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disease and defense > Dermatology > Flashcards

Dermatology Flashcards

1
Q

Skin + UVB=

A

Cholecalciferol (Vitamin D3)

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2
Q

The liver converts Vitamin D3 into

A

Calcidiol (25-hydroxy Vitamin D)

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3
Q

The Kidneys convert 25 hydroxy Vitamin D (Calcidiol) into

A

active 1,25 dihydroxy Vitamin D (Calcitriol)

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4
Q

Fitzpatrick Skin Types I and II

A

I. Never tans, always burns

II. Tans with difficulty, usually burns

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5
Q

Fitzpatrick skin types III and IV

A

III. Average tanning, sometimes burns

IV. Easily tans, rarely burns

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6
Q

Fitzpatrick skin types V and VI

A

V. Very easy to tan, very rarely burns

VI. Never burns

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7
Q

Types of cells present in the epidermis

A

Keratinocytes, Langerhans cells, Melanocytes

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8
Q

Two types f melanin produced by melanocytes

A

Eumalanin: black to brown pigment
Pheomelanin: yellow to red-brown pigment

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9
Q

Skin pigmentation is due to:

A

TYPE OF MELANIN PRODUCED,

AS WELL AS SIZE AND DISTRIBUTION OF MELANOSOMES

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10
Q

Distribution of melanosomes in Light skin vs dark skin

A

in light skin, the melanosomes are smaller and are distributed in clusters above the nucleus in the keratinocyte, in dark skin, the melanosomes are larger and distributed individually throughout the cytoplasm of the keratinocyte

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11
Q

The absence of melanocytes is called _____. Where is it commonly seen?

A

Vitiligo, commonly seen in periorifacial and acral locations

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12
Q

Layers of the epidermis

A

Stratum corneum
Stratum granulosum
Stratum spinosum
stratum basalis

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13
Q

How long does renewal of the epidermis take?

A

28 days

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14
Q

Hemidesmosome

A

Attachment point of basal cells to the basal lamina of the dermal epidermal junction

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15
Q

Bullous Pemphigoid

A

Autoantibodies to BP180 (type XVII collagen) or BP230, both found int he hemidesmosomes. Causes subepiderman blisters and tense bulla. Most common autoimmune bullous disorder. Treatment: prednisone

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16
Q

keratin,

A

a tough protective protein that makes up the majority of the structure of skin, hair and nails. MAde by keratinocytes of the epidermis

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17
Q

Desmosomes

A

structuresfor cell to cell adhesion (macula adherens)

• Contain intracellular keratin filaments and transmembrane proteins, desmogleins and desmocollins

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18
Q

Acquired antibodies to desmoglein 1 and desmoglein 3 cause ____ _____

A

pemphigus vulgaris

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19
Q

Pemphigus Vulgaris

A

-Primary skin lesions are flaccid bulla (Nickolsky sign positive)
-Pathology: Intraepidermal blisters
• painful oral erosions
• Other mucous membranes can be involved (eyes, GI and GU mucosa)
• Treatment: Prednisone or other immunosupressives

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20
Q

What cell layer do the cells start to lose their nuclei?

A

Statum granulosum

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21
Q

What do the granules of keratinocytes contain?

A

keratohyalin granules contain filaggrin, which X-links keratin, lamellar bodies excrete ceramics

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22
Q

What is the stratum corneum composed of? What keeps it moist?

A

dead and desquaming keratinocytes. Natural moisturizing factor (NMF) keeps it moist

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23
Q

Patients with ______ mutations have significantly reduced levels of the NMF in the stratum corneum and exhibit increased _______ water loss

A

filaggrin

transepidermal

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24
Q

Merkel cells

A

Small cells associated with nerve endings in epidermis. Their function has long been uncertain, but they seem to be involved in neural development and tactile sensation. Recent evidence supports a role for Merkel cells in light touch

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25
Q

Macule

A

Flat area of color change
Less than 1.0 cm
Can be hyper pigmented or hypopigmented

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26
Q

Patch

A

Flat area of color change
Greater than 1.0 cm
Can be hyper pigmented (think cafe au lait spot) or hypopigmented

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27
Q

Papule

A

Discrete,solid,elevatedbody
• Less than 1 cm in diameter
• May be further classified by surface change
– Scale, Crust

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28
Q

Plaque

A
  • Solid,flat-topped,elevated area of skin
  • Greater than 1cm and broader than thick
  • May be further classified by surface change
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29
Q

