110: Epithelial Precancerous Lesions Flashcards
(211 cards)
1
Q
What are actinic keratoses also known as?
A
Actinic keratoses are also known as solar keratoses or senile keratoses.
2
Q
What is a strong indicator of actinic keratoses (AKs)?
A
A strong indicator of actinic keratoses (AKs) is chronic exposure to UV radiation, which identifies patients at high risk of developing nonmelanoma skin cancer.
3
Q
What demographic is most commonly affected by actinic keratoses in the US?
A
In the US, actinic keratoses (AKs) are most commonly diagnosed among dermatology patients aged 45 years and older.
4
Q
What are some risk factors associated with developing actinic keratoses?
A
Risk factors for developing actinic keratoses include:
- Skin phenotype
- Cumulative UV exposure
- Age
- Gender
5
Q
How does the prevalence of actinic keratoses vary by gender?
A
The prevalence of actinic keratoses increases with age, and men are more likely to develop AKs than women.
6
Q
What are the typical clinical features of a patient with actinic keratoses?
A
A typical patient with actinic keratoses is an older, fair-skinned, light-eyed individual with a history of significant sun exposure, who burns and freckles rather than tans, and has significant solar elastosis on examination.
7
Q
What is the typical size and appearance of an erythematous actinic keratosis lesion?
A
An erythematous actinic keratosis lesion is typically 2 to 6 mm, erythematous, flat, rough, gritty, or scaly papule that is more easily felt than seen.
8
Q
What is field cancerization in the context of actinic keratoses?
A
Field cancerization refers to the presence of multiple actinic keratoses affecting a large area of sun-exposed skin alongside subclinical lesions. Definitions include having more than 2 AKs in one skin area with signs of solar damage, at least 3 AKs within 25 cm² of skin, or more than 5 AKs in one body region or field.
9
Q
A 55-year-old farmer presents with multiple erythematous, rough, scaly papules on his forearms. What is the most likely diagnosis, and what are the key risk factors for this condition?
A
The most likely diagnosis is actinic keratosis (AK). Key risk factors include chronic UV exposure, fair skin, outdoor occupation, and advancing age.
10
Q
A patient with Fitzpatrick skin type I reports frequent sunburns during childhood. How does this history influence their risk of developing actinic keratosis?
A
Frequent sunburns during childhood significantly increase the likelihood of developing actinic keratosis later in life.
11
Q
What are the clinical features of a typical erythematous actinic keratosis lesion?
A
A typical erythematous AK lesion is a 2-6 mm erythematous, flat, rough, gritty, or scaly papule, often found on sun-exposed skin with signs of photodamage.
12
Q
A patient with a history of organ transplantation presents with multiple AKs. Why are they at increased risk, and what is the recommended preventive measure?
A
Immunosuppression increases the risk of AKs and their malignant transformation. Preventive measures include consistent use of broad-spectrum sunscreen and regular dermatologic evaluations.
13
Q
What are the key risk factors associated with the development of actinic keratoses (AKs)?
A
Key risk factors for developing AKs include:
- Skin phenotype: Fair skin, red or blond hair, blue eyes (Fitzpatrick type I) are at higher risk.
- Cumulative UV exposure: High levels of UV exposure, especially in outdoor occupations.
- Age: Older individuals are more likely to develop AKs.
- Gender: Men are more likely to develop AKs than women.
- History of sunburns: A higher number of sunburns during childhood increases future risk.
- Immunosuppression: Immunosuppressed patients are at increased risk of developing AKs earlier in life and with more rapid malignant transformation.
14
Q
Describe the typical clinical features of a patient with actinic keratoses (AKs).
A
A typical patient with AKs is characterized by:
- Demographics: Older, fair-skinned, light-eyed individual.
- Sun exposure history: Significant history of sun exposure, often burns and freckles rather than tans.
- Physical examination findings: Presence of significant solar elastosis.
- Common locations: 80% of AKs are found on chronically sun-exposed areas such as the bald scalp, face, ears, neck, forearms, and dorsal hands.
- Symptoms: Mostly asymptomatic, but may experience pruritus, burning or stinging pain, bleeding, and crusting.
15
Q
What is field cancerization in the context of actinic keratoses (AKs)?
A
Field cancerization refers to the phenomenon where multiple actinic keratoses affect a large area of sun-exposed skin alongside subclinical lesions. Definitions of field cancerization include:
- More than 2 AKs within 1 skin area with signs of solar damage.
- At least 3 AKs within 25 cm² of skin.
- More than 5 AKs in 1 body region or field.
16
Q
What are the clinical features of hypertrophic actinic keratosis (AK)?
A
Hypertrophic AK is characterized by:
- Thicker, scaly, rough papule or plaque that is skin-colored, gray-white, or erythematous.
- Affects dorsal hands, arms, and scalp.
- A typical erythematous AK can progress into a hypertrophic AK.
- Induration, inflammation, pain, and ulceration are key indicators for distinguishing hypertrophic AK from squamous cell carcinoma (SCC).
17
Q
What is actinic cheilitis and its clinical presentation?
A
Actinic cheilitis represents confluent actinic keratoses on the lips, most often the lower lip. Its clinical presentation includes:
- Red, scaly, chapped lips with possible erosions or fissures.
- The vermilion border of the lip is often indistinct.
- Focal hyperkeratosis and leukoplakia may be observed.
- Individuals often complain of persistent dryness and cracking of lips.
18
Q
What are the main etiologic factors contributing to the formation of actinic keratoses (AKs)?
A
The main etiologic factors contributing to the formation of actinic keratoses include:
- Fair skin and exposure to UV radiation.
- Majority of lesions develop in areas with chronic exposure to sunlight, such as:
- Balding scalp
- Nose
- Ears
- Lips
- Dorsal hands
- Forearms
- Cumulative UV exposure, frequent sunburns, and poor use of sun protection.
- Other risk factors include male sex, advancing age, and immunosuppression.
19
Q
How does the Olsen classification categorize actinic keratosis?
A
The Olsen classification categorizes actinic keratosis into three grades based on clinical features:
Grade | Description |
|——-|————-|
| 1 (Mild) | Slight palpability; AK better felt than seen |
| 2 (Moderate) | Moderately thick AK; Easily seen and felt |
| 3 (Severe) | Very thick or obvious AK |
20
Q
What is the significance of the Roewert-Huber classification in actinic keratosis?
A
The Roewert-Huber classification is significant as it categorizes actinic keratosis based on histologic levels:
- Type AK I: Involvement of basal and suprabasal layers of the epidermis; nuclei hyperchromatic and variable in size; loss of nuclear polarity.
- Type AK II: Involvement of the lower two-thirds of the epidermis; alternation with zones of normal epidermis; buds of keratinocytes in the upper papillary dermis.
- Type AK III: Involvement of more than two-thirds of the full epidermal thickness; involvement of hair follicle, infundibula, and acrosyringium; buds of keratinocytes in the upper papillary dermis.
21
Q
A patient presents with a conical hypertrophic protuberance on their cheek. What is the likely diagnosis, and what percentage of such lesions represent actinic keratosis?
A
The likely diagnosis is a cutaneous horn, a type of hypertrophic AK. Approximately 21% of all cutaneous horns represent AKs.
22
Q
What are the histological differences between AK types I, II, and III according to the Roewert-Huber classification?
A
Type I: Atypical keratinocytes in basal and suprabasal layers. Type II: Atypical keratinocytes in the lower two-thirds of the epidermis. Type III: Atypical keratinocytes involve more than two-thirds of the epidermis and may extend to hair follicles.
