Cellulitis

Red Rash, PMH of arthritis

Erythematous plaque with illdefined borders, tender to

palpation with lymphatic
streaking

Always an infectious process

Common infection (3% per year), often an entry

for bacteria or fungi. Spreading erythematous,
non-fluctuant tender plaque. More commonly
found in lower leg. Lymphangitic spread to
draining
lymph nodes common
Risk Factors:

Local trauma
Underlying skin lesion
Inflammation
Edema and impaired lymph
flow in the area
Preexisting skin infection

Usually caused by
G + organisms like
Group A strep
and Staph Aureus
unless there have
been unusual
exposure

Treat Immediately with coverage for G +

bacteria!
Usually treat empirically against group A strep, and
maybe against staph aureus as well. Purulent

Erysipelas

Type of cellulitis Main Pathogen is

Strep pyogenes

Superficial cellulitis with Marked Dermal

Lymphatic involvement resulting in
Raised skin. Associated with high WBC
count, and can be preceded by chilld,
fever, headache, vomitting, and joint pain

Treat Immediately with Oral antibiotics

Usually treat empirically against group A strep,

Absess

History of dug use, painful enlarging mass on right

arm, history of MRSA infection and IVDU

Collection of pus within the dermis and deeper skin tissues,

presenting at painful tender, fluctuant and erythematous
nodules. Often it is surmounted by a pustule and surrounded by a
rim of erythematous edema. Spontanteous drainage of purulent
material can occur

Treat with incision and drainage! Can also

recommend antibiotics in pts with severe/extensive
disease, rapid progression or failure to improve
with I&D. ALWAYS SEND WOUND CULTURES

Furunculosis
Boil; Acute, round, tender, circumscribed, perifollicular abscess that generally
ends in central suppuration
Common areas include
the back of the neck,
face, axillae, and
buttocks
Caused by Staph
aureus.
Can used warm
compresses to
promote drainage
may be used for
single furunculosis

Carbunculosis
Carbuncle-coalescence of several inflamed follicles into a single inflammatory
mass with purulent discharge and multiple follicles

Folliculitis
Superficial bacterial infection of the hair follicles,
presenting as raised, erythematous,
occasionally pruritic pustules <5mm in
diameter. Genital folliculitis maybe sexually
Usually caused by Staph
transmitted.
Aureus unless there
exposure to hot tub or
qwimming pool, then
consider pseudomonas
folliculitis

Cleanse affected area with antibacterial soap and

water. Treat with oral and topical staphylococcal
agents may be used, deep lesions of folliculitis
represent small follicular absesses and should be

Impetigo

HONEY CRUSTEDMain Pathogen is

Strep pyogenes

Superficial bacterial skin infection commonly seen in children aged 25. Impetigo is easily spread by close contact. Most cases are due to
Staph, with some being due to GAS. 3 types: Non-bullous impetigo
(Impetigo contagiosum) , Bollous impetigo, Ecthyma

Impetigo ContagiosumLesions that begin as papules

surrounded by erythema that
then progress to enlarging
pustules that break down and
form thick, adherent, golden
Honey colored crusts

Bollous Impetigoseen in children and

characterized by
flaccid bullae with
clear yellow fluid, that
later becomes
purulent

Ecthyma- ulcerative form of

impetigo where the lesions
extend through the
epidermis and deep into the
dermis

IMPETIGO
Usually caused by Staph
aureus or Group A Strep
Non-bullous or Bullous
Vesicles and pustules with
honey-colored crusting
Tx:

Topical antibiotics for localized

infection (Mupirocin)
Cephalexin, Dicloxicillin,
Clindamycin for more
widespread or advanced
infections

Sequelae

Post-strep GN
Rheumatic Fever

Necrotizing Fasciitis
Life threating infection of the fascia just above the muscle. IT
progresses rapidly over the course of a few hours, may follow surgery
or trauma. Expanding dusky, edematous, red plaque with blue
discoloration. It may turn purple and blister. Anesthesia of the skin
of the affected area is a characteristic finding. Caused by GAS, Staph
Aureus

High mortality rate, and treatment includes:

widspread debridement and broad-spectrum
system antibiotics

Tinea Pedis

AKA Athletes foot

Most common fungal infection in developed countries, most

commonly by fungus Trichophyton rubrum. 3 Clinical Patterns:
Moccasin type, Vesiculobollous, Interdigital type
Moccasin type:
Chronic hyperkertotic
type with sharply
marginated scale,
distributed along
lateral borders of feet,
heels, and soles,
associated with
ecymycosis

Vesiculobollous type:
Grouped, 2-3 mm,
vesicles, often on the
arch or instep, can be
itchy or painful, type IV
hypersensitivity

Interdigital type: most

common, presenting
with scaling and
redness between the
toes, and may have
associated maceration

KOH exam is the most appropriate test in diagno

Used to see hyphae as its dissolves the keratinocytes
Clotriamazole cream twice daily for 4 weeks
First line- imidazoles, 2nd line- allylamines

Tinea Corporus

AKA Ringworm

Annular lesion with central clearing is typical, KOH scraping best from
the active margin, not the centrally clearing

KOH exam is the most appropriate test in

diagnosis from the active margin. Used to see
cream
twice daily for 4 weeks
hyphae as Clotriamazole
its dissolves the
keratinocytes
First line- imidazoles, 2nd line- allylamines

Intro

Neonatal
Rashes

Vascular
Lesions

Eczemato
id

Eruption
s

TINEA CORPORIS
Ringworm

Erythematous, pruritic, and

scaly lesions usually with an
annular shape that grows
outward leaving a central
clearing
Tx: topical antifungal
azoles

squamou
s
Disorder
s

Infectiou
s
Disorder
s

Infestation
s

sensitivi
ty

Syndrome
s

Tinea Cruris

AKA jock itch

Dermatophyte infection of the groin, may lack scale due to scrotal

occlusion. Can be alongside tenia pedis, so have to look for both

KOH exam is the most appropriate test in

diagnosis from the active margin. Used to see
cream
twice daily for 4 weeks
hyphae as Clotriamazole
its dissolves the
keratinocytes
First line- imidazoles, 2nd line- allylamines

TINEA CAPITIS
Fungal infection of the
scalp and hair follicle
Broken off hairs with
scaling

Black dot sign

Tricophytonwill

flouresce

not

Can form kerion

DDx: alopecia areata,
seborrheic dermatitis
Tx: oral griseofulvin for 6

8 wks

Onychomycosis

AKA jock itch

Chronic fungal infection of the nailbed that starts with tenia pedis and
responds poorly to topical antifungals
Distal Subungal onychomycosis:
Thickened nail, subungal debris, and
seperation of the nail plate from the nail
bed. Caused by Trichophyton rubrum.

