Cancer - Thomson/Curtin Flashcards
1
Q
What is the most common type of oral cancer
A
Squamous cell carinoma (>90%)
2
Q
5 Primary tumour types of oral cancer
A
SCC
Minor salivary gland carcinoma
Lymphoma
Malignant Melanoma
Sarcoma
3
Q
A
SCC
4
Q
ORAL CANCER acronym
A
Oral ulceration (non-healing)
Red/white patches
Abnormal swellings
Loss of tongue mobility
Cauliflower-like growths
Abnormal, localised tooth mobility
Non-healing sockets
Colour change in mucosa (brown/blue)
Erosions in mucosa
Reduced / altered sensation
5
Q
Why is SCC a lethal disease?
A
50% of patients seen with SCC will die within 5 years
- rising incidence
6
Q
Aetiology of SCC (7)
A
Tobacco / Alc
Poor nutrition
Infections (HPV)
Poor oral health
Low SES
Immunosuppression
Genetics
7
Q
What is the malignant transformation rate of oral epithelial dysplasia?
A
12.3%
8
Q
What is an OPMD?
A
Morphologically altered tissue in which oral cancer is more likely to occur than its normal counterpart
9
Q
Definition of leukoplakia
A
White patch which cannot be wiped off mucosa or ascribed to any other clinical or histo-pathological condition
- By definition, leukoplakia has a potentially malignant predisposition
10
Q
What has a higher risk of malignant transformation - homogenous or non-homogenous leukoplakia?
A
Non-homogenous
11
Q
What is the commonest type of OPMD?
A
Leukoplakia
12
Q
Female pt aged 63
A
Proliferative verrucous leukoplakia
13
Q
Features of Proliferative verrucous leukoplakia (5)
A
- Females > 60
- Not associated with tobacco or alc use
- Slow growing, progressive
- Fissured, warty-looking
- 70% malignant transformation rate
14
Q
What to be mindful with erythroplakia?
A
high chance of malignancy
- 40% of observed erythroplakia is already invasive OSCC
15
Q
A
Erythroleukoplakia
- White flecks or nodules on atrophic erythematous base
- More dangerous than leukoplakia, but not as likely to turn malignant as erythroplakia
- If in labial commissures, could be related to chronic hyperplastic candidosis
16
Q
A
Erythroleukoplakia
- White flecks or nodules on atrophic erythematous base
- More dangerous than leukoplakia, but not as likely to turn malignant as erythroplakia
17
Q
A
Oral Submucous Fibrosis
18
Q
A
Chronic hyperplastic candidosis
19
Q
How to treat chronic hyperplastic candidosis
A
Fluconazole (systemic antifungal)
20
Q
Why dont topical antifungals work on chronic hyperplastic candidosis (nystatin, amphotericin)
A
They have thickened hyperplastic epithelium above the fungi
- Topical antifungal will not be able to penetrate, requires a systemic antifungual (fluconazole)
21
Q
Why does chronic hyperplastic candidosis come back?
A
Pt keeps smoking
22
Q
A
Discoid lupus erythematous
23
Q
A
Actinic cheilitis
24
Q
A
Lichen planus / lichenoid lesions
- be very mindful if its seen on the tongue
25
Tertiary syphillis
26
What locations are the most high risk for malignant change?
* Floor of mouth
* Ventro-lateral tongue
* Retromolar regions
27
Managment goals of OPMD (7)
* Accurate diagnosis
* Prediction of clnical behaviour
* Early recognition of malignancy
* Removal of dysplastic mucosa
* Prevention of recurrence
* Prevent malignant transformation
* Minimal patient morbidity
28
What does sclerous mean?
Hard / bony
29
What defines a malignant tumour? (3)
The *appearance, behaviour & histology*
30
What is the appearance of cancer?
1. Ulcerated / non-healing
2. White or red in colour
3. Margins are fucked
4. Cirrous / Sclerous (hard and bony)
31
What is the primary mode of spread of oral cancer?
Lymphatic
32
What is the behaviour of cancer?
1. Grows locally invasively
2. Spreads regionally then distantly
3. “Parasitic”
4. “Anarchistic”
33
What is the role of lymph nodes?
LN are drainage ports, packed full of lymphocytes
34
What is cachexia?
Extreme weight loss and muscle wasting
35
What happens to the basement membrane cells when cancer occurs?
Basement membrane cells switch to mesenchymal cells
36
What is an adenoma carcinoma?
Adenocarcinoma is **a type of cancer that starts in mucus-producing glandular cells of your body**
* Salivary gland tumours
* Asymptomatic
37
What are the principles of management for oral oncology
* Establish diagnosis
* Establish extent of disease
* Classification
* Staging
* Treatment
38
What are the three parameters of cancer staging?
Tumour size
Lymph node involvement
Metastasis
39
Why do we use staging for oncology? (5)
Standardisation
Disease progression
Prognosis
Risk stratification
Disease management
40
What is prognostication?
Guessing the outcome based on statistics
41
What is the fatality rate for small, treatable **oral cancer** tumours
**25%**
42
General complications of cancer
CANCER acronym
Cachexia & wasting
Anaemia
Nutritional deficiency
Cutaneous manifestations
Endocrine disorders
Rare manifestations
43
3 common sites for metastases from jaws
Breast
Lung
Prostate
44
Effects of tumour metabolites (4)
Facial flushing
Pigmentations
Amyloidosis
Oral erosions
45
Changes caused by functional disturbances (4)
Purpura
Bleeding
Infections
Anaemia
46
What complications can radiotherapy have on periodontal tissues (4)
Mucositis
Ulceration
Periodontal disease
Candidosis
47
What complications can radiotherapy have on teeth?
