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Skin Flashcards

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Dermatology Board Prep flashcards
1
Q

What percentage of body weight does the skin make up?

A

20%

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2
Q

fxn of fibroblasts

A

lay down collagen, make skin rough

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3
Q

fxn of perivascular mast cells

A

degranulate, increase vascular permeability

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4
Q

fxn of dendrocytes

A

processing cells for anything that gets in the skin

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5
Q

In what layer do you find new keratinocytes with desmosomes?

A

stratum spinosum

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6
Q

In what epidermal layer will you find keratohyaline granules?

A

stratum granulosum

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7
Q

What is a dermatophyte infection and in what epidermal layer will you see this?

A

fungal infection that lives off decaying cells, will find in the stratum corneum layer

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8
Q

Cells in the epidermis

A

Keratinocytes, melanocytes, Langerhaan’s cells and dendrocytes, and merkel cells

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9
Q

What is “dermabrasion”?

A

getting dead cells off of the epidermis, from the corneum layer

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10
Q

Keratinocytes are squamous epithelial cells that can produce what?

A

Keratin and cytokines at times of injury

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11
Q

Melanocytes are derived from?

A

neural crest cells

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12
Q

Melanocytes are found in stratum?

A

basale

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13
Q

Why will people with PKU have very pale skin?

A

because they can’t process phenylalanine (can’t convert to tyrosine which is needed to produce melanin)

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14
Q

Besides production of melanin, what is tyrosine also important for?

A

catecholamine production

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15
Q

How is melanin formed?

A

comes from tyrosine being converted to DOPA by tyrosinase and then DOPA can be converted to melanin

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16
Q

Does the number of melanocytes differ between races?

A

NO!

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17
Q

What is responsible for AA to have more pigmented skin?

A

Whites have much faster melanin degradation and their melanosomes are concentrated in the basal layer, AA have melanosomes present throughout the skin layers and have larger melanocytes with more dendritic processes.

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18
Q

What is meant when you refer to Langerhaan’s cells as “immigrant cells”?

A

They are bone marrow derived, not formed embryonically but come from monocytes and migrate to the skin

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19
Q

Where are langerhaan’s cells prevalent? Where are they uncommonly found?

A

prevalent in the dermis, uncommon in epidermis

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20
Q

What cells play a role in contact hypersensitivity?

A

Langerhaan’s cells

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21
Q

Describe type IV hypersensitivity

A

No Abs involved, it is an altered T cell response, cytotoxic T cells go crazy and over respond to a noxious stimulus (poison ivy, perfume)

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22
Q

What specialized receptors/antigens to Langerhaan’s cells have?

A

They express MHC-1, MHC-II, Fc IgG, IgE receptors

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23
Q

What cells act like mast cells in the lower epidermis and dermis?

A

Dendrocytes

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24
Q

What is role of dendrocytes?

A

Can release histamine and contribute to the inflamm. response in the lower epidermis and in the dermis are involved in processing antigens

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25
Q

Why can people who come down with GVHD after a bone marrow transplant have skin discoloration and discoriation?

A

The langerhaan’s and dendrocytes are processing the graft cells and the proteins the graft cells are now producting, causing a skin reaction

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26
Q

Where do you find merkel cells?

A

specialized regions such as the lips, oral cavity, and palmar skin

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27
Q

What are merkel cells associated with?

A

a terminal neuronal axon

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28
Q

Where will you find eccrine sweat glands?

A

All over the body, greatest number on the face, chest and back

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29
Q

What type of sweat glands are most important in regulating our body temp?

A

Eccrine glands

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30
Q

Which sweat glands can be attributed to body odor?

A

Apocrine

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31
Q

Where will you find apocrine sweat glands?

A

They are fewer in number, found in axilla, groin, scalp, face, and abdomen

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32
Q

What happens when you use a steroid cream on a contact dermatitis?

A

you will slow down the activity of the langerhaan’s cells and also decrease the amount of local lymphocytes in that area, interfering with the whole immune process.

