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Dermatology > Pathophys/Path 4 > Flashcards

Pathophys/Path 4 Flashcards

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Dermatology Board Prep flashcards
1
Q

Effective treatment of skin disease requires?

A
  • timely identification or estimation of pathogen

- selection of treatment that is effective and good dosing

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2
Q

Natural Resistance of Skin

A
  • first line defense
  • physical barrier
  • secreting low pH, sebaceous fluid, fatty acids, antimicrobial peptides to inhibit growth of pathogens
  • possess normal flora, deterring others
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3
Q

Bacterial Skin Disease: Pathogenesis

A

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

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4
Q

2 Classes of Toxins

A

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

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5
Q

Impetigo

A
  • superficial, crusting epidermal skin infection that presents in bullous & nonbullous forms
  • “honey colored crusts” - superficial plack
  • young children, face, staph, strep
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6
Q

Erysipelas

A

streptococcal infection of superficial dermal lymphatics that is sharply demarcated, raised borders - strep

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7
Q

Cellulitis

A

deeper dermis and subcutaneous tissue with poorly demarcated borders
-strep

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8
Q

Cutaneous abscesses

A

collection of pus in the dermis and subcutaneous tissue

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9
Q

Folliculitis

A

superficial infection of hair follicle with pus accumulation in the epidermis

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10
Q

Furuncles

A

“boils”

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

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11
Q

Carbuncles

A

adjacent furuncles coalesce to form a single inflamed area

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12
Q

Super antigens

A

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)
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13
Q

Bacterial skin disease

A

most common type of skin infection
lots of conditions
classified by skin layer/structure it infects

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14
Q

Scalded Skin Syndrome

A

toxin-producing S. aureus
mostly infants/children
adults with renal failure/immunosuppression

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15
Q

Scalded Skin Syndrome Histology, Symptoms

A
  • 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
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16
Q

Scalded Skin Syndrome Treatment

A

Antibiotics (beta-lactmase resistant)

Supportive

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17
Q

Necrotizing Fasciitis

A

-insidious and deadly soft-tissue infection, widespread tissue necrosis
I-polymicrobial
II-strep “flesh-eating”
III-clostridial myonecrosis “gas gangrene”

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18
Q

Necrotizing Fasciitis Symptome

A
  • 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
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19
Q

Necrotizing Fasciitis Treatment

A

Surgery - widespread debridement

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20
Q

Toxic Shock Syndrome

A 
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
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21
Q

Puss forming infections

A

staph, except periorificial abscesses (anaerobic)

Majority is cellulitis

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22
Q

Bacterial Skin Disease Diagnosis

A

presentation, history, culture

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23
Q

Bacterial Skin Disease Treatment

A

Abx

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24
Q

Fungal Skin Disease Categories

A

1) Superficial
2) Deep
3) Systemic

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25
Q

Superficial fungal infections

A

most common
confined to dead keratinous tissue, epidermis, hair follicles
-caused by: dermatophytes, nondermatophyte molds, yeasts (candida, malassezia)

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26
Q

Deep fungal infections

A

all skin layers and extend into subcutaneous tissue

direct inoculation of skin: sporotrichosis, mycetoma, chromomycosis

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27
Q

Systemic Infection

A 
immunocompromised
not common
inhale spore (pulmonary)
-histo, blasto, coccidio -nonimmuno
-crypto, aspergill, fusariosis, mucormycosis- immune compromised
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28
Q

Dermatophytes

A

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

29
Q

3 general of Dermatophytes

A

1) Trichophyton - most common
2) Microsporum
3) Epidermophyton

30
Q

Tinea pedis

A

“athlete’s foot” -superficial of foot

  • worldwide increase, occlusive footwear
  • 95% from dermatophytes
31
Q

Tinea Unguium

A

(onchomycosis) - superficial infection of nail plate or bed

- nail bed deformity (onchodystrophy) with thickening (hyperkeratosis) and discoloration

32
Q

Tinea Corporis

A

“ring worm” - superficial infection of glabrous skin occurring most commonly on trunk and limb
-annular plaques or patches with red, raised, scaling border

