Dermatology Flashcards
Eccrine Glands
A type of sweat gland
opens directly onto skin
regulates body temperature through sweat
Apocrine Glands
A type of sweat gland opens directly into hair follicles found in axillae and anogenital areas becomes active during puberty, decrease in aging adult produce body odor
ABCDE Rule
For nevi A - asymmetry B - borders (regular vs irregular) C - color (uniformity; tan, black, blue, red) D - diameter (>6mm) E - evolution or elevation
Secondary Skin Lesion
Later evolution or result of external trauma to the primary lesion
ex. Erosion Ulcer Fissure Excoriation Atrophy Scaling Crusting
Most common types of skin cancer arise from which skin layer?
Epidermis
Remember the layers by “Come Lets Get Sun Burnt”
What are the two main cell types in epidermis?
Keratinocyte - (epithelial cells) starts out in the basal cell membrane and differentiates all the way to the corneum (dead cell layer) —keratinocyte carcinoma
Melanocyte - pigment cells - located in between the dermis and epidermis –melanoma
What is the difference between BCC and SCC?
Both types of keratinoctye carcinomas
Basal Cell Carcinoma - cancer originating from the stratum basale (or the basal cell layer)
Squamous Cell Carcinoma - cancer originating from corneum, lucidum, granulosum, or spinosum
Which type of skin cancer is most common?
Keratinocyte carcinomas (SCC, BCC) making up ~97% of skin cancer
melanoma makes up about 2% of skin cancer but is much more deadly
Acanthosis
abnormal thickness of epidermis (relative to the location on the body)
diffuse epidermal hyperplasia
Invasive SCC
this means that the squamous cells have invaded based the basal membrane and into the dermis
Hyperkeratosis
thickening of stratum corneum by abnormal keratin
often associated with a qualitative abnormality of the keratin
Parakeratosis
Retention of nuclei in stratum corneum
normal in mucous membranes
Hypergranulosis
Hyperplasia of stratum granulosum, usually caused by intense rubbing
Papillomatosis
Hyperplasia and enlargement of contiguous dermal papillae leading to surface elevation
common wart
Dyskeratosis
Abnormal keratinization occurring prematurely in cells below stratum granulosum
Acantholysis
loss of intracellular connections causing loss of cohesion between keratinocytes
Spongiosis
epidermal intracellular edema
First Degree Burn
erythema, swelling
transitory, reversible
Second Degree Burn
Blisters involving epidermis
Hair follicles, adenxa in dermis spared
Third Degree Burn
Full-thickeness burns; massive necorsis of epidermis and parts of dermis, subcutis
cannot heal spontaneously
Macule
flat, smaller than 2cm (ex. freckle)
Patch
similar to macule but larger
flat >2cm
Papule
slightly elevated, smaller than 1 cm
ex. eczema caused by allergy
Nodule
similar to papule but greater than 1 cm
(slightly elevated)
ex. nevus
Tumor
nodule greater than 5 cm
Vesicle
fluid-filled elevation of epidermis
smaller than 1 cm
ex. herpesvirus lesion on the lip
Bulla
vesicle measuring more than 1 cm (ex. burns)
Pustule
vesicle filled with pus (ex. impetigo)
Ulcer
defect of the epidermis (ex. syphilitic chancre)
Crust
skin defect covered with coagulated plasma (“scab”)
Scales
Keratin layers covering skin as flakes or sheets; can be scraped away
ex. psoriasis, seborrheic keratoiss
Squames
Large scales (ex. ichthyosis)
Excoritation
superficial skin defect caused by scratching
Fissure
sharp-edged defect extending deeper into dermis (ex. athlete’s foot)
Orthokeratosis
hyperkeratosis with just keratin, no nuclei
Parakeratosis
hyperkeratosis with keratin and nuclei
Effects on skin from chronic sun exposure
hyperpigmentation
atrophy of epidermis
dermal connective tissue degeneration
Folliculitis
bacterial infection of the hair follicule
Acne vulgaris
infiltration and destruction of follicular epithelium by neutrophilic exudate
Where are fungal infections mc?
Keratin layer (dead tissues)
Verruca Vulgaris
Common Wart
on microscope – papillomatosis
Auspitz sign
seen with psoriasis
bleeding points when scale is lifted from plaque d/t tortuous dilated vessels
What is the MC malignant skin tumor?
BCC
most commonly located on the FACE
What are telltale signs of skin cancer?
persistent, nonhealing ulcer
irregular shape
friable (crumbles), bleeds, multicolored
indurated (hardened) margins of an ulcer or tissue around it
Lentigo
macule or papule’ pigmented but does not respond to sun
Junctional nevus
mole just in the epidermis
Compound nevus
mole in both epidermis and dermis layers
Clinical Warning Signs for Melanoma
change in color, size, or shape of preexisting mole (typically >10mm)
itching or pain to nevus
new pigmented lesion developed in adult life
irregular notched borders
variegation of color (black, brown, red, blue, and gray)
What is the most important prognostic factor in melanoma?
tumor thickness
Radial vs vertical growth phase of melanoma?
Radial = (epidermis) tendency of melanoma cells to grow horizontally along the epidermis (no metastatic potential)
Vertical = (dermis) melanoma cells grow vertically in the deeper dermis with no maturation and acquire a metastatic potential
Onychogryphosis
hypertrophic nail
related to trauma
Koilonychia
thin and spoon nail
seen in Fe deficiency anemia
Onychomycosis
thicken, discolor, disfigure, and split nail, related to FUNGAL infection
Paronychia
soft tissue infection, pus formation around a fingernail
What is Impetigo?
superficial bacterial infection of the Epidermis
typically caused by a mix of staph and strep
How do people get impetigo?
minor breaks in the skin
preexisting dermatoses
Bites
wounds, burns, ulcers
HIGHLY contagious amongst close contacts
What is nonbullous impetigo?
“Classic impetigo”
Erythematous macules/papules that evolve into vesicles/pustules, rupture forming HONEY COLORED crusts
Where on the body is nonbullous impetigo most common?
face and extremities
Where on the body is bullous impetigo more common?
on the trunk and folds such as axillae
What is Ecthyma?
a type of impetigo that has extended into the dermis
the lesions are now coagulated and less honey-colored crusts
still considered a superficial infection since there is no systemic sxs
will heal with scarring
How do you dx impetigo?
Clinical dx
Microscope will help you determine if its staph or strep
Staph = clusters Strep = chains
What is the treatment for impetigo?
think if you want to go topical or oral depending on the extent of spread of infection
Topical: Bactroban (Mupirocin) - covers MRSA too - 2% ointment
Retapamulin (Altabax) 1% ointment (less commonly used)
Oral: Cephalexin (Keflex) second gen that covers both gram - and +
Clindamycin (covers MRSA)
Staph only = dicloxacillin
Augmentin (Amoxicillin - Clavulanate) -big guns
What is Erysipelas?
soft tissue infection involving the dermis and subcutaneous tissue and superficial lymphatics (similar to cellulitis)
MC in young children and the elderly
MC caused by Group A Strep (GAS)
How does erysipelas present?
actue painful onset
edematous, red, warm plaques with clear borders
MC on cheeks and ears (can also be seen on extremities but less common)
fever, chills, regional lymphadenopathy
What is the treatment for erysipelas?
outpt with oral ABX
remember you are doing broad spectrum to cover for both erysipelas and cellulitis
PCN (500mg every 6 hours)
Amoxicillin (500mg every 8 hours)
Keflex (250-500mg every 6 hours)
How does the age distribution differ between cellulitis and erysipelas?