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33
Q

What are the 2 major layers of the dermis?

A

Papillary and Reticular

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34
Q

Which dermal layer is closest to the epidermis with loose CT?

A

Papillary

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35
Q

Which dermal layer has dense dermal collagen and is more packed together?

A

Reticular

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36
Q

Components of the Dermis? (12)

A
  1. collagen 2. elastin reticulum 3. gel-like ground substance 4. hair follicles 5. sebaceous glands 6. sweat glands 7. blood vessels 8. nerves 9. lymphatic vessels 10. fibroblasts 11. mast cells 12. macrophages
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37
Q

What are the components of the subcutaneous fat layer?

A

Adipocytes, dermal, subcutaneous collagen (continuous with dermis, anchors dermis down)

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38
Q

What will you see with people with lots of subcutaneous fat in regards to the structure?

A

You will see layer of fat then layers of collagen and then more fat (collage in between fat layers), don’t know why this is

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39
Q

What are the theories behind why there is collagen separating fat layers in humans?

A

Your body thinks you are storing up for a period of hibernation or cold, your fat layers are separated by collagen to preserve more heat and contribute to greater thermogenesis.

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40
Q

What are the 4 structural units of nails?

A
  1. the proximal nail fold 2. the matrix from which the nail grows 3. the hyponichium (nail bed) 4. nail plate
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41
Q

Nail growth, how many mm per day?

A

1mm or less per day

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42
Q

If you removed a pt’s toenail, how long should you tell them it will take for their nail to grow back?

A

around a month

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43
Q

Lymphocytes in the skin express what specialized antigen?

A

Cutaneous lymphocyte associated antigen (CLA)

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44
Q

Describe the innate immune response in the skin

A

Dirt/dust in wound, gets taken up by Langerhaan’s cells, macrophage-like cells release cytokines, the cytokines activate other macrophage like cells in the dermal layer (dendritic cells, macrophages), these cells engulf and destroy the dust/dirt particle automatically.

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45
Q

Describe adaptive immunity of the skin

A

Langerhaan’s cells process a foreign antigen, present it to helper T cells which recognize it, produce cytokines (IL-2 + others) to recruit more T cells, from here an immune response is mounted.

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46
Q

What does DEJ stand for?

A

Dermal epidermal junction

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47
Q

Describe the skin changes that happen with aging

A

skin becomes thinner, drier, wrinkled, and demonstrates changes in pigmentation, shortening and decrease in number of capillary loops, fewere melanocytes and L cells, atrophy of sebaceous, eccrine, and apocrine glands, changes in hair color (hormonal), fewer hair follicles and growth of thinner hair.

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48
Q

What goes with each of these respectively as the “bigger” version? Macule, papule, vesicle

A

macule < patch, papule < plaque, vesicle < bullae

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49
Q

What are people usually referring to when they say they have a blister?

A

a bulla

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50
Q

Chronic dermatitis = ?

A

Lichenification

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51
Q

What is it called when you have separation of the nail plate from the nail bed?

A

Onycholysis

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52
Q

Hyperkeratosis = ?

A

Thickening of the stratum corneum, a QUALITATIVE abnormality of the keratin

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53
Q

What will you sometimes see in people who have had radiation to a section of skin? When was this discovered?

A

hyperkeratosis, when they used to use radiation to get rid of plantar’s warts, 20 years later lots of these people developed hyperkeratosis

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54
Q

Parakeratosis = ?

A

Keratinization with RETAINED NUCLEI of the stratum corneum, the cells are not maturing as they migrate up.

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55
Q

Is parakeratosis normal?

A

Yes on mucuous membranes (mouth, vaginal epithelium)

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56
Q

Hypergranulosis = ?

A

Hyperplasia of stratum granulosum, usually due to constant rubbing

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57
Q

Could you use the term acanthosis to describe a lesion?

A

No, would need path report to know this

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58
Q

Acanthosis = ?

A

Diffuse epidermal hyperplasia, increase # of cells in all layers, very difficult to distinguish from hyperkeratosis, won’t be raised.

