Derm Lecture 2 Flashcards
acne epidemiology
- Most common cutaneous disorder affecting adolescents & young adults
- Resolves in 3rd decade
- Post-adolescent acne affects women
- Adolescent acne affects males
acne is a disease of?
acne is a disease of pilosebaceous follicles
4 factors of acne pathology
- follicular hyperkeratinization (turning over of dead skin cells)
- increased sebum production
- Cutibacterium acnes w/in the follicle
- Inflammation
acne pathogenesis
- Sebaceous glands enlarge & sebum production increases during pre-puberty
- Sebum provides a growth medium for C. acnes
- Microcomedones (pores) provide an anaerobic lipid-rich environment for bacteria
- Inflammation results in the proliferation of C. acnes
what are the 3 types of acne lesions?
closed comedone - whitehead
open comedone - blackhead
inflammatory papules and nodules
what is a closed comedone?
whitehead - type of acne lesion
Accumulation of sebum and keratinous material converts a microcomedone into a closed comedone
what is a open comedone?
blackhead - type of acne lesion
follicular orifice is opened w/continued distension forming an open comedone – densely packed keratinocytes, oxidized lipids, and melanin all contribute to dark color
what are inflammatory lesions for acne?
type of acne lesion
follicular rupture contributes to this; proinflammatory lipids & keratin are extruded into the surrounding dermis leading into inflammatory papules & nodules
how do androgens contribute to the development of acne?
through stimulating the growth and secretory function of sebaceous glands
most circulating androgens are produced by what glands? and others, that aren’t, are produced by what glands?
most produced by adrenal glands, others produced by sebaceous glands
who and how does infantile acne occur in?
occurs as a result of elevated androgen levels produced by the adrenal glands in girls and by adrenal and testes in boys
androgen levels fall by age 2 and acne improves
how does puberty contribute to causing acne?
onset of acne correlates with the rise in serum DHEA-S levels that occur as puberty approaches
higher DHEA-S found in prepubertal girls with acne than those w/out
do the majority of pts with acne have androgen excess or normal androgen levels?
normal androgen levels
what conditions do you see hyperandrogenism in?
PCOS
congenital adrenal hyperplasia
adrenal or ovarian tumors
what external factors contribute to acne?
soaps, detergents and astringents - remove sebum from the skin surface BUT DO NOT ALTER SEBUM PRODUCTION
repetitive mechanical trauma like scrubbing may worsen acne by rupturing comedones and promoting inflammatory lesions
turtlenecks, bra straps, shoulder pads, and helmets may produce acne mechanica - occlusion of the pilosebaceous follicles leads to comedone formation
major causes of drug induced acne
- glucocorticoids
- phenytoin
- lithium
- isoniazid
- epidermal growth factor receptors inhibitors
- androgens
- corticotropin
- disulfiram
milk and acne
natural hormonal compounds of milk or other bioactive molecules in milk could exacerbate acne
consumption of milk has been associated with increased levels of insulin like growth factor (IGF)
family history and acne
- Case controlled studies show a more than 3 fold risk among individuals with affected first degree family members
- Twin studies support heritable nature of cases of severe acne
Insulin resistance and acne
-May stimulate increased androgen production and is associated with increased serum levels of IGF-1
diagnosis of acne
PE, Type and location of acne
Endocrine function
- Hyperandrogenism - PCOS is most common cause
- Sx’s of PCOS = menstrual irregularity, hirsutism, acne, ovarian cysts, insulin resistance, acanthuses nigrans
- May adrenal or ovarian tumor
labs to run for acne
- DHEA-S
- Total testosterone
- Free testosterone
First line tx for mild acne
Benzoyl Peroxide (BP) or topical retinoid
OR
Topical combination: BP + antibiotic or retinoid + BP or retinoid + BP + antibiotic
First line tx for moderate acne
Topical combination: BP + antibiotic or retinoid + BP or retinoid + antibiotic
OR
Oral abx + topical retinoid + BP
OR
Oral abx + topical retinoid + BP + topical abx
First line tx for severe acne
Oral abx + BP + abx
or
retinoid + BP
or retinoid + BP + abx
OR
isotretinoin
what is rosacea?
-common, chronic skin disorder characterized by relapses
where is rosacea localized to?
primarily localized to central face
what are the 4 types of rosacea?
