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Organ Pathology Exam 1 > Derm > Flashcards

Derm Flashcards

1
Q

What skin elements does ectoderm provide?

A

Epithelial elements: epidermis & sweat glands

Nerves and melanocytes (neuroectoderm)

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2
Q

What skin elements does mesoderm provide?

A

Fibrous tissue, blood vessels, muscle fat

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3
Q

What part of the surface does the epidermis arise from in the embryo? What about melanocytes?

A
  • from the single-layered surface embryonic ectoderm
  • Develops into a multilayered (stratified) epithelium
  • At around the 18th week it resembles neonatal epidermis with a superficial “cornified” layer
  • Melanocytes migrate during embryonic life from the neural crest to the developing epidermis
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4
Q

How does hair develop?

A

Hair develops primarily from epidermal cells, but require interactions with underlying mesenchymal cells

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5
Q

How do sweat glands develop?

A

As outgrowths of epidermal (eccrine) and follicular (apocrine) epithelia

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6
Q

Describe epidermis of the skin generally? What is the main cell type?

A

-outermost layer of the skin
-Stratified squamous epithelium
Thickness varies with location (

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7
Q

Where are melanocytes? What do they look like?

A
  • Melanocytes lay in basal layer
  • have dendritic processes to touch the different karatinocytes
  • Most deliver pigment to keratinoctyes and place it on top to protect their DNA from UV
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8
Q

Describe the Langerhans cell–where and what?

A
  • Positioned within the epidermis and dermis

- Involved in a wide range of T-cell mediated immunoreactions

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9
Q

Describe the Merkel cell–where and what?

A
  • Positioned in the lower epidermis

- Involved in touch sensation

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10
Q

What does the dermis do, generally?

A
  • Dense paucicellular fibrous and elastic tissue
  • Supports the epidermis and all of the adnexal structures
  • Also houses all of the vascular, nervous, muscular structures
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11
Q

What does the papillary dermis have?

A

numerous capillaries

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12
Q

What is the reticular dermis in relation to the papillary dermis?

A

less cellular with less capillaries

-mainly a structural function

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13
Q

What does the subcutis do?

A
  • Fat pad that underlies the skin
  • Fat cells in human contains mostly triglycerides
  • Thickness varies based on site (e.g. broad around the waist and barely present in the eyelid)
  • Functions: Insulator, cushion, metabolic storage, allows for movement
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14
Q

What do septa in the subcutis do?

A

They are Fibrous bands; they separate the subcutis into lobules
-house the nerves and larger vessels

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15
Q

What are adnexal structures?

A 
-appendages of the skin:
Hair follicles 
Sebaceous Glands 
Sweat Glands
Apocrine 
Eccrine
-think of them as mini-organs, each with specific functions
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16
Q

What are the three types of hair?

A

Lanugo: covers the fetus
Vellus: similar to lanugo, over most of our body
Terminal: Scalp, axilla, beard, pubic regions
-Vary in length, structure & hormonal responsiveness depending on site

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17
Q

What are the three parts of hair (from top to bottom)?

A

1) Infundibulum
2) Isthmus
3) Inferior

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18
Q

Describe the hair bulb and what it does

A
  • lies at the base of the follicle
  • where the hair growth occurs; “matrix cells” of the bulb are mitotically active (the cells that come out turn into the hair shaft)
  • Dermal papilla forms an invagination within matrix cells
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19
Q

Describe the cross-sectional layers of hair from outside in

A 
Fibrous sheath (continues w/basal membrane of epidermis)
Outer root sheath
Inner root sheath
Hair cuticle
Hair Shaft
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20
Q

How do sebaceous glands develop in utero. Describe sebaceous glands.

A

-Embryologically develop from outer root sheath of hair follicle
-Gland that produces lipids
-different functions have been proposed:
keeps stratum corneum pliable
In cold weather, hinders evaporation

On cutaneous surfaces, they have an associated hair follicle, but also found on buccal mucosa and lip w/o a hair = Fordyce’s spots (also w/o a hair on areola, prepuce, eyelids)

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21
Q

Where do you find sebaceous glands?

A

Everywhere on the skin surface EXCEPT palms and soles

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22
Q

What are Fordyce’s spots?

A

Sebaceous glands on buccal mucosa and lip; without hair

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23
Q

What are the two types of sweat glands? Where are they and what do they do?

A

1) Apocrine
Axilla, pubic/genital, perianal, periumbilical
Moll’s glnd of the eyelids and ear cerumen glnds
Function not entirely known, pheromone?

2) Eccrine
Present everywhere except mucocutaneous junctions
Produces hypotonic fluid and functions as evaporative cooling

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24
Q

What is the difference of the excretory duct function on eccrine vs. apocrine glands?