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59
Q

What is acanthosis usually caused by?

A

Chronic inflamm, irritation

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60
Q

Papillomatosis = ?

A

surface elevation caused by hyperplasia and enlargement of contiguous dermal papilla, this WILL be raised up in small area

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61
Q

How can you distinguish papillomatosis from acanthosis?

A

Acanthosis will not be raised up, papillomatosis will.

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62
Q

Acantholysis = ?, example?

A

Loss of intercellular cohesion between keratinocytes, ex. pemphigus vulgaris

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63
Q

How will acantholysis present?

A

As a papule over a macule

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64
Q

Spongiosis = ?

A

Intracellular edema of the epidermis

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65
Q

Hydopic swelling = ? what do you see this with?

A

(ballooning), intracellular edema of keratinocytes, seen in viral infections

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66
Q

Exocytosis = ?

A

Infiltration of epidermis by inflammatory cells from the dermis

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67
Q

How do you distinguish an erosion from an ulceration?

A

an ulceration will bleed because it goes through to the dermis, an erosion is only part of the epidermis and won’t bleed.

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68
Q

What is vacuolization?

A

Formation of vacuoles within or adjacent to cells

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69
Q

“lentiginous” refers to ?

A

Linear pattern of melanocyte proliferation within epidermal basal layer

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70
Q

What are the 3 broad issues that contribute to skin pathology?

A
  1. Degeneration 2. Inflammation (dermatoses) 3. Neoplasms
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71
Q

What is the most common type of vitiligo?

A

Non-segmented, found all over the body

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72
Q

What are the causes of vitiligo?

A

autoimmune (Abs destroy melanocytes), genetic component, and oxidative stress, immune system becomes more active during physiological stress

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73
Q

What is the hallmark of ephelis?

A

appear after sun exposure (or increase/become darker)

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74
Q

When can you see someone’s freckles the most?

A

If they become anemic

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75
Q

What causes freckles (ephelis)?

A

increased amount of melanin produced within basal keratinocytes, melanocytes may be SLIGHTLY enlarged but NORMAL density.

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76
Q

What condition looks like very large freckles?

A

Lentigo

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77
Q

Describe lentigo

A

benign localized hyperplasia of epidermal melanocytes (linear, non-nested hyperplasia, in this case there IS an increase in number of melanocytes

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78
Q

Which age group does lentigo affect?

A

All ages

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79
Q

Can you see lentigo in mucous membranes?

A

Yes

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80
Q

How large are lentigo patches?

A

small, 5-10 mm diameter

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81
Q

How do you distinguish lentigo from freckles?

A

they do not wax/wane, don’t get darker in sunlight

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82
Q

Melanocytes should only be in _________ and ___________?

A

epidermis and surrounding hair follicles

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83
Q

What is the difference between Becker’s nevus and Cafe au lait spots?

A

Becker’s nevi break up into smaller macules at the periphery, cafe au lait spots do not.

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84
Q

What is a becker’s nevus?

A

It is NOT nevocellular, it lacks nevus cells, but it is a developmental anomaly that shows up as a brown macular patch or patch of hair or both.

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85
Q

When do you need to get a neuro consult on an infant with cafe au lait spots?

A

If they have 6 or more, could have neurofibromatosis type 1

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86
Q

Describe the lesions assoc. with melasma

A

Dark, irregular, well-demarcated, hyperpigmented macules to patches

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87
Q

Where do you see melasma?

A

upper cheek, nose, lips, upper lip, and forehead

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88
Q

Cause of melasma?

A

Stimulation of melanocytes or pigment-producting cells by estrogen and progesterone to produce more melanin pigments when exposed to sun

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89
Q

Estrogen is a ___________ hormone?

A

trophic, stimulates other things to be active

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90
Q

Melanocyte nevus = ?

A

A mole!

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91
Q

Size of nevi?

A

2.0mm

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92
Q

Nevi can be _______ or ________? Which is more common?

