Preface

Agam is a group of budding medicos, who are currently doing their under graduation in
various Medical Colleges across Tamil Nadu and Pondicherry. The group was initiated on 18th
November 2017, in the vision of uniting medicos for various social and professional causes.

We feel delighted to present you Agam Pathology notes prepared by Agam Divide and Rule
2020 Team to guide our fellow medicos to prepare for university examinations.

This is a reference work of 2017 batch medical students from various colleges. The team
took effort to refer many books and make them into simple notes. We are not the authors of the
following work. The images used in the documents are not copyrighted by us and is obtained from
various sources.

Dear readers, we request you to use this material as a reference note, or revision note, or
recall notes. Please do not learn the topics for the 1st time from this material, as this contain just the
required points, for revision.
Acknowledgement

On behalf of the team, Agam would like to thank all the doctors who taught us Pathology.
Agam would like to whole heartedly appreciate and thank everyone who contributed towards the
making of this material. A special thanks to Vignesh M, who took the responsibility of leading the
team. The following are the name list of the team who worked together, to bring out the material in
good form.

• Vidhya Lakshmi M D
• Afrah Marzook
• Vimal. K
• Dhanshree Bakhru
• Amrutha Priya Devi B
• Vignesh. M
 THE SKIN
SHORT NOTES:
1. Basal cell carcinoma of skin
2. Malignant melanoma
3. Intradermal nevus

SHORT ANSWERS
1. Blue Nevus
2. Characteristic features of Mycosis Fungoides

UPDATES

PATHOLOGY AGAM
SHORT NOTES
1. BASAL CELL CARCINOMA
 Local aggressive cutaneous tumor
 Slow growing
 Rarely metastasize
 Multiple basal cell cancer – Nevoid Basal cell carcinoma syndrome or basal cell nevus or
Gorlin syndrome
 Accompanied by medulloblastomas, ovarian cancer, odontogenic keratocysts and
developmental abnormalities
 UV rays exposure can cause mutations C-T transitions.

PATHOGENESIS
 Mutations in the gene activate Hedgehog pathway signaling
 Gene: PTCH gene (tumor suppressor)
 Function of PTCH gene: PTCH Protein ,receptor for hedgehog determines hair follicle
formation and hair growth
 Action: suppression of PTCH gene

GROSS MORPHOLOGY
 Nodulo ulcerative- small nodules undergo central ulceration
 Pearly rolled margins are seen
 Tumor enlarges in size by burrowing and by destroying the tissues locally like a rodent
and hence named as Rodent Ulcer

MICROSCOPIC FEATURES
 Proliferation of basaloid cells
 Peripheral palisading is seen
 Basaloid cells are arranged in the form of island called tumour island

AGAM PATHOLOGY
2. MALIGNANT MELANOMA
 Deadly skin lesions arising from melanocytes
 Areas commonly affected in
 Males – trunk
 Females – leg
 Other than skin, melanoma is seen in orbit , uvea, meninges, oral cavity and esophagus
 Melanocytic tumors can be:
 Benign Nevus (mole)
 Malignant Melanoma

CAUSES:
 Family history
 High age
 Exposure of white skin to sunlight and UV light
 Genetic mutation

GENETIC MUTATIONS - PATHOGENESIS

 Familial and hereditary cases revealed germ line mutations in
 CDKN2A gene which encodes for cyclin dependent kinase inhibitor
 Mutational loss of PTEN gene
 Mutation in tumor suppressor gene but not p53 gene
PROTO- MODE OF ASSOCIATED
ONCOGENES ACTIVATION HUMAN TUMOURS
Growth factor like Melanoma
Fibroblast growth FGF3 Amplification Breast cancer
factors Bladder cancer
Melanoma
Cyclin dependent Amplification or point
CDK4 Glioblastoma
kinase mutation
Sarcoma
Tumour suppressor Suppression of tumour
CDKN2A Melanoma
gene suppressor genes
Telomerase activity TERT Activation Melanoma

PATHOLOGY AGAM
HISTOLOGY
 Junctional activity is seen
 Fine melanin pigments are present
 Eosinophilic nucleoli is present
 Mitotic figures are seen

ABCDE OF MELANOMA
 A – Asymmetry
 B – Border irregularity
 C – Colour variation
 D – Diameter > 6 mm
 E – Evolution & Elevation of size

