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Dermatology path > Infectious skin diseases > Flashcards

Infectious skin diseases Flashcards

pathogenesis of skin infections; bacterial, fungal, viral skin diseases;

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Dermatology Board Prep flashcards
1
Q

How does the skin offer a first line of defense against microbial infection?

A

physical barrier; low pH, sebaceous fluid, fatty acids; normal flora deters further colonization

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2
Q

What is the most common means bacteria infect the skin?

A

penetration of the skin barrier

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3
Q

What are the 3 steps of bacterial pathogenesis?

A

bacterial adherence to host; invasion of tissue w/ evasion of host; elaboration of toxins

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4
Q

Which organisms are produce superantigens?

A

virulent S. aureus and S pyogenes

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5
Q

How do superantigens work?

A

bind conserved portions of T cell receptors and activate large numbers of T cells leading to cytokine storm and inflam response

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6
Q

What is impetigo

A

a superficial cursting of epidermal skin infections presenting in bullous and nonbullous forms

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7
Q

Who/What/By whom/characteristic feature of impetigo

A

young children; face; S. aureus and S. pyogenes; honey colored crust

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8
Q

Define Erysipelas

A

streptococcal infection of superficial dermal lymphatics w/ sharply demarcated, raised borders

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9
Q

Define cellulitis and causative agent

A

infection of deeper dermis and subcutaneous tissue w/ poorly demarcated borders; majority streptococcal

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10
Q

cutaneous abscess

A

collections of pus in the dermis and subcutaneous tissue

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11
Q

Define folliculitis

A

superficial infection of hair follicles w/ pus accumulation in epidermis

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12
Q

Define furuncles

A

deeper involvement of hair follicles in which infection extends into the subcutaneous tissue

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13
Q

Define carbuncle

A

adjacent furuncles coalesce to form single inflamed area

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14
Q

Who/What/By whom of Staphyloccal scalded skin syndrome

A

infants/kids, adults w/ renal failure, immsprsd;
granular layer split of epidermis;
exotoxin producing S. aureus

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15
Q

What are the clinical features of Staph scalded skin syndrome?

A

diffuse generalized erythema, superficial desquamation w/ flural accentuation; uninvolved mucous membranes; perioral, periocular crusting, radial fissures

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16
Q

What is staph scalded skin syndrome Tx?

A

Antibiotics and supportive care

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17
Q

What is the pathogenesis of staph scalded skin syndrome?

A

exotoxin bind to desmoglein 1 and cleave leading to loss of cell-cell adhesion

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18
Q

define necrotizing fasciitis

A

insidious and deadly soft tissue infections associated w/ widespread tissue necrosis

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19
Q

Who is subject to necrotizing fasciitis?

A

patients after minor trauma and surgical wounds; most are immunocompromised, diabetic, alcoholic, or obese

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20
Q

What is an early warning sign of necrotizing fasciitis? What happens if it is ignored?

A

pain out of proportion to clinical findings; ignoring leads to rapid progression and delay may be fatal (red to purple skin w/in 36 hours)

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21
Q

What type of emergency is necrotizing fasciitis?

A

surgical emergency associated with debridement

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22
Q

What is toxic shock syndrome?

A

S. aureus caused disease that produces TSST-1 toxin classically from tampons, surgery or deep abscesses

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23
Q

How does toxic shock syndrome present?

A

sunburn-like erythema and sandpaper papules progressing to desquamation of hands and feet

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24
Q

Toxic shock syndrome Treatment

A

antibiotics and remove agent

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25
Q

What are general features of bacterial skin diseases?

A

pus forming infections: staphylococcal except in periorifical abscesses that are anaerobic

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26
Q

What accounts for the majority of serous bacterial SSTIs?

A

cellulitis

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27
Q

How is a diagnosis made in bacterial skin diseases?

A

clinical presentation and Hx; culture to confirm and base Tx from

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28
Q

In fungal diseases, where are superficial infections?

A

confined to dead keratinous tissue, epidermis and hair follicles

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29
Q

What causes superficial fungal diseases?

A

dermatophytes; nondermatophyte molds; yeasts (candida)

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30
Q

in fungal diseases, where are deep infections?

A

all skin layers and some extend into the subcutaneous tissue

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31
Q

How do deep infections typically occur?

A

direct inoculation of skin such as sporotrichosis, mycetoma, chromomycosis

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32
Q

Where are systemic fungal infections typically found?

A

since inhaled, least common cutaneous and have pulmonary focus even though a skin lesion may tip the infection

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33
Q

What does the most common cause of superficial fungal infections feed on?

A

dermatophytes digest keratin as nutrient source

34
Q

Where will dermatophytes likely colonize?

A

stratum corneum; nail plate; hair follicles

35
Q

What are the dermatophytes virulence factors?

A

enzymes: adherence to keratin; invasion of keratin by secretized enzymes

36
Q

What are the dermatophyte genera that cause superficial fungal infections?

A

Trichophyton (most common); microsporum; epidermophyton

37
Q

How is a tinea infection characterized?

A

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

38
Q

What is the most common cause of tinea pedis?

A

95% dermatophytes due to occlusive footwear

39
Q

What is the result of tinea unguium/onchomycosis?

A

infection of nail plate/bed leading to deformity with thickening and discoloration (onchodystrophy and hyperkeratosis)

40
Q

Where is tinea corporis located?

A

trunk and limbs

41
Q

Where is tinea cruris? clinical presentation?

