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osomop 4th > PMOL > Flashcards

PMOL Flashcards

1
Q

what is the most common malignant tumour to arise in the oral cavity?

A

squamous cell carcinoma

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2
Q

what are most OSCC not accompanied by?

A

recognised pre exciting mucosal lesions

> some mucosal lesions seem to show an increased association with subsequent OSCC than others, but inconsistent

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3
Q

what does potentially malignant mean?

A

the lesions are not “malignant” already and it is not inevitable that the OSCC will develop, there is a risk that tumour could arise, although that risk is difficult to evaluate for individual patients

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4
Q

what do PMOL generally look like?

A

> generally white, red or both
flat, nodular, warty or elevated
large or small
single or multiple
any site but lateral/ ventral of tongue, FOM

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5
Q

what are examples of white / red lesions which aren’t PMOL?

A

> inherited = white sponge naevus
irritational = frictional keratosis
immunological = LP/LR, LE, others
infective = caused by candida, Epstein-barr virus
iatrogenic = scars, skin grafts and flaps
idiopathic = leukoplakia

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6
Q

classification and definition of leukoplakia?

A
  • homogenous = flat, possibly fissured
  • non-homogenous = nodular, speckled or both
    proliferative verrucous leukoplakia is believed to be a subset of non homogeneous leukoplakia

def - a white patch which cannot be classified as any other disease and is associated with an increased risk of malignancy

in other words - not = acute candidiasis, frictional keratosis, LP/LR, WSN

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7
Q

definition of erythroplakia?

A
  • a white/red patch that can’t be diagnosed as anything else
  • similar to leukoplakia but refers to a red patch
  • sometimes called erythroplasia
  • diagnosis is based on exclusion and thus needs properly assessed
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8
Q

what intra oral disease have an association with OSCC?

A
  1. OLP/ LR
  2. LE
  3. patterson Kelly brown syndrome
  4. submucous fibrosis
  5. dyskeratosis congenita
  6. epidermolysis bullosa
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9
Q

what risk is a homogenous leukoplakia in developing into a OSCC?

A

low risk

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10
Q

what risk is a non homogenous leukoplakia at developing into an OSCC?

A

high risk

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11
Q

what risk is an erythroplakia at developing into an OSCC?

A

highest risk

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12
Q

what is the epidemiology of an OSCC?

A
  • variable and complicated
  • much uncerctaintity in diagnosis
  • rare
  • middle age and elderly
  • twice as common in males as females
  • developing countries = lots of tobacco use = Lots of OSCC = lots of precursors
  • less than 10 a year in NI
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13
Q

what are the common sites of OSCC?

A
  • VT
  • LT
  • FOM
  • RMP
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14
Q

what is the size of an OSCC?

A
  • larger
  • spanning multiple intraoral sites
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15
Q

what is the appearance of an OSCC?

A

non-homogenous
microscopic = dysplasia

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16
Q

when would you be more worried if someone had an OSCC?

A
  • in non smokers (absence of risk factors)
17
Q

what 3 things do you need to do to establish a diagnosis of an unknown lesion?

A
  1. history (duration, onset, habits, systemic disease?, medication, family history)
  2. examination
  3. special investigations
18
Q

what do you have to note during an examination of a PMOL?

A
  1. the nature
  2. the size
  3. the site
  4. the extent
  5. that it isn’t anything else
  6. homo or non-homogenous
19
Q

why is it important to palpate a PMOL?

A

to check for any change in the feel of the underlying, especially induration

20
Q

what laboratory investigation do you complete for a PMOL?

A
  1. MICROBIOLOGICAL - candida isolation
  2. HAEMATOLOGICAL - haematinic deficiencies/ anaemia, biochemistry, autoantibodies
  3. HISTOPATHOLOGICAL - morphological
21
Q

what makes a lesion white?

A
  • thicker keratin (hyperkeratosis)
  • thicker epithelium (hyperplasia)
  • fibrosis in the lamina propia
22
Q

what makes a lesion red?

A
  • thinner keratin
  • thinner epithelium (atrophy)
  • vascularity in the lamina propia
23
Q

what morphological changes may occur in a PMOL?

A
  • hyperkeratosis
  • epithelial thickness change
  • change in rete peg architecture
  • status of basal layer (hyperplasia, apoptosis)
  • dysplasia
  • changers in lamina propia
  • candida present
24
Q

what is dysplasia?

A

> a description of architectural and cytological changes in epithelium that resemble those of cancer but without invasion of the tissues

> a form of “intermediate step” in cancer development : a tissue disturbance that looks like a cancer but does not behave like a cancer

> the presence of dysplasia implies some disturbance of epithelial proliferation and/ or differentiation, its presence can assist in treatment

25
Q

what are the features of dysplasia ?

A
  • distorted rete peg architecture
  • irregular stratification
  • dyskeratosis
  • basal cell hyperplasia
  • loss of adherence
  • loss of polarity
  • hyperchromatism
  • increased N : C
  • anisocytsosis
  • pleomorphism
  • number, location and form of mitotic figures
26
Q

what are the 4 sub divisions of dysplasia?

A
  1. mild
  2. moderate
  3. severe
  4. carcinoma-in-situ
  • they’re are sometimes referred to low grade (mild) and high grade
27
Q

what is the sequence of cancer formation?

A

= progressive worsening of dysplasia

  • no dysplasia > mild
  • mild > moderate
  • mod > severe
  • severe > invasion
28
Q

what does the linear sequence of cancer formation never appear in real life?

A
  • cancer is a genetic disease
  • cellular morphology is a poor reflection of genetic changes
  • biopsies are small
  • the section biopsied will never turn to SCC
  • the past is a poor guide to the future
  • dysplasia assessment is too complex too be helpful
29
Q

what is the risk factor in the presence of dysplasia in developing an OSCC?

A

x10

30
Q

what is the chance of developing an OSCC from dysplasia from the different grades?

A

mild = <5%
mod = 10-20%
severe = 15-20%

31
Q

what are the important features of epithelial dysplasia?

A
  • some features are interrelated
  • none of the features are specific
  • not all the features are present
  • assessment is very subjective
  • sampling error is significant
32
Q

why is there lots of uncertainty in studying dysplasia for OSCC diagnosis?

A
  • studies are retrospective, intrinisicallu biased and not directly comparable
  • number of cases are small
  • OSCC may not develop for many years
33
Q

Management of PMOL?

A

> long term follow ups = life long

> get rid of the lesion (at least the worst part)
stabilise the intracellular biology
observation
combination

34
Q

what are the surgical treatment option of PMOL?

A
  • scalpel excision
  • laser excisions
  • CO2 laser ablation
  • photodynamic therapy
  • cryotherapy
35
Q

what are medical treatment options for PMOL?

A
  • retinoids
  • EGFR inhibitors/ antagonists (epidermal growth factor receptor)
  • COX2 antagonists
  • cell cycle interruption = p53 modulators
  • topical anti cancer agents = bleomycin
36
Q

what are the advantages of treatment?

A

> surgical = the most abnormal looking tissue can be removed or destroyed
medical = topical drug can be directed at the most abnormal site with less destruction and systemic medication may also manage other sites

37
Q

what are the disadvantages of treatments?

A

> local side effect - pain, infection, slow healing
sytemic side effects
no therapy prevents new lesions or OSCC

38
Q

what is the aim of management?

A
  • preventing the development of OSCC
  • detecting the patients first OSCC at the earliest opportunity

osomop 4th (18 decks)

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