Full mock viva: Anogenital warts
Use this as a spoken rehearsal. Keep answers short initially. Add the extra detail only if the examiner probes.
Opening case presentation
“This patient has multiple asymptomatic/symptomatic verrucous lesions over the anogenital region for [duration]. The lesions began as small papules and progressively increased in number and size. There is/there is no history of pruritus, pain, bleeding, discharge, dysuria, dyspareunia, or altered bowel habits. Relevant sexual history, history of similar lesions in the partner, prior STI, HIV risk, immunosuppression, pregnancy status, and previous treatment have been elicited.”
“On local examination, there are multiple discrete and coalescent, skin-coloured to pinkish, soft, non-tender, exophytic verrucous papules forming papillomatous plaques over the anterior commissure of the vulva. The lesions have a cauliflower-like surface, with no ulceration, induration, bleeding, or fixation.”
“Additionally, there is a pedunculated, verrucous, non-tender lesion in the perianal region. I would examine the remaining vulva, vaginal introitus, urethral meatus, vagina and cervix as appropriate, the anal canal where indicated, oral cavity, and inguinal lymph nodes. I would also screen for associated STIs and assess for immunosuppression.”
“My diagnosis is anogenital warts, or condylomata acuminata, involving the vulvar anterior commissure and perianal skin.”
One-line pathogenesis: “They are usually due to low-risk HPV, especially types 6 and 11, acquired through intimate skin-to-skin sexual contact.”
Part 1: Core viva questions
1. What is your diagnosis?
Answer: Anogenital warts, also known as condylomata acuminata, involving the vulva and perianal skin.
2. Why do you call these anogenital warts?
Answer: The lesions are multiple, soft, exophytic, verrucous papules and coalescent plaques with a papillomatous or cauliflower-like surface at typical anogenital sites. A pedunculated morphology can also occur.
3. What are the common morphologies of anogenital warts?
Answer: They may be:
- Papular
- Flat
- Filiform
- Pedunculated
- Verrucous or cauliflower-like
- Multiple confluent papillomatous plaques
They may look pale and macerated on moist mucosal surfaces, while lesions on drier skin can be more hyperkeratotic. Fitzpatrick’s describes lesions as often multiple, well-defined papules that can be flat, filiform, or larger protuberant lesions. Fitzpatrick’s Dermatology, p. 3132.
4. What is the causative organism?
Answer: Human papillomavirus, a non-enveloped, double-stranded DNA virus of the family Papillomaviridae.
5. Which HPV types commonly cause genital warts?
Answer: HPV types 6 and 11 cause approximately 90% of anogenital warts.
6. Are these HPV types oncogenic?
Answer: HPV 6 and 11 are low-risk, non-oncogenic types and are rarely associated with invasive cancer. However, a patient can have simultaneous infection with high-risk HPV types, so standard cervical screening should continue.
7. Which HPV types are high risk?
Answer: Most importantly HPV 16 and 18. Other high-risk types include 31, 33, 35, 45, 52, and 58.
8. What cancers are associated with high-risk HPV?
Answer: Cervical, anal, penile, vulvar, vaginal, and a proportion of oropharyngeal cancers.
9. What is the usual mode of transmission?
Answer: Predominantly intimate skin-to-skin sexual contact, including vaginal, anal, and oral sexual contact. Transmission can occur even if no visible warts are present.
10. What is the incubation period?
Answer: Variable, usually weeks to months, but visible warts can appear months or even longer after acquisition. Therefore, their appearance cannot reliably determine the timing of infection or identify a particular partner as the source.
Part 2: Focused history
11. What history would you take in this patient?
Answer:
- Lesion history: onset, progression, number, itching, pain, bleeding, discharge, ulceration.
- Sexual history: partners, new partner, barrier use, partner symptoms, prior STIs.
- Other genital symptoms: vaginal discharge, genital ulcers, dysuria, dyspareunia.
- Anal symptoms: pain, bleeding, discharge, tenesmus, altered bowel habits, receptive anal intercourse.
