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Clin Med I > Skin conditions I and II > Flashcards

Skin conditions I and II Flashcards

1
Q

how do cellulitis, erysipelas and abscesses normally present?

A
  • erythema
  • edema
  • warmth
  • d/t breach in skin barrier -> bacterial entry
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2
Q

where/who is erysipelas normally found

A
  • upper dermis and superficial lymphatics

- kids and older adults

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3
Q

where/who is cellulitis normally found

A
  • deeper dermis and subcutaneous fat

- middle aged and older adults

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4
Q

where are abscesses normally found

A

upper and deeper dermis

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5
Q

risk factors for cellulitis/ erysipelas

A
  • skin barrier disruption
  • preexisting skin conditions
  • skin inflammation i.e. d/t radiation
  • edema - lymphatic or venous insufficiency
  • obesity
  • immunosuppression
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6
Q

most common cause of erysipelas

A
  • beta hemolytic strep
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7
Q

most common cause of cellulutis

A
  • beta hemolytic strep

- staph aureus (including MRSA)

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8
Q

most common cause of skin abscess

A
  • staph aureus (including MRSA)
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9
Q

clinical manifestations of cellulitis

A
  • erythema, warmth, edema
  • unilateral almost always
  • common in lower extremities
  • +/- purulence
  • slower onset
  • localized sx develop over days
  • less distinct boarders
  • +/- drainage
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10
Q

clinical manifestations of erysipelas

A
  • erythema, warmth, edema
  • unilateral almost always
  • common in lower extremities
  • nonpurulent
  • acute onset sx
  • clear demarcation- butterfly involvement on face
  • systemic manifestations- fever/ chills
  • raised above level of surrounding skin
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11
Q

what does induration mean

A

hard surrounding

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12
Q

what does fluctuant mean

A

soft and moveable

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13
Q

what is a skin abscess

A
  • collection of pus

- in dermis or subcutaneous space

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14
Q

clinical presentation of skin abscess

A
  • painful
  • fluctuant
  • erythematous nodule
  • +/- cellulitis
  • surroudning induration
  • regional adenopathy
  • systemic sx rare
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15
Q

furuncle

A

infection of hair follicle -> abscess

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16
Q

carbuncle

A

infection of multiple hair follicles -> abscess

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17
Q

what are common areas for skin abscesses to develop?

A
  • neck
  • face
  • axillae
  • buttocks
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18
Q

what is LRINEC score?

A
  • lab risk indicator for necrotizing fasciitis

- distinguish NF from other soft tissue infections like cellulitis

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19
Q

when would you use the LRINEC score

A
  • concerning hx and exam
  • pain out of proportion to exam
  • rapidly progressive cellulitis
  • score >6 means NF
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20
Q

complications of cellulitis

A
  • NF
  • bacteremia and sepsis
  • osteomyelitis
  • septic joint
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21
Q

conditions that may be hard to distinguish from cellulitis

A
  • gout
  • DVT
  • venus stasis dermatitis
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22
Q

management of cellulitis/ abscess/ erysipelas

A
  • depends on severity
  • should see improvement in 24- 48 hours
  • tx duration of 7-10 days, up to 14
  • if no improvement consider underlying abscess
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23
Q

where does impetigo most commonly occur

A

on face of kids 2-5

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24
Q

what is the most common form of impetigo

A
  • non-bullous
  • papules progress to vesicles surrounded by erythema
  • dev into pustules which break down and form golden crust
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25
Q

ectyhma impetigo

A
  • ulcerative
  • extend deep into dermis
  • “punched out ulcers” with yellow crust
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26
Q

possible consequences of impetigo

A
  • post-strep glomerulonephritis

- rheumatic fever

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27
Q

sx of post-streph glomerulonephritis

A
  • edema
  • HTN
  • hematuria
  • occurs 1-2 weeks post infection
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28
Q

most common cause of impetigo?

A
  • s. aureus
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29
Q

most common cause of bullous impetigo?

A
  • s. aureus strain that produces toxin -> cleavage of superficial skin
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30
Q

most common cause of ecthyma impetigo?

