Pre-Malignant Conditions Flashcards

1
Q

What is a pre-malignant lesion?

A
  • morphologically altered tissue in which cancer is more likely to occur than in its apparently normal counterpart
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2
Q

What is a pre-malignant condition?

A
  • a condition w/ significantly increased risk of developing cancer
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3
Q

What is Leukoplakia?

A

= predominantly white lesion of the oral mucosa that cannot be
characterised as any other definable disease & not associated w
any physical or chemical causative agent except tobacco

~5% chance of malignant transformation

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4
Q

What are the two appearance types of Leukoplakia?

A
  1. Homogenous
    - uniform flat appearance
    - shallow cracks/smooth/corrugated surface w/ consistent texture
  2. Non- Homogenous (more concerning)
    -white or white+red lesion (erythroleukoplakia)
    - irregularly flat or nodular or exophytic

Nodular lesions = raised, rounded, red + or white

Excrescences exophyic lesions (cauliflower, polyp appearance) = irregular blunt or sharp projection

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5
Q

What is the aetiology of Leukoplakia?

A
  • 10% of oral leukoplakia = idiopathic
    90% assoc. w/ the use of tobacco/ Areca nut
    M > F
  • diagnosed in middle age +
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6
Q

What area of the mouth does Leukoplakia affect?

F^^^ing BMT

A
  • Buccal mucosa (~25% of cases)
  • Mandibular gingiva (~20% cases)
  • Tongue (~10% cases)
  • Floor of mouth (~10% cases)
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7
Q

What are the clinical features that suggest increased risk of malignant transformation of leukoplakia?

SSC AG

A

Surface = raised or nodular

Site- FoM, lateral border of tongue, retromolar region, buccal sulcus (esp paan chewers), labial commissure

Colour = red/ white (speckled)

Age (old)
Gender Female

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8
Q

What is the aetiology of Leukoplakia? (3)

A
  • Tobacco (chewing i.e. paan, or smokeless tobacco i.e. snuff ~ 60% of users develop keratosis at site of snuff placement)
  • Reverse smoking, pipe smoking, smoking cigarettes
  • Candida albican (30% of leukoplakia may contain contain candida aka CHC)
    lesion may show dysplasia, most commonly at corner of mouth, some lesions regress if candida treated systemically w oral fluconazole
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9
Q

What is Erythroplakia?

A

= bright red velvety plaque which cannot be characterised as any other definable lesion (disease)

~80% chance of malignant transformation

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10
Q

Is Eythroplakia always associated with dysplasia?

A

YES, high risk lesions + is always assoc. w/ dysplasia or carcinoma

Risk of malignant change is greatest in lesions showing severe dysplasia, in comparison to those w/ mild dysplastic change

MUST REFER VIA 2 WEEK OM URGENT REFERRAL PATHWAY

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11
Q

Other causes of white patches:

Name 2 conditions that are normal anatomy?

A

1) Fordyce spots

2) Leucoedema

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12
Q

Other causes of white patches:

Name a condition that is developmental ?

A
  • White sponge naevus
    (aka hyperkeratinisation of mucosa)
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13
Q

Other causes of white patches:

Name 3 conditions that are caused by trauma?

A

Frictional Keratosis

Cheek biting

Traumafrom dentures, cusps, restorations, ortho appliance

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14
Q

Other causes of white patches:

Name 2 conditions whose cause is chemical?

A

Aspirin burns

Smokers keratosis (on palate)

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15
Q

Other causes of white patches:

Name 2 conditions whose cause is autoimmune?

A

Lichen Planus

Lupus Erythematous

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16
Q

Other causes of white patches:

Name 2 conditions whose cause is ineffective?

A

CHC

Oral hairy leukoplakia

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17
Q

What are Fordyce Spots/Granules?

A

= common + BENIGN
= appear in childhood (increase at late puberty + adult life)

represent sebaceous glands
creamy-yellow papules (may coalesce on buccal or labial mucosa)

  • tx: reassure pt its normal anatomy
18
Q

What is Leucoedema?