A

Apocrine: empties into infundibulum of hair
Eccrine: empties directly onto skin surface

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25
Q

Describe the coiled secretary gland that eccrine and apocrine glands have. Where is it?

A

Present in the deep dermis / subcutis
Two cell layers
Apocrine gland is larger than eccrine overall and has pink excretory cells

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26
Q

What are the histologic patterns of skin disease?

A 
Histologic patterns organize diseases
Major
-Lichenoid (interface) pattern
-Psoriasiform pattern
-Spongiotic pattern
Vesiculobullous pattern 
Granulomatous pattern
Vasculopathic

Minor Patterns

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27
Q

What is lichenoid dermatitis generally?

A

A pattern of skin inflammation characterized by DAMAGE TO THE EPIDERMAL BASAL CELL LAYER
May see apoptosis (cell death) or vacuolization of basal cells

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28
Q

What are the two types of lichenoid dermatitis we discussed in class?

A

Lichen Planus
Erythema Multiforme

(but many others, including Lupus, GvsH, etc.)

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29
Q

Describe Lichen Planus.

A

Lichenoid Dermatitis:
5 P’s: Pruritic (itchy), Purple, Planar (flat surface), Polygonal Papules
-Wickham’s striae on mucosal surfaces (white lines)
-Classically on the wrists, ankles, and oral/genital mucosa
50% of women and 25% of men will have genital involvement

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30
Q

What are the four forms of Lichen Planus

A

Four distinct forms: (1) papules or plaques in the setting of generalized cutaneous lichen planus; (2) hypertrophic disease; (3) erosive disease; and (4) lichen planopilaris (hair loss)
Although cutaneous disease is often self-limiting, mucous membrane disease is more persistent-just annoying but often not a problem
Erosive lichen planus often involves multiple mucous membrane sites–in particular, the vulva, vagina and oral mucosa—more involved

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31
Q

Describe Lichen Planus on a microscope

A

Band of chronic inflammation
-Death of basal keratinocytes
-big band of blue inflammatory cells which are obscruting the dermal epidermal dermis
Apoptosis—damage to the basal epithelial cells—heart of this type of skin issue
-final diagnosis from secondary features

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32
Q

What are the causes of Lichen plans?

A

Unknown cause
Some suggest altered antigens are expressed in the basal layer
These cause a cytotoxic immune response (CD8-expressing lymphocytes)

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33
Q

What is Erythema Multiforme?

A

Self-limiting disorder
Can occur at any age
Patients present with a large variety of lesions
-Macules (flat patches), papules (small bumps), vesicles (blisters)
-Classic target-shaped lesion: red macule with pale center
-Often symmetric involvement of extremities, but can see more widespread lesions

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34
Q

What are the four categories of Erythema Multiform?

A
  • EM minor: no mucosal involvement
  • EM major: mucosal disease, but 30% surface area involvement
  • Toxic epidermal necrolysis: >30% surface area involvement
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35
Q

What causes Erythema Multiforme?

A

Reaction to:
-Infectious agents (herpes simplex, mycoplasma)
-Drugs (sulfonamides, penicillin, barbiturates)
-Cancer (carcinoma and lymphoma)
-Idiopathic connective tissue diseases (lupus)
Epidermal cell injury mediated by cytotoxic(CD8) cells

36
Q

What is Psoriasiform dermatitis?

A

Achanthosis with elongation of the rete ridges in a regular manner
Achanthosis = epidermal hyperplasia (thickening)
Heart of this is a thickening of the epidermis in a very regular fashipon
Elongation of the rete ridges
Psoriasis is one of the many types

37
Q

What is psoriasis?

A
  • Chronic relapsing disease
  • Affects about 1 in 50 people
  • Classically the plaque form presents as well-circumscribed erythematous patches with a silvery scale
  • Tends to involve the extensor surfaces (elbows & knees), scalp, sacral area and nails
  • Other clinical variants, i.e. Guttate, Pustular
  • Nail changes occur in about 1/3rd of patients
  • Yellow-brown discoloration, pitting, separation
38
Q

Describe the histology of psoriasis

A
  • Regular thickening of epidermis
  • Thickened and altered cornified layer
  • Elongated rete’s ridges are typical; inflammation also
  • Also replaced with thick scales; in psoriasis, the nuclei stay (unlike the others); this is what gives rise to the classic silvery scale
39
Q

What are the factors for psoriasis?

