Transcript Dermatologic Board Review - Lock Haven University of

Dermatologic Board
Review
Lane Bower, MHSc, PA-C
Which is the SK?
Seborreic Keratosis
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Most common benign cutaneous neoplasm
Origin unknown
No malignant potential
Easily and quickly removed
Vary in size shape, most oval
Most common on torso, lesser degree on face
Increasing numbers with age
Leser Tre’lat Sign
Nevus
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A benign, pigmented lesion that is not caused
by any outside catalyst.
There are many types of nevi; junctional,
compound, dermal. Refer to text
Main job is differentiating from dysplastic nevi
which have malignant potential
What to do?
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When in doubt, remove it and send it to
pathology.
Do a conservative full excision
If it just doesn’t look right, remove it
That’s the thing with dysplastic nevi, if you
can’t make up your mind as to whether it is
benign or a possible melanoma, it is probably
the middle ground of dyplastic
Actinic Keratosis
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Common, sun induced, pre-malignant, changes
that increase with age
Most common sites are forehead, shoulders,
back, and dorsum of arms
Start as an erythematous, rough, area, that
forms a yellow crust.
They are usually very symmetrical in
distribution.
……actinic keratosis
Basal cell and other
skin cancers can
develop in these
transitional type
lesions.
Treatment of AK
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5-FU get incorporated in to rapidly
reproducing cells and causes cell death
Retin-A has been helpful
Cryotherapy for early lesions is effective
Laser is excellent!
Avoidance of further sun damage is paramount
Explain the Course using 5-FU
Who’s the Mole?
Zosteriform
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Lesions arranged along the cutaneous
distribution of a spinal dermatome
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They are unilateral and denote
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herpes zoster
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metastatic carcinoma of the breast
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dermatomal hemangiomatous growths of SturgeWeber syndrome
Impetigo
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Level of Infection
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Port of Entry
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Epidermal superficial infection
Cuts, abrasions, bug bite
Likes moist areas (mouth, nose) and hot
moist climates
Susceptibility
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Common in infants & children
VERY Contagious!
Impetigo
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Symptoms
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Itch
Signs (Appearance)
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Vesicular
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Toxins cause epidermal cleavaging of stratum corneum
Some strains Strep. aureus cause thin-roofed bulla
Evolves to pustules and become “honey-crusted”
Satellite lesions on periphery (asymptomatic)
Impetigo
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Causative Agents
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Staphylococcus aureus (most usual)
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? 2wk incubation
Streptococcus pyrogenes (occ. alone OR
together)
Impetigo
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Course of Disease
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Self-limiting !!
But…
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may last weeks or months
Post streptococcal glomerulonephritis may
follow! Esp. 2 - 4 yo. Hematuria/proteinuria.
Osteomyelitis, septic arthritis & pneumonia from
otherwise seemingly innocuous impetigo
Impetigo
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Treatment
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(cover both Staph & Strep)
All
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Wash with anti-bacterial soap 1-2/d to remove crusts.
Wash entire body to prevent spread 1- 2/day
Non Bullous
Dicloxicillin 250-500 mg Qid
X5-10 days
Azithromycin 500mg QD for
1 day then 250 mg X 4days
Cloxicillin 500-1000 mg
Q6h X 5-10 days
Erythromycin 250-500 mg
TID X 5-10 days
2nd Generation
Cephalosporin
Bactroban
Bactroban apply TID X 5-10
days
Bullous
Dicloxicillin 250-500 mg Qid
X5-10 days
Keflex 250-500 mg QID X 10
days
Azithromycin 500mg QD for
1 day then 250 mg X 4days
Augmentin 875/125 mg BID
x 10 days or 500/125 mg TID
X 10 days
Erysipelas & Cellulitis
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Level of Infection
 Erysipelas  epidermis & dermis (defined border).
 Acute inflammatory version of Cellulitis with streaking.
 Cellulitis  dermis & subcutaneous tissue (diffuse)
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Symptoms
 Area is red, hot, swollen, tender, edema, ?malaise
 perhaps vesicles, bullae, petechiae/purpura
 Perhaps spread to lymphatics, “red streaks”
 lymph nodes may be swollen and tender
 chills and fever may be present
Erysipelas & Cellulitis
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A portals of entry
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Open lesion, trauma, surgical wound,
athletes foot, IV drug use, insect bite, fissure
Radiation therapy
Arms usually in young adults
Legs usually in children and older adults
Puerperal sepsis common form before
antibiotics
Peripheral vascular disease is a common
underlying factor
Erysipelas & Cellulitis
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Diagnosis
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Largely Clinical:
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Labs
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CBC
gram stain and culture wounds poor yield
needle aspiration (5% yield), biopsy (20% yield),
blood cultures (5% yield)
Films (?)
