Skin Pathology Flashcards
Layers of the epidermis
- Stratum Corneum
- Stratum Lucidum (palms and soles)
- Stratum Granulosum
- Stratum Spinosum
- Stratum Basalis
Microscopic terms associated with stratum corneum
Hyperkeratosis - thickened stratum corneum - abnormal keratin quality (scaly skin)
Parakeratosis - retention of nuclei in the stratum corneum
Microscopic terms associated with stratum granulosum
Hypergranulosis - hyperplasia of stratum granulosum due to intense rubbing
Dyskeratosis - premature abnormal keratinization below the stratum granulosum - EOSINOPHILIC
Microscopic terms associated with stratum basalis
Lentiginous - linear pattern of melanocyte proliferation within the epidermal basal cell layer
Lentiginous melanocytic hyperplasia - occurs as a reactive change or part of neoplasm
Vacuolization - vacoules within or adjacent to cells - refers to basal cell basement membrane zone area
Terms that apply to all levels of the epidermis
Exocytosis - infiltration of epidermis by inflammatory or circulating blood cells
Acanthosis - diffuse epidermal hyperplasia
Spongiosis - intercellular edema of epidermis
Hydropic Swelling - intracellular edema of keratinocytes - seen with INFECTIONS
Acantholysis - loss of intercellular connections –> loss of cohesion between keratinocytes
Erosion - discontinuois skin with INcomplete epidermis loss
Ulceration - discontinuous skin with complete epidermis loss
Describe Melanocytes
The melanocytes are scattered along the basal layer (every 4th — 6th cell). They have a clear cytoplasm distinguishing them from keratinocytes. They have long dendritic processes which form a complex pattern with adjacent keratinocytes allowing the transfer of melanin granules from melanocytes to keratinocytes
Etiology of Vitiligo
Loss of MELANOCYTES (partial or complete)
Must distinguish from Albinism which is due to abnormal melanin production - they have a normal number of melanocytes
Theories of Vitiligo
- Most supported = Autoimmunity. Autoantibodies against melanocytes
- Toxicity to Melanocytes
- Abnormal Macrophages and Tcells
Morphology of Vitiligo
Macules and Patches of well defined pigment loss.
Most Common Locations of Vitiligo
Hands, Axilla, Perioral, Periorbital, Anogenital
Tests for Vitiligo
Immunohisto Positive:
Tyrosinase
Melan-A
S-100
Treatment for Vitiligo
UVA Therapy + Photosensitizing Drug
Etiology of Melasma (Chloasma)
Altered Function of Melanocytes with PREGNANCY or ORAL CONTRACEPTIVES
Enhanced pigment transfer to basal keratinocytes
Histology Patterns of Melasma (there are 3)
Epidermal - Melanin Deposited in Basal Layer
Dermal - Melanin Pigment Incontinence
Mixed - A combination of Epidermal and Dermal
Morphology of Melasma
Macules and Patches
Cheeks, Temples, Forehead
“Mask of Preganancy”
What makes Melasma worse?
Sunlight.
Treatment of Melasma?
Resolves Spontaneously
May respond to topical bleaching agent
Etiology of Freckles (Ephelis)
Normal Number of Melanocytes
Increased Number of Melanosomes
Increased Amounts of Melanin Pigment in basal keratinocytes
Morphology of Frackles (Ephelis)
Macules
They are similar to NF-1 cafe au lait spots. However, NF-1 spots are independent from sun exposure and contain macromelanosomes
How do freckles differ from lentigo?
They have a cyclical presentation - intensify in the summer and fade in the winter. Lentigo maintains stable color and is independent of sun exposure.
And freckles do NOT have increased number of melanocytes whereas lentigo do have increased number of melanocytes
What is the most common pigmented lesion in light skinned people?
The freckle
Etiology of Lentigo
Benign
Localized
Melanocyte Hyperplasia ( increased number)
Who does Solar/Actinic Lentigo affect?
Older Adults (also referred to as Liver Spots) NOT precancerous
Morphology of Lentigo
Patches Linear Melanocytic Hyperplasia Hyperpigmented Basal Cell Layer Elongation and thinning of the rete ridges NOT Precancerous
How does Lentigo differ from freckles?
It does not darken when exposed to sunlight
Who does Lentigo affect?
Infants and Children
Name the varients of Nevocellular (Melanocytic) Nevi.
Congenital Nevus Halo Nevus Blue Nevus Spindle/Epithelial Cell Nevus (Spitz Nevus) Dysplastic Nevus
Describe a Congenital Nevus
Hairy - because they respect the hair follicle
Deep Dermal/SubQ Growth
Present at Birth
Describe a Halo Nevus
Lymphocytic Infiltration
Host immune response against Nevus Cells
Describe a Blue Nevus
Non-nested Dermal Infiltration w/ assoc fibrosis
Highly dendritic
Heavily Pigmented
Black/Blue Nodule - often confused for melanoma clinically
Describe a Spindle/Epithelial Cell Nevus (Spitz Nevus)
Fasicular Growth
Cytology - Large with Pink-Blue Cytoplasm
Clinical - Commmon in Children
Clinical - Red-Pink Nodule
Clinical - Confused with Hemangioma clinically
Describe a Dysplastic Nevus
Large Intraepidermal Nests
Cytology - Atypia
Clinical - Potential Precursor for Mal. Melano.