Erysipelas is bimodal (young and old)
Cellulitis is MC in middle-aged, elderly, and immunocompromised
Pasteurella multocida
organism responsible for cellulitis secondary to dog or cat bites
IV Drug users are more likely to get cellulitis secondary to what bacteria?
Staph Aureus
If you are palpating a pt you suspect having cellulitis and you hear crunching, what pathogen should you be thinking about?
Clostridia
Crepitant cellulitis
Haemophilus influenzae causing cellulitis commonly presents where on the body?
face and periorbital
What is the clinical manifestation of cellulitis?
abrupt or gradual onset
swelling, erythema, tenderness, and warmth (may also have bulla, vesicles, necrosis)
Borders are rough and less defined - expanding
Lower extremities MC location
Fever, chills, malaise, anorexia, lymphadenopahty, lymphagitis
can lead to sepsis
What is lymphagitis?
seen with cellulitis pts the red line showing the proximal spread of the infection this is a bad sign start on IV ABX right away this is a lymphatic spread
For which pts with cellulitis should you cover for Pseudomonas aeruginosa?
penetrating trauma (“stepped on a nail”)
immunocompromised
hospitalized
What is the treatment for Cellulitis?
Keflex
Augmentin (used for cat and dog bite - pasteurella)
Dicloxacillin
Clinda (MRSA)
Cipro (puncture wounds d/t covering pseudomonas)
When should you be suspecting MRSA for a pt with cellulitis?
(this is important because you would normally be treating with keflex but if you suspect MRSA you will change to clinda or something else)
Penetrating trauma IV Drug Users Abscess/Purulent Drainage Hx of MRSA close contacts with MRSA pts recent ABX use Hospitalization
MRSA treatment
Oral:
- Bactrim DS (double strength)
- Doxycycline
- Clinda
- Linezolid
IV:
- Clinda
- Linezolid
- Vancomycin (not first line)
- Daptomycin
What is folliculitis?
Inflammation of the superficial or deep portion of the hair follicle
bacterial infection is MC cause
What is the MC bacteria responsible for folliculitis?
Staph Aureus
Hot Tub Folliculitis
pseudomonas aeruginosa
rash presents 1-2 days after being in hot tub
Psuedofolliculitis barbae
“Razor bumps”
can occur over any shaved area
related to curved hair follicles, foreign-body type reaction
can be secondarily infected by staph aureus
What is a furuncle?
folliculitis that is deeper
tender, nodules/abscesses (boils)
What is a carbuncle?
deeper folliculitis where the infections are interconnecting under the skin
several contiguous hair follicles
What is the treatment for Folliculitis?
Topical:
- Mupirocin (Bactroban) - covers MRSA
- Retapamulin (Altabax)
Oral: Keflex Augmentin (if you needed to bump it up) Bactrim DS (MRSA) Doxy (MRSA) Clinda (MRSA)
Cipro (psuedomonas - Hot tub)
What is the treatment for Folliculitis?
Topical: (if this is just one small location)
- Mupirocin (Bactroban) - covers MRSA
- Retapamulin (Altabax)
Oral: Keflex Augmentin (if you needed to bump it up) Bactrim DS (MRSA) Doxy (MRSA) Clinda (MRSA)
Cipro (psuedomonas - Hot tub)
Acute Paronychia
acute infection caused by Staph Aureus of the nail fold
Chronic Paronychia
loss of cuticle, proximal nail fold becomes boggy, nail plate becomes irregular/discolored
A pt comes in with a red swollen, painful hand with some red streaking. After asking some questions you find out he has a new kitten. What do you think he has? How do you treat it?
Cellulitis
treat with Augmentin
A pt comes in with an itchy rash. After asking some questions you find out she was recently in a hot tub. What do you think she has and how would you treat?
folliculitis
treat with cipro to cover for psudomonas
What is pediculus humanus capitis?
Head louse
What is pdiculus humanus corporiss?
Body louse
What is phihirus pubis?
Crab or pubic louse
What is pediculosis?
Lice
What is the primary symptom of pediculosis and what causes it?
Itching due to an allergic reaction to louse saliva
What do you need to dx lice?
Must have at least one life louse
Eggs (nits) does NOT confirm active infection unless they are “viable”
What is the treatment for head lice?
Since developing embryos may survive initial topical treatment you must repeat a second course 7-10 days laters to kill newly hatched nymphs
Permethrin (Nix) Pyrethrin Malathion Benzyl Alcohol Ivermectin (topical and oral)
Other treatments might include shaving or suffocation with mayo or vaseline
Non-washable items should be sealed in plastic bags for 3-5 days
How do you treat crab lice?
Same as head lice
What diseases may be transmitted by body lice?
Typhus and trench fever
What is the treatment for body lice?
Wash entire body, topical treatment or oral ivermectin
What are the hallmark features of scabies?
Intense pruritic, papular rash with excoriations
Borrowing typical in hands and wrists
Typically the head and neck are spared
“Norwegian Scabies”
Crusted scabies
EXTREMELY contagious (primarily in older, immunocompromised, or homeless)
What is the treatment for scabies?
Permethrin
Lindane (risk of neurotoxicity)
Crotamiton
Oral Ivermectin
Cimex lectulrius
Bed bugs
What is the treatment for bed bugs?
Bites typically resolve within one or two weeks Topical or oral steroids Antihistamines Eradication -heating/steaming extermination -laundering of linens -vacuuming of furniture
Red, white, and blue sign
Seen with brown recluse spider bites
Red (peripheral erythema)
White (blanching)
Blue (violaceous center)
nits
pediculosis eggs
just the presence of eggs does not confirm dx because the shells might be empty
they must be viable
How do you tell the difference between head lice and dandruff?
dandruff should flake off while nits are attached to the shaft via protein
Where are you more likely to see head lice?
in the homeless
hair shafts
behind the ears and on the back of the neck
How to lice treatment drugs work?
toxic to the louse nervous system
however this might not kill the nits so you will need to do a second treatment 7-10 days later
What is the first line treatment for head lice?
Nix (permethrin 1%) OTC
apply to dry hair for 10 minutes and then wash hair and comb to remove nits and lice
repeat in 7-10 days
A pt comes in with a pruritic papular rash that is more itchy at night, what should you be thinking?
Scabies
What is the key characteristic of scabies?
Burrowing
typically in the webbed part of the hands and toes
Where are scabies rashes more commonly located?
Belt line
Buttocks
Genitalia
in between the fingers and toes
How do you instruct pts to treat their scabies?
Permethrin 5% cream that is applied from the neck down after pt has showered
washed off after 14 hours and then reapplied again in 1 week
How does treatment change for Norwegian scabies?
you do both topical and oral
Loxosceles reclusa
brown recluse spider
How do you treat a brown recluse spider bite?
most bites can be treated with rest, ice, and elevation
make sure tetanus is up to date
pain meds
most importantly make sure wound is kept clean
What is the age of onset for pityriasis rosea?
adolescence through adults
more common in spring and fall
What is pityriasis rosea?
often considered viral (but truly unknown) falls under the class of papulosqaumous
What is the prodrome phase of pityriasis rosea?