A

congenital or acquired, acquired is more common

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93
Q

What is “nevus” mean?

A

It denotes any congenital skin lesion, just a type of melanocyte. If use the term “nevus” means the melanocytes are nested together.

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94
Q

What do nevus cells NOT have?

A

dendritic processes, they won’t spread out into other layers

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95
Q

The earliest melanocyte nevus lesions are?

A

junctional, pretty flat, more pigmented and closer in association to melanoma

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96
Q

Describe the characteristics of junctional nevi

A

Located along the DEJ, uniform nuclei, with little or no mitotic activity

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97
Q

What do most junctional nevi do? What is this process called?

A

Grow into the underlying dermis, when they are then considered a “compound nevus”, this process is called maturation

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98
Q

Which nevi are more elevated, junctional or compound/demal?

A

Compound/dermal are more elevated than junctional

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99
Q

What are older nevi called? Why is this?

A

They are called intradermal, because eventually they have no epidermal nests and are just in the dermis

100
Q

When a stem cell factor binds to a cKIT receptor in the skin, what gets turned on?

A

RAS

101
Q

What does RAS play a role in?

A

cell life cycle and proliferation, makes cells live longer and proliferate more.

102
Q

What does p16 do?

A

Turns OFF cell proliferation

103
Q

What is BRAF?

A

encodes for serine/threonine kinase, a positive mediator of RAS signals

104
Q

When BRAF is mutated and stimulates increased cell proliferation, what is also stimulated?

A

p16, which turns the system back “off”

105
Q

Describe the appearance of a compound nevus.

A

Raised, dome-shaped, symmetry with uniform pigmentation (suggests benign), intraepidermal nevus cell nests with cords of nevus cells in dermis.

106
Q

What happens to a nevus after a long time that patients may confuse with melanoma?

A

the melanocytes lay down fibrotic tissue, it won’t change anymore

107
Q

What is the condition where you have nevi all over your body?

A

Dysplastic Nevus Syndrome

108
Q

What is the probability of developing melanoma if you have dysplastic nevus syndrome?

A

> 50% by age 60

109
Q

What are the similarities between mongolian spots and nevi of Ota/Ito?

A

Both are congenital (apparent w/in first year of life), have a “mottled” appearance, and occur more often in asians and AA.

110
Q

What are the differences between mongolian spots and Nevi of Ota/Ito?

A

Ota: trigeminal nerve, 1st and second divisions, Ito: posterior supraclavicular and lateral brachiocutaneous nerves.

111
Q

Dermal melanocytosis = ?

A

Mongolian spots, nevus of Ota and Ito

112
Q

In dermal melanocytosis, what occurs?

A

melanocytes in dermis actively synthesize melanin (this is abnormal).

113
Q

What is the “Tyndall effect”?

A

scattering of shorter wavelengths by dermal melanin that gives mongolian spots their blue color.

114
Q

What is “variegation”?

A

Variability in pigmentation, as seen in dysplastic nevi

115
Q

What are the characteristics of dysplastic nevi?

A

larger than acquired nevi (>5 mm), flat macules, slightly raised plaques, or target-like lesions with darker raised center (pebbly surface), irregular flat periphery, variability in pigmentation, irregular borders, usually compound, occur on BOTH sun-exposed and sun-protected areas.

116
Q

What does “cytologic atypia” mean?

A

irregularly shaped, dark staining nuclei, seen with dysplastic nevi

117
Q

CDKN2A = ?

A

P16

118
Q

Dysplastic nevus syndrome is autosomal _____?

A

Dominant

119
Q

What mutations are associated with Dysplastic Nevi Syndrome?

A

CDKN2A (p16) or CDK4/6 gene mutations

120
Q

Which pathway would you want to affect with drug therapy in treating dysplastic nevi syndrome?

A

the cell proliferation pathway (BRAF side)

121
Q

Explain what the CDKN2A mutation would do?

