PAMS: Dermatology -Other Dermatologic Disorders Flashcards
What is the Tx of Achrocordon ?
It is mainly cosmetic; cryosurgery, electrodessication, simple
excision, shave excision
What is the prognosis of Cafe-au-Lait Macule?
IF > 6 CAFE-AU-LAIT LESIONS:
▪ Tuberous sclerosis
▪ Neurofibromatosis
▪ McCune-Albright syndrome
▪ Fanconi anemia
What is the presentation of stage-01 pressure ulcer ?
Itis a Non-blanching erythema which should dissappear in 5-
10 minutes after repositionin. Persistent erythema indicates damage.
How to perform a Finger-tip pressure test?
With one finger, press over the area of erythema and relase the pressure. The skin will blanch or non-blanch depending on the type of pathology.
What is the presentation of Pressure Ulcers – Stage II?
These are shallow ulcers with red wound bed and no sloughing.
What is the clinical presentation of pressure ulcer stage-3?
Full Thickness Skin Loss
* SubQ fat may be visible
* Bone, tendons and
muscle NOT visible
* Slough may be present
What is the presentation of stage IV pressure ulcer ?
Full Thickness Tissue Loss
* Exposed and palpable
tendons, muscle and bone
* Slough or eschar may be
present
What is the management of stage 01 pressure ulcer ?
maintain good hygiene; daily wash with soap and water
What is the management of stage 02 pressure ulcer ?
daily cleaning with saline solution; cover with occlusive dressing.
What is the management of stage III and IV pressure ulcers ?
specialized moist to absorbent dressings (alginate, hydrocolloid)
* If necrotic → debridement
* If infected → topical antibiotic then dressing
* If persistent infection → culture
* If infected w/ systemic sx (e.g., fever) → IV/PO antibiotics
What is the clinical presentation of Dyshidrotic Eczema?
- Pruritic vesicles on the palms and lateral and dorsal aspects of the fingers
- Symmetrical Lesions may coalesce, forming bullae (risk for secondary infection)
- Recurrent, multiple episodes over years.
- Resolves with time
What is the management of dyshydrotic eczema ?
Avoid trigger (if known)
* General measures
* Topical steroids or calcineurin inhibitors (e.g., tacrolimus)
What is the clinical presentation of epidermal inclusion cyst?
discrete, freely-movable cyst or nodule with
central punctum.
What is the risk associated to multiple epidermal cysts ?
Colon cancer.
What is the pathophysiology of Hidradenitis Suppurativa?
It is caused by sebaceous gland atrophy causing Lymphocytic infiltration and hyperkeratosis of the pilosebaceous unit. Leading to cytokines mediated Hair follicle destruction and granuloma
formation. Healing is accompanied by sinus tract formation.
https://youtu.be/QRc8sEd46lg?si=PWAReqbqON7xj4j1
What is the epidemiology of Hidradenitis Suppurativa?
- Prevalence anywhere from < 1% to 4%
- Female 3:1
- Onset in 20s for most patients
What are the risk factors for Hidradenitis Suppurativa?
Family Hx – autosomal dominant pattern of inheritance in some cases
* Overweight
* Smoking
* Female sex.
What is the clinical presentation of Hidradenitis Suppurativa?
Pain, burning, itching and hyperhidrosis 24 to 48 Hrs prior to Lesions onset at the Intertriginous areas. The lesions are nodules and subcutaneous abscess with sinus tract formation and purulant discharge. Lasts days to months and heals with fibrotic scarring.
What is the presentation of Hurley stage 01 Hidradenitis Suppurativa?
localized and includes the formation of single or multiple
abscesses, without sinus tracts and scarring
What is the presentation of Hurley stage 02 Hidradenitis Suppurativa?
recurrent abscesses, with sinus tract formation and
scarring, occurring as either single lesions or multiple, widely
separated lesions
What is the presentation of Hurley stage 03 Hidradenitis Suppurativa?
diffuse or nearly diffuse involvement of the affected
region, with multiple interconnected tracts and abscesses across
the entire area
What is the medical management of Hidradenitis Suppurativa?
Topical antibiotics
* Oral antibiotics
* Monoclonal antibodies (MAB)
What is the pathophysiology of weals and pruritis in utricaria ?
Release of chemical mediators by mast cells and basophils
What is the pathophysiology of angioedema
Release of bradykinin.