HA
Malaise
mild constitutional sxs
What is the most common location on the body for pityriasis rosea?
the Herald patch - the trunk
the exanthem that appears weeks later - trunk and proximal extremities
Herald Patch
that initial patch of pityriasis rosea single oval lesion 2-10cm in diameter pink, salmon-red to erythematous slightly raised, fine collarette scale
Exanthem
In addition to the already present Herald rash, this new rash appears days to months later (typically 2 weeks later)
presents as a smaller lesion on the trunk/proximal extremities
“Christmas Tree” distribution of a rash
Pityriasis rosea exanthem rash that follow langer’s lines (cleavage lines of the body)
What is reverse pityriasis rosea?
when the lesions are on the extremities, sparing the trunk
What is atypical pityriasis?
herald patch may be absent or sole lesion
OR
multiple herald patches
OR
lesions may be present on face, neck, palsm and soles or unilateral
OR
vesicular, pustual, or urticarial variants
What are some of the DDx for pityriasis rosea?
lichen planus
erythema multiform
secondary syphilis
How do you dx pityriasis rosea?
clinically
can use KOH prep or RPR to rule out fugal infection and syphilis
What is the treatment for pityriasis rosea?
symptomatic
antihistamines, calamine lotion, steroids
+/- UVB phototherapy
the rash will last for about 4-10 weeks
What is the epidemiology of lichen planus?
acute or chronic
more common in females
~1% of the population
30-60 years of age
What is the cause of lichen planus?
idiopathic
however it can be associated with Hep C so screen pts with LP for HCV infection
can also be seen with drug reactions such as BB, HCTZ, ACEI, NSAIDs, antimalarial
What are the 6 Ps of lichen planus?
Purple Pruritic Polygonal Planar Papules Plaques
Where is lichen planus commonly found on the body?
flexor surfaces of the wrists, shins, lumbar, feet genitalia mouth hair nails
Koebner’s Phenomenon
new lesions of lichen planus (and psoriasis) at the sight of trauma
Besides the 6 Ps, what does lichen planus look like? (looking for a commonly used descriptive term)
wickham striae
white, lacy reticular pattern (especially oral lichen planus)
Pts with chronic oral lichen planus are at an increased risk for what?
SCC
What is the DDx for lichen planus?
drug induced psoriasis secondary syphilis pityriasis roasea lupus
What is the DDx for oral lichen planus?
candidiasis
leukoplakia
lupus
secondary syphilis
What types of drugs can cause lichen planus?
gold salts BB antimalaria pills HCTZ Furosemide spironolactone
How is lichen planus dx?
clinical presentation + punch biopsy (punch typically done by dermatologist)
in the meantime start them on steroids (since it doesn’t look fungal)
What is the treatment for lichen planus?
topical steroids if early and localized
- Clobetasol (Temovate)
- Bethamethason
- Deproprionate (Diprolene)
intralesional injections of Tiamcinolone Acetonide (Kenalog) for resistant or hyperkeratotic lesions
Oral steroids for generalized lesions
-Prednisone for 4-6 weeks then taper for 4-6 weeks
What is the prognosis of lichen planus?
majority of cutaneous LP spontaneously remit within 1-2 years
recurrences may occur
coin-shaped, disseminated, pruritic eczema lesions found on the extremities
nummular eczema
What is Tinea Corporis?
superficial fungal infection of the skin
typically from Trichophyton, Microsporum, Epidermophyton
T. RUBRUM MC
What are the risk factors for tinea corporis?
affects all ages
warm-hot environments
animals
contaminated soil
T. Rubrum
MC cause of tinea corporis
Pruritic lesions typically begin as erythematous scaly plaques with central resolution that is annular in shape
might scale or crust due to inflammation in advancing border
Tinea Corporis
Malassezia furfur
causes tinea versicolor
Well-demarcated macules/patches with fine scale
hypo-and hyperpigemention variable
MC on trunk
tinea versicolor
What does tinea versicolor look like on a KOH prep?
spaghetti and meatballs
What is the age group for acute guttate psoriasis?
children and adolescents
What is the rash distribution of acute guttate psoriasis?
mainly on the trunk
some on the face and scalp
usually spares palms and soles
What is associated with acute guttate psoriasis?
it is often precipitated by an acute strep infection
What does pityriasis mean?
scaling
Langer’s Lines
Skin cleavage lines of the body that pityriasis rosea tends to follow (Christmas tree distribution)
What do you use KOH prep for?
to determine if a rash is fungal
used in pityriasis to rule out fungal (since this rash looks fungal)
How does pityriasis rosea typically present?
Might have a prodrome of HA and malaise
Herald Patch is the first and largest patch
about 2 weeks later they might have a full blown rash
at what point with pityriasis rosea would you get a skin biopsy?
if 3 months has passed and no improvement (maybe misdx)
What is the RPR test used for?
tests for syphilis
this is a do not miss dx
know when its on the ddx
-pityriasis rosea
If a pt comes in with lichen planus, what should you screen them for?
Hep C
there is an association between these 2
If a pt has had a recent trauma and then presents with this papule like rash, what should you be thinking?
Lichen planus
Koebner’s Phenomenon
What age group is most common with erythema multiforme?
can occur in all ages but peaks between 20-40 years of age
M > F
What is the MC etiology of erythema multiforme?
HSV
What drugs can cause erythema multiforme?
barbiturates, NSAIDs, PCNs, metformin, cipro, bupropion
even vaccines (diptheria -tetanus, hep B)
What is the prodrome for erythema multiforme?
Fever
malaise
myalgia
sore throat and cough if d/t mycoplasma
What is the typical presentation of erythema mutliforme?
might have a prodrome
starts benign acutely and evolve over days
have a dark center –> target lesion (round with 3 concentric zones)
typically starts distal and moves proximal
loves palms and soles (think about secondary syphilis and lichen planus) loves elbows and knees (so does psoriasis)
What is the difference between erythema mutliforme major and minor?
Major is more commonly d/t drug erruption (think about steven johnson syndrome)
major always has mucus membrane involvement
minor usually confined to extremities and face with classic target lesions with little to no mucous membrane involvement, usually associated with HSV outbreak
What is Nikolysky sign?
seen with major erythema multiforme
when you rub the skin it comes off
this is why you are worried about stevens-johnsons syndrome
What is the prognosis of erythema multiforme?
usually resolves spontaneously within 3-5 weeks
may be recurrent (especially for those with recurrent HSV)
What is the treatment for erythema multiforme?
remove any offending drug
oral antihistamines and topical steroids for symptomatic relief
oral prednisone for severe cases
treat underlying etiology
- HSV: acyclovir
- Mycoplasma: macrolide
Where does secondary syphilis most commonly present on the body?
mucosal lesions
palms and soles
What is atopy?
eczema, hay fever, asthma
sometimes we add ASA allergy
typically in the family hx
What is the cause of pityriasis (tinea) versicolor?
yeast infection
overgrowth of the yeast on the body
What is the prevention for herpes zoster?
vaccine for those >60 years (~60% reduction)
What is the treatment for herpres zoster?
acyclovir within 72 hours of rash onset
5x/day for 7-10 days
Molluscum contagiosum
viral rash
caused by a pox virus
mostly in children or young adults
it’s self limited for about 2 months
Verruca Vulgaris (HPV)
common wart (from HPV, just a different strand) occurs weeks to months after skin to skin exposure
condylomata acuminata
anogenital warts
What is the treatment for HPV?
no treatment is curative
surgery is the most likely to be curative (and cheapest option)
QUIT SMOKING
How do you prevent HPV?
Gardasil vaccine protects against 9 different types -6 and 11 -16,18,31,33,45,52, and 58 ideally administered before the individual has become sexually active
umbilicated papules
discrete, solid, skin-colored papules 3-5mm
describes what kind of skin problem?
Molluscum contagiosum
What is the treatment of verruca vulgaris?
chemically or physically burn it off or just wait because they are self limiting
educate the pt not to spread it around (contagious)
What is respiratory papillamatosis?
caused by vaginal birth when someone has HPV
the infant inhaled the virus
How do you dx HPV?
warts if its type 6 or 11
dysplasia of epithelial cells on pap smear (type 16 and 18)
application of acetic acid solution (vinegar) –> colposcopy (not sure how common this is)
When do you see post-adolescent acne?
