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DS4101 > Cancer - Thomson/Curtin > Flashcards

Cancer - Thomson/Curtin Flashcards

1
Q

What is the most common type of oral cancer

A

Squamous cell carinoma (>90%)

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2
Q

5 Primary tumour types of oral cancer

A

SCC

Minor salivary gland carcinoma

Lymphoma

Malignant Melanoma

Sarcoma

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3
Q
A

SCC

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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

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5
Q

Why is SCC a lethal disease?

A

50% of patients seen with SCC will die within 5 years

  • rising incidence
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6
Q

Aetiology of SCC (7)

A

Tobacco / Alc

Poor nutrition

Infections (HPV)

Poor oral health

Low SES

Immunosuppression

Genetics

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7
Q

What is the malignant transformation rate of oral epithelial dysplasia?

A

12.3%

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8
Q

What is an OPMD?

A

Morphologically altered tissue in which oral cancer is more likely to occur than its normal counterpart

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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
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10
Q

What has a higher risk of malignant transformation - homogenous or non-homogenous leukoplakia?

A

Non-homogenous

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11
Q

What is the commonest type of OPMD?

A

Leukoplakia

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12
Q

Female pt aged 63

A

Proliferative verrucous leukoplakia

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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
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14
Q

What to be mindful with erythroplakia?

A

high chance of malignancy

  • 40% of observed erythroplakia is already invasive OSCC
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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
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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
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17
Q
A

Oral Submucous Fibrosis

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18
Q
A

Chronic hyperplastic candidosis

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19
Q

How to treat chronic hyperplastic candidosis

A

Fluconazole (systemic antifungal)

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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)
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21
Q

Why does chronic hyperplastic candidosis come back?

A

Pt keeps smoking

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22
Q
A

Discoid lupus erythematous

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23
Q
A

Actinic cheilitis

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24
Q
A

Lichen planus / lichenoid lesions

  • be very mindful if its seen on the tongue
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25
Q
A

Tertiary syphillis

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26
Q

What locations are the most high risk for malignant change?

A
  • Floor of mouth
  • Ventro-lateral tongue
  • Retromolar regions
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27
Q

Managment goals of OPMD (7)

A
  • Accurate diagnosis
  • Prediction of clnical behaviour
  • Early recognition of malignancy
  • Removal of dysplastic mucosa
  • Prevention of recurrence
  • Prevent malignant transformation
  • Minimal patient morbidity
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28
Q

What does sclerous mean?

A

Hard / bony

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29
Q

What defines a malignant tumour? (3)

A

The appearance, behaviour & histology

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30
Q

What is the appearance of cancer?

A
  1. Ulcerated / non-healing
  2. White or red in colour
  3. Margins are fucked
  4. Cirrous / Sclerous (hard and bony)
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31
Q

What is the primary mode of spread of oral cancer?

A

Lymphatic

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32
Q

What is the behaviour of cancer?

A
  1. Grows locally invasively
  2. Spreads regionally then distantly
  3. “Parasitic”
  4. “Anarchistic”
33
Q

What is the role of lymph nodes?

A

LN are drainage ports, packed full of lymphocytes

34
Q

What is cachexia?

A

Extreme weight loss and muscle wasting

35
Q

What happens to the basement membrane cells when cancer occurs?

A

Basement membrane cells switch to mesenchymal cells

36
Q

What is an adenoma carcinoma?

A

Adenocarcinoma is a type of cancer that starts in mucus-producing glandular cells of your body

  • Salivary gland tumours
  • Asymptomatic
37
Q

What are the principles of management for oral oncology

A
  • Establish diagnosis
  • Establish extent of disease
  • Classification
  • Staging
  • Treatment
38
Q

What are the three parameters of cancer staging?

A

Tumour size

Lymph node involvement

Metastasis

39
Q

Why do we use staging for oncology? (5)

A

Standardisation

Disease progression

Prognosis

Risk stratification

Disease management

40
Q

What is prognostication?

A

Guessing the outcome based on statistics

41
Q

What is the fatality rate for small, treatable oral cancer tumours

A

25%

42
Q

General complications of cancer

CANCER acronym

A

Cachexia & wasting

Anaemia

Nutritional deficiency

Cutaneous manifestations

Endocrine disorders

Rare manifestations

43
Q

3 common sites for metastases from jaws

A

Breast

Lung

Prostate

44
Q

Effects of tumour metabolites (4)

A

Facial flushing

Pigmentations

Amyloidosis

Oral erosions

45
Q

Changes caused by functional disturbances (4)

A

Purpura

Bleeding

Infections

Anaemia

46
Q

What complications can radiotherapy have on periodontal tissues (4)

A

Mucositis

Ulceration

Periodontal disease

Candidosis

47
Q

What complications can radiotherapy have on teeth?