33
Q

Tinea facei

A

“ring worm” superficial on face

-annular plaques or patches with red, raised, scaling border

34
Q

Tinea cruris

A

“jock itch” superficial infection on groin region

  • almost all male
  • erythematous patch involving inner thigh, inguinal folds
  • spares penis
35
Q

Tinea capitis

A

superficial infection of scalp and hair

-95% caused by T tonsurans

36
Q

Candidiasis

A

superficial

  • candida albicans-skin, mucus membranes, nails, GI tract
  • more in women (vulvovaginal)
  • immunosuppressed
37
Q

Tinea versicolor

A

superficial, harmless, tropical
-overgrowth of Malassezia species, formation of hypo/hyperpigmented patches and fine scale
“spagiattie and meatball”

38
Q

Viral Skin infection

A

most eliminated initially

some chronic

39
Q

HPV

A

genital warts

resistant

40
Q

Herpes Simplex Virus

A

HSV-1, HSV-2, VZV, EBV, CMV
most widespread human virus
produce latent, incurable infection

41
Q

HSV-1

HSV-2

A
  • 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)
42
Q

Herpes Labilis

A

most common form

  • vesicular or ulcerative lesions of oral cavity, perioral skin, mucosa
  • HSV-1 - oral secretion contact
43
Q

Herpes genitalis

A
  • genital mucosa

- most HSV-2 some HSV-1

44
Q

HSV-1,2 Symptoms

A

=Prodrome of tingling pain in region
HSV-1 asymptomatic
HSV-2 severe, painful vesicle formation and ulceration, constitutional (fever, lethargy)

45
Q

HSV-1 recurrence

A

painful, grouped vesicles on erythematous base on vermillion border of lip for 2-3 days-heal in 4 to 5 (crusting)

46
Q

HSV-2

A
  • similar skin findings, but less severe than primary infection
  • no constitutional symptoms
47
Q

HSV diagnosis

A

physical

Tsanck smear, viral culture, serologic testing, ab, tissue biopsy

48
Q

Eczema herpeticum

A

HSV superinfection of atopic dermatitis

49
Q

Herpetic whitlow

A

digital HSV infection

50
Q

Herpes gladiatorum

A

corporeal HSV from skin to skin contact in athletics

51
Q

Herpes Treatment

A

Acyclovir

Valacyclovir/famciclovir
Foscarnet/cidofovir

52
Q

Varicella Zoster Virus

A

“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

53
Q

Herpes Zoster

A

“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
54
Q

VZV Treatment

A

supportive, acyclovir
Vaccine, live, attenuated (varivax)
Zostavax (persons at least 60 years old)

55
Q

VZV Diagnosis

A

clinical
non-specific Tzanck, histology
Specific: DFA immunochem culture PCR
serology

56
Q

Molluscum contagiosum

A

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
57
Q

HPV

A 
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
58
Q

HPV live cycle

A

-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)

59
Q

Palmoplantar wart

A

HPV-1, volar aspect of palms/soles, tips of fingers and toes

60
Q

Flat warts

A

HPV 3, 10
verruca plana
smooth, skin-colored papules on face, arms, dorsal hands

61
Q

Common warts

A

HPV 2

62
Q

Genital warts

A

most common venereal disease
scaly and papular to smooth and flesh-colored
penis, vulva, perianal area
HPV-6 HPV-11

63
Q

Cervical Cancer

A

HPV-16,18,31,33

64
Q

Bowenoid papulosis

A

HPV-16,18
hyper pigmented papules on genitalia (look like genital warts)
HSIL or SCCIS

65
Q

Erythroplasia of Queyrat

A

HPV 16,18

-represents HSIL

66
Q

Buschke-Lowenstein tumor

A

HPV 6,11

“semi-malignant” verrucous carcinoma locally invasive and destructive rare metastasized

67
Q

Oral florid papillomatosis

A

HPV 6,11

smoking irradiation chronic inflammation

68
Q

Warts:treat prevent

A

most self-limited
Gardasil (6,11,16,18)
Cervarix (16,18)

69
Q

Digital SCC

A

HPV 16

Dermatology (9 decks)

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