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Dentistry year 3: Semester 6 > oral med - ALL OF NATS > Flashcards

oral med - ALL OF NATS Flashcards

1
Q
  1. What are the benign mucosal lesions caused by congenital defects?
A

Leukoedema, fordyce spots

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2
Q
  1. What are the benign mucosal lesions associated with trauma?
A

Aphthous ulcers,

frictional keratosis,

linea alba,

cheek biting,

polyps,

amalgam tattoo,

denture induced hyperplasia,

mucocele,

ranula,

melanotic macule

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3
Q
  1. What are the benign mucosal lesions associated with frictional keratosis?
A

Linea alba,

cheek biting

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4
Q
  1. What are the benign mucosal lesions associated with primarily fungal infection?
A

Pseudomembranous candidosis, chronic hyperplastic candidosis

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5
Q
  1. What is the benign mucosal lesions associated with viral infection?
A

Secondary herpes, papilloma

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6
Q
  1. What are the benign mucosal lesions of inflammatory cause?
A

Geographic tongue,

lichenoid lesion,

fibrous epulis,

pyogenic granuloma

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7
Q
  1. What are the benign mucosal lesions of autoimmune inflammatory cause?
A

Oral lichen planus, vesiculobullous conditions

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8
Q
  1. What is the metabolic disease that is presented as pigmentation intraorally, e.g. buccal mucosa?
A

Addison’s disease

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9
Q
  1. What is the condition that is associated with benign mesenchymal neoplasms?
A

Lipoma

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10
Q
  1. What are the conditions that are of idiopathic cause?
A

Lipoma,

melanotic macule

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11
Q
  1. What are the clinical features of leukoedema?
A

Bilateral diffuse, grey white on buccal mucosa

+/- folded, wrinkling, corrugation

X rub off, disappears when stretched

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12
Q
  1. What are the causes of fordyce spots?
A

Ectopic sebaceous glands,

hormonal - puberty

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13
Q
  1. What are the causes of leukoedema?
A

Secondary to lower grade mucosal irritation → intracellular oedema

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14
Q
  1. What is the epidemiology of leukoedema?
A

More common among smokers

24-90% prevalence

Blacks > whites

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15
Q
  1. What is the epidemiology of fordyce spots?
A

Adults > kids

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16
Q
  1. What are the signs and symptoms of fordyce spots?
A

Multiple yellow / yellow-white papules

Buccal mucosa & lateral portion of vermillion of upper lip > retromolar area & anterior tonsilar pillar

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17
Q
  1. What are the possible sequelae of fordyce spots?
A

May become hyperplastic

Form keratin-filled pseudocysts

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18
Q
  1. What are the histopathological features of fordyce spots?
A

No hair follicles

Otherwise normal sebaceous glands

Acinar (polygonal sebaceous cells) lobules beneath epithelial surface, communicate thru central duct

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19
Q
  1. What is the epidemiology of aphthous ulcers?
A

20% population

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20
Q
  1. What is the mnx for aphthous ulcers?
A

Remove source

HSMW

Deal with it bruh

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21
Q
  1. What are the causes of aphthous ulcers?
A

Traumatic stimulus - dentures, restorations, direct trauma etc

Haematinic deficiency, hormonal

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22
Q
  1. What are the causes of linea alba?
A

Pressure,

fictional irritation,

sucking trauma,

clenching

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23
Q
  1. What is the epidemiology of cheek biting?
A

Under stress, exhibit psychological conditions

35+

F>M

Glass blowers

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24
Q
  1. What are the clinical presentations of cheek biting?
A

Bilateral on anterior buccal mucosa

Unilateral / combined w/ lesions of lips / tongue

Thickened, shredded, white areas +/- interviewing zones of erythema, erosion, focal traumatic ulceration

Irregular ragged surface

Can remove shreds of white material

@ midportion of anterior buccal mucosa along occlusal plane

Not to be confused with dysplastic leukoplakia - have more sharply demarcated borders, periphery gradually blends w/ adj mucosa

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25
Q
  1. What is the cause of polyp?
A

Benign growth from mucosa

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26
Q
  1. How to treat polyp?
A

