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white

ghj rh4 English 199 cards

Cards in this deck (199)

  1. 1What are the three groups of white lesions based on their clinical features?1. White lesions due to epithelial thickening. 2. White lesions due to accumulation of necrotic debris on the mucosal surface. 3. White lesions due to sub-epithelial changes in the connective tissue.
  2. 2What contributes to the white appearance of lesions in the oral mucosa?Keratin absorbs moisture from saliva.
  3. 3What causes white lesions to appear white?The pink to red color of the blood vessels in the underlying connective tissue is masked by the increased thickness of the epithelium.
  4. 4What are the characteristics of white lesions?Asymptomatic, rough to palpation, cannot be rubbed off with a gauze, and appear flat white when dried.
  5. 5Are all white lesions potentially malignant?No, only a minority of white lesions are potentially malignant.
  6. 6Name three common benign chronic mucosal lesions.Leukoedema, Frictional keratosis, Cheek biting.
  7. 7Name one uncommon benign chronic mucosal lesion.Hairy leukoplakia.
  8. 8What is leukoedema?A normal anatomical variation.
  9. 9What is leukoedema?A generalized bilateral, grayish-white change in the appearance of oral mucosa.
  10. 10Is leukoedema a disease?No, it is a variation of normal.
  11. 11Where is leukoedema usually found?In the buccal mucosa.
  12. 12What causes the grayish-white appearance in leukoedema?A buildup of parakeratin at the surface.
  13. 13What percentage of the African population has leukoedema?About 90%.
  14. 14What is the etiology of leukoedema?Unknown, but it has been suggested to develop in areas of local irritation.
  15. 15What is the characteristic feature that decreases as the buccal mucosa is stretched?White appearance (Blanch Test).
  16. 16Where is the oral manifestation located?Buccal mucosa, extending onto the labial mucosa.
  17. 17In which region is the manifestation noticeable along the occlusal line?Buccal premolar & molar region.
  18. 18How is the manifestation distributed?Diffuse, symmetrically & bilaterally.
  19. 19What is the appearance of the manifestation?Grayish-white, opaque or milky.
  20. 20How does the manifestation appear in the early stage?Filmy opalescence of mucosa.
  21. 21How does the manifestation appear in the later stages?Grayish-white cast with coarsely wrinkled appearance.
  22. 22What are the symptoms of Leukoedema?Asymptomatic.
  23. 23Are patients often aware of the presence of Leukoedema?No, they are often not aware of its presence.
  24. 24Is treatment necessary for Leukoedema?No, no treatment is necessary.
  25. 25Is Leukoedema a premalignant lesion?No, it is not premalignant.
  26. 26What happens to the lesion in tobacco users if tobacco use is ceased?There can be a considerable decrease in the lesion.
  27. 27What is another name for hereditary benign intraepithelial dyskeratosis?Darier's disease
  28. 28What are the characteristics of white sponge nevus?Thick, white, velvety patches in the mouth
  29. 29What are the characteristics of follicular keratosis?Small, red or flesh-colored bumps on the skin
  30. 30What is White Sponge Nevus?A rare genetic condition with autosomal dominant pattern of inheritance.
  31. 31Is White Sponge Nevus cancerous or non-cancerous?Non-cancerous (benign) overgrowth of cells.
  32. 32What are the white patches of tissue called in White Sponge Nevus?NEVI.
  33. 33Where are the white patches of tissue typically found in White Sponge Nevus?On mucous membranes, especially in the mouth.
  34. 34At what age does White Sponge Nevus usually first appear?During early childhood.
  35. 35Which body parts does White Sponge Nevus affect?Oral cavity, nose, esophagus, external genitalia, anorectal area.
  36. 36What causes the condition related to KRT4 or KRT13 gene mutations?Mutation in KRT4 or KRT13 gene.
  37. 37What do KRT4 and KRT13 genes code for?Keratins.
  38. 38How do mutations affect keratins?They disrupt the structure of keratins.
  39. 39What is the function of keratin filaments in mucosae?To protect from damage due to friction or physical stresses.
  40. 40What happens when fragile keratin filaments are damaged?Leads to inflammation.
  41. 41What is the consequence of inflammation in this condition?Promotes abnormal growth & proliferation of epithelial cells.
  42. 42What is the end result of abnormal growth and proliferation of epithelial cells?Thickening of mucosa leading to white spongy nevus.
  43. 43What are the characteristics of the oral lesions?Bilateral, sometimes symmetrical, soft, raised white lesions on the mucosa.
  44. 44Where do the lesions usually appear?Buccal mucosa (may be localized or covering entire oral mucosa).