A

jock itch of groin: erythematous patch of inner thigh and inguinal folds spares scrotum and penis

42
Q

What is the common cause of tinea capitis?

A

infection of scalp and hair from superficial infection w/ T. tonsurans

43
Q

What are 3 distinctive features of superficial fungal diseases regarding histopathology?

A

neutrophils present in stratum corneum;
hyphae in corneum visible on PAS stain (pink-red);
culture material scraped from area for ID

44
Q

Where does candidiasis typically present?

A

skin, mucus membranes, nails or GI tract

45
Q

Who is candidiasis more common in?

A

women (vulvovaginal candidiasis); immunosuppressed

46
Q

What is a typical presentation of tinea versicolor?

A

recent tropical visit; Malassezia overgrowth causing harmless hypo/hyper pigmented patches with fine scaling

47
Q

What disease presents as off-white/pink macules and papules with a spaghetti and meatball appearance?

A

Tinea versicolor

48
Q

What is significant about most viruses affecting the skin?

A

produce chronic/life long infection

49
Q

Describe the infection and reactivation of HSV 1,2 infections

A

initial via mucosa or abraded skin; travel retrograde along sensory neuronal axons to nuclei during latency; reactivate at previous primary infection site

50
Q

HSV reactivations lead to what?

A

shedding of viral particles w/o symptomatic disease contributing to disease spread

51
Q

What causes herpes labialis? how is it spread?

A

HSV-1 and spread through contact with oral secretions

52
Q

What causes herpes genitalis?

A

HSV-2 (increasing overlap from HSV-1)

53
Q

What is the typical presentation of HSV infection?

A

variable depending on immune status of host with prodrome tingling or pain in diseases region

54
Q

How could HSV-1 and HSV-2 infections be differentiated other than location?

A

HSV-1: asympptomatic

HSV-2: severe, painful vesicle form, ulceration, fever, lethargy

55
Q

How does HSV-1 reactivations typically present?

A

grouped vesicles on erythematous base for 2-3 days; lesions develop ulceration w/ crusting then heal in 4-5 days

56
Q

How are HSV infections diagnosed?

A

most clinical eval alone; Tsanck smear, viral culture, direct fluorescnt Ab study; serologic testing

57
Q

What are the dermatologic disease manifestations of HSV infections?

A

eczema herpeticum (atopic dermatitis); herpetic whitlow (digital infection); herpes gladiatorum (corporeal)

58
Q

How should a HSV infection be treated?

A

Acyclovir; valacyclovir; famciclovir; foscarnet; cidofovir

59
Q

What is the MOA of acyclovir?

A

inhibits viral DNA polymerase after phosphorylation by herpes specific thymidine kinase

60
Q

How does resistance arise to acyclovir?

A

viral thymidine kinase deficiency

61
Q

How is VZV transmitted and incubation period?

A

very contagious airborne or direct contact with incubation 11-20 days

62
Q

What describes the primary infection of VZV?

A

pruritic eruption spreading from face/scalp to trunk/ to extremities resembling drops on a rose petal

63
Q

VZV under histology has what characteristic finding?

A

multinucleated acanthoytic keratinocyte

64
Q

What are the vaccines for VZV?

A

varivax (live attenuated prevents/decreases risk)

Zostavax (persons at least 60y/o)

65
Q

What causes molluscum contagiosum? What does it look like?

A

DNA poxvirus of the molluscipox genus;

smooth, dome-shaped, umbilicated papules

66
Q

What does molluscum contagiosum look like on histologic exam?

A

Henderson-Patterson bodies => intracytoplasmic inclusions within keratinocytes

67
Q

How does molluscum contagiosum progress?

A

self limited disease in healthy patients

68
Q

What is the genome of HPV?

A

icosahedral, naked, circular ds DNA

69
Q

HPV are very genetically simple. How does this help the virus?

A

implies strong host dependence and few targets for anti-virals

70
Q

What are the 3 domains of the HPV genome?

A

upstream regulatory region; early and late regions;

71
Q

What proteins of HPV may lead to cancer? How?

A

E6 protein leads to degradation of p53; E7 inactivates Rb protein

72
Q

How does HPV infect a person?

A

through basal keratinocytes through minor abrasions in skin/mucosa => direct contact; cell entry L1/L2 proteins and cell surface receptors

73
Q

How does the virus replicate and divide?

A

replicates in nucleus; divides and spreads laterally and migrates upward to suprabasal cell layers

74
Q

What does HPV-1 cause?

A

palmoplantar warts on volar aspect of palms/soles and fingers/toes

75
Q

What does HPV-2, 4 cause?

A

common warts => verrucous papules on glaberous skin

76
Q

What does HPV-3, 10 cause?

A

flat warts=> slightly elevated flesh colored papules that are smooth or hyperkeratotic

77
Q

What does HPV-6, 11 cause?

A

genital warts=> scaly and papular to smooth and flesh colored

78
Q

How will the histology of the HPV-6, 11 be viewed?

A

hyperkeratosis; papillomatosis; hypergranulosis

koilocytes: vacuolated superficial keratinocytes w/ pyknotic raisin like nuclei

79
Q

How should warts from HPV be treated?

A

most are self limited in healthy patients but Tx tailored to site involved

80
Q

What causes an increase risk in cervical cancer?

A

condylomata associated with HPV will increase cervical cancer risk

81
Q

What are the 2 types of vaccines associated with HPV?

A

Quadrivalent composed of L1 VLP from 6, 11, 16, 18;

bivalent HPV 16, 18 that is a VLP vaccine

Dermatology path (11 decks)

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