EXCISION

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27
Q
  1. How is amalgam incorporated into oral mucosa?
A

Previous areas of mucosal lesion contaminated w amalgam dust w/n oral fluids

Broken amalgam pieces fall into extraction sites

Floss contaminated w amalgam particles of a recently placed restoration

Amalgam from endo retrofill left w/n soft t/s at surgical site

Fine metallic particles driven thru oral mucosa from P of high speed air turbines

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28
Q
  1. What are the clinical features of amalgam tattoo?
A

Macules / slightly raised lesions

Black / blue / grey

Borders - well defined / irregular / diffuse

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29
Q
  1. What can you see in the R/G of amalgam tattoo?
A

R/O

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30
Q
  1. What to do if you can’t find any R/O in the R/G of a suspected amalgam tattoo?
A

Biopsy to rule out possibility of melanocytic neoplasia

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31
Q
  1. What happened in mucocele?
A

Submucosal cystic swelling d/t damage to minor salivary gland / ducts - mucous extravasation cyst

Saliva escapes from damaged duct into surrounding lip → swelling

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32
Q
  1. Is mucocele more commonly found in the lower or upper lip?
A

Lower lip

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33
Q
  1. If mucocele is found in the upper lip, what is it more likely to be?
A

Minor salivary gland tumour

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34
Q
  1. What are the clinical features of mucocele?
A

Bluish translucent hue d/t swelling, dome shaped, range from 1-2mm - few cm, some firm to palpation but can be fluctuant

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35
Q
  1. What is the treatment of mucocele?
A

Excision of cyst & associated gland under LA

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36
Q
  1. What is a ranula?
A

Mucocele of sublingual gland and its draining ducts

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37
Q
  1. What are the clinical features of ranula?
A

Painless swelling

Blue, dome shaped, fluctuant swelling in FOM

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38
Q
  1. What is the non-oral presentation of ranula?
A

Plunging ranula passes thru mylohyoid m/s → neck swelling

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39
Q
  1. How to manage ranula?
A

Excision (i/o or e/o approach) under GA

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40
Q
  1. What is the complication associated with mucocele?
A

Reduced sensation to region d/t damaged sensory nerve branch

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41
Q
  1. What are the causes of denture induced hyperplasia?
A

Ill-fitting denture, worn 24/7

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42
Q
  1. What are the clinical features of denture induced hyperplasia?
A

Tumour like hyperplasia of fibrous c t/s

Single / multiples folds of hyperplastic t/s in alveolar vestibule

Most often - 2 folds of t/s, flange of denture fits into fissure b/w folds

Redundant t/s - firm, fibrous

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43
Q
  1. How do you Mx denture induced hyperplasia?
A

Excision,

new dentures

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44
Q
  1. What is pseudomembranous candidosis associated with?
A

Candida albicans

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45
Q
  1. What are the local and / or systemic predisposing factors associated with pseudomembranous candidosis?
A

Dry mouth, steroid inhaler, anaemia, nutritional deficiency,

DM, immunosuppressed / immunocompromised,

extremes of age,

dentures,

broad-spectrum antibiotics,

systemic / inhaled corticosteroid

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46
Q
  1. What are the signs and symptoms of pseudomembranous candidosis?
A

Relatively mild, burning sensation of oral mucosa,

unpleasant taste - salty / bitter, ℅ ‘blisters’ - in fact the elevated plaques rather than true vesicles

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47
Q
  1. What are the clinical features of pseudomembranous candidosis?
A

White (cottage cheese PANEER / curdled milk)

Removable patches

Erythematous / bleeding base / normal

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48
Q
  1. How to investigate pseudomembranous candidosis?
A

Culturing w KOH prep - budding yeasts, hyphae, pseudohyphae

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49
Q
  1. What are the local measures for pseudomembranous candidosis?
A

if on corticosteroid inhaler - rinse mouth w/ water / brush teeth STAT after use

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50
Q
  1. What are the treatment options for pseudomembranous candidosis?
A

