1/86
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced |
---|
No study sessions yet.
population affected by hidradenitis suppurtiva
women of reproductive age (shortly after puberty)
cause of hidradenitis suppurtiva
-occlusion of hair follicle via hyperkeratosis
-TNF-alpha significantly increased
-hormones, comorbidities
manifestation of hidradenitis suppurtiva
-gradual onset, chronic flares
-persistent/recurrent boil-like lesions in axillae/inguinal area
-painful
-can progress to open "tombstone" comedones
hidradenitis suppurtiva diagnosis
hidradenitis suppurtiva
definitive hidradenitis suppurtiva diagnosis requires presence of 3 criteria:
typical lesion (1+)
typical distribution
chronic/recurrent sx
hidradenitis suppurtiva typical lesions
painful nodule
abscess
draining sinuses
double open comedones
bridged scars
hidradenitis suppurtiva typical distribution
axillae
groin
buttocks
perineal
inframammary
how to determine treatment for hidradenitis suppurtiva
hurley staging of severity
hurley stage 1
mild
recurrent abscesses without scarring or sinus tract formation (tunnels)
hurley stage 2
moderate
recurrent abscesses with scarring and sinus tract formation separated by normal skin
hurley stage 3
severe
recurrent abscesses with scarring and sinus tract formation with no intervening normal skin
why do GS and culture for hidradenitis suppurtiva?
if secondary infection (staph aureus) suspected
treatment hurley stage 1
topical clinda +
1) doxy
2) oral clinda + oral rifampin
3) spironolactone (females with comorbid pcos/premenstrual flares)
treatment hurley stage 2
same as hurley stage 1, plus:
1) immunosuppressives (humira, remicade)
2) other options: (dapsone, cyclosporin, acitretin)
treatment hurley stage 3
pharm tx for stages 1 and 2, then:
1) surgical interventions
2) pain control
pt's with hidradenitis suppurtiva are at an increased risk of
cardiovascular events and malignancies
hidradenitis suppurtiva remission is more common in
non-smokers, those who have quit smoking, non-obese individuals
acrochordon aka
skin tag
population affected by acrochordons
mid 40s-60s
weight gain
manifestation of acrochordons
asymptomatic, soft, flesh-colored papules on thin stalk (contains central BV)
acrochordon diagnosis
clinical
acrochordon biopsy would show
loose fibrous tissue in dermis of a polyp with thin epidermis
tx options for acrochordon
cryo
shave excision
scissors +/-cauterization
lipoma
benign localized overgrowth of fat cells under the skin (trunk, neck, arms, axillae)
lipoma diagnosis
clinical
lipoma histopathology results
well-circumscribed adipose tumor with a thin capsule
angiolipoma histopathology results
adipose collections containing a proliferation of capillary-sized vessels
epidermal inclusion cyst
benign growths of upper portion of hair follicle, capsule filled with keratin debris
cause of epidermal inclusion cyst
plugging of follicular openings, arise from infundibulum of hair follicle
epidermal inclusion cyst affect what areas (most commonly)
central trunk and face
hallmarks of inflamed epidermal inclusion cyst
swelling, pain, purulent drainage (cheesy, foul odor)
hallmarks of non-inflamed epidermal inclusion cyst
asymptomatic, central punctum (black)
epidermal inclusion cyst diagnosis
clinical
epidermal inclusion cyst biopsy results
cyst in dermis lined with stratified squamous epithelium and filled with keratin flakes
epidermal inclusion cyst culture of contents will be _____
sterile
standard of care for non-inflamed epidermal inclusion cyst
surgical removal of entire capsule
standard of care for inflamed epidermal inclusion cyst
hypertrophic scar
symptomatic scar, does not extend beyond border of original injury
keloid
type of hypertrophic scar that will grow beyond the borders of original injury
keloid biopsy results
whorls of fibroblasts, think bands collagen
(biopsy has risk of scarring!)
