PRIMARY LESIONS:

LALALA-LALA

original skin lesions; unaltered by any factors

FLAT LESIONS
1.

MACULE

2.

PATCH

Flat discoloration
< 1 cm
Larger (> 1cm) macule
Ex. vitiligo, nevus flammeus

Elevated, circumscribed, solid

No visible fluid
< 1cm in size
May appear white (milia), red (eczema), yellowish
(xanthoma), black (melanoma)
Usually found in the dermis
o Opening of sweat ducts
o Root of hair follicles
If associated w/ scales: papulosquamous
May last for a year
Papules that are equidistant: follicular papules (ma y also see
hair sticking out)
Broad papule or confluence of papules
>1cm
Center may be depressed or may have normal skin
May also be centrally depressed

ELEVATED SUPERFICIAL
3.

PAPULE

4.

PLAQUE

ELEVATED DEEP
5.

NODULE

6.

TUMOR

7.

WHEALS (HIVES)

Large papule (>1cm)

Deep on palpation (centered in dermis and subcutaneous fat)
Soft/firm, fixed/movable, elevated/deep/pedunculated
(fibromas)
Usually >2cm
Usually round
Plateau like, edematous elevations
Evanescent (do not last > 1 day)
Associated with angioedema
May be pink to red, surrounded by a flare of macular
erythema
May be discrete/coalesce
Prototype lesion of urticaria
Dermatographism or pressure induced whealing may be
seen

LALALA-LALA
FLUID CONTAINING
8.

VESICLES (BLISTERS) superficial

9.

BULLAE superficial/deep

10. PUSTULES

Circumscribed, fluid containing

Epidermal
May contain serous fluid or blood mixed with serum
Apex may be rounded, acuminate, or umbilicated
< 1cm size (usually 1 10mm)
May arise directly from macule/papule and may develop into
bullae or pustules
When vesicles rupture, it may form an erosion.
Findings
o Umbilicated: eczema herpeticum
o Grouped: herpes zoster
o Linear: allergic contact dermatitis from uroshiol
(poison ivy)
If with seropurulent contents -> vesicopustules
May consist of a single cavity (unilocular) or multiple
compartments (multilocular) containing fluid
>1cm
Round/irregularly shaped blisters containing
serous/seropurulent fluid
Usually unilocular
If superficial (epidermal), it may have thin walls = prone to
rupture
o Remnants of the thin wall may form a crust
If subepidermal, usually tense; ulceration & scarring may
result
Nikolskys sign: diagnostic maneuver of putting lateral
pressure on unblistered skin in a bullous eruption & having
the epithelium sheared off
Asboe Hansens sign: extension of a blister to adjacent
unblisteredskin when pressure is put on top of the blister
Hemorrhagic bullae may be seen in : pemphigus, herpes
zoster, severe bullous drug reactions, lichen sclerosus et
atrophicus
Small elevations of the skin which contain pus (necrotic
inflammatory cells)
May see neutrophils
With inflammatory areola
Usually white or yellow centrally (may be red if with blood)
May originate as pustules or papules or vesicles (may
represent a transitory early stage papulopustules or
vesicopustules)

Ex. acne

LALALA-LALA
SECONDARY LESIONS:
1.

altered by external factors (ex. scratching); modified by evolution, regression, trauma or other external factors

SCALES (exfoliation)

2.

CRUSTS/SCABS

3.

EXCORIATIONS & ABRASIONS

4.

FISSURES (CRACKS/CLEFTS)

Implies a pathologic process in epidermis

Parakeratosis (persistence of nuclei in keratinocytes in
stratum corneum of skin) often present
Dry, greasy, laminated masses of keratin
We normally shed little amounts of stratum corneum
Occurs due to:
o Rapid epidermal cell formation
o Interruption in the normal process of keratinization

Fine & branny or powdery: Tinea versicolor

Coarser: eczema, ichthyosis
Stratified: scalded skin syndrome & infection
associated desquamations (scarlet fever)
Silvery squames (due to trapping of air between
layers): psoriasis described as plaque with thick
scales

Dried serum, pus, ,or blood with epithelial/bacterial debris

When removed, there is erosion/ulcer/wound underneath

Dry, superficial, golden yellow: impetigo

Hard and tough: third degree burns
Elevated brown/black/green masses: late
syphilis (oyster shell crusts: rupia)

Excoriations
Punctate/linear abrasions
Superficial (usually only involves epidermis but may reach
papillary dermis)
Due to scratching with fingernails in an effort to reduce
itchiness
Inflammatory areola
May allow entry of microorganisms -> may cause crusting,
pustules, cellulitis & enlargement of neighboring lymph
glands
Elevated, long & deep excoriations = severe pruritus
(except lichen planus where there is severe pruritus but rare
excorations)
Abrasions
If due to mechanical trauma or constant friction
Linear cleft in epidermis or dermis following skin lines
Common in skin that is thickened & inelastic from frequent
inflammation & dryness (especially in areas of frequent
movement)
o Ex. tips & flexural creases of thumb, fingers, palms;
edges of heels; clefts between fingers & toes, angles
of mouth, lips, nares, auricles, anus
May be single or multiple
Exposure to cold, wind, water, or cleaning products may
produce a stinging burning sensation = indicates microscopic
fissuring
o Referred to as chapping (chapped lips)
Pain often produced by movement of the parts involved ->
may open, deepen or form new fissures
Painful but NOT bacterial! No need for oral antibiotics. May
apply topical antibiotics or wait it out

LALALA-LALA
5.

EROSIONS

6.

ULCERS

7.

SCARS

Produced by a loss of all or portions of the epidermis alone

Heals without a scar
Rounded or irregularly shaped excavations due to complete
loss of epidermis + some part of the dermis
Heal with scarring
Composed of new connective tissue that replaced the lost
substance in the dermis or deeper parts as a result of
injury/disease, as part of the normal reparative process
Shape & size determined by form of previous destruction
May be diagnostic
o Lichen planus & discoid lupus erythematosus: same
inflammation anatomically but DLE produces
scarring as it resolves while LP rarely does
May be atrophic or fibrotic (keloid)
May also present as discoloration
o True discolorations disappear with time or tx
o Discolorations due to a scar: do not disappear; they
only improve
Scars will have no skin lines & follicular openings making
them appear shiny

**Anything that involves the dermis will leave a scar. Bleeding also indicates that you have reached the dermis.
**Laser: used as a treatment for some skin lesions because it can penetrate up to the dermis without damaging the epidermis
**Things to discuss when describing skin lesions: count, color, size, characteristic configuration, location, surface, elevation, discrete/coalescing

LALALA-LALA
1A & 1B: NAIL LESIONS
SKIN LESION
Dermatophyte
onychomycosis

Description
Yellow discoloration
Nail becomes thick &
brittle due to
keratin
Nail may separate
from nail bed
May involve skin of
the toe & soles
(scaling,
erythematous, well
defined patches may
appear)
Usually starts distally
going proximally
Superficial without
paronychial
inflammation
Chalky white spots on
or in the nail plate that
is easily shaved off

Cause/Precipitating
Factors/Risk
Factors
Fungal infection by a
dermatophyte

Age & Area of

Predilection

Diagnosis
Scrape on top of nail:
do KOH test & look
for long, septate
hyphae

T. rubrum most
cases

If subungual: get
keratin under brittle
nail
REMEMBER: KOH is
not highly reliable
because it has poor
yield since keratin
has to be dissolved to
actually see the
hyphae

T. mentagrophyte

Treatment
Oral:
Itraconazole
Ketoconazole
only give for 10
days for tinea
versicolor due to
hepatotoxicity
Terbinafine
Fluconazole
2 4mos: time
needed to grow
fingernails
4 6 mos: grow
toenails

Pain or swelling in
proximal fold
Pink & tender
Described as a yucky
nail
Gradual thickening &
brownish
discoloration of nail
plates

Onychomycosis is fungal
infection of the nail
Onycholysis is separation
of the nail from the nail bed
3 types:
1. Distal subungual
most common
- usually caused
by T rubrum
2.

Duration of anti
fungal treatment
3.

Asymptomatic in the
nails (reservoir for
infection); Px will
usually complain of
the alipunga than the
changes in the nail

Candida
onychomycosis

Also know this

Candida albicans
Common in
homemakers, and
frequent/prolonged
exposure of hands
to water
Usually seen in DM
px

Fingernails
commonly
affected

See
pseudohyphae/yeasts

Anticandidal
agents + topical
corticosteroid
Avoidance of wet
work & other
irritants
If topical tx fail,
give oral
fluconazole 1x/wk
or itraconazole

White superficial
- leukonychia
trichophytica
- usually due to T
mentagrophytes
- invasion of
toenail plate on
nail surface
Proximal
subungual
- involves nail
plate from
proximal nailfold
- usually due to T
rubrum & T
megninii
- may be an
indication of HIV
infection

Check proximal part first

when treating candida
With paronychia (swelling
of nail fold; pressing on it
makes fluid come out)

Other info

LALALA-LALA
Produces destruction
of the nail & massive
nailbed
hyperkeratosis
**Remember, it is very important to differentiate a dermatophyte type of onychomycosis from a candidal one.
Dermatophyte
onychomycosis
Brittle
No paronychia
Long septate hyphae
SKIN LESION
Psoriatic
onychomycosis

Candida onychomycosis
Not brittle
With paronychia
Pseudohyphae
Description

Pits on the nails

Furrows/transverse
depressions (Beaus
lines)
Nail bed splinter
hemorrhages
Yellowish green
discoloration may
occur in area of
onycholysis
Oil spots (start in the
middle)
Pathology is in the
nail plate

Cause/Precipitating
Factors/Risk
Factors
86.5% of patients
have psoriatic
arthritis

Why is it important to differentiate?