A
  • strep pyogenes
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31
Q

urticaria

A
  • hives, welts, wheels
  • common
  • intensely pruritic
  • usually no identifiable trigger
  • sometimes accompanied by angioedema
  • anyone can get it
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32
Q

acute urticaria

A
  • less than 6 weeks
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33
Q

chronic urticaria

A
  • recurrent

- signs and sx recur most days of week for more than 6 weeks

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34
Q

clinical manifestations of urticaria

A
  • circumscribed, raised, erythematous plaque with central palor
  • round/oval
  • very itchy
  • most severe at night
  • any area of body
  • transiently appearing
  • can get angioedema in lips, extremities, genitals
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35
Q

pathophys of urticaria

A
  • mediated by mast cells in dermis
  • release histamine -> itching
  • release vasodilatory mediators -> swelling
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36
Q

dx of urticaria

A
  • mainly clinical exam and history
  • signs and sx of allergic reaction
  • any underlying disorders
  • allergy test
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37
Q

management of urticaria

A
  • focused on short term relief
  • 2/3 spontaneously resolve and are self limited
  • can use H1 and H2 antihistamines
  • may use steroids
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38
Q

lipomas

A
  • most common benign soft tissue neoplasm
  • mature fat cells enclosed by fibrous capsule
  • dx based on history and PE
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39
Q

where are lipomas usually found?

A
  • most common in upper extremities and trunk
  • can be found anywhere
  • range in size
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40
Q

pathophys of lipomas

A
  • > 50% develop in subcutaneous tissue

- cause unknown but associated with gene rearrangement of chromosome 12

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41
Q

clinical manifestations of lipomas

A
  • superficial
  • soft
  • painless
  • round, oval, multilobulated
  • pt may confuse them for enlarged lymph nodes
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42
Q

management of lipomas

A
  • if stable/asymptomatic then no tx

- can surgically excise

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43
Q

epidermal inclusion cyst

A
  • most common cutaneous cyst
  • skin colored dermal nodules
  • visible central punctum
  • usually small in size
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44
Q

where are epidermal inclusion cysts usually found

A
  • face
  • scalp
  • neck
  • trunk
  • can occur anywhere
  • 2X more common in men
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45
Q

what disease is epidermal inclusion cysts associated with?

A

gardener syndrome- predisposition to colon polyps

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46
Q

pathophys of epidermal inclusion cysts

A
  • d/t trauma
  • implantation and proliferation of epithelial elements into dermis
  • spontaneous rupture can occur
  • cheesy material
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47
Q

clinical manifestations of epidermal inclusion cysts

A
  • firm
  • asymptomatic
  • overlyting a punctum (where hair follicle comes out)
48
Q

management of epidermal inclusion cysts

A
  • asymptomatic- none
  • excesion of cyst or incision and drainage
  • intralesional injection with triamcinolone
49
Q

tetanus cause

A
  • clostridium tetani
  • found in soil
  • rarely seen in US d/t vaccine
  • incidence increases after natural disasters
50
Q

pathophys of tetanus

A
  • c. tetani produces matalloprotease tetanospasmin (toxin)
  • toxin released in brain stem -> blocks neurotransmission that modulates muscle contraction
  • result- increased muscle tone, painful spasm, widespread autonomic instability
51
Q

what is the incubation period for tetanus?

A
  • 8 days

- further the inoculation site is from CNS the longer the incubation pd

52
Q

clinical manifestations of tetanus

A
  • trismus (lock jaw)
  • massester muscle reflex . spasm
  • tonic contractions of skeletal muscles
  • no impairment in consciousness
53
Q

when does acne typically resolve?

A
  • 3rd decade

- post adolescent usually impacts women

54
Q

pathogenesis of acne

A
  • inflammation of pilosebaceous follicles
  • follicular hyperkeratinization
  • increased sebum production
  • cutibacterium acnes
  • inflammation
55
Q

sebaceous gland changes in ance

A
  • gland enlarges
  • sebum production increases during puberty -> medium for c. acne
  • micromedones = enviornment for bacteria
56
Q

closed comedone

A
  • white head

- accumulation of sebum and keratinous material

57
Q

open comedone

A
  • black head
  • keratinocytes
  • oxidized lipids
  • melanin
58
Q

pathogenesis of inflammatory acne

A
  • follicle ruptures -> proinflammatory lipids and keratin released into surrounding dermis
  • family history has 3X risk
  • stress doesnt appear to be associated
59
Q

androgens and acne

A
  • stimulates growth of secretory fn of sebaceous glands
  • high levels at birth -> acne until about 2 y/o
  • acne onset correlated to DHEA-s levels
  • most pts with acne have normal androgen levels*
60
Q

external factors that cause acne

A
  • soaps/ detergents/ astrigents
  • repetitive mechanical trauma like scrubbing
  • bra straps, shoulder pads, helmets
61
Q

milk and acne

A
  • milk can exacerbate acne d/t increased levels of IGF
62
Q

insulin resistance and acne

A
  • stimulates androgen production
  • associated with increased IGF-1
  • increased facial sebum production
  • normal rise in insulin resistance and IGF-1 in puberty
63
Q

