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The Skin Under Attack Flashcards

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Dermatology Board Prep flashcards
1
Q

Describe the natural resistance properties of the skin

A
  1. physical barrier
  2. low pH (due to secretion of sebaceous fluid and FA)
  3. secretion of anti-microbial peptides
  4. normal flora
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2
Q

Describe the general mechanism of pathogenesis for bacterial skin infections

A
  1. invasion of bug through wound or pre-existing skin condition
  2. bacteria adheres to host cells
  3. bacterial evades host immune defenses
  4. invasion into tissues
  5. release of toxins
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3
Q

actively secreted proteins that cause tissue damage or dysfunction

A

exotoxins

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4
Q

how do exotoxins cause tissue damage?

A

enzymatic reactions cellular dysfunction pore formation –> cell lysis

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5
Q

superantigens are (exo or endo toxins)

A

exotoxins

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6
Q

MOA superantigens

A

bind conserved portion of TCR and therefore actives a large % of T cells –> cytokine storm

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7
Q

assc with severe tissue necrosis and rapid development of skin infection

A

superantigens

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8
Q

What bugs are superantigens assc with?

A

Staph aureus Strep pyogenes

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9
Q

superficial, crusting epidermal skin infection bullous and non-bullous forms usually in young chilfren usually affects the face honey colored crust

A

impetigo

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10
Q

What bugs are noted to cause impetigo?

A

Staph aureus Strep pyogenes

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11
Q

streptococcal infection of the superficial dermal lymphatics

A

Erysipelas

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12
Q

presentation of erysipelas

A

areas of erythema that demonstrate sharply demarcted, raised boarders

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13
Q

erythema with poorly demarcated boarders (infectious in nature)

A

cellulitis

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14
Q

What layers of the skin are involved in cellulitis?

A

deeper dermis and subcutaneous

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15
Q

bacterial origin of cellulitis

A

streptococcal

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16
Q

abscesses are collections of pus in the _____

A

dermis and subcutaneous tissue

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17
Q

superficial infection of the hair follicles with puss accumulation in the epidermis

A

folliculitis

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18
Q

aka boils

A

furuncles

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19
Q

how are furuncles different than folliculitis

A

deeper involvement of the hair follicle that extends to the subcut

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20
Q

term for when adjacent furuncles coalesce to form a single inflamed area

A

carbuncles

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21
Q
  • Diffuse generalized erythema superficial desquamation with flexural accentuation
  • Perioral and periocular crusting and radial fissuring with mild facial swelling
  • Mucous membranes – uninvolved
A

scalded skin syndrome

*S aureus exotoxin

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22
Q

pathogenies of scalded skin syndrome

A

infection with Staph aureus EXOTOXIN which binds desmoglein-1 and cleaves it

–> loss of cell cell adhesion

–> superficial desquamation

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23
Q

Who usually gets scalded skin syndrome?

A

infants, young children, adults in renal failure (prob due to decreased clearance of toxin)

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24
Q
  • granular layer split in epidermis
  • dermis lacks inflammatory cell infiltrate
A

histo findings of scalded skin syndrome

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25
Q

insidious onset of widespread tissue necrosis

A

necrotizing fasciitits

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26
Q

how is necrotising fasciitis different than cellulitis?

A

it is deeper! infection spreads along fascial plane beneath subcut

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27
Q

pain out of proportion to clinical finding

A

necrotizing fasciitits **usually following minor trauma

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28
Q

color change seen in NF

A

erythema –> red-purple–> gray-blue **within 36 hrs

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29
Q

What are the 3 subtypes of NF and what ate the orgs assc with them?

A

I: polymicrobial

II: streptococcal (“flesh eating strep”)

III: clostridial myonecrosis (gas gangrene)

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30
Q

fever, strawberry tongue, sunburn-like erythema and sandpaper papules, later get desquamation of hands and feet

A

Toxic shock syndrome

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31
Q

What is the pathogenesis of TSS?

A

Staph aureus’s exotoxin TSST-1 (less commonly GAS)

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32
Q

Tx for TSS?

A

abx to remove nidus of infection

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33
Q

sunburn-like erythema and sandpaper papules

A

TSS

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34
Q

Pus-forming infections tend to be_____ in origin, except for periorificial abscesses, which are often______.