Oral terbinafine

Tinea Reversicolor
NOT caused by a dermatophyte. Colonization caused by species of
malassezia, a lipophilic yeast which is a normal resident of the skin.
Tends to Recur anually during the summer months. Well
demarcated, tan, salmon, or hypopigmented or
hyperpigmented patches, on thrunk and arms. Scale often
only seen when rubbed, and Revert after treatment

Spagetti and meatball

pattern corresponding
to hyphae and spores

Not curable!!
KOH exam is the most appropriate test in
diagnosis from the active margin. Treat with
First line- imidazoles, 2nd line- allylamines
Antifungal shampoo

Intertrigo

AKA jock itch

Inflammation of large skin folds, up to 10% complicated by candida

yeast colonization. It will Burn more than itch, Satellite macules,
and KOH exam may reveal pseudohyphae
Sharply defined red plaques involving
the skin folds with surrounding satellite
macules

Clotreimazole cream is treatment of choice since it

works better than nystatin. Encourage weight loss,
wear looser clothing

Seborrheic Dermatitis
Common inflammatory rxn to Malassezia furfur yeast (normal flora)
that thrive on oily skin. Erythematous scaling patches on the
scalp and face. Worse in HIV pts.
Favors the central chest

Common chronic skin condition, characterized by Redness and scaling

occuring in places where sebaceous glands are present, Face and
scalp, presternal area, and body folds. Dandruff is an example of mild
seborrheic
dermatitis
nfancy,
puberty,
>20 years old, more common in males (think males sweat more
Orange-red or Gray white
lesions that are sharply
marginated and with greasy
or white
drying
scaling
Behind
external
ear
= Sticky crusts
macules
and fissures
Scalp = diffuse, marked scaling
("dandruff")
Face & trunk = scattered, discrete
lesions
Cannot bepolycyclic,
cured, only
Control
Nummular,
andcontrolled.
even
with Desonide
Cream for flares (mild steroid
annular
on the trunk
with low potency) and topical ketoconazole
or topical corticosteroids.

SEBORRHEIC DERMATITIS

Common (cradle cap)

Chronic disorder marked by
redness and scaling in areas
with dense concentrations of
sebaceous glands (scalp,
eyebrows, body folds)
Fine flaky to thick greasy
yellow scales with or without
an underlying erythematous
patch or plaque base.
Usually resolves by one year
old.
Tx:

Manual removal of scales

Medicated shampoos (tar,
selenium, ketoconazole)
Topical corticosteroids

Summary: Adult Fungal

Treatment
1 line
2 line
st

Tinea pedis
Tinea corporis
Tinea cruris
Tinea versicolor

Candida

Seborrheic dermatitis

nd

Clotrimazole
Miconazole cream

Terbinafine
Naftifene
Butenafine
cream or gel

Selenium sulfide, zinc

pyrithione shampoos

Oral fluconazole or
itraconazole

Clotrimazole
Miconazole cream
or
Nystatin powder,
ointment

Desonide or 1%
hydrocortisone
ointment

Ketoconazole cream

Desonide or 1%
hydrocortisone for
flares
20

Verruca Vulgaris
Hyperkeratotic, exophytic, dome shaped papuples or nodules.
Common on the fingers, dorsal hands, knees or elbows but can occur
anywhere. Punctate black dots that represent thrombosed capillaries.
Can Koebnerize or spread with skin trauma. Caused by HPV
Type of Wart

HPV Type

Verruca vulgaris: common

warts

HPV 2,4

Verrucae plana: flat warts

HPV 3, 10

Palmoplantar warts

HPV 1

Condylomata acuminata:
external genital warts

HPV 6, 11, 16,

18, 31, and
more

Number
of Warts

Hand & Foot

Face

Other Sites

Few

Cryotherapy
Salicylic acid
Adhesive tape
Laser

Cryotherapy
Exicision

Cryotherapy
Salicylic acid

Many

Salicylic acid
Cryotherapy
First
lineSquaric acid or
DCNB
Laser

Cryotherapy
Tretinoin creamnd

imidazoles, 2

Imiquimod
Tretinoin cream
line-Squaric
allylamines
acid or DCNB

Verrucae Planae: Flat Warts

Skin-colored or pink
Smooth-surfaced,
slightly elevated, flattopped papules
Dorsal hands, arms,
face (exposed
surfaces)

22

Palmoplantar
Verruca

Thick, endophytic (depressed

into skin of sole) papules
Mosaic warts: plantar warts
coalescing into large plaques
Can accumulate a thick callus
over and around the wart
Plantar warts may be painful
when walking

23

External Genital Warts

Soft hyperkeratotic, sessile papules. HPV is one of the most common
STIs, peak prevalence in women 20-24 yo, men 25-29 yo.
Favors the central chest
Warts are caused by human
papilloma viruses
Numerous morphologies exist:
common, flat, palmoplantar, external
genital
Treatment is difficult and there are
many options available
Vaccines have been developed to
reduce HPV-associated neoplasia, and
some have efficacy for external
genital warts
Cannot be cured, only controlled. Control
with Desonide Cream for flares (mild steroid
with low potency) and topical ketoconazole.

Psoriasis Vulargis
Peaks in mid 20s or mid 50s, and even in kids with mean age of onset
at 8 yo. 1.5-2% of population in western countries. ERYTHEMATOUS
BORDER,component.
sharp margin,
skaly
Psoriasis vulgaris (and
Hereditary
Incredibly
rapid
shortening of the normal cell cycle,
reulting in increased proliferation of
epidermal cells. Overwhelming T cell
population
in lesions.type:
Eruptive inflammatory
Acute Guttate, with multiple small
nummular lesions and a greater
tendency toward spontaneous
resolution Rare. Salmon-pink
papules with or without
scales, localized on trunk
Chronic stable plaque psoriasis:
majority. Erythematous base
with silvery while lamellar
scale that bleeds when
pulled off (auspitz)

variants)
Plaques, erythematous, sharply
marginated
Scales, silvery-white flaky
Observe blood droplets w/scale
removal (Auspitz sign)
Race and heredity (1 parent +,
2 parents ++)
Inverse: No scales (moist areas)
Arthritis in 10-25% of patients
Systemic methotrexate and
biologicals
Inpatient Rx for erythroderma
variant
Steroids topically
Variants of psoriasis: pustular &
erythroderma
UVB and PUVA
Laser
Guttate
Adult onset in 20s and 50s
Retinoids topically and
systemically
Injury to skin is trigger
(Koebner phenomenon)

Inverse psoriasis
Psorasis in warm and moist
environments not scaly,
but more macerated,
often bright red and
fissured due to scale
coming
SHARP off
DEMARCATIONS

Fingernails pitting, yellowish brown Oil sp

Pustular psoriasis:
Pustiules that have PNLs, either
generalized or palmoplantar

important for distinction

Management:
Emollients
Topical corticosteroids
Laser therapy
Phototherapy
UVB
Psoralen and UVA

Psoriatic Arthritis: Seronegative, can

be present in people without the
skin manifestations

Pityriasis Rubra Pilaris

Reddish orangy scaly plaques, palmoplantar keratoderma,
keratotic follicular papules. Eyrthroderma
with
Islands of
Craniocaudal
distribution
sparing
Pityriasis rubra P I L A R I S
Nail involvement without oil