83% of women have pre-menstrual flares
What is oral isotretinoin used to treat?
aka accutane
used for severe acne (6 months of treatment)
works by shrinking sebaceious glands and decrease sebum secretions
What topical agents can be prescribed for acne?
retinoids such as tretinoin, adapalene, tazoratene
What is the most mild form of acne?
comedonal acne
What is the worst form of acne?
nodulocystic
What is the treatment for pts with acne around their periods?
OCPs
spironolactone
(decrease sebum production)
What are the side effects of accutane?
be sure this is monotherapy (no other acne meds)
- dry skin and lips
- photosensitivity
- teratogenicity (iPLEDGE) –> must have monthly pregnancy tests
- hypertriglyceridemia
- hepatotoxicity
- myalgia
- Pysch effects
What is rosacea?
facial flushing
inflammatory papulopustual eruption
unknown cause
chronic and relapsing
What is the classic form of rosacea?
papulopustual
erythematotalangiesctatic is central facial flushing (not classic)
What is phymatous?
Rosecea
thickened and irregular surface of nose, chine, forehead, ears, eyelids
What treatements for rosecea help with the redness?
topical brimonidine and oxymetazoline
What is hidradenitis suppurativa?
follicular occlusive disease found in the skin folds
What is the epidemiology of hidradenitis supporativa?
rare
1-4%
onset: puberty - 40y/o
W > M
What is the pathogenesis of hidradenitis suppurativa?
hormones increase follicular epithelial hyperplasia that leads to nodule that can turn into an abscess
this can lead to comedones or scarring
What is stage 1 of hidradenitis suppurativa?
abscess formation without sinus tracts or scarring
What is stage 2 of hidradenitis suppurativa?
recurrent abscesses with sinus tracts, scarring
What is stage 3 of hidradenitis suppurativa?
diffuse involvement, multiple interconnected sinus tracts and abscesses
What is the treatment of hidradenitis suppurativa?
No cure Lifestyle modification: -avoid skin trauma (wear loose clothing) -daily gentle cleansing -smoking cessation -no dairy
Mild:
- topical treatment - CLINDA
- punch debridement
- intralesional corticosteroid injections
- 7-10 day course of PO ABX (doxy)
Moderate:
- PO ABX up to 3 months
- spironolactone
- punch debridment
Severe:
- prednisone
- humera
- PO isotretinoin
Anagen
growth phase of hair cycle
2-6 years
80-90% of hairs on normal scalp
Catagen
involutional phase of hair cycle
2-3 weeks
5-10% of hairs on normal scalp
Telogen
resting phase of hair cycle
2-3 months
1-3% of hairs on normal scalp
How many hairs is normal to loose a day?
100
Alopecia Areata
Chronic immune mediated disorders
target anagen hair follicles
non-scarring hair loss
very smooth round patch of skin
What is the age group for alopecia areata?
usually before the age of 30
M = F
alopecia totalis
complete loss of scalp hair
alopecia universalis
loss of scalp and body hair
What is the treatment for alopecia areata?
intralesional corticosteriods (triamcinolone) injected into upper subQ of scalp
potent topical steroids
topical immunotherapy
What is telogen effluvium?
diffuse non-scarring alopecia
sometimes bitemporal hair loss
<50% hair loss, no balding occurs
What are the typical causes of telogen effluvium?
major surgery serious illness childbirth protein or caloric malnutrition thyroid disorders drugs emotional stress
What is the pathogenesis of telogen effluvium?
# of hairs in telogen phase increases unknown why
What is the treatment for telogen effluvium?
removal or treatment of underlying cause
minoxidil is controversial
usually is self-limited in 6-12 months
What is androgenetic alopecia?
typically in men
progressive loss of terminal hairs on anterior scalp, mid-scalp, temporal scalp
Malassezia
yeast that causes tinea versicolor
What is pityriasis alba?
small white scaly “patches” typically on the faces of kids after summer
Tinea capitis
infection of scalp hair
typically seen in children
caused by direct contact with an infected individual
pruritic
What is tinea corporis?
pruritic circular or oval, erythematous scaling plaque that usually has a central clearing and a raised border
What is tinea cruris?
fungal infection of the groin
What is tinea pedis?
fungal infection of the foot
“athletes foot”
What is tinea unguium?
Fungal infection of the nail
“onychomycosis”
What is the treatment for tinea capitis?
oral antifungals
griseofulvin for 6-12 weeks
What is the treatment for tinea cruris?
topical antifungals
terbinafine PO
Itraconazole PO
What pathogen causes impetigo?
staph and strep
What is considered “classic impetigo?”
nonbullous impetigo
erythematous macules/papules that evolve into vesicles that rupture –> honey-colored crust
Where is classic impetigo more commonly located on the body?
face and extremities
Bulla
vesicle greater than 1 cm
Why might you prescribe clinamycin for impetgio and what are the possible side effects?
if you think the impetgio is MRSA
SE: C. Diff (so be cautious in older pts)
What is the likelihood that someone who is allergic to PCN will be allergic to cephalopsorins?
since PCNs and cephs are cousins there is a 10% chance that someone allergic to PCN will be allergic to cephs
What do you do if a pt has recurrent infections of impetigo?
do a nasal swab (MRSA likes to hang out in the nares)
treat with bactroban intransal
What is a potential complication of impetigo?
poststrep glomerulonephritis
What pathogen is most commonly responsible for erysipelas?
GAS - group A strep
“I went to bed last night fine and woke up this morning with the huge rash on face”
typical presentation of erysipelas
very acute painful onset
How can you tell the difference between erysipelas and cellulitis?
Erysipelas has very clear borders
acute onset
typically on the face
Cellulitis does not have clear borders and is less of an acute onset
can be anywhere on the body but lower extremities are more common
in some cases it will be hard to tell the difference between these two but you are going to treat it more broadly so you cover both
Where is erysipelas more commonly located on the body?
cheeks and ears
Why would you get imaging (Xray, MRI, CT) on a pt you suspect has cellulitis?
- to rule out osteomyelitis
- if pt has periorobital cellulitis you want to see if they have proptosis and aggressively treat right away
You’re in the ER with a pt who you suspect has cellulitis of the lower right calf. What will your discharge notes report?
first mark their leg with a skin marker around the rash so you can compare at a later date to see if it has improved
1) take kephlex (cephalexin)
2) elevate the leg
3) use Tylenol and warm compresses PRN
4) return in 2 days for wound check or set up a phone appointment to make sure the rash has improved
inform the pt that at first the rash might get worse due to the bacteria dying a releasing more toxins but that shortly after that it should improve
if the follow up will not be with you consider printing out their chart for the pt to give the next MD they see
What pathogen should you be thinking about with ciprofolxacin?
psuedomonas
What is the treatment for acute paronychia?
warm soaks
I and D
ABX
make sure their tetanus is up to date
What is the treatment for chronic paronychia?
encourage good nail hygiene
stop nail bitting
no ABX
Terms to describe the common wart?
Papillomatosis (microscopic term)
verruca vulgaris (HPV)
What is telangiectasia?
spider veins
sometimes seen with BCC
How do you differentiate rosacea from acne?
rosacea doesn’t have comedones and is more redness localized to the central part of the face (not usually on chest or back)
When should you be concerned about hyperandrogenism?
it can be normal for women to get acnea around their periods, however if you see these other signs you should be concern (you want to rule out PCOS):
- hair loss
- irregular menses
- infertility
- abrupt onset of severe acne
- cushingoid features
- acne refractory to therapy
- acanthosis nigricans
- obesity
Which treatments are used to attack the follicular hyperkeratiniazation part of acne?
topical retinoids and isotretinoin
azelaic acid
salicylic acid
Which treatments are used to treat the increased sebum production part of acne?
oral isotretinoin hormone therapies (OCP, spironolactone)
Which treatments are used to treat the P. Acnes proliferation part of acne?
