Pathophys/Path 4 Flashcards
Effective treatment of skin disease requires?
- timely identification or estimation of pathogen
- selection of treatment that is effective and good dosing
Natural Resistance of Skin
- first line defense
- physical barrier
- secreting low pH, sebaceous fluid, fatty acids, antimicrobial peptides to inhibit growth of pathogens
- possess normal flora, deterring others
Bacterial Skin Disease: Pathogenesis
2 step process:
1) Invasion- penetrate skin (break most common)
2) adherence to host, invasion of tissue with evasion of host defense, elaboration of toxins
2 Classes of Toxins
1) exotoxins-actively secreted proteins that cause tissue damage or dysfunction through various mechanisms (enzymatic rxns, cellular dysregulation/ pore formation w/cell lysis)
2) endotoxins
Impetigo
- superficial, crusting epidermal skin infection that presents in bullous & nonbullous forms
- “honey colored crusts” - superficial plack
- young children, face, staph, strep
Erysipelas
streptococcal infection of superficial dermal lymphatics that is sharply demarcated, raised borders - strep
Cellulitis
deeper dermis and subcutaneous tissue with poorly demarcated borders
-strep
Cutaneous abscesses
collection of pus in the dermis and subcutaneous tissue
Folliculitis
superficial infection of hair follicle with pus accumulation in the epidermis
Furuncles
“boils”
deeper involvement of hair follicles in which the infection extends into the subcutaneous tissue
Carbuncles
adjacent furuncles coalesce to form a single inflamed area
Super antigens
special exotoxins seen in S aureus & S pyogenes
- bind conserved portions of T cell receptors and activate large numbers
- cause huge inflammatory response (severe tissue necrosis)
Bacterial skin disease
most common type of skin infection
lots of conditions
classified by skin layer/structure it infects
Scalded Skin Syndrome
toxin-producing S. aureus
mostly infants/children
adults with renal failure/immunosuppression
Scalded Skin Syndrome Histology, Symptoms
- granular layer split in epidermis; dermis lacks inflammatory infiltrate
-diffuse generalized erythema and superficial desqumation with flexural accentuatuin
-mucus membranes NOT involved
perioral and periocular crusting and radial fissuring with mild facial swelling
Scalded Skin Syndrome Treatment
Antibiotics (beta-lactmase resistant)
Supportive
Necrotizing Fasciitis
-insidious and deadly soft-tissue infection, widespread tissue necrosis
I-polymicrobial
II-strep “flesh-eating”
III-clostridial myonecrosis “gas gangrene”
Necrotizing Fasciitis Symptome
- rapid progressoin, spreads on deep plane b/w subcutis and fascia
- pain out of proportion to clinical findings
- tender, warm, swelling, red
- red and purple to grey-blue patches in 36hrs
- violaceous/hemorrhagic bullae
Necrotizing Fasciitis Treatment
Surgery - widespread debridement
Toxic Shock Syndrome
S. aureus - TSST-1 toxin cause: tampon, surgery, deep abscesses features: fever, strawberry tongue, sun-burn like erythema, sandpaper papules, desquamatioin of hands and feet -can go to shock Treat: Abx and remove nidus of infection
Puss forming infections
staph, except periorificial abscesses (anaerobic)
Majority is cellulitis
Bacterial Skin Disease Diagnosis
presentation, history, culture
Bacterial Skin Disease Treatment
Abx
Fungal Skin Disease Categories
1) Superficial
2) Deep
3) Systemic
Superficial fungal infections
most common
confined to dead keratinous tissue, epidermis, hair follicles
-caused by: dermatophytes, nondermatophyte molds, yeasts (candida, malassezia)
Deep fungal infections
all skin layers and extend into subcutaneous tissue
direct inoculation of skin: sporotrichosis, mycetoma, chromomycosis
Systemic Infection
immunocompromised not common inhale spore (pulmonary) -histo, blasto, coccidio -nonimmuno -crypto, aspergill, fusariosis, mucormycosis- immune compromised
Dermatophytes
superficial fungus
digest keratin as nutrient
-colonize highly kertinized stratum corneum, nail plate, hair follicles
-don’t invade, not deep, not lethal
-virulence: adhear to keratin, invade by secretized enzymes
3 general of Dermatophytes
1) Trichophyton - most common
2) Microsporum
3) Epidermophyton
Tinea pedis
“athlete’s foot” -superficial of foot
- worldwide increase, occlusive footwear
- 95% from dermatophytes
Tinea Unguium
(onchomycosis) - superficial infection of nail plate or bed
- nail bed deformity (onchodystrophy) with thickening (hyperkeratosis) and discoloration
Tinea Corporis
