Neoplasia Practical Flashcards

1
Q

Most benign tumours are not life threatening, can you think of an example of when a benign tumour may be deadly? What factors do you think may influence the prognosis (outlook for the patient)?

A

Benign tumours of the brain can be lethal if they cannot be completely surgically excised. A tumour that is deep within the brain or close to major blood vessels will not be easily cut out but will respond well to treatment if the cells of the tumour are proliferating (multiply) rapidly.

However, slow growing tumours will be more resistant to current treatments that just target rapidly dividing cells

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2
Q

characteristic of benign tumours (4/5)

A

never metastasize

encapsulated

homogenous

well-differentiated

GENERALLY, slower growing but many exceptions

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3
Q

characteristics of malignant tumours (4 important/5)

A

Can potentially metastasize

Infiltrative/invasive growth pattern

Heterogeneous (pleomorphic, cells lack uniformity)

well-differentiated or poorly/undifferentiated (anaplastic)

Some populations within the malignancy will grow quickly sometimes outstripping the growth of their blood supply and thus undergoing necrosis in areas. many mitotic cells

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4
Q

Sarcomas are VERY rare cancers but of all of the different types of sarcoma, osteosarcoma is the most common, can you explain why osteosarcomas are more commonly found in young people?

A

The bones of young people are still growing & are therefore at greater risk (increased proliferation). We stop growing taller soon after puberty at which point the risk of osteosarcomas diminishes.

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5
Q

Squamous cell carcinoma of the skin
Squamous cell carcinoma of the penis
Squamous cell carcinoma of the vulva
Squamous cell carcinoma of the mouth
Squamous cell carcinoma of the cervix

Similarities between these cancers?

A

All the SCCs have a similar pathogenesis, they all began in stratified squamous epithelium that acquired mutations most likely from carcinogens from cigarettes, &/or alcohol, HPV infection or UV.

Please note that simple squamous epithelium is very delicate and so will die when stressed whereas stratified squamous epithelial cells line area exposed to physical stress and the cells are labile

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6
Q

It is possible to get two different carcinomas at the end of the oesophagus. squamous cell carcinomas tend to occur in the upper third proximal to the oral cavity while adenocarcinomas occur in the lower third of the oesophagus. why is this the case?

A

Upper oesophagus: The oesophagus is lined by stratified squamous epithelium and is essentially a transit tube carrying boluses of food from the oral cavity to the stomach. The stratified squamous epithelium is good at withstanding physical stress including
abrasion from dietary constituents. However, the cells may be mutated by carcinogens in cigarette smoke, alcohol & infection with HPV. The upper oesophagus is most likely to develop a squamous cell carcinoma because of these carcinogens.

lower oesophagus: In people with chronic gastric reflux, the stratified squamous cells are damaged by the stomach acid & the cells undergo metaplasia to become a simple glandular epithelium which secretes mucous that provides a protective layer against the stomach acid. If mutations occur in these glandular epithelial cells they can form an adenocarcinoma

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7
Q

What type of epithelium normally lines the conductive regions of the airways?

A

Simple ciliated (initially pseudo-stratified columnar, then columnar then cuboidal) with goblet cells producing mucous interspersed

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8
Q

The chronic irritation caused by smoking results in what type of cellular adaptations (changes)?

A

Ciliated epithelium undergoes metaplasia to become stratified squamous epithelium. Goblet cells undergo hyperplasia.

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9
Q

metaplasia means?

A

change from one normal and well-differentiated cell type into another normal and well-differentiated cell type.

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10
Q

hyperplasia means?

A

increase in cell number.

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11
Q

Positive and negative consequences of metaplasia and hyperplasia? Reversible?

A

Metaplasia is good as it allows the cells to survive but they lose their original function, they no longer filter the air or remove mucous effectively thus smokers are more prone to infections and must cough up mucous.

Metaplasia and hyperplasia are normal, the cells are genetically & phenotypically normal but if they get mutations, they can become dysplastic or pre-cancerous.

Unlike metaplasia and hyperplasia, in dysplasia the cells are genetically & phenotypically abnormal; dysplasia is NOT a cellular adaptation.

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12
Q

What must take place before cancer develops?

A

Mutations lead to dysplasia (abnormal cell presence), which the immune system may destroy and in some parts of the body may be screened for.

In the lungs the dysplasia, which gives no signs/symptoms progresses from mild, moderate to severe where it starts to overlap with carcinoma-in-situ, which is the name for an epithelial malignancy that has yet to penetrate through the basement membrane which sits beneath the epithelial layer. It is now a matter of time before some of the cancer cells start to secrete enzymes that breakthrough the connective tissue thus allowing the cancer to invade and later metastasize.

If the cell that sustained the mutations is a goblet cell, it becomes an adenocarcinoma whereas if the last normal cell was a stratified squamous cell, it forms a squamous cell
carcinoma.

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13
Q

dysplasia means?

A

Presence of abnormal cells within tissue/organ. not cancer, but can become cancer.

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14
Q

Which part of the cervix is most vulnerable to forming dysplastic lesions?

A

The transformation zone where metaplasia occurs during the female’s reproductive life:
The inner simple glandular cells in the endocervix undergoes metaplasia when exposed to the ectocervix & becomes stratified squamous like the ectocervix & vagina. Metaplasia does not always lead to dysplasia but it increases the risk & so is the site of cell sampling in Pap smears.

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15
Q

Does metaplasia always precede dysplasia?

A

No. Metaplasia may precede the development of dysplasia in the cervix, lower oesophagus & conductive airways as described above. In other tumours, normal cells undergo mutations & become a benign tumour, which in some cases get further mutations becoming malignant (the example I used in the lecture was bowel cancer). In other cases, the normal cells in the area get mutated and become dysplastic & then
cancerous e.g. SCC of the skin, mouth, upper oesophagus, melanoma, mesothelioma etc.

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16
Q

“Adeno” means?

A

glandular (secretory), epithelial cell of origin.

17
Q

Metastasis means?

A

When some of the cancer cells move to distant sites and set up secondary growths.

18
Q

3 ways cancer can spread?

A

lymph/lymphatic spread

blood/haematogenous

direct seeding (e.g. floating in fluid in pleural/peritoneal fluid)

19
Q

Which organs are frequently affected by metastatic or secondary cancers?

A

Lungs, then liver, brain, bones.

The lungs are the most commonly affected organ as all venous blood returns to them & cancers usually spread first in the lymphatic & venous systems.

The liver is our largest visceral organ & thus gets a large amount of arterial blood but it is also the major metabolic organ when it comes to nutrients/food, drugs and hormones. Everything that we ingest, that enters our system (crosses the epithelium of the GIT) are carried to the liver via the portal venous system for processing. Many cancers first enter the blood at capillary beds or through thin-walled venules and get carried in venous blood to the liver and lungs. Once we have more haematogenous mets (clumps or emboli of cancer cells travelling in the blood) they go to
areas that get a lot of arterial blood like the brain & bones.

(Notes: The liver rarely develops primary cancers unless affected by cirrhosis. Cirrhosis, like all chronic inflammatory conditions involves continued injury & repeated attempts at repair. Cancers only form in dividing cells & if cells are forced to divide more frequently, they are more likely to make a mistake and pass that mistake or mutation onto their daughter cells which can become dysplastic. In addition, there is increased level of oxidants and other chemical mediators capable of damaging DNA at sites of chronic inflammation.)

20
Q

(TABLE OF CANCERS)

A

(Table of cancers)