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Disease And Defense > Dermatology > Flashcards

Dermatology Flashcards

1
Q

how much does the skin weight?

A

approximately 4 kg

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2
Q

Surface area of skin

A

2 m2

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3
Q

Function of skin

A

1) decoration 2) barrier 3) vitaminD synthesis 4) water homeostasis 5) thermoregulation 6) insulate/calorie reservoir 7) touch/sensation

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4
Q

Fitzpatrick Skin Scale

A

way to categories skin types based on color and ability to sunburn

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5
Q

Fitzpatrick 1

A

Red/blond hair, with blue/green eyes, white skin with lots of freckles, always sunburns and enver tans

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6
Q

Fitzpatrick 2

A

Blond/brown hair, light to medium eyes, fair skin with some freckles, sunburns easily and minimally tans

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7
Q

Fitzpatrick 3

A

Brown hair, medium to dark eyes, light brown skin, minimal freckles, sunburns initially, and tans gradually

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8
Q

Fitzpatrick 4

A

Medium to dark hair, dark eyes, moderate brown skin, no freckles, minimal sunburn, tans well

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9
Q

Fitzpatrick 5

A

dark hair and eyes, dark brown skin, no freckles, rarely sunburns, dark tan

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10
Q

Fitzpatrick 6

A

dark hair and eyes, black skin, no freckles, never sunburns, always tan

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11
Q

what gives our skin its color?

A

due to the type, size and distribution of melanosomes

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12
Q

Eumelanin

A

brown to black pigment

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13
Q

Pheomelanin

A

yellow to red-brown pigment; not as effect a eumelanin at blocking light

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14
Q

Distribution of melanosomes in light skin

A

small melanosomes, distributed in clusters above nucleus of keratinocyte

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15
Q

Distribution of melanosomes in dark skin

A

large melanosomes, distributed individually through cytoplasm of keratinoctye

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16
Q

Albinism

A

defect in tyrosinase gene that is involved in melanin production

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17
Q

Vitiligo

A

autoimmune response to melanocytes. It is acquired depigmentation so there is a complete lack of melanocytes. Most seen in periorificial and aural locations.

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18
Q

Sources of Vitamin D

A

Sun exposure, fish, fish liver oil, egg yolks, fortified dairy, grains

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19
Q

Vitamin D Deficiency

A

Rickets - weakened bones causing skeletal abnormalities

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20
Q

How does Vitamin D get converted to active form in the skin?

A

Skin + UVB from the sunlight stimulates 7-dehydrocholesterol to convert to Cholecalciferol (Vit D3) in the skin.

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21
Q

7-dehydrocholesterol

A

enzyme that when stimulated with by UBV is covered to cholecalciferol (Vitamin D3)

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22
Q

what forms of Vitamin D do we get in our diet

A

Cholecalciferol (D3) and Ergocalciferol (D2), absorbed through intestines

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23
Q

What happens to Vitamin D in the liver?

A

D2 and D3 are covered to Calcidiol (25-hydroxy)

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24
Q

Calcidiol

A

25-hydroxy that is converted from Vitamin D3 and D2 in the liver and it transfered to the kidney

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25
Q

What happens to vitamin D in the kidney

A

it is converted to 1,25- dihydroxy Vitamin D (calcitrol) which is the active form.

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26
Q

Calcitrol

A

is the active form of vitamin D from the kidney, increases calcium absorption, PTH mediated bone resorption, decreases renal Ca2+ and phosphate excretion

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27
Q

Epidermis cell type

A

stratified squmaoue epithelial

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28
Q

Components of the dermis

A

Papillary Dermis: loose connective tissue just under epidermis; Reticular Dermis: dense connective tissue further down

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29
Q

Adnexal structures

A

Apocrine, eccrine gland, hair follicles, nails, subcutaneous fat

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30
Q

Where is thick skin found?

A

On palms and soles, hairless

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31
Q

Keratinocytes

A

Barrier layer in epidermis that synthesize keratin, the intracellular fibrous skin protein

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32
Q

Melanoctyes

A

pigment producing neural crest cells located on basal layer of epidermis near hair follicles; 1 melanocyte provides pigment to many more keratinocytes via dendritic branches

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33
Q

Melanin

A

pigment derived from tyrosine, packed in melanosomes. Protective of DNA and UV damage.

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34
Q

Langerhan Cells

A

Endogen presenting - cells of the immune response in the skin. There is a small number in the epidermal layer. Essentially Dendritic cells in epidermis that are BM derived

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35
Q

Merkel Cells

A

Never endings in epidermis, involved in neural development and tactile sensation; rarely become neoplastic and cause merkel cell carcinoma

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36
Q

How long is the life cycle of keratinocytes?

A

28 days!

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37
Q

What are the layers, form Bottom to Top of the epidermis?

A

Stratum basalis, Stratum Spinosum, Stratum Granulosm, Stratum Corneum

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38
Q

Stratum Basalis

A

deepest layer of the epidermis; single layer of columnar or cuboidal keratinocytes that are attached via hemidesmosomes to the basal lamina of dermal epidermal jungion; houses the stem cells of epidermis

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39
Q

What attaches the keratinocytes to basal lamina?

A

hemidesmosomes

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40
Q

Bullous Pemphigoid

A

autoimmune disease with Ab to BP230 or BP180 that attach Type XVII collage to make hemidesmosomes ineffective and lead to sub-epidermal blisters. Increased risk of infection. Occurs in older adults

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41
Q

Epidermolysis Bullosa

A

group of inherited disorders that results in blistering due to trauma at that sub epidermal junction. Two types: Junctional and Dystrophic

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42
Q

Junctional Epidermolysis Bullosa

A

Collagen XVII or Laminin 5 mutation; blistering disorder a subepidermal junction due to trauma/friction, improves with age

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43
Q

Dystrophic Epidermolysis Bullosa

A

mutation in Collagen VII which leads to psedosyndactylyl (mitten hand), flexion contractures, increased risk of squamous cell carcinoma, infection; recessive form is most severe.

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44
Q

Stratum Spinosum

A

Full of desmosomes that attach keratinocytes together (cell to cell adhesion)

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45
Q

Desmosomes

A

Cell to cell adhesion in stratum spinosum layer composed of intracellular Keratin Filaments (5 and 14) and Desmogleins

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46
Q

Pemphigus Vulgaris

A

autoAb to desmogelin 1 and 3 that produces flaccid bulla with intraepidermal blistering.

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47
Q

Epidermolysis Bullosa of the Stratus Spinosum layer?

A

Epidermolysis Bullosa Simplex; genetic defects in Keratin 5 and 14, generalized onset of blisters shortly after birth

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48
Q

Stratum Granulosum

A

2nd layer from the stop of the epidermis; cells start to loose their nuclei and keratohyalin granules contain filaggrin which cross links to form cornfield cell envelope, Contains lamellar bodies

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49
Q

Filaggrin

A

located in stratum granulosum of epidermis, is important for barrier formation

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50
Q

Lamellar bodies

A

located in stratum granulosum of epidermis, important for excretion of ceramics to form barrier

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51
Q

Stratum Lucidum

A

a layer seen only in thick skin, with no hair follicles. Cells no longer have nuclei or organelles. This layer helps reduced friction and shear forces

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52
Q

Stratum Corneum

A

Top most layer of the epidermis, with dead and desquamating keratinocytes. Breakdown of filaggrin forms Natural Moisturizing factor

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53
Q

Natural Mousturizing Factor

A

formed from the breakdown of filaggrin in the stratum corneum layer, binds to H20 to keep skin moist; levels decline with age.

