Bacterial Infx Of Skin

Front 1

What caused this skin lesion?

Back 1

Folliculitis

Front 2

Identify this skin lesion.

Back 2

furuncle

Front 3

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Back 3

Carbuncle

Front 4

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Back 4

Hidradenitis supprativa

Front 5

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Back 5

Impetigo

Front 6

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Back 6

Cellulitis

Front 7

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Back 7

Bullous impetigo

Front 8

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Back 8

Necronizing fasciitis

Front 9

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Back 9

Erysipelas

Front 10

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Back 10

Verruca vulgaris

Front 11

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Back 11

Condyloma acuminatum (female)

Front 12

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Back 12

Herpes simplex virus type I

Front 13

Identify this skin lesion.

Back 13

Herpes simplex virus type II (affecting a male)

Front 14

Identify this skin lesion.

Back 14

Varicella zoster virus. (chickenpox- child)

Front 15

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Back 15

Eczema herpeticum

Front 16

Idenify this skin lesion.

Back 16

molluscum contagiosum

Front 17

Identify this skin lesion.

Back 17

pityriasis rosea

Front 18

What is folliculitis?

Back 18

acute pustular infx of the infundibulum.

Front 19

Decribe the appearance of folliculitis.

Back 19

follicular papule, pustule, or crust in hear bearing areas*. Lesions are mostly grouped and clustered. May be pruritic, mildly tender and surrounded by erythematous halo. Only small portions of folliciles in a region are affected *

Front 20

Will folliculitis scar?

Back 20

NO, not in most cases.

Front 21

Will folliculitis cause lymphadenopathy?

Back 21

NO

Front 22

What is a furuncle?

Back 22

acute, deep seated red, hot, tender nodule or abscess that evolves from a folliculitis.

Front 23

Describe the appearance of a furuncle.

Back 23

Can occur anywhere on the body (butt, thigh, axilla, face, neck = MC). Firm tender nodule (1-2cm) with central necrotic plug with surrounding cellulitis and central abscess formation.

Front 24

Will a furuncle scar?

Back 24

YES- has high potential for scarring. Cavitation (crater) will remain.

Front 25

What is a carbuncle?

Back 25

deeper infection that is comprised of interconnecting abscesses usually arising from several contiguous hair follicles. Large, painful, superating mass.

Front 26

Describe the appearance of a carbuncle.

Back 26

Several, adjacent, coalescing furuncles that coalesce into dermal and subQ abscesses, superifcial pustules and necrotic plugs. Draining pus may be observed.

Front 27

Will a carbuncle cause systemic symptoms and/or lymphadenopathy?

Back 27

YES

Front 28

What is the most common organism is the cause of folliculitis and the lesions that it can give rise to?

Back 28

stapholococcus aureus

Front 29

What other organisms can give rise to a bacterial folliculitis?

Back 29

pseudomonas aeruginosa, p. acnes.

Front 30

What organisms can give rise to fungal folliculitis?

Back 30

tinea, candida

Front 31

What viruses give rise to viral folliculitis?

Back 31

herpes simplex virus

Front 32

What are some risk factors for developing folliculitis?

Back 32

shaving, plucking, waxing, high temperatures/humidity, steroid use, diabetes mellitus, immunosuppression, obesity, poor hygiene, sweating, occlusion of hear bearing area

Front 33

How would you diagnose a folliculitis?

Back 33

Clinically, to confirm use culture and gram stain or KOH prep. or Tzanck smear

Front 34

Tx of folliculitis

Back 34

gentle cleansing and topical antibx (arythromycin, clindamycin). Patient education to improve hygiene.

Front 35

Tx of carbuncles and furuncles caused by bacterial infx

Back 35

Incision and drainage* (all abscesses), topical antibx (bactroban, neomycin), systemic antibx (naf, ox, clox, diclox, erythromycin for PCN allergy, cipro for severe pseudomonas)

Front 36

Tx of carbuncles and furuncles caused by herpes

Back 36

acyclovir (valtrex)

Front 37

What is hidradenits suppurativa?