A

p16 usually gets turned on when BRAF is turned on to stop the cell proliferation from getting out of control, when it is mutated, it can’t turn this cell proliferation off (can’t turn off CDK 4/6)—>dysplastic nevi

122
Q

Explain what the CDK 4/6 mutation would do?

A

In this case, p16 can do its job and down regulated CDK 4/6 as it is supposed to but this mutation causes CDK 4/6 to be resistent to this input.

123
Q

Can you screen people who may potentially have the CDK 4/6 or CDKN2A mutations?

A

Yes, starting to do more of this.

124
Q

Why is it so important to not miss a potential malignant melanoma?

A

B/c once it has metastasized it is very resistent to treatment

125
Q

What is the only primary skin cancer than can kill you?

A

Malignant melanoma and RARE merkel cell tumor

126
Q

Prognosis for MM is related to ?

A

VERTICAL growth (breslow staging)

127
Q

A nevus lesion that is >?? raises concern for MM?

A

6 mm

128
Q

At presentation, (when people usually come in concerned about a mole), how big are they usually?

A

> 10 mm

129
Q

ABCDE?

A

A=Asymmetry B=Borders/Bleeding C=Colors D=Diameter E=Erythema/Evolving?

130
Q

Lentigo maligna?

A

indolent type, usually on the face, seen in elderly, growing slowly radially, not changing very much

131
Q

Most common type of MM?

A

Superficial Spreading

132
Q

Acral/mucosal lentiginous MM?

A

UNrelated to sun exposure, could be anogenital

133
Q

What does the appearance of a nodule within a mole indicated?

A

correlates with the emergence of a clone of cells w/ metastatic potential.

134
Q

If you are concerned about MM and the lesion feels more nodular, what does this mean?

A

More chance of metastasis, as the melanoma grows deeper (vertical growth), tend to feel more nodular.

135
Q

Do males or females have a worse prognosis with MM?

A

males have worse.

136
Q

What are “Clark’s Levels”?

A

A scale for MM 10 year survival rate based on Breslow Depth (1-5), 5 being worst.

137
Q

<____mm in depth = good prognosis for MM?

A

<1.7 mm depth

138
Q

What percentage of MM are familial?

A

10-15%, many have dysplastic nevi syndrome

139
Q

What is mutated in 40% of familial melanoma?

A

CDKN2A (p16)

140
Q

What 3 tumor suppressors does p16 code for?

A

p15/INK4b, p16/INK4a, p14/ARF

141
Q

What does p16/INK4a normally do?

A

It normally enhances activity of TSGs of Rb family by inhibiting CDK4.

142
Q

What does p14/ARF normally do?

A

Enhances activity of p53 by inhibiting activity of MDM2.

143
Q

What are the other gene mutations they have found in fair skinned individuals that may make them more susceptible to MM?

A

MC1R (melanocortin-1-receptor), ASIP (regulator of melanocortin receptor signaling), TYR (tyrosinase enzyme).

144
Q

BENIGN epidermal tumors are derived from?

A

keratinizing stratified squamous epithelium of the epidermis and hair follicles, these are NOT due to melanocytes

145
Q

How will benign epidermal tumors have increased pigmentation?

A

d/t to the accumulation of keratin

146
Q

Appearance of Seborrheic Keratosis?

A

Round, flat, coin-like, waxy plaques, “stuck-on appearance”

147
Q

What is the surface of seborrheic keratosis like?

A

velvety to granular

148
Q

What is a keratin filled horn cyst and pseudocyst? What are they assoc. with?

A

assoc. with seborrheic keratosis, keratin filled pocket at skin surface, if open to surface, called “pseudocyst”

149
Q

What age group gets seborrheic keratosis? What population is it enhanced in?

A

middle aged or older, enhanced in people of color

150
Q

What is Dermatosis papulosa nigra?

A

multiple small seborrheic keratosis lesions on the face (Morgan Freeman)

151
Q

What mutation is assoc. with Seborrheic Keratosis?

A

Mutation in FGFR3 gene (fibroblast growth factor receptor 3)

152
Q

Explain what happens with the FGFR3 mutation.