Nodule

A
  • Firm and well-defined lesion
  • May be dermal or subcutaneous
  • Greater than 1.0 cm
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30
Q

Scale

A
  • Excess stratum corneum (outermost layer)
  • May appear as flakes or plates
  • Color usually white or gray
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31
Q

Crust

A

• Dried blood, serum or purulent exudate that
forms on the skin surface
• May be thick or thin
• Color determined by type of dried fluid

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32
Q

Vesicles

A
  • Fluid filled cavity or elevation
  • Form within or just below epidermis
  • Less than 1.0 cm in diameter
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33
Q

Bulla

A
  • Fluid filled “blister”

* Greater than 1.0 cm in diameter

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34
Q

Pustule

A
  • Circumscribed elevation that contains pus
  • Less than 1.0 cm in diameter
  • Color usually whitish-yellow
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35
Q

Erythema

A
  • Localized, blanchable redness

* Caused by increased blood flow

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36
Q

Erythroderma

A
  • Generalized, blanchable redness
  • Caused by increased blood flow
  • May be associated with desquamation or extensive scaling
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37
Q

Telangiectasias

A

• Visible, persistent, dilation of small, superficial cutaneous blood vessels

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38
Q

Palpable purpura

A

• Raised and palpable discoloration
• Due to vascular inflammation and
extravasation of red blood cells (vasculitis)
• Color is red or violaceous

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39
Q

Erosion

A
  • Localized loss of epidermal or mucosal epithelium

* Causes can include injury or denuding of vesicle or bulla roof (removal)

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40
Q

Ulcer

A

• Circumscribed loss of epidermis and at least upper dermis
– Depth: can extend to subcutaneous, muscle or
bone areas
– Edge: clean, ragged, undermined
– Tissue at base: necrotic, purulent or healthy granulation tissue

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41
Q

Eschar (crust)

A

•”Scab”
• Adherent,thick,dry crust
• Causes: trauma, infection, or excoriating skin disease
• Black

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42
Q

Intertriginous distribution

A

Regions where opposing skin surfaces come in contact that may cause friction

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43
Q

Flexural distribution

A

• Pertaining to the skin surface overlaying muscles that flex joints, such as biceps

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44
Q

Does the epidermis contain blood vessels?

A

The epidermis contains no blood vessels, it depends upon the dermis for all its nutritional support.

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45
Q

The dermis also provides the _____, _____ and _____ of the skin

A

strength, resiliency and plasticity

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46
Q

Two zones of the dermis

A

: a) the papillary dermis (located immediately beneath the epidermis), and b) the reticular dermis located deeper in the tissue.

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47
Q

Dermal matrix consists of

A

mixture of collagen fibers, elastic fibers and ground substance all of which are synthesized by dermal fibroblasts.

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48
Q

skin appendages or adnexal structures

A

hair follicles, sebaceous glands (oil glands), and sweat glands found in the skin that are vital to protection and homeostasis.

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49
Q

dermal papillae

A

The downward projections of epidermis interdigitate with upward projections of the dermal papillae

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50
Q

What is the main function of collagen in the skin?

A

It provides essentially all the tensile strength of the skin.

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51
Q

What type of collagen comprises >85% wt % of the adult dermis?

A

Collagen I

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52
Q

What type of collagen is present in large quantities in the fetal dermis?

A

Collagen III

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53
Q

Structure of collagen

A

three chains of proteins arranged in an α-helical structure, electron microscope yields a characteristic pattern of striations with 68 nm intervals. The chains consist of repeated strings of glycine and two other proteins, forming a Gly-X-Y structure. The X and Y are usually proline and hydroxyproline.

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54
Q

Where/how is collagen synthesized?

A

The synthesized collagen proteins are secreted and then are assembled into collagen fibrils EXTRACELLULARLY.

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55
Q

classic example of an acquired abnormality in collagen production

A

Scurvy

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56
Q

Ehlers-Danlos syndrome (EDS)

A

genetic disorders of collagen synthesis, all of the subtypes share 4 major clinical features including:

  • skin hyperextensibility
  • joint hypermobility
  • tissue fragility
  • poor wound healing
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57
Q

Collagen fibers provide the skin with tensile strength, but elastic fibers provide the skin with ________

A

resiliency

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58
Q

elastic fibers are ______ (silver-loving) and special silver stains (such as the ______) may be performed to accentuate the presence of elastic fibers

A

argyrophilic

Verhoff-Van Gieson stain

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59
Q

The most common acquired disorder of elastic is

A

solar elastosis
Over a lifetime, a person accumulates sunlight exposure, leads to degeneration of the elastic. collagen bundles become dystrophic tend to “clump”sun-damaged elastic fibers become easy to appreciate on routine microscopy, as basophilic (blue) staining material within the superficial portions of the dermis.

