The Skin Under Attack Flashcards
1
Q
Describe the natural resistance properties of the skin
A
- physical barrier
- low pH (due to secretion of sebaceous fluid and FA)
- secretion of anti-microbial peptides
- normal flora
2
Q
Describe the general mechanism of pathogenesis for bacterial skin infections
A
- invasion of bug through wound or pre-existing skin condition
- bacteria adheres to host cells
- bacterial evades host immune defenses
- invasion into tissues
- release of toxins
3
Q
actively secreted proteins that cause tissue damage or dysfunction
A
exotoxins
4
Q
how do exotoxins cause tissue damage?
A
enzymatic reactions cellular dysfunction pore formation –> cell lysis
5
Q
superantigens are (exo or endo toxins)
A
exotoxins
6
Q
MOA superantigens
A
bind conserved portion of TCR and therefore actives a large % of T cells –> cytokine storm
7
Q
assc with severe tissue necrosis and rapid development of skin infection
A
superantigens
8
Q
What bugs are superantigens assc with?
A
Staph aureus Strep pyogenes
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
10
Q
What bugs are noted to cause impetigo?
A
Staph aureus Strep pyogenes
11
Q
streptococcal infection of the superficial dermal lymphatics
A
Erysipelas
12
Q
presentation of erysipelas
A
areas of erythema that demonstrate sharply demarcted, raised boarders
13
Q
erythema with poorly demarcated boarders (infectious in nature)
A
cellulitis
14
Q
What layers of the skin are involved in cellulitis?
A
deeper dermis and subcutaneous
15
Q
bacterial origin of cellulitis
A
streptococcal
16
Q
abscesses are collections of pus in the _____
A
dermis and subcutaneous tissue
17
Q
superficial infection of the hair follicles with puss accumulation in the epidermis
A
folliculitis
18
Q
aka boils
A
furuncles
19
Q
how are furuncles different than folliculitis
A
deeper involvement of the hair follicle that extends to the subcut
20
Q
term for when adjacent furuncles coalesce to form a single inflamed area
A
carbuncles
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
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
23
Q
Who usually gets scalded skin syndrome?
A
infants, young children, adults in renal failure (prob due to decreased clearance of toxin)
24
Q
- granular layer split in epidermis
- dermis lacks inflammatory cell infiltrate
A
histo findings of scalded skin syndrome
25
insidious onset of widespread tissue necrosis
necrotizing fasciitits
26
how is necrotising fasciitis different than cellulitis?
it is deeper! infection spreads along fascial plane beneath subcut
27
pain out of proportion to clinical finding
necrotizing fasciitits \*\*usually following minor trauma
28
color change seen in NF
erythema --\> red-purple--\> gray-blue \*\*within 36 hrs
29
What are the 3 subtypes of NF and what ate the orgs assc with them?
I: polymicrobial
II: streptococcal ("flesh eating strep")
III: clostridial myonecrosis (gas gangrene)
30
fever, strawberry tongue, sunburn-like erythema and sandpaper papules, later get desquamation of hands and feet
Toxic shock syndrome
31
What is the pathogenesis of TSS?
Staph aureus's exotoxin TSST-1 (less commonly GAS)
32
Tx for TSS?
abx to remove nidus of infection
33
sunburn-like erythema and sandpaper papules
TSS
34
Pus-forming infections tend to be\_\_\_\_\_ in origin, except for periorificial abscesses, which are often\_\_\_\_\_\_.
staphylococcal anaerobic
35
\_\_\_\_\_ accounts for the majority of serious bacterial SSTIs.
cellulitis
36
how is the Dx of a bacterial skin infection made?
usually made on the clinical presentation and historical information culture may confim dx
37
What layers of the skin are superficial fungal infections limited to?
* dead keratinous tissue
* epidermis
* hair follicles
38
What orgs cause superficial fungal infections?
* dermatophytes
* non-dermatophyte molds
* yeasts (candida and malassezia)
39
WHat layers of the skin do deep fungal infections involve?
all layers and can extend into the subcut
40
What fungi are assc with deep infections
* sporotrichosis
* mycetoma
* chromomycosis
\*\*require direct inoculation of the skin
41
are fungi that digest keratin as a nutrient source
dermatocytes
42
Where do dermatocytes colonize?
stratum corneum,, nail plate, and hair follicles \*\*the keratinized structures!
43
Are dermatocyte infections lethal?
No, they rarely invade viable tissue
44
What are the dermatocyte virulence factors?
enzymes that allow them to adhere to keratin and then invade keratin (secreted enzymes) \*\*the digestive products serve as the nutrients for the fungi
45
What are the 3 genera of dermatophytes
trichophyton; microsporum; epidermophyton
46
intensely pruritic, annular lesions with peripheral scale, central clearing, and variable inflammation
tinea infection
47
superficial fungal infection of the foot.
tinea pedis
48
Fungal infection leading to nail bed deformity (onchodystrophy) with thickening (hyperkeratosis) and discoloration
tinea ungium (aka onchomycosis)
49
superficial fungal infection of glabrous skin occurring most commonly on the trunk and limbs
tinea corporis
50
superficial fungal infection of glabrous skin occurring on the face
tinea facei
51
erythematous patch involving the inner thigh and inguinal folds while sparing the scrotum and penis.