- erythematotelangiectatic
- papulopustular
- phymatous
- ocular rosacea
rosacea epidemiology
- Fair-skinned ppl
- Celtic & Northern European origin greatest risk
- Adults over 30
- Female predominance except for phymatous form
- Phymatous form: adult men
erythematotelangiectatic rosacea clinical features
persistent central erythema flushing
telangiectasias (enlarged cutaneous blood vessels)
roughness & scaling, skin sensitivity-stinging or burning
erythema congestivum (after an exacerbation of facial redness, return to baseline to slow)
papulopustualar rosacea clinical features
presence of papules and pustules in central face
- may be mistaken for acne
- Unlike acne, comodones do NOT occur
inflammation extends well beyond follicle
phymatous rosacea clinical features
exhibits tissue hypertrophy which manifests as thickened skin w/irregular contour
-common on nose, but can be on chin, cheeks & forehead
ocular rosacea clinical features
occurs in more than 50% of pts w/rosacea
- may precede, follow or occur concurrently w/disease
- exhibits conjunctival hyperemia, blepharitis, keratitis, lid margin, teleangiectasias, abnormal tearing, chalazion, hordeolum
rosacea exacerbating factors
- Exposure to extreme temps
- Sun exposure
- Hot beverages
- Spicy food
- Alcohol
- Exercise
- Irritation from topical products
- Emotions-anger, rage, embarrassment
- Drugs- nicotinic acid, vasodilators
- Skin barrier disruptions
rosacea pathogenesis factors
- abnormalities in innate immunity
- inflammatory rxns to cutaneous microorganisms
- UV damage
- vascular dysfxn
rosacea dx
- Clinical assessment is sufficient
- Skin biopsies rarely indicated
- No serologic studies useful
rosacea ddx
acne (has comedones)
-rosacea is different from acne by the presence of the neurovascular component and the absence of comedones
erythematotelangiectatic rosacea tx
1st-line interventions- behavioral changes, avoid triggers (e.g. sun protection, decr ETOH)
2nd-line- laser & light-base therapy;
pharmacotherapy - alpha-adrenergic agonists
-Topical Brimoidine (Mirvaso)
-Topical Oxymetazoline (Rhofade)
papulopustular rosacea tx
- Topical Metronidazole
- Topical Azelaic acid
- Topical Ivermectin (Soolantra, Sklice)
- Oral Tetracycline, Doxycycline, Minocycline
- Oral Isotretinoin
ocular rosacea tx
- Lid scrubs
- Warm compresses
- Topical antibiotics (Ilotycin ointment)
- Referral to Ophthalmologist
phymatous rosacea tx
- Oral Isotretinoin in early disease
- Laser ablation & surgery in advanced disease (e.g. rhinoplasty)
what is psoriasis and what is it characterized by?
- Common chronic inflammatory skin disease
- Characterized by well-demarcated, erythematous plaques with silver scale, “silver scaley plaques”
psoriasis epidemiology?
- Associated w/variety of comorbidities
- Prevalence increases w/distance from equator
- Any gender
- 2 peaks for age of onset: 20-39 & 50-69 y/o
types of psoriasis
chronic plaque psoriasis (most common)
guttate psoriasis
pustular psoriasis
erythrodermic psoriasis
inverse psoriasis
nail psoriasis
chronic plaque psoriasis clinical features
- most common
- symmetrically distributed cutaneous plaques
- scalp, extensor elbows, both knees and gluteal cleft common sites
- plaques may be asymptomatic but pruritis is common
what are the common sites of chronic plaque psoriasis?
scalp, extensor elbows, both knees and gluteal cleft
what is present in chronic plaque psoriasis?
pruritis
guttate psoriasis clinical features
- abrupt appearance of multiple small psoriatic papules & plaques usually <1cm
- trunk & proximal extremities most common
- child or young adult with no hx of psoriasis
- strong association with recent infection (post strep complication)
guttate psoriasis seen in who?
child or young adult with NO hx of psoriasis
guttate psoriasis has a strong associated with what?
strong association with recent infection (post strep complication)
where does guttate psoriasis commonly occur on the body?
trunk & proximal extremities most common
pustular psoriasis clinical features
- life-threatening complications
- most severe variant (von Zumbusch type)
- acute onset wide-spread erythema, scaling and sheets of superficial pustules
- associated w/malaise, fever, diarrhea, leukocytosis, hypocalcemia
what psoriasis has life-threatening complications?
pustular psoriasis
what is the most severe variant of pustular psoriasis?
von Zumbusch type
what are causes of pustular psoriasis?
reported causes include pregnancy, infection & withdrawal of glucocorticoids
erythrodermic psoriasis clinical features; complications related to what?
