Brown nail discoloration Pitting of nails 5 – 10% of cases associated with psoriatic arthritis (psoriasis, arthritis & spondylosis) 10 Psoriasis 11 Blistering Dermatoses Pemphigus Vulgaris Bullous Pemphigoid Dermatitis Herpetiformis 12 Blistering Dermatoses Group of conditions in which blisters are the primary and most distinctive feature Autoantibodies to specific cell adhesion molecules Can occur at multiple levels within the skin Their location is essential for histological diagnosis Examples: Pemphigus Vulgaris Bullous Pemphigoid Dermatitis Herpetiformis 13 Blistering Dermatoses Features Pemphigus Vulgaris Bullous Pemphigoid Dermatitis Herpatiformis Antibody target Desmosome Hemidesmosomes Gliadin, reticulin Pattern on IF Net-like pattern Linear pattern at the IgA positive clusters at the basement membrane tips of dermal papillae Bullae Suprabasal Subepidermal Subepidermal 14 Blistering Disorders Robbins Basic Pathology, 10 e 15 Disorders of Skin Pigmentation Vitiligo Albinism Naevi 16 Vitiligo An autoimmune process in which in which there is partial or complete loss of melanocytes The patient develops white, non-tanning, geographic macules and patches Vitiligo affects 1% of population Site: Hands, wrists, and perioral and anogenital regions May occur alone or in association with autoimmune disease – autoimmune addisonism, autoimmune atrophic gastritis, Hashimoto thyroiditis, DM 1 17 Albinism Congenital lack of pigmentation Due to an enzyme defect (Tyrosinase) that impairs melanin production Ocular and oculocutaneous forms Increased risk of cutaneous malignancies due to reduced protection against UV rays 18 Melanocytic Naevi Aka mole Benign neoplasm of melanocytes Congenital naevus Present at birth Large: 6 – 15 mm Often associated with hair Acquired naevus Appear after birth, usually around puberty Begins as nests of melanocytes at the dermoepidermal junction – junctional naevus Most common mole in childhood Grows by extension into the dermis – compound naevus Junctional component is eventually lost resulting in an intradermal naevus Most common mole in adulthood Tend to involute spontaneously in old age Macule or papule, small diameter (< 6 mm), symmetrical, well-defined borders, evenly pigmented Dysplasia may arise, precursor to melanoma 19 Melanocytic Naevi 20 Neoplastic Disorders Squamous Cell Carcinoma Basal Cell Carcinoma Melanoma 21 Squamous Cell Carcinoma A locally invasive malignant tumour that Prolonged exposure to arsenic can metastasize Betel chewing Occurs in sun-exposed skin HPV Familial Commoner in fair-skinned people Genetic syndromes Most often on the face, preferentially Xeroderma pigmentosum involving the lower lip Often preceded by pre-invasive lesions Pathogenesis related to UV exposure (actinic keratosis, CIS, Bowen disease) Risk factors Gross nodular mass, ulcerated Prolonged exposure to sunlight Micro Burn scars Malignant epithelial cells that tend to Chronic skin ulcers keratinise and form keratin pearls Sites of draining sinuses Histologically indistinguishable from SqCC in Albinism mucosal sites Following radiation Rx Rx – excision Immunosuppressive therapy 22 Squamous Cell Carcinoma Robbins Basic Pathology, 10e 23 Basal Cell Carcinoma Malignant proliferation of basal cells of the epidermis Most common cutaneous malignancy in Caucasians? Risk factors stem from UVB-induced DNA damage Prolonged exposure to sunlight Albinism Xeroderma pigmentosum Gross: elevated nodule surrounded by telangiectatic vessels Histology: basal cells with peripheral palisading Rx – surgical excision 24 Basal Cell Carcinoma Robbins Basic Pathology, 10e 25 Melanoma Malignant tumour of melanocytes Dysplastic naevus syndrome DEADLIEST of all cutaneous malignancies Gross: mole-like cutaneous growth with Only 4% of skin cancers but majority of skin “ABCD’ cancer deaths Asymmetry Most often originate in the skin but can Borders are irregular arise elsewhere too e.g. in the eyes, ears, Colour is not uniform GIT, meninges Diameter > 6 mm Quickly metastasizes Micro: 2 main growth patterns: Regional LNs, lung, liver, GIT, bone, CNS, Radial growth – horizontally along the skin epidermis and superficial dermis Risk factors: Low risk of metastasis UVB-induced DNA damage Vertical growth – into the deep dermis Prolonged exposure to sunlight Increased risk of metastasis Albinism Xeroderma pigmentosum 26 Melanoma: Clinicopathological Forms Superficial spreading melanoma Nodular melanoma Most common subtype (75%) 15% Dominant early radial growth Early vertical growth Stays in-situ for months only Poor prognosis Lentigo maligna melanoma Acral lentiginous melanoma 5% 2 – 3% Sun-exposed skin of the face and Palms and soles; nail bed head and neck region Commonest form in dark-skinned Older people; peak incidence is 70 people years Not related to UV light exposure Stays in-situ for years 27 Melanoma: Morphology 28 Melanoma: Staging T N M T0 No evidence of primary tumour N0 No regional lymph node metastasis M0 No distant metastasis Tis Melanoma in situ N1 Spread to 1 regional lymph node M1 Distant metastasis T1 Melanoma ≤ 1 mm in thickness N2 Spread to 2 – 3 regional lymph nodes T2 Melanoma 1.01 – 2 mm in thickness N3 Metastasis to ≥ 4 regional lymph nodes T3 Melanoma 2.01 – 4 mm in thickness T4 Melanoma > 4 mm in thickness Stage Grouping T N M 0 Tis N0 M0 I T1 - T2a N0 M0 II T2b - T4b N0 M0 III T1 – T4b ≥ N1 M0 IV Any T Any N M1 29 References Fundamentals of Pathology, 2017 Robbins Basic Pathology, 10e 30

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