Radiation caries
Dental hypersensitivity
Loss of taste
48
What complications of radiotherapy can affect your tx plan? (3)
Trismus
Osteoradionecrosis
Craniofacial defects (in younger pts)
49
Path of radiation in radiotherapy case
50
Radiation caries
51
Osteoradionecrosis
52
How to manage patient **during** head & neck radiotherapy (5)
1. Discourage smoking and alcohol
2. Elimate infections
3. Relieve mucositis
4. Saliva substitutes
5. Physiotherapy for trismus
53
Managment of patients **after** receiving head & neck radiotherapy (6)
1. Continue OH/preventive care
2. Antibiotics for infections
3. Refer to OMFS for exo/oral surg
4. Topical fluoride
5. Avoid mucosal trauma
6. Saliva substitutes
54
Saliva substitute
Biotene
55
Oral complications of chemotherapy
Infections
Ulcers / mucositis
Lip cracking
Bleeding
Xerostomia
Periodontal disease
Delayed / abnormal development
56
Management of patients befor Chemotherapy (2)
Oral and dental assessment
OH
57
Management of patients during chemotherapy (6)
* Folic acid to reduce ulcers
* Ice cold water / sucking ice
* CHX (diluted)
* Nystatin (for candidosis)
* Aciclovir (herpes infection)
* AB for infections
58
What drug interaction should wartch out for with methotrexate? (chemotherapy drug)
Methotrexate exacerbates the effect of **NSAIDs and Aspirin**
\*Patients suffering from rheumatoid arthritis often also take methotrexate as a medication
59
Features of oral mucositis
Widespread erythema
Ulceration
Soreness & bleeding
60
WHO mucositis scale
1- Soreness / erythema
2- Erythema & ulcers / able to eat solids
3- Ulcers / requires liquid diet
4- Oral intake not possible
61
Management of patients with Oral Mucositis (5)
PCA / opioids
Avoid smoking, alc, spices
Good OH
Cold water / ice
Topical analgesics
62
Why do cancer treatments have the potential to significantly impact oral tissues?
Treatments are aimed at rapidly dividing cells (skin, mucosa, blood, etc)
Chemo - systemic
Radio - localised
63
Why do th things sometimes not go according to plan with cancer treatment?
Altered pt priorities
Pt capacity
Altered oral physiology
Cannot get to dentist
Financial problems
64
What needs to be done **before** cancer patient receives treatment? (6)
* Clinical exam
* Identify problem teeth
* Pulp testing
* radiography
* OPG
* Perio issues
65
Consideration for exos post cancer treatment
Radiotherapy damages bone permanently
If tooth needs to come out, be very careful - atraumatic resto
66
Oral consideration for Radiotherapy? Management?
Xerostomia
Cells of salivary glands are affected greatly
* Leads to dental, mucosal and eating issues
* Infection
* Mucosa becomes atrophic
Management: do surgery first so tissues can heal - will be permanently affected after radiotherapy
67
Mechanism of action radiotherapy vs chemo
Radiotherapy - locallised radiation doses stops growth of cancer cells
Chemotherapy - uses drugs to stop growth (killing or stopping cell division)
68
Systemic effects of chemotherapy
Myelosuppression (mucositis)
Neutropenia (infections)
Fungal (thrush)
Viral (herpes, cytomegalovirus)
69
Oral impacts of chemotherapy
Mucositis
Oral thrush
Sloughing of mucosa
70
What is involved in CO2 laser surgery? (7)
Rapid dissection
Haemostasis
Post-operative analgesia
Excision allows histopathological dx
Low morbidity
Reduced scarring
Good patient acceptance
71
What are the 3 surgical interventions for OPMD's
1. Scalpel excision
2. Laser therapy
3. Photodynamic therapy
72
Histopathological features of OED
## Footnote
**Cytology features (4)**
Variation in:
* Nucleus size & shape
* Cell size & shape
Hyperchromasia
Increased # and size of nucleoli
Atypical mitotic figures
73
Histopathological Features of OED
## Footnote
**Tissue Architecture (IDLAK)**
Irregular epithelial stratification
Drop-shaped rete ridges
Loss of polarity of basal cells
Abnormally superficial mitoses
Keratin pearls within rete ridges
74
What is dysplasia?
Histopathological term describing a **range of tissue dysmaturation and disorganisation** changes seen in biopsy specimens
Associated with an increased risk of malignant transformation
75
What are the 2 systems of grading OED
WHO (mild, mod, severe, carcinoma in situ)
Binary System (high/low grade/risk)
76
Describe the Binary System's method of grading OED
High risk lesions
* Lesions presenting with at least **4 architectural changes** and **5 cystological changes**
* Low-risk lesions present with **\<4 architectural changes** and **\<5 cytological changes**
77
Describe what cancer is (features, how)
**Invasive tumour from epithelial lining tissue**
accumulation of **multiple mutations** in DNA
Disruption of **cell proliferation, differentiation and development**
**Abnormal, uncoordinated growth**
Due to **Carcinogens or spontaneous mutation**
**Local tissue invasion and destruction**
**Crab-like**
**Metastasis**
78
3 high risk and 3 low risk aetiology of OSCC
HIGH risk
1. Tobacco/alc
2. Age
3. Immunodeficiency
LOW risk
1. Poor OH
2. Low SES
3. HPV