A

= variation of normal
= BILATERAL, diffuse, translucent, greyish appearance on OM
= optical illusion, white patch disappears on stretching of mucosa

mostly affecting black population, occurring in white population too

19
Q

What is Oral Hairy Leukoplakia?

A

= not malignant
- painless
- usually involving lateral borders of tongue
- assoc w. EBV
- If assoc. w/ AIDS, resolves w/ HAART
- may mimic other mucosal diseases

20
Q

What is Lichen Planus?

Naani iss ACE

A

= a pre-malignant condition

  • Pts w/ long standing OLP may develop oral SCC (monitor pts)

Changes to look out for?
-isolated areas of increasing whiteness
- speckling (areas of redness + whiteness)
- solitary ulceration (unlikely to reflect trauma)

Advice given to OLP pts:
- make aware of malignant potential
- Avoid tobacco + alcohol
-Diet rich in Vit A,C, E/ antioxidants
- Good OH + regular visits to GDP

21
Q

What is Chronic Hyperplastic Candidosis?

A
  • uncommon
  • assoc w tobacco use
  • rx to immunodeficiencies sometimes
  • Resistant to topical anti-fungal tx (need to use systemic anti-fungals for 6 weeks)
  • Tx: candida organisms, as they produce malignant compounds
22
Q

Pre-Malignant Conditions:

What is Syphilis + how does it present?

A

= bacterial STI caused by Treponema pallidum Treponema palladium
(primary, secondary, latent + tertiary types)

  • IO pres:
    Syphilitic leukoplakia, presenting on central dorsum of tongue (rare)
    Glossitis w mucosal atrophy

Other oral pres:
painless ulcers (chancres),
mucous patches/maculopapular lesions
on = tongue, lips, + buccal mucosa

Diagnosis: dark-field microscopy, UV microscopy or phase contrast

23
Q

Pre-Malignant Conditions:

What is Sideropenic Dysphagia + how does it present?

aka Patterson Kelly or Plummer Vinson Syndrome

A

aka Patterson Kelly or Plummer Vinson Syndrome

  • Fe def anemia
  • generalised mucosal atrophy
  • oesophageal web
  • middle aged women
24
Q

Pre-Malignant Conditions:

What is Oral Submucous Fibrosis + how does it present?

Prahlaad

A
  • Fibrosis of OM + difficulty opening mouth
  • Marbled mucosa
  • Paan + Betal nut chewers!
    ~ 30% may develop OSCC !
25
Q

Pre-Malignant Conditions:

What is Actinic Keratosis + how does it present? 🌞

A
  • sunlight induced changes in the lip (normally lower lip)
  • increased risk of OSCC!
26
Q

Management of Leukoplakia + Erythroplakia:

What clinical information should you gather about the lesion as GDP? (step 1)

SSS CH

A

Determine the level of RISK, depending on the:

site
size
surface
colour
habits

27
Q

Management of Leukoplakia + Erythroplakia:

After gathering clinical information, what should you do next as GDP? (step 2)

A

Urgent referral to OMFS

(Do not biopsy the lesion yourself!)

(If lesion very suspicious, mark the letter as urgent or tx within two week
rule & phone relevant consultant. Fax letter & send through post too)

28
Q

What is the survival rate for Oral Cancer?

A

= only 40% survival, therefore early detection is KEY πŸ”‘

29
Q

Management of Leukoplakia + Erythroplakia:

What type of biopsy would OMFS conduct in hospital setting ? (step 3)

A
  • Always biopsy most suspicious part & include margin of normal tissue!
  • Incisional biopsy for LARGE LESIONS (multiple biopsies if necessary)
  • Exicisonal biopsy if lesion= SMALL
30
Q

Management of Leukoplakia + Erythroplakia:

What key information should you make the pt aware about post tx/ biopsy?

A

Regardless of tx, leukoplakia can REOCCUR (current tx, will not prevent progression of future leukoplakia to SSC)

Therefore, MODIFICATION OF HABITS is key πŸ”‘

31
Q

What lesions are regarded as high risk?