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54
Q

What disorders arrise from loss of function of filaggrin?

A

Icthyosis Volgaris and Atopic Dermatitis

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55
Q

Small, light colored hair

A

Villous hair

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56
Q

Thicker hair

A

Terminal har

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57
Q

Allopecia Ariata

A

attack of hair follicles, can range form moderate to severe

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58
Q

Macule vs. Patch

A

both are flat areas of color change, macules are

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59
Q

Papule vs. Plaque

A

both are elevated bodies, Papules are

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60
Q

Nodule

A

firm and well-defined lesions that are dermal or subcutaneous >1 cm

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61
Q

Scale

A

excess stratum corneum, appears as white or gray flakes

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62
Q

Crust

A

dried blood, serum, or purulent exudate

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63
Q

Vesicles Vs. Bulla. vs pustule

A

Vesicle and bulla are both fluid filled, Vesicles is

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64
Q

Erythma vs. Erythroderma

A

Erythema is localized redness caused by increased blood flow; Erythroderma is generalized blanchable redness all over that is blanachable.

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65
Q

Telangiectasia

A

visible persistent dilation of superficial blood vessles

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66
Q

Ecchymoses

A

bruise, discoloration of skin or MM due to extravascular blood

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67
Q

Petichiae

A

tiny 1-2mm hemorrhages

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68
Q

Vasulitis

A

raised discoloration of palpable purport due to vascular inflammation and extravascular RBCs. can be red or violaceous

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69
Q

Atrophy vs Erosion

A

Atrophy is loss of epidermal, dermal or SC; Erosion, loss of epidermal or mucosal epithelium due to injury, denuding veiscle, bulla removal

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70
Q

Ulcer

A

Circumscribed loss of epidermis and at least some part of upper dermis; depth can extend to bone. Edge is clean or ragged. Tissue can be necrotic, purulent, healthy.

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71
Q

Fissure

A

deep linear crack found in thickened skin

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72
Q

Eschar

A

crust or scab that is black in color; due to trauma, infection, skin disease

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73
Q

Types of distribution of skin findings

A

Lyphagetic, dematomal, palmoplantar, photodistrubted

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74
Q

Intertriginous Distribution

A

skin surfaces that come into contact with eachother

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75
Q

Flexural Distrubition

A

overlapping muscles that flex joints

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76
Q

Dermatitis

A

Essential Eczema or inflammation of the skin

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77
Q

Types of Dermatitis

A

Stasis, Atopic, Irritant Contact, Allergic Contact, Drug erruptions, Psoriasis

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78
Q

Stasis Dermatitis is due to….

A

venous insufficiency of lower extremities that causes edema

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79
Q

Stasis Dermatitis looks like

A

dry, itchy, could be due to contact allergic due to topical application or irritant due to wound exudates

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80
Q

Complications of Stasis Dermatitis

A

stasis ulcers

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81
Q

Treatment of stasis ulcers

A

compression, elevation, exercise of calves, vascular surgery, topical steroids, avoid allergens

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82
Q

Major differences in Stasis Dermatitis vs. Cellulitis

A

Derm: causes erythmatous papules and plaques with scale that affect dermis and epidermis bilaterally! Cellulitis cases warm, tender erythematous patches or plaques to the dermis or subcutanoues regions Unilaterally

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83
Q

Atopic Determatitis

A

Due to a filaggrin mutation that is associated with Xeroxes and asthma and allergies. Most provolone in Children under 5; most often in flexture of joints like antecubital fossa, popliteal fossa, neck, wrist, ankle

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84
Q

Types of Atopic Dermatitis

A

Infantile, childhood, adulthood

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85
Q

Infantile Dermatitis

A

dry, red, scaly cheeks, flushed in gold.

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86
Q

Diagnosis of Atopic Dermatitis

A

Itchy skin with 3 or more of the follow: onset under 2 years; Hx of involvement in skin creases; Hx of asthma or hay fever; Hx of dry skin in last year; visible flexture eczema

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87
Q

Irritant Contact Dermatitis

A

Not immunologically mediated due to a single or repeated exposure of strong of weak irritants

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88
Q

Strong irritant

A

a small amount causes irritant contact dermatitis

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89
Q

Weak irritant

A

takes frequent exposure (large dose) to cause dermatitis, harmless by itself or single exposure

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90
Q

Allergic Contact Dermatitis

A

Contact exposure that initiates an immune response with memory T-cells; Delayed Type IV hypersensitivity. Small molecules penetrate the skin and elicits a TNFalpha and IL-1 cytokine release

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91
Q

What are the most common allergic contacts in Allergic contact dermatitis?

A

Nickel and balsam of Peru (fragrance)

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92
Q

Risk factors for nickel allergy?

A

female, young, pierced ears

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93
Q

Neomycin sulfate and bacitracin

A

allergens in topical antibiotic solutions

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94
Q

Ezcematous Eruptions

A

Drug eruptions; most common in adults due to use of drugs; being 7-14 days after beginning new med

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95
Q

Common drug eruption reactions occur with..

A

aminopenicillin, sulfonamide, cephalosporin, anticonvulsants, eallpurional

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96
Q

Treatment of drug eruptions

A

discontinue drug, topical steroids and antihistamine

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97
Q

Urticaria

A

hives, wheels (an immediate Type I hypersensitiviey_ by IgE due to physical and chemical triggers. the lesions last for less than 24 hours. Can be acute (6 weeks).

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98
Q

Nummular Dermatitis

A

Excess dry skin, red,scaly crusty patches most often seen on legs (somtimes arms and trunk) in Men over 50.

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99
Q

Treatment of nummular dermatitis

A

moisturizer, minimize soap, sometimes steroids

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100
Q

Suborrheic Dermatitis

A

sharply demarcated patches with pick or orange-yellow erythema seen in infancy or post-pubery when sebaceous glands are active. Most commonly seen on face, scalp, ears, and chest. Also known as Cradle Cap. Due to overproduction of skin oil and yeast irritation. Due to Malessazia Furfur.

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101
Q

Psoriasis

A

hyperproliferation of epidermis, elongation of rete ridges that occurs on the extensor surfaces. Often associated with a family history

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102
Q

Types of Psoriasis

A

Chronic Plaque disease, Guttate (strep throat), erythroderma, Pustular psorasis

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103
Q

Co-morbidities of psoriasis

A

Arthritis, Cardiovascular disease, anxiety, insulin resistance

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104
Q

Treatment of Psoriasis

A

Vitamin D3 analog, steroids, phototherapy, anti-T lymphocytes, Anti TNFalpha

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105
Q

what is the purpose of epidermal Rete?

A

Shear strength

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106
Q

what is located in the dermis

A

hair glands, sweat glands, sebaceous glands, vessels, nerves

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107
Q

Papillary Dermis

A

Thin collagen bundles that locks with epidermal rete to increase strength and surface area

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108
Q

Reticular Dermis

A

thick collagen bundles with visible elastic fibers that cause reliance

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109
Q

what is the purpose of elastin?