- uncommon- acute or chronic
- characterized by generalized erythema and scaling from head to toe
- complications related to loss of adequate skin barrier & electrolyte abnormalities
inverse psoriasis clinical features
- presentation involving intertriginous areas
- inguinal, perineal, genital, intergluteal, axillary, inflammatory
- sometimes misdiagnosed as a fungal or bacterial infection
nail psoriasis clinical features
- often noted after onset of cutaneous disease
- more common in pts w/psoriatic arthritis
- most common abnormalities is nail pitting
who is nail psoriasis most common in?
in pts w/psoriatic arthritis
what is the most common abnormality of nail psoriasis?
nail pitting
psoriasis risk factors
Genetics
-40% have a family hx
concordant among monozygotic twins
-multiple susceptibility loci
Smoking
Obesity-increased levels of proinflammatory cytokines
Drugs- beta blockers, lithium, antimalarial
Infections- Poststrep flares & HIV well kown contributers to worsening sx
Alcohol- associated w/risk of development of psoriasis
Vit D Def- lower in pts w/psoriasis
what drugs are risk factors for psoriasis?
beta blockers, lithium, antimalarial
obesity and psoriasis
increased levels of proinflammatory cytokines
vit d and psoriasis
vit d is lower in pts w/psoriasis (vit d def)
psoriasis pathogenesis
- Complex immune-mediated disease
- Typical clinical findings of scaling, induration, & erythema, hyperprolifration & abnormal differentiation of the epidermis, inflammatory cell infiltrates, vascular dilitation
psoriasis dx
- Family hx
- Clinical exam
- Skin biopsy
- No lab tests
psoriasis mild to moderate txs
- Emollients (e.g. Ucerin)
- Topical corticosteroids:
1. hydrocortisone
2. triamcinolone
3. fluocinonide
4. betamethasone diproprionate
5. clobetasol
Vitamin D Analogs:
- calcipotriol (Calcitrene, Dovonex)
- calcitrol (Vectical)
- tacalcitol
- Tar- T/Gel (Neutrogena)
- Topical retinoids- Tazarotene cream
- Anthralin (Dritho-Crème HP, Zithranol) shampoo
- Tacrolimus (Protopic) or pimecrolimus (Elidel) for face
topical corticosteroids for psoriasis tx
- hydrocortisone
- triamcinolone
- fluocinonide
- betamethasone diproprionate
- clobetasol
vitamin d analogs for psoriasis tx
- calcipotriol (Calcitrene, Dovonex)
- calcitrol (Vectical)
- tacalcitol
psoriasis moderate to severe tx
- Phototherapy: good for widespread disease
- Photochemotherapy (PUVA)- txt w/oral or bath psoralen followed by UVA radiation
- Home phototherapy machines UVB- $3000
Systemic therapies:
- Methotrexate (folic acid antagonist)
- Cyclosporine (T-cell suppressor)
- Apremilast (Otezla) (phosphodiesterase-4 inhibitor)
Biologics:
- Entanercept (Enbrel) (TNF-alpha inhibitor)
- Infliximab (Remicade) (TNF-alpha inhibitor)
- Adalimumab (Humira) (human monoclonal antibody, also TNF-alpha inhibitor)
- Ustekinumab (Stelara) (human monoclonal antibody targets IL12 and IL23)
- Secukinumab (Cosentyx) (monoclonal antibody anti IL-17A)
- Ixekizumab (Taltz) (monoclonal antibody anti IL-17A)
- Brodalumab (Siliq) (monoclonal antibody anti 17A)
- Guselkumab (Tremfya) (human immunoglobulin G1 monoclonal antibody)
what is alopecia?