- Past history: prior warts, STI treatment, HIV, diabetes, transplant, systemic immunosuppression.
- Drug and allergy history.
- Pregnancy and obstetric history, where relevant.
- Cervical screening and HPV vaccination status.
- Psychosocial impact, including distress, relationship issues, and stigma.
12. Why ask about pregnancy?
Answer: Warts may enlarge, become friable, and bleed more easily in pregnancy. Several agents are unsuitable in pregnancy, including podofilox, podophyllin, and sinecatechins. Imiquimod is generally avoided because pregnancy data are limited. Cryotherapy, TCA/BCA, or surgical removal can be considered depending on the lesion burden.
13. Why ask about HIV or immunosuppression?
Answer: Immunosuppressed patients can develop more numerous, extensive, persistent, recurrent, or treatment-resistant warts. They also need a lower threshold for biopsy because atypical lesions or malignancy can mimic warts.
14. Does a wart diagnosis establish recent infidelity?
Answer: No. HPV can remain clinically inapparent for an unpredictable period. Visible warts do not determine when infection was acquired or from whom.
Part 3: Examination questions
15. How would you examine this patient?
Answer: I would ensure privacy, obtain consent, offer a chaperone, and position the patient appropriately. I would:
- Inspect the external genitalia, vulva, perineum, and perianal region.
- Describe lesions by number, size, colour, surface, consistency, base, tenderness, distribution, and secondary changes.
- Look for ulcers, pigmentation, induration, fixation, bleeding, discharge, or features suggesting malignancy.
- Examine vaginal introitus and urethral meatus.
- Arrange speculum examination and cervical assessment when indicated.
- In a patient with perianal lesions, assess for intra-anal disease with digital rectal examination and anoscopy when appropriate.
- Examine oral mucosa if indicated.
- Palpate inguinal lymph nodes.
- Perform a general examination for other STIs and evidence of immunosuppression.
16. Why is examination of the anal canal relevant here?
Answer: External perianal warts can coexist with intra-anal warts, even without a history of receptive anal intercourse. Digital anorectal examination and anoscopy may be appropriate. The CDC specifically recommends considering inspection of the anal canal in people with external anal or perianal warts.
CDC STI guideline
17. What would make you suspect malignant transformation or an alternative diagnosis?
Answer: Pigmentation, induration, ulceration, bleeding, fixation to underlying tissue, rapid destructive growth, marked pain, atypical morphology, enlarged hard nodes, or failure to respond to appropriate treatment.
Part 4: Differential diagnosis
18. What are your differentials?
Answer:
- Condyloma lata of secondary syphilis
- Molluscum contagiosum
- Vestibular papillomatosis
- Skin tags or fibroepithelial polyps
- Seborrhoeic keratosis
- Verruca vulgaris
- Bowenoid papulosis / high-grade squamous intraepithelial lesion
- Vulvar intraepithelial neoplasia
- Squamous cell carcinoma, including verrucous carcinoma
- Lichen planus or other papular genital dermatoses, depending on morphology
19. Differentiate condyloma acuminata from condyloma lata.
Answer:
| Feature | Condyloma acuminata | Condyloma lata |
|---|
| Cause | HPV, usually 6 and 11 | Treponema pallidum, secondary syphilis |
| Surface | Verrucous, papillomatous, cauliflower-like | Smooth, flat-topped, moist |
| Consistency | Soft, exophytic | Broad, flat, moist plaques |
| Sites | Vulva, penis, perineum, perianal region | Warm, moist intertriginous areas, often perianal |
| Infectivity | Infectious | Highly infectious |
| Associated signs | Usually isolated local lesions | May have rash, lymphadenopathy, mucous patches, systemic features |
| Tests | Usually clinical diagnosis | Syphilis serology and lesion testing where available |
20. What is vestibular papillomatosis and how is it different?
Answer: Vestibular papillomatosis is a normal anatomical variant. It consists of multiple small, soft, symmetrical, flesh-coloured papillae on the vestibule, each with a separate base. It is not an STI and requires reassurance, not destructive treatment. In contrast, warts are irregular, asymmetrical, often coalesce, and have a common base.