GROSS MORPHOLOGY: (Here the prognosis gets worse as we go down)

S.NO TYPE FEATURES
 Insitu
Lentigo Maligna
1  Slow growing tumour
Melanoma
 Good prognosis
 Slightly elevated
Superficial
 Variegated color
2 spreading
 Ulcerated surface
melanoma
 Poor prognosis
 Ulcerated
Acral lentigenous  Metastasize
3
melanoma  Bad prognosis
 Palms, soles, mucosal surfaces are involved
 Deeply pigmented
 Ulcerated
Nodular
4  Elevated
melanoma
 Nodular
 Worst prognosis
 Neural invasion
Desmoplastic
5  Fibrotic stroma
melanoma
 Worst prognosis

AGAM PATHOLOGY
BRESLOW THICKNESS
It is the measurement of the depth of
the melanoma from the surface of skin to the
deepest point of the tumour. It is measured in
millimeters

CLARKS STAGING OF MELANOMA

PROGNOSTIC FACTORS
 Tumour depth (Breslow thickness)
 Mitotic figures
 Ulceration of overlying skin
 Gender
 Location

MANAGEMENT:
 Resistant to chemotherapy and radiotherapy
 Anti-CTLA4 blocking antibodies and Anti-PD1 blocking antibodies are used

PATHOLOGY AGAM
3. INTRADERMAL NAEVUS
 An intradermal nevus (also called an intradermal melanocytic nevus) is simply a classic
mole or birthmark.
 It typically appears as an elevated, dome-shaped bump on the surface of the skin.
 It’s estimated that about one percent of newborns are born with an intradermal nevus.
 “Nevus” refers to the mole. “Intradermal” means that the cells of the mole are located
beneath the most external layer of skin.
 In most cases, intradermal nevi appear after adolescence and are benign (noncancerous)
skin growth.

GROSS MORPHOLOGY
 Appears as a small lump on the skin
 Has the same degree of pigmentation as the surrounding skin
 Sometimes hair follicles are found coming out
 In some cases, brown spots are seen due to the presence of blood vessels
 Commonly found in scalp, neck, eyelid, upper arms and legs
 Normal size: 5mm – 1cm
 Typically round and well defines, sometimes appear warty and domed

MICROSCOPIC FEATURES
 Symmetrical lesion
 Matures with depth
 Rare mitosis (superficial)
 No nucleoli

CAUSES OF INTRADERMAL NAEVUS

 Sun damage
 Genetic factors
 Immunosuppressive treatments

AGAM PATHOLOGY
SHORT ANSWERS
1. BLUE NEVUS
 Collection of Type-C melanocytes in the dermis
 They are heavily pigmented nevus cells
 Blue color is due to the Tyndall effect exhibited by the deeply present melanin pigment
 Common sites – head, neck and upper extremity
 Microscopic features
 Deep dermal proliferation of type C melanocytes,
 No junctional or superficial dermal involvement
 Clinically confused with melanoma

2. MYCOSIS FUNGOIDES
 Also known as Cutaneous t cell lymphoma
 They are peripheral T cell lymphoma derived from mature post thymic T lymphocyte
 Lesions involve truncal areas, and include scaly, red brown patches, scaling plaques that
may be confused with psoriasis.
 Fungating nodules also seen
 Eczema like lesions raised, indurated, irregular outlines and erythematous plaques
supervene.
 Sezary Syndrome: There is seeding of blood by malignant T cells accompanied by diffuse
erythema and scaling of entire body surface (erythroderma)
 Sezary-Lutzer cells: Band like aggregates may invade epidermis as single cells and form
clusters (Pautrier microabcesses)

UPDATES
1. BENIGN FIBROUS HISTIOCYTOMA (DERMATOFIBROMA)
 Several fusion genes, including one in which one partner is the gene for the receptor
tyrosine kinase ALK, have been identified in a subset of cases, suggesting that these
proliferations are best considered true neoplasms.
 These tumors appear to be composed at least partially of dermal dendritic cells.
2. ONE LINER:
 Metastasis of Dermatofibrosarcoma Protuberans is seen with tumors that exhibit greater
cytologic atypia.

PATHOLOGY AGAM
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AGAM PATHOLOGY