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60
Q

pseudoxanthoma elasticum (PXE)

A

caused by mutation in a gene encoding part of the “multidrug resistance complex”, responsible for pumping compounds out of cells. The elastic fibers of the dermis become enlarged, tangled, calcified–> characteristic purple-blue color on histo. Skin of the flexural areas= “plucked chicken.” Elastic fibers of the blood vessels are also damaged leading to hypertension and bleeding disorders, particularly in the eye.

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61
Q

Ground substance

A

a gelatinous material intercalated between and amongst the collagen bundles, elastic fibers, and appendageal structures of the dermis. It consists principally of two glycosaminoglycans: hyaluronic acid and dermatan sulphate.

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62
Q

Is ground substance static?

A

No, ground substance is constantly being destroyed, by enzymes like hyaluronidase, and then renewed via production from fibroblasts

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63
Q

Restylane

A

pure hyaluronic acid, placed under skin to augment the tissue and remove lines. It is well-suited for this purpose for two reasons: a) it is a natural substance that is already present in the skin and it does not engender an immune response (unlike some bovine collagen fillers) and b) it absorbs a tremendous amount of water and amplifies the augmentation. Just like endogenously produced hyaluronic acid, Restylane is broken down by tissue hyaluronidases and it is not a permanent augmentation.

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64
Q

verruca

A

warts. They are benign, virally induced neoplasms (growth) that require an increased blood supply simply to support the virally-proliferating cells. These proliferating vessels may be identified as brownish, thrombosed capillary structures in the center of the verruca

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65
Q

leukocytoclastic vasculitis. How does it manifest clinically?

A

A common disease involving the post-capillary venules due to the precipitation of immune complexes in the walls of vessels.
. Clinically, vasculitis manifests as “palpable purport” (non blanch able). PMNs attach to vessel wall and degranulate, yielding damage and the extravasation of RBCs into the dermis. This deposition in the vessel walls, w/ infiltrating neutrophils and PMNs debris is called leukocytoclasia.

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66
Q

Free nerve endings pass through the upper dermis to terminate at the:

A

dermoepidermal junction

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67
Q

Nerves and conduction rate of pruitus

A

slow, umyelinated C fivers

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68
Q

Pacinian corpuscles

A

are structures which resemble an onion in cross-section. They are involved in pressure and vibratory sensation. most concentrated in the genital area.

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69
Q

Meissner’s corpuscles

A

resemble a pine-cone and are thought to be involved in fine touch and tactile discrimination. Such receptors are in highest concentration on the distal aspects of the digits, particularly the pulps of the fingers

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70
Q

Terminal Hairs

A

large, thick, coarse, pigmented. Ex: scalp, a man’s beard area and possibly chest/back, and the pubic area, begin deep in the dermis at/near the dermal-subcutaneous junction.

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71
Q

Vellus Hairs

A

small, fine, and apigmented. Such hairs are located diffusely on the body, and represented the types of hairs often on the ear, the lateral face of women, and the body in general.

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72
Q

It is common to divide the hair follicle into thirds:

A

infundibulum=upper third
isthmus= middle third (from the sebaceous duct to the insertion of the arrector pili)
martial area= lower third.

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73
Q

Phases of hair life cycle

A

~85%-anagen (the growth phase),
10-15% telogen (the resting phase)
(1-5%) in catagen (transition phase between anagen and telogen)

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74
Q

androgenic alopecia

A

hairs become miniaturized, finer and lie higher in the dermis. Ultimately they come to resemble vellus hairs. Conversion of testosterone to 5-dihydrotestosterone is important in promoting this change

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75
Q

treatments of male pattern baldness

A

finasteride, a 5-α-reductase inhibitor

minoxidil, a drug known to promote the anagen phase

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76
Q

holocrine gland

A

(sebaceous glands are and example) the method of secretion involved entire sebocytes (sebaceous gland cells) being secreted and in the process breaking-down to extrude the contents.

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77
Q

Acne is a ubiquitious disorder of the _______ unit

A

pilosebaceous

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78
Q

comedones

A

Blocked pores that are further classified to be: open - “black heads” or closed - “white heads”.