Fluconazole 50mg OD max 14/7 for oropharyngeal candidosis

c/i warfarin & statins

Miconazole 20mg/g pea sized after food QDS

Continue for 7/7 after lesions healed

c/i warfarin & statins

Nystatin 1ml after food QDS for 7/7

Rinse around mouth for 5 mins before swallowing

Continue for 48 hours after lesions healed

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51
Q
  1. What is a significant aetiological factor in chronic hyperplastic candidosis?
A

Smoking

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52
Q
  1. What are the clinical features of chronic hyperplastic candidosis?
A

Firmly adherent (x scrapable) white plaques

+/- intermingled erythema & nodularity

@ commissure / anterior region of buccal mucosa

Bilateral, may also affect tongue

Fine intermingling of red & white areas → speckled leukoplakia

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53
Q
  1. How do you diagnose chronic hyperplastic candidosis?
A

Biopsy

Swab may be non-diagnostic cuz candida infiltrates deeply into epithelium

Presence of candidal hyphae + complete resolution post antifungal Tx

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54
Q
  1. Is chronic hyperplastic candidosis a malignant mucosal disorder?
A

NO - so x call candida leukoplakia

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55
Q
  1. What is papilloma associated with?
A

HPV

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56
Q
  1. What are the clinical features of papillomas?
A

Sessile (immobile) / pedunculated

Can become traumatised; look like pomelo flesh

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57
Q
  1. How do you manage papilloma?
A

Excision

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58
Q
  1. What is secondary herpes caused by?
A

Reactivation of latent virus in the trigeminal system

E.g. UV light, stress, immunocompromised

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59
Q
  1. What are the signs and symptoms associated with secondary herpes?
A

Tingling sensation before vesicles develop on the lip

Cold sore

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60
Q
  1. How to mnx secondary herpes?
A

Topical antivirals

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61
Q
  1. What is geographic tongue also associated with?
A

Fissured tongue, vitamin B

Possible a/w psoriasis

Hereditary but unclear genetic links

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62
Q
  1. What is the epidemiology of geographic tongue?
A

1-2% population

M=F

All ages, less common in kids

Fam Hx

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63
Q
  1. What are the signs and symptoms of geographic tongue?
A

Sore / sensitive tongue when eating spicy / acidic foods

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64
Q
  1. What are the clinical features of geographic tongue?
A

Affect tongue surface

Can move around tongue → erythema migrans

Map looking, irregular outlined red patches

Red areas surrounded by white / yellow / cream border

Can disappear / return after some time

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65
Q
  1. Where else can geographic tongue affect?
A

Lips / cheeks / palate

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66
Q
  1. How to diagnose geographic tongue?
A

Hx, C, x need special investigations

Some pt may have ‘fissured tongue’ a/o psoriasis

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67
Q
  1. How to manage geographic tongue?
A

Analgesic m/w or lozenges to numb tongue before meals is sore

Avoid alcohol containing m/w

Use sugar free lozenges

Avoid spicy / acidic foods, carbonated drinks, vinegars, tomatoes

Stop / cut down on smoking

Confine alcohol intake

Regular dental visits

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68
Q
  1. What is a lichenoid reaction?
A

Inflammatory reaction to metal / medication

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69
Q
  1. What are the causes of lichenoid reaction (medication)?
A

Antihypertensives

  • ACEi - captopril
  • ARBs - losartan
  • Beta-blocker - propranolol, atenolol
  • CCBs - amlodipine, nifedipine, verapamil
  • Thiazide diuretics - hydrochlorothiazide
  • Loop diuretics - furosemide

Oral hypoglycaemics

  • Tolbutamide
  • Chlorpropamide (sulphonylureas)

NSAIDs

  • Ibuprofen, naproxen, phenylbutazone
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70
Q
  1. What are the clinical features of lichenoid reaction?
A

White lesion next to possible source

X wipeable

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71
Q
  1. What is fibrous epulis?
A

Growth on gum, chronic irritation

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72
Q
  1. What are the clinical features of fibrous epulis?
A