Drug of Choice
Dermatophyte: Terbinafine
Fluconazole & Itraconazole can be used for
both dermatophytes and candida

Age & Area of

Predilection

Diagnosis
Characterized by
pitting of nails +
symptoms of
dermatophyte
onychomycosis
The px usually comes
with psoriatic plaques
in other parts of the
body (ex. scalp)

Treatment
Intralesional
injection of
Triamcinolone
acetonide
suspension, 3 5
mg/ml
Topical 1% 5 F U
solution, MTX,
PUVA,
cyclosporine or
acitretin

Also know this

Features of psoriasis:
1. Distal
onycholysis
2. Brittle
3. Nail pits
4. Oil spots

Other info

LALALA-LALA
2A: ERYTHEMATOUS LESIONS: Non Scaly Papules
SKIN LESION
Miliaria Rubra
(prickly heat,
heat rash)

Description
Discrete, extremely
pruritic,
erythematous
papulovesicles
May also become
confluent

Cause/Precipitating
Factors/Risk Factors
Retention of sweat as
a result of occlusion
of eccrine sweat ducts
and pores
S. epidermidis

Accompanied by
prickling, burning, or
tingling sensation

Scabies

Pruritic papular
lesions, excoriations
& burrows w/c house
the female mite & her
young (burrows appear
as slightly elevated,
grayish, tortuous lines
in the skin)

Vesicle or pustule
containing mite may
be seen at end of
burrow

Sarcoptes scabei (itch

mite, causative
organism)
Close personal
contact, fomites
(clothing, bedsheet)
Immunocompromised,
institutionalized,
malnourished patients

Age & Area of

Predilection
Infants due to
immature eccrine
gland
Antecubital & popliteal
fossae, trunk,
inframmary areas,
abdomen (waistline),
inguinal region ->
areas usually
macerated due to
impedance in the
evaporation of
moisture
Young children
M=F
Circle of Hebra:
axillae, elbow,
flexures, wrists, hands,
crotch
Finger webs
Scalp & face spared
(adults)
Entire cutaneous
surface involved
(infants)

Diagnosis

See mite under

microscope (usually
burrows in stratum
corneum & deposits
eggs here)
Majority of mites
found on hands &
wrists
Less frequently in
(decreasing order):
elbows, genitalia,
buttocks, axillae
India ink or gentian
violet applied to
infested area =
allows identification
of burrows easily

Presentation:
F itching of nipples
M itchy papules on
scrotum & penis

Treatment

Also know this

Other info

Control temperature to
decrease sweating
Good aeration
Anhydrous lanolin
resolves occlusion of
pores
Calamine lotion
Antihistamines
Topical corticosteroids

Non follicular
distribution
No hair is
coming out,
therefore does
not involve hair
follicles

Problem in kids
due to itching
(may present
with bacterial
infection
already)

Permethrin 5% cream
- safest, most effective
(C/I: pregnancy)
- apply neck down
because most lesions are
here
- treat all household
contacts
- repeat after 1 week
(wait for eggs to hatch
again)

Features of scabies:
1. Circle of Hebra
2. Nocturnal itch
3. Contact w/
person at home

May be
mistaken for
Langerhans cell
histiocytosis

6 10% precipitated
sulphur in petrolatum
- safe in pregnancy
- doesnt smell good
Ivermectin not used

2 4 wks after
infection:
sensitization period
Nodular scabies:
Dull red nodules (3
5mm diameter)
appearing during
active scabies,
may/may not itch

Nodular scabies:
Scrotum, penis, or
vulva

For nodular scabies:

Intralesional steroids, tar,
excision

Reinfections may occur

earlier and in more
severe forms

Suspect scabies
if more than 1
famly member
has pruritus
In animal or
zoonotic
scabies,
burrows are
usually absent &
is self limited

LALALA-LALA

Acne Vulgaris

Crusted scabies
(Norwegian or
hyperkeratotic): seen
in
immunocompromised
or debilitated px
Chronic inflammatory
disease of the
pilosebaceous
follicles
Comedo (primary
lesion of acne) non
inflammatory lesion
(ex. blackhead or
open comedo;
whitehead or closed
comedones)
May also present as
papules, pustules,
cysts, nodules, scars
Remember that all
lesions of acne will
ALWAYS have a
plug

Crusted scabies:
Face & scalp,
genitalia, buttocks,
pressure bearing
areas
Propionibacterium
acnes
- metabolize sebum to
free fatty acid ->
cause inflammation of
cyst wall -> rupture
Androgenic
stimulation of
sebaceous gland
External factors:
mechanical trauma,
cosmetics, topical
corticosteroids
Hereditary (keratinous
plug in lower
infundibulum of hair
follicle primary
defect)

Begins at puberty (sign

of increased sex
hormone production)
usually 8 12 y/o
Lesions are
comedonal in
character
Adolescents (15 - 18
y/o) majority of cases
Lesions
become
inflammatory
pustules
Involution of
disease
before 25 y/o
Acne may also begin
at 20 35 y/o in
people who did not
have teenage acne

No pruritus in acne!
Face (most common in
cheeks), neck, upper
trunk, upper arms and
other oily seborrheic
areas

TOPICAL (long term

usage is the rule, and apply
to entire acne affected
area, not just the lesions; 6
8 wks)

Benzoyl peroxide (most

effective for inflammatory
acne)
Topical retinoids
Clindamycin
Erythromycin + benzoyl
peroxide
Sulfur, resorcin, salicylic
acid
Azeleic acid
SYSTEMIC (inhibits
formation of new lesion; for
moderate to severe acne;
usually 3 6 months
duration)

Tetracycline (safest &

cheapest; may cause
staining of teeth if taken
by kids < 9 or 10 y/o)
Minocycline (most
effective oral antibiotic in
treating acne vulgaris)
Doxycycline
Erythromycin
Clindamycin
Sulfonamides
OCPs
Spironolactone
Dexamethasone
Isotretinoin (do not give
in childbearing age due
to teratogenicity)
Indicated for
severe acne that
improves by less
than 50% after 6
mos of therapy
w/ combined

Remember that acne is

one of the follicular
diseases

Keep px disease free for

1 2 mos first, before
decreasing dosage to
prevent flaring

Major advantage: ONLY

acne therapy that is not
open ended (leads to
remission of months or
years)

LALALA-LALA
oral & topical
antibiotics
Give keratolytics to
slough off corneum w/
hopes of removing
comedones
SKIN LESION
PEDICULOSIS
(Phthiriasis)
Pediculosis
Capitis

Description

Intense pruritus of
the scalp w/ posterior
cervical
lymphadenopathy
Affected hair
becomes lustreless &
dry
Visible nits whitish
concretions on the
hair shaft but most
common in the
retroauricular area

Cause/Precipitating
Factors/Risk Factors
Pediculus humanus
var. capitis (head
louse)

Age & Area of

Predilection

Diagnosis

Children (but may also

occur in adults)

Treatment

GOAL: eliminate both lice

& ova
Permethrin (most widely
used pediculicide)
Some
association with
congenital
leukemia in
permethrin
abuse
Pyrethrins + piperonyl
butoxide

Pediculosis
corporis
(pediculosis
vestimenti,
vagabonds
disease)

Generalized itching +
erythematous &
copper colored
macules or urticarial
wheals and
lichenification
See nits on clothing
or beddings
Pediculid reaction

Pediculus humans
var. corporis (body
louse)
Due to body lice that
lay their eggs in the
seams of clothing

Indigent, homeless
individuals
Upper back; no
involvement of hands
& feet

Also know this

Established by
generalized itching
+ parallel linear
scratch marks +
hyperpigmentation +
erythematous
macules
2 6wks:
sensitization period
for first time
infections
Supported by finding
lice in the seams of
clothing or in
beddings

Enzymatic egg remover

(Clear)
Bathe thoroughly with
soap & water
Destruction of lice
Wash bedding &
clothing
Disinfection
(placing clothes
in dryer for 30
mins at 65oC or
ironing them)

Problem: Knockdown
Resistance (common
mechanism of resistance
that manifests as lack of
immobilization of lice

Secondary complications
with impetigo &
furunculosis common
during itching

Body louse infestation is

different from scabies, in
that there is no
involvement of hands &
feet
Body lice vectors for
relapsing fever, trench
fever, epidemic typhus
Secondary impetigo &
furunculosis are common

Other info

LALALA-LALA
SKIN LESION
Pediculosis
pubis (crabs)

Description
Nits are attached to
hairs at an acute
angle
See sky blue
macules (maculae
ceruleae) in side of
trunk and inner
aspects of thighs
(due to altered blood
pigments)

INSECT BITES

Immediate reaction:
inflammatory reaction
at the site of the
punctured skin, to
the insects venom or
saliva containing
histamine, enzymes,
agglutinins,
serotonin, formic
acid, or kinins.
Accompanied by
pruritic local
erythema & edema
Delayed reaction:
hosts immune
response to
proteinaceous
allergens

Bedbug
bites/Cimicosis
(Order
Hemiptera)

Present as pruritic
red papules typically
with a surrounding
swelling & a central
punctum (minute
round spot indicating
an opening)
Several
erythematous
papules or urticarial
lesions grouped
together or in rows
(breakfast, lunch,
dinner)

Cause/Precipitating
Factors/Risk Factors
Phthirus pubis

Age & Area of

Predilection
Adults

Transmission through
sexual intercourse &
close physical
contact; not
infrequently from
bedding

Genital region &

hypogastrium
hairy areas of the legs,
abdomen, chest, arms,
axillae (rare)

Diagnosis
If diagnosed with
crabs, search for
other STDs

Treatment

Also know this

Permethrin
Pyrethrins combined w/
piperonyl butoxide
Enzymatic egg remover
(Clear)
Retreatment in 1 week
recommended

CLASS INSECTA
Order Lepidoptera
(caterpillar, moth)
Order Hemiptera
(bedbug, reduviid
bugs)
Order Anoplura
(louse)
Order Diptera
(mosquito, flies)
Order Coleoptera
(beetles)
Order Hymenoptera
(bees, wasps, ants)
Order Siphonaptera
(fleas)

Cimex lectularius:
most common in
temperate
C hempiterus: tropical
climates
Suspected vectors for
Chagas disease &

a) Pruritus: camphor,
menthol lotions, gel
formulations, topical
anesthetic preparations
b) Persistent bite
reactions: topical
corticosteroid
preparations
c) If topical agents fail,
give intralesional injection
of corticosteroids or
excision of pruritic nodule
Prevention: Protective
clothing & inset repellant

Arms, legs, ace

Diascopic exam
shows hemorrhagic
dot (site of bite) in
the middle of most
lesions