21. How would molluscum contagiosum differ?
Answer: Molluscum lesions are dome-shaped, smooth, pearly papules with central umbilication. Genital lesions in adults can be sexually acquired. They lack the verrucous, papillomatous surface of condylomata.
22. What is Bowenoid papulosis?
Answer: It is now generally classified as high-grade squamous intraepithelial lesion. It presents as multiple pigmented or erythematous papules in the genital or perianal area, commonly associated with high-risk HPV, especially HPV 16. Histologically it resembles squamous cell carcinoma in situ, so biopsy is required.
Part 5: Investigations
23. Is HPV testing required to diagnose genital warts?
Answer: No. The diagnosis is generally clinical. HPV testing does not confirm the clinical diagnosis of genital warts and does not change wart management. It is not recommended for evaluating partners of persons with genital warts.
24. When would you do a biopsy?
Answer: I would biopsy if:
- The lesion is pigmented, ulcerated, bleeding, indurated, fixed, or atypical.
- The diagnosis is uncertain.
- There is poor response to standard treatment.
- The disease worsens during therapy.
- The patient is immunocompromised, particularly with HIV.
- I suspect intraepithelial neoplasia or invasive malignancy.
25. What histopathology do you expect in condyloma acuminatum?
Answer: Papillomatosis, acanthosis or epidermal hyperplasia, parakeratosis, and koilocytosis. Koilocytes are squamous cells with perinuclear cytoplasmic halos and abnormal, enlarged hyperchromatic nuclei. Dermatology, 5e, p. 1672.
26. What is the significance of koilocytosis?
Answer: It is the characteristic cytopathic effect of HPV infection. It supports HPV-associated epithelial change, but it must be interpreted in anatomical and histological context.
27. What STI tests would you offer?
Answer: Based on risk assessment, local protocols, and consent:
- HIV testing
- Syphilis serology
- Gonorrhoea and chlamydia NAAT from appropriate genital, rectal, or pharyngeal sites
- Hepatitis B and C testing where indicated
- Pregnancy testing when relevant
I would also ensure the patient is up to date with routine cervical cancer screening according to national guidelines.
28. Do genital warts themselves require a Pap smear or colposcopy?
Answer: External uncomplicated warts do not by themselves require more frequent cervical screening than the routine screening schedule. However, visible cervical lesions require specialist assessment and biopsy before treatment to exclude high-grade squamous intraepithelial lesion.
Part 6: Management
29. What are your management principles?
Answer:
- Confirm the clinical diagnosis and biopsy atypical lesions.
- Assess the extent, including genital and anal involvement.
- Screen for other STIs and assess immunosuppression.
- Discuss that observation is acceptable because some warts regress spontaneously.
- If treatment is desired, choose therapy based on size, number, site, pregnancy status, cost, adverse effects, access, and patient preference.
- Counsel regarding recurrence, transmission, condoms, partner notification, and HPV vaccination.
- Review treatment response and reconsider diagnosis or biopsy if treatment fails.
30. Is treatment mandatory?
Answer: No. Untreated warts may regress, persist, or enlarge. Treatment is offered to relieve symptoms, reduce lesion burden, address cosmetic or psychosocial concerns, and reduce local trauma. Treatment removes visible warts but does not reliably eradicate HPV.
31. What treatment would you choose in this case?
Answer: With plaque-like vulvar lesions and a pedunculated perianal lesion, I would first assess lesion extent, pregnancy status, and anal canal involvement. Reasonable options include:
- Cryotherapy for accessible external lesions.
- TCA 80% to 90%, carefully applied by a clinician, especially for small moist lesions.
- Surgical removal, electrosurgery, or laser for a pedunculated lesion or bulky disease when rapid clearance and histology are needed.
- Patient-applied therapy can be considered for suitable external lesions if the patient can identify and reach them correctly.
For a pedunculated perianal lesion, snip excision or electrosurgery may give rapid clearance and allows histopathological examination if there is diagnostic concern.