  45. 45How does the surface of the lesion appear?Folded.
  46. 46How does the thickened tissue feel to the touch?Spongy.
  47. 47Are the lesions generally painful?No, generally painless.
  48. 48What risk can the folds of extra tissue pose?Promote bacterial growth and lead to infection.
  49. 49What is the only treatment of utmost importance for management?Reassurance.
  50. 50What is the effectiveness of most drug therapy treatments?Ineffective or inconsistent.
  51. 51What is the result of antibiotic treatment for some patients?Complete or partial remission.
  52. 52What is Hereditary Benign Intraepithelial Dyskeratosis?A rare genetic disorder affecting the mucous membranes of the mouth and throat.
  53. 53What is the name of the disorder characterized by elevated plaques on oral and ocular mucous membranes?Hereditary Benign Intraepithelial Dyskeratosis
  54. 54How is Hereditary Benign Intraepithelial Dyskeratosis inherited?Autosomal dominant
  55. 55When do the symptoms of Hereditary Benign Intraepithelial Dyskeratosis typically appear?Early childhood
  56. 56What pattern do the symptoms of Hereditary Benign Intraepithelial Dyskeratosis follow throughout life?Waxing and waning
  57. 57What are the typical symptoms of oral manifestations?Asymptomatic.
  58. 58How do oral manifestations appear?As thick, soft, white papules and plaques of various sizes.
  59. 59Which parts of the oral cavity can be involved by oral manifestations?Any part, especially buccal mucosa, tongue, and lips.
  60. 60Are oral manifestations precancerous?No, they are not precancerous.
  61. 61What is the main difference between white sponge nevus and HBID?HBID involves the eye, while white sponge nevus does not involve the eye but instead involves nose, external genitalia, and rectum.
  62. 62What is the condition called?Hereditary Benign Intraepithelial Dyskeratosis
  63. 63Is there a cure for the condition?No, there is no cure.
  64. 64What is the result of medical management with topical corticosteroids and systemic immunosuppression?Only minimal improvement in symptoms.
  65. 65What happens after plaque excision in surgical treatment?Exuberant recurrence.
  66. 66What is the alternative name for Follicular Keratosis?Darier Disease
  67. 67Is Follicular Keratosis a common or rare disorder?Rare
  68. 68How is Follicular Keratosis inherited?Autosomal dominant
  69. 69What gene is associated with mutations in Follicular Keratosis?ATP2A2
  70. 70What are the characteristics of the blemishes in Follicular Keratosis?Wart-like, yellowish, hard, mildly greasy, and emit a strong odor
  71. 71At what age does Follicular Keratosis typically onset?Late childhood to early adulthood
  72. 72What percentage of patients have mucosal lesions?15%
  73. 73What are the affected areas of the oral cavity?Palate, tongue, buccal mucosa, gingiva, and throat.
  74. 74What kind of pattern or small papules are found in the oral cavity?White cobblestone pattern or small papules.
  75. 75What is also seen in addition to mucosal lesions in the oral cavity?Overgrowth of gingiva.
  76. 76When is treatment necessary for this condition?Only if troublesome symptoms exist.
  77. 77What is the recommended treatment for mild disease of the skin?Moisturizers, sun protection, selection of right clothing to avoid heat & sweating.
  78. 78What treatment may be effective for localized disease of the skin?Dermabrasion & topical retinoids.
  79. 79What is the recommended treatment for severe disease of the skin?A trial of an oral retinoid medication (acitretin, isotretinoin).
  80. 80What should be considered before using oral retinoid medication for severe disease?The troublesome side effects of these drugs.
  81. 81What is focal (frictional) hyperkeratosis?A type of white patch found on oral mucosa.
  82. 82What causes focal (frictional) hyperkeratosis?Constant/chronic irritation stimulating excessive keratin production.
  83. 83What are the most common factors associated with focal (frictional) hyperkeratosis?1. Tissue chewing (buccal & labial mucosa) 2. Ill-fitting or irregularly surfaced dentures 3. Fractured or malposed teeth 4. Improper tooth brushing 5. Constant mastication on edentulous alveolar ridges 6. Orthodontic appliances 7. Poorly adapted dental restorations
  84. 84What are the characteristics of oral manifestations in most patients?Free of symptoms.
  85. 85How do the oral manifestations appear?Rough, white, non-painful patches that are not removable.
  86. 86What is linea alba in the context of oral manifestations?Horizontal thickening of buccal mucosa along the occlusal line.
  87. 87What habit do patients often develop with elevated mucosal sites?Chewing at the thickened mucosal sites.
