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HANA Part 4 – PM4B > (SYNOPTIC) Cancer Metastases > Flashcards

(SYNOPTIC) Cancer Metastases Flashcards

1
Q

What is a metastasis?

A

Secondary involvement of cancer spreading across the body

Cells within metastases resemble the 1y tumour

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2
Q

What are the main routes of metastatic spread?

A

(1) Lymphatic system

(2) Haematogenous spread
- via blood

(3) Transcoelomic
- through body walls into abdominal/ chest cavities

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3
Q

What is the process of carbohydrate interactions in disease pathways of metastatic cancers?

A

(1) Leukocyte captures chemo-attractants
(2) Leukocyte rolls
(3) Rolling slows
(4) Leukocyte adhesion to endothelium
(5) Transmigration + release of chemo-attractants into tissue

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4
Q

What is lymphatic spread?

A

Follows lymphatic system

Lymphadenopathy

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5
Q

What is lymphadenopathy?

A

Spread + growth of cancer cells/ reactive hyperplasia

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6
Q

What is haematagenous spread?

A

Spread of metastases via circulatory system

Veins more readily invaded than arteries

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7
Q

What will a cancer metastases invasion of the inferior vena cava likely cause?

A

Lung metastases

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8
Q

What is transcoelomic spread?

A

Spread of metastases across peritoneal cavity

Often associate with fluid buildup

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9
Q

Name two types of cancer metastases that have arisen from transcoelomic spread?

A

(1) Ovarian cancer - across peritoneum

(2) Lung cancer - across pleural cavity

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10
Q

State the likely location of cancer metastases based on the location of the primary cancer.

Bladder

A
  • Bone
  • Liver
  • Lung
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11
Q

State the likely location of cancer metastases based on the location of the primary cancer.

Breast

A
  • Bone
  • Brain
  • Liver
  • Lung
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12
Q

State the likely location of cancer metastases based on the location of the primary cancer.

Colon

A
  • Liver
  • Lung
  • Peritoneum
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13
Q

State the likely location of cancer metastases based on the location of the primary cancer.

Kidney

A
  • Adrenal gland
  • Bone
  • Brain
  • Liver
  • Lung
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14
Q

State the likely location of cancer metastases based on the location of the primary cancer.

Lung

A
  • Adrenal gland
  • Bone
  • Brain
  • Liver
  • Other lung
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15
Q

State the likely location of cancer metastases based on the location of the primary cancer.

Melanoma (skin)

A
  • Bone
  • Brain
  • Liver
  • Lung
  • Skin
  • Muscle
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16
Q

State the likely location of cancer metastases based on the location of the primary cancer.

Ovary

A
  • Liver
  • Lung
  • Peritoneum
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17
Q

State the likely location of cancer metastases based on the location of the primary cancer.

Prostate

A
  • Adrenal gland
  • Liver
  • Bone
  • Lung
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18
Q

How are metastases diagnosed?

A
  • CT Scans
  • X-ray
  • Tumour markers
  • Biopsy
  • Cytology
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19
Q

What is the pharmacological symptomatic treatment of bone metastases?

A

Bisphosphonates

To reduce calcium

As bone metastases are often linked to hypercalcaemia

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20
Q

How is spinal cord compression, due to bone metastases, treated?

A

Dexamethasone with PPI cover

Radiotherapy to bone

Pain relief + laxatives

21
Q

What is the pharmacological treatment of brain metastases?

A

Dexamethasone + PPI

Often causes seizures - anti-epileptics

22
Q

What is the pharmacological treatment of lung metastases?

A

Dexamethasone + PPI

Salbutamol to open airways (if required)

May require tranexamic acid to reduce bleeding

23
Q

What is the pharmacological treatment of liver metastases for symptomatic relief?

A

Dexamethasone
- useful for pain

Drain ascites

24
Q

What is primary chemotherapy resistance?

A

Intrinsic resistance to chemotherapy, regardless of drug exposure

25
Q

What is acquired chemotherapy resistance?

A

Natural selection of tumour cells that are sensitive to chemotherapy drug die, but this does not affect the tumour as a whole

26
Q

What are some mechanisms of metastases resistance?