23
Q
What are the clinical features of actinic cheilitis, and which lip is most commonly affected?
A
Actinic cheilitis presents as red, scaly, chapped lips with erosions or fissures, most commonly affecting the lower lip.
24
Q
What are the key features of the Olsen classification for actinic keratosis?
A
Grade 1: Slightly palpable AK. Grade 2: Moderately thick AK. Grade 3: Very thick or obvious AK.
25
What are the clinical features that differentiate hypertrophic actinic keratosis (AK) from squamous cell carcinoma (SCC)?
Hypertrophic AK is characterized by:
- Thicker, scaly, rough papule or plaque that is skin-colored, gray-white, or erythematous.
- Affects areas such as dorsal hands, arms, and scalp.
- Clinical clues indicating a transition to SCC include:
- Induration
- Inflammation
- Pain
- Ulceration
26
How does the classification of actinic keratosis (AK) differ between the Olsen and Roewert-Huber systems?
The classification of AK differs as follows:
| Classification System | Criteria |
|----------------------|----------|
| Olsen Classification | Based on palpable thickness of AK lesions (Grade 1 to 3) |
| Roewert-Huber Classification | Based on histologic level, with types AK I to III indicating the extent of atypical keratinocytes in the epidermis |
27
What are the primary etiologic factors contributing to the development of actinic keratosis (AK)?
The primary etiologic factors for AK include:
- **Fair skin** and **exposure to UV radiation**.
- Majority of lesions develop in areas with chronic sun exposure such as:
- Balding scalp
- Nose
- Ears
- Dorsal hands
- Other contributing factors:
- Cumulative UV exposure
- Frequent sunburns
- Poor use of sun protection
- Male sex
- Advancing age
- Immunosuppression.
28
What are the rare exogenous factors that can lead to actinic keratoses?
Rare exogenous factors include **ionizing radiation** and **radiant heat**.
29
What genetic disorders are associated with increased risk for actinic keratoses due to impaired DNA damage repair mechanisms?
Genetic disorders associated with increased risk include **xeroderma pigmentosum**, **Bloom syndrome**, and **Rothmund-Thompson syndrome**.
30
What is the role of UV radiation in the pathogenesis of actinic keratoses?
Chronic **UVB radiation** induces genetic alterations in keratinocytes in the basal layer, leading to the formation of **cyclobutene pyrimidine dimers** that modify DNA structure (photomutagenesis).
31
What are common indications for biopsy in suspected actinic keratoses?
Common indications for biopsy include:
1. Rapidly enlarging lesions
2. Bleeding or ulceration
3. Inflammation
4. Strong induration
5. Lesions extending beyond 1 cm in size
6. Resistance to treatment.
32
What histopathological features are observed in actinic keratoses?
Histopathological features include:
- Compact packing of basal and suprabasal atypical keratinocytes with **hyperchromatic** and **pleomorphic nuclei**.
- Atypical mitotic figures, apoptotic cells, and dyskeratosis may be present.
- Architecture is increasingly lost in the basal layers but not the full thickness of the epidermis.
33
What dermoscopic features are characteristic of nonpigmented lesions in actinic keratoses?
Common features of nonpigmented lesions include:
- Scales appearing as **whitish or yellowish crystalline structures**.
- Reddish pseudonetwork with erythema and wavy configuration of **telangiectasias** between enlarged hair follicles, resulting in a **'strawberry pattern'**.
34
What are the features of hyperkeratotic lesions on the face as seen in actinic keratoses?
Hyperkeratotic lesions on the face may exhibit:
- **Targetoid-like pattern**: Prominent keratotic plugs within hair follicles.
- **Rosette sign**: White dots localized inside the follicular openings, reflecting alternating ortho- and parakeratosis.
35
What is the role of HPV in the pathogenesis of actinic keratosis?
HPV infection (types 5, 8, 21, 39) is debated as a contributing factor to AK development.
36
What molecular events are commonly associated with the pathogenesis of actinic keratosis?
Common molecular events include p53 inactivation, H-ras activation, and decreased Notch1 signaling, leading to uncontrolled keratinocyte proliferation and atypia.
37
What are the dermoscopic features of nonpigmented actinic keratosis lesions?
Nonpigmented AK lesions show whitish or yellowish crystalline scales, a reddish pseudonetwork, and wavy telangiectasias forming a 'strawberry pattern.'
38
What are the histopathological features of actinic keratosis?
Features include compact packing of atypical keratinocytes, hyperchromatic nuclei, dyskeratosis, and a 'pink and blue' flag sign with alternating orthokeratosis and parakeratosis.
39
What is the significance of the 'strawberry pattern' in dermoscopy of actinic keratosis?
The 'strawberry pattern' indicates whitish or yellowish crystalline scales and a reddish pseudonetwork with wavy telangiectasias, characteristic of nonpigmented AKs.
40
What are the clinical indications for performing a biopsy on an actinic keratosis lesion?
Indications include rapid enlargement, bleeding, ulceration, inflammation, strong induration, size >1 cm, and resistance to treatment.
41
What is the significance of the 'pink and blue' flag sign in actinic keratosis histopathology?
The 'pink and blue' flag sign indicates alternating orthokeratosis and parakeratosis, a common feature in later stages of AK.
42
What are the rare exogenous and endogenous factors that predispose individuals to actinic keratoses?
Rare exogenous factors include **ionizing radiation** and **radiant heat**. Rare endogenous predisposing conditions are genetic disorders with impaired DNA damage repair mechanisms after UV exposure, such as **xeroderma pigmentosum**, **Bloom syndrome**, and **Rothmund-Thompson syndrome**.
43
How does chronic UVB radiation contribute to the pathogenesis of actinic keratoses?
Chronic **UVB radiation** induces genetic alterations in keratinocytes in the basal layer, leading to the formation of **cyclobutene pyrimidine dimers** that modify DNA structure (photomutagenesis).
44
What indicates alternating orthokeratosis and parakeratosis?
It is a common feature in later stages of actinic keratosis (AK).
45
What are the rare exogenous factors that predispose individuals to actinic keratoses?
Rare exogenous factors include ionizing radiation and radiant heat.
46
What are the rare endogenous factors that predispose individuals to actinic keratoses?
Rare endogenous predisposing conditions are genetic disorders with impaired DNA damage repair mechanisms after UV exposure, such as xeroderma pigmentosum, Bloom syndrome, and Rothmund-Thompson syndrome.
47
How does chronic UVB radiation contribute to the pathogenesis of actinic keratoses?
Chronic UVB radiation induces genetic alterations in keratinocytes of the basal layer, leading to the formation of cyclobutene pyrimidine dimers that modify DNA structure and can result in mutations of the tumor-suppressor gene p53.
48
What are the common clinical indications for performing a biopsy on suspected actinic keratoses?
Common indications for biopsy include:
1. Rapidly enlarging lesions
2. Bleeding or ulceration
3. Inflammation
4. Strong induration
5. Lesions extending beyond 1 cm in size
6. Resistance to treatment
49
What histopathological features are observed in actinic keratoses?
Histopathological features include:
- Compact packing of basal and suprabasal atypical keratinocytes with hyperchromatic and pleomorphic nuclei.
- Presence of atypical mitotic figures, apoptotic cells, and dyskeratosis.
- Loss of architecture in the basal layers but not the full thickness of the epidermis.
- Flag sign or Pink and Blue indicating alternation of orthokeratosis and parakeratosis in later stages.
50
What dermoscopic features are characteristic of nonpigmented lesions in actinic keratoses?
Common dermoscopic features of nonpigmented lesions include:
- Scales appearing as whitish or yellowish crystalline structures.