A

Genetic factors
-Those with HLA-C have increased risk
Environmental factors
-Only a small percentage with HLA-C will develop
End up with marked keratinocyte proliferation
-Probably from cytokines and growth factors elaborated by inflammatory cells drawn to the skin

40
Q

What is Spongiotic (eczamtous) dermatitis generally?

A
  • Intraepidermal intercellular edema (aka spongiosis)
  • Histologically spongiosis appears as widened spaces between keratinocytes
  • can vary from a subtle, only seen microscopically to clinically visible vesicles
  • eczema is a type but often used to describe the whole category
41
Q

What are the two types of spongiotic (eczamtous) dermatitis we discussed?

A

Allergic contact dermatitis

Atopic dermatitis

42
Q

What is allergic contact dermatitis?

A
  • from contact with an allergen to which the person has previously been sensitized
  • > 3000 chemicals have been implicated
  • Uncommon in children
  • Rash develops 12–48 hrs after exposure
  • Erythematous papules, small vesicles or weeping plaques
  • Pruritic (itchy)
  • can see a plaque with vessels histologically
  • lots of eosinophils
43
Q

Describe the mechanism of allergic contact dermatitis

A
  • Antigens captured by Langerhans cells within epidermis
  • Langerhans cells migrate through lymphatic vessels to lymph nodes
  • Antigens are presented to T-cells
  • Upon re-exposure memory T-cells migrate to area of exposure & release cytokines –> inflammatory cells and causes leaky vessels
44
Q

Describe atopic dermatitis

A
  • Affects up to 25% of the population
  • “The itch that rashes”
  • Most often a family history
45
Q

What is the atopic triad?

A

The “Atopic Triad”-these three tend to go together

  • Atopic dermatitis
  • Allergic rhinitis/conjunctivitis
  • Asthma
46
Q

What can you see in the chronic form of atopic dermatitis?

A

Lichenification

47
Q

Describe infantile atopic dermatitus

A

2 months – 2 years of age
Head
Diaper area
Flexor AND extensor surfaces

48
Q

Describe childhood atopic dermatitis

A

2 years – 12 years
Flexor surfaces: antecubital, popliteal fossae, neck, trunk
Less involvement of face
50% of patients will resolve by adolescence

49
Q

Describe adult atopic dermatitis

A
  • Continuation of childhood eczema appearance
  • Symptoms may have resolved or improved during adolescence
  • May return later in life at any point in patients with atopic predisposition, wax and wane
  • May return in a variety of forms, including hand dermatitis
50
Q

Describe skin susceptibility to infections

A 
Bacterial: Staph > Strep = Impetiginized Eczema
Viral
Herpes Simplex Virus
Poxvirus (Molluscum contagiosum)
Human papillomavirus (common warts)
51
Q

What is impetiginized eczema?

A
  • Very common exacerbating factor
  • Staph aureus > Strep
  • S. aureus colonizes 90% of atopic skin
  • Treat with topical or oral antibiotics
  • May see improvement in clinical non-impetiginized eczema
52
Q

What is Actinic Keratosis? What type of skin tumor is it?

A 
“pre-malignant”
Keratosis: have hyperkeratosis
Feels scaly or rough on clinical exam
Actinic: related to the sun
Occur more frequently in lightly pigmented people
Occur in sun exposed areas
53
Q

What is the etiology of actinic keratosis?

A

Exposure to UVB radiation-most of the radiation that has significant energy
Changes indicating clonality in keratinocytes
Frequently p53 (tumor suppressor) mutations

54
Q

What do you see clinically for actinic keratosis?

A

Red or yellow-brown scaly lesions (occasionally may be more darkly pigmented)
Increased incidence with age, fair skin and in males
Sun damaged skin: head and neck, backs of hand and arms
Exposure to ionizing radiation, arsenic and hydrocarbons may cause similar lesions

55
Q

Describe what you see from a histopathological standpoint for actinic keratosis.

A
  • changes in the lower portion of the epidermis where the cells appear disorganized and have dark nuclei
  • The epidermal thickness is usually altered, it may be thickened or atrophic
  • The stratum corneum may abnormally retain nuclei (termed parakeratosis)
56
Q

What is the outcome of actinic keratosis?

A
  • between 1/10 and 1/100 are thought to progress to invasive squamous cell carcinoma
  • Some regress and others may remain stable
  • Because of small risk of progression, generally recommended that they be eliminated (frozen, topical medication, cut out)
57
Q

What is squamous cell carcinoma? (SCC)

A
  • tumor that can arise at many sites (Cervix, oral cavity, lung), usually from stratified squamous epithelium-anywhere with SCC or WHERE SCC CAN DEVELOP (e.g. lung doesn’t normally have SCC but with repeated injuries can change to SCC and then get SCC carcinomas)
  • Cutaneous SCCs are extremely common tumors (2nd only to basal cell carcinomas)
  • Can be in situ and invasive
58
Q

What are the causes of SCC?