BMI and acne

A
  • possible that low BMI reduces risk of acne in males

- increased risk of high BMI and acne only in women

64
Q

ways to classify acne

A
  • comedonal acne- noninflammatory
  • inflammatory acne- papules, pustules
  • nodular acne- aka cystic acne
65
Q

dx of acne

A
  • PE
  • type and location
  • medication hx
  • endocrine fn
  • DHEA-S, total testosterone, free testosterone
66
Q

counseling points for acne tx

A
  • no cure
  • 4-6 weeks for improvement
  • may get worse before better
67
Q

Rosacea

A
  • chronic disorder
  • relapses
  • primarily in central face
  • 4 main subtypes
  • more common in fair skinned and adults (F) >30
68
Q

main subtypes of rosacea

A
  • erythematotelangiectatic
  • papulopustular
  • phymatous
  • ocular
69
Q

pathogenesis of rosacea

A
  • abnormalities in innate immunity
  • inflammatory reactions to cutaneous microorganisms
  • UV damage
  • vascular dysfunction
70
Q

erythematotelangiectatic rosacea

A
  • presistant central erythma
  • flushing
  • rough and scaling
  • enlarged cutaneous BV
  • skin sensitivity
  • erythema congestivum
71
Q

erythema congestivum

A

after exacerbation of facial redness in rosacea, return to baseline is slow

72
Q

papulopustular rosacea

A
  • papules and pustules in central face
  • can be mistaken for acne
  • comedones dont occur
  • inflammation extends beyond follicle
73
Q

phymatous rosacea

A
  • tissue hypertrophy
  • irregular contours
  • usually on nose
  • can occur on chin, cheeks, forehead
  • most common in men
74
Q

ocular rosacea

A
  • happens in more than 50% of pts
  • conjunctival hyperemia
  • blepharitis
  • keratitis
  • lid margin teleangiecstasis
  • abnormal tearing
  • chalazion
  • refer to ophthalmologist
75
Q

rosacea exacerbating factors

A
  • extreme temps
  • sun exposure
  • hot drinks
  • spicy food
  • alcohol
  • exercise
  • irritation from topical products
  • emotions
  • drugs
  • skin barrier disruption
76
Q

dx for rosacea

A
  • clinical assessment

- no biopsy or serologic studies

77
Q

management of erythematotelangiectatic rosacea

A
  • first line- behavioral changes/ avoid triggers

- second line- laser and light based therapy

78
Q

psoriasis

A
  • well demarcated plaques with silver scales
  • associated with many comorbidities
  • peak age onset: 30-39 and 50-69
79
Q

risk factors for psoriasis

A
  • genetics *
80
Q

exacerbating factors for psoriasis

A
  • smoking
  • obesity
  • drugs
  • infection- post strep flaares and HIV
  • alcohol
  • vit D deficiency
  • stress
81
Q

pathophys of psoriasis

A
  • immune mediated
  • scaling, induration, erythema hyperproliferation
  • abnormal differentiation of epidermis
  • inflammatory cell infiltrates
  • vascular dilitation
82
Q

categories of psoriasis

A
  • chronic plaque psoriasis
  • guttate
  • pustular
  • erythrodermic
  • inverse
  • nail
83
Q

chronic plaque psoriasis

A
  • most common
  • symmetrical distribution
  • asymptomatic or pruritis
84
Q

common places for plaque psoriasis

A
  • scalp
  • extensor elbows, knees
  • gluteal cleft
85
Q

guttate psoriasis

A
  • multiple small papules and plaques
  • trunk and proximal extremities common
  • strong assoc with recent strep infection
  • child or YA with no hx psoriasis
86
Q

pustular psoriasis

A
  • life threatening
  • acute onset
  • wide spread erythema, scaling, and sheets of superficial pustules
  • maialse, fever, diarrhea, leukocytosis, hypocalcemia
87
Q

causes of pustular psoriasis

A
  • pregnancy
  • infection
  • withdrawal from glucocorticoids
88
Q

erythrodermic psoriasis

A
  • uncommon
  • acute or chronic
  • generalized erythema and scaling from head to toe
  • complications d/t loss of adequate barrier
89
Q