Types of Melanocytic Nevus
- Junctional
- Compound
- Intradermal
Describe Junctional Nevus
Round Nests of Melanocytes
Pigmented and Flat
It matures - which indicates benign
Junctional –> Compound –> Intradermal
Describe Compound Nevus
Junctional Nevus that starts to grow into dermis as nests/cords
Describe Intradermal Nevus
Old Lesion Nests are lost and cells shrink Matured lesion Flesh Colored Slightly more raised
Maturation of Melanocytic Nevus
Flat –> Raised
Colored –> Flesh Colored
Junctional –> Compund –> Intradermal
Steps of tumor progression in Dysplastic Nevus
Melanocytic Hyperplasia –> Junctional Nevus –> Dysplastic Nevus (BUZZ** Abnormal Archetecture and Cytologic Features) –> Early Melanoma (Radial Growth Phase) —> Advanced Melanoma (Vertical Growth Phase) with malignant spread into dermis and vessels
Clinical Features of Dysplastic Nevus
- Can occur on Sun or NON-Sun exposed skin
- MOST are clinically stable - will not progress
- Trunk has worse prognosis than extremeties
- Dysplastic Nevus is a precursor to malignant melanoma
Morphology of Dysplastic Nevus
- Flat with “pebbly” surface
or - Target like with a darker raised center
- irregular borders
What will make more likely a progression from Dysplastic Nevus –> Malignant Melanoma
Increase in 1) abnormal architecture and 2) abnormal cytologic features
What has the ability to progress to Malignant Melanoma?
Dysplastic Nevus (recognize that the Melanocytic Nevus - junctional, compound, intradermal - does not progress)
NOT ALL PROGRESS
Heritable Melanoma Syndrome
Prone to develop melanoma
Can have rapid progression of lesion
How do you sample a pigmented lesion?
NOT with a punch biopsy
How is prognosis determined in malignant melanoma?
By the depth of the lesion - more deep is more bad
Describe Radial Phase as it pertains to Malignant Melanoma
Cells proliferate laterally
Grow horizontally within epidermis
Do not have metastatic ability in this phase
Types:
Lentigo Maligna
Superficial Spreading
Acral/mucosal Lentiginous
Describe Vertical Phase as it pertains to Malignant Melanoma
- Advanced Phase
- Cells proliferate as expansile balloon like nodules
- Going into dermis (depth of invasion determines prognosis)
- No cellular maturation
- Nodular phase
What locations have worse prognosis for malignant melanoma?
- Trunk and face have worse prognosis when compared to extremities
What are the items to look at when deciding the prognosis of Malignant Melanoma?
- measurement of tumor depth in mm
- number of mitosis per square mm
- presence of immune response
- presence of tumor infiltrating lymphocytes
- Gender
- Location (trunk vs extremeity)
Describe Breslows Level
Used in measuring malignant melanoma depth
Measure from the top of the granular layer to the bottom of the melanoma
(old version was Clark’s Levels)
At what depth is metastasis not yet a concern?
3mm = 84% chance)
Lesions >1.7 mm have potential to spread via Lymph Nodes
What is the most commonly mutated gene in FAMILIAL melanoma?
p16INK4A (also known as cyclin-dependent kinase inhibitor 2, or CDNK2) is the most commonly mutated gene in familial melanoma, in one study affecting 92% of melanoma patients from families with FMS
How should you sample melanoma?
Not with punch biopsy.
You should do an excision that contains the entire lesion plus normal tissue on all edges.
What procedures are utilized in determining stage of melanoma?
- Wide Local Excision
- Lymph Node Mapping w/ Sentinel Node Biopsy - ). The surgeon removes only the nodes with the radioactive substance or dye. A pathologist then checks the sentinel lymph nodes for cancer cells. If no cancer cells are detected, it may not be necessary to remove additional nodes.
What imaging techniques are utilized with melanoma?
CXR
CT Scan
MRI
PET Scan
Histologically Describe Epidermal Inclusion Cyst
Lined by stratified squamous epithelium that contains a granular layer
Cyst is filled with concentric layers of lamellated keratin
Describe a Pilar/Trichilemmal Cyst
Similar to Epidermal Inclusion Cyst
Except resembles follicular epithelium w/o granular layer
Occurs in scalp
Filled by homogenous mixture of keratin and lipid
Has a pilosebacous structure attached to cyst
Describe Acanthosis Nigricans
Zone of hyperpigmentation
Velvet like texture
Common in areas of flexion
Insulin Resistant Syndromes
Describe Seborrhetic Keratosis
Basal Cells with HORN CYSTS
MC benign epidermal tumor
appear STUCK ON
PIGMENTED
Describe Keratoacanthoma
RAPID GROWING
NODULE - Benign CRATERIFORM
looks like well differentiated squamous cell carcinoma
Describe Actinic (Solar) Keratosis
Solar - SUN EXPOSED SKIN Precursor for Squamous Cell Carcinoma PEARLY GREY SUPERFICIAL SHAVE BIOPSY SCALY - due to dysplasia in epidermis - maintain nucleus