- Reddish pseudonetwork with erythema and wavy configuration of telangiectasias between enlarged hair follicles, resulting in a strawberry pattern.
51
What are the clinical implications of the annual progression rate of actinic keratosis (AK) to squamous cell carcinoma (SCC)?
The annual progression rate of a single lesion of AK to SCC is reportedly below 1%, ranging from 0 to 0.53%. This indicates that while the risk is low, it is essential to monitor AKs closely.
52
What are the advantages and disadvantages of cryosurgery as a treatment for actinic keratoses?
| Advantages | Disadvantages |
|------------|---------------|
| Short treatment duration (seconds to minutes) | Little standardized procedure |
| No need for local anesthesia | Frequent blister formation |
| Efficient in clearing single lesions | Hypopigmentation |
| Easy to administer | Risk of nerve damage and scarring |
53
How does the risk of progression to squamous cell carcinoma (SCC) vary among actinic keratosis (AK) lesions?
The risk of progression to SCC varies from less than 1% to 20%. Factors influencing this risk include the duration of the AK's presence, total lesion count (greater than 5), and individual patient characteristics.
54
What are the key differences between lesion-targeted therapies and field-targeted therapies for actinic keratoses?
| Therapy Type | Description |
|--------------|-------------|
| Lesion-Targeted Therapies | Focus on specific lesions, often using destructive methods like cryosurgery or ablative lasers. |
| Field-Targeted Therapies | Treat larger areas of skin to address multiple lesions, often using topical medications or photodynamic therapy. |
55
What is the significance of spontaneous regression in actinic keratosis lesions?
Spontaneous regression of actinic keratosis lesions may occur, with annual regression rates for single lesions ranging from 20% to 30%. However, lesions that have regressed can relapse, with recurrence rates ranging from 15% to 53%.
56
What diagnostic step is warranted for a patient with a rapidly enlarging, painful lesion on their scalp?
A biopsy is warranted to rule out progression to squamous cell carcinoma (SCC), as rapid enlargement and pain are concerning features.
57
What is the estimated annual progression rate of a single actinic keratosis lesion to invasive squamous cell carcinoma?
The annual progression rate of a single AK lesion to invasive SCC is below 1%, ranging from 0 to 0.53%.
58
What is the annual regression and recurrence rate for untreated actinic keratosis lesions?
Annual regression rates for untreated AK lesions range from 20% to 30%, while recurrence rates range from 15% to 53%.
59
What are the distinguishing features between pigmented actinic keratosis (AK) and facial lentigo maligna?
Pigmented AK is characterized by white evident follicles, scales, and red color, while facial lentigo maligna shows intense pigmentation and gray rhomboidal lines.
60
What factors increase the risk of progression from actinic keratosis to squamous cell carcinoma?
The risk for SCC formation increases with the duration of presence of the lesions, total lesion count (greater than 5), and individual patient characteristics.
61
What are the advantages and disadvantages of using liquid nitrogen cryosurgery for treating actinic keratoses?
Advantages: Short treatment duration, no need for local anesthesia. Disadvantages: Little standardization, frequent blister formation, risk of hypopigmentation, and potential nerve damage.
62
What is the significance of early and consequent therapy in the management of actinic keratoses?
Early and consequent therapy helps minimize symptoms like scaling, pain, or pruritus, improves cosmetic appearance, and ultimately enhances the quality of life for patients.
63
What is the primary benefit of liquid nitrogen cryosurgery in treating actinic keratoses?
The primary benefit of liquid nitrogen cryosurgery is the lack of need for local anesthesia and the simple post-treatment care it offers.
64
What are some short-term complications associated with cryosurgery?
Short-term complications of cryosurgery include:
1. Procedure-related discomfort with pain and hemorrhage
2. Blister formation
3. Risk of nerve damage
4. Pigmentary changes from destruction of adjacent melanocytes
5. Scarring
65
How do surgical approaches compare to other destructive treatments for actinic keratoses in terms of recurrence rates?
Some studies suggest that surgical therapies show lower rates of recurrence than other destructive treatments for actinic keratoses.
66
What are the potential disadvantages of surgical procedures for treating actinic keratoses?
Disadvantages of surgical procedures include:
1. Need for local anesthesia
2. Potentially prolonged wound healing
3. Risk of infection
4. Bleeding
5. Dyspigmentation
6. Scarring
7. Poor cosmetic outcomes
67
What is the mechanism of action for photodynamic therapy using 5-Aminolevulinic acid (ALA)?
The mechanism of action for photodynamic therapy using 5-Aminolevulinic acid (ALA) involves:
1. ALA is absorbed by the epidermis and accumulates in atypical cells.
2. It is processed to protoporphyrin IX.
3. Subsequent exposure to a specific wavelength light activates protoporphyrin IX.
4. This results in a phototoxic reaction with the release of reactive oxygen species (ROS), leading to destruction of target cells by necrosis and apoptosis.
68
What are the adverse events associated with laser therapies for actinic keratoses?
Adverse events associated with laser therapies for actinic keratoses include:
1. Hypopigmentation
2. Atrophic scarring
3. Potential for actinic keratoses to relapse after laser treatment
69
What are the advantages of surgical approaches for treating actinic keratosis?
Advantages include histopathologic assessment and low recurrence rates.
70
What are the advantages and disadvantages of cryosurgery for treating actinic keratoses?
Advantages: Short treatment duration, no need for local anesthesia, and simple post-treatment care. Disadvantages: Risk of nerve damage, pigmentary changes, scarring, and frequent blister formation.
71
What are the benefits and drawbacks of surgical treatment for hypertrophic AKs?
Benefits: Allows histopathologic assessment and has low recurrence rates. Drawbacks: Requires local anesthesia, prolonged wound healing, and risks of infection, scarring, and poor cosmetic outcomes.
72
What are the advantages and disadvantages of ablative laser therapy for actinic keratosis?
Advantages: Short treatment duration. Disadvantages: Risk of dyspigmentation, scarring, and high equipment costs.
73
What is the mechanism of action of photodynamic therapy (PDT) in treating actinic keratosis?
PDT involves applying a photosensitizing agent (e.g., 5-ALA), which accumulates in atypical cells. Light exposure activates the agent, causing phototoxic reactions and cell destruction.
74
What are the common adverse events of cryosurgery for actinic keratosis?
Adverse events include pain, hemorrhage, blister formation, nerve damage, pigmentary changes, and scarring.
75
What are the advantages and disadvantages of cryosurgery for treating actinic keratoses?
Advantages: Commonly performed with a spray device, cotton swab, or probe. Suitable for a limited number of clinically perceptible or symptomatic lesions. No need for local anesthesia and simple post-treatment care. Disadvantages: Short-term complications include discomfort, pain, hemorrhage, and blister formation. Risk of nerve damage and pigmentary changes from destruction of adjacent melanocytes, leading to scarring.
76
How do laser therapies differ in their application and potential outcomes for actinic keratoses?
Laser Therapies: Types: Carbon dioxide (CO2) and erbium:yttrium aluminum garnet (Er:YAG) lasers. CO2 Laser: Higher penetration depth, advantageous for thicker and hyperkeratotic lesions. Adverse events include hypopigmentation and atrophic scarring. Outcomes: Actinic keratoses (AKs) can relapse after laser treatment, indicating the need for ongoing management.
77
What is the mechanism of action for lesion-directed photodynamic therapy (PDT) in treating actinic keratoses?