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79
Q

Eccrine glands

A

“general sweat glands”. The primary function of the eccrine unit is thermoregulation, which is accomplished through the cooling effects of evaporation of this sweat on the skin surface.

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80
Q

Merocrine glands/secretion

A

secrete WITHOUT either the apocrine blebbing, or holocrine shedding. Eccrine glands are a classic example of a merocrine secretion.

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81
Q

that even though sweating is mediated by the _____ portion of the autonomic nervous system it is triggered via _______ secretion. This is a chemical otherwise associated with the ________ nervous system.

A

sympathetic
acetylcholine
parasympathetic

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82
Q

Apocrine glands

A

outgrowths of the upper bulge of the primitive ectodermal germ, a fetal structure which yields the follicular unit. The apocrine glands are located only in the axillary and anogenital area.

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83
Q

Specialized variants of apocrine glands include

A

Moll’s glands on the eyelids, the cerumen (ear wax) glands of the external auditory canal, and the lactation glands of the breasts. At puberty, hormonal stimulation causes apocrine glands to become functional, and the glands respond mainly to sympathetic adrenergic stimuli initiated by emotional stress.

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84
Q

The predominant mode of apocrine secretion is

A

decapitation, a process where the apical portion of the secretory cell cytoplasm pinches-off and enters the lumen

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85
Q

Apoeccrine glands

A

hybrid sweat glands that are found chiefly in the axilla. Apoeccrine glands may play a role in axillary hyperhidrosis. These hybrid glands have both a small diameter portion, similar to an eccrine gland, and a larger diameter portion that resembles an apocrine gland. Similar to eccrine glands, they respond mainly to cholinergic stimulihybrid sweat glands that are found chiefly in the axilla. Apoeccrine glands may play a role in axillary hyperhidrosis. These hybrid glands have both a small diameter portion, similar to an eccrine gland, and a larger diameter portion that resembles an apocrine gland. Similar to eccrine glands, they respond mainly to cholinergic stimuli

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86
Q

Which secretes more, an apoeccrine gland or an eccrine glands

A

apoeccrine glands secrete nearly ten times as much sweat as eccrine glands

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87
Q

hyperhidrosis

A

focal excessive sweating. may be eccrine, particularly “clammy hands” or “sweaty feet, or may be due to apoeccrine glands in the axilla. generally do not sweat during sleep, most authorities consider it a disease of autonomic dysfunction.

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88
Q

What is an ointment comprised of?

A

water in and oil emulsion

89
Q

What is the potency of an ointment? Is it hydrating or drying? what is the irritation risk?

A

Ointments are HIGH potency
HYDRATING
LOW irritation risk

90
Q

Where can ointments be used?

A

Use in non-intrigenous sites.

Do not use on face, hands, groin

91
Q

A cream is comprised of….

A

Oil in water emulsion

92
Q

Cream:

  • potency
  • hydration
  • sensitization risk
  • irritation risk
A

Cream:

  • MODERATE potency
  • Some hydration (not as good as ointments)
  • HIGH sensitization risk
  • LOW irritation risk
93
Q

Where can a cream be used?

A

virtually all body sites

94
Q

Gels:

  • Potency
  • Hydration
  • sensitization risk
  • irritation risk
A

Gels

  • HIGH potency
  • Gels are DRYING
  • SIGNIFICANT sensitization risk
  • -HIGH irritation risk
95
Q

Where can gels be used?

A

oral mucosal surfaces, scalp

Do not use in fissures, erosions, macerated regions

96
Q

Lotion/solutions

  • Potency
  • Hydration
  • Sensitization risk
  • irritation risk
A

Lotion/solution:

  • LOW potency
  • VARIABLE drying
  • SIGNIFICANT sensitization risk
  • MODERATE irritation risk
97
Q

Where can lotion/solution be used?

A

Can be used in scalp, intertriginous areas.

Do not use in fissures/erosions

98
Q

What is a foam?

A

Pressurized collection of gas bubbles in liquid film matrix. Stable at RT, melts at 37 degrees (volatile). Components evaporate and leave supersaturated active ingredient. Stain free, quick drying, no residue

99
Q

Foam:

-Potency

A

Foam:

-STRONG potency

100
Q

Where can foam be used?