“ring worm” - superficial infection of glabrous skin occurring most commonly on trunk and limb
-annular plaques or patches with red, raised, scaling border
Tinea facei
“ring worm” superficial on face
-annular plaques or patches with red, raised, scaling border
Tinea cruris
“jock itch” superficial infection on groin region
- almost all male
- erythematous patch involving inner thigh, inguinal folds
- spares penis
Tinea capitis
superficial infection of scalp and hair
-95% caused by T tonsurans
Candidiasis
superficial
- candida albicans-skin, mucus membranes, nails, GI tract
- more in women (vulvovaginal)
- immunosuppressed
Tinea versicolor
superficial, harmless, tropical
-overgrowth of Malassezia species, formation of hypo/hyperpigmented patches and fine scale
“spagiattie and meatball”
Viral Skin infection
most eliminated initially
some chronic
HPV
genital warts
resistant
Herpes Simplex Virus
HSV-1, HSV-2, VZV, EBV, CMV
most widespread human virus
produce latent, incurable infection
HSV-1
HSV-2
- initial through mucosa or abraded skin
- virus travel retrograde to sensory neuronal axon to nuclei - replicate/latent
- reactivation: stress, fever, trauma (local), UV light, period, immunosuppression
- shed w/o symptoms (1-5% of time)
Herpes Labilis
most common form
- vesicular or ulcerative lesions of oral cavity, perioral skin, mucosa
- HSV-1 - oral secretion contact
Herpes genitalis
- genital mucosa
- most HSV-2 some HSV-1
HSV-1,2 Symptoms
=Prodrome of tingling pain in region
HSV-1 asymptomatic
HSV-2 severe, painful vesicle formation and ulceration, constitutional (fever, lethargy)
HSV-1 recurrence
painful, grouped vesicles on erythematous base on vermillion border of lip for 2-3 days-heal in 4 to 5 (crusting)
HSV-2
- similar skin findings, but less severe than primary infection
- no constitutional symptoms
HSV diagnosis
physical
Tsanck smear, viral culture, serologic testing, ab, tissue biopsy
Eczema herpeticum
HSV superinfection of atopic dermatitis
Herpetic whitlow
digital HSV infection
Herpes gladiatorum
corporeal HSV from skin to skin contact in athletics
Herpes Treatment
Acyclovir
Valacyclovir/famciclovir
Foscarnet/cidofovir
Varicella Zoster Virus
“chicken pox”
airborn/contact very contagioius (11-20 day inc)
-primary: fever, malaise, myalgia by pruritic eruption, spreading from face/scalp to trunk
“dew drops on rose petal”
-affects 90% unvaccinated before age 10
-self-limited, benign in children
bad for adults & immunocompromised
Herpes Zoster
“shingles”
- reactivation of latent VZV in any dorsal root ganglion
- lifetime risk is ~20%, increase with age & immunocompromised
- lesions are contagious until they have crusted
VZV Treatment
supportive, acyclovir
Vaccine, live, attenuated (varivax)
Zostavax (persons at least 60 years old)
VZV Diagnosis
clinical
non-specific Tzanck, histology
Specific: DFA immunochem culture PCR
serology
Molluscum contagiosum
DNA poxvirus (molluscipox)
- in healthy, disease of children
- smooth, dome-shaped, umbilicated papules
- intracytoplasmic inclusions within keratinocytes (Henderson-Paterson bodies)
- self-limited (healthy)
- destructive or medical therapies may hasten resolution
HPV
icosahedral, naked, ~55nm in diameter small closed circular double-stranded DNA Upstream regulatory region -early region -E1-8 -late-L1-L2 E6-leads to degradation of p53 E7-inactivates Rb protein *over-expression of E6 and E7 proteins in malignant tumors
HPV live cycle
-tissue/species specific
-gain access to basal keratinocytes through minor abrasians in the skin/mucosa
-direct/sexual contact
-entry b/w L1/L2 proteins & cell surface receptors
-replicated in nucleus (dep on host cell)
spreads laterly then migrates upward suprabasal cells where mature virus continues (shed with desqumation)
Palmoplantar wart
HPV-1, volar aspect of palms/soles, tips of fingers and toes
Flat warts
HPV 3, 10
verruca plana
smooth, skin-colored papules on face, arms, dorsal hands
Common warts
HPV 2
Genital warts
most common venereal disease
scaly and papular to smooth and flesh-colored
penis, vulva, perianal area
HPV-6 HPV-11
Cervical Cancer
HPV-16,18,31,33
Bowenoid papulosis
HPV-16,18
hyper pigmented papules on genitalia (look like genital warts)
HSIL or SCCIS
Erythroplasia of Queyrat
HPV 16,18
-represents HSIL
Buschke-Lowenstein tumor
HPV 6,11
“semi-malignant” verrucous carcinoma locally invasive and destructive rare metastasized
Oral florid papillomatosis
HPV 6,11
smoking irradiation chronic inflammation
Warts:treat prevent
most self-limited
Gardasil (6,11,16,18)
Cervarix (16,18)
Digital SCC
HPV 16