Topical antipruritics or
corticosteroids
Zinc lotion with 2 4%
polidocanol or 1%
methanol
Severe cases: systemic
antihistamines

Recurrent bacterial
infection may be due to
insect bites

Other info

LALALA-LALA
Hepa B

Eliminate bird nests & bat

roosts, cracks & crevices
Treat area with
insecticide (dichlorvos &
permethrin)

Often infest bats &

birds & usually reside
in cracks & crevices
and descend to feed
while victim sleeps

SKIN LESION

Typically painless
Romanas sign:
unilateral eye
swelling after a
nighttime encounter
with Trypanosoma
cruzi (transmitted by
feces & rubbed into
bite)
Description

Mosquito bites
(Order Diptera)

Multiple pruritic often

excoriated papules

Reduviid bites
(Order
Hemiptera)

Bullous reaction
(culicosis bullosa)

Permethrin
impregnated bednets:
effective in tropical
climates

Poor housing
conditions

Exposed areas of skin

Cause/Precipitating
Factors/Risk Factors
Moisture, warmth,
CO2, estrogens, lactic
acid in sweat, drinking
alcohol attract
mosquitos

Age & Area of

Predilection
Exposed areas of the
body; arms & legs

Diagnosis

Antipruritics/corticosteroid
creams
Oral antihistamines
Insect repellatns (diethyl
toluamide)

Large blisters
(pemphigus
hystericus)

Flea
bites/Pulicosis
(Order
Siphonaptera)

Multiple, irregularly
distributed wheals &
papules that are
grouped and may be
arranged in zigzag
lines
Hypersensitive
reactions appear as
nodules or bullae

Treatment

Protective clothing &

mosquito netting
Attack mosquito habitats
(sprays/disposing
stagnant water)

4 species that most

commonly attack
humans:
1. Cat flea
(Ctenocepha
lides felis)
2. Human flea
(pulex
irritans)
3. Dog flea (C
canis)
4. Oriental rat
flea

Legs & covered body

regions (waist)

Diascopic exam:
central hemorrhagic
bite site (purpura
pulicosa)

Topical & systemic

antipruritic treatment;
corticosteroids
Pet grooming :D
Insect repellent

Also know this

Secondary infection
common in children
Mosquito bites are a
common cause of papular
urticaria & may also play
a role in reactivation of
latent EBV infection
Severe local reactions
seen in young children,
immunodeficient
individuals

Other info

LALALA-LALA
(Xenopsylla
cheopis)
Usually present in
houses with cats or
dogs
Ant bites (Order
Hymenoptera)

Painful stings within

seconds of bite
accompanied by
whealing

Any body part

Later: intense pruritic

sterile pustule
develops at the site
with an erythematous
hemorrhagic halo

Bee (Order
Hymenoptera)

Severe cases may

cause anaphylaxis,
seizures,
mononeuropathy
Reaction to venom =
ranges from pain &
mild local edema to
exaggerated
reactions that may
last for days
Serum sickness
(fever, urticaria, joint
pain) occur 7 10
days after sting
Severe anaphylactic
shock and death may
occur w/in minutes of
sting

Ice packs
Oral antihistamines
Topical antipruritics or
corticosteroids
If w/ secondary infection:
antibiotics

Bee venom contains

histamine, mellitin,
hyaluronidase, HMW
substance with acid
phosphatase, &
phospholipase A

Usually exposed areas

For local reactions:

Immediate application of
ice packs or topical
anesthetics
For chronic reactions:
Injection with
Triamcinolone
suspension diluted to
5mg/mL with 2%
lidocaine
For severe reactions:
Oral prednisone
For severe systemic
reactions:
0.3mL of epinephrine IM
Corticosteroids

LALALA-LALA
2B: ERYTHEMATOUS LESIONS: Non Scaly Nodules
SKIN LESION
Furuncle (boil)/
Caruncle

Description
Furuncle
Acute, round, tender,
circumscribed
perifollicular
staphylococcal abscess;
nodular & with central
suppuration
Carbuncle
2 or more confluent
furuncles, w/ separate
heads
Lesions begin in hair
follicles, continue by
autoinoculation (carriers
in nose/groin)
Most will undergo central
necrosis & rupture thru
skin

Cause/Precipitatin
g Factors/Risk
Factors
S aureus
Predisposing
factors:
Disruption of skin
surface integrity
(pressure, irritation,
friction, dermatitis,
shaving, etc)
Systemic disorders
(alcoholism,
malnutrition, blood
dyscrasias,
immunosuppression)
Atopic dermatitis
(predisposes
individual to carrier
state)
Nasal carriers are at
risk for chronic
furunculosis

Age & Area of

Predilection
Nape, axillae,
buttocks (but may
occur anywhere)

Diagnosis

Treatment

Also know this

Warm compress may arrest

early furuncles

Vs. acne: furuncle is extremely

painful

Penicillinase resistant
penicillin or 1st gen
cephalosporin (1 2g/day)
oral!

Furuncle is deep so topical meds

will not work

Bactobran applied to
anterior nares to prevent
recurrence (apply daily for 5
days)
If localized with definite
fluctuation: incision &
drainage
If lesion is in EAC, upper lip
or nose, I & D will only be
done if antibiotics fail
To eradicate carrier state:
1. Daily use of
chlorhexidine wash
2. Rifampin +
Dicloxacillin (10
days)
3. Sulfa TMP for
MRSA (10 days)
4. Low dose
clindamycin (3 mos)

Similarities between erysipelas &

furuncle:
1. + signs of inflammation
2. Painful
3. Acute

DO NOT do I & D if
acutely inflamed, give
moist heat instead.

LALALA-LALA
2C: ERYTHEMATOUS LESIONS: Non Scaly Plaques
SKIN LESION

Description

Fixed Drug
Eruption (FDE)

Begins as a red patch that

soon evolves to an
iris/target lesion (~1cm),
identical to erythema
multiforme & may
eventually blister & erode

Cause/Precipitating
Factors/Risk Factors
Medications taken
intermittently

Age & Area of

Predilection
Young boys

Diagnosis

Treatment
Stop taking
offending drug.

Oral & genital

mucosa (50%)
NSAIDS:
usually lips
Sulfa
TMP:
usually
genital

HLA B22

Known as fixed because

it occurs at the same site
w/ every exposure to
medication

Erythema
Multiforme
(EM)

Target or iris lesions with

3 zones:
1. Central dusky
purpura
2. Elevated,
edematous, pale
ring
3. Surrounding
macular
erythema
Px may present with
conjunctivitis

Features:
1. Normal stratum corneum
2. Chronic changes in
dermis:
a. Papillary fibrosis
b. Pigment
incontinence
3. Eosinophils & neutrophils
4. No anesthesia or
hyposthesia
With first intake of drug:
1. Redness
2. Hyperpigmentation
3. Redness + increasing size
+ pruritus

Usually causes
prolonged/permanent
postinflammatory
hyperpigmentation
A non pigmenting FDE
is usually caused by
Pseudoephedrine HCl
(Baboon syndrome
buttocks, groin, axilla)
Begin as sharply
marginated, erythematous
macules, which become
raised, edematous
papules over 24 48 hrs

Also know this

FDEs may progress to Steven

Johnsons syndrome
Usually associated with
anticonvulsant intake
Herpes simplex
infection (usually
orolabial HSV)
In the Phils: usually
drug induced
HLA DQ3

Young adults
Dorsal hands (initial
involvement), dorsal
feet, extensor limbs,
elbows & knees,
palms & soles (site
of typical iris/target
lesions)

Prevention:
cornerstone of
treatment (if due to
HSV)

Sunblock creams
(may prevent UVB
induced outbreaks)

Antiherpetic
antibiotic (in oral,
chronic, suppressive
doses)
Acyclovir
may prevent
lesions

Prednisone (may
reactivate HSV and
increase frequency
of attacks)

Features:
1. Target/iris lesions
2. Cellular necrosis
3. Basketweave stratum
corneum
4. Mononuclear infiltration
FDE vs. EM
FDE: < 6 lesions
EM: many generalized lesions

For severe erythema multiforme,

give oral steroids.

LALALA-LALA
SKIN LESION
Erysipelas (St.
Anthonys fire or
ignis sacer)

Description
Fiery red swelling with
characteristic raised,
indurated border; onset
usually w/ prodromal sx
Distinctive feature:
advancing edge of patch

Cause/Precipitating
Factors/Risk Factors
Any inflammation of
the skin (esp if
fissured/ulcerative)
may provide entrance
for beta hemolytic
streptococcus

Age & Area of

Predilection
Newborn, postpartum
women

S pyogenes/ S aureus

Leg: Tinea pedis as

mode of entry

PAINFUL!

Cellulitis

Spreads peripherally;
more superficial than
cellulitis
Suppurative inflammation
involving the
subcutaneous tissue

Diagnosis

Treatment
Systemic penicillin
(vigorous tx for 10
days; improvement
seen in 24 48h)

Face (lesion starts in

cheek near nose & in
front of ear lobe)
Legs (more likely to
need hospitalization)
Perineum &
abdomen (in
postpartum women)

Urticaria

May be accompanied by
angioedema
Rarely lasts >12 hrs
Mast cell degranulation =
increased histamine

Exfoliative
Dermatitis
(erythroderma,
pityriasis rubra)

Extensive erythema &

scaling; may ooze a straw
colored exudates
Itching appears w/
systemic toxicity (fever)

Acute tuberculoid leprosy may look

like erysipelas BUT acute
tuberculoid leprosy has no fever,
pain, or leukocytosis.

Erythromycin
Locally: ice bags &
cold compresses

IV penicillinase
resistant penicillins
or 1st gen
cephalosporin (oral!)

Usually follows some

discernible wound

No central suppuration
(Sinong may central
suppuration?
Furuncle/carbuncle )
Ill defined border
indicates deepness
Wheals, white/red
evanescent plaques,
surrounded by a red halo
or flare; pruritic!