A

Can be used in hair bearing areas. Avoid fissures or erosions

101
Q

1 gram of cream covers:

A

10cm X 10cm

102
Q

How much further does 1 gram of ointment spread than 1 gram of cream

A

1 gram of ointment spreads 10% further than 1gram of cream

103
Q

How many topical grams are needed to cover a man’s entire body?

A

20g

104
Q

FTUs for 1 hand, both sides

A

A single hand, both sides requires 1 FTU

105
Q

Is topical steroid class I or class VII more potent?

A 
Class I is the most potent class
Class VII is the least potent class
106
Q

Hydrocortizone 2.5%

A

cream or ointment, class VII used to treat mild eczema, inflammatory dermatoses on face, intertriginous areas, groin

107
Q

Triamcinolone Acetonide 0.1%

A

cream or ointment. Class IV used in moderate spongiotic dermatoses:
eczematous dermatitis, atopic dermatitis, allergic contact dermatitis, bug bytes, drug reactions
Use on TRUNK or EXTREMITIES
Long term can’t use on face, intertriginous, groin

108
Q

Clobetasol Propionate 0.05%

A 
Cream or ointment, class I used in acute eruptions needing a quick fix like contact dermatitis, acute drug eruptions
Can't use on face, intertrigious areas, groin
* long term adverse effects possible
109
Q

Adverse local effects of topical steroids

A

Skin atrophy, generally from long term use, can cause shiny, thick skin, telangiectasia, stria. Baseline skin is more susceptible, as are intertriginous areas

110
Q

Adverse systemic effects of topical steroids

A

Happens with longterm use of potent/superpotent
-adrenal suppression
-Cushing’s
Growth retardation in kids

111
Q

What’s the max dose of a class I steroid every week?

A

50g/wk

112
Q

Mechanisms of Penetration of Topical Medication through Stratum Corneum

A

passive diffusion
channels or pores
through appendageal structures

113
Q

What is a gel?

A

Semisolid emulsion in alcohol base

114
Q

What are Lotions/Solutions?

A

Powder in water (some oil in water)

115
Q

Which vehicles contain preservatives that may increase the risk of contact allergy and sensitization?

A

Water-based vehicles (such as creams, lotions, and solutions)

116
Q

Eczema is a more broad term that can encompasses what common skin condition?

A

Atopic dermatitis

117
Q

Dx criteria for atopic dermatitis

A

Itchy skin + 3 or more of the following:

involvement of skin creases, history of asthma or hay fever, dry skin, visible flexural eczema, onset under the age of 2

118
Q

The etiology behind atopic dermatitis has to do with a _____ mutation

A

filaggrin

119
Q

While babies commonly exhibit atopic dermatitis on the cheeks, in childhood, many kids have eczema on the ____ skin

A

flexural

antecubital fossa, neck, wrists, ankles

120
Q

What other conditions are associated with atopic dermatitis?

A

asthma and allergi rhinits

121
Q

Irritant contact dermatitis

A

Most common kind of contact dermatitis

non-immune reaction from direct cytotoxic effects from common irritants.

122
Q

Allergic contact dermatitis is what kind of immunopathology?

A

Type IV hypersensitivity

123
Q

How is allergic contact dermatitis diagnosed?

A

patch test

124
Q

What is the ideology behind allergic contact dermatitis?

A

common allergens. Ex: nickel

125
Q

Stasis dermatitis

A

skin change that occurs from stasis (blood pooling in the veins of LOWER LEG)

126
Q

What is the etiology of stasis dermatitis?

A

lower extremity edema

127
Q

Nummular dermatitis

A

“discoid eczema” commonly on legs but can appear on trunk or arms, common in men 50+

128
Q

Seborrheic Dermatitis

A

Commonly occurs on SCALP, symmetrically over face including nasolabial folds, ears, chest.
Flaky, greasy scales

129
Q

etiology of seborrheic dermatitis

A

overproduction of skin oil + yeast malasseria furfur

130
Q

Describe psoriasis

A

hyper proliferation of epidermis with elongation of tete ridges and dilated capillary loops in dermal papillae

131
Q

Seborrheic dermatitis id linkrf yo

A

neurological conditions, parkinsons, head injury

132
Q

Psoriasis is a risk factor for what diseases?