A

staphylococcal anaerobic

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35
Q

_____ accounts for the majority of serious bacterial SSTIs.

A

cellulitis

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36
Q

how is the Dx of a bacterial skin infection made?

A

usually made on the clinical presentation and historical information culture may confim dx

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37
Q

What layers of the skin are superficial fungal infections limited to?

A
  • dead keratinous tissue
  • epidermis
  • hair follicles
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38
Q

What orgs cause superficial fungal infections?

A
  • dermatophytes
  • non-dermatophyte molds
  • yeasts (candida and malassezia)
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39
Q

WHat layers of the skin do deep fungal infections involve?

A

all layers and can extend into the subcut

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40
Q

What fungi are assc with deep infections

A
  • sporotrichosis
  • mycetoma
  • chromomycosis

**require direct inoculation of the skin

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41
Q

are fungi that digest keratin as a nutrient source

A

dermatocytes

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42
Q

Where do dermatocytes colonize?

A

stratum corneum,, nail plate, and hair follicles **the keratinized structures!

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43
Q

Are dermatocyte infections lethal?

A

No, they rarely invade viable tissue

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44
Q

What are the dermatocyte virulence factors?

A

enzymes that allow them to adhere to keratin and then invade keratin (secreted enzymes) **the digestive products serve as the nutrients for the fungi

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45
Q

What are the 3 genera of dermatophytes

A

trichophyton; microsporum; epidermophyton

46
Q

intensely pruritic, annular lesions with peripheral scale, central clearing, and variable inflammation

A

tinea infection

47
Q

superficial fungal infection of the foot.

A

tinea pedis

48
Q

Fungal infection leading to nail bed deformity (onchodystrophy) with thickening (hyperkeratosis) and discoloration

A

tinea ungium (aka onchomycosis)

49
Q

superficial fungal infection of glabrous skin occurring most commonly on the trunk and limbs

A

tinea corporis

50
Q

superficial fungal infection of glabrous skin occurring on the face

A

tinea facei

51
Q

erythematous patch involving the inner thigh and inguinal folds while sparing the scrotum and penis.

A

Tinea cruris

52
Q

fungal infection of the scalp and hair.

A

tinea capitis

53
Q

Ninety-five percent of cases of tinea capitis are caused by superficial infection with ____

A

T tonsurans

54
Q

histo findings of superficial fungal infection

A
  • neutrophils in stratum corenem
  • fungal hyphae in stratum corneum or follicles
55
Q

formation of hypopigmented or hyperpigmented patches with associated fine scale

A

Malassezia overgrowth (tinea versicolor)

56
Q

yeast in skin, mucus membranes, nails, or gastrointestinal tract

A

candida albicans

57
Q

spaghetti and meatballs in histo (PAS stain) = short curved hyphae and clusters of round spores

A

tinea versicolor

58
Q

Herpes viruses are unique in their ability to…

A

produce latent, incurable infections

59
Q

HSV1 and HSV2 establish initial infection through: What occurs following this initial infection?

A

mucosa or abraded skin virus travels retrograde from point of inf along sensory neuronal axons to nuclei, where they multiply and remain latent

60
Q

Possible causes of HSV reactivation: Possible effects of HSV reactivation:

A

stress, fever, localized trauma, UV, menstruation symptomatic disease OR asymptomatic viral shedding

61
Q

HSV1 infection, presents as vesicular or ulcerative lesions of oral cavity or perioral region; spread through contact with oral secretions

A

herpes labialis

62
Q

Infection caused by HSV-2 (most of the time, but some HSV1 overlap)

A

herpes genitalis

63
Q

HSV infections often present with:

A

tingling or pain in the region of subsequent disease

*note: presentation depends on immune status of host

64
Q

Primary HSV1 infections? Recurrences?

A

–asymptomatic

–painful, grouped vesicles on erythematous base (lip) x2-3 days; ulceration crusts over and heals in 4-5days

65
Q

Primary HSV2 infections? Recurrences?

A
  • severe, painful vesicle formation and ulceration, fever, lethargy
  • painful, vesicles with ulceration, but no fever/lethargy
66
Q

HSV diagnosis?