Also know this

Erysipelas & cellulitisare both deep

see neutrophils reaching the
dermis w/c is why topical meds
wont work :(
Possible complications:
Gangrene
Metastatic abscess
Sepsis

Drugs (most frequent

cause: Penicillins)
Aspirin may
exacerbate
chronic
urticaria
Food, food additives,
emotional stress,
menthol, neoplasms
(carcinomas,
Hodgkins, CLL),
inhalants, infections
(acute urticaria: strep,
TB; chronic urticaria:
hep B & C)
Possible causes:
1. Generalizatio
n of a pre
existing
chronic
dermatoses
2. Drug

Covered areas:
trunk, buttocks, chest

If individual wheal persists

for > 24 hrs = do skin
biopsy

Antihistamines
Avoidance of the
trigger
For chronic:
antihistamine daily

May present with chills & fever

Features:
1. Mild dermal edema
2. Margination of neutrophils
w/in postcapillary venules
3. No karyorrhexis & fibrin
deposition (compared to
vasculitis)
Acute: < 6wks
Chronic: >6wks

Face & extremities

Topical steroids,
soaks, compresses
Systemic
corticosteroids
Immunosuppresants

Features:
No vesicles or pustules
Course of disease may be
protracted, last years, or may
persist & resist therapy

LALALA-LALA

SKIN LESION
Hansens
Disease
(Leprosy)

Description
Important feature:
Neurotropism

eruptions
3. Idiopathic
Predisposing Factors:
Psoriasis, eczema,
drug allergy, other
dermatoses
Cause/Precipitating
Factors/Risk Factors
Mycobacterium leprae
Weakly acid
fast
Grows best
(30oC)
Intracellular

Age & Area of

Predilection
2 peaks of
presentation:
1. Children 10
20 yrs
2. Adults 30
60 yrs
Areas of predilection:
Cooler areas of the
body (spares scalp &
midline)

Diagnosis
Early diagnosis is
essential!

Dapsone
(cornerstone of tx)

Lepromin skin test (to

determine type of leprosy)
Multibacillary (if
+ organisms on
skin smear)
Paucibacillary (if
skin smear is (-)
or px has < 5
lesions)

Dapsone + Rifampin

PGL 1 (for pure neural

leprosy)

Early &
Indeterminate
Leprosy
(indeterminate
because course of
disease cannot be
predicted yet)

First lesion: solitary, ill

defined hypopigmented
patch w/ slight anesthesia

Cheeks, upper arms,

thigh, buttocks

Treatment

Clofazimine (side
effect: skin
discoloration)
Compared to TB tx
regimens, meds are
given once a month
for leprosy.

Usually no/few bacilli

Also know this

Before starting tx, do a CBC
because Dapsone may
cause hemolytic anemia

Do liver function tests &

chest xray (check for TB)

Leper reaction:
Upon starting tx, px may experience
the ff:
Fever
Joint pains
Nerve damage due to
inflammation of nerve
Skin becomes swollen &
erythematous
New lesions appear
Management of leper reaction:
Prednisone
Peripheral nerves not enlarged
No plaques/nodules
Few cases stay in this state; most
will become lepromatous,
borderline, or tuberculoid. Some
may spontaneously resolve.

90% initially present with

numbness (cutaneous
findings may appear years
later)
Loss of cold & light touch
earliest sensory
changes (usually
feet/hands)

SKIN LESION

Description

Cause/Precipitating
Factors/Risk Factors

Age & Area of

Predilection

Diagnosis

Treatment

Also know this

LALALA-LALA
Tuberculoid
Leprosy (TT)

Typical lesion: large,

erythematous plaque w/ a
sharply defined & elevated
border that slopes down to
a flattened atrophic center
(saucer right side up)

Face, limbs, trunk

High chance for

spontaneous cure
over the years

Lesions are solitary or few

in number (< 5) because
cell mediated immunity
is high
Paucibacillary

Borderline
Tuberculoid
Leprosy (BT)

Borderline
Leprosy (BB)

Nerve involvement is early

& permanent (may cause
muscle atrophy)
Lesions similar to
tuberculoid lesions except
they are smaller & more
numerous
Satellite lesions around
large macules/plaques
Lesions numerous but
countable, red irregularly
shaped plaques

Features:
1. Presence of palpable
induration & neurologic
findings differentiates
indeterminate from
tuberculoid lesions
2. Lesions are
anesthetic/hypesthetic,
anhidrotic.
3. Superficial peripheral
nerves serving/proximal to
lesion = enlarged/tender
(visible in greater auricular
nerve & superficial
peroneal nerve)

Moderate anesthesia in lesions

Nerves may be enlarged or
thickened

Generalized lesions but

asymmetrical

Borderline
Lepromatous
Leprosy (BL)

SKIN LESION
Lepromatous
Leprosy

Borders not so well

defined compared to
tuberculoid
Lesions symmetrical, too
numerous to count, may
include macules, papules,
plaques, nodules
Description
Lesions: may appear as
1)pale lepromatous
macules or 2) infiltrations
with numerous bacilli in
lesions

Small lepromatous lesions more

than borderline type lesions

Cause/Precipitating
Factors/Risk Factors

Age & Area of

Predilection

Diagnosis

Treatment
May become
progressively worse
w/o treatment

Nerve involvement later

Sensation & sweating over lesions
is normal
Also know this
Clues to leprosy:
1. Permanent anesthesia
doesnt disappear with
treatment
2. Nerve involvement &
clawing appear late in the

LALALA-LALA
Lepromatous macules
Symmetrical & diffusely
distributed over the body
Small & numerous
Ill defined, blend into
surrounding skin
Little or no loss of
sensation, no nerve
thickening, no sweating

Present with loss of hair in

eyebrows (madarosis) ->
eyelashes -> body (scalp
hair spared)

Misdiagnosed as diabetic

Lepromatous
neuropathy
infiltrations
3 types: diffuse, plaque,
nodular
**Diffuse diffuse
infiltration of face,
madarosis, waxy/shiny
appearance of skin
May manifest as lepromas
(ill defined nodules
occurring in acral parts:
ears, brows, nose, chin,
elbows, hands, buttocks,
knees)
Nerve disease is bilateral
& symmetrical (stocking
glove pattern)

3.

4.

disease
Anesthesia on a lesion
leprosy is the only
dermatologic disease that
will cause this
Hypopigmented patches in
kids early sign!

LALALA-LALA
2D: ERYTHEMATOUS LESIONS: Non Scaly Patch
SKIN LESION
Phototoxic
Dermatitis

Description
Exaggerated sunburn
reaction: erythema, edema,
vesicles, bullae, burning,
stinging
Frequently resolves with
hyperpigmentation
Mechanism: Direct tissue
injury

Photoallergic
Dermatitis

Rash
Usually eczematous
lesions & pruritic
Mechanism: Type IV
delayed hypersensitivity
reaction

Cause/Precipitating
Factors/Risk Factors
Phototoxic agents:
Coal tar
(cosmetics, drugs,
dyes, insecticides,
disinfectants)
Furocoumarins in
plants
Bergapten (lotion,
aftershave)
Yellow cadmium
sulfide (tattoos)
Drugs:
doxycycline,
naproxen,
ibuprofen,
amiodarone,
phenothiazine

Age & Area of

Predilection
Sun exposed areas:
Face
V of neck
Extensors of
upper
extremities
Dorsum of
hands
Often lower
legs & feet

Photoallergic agents:
Drugs:
phenothiazines,
chlorpromazine,
quinidine,
sulfonylureas,
NSAIDs
Topical
antimicrobials/
antibacterial
soaps(hexachloro
phene, bithionol)
Sunscreens
(PABA,
benzophenones)
Fragrances (must
ambrette, 6
methylcoumarin)
Aftershave (oil of
sandalwood)

Sun exposed areas:

Face
V of neck
Extensors of
upper
extremities
Dorsum of
hands
Often lower legs & feet

Diagnosis
Topical agent: clinical
Systemic agent:
clinical + phototests

Treatment
Symptomatic tx:
corticosteroids

Also know this

Onset: minutes to hours after
exposure; usually occurs after
1st exposure

Avoid sun exposure

Protective clothing is
essential
Sunscreen with broadest
UVA coverage

Topical agent:
photopatch tests
Systemic agent:
clinical + phototests;
photopatch tests

Same

Onset: 24 48hrs after

exposure
No occurrence after 1st
exposure

LALALA-LALA
2E: ERYTHEMATOUS LESIONS with Eczema
SKIN LESION
Atopic
Dermatitis

Description
Hallmark of AD: pruritus
(itching usually precedes
lesions)
Diagnostic criteria of
Hanifin & Rajka:
Major criteria:
Pruritus
Typical morphology &
distribution (adults: flexural,
infants: facial & extensors)
Chronically relapsing
dermatitis
Personal or family hx of
atopic disease
Minor criteria (at least 3):
Xerosis
Ichthyosis
Elevated serum IgE
Early age of onset
Nipple eczema
Cheilitis
Recurrent conjunctivitis
Dennie Morgan folds
Keratoconus
Anterior subcapsular
cataract
Periorbital darkening
Pityriasis alba
Itch when sweating
Blanching phenomenon
White dermographism
Food hypersensitivity
Susceptibility to infection (S
aureus, eczema
herpeticum HSV 1, HIV)

Cause/Precipitating
Factors/Risk Factors
Risk factors:
1. Polygenic
inheritance/person
al or family hx of
atopic disease
2. Environmental
factors
3. High level of IgE
antibodies to
housemites

Age & Area of

Predilection
Adults: flexural
lichenification
Infants: facial &
extensors

Diagnosis

Treatment
Topical therapy
1. Corticosteroids
dominant method of
tx for AD
Potent steroid
during
weekend, milder
steroid during
the week
2. Calcineurin inhibitors
(Tacrolimus)
alternative to
steroids
Systemic therapy
1. Antihistamines for
sedative effect
2. Antistaph antibiotics
during flares
(cephalosporins &
semisynthetic
penicillins)
3. Systemic steroids
only for controlling
acute exacerbations
4. Azathioprine,
mycophenolate
mofetil,
methotrexate for
debilitating disease
unresponsive to
other tx
5. Phototherapy
hospital based; good
for control of severe
AD

Also know this

Associated features &
complications:
1. Dennie Morgan folds
Linear transverse fold
below edge of lower
eyelids
2. Hertoghes sign
Thinning of lateral
eyebrows
3. Headlight sign
Perioral, perinasal &
periorbital pallor
4. Pityriasis alba
Subclinical dermatitis
Poorly marginated,
hypopig mented
slightly scaly patches
5. Keratosis pilaris
Horny follicular
lesions
Refractory to tx