A

Multiple:

  • UV and ionizing radiation (>80% develop in association with actinic keratosis)
  • Chemicals, notably arsenic
  • HPV infections, especially in anogenital sites
  • Chronic inflammation, such as near burn sites
  • Immunosuppression also increases risk
59
Q

What is the clinical appearance of SCC?

A
  • More in men, older people and light-skinned people
  • As most are related to sun-exposure, most arise in locations similar to actinic keratosis
  • Other sites include nail bed and genital (HPV)
  • often presents a hard, slowly progressive tumor, may be painless
60
Q

What is the histopathology for the two kinds of SCC?

A

In situ: Atypical, neoplastic keratinocytes have filled the entire epidermis, but are contained by the basement membrane
Disorganized cells
Enlarged hyperchromatic nuclei

Invasive: The atypical keratinocytes have invaded through the basement membrane into the dermis
Range of appearances depending on degree of differentiation

61
Q

What is the clinical outcome of SCC?

A
  • Although common, infrequently metastasize (overall 10% metastasize)
  • Tumor that arise from burn site are higher risk tumors
  • Penis, scrotum and anus sites metastasize more frequently
62
Q

What is Basal Cell Carcinoma (BCC) generally?

A

Most common invasive cancer in humans

Termed “basal cell” because the tumor cells resemble cells of the lowest (basal) layer of the epidermis

63
Q

What is the etiology of BCC?

A
  • Like actinic keratosis and SCC, exposure to UV radiation accounts for most cases
  • Rare genetic syndrome: Nevoid Basal Cell Carcinoma (Gorlin-Goltz) Syndrome from mutation in PTCH1 tumor suppressor gene
  • Similar defects may be found in sporadic BCCs
  • PTCH1 is a receptor for SHH
  • W/O PTCH-SHH, SMO cannot be inactivated
  • SMO produces transcription factors that stimulate growth
64
Q

What are the clinical symptoms of BCC?

A
  • Slightly more common in men then women
  • Amount of sun exposure correlates with BCC
  • at higher latitudes/lower elevations–older people; in sunny or higher elevation climates may develop in middle aged
  • Face is most common, back of the hand is infrequent. —Also less common on extremities
65
Q

What are the varieties of BCC?

A

Ulcerative variant: Starts as a “small pearly papule” with central ulceration developing as it enlarges
Superficial variant: presents as a slowly growing red patch
Pigmented variant: Carcinoma is associated with excess pigment, more common in Asian populations
Other variants…

66
Q

Histopathology of BCC

A

microscopic appearance: rounded nodules of cells w/ dark nuclei separating from surrounding stromal tissue.

  • The assorted variants also may have a characteristic microscopic appearance
  • Superficial variant has multiple small tumor lobules that only involve the superficial dermis
  • Pigmented variant has conspicuous pigment
  • huge separation from surrounding stoma
67
Q

Outcome of BCC

A

Though extremely common, they only rarely metastasize
Lesions of the scrotum are a notable exception, with approx 1/10 metastasizing
If left untreated they can cause extensive local destruction

68
Q

What is melanoma generally?

A
  • Melanocyte: Cell that originates at the neural crest and migrates to tissues during development
  • Melanomas arise from this type of cell
  • Melanomas can arise in mucosal surfaces (mouth, anogenital), eye, meninges, but most arise in the skin
69
Q

What is the etiology/cause of melanoma?

A

Sun exposure:
-Most common on sun exposed surfaces
-Not straightforward (?sun exposure in early life)
-Non sun-exposed surfaces sometimes also involved
Inherited factors:
-FAMM / Dysplastic Nevus Syndrome
-Mutation of p16 gene
-Patients get melanoma at a young age
-Other genes (15% of melanomas are familial)

Note: Sun exposure plays a role, but not as straightforward as in other epidermal tumors; some have found that sun exposure early in life may be important. Severe sunburns early in life may be of significant risk. Familial causes of melanoma are also known, FAMM is the most well-known, but this accounts for less than half of familial melanoma. The genes ID’ed in familial melanoma have also been in sporadic melanomas.

70
Q

What are the clinical risk factors of melanoma?

A

-Increased exposure of fair skin to sun
-Exposure during childhood
-Episodic exposure (SSM)
M:F 3:2 (a little heavily weighted toward males)
-Persons with previous melanoma have 5X risk for developing second melanoma—remember, same genetics and environmental factors
-Immunosuppressed patients
-XP: AR condition with inability to repair DNA
-Congenital bathing-suit nevus

71
Q

What is the clinical appearance of melanoma?