treatment of hypertrophic scars
will become more supple over the years
intralesional steroid injections
surgical correction
treatment of keloids
will not become more supple over the years
intralesional steroid infections
surgical correction
referral required for management
population affected by pilonidal disease
3:1 male: female
peak between 16-20 y/o
cause of pilonidal disease
hair follicles become blocked > foreign body granuloma reaction and drainage
manifestation of pilonidal disease
acute abscess midline in upper gluteal cleft
-+/- pain, drainage, systemic sx possible
pilonidal disease diagnosis
clinical
pilonidal disease culture
if purulence present to direct treatment
treatment of pilonidal disease painless cyst
monitor
treatment of pilonidal disease acute abscess
1) I&D
2) abx for concomitant cellulitis:
-1st gen ceph + metronidazole
3) refer to general surgery
post-inflammatory hyperpigmentation
acquired disorder causing darkening of the skin secondary to inflammation/trauma, epi or dermis
post-inflammatory hyperpigmentation diagnosis
clinical
post-inflammatory hyperpigmentation wood's lamp exam results
epidermal pigmentation will enhance
dermal pigmentation does not enhance
post-inflammatory hyperpigmentation biopsy
increase in epidermal melanin +/- dermal melanophages
post-inflammatory hypopigmentation
acquired disorder causing lightening of the skin secondary to inflammation/trauma, epi or dermis
post-inflammatory hypopigmentation wood's lamp
may be more visible but won't be as bright as other disorders
post-inflammatory hypopigmentation biopsy
non specific: decrease melanin in epi, decrease melanophages in upper dermis
melasma
acquired hypermelanosis characterized by symmetric hyperpigmented patches with irregular borders on sun exposed regions of face
causes of melasma
sun exposure and hormones
melasma dx
clinical
melasma biopsy (if atypical or dx uncertain)
epidermal: enlarged melanocytes
dermal: melanophages/somes in dermis, limited melanin in epidermis
acanthosis nigricans
cutaneous manifestation of insulin resistance (often secondary to DM)
manifestation of acanthosis nigricans
thick velvety brown/black plaques, symmetrical, gradual onset
("looks dirty but can't wash it off")
affected areas of acanthosis nigricans
neck, axillae, groin, intertriginous areas
acanthosis nigricans palmar involvement may be a sign of
malignancy
acanthosis nigricans diagnosis
clinical
acanthosis nigricans biopsy
hyperkeratosis with increased pigmentation of basal layers
acanthosis nigricans labs
to ID underlying etiology
treatment of acanthosis nigricans should focus on
ID and tx of underlying disease
manifestation of pityriasis alba
round/ovoid, scaly, hypopigmented macule/patches that fade over the course of weeks, usually asymptomatic
population affected by pityriasis alba
children/adolescents > adults (<12 y/o)
areas affected by pityriasis alba
face, neck, trunk
pityriasis alba diagnosis
clinical
pityriasis alba biopsy (if dx unclear)
decrease # active melanocytes, smaller/fever melanosomes, less melanin in basal layer
peak onset of vitiligo
10-20 y/o
manifestation of vitiligo
slow progression of white, well-circumscribed spots, smooth (most common type = generalized)
cause of vitiligo
CD8+ T cells destroy melanocytes > loss of pigment
vitiligo wood's lamp
accentuates areas of non-scaly depigmentation
vitiligo biopsy
absence of melanocytes
what are more likely to develop in areas of depigmentation
actinic keratoses and skin cancer
post-inflammatory hyperpigmentation conservative treatment
treat underlying cause
sun protection
post-inflammatory hyperpigmentation gold standard
hydroquinone (gold standard)
topical retinoids +/- low potency topical steroid
post-inflammatory hypopigmentation treatment
1) treat underlying inflammatory disorder
2) repigmentation from sun (caution)
melasma conservative treatment
sun protection
minimize exogenous hormone exposure
melasma 1st line treatment
topical lightening agents
-hydroquinone, topical tretinoin +/- low potency topical steroid
acanthosis nigricans treatment
1) treat underlying disease!
2) topical agents (retinoids, hydroxyquinone, topical steroids, etc)
pityriasis alba treatment
1) proper moisturization and sun protection
2) topical steroids prn
vitiligo pharmacological treatment options
1) topical steroids (high or super high potency)
2) topical calcineurin inhibitors
3) topical vitamin D analogs