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Skin Pathology Flashcards

1
Q

Layers of the epidermis

A
  1. Stratum Corneum
  2. Stratum Lucidum (palms and soles)
  3. Stratum Granulosum
  4. Stratum Spinosum
  5. Stratum Basalis
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2
Q

Microscopic terms associated with stratum corneum

A

Hyperkeratosis - thickened stratum corneum - abnormal keratin quality (scaly skin)

Parakeratosis - retention of nuclei in the stratum corneum

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3
Q

Microscopic terms associated with stratum granulosum

A

Hypergranulosis - hyperplasia of stratum granulosum due to intense rubbing

Dyskeratosis - premature abnormal keratinization below the stratum granulosum - EOSINOPHILIC

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4
Q

Microscopic terms associated with stratum basalis

A

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

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5
Q

Terms that apply to all levels of the epidermis

A

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

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6
Q

Describe Melanocytes

A

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

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7
Q

Etiology of Vitiligo

A

Loss of MELANOCYTES (partial or complete)

Must distinguish from Albinism which is due to abnormal melanin production - they have a normal number of melanocytes

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8
Q

Theories of Vitiligo

A
  1. Most supported = Autoimmunity. Autoantibodies against melanocytes
  2. Toxicity to Melanocytes
  3. Abnormal Macrophages and Tcells
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9
Q

Morphology of Vitiligo

A

Macules and Patches of well defined pigment loss.

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10
Q

Most Common Locations of Vitiligo

A

Hands, Axilla, Perioral, Periorbital, Anogenital

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11
Q

Tests for Vitiligo

A

Immunohisto Positive:
Tyrosinase
Melan-A
S-100

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12
Q

Treatment for Vitiligo

A

UVA Therapy + Photosensitizing Drug

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13
Q

Etiology of Melasma (Chloasma)

A

Altered Function of Melanocytes with PREGNANCY or ORAL CONTRACEPTIVES

Enhanced pigment transfer to basal keratinocytes

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14
Q

Histology Patterns of Melasma (there are 3)

A

Epidermal - Melanin Deposited in Basal Layer
Dermal - Melanin Pigment Incontinence
Mixed - A combination of Epidermal and Dermal

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15
Q

Morphology of Melasma

A

Macules and Patches
Cheeks, Temples, Forehead
“Mask of Preganancy”

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16
Q

What makes Melasma worse?

A

Sunlight.

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17
Q

Treatment of Melasma?

A

Resolves Spontaneously

May respond to topical bleaching agent

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18
Q

Etiology of Freckles (Ephelis)

A

Normal Number of Melanocytes
Increased Number of Melanosomes
Increased Amounts of Melanin Pigment in basal keratinocytes

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19
Q

Morphology of Frackles (Ephelis)

A

Macules
They are similar to NF-1 cafe au lait spots. However, NF-1 spots are independent from sun exposure and contain macromelanosomes

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20
Q

How do freckles differ from lentigo?

A

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

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21
Q

What is the most common pigmented lesion in light skinned people?

A

The freckle

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22
Q

Etiology of Lentigo

A

Benign
Localized
Melanocyte Hyperplasia ( increased number)

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23
Q

Who does Solar/Actinic Lentigo affect?

A 
Older Adults (also referred to as Liver Spots)
NOT precancerous
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24
Q

Morphology of Lentigo

A 
Patches
Linear Melanocytic Hyperplasia
Hyperpigmented Basal Cell Layer
Elongation and thinning of the rete ridges
NOT Precancerous
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25
How does Lentigo differ from freckles?
It does not darken when exposed to sunlight
26
Who does Lentigo affect?
Infants and Children
27
Name the varients of Nevocellular (Melanocytic) Nevi.
``` Congenital Nevus Halo Nevus Blue Nevus Spindle/Epithelial Cell Nevus (Spitz Nevus) Dysplastic Nevus ```
28
Describe a Congenital Nevus
Hairy - because they respect the hair follicle Deep Dermal/SubQ Growth Present at Birth
29
Describe a Halo Nevus
Lymphocytic Infiltration | Host immune response against Nevus Cells
30
Describe a Blue Nevus
Non-nested Dermal Infiltration w/ assoc fibrosis Highly dendritic Heavily Pigmented Black/Blue Nodule - often confused for melanoma clinically
31
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
32
Describe a Dysplastic Nevus
Large Intraepidermal Nests Cytology - Atypia Clinical - Potential Precursor for Mal. Melano.
33
Types of Melanocytic Nevus
1. Junctional 2. Compound 3. Intradermal
34
Describe Junctional Nevus
Round Nests of Melanocytes Pigmented and Flat It matures - which indicates benign Junctional --> Compound --> Intradermal
35
Describe Compound Nevus
Junctional Nevus that starts to grow into dermis as nests/cords
36
Describe Intradermal Nevus
``` Old Lesion Nests are lost and cells shrink Matured lesion Flesh Colored Slightly more raised ```
37
Maturation of Melanocytic Nevus
Flat --> Raised Colored --> Flesh Colored Junctional --> Compund --> Intradermal
38
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
39
Clinical Features of Dysplastic Nevus
1. Can occur on Sun or NON-Sun exposed skin 2. MOST are clinically stable - will not progress 3. Trunk has worse prognosis than extremeties 4. Dysplastic Nevus is a precursor to malignant melanoma
40
Morphology of Dysplastic Nevus
1. Flat with "pebbly" surface or 2. Target like with a darker raised center - irregular borders
41
What will make more likely a progression from Dysplastic Nevus --> Malignant Melanoma
Increase in 1) abnormal architecture and 2) abnormal cytologic features
42
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
43
Heritable Melanoma Syndrome
Prone to develop melanoma | Can have rapid progression of lesion
44
How do you sample a pigmented lesion?
NOT with a punch biopsy
45
How is prognosis determined in malignant melanoma?
By the depth of the lesion - more deep is more bad
46
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
47
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
48
What locations have worse prognosis for malignant melanoma?
- Trunk and face have worse prognosis when compared to extremities
49
What are the items to look at when deciding the prognosis of Malignant Melanoma?
1. measurement of tumor depth in mm 2. number of mitosis per square mm 3. presence of immune response 4. presence of tumor infiltrating lymphocytes 5. Gender 6. Location (trunk vs extremeity)
50
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)
51
At what depth is metastasis not yet a concern?
3mm = 84% chance) | Lesions >1.7 mm have potential to spread via Lymph Nodes
52
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
53
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.
54
What procedures are utilized in determining stage of melanoma?
1. Wide Local Excision 2. 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.
55
What imaging techniques are utilized with melanoma?
CXR CT Scan MRI PET Scan
56
Histologically Describe Epidermal Inclusion Cyst
Lined by stratified squamous epithelium that contains a granular layer Cyst is filled with concentric layers of lamellated keratin
57
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
58
Describe Acanthosis Nigricans
Zone of hyperpigmentation Velvet like texture Common in areas of flexion Insulin Resistant Syndromes
59
Describe Seborrhetic Keratosis
Basal Cells with HORN CYSTS MC benign epidermal tumor appear STUCK ON PIGMENTED
60
Describe Keratoacanthoma
RAPID GROWING NODULE - Benign CRATERIFORM looks like well differentiated squamous cell carcinoma
61
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 ```

Skin Pathology (1 decks)

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