Description of lesions Macule / Patch Papule Nodule plaque Vesicle & Bullae Scale dry, flaky area on skin Lichenification thickened and rough skin characterized by prominent skin markings

1. Dermatopathology

2. Skin - Histology

3. Skin - Histology

4. Skin - Histology
• Langerhans cells:
– antigen-processing histiocytic cells located in the
epidermis that contain Birbeck granules
• Merkel cells
– Neuroendocrine cells in the basal layer of the
epidermis that have neuroendocrine granules
– May have tactile function

5. Description of lesions
– Macule / Patch
A circumscribed area of any size
characterized by its flatness and usually
distinguished from surrounding skin by
its coloration

6. Description of lesions
Papule Elevated solid area 5 mm or less
across

7. Description of lesions
Nodule
Elevated solid area greater than 5
mm across

8. Description of lesions
• Plaque Elevated flat-topped area, usually
greater than 5 mm across

9. Description of lesions
• Vesicle & Bullae
Vesicle
A fluid-filled raised area 5 mm or less
across
Bulla
Fluid-filled raised area greater than 5
mm across

10. Description of lesions
• Pustule
pus
Pustule – discrete, pus-filled raised area

11. Description of lesions
• Scale dry, flaky area on skin
• Lichenification thickened and rough skin
characterized by prominent skin markings
(repeated rubbing)

12. Description of lesions
• Wheal (urticaria)
Itchy, transient, elevated area with
variable blanching and erythema
formed as the result of dermal edema

13. Erosions & Ulcer

14. Skin Pathology
Microscopic - Definitions
• Hyperkeratosis
– Hyperplasia of the stratum corneum often associated
with a qualitative abnormality of the keratin; clinically
presents as a white patch (leukoplakia)
• Parakeratosis
– Keratinization characterized by retention of the nuclei in
the stratum corneum
• Acanthosis
– Epidermal hyperplasia(Squamous cell layer or prickle cell
layer) usually due to hyperkeratosis

15. Hyperkeratosis

16. Parakeratosis

17. Acanthosis

18. Skin Pathology - Definitions
• Dyskeratosis
– Abnormal keratinization occurring prematurely within
individual cells or groups of cells below the stratum
granulosum
• Acantholysis
– Loss of intercellular connections resulting in loss of
cohesion between keratinocytes; may be due to
immunologic destruction of the intercellular bridges as in
pemphigus
• Papillomatosis
– Hyperplasia of the papillary dermis with elongation and/or
widening of the dermal papillae

19. Dyskeratosis

20. Acantholysis

21. Papillomatosis

22. Disorders of pigmentation and
melanocytes

23. Vitiligo
• Partial or complete loss of melanocytes in epidermis
• Auto-immune disorder associated with pernicious
anemia, Addison’s disease, and thyroid diseases
• Clinical : More noticeable in dark skinned
Flat, well demarcated macules of pigment loss in
Hands, wrists, axilla, perioral, periorbital areas of skin
• Histology : Loss of melanocytes in epidermis and
confirmed by EM
• Differential Diagnosis : Albinism, where melanocytes
are normal but basal keratinocytes contains no
pigment due to deficient tyrosinase enzyme

24. Vitiligo

25. Freckles (Ephelis)
• Most common pigmented lesions
of childhood in fair-skinned
individuals
• Small tan red macules, first
appear in early childhood after
sun exposure
• Tend to fade and reappear in a
cyclic fashion with winter and
summer, respectively
• Histology – increased
pigmentation of basal
keratinocytes with normal
number of melanocytes

26. Melasma
• A mask-like zone of facial
hyperpigmentation commonly
associated with pregnancy
• Presents as poorly defined, blotchy
macules involving the cheeks,
temples, and forehead bilaterally
• May darken with sun exposure;
often resolves after end of
pregnancy; also associated with oral
contraceptives
• 2 types – epidermal type & dermal
type
• Pathology – Enhanced pigment
transfer

27. Nevi
• A nevus is any congenital lesion of the skin
• A nevocellular nevus (Moles)- refers to any
congenital or acquired neoplasm of the
melanocytes
• Nevocellular nevi are generally tan to deep
brown, uniformly pigmented, small papules
with well-defined, rounded borders (usually
less than 6 mm)

28. Nevocellular Nevi
• Most are subdivided into junctional,
intradermal, or compound types
• Most nevocellular nevi begin as junctional
nevi
–Junctional-->compound-->intradermal
nevus
–Shows maturation with loss of melanin
and becoming more spindle

29. Junctional Nevi

30. Compound Nevus

31. Intradermal Nevus

32. Nevocellular Nevus: variants
• Congenital nevus
• Blue nevus
• Spindle and epithelioid cell nevus
• Halo nevus
• Dysplastic nevus

33. Congenital Nevus
• This lesion is large and
has some color
variability but it’s
edges are smooth.
• As it’s name implies,
they are often present
from birth.
• Because of their large
size, they may
simulate melanomas.

34. Congenital Nevus -Giant Hairy Type
• Rarely congenital nevi are large and cover large
areas of the body .A typical such distribution is
in the bathing trunk area (Bathing trunk nevus)
• These extend deeply into subcutaneous fat and
deeper tissues.
• In addition to causing severe disfigurement
they represent an increased risk of melanoma.