A

located in reticular dermis provides resilience or springs back after distortion

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110
Q

Collagen Structure

A

Triple alpha helix that is made up of Gly- Porline- Hydroxyproline. There are a number of different types

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111
Q

Collagen I

A

most common in adult dermis, >85% of collagen in adults

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112
Q

Collagen III

A

fetal collagen

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113
Q

Collagen IV

A

collagen in basement membrane

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114
Q

Collagen VII

A

collagen in anchoring fibers

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115
Q

synthesis of Collagen

A

Procollagen is synthesized in fibroblasts and is excreted. Cleaved outside of fibroblasts convert it to tropocollagen where with the help of vitamin C, is cross linked to form final collagen network

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116
Q

Ground Substance

A

made up of glycosaminoglycans like hyaluronic acid and dreamt sulfate, fibronectins. This promotes diffusion of blood and other contents

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117
Q

Disorders of collagen production

A

1) Scurvy (Acquired) 2) Ehlers Danlos Syndrome (inherited)

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118
Q

Scurvy

A

Vitamin C deficiency causes decreased mature collagen production with signs and symptoms developing 1-3 months follow time of deficiency

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119
Q

Scurvy Signs and Symptoms

A

Keratotic plug, perifollicular hemorrhage, corkscrew hair, hemohorrhagic gingivitis, weakness, delayed wound healing

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120
Q

why is hemorrhage common in scurvy?

A

lack of collagen support for blood vessels

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121
Q

Ehlers Danlos Syndrome

A

inherited disorder in collagen formation

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122
Q

Ehlers Danlos Syndrome Signs/Symptoms

A

Hyper-extensible joints and skin, fragile blood vessels, poor wound healing, absent inferior labial and inguinal frenulum, Gorlin’s Sign, molluscoid pseudoturmors

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123
Q

Gorlin’s Sign

A

ability to touch tip of nose with tongue, sign of EDS

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124
Q

Mullucoid Pseudotumors

A

scar like nodules on knees, common in EDS

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125
Q

Elastin Disorders

A

Solar Eslastosis (acquired) and Psedoxanthoma Elasticum (inherited)

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126
Q

Solar Elastosis

A

an acquired disorder of elastase that is due to sun damage; ineffective remodeling and basophilic. Indicative of a persons age at biopsy

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127
Q

Pseudoxanthoma Elasticum

A

inherited disorder of elastin, due to mutation in MDR gene that causes brittle and calcified elastin.

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128
Q

Pesudoxanthoma elasticum signs/symptoms

A

Plucked chicken skin, systemic hypertension, angioid retina streaks, arterial rupture in eye

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129
Q

Ground Substance disorders

A

Restylane and NO congenital disorders

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130
Q

Restylane

A

a hyaluronic acid used a ground stubance filler to fill in wrinkles

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131
Q

Blood supply in the skin

A

Epidermis has no individual blood supply, so dermis must supply it with blood. Dermis has two levels of blood supply the Superficial plexus (supplies dermis) and the deep plexus

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132
Q

What diseases causes disorder capillary loops in the dermis blood supply?

A

Psorasis and verruca worts (disease with increased epidermal turnover)

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133
Q

Vascultis

A

inflammation of capillaries and venues that causes palpable purpura; due to drug hypersensitivity, infection, neoplasm, collagen vasculature diseases

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134
Q

Nerve supply in the dermis

A

Contain both Specialized and Free nerve endings

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135
Q

Type A nerves

A

heavily myelinated nerves with rapid salutatory conduction; involved in proprioception, touch, stretch, pain

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136
Q

Type C nerves

A

unmyelinated nerves with slow conduction; involved in dull, non-localized, diffuse sensation like temperature and pruritus

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137
Q

Meissner’s Corpuscles

A

Nerve receptors that look like leaves near Dermal-Epidermal junction that are used in find-touch sensation like in digits.

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138
Q

Pacinian Corpuscles

A

Nerve receptors that look like onions located deep in the dermis and are sensitive to pressure and vibrations, most prevalent in genitals

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139
Q

Hair Follicle Structure

A

Infundibulum: top most above/level with sebaceous duct; Isthmus: between sebaceous duct and arrector pili; lowest part is the bulb or the martial area

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140
Q

How are hair follicles formed during embryology?

A

Primitive edtodermal gland is induced by underlying dermal mesenchyme and forms 3 buldges. The lower budge mask up the attachment to arrector pili, middle budge forms sebaceous gland, upper part forms apocrine gland

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141
Q

hair cycle

A

Anagen, telogen, catagen, all random stages in which the hair is in

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142
Q

Anagen

A

growth stage of hair cycle; 85% of hairs are here, lasts for 3 years

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143
Q

Telogen

A

rest stage of hair cycle; 10-15% of hairs are here; lasts 3 months

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144
Q

Catagen

A

involution stage of hair cycle; 1-5% of hair is here; lasts 3 weeks

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145
Q

Androgenic hair loss

A

patterned baldness due to conversion of testosterone to dihydrotestosterone that leads to miniaturization of the hair follicles.

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146
Q

Treatment of Androgenic hair loss

A

Finasteride which blocks the DHT synthesis and moves follicles deeper and maintains the size of hair follicles. Dangerous in women, especially during menstrual years

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147
Q

Sebaceous glands

A

used to lubricate terminal hair

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148
Q

Acne

A

is due to pilosebaceous unit; abnormal follicular maturation which leads to a plugged follicle and overgrowth of P. Acnes which liberate Free Fatty Acids and/or ruptures follicles that leads to dermal inflammation.

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149
Q

Holocrine Gland

A

is a gland where secretion occurs of the entire cells. Example is Sebaceous gland where entire sebocyte is secreted to release its contents

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150
Q

Eccrine gland

A

sweat glands that are used in thermoregulation; most prevalent on forehand, upper lip, palms, and soles

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151
Q

Structure of eccrine gland

A

1) coiled secretory component deep in dermis 2) intradermal duct 3) acrosyringium (intraepidermal)

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152
Q

How is sweat released?

A

mediated by sympathetic Autonomic nervous system, but triggered by ACh (a parasympathetic Neurotransmitter)

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153
Q

Secretion from eccrine glands are…

A

watery and odorless

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154
Q

Merocrine

A

secretion of tiny vesicles like in eccrine glands

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155
Q

Acquired disorder of eccrine glands

A

heat shock, antipersperents

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156
Q

Miliaria

A

Aquired disorder of eccrine gland, blocked sweat ducts that cause heat rash

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157
Q

Anhidrotic Ectodermal Dysplasia

A

inherited eccrine disorder that is due to mutation in EDA gene, so that have decreased thermoregulation, decreased sweat, spare hair and malformed teeth

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158
Q

Apocrine Gland

A

located in axially and anogenital regions that release sialomucin. These are small and nonfiction until puberty

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159
Q

Sialomucin vs. eccrine secretion

A

stickier, but still odorless. Develops odor by contact with bacteria

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160
Q

Apocrine Secretion

A

secrets apex of cell to release contents

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161
Q

Apoeccrine Gland

A

hybrid sweat gland in axilla.

