Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Oral pathology > OP07 premalignant conditions of oral mucosa > Flashcards

OP07 premalignant conditions of oral mucosa Flashcards

(52 cards)

Start Studying
1
Q

What does cancer imply?

A

Tissue invasion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is key to the difference between premalignancy and cancer?

A
  • Pathology feature are not as severe as in cancer,
  • There is a risk of future transformation, and
  • There is no invasion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is a Carcinoma in situ?

A

The tissue has transformed - showing features of cancer through all the thickness of the tissue, but it is still not invasive.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Summarise evidence for precancer

A
  1. Precancerous areas have undergone malignant change
  2. Alterations are seen at the margins of overt OSCC’s
  3. Precancer changes are seen the same in epithelial malignancies, just without invasion
  4. Chromosomal, genetic and molarcular alterations are seen in both invasive and premalignant stages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the premalignant lesion?

A

A morphologically altered tissue in which oral cancer is more likely to occur in its apparently normal counterpart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Give some examples of potential premalignant lesions

A

Leukoplakia
Erythroplakia
Palatal lesions in reverse smokers
Proliferative verrucous leukoplakia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is a premalignant condition?

A

A generalised state associated with a significantly increased risk of cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Give some examples of premalignant conditions

A

Oral submucous fibrosis
Actinic keratosis
Lichen planus
Discoid lupus erythematous
Sideropenic dysphagia
Hereditary epidermolysis bullosa
Xeroderma pigmentosum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is hyperplasia?

A

Increased cell number in response to a stimulu

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Do all premalignant disorders show epithelial hyperplasia?

A

No, some do but some PMD show epithelial atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What parts of the epithelium undergo hyperplasia in premalignancy?

A

Basal cell hyperplasia
Acanthosis (prickle cell layer thickening)
Hypergranulosis - granular cell layer
Hyperorthokeratosis - stratum corneum
Hyperparakeratosis - parakeratinised layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is dysplasia in general?

A

Disturbance in the maturation of a tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is epithelial dysplasia?

A

Cyto/histological changes within the epithlium which indicate a risk of malignant change.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the relationship between premalignancy and dysplasia?

A

In pregmalignancy (no invasion), the severity of dysplasia correlates with the risk of transformation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the relationship between malignancy and dysplasia?

A

In malignancy (invasive), the severity of dysplasia correlates with prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the features of dysplasia on a cellular level? (8)

A
  • Anisonucleosis - variability in nucleus size
  • Increase nuclear size
  • Nuclear pleomorphism (variability in shape)
  • Anisocytosis - variability in cell size
  • Nuclear hyperchromatism (very darkly stained)
  • Cellular pleomorphism
  • Atypical mitotic figures
  • Increased number and size of nucleoli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the features of dysplasia on an architectural level? (8)

A
  • Irregular epithelial stratification
  • Disturbed/loss of polarity (of basal cells eg nucleus is pushed to one size)
  • Basal cell hyperplasia
  • Drop-shaped rete pegs (wide at bottom)
  • Increased mitoses
  • Superficial mitoses (eg in prickle cell layer instead of basal)
  • Premature keratinisation (dyskeratosis)
  • Keratin pearls in rete ridges
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How is dysplasia classically graded?

A

Mild: lower third of epithelial thickness
Moderate: extends into the middle third, atypical changes more marked
Severe: more than 2/3, marked cytological atypical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the WHO suggestions for risk of dysplasia?

A
  1. ‘no/questionable/mild’ - low risk
  2. ‘moderate/severe’ - high risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What factors affect dysplasia?

A

Candida (upto 50% of CHC have dysplasia)
Viral infections (HPV)
Tobacco
Alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What can happen to the progress of dysplasia?

Study These Flashcards
A

Might worsen, remain, improve or resolve

22
Q

What are some differentials for dysplasia - might look like dysplasia but are other epithelial changes?

Study These Flashcards
A

Response to trauma
Ulceration
Inflammation
Irradiation
Nutritional deficiencies (iron, folate, B12)

23
Q

What is the definition of leukoplakia?

Study These Flashcards
A

White plaques of questionable risk, excluding (other) known diseases or disorders that carry no increased risk for cancer.
Clinical term, no specific histology, not a diagnosis. Biospy is mandatory.

24
Q

What are the classic clinical types of leukoplakia?