  88. 88What is occasionally observed with recent trauma to the site of oral manifestations?Patchy erythema with or without petechiae.
  89. 89What is the first step in management?Ensure the removal of the frictional irritant.
  90. 90What habits should be stopped during management?Biting, sucking, or chewing habits.
  91. 91What should be done about fractured or rough tooth surfaces?They should be corrected.
  92. 92When should the patient be re-evaluated for signs of lesion regression or resolution?In 2-3 weeks.
  93. 93What should be done if there is no resolution even after eliminating the cause?Obtain a biopsy specimen of the tissue to confirm the absence of dysplastic or neoplastic change.
  94. 94What are the white lesions associated with smokeless tobacco known as?Leukoplakia.
  95. 95What are the white lesions associated with smokeless tobacco use?Leukoplakia, speckled leukoplakia, and erythroplasia.
  96. 96Name a lesion associated with smokeless tobacco that is a type of carcinoma in situ.Tobacco-associated keratosis.
  97. 97What is the full form of CIS?Carcinoma in situ.
  98. 98Name a type of carcinoma associated with smokeless tobacco.Verrucous carcinoma and invasive squamous cell carcinoma (SCC).
  99. 99What are the clinical features of leukoplakia?Filmy white or yellow patch involving the oral mucosa. May appear translucent or opaque and raised, or ulcerated. Ill-defined areas of white thickening at the sites where oral smokeless tobacco is habitually placed.
  100. 100What are the characteristics of tobacco-associated keratosis?White patches with interspersed areas of erythema. Normally located on buccal mucosa. Ill-defined areas of white thickening at the sites where oral smokeless tobacco is habitually placed. Most common areas: mandibular labial and buccal mucosal folds. Continued use causes affected areas to become grayer & corrugated.
  101. 101What are the distinguishing features of verrucous carcinoma?Exophytic growths with papillary projections. Rough surfaced with a broad-base attachment. Mixed red and white appearance. Ulceration or inflammation in some cases. Found on the floor of the mouth & on the ventral + lateral surfaces of the tongue. May arise in differing locations associated with placement of tobacco & buccal folds.
  102. 102What are the characteristics of squamous cell carcinoma?May appear translucent or opaque and raised, or ulcerated. Mixed red and white appearance. Ulceration or inflammation in some cases. Found on the floor of the mouth & on the ventral + lateral surfaces of the tongue. May arise in differing locations associated with placement of tobacco & buccal folds.
  103. 103What is Leukoplakia?A condition characterized by thickened, white patches on the mucous membranes of the mouth and tongue.
  104. 104What is Speckled Leukoplakia?A type of leukoplakia characterized by white and red patches in the mouth.
  105. 105What is Tobacco-associated keratosis?White patches on the gums or mouth caused by tobacco use.
  106. 106What is Verrucous carcinoma?A slow-growing, low-grade type of squamous cell carcinoma.
  107. 107What is Squamous cell carcinoma?A common form of skin cancer that develops in the squamous cells.
  108. 108What can help minimize or cease tobacco use?Education, behavior intervention & 4mg nicotine lozenges.
  109. 109What is recommended for lesions suggestive of cancer?Biopsies.
  110. 110How are premalignant lesions and carcinomas treated?With a multidisciplinary approach.
  111. 111What is another name for Nicotine Stomatitis?Smoker's palate
  112. 112Where does Nicotine Stomatitis occur?On the hard palate.
  113. 113What causes Nicotine Stomatitis?Concentrated heat stream from smoking a pipe, cigar or cigarettes.
  114. 114Who does Nicotine Stomatitis mainly affect?Patients who smoke tobacco.
  115. 115How aware are patients of Nicotine Stomatitis?Patients are typically unaware of the lesion or have it for many years without changes.
  116. 116Where is the oral manifestation primarily found?Exclusively on the palate, primarily posterior hard palate, and less often on the adjacent soft palate.
  117. 117How does the oral manifestation first appear?As a reddened area.
  118. 118What does the oral manifestation progress to in appearance?A white, thickened, and fissured appearance.
  119. 119What does the white, rough, and leathery oral manifestation contain?Numerous red dots or macules, which represent inflamed salivary gland duct orifices.
  120. 120What is the only definitive treatment for nicotine stomatitis?Smoking cessation
  121. 121Is nicotine stomatitis considered a premalignant lesion?No
  122. 122What is the recommended evaluation for oral mucosa with nicotine stomatitis?Periodic evaluation
  123. 123What is the prognosis for nicotine stomatitis?Good
  124. 124What risk does a patient with nicotine stomatitis have?Increased risk of developing cancer in other locations in the upper aerodigestive tract
  125. 125What is Solar Cheilitis?A degenerative condition of the tissue of the lips.