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162
Q

Axially Hyperhidrosis

A

focal excessive sweating, except during sleep. Treatment is botulinum toxin to prevent ACh release

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163
Q

Senile Cherry Angioma

A

Vascular tumor that occurs mostly in adults that leads to a bright red, smooth, papule on skin; mostly located on trunk

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164
Q

Treatment of Cherry Angiomas

A

Superficial Electrodessication, Liquid N2, Shave biopsy, pulse dye laser

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165
Q

Infantile Hemangioma

A

also called capillary or straberry hemangioma; is a benign endothelial neoplasm that can occur anywehere. Cells stain positive for GLUT-1, a placental vascular marker.

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166
Q

Onset of Infantile Hemangiomas

A

Could be born with it, or appear within first 2 months of life; grows rapidly for first few weeks and then involutes 10% each year. Most prevalence in girls, premature babies, and those with post-crionic villous sampling

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167
Q

Complications of infantile hemangioma

A

1) location: visual or airway interruptions 2) size 3) ulceration 4) Over 5 (visceral or CNS) 5) can cause systemic disease with Congestive heart fialure, Kasabach Merritt 6) Congential: PHACES

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168
Q

Kasabach-Merritt

A

Thromocytopenic Coagopathy - associated with infantile hemangiomas

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169
Q

PHACES

A

Posterior fossa abnormalities, hemangioma, arterial aorta abnormalities, cardiac, eye, and sternal defects - all complications of infantile hemangioma

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170
Q

Infantile hemangioma treatment

A

observation, local wound care, pulse dye laser, topic and systemic steroids, beta blockers

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171
Q

Port wine Stain

A

a capillary malformation within dermis that is lined by flat continuous endoethlium, NO GLUT-1 mutation, but somatic mutation in GNAQ. Presents as pink patch and can progress to purple with modularity.

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172
Q

Areas of port wine stain

A

trigeminal nerves, mid dorsal, lumobsacral, nape of neck

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173
Q

Age of onset for Port Wine Stain

A

present at birth and persists until adulthood

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174
Q

Klippel-Trenaunay Syndrome

A

complication of port wine stain; overgrowth of extremity covered with port wine. Complications of varicose veins, venous stasis, edema, ulceration

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175
Q

Sturge Weber Syndrome

A

Complication of Port Wine Stain; ocular and neurologic abnormalities - glaucoma, seizure, Developmental delay

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176
Q

Complications of Port Wine

A

Klippel-Trenaunay and Sturge weber

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177
Q

Treatment of Port Wine

A

Pulse dye laser to prevent thinking or darkening with time

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178
Q

nevus Sebaceous

A

hamartoma of sebaceous bland on face or scalp, appears papillomatous yellow-orange linear plaque with absent hairgrowht

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179
Q

Onset of Nevous Sebaceous

A

Rapid growth at puberty due to enlargement of sebaceous glands

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180
Q

Complications of Nevous Sebaceous

A

Neurological abnormalities (epidermal nevous syndrome) and potenital for epithelial neoplasm

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181
Q

Treatment of Nevus Sabeceous

A

Observation, surgical excision

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182
Q

Sebaceous Hyperplasia

A

Bengin tumor of sebaceous gland most prevent on face>trunk>extremities. Appears as a yellow-hits papule with central dull. Increased in frequency after middle age due to possible sun exposure

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183
Q

Treatment of Sebaceous hyperplasia

A

No treatment often; electrodessication, trichloroacetic acid, liquid N2, laser therapy

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184
Q

Acrochordon

A

also known as skin tags, or fibroepithelail polyps, benign skin grows that are soft, flesh colored (tan or brown) exophytic papules with narrow base. Occurs in areas of rubbling like neck, axially, inframammary

185
Q

Acrochordon prevalence

A

1/4 of adults have these

186
Q

Complications of Acrochordons

A

recurrent trauma or torsion

187
Q

Treatment of Acrochordons

A

No treatment, snip excision, removal by cryosurgery with liquid N2, electrodessication

188
Q

Dermatofibroma

A

Fibrous histiocytoma, a benign histiocytoma that appears as a brown, firm papule that has dimple sing when pinched. occurs most often on legs in adults

189
Q

Complications of Dermatofibroma

A

large and enlarging may be malignant (dermatofibrosarcoma protuberans). can be painful or pruritus

190
Q

Treatment of Dermatofibromas

A

no treatment, if necessary biopsy to rule out malignancy

191
Q

Lipoma

A

Begnin adipose tumor that is soft to touch movable and painless, usually greater than 1 cm. Occurs in Adults, rare in children

192
Q

Treatment of lipoma

A

not treatment often, sometimes surgical excision

193
Q

Keloid scar

A

Overgrowth of granulation tissue. Early stage full of collagen III, later stage collage I. Firm, rubbery, shiny nodule that expands border of wound. Can be pink to dark brown in color.

194
Q

Treatment of keloid scars

A

topical steroids, intralesional steroids, surgical excision (if prone to keloids, but not be beneficial), surgery +/- radiation

195
Q

Seborrheic Keratosis

A

Branacle, benign tumor of hair follicle; a white, gray, brown of black exophytic papule that is sunk in. Can be smooth or verrucous, friable, and studied with small pits. Occurs on head, neck, or trunk

196
Q

Types of Seborrheic Keratosis

A

1) dermatosis Papulos nigra (black and asians) 2) stucco keratosis (acral areas) 3) inflamed seborrheic keratosis 4) leser-Trelat: increased in size, number, and internal malignancies (adenocarcinoma of stomach)

197
Q

Treatment of seborrheic keratosis

A

moisturizers (alpha-hydroxy-acids, lactic acid), cryosurgery, surgical removal

198
Q

Nevocellular nevi

A

moles that can occurs in on any skin area or mucosal membranes. Increase in number with age of person.

199
Q

Treatment of Nevocellular nevi

A

no treatment necessary; for atypical appearing/evolution: shave or punch biopsy and excision. DO not electrodissicate, cryotherapy, dermabrasion, or laser

200
Q

Types of Nevocellular nevi

A

Intradermal, junctional, compound

201
Q

Intradermal Nevus

A

Less than 6 mm papule or nodule, dome shaped, pedunulated cerebriform, located on head and neck

202
Q

Junctional Nevis

A

1-5 mm macule, smooth surface, tan to brown/black. Can ben anywhere, common on plantar and palmar surfaces

203
Q

Compound Nevus

A

varaible in size, papule or nodule, dome shpaed tan to brown to black, found on trunk and proximale extremities

204
Q

Blue Nevus

A

Dermal proliferation of melanoctyes to produce abundant melanin, tyndall effect to have blue color

205
Q

Blue Nevus onset

A

congenital; 1:3000 or acquired; common in asians or caucasians

206
Q

Complications of blue nevus

A

malignancy is rare

207
Q

Treatment of blue nevus

A

no treatment if unchanging, surgical removal, punch biopsy, excision

208
Q

Congential Nevi

A

1mm to lauge, darkened patch with dark hair on step.. could be solitary or multiple on cutaneous surface.

209
Q

Complications of congenital nevi

A

head, neck, posterior midline, leptomeningeal melanocytosis could be increased risk of melanoma

210
Q

Treatment of congenital nevi

A

elective surgical excision - controversial

211
Q

Dysplastic Nevus

A

acquired melanocyte proliferation to have oval or irregular shape, color variation, indistinct margins with no size limits. Could appear to any skin area.