A

It is always on, it stimulates cells to continuously produce keratin, drives the growth of the sebrorrheic keratoses.

153
Q

What should you be concerned about if someone with previously clear skin comes in with a huge outbreak of seborrheic keratosis?

A

Paraneoplastic syndrome—>GI carcinoma releasing growth factors out of control

154
Q

What is the Leser-Trelat sign?

A

Explosive development of seborrheic keratosis

155
Q

Thickened hyperpigmented skin with velvet-like texture is?

A

Acanthosis Nigricans

156
Q

What are the 2 types of acanthosis nigricans?

A

Benign (80%) and Malignant

157
Q

Describe benign acanthosis nigricans

A

Autosomal dominant with variable penetrance, is assoc. with obesity or endocrine abnormalities (pituitary or pineal tumors and DM), is part of several rare congenital syndromes

158
Q

When does malignant acanthosis nigricans occur? What is associated with?

A

Occurs quickly in middle aged to older people, is assoc. with underlying cancers (GI adenocarcinomas—>stimulate fibroblasts to lay down more keratin (what causes the hyperpigmentation)

159
Q

When you see numerous, repeated PEAKS and VALLEYS in the epidermis, what should you think of?

A

Acanthosis Nigricans

160
Q

What other conditions can the familial type of Acanthosis Nigricans be assoc. with?

A

Achondroplasia (mutation in FGFR3), Thanatophoric dysplasia (mutation in FGFR3)

161
Q

Fibroepithelial polyp = ?

A

Skin tag, acrochordon, squamous papilloma

162
Q

A soft, flesh-colored, “bag-like” tumor is?

A

a fibroepithelial polyp (skin tag)

163
Q

What should you think of when you see “fibrovascular cores”?

A

Fibroepithelial polyp

164
Q

Disorders assoc with fibroepithelial polyps?

A

Diabetes, Obesity, Intestinal polyposis

165
Q

What happens to fibroepithelial polyps during pregnancy?

A

They become more numerous or prominent (like melanocyte nevi and hemangiomas)

166
Q

What is a “wen”?

A

An epidermal (inclusion) cyst

167
Q

What is inside a wen?

A

keratin and lipid debris

168
Q

Wall: Resembles normal epidermis
Center: Filled with laminated strands of keratin and lipid debris

A

Epidermal Inclusion cyst

169
Q

Wall: resembles follicular epithelium withOUT granular cell layer
Center: Filled with homogenous mixture of keratin and lipid

A

Pilar or trichilemmal cyst

170
Q

Wall: Similar to epidermal inclusion with multiple appendages budding outward

A

Dermoid Cyst

171
Q

Resembling sebaceous gland duct from which numerous compressed sebaceous lobules originate

A

Steatocystoma simplex

172
Q

What is steatocystoma multiplex?

A

a missense mutation in keratin, causing keratin to be produced in abnormal amounts

173
Q

Tumors that arise from structures that stick out from epidermis are termed?

A

Benign adnexal (appendage) tumors

174
Q

Benign adnexal (appendage) tumors are benign but can be confused with?

A

BCC

175
Q

Some benign adnexal (appendage) tumors have a mendelian inheritance pattern, with mutations in which genes? What will these types be like?

A

TSG, PTEN; more aggressive if inherited mutation

176
Q

If someone inherits a mutation causing benign adnexal tumors, what will they have a predisposition for?

A

internal malignancy

177
Q

Benign adnexal tumors can involve?

A

Hair follicles, sebaceous glands, and sweat glands

178
Q

Apocrine sweat glands secrete their fluid how?

A

Through membrane bound vesicles

179
Q

General characteristics of benign adnexal tumors?

A

Flesh colored, solitary or multiple, papules and nodules, some have predisposition for certain body surfaces.

180
Q

When thinking of names of benign adnexal tumors what should you keep in mind?

A

They are usually named based on location

181
Q

Where will you find eccrine poromas?

A

On the palms and soles

182
Q

What are the “turbin-type tumors”?