Mechanism of Action for PDT: 1. Topical application of a photosensitizing agent (e.g., 5-Aminolevulinic acid (ALA) or methyl aminolevulinate (MAL)). 2. These agents are absorbed by the epidermis and accumulate in atypical cells. 3. They are processed to protoporphyrin IX. 4. Subsequent exposure to a specific wavelength of light activates protoporphyrin IX. 5. This results in a phototoxic reaction, releasing reactive oxygen species (ROS) that lead to necrosis and apoptosis of target cells.
78
What is the mechanism of action of Diclofenac in the treatment of Actinic Keratoses?
Diclofenac is an inhibitor of cyclooxygenase and belongs to nonsteroidal anti-inflammatory drugs. It is protective against the appearance of new Actinic Keratoses (AKs) and acts against subclinical lesions.
79
What are the common adverse events associated with the use of 5-Fluorouracil (5-FU) for Actinic Keratoses?
Common adverse events of 5-Fluorouracil (5-FU) include erythema, erosion, and discomfort at the site of application.
80
How does Imiquimod function in the treatment of Actinic Keratoses?
Imiquimod acts as a Toll-like receptor 7 agonist, activating innate immune cells to produce interferon-alpha and other cytokines, which helps in the treatment of Actinic Keratoses.
81
What is the recommended dosage for 3% Diclofenac gel in the treatment of Actinic Keratoses?
The recommended dosage for 3% Diclofenac gel is twice daily for 90 days.
82
What formulation of 5-Fluorouracil is suggested for hypertrophic lesions and why?
A formulation of 0.5% 5-Fluorouracil with 10% salicylic acid is suggested for hypertrophic lesions because salicylic acid has a keratolytic effect and improves the penetration of 5-FU.
83
What is the mechanism of action of 5-fluorouracil (5-FU) in treating actinic keratosis?
5-FU acts as an anti-metabolite by inhibiting thymidylate synthetase, leading to cytostatic effects on atypical keratinocytes.
84
What is the recommended dosage and duration of treatment for a patient prescribed 3% diclofenac gel for actinic keratosis?
The recommended dosage is twice daily application for 90 days.
85
What are the common adverse events associated with imiquimod therapy for actinic keratosis?
Common adverse events include local irritation, pain, pruritus, swelling, and systemic symptoms like flu-like symptoms in rare cases.
86
What is the role of cyclooxygenase inhibitors like diclofenac in treating actinic keratosis?
Diclofenac inhibits cyclooxygenase, reducing inflammation and acting against subclinical AK lesions.
87
What are the potential systemic adverse events of imiquimod therapy for actinic keratosis?
Systemic adverse events include cardiovascular disorders, myalgia, arthralgia, and flu-like symptoms.
88
What are the advantages of using 5-FU plus salicylic acid for hypertrophic actinic keratosis?
Salicylic acid enhances keratolysis and improves 5-FU penetration, making it more effective for hypertrophic lesions.
89
What are the key adverse events associated with the use of 3% diclofenac in 2.5% hyaluronic acid gel for treating actinic keratoses?
Adverse events may include erythema, scaling, burning sensation, and pruritus at the site of application.
90
How does the formulation of 5-Fluorouracil (5-FU) with salicylic acid differ in its application compared to standard 5-FU treatments?
The combination of 0.5% 5-FU with 10% salicylic acid is applied once daily for up to 12 weeks on an area not larger than 25 cm², which may be more suited for hypertrophic lesions due to the keratolytic effect of salicylic acid that improves penetration of 5-FU.
91
How does the formulation of 5-Fluorouracil (5-FU) with salicylic acid differ in its application compared to standard 5-FU treatments?
The combination of **0.5% 5-FU with 10% salicylic acid** is applied **once daily for up to 12 weeks** on an area not larger than 25 cm², which may be more suited for **hypertrophic lesions** due to the keratolytic effect of salicylic acid that improves penetration of 5-FU.
92
What is the recommended dosage and application frequency for Imiquimod in the treatment of actinic keratoses?
Imiquimod is available in different concentrations:
1. **5% cream**: applied **3 times per week for 4 weeks**.
2. **3.75% cream**: applied **once daily for 2 weeks**.
3. **2.5% cream**: applied **once daily for 2 weeks**.
93
What is the mechanism of action of Imiquimod in the treatment of actinic keratoses?
Imiquimod acts as a **Toll-like receptor 7 agonist**, activating innate immune cells to produce **interferon-alpha** and other **cytokines**, which help in the treatment of actinic keratoses.
94
What is the preferred concentration of imiquimod for treating single actinic keratosis (AK) lesions?
3.75% imiquimod is commonly preferred for treatment of single AK lesions as well as for field-directed therapy.
95
What are the local adverse events associated with Ingenol mebutate treatment?
Local adverse events include irritation, pruritus, inflammatory changes such as erythema, blister, edema, erosion, scaling, and crusting. These reactions usually appear early and subside within 14 days.
96
What is the effectiveness of cryopeeling in treating actinic keratosis?
Cryopeeling is effective for hypertrophic AK and helps reduce recurrence rates, although it bears a higher risk for hypopigmentation of treated areas.
97
What are the common side effects of medium-depth chemical peels for actinic keratosis?
Common side effects include stinging, burning sensation, erythema, and scaling. They can cause skin damage in the superficial papillary dermis and induce a wound reaction with exfoliation of atypical keratinocytes and reepithelialization.
98
Why are deep chemical peels rarely used for treating actinic keratosis?
Deep chemical peels using phenol or higher concentrations of TCA are rarely used due to potential cardiac and renal toxicity of phenol and a higher risk of scarring, infection, and hypopigmentation.
99
What is dermabrasion and how is it performed?
Dermabrasion, also known as surgical skin planning, involves physical ablation of lesions with superficial abrasion of the epidermis. It is performed under sedation or general anesthesia due to pain.
100
What is the role of field-targeted photodynamic therapy in treating actinic keratosis?
Field-targeted photodynamic therapy is performed with 5-ALA cream or MAL nanoemulsion as photosensitizing agents.
101
What are the common adverse events associated with chemical peeling for actinic keratosis?
Adverse events include stinging, burning sensation, erythema, and scaling.
102
What is the preferred treatment for single actinic keratosis (AK) lesions and field-directed therapy?
3.75% imiquimod is commonly preferred for treatment of single AK lesions as well as for field-directed therapy.
103
What are the local adverse events associated with Ingenol mebutate treatment for actinic keratosis?
Local adverse events include irritation, pruritus, inflammatory changes such as erythema, blister, edema, erosion, scaling, and crusting. All adverse reactions appear early and usually subside within 14 days.
104
How does cryopeeling work in the treatment of actinic keratosis and what are its risks?
Cryopeeling involves extensive application of liquid nitrogen to a complete field of manifest and subclinical AK. It is effective for hypertrophic AK but bears a higher risk for hypopigmentation of treated areas.
105
What are the common side effects of medium-depth chemical peels in treating actinic keratosis?
Common side effects include stinging, burning sensation, erythema, and scaling. They cause skin damage in the superficial papillary dermis and induce a wound reaction with exfoliation of atypical keratinocytes and reepithelialization.
106
What is the significance of using deep chemical peels for actinic keratosis treatment?
Deep chemical peels using phenol or higher concentrations of TCA are more effective in treating hyperkeratotic AK or AK with appendageal epithelial atypia, but they are rarely used due to potential cardiac and renal toxicity, as well as a higher risk of scarring, infection, and hypopigmentation.
107
What is dermabrasion and why is it rarely used nowadays in the treatment of actinic keratosis?
Dermabrasion, also known as surgical skin planning, is based on physical ablation of lesions with superficial abrasion of the epidermis. It is rarely used nowadays due to the need for sedation or general anesthesia because of pain.