At gingival margin of teeth

Normal overlying mucosa & fibrous centre

73
Q
  1. How to treat fibrous epulis?
74
Q
  1. What is pyogenic granuloma?
A

Growth on gum

Local irritation or trauma

NOT a true granuloma

75
Q
  1. What is the epidemiology of pyogenic granuloma?
A

a/w F during pregnancy - possible hormonal association

76
Q
  1. What are the clinical features of pyogenic granuloma?
A

At gingival margin of teeth

More vascular lesion, appears blueish / blackish

77
Q
  1. What happens in Addison’s disease?
A

Oral mucosal pigmentation associated with systemic condition

78
Q
  1. What is the epidemiology of melanotic macule?
79
Q
  1. What are the clinical features of melanotic macule?
A

Round / oval brown / black pigmented area on lip / any mucosal surface

80
Q
  1. What are the clinical features of oral lichen planus?
A

Bilateral white, lace like pattern on buccal mucosa & tongue

Desquamative gingivitis on gums - red, shiny

White / red patches

Ulcers

81
Q
  1. What is the epidemiology of oral lichen planus?
A

1-2%

Middle aged to elferly F

Some cases a/w Hep C but x common in the UK

82
Q
  1. What are the signs and symptoms of oral lichen planus?
A

Burning / stinging when eating / drinking

Exacerbated by spicy foods, citrus fruits, alcohol

If gums affected → tender & uncomfy t/b

Ulcers

83
Q
  1. What are other sites affected by lichen planus?
A

Skin, nails, genitals, scalp

Less common - oesophagus, larynx, anus, bladder, eyelids, lacrimal glands

84
Q
  1. What are the types of OLP?
A

Erosive / papular,

reticular,

atrophic,

plaque,

bullous

85
Q
  1. How to diagnose OLP?
A

C, biopsy,

swab if suspect super-added candida

Blood tests if associated d/s suspected

86
Q
  1. How to treat OLP?
A

Baseline photos,

topical,

systemic,

pt advice,

referral

87
Q
  1. How to treat OLP topically?
A

Analgesic m/w (difflam / benzydamine)

Topical steroids - m/w / sprays / pastes

Topical tacrolimus (immunosuppressant)

Daily H2O2 m/w or occasionally CHX 2x/week (avoid m/w containing alcohol)

88
Q
  1. How to treat OLP systemically?
A

For severe OLP

Regular blood tests to screen for drug toxicity

On bone protection if on long term oral corticosteroids

Azathioprine, mycophenolate mofetil - to further dampen down immune system so that dose of corticosteroid can be reduced ASAP

89
Q
  1. How to advise pt w OLP?
A

Maintain OH - soft brush, TePe, mild flavour / SLS-free t/p

Regular dental checkups

Avoid spicy, acidic, salty foods

Stop smoking, reduce alcohol intake - main RF for mouth cancer

90
Q
  1. When to refer a pt w OLP?
A

Possible malignancy; cant Dx, cant mnx in primary care

91
Q
  1. What are the signs and symptoms of vesiculobullous conditions?
A

Painful blisters

92
Q
  1. What are the other sites involved in vesiculobullous conditions?
A

Iips,

lacrimal glands

93
Q
  1. What are the clinical features of vesiculobullous conditions?
A

Blisters can rupture into erosion & ulcers

94
Q
  1. How to diagnose vesiculobullous conditions?
95
Q
  1. What are the clinical features of lipoma?
A

Fat cells surrounded by thin fibrous capsule

96
Q
  1. How to manage lipoma?
97
Q
  1. What are the causes of genodermatoses (white sponge naevus)?
A

Inherited (autosomal dominant)

Defect in normal keratinisation of oral mucosa

98
Q
  1. What is the epidemiology of genodermatoses?
A

F=M; birth to adolescence

99
Q
  1. What are the signs and symptoms of genodermatoses?
A

Roughness, white area

100
Q
  1. What are the clinical features of genodermatoses?
A

White / greyish white patches

Merge w surrounding normal appearing mucosa

Firmly adherent

X associated erythema / ulceration

Surface folded, soft, spongy

101
Q
  1. Where else does genodermatoses affect?
A

Oesophageal, nasal, genital, aro-rectal

Skin, nails, hair

Teeth x affected

102
Q
  1. How to diagnose genodermatoses?
A

C, +ve fam Hx, biopsy if in doubt

Genetic mutation testing - keratin 4 a/o 13

103
Q
  1. How to treat genodermatoses?
A

Benign, x Tx needed, x potentially malignant disorder

104
Q
  1. What is the cause of epitheliolysis?
A

Secondary to mucosal irritation by toothpaste, mouthwash

105
Q
  1. What are the clinical features of epitheliolysis?
A

Strands of gelatinous milk white

Removable by wiping

X sig abnormality of underlying t/s

106
Q
  1. How to mnx epitheliolysis?
A

Cease m/w use

Avoid SLS containing products (sodium lauryl sulphate)