Chronic immune T cell mediated disorder that targets anagen (active) hair follicles causing nonscarring hair loss
how does alopecia commonly present?
with discrete patches on the scalp
but can lose body hair too
alopecia epidemiology
Onset is usually before age 30
Men and women equally affected
alopecia classification
Alopecia areata - Discrete patches
Alopecia totalis - Entire scalp
Alopecia universalis - Entire body
alopecia pathophysology
T cell mediated inflammation disrupting the normal hair cycle
-Does not lead to destruction of the hair follicle
Premature transition of active follicle to inactive
Collapse of immune privileged status of hair follicles
Inappropriate trigger of immune response against follicular antigens
alopecia risk factors
- Genetics
- Severe stress
- Drugs and vaccinations
- Infections
- Vitamin D deficiency
alopecia clinical manifestations
- Smooth, circular discrete patches of complete hair loss that develops of period of 2-3 weeks
- Occasionally pruritis or burning may precede
- Can spread in bizarre patterns
- Can involve any or all body hair
-Nail abnormalities - Onychorrhexis (Longitudinal fissuring of nail plate)
if men have alopecia, what may be the only or initial involvement?
their beard
alopecia nail abnormalities
called onychorrhexis - longitudinal fissuring of nail plate
what may precede alopecia?
pruritis or burning may precede
alopecia associated diseases
- Lupus
- Vitiligo
- Atopic dermatitis
- Thyroid disease
- Allergic rhinitis
- Psoriasis
- Down syndrome
- Polyglandular autoimmune syndrome type 1
alopecia clinical course
- 50% of patients with limited patchy hair loss will recover spontaneously within 1 year
- Some experience multiple episodes
- 10% progress to alopecia totalis or universalis
alopecia dx
PE
Exclamation point hair at margins
Pathology: Peribulbular lymphatic inflammatory infiltrates surrounding follicles - Swarm of bees
limited alopecia/patchy hair loss tx and adrs
Topical or intralesional sterioids
-Triamcinolone or betamethasone
-ADRs: skin atrophy and hypopigmentation
extensive alopecia topical immunotherapy tx
- DPCP
- SADBE
- DNCB (Not used much anymore, may be mutagenic)
extensive alopecia second line tx
- Minoxidil (rogaine)
- Anthralin
- Phototherapy – PUVA
extensive alopecia systemic therapies
- Oral steroids
- Sulfasalazine
- Methotrexate
- Cyclosporine
- Biologics
what is hidradenitis suppurativa?
aka acne inversa
- Chronic, inflammatory skin condition
- Primary lesion is a solitary, painful, deep-seated inflamed nodule
- Develop sinus tracts w/chronic disease
- Scarring
what do you develop with hidradenitis suppurativa?
sinus tracts and scarring
what is the primary lesion of hidradenitis suppurativa?
a solitary, painful, deep-seated inflamed nodule
hidradenitis suppurativa epidemiology
- Onset usually from puberty-40 yo
- Women > men
- Anecdotally- AA women
what is the most common site of involvement for hidradenitis suppurativa?
axillae
hidradenitis suppurativa sites of involvement
- Primary sites of involvement are the intertriginous areas
- Axillae most common site
- Inguinal, inner thigh, perianal, inframammary, buttocks, scrotum, vulva
hidradenitis suppurativa pathogenesis
- Apocrine glands (sweat glands)
- Follicular occlusion, follicular rupture & associated immune response
- Ductal keratinocyte proliferation, ductal plugging then expansion which leads to rupture & release of contents
- Stimulating immune response & leading to sinus tracts in the skin
hidradenitis suppurativa clinical staging
- Stage I- abscess formation
- Stage II- recurrent abscess formation w/sinus tract formation and scarring
- Stage III- diffuse involvement multiple interconnected sinus tracts
hidradenitis suppurativa dx
-Pt hx
- PE -> typical lesions are deep-seeded inflamed nodules, sinus tracts, abscess, and/or scars
- > typical locations (axillae, groin, etc.)
- > relapse and chronicity
-Skin biopsy not necessary
Hidradenitis suppurativa tx
- Avoidance of skin trauma
- Smoking cessation
- Weight management
- Antiseptics- chlorhexidine 4% 1x/wk
- Emollients
- Management of comorbidities
Hidradenitis suppurativa Stage 1 Management
- Topical clindamycin 1% BID
- Intralesional corticosteroid (triamcinolone)
- Punch debridement to evacuate inflammation
- Topical resorcinol 15% (chemical peel)
Hidradenitis suppurativa Stage 2 Management
- Oral tetracyclines for several months (doxycycline, tetracycline, minocycline)
- Clindamycin and Rifampin
- Oral retinoids
- Antiadrenergic therapies- oral contraceptives, spironolactone
- Punch biopsy of fresh lesions
Hidradenitis suppurativa Stage 3 Management
- TNF-alpha inhibitors (adalimumab, infliximumab)
- Systemic glucocorticoids- prednisone
- Cyclosporine
- Surgery