Benzoyl Peroxide (BPO)
Topical antimicrobials
Oral ABX: doxy or minocycline (limited to 3 months)
Azelaic acid
Which treatments are used to treat the inflammation part of acne?
oral isotretinoin
oral ABX
Topical retinoids
azelaic acid
Hydroquinone plays what role in acne treatment?
post-inflammatory hyperpigmentation
helps lighten dark spots
What treatments help with the rosacea bumps?
topical metronidazole topical azelaic acid sulfacetamide topical acne meds retinoids ABX (targeting inflammation more than bacteria)
How can you tell rosacea from lupus?
both can be on the face
lupus is more purple and has more demarcated borders
Alopecia universalis
a type of alopecia areata where there is loss of scalp and body hair including the eyelashes
What is the best treatment for onychomycosis?
Oral antifungals since topical antifungals take almost a year to work
Lichen Planus genital lesions are most commonly seen where?
glans penis
vulva/vagina
remember this may be associated with SCC –> long term follow up
Lichen Planus hair lesions if left untreated…
can result in scarring alopecia
Which lesions of lichen planus represent a more advanced lesion?
esophageal lesions
A pt comes in with oral lesions and body lesions, what should you be thinking?
lichen planus
but also lupus!
What do you see on microscope with lichen planus?
hyperkeratosis
both para and ortho
What is Nikolsky sign and when might it be positive?
its when you take a pencil eraser to the pts rash and gently twirl it back and forth. if a blister appears within minutes its a positive sign
seen often with Erythema multiforme major (typically d/t drug eruption)
Where is erythema multiforme commonly seen on the body?
the distal extremities moving proximally and the face
Risk factors of tinea corporis?
ringworm basically
warm-hot environments
animals
contaminated soil
Who is more likely to get mooluscum contagiosum?
children, sexually active adults, pts with HIV
What lesion is caused by pox virus?
molluscum contagiosum
How would you describe a molluscum contagiousm lesion?
discrete, solid, skin-colored papule 3-5mm on the chest
red halo regressing spontaneously
UMBILICATED papules
Condylomata acuminata
angogenital warts
How do you dx HPV?
acetic acid solution application with whitening of the lesions
Phthirus pubis
crab or pubic louse
Pediculus humans corprois
body lice
Which type of pediculosis run the risk of causing a systemic disease?
body lice
typhus and trench fever d/t louse feces (note even scabies runs this risk)
By the time a pt is scratching due to head lice, how long have they had the infestation?
it takes 2-6 weeks to develop a reaction
the more times (# of times) you are exposed the shorter time it takes to mount a response
Where are you likely to see nits are what do they look like?
close to the scalp on the shaft of the hair (they need the warmth of the head so they are close to the scalp) –they hold on using a protein matrix and do not easily flake off like dandruff would
brown colored indicates an active nit
Permethrin is used for what?
OTC treatment for head lice
How do you treat pediculus humansus capitus for a pregnant pt?
benzyl EtOH 5%
apply to dry hair for 10 minutes –wash hair – comb hair to remove nits and lice
repeat in 7-10 days
How does mayonnaise, olive oil, and vaseline work for head lice?
considered suffocating but what’s really happening is that you are slowing them down enough to allow you to effectively comb them out
What must you keep in mind for anyone with crab lice?
that this is considered an STI and you should screen them for STIs
Ivermectin is used for what?
PO treatment for body lice and scabies
Why is dx body lice sometimes difficult?
body lice are only on the body when they are feeding
so be sure to check clothing for fece marks
How long can scabies survive off the body?
4 days
How do you treat Norwegian scabies?
topical + oral drugs
such as permethrin and ivermectin
Cimex lecturlrius
common bed bug
General characteristcs of drug induced rashes
symmetrically start on the trunk and move distally
Immediate reactions (drug-induced)
Occur less than 1 hr of the last administered dose Type 1 hypersensitivity Uritcaria Angioedema Anaphylaxis
Delayed reaction (drug-induced)
Occurring after 1 hour, but usually more than 6 hours and occasionally weeks to months after the start of administration
Exanthematous eruptions
Fixed drug eruption
Systemic reactions (DIHS, SJS, TEN)
Which drug do we do allergy drug testing for?
PCN
What is the most important information in determining if a rash is medication-related?
TIMING
For exantheamtous drug eruptions, initiation of the medication is often ____days before the rash
7-10 days
What are risk factors for drug reactions?
Females Prior history of drug reaction Recurrent drug exposure HLA type Certain disease states (EBV, HIV)
Exanthematous Drug Eruption
Most common of all cutaneous drug eruptions
Does not blister
Macularpapular
Pruritic +/- fever
Rash appears more than 2 days after drug has been started (commonly around day 8-11) will persist 2-3 days after stopping the drug
Where are the greatest areas of steroid absorption on the body?
thin areas
eyelids, genitals, skin creases
use lower potency in these areas
Where are the least areas of steroid absorption on the body?
palms and soles
require higher potency drugs
What are the characteristics and benefits of ointments?
best for dry, thickened areas due to being oil based and helps trap in the water (moisturizer)
best for dry, non-hairy skin
avoid thin areas (face, armpits)
What are the characteristics and benefits of creams?
water based with oil
less potent than ointments
easy to wash off
more cosmetically appealing
have preservatives (might cause side effects)
used for exudative types lesions and intertriginous areas
What are the characteristics and benefits of gels?
alcohol base with water and oil has drying effect greaseless, transparent may be used on hair-bearing area will caused stinging to inflamed skin
What are the characteristics and benefits of lotions?
powder in water (have pt shake the bottle)
least potent of topical steroids
good for large body areas (including hairy areas)
provide cooling, drying effect as they evaporate
What are the 7 groups of topical steroid potency?
super potent (Group 1) high (2 and 3) medium (group 4) lower - mid (group 5) low (group 6) least potent (group 7)
What conditions are treated with high potency steroids (group 1-2)?
alopecia areata atopic dermatitis (only if resistant) discoid lupus lichen planus nummular eczema (only if resistant) hyperkeratotic eczema psoriasis
What conditions are treated with medium potency steroids (group 3-5)?
anal inflammation
atopic dermatitis
nummular eczema
seborrheic dermatitis
What conditions are treated with low potency steroids (group 6-7)?
diaper dermatitis
eyelid and facial dermatitis
What is the most common side effect of topical steroids?
skin atrophy
other side effects:
- striae
- easy bruising or tearing of the skin
- telangiectasias
- hypopigmentation
- acneiform eruption, steroid - induced rosacea
- cushing syndrome or hyperglycemia
- glaucoma or cataracts
- tachyphylaxis
Path of atopic dermatitis
genetic defect that disrupts skin barrier function making the skin more sensitive to irritants
What is the epidemiology of atopic dermatitis?
very common
11-19%
all cases start within first decade of life
only 5% of cases develop after 5 years of age
this is an infant/toddler disease
How does the rash distribution of atopic dermatitis differ between age?
children: face
older: flexor surfaces
What is a long term treatment to decrease skin infections d/t atopic dermatitis?
bleach baths
Exanthematous Drug Eruption
Most common of all cutaneous drug eruptions
Does not blister
Macularpapular
Pruritic +/- fever
Rash appears more than 2 days after drug has been started (commonly around day 8-11) will persist 2-3 days after stopping the drug
Fixed Drug Eruption
Solitary erythematous patch or plaque that will recur at the same site with re-exposure to the drug
What drugs are associated with fixed drug reaction?