Back 37

chronic and relapsing condition of the apocrine sweat glands*

Front 38

What is the etiology and pathophysiology of hidradenitis supprativa?

Back 38

occlusion of the follicular infundibulum and apocrine duct with subsequent dilation and severe inflammatory changes to a single gland. Bacterial growth within dilated duct with rupture resulting in exatension of inflammation and infection, ulceration, and fibrosis with sinus tract formation.*

Front 39

What are the risk factors of hidradentitis supprativa?

Back 39

smoking, obesity, genetic predisposition to an acne or apocrine duct obstruction. May be associated with follicular occlusion syndrome*

Front 40

What are the most common regions for hidradenitis supprativa to occur?

Back 40

axilla and anogenital region*

Front 41

What are the clinical manifestations of hidradenitis supprativa?

Back 41

tender inflammatory nodules and abscesses, hypertrophic scars, sinus tract development, chronic perulent bloody discharge. Pt will have double open comedones*

Front 42

Dx for hidradentitis supprativa

Back 42

clincal, biopsy- keratin occlusion of the apocrine duct and hair follicle, ductial dilation and inflammatory changes, destruction and fibrosis. increased WBC, ESR, CRP

Front 43

Tx for hidradenitis supprativa

Back 43

cominations of
1. intralesional glucocorticoids (tiamicinolone) and antibx
2. surgery to remove the affected gland and incision/drainage of abscess

Front 44

What antibx should be used to treat hidradenitis supprativa?

Back 44

tetracycline, clindamycin, erythromycin

Front 45

What should be included in patient education about hidradenitis supprativa?

Back 45

reaasurance and psychological management (depression), weight reduction, reduce friction and moisture, absorbent powders

Front 46

What are the most common microbes to colonize the skin?

Back 46

staph epidermidis, staph aureus, strep pyogenes (first skin then throat-GABHS)*

Front 47

What is impetigo?

Back 47

superficial skin infection that is contageous and limited to the epidermis- crusted errosions or ulcers.

Front 48

What is needed for impetigo to occur?

Back 48

Minor skin trauma* Intact skin is the most important defense against invasion of pathogenic bacteria

Front 49

Who are most commonly affected by impetigo?

Back 49

children, yound adults with prevalence in late summer and early fall

Front 50

Where does impetigo most commonly occur on the body?

Back 50

face (mouth and nose)

Front 51

Decribe non-bullous impetigo.

Back 51

transient superficial small papule, vesicles and pustules which rupture and result in erosion and crust formation (gold/yellow)* scattered and discrete- spread rapidly by autoinnoculation. may have localized lymphadenopathy.

Front 52

What indicates that an impetigo has been caused by staph?

Back 52

golden yellow exudate

Front 53

Describe bullous impetigo.

Back 53

vesicles and bullae containing clear or turbid flid without surrounding erythema arise on normal appearing skin- mediated by toxins. With rupture, shallow moist erosion forms.

Front 54

What is cellulitis?

Back 54

acute inflammatory diffuse spreading infx of dermis and subQ tissue accompanied by systemic symptoms (fever chills malaise)

Front 55

Describe the appearance of cellulitis.

Back 55

hot, bright red, painful skin lesion, swollen erythematous plaque with raised borders.

Front 56

What is an ascending lymphangitis?

Back 56

Associated red streak in skin proximal to cellulitis. Infx spreading via lymphatic system-- streak = route of infx.

Front 57

What is erysipelas?

Back 57

superficial cellulitis involving only superficial dermal tissue. Conjunctival entry.

Front 58

What causes cellulitis?

Back 58

local trauma or hematogenous spread (if no local trauma)- most commonly caused by staph or GABHS

Front 59

Where is cellulitis most commonly found?

Back 59

face, legs

Front 60

Is cellulitis usually unilateral or bilateral?

Back 60

unilateral*

Front 61

What are some risk factors for cellulitis?