  126. 126How does Solar Cheilitis present?As diffuse or patchy dryness and variable thickening of the vermilion of the lower lip.
  127. 127What causes Solar Cheilitis?Years of exposure to ultraviolet (UV, mainly UVB) light, e.g. sunlight.
  128. 128Who is more commonly affected by Solar Cheilitis?Adults, with the risk increasing with age.
  129. 129Which gender is more commonly affected by Solar Cheilitis?Men.
  130. 130Which lip is most commonly affected by Solar Cheilitis?Lower lip (90%).
  131. 131What are some oral manifestations of the condition?Dryness, thinned, fragile skin, thickened, scaly papules and plaques, swelling, redness, soreness, fissuring, focal ulceration, crusting, loss of demarcation between the vermilion border of the lip and its adjacent skin, white thickened patches (leukokeratosis), discolored skin with pale or yellow areas, prominent folds and lip lines, difficulty applying lipstick which tends to 'bleed' into the surrounding lines.
  132. 132What is the management for the pre-malignant condition?Close monitoring and regular follow-up.
  133. 133What does the pre-malignant condition predispose to?Intraepidermal carcinoma (squamous cell carcinoma in situ) and Invasive squamous cell carcinoma.
  134. 134When should invasive squamous cell carcinoma be suspected?If the lip is focally tender, or a persistent ulcer or enlarging nodule develops.
  135. 135Who is more prone to developing cancer in this condition?Smokers.
  136. 136What are some measures for smoking cessation?Management
  137. 137What is essential for lifelong, year-round, daily sun protection?Limiting sun exposure
  138. 138What should be worn for sun protection?A hat with a wide brim
  139. 139How can sunscreen be applied for sun protection?Frequently, including lip balm
  140. 140What can men consider for sun protection?Growing a mustache
  141. 141What are the two types of white lesions?1. Idiopathic leukoplakia, 2. Hairy leukoplakia
  142. 142What is idiopathic leukoplakia?A white precancerous lesion firmly attached to the oral mucosa.
  143. 143What is the estimated risk for malignant transformation of idiopathic leukoplakia?4% to 6%.
  144. 144Which areas of the oral cavity are most commonly affected by idiopathic leukoplakia?Buccal mucosa, tongue, floor of the mouth, gingiva, and lower lip.
  145. 145What are the different subtypes of Idiopathic Leukoplakia?Homogeneous or 'Thick' Leukoplakia, Speckled Leukoplakia, Verrucous or Verruciform Leukoplakia
  146. 146What is the main predisposing factor for Idiopathic Leukoplakia?Smoking, especially smoking tobacco.
  147. 147Name an important etiologic agent for Idiopathic Leukoplakia apart from smoking.Alcohol.
  148. 148Apart from smoking and alcohol, what other etiologic agent is associated with Idiopathic Leukoplakia?Chronic local friction and Candida albicans.
  149. 149What is the common form of Idiopathic Leukoplakia?Homogenous or 'Thick' Leukoplakia.
  150. 150Which part of the mouth does Homogenous Leukoplakia most commonly affect?The buccal mucosa.
  151. 151What is the malignant transformation potential of Homogenous Leukoplakia?Low.
  152. 152What is the appearance of homogenous leukoplakia?A well-defined white patch.
  153. 153What are the clinical features of homogenous leukoplakia?Localized or extensive lesion, slightly elevated, wrinkled or fissured surface, leathery dry or mud-like on palpation.
  154. 154What is Speckled Leukoplakia?A less common form of Idiopathic Leukoplakia.
  155. 155Which subtype of leukoplakia poses a greater risk for malignant transformation?Speckled Leukoplakia.
  156. 156How is the speckled form of leukoplakia described?Non-homogenous with white nodules over an atrophic erythematous surface.
  157. 157What is Verrucous Leukoplakia?A rare form of Idiopathic Leukoplakia.
  158. 158Who is commonly affected by Verrucous Leukoplakia?Older adults in their sixties to eighties.
  159. 159What risk does Verrucous Leukoplakia pose compared to the homogenous subtype?Greater risk for malignant transformation.
  160. 160How does Verrucous Leukoplakia present?Thick white lesions with papillary surfaces.
  161. 161What is the nature of the lesions in Verrucous Leukoplakia?Highly keratinized.
  162. 162What is the proliferative nature of some Verrucous Leukoplakia?Very extensive and has a high risk for malignant transformation.
  163. 163How is Idiopathic Leukoplakia diagnosed?Through clinical examination and biopsy.