Phenophthalein (laxatives) Tetracyclines Sulfa drugs NSAIDs Barbiturates Food coloring (yellow)
Where are the common locations for fixed drug reaction rashes?
Mouth
Genitalia
Face
Acral areas
Remember this is one solitary lesion
What is the time of onset for fixed drug reactions?
30 minutes to 8 hours after ingesting the drug (for previously sensitized individuals)
What is the treatment of fixed drug reactions?
Lesions resolve days to weeks after the drug is discontinued
Non-eroded lesions can be treated with an antimicrobial ointment and a dressing until the site is reepithelized
Address pain
Drug-induced hypersensitivity syndrome
Also known as drug reaction with eosinophilia and systemic symptoms (DRESS)
Skin eruption with systemic sxs and internal organ involvement (liver, kidney, heart)
Typical sxs: macular exanthema, erythematous centrofacial swelling, fever, malaise, lymphadenopathy, involvement of other organs
> 70% of pts have an eosinophilia
When are you going to stop all medications for a pt with a skin rash?
If you suspect DIHS and they’re basically on their way to the ICU
What is the treatment for DIHS?
Get Dermatology involved
Stop medications if severe
Start systemic steroids if severe (topical + antihistamines if moderate)
What medications can cause DIHS?
Allopurinol ABX (sulfas, PCNs) NSAIDs AntiTB drugs Anticonvulsants AntiHIV drugs
What is the clinical course of DIHS?
typically starts 3 weeks post drug
macular exanthem erythematous centrofacial swelling fever, malaise lymphadenopathy >70% have eosinophilia
Epidermal Necrolysis Spectrum
A spectrum that includes SJS and TEN
What is the mortality rate of SJS/TEN?
SJS 5-12%
TEN >20%
Which drugs have higher risk of SJS/TEN?
Sulfa ABX Allopurinol Tetracyclines Anticonvulsants NSAIDs Nevirapine Thiacetazone
(Mnemonic SATAN)
What is the time frame of SJS/TEN?
Clinically begins within 8 weeks after onset of drug exposure
What clinical findings do you see with SJS/TEN?
Fever
HA
Rhinitis
Myalgias
May precede the mucocuutaneous lesions by 1-3 days
Eruption is initially symmetric and distributed on the face, upper trunk, and proximal extremities
Rash can rapidly extend to the rest of the body
Erythematous, irregularly shaped, dusky red to purpuric macules (atypical targets) which coalesce
NIKOLSKY sign
How do you determine the difference between SJS and TEN?
Based on the TBSA which is determined by counting ALL skin lesions, ruptured and unruptured blisters
For a pt you suspect has SJS/TENs which consults will you be contacting?
Derm
Ophthamology
Gynecology
SSSS
Staph Scalded Skin Syndrome
Infant disease most commonly
Staph bacteremia
Bright red confluent painful rash with large blisters. Sandpaper texture.
SSSS
What is the path behind SSSS?
Staph exfoliative exotoxin cleaves the desmoglein 1 complex
5% of all Staph Auerus strains produce this endotoxin
Spread person - person
What is the mortality rate of SSSS?
Infants 4%
Older children/adults 60%
What is the prodrome for SSSS?
Fever
Sorethroat
Conjunctiviits
What is the time frame for SSSS?
Rash develops within 48 hours of prodrome
How do you differentiate SJS/TEN from SSSS?
Biopsy
SSSS - epidermal cleavage
SJS/TENS - subepidermal cleavage w/ epidermal necrosis
What is the treatment for SSSS?
Penicillinase-resistant PCN
- Nafcillin, oxacilin
- Vanco for MRSA
Wound care
Monitor fluid status
Pemphigus
Bullous disease
Autoimmune disease
Painful, generalized flaccid blisters with mucosal involvement
Acute and chronic forms
Can be confused with SJS
4 types:
- Pemphigus vulgaris (70%)
- pemphigus foliaceus
- IgA pemphigus
- Paraneoplastic pemphigus
What is the path behind pemphigus vulgaris?
Acanthloysis (loss of adhesion from keratinocyte to keratinocyte) results d/t circulating autoantibodies (IgG) against epithelial cell surface antigens (desmoglein 1 and 2) leading to intra epithelial cutaneous and mucosal lesions
What is the epi for pemphigus vulgaris?
Rare (0.1 per 100,000)
Higher risk in Ashkenazi jews, indian, mediterranean, middle east decent
Age 40-60 years
M = F
Genetics
Contributing factors of pemphigus?
Genetic -HLA class 2
Drugs - penicllamine, captopril, NSAIDs, cephs
Infections - Herpes, coxsackivirus
Clinical picture of pemphigus vulgaris
usually starts with painful excoriated mouth blisters
can be months before cutaneous signs
flaccid irregular border and varying size blisters begin to form on normal appearing tissue
blisters usually coalesce and rupture easily
PAINFUL
How do you dx pemphigus vulgaris?
Skin biopsy - intraepithelial seperation and acanthloysis
“Tombstone” appearance d/t retention of keratinocytes
What is the treatment for Pemphigus vulgaris?
Corticosteroids
Immunosuppressive drugs -rituximab, sulfasalazine, methotrexate
IVIG
What is the difference between bullous pemphigoid?
Both are autoimmune
Bullous pemphigoid is sub-epidermal blister while PV is intra-epidermal blistering
Bullous is less deadly and rarely involves mucous and higher age of onset (65-70)
Both are prone to relapse
What is necrotizing fasciitis?
Invasive bacterial infection of the soft tissue and deep tissue invading the fat, fascia, and at times underlying muscle causing death of tissues
Bacteria spread occurs across fascial plane
What are risk factors for necrotizing fasciitis?
DM immune compromised (CA, organ transplants) Obesity Surgery Traumatic wounds
Necrotizing Fasciitis type 1
Polymicrobial
Anaerobes: one of (bacteroides, clostridium, peptostreptococcus)
PLUS
Facultative anaerobes (e. Coli, entrobacter, klebsiella, proteus)
Necrotizing Fasciitis type 2
Monomicrobial GAS Staph MRSA Vibro vulnificus
What is the presentation of necrotizing fasciitis?
Fever
Intense pain (early on its out of proportion to PE findings)
Systemic toxicity
+/- site of introduction
Local edema, cerpitus
Skin abnormality, red, purple, or necrotic tissue
SPREADS RAPIDLY
What is the treatment for necrotizing fasciitis?
ABX
- carbapenems
- anaerobic coverage - clindmycin
- MRSA coverage (Vanco, linezolid)
NPO because they are going to the OR TODAY
Fournier Gangrene
Necrotizing fasciitis of the perineum or scrotum
What pathogens are responsible for fournier gangrene?
E. Coli (aerobe)
Bacteroides (anaerobe)
What is the Epi of fournier gangrene?
80% have DM
Trauma to genitalia frequently associated
M > F
Age: 30-60 years
What is the path of fournier gangrene?
Effects superficial and deep tissues of genitalia and perineum
Infection can originate from anorectum, urogenitalia tract, or skin of the genitalia
Can spread across the Colles fascia of the abdominal wall and Scarpa’s fascia of the inguinal area
What is the treatment of fournier gangrene?
Fluid support
ABX (cover gram -, +, anaerobes, MRSA)
REMOVE DEAD TISSUE ASAP
+/- IVIG
What are complications of Fournier Gangrene?
Pain with erection (50%) Genitial scarring Impotence Psych consideration Extensive reconstruction needs NSQIP mortality rate: 10%
Purpura fulminans
Thrombotic disorder with purple hue enlarging lesions and necrotic distal digits caused by hemorrhagic skin necrosis and coagulation impairment rapidly leading to DIC
Idiopathic vs underlying infectious caused (meningococcal meningitis - Neisseria)
Protein C deficiency is associated with which type of skin disorder?