A

Cylindromas (found on forehead and scalp)

183
Q

Which benign adnexal tumors look like acne vulgaris?

A

cylindromas

184
Q

What causes cylindromas (physiologically)?

A

dominantly inherited, inactivation of TSG CYLD

185
Q

What will a cylindroma look like on biopsy?

A

islands of cells resembling normal epidermal or adnexal, fit together like a jigsaw puzzle

186
Q

What type of adnexal tumors do you get on your T-zone?

A

Trichoepitheliomas

187
Q

What causes trichoepitheliomas?

A

Proliferation of basaloid cells that form primitive structures resembling hair follicles

188
Q

Describe syringomas?

A

benign adnexal tumors of eccrine sweat glands that affect the lower eyelids (multiple small tan papules)

189
Q

Sebaceous adenomas can convert to what on rare occasion?

A

adenocarcinoma

190
Q

This adnexal tumor can be associated with internal malignancy in Muir Torre syndrome (a subset of hereditary nonpolyposis carcinoma syndrome)?

A

Sebaceous adenomas

191
Q

These are precursors for SCC?

A

Actinic Keratosis

192
Q

The number one cause for AK is sun exposure, what are the other things that could cause it?

A

ionizing radiation, industrial hydrocarbons, arsenicals

193
Q

What is the “hallmark” of AK?

A

parakeratosis

194
Q

What is Imipuimod?

A

activates immune system by stimulating toll-like receptors; helps body take care of AK before it becomes SCC

195
Q

What is called when you have keratosis on the lips?

A

Actinic chelitis

196
Q

What will the basal layer look like with AK?

A

Atypical, have huge nuclei

197
Q

SCC is the ___ most common tumor from “sun exposure”.

A

2nd, BCC is first

198
Q

What percentage of SCC will metastasize to nodes?

A

<5%

199
Q

These tumors can cause skin ulceration, have atypical nuclei and infiltrating margins?

A

SCC

200
Q

SCC in situ = ?

A

Bowen’s Disease; if no invasion through DEJ

201
Q

What levels of epidermis do SCC lesions involve?

A

ALL of them

202
Q

The pathogenesis of SCC usually involves what mutation?

A

DNA damage due to UV light which mutates p53, can no longer do its job of killing off atypical cells

203
Q

UV light can cause mutations in p53, what else does it do?

A

dampens the immune surveillance (LH cells or lymphocytes, lessens their effect)

204
Q

What happens with DNA damage due to the sun, what “senses” this damage?

A

The DNA damage is sensed by kinases (ATM and ATR) which normally then upregulate p53 to destroy the damaged cells but if p53 is mutated this doesn’t work

205
Q

Incidence of SCC is proportional to what?

A

degree of lifetime sun exposure

206
Q

SCC also has an association with ?

A

Immunosuppression

207
Q

Which types of HPV are assoc. with SCC?

A

5 and 8

208
Q

What is the difference between a tumor being “invasive” and having “metastatic potential”?

A

Invasive refers to spread locally in the area where the lesion originated. Metastasis refers to spreading to other parts of the body.

209
Q

What is a glioblastoma multiforme?

A

one of the most invasive malignant type of brain tumors, but will never metastasize, stays in brain.

210
Q

What will you see on a path report if the lesion in question is a BCC?

A

BLUE palisading nests

211
Q

What is an inherited disorder that involves lacking DNA repair?

A

Xeroderma pigmentosum, kids cannot go out in the sun bc instead of the sun mutating their DNA repair genes, they are born with the mutations

212
Q

What is the most common invasive cancer in humans?

A

BCC

213
Q

Most common appearance of BCC?

A

pearly papules with telangiectasis

214
Q

Can BCC contain melanin?

A

Yes, they can, don’t always

215
Q

Advanced BCC lesions can?

A

ulcerate, become locally invasive

216
Q

How do the tumor cells of BCC look?

A

They resemble normal basal layer of epidermis but are squished together (palisade)

217
Q

What are the 2 patterns of BCC growth?