212
Q

Complications of dysplastic nevi

A

melanoma, FAMM

213
Q

FAMM

A

familial atypical moles and melanoma: melanoma in 1 or more 1st of 2ned degree relatives, numerous nevi

214
Q

Treatment of Dyplastic nevi

A

mole mapping, total body photography, remove atypical

215
Q

Cafe Au lait macules

A

subtle increase in melanocytes with increase melanin production on trunk and extremities. Associated with early childhood.

216
Q

Complications of Cafe au Lait

A

Neurofibromatoosis: while with 6 mor more >5mm cafe au lait spots

217
Q

Crowe’s Sign

A

child with six of more cafe au lait spots; sign of NF

218
Q

Neurofibromas

A

soft, flesh colored papules with buttons hole sign, deep, form subcutaneous nodules.

219
Q

Development of Neurofibromas

A

AD with variable expression, 50% sporadic mutation in NF-1 on Ch17

220
Q

Diagnosis of NF

A

2 or more of the following: >6 café au lait macules; >2 neurofibromas; crow’s sign (axially, inguinal freckling); optic glioma; >2 lisch nodules; osseous lesion; first-degree relative with disorder

221
Q

Proximal Subungual white Onychomycosis

A

white on the nail; associated with HIV due to trichophyton rubrum

222
Q

Anagen Effluvium

A

loss of growing hair, most due to chemo

223
Q

Telogen Effluvium

A

hair goes into resting cycle; may be due to medications and post-patrum

224
Q

Intertrigo

A

irritant dermatitis

225
Q

malassezia furfur

A

suborrheic dermatitis

226
Q

Dermatomyositis

A

Photodistrubted violaceous poikiloderma that favors scalp and extensor skin sites. Heliotrope, samitz sign, Guttron’s papule, shawl sign

227
Q

Heliotrope

A

eruption on upper eyelipds +/- periorbital edema

228
Q

samitz sign

A

ragged cuticles

229
Q

Guttron’s Papules

A

Lichenoid papules overlying knuckles, elbows, knees - dermatomyositis

230
Q

Shawl sign

A

poikiloderma across back and shoulder

231
Q

Tuberous Sclerosis

A

hypomelanotic macules, adenoma sebaceum, shagreen patch,

232
Q

Pyoderma Gangrenosum

A

avoid surgery and debridement - oral and topical anti-inflammatory agents!

233
Q

Pyoderma Gangrenosum associations

A

IBD, Arthritis, Monoclonal gammopathy, hematologic disorders

234
Q

Lichen Planus

A

purple, polygonal pruritic papules with wickham’s striae

235
Q

Wickham’s Striae

A

overlying lace-like patterns of white lines of surface

236
Q

Lichen Planus Associations

A

Hepatits C

237
Q

Ancanthosis Nigricans

A

velvety hyperpigmentation of intertriginous surfaces (sometimes extensor) Most foten nick, axillae, dorsal hands; due to stimulating epidermal keratinocyte and dermal fibroblast proliferation

238
Q

Acanthosis Nigricans associations

A

AD, rare, onset in childhood; associated with DM,, Endocrinopathies (hyperandogren, cushings, PCOS) and really drugs

239
Q

Acanthosis Nigricans and malignancy

A

many precede or accompany or follow internal cancer, due to malignancy of stomach, lunch, breast

240
Q

Treatment of acanthuses nigricans

A

treatment of underlying disorder, keratolytics (ammonium lactate or urea cream)

241
Q

Brick and Mortar model of the skin

A

in the stratum corneum, the bricks are the keratinocytes and the mortar is the lipids in the extracellular space

242
Q

How do topical penetrate through the skin?

A

Passive diffusion, movement through channels or pores int he lacunar system, transported via apendegeal system like hair follicles

243
Q

What drug factors influence topical absorption?

A

1) active drug concentration, molecular size, liophilicity, composition of vehicle

244
Q

Molecular size and topicals

A

diffusion is inversely proportional to molecular size

245
Q

Lipophilicity and topicals

A

lipophilic are more likely to permeate skin to get into lacunar region

246
Q

Patient factors to topic use

A

complicance, barrier disruption, anatomical location, skin hydration, occlusion

247
Q

What are potenital barrier disruptions in skin?

A

atopic dermatitis - in addition to the drug penetrating easily, so can infections

248
Q

Anatomical locations that are very sensitive to topicals

A

face, jaw, scrotum, eyelids - must not use high potency steroids

249
Q

Anatomical locations that are resistant to topicals

A

plantar surface

250
Q

Skin hydration and topical penetration

A

good hydration equates to good penetration

251
Q

Occlusion and topical penentration

A

use wet wraps to optimize absorption

252
Q

what is the cross between a powder and a grease?

A

Protective paste

253
Q

what is the cross between a powder and a liquid?

A

drying paste, gels, shake lotions and suspensions

254
Q

what is the cross between a liquid and a grease?

A

ointments, creams, lotions

255
Q

Cream

A

oil in water, moderate potency, some hydration, but less than ointments, significant sensitization and irritation risk, can be used on all body sites except macerations

256
Q

Ointments

A

water in oil, strongest potency, hydrating, low sensitization and irritation risk. Use best on non-intertriginous sites - avoid face, hands groin. greasy and staining

257
Q

Gels

A

alcohol based, drying. Strong potency, but significant sensitization and irritation risk. Best on oral and mucosal surfaces and scalp, avoid on fissures, erosions, macerated regions.

258
Q

Lotions

A

powder in water (some oil in water), low potency, variability in drying. Avoid on fissures or erotions. Highest patient acceptance.

259
Q

Foam

A

pressurized collection of gaseous bubbles in matrix, maximal delivery of active ingredient, strong potency, quick dry, use on hair bearing areas, avoid issues or erosions.

260
Q

What topical is most potent?

A

Oinments, Gels, Foams

261
Q

what topics are not very potent

A

lotions

262
Q

What topicals have moderate potency

A

cream

263
Q

which topicals are have greatest sensitization/irritation risk?

A

Cream, Gels

264
Q

what do you consider when choosing a topical?

A

anatomic location, contact allergy/sensitization

265
Q

A fingertip unit is how many grams?

A

0.5g

266
Q

Face and neck, how many FTU?

A

2.5 FTU

267
Q

Trunk - front and back FTU

A

7

268
Q

One arm FTU

A

3

269
Q

One hand - both sides FTU

A

1 FTU

270
Q

One Leg FTU

A

6 FTU

271
Q

One foot FTU

A

2 FTU

272
Q

how much does 1 g of cream cover

A

10cm x 10cm area

273
Q

how much does 1 g of ointment ocver

A

10% further than cream

274
Q

how many grams is necessary to treat an adult man?

A

20g

275
Q

Basic action of glucocorticoids

A

bind to cells and cause the release of HSP90 to dimerize and inhibit the transcription of NFkB to control inflammation and increase levels of IkB to inhibit NFkB directly.

276
Q

Alternative Methods for antiinflammation to be used with steroids?