Mucous embrane
winvolvement with
extropion

Progresses cranial to caudal

(face, scalp, trunk)
Islands of sparing
spot
Location also + nails, mucous
membranes, eyes
Acute onset in sporadic cases
Retinoids (systemic) for
extensive disease
Initial Rx: emollients, topical
steroids
Salmon or orange-red scaly
plaques

NO CLEAR BORDER

Treat with MTX if extensive, or

phototherapy or even extracorporeal
photochemotherapy

Pityriasis Rosea
Self limiting (4-6 weeks) exanthematous skin disease
characterized by appearance of slightly inflammatory, oval,
papulosquamous lesions on the trunk and proximal areas of
the
extremities
Begins
with HERALD PATCH- single round or oval, PatchHerald patch
sharply delimited, pink or salmon-colored lesion on
chest, neck, or back that becomes scaly with
central cleaning
1-2 weeks later smaller oval lesions appear on
trunk and extremities ALONG THE CLEVAGE OF
SKIN, CHRISTMAS TREE PATTERN ON BACK

Herald patch

Involves trunk and proximal

extremities
Treeclassic Christmas tree on
back
Youths have atypical
distribution (face and scalp)
R/O tinea (esp. herald patch)
Itchy
Acute
Self-limited
Inflammatory oval lesions
Scaly with central clearing
Reactivation of herpes virus
postulated
One large initial lesion = Herald
patch
Sometimes takes months to
resolve
Exanthematous
After herald patch, 1-2 weeks to
appearance

Lichen planus
Uncommon disorder affecting Middle aged adults. Buccal
mucosal or genital involvement/pain that is severe and
dehabilitating.
4
Ps:
Lacelike Wickhams striae
Papule, Purple, Polygonal, Pruritus
Wickhams Striae- white lacelike patterns on
surface of the papules and plaques
Affects skin, nails, mucous membranes, and
vulva and penis
Flexor surfaces are common involvement
Severe prurtits

Scalp involvement leads to hair

Involves skin, nails, mouth,

vulva, penis
Clinical diagnosis
Hyperpigmentation after
healing
Expect remission within 1-2
years
Normally in middle-aged adults
Purple, papules/plaques,
polygonal, purple
Located in flexor sites
Association with hepatitis C
postulated
Nails may be lost if
involvement is severe
Koebner
Usual
initial Rx is topical
corticosteroids
reaction, the
Severe
pruritis, painofif
development
loss!!
ulceration

skin lesions in
areas of trauma,
as a result of
Usually remits w/I 1-2 years, treat with topical
corticosteroids
scratching

Acne Vulgaris
Multiple type of skin lesions: Comedo (black head or white head),
Papules, Pistules. If severe: Nodules, sinus tracts.
Common disorder, usually in adolescents and young adults, usually more
severe in males. Caused by androgens stimulating sebum production and
keratin becoming more dense
Family History in Nodular acne!!; NO
RELATION TO DIET
Want to remove the plugs, reduce
production, treat bacterial colonization.
Think about PCOS. If using isotretinoin, do
LFTs.

Open Comedo:
Blackhead
Dilated pore,
oxidized oily
debris

Closed
Comedo:
Whitehead, 12 mm pebbly
while papule

Treat with a combination of Benzoyl peroxide

gels, topical antibiotics, and topical retinoids
(starting at higher strength and then
bringing it down.

31

Acne vulgaris
The follicular orifice becomes
blocked by keratinous material and
sebum (=microcomedones then
comedones=hallmark of acne)
Propionibacterium acnes
(bacterium) acts to release free
fatty acids from sebum
Causes sterile inflammation within
the comedones and results in
rupture of the nodule wall
Further inflammatory reaction
results as oily and keratinous
debris from the nodule are
extruded into the dermis

32

ACNE CONGLOBATA
Severe form of nodular acne

Characteristics:
Nodules (may be very
painful), sinus tracts
(tunnels of pus under the
skin)
May result in severe
scarring

Differential diagnosis:

Bacterial folliculitis
Granulomatous rosacea
Sarcoidosis
Lupus vulgaris
http://www.hkma.org/english/cme/clinicalcase/200904a_set.htm

33

Is it chloracne?
May mimic acne vulgaris
Open and closed comedones
Nodules with no/less
inflammation
Caused by exposure to
halogenated aromatic
hydrocarbons (fungicides,
insecticides, herbicides, wood
preservatives)

Patient exposed in
industrial explosion
in Meda, Italy
1976
(now known
as the
Seveso
accident)
Significant dioxin
exposure for both
workers and
inhabitants of region
http://www.hrdpidrm.in/e5783/e17327/e24075/e27316/

Most common skin sign of

dioxin poisoning
(occupational, environmental,
deliberate)
TCDD
2,3,7,8-Tetrachlorodibenzo-p-dioxin

Former president of the Ukraine,

Viktor Yushchenko, 2004
http://vets.yuku.com/topic/27173

34

Other conditions may mimic or cause

acne
Steroid acne
Prolonged topical or
systemic use of
glucocorticoids
Acneiform (not true
acne)- because not same
pathology
Appearance:

Other medicationrelated acne

True acne (hormonal)
Androgens
Testosterone
Danazol
Oral contraceptives

Acneiform

Monomorphous folliculitis
Phenytoin
small erythematous papules
Lithium
and pustules
Isoniazid
NO COMEDONES
Iodides
Treatment: stop or reduce
glucocorticoids
Bromides
http://0-www.accessmedicine.com.library.touro.edu/content.aspx?aID=5185720

Rosacea
Red fascial rash with PERIORBITAL SPARING, no Comedones!
Chronic inflammation of sebacesous glands
middle age adults; usually women., flushing and blushing. Response to
certain stimuli.

36

Classificationn
Staging (Plewig and Kligman)

Sub-types (CURRENT)

Stage I: Persistent erythema

with telangiectases

Erythematotelangiectatic
rosacea (ETR)- red face

Stage II: Persistent

erythema, telangiectases,
papules, tiny pustules

Papulopustular rosacea

Phymatous rosacea- werd nose

Stage III: Persistent deep

erythema, dense
telangiectases, papules,
pustules, nodules; rarely
persistent "solid" edema of
the central part of the face

Ocular rosacea- present before

presentation of others refer
to optho

http://0-www.accessmedicine.com.library.touro.edu/content.aspx?aID=5185754

Perioral Dermatitis
Chronic Papulopustular and eczematous facial dermatitis affecting
young women. Hallmark is exacerbation when treate with
Involves
nasolabial folds and nares, Can present in periorbital area
corticosteroids.

