47: Verruca Plantaris - Mahoney Flashcards
describe virus of verruca plantaris
HPV double stranded DNA icoshohedral capsule (20 sides)
why are some people more susceptible to verruca than others?
Persistence of disease may be attributable to a lack of Langerhans’ cells at site of lesion, leading to decreased T-cell response
More common in children, rare over the age of 50, common in immunosuppressed pts
pathognomonic characteristics
***
- acanthosis
- thickening of stratum spinosum
- hyperkeratosis
- thickening of stratum corneum
- interpapillary projections (papillomatosis)
- upward proliferation of epidermis and subepidermal papillae causing surface of epidermis to show irregular undulation
- ***purely epidermal
where does DNA and prtn production occur?
final virus assembly?
spinosus layer
granular layer
what causes the “black dots” or “petechia” seen clinically w/i white, fibrotic base of wart?
Papillomatosis result in the characteristic “black dots” or “petechia” that are seen clinically within the white, fibrotic base of the wart
HPV forms that cause plantar warts
- HPV-1 (common wart)-occurs most frequently
- HPV-2 (mosaic wart)
- HPV-4 (common wart)
- HPV-10
(HPV-63 has also been implicated)
After removing overlying hyperkeratosis from a wart, will see …
a white, fibrotic-like area with presence of “dots” that interrupts the normal skin lines and bleeds easily upon debridement
IPK vs. porokeratosis location
- IPK’s most often confined to weight-bearing areas and covered by thick plug of hyperkeratosis
- Porokeratosis found anywhere on plantar surface, similar to verruca
describe porokeratosis
- Porokeratosis is actually a small clonal projection of keratinizing squamous cells
- Have a coronoid lamellae-columns of parakeratotic keratin that overlie a depression in the surface epithelium
- this leads to a prominent rim around the lesion
what cancer can warts become?
- Some evidence to suggest that verrucae may undergo transformation to squamous cell carcinoma
- very uncommon
- consider this possibility if you have a resistant wart that looks more “fleshy” than normal and perform biopsy
chemical ablation tx
- topical salicylic acid is most common
- keratolytic agent
- applied once or twice daily by pt under occluison and turns skin white
- cantharidin (blister beetle) and pdophyllin (american mandrake) applied in office under 24-48 hr occlusion causing severe blister
cryosurgery
- liquid nitrogen in spray canister best, can use q-tips dipped
- cell death occurs below -20 C
- triple freeze technique
- administer for 30 sec or until pain, wait until regains color and then refreeze 2 times
- will form hemorrhagic blister, follow in 2 wks
topical treatments
- Topical corticosteroid under occlusion
- inhibits cell division and synthesis of DNA in epidermis-apply bid
- Tretinoin topical vit A
- increases differentiation and proliferation of epidermis-apply bid under occlusion
- 5FU
- inhibits DNA synthesis, apply BID under occlusion
oral medications
- systemic etretinate at dose 1 mg/kg dialy for no more than 3 mo
- systemic retinoid for psoriasis
- tagamet/cimetidine 25-40 mg/kd/day
- interferes with suppressor t-cell function so inflammatory response against virus prolonged
intralesional injection therapy
- 0.1% bleomycin (cancer drug)
- inhibits DNA synthesis
- no more than 0.25 cc injected into wart, numb with local first
- candida antigen
- Introduce antigen into base of wart with needle in same concentration as with allergy testing, then puncture wart aggressively
- Induces immune response
