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Skin Pathology > Skin Pathology > Flashcards

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
Q

How does Lentigo differ from freckles?

A

It does not darken when exposed to sunlight

26
Q

Who does Lentigo affect?

A

Infants and Children

27
Q

Name the varients of Nevocellular (Melanocytic) Nevi.

A 
Congenital Nevus
Halo Nevus
Blue Nevus
Spindle/Epithelial Cell Nevus (Spitz Nevus)
Dysplastic Nevus
28
Q

Describe a Congenital Nevus

A

Hairy - because they respect the hair follicle
Deep Dermal/SubQ Growth
Present at Birth

29
Q

Describe a Halo Nevus

A

Lymphocytic Infiltration

Host immune response against Nevus Cells

30
Q

Describe a Blue Nevus

A

Non-nested Dermal Infiltration w/ assoc fibrosis

Highly dendritic
Heavily Pigmented

Black/Blue Nodule - often confused for melanoma clinically

31
Q

Describe a Spindle/Epithelial Cell Nevus (Spitz Nevus)

A

Fasicular Growth
Cytology - Large with Pink-Blue Cytoplasm
Clinical - Commmon in Children
Clinical - Red-Pink Nodule
Clinical - Confused with Hemangioma clinically

32
Q

Describe a Dysplastic Nevus

A

Large Intraepidermal Nests
Cytology - Atypia
Clinical - Potential Precursor for Mal. Melano.

33
Q

Types of Melanocytic Nevus

A
  1. Junctional
  2. Compound
  3. Intradermal
34
Q

Describe Junctional Nevus

A

Round Nests of Melanocytes
Pigmented and Flat
It matures - which indicates benign
Junctional –> Compound –> Intradermal

35
Q

Describe Compound Nevus

A

Junctional Nevus that starts to grow into dermis as nests/cords

36
Q

Describe Intradermal Nevus

A 
Old Lesion
Nests are lost and cells shrink
Matured lesion
Flesh Colored
Slightly more raised
37
Q

Maturation of Melanocytic Nevus

A

Flat –> Raised
Colored –> Flesh Colored
Junctional –> Compund –> Intradermal

38
Q

Steps of tumor progression in Dysplastic Nevus

A

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
Q

Clinical Features of Dysplastic Nevus

A
  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
Q

Morphology of Dysplastic Nevus

A
  1. Flat with “pebbly” surface
    or
  2. Target like with a darker raised center
  • irregular borders
41
Q

What will make more likely a progression from Dysplastic Nevus –> Malignant Melanoma

A

Increase in 1) abnormal architecture and 2) abnormal cytologic features

42
Q

What has the ability to progress to Malignant Melanoma?

A

Dysplastic Nevus (recognize that the Melanocytic Nevus - junctional, compound, intradermal - does not progress)

NOT ALL PROGRESS

43
Q

Heritable Melanoma Syndrome

A

Prone to develop melanoma

Can have rapid progression of lesion

44
Q

How do you sample a pigmented lesion?

A

NOT with a punch biopsy

45
Q

How is prognosis determined in malignant melanoma?

A

By the depth of the lesion - more deep is more bad

46
Q

Describe Radial Phase as it pertains to Malignant Melanoma

A

Cells proliferate laterally
Grow horizontally within epidermis
Do not have metastatic ability in this phase

Types:
Lentigo Maligna
Superficial Spreading
Acral/mucosal Lentiginous

47
Q

Describe Vertical Phase as it pertains to Malignant Melanoma

A
  • Advanced Phase
  • Cells proliferate as expansile balloon like nodules
  • Going into dermis (depth of invasion determines prognosis)
  • No cellular maturation
  • Nodular phase
48
Q

What locations have worse prognosis for malignant melanoma?

A
  • Trunk and face have worse prognosis when compared to extremities
49
Q

What are the items to look at when deciding the prognosis of Malignant Melanoma?

A
  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
Q

Describe Breslows Level

A

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
Q

At what depth is metastasis not yet a concern?

A

3mm = 84% chance)

Lesions >1.7 mm have potential to spread via Lymph Nodes

52
Q

What is the most commonly mutated gene in FAMILIAL melanoma?

A

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
Q

How should you sample melanoma?

A

Not with punch biopsy.

You should do an excision that contains the entire lesion plus normal tissue on all edges.

54
Q

What procedures are utilized in determining stage of melanoma?

A
  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
Q

What imaging techniques are utilized with melanoma?

A

CXR
CT Scan
MRI
PET Scan

56
Q

Histologically Describe Epidermal Inclusion Cyst

A

Lined by stratified squamous epithelium that contains a granular layer
Cyst is filled with concentric layers of lamellated keratin

57
Q

Describe a Pilar/Trichilemmal Cyst

A

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
Q

Describe Acanthosis Nigricans

A

Zone of hyperpigmentation
Velvet like texture
Common in areas of flexion
Insulin Resistant Syndromes

59
Q

Describe Seborrhetic Keratosis

A

Basal Cells with HORN CYSTS
MC benign epidermal tumor
appear STUCK ON
PIGMENTED

60
Q

Describe Keratoacanthoma

A

RAPID GROWING
NODULE - Benign CRATERIFORM
looks like well differentiated squamous cell carcinoma

61
Q

Describe Actinic (Solar) Keratosis

A 
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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