108
What is the role of field-targeted photodynamic therapy in treating actinic keratosis?
Field-targeted photodynamic therapy is performed with 5-ALA cream or MAL nanoemulsion as photosensitizing agents, providing a targeted approach to treating actinic keratosis.
109
What is the effectiveness of natural daylight PDT compared to conventional PDT for treating actinic keratoses (AKs)?
The effectiveness of natural daylight PDT for treating mild to moderate AKs is noninferior to conventional PDT in several trials.
110
What are the primary prevention measures to decrease the risk of actinic keratoses (AKs)?
Primary prevention measures include:
1. Minimizing UV radiation exposure.
2. Avoiding intense midday sun.
3. Consistently applying and reapplying broad spectrum sunscreens.
4. Wearing UV protective clothing, hats, and sunglasses.
5. Installing UV protective windows where indicated.
6. Taking oral vitamin D supplements if necessary to avoid vitamin D insufficiency.
111
What is the recommended use of sunscreens to prevent actinic keratoses (AKs)?
The recommended use of sunscreens includes:
- Using a broad spectrum sunscreen against UVB and UVA radiation with a minimum sun protection factor of 30.
- Applying sunscreen in sufficient amounts at least 20 minutes before going outside and reapplying every 2-3 hours.
112
What evidence supports the use of systemic retinoids in the prevention of nonmelanoma skin cancer and actinic keratoses (AKs)?
There is strong evidence for the use of systemic retinoids in preventing nonmelanoma skin cancer and AKs; however, they are only effective while being taken and are limited by frequent occurrences of systemic toxicities.
113
What was the effect of oral nicotinamide (vitamin B3) on actinic keratoses (AKs) in high-risk patients?
Oral nicotinamide (vitamin B3) was reported safe and effective in reducing rates of new nonmelanoma skin cancer and AK in high-risk patients, with a 13% reduction in the number of AKs in those who took 500mg of nicotinamide BID for 12 months compared to placebo. However, the beneficial effects disappeared when treatment was discontinued.
114
What are the advantages of natural daylight photodynamic therapy (PDT) over conventional PDT for actinic keratosis?
Natural daylight PDT is less painful, has shorter incubation times, and is equally effective for mild to moderate AKs compared to conventional PDT.
115
A patient with multiple AKs is advised to use sunscreen. What are the key recommendations for effective sunscreen use?
Use broad-spectrum sunscreen with SPF 30 or higher, apply 20 minutes before sun exposure, and reapply every 2-3 hours.
116
What chemopreventive agent has been shown to reduce the number of actinic keratosis lesions by 13% in high-risk patients?
Oral nicotinamide (vitamin B3) at a dose of 500 mg twice daily for 12 months has been shown to reduce AK lesions by 13%.
117
What is the role of systemic retinoids in preventing actinic keratosis, and what are their limitations?
Systemic retinoids prevent AKs and nonmelanoma skin cancer but are limited by systemic toxicities like hyperlipidemia and liver dysfunction.
118
What are the common adverse events of natural daylight photodynamic therapy (PDT)?
Adverse events include local erythema, edema, blistering, sterile pustule formation, and crusting.
119
What are the primary prevention measures for actinic keratosis?
Primary prevention includes minimizing UV exposure, using sunscreen, wearing protective clothing, and avoiding intense midday sun.
120
What are the primary measures for preventing actinic keratoses (AKs)?
Primary prevention measures for AKs include:
1. **Minimizing UV radiation** exposure, which is the most effective means of decreasing the risk of AKs.
2. **Avoiding intense midday sun**.
3. **Consistently applying and reapplying broad spectrum sunscreens**.
4. **Wearing UV protective clothing, hats, and sunglasses**.
5. **Installing UV protective windows** where indicated.
6. **Taking oral vitamin D supplements** if necessary to avoid vitamin D insufficiency.
121
What is the recommended use of sunscreens to prevent actinic keratoses?
To effectively prevent actinic keratoses, it is recommended to:
1. Use a **broad spectrum sunscreen** that protects against both UVB and UVA radiation.
2. Ensure a **minimum sun protection factor (SPF) of 30**.
3. Apply sunscreen in sufficient amounts at least **20 minutes before going outside**.
4. Reapply sunscreen every **2-3 hours** while outdoors.
122
What evidence supports the use of systemic retinoids in the prevention of nonmelanoma skin cancer and actinic keratoses?
There is **strong evidence** supporting the use of **systemic retinoids** in preventing nonmelanoma skin cancer and actinic keratoses (AKs). However, their effectiveness is limited to the duration of treatment, and they are associated with **systemic toxicities** such as:
- Hypercholesterolemia
- Hypertriglyceridemia
- Mucocutaneous xerosis
- Musculoskeletal abnormalities
- Alterations in liver function
123
What role does oral nicotinamide play in the prevention of actinic keratoses?
Oral nicotinamide (vitamin B3) has been reported to be **safe and effective** in reducing the rates of new nonmelanoma skin cancer and actinic keratoses in high-risk patients. Specifically:
- The number of AKs was reduced by **13%** in patients taking **500mg of nicotinamide BID for 12 months** compared to placebo.
- However, the beneficial effects **disappeared** when treatment was discontinued.
124
What are the primary risk factors associated with the development of actinic keratosis (AK)?
The primary risk factors for actinic keratosis (AK) include:
- **Fair skin**
- **Ultraviolet (UV) radiation**
- **Immunosuppression**
- **Human papillomavirus (HPV) infection**
- **Exposure to tar, arsenic, and X-rays**
125
Describe the progression of actinic keratosis from early lesions to invasive squamous cell carcinoma (SCC).
The progression of actinic keratosis (AK) follows a stepwise pathway:
1. **Normal skin**
2. **AK I**: Early lesions confined to the basal layers of the epidermis.
3. **AK II**: Intermediate lesions.
4. **AK III**: Late lesions that may progress to invasive squamous cell carcinoma (SCC).
This progression is often associated with genetic alterations such as loss of the tumor-suppressor gene **p53** and mutations in **p16**.
126
What role does Notch signaling play in the development of actinic keratosis?
Decreased **Notch signaling** in the underlying dermis may contribute to the formation and progression of actinic keratosis (AK). This signaling pathway is important for maintaining normal skin homeostasis, and its disruption can lead to the development of AK lesions.
127
What are the two proposed pathways for the progression of actinic keratosis to squamous cell carcinoma (SCC)?
There are two proposed pathways for the progression of actinic keratosis (AK) to squamous cell carcinoma (SCC):
1. **Classic pathway**: Involves a stepwise progression from AK I to AK II and then to AK III, ultimately leading to SCC.
2. **Alternative pathway**: Suggests that any AK, including low-grade lesions, has the potential to directly progress to invasive SCC.
128
What are the key risk factors associated with the development of actinic keratosis (AK)?
The key risk factors for actinic keratosis (AK) include:
- **Fair skin**
- **Ultraviolet (UV) radiation**
- **Immunosuppression**
- **Human papillomavirus (HPV) infection**
- **Exposure to tar, arsenic, and X-rays**
129
Describe the sequential progression of actinic keratosis from normal skin to squamous cell carcinoma (SCC).
The sequential progression of actinic keratosis (AK) is as follows:
1. **Normal skin**
2. **AK I**: Early lesions confined to the basal layers of the epidermis.
3. **AK II**: Intermediate lesions.
4. **AK III**: Late lesions that may progress to invasive squamous cell carcinoma (SCC).
130
What molecular events are commonly associated with the progression of actinic keratosis?