32. What patient-applied treatments are available?
Answer:
- Imiquimod 3.75% or 5% cream
- Podofilox 0.5% solution or gel
- Sinecatechins 15% ointment
They are for external anogenital warts and require proper patient instruction.
33. Give the regimen for imiquimod 5%.
Answer: Imiquimod 5% cream is applied as a thin layer to visible external warts at bedtime three nights per week, left on for approximately 6 to 10 hours, then washed off. It is used until clearance or for a maximum of 16 weeks.
Its mechanism is local immune activation through toll-like receptor 7, inducing cytokines including interferon-alpha.
34. Give the regimen for podofilox 0.5%.
Answer: Apply twice daily for 3 consecutive days, followed by 4 treatment-free days. The cycle may be repeated for up to four cycles. It should only be applied to visible external warts, with a total treated area not exceeding 10 cm² and total daily volume not exceeding 0.5 mL. It is contraindicated in pregnancy.
35. How does podofilox work?
Answer: Podofilox, or podophyllotoxin, is an antimitotic cytotoxic agent. It disrupts microtubule assembly and causes wart necrosis.
36. What is the role of cryotherapy?
Answer: Cryotherapy with liquid nitrogen is a clinician-applied first-line option. It destroys lesions by freezing and tissue necrosis. It is useful for multiple external lesions and can be used during pregnancy. Pain, blistering, ulceration, and pigmentary changes can occur.
37. What is the role of TCA?
Answer: TCA or BCA 80% to 90% is a clinician-applied chemical destructive treatment. It causes protein coagulation and tissue necrosis. It can be used in pregnancy. It must be applied sparingly because excess acid can damage adjacent normal tissue.
38. When would you use surgery or electrosurgery?
Answer: For large, pedunculated, extensive, keratinized, refractory, or rapidly removable lesions; when a single-session approach is preferred; or when a biopsy is needed. Surgical methods include scissor excision, shave excision, curettage, electrosurgery, and laser.
39. What is the disadvantage of ablative treatment?
Answer: It removes visible lesions but may not remove subclinical HPV infection, so recurrences are common. It can also cause pain, scarring, pigmentary alteration, and, rarely, chronic pain syndromes if treatment is excessive.
40. When do you change the treatment modality?
Answer: If there is no substantial improvement after a complete course, if side effects are severe, if adherence is poor, if lesion morphology changes, or if the diagnosis becomes doubtful. Re-examine, consider biopsy, assess immunosuppression, and use an alternative modality.
41. How soon should warts respond to treatment?
Answer: Most respond within about three months of therapy. Immunosuppression, poor adherence, extensive disease, and difficult anatomic sites may reduce response.
CDC treatment guidance
Part 7: Special situations
42. How would you manage anogenital warts in pregnancy?
Answer: Avoid podofilox, podophyllin, and sinecatechins. Imiquimod is generally avoided because there are insufficient pregnancy data. Use cryotherapy, TCA/BCA, or surgical removal if treatment is required. Warts may become larger and more friable during pregnancy.
Caesarean delivery is not performed solely to prevent neonatal HPV infection. It is considered if the lesions obstruct the pelvic outlet or if vaginal delivery would cause excessive bleeding.
43. What is giant condyloma of Buschke-Löwenstein?
Answer: It is a rare, large, locally aggressive, destructive verrucous tumour arising in the anogenital region, often associated with HPV 6 and 11. It may invade locally, recur frequently, and can undergo malignant transformation to squamous cell carcinoma, though distant metastasis is uncommon. Management usually requires wide surgical excision and multidisciplinary care.
44. How does HIV alter disease and management?
Answer: Warts may be more extensive, atypical, recurrent, and resistant to treatment. Standard therapies can still be used, but there should be a lower threshold for biopsy. HIV care and effective antiretroviral treatment are important, alongside careful follow-up.
45. What is your approach if the lesions are in the anal canal?
Answer: Assess extent with anoscopy and involve an experienced colorectal or sexual-health specialist. Intra-anal warts can be treated with cryotherapy, surgical removal, or carefully administered TCA/BCA. Patient-applied agents are not used inside the anal canal.