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typical presentation and appearance
Plain / CT / MRI: underlying fasciitis or
osteomyelitis
Referrals: (?) Ortho if over joint
Erysipelas & Cellulitis
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Differential Diagnosis
 Necrotizing Fasciitis: deeper and much more virulent.
Consider if patient doesn’t respond to antibiotics
within 48 hours.
 Deep vein thrombosis
Course
 Antibiotics
 possible abscess (I&D), sepsis, fasciitis (rare)
 Erysipelas  Endocarditis
 Recurrent cellulitis  persistent lymphedema
Erysipelas & Cellulitis
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Differential Diagnosis
 Necrotizing Fasciitis: deeper and much more virulent.
Consider if patient doesn’t respond to antibiotics
within 48 hours.
 Deep vein thrombosis
Course
 Antibiotics
 possible abscess (I&D), sepsis, fasciitis (rare)
 Erysipelas  Endocarditis
 Recurrent cellulitis  persistent lymphedema
Erysipelas & Cellulitis
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Inpatient
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IV methacillinase-resistant penicillin (nafcillin) or cephazolin
Consider pseudomonas in immunocompromised patients--ticarcillin,
piperacillin
Others: Elevate limbs, treat sources
Warning: May get worse first day or two of tx. Draw on pt.
Cellulitis Pitfalls
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Necrosis
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Devitalized tissue (tense, cyanotic, necrotic, bronzing
of the skin, blanched) will not be perfused, so
antibiotics will not get to the site.
If not improvement on ABX, consider devitalized
tissue & surgical
debridement
Cellulitis Pitfalls (cont.)
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Facial Cellulitis in adults
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H. Flu in adult is rare and may be toxic with
airway compromise. (usually >50yo) Admit &
tx (cefuroxime IV)
Facial Cellulitis in children
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Potentially serious !!!!
If no obvious entry for, probably H. Flu
 ? Meningitis (8% infants) ?tap.
Cellulitis Pitfalls (cont.)
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Cellulitis around the eye
Dangerous !!!
 Orbital vs. Peri-orbital cellulitis
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Periorbital (more common)
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Limited to eyelids in the preseptal region
Treat aggressively with IV abx
Orbital is EMERGENCY
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Infection spreads both by extension and retrograde
H. Flu usual
IV abx, admit, ? CT (globe displacement)
Cellulitis Pitfalls (cont.)
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Necrotizing Fasciitis
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Dangerous !!!
S. pyrogenes or others
Sx: painful, edema, necrosis,
widespread
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Occlusion of small blood
vessels to gangrene (growth
of anaerobes - eg
Bacteroides).
Risk factor: DM
Dx: x-rays show gas
Mortality 30% ! Surgical
treatment
Upper lid avulsion
Animal Bites
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Cats- Pasteurella multocida, S. aureus
Primary Antibiotic Augmentin 875mg BID x
10 days
Alternative- Cefuroxime 500 mg TID x 7dyas
80% of all cat bites become infected!
DO NOT USE KEFLEX!!!!!!
Animal Bites
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Dogs- Pasteurella mutlicoda,S. aureus
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Primary- Augmentin 875 mg BID
Alternative- Clindamycin 300 mg QID plus a
flouroquinolone
ONLY 5% become infected.
Tinea of the Foot
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Uncommon in women!
Uncommon in prepubertal children
Inevitable in immunocompromised patients
Acquired from locker-room floors and
communal baths
Once infected, patient becomes a carrier and is
at risk for recurrence
Tight fitting shoes and work-boots
Tinea Pedis
Treatment
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Promote dryness
Drysol 20% (aluminum chloride) H.S.
Topical antifungal (Loprox, Lotrimin, Spectazole)
Sometimes oral if refractory (Lamisil tablets)
Shoes that “breathe” and socks that wick away
moisture
Lamb’s wool between the toes
Treat secondary infection!!!!! (staph &
pseudomonas)
Special Treatment Considerations
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Tinea Capitis is not responsive to topical
agents. You must use an oral drug such as
Giseofulvin 500 mg. po qd.
Pediatric dosing: 10-20 mg/kg po qd X 4 – 6
weeks. Max 1 g/d. Absorption is better with a
fatty meal.
Tinea Cruris
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Warm, moist, dark, environment most
conducive to growth
If any dermatitis is treated with
topical steroids, it will initially
look better and lead to what is
called, “tinea incognito”
How Do We Know?
