DCNP - Adnexal Disorders Flashcards
acne: male/female differences
Males tend to develop acne later in adolescence but develop greater severity
Females tend to have a less severe, but a more chronic course
acne: triggering/exacerbating factors & medications
stress, hormonal fluctuations, endocrine disorders, smoking, and ultraviolet radiation
medications include topical and systemic corticosteroids, progesterone, testosterone, antidepressants, anti-seizure medications, isoniazid, and epidermal growth factor receptor (EGFR) drugs
acne: 4 key factors
follicular hyper-keratinization
microbial colonization with Propionibacterium/Cutibacterium acnes
sebum production
Inflammatory mechanisms
acne: contributing factors
diet
genetics
neuroendocrine regulatory mechanisms
increased sebum production
altered follicular differentiation
acne: subsets
Acne excoriee - Habitual picking, usually by young women
Acne mechanica - Caused by friction or chafing from chin straps, sports padding or equipment
Chloracne - Due to occupational exposure to toxins like chlorinated or halogenated chemicals. Large comedones and pustules on face, trunk, genitals and extremities.
Acne Cosmetica - Adolescent females who wear a lot makeup. Comedones, papules pustules
Acne associated w/endocrine abnormalities - Often accompanied by hirsutism, menstrual irregularities, and virilizing characteristics. Pustules and cysts.
Conglobata - Most severe form of acne, usu. young adult males, inflammatory, deep nodules & cysts developing sinus and abscesses. Severely disfiguring
Fulminans - Explosive onset, usu. young adult males, febrile, constitutional symptoms incl. polyarthralgia, leukocytosis, anemia & hepatomegaly
acne: neonatal
< 6 weeks
AKA neonatal cephalic pustulosis
common inflammatory response to Malassezia yeast affects up to 20% of infants
consists of papules and pustules on forehead, cheeks, eyelids, and chin. Less common on neck and trunk. Spontaneous resolution typically occurs by four months of age
acne: infantile
6 weeks – 1 year
Lesions include papules, pustules, comedones, nodules, and cysts primarily onthe face.
Be aware for additional signs of virilization as it can be linked to underlying endocrinopathies
It has been linked to increased incidence of severe adolescent acne
Can result in scarring, so treatment is encouraged with use of topical BPO and off-label use of adapalene.
acne: mid-childhood
age 1 – 7 years
When observed in children aged 18 months to 7 years and is the MOST concerning age group. Acne in this age range is rare and implies more significant systemic problems such as Cushing syndrome, premature adrenarche, congenitaladrenal hyperplasia, gonadal/adrenal tumors, or true precocious puberty
It is often misidentified as keratosis pilaris, rosacea, perioral dermatitis, or Demodex
Patients in this age group who present with chronic, severe, or virilizing acnerequire further evaluation for systemic disease. An appropriate evaluation wouldinclude use of growth charts, bone scans, total/free testosterone, dehydroepiandrosterone (DHEAS), prolactin, LH/FSH, 17-OH progesterone levels,and androstenedione
Both topical and oral therapies are advised, with the exception of prescribed tetracycline products, which are not recommended to children age 8 years and younger.
acne: pre-adolescent
encompasses ages 8 to 12 years
Typically, comedones are evident on the face and neck, but are less common on the torso
This may be an indicator of emerging puberty as it corresponds to additional sebum production and increase in the size of sebaceous follicles
There is some evidence to suggest that the severity and prevalence of acne in the preteen years is predictive of advanced prepubertal maturity
Treatment with traditional topical therapies is advised until the individual’s level of severity and potential for scarring can be assessed.
acne: adolescent
lasts approximately 5 years
acne: conglobata
most severe form of acne and typically arises in adolescent males, although it does not exclude females. It distinguishes itself with nodules, abscess formation, and scars. Comedones may have more than one opening, and cystic lesions often drain. Sinus tracking is not uncommon. Keloid scars, depressed, hypertrophic, boxcar, or ice pick scars may be evident.
acne: fulminans
occurs uncommonly, but with an explosive onset in the teenage male population. It is accompanied by bone pain at the clavicle and sternum. Patients may experience fever and leukocytosis as well as joint pain, anemia, and liver enlargement. Other acne variants develop as a result of secondary changes imposed by external factors
acne: diagnostics
bacterial culturesof a pustular lesion if gram negative folliculitis is suspected
Testing is indicated for those with clinical features of hyperandrogenism and include DHEAS and free testosterone as initial screening laboratory studies to evaluate hormonal influences
acne: differentials
Milia – appear similar to closed comedo, but there is an absence of open comedo, papules, pustules, cysts and erythema
Sebaceous hyperplasia – these bumps are often indented in the center
Perioral dermatitis – location is primarily around the mouth with an absence ofcomedo
Rosacea – has an absence of comedo
Folliculitis (gram positive and gram negative; Pityrosporum) – gram negative -monomorphic eruptive papules and pustules; gram positive appears similarly toacne, but should be considered if eruptions are acute
Pseudofolliculitis barbae – has an absence of comedo and primary affects onlyhair bearing areas.
Angiofibromas – have violaceous hue
Keratosis pilaris – absence of comedo
acne: benzoyl peroxide
antibacterial agent that kills C. acnes
mildly comedolytic
no resistance reported
not only enhances antibiotic therapy, it may reduce bacterial resistance.