Pupura fulminans
Which infection is most commonly associated with purpura fulminans?
Neisseria meningococcal meningitis
What is the presentation of purpura fulminans?
7-10 day onset after infection
Starts DISTALLY symmetric
Systemically ill - fever, hypotension
What is the treatment for purpura fulminans?
Fluid management ABX broad spectrum DIC management Heparin vs protein C concentrate Remove dead tissue —typically amputation
For a pt with atopy, which part of the triad typically started first?
Atopic dermatitis when they were an infant
What is the most common treatment for atopic dermatitis?
Emollients (thicker form of lotion OTC)
What is the epi of atopic dermatitis?
Common. 11-19% prevalence
All cases start within the first decade of life
Only 5% of cases develop after 5 years of age
What is the lesion distribution by age for atopic dermatitis?
Infants: face
Older: flexor surfaces
What other skin condition might present with a pt who has atopic dermatitis and why?
Impetigo due to these pts having more staph on their skin
What are the characteristics of the rash for chronic atopic dermatitis?
Lichenification (leather like fibrosis d/t chronic scratching)
Hyperpigmentation (if active)
Depigmentation (overtime)
On your differential for atopic dermatitis is contact dermatitis. How can you tell these two apart?
Contact dermatitis (whether allergic or irritant) is always related to the location in which the pt was exposed
How can you tell scabies apart for atopic dermatitis?
Atopic dermatitis in infants is always on the face while scabies typically is seen on the trunk (belt line) and genitalia
How can you tell atopic dermatitis from seborrheic dermatitis?
Seborrheic dermatitis is commonly found in the nasolabial folds but has more flaking as opposed to the pustule appearance of atopic dermatitis
What is first line treatment for atopic dermatitis?
Ideally using emollients often enough to decrease flare ups and thus the need for steroids
STEROIDs are first line treatment for flare-ups —mid potency (grade 5-7) apply 2-3 times a day
Second line - TCIs (Topical Calcineurin Inhibitors)
Rank in order from most potent to least potent vehicles of steroids
Ointment > cream > lotion
What are the major side effects of long term use of high dose steroids?
Skin atrophy!!
Telangiectasia
Striae
What is an appropriate long term treatment/prevention for atopic dermatitis?
Bleach baths
What determines potency of a topical steroid?
Vasoconstricitve effect
Grade 1 = most potent
Grade 7 = least potent
Super high potency topical steroids (group 1) are best for use where?
Palms and sole, hyperkeratotic lesions
Short term use - no longer than 3 weeks
How do you determine how much steroid to prescribe a pt?
You will be doing once or twice dosing daily
FTU - fingertip unit application method
1 fingertip unit = 0.5 grams
Multiply that by how many FTUs are needed to treat specific area (numbers given on a chart)
This will tell you how much is needed for 1 application
For ex.
0.5g x 7 FTUs needed for trunk = 3.5 gms needed per application
2 applications a day for 1 week = 49g tube needed
Which steroids can be used for intralesional injections and for which conditions is this done?
Triamicinolone acetonide
Methylprednisone acetate
Hyperkeratotic lesions
Cystic acne
Keloids
Immediate reactions to drugs
Occur less than 1 hour after last administered dose
Type 1 hypersensitivity reaction
Urticaria
Angioedema
Anaphylaxis
Delayed reactions to drugs
Occurring after 1 hour but usually more than 6 hours and occasionally weeks to months after the start
- exanthematous eruptions
- fixed drug eruption
- systemic reactions (DIHS, SJS, TEN)
What is angioedema?
Leaky blood vessels in the lower dermal layer caused by histamine release
Erythematous patch with central bulla
Fixed drug eruption
What is the path of psoriasis?
Autoimmune
Multifactorial (genes + environment)
HLA-Cw*0602
Bad MHC-1 receptor that the body sees as foreign and attacks
This results in hyperkeratosis
What do you see microscopically with psoriasis?
Acanthosis - “Test tubes in a row”
Hyperkaratosis with parakaratosis
Who gets psoriasis?
2-3%
W > M (or is it that women are more likely to seek help?)
Onset 15 - 30 y/o (median age 28)
10-15% begin in children young than 10
Erythematous scaly patches, plaques. Might be painful. Well defined round or oval plaques.
Symmetrically found on the extensor surfaces of arms, legs, scalp, buttocks, and trunk.
Psoriasis
90% are plaque
Silvery scale unique to psoriasis
What is the most common ocular finding in psoriasis?
Blepharitis
Plaques forming at the glands that lead to the eye
Eyelid erythema, edema, and psoriatic plaques
What nail findings might you see with a psoriatic pt?
Onychodystrophy
Pitting
Fingernails > toenails
Does not respond well to tx
What is the time frame of psoriatic arthritis?
~12 years after onset of skin disease
This puts the onset to about 30-40 years of age
This is not typical for arthritis so it helps you narrow you ddx to psoriatic arthritis
If you treat it early you help prevent it from progressing to full blown arthritis
How do you dx psoriasis?
Clinical dx
Unless its not the typical plaque psoriasis
Ddx
- syphilis
- pityriasis rosea
- pityriasis alba
- tine
- atopic dermatitis
What defines the difference between mild and severe psoriasis?
Mild: <5% of BSA
Severe: >5% of BSA
What are recommendations to help manage psoriasis for all forms and severity?
Daily sun exposure Topical moisturizers Sea bathing (order salt for salt baths at home) Relaxation Salicylic acid lotions OTC “tar” preparations
What is the treatment for mild psoriasis?
Topical steroids
Vitamin D analogs (calcipotriol, calcitriol)
Tazarotene (Tazorac)
Calcineurin inhibitors (tacrolimus, pimecrolimus)
Always consider PSYCH help for those that struggle with the social part or have genital plaques
What is the treatment for severe psoriasis?
Severe (>5%)
Mainstay of treatment = systemic therapy +/- phototherapy
-methotrexate (immunosuppressant)
SE: bone marrow suppression
-Acitretin (retinoid) - particularly good for pustular or palmoplantar forms
SE: teratogen
-Cyclosporine (calcineurin inhibitor) - used for rapid relief, “crisis therapy”
-Apremilast (PDE4 inhibitor) —good for arthritis
Cyclosporine is used for what?
Rapid relief, bridge therapy or “Crisis” therapy for severe psoriasis
SE: GI intolerance, renal impairment
What other options do you have if a pt with severe psoriasis isn’t responding to topical + systemic meds?
Biologics - all injections
TNF-a inhibitor (Humira - Adalimumab - SC injections q2 weeks)
IL-12/IL-23 inhibitors
IL - 17 Inhibitors
On these injections for LIFE
$$$$$
Insurance will only cover it if you have exhausted every other option of psoriasis treatment
Fitzpatrick Skin type 6
Black
Never burns, tans very easily
Fitzpatrick skin type 1
White; very fair; red or blonde hair; blue eyes; freckles
Always burns, never tans
What is the path of vitiligo?
Multifactorial disorder
Immune-mediated melanocyte destruction
Absence of melancytes within lesions
Must have some type of exposure before the disease starts (not sure what that exposure is but this isn’t seen at birth)
Associated with other autoimmune disorder
Who gets vitiligo?
It’s the most common depigmentation disorder 1% of general population Family hx in 25 - 30% of pts Adults = children F = M
Age of onset typically ~10 years
Pts commonly have DM
What are precipitating factors of vitiligo?
Usually nothing but sometimes:
Illness
Emotional stress
Sunburn
How do you dx vitiligo?