A

**clinical.

–available: Tsanck smear, viral culture, serology, fluorescent antibodies, tissue biopsy

67
Q

Digital HSV infection

A

herpetic whitlow

68
Q

HSV superinfection of atopic dermatitis

A

eczema herpeticum

69
Q

corporeal HSV infection related to direct skin-to-skin contact during athletics

A

herpes gladiatorum (get it, gladiator?)

70
Q

Treatment for HSV:

A

acyclovir valacyclovir famciclovir foscarnet cidofovir

71
Q

Reactivation of latent VZV in any DRG, contagious until crusty

A

herpes zoster

72
Q

What are the herpes histology buzz words?

A

multinucleated acantholytic keratinocyte (there’s also molding, nuclear dust of neutrophils, keratinocyte necrosis)

73
Q

Live, attenuated VZV vaccine

A

varivax

74
Q

Indicated for people at least 60 y/o to prevent/lessen shingles

A

zostavax

75
Q

Self-limting infection caused by poxvirus that usually affects children; produces smooth, dome-shaped umbilicated papules

A

molluscum contagiosum

76
Q

Histologic molluscum findings

A

intracytoplasmic inclusions within keratinocytes (Henderson-Paterson bodies)

77
Q

Describe the HPV structure.

A

icosahedral naked small circular dsDNA

78
Q

Why are there few HPV anti-viral targets?

A

genetically simple = strong host dependence and few drug targets

79
Q

HPV protein that leads to p53 degradation

A

E6

80
Q

HPV protein that inactivates Rb

A

E7

81
Q

What causes malignant tumors from HPV?

A

E6 and E7 overexpression

82
Q

How is HPV transmitted, and how does it actually enter cells?

A
  • sexually transmitted
  • entry via interaction between L1/L2 proteins and cell surface receptors (access to keratinocytes)
83
Q

Where does HPV replicate, and how does it spread?

A

nucleus (using all the host cell’s equipment)

–infected cell divides; population spreads laterally and migrates upward as the virus matures

–as top skin layer is shed, so are viruses

84
Q

Causes palmoplantar warts; palm, soles, tips of fingers, etc

A

HPV1

85
Q

Causes flat warts, “Verruca plana”; smooth or slightly keratotic, skin-colored papules on face, arms, dorsal hands

A

HPV3, HPV10

86
Q

Causes common warts; verrucous papules on glaberous skin, like legs

A

HPV2, HPV4

87
Q

Causes Condylomata acuminata; most distinguishable by location on penis, vulva, perianal area

A

HPV6, HPV11 (can also be due to HPV 16, 18, 31, 33)

88
Q

Associated with an increased risk of cervical cancer

A

uncommon variants of genital warts-causing HPV: 16, 18, 31, 33, 51

89
Q

Histology of HPV infections:

A
  1. hyperkeratosis 2. papillomatosis 3. hypergranulosis 4. vacuolated superficial keratinocytes with pyknotic nuclei (“koilocytes”)
90
Q

How do HPV vaccines prevent infection?

A

noninfectious recombinant virus-like particles, assembled from L1 capsid proteins *these trigger an antibody response = protection

91
Q

Quadrivalent HPV recombinant vaccine; protects against 6, 11, 16, 18

A

gardasil

92
Q

Bivalent HPV recombinant vaccine; protects against 16, 18

A

cervarix

93
Q

Causes digital squamous cell carcinoma

A

HPV16

94
Q
A

Molluscipox virus

95
Q
A

impetigo

96
Q
A

Folliculitis

97
Q

What causes this?

A

An exotoxin

(Staphloccal Scalded Skin Syndrome)

98
Q

most common cause?

A

HPV-6 and 11

99
Q
A

Tinea unguium

100
Q
A

Herpes simplex virus 1

101
Q
A

herpes zoster

102
Q
A

Basal cell carcimoma

103
Q
A

Molluscum contagiousum

104
Q

Protects against both anogenital warts and cervical cancer

A

gardasil

105
Q
A

herpes

106
Q
A

furuncle

107
Q
A

abscess

108
Q
A

folliculitis

109
Q
A

tinea versicolor

110
Q
A

warts

111
Q
A

koebner phenomenon

Derm (12 decks)

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