Flare may occur after steroids discontinued with gradual improve

Use calineurin inhibitors to trea

Hidradentitis suppuativa
Large tender, fluctuant erythematous cyst with multiple round and
oval erythematous firm tender nodules. Localized to central axilla,
Disorder
the apocrine sweat glands, budding glands with the product
nodules of
around
Treat with topical antibiotics before then systemic anti-inflammatory, can
even use steroids. ORAL RETINOIDS USEFUL EARLY
Chronic suppurative cicatrical
disease of the apocrine glandbearing skin
Disorder of the FOLLICLE, not
solely infectous. Can be
associated with severe nodular
acne
Puberty to midlife, females more
likely
Family history of this or nodular
acne important

Hand and exfoliative

dermatitis excessive
washing, can result with
2ndary infection with
Can be acute, subacute, or chronic relapsing skin staph aureus and HSV
Treat with
disorder caused by a genetic defect. Typical onset in
antihistamines,
children before age 5-7
emollients, use
of mild soap,
Water loss due to impaired epidermal barrier.
wet dressing
xerosis (dry skin)
Immune dysregulation (IgE mediated). Allergen
passes epidermis
and binds
to Langerhans
Infantile (0-2)on extensor
surface and rough red and scaly
presents note
to Th2
inflammatory
response
sparing
of the diaper
area
Child and adult groups- Flexor surfaces mainly (Antecubital and
popliteal fossae mainly), and on palms. In adults it is more
localized and lichenified, papules sometimes presesnt as
well
White
dermatog
raphism

Atopic dermatitis
(Eczema)

ITCH

40% spont remission

ATOPIC DERMATITIS

Chronic Inflammatory condition

Genetic Component

Starts around 3 months

Infants- on face and on

Extensor surfaces

Later: Flexor surfaces, neck

Treat with topical steroids

Complicated with Staph or even

HSV infection

Asteatotic (xerotic) eczema

Winter itch

Seen in winter months, in elderly or those with

very dry skin. Development of dry, scaly skin
resulting in erythema,
and dermatitis
fissuring. with
Treatcracks,
like atopic
antihistamines, emollients, use of
mild soap, wet dressing

Nummular exczema
Coin shaped lesions found on trunk and lower
extremities with sparing of the head. Start as
papules, then coalescing into plaques. Rare in
children, common in 60s-70s.

Dyshidrotic Eczema

Recurrent form of Vesicular Palmoplantar

Dermatitis in young adults, atopic dermatitis and
exposure to irritants are presdisposing factors.
Tapioca vesicles on the sides of fingers palms
and soles. Mild form is Red, scaly, weeping and
pruritic vesicles. Severe form occurs as large
bullae on palms and feet Burning pain and
Clinical
diagnosis, treat with topical corticosteroids
intense
pruritis

Contact Dermatitis

Acute or chronic inflammatory reactions to substances

that come in contact with the skin.
Irritant contact Dermatitis is caused by chemical
irritant and occurs in everyone and confined to area
of exposure.
mostand
common
Treat Hands
with topical
systemic GCs, lubricating
creams, abx, wet dressings
Evolution of Lesions Erythema with a dull, nonglistening surface
vesiculation (or blister formation) erosion crusting shedding of
crusts and scaling or (in chemical burn) erythema necrosis
shedding of necrotic tissue ulceration healing
Allergic Contact Dermatitis is defined by haptenspecific Tcell-mediated inflammation caused by an
antigen (re-exposure) that elicits a type IV
hypersensitivity rxn, occuring only in sensitized
individuals, and can spread beyond affected Acute Well-demarcated
erythema and edema with
areas and can Generalize.
nonumbilicated vesicles, and/or
Starts in a sensitized individual 48h-days
papules
after contact with allergen. Repeated
In severe reactions, bullae,
exposure leads to Crescendo reaction.
confluent erosions exuding
Eruption is confined to site. Subjective
serum, and crusts
symptoms are Intense pruritis which can be Subacute Plaques of mild
erythema showing small, dry
severe leading
to
stinging
and
pain
along
with
Nickel sulfate most common in
scales
constitutional
symptoms
Chronic Plaques of
jewelry, also bacitracin

Allergic Phytodermatitis

Poison IVY exposure

Essentially specialized allergic contact

dermatitis specifically for plant allergan
sOccurs in sensitized individuals after
exposure to plant allergens.
Characterized by an acture, VERY
pruritic,
eczematous
dermatitis,
Clinical diagnosis
that resolves
in 1-2in a
linear
weeks. arrangement
Acute: Erythema papules
vesicles erosions crusts
scaling.
Chronic:
Papules with
scaling

Chronic inflammation
thickening,
fissuring, scaling, and crusting results.
lichenification
excoriations
Patch Test- Positive
test showing erythema, papules, and possible vesicles

Treat all allergic contact dermatitis

using class I or II steroids, and
systemic steroids if wide spread

DIAPER DERMATITIS

Most commonly irritant

contact dermatitis.
Due

to mechanical irritation from

diaper material and skin breakdown
from exposure to urine and feces.
Spares skin folds
Treat with Zinc oxide

Second most common is

candidal dermatitis.
Usually

secondary to skin
breakdown from irritant contact
dermatitis. May occur following
antibiotic use.
BEEFY erythema, skin folds
involves with Satellite lesions
Treat with nystatin

45

Differences Between Irritant and Allergic Contact Dermatitis

Symptoms

Acute
Chronic

Lesions

Acute
Chronic

Margination
and site

Acute
Chronic

Evolution

Acute
Chronic

Causative
agents
Incidence

Irritant CD

Allergic CD

Stinging, smarting itching

Itching/pain
Erythema vesicleserosions
crusts scaling
Papules, plaques, fissures,
scaling, crusts

Itching pain
Itching/pain
Erythema papules
vesicleserosions crust scaling

Sharp, strictly confined to

site of exposure
Ill-defined
Rapid (few hours after
exposure)
Months to years of repeated
exposure
Dependent on concentration
of agent and state of skin
barrier; occurs only above
threshold level
May occur in practically
everyone

Papules, plaques, scaling, crusts

Sharp, confined to site of exposure but
spreading in the periphery; usually
tiny papules; may become
generalized
Ill-defined, spreads
Not so rapid (12-72 h after exposure)
Months or longer; exacerbation after
every reexposure
Relatively independent of amount
applied, usually very low
concentrations sufficient but
depends on degree of sensitization
Occurs only in the sensitized

ERYTHEMA TOXICUM NEONATORUM OR ETOX

Self limiting, BENIGN, fairly common. Presents with Erythematous macules
containing eosinophils. And look like Flea Bites. Occurs EVERYWHERE
Red macule white pustule on a erythematous base

No signs of systemic illness, Onset on

the first 4 days ( not present at birth).
Duration for 2-3 weeks, and Treat with
Reassurance

TRANSIENT NEONATAL PUSTULAR MELANOSIS

Self limiting and BENIGN. Pustules with NO ERYTHEMATOUS BASE

(vs. ETOX) rupture leaves hyperpigmented macules NEUTROPHILS
vs. EO (Etox)

Onset: Birth or first

24 hours of life
Duration: 3 wks 3
mo
Tx: reassurance

CUTIS MARMORATA

Benign and transient mottling of the skin when cold that resolves with warmth

Lacy
Possibly exaggerated
vasomotor response
to decreased core
temp.
Blanching mottled or
lacy erythema on
trunk and extremities.
Tx: Reassurance,
rewarming

MILIA
Up to 50% of newborns.
Small 1-2mm superficial
keratin cyst forming
nonconfluent pearly
papules with minimal
surrounding erythema;
typically on face, eyes, nose;
occasionally trunk.
Usually disappear in 2-4
weeks, may have recurrences.
DDx:

Pustular

melanosis, seborrheic
dermatitis.