Back 61

1. Trauma- wounds, abrasion, laceration, bites, burns
2. Local factors- PVD, poor hygiene, DM, ischemic ulcer, chronically edematous skin
3. Systemic factors- immunocompromised, cancer, alcoholic, IV drug user
4. Pre-exisiting dermatitis- fungal infx, sunburn, inflammatory condition

Front 62

Dx for cellulitis

Back 62

gram stain and culture- gram +, CBC with increased WBC with left shift, UA indicates post trep glomerulonephritis

Front 63

Tx for cellulitis

Back 63

systemic (GABHS- Pen VK, staph- diclox (adult) Keflex (kids) Unasyn (DM)) + topical antibx (bactroban*)

Front 64

Tx of bullous impetigo

Back 64

antibx PO

Front 65

If oral anitbx fail, what could be an indication?

Back 65

MRSA- use vancomycin

Front 66

What is necronizing fasciitis?

Back 66

Flesh eating bacteria. Acute rapidly progressive life-threatening secrosis of subQ fat and fascia

Front 67

What type of pt does necronizing fasciitis usually occur in?

Back 67

otherwise healthy

Front 68

What is the clinical presentation of necronizing fasciitis?

Back 68

initially exquisitely tender, erythematous, hot, swollen cellulitis that is unresponsive to therapy*, progresses alarmingly quickly from red -> purple -> grey-blue. Necrosis of fascia and fat produces thin, watery malodorous discharge.

Front 69

Dx of necronizing fasciitis

Back 69

fever, chills, leukocytosis, shock, tachycardia. Increased WBC with left shift

Front 70

What regoins of the body are mostly affected by necronizing fasciitis?

Back 70

perineum and genitalia (Fournier's gangrene)

Front 71

Tx of necronizing fasciitis

Back 71

Early detection. Extensive surgical debridement, possible amputation, systemic abx (PCN G, metronidazole). Increased oxygen if anaerobe.

Front 72

How are viral skin infx transmitted?

Back 72

direct contact with infectious lesions or contaminated surfaces.

Front 73

What is a common place where a person can contract a viral skin infection?

Back 73

gym locker room

Front 74

What is the pathophysiology behind viral skin infections?

Back 74

Replication of HPV is associated with proliferation of all epidermal layers except the basal layer and produces thickening and hyperkeratosis. Keratinocytes are being vacuolated due to being infected with the virus

Front 75

When a wart is de-roofed, what is revealed?

Back 75

studded brown-black dots (thrombosed capillaries)

Front 76

Can normal appearing epithelium contain HPV DNA?

Back 76

YES- residual DNA is associated with recurrence

Front 77

How is HPV associated with cervical cancer?

Back 77

HPV causes squamous cell abnormalities which are detected on PAP smears and often leads to development of cervical dysplasia and cancer.

Front 78

Which HPV types are associated with cervical cancer?

Back 78

16, 18, 31

Front 79

Describe verrca vulgaris

Back 79

firm 1-10 mm, flesh coloted to brown dome shaped papules or nodules.* Disrupt the lines of the finger prints*

Front 80

Describle verruca planae

Back 80

multiple smooth, flat topped papules, often slightly red or brown in color most common on the face and dorsum of the hands

Front 81

Describe verruca plantaris

Back 81

on soles of the feet and pressure points: metatarals, heels, toes. Painful small shiny sharply marginated papules with rough callus hyperkeratotic surface

Front 82

Describe condyloma acuminatum

Back 82

skin and mucosal surfaces of external genitalia and perineum. Appear small, discrete lesions or coalesce into large cauliflauer or raspberry like lesions.

Front 83

Describe attributes specific to males with condyloma acuminatum

Back 83

on shaft, may occur at urethral meatus, in homosexual men, may involve the perianal area.

Front 84

Describe attributes specific to women with condylum acuminatum

Back 84

warts affect the vulva, perineum, cervix, and vagina. may have internal lesions but not external.