LALALA-LALA
SKIN LESION
Infantile AD

Description
60% present in 1st yr of life
(usually >2 mos of age)

Cause/Precipitating
Factors/Risk Factors
Worsened after
immunizations & viral
infections

Usually begins as erythema

& scaling of cheek

Cheek, scalp, neck,

forehead, wrists,
extensor extremities
(areas involved
correlates with
capacity of child to
scratch/rub site & with
babys activities like
crawling)

Lesions may be papular or

exudative

Childhood AD

Age & Area of

Predilection
2 mos 2 yrs of age

Less exudative
Often lichenified, indurated
plaques

Diagnosis
Blinded food
challenges
Assays for food
specific IgE
Prick testing

Treatment
Partial remission during
summer & relapse during
winter (due to therapeutic
effects of UVB and humidity
& aggravation by wool & dry
air)
Evaporation barrier
immediately after bathing
White petrolatum
Aquaphor & vegetable
shortening
Protection of affected part
from scratching & rubbing

Antecubital & popliteal

fossa, flexor wrists,
eyelids, face, neck

Scratching impulse is usually

beyond control of px (itching is
same as lichen simplex
chronicus -> compelling,
paroxysmal) inability to feel
pain during paroxysms

Itch scratch cycle:

Pruritus leads to scratching
& scratching causes
secondary changes that
causes itching

Adult AD

Localized, erythematous,
scaly, papular, exudative,
or lichenified plaques

1.

Staphylococcal colonization
is universal

2.
3.

Hand dermatitis: most

common problem for adults
w/ hx of AD

Wet work
Especially
implicated in hand
eczema
st
After birth of 1 child
Soaps

Adolescents:
Antecubital & popliteal
fossa, front & sides of
neck, forehead, area
around eyes
Adults: chronic hand
eczema is common

Also know this

Dermatitis is uncommon
after middle life
Topical corticosteroid:
mainstay of tx
Avoid extremes of cold &
heat
Avoid overbathing
Tepid showers, not hot

Severe AD (>50% body

surface area involved)
associated with growth
retardation
Topical calcineurin
inhibitors
(macrolactams)/photo
therapy may allow for
rebound growth
Itching usually occurs in
response to heat/stress, during
the evening when trying to
relax, or at night
Flares may be due to acute
emotional stress (decreases
itch threshold)
Mild stigmata of dry skin &
irritation remain even after
recovery

LALALA-LALA
SKIN LESION
Seborrheic
Dermatitis

Description
Moist plaques w/ chronic,
superficial, inflammatory
disease of the skin

Cause/Precipitating
Factors/Risk Factors
Pityrosporum ovale

Scaling on an
erythematous base +
severe itching

Nummular
Eczema

Discrete, coin - shaped,

well circumscribed
erythematous, edematous,
vesicular & crusted plaques

Emotional stress
Alcohol
Atopy
Trauma (Koebners
phenomenon)

+ Koebners phenomenon:
formation of lesions after
trauma

Widespread dermatitis or
dermatitis distant from a
local inflammatory focus
Generalized acute
vesicular eruptions
associated with chronic
eczema of the legs w/ or
w/o ulceration
Often in linear configuration

Cradle cap seen in

infants as
yellow/brown scaling
lesions of the scalp
with adherent epithelial
debris
Young adulthood & old
age
Lower legs, dorsa of
hands, extensor
surfaces of arms
Lower legs (older men)
Trunk, hands, fingers
(younger females)

Severe, paroxysmal &

nocturnal pruritus

Infectious
Eczematous/
Autosensitization
Dermatitis

Age & Area of

Predilection
Scalp, eyebrows,
eyelids, nasolabial
creases, lips, ears,
sterna area, axillae,
submammary folds,
umbilicus, groin,
gluteal crease

Cause of the distant

dermatitis is not the same
as the cause of the local
one
Autosensitization to the
discharge
Precipitating factors:
Diabetics w/ non
healing wounds
Chronic otitis
media, eye, nose,
vaginal discharge

Diagnosis

Treatment

Also know this

Differentiate from
psoriasis (more
severe scaling, +
Auspitz sign: removal
of scales discloses
bleeding points, nail
pitting)

Antifungal agents
(Ketoconazole) & topical
calcinearia inhibitors mainstay

Dandruff (pityriasis sicca)

mild form of SD

Corticosteroid creams,
gels, sprays, foam
Be careful with use of
steroids due to side
effect of steroid rosacea

Initial tx: simple soaking

& greasing w/ occlusive
ointment OR application
of potent steroid
Antihistamine
Antibiotics if w/ staph
infection
Intralesional or systemic
steroids (if refractory to
topical meds)

Antibiotics
Oral glucocorticoids

Lesions may become

generalized -> generalized
exfoliative erythroderma/
erythroderma desquamativum
(esp in infants)
Atopic D has more severe
itching than seborrheic

Recurrent staph infection may

be present
As new lesions appear, old
lesions expand by tiny
papulovesicular satellite
lesions at the periphery fusing
with the main plaque
May be very similar to AD but
different in site of predilection
& presentation (coin shaped).
Although AD may be
nummular in adolescents, AD
is more chronic & lichenified.
Usually develops about a:
Discharging abscess
Ulcer
Sinus
Fistula

LALALA-LALA
SKIN LESION
Contact
Dermatitis
Irritant CD

Allergic CD

Description

Inflammatory reaction to a
substance that causes
eruptions in most people

Cause/Precipitating
Factors/Risk Factors

Hallmark: Pain & burning!

Acids
Alkaline materials
(soaps/detergents)
Solvents
Diaper

Lesions: necrosis &

ulceration

Acute: direct cytotoxic

damage to keratinocytes

Inflammatory reaction only

among people who have
been previously sensitized
(delayed reaction)
Delayed contact
hypersensitivity
Acquired sensitivity to
various substances
Erythematous papules,
vesicles, linear &
symmetrical lesions w/in
scratch marks

Chronic: slow damage to

cell membranes by CHON
denaturation & cellular
toxicity
Poison ivy, poison oak,
poison sumac
Nickel/other metals
Medications (antibiotics,
anesthetics, topical meds)
Rubber/latex
Cosmetics
Fabric & clothing
Detergents
Adhesives
Perfumes
Jewelry
Shoes

Age & Area of

Predilection
Hands
Lesions sharply
circumscribed to
contact area; no
distant lesions

Diagnosis

Treatment

Topical steroids
(betamethasone,
clobetasol propionate)

More intense in
contact areas but may
have distant lesions

Topical steroids

Highest incidence :6
12 mos of age

Use diaper w/
superabsorbent gel

Lower abdomen,
genitals, thighs,
convex surfaces of
buttocks

Frequent change of
diaper

Lesions: edema, vesicles,

Alkaline irritative effects of
ammonia formed in wet
diaper
Risk factor: frequent
maceration
Irritant Hand
Dermatitis/
Housewifes
Eczema

Dryness/redness of fingers
Chapping at back of hands,
erythematous hardening of
palms, fissuring

Under rings when not

removed during
washing

This is a non allergic

inflammatory response. No
previous exposure necessary.
Effect is evident w/in mins/hrs

Hallmark: Itch!
Diaper/Napkin
Dermatitis

Also know this

Topical hydrocortisone
Zinc oxide paste
Betamethasone
dipropionate
Clobetasol proprionate
Triamcinolone

Lesions appear 24 72 hrs

after exposure, but may
develop as early as 5 hrs or as
late as 7 days after exposure

LALALA-LALA
SKIN LESION
Intertrigo

Description
Superficial inflammatory
dermatitis occurring where
2 skin surfaces are in
apposition

Cause/Precipitating
Factors/Risk Factors
Hot & humid weather
Obesity
DM & hyperhidrosis

Result of friction, heat,

moisture -> affected fold
becomes erythematous,
macerated, secondarily
infected

Stasis
Eczema

Erythema/yellowish/ light
brown pigmentation of
lower 1/3 of legs esp
superior to medial
malleolus
Hyperpigmentation due to
melanin & hemosiderin
Cutaneous marker for
venous insufficiency

Venous insufficiency
Persons with heart failure,
varicose veins, recent
trauma of legs greater
risk

Age & Area of

Predilection
Children & elderly
Retroauricular areas,
folds of upper eyelids,
creases of neck,
axillae, antecubital
areas, finger webs,
inframammary areas,
umbilicus, popliteal
spaces, toe webs,
gluteal folds
Inframammary area in
obese women: most
frequent site of
intertriginous
candidiasis
Groin: fungal infection
Elderly (rarely occurs
before 5th decade of
life)
Lower 1/3 of lower leg
(superior to medial
malleolus)

Diagnosis

Treatment

Also know this

Eliminate maceration
Local
antibiotics/fungicides
Separate apposing skin
surfaces w/ gauze or
other dressings
Castellani paint,
polysporin ointment, low
potency topical steroid

Symptom relief
Tx of underlying venous
insufficiency
Emollients for pruritus
& eczema
Topical corticosteroids
Support stockings

Swelling may be noted late in

the afternoon with
spontaneous resolution in the
morning

LALALA-LALA
2E: ERYTHEMATOUS LESIONS: Dry, Chronic Eczema
SKIN LESION

Description

Lichen
Simplex
Chronicus
(Neurodermatitis
Circumscripta)

Paroxysmal pruritus
Criss cross pattern:
between is a mosaic
composed of flat topped,
shiny, smooth, quadrilateral
facets (lichenification)

Cause/Precipitating
Factors/Risk Factors
Chronic rubbing &
scratching
Associated with topic or
allergic contact dermatitis,
anxiety, nervousness,
depression

Age & Area of

Predilection
Nuchal area (female),
scalp, ankle, lower
legs, upper thighs,
exterior forearms,
vulva, pubis, anal area,
scrotum, groin

Diagnosis

Goal: cessation of
pruritus

Circumscribed, lichenified,
pruritic patches

Prurigo
Nodularis

Excoriated papules
(sometimes w/ bleeding),
slightly scaly & moist, rarely
nodular
Multiple severe itching
nodules (pea sized or
larger; 3 20mm)
Chronic disease, lesions
evolve slowly
Symmetrical & usually
linear arrangement