Melanoma
 A. One-half of the mole does not match the
other half (i.e. it is asymmetric)
 B. The edge (border) of the mole is jagged or
irregular
 C. More than one color is present in a mole
 D. It is larger than 5mm in diameter (the size
of a pencil eraser
How Can I Determine My
Personal Risk?
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It is estimated that 1 out of 7 people in the
United States will develop some form of this
cancer during their lifetime. One serious
sunburn can increase the risk by as much as
50%.
These early studies are coming into
question. Risk determination is complex
Pathologic Staging
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Depth of invasion offers the greatest
prognostic value in determining survival
Depth of invasion determines need for therapy
up and above surgical excision
Treatment
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Wide excision
Regional lymph node dissection for higher
stage disease
Chemotherapy for higher stage disease
Psoriasis
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Extensor surfaces most common
Palms and soles not commonly involved but
can be. R/O Reiter Syndrome
Localized plaques may be confused with
eczema or seborrheic dermatitis
Guttate form may be confused with secondary
syphilis or pityriasis rosea
Principles of Treatment
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Control stress
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Stress reduction techniques are effective in
controlling flares in certain patients
Determine end of treatment
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Patients perceive discoloration after clearing
plaques as continued disease
Principles of Treatment
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Calcipotriol (Dovonex)
Discovered in 1985 by chance-Women taking
Vitamin D for osteoporosis noted marked
improvement in psoriasis
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Vitamin D3 analogue
Inhibits cell proliferation and induces terminal
differentiation
Inhibits epidermal cell proliferation
Safe and effective
Applied BID in amounts up to 100 grams per week
Rx for 6-8 weeks gives 60% improvement
Does not effect ca++ or bone metabolism
Principles of Treatment
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Topical steroids
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Control itching
Results very gratifying early
Tachyphylaxis occurs
Skin atrophy and tangelectasias limit extensive use
Useful for treating intertriginous plaques and inflamed
areas
Plastic occlusion potentiates
Diprolene, Temovate
Principles of Treatment
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Intralesional steroids
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Kenalog 5-10 mg.Ml (atrophy with 10 mg
strength)
Anthralin (Anthra-Derm)
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Used only for chronic plaques
Messy stains long treatment times
Best used in combination with UVB
Principles of Treatment
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PUVA
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Methotrexate
Cyclosporine
Retinoids
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Psoralens and UVA radiation in combination
Etretinate (Tegison)
Hydrea
Psoralin UVA Treatment
UVB Treatment – Before and After
Contact Dermatitis
contact dermatitis, Skin
rash resulting from
exposure to either an
irritating or allergic
substance. In the first
type, an irritant, as
detergent or acid, causes
a sore much like a burn.
In the allergic type, the
reaction is delayed.
Symptoms are swelling,
blisters, and large
amounts of fluid in the
body tissues. Poison ivy
is a common example of
this type.
Contact Dermatitis
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Rhus dermatitis – (allergic)
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poison ivy, poison oak and
poison sumac account for
more cases of allergic
contact dermatitis than all
other contactants
combined
Occurs from contact with
the leaf,or internal parts of
the stem or roots
Occurs from direct contact
with the oleo resin
Can not be spread via the
blister fluid of current
lesions
Contact Dermatitis
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Metal dermatitis
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Nickel is the most common contact allergen
Women >men
Jewelry most often the source
Contact Dermatitis
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Diagnosis –
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History – persistent questioning may eventually
uncover the offending antigen
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Physical exam
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Date of onset
Relationship to work
Skin care products
Jewelry
Distribution
Types of lesions
Distribution
Distribution
Patch testing – indicated in cases in which
inflammation persists despite avoidance and
appropriate topical therapy
Contact Dermatitis
Fundamental principals of dermatological
therapy :
Avoid the offending agent
Wet lesions dried
Dry lesions hydrated
Inflammation treated with corticosteroids
Contact Dermatitis
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Treatment –
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the aim of treatment is to decrease erythema, pruritis and
edema
Prevent secondary infection – keep clean
Remove/avoid causative agents
Topical steroids
Oozing lesions should be dried with Burrow’s solution
compresses 3 to 4 times daily
Oral prednisone may be necessary for severe cases (tapering
dose)
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Topical corticosteroid precautions
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Wide variation in potency
Vehicle affects potency
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Ointments more potent than creams
Occlusive dressing
increases potency (do not
use ointments – folliculitis)
Adverse effects –
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Atrophy
Telangiectasia /tlan'je-ekta'zh/,
permanent widening of groups of
superficial capillaries and small vessels
(venules). Common causes are damage
due to excess sunlight, some skin diseases,
as rosacea, too-high levels of female
hormone, and collagen blood vessel
diseases.
Contact
Dermatitis
THE END