Tinea cruris
52
fungal infection of the scalp and hair.
tinea capitis
53
Ninety-five percent of cases of tinea capitis are caused by superficial infection with \_\_\_\_
T tonsurans
54
histo findings of superficial fungal infection
* neutrophils in stratum corenem
* fungal hyphae in stratum corneum or follicles
55
formation of hypopigmented or hyperpigmented patches with associated fine scale
Malassezia overgrowth (tinea versicolor)
56
yeast in skin, mucus membranes, nails, or gastrointestinal tract
candida albicans
57
spaghetti and meatballs in histo (PAS stain) = short curved hyphae and clusters of round spores
tinea versicolor
58
Herpes viruses are unique in their ability to...
produce latent, incurable infections
59
HSV1 and HSV2 establish initial infection through: What occurs following this initial infection?
mucosa or abraded skin virus travels retrograde from point of inf along sensory neuronal axons to nuclei, where they multiply and remain latent
60
Possible causes of HSV reactivation: Possible effects of HSV reactivation:
stress, fever, localized trauma, UV, menstruation symptomatic disease OR asymptomatic viral shedding
61
HSV1 infection, presents as vesicular or ulcerative lesions of oral cavity or perioral region; spread through contact with oral secretions
herpes labialis
62
Infection caused by HSV-2 (most of the time, but some HSV1 overlap)
herpes genitalis
63
HSV infections often present with:
tingling or pain in the region of subsequent disease
\*note: presentation depends on immune status of host
64
Primary HSV1 infections? Recurrences?
--asymptomatic
--painful, grouped vesicles on erythematous base (lip) x2-3 days; ulceration crusts over and heals in 4-5days
65
Primary HSV2 infections? Recurrences?
- severe, painful vesicle formation and ulceration, fever, lethargy
- painful, vesicles with ulceration, but no fever/lethargy
66
HSV diagnosis?
\*\*clinical.
--available: Tsanck smear, viral culture, serology, fluorescent antibodies, tissue biopsy
67
Digital HSV infection
herpetic whitlow
68
HSV superinfection of atopic dermatitis
eczema herpeticum
69
corporeal HSV infection related to direct skin-to-skin contact during athletics
herpes gladiatorum (get it, gladiator?)
70
Treatment for HSV:
acyclovir valacyclovir famciclovir foscarnet cidofovir
71
Reactivation of latent VZV in any DRG, contagious until crusty
herpes zoster
72
What are the herpes histology buzz words?
multinucleated acantholytic keratinocyte (there's also molding, nuclear dust of neutrophils, keratinocyte necrosis)
73
Live, attenuated VZV vaccine
varivax
74
Indicated for people at least 60 y/o to prevent/lessen shingles
zostavax
75
Self-limting infection caused by poxvirus that usually affects children; produces smooth, dome-shaped umbilicated papules
molluscum contagiosum
76
Histologic molluscum findings
intracytoplasmic inclusions within keratinocytes (Henderson-Paterson bodies)
77
Describe the HPV structure.
icosahedral naked small circular dsDNA
78
Why are there few HPV anti-viral targets?
genetically simple = strong host dependence and few drug targets
79
HPV protein that leads to p53 degradation
E6
80
HPV protein that inactivates Rb
E7
81
What causes malignant tumors from HPV?
E6 and E7 overexpression
82
How is HPV transmitted, and how does it actually enter cells?
- sexually transmitted
- entry via interaction between L1/L2 proteins and cell surface receptors (access to keratinocytes)
83
Where does HPV replicate, and how does it spread?
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
Causes palmoplantar warts; palm, soles, tips of fingers, etc
HPV1
85
Causes flat warts, "Verruca plana"; smooth or slightly keratotic, skin-colored papules on face, arms, dorsal hands
HPV3, HPV10
86
Causes common warts; verrucous papules on glaberous skin, like legs
HPV2, HPV4
87
Causes Condylomata acuminata; most distinguishable by location on penis, vulva, perianal area
HPV6, HPV11 (can also be due to HPV 16, 18, 31, 33)
88
Associated with an increased risk of cervical cancer
uncommon variants of genital warts-causing HPV: 16, 18, 31, 33, 51
89
Histology of HPV infections:
1. hyperkeratosis 2. papillomatosis 3. hypergranulosis 4. vacuolated superficial keratinocytes with pyknotic nuclei ("koilocytes")
90
How do HPV vaccines prevent infection?
noninfectious recombinant virus-like particles, assembled from L1 capsid proteins \*these trigger an antibody response = protection
91
Quadrivalent HPV recombinant vaccine; protects against 6, 11, 16, 18
gardasil
92
Bivalent HPV recombinant vaccine; protects against 16, 18
cervarix
93
Causes digital squamous cell carcinoma
HPV16
94
Molluscipox virus
95
impetigo
96
Folliculitis
97
What causes this?
An exotoxin
| (Staphloccal Scalded Skin Syndrome)
98
most common cause?
HPV-6 and 11
99
Tinea unguium
100
Herpes simplex virus 1
101
herpes zoster
102
Basal cell carcimoma
103
Molluscum contagiousum
104
Protects against both anogenital warts and cervical cancer
gardasil
105
herpes
106
furuncle
107
abscess
108
folliculitis
109
tinea versicolor
110
warts
111
koebner phenomenon