35. Giant Hairy Nevus (Congenital)

36. Halo Nevus
• White depigmented halos surrounding
compound nevi.
• Represents a host immune response against
nevus cells and surrounding normal
melanocytes
• Microscopic infiltrates of lymphocytes
surrounding nevus cells
• Nevi tend to disappear leaving only the white
macular portion

37. Halo Nevomelanocytic Nevi

38. Blue Nevus
• A black-blue nodule
• Often confused clinically with melanoma
• Non-nested dermal infiltration, fibrosis,
heavily pigmented nevus cells

39. Blue Nevus
• Note the distinctly bluish appearance of this lesion.

40. Blue Nevus
• Note the spindle shaped cells with the deep melanin
pigmentation. The latter by the Tindell effect produces
the bluish color to this type of nevus.

41. Spitz Nevus
Red-pink nodule
• May be confused with hemangioma
• Junctional nests with dermal maturation
• Large spindle and epithelioid cells
(Confused with melanoma)

42. Dysplastic nevus
• Synonyms – BK mole, Clark’s melanocytic nevi
(CMN)
• Tend to occur on sun exposed and non-sun-exposed
skin
• Familial dysplastic nevus syndrome is inherited in an
autosomal dominant pattern
• In patients with dysplastic nevi and a family history of
melanoma, the lifetime risk of developing melanoma is
near 100%
• Patients with sporadic dysplastic nevi have only a slight
increased risk of developing melanoma

43. Dysplastic Nevus Syndrome
• Dysplastic nevi are commonly associated with
patients who have multiple scattered nevi over the
entire body (dysplastic nevus syndrome) with
individual lesions that have a diameter of greater
than 1 cm.
• Histology – Compound nevi with fusion of adjacent
nests.
• Nevus cells replace the basal cells in dermo-
epidermal junction (lentiginous hyperplasia)
• Cytological atypia of melanocytes, melanin
incontinence
• Peculiar linear fibrosis surrounding rete ridges

44. Dysplastic Nevus
Syndrome

45. Dysplastic Nevus (left); five years later,
melanoma-in-situ

46. Malignant Melanoma
• Derived from melanocytes
• Risk Factors: Caucasians
• Dysplastic nevi
• Large congenital nevi
• Past history of melanoma
• Family history of melanoma
• Xeroderma pigmentosa
• Fair skin – regardless of sunburn history
• Severe sunburns in childhood
• Brief, intermittent, intense UV exposure, especially
during 10 –24 yr of age

47. Tumor progression in dysplastic nevi
A, Lentiginous melanocytic hyperplasia. B, Lentiginous junctional nevus.
C, Lentiginous compound nevus with abnormal architectural and cytologic features (dysplastic nevus).
D, Early melanoma, or radial growth phase melanoma (large dark cells in epidermis).
E, Advanced melanoma (vertical growth phase) with malignant spread into the dermis and vessels

48. Melanoma growth
• Radial
– Flat lesion
– Histologic horizontal pattern
– Do not metastasize
• Vertical
– Nodular lesion
– Histologic downward growth pattern
– Metastatic potential related to depth of tumor

49. Types of Melanoma
– Superficial spreading melanoma (70% of cases) -
Most common type presents usually on lower
extremities and back
– Nodular melanoma = vertical growth phase when
first encountered (15% of cases)-most aggressive
– Acral lentiginous melanoma – normally seen in the
palms, soles, and sub-ungual regions (8% of cases).
More common in dark-skinned individuals.
– Lentigo Maligna Melanoma – a large superficial
spreading melanoma occurring in the elderly (radial
growth phase), sun exposed regions (face)

50. Malignant Melanoma
• Asymmetry
• Border irregularity
• Color variability (Variegation)
• Diameter > 6 mm
• Elevation (usually but not always present)

51. Malignant Melanoma

52. Superficial Spreading Melanoma

53. Nodular Melanoma

54. Acral Lentiginous Melanoma

55. Lentigo Maligna(Hutchinson’s Freckle)
• Lentigo Maligna is a subtype of malignant
melanoma which typically occurs on sun exposed
skin of the face. It is slow growing and stays in the
in-situ stage for a long time. If neglected it will
become invasive.

56. Malignant Melanoma

57. Malignant Melanoma

58. Amelanotic melanoma

59. Melanomas – Prognosis
• 5 yr survival rate – 81%
• Mitoses
• Evidence of immune response – TILs
• Location – Central Vs Extremities
• Gender
• Depth of the tumor
– Breslow’s system 0.76mm Vs 1.7 mm

60. Benign neoplasms & Cystic disorders
of epidermis

61. Keratoses (Horny Growth)
• Seborrheic keratosis (Basal cell papilloma)
– Common benign epidermal tumor affecting middle-
aged or older individuals seen more in trunks
– Gross –Round, flat, pigmented,coin like plaques
with “stuck-on” appearance
– Easily scraped from the skin’s surface
– Closer observation will show small pores impacted
with keratin differentiating from melanomas
– Microscopically- Exophytic mass composed of
sheets of small cells (Basaloid cells) with variable
melanin pigmentation along with Hyperkeratosis of
surface and horn cysts (Keratin filled cysts) in
deeper areas

62. Seborrheic Keratosis

63. Seborrheic Keratosis

64. Seborrheic Keratosis -This field has the
classical features of a seborrheic keratosis

65. Seborrheic Keratosis
• Sudden appearance of large numbers of
seborrheic keratoses is a possible indication of
an internal malignancy (Leser-Trelat sign) as a
part of paraneoplastic syndrome
• TGF-alpha produced by tumours may result in
the skin lesions