A

Local disease usually asymptomatic
Signs (often to differentiate from a mole)
Asymmetry
Borders irregular, not smooth and rounded
Color, may be black, brown, red, blue, grey, white
Diameter, most lesions are larger
“E”-evolution–Changes to appearance of lesion
F: Leg
M: Back

72
Q

What are the different types of melanoma?

A 
--Melanoma in situ
Lentigo maligna
Superficial spreading
Acral lentiginous 
---Invasive (Traditional 4)
Superficial Spreading Melanoma (SSM)
Lentigo maligna melanoma
---Acral Lentiginous melanoma
Nodular melanoma
Miscellaneous
Including desmoplastic
73
Q

What is melanoma in situ generally?

A

-Radial or Horizontal growth phase
-Tumor grows along the skin surface and not down into deeper tissue
Subtypes:
Lentigo Maligna
SSM
Acral Lentiginous

74
Q

Describe lentigo maligna (a type of melanoma in situ).

A

Terminology
Lentigo maligna: type of in situ melanoma
Lentigo maligna melanoma: invasive melanoma arising from “lentigo maligna”
Lentigo simplex, solar lentigo, or just “lentigo” are all benign spots of hyperpigmentation

Chronic sun damaged skin of elderly
Brown / black macule-can have long horizontal growh phase
The in situ lesion often present for 10-15 years before invasive develops

75
Q

Describe the superficial spreading of melanoma in situ

A

Most common variant
Equal sex incidence
Leg (F) Back (M)
Dark macule

76
Q

Describe Melanoma in situ–Acral Lentiginous

A

1/10 melanomas in Caucasians
Predominant subtype in African Americans, Asians
Unrelated to sun exposure
Heel is most common site

77
Q

Describe Invasive Melanoma—Lentigo Maligna Melanoma

A

Invasive tumor is termed “Lentigo Maligna Melanoma” vs. “Lentigo Maligna” for in situ lesions

With progression to invasion become ulcerated, blue / black nodular lesions

78
Q

Describe Invasive Melanoma–Desmoplastic Melanoma

A

-Usually presents as asymptomatic amelanotic nodule on sun damaged skin
-Head and Neck
-Older adult, mean age 63
-50% arise in lentigo maligna
-61% five year survival for lesions > 4mm
-Compare to 40% for other types of melanoma > 4mm
(kind of looks like a scar)

79
Q

Describe Invasive Melanoma–Superficial Spreading Melanoma

A
  • Macule develops a blue or blue-black nodule

- Hypopigmented or amelanotic variants are flesh colored or erythematous

80
Q

Describe Invasive Melanoma—Acral Lentiginous Melanoma

A

Gradually enlarging macule with progression to frequently ulcerated, blue or black nodules
Associated with a poor prognosis (often thick at the time of Dx)

81
Q

Invasive Melanoma–Nodular Melanoma

A

No radial growth phase
Poor prognosis (thick at Dx)
M:F 2:1
(lack of surrounding macule in pictures)

82
Q

What are the prognostic factors of melanoma?

A

Some clinical features have prognostic implications
-Gender: males do worse
-Location: Central body is worse
Several characteristics from the pathologic exam are used to gauge prognosis and guide treatment
-Depth of invasion, the “Breslow Thickness”
-The number of mitotic figures
-Ulceration
-Lymph node involvement (sentinel lymph node)

83
Q

What are the outcomes of melanoma?

A
  • Tumors that have invaded deeply or spread beyond the initial location are deadly and often resistant to treatment
  • Most are now cured surgically
  • Increased public awareness
  • Early detection and treatment
  • Complete excision of early lesions is critical
84
Q

What is Mycosis fungoides (Cutaneous T-cell lymphoma)?

A
  • A T-cell lymphoma that begins in the skin–Clonal proliferation of CD4 T-cells
  • Most patients have disease that stays in the skin for years (decades), but some progress to systemic disease
  • Typically presents as a scaly “rash” on the trunk, progresses to plaques and nodules
  • Early lesions can be treated with light and topical steroids
  • Characteristically they extend into the epidermis as individual and small collections of cells.
85
Q

What is Merckel cell carincoma?

A
  • Long thought to be derived from the Merkel cells that reside in the skin, or it may arise from a stem cell
  • Frequently seen in sun damaged skin (head, neck and extremities)
  • Recently, found an association with a polyoma virus
  • Typically a hard nodule in an older (>60 yrs) patient
  • Usually a poor outcome (55% 3-year survival)

Organ Pathology Exam 1 (4 decks)

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