A
  • efficient repair to damaged DNA
  • decreased intracellular activation
  • increased intracellular breakdown
  • bypass biochemical pathways
  • overproduction of blocked enzyme
  • changes to receptor
27
Q

What is a cellular mechanism of defence, of a cancer cell, to alkylating agents?

A

Efficient repair to damaged DNA

28
Q

What is a cellular mechanism of defence, of a cancer cell, to methotrexate?

A

(1) Decreased uptake by cell
(2) Bypass biochemical pathways
(3) Gene amplification/ overproduction of blocked enzyme

29
Q

What is a cellular mechanism of defence, of a cancer cell, to doxorubicin?

A

Decreased uptake by cell

30
Q

What is a cellular mechanism of defence, of a cancer cell, to vinca alkaloids?

A

Increased drug efflux

31
Q

What is a cellular mechanism of defence, of a cancer cell, to anthracyclines?

A

Increased drug efflux

32
Q

What is a cellular mechanism of defence, of a cancer cell, to 5-fluorouracil?

A

Decreased intracellular activation

33
Q

What is a cellular mechanism of defence, of a cancer cell, to cytarabine?

A

Increased intracellular breakdown

Increased intracellular breakdown is a cellular resistance mechanism in which cells increase the rate of breakdown or metabolism of a drug, thereby reducing its concentration and effectiveness.

34
Q

What is an oncogene?

A

Gene that gains function when mutated

35
Q

What is a tumour suppression gene?

A

Gene that loses function when mutated

36
Q

What is EGFR, with regard to cancer?

A

Oncogene

37
Q

What does mutated EGFR do, with regard to cancer?

A

Promotion of angiogenesis

38
Q

What is p53?

A

Tumour suppressor gene

Mutated p53 suppresses apoptosis

39
Q

What is PGP?

A

p-glycoprotein

Increases drug efflux from a cell

40
Q

What does upregulation of MDR1 gene do?

A

Codes for PGP

Indirectly increases drug efflux from a cell

41
Q

What is the MoA of cisplatin?

A

Forms crosslinks with purine bases on DNA

Interferes with DNA repair mechanisms

Induces apoptosis

42
Q

Which receptor influences cisplatin uptake in a cell?

A

CTR1

43
Q

What is 5-fluorouracil?

A

Antimetabolite chemotherapy drug

Metabolites inhibit thymidylate synthetase
- stops DNA synthesis

44
Q

How does resistance to 5-fluorouracil occur?

A

Decreased intracellular activation of 5-FU to active metabolite

45
Q

What does methotrexate inhibit?

A

DHFR

46
Q

What effect is an overexpression of DHFR likely to have on methotrexate efficacy?

A

Cancer cell resistance to methotrexate

47
Q

With regard to chemotherapy, what is FEC?

A

3 complementary chemotherapy drugs

F - Fluorouracil

  • inhibits thymidylate synthetase
  • stops DNA synthesis

E - Epirubicin
- forms a complex with DNA

C - Cyclophosphamide
- forms DNA + RNA crosslinks

48
Q

What is chemotaxis

A

Chemotaxis, the process by which leukocytes are attracted to the site of cancer cells and release chemokines, involves various molecular interactions, including carbohydrate interactions. Carbohydrates are complex molecules composed of sugars and are present on the surface of cancer cells. These molecules can interact with other molecules, such as lectins, which are proteins that can bind to specific carbohydrate structures.

Lectins are present on the surface of leukocytes and are involved in the recognition and binding of carbohydrates on cancer cells. The binding of lectins to cancer cell carbohydrates can activate signaling pathways that lead to the recruitment of immune cells to the site of the tumor. This process is considered a carbohydrate interaction since it involves the recognition and binding of carbohydrates by proteins.

Chemotherapy drugs can also interact with carbohydrates on cancer cells. For example, some chemotherapy drugs are designed to target specific carbohydrate structures that are overexpressed on the surface of cancer cells. These drugs can bind to these carbohydrates and selectively kill cancer cells while sparing normal cells.

In summary, the interactions between carbohydrates on cancer cells and other molecules, such as lectins and chemotherapy drugs, play an important role in the process of chemotaxis and the targeting of cancer cells.

HANA Part 4 – PM4B (28 decks)

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