A

ALL red patches (erythroplakia)

Non-homogenous leukoplakia i.e. speckled + nodular appearance

All lesions showing dysplasia (risk of malignant transformation is directly linked to degree of dysplasia identified on histological exam)

32
Q

Management according to level of dysplasia:

What is management for a lesion displaying MILD dysplasia?

N A R (mild)

A
  • Advice on tobacco + alcohol cessation
  • Nutritional assessment
  • Review every 3-6m (biopsy at 3m to re-assess dysplasia + further biopsy at 2-3yr mark)
33
Q

Management according to level of dysplasia:

What is management for a lesion displaying MODERATE dysplasia?

A

Surgical excision if:
lesion = small
OR
if, pt unlikely to modify RFs

For candidal leukoplakia:
- Fluconazole tx for 6weeks
- VBA for smoking
- Re-biopsy after 3m to re-assess dysplasia

34
Q

Management according to level of dysplasia:

What is management for a lesion displaying SEVERE dysplasia?

SP

A

1) Surgical excision by:
scalpel, laser or cryotherapy

2) Photodynamic therapy:
useful for multiple lesions
has systemic effect, therefore need to stay in darkened room due to photosensitivity

35
Q

Summary:

state 4 crucial facts about leukoplakia + erythroplakia:

A
  1. Both are conditions assoc. w/ varying risk of malignant transformation
  2. Degree of dysplasia within the biopsy is a better indicator of malignant potential
  3. Erythroplakia almost ALWAYS shows dysplasia or carcinomaon biopsy
  4. Leukoplakia will show a more varied degree of dyplasia (non-homogenous pres. more sinister than homogenous)
36
Q

Histology:

Key definitions + terminology (8):

[don’t need to memorise, just here to refresh memory a little]

A

Keratosis = keratinisation in an epithelium that is not normally keratinised (ie non keratinised epithelium, eg buccal mucosa)

Hyperkeratosis = Increased thickness of the keratinised layer

Orthokeratosis = increased keratin w flat, anucleate superficial cells w homogenous eosinophilc cytoplasm

Parakeratosis = flat, homogenous eosinophilc superficial cells BUT w pyknotic nuclei

Acanthosis = Increased number of cells in prickle cell layer 🌡
-Associated w broadening of rete ridges & thicker epithelium

Atrophy = decreased epithelial thickness (thinning epithelium)
- Associated w loss of rete ridges
- Epithelium may be roughly equal thickness throughout

Atypia = changes to individual cell

Dysplasia = changes in whole epithelium

37
Q

What are the 10 histological features of oral dysplasia?

A
  1. Nuclear Hyperchromatism (increased DNA content)

2.Nuclear + cellular PLEOMORPHISM (variation in size+shape)

  1. Inc.nuclear: cytoplasm ratio
  2. Inc. no. of BIZARRE MITOSES
  3. Mitosis in prickle cell layer (normally found in basal cell layer which is lower down)
  4. Premature keratinisation in prickle cell layer (Acanthosis)

7.Loss of polarity of basal cells (nuclei in unusual positions)

  1. Loss of epithelial stratification
  2. Drop shaped rete ridges
  3. Loss of cell adherence
38
Q

What are the histological features of Leukoplakia? (6)

VICAAH

A

Hyperkeratosis or parakeratosis (responsible for white colour)

Variable hyperplasia

Acanthosis (inc. thickness of prickle cell layer) 🌡

Atrophy

Candidal Hyphae (~30%)

Inflammation

(may show one of more features of dysplasia listed on other cards)

39
Q

What are the histological features of Erythroplakia?

(oh) DIA

A

Dysplasia

Inflammation

Atrophy (responsible for red colour)

40
Q

State the grading + features of dysplasia for each grade?

A

None= Epithelial cells
appear normal

Mild=Few epithelial cells in the
basal layers show atypia

Moderate= Most cells in the basal layers & some suprabasally show atypia

Severe=Almost all cells show atypia but there is no evidence of invasion into the underlying tissues