Prurigo Mitis

Mild form of chronic

dermatitis characterized by
recurrent, intensely itching
papules & nodules
Severe itching ->
excoriation, eczematisation

Unknown
Atopic dermatitis, anemia,
Hep C, pregnancy, stress,
etc.
Chronic renal failure:
most common internal
cause of pruritus

Worsened after
immunizations & viral
infections

Any age but mainly in

adults (20 60 y/o)
M=F
Anterior surfaces of
thighs & legs
Forearms, trunk, neck

Early childhood

Treatment

Visual examination
Biopsy
Blood tests, liver,
kidney, thyroid fxn
tests

Blinded food
challenges
Assays for food
specific IgE
Prick testing

Stop scratching!
Cover affected areas at
night to prevent
scratching while asleep
Topical steroids:
Clobetasol propionate,
betamethasone
dipropionate
cream/ointment used
initially
Triamcinolone
suspension
Initial tx: intralesional or
topical administration of
steroids
Other measures:
Keep in cool areas,
avoid hot baths or
showers and wool
clothing
Use soap only in axilla
& inguinal area
Antihistamines
Antipruritic
lotions/emollients
PUVA
Vit D3, tacrolimus
Cryotherapy
Same

Also know this

With habitual itch scratch
cycle

LALALA-LALA
2F: ERYTHEMATOUS LESIONS: Papulosquamous Disease
SKIN LESION
Tinea Capitis

Description
Scalp ringworm

Cause/Precipitating
Factors/Risk Factors
Pathogenic dermatophytes

Incubation period: 2 4
days

(Except: Epidermophyton
floccosum &Trichophyton
concentricum)

Most common: T tonsurans

& M canis

T tonsurans

Age & Area of

Predilection
Children
Boys > Girls
Scalp, glabrous skin,
eyelids, lashes

Black dot ringworm

Subtle seborrheic like
scaling
Inflammatory lesion

Tinea
Corporis
(Tinea
Circinata)

With progressive central

clearing
Depth of infection usually
limited to epidermis & its
appendages
See annular outlines
(ringworm)

Also know this

Kerion celsii: deep tender
boggy plaques exuding pus;
cause scarring & permanent
alopecia

10 2% KOH solution
Findings: pattern of
endothrix/ ectothrix

Griseofulvin (2 4 mos)
Terbinafine (for
tricophyton infections; 1
4 wks)
Itraconazole/fluconazole
(2 3 wks)
Selenium sulfide
shampoo or
ketoconazole shampoo
(adjunct)

Culture (growth in 1
2 wks)

Kerion celsii: systemic

steroids + antifungal

Scutulae: cupshaped crust on

glabrous skin, < 2cm, mousy
odor

TOPICAL: localized
disease w/o fungal
folliculitis
Sulconazole,
miconazole,
itraconazole
(give 2 4
wks)
Terbinafine,
Ketoconazole
give for 1 wk

Variants:
1. Fungal folliculitis
(Majocchi granuloma)
Infection of hair
follicles w/ granuloma
formation
Usually in F who
shave legs
T rubrum/
mentagrophyte
2. Tinea imbricate
Concentric ring of
scales, extensive
patches w/ polycyclic
borders
T concentricum
3. Tinea incognito

Woods light
Fungal fluorescence
Fluorescent
substance: pteridine
(+) if bright green or
yellow green

Favus: concave, sulfur

yellow crusts around loose,
wiry hairs; atrophic scarring
results to smooth, glossy,
paper white patch

Culture:
granular/powdery,
yellow to red, brown
colony
(+) fluorescence in
Woods light

Scaly, erythematous,
papular eruptions with
loose & broken off hairs > inflammatory
Small spore ectothrix
1 or more circular, sharply
circumscribed, slightly
erythematous, dry, scaly,
hypopigmented patches

Treatment

(-) fluorescence in
Woods light

Large spore endothrix

M canis

Diagnosis

T rubrum most common

M canis causes moist
type
T mentagrophytes
Mode of transmission:
Contact w/ infected human
(most common)
Contact w/ contaminated
household pets, farm
animals, fomites
Widespread tinea corporis
may be a presenting sign of
AIDS or related to the use
of a topical steroid or
calcineurin inhibitor

Preadolescents
F>M
Neck, extremities,
trunk

Culture: profuse,
cottony, aerial mycelia;
buff to light brown
KOH exam of skin
scrapings (get from
active border of lesion
-highest yield of fungal
elements)
Fungal culture
PCR
Skin biopsy (see
septate branching
hyphae in stratum
corneum)

Combination with a
potent corticosteroid
may cause widespread
tinea & fungal
folliculities so avoid

LALALA-LALA
using CS!

Tinea Cruris
(jock itch,
crotch itch)

Begins as small,
erythematous scaling or
vesicular & crusted patch
that spreads peripherally
and partly clears in center
Patch: curved, well
defined border, particularly
on lower edge

T rubrum common
Epidermophyton floccosum
T mentagrophytes
They produce keratinases
that allow invasion of
cornified cell layer of
epidermis

Adult men
Upper & inner surface
of thighs
Perineum & perianal
areas

KOH wet mount

Growth on
Mycosel/Saboraud
agar plates

SYSTEMIC: for
extensive
disease/fungal folliculitis
Griseofulvin, terbinafine,
itraconazole,
fluconazole
Treat all areas of active
infection
Keep groin area clean &
dry
Loose fitting clothing
Lose weight
Use plain talcum
powder
Antifungal creams

4.

Atypical presentation
due to corticosteroid
tx
Tinea gladiatorum
Skin to skin contact in
wrestlers

Candidal infection may mimic

this (difference is the presence
of satellite pustules in candida)

Risk factors:
Warm & moist areas
Tight fitting clothes
Autoinoculation (athletes
foot & ringworm)
Direct skin-to-skin
contact/fomites
Obesity, DM,
immunocompromised
SKIN LESION

Description

TINEA PEDIS
(athletes foot)

Dermatophytosis of the feet

Characterized by erythema,
scaling, vesicular & crusted
patch spreading
peripherally with partial
central clearing
Most common fungal
disease
Chronic w/ exacerbations in
hot weather

T rubrum

Moccasin type lesions:

non inflammatory type w/
dull erythema &
pronounced scaling that
may involve entire sole and

Cause/Precipitating
Factors/Risk Factors
T rubrum cause
majority of infection;
usually non
inflammatory type
T mentagrophytes
cause inflammatory
lesions
Risk factors:
Hyperhidrosis (sweat
between toes and soles)
Hot, humid weather
Occlusive footear

Age & Area of

Predilection
Late childhood to young
adulthood
Younger indvls:
inflammatory
Older: non - inflammatory
M>F

Diagnosis

Treatment
Dry toes thoroughly
after bathing
Good antiseptic powder
Fungicides

Also know this

May become a portal of entry
for lymphangitis when
pyogenic cocci infect fissures
between toes & in the vesicles

Site: usually 3rd toe web

Distribution: usually
bilateral; may involve one
hand, both feet

This type of lesion may also be

caused by E floccosum

LALALA-LALA

SKIN LESION

sides of foot =
moccasin/sandal
appearance
A. Inflammatory/ bullous
type
Plantar arch &
along sides of feet
Burning/itching
sensation
Least common
Involves sole,
instep, webspaces
B. Interdigital type
Erythema, scaling,
maceration extend
up to dermis
Complicated by
secondary
bacterial infection
Description

TINEA
MANUM

Dermatophytosis of the
hands

T mentagro phytes

Dry, scaly, erythematous

type OR moist, vesicular,
eczematous type

PITYRIASIS
ROSEA

Usually begins with single 2

4cm thin oval plaque w/
fine collarette of scale
inside the periphery
(herald patch/mother
patch)
Salmon colored papules
& macules., oval/circinate
patches, covered with finely

C. White superficial
onychomycosis

Cause/Precipitating
Factors/Risk Factors
T rubrum more
common; produces dry,
scaly erythematous type
T mentagrophytes
dermatophytosis of hand
secondary to tinea of feet;
produces vesicular type;
both hands involved

Unknown
Some evidence points to a
viral cause reactivation
of HHV7 & HHV6
Spring & autumn months

Age & Area of

Predilection

Unilateral if associated with

tinea pedis & cruris
Often associated with tinea
unguium of fingernails (if
chronic)

15 40 y/o
F>M

Diagnosis

Treatment

Direct microscopic
exam of scrapings
(instep, heel, sides
of foot, palms)

Oral antifungal agents

(topical dont usually
work because of the
thick palmar stratum
corneum)
Griseofulvin, terbinafine,
itraconazole,
fluconazole

10 20% KOH
solution
Fungal culture

KOH wet mount

Growth on
Mycosel/Saboraud
agar plates

Prevention:
Dry toes thoroughly
after bathing
Good antiseptic powder
between toes (tolnaftate
or zeasorb powder)
Plain talc, cornstarch
dusted into socks
Supportive
Topical CS or
antihistamines for
associated pruritus
UV treatment may
expedite involution of
lesions

Also know this

Usually asymptomatic but may

be pruritic & have
constitutional symptoms

LALALA-LALA
TINEA
VERSICOLOR

crinkled, dry epidermis that

often desquamate
Hypopigmented,
coalescing, scaly macules
(due to abnormally small &
poorly melanised
melanosomes) in dark skin
Hyperpigmented on pale
skin

SKIN LESION
PSORIASIS

Description
Common, chronic,
recurrent, inflammatory
disease of the skin
Round, circumscribed,
erythematous, dry scaling
plaques of various sizes,
covered by gray or silvery
white imbricated lamellar
scales

Malassezia furfur (skin

lesions area produced
when in hyphal phase)
Risk factors:
Genetic predisposition
Warm, humid envt
Immunosuppression
Malnutrition
Cushing disease

Cause/Precipitating
Factors/Risk Factors
Unknown

Sterna region, sides of

chest, abdomen, back,
pubis, neck, intertriginous
areas, oily areas of skin
Face & scalp (usually in
infants &
immunocompromised px)