A

Calcineriun inhibitors, Retinoid, Vitamin D analog

277
Q

Calcineriun inhibitors

A

NF-ATn inhibition; good for use of dermatitis on groin

278
Q

Retinoid

A

inihibits AP-1 transcription factor to be anti-inflammatory, but cant be used with Vitamin D analog

279
Q

Vitamin D Analog- mechanism

A

inhibits AP-1 Transcirption factor to be anti-inflammatory

280
Q

Classes of steroid

A

7 classes, 7 is least potent and 1 is most potent.

281
Q

Hydrocortisone

A

class 7; low potency, good for children and adults with mild dermatits. Good for face, intertriginous areas, groin.

282
Q

Triamcinolone

A

all purpose steroid, class 4; good for spongiotic dermatoses, trunk, extremities, long term use not recommended for face, intertriginous and groin regions

283
Q

Clobetasol

A

high effectiivity and high potency steroid, high side effects, but good for severe dermatitis

284
Q

Adverse affects of glucocorticoid use

A

skin atrophy, shiny, thinning, telangiectasia. if used long enough can cause systemic side effects like adrenal suppression, cushion’s growth retardation.

285
Q

Which UV light has shortest wavelength?

A

UVC

286
Q

why does UVC damage our skin?

A

it is absorbed by the upper and middle atmosphere

287
Q

Results of UVB

A

sunburn, tan, formation of Vitamin D, eye damage, NMSC, DNA damage, immunosupression. Only penetrates the superficial tissue layer.

288
Q

What tissues are affected by UVB?

A

superificial layers - keratinocytes, melanocytes, langerhans

289
Q

Results of UV-A Damage

A

premature aging, loose skin, wrinkles, dark patches, DNA damage, ROS, Immunosuppression.

290
Q

What tissues are affected by UVA?

A

dermis, everything above plus fibroblasts and connective tissue

291
Q

Erythemal Action spectrum

A

carcinogenesis effectivenss of UV-B is much higher than at larger wavelengths

292
Q

Direct results of UVR damage

A

1) Damage to DNA, RNA, lipids 2) pro-inflammatory response 3) Immunosupresive 4) induction of innate defense 5) induction of apoptosis 6) Vitamin D synthesis

293
Q

DNA damage due to UVR

A

thymine dimers (UBV), primidine-6-4-pyromidone (UVB) and hydroxyguanosine (UVA)

294
Q

what DNA damage is due to UVB?

A

thymine dimers and primidine-6-4-pyrimidone

295
Q

what DNA damage is due to UVA?

A

Hydroxyguanosine

296
Q

what UVR causes NMSC

A

UVB

297
Q

What UVR causes melanoma?

A

UVB and UVA

298
Q

What are the primary pro-inflammatory cytokines released with UVR?

A

IL-1 and TNF Alpha

299
Q

What are secondary pro-inflammatory cytokines release with UVR?

A

IL-6, IL8, IL-10, GM-CSF

300
Q

What are the lipid mediators (pro-inflammaotry) released with UVR?

A

PAF

301
Q

What do mast cells release with UVR?

A

histamine

302
Q

How does UVR lead to immunosuppression?

A

1) UVR decrease langerhan cell populations 2) inducted inhibitor cytokines like IL-10 and TH2 3) induces tolerance to Tregs and NKT 4) induces keratinocyte to release certain cytokines

303
Q

UVR stimulates the keratinocyte to release..

A

Ci-Urocanic acid to activate mast or Bcells to make IL-10

304
Q

what does PAF do with UVR stimulation?

A

stimulates release of prostaglandin E2 to lead to IL10 and IL-12 (Blocked) production

305
Q

what are the skin’s defenses against UVR?

A

DNA repair, Activation of p53, Apoptosis of Cells with DNA damage, Defense against ROS, Melanin

306
Q

XPC

A

recognizes DNA damage

307
Q

XPB

A

incision and release DNA Damage

308
Q

Incision and release of DNA damage is due to…

A

XPB, XPD, XPF, XPG

309
Q

what is responsible for gap filling and ligation of DNA damage

A

PCNA, and DNA pol

310
Q

what enzymes make DNA repair possible after UV damage

A

Recognition of DNA damage, incision and release of NT, Gap filing and ligation

311
Q

what enzymes are responsible for defense against ROS?

A

peroxidase, catalse, superoxide dismutase, glutathione reductase, thioredoxin reductase

312
Q

UVR and Melanin

A

UVR stimulates karatinocytes to signal for melanogensis, which produces ROS as a byproduct

313
Q

Tyrosinase

A

rate limiting, involved in controlling pigmentation

314
Q

tyrosinase related protein 2

A

regulates eumelanin production

315
Q

Agouti signlaing peptide

A

Eumelanin production vs. phomelanin production

316
Q

Photodermatoses

A

are mostly idiopathic, or due to DNA repair defects, chemical photosensitivity, photoaggrevated, Connective tissue disease

317
Q

Disease with DNA repair defects

A

Xerderma Pigmentosum

318
Q

Disease with Chemical photosensitivity

A

Drug induced, prophyria

319
Q

Diseases that are photoaggrevated

A

psoriasis, atopic dermatitis

320
Q

Connective tissue diseases with UVR sensitivity

A

Lupus erythematous, dermatomyositis, mixed connective tissue disease

321
Q

Seborrheic Dermatitis - systemic diseases

A

Neurological disorders (PD), head trauma, PTSD, HIV

322
Q

Skin Signs of HIV

A

Seborrheic Dermatitis, Proximal nail fungal infections, psoriasis

323
Q

Velvet neck

A

acanthosis nigricans

324
Q

Acanthosis Nigricans

A

velvet neck - a rare AD disorder, but associated with obesity, DM, insulin resistance, endocrinopathies, drugs, cancer (malignancy and adenocarcinoma)

325
Q

Skin signs of Diabetes

A

brown patches over legs, thinning skin, ulcers, disseminated granuloma anulares (lots!)

326
Q

Skin signs of Endocarditis

A

Splinter hemoorhages, Janeway lesions, Osler nodes, Roth spots in eyes, Strep viridian’s from teeth

327
Q

Janeway lesions

A

Bruiselike manifestations on hand - sign of endocarditis

328
Q

Osler nodes

A

red, painful vascultiis - sign of endocarditis

329
Q

PHACES skin signs

A

Hemangioma on face and neck, + associated cardiac problems

330
Q

Ehler-Danos Skin signs

A

increased joint and skin elasticity, poor wound healing with large scars, increased ecchymoses

331
Q

Marfan’s skin signs

A

habitus, decreased subcutaneous fat - stretchy skin.

332
Q

Pulmonary Systemic Skin diseases

A

Scleroderma, Sarcoidosis

333
Q

Scleroderma Skin manifestations

A

Thickened skin over fingers and hands, skin tightening over mouth, salt and peper changes, Raynoud’s sign

334
Q

Raynoud’s Sign

A

fingers and toes feeling numb or tingling

335
Q

Sarcoidosis skin manifestations

A

looks lik an inflammatory response, altitiude is protective Hyperpigmented plaques, erosive, ulcerated plaques, granulomatous reactions in tattoos, bilateral hilar lymphadenopathy.