Tx: Reassurance

MILIA

Epsteins pearl

Penile pearl

MILIARIA
Sweat retention when eccrine
glands partially close sweat
infiltration.
Typically in intertriginous or
occluded areas.
Miliaria crystallina

Stratum corneum collection of swear

Small non-inflammatory
vesicles, that ruptures and
desquamates within days.

Miliaria rubra

Sub-epidermal
Heat rash
Pruritic erythematous macules and
vesicles on warm skin.

Tx: Reassurance; avoid occlusion;

cool environment

ACNE NEONATORUM
Acneiform eruption (comedones,
papules, pustules) on forehead,
cheeks, and nose in newborns and
infants.
Pearly papules with surrounding
erythema.

Unlike

milia

Possibly due to heightened sensitivity

of skin due to maternal hormones.
Peaks around 2 months. Wanes with
maternal hormones around 3-4
months.

DDx: other common neonatal skin

findings, infection,
hyperandrogenism.
Tx: Reassurance.

MONGOLIAN SPOT
AKA Congenital Dermal
Melanocytosis
Large benign bluishgray/black pigmented
nevus of lower back,
buttocks, thighs.
More common in darker skin
individuals.
Most start to fade by 2
years old and many
completely disappear
between 7 and 12 years.
DDx: ecchymosis, nonaccidental trauma
Tx: Reassurance, good
documentation to
differentiate from bruise.

Melanocytes fail to distribute properly

Intro

Neonatal
Rashes

Vascular
Lesions

Eczemato
id

Eruption
s

squamou
s
Disorder
s

Infectiou
s
Disorder
s

VASCULAR LESIONS

Infestation
s

sensitivi
ty

Syndrome
s

HEMANGIOMAS
Vascular tumor of proliferating
immature capillaries
Not usually present at birth
Note the distribution
Start as a red macule then
Reddish-purple raised nodule
on skin Expand during first
one to two years, then involute

50% by 5 years
90% by 9 years

BEARD DISTRIBUTION BAD

casue can obstruct airway
Tx:
Observation usual treatment of
choice
Systemic propranolol for severe
Steroids (topical, systemic,
intralesional)
Pulse-dye laser
Surgery

CAPILLARY MALFORMATION
Nevus Flammeus
AKA Port Wine stain
Collection of dilated
mature capillaries
Present at birth, some
persist throughout life
Pink to purple macular
lesion
May darken when child
cries
Do not regress
Associations:

Sturge Weber Syndrome

Klippel Trenaunay Weber

Tx: observation; pulsed

dye laser

CAPILLARY MALFORMATION
Nevus Simplex

AKA stork bite/angels

kiss, salmon patches
Present in some form in
almost all newborns
Present at birth, most
resolve by 18 months of
age
May darken when child
cries
Tx: observation

Intro

Neonatal
Rashes

Vascular
Lesions

Eczemato
id

Eruption
s

Papulosquamou
s
Disorder
s

Infectiou
s
Disorder
s

PAPULOSQUAMOUS
DISORDERS

Infestation
s

sensitivi
ty

Syndrome
s

PITYRIASIS ROSEA
Characteristic Herald
Patch followed by
patches in a Christmas
Tree distribution
Possible viral etiology
May have pruritus

Topical

steroids

Self resolves

ICHTHYOSIS

Congenital disorders of
keratinization leading to dry
scaly skin
Ichthyosis vulgaris

Most common
Autosomal dominant
Onset in early childhood

(normal at birth)
Dry, rough scaly skin by age 5
Improve with age

Sex linked Ichthyosis

X-linked recessive
Onset at or around birth
Dirty brown scales
Same or worse with age

Neonatal
Rashes

Intro

Vascular
Lesions

Eczemato
id

Eruption
s

ICHTHYOSIS

Lamellar Ichthyosis

Autosomal recessive
Onset at birth

Collodion membrane
Shed with emollients to
scales

Diffuse thick hyperpigmented

plate-like scales

Harlequin Ichthyosis

More severe
High mortality late,
ectropion, ex- labian

Papulosquamou
s
Disorder
s

Infectiou
s
Disorder
s

Infestation
s

sensitivi
ty

Syndrome
s

Neonatal
Rashes

Intro

Vascular
Lesions

Eczemato
id

Eruption
s

squamou
s
Disorder
s

Infectiou
s
Disorder
s

Infestation
s

STAPH SCALDED SKIN SYNDROME

Epidermolytic toxin
produced by Staph aureus
Usually in children <5 years
age
Fever
Perioral and periorbital
crusting
Generalized tender erythema
Fragile bullae with
superficial desquamation
initially

Nikolsky sign desquamation

with traction of skin/bullae

Rx:

IV antibiotics
Replace fluids/electrolytes

sensitivi
ty

Syndrome
s

Intro

Neonatal
Rashes

Vascular
Lesions

Eczemato
id

Eruption
s

squamou
s
Disorder
s

Infectiou
s
Disorder
s

MOLLUSCUM CONTAGIOSUM
Caused by a pox virus
(molluscum contagiosum)
Flesh colored to pink
dome-shaped
umbilicated papules
Usually seen ages 3-16
years
Tx:

Observe (usually resolves

in 6-18 months)
Destructive techniques

Infestation
s

sensitivi
ty

Syndrome
s

Intro

Neonatal
Rashes

Vascular
Lesions

Eczemato
id

Eruption
s

squamou
s
Disorder
s

INFESTATIONS

Infectiou
s
Disorder
s

Infestation
s

sensitivi
ty

Syndrome
s

Intro

Neonatal
Rashes

Vascular
Lesions

Eczemato
id

Eruption
s

SCABIES

Caused by Sarcoptes scabiei

mite
Highly contagious
Extremely pruritic
erythematous papules or scaly
linear burrows in web spaces,
groin, buttocks, axillae, arms, or
trunk
Diagnosed clinically or with skin
scrapings looking for mites,
eggs, or feces
Tx: permethrin 5% cream for all
household contacts, and
cleaning of all clothing and
linens.

squamou
s
Disorder
s

Infectiou
s
Disorder
s

Infestation
s

sensitivi
ty

Syndrome
s

Intro

Neonatal
Rashes

Vascular
Lesions

Eczemato
id

Eruption
s

LICE (PEDICULOSIS)

Arthropods that infest the hair of the

scalp (capitis), body (corporis), and
pubic area (pubis).
Attach to skin, feed on blood, lay eggs
(nits) on hair shaft.
Rarely, can be disease vectors (epidemic
typhus, relapsing fever) not head lice.
Lice infestation is contagious (direct
contact).
May have intense itching, may see
nits or lice. Diagnosis may require
repeated examinations.
Treatment: Permethrin 1% (lower
dose); Malathion for resistant
infestations. Repeat treatment in one
week. Nit comb.

squamou
s
Disorder
s

Infectiou
s
Disorder
s

Infestation
s

sensitivi
ty

Syndrome
s

Neonatal
Rashes

Intro

Vascular
Lesions

Eczemato
id

squamou
s
Disorder
s

PINWORMS (ENTEROBIUS
VERMICULARIS)

Most common helminth in

US.
Usually ages 4-14 yrs; fecal-oral
transmission of eggs.