A

cardiovascular disease

133
Q

Most common location for psoriasis

A

extensor surfaces, may include arthritis

134
Q

Cellulitis is characterized by

A

warm, tender erythematous patches or plaques. Located in dermis and subcutaneous tissue

135
Q

The most common vascular tumor in adults

A

cherry hemagiomas, not associated with any underlying disease. Primarily truncal

136
Q

Treatment for cherry hemangiomas

A

Superficial electrodesiccation

best for small lesions

137
Q

An infantile hemangioma is…

A

The most common soft tissue tumor of infancy
Benign endothelial cell neoplasm
Rapid proliferation in the first 1-3 months of life
Spontaneous involution over years

138
Q

Port Wine Stain

A

Vascular malformation
Present at birth
Persists into adulthood
No gender or gestational predilection

139
Q

Somatic mutation in port wine stains

A

GNAQ

140
Q

Klippel-Trenaunay syndrome

A

Overgowth of an extremity covered by alorge port wine stain

Varicose veins, venous stasis, edema, ulceration

141
Q

Sturge Weber Syndrome

A

Port wine stain + ocular and neurologic abnormalities including glaucoma, seizures and developmental delay)

142
Q

Why treat a port wine stain?

A

Persist into adulthood
Get worse with time
Dark purple, nodular, bleeding blebs

143
Q

Nevus Sebaceus

A

-papillomatous yellow-orange linear plaque on face or scalp
Scalp Lesions associated with alopecia
Rapid growth occurs at puberty

144
Q

Somatic mutations seen in nevus sebaceous

A

Somatic mutations in HRAS and KRAS

145
Q

Complication of nevus sebaceous

A

Epidemal nevus syndrome (neurologic abnormalities)

Epithelial neoplasms occur in 10-30% (Basal cell carcinoma, syringocystadenoma papilliferum)

146
Q

Sebaceous Hyperplasia

A

Common benign tumor of oil gland
Increasing freq. after middle age
face>trunk>extremities
1-6 mm yellowish-white papule (globules) with central dell

147
Q

Acrochordon

A

“skin tag” not treated unless causing irritation, then snip

148
Q

Dermatofibroma

A

Round to oval firm nodule- depressed or dome-shaped
Several mm to 1 cm, rarely larger
Color- skin-colored to tan to brown, rarely red, blue
Surface may demonstrate scale

149
Q

A keloid is a type of scar, which depending on its maturity, is composed of mainly either type ___ (early) or type___ (late) collagen.

A

III (early)

I (late)

150
Q

Seborrheic Keratosis

A

Benign tumor of the hair follicle
Exophytic papule- “stuck-on appearance
moisturize with a-hydroxy acids, lactic acid
cryosurgery

151
Q

Leser-Trélat

A

Rapid increase in size or number of seborrheic keratosis

Associated with internal malignancies, especially adenocarcinoma of the stomach (60%)

152
Q

Nevocellular Nevi

A

Moles that can be an:
Intradermal nevus
Junctional nevus
Compound nevus

153
Q

Appropriate treatment for nevocellular nevi

A

shave biopsy, punch biopsy, excision biopsy

NOT electrodessication, cryotherapy, dermabrasion, laser

154
Q

Blue Nevus

A

dermal proliferation of melanocytes that produce abundant melanin
Blue color- optical effect where longer wavelengths are absorbed and shorter wavelengths are reflected back (Tyndall effect)

155
Q

Congenital nevi are common in newborns, they look like large birthmarks.

A

.

156
Q

Risks associated with large congenital nevi

A

malignant melanoma

Risk 1% per year in large congenital nevi (>40 cm diameter)

157
Q

Dysplastic Nevi

A

Round to oval to irregular
color- tans, brown, black, reds
Margins- often indistinct (fuzzy), pigment bleeds into surrounding skin, irregular margins
Size- no limi

158
Q

Clinical importance of dysplastic nevi

A

Melanomas are contiguous with dysplastic nevi

6.6%-70.3% in ten studies

159
Q

FAMM Syndrome criteria

A

The occurrence of malignant melanoma in 1 or more first- or second-degree relatives
The presence of numerous (often >50) melanocytic nevi, some of which are clinically atypical
Many of the associated nevi showing certain histologic features

160
Q

Germline mutations in 3 genes have been linked to a subset of FAMM syndromes:

A

CDK2NA
CDK4
CMM1

161
Q

NMSC risk factors

A

fair skinned
areas with higher UV exposure
(UV radiation is the most common cause of BCC)
ionizing radiation, arsenic or polycyclic hydrocarbon exposure

162
Q

Most common malignancy in the US

A

Basal cell carcinoma. Rarely fatal, but can be disfiguring

163
Q

The majority of BCCs have a loss of function of the ____Gene which normally blocks the smoothened (SMO) transmembrane protein

A

PTCH1

164
Q

What can be sued to treat advanced BCC?