336
Q

Skin associations with Hepatitis B and C

A

Lichen planus, Vasculitis, Cryoglobliemia, Pruritius

337
Q

Lichen Planus

A

purple, polygonal pruritic papules with Wickham’s Straie. Associated with oral lesions (could be due to fillings) and Hep B And C

338
Q

Wickham’s Striae

A

overlying lace like pattern on Lichen Planus

339
Q

Porhuria Cutanea Tarda skin manifestations

A

blistering lesions on hands with sun expsoure, hypertrichosis, and atrophic scars. Associated with hepatitis, deficiency of uroprohyinogen decarboxylase. Treatment is serial phlebotomy to decrease iron load

340
Q

Hypertrichosis

A

excessive hair growth on face

341
Q

Osler Webber Rendu

A

Vascular blebs in mouth, indicative of GI manifestations

342
Q

Pyoderma Grangrinosum

A

lesions or pustules that form on an erythematous base that rapidly enlarge. Most commonly associated with Crohns or UV, arthritis, monoclonal gammopathy, hematological disorders (myelogenous leukemia, hairy cell leukemia). AVOID surgery or debridement.

343
Q

Cullen’s Sign

A

sign of an abdominal bleed, pancreatitis, trauma

344
Q

Grey Turner

A

ign of an abdominal bleed, pancreatitis, trauma

345
Q

Chronic Iron Deficiency Skin manifestations

A

Koilonychia, hair loss, angular chelties

346
Q

Koilonychia

A

spoon nails, associated with Fe def

347
Q

Angular Cheilitis

A

inflammation of the corners of the mouth

348
Q

Lindsay’s Sign

A

when 1/2 of the nail bet is white, sign of renal dysfunction

349
Q

Terry’s Sign

A

when just the tip of the nail bed is red, sign of cirrhosis or CHF

350
Q

Ectodermal Dysplasia skin signs

A

hair loss, nail changes, teeth malformation, no sweat glands

351
Q

Systemic Lupus Erythematous Skin signs

A

Molar rash, Discoid Rash, Oral Ulcers, Photosenstiivty,

352
Q

Systemic Lupus Erythematous signs

A

Molar, Discoid rash, Serositis, Oral unlcers, ANA+, Photosensitivity, blood disorders, renal involvement, arthritis, immunological, nuerological

353
Q

Skin signs in lung cancer

A

Erythema Gryatum Repens, Hyptertrichosis Lanuginosa Acquisita

354
Q

Erythema Gryatum Repens

A

wood grain appearance, associated with lung cancer

355
Q

Hypertrichosis Languiosa Acquisita

A

Fuzzy face

356
Q

Skin Signs associated with Adenocarcinoma/GI cancer

A

tripe palms

357
Q

Leser Trellat Sign

A

multiple erruptive suberrohetic keratosis, sign of colon cancer

358
Q

Dermatomyositis

A

shall like rash, that is associated with malignancies on reproductive organs

359
Q

Sister Mary Joseph Node

A

papule nodule near umbilicus; sign of pancreatic or GI cancer

360
Q

Where do drug rashes occur?

A

Most often on trunk, but also on palms, eye, mouth

361
Q

Risk factors for Non-Melanoma SC

A

Fair skin, high UV exposure, Ionizing radiation, arsenic, polycyclic hydrocarbon, phototherapy, prior skin cancer, genetic skin ease, smoking

362
Q

Smoking is a risk for what type of skin cancer

A

SCC

363
Q

Which gender is most likely to get skin cancer?

A

Men

364
Q

What type of UVR exposure causes SCC?

A

Total UVR

365
Q

what type of UVR exposure causes BCC

A

intermittent exposure and sunburns

366
Q

Types of Basal Cell Carcinomas

A

Superficial, Nodular, Infiltrative, Sclerosing/morpheaform

367
Q

What types of BCC is most prevalent?

A

Nodular

368
Q

Clinical Appearance of BCC

A

Flat, firm, pale or small pink, raised, very shiny, maybe areas of bleeding of abnormal vessels. Coulld have some crust or oozing

369
Q

Pathophysiology of BCC

A

lower layer of epidermis (Basal layer) due to mutations in sonic hedgehog pathway.

370
Q

Sonic Hedgehog pathway mutation in BCC

A

Mutation in PTCH1 which normally blocks Smoothed, a transcription factor that promotes tumor growth.

371
Q

Growth/metastases pattern in BCC?

A

very slow growing, rarely metastesizes, can infiltrate into nearly areas if left untreated. Increased risk of other types of skin cancer

372
Q

Treatment of BCC

A

Shaved biopsy, creams, burning, Moh’s Micrographic surgery. Vismedogib

373
Q

Visbodegib

A

drug to inhibit SMO; used only on metastatic of inoperable cancer types.

374
Q

Actinic Keratosis

A

premalignant skin lesion that develops into SCC (65%) or BCC (36%)

375
Q

Actinic Kerotosis Appearance

A

intradermal neoplasia on areas of sun exposure; hyperatosis and erythmatous papules

376
Q

Treatment of Actinic Kerotosis

A

Freezing, cream, photodynamic therapy, flurorescent light, sun protection

377
Q

Squamous Cell Carcinoma location

A

near site of sun exposure - face,e ar, neck, lips, back, or in scars, ulcers, injury

378
Q

Risk factors for SCC

A

immunosuppresion (transplant patients), UV damage, thermal injury, radiation, HPV, burns, chronic injury

379
Q

SCC appearance

A

hyperkeratotic papule, variable size and thickness, flat, reddish patches that grow slowly

380
Q

Clinical course of SCC

A

part of the epidermis, 03.-5% metastesize. most common sites occur to lymph nodes or dispant parts. More malignant than BCC, but not much.

381
Q

SCC in situ

A

Bowen’s Disease, earliest form of SCC, only invaded into the epidermis. Appears scaly, reddish, with patches of crust. Due to too much sun exposure and HPV

382
Q

Keratacanthoma

A

type of SCC with solitary lesion that growth rapidly over 6-8 weeks, crateriorn endophytic and exophytic nodules with keratin plug. Deep invasion in 10-20% of cases.

383
Q

Invasive SCC

A

hyperkeratotic papule with variable size and thickness, found on sun damaged skin that mtastaes.

384
Q

Transplant patients risk of skin cancer

A

Kaposis>SCC>BCC>melanoma

385
Q

Factors for SCC

A

Age, Skin type, UV, Genetics, HPV (65-90% in SCC), level of immunosuppression (CD4, medications, Heart>kidney>liver)

386
Q

Normal ratio vs translant ration risk of SCC to BCC

A

Norma: 1SCC:4BCC; Translplant 4SCC: 1BCC

387
Q

Treatment of SCC

A

topical 5-flurouracil, topical imiquidmod, cryosurgery, electrodessication, excision, Moh’s micrographic surgery, radiation

388
Q

Risk Factors of malignant melanoma

A

Middle age, history of melanoma, numbers common acquired nevi, history of blistering sunburns

389
Q

Common areas of Malignant Melanoma for Africans

A

acral, mucosa

390
Q

Common malignant melanoma areas for men and women?

A

men: back women: legs and back

391
Q

Pathophysiology of Malignant melanoma

A

bening nevus with a BRAF mutation that activates MAPK. Mutations also in NRAS. Most arrive de novo, 30% are from a previous nevus.

392
Q

Risk factors of melanoma

A

FAMM> sproadic dysplastic nevus syndrome > large congenital nevus > white skin, MM in first degree relative, immunosuppression, UV exposure, Tanning, fair skin

393
Q

what is the increased risk of Malignant melanoma if using a tanning bed?