Larvae hatch in duodenum, live in

ascending colon; females migrate
to perineum at night to lay eggs.
Presents with perianal,
perineal, or vaginal irritation
and intense pruritis, worst at
night.

DDx:

Eruption
s

scabies, perianal strep, diaper

dermatitis, sexual abuse

Diagnostic test: scotch tape test

Tx: single dose of
albendazole, may repeat in 2
weeks. Treat household
contacts, clean linens.

Infectiou
s
Disorder
s

Infestation
s

sensitivi
ty

Syndrome
s

Intro

Neonatal
Rashes

Vascular
Lesions

Eczemato
id

Eruption
s

squamou
s
Disorder
s

Infectiou
s
Disorder
s

HYPERSENSITIVITY
SYNDROMES

Infestation
s

Hypersensitivi
ty

Syndrome
s

ERYTHEMA MULTIFORME

Erythema multiforme
minor
Usually associated with
infection (possibly
medications)HSV, EBV,
mycoplasma
Fixed, typically nonpruritic annular red
macules, papules, and
plaques symmetrically on
trunk, extensor surfaces of
arms and legs, palms and
soles
Tx: supportive, treat
underlying infection

STEVENS JOHNSON SYNDROME

Erythema multiforme major

Usually associated with
medications (possibly infection)
sulfa, NSAIDs, anticonvulsants
Similar to EM but also
vesiculobullous and involve 2
or more mucous membranes;
often a more protracted and
severe course than EM
High mortality rate
Tx: supportive; remove
offending agent

Definitions
Exanthem:

A skin eruption (rash)

occurring as a symptom of a general
disease
Comes from the Greek "exanthema"

which means "a breaking out"

Enanthem:

Eruptive lesions on the

mucous membranes occurring as a
symptom of a general disease
71

Major viral infections of childhood

Paramyxoviruses Enveloped RNA viruses.

measles (rubeola)
mumps (covered in GI Viral Infections lecture)
croup (covered in Viral Respiratory Infections lecture)
RSV (covered in Viral Respiratory Infections lecture)
metapneumovirus (covered in Viral Respiratory Infections lecture)

Togaviruses Enveloped RNA viruses.

rubella (German measles)
Parvoviruses Non-enveloped ssDNA viruses
parvovirus B19 (erythema infectiosum, slapped cheek or fifth disease)
Picornaviruses Non-enveloped RNA viruses.
Coxsackievirus A (hand-foot-mouth disease)
Herpesviruses Enveloped DNA viruses
HHV-6 (roseola)
chicken pox (covered in Viral Skin Infections lecture)
72

Classic Childhood
Exanthems
1. Measles
2. Scarlet fever *
3. Rubella (German measles)
4. Atypical scarlet fever*
5. Erythema Infectiosum
6. Roseola
(These were identified from what was once called measles)
* Streptococcal bacterial infectious diseases, the others listed are viral
There are MANY other exanthematous diseases of childhood do not
limit your differential to these classic childhood exanthems
Enterovirus

exanthems - Coxsackievirus, Mycoplasma pneumoniae exanthems,

Meningococcal dx, Variola (Smallpox), Mononucleosis, Rickettsial diseases,
Asymmetric periflexural exanthem of childhood, Gianotti-Crosti syndrome, Papularpurpuric gloves and socks syndrome, Pityriasis rosea, etc.
73

Other Conditions to Consider When Presented

with Generalized Erythematous/Purpuric Rashes

Kawasaki Disease or other rheumatic

diseases
Erythema Multiforme
Urticaria
Drug reactions
Henoch- Schonlein purpura
Other

74

Diagnosis of
Exanthems

Appearance of rash alone is often not specific

enough to make the diagnosis
Detailed history and physical, selected lab tests
Rash history:When did it start?
Where did it start?
How
has it changed?
Itchy? Painful?
Any treatment tried?
Associated symptoms?
Fever, cough, coryza, conjunctivitis, joint pain or swelling,

diarrhea, etc

Immunization history, travel history, ill contacts,

tick or other bites, pets, medications, etc
75

Measles- KOPLIK SPOTS

Potent global pathogen; infects 20 million

people worldwide annually, with 164,000 deaths in
2008. Measles is still endemic in many countries and
unvaccinated travelers may introduce the disease and
spread the infection before it is recognized.
Spread by contact with an infected person, through
coughing and sneezing.
Causes an acute generalized infection; virus infects
multiple organ systems and targets epithelial,
reticuloendothelial and white blood cells.
76

Measles: pathogenesis
Has one of the highest attack rates among all viruses.
Virus remains active and contagious in the air or on infected surfaces for up to 2
hours
Virus is shed during prodromal and acute phases (up to 4 days before and 4
days after rash).

77

Measles-pathogenesis-II

Despite generating an efficient immune response, measles virus

causes a transient, profound immunosuppression during

and after infection.
Immunosuppression is marked by CD4 and CD8
lymphopenia (cause still unknown). May result in false-negative
PPD test for TB, and poor vaccine responses
Measles-induced immunosuppression increases susceptibility to
secondary bacterial and viral pneumonia and diarrhea, leading to
increases in measles-related morbidity and mortality.

Treatment of measles is supportive (fluids and

antipyretics) .

78

Measles Prodrome

Fever 4 days
3 Cs
Cough
Coryza
Conjunctivitis
Photosensitivity
Koplik Spots
Pathognomonic

79

Measles Prodrome
Koplik Spots =
small, white spots
(often on a reddened
background) that
occur on the buccal
mucosa =
diagnostic &
pathognomonic

80

Measles
Exanthem
Brightly

erythematous
macules and papules
that become confluent
as rash progresses
Typically begins at the
hairline and spreads
caudally
Lasts 4-7 days and then
fades from the head
downward

81

Measles

Fever and other

prodromal symptoms
begin to resolve after 3
days of rash

Resolution of rash may

be accompanied by a
fine desquamation
cephalad to caudad

82

Diagnostic Criteria for

Measles
Clinical case definition
Illness with generalized exanthem of at least 3
days
Temperature of >38.3C (101 F)
Cough, coryza, or conjunctivitis
and

Epidemiologic link to a serologically confirmed

case

Or any of the following

Isolation of measles virus from a clinical
specimen
Positive serologic test for measles IgM antibody
A fourfold increase in acute to convalescent

83

Differential Diagnosis of
Measles
Rubella
Roseola
Scarlet fever
Kawasaki disease
Erythema infectiosum
Secondary syphilis
Sensitivity reactions (erythema
multiforme, drug reactions)
Rocky mountain spotted fever

84

Measles-Intervention
Treatment
Supportive care/Treat complications
Vitamin A supplements have been shown to
decrease mortality by 50%

Malnourished, Hospitalized, Immunocompromised, Evidence of

vitamin A deficiency

Isolation
Inform Health Department

Prevention
Droplet & contact precautions
Measles immunization (available within the
attenuated MMR vaccine). Live vaccine along
with Vericella In 2011, there were 17 measles outbreaks with
222 confirmed cases were reported in the US, the highest number
since 1996.