A

Vismodegib, an inhibitor of smoothened

165
Q

Actinic Keratosis

A

most common precancer- 58 million Americans

65% of all SCC and 36 percent of BCCs arise from AKs

166
Q

Treatment for actinic keratosis

A 
Cryosurgery
Liquid nitrogen (boiling point of -196 C)
Topical 5-fluoruracil
Topical Imiquimod
Topical Diclofenac
Photodynamic therapy
Sun protection
167
Q

___ is the second most common cutaneous malignancy

A

Squamous cell carcinoma

168
Q

What special group is prone to getting SCCs?

A

immunosuppressed pts, especially organ transplant pts

169
Q

Risk factors for SCC

A

UV damage, thermal injury, radiation, HPV, burn scars (Marjolin’s ulcer) and chronic injury (i.e. EB)

170
Q

Subtypes of SCC

A

SCC in situ (Bowen’s disease)
Keratoacanthoma
Invasive SCC

171
Q

Keratoacanthoma

A

A type of SCC
primarily sun-exposed skin
Rapid growth over 6-8 weeks
Size- 1-3 cm
Crateriform endophytic and exophytic nodule with central keratin plug
Complications- deep invasion without regression in 10-20%

172
Q

Can SCC metastasize?

A

Metastasis occurs infrequently, but is more common in SCC of the lip (10-30%)

173
Q

Skin cancer and transplant patients

A

SCC = 65 fold risk
BCC = 10 fold risk
Melanoma = 3.4 fold risk
Kaposi’s sarcoma = 84 fold risk

174
Q

Ratios of SCC:BCC in normal and transplant patients

A

Non-transplant pts SCC:BCC = 1:4
Transplant pts SCC:BCC = 4:1
Incidence of skin cancer increases with number of years post-transplant:

175
Q

Non-melanoma Skin CancerTREATMENT

A 
Topical 5-fluoruracil
Topical Imiquimod
Cryosurgery
Electrodessication and Curettage
Excision
Mohs micrographic surgery
Radiation
176
Q

ABCD guidelines for melanoma

A 
A = Asymmetry
B = Border irregularity 
C = Color variation 
D = Diameter greater 	than 6 mm
E = Evolution (or 	change)
\+ "ugly ducking" rule
177
Q

What mutation is commonly associated with melanoma?

A

BRAF

178
Q

What drug can be used for melanoma patients with BRAF mutations?

A

Vemurafenib, a BRAF inhibitor

179
Q

Common race and sex specific locations for melanoma

A

Blacks- acral and mucosa
Men- back
Women- legs (torso in females age 15-29, perhaps due to tanning)

180
Q

The breslow depth measures…

A

the depth of the melanoma in mm

181
Q

Other mutations common in melanoma

A
  • BRAF 50%
  • NRAS 20%
  • Kit 2%
  • GNAQ 2%
182
Q

Windows protect against ___, but do not filter ___ and ____ of the sun’s UV rays pass through clouds on a cloudy day.
Sand reflects __% and snow reflects __% of the sun’s UV rays.

A 
UVB
UVA
80%
\_\_\_\_\_\_
25%, 80%
183
Q

Sunscreen should be applied to dry skin ______minutes before going outdoors.

___ ounce of sunscreen is enough to cover the exposed areas of the body.

Sunscreen should be reapplied at least every __ hours or after swimming or sweating heavily.

A

15-30

1, enough to fill a shot glass

2

184
Q

UVR Effects on the Skin

A
  • Damage to DNA, RNA, lipids, proteins
  • Pro-inflammatory effects
  • Immunosuppressive effects
  • Induction of innate defenses
  • Induction of apoptosis
  • Vitamin D synthesis
185
Q

How does UVR induces the synthesis of cholecalciferol (VitD3) and ergocalciferol (VitD2)?

A

non-enzymatically

186
Q

DNA damage induced by UVR

A

Thymine dimer : UVB

  • Pyrimidine-6-4 pyrimidone: UVB
  • Hydroxyguanosine (UVA and singlet oxygen)
187
Q

Primary and secondary cytokines released as a result of UVR

A

Primary Cytokines: IL-1a, TNF-a
-Secondary cytokines:
IL-6,IL-8,IL-10, GM-CSF

188
Q

UVR Induces Both ____ and ____

A

Inflammation

Immunosuppression

189
Q

How does UVR induce immunosuppression?