Clinically
Might need woods lamp in fair skinned individuals —the lesions will illuminate
What is the typical distribution of vitiligo?
Neck, clavicle Arm pits Genitalia Fingertips Knees Feet
Might also see it at sites of “trauma” - Koebner’s Phenomenon
What is the treatment for vitiligo?
Sun protection - SPF 50 min —need to protect from SCC, BCC
Cosmetic coverage
Topical steroids - Betamethasone (0.05%) - for actively growing lesions
Phototherapy - to kill off the expansion
Depigmentation
Surgical grafting (not a good option)
Oculocutaneous albinism
Skin, hair, and eyes without melanin production
What is the inheritance pattern of albinism?
Autosomal recessive
What is the path of albinism?
Autosomal recessive
Mutation of tyrosinase - enzyme used in melanin production
Results in no melanin production
What is the treatment of albinism?
Prevention of sun damage
SPF 50
UVR blocking clothes
Regular follow up with dermatology and ophthamology
Solar lentigines
“Liver spots”
Localized proliferation of melanoctyes and melanization
Hperpigmented, well-circumscribed lesions
Sun exposed areas
Skin Types 1-3 most at risk
What do you have to keep in mind when dx solar lentigines?
Must differentiate from actinic kertosis and lentigo maligna
- premalignant condition
- warning signs: rapid growth, pain, itching, bleeding, poor healing
Can be difficult to distinguish from early seborrheic keratosis
Solar lentigines will just show up over a few days and will stop growing …no pigmentation change, no growth, no elevation
If it does change be weary that this is no liver spots
What is the treatment/prevention of solar lentigines?
Basically just make sure this isn’t precancerous
Albative therapies - chemical peels, cryotherpay, laster therapy
Topical theapies - hydroquinone, retinoids
Prevention: regular sunscreen use and limiting sun exposure
Melasma
Progressive, macular, nonscaling hypermelanosis of sun-exposed areas (face)
Associated with:
- pregnancy
- oral contraceptive use
- phenytoin
Skin types 4-6
What is the treatment of melasma?
Hydroquinone 3% or 4%
Glycolic or Azelaic acid peel
Retinoids
Prevention:
- sunscreen
- discontinue oral contraceptive
Freckles
Ephelides
Small 1-2mm sharply defined macular lesions, uniform color
Face, neck, chest, arms
Childhood onset
Fade in winter
Can be treated in same manner as lentigo if necessary
Cafe-au-Lait macules
Tan or brown macule 1-20 cm (HUGE) Present at birth or early childhood 10-30% of general population has isolated cafe-au-lait Increase in melanin production Usually found on trunk
IF >6 CAFE-AU-LAIT LESIONS: Think about other underlying conditions (This can be a precursor) -fanconi anemia -neurofibromatosis -tuberous sclerosis -albright syndrome
Acanthosis Nigricans
Seen in DM or obese pts
Dark, hyperkeratosis streaks in skin folds:
- neck
- axilla
- groin
- body folds
What is the treatment of acanthosis nigricans?
Treat the underlying condition
DM or weight loss
Post-inflammatory hyperpigmentation
Irregular, dark pigmented macules and patches at site or previous injury or inflammation
- acne
- psoriasis
- lichen planus
- atopic dermatitis
- contact dermatitis
- trauma
All skin types
More obvious in 4-6 skin types
Lesions persist for months to years
Treatment: hydroquinone or azelaic acid
Nevi
Pigmented and no-pigmented tumors of the skin Contain nevus cells Any location on the body # increase with age Type/number genetically determined
Borders are regular and color even throughout lesion
What is a mole?
A collection of nevus cells
Keloids
Overgrowth of fibrous tissue Extends beyond the site of injury Can also occur spontaneously Family hx, genetic predisposition 4x more common in persons of afrobarribbean descent
Where are the common sites of keloids?
Head, neck, chest, and arms
Can be painful, itchy, stingy
What is the treatment for keloid?
Topical steroids - gels, locations, creams, ointments
Intralesional injections - kenalog, 5FU
Surgical excision
Recurrence is common
What is the rule of thumb for hairs growing out of nevi?
If hairs grow out of nevi they are probably benign
Epidermal cyst
“Balloon containing degraded skin contents”
Nodule with central pore (punctum)
Can originate from invagination of epidermis into the dermis or spontaneously
What is the treatment for epidermal cyst?
Intralesions kenalog injection
Incision and drainage
Surgical excision
Lipoma
Most common connective tissue tumor
Occurs most commonly in middle and later aged adults
F > M
Locations: back, chest, abdomen, neck
Cause - unknown
Asymptomatic
No treatment necessary - cosmetic surgery only reason usually
What is the most common connective tissue tumor?
Lipoma
Dermatofibroma
Very common F > M Trauma may play a major role -insect bites -folliculitis -injury to the skin
Painless, slow growing
No treatment needed
Surgery is curative - cosmetic reasons
Acronchordons
Skin tags
Soft tumors of normal skin
Location: neck, axillae, groin
Removal - cosmetic, irritation, and infection
What is the treatment for skin tags?
(Aka acrochordons)
Electrodessication (destruction) or surgical excision
Hemangioma
Vascular abnormalities
Not hereditary
Present at birth or develop in infancy
Can cause obstruction-eye, urogenital area, nose, mouth
Spontaneous involution may occur after a few years
Does not become cancerous
No treatment needed unless bleeding:
- systemic steroids
- arterial embolization
- surgery
Neurofibroma
Most common type of neural sheathe tumor
Nodular lesion located on the skin
Consider evaluation for neurofibromatosis
Neurofibromatosis
- autosomal dominant
- congenital and acquired tumors of CNS, skin, eyes, bones, endocrine glands, and Cafe au lait macules
What is the most common type of neural sheath tumor?
Neruofibroma
Actinic keratosis
Precancerous lesions Red scaly plaques located on the skin Occur on sun exposed areas - face, ears, hands, scalp Common in fair skinned 5-10% lesions become SCC
What is the clinical sxs of actinic keratosis and how do you treat it?
Precancerous!
Tender, burny or itchy, or even no sxs
Tx:
- cryosurgery
- curettage
- electrosurgery
- topical chemotherapy
What are the common locations for actinic keratosis?
Sun exposed areas - face, ears, hands, neck, scalp
What are the malignant and precancerous lesions?
Actinic Keratosis
BCC
SCC
Malignant melanoma
What is the most common type of skin cancer?
BCC
Where are the common locations to find BCC?
Face and neck
What are the clinical manifestations of BCC?
Translucent papule or lesions that will not heal
Become a large sore or ulcer that will not heal if untreated
Very rare metastasis
What is the second most common type of skin cancer?
SCC
What age group is more likely to get SCC?
Pts over 50
Can have a genetic tendency to develop lesions
Malignant Melanoma
Most DEADLY form of skin cancer
Can metastasize to other organs
ABCDE rule of melanoma
What are the 4 types of malignant melanoma?
Acral lentiginous
Nodular
Superficial spreading
Lentigo maligna
70% are superficial spreading type
What is the treatment for malignant melanoma?
Same for all skin cancers
- surgical excision
- Mohs surgery
- Electrodessication and curettage - not recommended
- Cryosurgery - not recommended
- Chemotheraperutic drugs - topical and oral
“Test tubes in a row”
microscopic evaluation of PSORIASIS - epidermal acanthosis
MC locations for psoriasis plaques?
extensor surfaces
“beefy red”
intertrigo - candidiasis
What is the treatment for intertrigo?
topical antifungals (clotrimazole, miconazole, nyastatin)
steroids
keep area dry
Who gets intertrigo?
F > M
DM
Obese
located in the skin folds
Tense bullae
bullous pemphigoid
treat with steroids