85

Complications of measles
Hospitalization: 30%
Young children (<5 yrs) and adults >20)

Death: 1-3/1000 cases

Encephalitis (leading cause of death in adults): ~1/1000
cases
Can have residual neurologic deficit or blindness
High mortality rate (25-50%)
Pneumonia: ~6% of children & 5-30% of adults
Diarrhea: ~8% of cases
Otitis media: 7-9% of pts
Higher risk of premature labor, lower birth weights, and

86

Rubella- FORCHHEIMER SPOTS

A mild disease of children, but dangerous to the fetus

during an intrauterine infection [TORCH infections].
Historically affected mostly children <10 yrs. About 25-50% of
infections are asymptomatic.
Rubella has been eliminated in the US, but is still endemic in
many parts of the world.
Spread similar to measles. Virus replicates in the oropharynx,
then local lymph nodes, then spreads systemically via the blood.
Incubation period:14-21days. Virus is shed from 1 week before to 2
wks after the onset of the rash.
87

Rubella-II

Causes a lacy, maculopapular, erythematous rash, lasting 35 days. Adolescents and adults are more likely to be symptomatic
and have fever.
Lymphadenopathy is prominent, esp. above the neck; may
last for a few weeks.
The most common complications in post-pubertal women
(50-70% of pts) are arthropathies of the fingers, wrists, and
knees that persist for up to a month [one of the few viral
arthritides, along with parvovirus B19 and chickungunya]. Rash and
arthropathy are probably immune-complex mediated
Encephalitis occurs in 1/5000-10000 cases, is usually mild, and
followed by complete recovery.
88

Rubella (German Measles)

Prodrome

Malaise
Fever slight or absent
Lymphadenopathy
(highly variable and
not specific)
Tender enlargement of

retroauricular, posterior
cervical, and
postoccipital nodes

Forchheimer spots
(pinpoint red macules
on soft palate)
Mild inflammation
of pharynx and
conjunctiva
89

Rubella: Exanthem
Erythematous,

maculopapular rash
Begins on face (Measles
begins at hairline) and moves
caudad
Whole body covered by 24
hours, confluent
Usually disappearing by day 3
AKA three day measles
Arthropathies of fingers,
wrists and knees common in
post-pubertal women (50%)
90

Rubella

Forscheimer Spots note

these are red vs. the
while spots of measles

91

Congenital Rubella Syndrome

Birth defects if acquired by a pregnant woman
Cardiac defects
Intrauterine
Hepatosplenomega
growth
ly
restriction
Bone
Microcephaly
radiolucencies
Meningoencepha
Thrombocytopenia
litis
with purpura
Cataracts
Dermal
Retinopathy
erythropoiesis
Hearing loss
Up to 85% of infants born to mothers
(Blueberry
who had rubella
during theirMuffin
first 11
weeks of Baby)
pregnancy develop
congenital rubella syndrome

100,000 cases worldwide

92

Congenital Rubella

93

Rubella: Diagnosis
Clinical
NP

swab (or blood, urine, of CSF)

for culture
Acute and convalescent sera for
antibody titers
IgM rubella specific antibody

94

Rubella: Intervention
Treatment
Supportive care
Isolation
Report to health department

Prevention
Droplet & contact precautions
Rubella vaccine (contained in MMR vaccine) -

Vaccine should NOT be given to pregnant

women
Testing of all pregnant women for immunity
Immediate post delivery vaccination for the nonimmune
95

ToRCHeS
Infections

thatcross the placenta

Toxoplasma gondii
O = other = HIV
Rubella
Cytomegalovirus (CMV)
Herpes simplex virus (HSV)
HSV-2 is more common, although HSV-1 is
also possible
Syphilis
96

Parvovirus B19 and erythema infectiosum

Spread primarily via aerosolized respiratory droplets. Also

occurs through blood products and vertical transmission,
from mother to fetus
Infection is most common in school-age children (5-15 yrs).
~60-65% of population is infected by age 40.
Outbreaks

occur in late winter and early spring.

Has an incubation period of 4-14 days

Virus infects erythroid precursors, and pts may have

slight decrease in hemoglobin levels.

Most infections are asymptomatic or give mild, nonspecific, cold-like

symptoms.
97

Erythema Infectiosum
Exanthem

Mild prodrome:
HA, coryza, low-grade fever, pharyngitis, and malaise

Within 7 days:
Characteristic brightly erythematous maculopapular rash
(slapped cheek disease) over the cheeks

19 year old parvati slapping shiva on the cheeks and wearing a lacy dress

Marked by nasal, perioral, and periorbital sparing

Can look like a sunburn
Typically fades over 2-4 days

1-4 days later erythematous macular-to-morbilliform

eruption occurs primarily on the extremities
Fades into a lacy pattern
May be the only manifestation of the disease
Lasts 3 days 3 weeks

May recur for weeks (sun, exercise, hot water, etc)

98

Parvovirus B19 infections in adults

60% of adults may have arthralgia
Middle-aged women and adolescents
May be the only clinical manifestation of infection
Both rash and arthralgia appear to be immune-complex mediated
Arthropathy resolves in a few weeks
B19 infection has been associated with gloves and socks syndrome:
Papular, purpuric eruptions manifesting as a painful rash and swelling in
the hands and feet

99

Parvovirus B19:
severe outcomes
Severe outcomes may occur in three groups of patients:
Pts with chronic anemias (i.e., sickle cell), may develop
severe but self-limiting anemia (transient aplastic crisis).
In immunosuppressed pts or in infants <1-year-old, persistent B19
infection can develop and cause a serious prolonged chronic anemia
owing to persistent lysis of RBC precursors.
Fetuses are at risk (~1.5-2.5%) for severe anemia, generalized edema
and possible myocarditis, leading to congestive cardiac
failure (hydrops fetalis), and fetal death if a
seronegative woman is infected while pregnant.
There is 5-10% risk of fetal loss secondary to B19
infection. Most reported fetal losses have occurred in
the first or second trimesters. B19 is the most
common viral cause of stillbirth.