A

-decrease in Langerhans Cells
-induction of inhibitory cytokine network:
-Tolerance induced by Suppressor cells
Treg (CD4+CD25+)
NKT cells

190
Q

UVR Immunosuppression Cascade

A

UVR Induces keratinocyte release of PAF and Cis-UCA> activates mast/B cells>IL-10 production

  • PAF induces PGE2 > activates B cells >IL10
  • IL-10 blocks IL-12 production by DC
  • T cells cannot be activated to form cytotoxic cells, but NKT and Treg induce tolerance
191
Q

IS UVR inhibited by high melanin content?

A

Not inhibited by high melanin content

It Potentiates induction of NMSC

192
Q

Example of genetic condition with DNA repair mechanism mutation

A

Xeroderma Pigmentosum is a family of diseases in which genetic defects in DNA repair lead to premature aging of the skin and fatal induction of UVR-induced skin cancers

193
Q

DNA Repair Enzymes

A

Excision of mutated strand of DNA
UVR ABC nuclease

Repair replication
DNA Polymerase

Rejoining
DNA Ligase

194
Q

Defenses against Reactive Oxygen in the Epidermis

A
  • Peroxidases and catalases
  • Superoxide dysmutase
  • Glutathione reductase
  • Thioredoxin reductase
195
Q

Rate limiting step in melanin production

A

Tyrosinase

196
Q

What explains 25-38% 0f European/African differences in pigmentation?

A

SLC24A5, a K-dependent Na/Ca ion exchanger

197
Q

In terms of pigmentation, Potential differences in signalling pathways that control MITF

A

MSH, WNT, SCF/Kit

198
Q

Viral characteristics of HPV

A

Non-enveloped double-stranded DNA virus

MANY, many types

199
Q

HPV lesions are named

A

Verruca_______

200
Q

What can be given if herpes are acyclovir resistant?

A

Foscarnet

201
Q

Potential complication of streptococcal impetigo

A

Up to 5% of streptococcal impetigo associated with acute post-streptococcal glomerulonephritis

202
Q

Who is at increased risk for cellulitis?

A 
– Very young
– Elderly
– Immunocompromised
– Intravenous drug users
– Patients with chronic ulcers
203
Q

Two most common organisms causing cellulitis

A

strep and staph

204
Q

Erysipelas

A

cellulits on the face

“Cliff drop border”

205
Q

Staphylococcal cellulitis can exhibit lymphatic _____

A

streaking

206
Q

syphilis is caused by

A

Treponema pallidum
• Spirochete- 6-14 spirals
• Never cultured

207
Q

Primary syphilis characteristics

A

chancre-ulcer full of spirocetes, goes away in a few weeks, characteristically PAINLESS!!! But lymphadenopathy is present

208
Q

Secondary syphilis can be latent for

A

1-2 years

209
Q

tertiary syphilis is characterized by

A

neuropathy

210
Q

Rash + Lymphadenopathy =

A

think syphilis

211
Q

Types of secondary skin lesions (4-10 weeks after chancre)

A 
– Non-pruritic papulosquamous lesions – Condylomata lata
– Nonscarring “moth-eaten” alopecia
– Split papules at oral commissures
– Annular lesions on face
– Oral lesions
212
Q

What do the dermatophytes eat and where are their infestations common?

A

they eat keratin, they live int he skin, hair, nails (not very deep)

213
Q

annular plaques with raised border and central clearing outward are often called “ringworm” but they are really:
Diagnosis?

A

tinea corporis,

DDx: KOH prep from leading edge

214
Q

Increased candidiasis is seen in the following conditions:

A

– Diabetes mellitus
– Occlusion
– Corticosteroid use
– Broad-spectrum antibiotics

215
Q

What does candida eat?

A

glucose or serum

216
Q

Malassezia furfur like to eat

A

follicular lipids.
asymptomatic, tan- colored subtly scaly macule or patch
• Clinical variants
– Hypopigmented variant – Folliculitis

217
Q

Scabies distribution

A

symmetric- interdigital web space, flexural wrist, waist, axillae, genitalia and breast (soft skin distribution)

218
Q

Symptoms of scabies

A

Symptoms- pruritus (nocturnal accentuation)
– Erythematous papules
– Erythematous burrows
– Nodular lesions on genitalia

219
Q

DDX of scabies

A

wet mineral oil prep

disease and defense (2 decks)

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