A

up 20% first time, 2% each time after

394
Q

where does malignant melanoma metastasize?

A

draining lymph nodes, skin between primary site and notes, lung, liver, brain, GI

395
Q

prevalance of malignant melanoma

A

increasing annually

396
Q

types of malignant melanomas

A

superficial spreading, nodular, letigo maligna melanoma, acral letiginous

397
Q

Clark’s Level

A

rating for melanoma about how many layers the melanoma has spread. Not very indicative of prognosis

398
Q

Breslow Depth

A

thickness of the invasion, most indicative for prognosis of malignant melanoma

399
Q

Treatment of a

A

Excision with 1 cm margin with fascia

400
Q

treamtnet of MM in situ

A

0.5 cm margins with subcutaneous tissue

401
Q

treatment of MM >1 mm

A

1-2 cm margins with fascia and sentinal node biopsy

402
Q

Vemuafenib

A

BRAF inhibitor, treatment of MM,

403
Q

Trametinib or Cobimetinib

A

MEK inhibitor, used in combo with BRAF for MM

404
Q

imatinib

A

Gleevec, cKIT inhibits

405
Q

pembrolizumab

A

PD-1 inhibitors. Block the death receptor on Tcells to boost immune response in MM

406
Q

Ipilimumab

A

CTLA-4 inhibitor. Blocks CTLA-4 to allow stronger immune response

407
Q

Kapois’s Sarcoma

A

endothelial malignancy of lymph or blood vessles trigger by HHV-8

408
Q

Appearnce of Kaposis

A

on skin, musocal membranes (mouth) lymph nodes, lungs, GI, form purple, red, brown blotches on skin. Most often on legs and face.

409
Q

Symptoms of kaposis

A

asymptomatic

410
Q

Classical Kaposis

A

Mediterranean - elderly men on legs, ankles, soles of eet, slightly weaker immune system

411
Q

Endemic Kaposis

A

lymphadeopathic, aggressive in Africa, young men, rapidly fatal. due to weakened immune system

412
Q

Iatrognic Kaposi’s

A

Transplant related due to immuneosuppression

413
Q

Epidemic Kaposi’s

A

AIDs associated

414
Q

Treatment of Kaposi’s Sarcoma

A

radiation, excision, INFalpha, chemo

415
Q

Ages for Impetigo

A

most common in children, but all ages

416
Q

Acquired by - impetigo

A

Staph, Strep, S. pyrogens due to direct contact more so than fomites

417
Q

Predisposing factors for imeptigo

A

high humidity, cutaneous carriage, poor hygiene

418
Q

Impetigo Contagiosa

A

Non-bullous impetigo of the face (sometimes extremities). One single erythematous macule + superficial blister that forms in multiple honey colored lesions. Variable lymphadenopathy. 5% associated with post-strep glomerulonephiritis

419
Q

Non-Bollous - staph impetigo

A

Face of person of any age, secondary lesions due to injury or dermatitis, with yellow crust with variable erythema.

420
Q

Bullous Impetigo

A

can occur anywhere with single superficial flaccid blister and layered pus that transforms into multiple blisters. Most often due to staph infection.

421
Q

Scalded Skin Syndorme

A

Staph infection in children

422
Q

Diagnosis of Impetigo

A

CP, culture, gram stain of crust/fluid, rarely skin biopsy

423
Q

which impetigo is associated with glomerulonephritis?

A

Impetigo contagiosa

424
Q

Cellulitis is acquired by..

A

bacterial infection of Beta-heylolytic strep, staph, H, influenza, through breaks in skin in elderly, immunocompromised, IV drug users, ulcers, post surg.

425
Q

Erysipeals

A

St. Anthony’s fire- cellulitis of the face. Appears as cliff border with non-pitting edema. Associated with pain, region lyphadenompathy. Rarely is there bullae, pustules or nerosis

426
Q

Cellulitis

A

Located on extremities, ill defined, warmth, painful, lypthatic streaking, variable lymphadenopathy. Progresses to septicemia.

427
Q

Diagnosis of Cellulti

A

CP, CBC with leukoctyosis, biopsy for edema and increased PMNS, not usually culture or gram staning

428
Q

Dermatophytus

A

fungal infections due to contact with humans, animals, fomites and soil.

429
Q

Trichophyton rubrum

A

cutaneous pathogen

430
Q

Trichophyton mentagrophytes

A

tinea pedia

431
Q

trichophyton tonsurans

A

tinea capitis

432
Q

Microsporum canis

A

fluorescent tinea capitis

433
Q

Epidermophyton fluccosum

A

tinea cruris

434
Q

Scalp or hair fungal infections

A

tinea capitis with grey patch or black dots, associated with Kerion: abscess formation

435
Q

Body fungal infections

A

Tinea corporis, occurs on glabrous skin (non hair bearing) Associated with Majoochi’s Granuloma

436
Q

Majoochi’s Granuloma

A

follicular pus + Glanulomas associated with tinea corporis

437
Q

Tinea Cruris

A

genital fungal infection

438
Q

Onychomycosis

A

nail fungal infection

439
Q

Candidasis Finections

A

Fungal infections on skin, MM

440
Q

Predispoing factors to Candidasis

A

Diabetes, occlusion, corticosteroid, broad spectrum antibiotics

441
Q

Food source of candidas

A

glucose and serum

442
Q

Thrus

A

oral candidas infection

443
Q

Perleche

A

Angular cheilitis or angles of mouth, candida infection

444
Q

Erosio interdigalis Bastomyce

A

Interdigital candida infection

445
Q

Tinea Versicolor

A

Melazzesi Furfur, occurs in post-Pubertal in warm/humid areas. most often occurs on cutaneous surfaces like the trunk. Has subtly scaly macules with patches. Mostly asymptomatic

446
Q

Complications of Tinea Versicolor

A

Hypopigmented, Folicultiis: follicular papules.

447
Q

Diagnosis of Tinea Versicolor

A

CP, KOH: spagetti and meatballs

448
Q

What do Dermatophytus infections eat?

A

Keratin

449
Q

what does candidas eat?

A

Glucose and serum

450
Q

what does Tinea Versicolor eat?

A

Follicular Lipids

451
Q

Scabies

A

Sarcropetes scabiei infection by direct contact which leads to interdigital, flextures, genitals or breast manifestations. Skin finginds: erythematous papules with burrows, scale, nodules. Pururitis that occurs at night or after bathing

452
Q

Norwegian Scabies

A

massive hyperkeratosis in immunosuppressed people or with decreased sensation.

453
Q

Scalp Lice

A

Pediculus Hamanus Va. Capitis

454
Q

Body lice

A

pediculus hamanus var. corporis

455
Q

Pubic Louse

A

Phthirus pubis

456
Q

Head lice

A

scalp, post auricular, posterior neck, with nits. Lice are brown with six legs and difficult to find. Associated with intense puritus and erythymatous scale

457
Q

Body lice

A

Only found on clothes similar appearnce to head, pruritus, erythemyatous papules and macules

458
Q

Crab or pubic lice

A

Genital, eyelash, bear, axially found easily on hairy attachments causes pruritus

459
Q

Diagnosis of scabies

A

mineral oil for scraping or skin biopsy

Disease And Defense (7 decks)

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