100

Erythema Infectiosum

101

Erythema Infectiosum:
Intervention

Diagnosis
Clinical
Can do blood work (Specific IgM antibody or
virus by PCR) on exposed pregnant women
Then follow their pregnancy closely with serial US

Treatment
Supportive Care (severe outcomes may require
supportive therapy with blood transfusions until
neutralizing antibody responses can clear the virus and
hematopoiesis is restored)

Prevention
Droplet & contact precautions

102

Roseola
Prodrome and Exanthem
3-5 days of high fever & irritability
Within 24 to 48 hours of defervescence a faint
pink maculopapular rash appears
Typically beginning on the trunk (hairline
is measels, face is rubella, trunk is
roseola & may spread to involve the neck
and extremities
Non-pruritic, blanching
May last for hours to several days
Diagnosis- Clinical

Often have associated transient leukopenia

103

HHV-6 pathogenesis
Caused by two serologic variants of HHV-6 (A and B)
HHV-6A is mostly associated with infection in immunocompromised adults, causing an abrupt onset of symptoms,
with fever, malaise, encephalitis and other organ system
involvement, especially pneumonitis.
Common cause of febrile illness in children, typically < 1 yr
old. Causes febrile seizures in 10-20% of pts (ages 6-24 mos); accounts
for up to 20% of visits to ERs for pediatric febrile illnesses.

Rarely affects healthy adults, in which it causes a mild mono-like

illness.
Transmission is horizontal via saliva of siblings or adult family
members.
Latent infection and replication occurs in T cells and monocytes.

104

Roseola: Intervention

Treatment
Supportive care (unless pt is a stem cell transplant
recipient; foscarnet and ganciclovir are used prophylactically in
these).

Prevention
Difficult; No vaccine
Droplet and contact precautions during febrile

phase

105

Varicella
Prodrome and Exanthem
Typically

affects unvaccinated children ages 1-6 yrs

Prodrome
Incubation period ~10-14 days
Low grade fever, malaise, abdominal pain, pruritis, cough,

coryza, sore throat

Exanthem
Each lesion starts as an erythematous macule and passes

through stages of papule, vesicle, pustule, and crust

Lesions appear in crops
Hallmark is the presence of lesions in various stages
Dew drop on a rose petal
Lesions usually crust by 6 days, completely heal by 16 days
Usually start on trunk and spreads to face & extremities
106

Varicella

Diagnosis = clinical
Transmission
Primarily by airborne droplets
Infectious period begins 2 days before
skin lesions appear and ends when
the lesions crust
No longer considered contagious when

107

Varicella

Treatment
Supportive care/treat
complications
Manage pruritis!
Prevention
Droplet & contact
precautions
Varicella vaccine

108

Complications of Varicella
Secondary bacterial infections of
the skin
Remember:
Pneumonia
reactivation
Encephalitis
infections later in
Cerebellar ataxia
life can manifest
Transverse myelitis
as herpes zoster
or post-herpetic
Otitis media
neuralgia
Death
Inutero infection:

Congential Varicella - intrauterine growth

retardation, microcephaly, cortical atrophy, limb

hypoplasia, microphthalmia, cataracts, chorioretinitis,
and cutaneous scarring

109

Hand-foot-mouth disease
A common acute illness, affecting mostly children.
Most commonly caused by Coxsackie A group viruses.
Spread by direct contact, via respiratory droplets. Most contagious
during first week of illness. Pts can continue to shed virus weeks after
symptoms resolve. Asymptomatic carriers can shed virus as well

Characterized by mild fever, anorexia, malaise, and tender

vesicular lesions first appearing on the hard palate, tongue,
and buccal mucosa and 1-2 days later, progresses to small,
tender cutaneous lesions on the hands, feet or buttocks.
Disease is mild and resolves in a week
Systemic appearance contrasts with herpangina, which affects
mouth only.
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Hand, Foot, and Mouth Disease

111

Hand, Foot & Mouth

Disease:
Intervention
Diagnosis

usually clinical

Treatment
Supportive care (complications are extremely rare
meningitis/encephalitis)

Magic Mouthwash (Keep pt Hydrated!)

Prevention
Droplet & contact precautions
No vaccine
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Shubrook Metabolic
Diseases

Diabetes Mellitus type 1

Vitiligo- areas lacking melanin, patches of white skin

Necrobiosis lipoidica- collagen degeneration with

granulomatous response. Common in T1D but not
exclusice

Limited joint mobility/ Diabetic Cheiropathy

Tendon shorting due to gycosylation

Prayer Sign

Aquired performating dermatitis- prurits papules usually

found on the limbs, but can move
Scleroderma Dibeticorum- Conntective tissue disorder
caused by poor metabolic control

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Diabetes type 2

Diabetes Mellitus type 2

Acanthosis nigricans

Acrochordans

Common for sever insulin resistence, thickening of

the skin

Skin tags

Diabetic dermopathy- trauma leading to

thicking of the skin and is chronic and
permanent, treatment is observation

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Hashimotos Thyroiditis

Hashimotos Thryoiditis
Myxedema

Gained substantial weight and face and entire body

because buffy, Treat hypothyroidism and it goes
away

Loss of eyebrows

loss of lateral third of the eyebrow

115

Graves disease

Graves
Proptosis of the lid
Get treatmetn for the thyroid and cen go
away

116

Hyperlipidemia
syndromes

Hyperlipidemia syndromes
Xanthlamas

Eruptive xanthomas

Associated with lack of metabolic control leading to

a popcorn rash

Tendinous xanthomas

Lipid deposits on eyelids that dont go away, can be

genetic hyperlidemia

Classic for genetically based hyperlipidemia

Arcus Senilis

117

Addisons Disease

Addisons Disease
Hyperpigmentation of skin on sun
exposed areas on joint lines and gums

118

Hyperpigmentation
Post

Inflammatory hyperpigmentation

Result of an infection, irritation, or trauma to the

skin. Arachadoinic acid to LT. more common in

darker skin, and bad in sun exposure
Melasma
Tanning and darkening of skin along cheeks

facial bones and jaw line. Common during

pregnancy, so more likely in women taking birth
control pills, dispears spontaneously over time
Addisons

Disease

Darking on palmar creases, friction points, gums

and lips
Caf

Au Lait spots

Hyper pigmented macules that vary in color

from light to dark brown, can be released to NF1

Variation is a coast of maine border seen in
McCune Albright syndrome
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Hypopigmentation
Vitiligo
Post

inflammatory
Leprosy
Hypestheic as well cause

leprosy attacks the nerves as

well
Pinta
Tinea

Versicolor
Pellagra
Pityriasis Alba
Albinism:
Hereditary inability to

synthesize melanin due to

tyrosine kinase defects
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Skin Cancers
Melanoma
Transformation of the melanocytes

Squamous

cell

Transformation of the most superficial layer of the epidermis

Basal

cell

Transformation of the basal cells originating from the hair follicles

121

Basal cell
Slow

growing waxy bump on skin

Pearly, Smooth, Rolled edge,
Ulcerate, on Sunexposed areas
Clasically raised
Locally destructive but rarely
metastize

122

Squamous cell
carcinoma
Either

Well or poorly
differentiated types
Metasitize
Poorly Differentiated
Fleshy, Granulomatous,

Ulcerated with everted

edge, Surrounding
erythema
Well

Differentiated

Hyperkeratosis, firm and

hard, looks like a

keratoacanthoma
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Melanoma
Most

serious of
skin cancers
Acral Melanomas
Seen in dark skin
Fall in distal

aspect of the
limbs
Most on on the
plantar surface,
NON SUN
EXPOSED AREA
124