A

Radiation caries

Dental hypersensitivity

Loss of taste

48
Q

What complications of radiotherapy can affect your tx plan? (3)

A

Trismus

Osteoradionecrosis

Craniofacial defects (in younger pts)

49
Q
A

Path of radiation in radiotherapy case

50
Q
A

Radiation caries

51
Q
A

Osteoradionecrosis

52
Q

How to manage patient during head & neck radiotherapy (5)

A
  1. Discourage smoking and alcohol
  2. Elimate infections
  3. Relieve mucositis
  4. Saliva substitutes
  5. Physiotherapy for trismus
53
Q

Managment of patients after receiving head & neck radiotherapy (6)

A
  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
Q

Saliva substitute

A

Biotene

55
Q

Oral complications of chemotherapy

A

Infections

Ulcers / mucositis

Lip cracking

Bleeding

Xerostomia

Periodontal disease

Delayed / abnormal development

56
Q

Management of patients befor Chemotherapy (2)

A

Oral and dental assessment

OH

57
Q

Management of patients during chemotherapy (6)

A
  • Folic acid to reduce ulcers
  • Ice cold water / sucking ice
  • CHX (diluted)
  • Nystatin (for candidosis)
  • Aciclovir (herpes infection)
  • AB for infections
58
Q

What drug interaction should wartch out for with methotrexate? (chemotherapy drug)

A

Methotrexate exacerbates the effect of NSAIDs and Aspirin

*Patients suffering from rheumatoid arthritis often also take methotrexate as a medication

59
Q

Features of oral mucositis

A

Widespread erythema

Ulceration

Soreness & bleeding

60
Q

WHO mucositis scale

A

1- Soreness / erythema

2- Erythema & ulcers / able to eat solids

3- Ulcers / requires liquid diet

4- Oral intake not possible

61
Q

Management of patients with Oral Mucositis (5)

A

PCA / opioids

Avoid smoking, alc, spices

Good OH

Cold water / ice

Topical analgesics

62
Q

Why do cancer treatments have the potential to significantly impact oral tissues?

A

Treatments are aimed at rapidly dividing cells (skin, mucosa, blood, etc)

Chemo - systemic

Radio - localised

63
Q

Why do th things sometimes not go according to plan with cancer treatment?

A

Altered pt priorities

Pt capacity

Altered oral physiology

Cannot get to dentist

Financial problems

64
Q

What needs to be done before cancer patient receives treatment? (6)

A
  • Clinical exam
  • Identify problem teeth
  • Pulp testing
  • radiography
  • OPG
  • Perio issues
65
Q

Consideration for exos post cancer treatment

A

Radiotherapy damages bone permanently

If tooth needs to come out, be very careful - atraumatic resto

66
Q

Oral consideration for Radiotherapy? Management?

A

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
Q

Mechanism of action radiotherapy vs chemo

A

Radiotherapy - locallised radiation doses stops growth of cancer cells

Chemotherapy - uses drugs to stop growth (killing or stopping cell division)

68
Q

Systemic effects of chemotherapy

A

Myelosuppression (mucositis)

Neutropenia (infections)

Fungal (thrush)

Viral (herpes, cytomegalovirus)

69
Q

Oral impacts of chemotherapy

A

Mucositis

Oral thrush

Sloughing of mucosa

70
Q

What is involved in CO2 laser surgery? (7)

A

Rapid dissection

Haemostasis

Post-operative analgesia

Excision allows histopathological dx

Low morbidity

Reduced scarring

Good patient acceptance

71
Q

What are the 3 surgical interventions for OPMD’s

A
  1. Scalpel excision
  2. Laser therapy
  3. Photodynamic therapy
72
Q

Histopathological features of OED

Cytology features (4)

A

Variation in:

  • Nucleus size & shape
  • Cell size & shape

Hyperchromasia

Increased # and size of nucleoli

Atypical mitotic figures

73
Q

Histopathological Features of OED

Tissue Architecture (IDLAK)

A

Irregular epithelial stratification

Drop-shaped rete ridges

Loss of polarity of basal cells

Abnormally superficial mitoses

Keratin pearls within rete ridges

74
Q

What is dysplasia?

A

Histopathological term describing a range of tissue dysmaturation and disorganisation changes seen in biopsy specimens

Associated with an increased risk of malignant transformation

75
Q

What are the 2 systems of grading OED

A

WHO (mild, mod, severe, carcinoma in situ)

Binary System (high/low grade/risk)

76
Q

Describe the Binary System’s method of grading OED

A

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
Q

Describe what cancer is (features, how)

A

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
Q

3 high risk and 3 low risk aetiology of OSCC

A

HIGH risk

  1. Tobacco/alc
  2. Age
  3. Immunodeficiency

LOW risk

  1. Poor OH
  2. Low SES
  3. HPV

DS4101 (43 decks)

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