Study These Flashcards
A
  1. Homogenous: uniformly flat, thin, shallow cracks
  2. Non-homogenous - speckled, nodular, verrucous
25
Describe the types of non-homogenous leukoplakia's
Speckled - mixed red and (predominantly) white (erythroleukoplakia) Nodular - small polypoid outgrowths rounded red or white excrescences Verrucous - wrinkled or corrugated appearance
26
What are the potentials to exclude before calling something a leukoplakia?
White sponge naevus Frictional keratosis Cehmical injury Acute pseudomembranous candidosis Leukoedema (change of tissues, ground glass mucosa) Lichen planus Lichenoid reaction Discoid lupud erythematous Skin grafts Hairy leukoplakia Leukokeratosis nicotina palate - smokers get irritation of palate with red pinpoints (minor salivary glands irritated)
27
What is an erythroplakia?
A fiery red patch that cannot be characterised clinically or pathologically as any other definable disease Clinical term, no specific histology
28
What do erythroplakias look like?
Clinically flat, smooth, granular or velvety surface
29
Why are red lesions red?
Red due to epithelial atrophy and thinning
30
How often to erythroplakias show severe dysplasia and invasive carcinoma?
They show severe dysplasia in 40% of cases And show invasive carcinoma in 50% of cases
31
What should you exclude before calling something an erythroplakia?
Desquamative gingivitis Erythematous lichen planus (atrophic/erosive) Discoid lupud erythematosus Pemphigoids Hypersensitivity reactions Reiter's disease (reactive arthritis) Erythematous candidiasis (acute or chronic) Histoplasmosis Haemangioma Kaposi's sarcoma Leukokeratosis nicotina palate
32
What is the puzzle of CHC?
Whether candida induces dysplasia or if the dysplastic epithelium is more easily colonised by candida?
33
How do you find out whether candida is the cause of dysplasia?
Treat for the candida and follow up with the patient to see if the lesion disappears or not If not - rebiopsy, and see whether the fungal treatment has been successful or not
34
What are reverse smoking palate lesions?
When you smoke with the burning end inside the mouth Smoke carcinogens dissolve in saliva
35
What is sublingual keratosis?
Anterior floor of mouth and ventral surface of tongue with 'ebbing tide' (wrinkly) appearance
36
Does sublingual keratosis have a high rate of transformation?
Sublingual keratosis has a high rate of transformation and a thin epithelium at this location.
37
What is oral submucous fibrosis and what causes it?
Disorder of the mouth, pharynx, oesophagus Associated with areca nut (paan) chewing - malignant transformation rate approx 8% over 15-20yrs.
38
What clinical symptoms present with oral submucous fibrosis?
Stiffening of mucosa, fibrosis, blanched appearance, reduced mouth opening, deformed uvula, marble mucosa appearance
39
What are the histological features of oral submucous fibrosis?
Hyalinsation of subepithelial CT Few fibroblasts Narrow/obliterated blood vessels Chronic inflammatory cells Atrophic epithelium (less common) with epithelial dysplasia in about 15% of biopsies
40
Why does chewing areca nut cause this?
Areca nut + slaked lime wrapped in betel leaf + spices, chewed and kept in vestibular sulcus, sometimes with tobacco Areca nut contains: - Arecoline hydrolysed by lime --> arecaidine (carcinogen) - Arecoline induces fibroblast proliferation - Flavinoids and tannins stabilise collagen - Copper --? lysil oxidase cross-links collagen
41
What is actinic keratosis and what is it characterised by?
Important in the development of lip cancer (SCC) Dryness, atrophy, erythema, swelling, scaly lesions, blurring of vermillion demarcation, pallor areas
42
Who is at highest risk of actinic keratosis?
Fair skinned people who do outdoor activities
43
What does histology in actinic keratosis show?
Dysplasia, elastosis, inflammatory infiltration, hyperplasia, acanthosis
44
Which types of lichen planus are most likely to transform?
Any can, but erosive and atrophic are the most likely
45
Read over these hereditary conditions, rare, that can cause malignant transformations
o Epidermolysis bullosa – blister formation at minimal trauma o Xeroderma pigmentosum – defective DNA repair mechanism to UV light injury, tip of the tongue, x20000 risk of malignant transformation o Dyskeratosis congenita (DC) – Most cases are X-linked (affects males)  Defective telomere maintenance  cell ageing?  Patients often develop * White plaques on the dorsal tongue (can be confused with leukoplakia, but absence of habits and young age may point to their hereditary nature) * Abnormal skin pigmentation, nail dystrophy, pulmonary disease, malignancies * Malignant change within the areas of white patches has been reported. o Fanconi anemia ~ 19 genes affected, short median life span (33yrs) leads to bone marrow failure (aplastic anemia) and cancer: acute myeloid leukemia, HNSCC (x500) o Bloom syndrome – BLM gene codes for helicases (unwind DNA). Patients have short stature, high pitched voice, long narrow face, small lower jaw, prominent nose & ears, skin rash after exposure to the sun, and a greatly increased risk of cancer, telangiectases, hyper/hypo pigmentation patches, male often infertile. o Ataxia telangiectasia – primary immunodeficiency disease. Delayed development of motor skills, poor balance, and slurred speech, usually occur during the first decade. Sensitive to radiation. ~20% acute lymphocytic leukemia/lymphoma, susceptible to infections, mild diabetes mellitus and some cancers. Normal or above intelligence. o Li-Fraumeni syndrome – rare disorder with greatly increased risk of developing several types of cancer, in children and young adults. CHEK2 & P53 genes
46
In what conditions does epithelial atrophy occur?
Syphilitic leukoplakia Siderpenic dysphagia Lichen planus - erosive/atrophic
47
What does epithelial atrophy do?
A thin epithelium becomes less of a barrier to diffusing carcinogens
48
What is syphilitic leukoplakia and how does it cause epithelial atrophy?
Causes endarteritis = the lumen of arteries gets narrowed down, leading to less blood supply and hence epithelial atrophy
49
What is sideropenic dysphagia and how does it cause epithelial atrophy?
Causes iron deficiency causing atrophy of epithelium
50
What features in about 4-6% of cases cause increased risk of malignant trasnformation in dysplastic conditions?
Speckled > homogenous Floor of mouth > other sites
51
What is the treatment for dysplasia?
Biospy --> review --> remove risk factors If severe dysplasia --> excision, otherwise frequent review
52
Describe some trends in transformation rates
Transformation increases for high grade Surgical excision decreases transformation rate but does not eliminate the risk Not excised lesions lead to higher transformation rates Time to transformation is variable Tongue is a high risk site

Oral pathology (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions