47: Verruca Plantaris - Mahoney Flashcards Preview

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Flashcards in 47: Verruca Plantaris - Mahoney Deck (22)

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-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



  • 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



  • theory: induce a delayed cutaneous hypersensitivity reaction against the wart by sensitizing the patient with squaric acid dibutylester (SADBE)
    • Apply 3% topical SADBE in acetone to lesions (or to normal skin close to wart) under occlusion for 48-72 hours; After 2 weeks, serial dilutions of SADBE (.03%-3%) are applied to the lesions twice a week; If no response after 10 weeks, patient is a nonresponder
  • imiquimod/aldara cream
    • recruits cytokines and interferon-alpha to wart to induce keratinocytes to produce enzymes to block viral replication


name MOA for following tx



Salicylic acid



a. keratolytic

b. inhibits suppressor t-cell response

c. recrutis cytokines to area

d. inhibits DNA synthesis

e. initiates delayed hupersentivity reaction







surgical ablation techniques

  • Needling
    • works by destruction of tissue and induction of inflammatory response
  • Curettage
    • blunt dissection with tissue nipper, curette down to superficial fascia, cauterize base
  • Hyfercation
    • spark-gap, tissue dehydration precedes charring, and cell death ensuses with thrombosis of blood vessels
  • Sharp surgical excision
    • high rate recurrence and scar formation


laser ablation techniques

  • CO2 or pulsed dye lasers
    • Light passed through a CO2 gas chamber is absorbed primarily by water, while light passed through dye emits light absorbed primarily by red pigment (i.e. blood hemoglobin)

    • CO2 needs local anesthetic, pulsed dye does not


which is true?

1.The CO2 laser is attracted to hemoglobin

2.The pulsed dye laser is attracted to water

3.The pH of a chlorinated pool is verruccacidal

4.The verruca virus is a double-stranded RNA HPV

5.The verruca virus does not spread into the dermis



recommendation for children

I recommend mixture of 5-FU and 17% sal acid under occlusion with duct tape, followed by imiquimod, then oral Tagamet®, and lastly, pulsed dye laser

If you cause pain in a child, you’ll only have that one chance, so make it work

In adults, I would start out with liquid nitrogen and once daily application of 5-FU plus 17% sal acid under occlusion with duct tape, followed by Aldara®, followed by pulsed dye laser plus Aldara® if unsuccessful

Remember you are dealing with a benign lesion, so “firstly, do no harm”


always use ...

combination tx

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