46. How do you approach warts in a child?
Answer: Assess sensitively and without presumption. Transmission can be perinatal, nonsexual, or sexual. However, sexual abuse must be considered, particularly in older children or if there are concerning clinical or social findings. Follow safeguarding protocols and involve paediatrics and child-protection teams as appropriate.
Part 8: Counselling viva
47. What will you counsel this patient?
Answer:
- These are common lesions caused most often by low-risk HPV.
- The virus can be passed to partners even if lesions are not visible.
- Treatment removes visible warts but may not eliminate the virus completely.
- Recurrence is common, particularly in the first few months.
- Avoid shaving or waxing through active lesions because this can cause trauma and autoinoculation.
- Condoms reduce, but do not eliminate, HPV transmission because uncovered skin can carry HPV.
- Inform current sexual partner(s).
- Partner HPV testing is not recommended, but partners may benefit from clinical examination and testing for other STIs.
- Continue routine cervical screening.
- Offer HPV vaccination if eligible or not adequately vaccinated.
48. Should the partner be treated?
Answer: Treat visible lesions if present. Routine treatment or HPV testing of an asymptomatic partner is not recommended. They should be examined if symptomatic or concerned and offered screening for other STIs according to risk.
49. Should the patient abstain from sex?
Answer: During treatment, it is sensible to avoid sexual contact if lesions are painful, treatment is on the skin, or skin is inflamed. Condoms reduce but do not fully prevent transmission. For sinecatechins, genital, anal, and oral sexual contact should be avoided while the ointment remains on the skin.
50. Does the HPV vaccine treat existing warts?
Answer: No. HPV vaccines are preventive, not established therapeutic treatment for existing HPV infection or visible warts. However, vaccination can still protect against HPV types not yet acquired and should be offered according to local age and eligibility recommendations.
A 2024 systematic review evaluated therapeutic use of HPV vaccines for active anogenital warts but does not establish vaccination as standard wart therapy (
PMID 38453661). Continue to describe vaccination as prevention, not treatment, in your viva.
Part 9: Hard and very hard viva questions
51. Why does treatment not necessarily prevent HPV transmission?
Answer: Treatments remove clinically visible lesions but may not eradicate HPV from adjacent clinically normal epithelium. Therefore, subclinical infection and viral shedding may persist. The effect of treatment on future transmission is uncertain.
52. Explain high-risk HPV carcinogenesis.
Answer: Persistent infection with high-risk HPV can lead to viral genome integration into host DNA and overexpression of viral oncoproteins:
- E6 promotes degradation of p53, impairing DNA-damage response and apoptosis.
- E7 inactivates the retinoblastoma protein, pRb, releasing E2F transcription factors and driving cell-cycle progression.
High-risk HPV E6 and E7 have stronger effects on p53 and pRb than low-risk HPV types, explaining their greater oncogenic potential.
53. Why do HPV 6 and 11 cause exophytic warts but rarely cancer?
Answer: Their E6 and E7 proteins have much weaker affinity for p53 and pRb and usually remain episomal rather than integrating into the host genome. They promote epithelial proliferation sufficient for wart formation but have a low propensity for malignant transformation.
54. Why might lesions recur after apparently successful treatment?
Answer: Recurrence may reflect:
- Persistent subclinical HPV infection in adjacent epithelium
- Reinfection or exposure from a partner
- Incomplete treatment of visible lesions
- Immunosuppression
- Large initial lesion burden
- Poor adherence to patient-applied therapy
55. Can you use acetic acid whitening to diagnose warts?
Answer: Acetic acid may produce acetowhitening of HPV-infected epithelium, but it lacks specificity and is not recommended as a routine diagnostic test. It may also whiten inflamed, traumatised, or non-HPV epithelium.
56. What does p16 immunostaining signify?
Answer: Diffuse “block-positive” p16 staining is a surrogate marker of transforming high-risk HPV infection in appropriate lesions, reflecting disruption of the pRb pathway by E7. It is useful in histopathological assessment of HPV-associated high-grade squamous lesions, not in routine clinical diagnosis of ordinary genital warts.