  164. 164What are the possible differential diagnoses for Idiopathic Leukoplakia?Lichen Planus, Cinnamon Contact Stomatitis, Candidiasis, Hairy Leukoplakia, Chronic Biting, Tobacco Pouch Keratosis, Leukoedema, Chemical Burn, Uremic Stomatitis, Skin Graft, Discoid Lupus Erythematosus.
  165. 165How is Idiopathic Leukoplakia definitively diagnosed?Through Tissue Biopsy.
  166. 166What examination is used for a definite diagnosis of Idiopathic Leukoplakia?Histopathological Examination.
  167. 167What is the treatment approach for Idiopathic Leukoplakia?Elimination of predisposing factors, use of systemic retinoid compounds, and surgical excision as the preferred treatment.
  168. 168What is Hairy Leukoplakia?A lesion often found in individuals with weakened immune systems, particularly characteristic of HIV infection.
  169. 169Is Hairy Leukoplakia precancerous?No.
  170. 170When does Hairy Leukoplakia rarely occur?After organ transplantation in immunosuppressed patients.
  171. 171What causes Hairy Leukoplakia?Conditions that weaken the immune system.
  172. 172Which virus plays an important role in the pathogenesis of Hairy Leukoplakia?Epstein Barr Virus (EBV).
  173. 173Where is Hairy Leukoplakia commonly found?Bilaterally on the lateral margins of the tongue.
  174. 174What are the clinical features associated with Hairy Leukoplakia?White patches, hairy appearance, asymptomatic, unremovable, corrugated surface, vertical orientation, smooth surface, flat surface.
  175. 175How do we diagnose Hairy Leukoplakia?Through clinical examination and history taking.
  176. 176What are the possible differential diagnoses for Hairy Leukoplakia?Chronic biting, Lichen Planus, Frictional Keratosis, Cinnamon Contact Stomatitis, Candidiasis, Uremic Stomatitis.
  177. 177How do we diagnose Hairy Leukoplakia?Through Histological Examination, In situ Hybridization, Polymerase Chain Reaction, and Electron Microscopy.
  178. 178Is treatment required for Hairy Leukoplakia?Not required.
  179. 179What antivirals may be used for Hairy Leukoplakia?Acyclovir and Valacyclovir.
  180. 180What is Hairy Tongue?A common, temporary, and harmless disorder involving the tongue.
  181. 181What percentage of the population does Hairy Tongue occur in?Up to 13%.
  182. 182Who is more frequently affected by Hairy Tongue?Older males.
  183. 183What causes the hair-like appearance of Hairy Tongue?Accumulation of keratin on the filiform papillae.
  184. 184What are the predisposing factors for Hairy Tongue?Poor oral hygiene, Oxidizing Mouthwashes, Antibiotics, Smoking, Radiation Therapy, Emotional Stress, Bacterial and Fungal Infections, Edentulousness, Excessive Use of Coffee or Tea.
  185. 185Is the exact cause of Hairy Tongue known?No, it is unknown.
  186. 186What are the clinical features of Hairy Tongue?Asymptomatic elongation of filiform papillae.
  187. 187What is the range of colors for the coating of Hairy Tongue?White to brown or black.
  188. 188How is Hairy Tongue diagnosed?By clinical examination.
  189. 189What are the treatment methods for Hairy Tongue?Elimination of predisposing factors, brushing of the tongue, and use of keratolytic agents like trichloroacetic acid and podophyllin.
  190. 190What is Geographic Tongue?A common, harmless benign disorder of the dorsal surface of the tongue.
  191. 191What are the other names for Geographic Tongue?Erythema Migrans and Benign Migratory Glossitis.
  192. 192What is the characteristic appearance of Geographic Tongue?Map-like appearance.
  193. 193Who does Geographic Tongue mainly affect?Mainly middle-aged or older females.
  194. 194Is the exact cause of Geographic Tongue known?No, it is unknown.
  195. 195What are the clinical features of Geographic Tongue?Multiple, well defined erythematous, depapillated patches with a slightly elevated whitish border, commonly appearing on the dorsum of the tongue.
  196. 196Are the patches in Geographic Tongue painful?No, they are asymptomatic.
  197. 197What often accompanies the patches in Geographic Tongue?A fissured tongue.
  198. 198Do the lesions in Geographic Tongue stay in one area for a long time?No, they usually stay in one area for a short time, then disappear and reappear in a different area.
  199. 199How is Geographic Tongue diagnosed?Through clinical examination.

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Flashcards on white, created by ghj rh4 on 10/12/2023.
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