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Foundations of Medicine > Tumour pathology > Flashcards

Tumour pathology Flashcards

1
Q

What is hypertrophy?

A

Increase in cell size but not number of cells

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2
Q

What is hyperplasia?

A

Increase in cell number but not size.

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3
Q

What is squamous metaplasia?

A

The change from one type of epithelial cell to a squamous cell.

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4
Q

What is the process of cell division called?

A

Mitosis

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5
Q

What are the stages in mitosis?

A

G1 - Growth
S- DNA replication
G2 - Growth
M - Cell division (PMATC)

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6
Q

What happens at the G1/S checkpoint?

A

It is a restrictive checkpoint.
Cyclin proteins that accumulate during the cell growth combine with cyclin dependant kinases which then phosphorylate pRb. pRb is inhibited and loses affinity for the e2F transcription factor. This allows the cycle to continue.

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7
Q

What three molecules inhibit cyclin CDK?

A

p16
p21
p27

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8
Q

What is p53?

A

An internal signal that results from cell damage and causes apoptosis. If a cell have a broken p53 then it can result in cancer. It is therefore an anti-oncogene. This is found at checkpoint 2 in the G2 phase.

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9
Q

What is carcinogenesis?

A

Failure of cell cycle control where there is a disturbance between the amount of proliferation and apoptosis.

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10
Q

What can cause carcinogenesis?

A

Environmental factors such as:

  • Chemicals (Oxidising and alkylating agents cause DNA base damage)
  • Radiation (DNA base damage)
  • Viruses (Viral genome effects the regulatory genes of the host)
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11
Q

Examples of viruses that give rise to cancer

A

Type 16 - Human papilloma virus leading to cervical cancer. Treated with the HPV vaccine.
EBV - Herpes virus causes stomach cancer, nasopharyngeal cancer, lymphoma.

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12
Q

Examples of inherited mutations that can cause cancer

A

APC - Signal transduction - Colon cancer
p53 - Cell cycle - carcinomas and sarcomas, Li-Fraumeni syndrome.
Rb - Cell cycle - Retinoblastoma and osteosarcoma
p16 - Inhibits CDKs - Melanoma.

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13
Q

Diseases can be …., ….. or …..?

A

Self-limiting, chronic or progressive.

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14
Q

What are the different elements of pathology?

A

Aetiology (cause)
Pathogenesis’s (Why the cause caused the disease)
Pathological features (macroscopy and microscopy)

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15
Q

What is a tumour?

A

An abnormal growing mass of tissue. Uncontrolled and uncoordinated growth.

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16
Q

How will malignant tumours appear under microscopy?

A

Cellular and with nuclear pleomorphism.

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17
Q

What are anti-angiogenic factors and what are some examples?

A

They prevent angiogenesis. i.e. Endostatin and p53

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18
Q

What are pro-angiogenic factors and what are some examples?

A

VEGF (which is phosphorylated to activate) and placental growth factor. Tumour cell can be induced to release these by neighbouring cells.

19
Q

How is apoptosis regulated?

A

Caspases.

20
Q

What is a benign tumour ?

A 
Non-invasive 
Usually encapsulated 
No evidence of invasion or metastases
Well differentiated 
Similar function to surrounding tissue 
Rarely kill people
21
Q

What is a malignant tumour?

A 
Invasive growth
No capsule 
Metastasis 
Poorly differentiated 
Loss of normal function 
Frequently kills people
22
Q

What are the three types of cancer?

A
  • Epithelial cells. Squamous, cuboidal, columnar. Carcinomas.
  • Mesoderm cells. Bone and muscle. Sarcomas.
  • Glandular cells. breast, oesophagus, lung. Adenocarcinomas.
23
Q

Table of cancers

A

-

24
Q

How can cancers be minitored and detected?

A

Using biomarkers which are properties of cancer cells.

25
Q

Examples of biomarkers present in someone with cancer

A

Alpha-fetoprotein -> Teratoma of the testis and hepatocellular carcinoma
CEA -> Colorectal cancer
Oestrogen receptor -> breast cancer
prostrate specific antigen -> Prostate cancer

26
Q

Examples of biomarkers present when someone might develop cancer

A 
Kras -> Colorectal cancer 
Braf -> Melanoma 
EGFR -> Lung cancer 
PD-L1 -> Lung cancer 
Her2 -> breast cancer and gastric cancer
27
Q

What happens to allow for the spread of cancer?

A

Degradation of the tumour matrix by proteolytic enzymes.

28
Q

What are the two types of cancer spread?

A

Invasion (spread to an area immediately next to the cancer)

metastasis (spread to a different part of the body)

29
Q

Where are the common sites of cancer spread?

A

Bone
Brain
Liver
lungs

30
Q

Where are unusual sites for cancer spread?

A

Kidneys

Heart

31
Q

What is EMT?

A

The process by which cells become independent.

32
Q

What are the different methods of cancer spread?

A

Local spread (Invasion). Invasion into neighbouring connective, lymph, blood vessels.
Lymphatic spread. Invasion in to the lymphatics of lymph nodes.
Blood spread. Invasion into blood vessels allowing invasion into other tissues.
trans-coelomic spread. From the local spread tumours spread across body cavities.

33
Q

Describe the process of metastasis

A

Invasion
Intravasation (Entry to lymphatics, blood etc)
Transport
Extraversion (Entry into tissue)
Colonisation (Can metastasise and then lie dormant)

34
Q

What are some common metastasis pathways?

A 
Breast to bone 
Prostate to bone 
Colorectal to liver 
Ovary to Omentum/peritoneum 
Osteosarcomas to lungs
35
Q

How do some cancer cells hide?

A

They hijacks the immune checkpoints and alter immune responses using Sting5

36
Q

What are the effects of benign tumours?

A
  • pressure and obstruction. This causes bleeding, pain, weight loss,
37
Q

What are the effects of malignant tumours on the health of a person ?

A
  • Inappropriate hormone production i.e. ACTH or ADH
38
Q

What is the earliest change indicating malignancy?

A

Dysplasia - looked like cell disorganisation.

39
Q

What are preventative measure that can be taken?

A 
Good diet 
Exercise 
Not smoking 
Drinking within recommended units 
Drinking enough water 
Getting vaccinated 
Assess to good health care 
Attending screening
40
Q

What are the different treatment options for cancer?

A 
Surgery 
Radiotherapy 
Hormone therapy 
Chemotherapy 
Biological therapy 
Immunotherapy
41
Q

What is chemotherapy?

A

Compound targeting DNA, RNA and proteins. It aims to forces cells into apoptosis and is effects all rapidly dividing cells.
It can be IV or oral.
Often chemo is neoadjuvant (before surgery) or adjuvant (along side surgery)

42
Q

What are the three main types of chemo?

A

Alkylating agent and platinum drugs which block DNA replication
Antimetabolites which are competitive inhibitors of the S phase of cell division
Organic drugs which prevent microtubule assembly.

43
Q

What are examples of personalised systemic therapies?

A

Hormonal therapies.
Targeted therapies.
Immunotherapy.

44
Q

What are the 5Rs of radiotherapy?

A

Radiosensitivty - Are the cells receptive to radiotherapy
Repair - Will the body repair the tumour damage
Re-population - will the cell just grow back
Re-oxygenation - Cancer cells with more oxygen in them will be damaged more by radiotherapy than cells which lack oxygen
Re-assortment - Cells will be more sensitive at different points in there cell cycle. I.e. G2 and M

Foundations of Medicine (25 decks)

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