107
Q
  1. What are the causes of traumatic keratosis?
A

Secondary to physical (frictional) / chemical / thermal irritation

108
Q
  1. What are the signs and symptoms of traumatic keratosis?
A

Rough / ridged to pt’s tongue

109
Q
  1. What are the clinical features of traumatic keratosis?
A

X removable

+/- shaggy surface

Appear macerated / a/w ridging

110
Q
  1. How to diagnose traumatic keratosis?
A

Should match cause, biopsy if not sure

111
Q
  1. How to mnx traumatic keratosis?
A

Remove cause

112
Q
  1. What are the causes of nicotinic stomatitis?
A

Smoking - 60% pipe, 30% cigarette

113
Q
  1. What is the epidemiology of nicotinic stomatitis?
114
Q
  1. What are the clinical features of nicotinic stomatitis?
A

Generalised white / greyish white on hard palate extending onto soft palate

Small red dots <=1mm

115
Q
  1. What are the red dots found on nicotinic stomatitis?
A

Inflamed openings of minor salivary glands

116
Q
  1. How to manage nicotinic stomatitis?
A

Smoking cessation

117
Q
  1. What is graft vs host disease?
A

Immune response of donor-derived cells against recipient tissues

118
Q
  1. What are the signs and symptoms of graft vs host disease?
A

Pain, sensitivity, taste changes, trismus

119
Q
  1. What are the clinical features of graft vs host disease?
A

Dry mouth

For acute GVHD - depends on severity - mild rash to diffuse severe sloughing that resembles toxic epidermal necrolysis

Diarrhoea, nausea, vomiting, abdominal pain, liver dysfunction

120
Q
  1. What is the epidemiology of discoid lupus erythematosus?
121
Q
  1. What are the clinical features of discoid lupus erythematosus?
A

Central erythematous mucosa surrounded by slightly elevated white border

Fine perpendicular white ‘paint-brush’-like lines

@ palatal, buccal, vestibular mucosa

122
Q
  1. Where else does discoid lupus erythematosus affect?
A

SLE (systemic lupus erythematosus) - facial butterfly rash

123
Q
  1. How to diagnose discoid lupus erythematosus?
124
Q
  1. How to mnx discoid lupus erythematosus?
A

Topical steroids, treat the candida as well

125
Q
  1. What are the causes of hairy leukoplakia?
A

Epstein barr virus (HPV 4), strongly a/w HIV

Often super added candida

Any immunosuppressed / immunocompromised

Pt on topical corticosteroids

126
Q
  1. What are the clinical features of hairy leukoplakia?
A

Firmly adherent, corrugated surface

@ lateral border of tongue

127
Q
  1. How to diagnose hairy leukoplakia?
A

C, biopsy, HIV testing

128
Q
  1. What is the risk factor of acute erythematous candidosis?
129
Q
  1. What are the signs and symptoms of acute erythematous candidosis?
A

Burning sensation - ‘as if a hot drink had scalded it’

NOT same as burning mouth syndrome cuz x abnormal filiform papillae

130
Q
  1. What are the clinical features of acute erythematous candidosis?
A

Diffuse loss of filiform papillae of dorsal tongue

Reddened, ‘bald’ appearance of tongue

131
Q
  1. What are the types of chronic erythematous candidosis?
A

Angular cheilitis, denture stomatitis, median rhomboid glossitis

132
Q
  1. What are the causes of angular cheilitis?
A

Chronic erythematous candidosis

May be underlying anaemia / haematinic deficiency

May be candida alone / staph aureus or both

Beta-haemolytic streptococci

133
Q
  1. What are the clinical features of angular cheilitis?
A

Erythema, cracking, crusting, bleeding of skin at angles of mouth

Always check for accompanying sings of i/o candidosis, often a/w denture stomatitis