Common molecular events associated with the progression of actinic keratosis include:
- **Loss of the tumor-suppressor gene p53**
- **Ras activation**
- **Chromosomal aberrations**
- **Defective apoptosis**
- **Loss of p16 and other mutations**
131
How does decreased Notch signaling contribute to the development of actinic keratosis?
Decreased Notch signaling in the underlying dermis may contribute to the formation and progression of actinic keratosis (AK) by disrupting normal cellular communication and differentiation processes, potentially leading to the development of AK lesions.
132
What are the implications of the alternative pathway in the progression of actinic keratosis to squamous cell carcinoma?
The alternative pathway suggests that any actinic keratosis (AK), including low-grade lesions, has the potential to directly progress to invasive squamous cell carcinoma (SCC). This highlights the importance of monitoring and managing all AK lesions to prevent malignant transformation.
133
What is Bowen Disease and its potential progression?
Bowen Disease is a distinct type of squamous cell carcinoma (SCC) in situ that affects both skin and mucous membranes and has the potential to progress to invasive SCC.
134
What are the common clinical features of Bowen Disease?
Common clinical features include slow-growing lesions that may be asymptomatic, erythematous plaques with irregular, clearly demarcated borders, scaly, crusted, or hyperkeratotic surface, lesions may grow to several centimeters, flat plaques may transform into nodular or verrucous forms, and color variations: pink or reddish for flat plaques, gray or brownish for crusty lesions.
135
What are the main etiologic factors associated with Bowen Disease?
The most important etiologic factors include long history of significant UV exposure, HPV infection (subtypes 16, 18, 31, 34, 35, 54, 58, 61, 62, and 73), increased frequency in patients undergoing psoralen plus UVA therapy, higher incidence in immunosuppressed patients, and other factors like arsenic exposure and ionizing radiation.
136
What is the typical diagnostic approach for Bowen Disease?
The diagnostic approach includes clinical picture and typical history indicating high suspicion for BD, biopsy and histologic examination for final diagnosis, and histologic findings such as full-thickness epidermal atypia, abnormal mitoses, acanthosis, hyperkeratosis, and variable cytologic atypia.
137
What are the histopathologic subtypes of Bowen Disease?
The histopathologic subtypes include Psoriasiform BD (parakeratosis and marked acanthosis), Atrophic BD (thinned epidermis), Acantholytic BD (acantholysis in the epidermis), Epidermolytic BD (epidermolytic hyperkeratosis), and Pagetoid BD (nesting of atypical cells within the epidermis).
138
What are the clinical differential diagnoses for Bowen Disease?
Differential diagnoses include superficial BCC, patches of psoriasis, atopic dermatitis, or lichen planus, viral warts, seborrheic keratosis, SCC, melanoma, amelanotic melanoma, and sexually transmitted Bowenoid papulosis.
139
What are the key histological findings in Bowen Disease?
Key histological findings include full-thickness epidermal atypia, loss of stratified epidermal architecture, abnormal mitoses, acanthosis, hyperkeratosis, parakeratosis in the upper epidermal layers, variable cytologic atypia, and infiltration of upper dermis with inflammatory cells.
140
What are the key epidemiological characteristics of Bowen Disease in the United States?
Key epidemiological characteristics include unknown exact incidence, 142/100,000 persons in Hawaii, occurrence mainly in adults (>60 years old), male preponderance, higher recurrence rate in immunocompromised individuals, and women more affected on cheeks and lower legs.
141
What are the clinical features of Bowenoid Papulosis?
Bowenoid Papulosis presents with multiple flat verrucous papules and plaques that have a red-to-brownish color, most common among young to middle-aged sexually active individuals, with lesions typically found on the glans penis, prepuce, and penile shaft in males, and around the labia minora and majora in females.
142
What is the clinical course and prognosis of Bowen Disease?
The clinical course is characterized by rare recurrence, approximately 5% risk of progression to invasive cancer if untreated, higher risk in immunocompromised patients, and higher risk of nonmelanoma skin cancer but not usually associated with higher risk for internal malignancies.
143
What are the treatment options for Bowen Disease?
Treatment options include surgical and destructive therapies (excision, Mohs micrographic surgery, curettage, chemoblation, cryosurgery), topical therapies (5-FU, imiquimod cream, ingenol mebutate), and nonsurgical ablative therapies (photodynamic therapy, laser ablation, radiation therapy).
144
What factors increase the risk of recurrence and transformation in immunocompromised patients with Bowen Disease?
Immunosuppression increases the risk of recurrence, multiple BD lesions, and transformation to invasive carcinoma.
145
What is the diagnosis and risk of malignant transformation for Bowenoid papulosis?
The diagnosis is Bowenoid papulosis, with a low risk of malignant transformation ranging from <1% to 2.6%.
146
What factors influence the clinical course and prognosis of Bowen Disease?
Factors include recurrence risk, immunocompromised status, location of lesions, and association with internal malignancies.
147
What are the main categories of treatment options for Bowen Disease?
The main categories include surgical and destructive therapies, topical therapies, and nonsurgical ablative therapies.
148
What are the histopathologic findings associated with Bowenoid Papulosis?
Histopathologic findings include SCC in situ-like changes, hyperplastic epidermis with acanthosis, signs of cellular atypia, dyskeratotic keratinocytes, and HPV detection via PCR.
149
How does the clinical course of Bowenoid Papulosis compare to that of invasive squamous cell carcinoma (SCC)?
Bowenoid Papulosis is generally more benign with low malignant transformation risk, while SCC is invasive and requires aggressive treatment.
150
What are the two different morphologies of skin lesions associated with Epidermodysplasia Verruciformis (EV)?
The two morphologies are EV-plane warts (thin, pink, flat-topped papules) and widespread scaly lesions (erythematous or hypopigmented macules).
151
What is the significance of HPV vaccination in relation to Anal Intraepithelial Neoplasia (AIN)?
HPV vaccination may reduce the incidence of Anal Intraepithelial Neoplasia (AIN).
152
What are the three categories of Vulvar Intraepithelial Neoplasia (VIN)?
The categories are VIN usual type (associated with high-risk HPV), VIN differentiated type (not associated with HPV), and unclassified type.
153
What are the risk factors associated with Vulvar Intraepithelial Neoplasia (VIN)?
Risk factors include smoking, sexual promiscuity, HPV infection, and immunosuppression.
154
What are the treatment options for patients with high-grade squamous intraepithelial lesions (HSIL) of Anal Intraepithelial Neoplasia (AIN)?
Treatment options include topical treatments like trichloroacetic acid, infrared coagulation, 5-FU, intraanal imiquimod, or electrocautery.
155
What are the usual risk factors for high-grade squamous intraepithelial lesions (HSIL) of Anal Intraepithelial Neoplasia (AIN)?
Risk factors include smoking, sexual promiscuity, HPV infection, and immunosuppression.
156
What are the treatment options for patients with high-grade squamous intraepithelial lesions (HSIL) of Anal Intraepithelial Neoplasia (AIN)?
Treatment options include topical treatments such as trichloroacetic acid, infrared coagulation, 5-FU, intraanal imiquimod, or electrocauterization, and surgical options like surgical excision or other ablative therapies.
157
What is the diagnosis for multifocal reddish patches on the vulva, and what HPV types are commonly associated?
The diagnosis is vulvar intraepithelial neoplasia (VIN) usual type, commonly associated with high-risk HPV types 16, 18, and 31.
158
What is the diagnosis for flat-topped papules resembling tinea versicolor in a patient with HIV, and what genetic mutations are associated?