Age & Area of

Predilection
Mean: 27 y/o
Scalp, nails, extensor
surfaces of limbs
(shins), elbows, knees,
umbilical & sacral
region

Symmetrical, solitary
macule to > 100 macules

Nail pitting & oil spots

Types
W/ prominent features of
seborrheic dermatitis

Inverse
psoriasis

W/ minimal amount of soft

& greasy micaceous scales
flexural psoriasis palms
& toes
volar psoriasis

Anti fungal agents

(selenium sulfide,
imidazoles, triazoles,
sulfur preparations,
salicylic acid, benzoyl
peroxide, etc)

Flexure areas
(antecubital areas,
axillae, under breast)
Folds, recesses, flexor
surfaces: ears, axillae,
groin, inframammary
fold, palms, soles, nails

Hypopigmentation may persist

for wks/mos after fungal
disease is cured
Most cost effective tx:
selenium sulfide & zinc
pyrithione soap

Ketoconazole:
400mg/1x a month
Itraconazole: 200mg for
7 days
Terbinafine: topical

Diagnosis

Treatment
Depends on site,
severity, duration, age
Topical:
-

Corticosteroids
Tars
Vit D
Salicylic acid
UV
Tazarotene

Systemic
CS
Methotrexate

May be accompanied by
itching/burning

Seborrheic
like psoriasis

Woods light exam

Culture (rarely used
for dx)

Also know this

Koebners phenomenon:
appearance of lesions at areas
of injuries
Auspitzs sign: bleeding points
secondary to thinning of
epidermis over dermal
papillae; bleeding upon
removal of scales
Woronoff ring: concentric
blanching of erythematous skin
near periphery of healing
psoriatic plaque

LALALA-LALA
Napkin
psoriasis
Psoriatic
arthritis

Guttate
psoriasis

Generalized
pustular
psoriasis

Increases risk for adult

psoriasis infection
5 clinical patterns:
1. asymmetrical distal
interphalangeal joint
involvement w/ nail
damage
2. arthritis mutilans w/
osteolysis of phalanges &
metacarpals
3. symmetrical polyarthritis
like RA, with claw hands
4. oligoarthritis w/
swelling & tenosynovitis
of 1 or few hand joints
most common
5. ankylosing spondylitis
alone or with peripheral
arthritis
Typical lesions: size of
water drops (2 5mm)
Abrupt erosion following an
infection (ex. strep
pharyngitis)
Sudden onset, with
formation of lakes of pus
periungually, on palms &
edges of psoriatic plaques
Erythema in flexures before
eruptions appear
w/ pruritus & burning
sensation

Infants between 2 8
mos of age
Distal & proximal
interphalangeal joints
(relative sparing of
metacarpal &
metatarsal phalangeal
joints)

Usually px <30 y/o

Px usually have hx of
psoriatic arthritis
Linked with pneumonia,
CHF, ARDS

Aspirin, NSAIDs, oral

retinoids, PUVA

Topical steroids
UVB

Acitretin

LALALA-LALA
3: SKIN COLORED PAPULES
SKIN LESION
Verruca
vulgaris
(common wart)

Description
Benign epidermal
proliferations
Elevated round papules w/
a rough grayish surface
(verrucous)
If in palms &
soles, not very
verrucous
Linear configuration of
verruca

Cause/Precipitating
Factors/Risk Factors
HPV type 1, 2, 4, 27, 57,
63
Transmission: simple
direct contact;
autoinoculation

Age & Area of

Predilection
5 20 y/o
Hands, peri ungal
(esp in nail biters),
elbows, knees, plantar
surfaces, anogenital
areas

Predisposing factors:
Frequent immersion of
hands in water
(makes skin soft, easier
for virus to enter)
Meat handlers

See black dots

(thrombosed dilated
capillaries) on surface
Verruca Plana
(flat warts)

Flat topped papules that

are slightly erythematous
Brown on light skin &
hyperpigmented on dark
skin
Multiple & grouped

HPV type 3, 10, 28, 41

Children & young adults

Transmission: direct
contact & autoinoculation
(in men who shave
beards, women who
shave their legs)

Forehead, cheeks,
nose, neck, dorsa of
hands, wrists, elbows or
knees

Painless, itching not

prominent
Smooth surface, firm,
dome shaped pearly
papules (3 5mm) with
central umbilication

Poxvirus (MCV 1 4)
MCV 1: children
MCV 2: HIV

Treatment
Generally self limited
In the Phils:
Electrocautery (complete
removal)
Give xylocaine
before doing
this because
warts in palms
are painful
(many pain
receptors
Meissner &
Pacini)
Topical keratolytics
(salicylic acid/lactic acid
preparations)
Light cryotherapy (may
produce loss of color)
because nitrogen can
cause death of
melanocytes in colored
skin
Topical salicylic acid
(may cause burning of
normal skin = apply
petroleum jelly)

No rough surface, no black

dots
Molluscum
contagiosum

Diagnosis

Usually in kids, sexually

active individuals,
immunosuppressed px
(HIV infected)
Kids: face, trunk,
extremities
Adults: lower abdomen,
upper thighs, penile
shaft in men
Immunosuppressed:
face (cheeks, neck,
eyelids), genitalia

Topical tretinoin
If px is healthy: usually
self limited
Kids: no tx OR topical
tretinoin/cantharidin (4 6
hrs)
Adults: cryotherapy or
curettage; sexual partners
should be examined
Immunosuppressed:
aggressive tx with HAART;
curettage or core removal w/
blade; cantharone or 100%
trichloroacetic acid;
cryotherapy

Also know this

Usually asymptomatic:
painless & no itching
Larger than verruca plana
No dermatoglyphics
(fingerprint folds) in calluses,
these lines are accentuated

W/ Koebnerization (also
found in psoriasis) tend to
form linear, slightly raised
papular lesions
Lesions are small and
numerous & spread fast
Of all HPV infections, flat warts
have the highest rate of
spontaneous remission
DO NOT DO CAUTERY. Do
curettage! Scrape off infected
area with curette w/c will
remove abnormal tissue. Try to
also remove the molluscum
body

4: PUSTULAR DISEASE
LALALA-LALA
SKIN LESION
Acne Vulgaris
(review nalang
:D)
Miliaria
Pustulosa

Description
Comedo as basic lesion

Cause/Precipitating
Factors/Risk Factors
Propionibacterium acnes

Follicular disease w/ a
keratinous plug
Distinct, superficial
pustules that are
independent of the hair
follicle

Preceded by another
dermatitis that has
produced injury,
destruction, or blocking
of the sweat duct

Pruritic

Age & Area of

Predilection
Adolescents (15 18
y/o)
Involution of disease
before 25 y/o
No particular age
Intertriginous areas,
flexure surfaces of
extremities, scrotum,
back of bedridden px

Commonly associated
diseases:
Contact dermatitis
Lichen simplex chronicus
Intertrigo

Gram (-)
Folliculitis

P Aeruginosa
Folliculitis

Staphylococcal
Folliculitis

Superficial pustules (3
6mm)
Fluctuant, deep seated
nodules

Pruritic, follicular,
maculopapular, vesicular,
or pustular lesions

Atypical plaque
Pustular erythematous
follicular lesion

Enterobacter, Klebsiella,
Proteus, Serratia
Predisposing factors:
Long term antibiotic
therapy
Continuous scratching
Occurs in areas of
irritation (shaving,
friction, clothes rubbing)
Usually occurs 1 4
days after bathing in hot
tub

S aureus

Anterior nares, face

Sides of trunk, axilla,

buttocks, proximal
extremities, apocrine
areas of breast & axilla
Eyelashes, axilla, pubis,
thighs

Diagnosis

Treatment

Also know this

See acne vulgaris (p. 8)

Usually self limited

Place px in cool envt
Circulating air fans
Anhydrous lanolin help
resolve occlusion of
pores & helps restore
normal sweat secretions
Hydrophilic ointment
Soothing, cooling baths
Dusting powders

Recurrent episodes may be a

sign of type I
pseudohypoaldosteronism
(salt losing crises may
precipitate miliaria pustulosa or
rubra)
Difference from acne: no
keratinous plug

No need for antibiotics

(because pustules are
sterile; contain nonpathogenic cocci)
Isotretinoin
Sulfa TMP

Involutes w/in 7 14
days
3rd gen cephalosporins
(oral), fluoroquinolones if
w/ fever
Thorough cleansing of
affected area with
antibacterial soap and
water (3x/day)
Deep lesions should be
drained
Mupirocin ointment
topically
st
1 generation
cephalosporin (if

Some may present with fever

& prolonged disease (hot foot
syndrome)

LALALA-LALA
drainage or topical
therapy fail)
Anhydrous formulation of
aluminum chloride (for
chronic folliculitis)
SKIN LESION
Superficial
Pustular
Folliculitis
(impetigo of
Bockhart)
Ecthyma

Description
Superficial folliculitis w/ thin
walled pustules at follicle
orifice
Fragile, yellowish white,
domed pustules
Begins with vesicle or
vesicopustule w/
erythematous base &
surrounding halo that
enlarges over days &
crusts
Becomes superficial saucer
shaped ulcer with raw
base

Pyogenic
Paronychia

Indurated ulcer margin;

granulating base may
extend deeply into dermis
Inflammatory reaction of
the nail folds
Purulent, painful swelling of
tissues around the nail
May be acute/chronic

Cause/Precipitating
Factors/Risk Factors
S aureus

Age & Area of

Predilection
Extremities, scalp, face

Diagnosis

May secondarily arise in

scratches, insect bites,
other skin injuries
Beta hemolytic
streptococcus
S aureus

Children

Lesions may heal but

may leave a scar

Lower extremities,
shins, dorsal feet

Good hygiene
Muciprocin or bacitracin
ointment
1st generation
cephalosporin or oral
dicloxacillin

Predisposing factors:
Uncleanliness
Malnutrition
Trauma
IV drug users
HIV infection
DM

Primary predisposing
factor: separation of
eponychium from nail
plate (due to
trauma/frequent wetting
of hands)
Manicure/pedicure