Reduced OVD

Accentuated folds @ angle of mouth

SO saliva pools in the area → keeping moist → favours yeast infection

134
Q
  1. How to mnx angular cheilitis?
A

Miconazole cream 2% apply to angles of mouth BD, continue use for 10/7 after lesions have healed; c/i warfarin, statin

Miconazole 2% + Hydrocortisone 1% cream / ointment apply to angle of mouth BD; c/i warfarin, statin

Sodium fusidate ointment 2% apply to angelus of mouth QDS

135
Q
  1. What is the cause of denture stomatitis?
A

Any appliance w mucosal coverage

s/t w petechial haemorrhage

Localised to denture-bearing area of upper denture

136
Q
  1. What are the clinical features of denture stomatitis?
A

Palatal mucosa m/c affected

Erythema classification (newton)

  • Type I - patchy
  • Type II - generalised
  • Type III - papillary hyperplasia if long standing condition, a/o pt taking medication that predisposes to hyperplasia, e.g. nifedipine, ciclosporin, phenytoin
137
Q
  1. What are the signs and symptoms of denture stomatitis?
A

Soreness / burning

138
Q
  1. How to diagnose denture stomatitis?
A

If doing swab / imprint → sample should be taken from fitting surface

139
Q
  1. How to treat denture stomatitis?
140
Q
  1. What is the epidemiology of median rhomboid glossitis?
A

Rare in kids

141
Q
  1. What are the clinical features of median rhomboid glossitis?
A

Rhomboidal shaped depapillation & erythema in the middle of mid dorsum of tongue

May be a/w hyperplasia → lobular appearance

Corresponding area of erythema affecting palatal mucosa → chronic multifocal candidosis

142
Q
  1. What is oral leukoplakia?
A

White plaque of QUESTIONABLE risk - one of the potentially malignant disorders

Non-scrapable

Excluded other known diseases or disorders

143
Q
  1. What is the epidemiology of oral leukoplakia?
A

SEA - influenced by betel nut chewing

M>F

2.6% globally; 3% in developed countries

144
Q
  1. What are the causes of oral leukoplakia?
A

Secondary to smoked / smokeless tobacco, alcohol, betel quid use

If no RF → idiopathic leukoplakia - possible underlying genetic basis development

145
Q
  1. How to diagnose oral leukoplakia?
A

Clinical & biopsy - histopathology to rule out other Dx

Ix for 2-week referral

  • Swelling, ucleration, speckling, induration
  • Additional clinical concern
  • Red a/o white patch consistent w erythroplakia / erythroleukoplakia
146
Q
  1. What are the differential diagnoses of white lesions?
A

Smoker’s palate, leukoedema, frictional keratosis, hairy leukoplakia, oral lichen planus, white sponge naevus

147
Q
  1. What are the types of oral leukoplakia?
A

Homogenous leukoplakia,

non-homogenous leukoplakia,

speckled leukoplakia,

erythroplakia

148
Q
  1. What are the clinical presentations of homogenous leukoplakia?
A

Uniformly white, relatively flat

Superficial & clear demarcated margins

149
Q
  1. What are the clinical presentations of non-homogenous leukoplakia?
A

Fissured, erythematous

Nodular, verrucous, irregular surface

Less well demarcated margins

Represents a higher risk lesion than homogenous

150
Q
  1. What are the clinical presentations of speckled leukoplakia?
A

Speckled areas / islands of red patches

151
Q
  1. What are the clinical presentations of erythroplakia?
A

Fiery red patch x clinically / pathologically characterised as any other conditions

Rare

Middle aged, elderly

Similar RF to OL

Malignant transformation rate 14-50% - highest out of all oral potentially malignant disorders

152
Q
  1. What is the relationship between HPV & OL?
A

Less evidence on link b/w HPV & OL

Many reports on link b/w HPV & OSCC

153
Q
  1. What is the transformation rates of OL?
A

Pt specific, x accurately predicted

Annual transformation rate (ATR) - % of pt that will see a malignant change in their OL in a year, around 2-3%