57. Why should you not use podophyllin resin indiscriminately?
Answer: Podophyllin resin has unpredictable concentrations of active compounds and can cause severe local and systemic toxicity, especially when applied to large areas, friable tissue, or if not washed off appropriately. Safer alternatives such as podofilox are preferred.
58. Why might a “wart” not respond to therapy?
Answer: The possibilities are:
- Incorrect diagnosis, such as condyloma lata, molluscum, skin tag, VIN, or SCC
- Inadequate application or poor adherence
- Inadequate freezing or incomplete destruction
- Immunosuppression
- Very keratinized or extensive lesions
- Repeated trauma or reinoculation
The next step is to reassess the diagnosis and consider biopsy, rather than repeatedly using the same destructive therapy.
59. How do you distinguish giant condyloma from ordinary genital warts clinically?
Answer: Giant condyloma is much larger, bulky, malodorous, locally destructive, recurrent, and may invade adjacent structures. It can produce fistulae, obstruction, bleeding, or secondary infection. It requires imaging and histological assessment to evaluate deep invasion and exclude carcinoma.
60. What is the most important practical message in this patient with perianal disease?
Answer: Do not limit the assessment to visible perianal skin. Consider intra-anal involvement, evaluate for other STIs and immunosuppression, and biopsy if lesions are atypical or treatment-resistant.
Examiner-style rapid-fire round
| Question | Model answer |
|---|
| Is genital wart diagnosis clinical? | Yes, usually by visual inspection. |
| Common HPV types? | 6 and 11. |
| Are 6 and 11 high risk? | No, low risk. |
| Common high-risk types? | 16 and 18. |
| HPV test for wart diagnosis? | No. |
| Biopsy indications? | Atypical, pigmented, indurated, fixed, bleeding, ulcerated, uncertain, refractory, worsening, or immunocompromised patient. |
| Can warts resolve spontaneously? | Yes. |
| First-line patient-applied drugs? | Imiquimod, podofilox, sinecatechins. |
| Clinician-applied options? | Cryotherapy, TCA/BCA, excision, curettage, electrosurgery, laser. |
| Podofilox in pregnancy? | Contraindicated. |
| Imiquimod in pregnancy? | Generally avoid. |
| TCA in pregnancy? | Can be used. |
| Cryotherapy in pregnancy? | Can be used. |
| C-section solely for HPV prevention? | No. |
| Partner HPV test? | Not recommended. |
| Condom protection? | Reduces but does not eliminate risk. |
| Do warts prove recent infection? | No. |
| Do ordinary warts require more frequent Pap tests? | No, routine screening schedule applies unless another indication exists. |
| External anal wart: what else to assess? | Intra-anal warts. |
| Histology? | Papillomatosis, acanthosis, parakeratosis, koilocytosis. |
A strong final answer if asked, “How will you manage this exact patient?”
“I would first confirm that the lesions are clinically typical and assess the complete anogenital extent, including possible anal canal involvement because there is a perianal lesion. I would take a sexual and STI risk history, assess pregnancy status and immunosuppression, offer testing for HIV, syphilis, and other STIs according to risk, and ensure routine cervical screening is current. I would biopsy any atypical, pigmented, ulcerated, indurated, fixed, bleeding, or refractory lesion.”
“For treatment, I would discuss observation versus active therapy. Given the plaque-like vulvar lesions and a pedunculated perianal lesion, cryotherapy or careful TCA may be used for suitable external lesions; excision or electrosurgery is a practical option for the pedunculated lesion, particularly if histology is needed. Choice depends on lesion size, exact location, pregnancy, patient preference, and available expertise.”
“Finally, I would counsel about recurrence, partner notification, condom use, HPV vaccination, and the fact that treatment clears visible warts but may not eradicate HPV infection.”
Key references:
Fitzpatrick’s Dermatology, p. 3132;
Dermatology, 5e, p. 1672; and the current
CDC anogenital-warts guidance.