The diagnosis is epidermodysplasia verruciformis (EV), associated with mutations in the TMC6 (EVER1) and TMC8 (EVER2) genes.
159
What is the diagnosis for a unifocal lesion on the vulva associated with lichen sclerosus, and how does it differ from the usual type?
The diagnosis is VIN differentiated (simplex) type, which is less common, not associated with HPV, and typically affects postmenopausal females.
160
What is the diagnosis for a well-demarcated erythematous plaque on the perianal region, and what is the risk of progression to invasive SCC?
The diagnosis is perianal intraepithelial neoplasia (PaIN), with only 5% of patients potentially progressing to invasive SCC.
161
What is the diagnosis for anal pruritus in a patient with a history of high-risk sexual behavior, and what are the treatment options for high-grade lesions?
The diagnosis is anal intraepithelial neoplasia (AIN). Treatment options for high-grade lesions (AIN 2 or AIN 3) include topical trichloroacetic acid, infrared coagulation, 5-FU, intraanal imiquimod, or electrocauterization.
162
What are the two different morphologies of skin lesions associated with Epidermodysplasia Verruciformis (EV)?
1. EV-plane warts: Numerous thin, pink, flat-topped papules and plaques resembling flat warts on knees, elbows, and trunk. 2. Widespread scaly lesions: Erythematous or hypopigmented macules and flat papules that resemble tinea versicolor.
163
What is the significance of HPV vaccination in the context of Anal Intraepithelial Neoplasia (AIN)?
HPV vaccination with a quadruple vaccine against HPV types 6, 11, 16, and 18 may reduce the incidence of AIN, particularly in patients with high-risk factors such as HPV infection and immunosuppression.
164
What are the three categories of Vulvar Intraepithelial Neoplasia (VIN) and their associations with HPV?
| Category | Description | HPV Association |
|----------|-------------|-----------------|
| VIN usual type | Associated with high-risk HPV (types 16, 18, 31); occurs in younger premenopausal females with multifocal lesions. | High-risk HPV |
| VIN differentiated (simplex) type | Less common, usually not associated with HPV; affects postmenopausal females with unifocal presentation. | Not associated with HPV |
| Unclassified type | Varies in presentation and risk factors. | Varies |
165
What are the risk factors and clinical presentation of Vulvar Intraepithelial Neoplasia (VIN) associated with the usual type?
Risk factors include smoking, sexual promiscuity, HPV infection, and immunosuppression. Clinical presentation includes reddish patches to gray-white plaques, verrucous wart-like papules, and may be asymptomatic or cause vulvar pain, burning sensation, dysuria, or pruritus.
166
What are the histopathological features of leukoplakia?
Leukoplakia exhibits hyperkeratosis, epithelial hyperplasia, and dysplasia, including atypical mitosis, polymorphic cells, hyperchromatic and polymorphic nuclei. Different growth patterns may be observed, including clinically flat, papillary endophytic, papillary exophytic, and verrucous proliferation.
167
What is the most likely diagnosis for a white lesion on the oral mucosa that cannot be rubbed off, and what are the next steps in management?
The most likely diagnosis is leukoplakia. Next steps include identifying and eliminating causative agents, followed by a biopsy if the lesion does not regress within 2-6 weeks.
168
What subtype of leukoplakia is characterized by a white, flat lesion on the oral mucosa with shallow cracks, and what is the risk of malignant transformation?
This is the homogeneous form of leukoplakia, which has a lower risk of malignant transformation compared to nonhomogeneous forms.
169
What is the diagnosis for a rare form of leukoplakia characterized by high recurrence and malignant transformation rates?
The diagnosis is proliferative verrucous leukoplakia, which has a high rate of malignant transformation and recurrence.
170
What etiological factors should be considered for a white lesion on the oral mucosa in a patient with a history of chewing tobacco, and what is the role of tobacco cessation?
Etiological factors include chronic chemotoxic exposure from tobacco. Tobacco-related white lesions may disappear once use is discontinued.
171
What is the diagnosis for a well-demarcated, glistening erythematous plaque on the glans penis, and what is the associated HPV type?
The diagnosis is erythroplasia of Queyrat (EQ), a type of penile intraepithelial neoplasia (PIN), commonly associated with HPV 16.
172
What are the two clinical variants of penile intraepithelial neoplasia (PIN), and which has a higher risk of progression to invasive SCC?
The two clinical variants are genital Bowen disease (GBD) and erythroplasia of Queyrat (EQ). EQ has a higher risk of progression to invasive SCC (approximately 30%).
173
What are the clinical features and risk factors associated with the progression of leukoplakia to invasive squamous cell carcinoma (SCC)?
Clinical features include predominantly white lesions of the oral mucosa that cannot be rubbed off, with homogeneous and nonhomogeneous forms. Risk factors include tobacco use, chronic chemotoxic exposure, HPV infection, alcohol consumption, and previous malignancy or premalignancy of the upper aerodigestive tract.
174
How does the presence of HPV influence the risk and characteristics of penile intraepithelial neoplasia (PIN)?
PIN associated with HPV infection is more aggressive and may develop into warty and basaloid subtypes of penile SCC. PIN without HPV is morphologically associated with the usual or differentiated type of penile SCC.
175
What diagnostic steps should be taken when leukoplakia is suspected, and what are the implications of biopsy results?
Diagnostic steps include clinical diagnosis, identifying and eliminating causative agents, and proceeding to biopsy if regression does not occur. Biopsy results are crucial to rule out malignant transformation into invasive SCC.
176
What is erythroplakia and how is it characterized?
Erythroplakia is a red macule or patch on a mucosal surface that cannot be categorized as any other known disease entity. It is characterized by being asymptomatic, solitary, sharply demarcated, smooth, and homogeneous in color.
177
What are the risk factors associated with erythroplakia?
Risk factors include consumption of tobacco products, alcohol consumption, chewing carcinogenic nuts like areca nuts, and genetic predisposition with a high mutation rate of p53.
178
What is the clinical course and prognosis of erythroplakia?
Erythroplakia is considered one of the most dangerous potentially malignant lesions in the oral cavity, carrying the greatest risk of progressing to or harboring invasive carcinoma.
179
What are arsenical keratoses and their clinical implications?
Arsenical keratoses result from chronic intake or intoxication with arsenic, considered precancerous lesions with potential to progress into invasive SCC. They commonly appear on palms and soles as gray-to-yellow keratotic papules.
180
What are the treatment options for arsenical keratoses?
Treatment options include surgical excision, cryosurgery, curettage, ablative resurfacing, topical and systemic retinoids, and regular follow-up every 6-12 months.
181
What are thermal keratoses and their potential risks?
Thermal keratoses are precancerous lesions from long-term exposure to infrared radiation, which can progress to SCC. The risk of progression is currently unknown.
182
What are hydrocarbon keratoses and their associated risks?
Hydrocarbon keratoses are precancerous lesions from prolonged exposure to tar, containing highly cancerogenic polycyclic aromatic hydrocarbons. They can progress to SCC, but the rate of progression is unknown.
183
What is the diagnosis for a red macule on the buccal mucosa that is sharply demarcated and velvety on palpation?
The most likely diagnosis is erythroplakia, which carries the greatest risk of progressing to or harboring invasive carcinoma among oral lesions.
184
What is the diagnosis for a gray-to-yellow keratotic papule on the palm in a patient with chronic arsenic exposure, and what are the management steps?
The diagnosis is arsenical keratosis. Management includes identifying and discontinuing arsenic sources, thorough skin examination, and treatment of lesions.
185
What is the diagnosis for hyperkeratotic papules on the face and neck after prolonged exposure to tar, and what occupations are at risk?