inverse psoriasis

A
  • inguinal, perineal, genital, intergluteal, axillary and inframammory areas
  • sometimes misdx as fungal or bacterial infections
90
Q

nail psoriasis

A
  • more common in pts with psoriatic arthritis

- nail pitting

91
Q

dx of psoriasis

A
  • family hx*
  • clinical exam
  • skin biopsy
92
Q

management of psoriasis

A
  • emollients
  • topical corticosteroids
  • vit D analogs
  • Tar- T/gel
  • topical retinoids
  • UVB light therapy
  • photochemothearpy
  • excimer laser
  • biologics
93
Q

alopecia

A
  • targets anagen hair follicles -> non-scarring hair loss
  • usual onset before 30
  • men and women equally affected
94
Q

classifications of alopecia

A
  • areata
  • totalis
  • universalis
95
Q

alopecia areata

A

discrete patches

96
Q

alopecia totalis

A

entire scalp

97
Q

alopecia universalis

A

entire body

98
Q

pathophys of alopecia

A
  • T cell mediated inflammation disrupts normal hair cycle
  • no destruction of hair follicle
  • premature transition of active follicle to inactive
  • collapse of immune privileged status
  • inappropriate trigger of immune response vs follicular antigen
99
Q

alopecia risk factors

A
  • genetics
  • severe stress
  • drugs and vaccines
  • infections
  • vit D def
100
Q

clinical manifestations of alopecia

A
  • smooth, circular, discrete patches of hair loss
  • dev over 2-3 weeks
  • pruritis or burning may precede
  • beard may be first site in men
  • can spread in bizarre patterns
  • nail abnormalities possible
101
Q

onychorrhexis

A
  • longitudinal fissuring of nail plate

- can occur in pts with alopecia

102
Q

diseases associated with alopecia

A
  • thyroid disease***
  • lupus
  • vitiligo
  • atopic dermatitis
  • allergic rhinitis
  • psoriasis
  • down syndrome
  • polyglandular autoimmune syndrome type I
103
Q

clinical course of alopecia

A
  • 50% with limited patchy hair loss spontaneously recover in 1 yr
  • some have multiple episodes
  • 10% progress to totalis or universalis
104
Q

dx of alopecia

A
  • clinical exam
  • exclamation point hair at margins
  • skin biopsy only in uncertain cases- show inflammatory infiltrates surrounding follicles aka swarm of bees
105
Q

management of alopecia

A
  • topical or intralesional corticosteroids (caution skin atrophy and hypopigmentation)
  • topical immunotherapy for severe
  • rogaine
  • phototherapy
  • oral steroids or biologics as last line
106
Q

hidradenitis supprativa

A
  • chronic follicular occlusive skin condition
  • aka acne inversa
  • inertriginous area involvement
  • onset usually puberty to 40, women more than men
107
Q

pathogenesis of HS

A
  • follicular occlusion, follicular rupture and associated immune response
  • ductal keratinocyte proliferation
  • ductal plugging then expansion -> rupture
  • stim immune response leading to sinus tracts
108
Q

risk factors and exacerbating factors of HS

A
  • genetics*
  • mechanical stress
  • obesity
  • smoking
  • hormones- perimenstrual flares, goes away during pregnancy
  • bacteria- staph and strep
  • drugs
109
Q

clinical manifestations of HS

A
  • axilla most common site
  • inguinal, inner thigh, perianal, inframammary, buttock, scrotum, vulva
  • primary lesion is solitary, painful, deep seated inflamed nodule
  • dev sinus tracts with chronic disease
  • scarring
110
Q

what is the staging system called for HS?

A

hurley staging

111
Q

Stage I hurley manifestation and management

A
  • abscess formation
  • topical clindamycin
  • intralesional corticosteroid
  • punch debridement
  • chemical peel
112
Q

stage II hurley manifestation and management

A
  • recurrent abscess
  • sinus tract formation and scarring
  • oral tetracyclines for several months
  • clindamycin or rifampin
  • oral retinoids
  • antiadrenergics
  • punch biopsy of fresh lesions
113
Q

stage III hurley manifestation and management

A
  • diffuse involvement
  • multiple interconnected sinus tracts
  • TNF alpha inhibitors
  • systemic glucocorticoids
  • cyclosporine
  • surgery
114
Q

dx of HS

A
  • patient history
  • clinical exam
  • skin biopsy not necessary
115
Q

prevention of HS

A
  • avoid skin trauma
  • stop smoking
  • weight management
  • antiseptics
  • emollients
  • management of comorbidities

Clin Med I (16 decks)

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