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Part 4 – PM4B Ali > (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

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

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

Part 4 – PM4B Ali (19 decks)

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