W16 58 tumour growth, management and prognosis Flashcards

1
Q

When is the cell vulnerable?

A

During the process of DNA replication, the cell is vulnerable to mutations etc

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2
Q

Describe briefly the cell cycle

A

Most of the time cells are in M0 and functioning. In response to external signals and on the absence of suppression signals, the cell ‘decides’ to divide and enters the cell cycle. It first undergoes checks to make sure that it is healthy (G1), makes a full copy of all its DNA (S), makes another check to ensure that both copies are healthy (G2), and then it splits into 2, with one copy in each cell.

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3
Q

What are the 6 hallmarks for cancer? (READ PG569 AFTER FLASHCARD!)

A
  1. Sustained proliferation signalling
  2. Evading growth suppressors
  3. Resisting apoptosis
  4. Replication immortality
  5. Angiogenesis
  6. Invasion and metastasis
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4
Q

What are the emerging hallmarks of cancer?

A

Avoiding the immune system
Deregulating cellular mechanism

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5
Q

What are the enabling characteristics for cancer?

A
  1. Genomic instability (mutations acquiring rapidly)
  2. Promoting inflammation (factors encouraging repair can encourage cancer growth)
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6
Q

What is atrophy?

A

Acquired decrease in organ size due to decreasing size or number of cells

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7
Q

Why is hypertrophy?

A

Increase in the organ size due to increasing size of individual cells

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8
Q

What is hyperplasia?

A

Increase in organ size due to increase number of individual cells

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9
Q

What is metaplasia?

A

A reversible change in differentiation within an organ from one cell type to another, usually in response to persistent injurious stimuli

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10
Q

What is dysplasia?

A

Abnormal maturation of cells that is not reversible. Is generally considered to be on a spectrum with neoplasia, and often has malignant potential.

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11
Q

What is neoplasia?

A

‘New growth’. Uncontrolled growth of abnormal cells. Can be benign or malignant.

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12
Q

What is cancer?

A

Malignant neoplasia

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13
Q

What is a carcinoma-in-situ?

A

Has all the features of malignant neoplasia, but does not invade or breach the original basement membrane. May represent the ‘missing link’ between dysplasia and cancer.

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14
Q

What investigations should you do of suspecting cancer?

A

History
Examination
Investigation (staging)
Treatment planning

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15
Q

Are benign tumours bad?

A

Yes although they cant invade structures and metastasise, they can still grow and press on important structures.

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16
Q

What are the macroscopic differences between benign and malignant tumours?

A

Benign - slow growing, clearly demarcated, smooth and rounded, displaces adjacent structures
Malignant - grow rapidly, not easily distinguished from surrounding tissue, hard ulcerate and necrotic, invades local tissue and metastasizes.

17
Q

What are the microscopic differences between benign and malignant tumours?

A

Benign - normal mitotic rate, normal nuclei
Malignant - high mitotic rate, pleomorphic, hyperchromatic nuclei

18
Q

What are epithelial tumours called?

A

Carcinomas

19
Q

What are the naming mechanisms for different benign neoplasms arising from different kinds of epithelium?

A

squamous - papilloma
glandular - adenoma
skin - papilloma
melanocytes - naevus

20
Q

What are the naming mechanisms for different malignant neoplasms (cancers) arising from different kinds of epithelium?

A

squamous - squamous cell carcinoma
glandular - adenocarcinoma
skin - squamous cell/basal cell carcinoma
melanocytes - melanoma

21
Q

what are malignant mesenchymal (connective tissue) tumours called?

A

sarcomas

22
Q

what are the names for different mesenchymal (connective tissue) benign tumours?

A

bone - osteoma
cartilage - chondroma
fat - lipoma
smooth muscle - leiomyoma
fibrous tissue - fibroma

23
Q

what are the names for different mesenchymal (connective tissue) malignant tumours?

A

bone - osteosarcoma
cartilage - chondrosarcoma
fat - liposarcoma
smooth muscle - leiomyosarcoma
fibrous tissue - fibrosarcoma

24
Q

what is the grade of a tumour?

A

a classification system of how well-differentiated a tumour is (how much of the characteristics of the original tissue it retains)
(AKA how disorganised )
A measure via microscopy (rather than clinical)

25
Q

Are well-differentiated or poorly differentiated tumours more aggressive?

A

Well-differentiated tumours generally are less aggressive and have a better prognosis than poorly-differentiated tumours.

26
Q

What is the staging of a tumour?

A

A classification system of how advanced a tumour is. The higher the score, the worse the tumour.
(clinical measure)

27
Q

What is the TNM system?

A

Staging system - assigns a score to the Tumour, the spread to the local lymph Nodes and whether or not the tumour has metastasised.

28
Q

You don’t need to know all of the different stages for tumours. But what does a higher stage score mean? (images pg573)

A

The higher the score, the higher the odds of dying from the disease
The bigger the tumour and the deeper it invades, the worse the prognosis
Nodal stage - the more nodes you have, the bigger you have and the more they have spread, the worse the prognosis. Or burst and invading locally in the neck.

29
Q

How does HPV affect cancers?

A

HPV affects (can drive) oropharyngeal cancer
It can be involved in but does not drive or cause oral cancer

30
Q

What does oropharyngeal cancer involve?

A

The base of the tongue (posterior third)
Soft palate
Tonsils

31
Q

Are HPV+ cancers more or less survivable?

A

HPV+ tumours are much more amenable to treatment - survival is better

32
Q

What are the 4 treatment options for cancer?

A

Chemotherapy
Radiotherapy
Immunotherapy
Surgery

33
Q

How does radiotherapy work?

A

Works via the cell cycle. When DNA is opened up, it is vulnerable and more likely to be damaged. So when open, it can be attacked by the ionising rays from radiotherapy, and disrupt the DNA so it destroys it. Cells in the process are dividing are disproportionately affected by radiotherapy compared to those that aren’t. Eg cancer cells that are rapidly dividing are more affected than those that aren’t. Cells targeted undergo necrosis or apoptosis.

34
Q

What are the dentally relevant side effects of radiotherapy?

A

Xerostomia - leading to radiation caries - VERY HIGH RISK! (because affects the salivary glands)
Osteoradionecrosis - frequently the bone is intact but the osteocytes have been killed, so a tooth extraction eg fracturing the buccal plate means the bone is unable to heal, causing osteonecrosis of the jaw.

35
Q

What is chemotherapy?

A

Poisoning the cancer cells. Mostly work on DNA replication. Targets rapidly dividing cells. Component cyclophosphonide - will shrink the cancer rapidly and reliably. Disproportionately affects cells that are undergoing replication and multiplication.

36
Q

What is the problem with chemotherapy and how does this cause the side effects?

A

There are a lot of cancer cells and they are surrounded by healthy cells.
Eg in chemotherapy patients often lose their hair since hair cells are rapidly multiplying. They become neutropenic and anaemia - get a poor immune system since blood cells are rapidly multiplying and these are poisoned.
Orogastric mucosa causing mouth ulcers.

37
Q

What is immunotherapy?

A

New and complex. This method restimulates the immune system to recognise cancer cells (which appear as alien to the immune system).
eg nivolumab - might be able to help a metastasising cancer from growth - allowing people to die with cancer rather than from it

38
Q

What are the stages of surgery to treat cancer?

A

Resection - remove the tumour completely without leaving any cells behind
Regional clearance - if tumour has spread locally, you can remove it and all of the spread
Reconstruction - restore function of what you have taken out with the tumour
Palliate - making someone comfortable