The diagnosis is hydrocarbon keratosis. Occupations at risk include tar distillers, roofers, asphalt workers, and chimney sweeps.
186
What is the diagnosis for a red macule on the oral mucosa and a history of chewing areca nuts, and what genetic mutation is commonly associated?
The diagnosis is erythroplakia, commonly associated with a high mutation rate of p53.
187
What is the diagnosis for a hyperkeratotic papule on the neck after prolonged exposure to infrared radiation, and what is the precursor lesion?
The diagnosis is thermal keratosis, with the precursor lesion being erythema ab igne.
188
What is the diagnosis for a hyperkeratotic papule on the forearm after prolonged exposure to tar, and what are the cancerogenic substances in tar?
The diagnosis is hydrocarbon keratosis. Cancerogenic substances in tar include polycyclic aromatic hydrocarbons such as benzpyrene and dibenzanthracene.
189
What is the diagnosis for a hyperkeratotic plaque on the sole after chronic arsenic exposure, and what are the histopathological features?
The diagnosis is arsenical keratosis. Histopathological features resemble hypertrophic AKs with more cellular atypia and prominent vacuolization of keratinocytes.
190
What is the diagnosis for a hyperkeratotic papule on the scrotal skin after prolonged tar exposure, and what cofactor increases the risk of progression?
The diagnosis is hydrocarbon keratosis. UV exposure acts as a cofactor, increasing the risk of progression.
191
What is the diagnosis for a red macule on the soft palate that is less than 1.5 cm in diameter, and what clinical feature suggests transformation to invasive SCC?
The diagnosis is erythroplakia. Induration is a clinical feature that suggests transformation to invasive SCC.
192
What is the diagnosis for a hyperkeratotic papule on the forearm after prolonged exposure to tar, and what occupations are at risk?
The diagnosis is hydrocarbon keratosis. Occupations at risk include tar distillers, roofers, and asphalt workers.
193
What is the latency period for lesion development in hydrocarbon keratosis?
The latency period for lesion development ranges from 2.5 to 45 years.
194
What is the diagnosis for a hyperkeratotic papule on the neck after prolonged exposure to infrared radiation, and what is the precursor lesion?
The diagnosis is thermal keratosis. The precursor lesion is erythema ab igne.
195
What are the histopathological features of a hyperkeratotic plaque on the sole after chronic arsenic exposure, and what is the risk of progression?
Histopathological features resemble hypertrophic AKs with more cellular atypia and prominent vacuolization of keratinocytes. Progression to invasive SCC is relatively rare.
196
What are the key clinical findings associated with erythroplakia?
- Erythroplakia typically presents as an asymptomatic, solitary, subtle, erythematous macule or patch.
- It is sharply demarcated from surrounding pink mucosa, with a smooth and homogeneous surface.
- Some lesions may have a pebbled or stippled surface and feel soft and velvety on palpation.
- Induration is a significant indicator suggesting transformation to invasive SCC.
- Most common areas affected include the soft palate, floor of the mouth, and buccal mucosa.
- Lesions are usually less than 1.5 cm in diameter.
197
What are the recommended treatment options for erythroplakia?
- The first treatment of choice for erythroplakia is surgical excision or excision with CO2 laser, allowing for histologic workup.
- Early treatment is warranted to reduce the risk of malignant transformation.
- If recurrence occurs, cryotherapy or CO2 laser may be useful.
- Other treatment options include PDT, herbal extracts, beta-carotene supplements, anti-inflammatory drugs, and vitamin A.
- Patients should be followed closely for any signs of recurrence.
198
What are the characteristics and risks associated with arsenical keratoses?
- Arsenical keratoses result from chronic exposure to arsenic, presenting as gray-to-yellow keratotic papules, commonly on palms and soles.
- They may resemble vulgar warts or hypertrophic lichen planus and can persist for many years, but progression to invasive SCC is relatively rare.
199
What are the potential risks and management strategies for thermal keratoses?
- Thermal keratoses are precancerous lesions resulting from long-term exposure to infrared radiation, which can progress to SCC.
- Common sources include open fires, railway engines, wood-burning stoves, and heating pads.
- The precursor lesion is erythema ab igne, and biopsy should be performed on any hyperkeratotic papule or plaque within such a patch.
200
What are the occupational risks associated with hydrocarbon keratoses?
- Hydrocarbon keratoses, also known as pitch keratoses, result from prolonged exposure to tar, which contains highly carcinogenic polycyclic aromatic hydrocarbons.
- Occupations at risk include tar distillers, roofers, asphalt workers, and others exposed to tar products.
201
What are chronic radiation keratoses and their potential risks?
Chronic radiation keratoses are precancerous lesions that may arise at irradiated sites years after exposure to ionizing radiation sources such as X-rays and grenz rays. They can present as hyperkeratotic papules or plaques and may progress to squamous cell carcinoma (SCC). Patients with these keratoses are also at risk for internal malignancies.
202
What are chronic scar keratoses and their associated risks?
Chronic scar keratoses, also known as cicatrix keratoses, are precancerous lesions that arise in longstanding scars from various causes, such as burn scars and chronic wounds. Approximately 2% of burn scars may undergo malignant changes, leading to conditions like Marjolin ulcer.
203
What is the significance of Marjolin ulcer in chronic scar keratoses?
Marjolin ulcer refers to malignant changes that occur within a scar. Acute Marjolin ulcer develops within 1 year of injury, while chronic Marjolin ulcer develops more than 1 year after. It is significant because it can lead to invasive carcinomas, including SCCs, which have an aggressive growth pattern and a high propensity to metastasize.
204
What are the therapeutic options for Bowen Disease?
Therapeutic options for Bowen Disease include surgical and destructive therapies such as excision, curettage, and ablative lasers (CO2, Er:YAG). Topical therapies like 5-Fluorouracil are also used.
205
What is the diagnosis for hyperkeratotic papules on the palms after chronic radiation exposure, and what is the latency period for lesion development?
The diagnosis is chronic radiation keratosis. The latency period for lesion development can be up to 50 years after exposure.
206
What is the diagnosis for a persistent ulceration within a longstanding burn scar, and what is the risk of malignancy?
The diagnosis is chronic scar keratosis (Marjolin ulcer). Approximately 2% of burn scars undergo malignant changes, most commonly to SCC.
207
What is the diagnosis for a persistent lesion within a scar from a chronic wound, and what is the most common type of invasive carcinoma associated?
The diagnosis is chronic scar keratosis. The most common type of invasive carcinoma associated is SCC.
208
What are the common sites for chronic radiation keratoses and how do they present clinically?
Common sites for chronic radiation keratoses include palms, soles, and mucosal surfaces. They present as hyperkeratotic papules or plaques within areas of chronic radiation dermatitis and occasionally on clinically normal skin.
209
What is the latency period for the development of lesions in patients exposed to ionizing radiation?
The latency for the development of lesions in patients exposed to ionizing radiation can be up to 50 years after exposure.
210
What are the characteristics and risks associated with chronic scar keratoses?
Chronic scar keratoses, also known as cicatrix keratoses, are precancerous lesions that arise in longstanding scars from various causes. Key characteristics include approximately 2% of burn scars will undergo malignant changes. Marjolin ulcer can develop from any scar, with acute forms appearing within 1 year and chronic forms developing more than 1 year after an injury.
211
What preventive measures can be taken to reduce the risk of malignant changes in chronic scar keratoses?
Preventive measures to reduce the risk of malignant changes in chronic scar keratoses include wound care, early skin grafting, avoidance of contractures, and early excision of any tissue showing degenerative changes.