Front 85

Dx for common, plane, and plantar warts

Back 85

Clinical. Upon removal of wart, characteristic red-brown dots (thrombosing capillary loops) are seen.

Front 86

Dx for anogenital warts

Back 86

colposcopy and proctoscopy are need e to identiy and treat rectal or cervical warts. Pap smears prepared from cervical scrapings often show cytologic evidence of HPV, Biopsy of lesions, PCR to indicate virus type

Front 87

Tx for warts

Back 87

No cure.

Front 88

Cosmetic tx of warts

Back 88

cryogenic surgery, adhesiotherapy, hypnosis, topical, curettage, electrocautery, laser ablation

Front 89

Describe a herpes virus infx

Back 89

very common acute self limiting vesicular opening

Front 90

How is the herpes virus transmitted?

Back 90

skin-skin/skin-mucosal contact
Most transmission (70%) occurs during asymptomatic shedding.

Front 91

Risk factors of HSV

Back 91

many sexual partners, unprotected intercourse, asymptomatic infx

Front 92

Type I is usually ________ and type II is usually _______.

Back 92

I: facial or non genital (spread by saliva)
II: usually genital

Front 93

Pathogenesis for HSV

Back 93

virus penetrates the epidermis or mucus membranse and replicates in epithelial cells. After primary infx latent non replicating virus ascends peripheral sensory nerves and resides within the dorsal root ganglia.

Front 94

Which cranial nerves pertain to HSV-I and HSV-II?

Back 94

HSV-I: trigeminal
HSV-II: sacral nerve

Front 95

What does NLR stand for pertaining to HSV?

Back 95

Neurovirulence, Latency reside in ganglia, Reactivation in stress

Front 96

Is HSV recurrent?

Back 96

Yes- hallmark trait of disease. Occurs at a similar site each time- usually the face, lips, or genitals.

Front 97

What precipitates an HSV attack?

Back 97

stress, hormonal change, sunlight, local trauma, URI

Front 98

Clinical presentation of HSV

Back 98

classically painful grouped vesicles on erythematous base- may evolve to pustules that beomce eroded as overlying epidermis sloghs. Erosions are punched out* and may enlarge to ulcerations which may be crusty or moist. Pain, burning or tingling at site. Rarely scar.

Front 99

Clinical presentation specific to HSV-I

Back 99

acute gingivostomatitis- circumerential around the mouth. Vesicles on lips and mucus membranes quicly erode and are painful.* Cornea can be involved- dedritic ulcer (olive branch looking). Fever, malaise, local lymphadenopathy (2 wks)

Front 100

Clinical presentation of herpetic whitlow

Back 100

painful vesicle or pustule found on the finger

Front 101

What is eczema herpeticum?

Back 101

HSV 2nd infx occuring from erosion caused by eczema

Front 102

Clinical presentation specific to HSV-II

Back 102

acute vuvlovaginitis, penile or perianal lesions are common. Male- shaft, meatus, glans, anus, thighs, scrotum.
Female- labia, perineum, inner thighs and butt.

Front 103

If a women with genital herpes were to give birth, what procedure would be called for at the time of delivery?

Back 103

C-section

Front 104

Dx of HSV

Back 104

clinical presentation, viral culture*, direct fluorescent antibody for antigen detection from vesicle fluid, Western blot* gold standard for serological testing. *Tzanck smear

Front 105

What is a Tzanck Smear?

Back 105

Viral testing- fluid from intact vesicle smeared on a slide, positive result = GIANT MULTI NUCLEATED CELLS*

Front 106

Tx for HSV

Back 106

NO CURE. Acyclovir cream applied 5 x daily for 5 days. Pts with high recurrence get long term oral antivirals

Front 107

What foods have been found to bring on HSV outbreaks?

Back 107

peanut butter and chocolate

Front 108

Immunization for HHV-3?