A

Multifocal and Nodular

218
Q

Where do multifocal BCC growths arise from?

A

Epidermis, extend over several square cm

219
Q

Which BCC lesions start in the follicular epidermis and grow downward into the dermis?

A

Nodular lesions

220
Q

Nevoid basal cell carcinoma syndrome = ?

A

Gorlin Syndrome, an autosomal dominant disorder on Chm 9, PTCH gene mutation

221
Q

What syndrome led to finding the genes that cause BCC?

A

Gorlin Syndrome (Nevoid basal cell carcinoma syndrome)

222
Q

When someone has Gorlin syndrome, they have a mutation where? and what has to occur for them to have a BCC?

A

They have a PTCH gene mutation on Chm 9, they have one normal allele, so this normal allele must become inactivated by UV light for them to have symptoms.

223
Q

Usually people with Gorlin Syndrome have BCC by age?

A

before age 20

224
Q

What is Gorlin Syndrome assoc. with?

A

medulloblastomas and ovarian fibromas

225
Q

What is the normal action of p53?

A

To turn on apoptosis and to repair a cell that is abnormal (signal DNA repair)

226
Q

What genetic defects do kids with xeroderma pigmentosa have?

A

Defects in PTCH and p53

227
Q

What does the PTCH gene encode for?

A

a receptor for Sonic Hedgehog gene

228
Q

Absence of PTCH causes what?

A

activation of SMO which leads to BCC

229
Q

What happens in normal people when the sonic hedgehog protein binds to PTCH?

A

It dissociates from SMO so SMO becomes activated and initiates cell proliferation

230
Q

Pts with NON NBCCS have which type of mutations?

A

30% have PTCH mutations, 40-60% have p53 mutation

231
Q

What tumor can look like small cell cancer of the lung?

A

Merkel cell carcinoma (very rare)

232
Q

How is angioedema different from urticaria?

A

It is closely related by characterized by deeper edema of both the dermis and subcutaneous fat

233
Q

What does histamine specifically cause at the capillary level?

A

causes endothelial cell retraction (causes the endo cells to pull away from each other) increasing vascular permeability.

234
Q

Why is IgG the best Ab?

A

b/c it is so heavily recognized by our phagocytic cells (neutrophils, macrophages)

235
Q

Define Dermatoses

A

Inflammatory processes that occur within the skin

236
Q

Why do some people get urticaria?

A

Some people are just genetically prone to produce more IgE in response to certain stimuli, and there are a TON of receptors on mast cells for IgE—->bind them, release histamine

237
Q

Besides production of IgE in response to a stimulus, how else can mast cells be stimulated to release histamine?

A

C3A and C5A (part of complement) can activate mast cells and cause them to de granulate

238
Q

What are the two ways to activate complement?

A

C1—–>everything else

C3——>everything else (this way bypasses C1 and C2)

239
Q

What can the lesions of urticaria look like?

A

they can vary from small pruritic papules to large edematous plaques

240
Q

What can be an instigator for urticaria?

A

ASA

241
Q

What is complement mediated urticaria?

A

hereditary angioneurotic edema (inherited deficiency of C1 inhibitor, causing C1 to constantly be active, constantly degranulating mast cells), in a majority of cases there is no underlying cause. So anytime complement is activated these pts will have urticaria-like lesions/symptoms.

242
Q

If pt has persistent urticaria, what underlying diseases could they potentially have?

A

collagen vascular disorders, Hodgkin lymphoma

243
Q

Eczema is greek for ?

A

“to boil over”

244
Q

All forms of eczema are characterized by?

A

red, papulovesicular, oozing, and crusted lesions

245
Q

If eczema is persistent what can the lesions transform into?

A

raised, scaling plaques due to acanthosis and hyperkeratosis

246
Q

epidermal ________ is a hallmark of acute eczema

A

spongiosis

247
Q

What cells play a central role in contact dermatitis?

A

Langerhaan’s cells

Pathophys-Derm (3 decks)

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