Refer to factors influencing malignant change

154
Q
  1. How to lower risk of developing OL?
A

Reduce / stop tobacco use & alcohol consumption

Stop using snuff, betel, areca nut

Vaping & electronic nicotine ‘safer’

155
Q
  1. How to mnx OL?
A

Surgical excision, esp high risk of malignant transformation

Annual recurrence following surgical excision - 5-10%

Cochrane - lack of evidence to support routine surgical mnx

156
Q
  1. What is the follow up interval for OL?
A

3-6/12 follow up

157
Q
  1. What are the factors influencing malignant change?
A

Surface architectural changes - nodularity / verrucous changes

Presence of areas of erythema w/n leukoplakia (erythroleukoplakia / speckled leukoplakia)

Female

Increased age

Idiopathic leukoplakia - if OL develops w/o aetiological factor → higher risk of malignancy

Site - FOM, ventrolateral tongue, soft palate

Size - >200mm (20cm)

Dysplasia grade / severity

  • Confirmed by histopath assessment
  • Dysplasia = abnormal epithelial growth → cytologic, maturational, architectural changes w/n epithelium

Candidal infection in OL

  • Carcinogens - certain candida strains can form nitrosamines
  • Chronic hyperplastic candidosis - typically involves commissures, smokers, Dx - fungal hyphae on histopath + C
158
Q
  1. What is haemangioma?
A

Benign vascular tumour derived from b v/s cell types

When excising, be careful - potential profuse bleeding

Alternative excision - bipolar

159
Q
  1. What is peripheral giant cell lesion?
A

Red purple nodules located on gums

160
Q
  1. What are the biopsy techniques?
A

Excisional, incisional, punch, aspiration, cytology

161
Q
  1. What is excisional biopsy technique?
A

Complete removal of lesion w surrounding normal t/s

Width & depth >1-2mm

Can be examined histologically

162
Q
  1. What is an incisional biopsy technique?
A

Removal of portion of lesion / sample of abnormal t/s for diagnostic purposes

163
Q
  1. What is punch biopsy ?
A

Removal of a cylinder of t/s w a disposable instrument PUNCH

A form of incisional biopsy

164
Q
  1. What is an aspiration biopsy technique?
A

Fine needle cytology for deep soft t/s lesions / aspirations of fluid for microscopes / other exam

165
Q
  1. What is cytology biopsy technique?
A

Obtain sample of cells for microscopic / other examination, often but not exclusively by scraping the lesion surface

166
Q
  1. How to handle specimen?
A

Small piece of blotting paper

In neutral buffered formalin at least 10x of specimen vol

Accurate labelling

167
Q
  1. What is cryosurgery?
A

Freezing t/s → controlled necrosis

168
Q
  1. What is diathermy?
A

Electrical current to destroy t/s, e.g. bipolar, polar diathermy

169
Q
  1. What is laser surgery?
A

Electromagnetic energy & topical amplification → cutting, t/s evaporation, coagulation, protein gene naturation → cell death

170
Q

what causes Pyogenic granuloma

A

Pregnancy

Poor OH

Gingival irritation & inflammation

clinical presentation - bright red

171
Q

what causes Peripheral giant cell granuloma

A

Local irritation / trauma

clincial presentation - blue purple

172
Q

what causes fibrous epulis

A

chronic irritation

clinical presentation - pink

173
Q
  1. What is oral erythroplakia?
A

Red pre-cancerous lesion;

Dx by exclusion; fiery red patch (sharply demarcated) that x be characterised otherwise

174
Q
  1. Where is oral erythroplakia commonly found?
A

Buccal mucosa, palatal mucosa, FOM, soft palate

175
Q
  1. What are the causes of oral erythroplakia
A

Similar to oral leukoplakia

Tobacco chewing / smoking, betel quid chewing +/- tobacco, alcohol; possible link b/w HPV & erythroplakia

176
Q
  1. What is the prevalence of oral erythroplakia
A

Around 0.3% outside hospital

177
Q
  1. Why is oral erythroplakia considered as a premalignant lesion
A

Greater cancer risk than white lesions

Precursor lesions - altered epithelium w/ increased chance of progression to cancer

Dentistry year 3: Semester 6 (16 decks)

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