Back 108

varivax- 80% effective in preventing symptomatic primary VZV infx

Front 109

Risk factors for Primary VZV

Back 109

winter/spring, person with Zoster can give another person primary varicella but not vice versa. Close proximity.

Front 110

How is Primary VZV transmitted?

Back 110

air borne droplets, direct contact with vesicular fluid

Front 111

What causes a secondary VZV infx?

Back 111

stress, immunosuppression, malignancy, AIDS

Front 112

Clinical manifestations of Primary VZV

Back 112

prodromal symptoms precede eruption of disseminated pruritic erythematous macules and papules starting on the scalp and face* then spreading to the trunk and extremities. Dew drops on a rose petal*

Front 113

Tx for Primary VZV

Back 113

symptomatic therapy: antipyretics, antihistamines, calamine lotion, warm baths. Using antiviral agents 24-72 hours after onset decreases severity and duration.

Front 114

In what kind of pattern do Primary VZV lesions appear?

Back 114

In crops- may in one location at one time.

Front 115

Should aspirin be given to children under the age of 16?

Back 115

NO. Possibility of developing Reye's Syndrome.

Front 116

Complications of Primary VZV

Back 116

superinfx by staph, strep, varicella encephalitis, or Reye's syndrome

Front 117

Is primary VZV more severe in adults or children?

Back 117

Adults

Front 118

Clinical manifestations of Variella Zoster: shingles?

Back 118

Prodromal symptoms = sharp, lancing pain or burning, fever, headache, malaise, pruritis, tingling or tenderness at the site of future lesions-- dermatomal pattern*. Painful eruption of grouped vesicles on erythematous base, unilateral dermatome- thoracic (MC), cervical, trigeminal, lumbosacral.

Front 119

Transmission of shingles

Back 119

aerosolized from skin of individuals with herpes zoster

Front 120

Dx of VZV

Back 120

H&P, viral culture, VZV antigen detection smear of vesicle fluid, VZV antibody titers, direct fluorescent antibody test

Front 121

Tx of VZV

Back 121

administer antivirals <72 hours of onset of lesions, result in decreased duration and pain. Use acyclovir, famcyclovir, valacylovir- used mostly in patients with high risk of recurrence.

Front 122

Complications of VZV

Back 122

post herpetic neuralgia (pain at rash site for mos-yrs), 2nd bacterial infx

Front 123

Ramsay-Hunt syndrome

Back 123

Result of VZV. CN VIII involvement vesicles in pharynx and ear affected, possible hearing loss.

Front 124

Opthalamic zoster

Back 124

CN V affected (vesicles on side and tip of nose) possible loss of vision.

Front 125

What is molluscum contagiosum?

Back 125

self limited epidermal viral infx, characterized by round or oval firm, skin colored umbilicated perarly papules with a waxy surface. Large lesions have central keratotic plug which gives central umbilication*, pressure on plug causes extrusion.

Front 126

Where is molluscum contagiosum usually found in healthy individuals? In individuals with HIV?

Back 126

healthy- face, eyelids, neck, trunk, axilla*, anogenital area.
HIV- face (large) can be spread via shaving. Enlarge and cause disfigurement- response to HAART

Front 127

What causes molluscum contagiosum?

Back 127

molluscum contagiosum virus (MCV)- poxvirus that shares 30% homology with small pox.

Front 128

Dx of molluscum contagiosum

Back 128

biopsy, smear of keratotic plug (reveals inclusion bodies)

Front 129

Tx of molluscum contagiosum

Back 129

In most cases is spontaneous resolution. Cerratage, electrocaudery, cryosurgery

Front 130

What is pityriasis rosea

Back 130

acute self limited HHV infx-- HHV 7

Front 131

Describe pityriasis rosea.

Back 131

single oval slightly raised (2-5 cm) red herald patch precedes a 1-2 week long exanthem. Rash has typical christmas tree pattern on trunk , NO FACE. spontaneous resolution.

Front 132

Tx of pityriasis rosea

Back 132

antihistamine, steroid as necessary