No particular age
Folds of skin
surrounding nail

Smears of purulent
material will confirm
impression

Pruritic pink to red

intertriginous moist patches
surrounded by a thin
collarrette scale & pustules

Candida albicans
(seen in
immunocompromised
px,& conditions that favor

Protection against
trauma & keeping hands
dry
Acutely inflamed
pyogenic abscess:
incision & drainage (do
this first before giving
penicillin or
cephalosporin)

Secondary bacterial
infection due to: S
aureus, Strep pyogenes,
Candida albicans

Intertriginous
Candidiasis

Treatment

No particular age
Inframammary area (for
obese women)

10% KOH microscopic

exam (see
pseudohyphae)

Candida (usually
implicated in chronic
paronychia) topical/oral
antifungal (miconazole) +
topical steroids
Goal: reduce
inflammation!
Topical terbinafine will

Also know this

LALALA-LALA
closely adjacent to the
patches
Hallmark: Satellite lesions
on surrounding healthy skin
(satellite pustules)

growth: warm, moist,

high skin pH, reduced
microbial flora due to
antibiotic therapy),
obesity, poor hygiene,
restrictive clothing

Axilla, groin,
overhanging abdominal
folds, intergluteal folds,
interdigital spaces,
umbilicus

not work; only AZOLES

will work

LALALA-LALA
5: VESICULAR
VESICULAR DISEASE
DISEASE
5:
SKIN LESION
Miliaria
Crystallina

Description
Small, clear, very
superficial vesicles w/ no
inflammatory reaction
Asymptomatic, short
lived, self limited

Impetigo
Contagiosa

Discrete, thin walled

vesicles that become
pustular & rupture
Very weepy lesions (fresh
exudates) covered by
yellow/orange crusts
Gyrate pattern/gyrate
erythema (round, ring
like polycyclic or arcuate)

Steven
Johnsons
Syndrome

Flat, erythematous,
purpuric macules that form
incomplete atypical
targets that may blister
centrally
(Erythema multiforme minor
may also appear as target
lesions, may be drug induced,
and may have the same areas
of predilection. Difference is in
Nikolsky sign)

Evolution of lesions:
Macules -> vesicles &
bullae
Fever & influenza like
symptoms precede

Cause/Precipitating
Factors/Risk Factors
Increased perspiration
Clothing that prevents
dissipation of heat &
moisture
Bedridden px & bundled
children

Age & Area of

Predilection
Neonates ( < 2 wks)

S aureus (most common)

Streptococci
(group B strep newborn
impetigo)

Children

Predisposing factors:
Temperate zones

Exposed body parts:

face, hands, neck,
extremities (palms &
soles spared)

Treatment
Self limited
No medical treatment
required
Symptom relief (keep px
in cool envt)

Infants: head, neck,

upper trunk
Adults: trunk

Sources of infection:
Kids: pets, dirty
fingernails, other kids
Adults: barber shops,
beauty parlors, swimming
pools, etc

Drug allergy (1day 3

wks latent period):
antibiotics, NSAIDs,
allopurinol,
anticonvulsants

Diagnosis

Histopathology:
1. Superficial
inflammation in
upper part of
pilosebaceous
follicles
2. Subcorneal
vesicopustule
3. Mild inflammation
in dermis (PMNs,
edema)

Clean area before

applying meds
Systemic antibiotics
(semisynthetic penicillins
or 1st gen
cephalosporins) w/
topical therapy
(Bacitracin & muciprocin
ointment)

Also know this

Impt features to remember:
1. Rupture spontaneously
2. Normal skin w/
desquamation
3. No mucosal involvement
4. Acute
5. No target lesions
6. No erythema! most
important
Impetigo on the scalp:
complication of pediculosis
capitis
Acute glomerulonephritis
complication following beta
hemolytic strep skin infection
Usually in kids <
6y/o
Absent in staph
impetigo

Recurrent: 10 days
Rifampin (600mg/d)

Oral mucosa &

conjunctiva

Skin biopsy:
Lymphocytic infiltrate
at dermoepidermal
junction w/ necrosis of
keratinocytes

Similar to px with
extensive burn
1. IV immunoglobulin
2. Systemic
corticosteroids
(dexamethasone,
methylprednisolone)
Stops spread &
skin loss
3. ICU
4. Increase caloric
enteral intake

Cause of mortality in
dermatology
Px usually go to the hospital
because of pain
+ Nikolsky sign: application
of very slight pressure causes
the skin to slough off; usually
seen in vesicular lesions (due
to weakening of intercellular
attachments)
This is absent in
erythema multiforme
minor because
lesions here are
more papular

LALALA-LALA
eruption/skin lesions
(rapidly spread w/in 4 days)

2 causes of mortality in SJS:

1. Sepsis
2. Electrolyte
imbalance

Mucosal involvement (>2

mucosal surfaces eroded
oral or conjunctiva)
Not pruritic
Herpes
Simplex

Intraepidermal vesicles
Acantholysis (ballooning
degeneration of epidermal
cells)
Types of infection:
Primary infection: virus
replicates in site of
infection; usually resides in
trigeminal ganglion
Nonprimary initial
episode: initial clinical
lesion in a person
previously infected w/ the
virus
Recurrent infection

HSV 1: orolabial herpes;

more common
HSV 2: genital herpes
Risk factors:
Immunocompromised
Prior infection
Occupation (esp in
herpetic whitlow)
Minor trauma & sun
exposure
Transmission: intimate
skin to skin contact, bodily
fluids

Tzanck smear most

common procedure
- Not specific (HSV,
VZV)
- Multinucleated
epidermal giant cells
Direct fluorescent
antibody test more
accurate
Viral culture very
accurate & rapid
(results ini 48 72 hrs)
PCR
Skin biopsy
Serology

Drug of choice:
Acyclovir (oral)
Indications for oral meds:
Recurrence
Dissemination
(in
immunocompro
mised)

SJS involves less than 10%

body surface. (Toxic
epidermal necrolysis involves
>30% body surface & its a
more severe SJS)
Features:
1. Acute
2. Clustered lesions (In
SJS, not clustered)
3. Can have mucosal
involvement
Other manifestations:
Herpetic whitlow
Infection of digits
Tenderness &
erythema of lateral
nail fold
Herpetic
keratoconjunctivitis
Punctate/marginal
keratitis
May impair vision
Herpes gladiatorum
HSV 1
Seen in wrestlers,
rugby players
Face, sides of neck,
inner arms
Herpes Sycosis
Affect primarily the
hair follicle
Close razor shaving
Recurrent Ecthyma
Multiforme
Presents with
papules later
become target
lesions in palms,
elbows, knees and
oral mucosa
Neonatal Herpes
Passage through
birth canal

LALALA-LALA
-

Skin lesions,
microphthalmos,
encephalitis,
chorioretinitis,
intracerebral
calcifications

HSV
Encephalitis/Meningitis
Headache, fever,
mild photophobia,
autonomic
dysfunction
Orolabial
Herpes

Lesions in mouth: broken

vesicles that appear as
erosions or ulcers covered
w/ white membrane

95%: recurrent HSV1

infection

Lips near vermillion

border

If untreated, may last 1

2 wks

Upon onset: high fever,

lymphadenopathy, malaise

Labia, vulva,
perineum, perianal
areas, shaft, glans
penis

Usually resolves in 21
days

Asymptomatic shedding may

occur between outbreaks

Frequent trigger: UVB

exposure

Frequent manifestation:
cold sore or fever blister

Genital
Herpes

Erosions may spread to

oral mucosa, tongue,
tonsils = herpetic
gingivostomatitis
Vesicles in erythematous
base that ulcerate & crust
Grouped blisters &
erosions w/ continued
development of new
blisters over 7 14 days
Course:

HSV2
Spread by skin-to-skin
contact during sexual
intercourse

Can present as severe

systemic illness
Fever & flulike
illness
Vaginal pain &
dysuria (herpetic
vulvovaginitis)

LALALA-LALA
SKIN LESION
Herpes Zoster

Description
Shingles
Cutaneous eruptions
frequently preceded by one
to several days of pain in
affected area
Papule & plaques of
erythema -> blisters

Cause/Precipitating
Factors/Risk Factors
Reactivation of varicella
zoster virus
Risk factors:
Age
Immunosuppression

Age & Area of

Predilection
F>M
Sensory dorsal root
ganglion cells
Usual sites:
Thoracic (55%)
Cranial trigeminal
(20%)
Lumbar 15%
Sacral 5%
Ophthalmic zoster:
involvement of
ophthalmic division of
5th CN
Ramsay hunt
syndrome:
involvement of facial &
auditory nerves

Scabies

See page 7 for complete

details
Features:
1. Pruritic
2. No target lesions
3. No mucosal
involvement
4. Px usually comes
to you the lesion
has been there for
several weeks
duration

Diagnosis
Tzanck smear

Treatment

Also know this

Acyclovir
Indications:
Immunocompro
mised px
To prevent
complications in
elderly (give 1st
3 days)
Ophthalmic
involvement

Features:
1. More painful than
simplex
2. Dermatomal
3. Not recurrent
4. Unilateral w/in
distribution of
cranial/spinal nerve
5. Neuralgic
Postherpetic Neuralgia
Major complication; occurs 1
month after onset of zoster
infection

LALALA-LALA
6: BULLOUS DERMATOSIS
SKIN LESION
Fixed Drug
Eruption (FDE)
Contact
Dermatitis
Bullous
Impetigo

Description

Cause/Precipitating
Factors/Risk Factors

Age & Area of

Predilection

Diagnosis

Treatment

See p 13/14
See p. 22
Strikingly large, fragile
bullae
Ruptures & leaves
circinate, weepy or
crusted lesions (impetigo
circinate)

S aureus
Predisposing factor:
Insect bites
Cuts
Nursery w/ infected
children

Other manifestations:
Constitutional symptoms
appear later
Diarrhea w/ green stools
Bacteremia, pneumonia,
or meningitis
Sources:
Andrews Clinical Dermatology
Dra. Ismaels lec
The original megatable from MH :D Thank you <3

Any age but usually in

newborn infants
Neonatal type is
highly contagious
Begins in 4th
10th days of life
w/ appearance of
bullae
Early: face & hands
Adults: axillae, groin,
hands
(spares scalp)

Systemic antibiotics
IV fluid resuscitation
if w/ large areas of
involvement w/
denuded skin from
ruptured bullae

Also know this