Oncology 1 Flashcards

1
Q

What is cancer?

A

A seemingly diverse range of conditions but with a common theme – ‘the persistent, purposeless proliferation’ of host cells, often (but not always) to the detriment of the host.

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2
Q

Is cancer genetic?

A

Yes, but it is rarely heritable.

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3
Q

How does cancer arise?

A

From the accumulation of mutations that eliminate the normal constraints of proliferation.
Arise from errors in mutation.
– Errors mostly genetically silent w/ no clinical repercussions.
– Some may have effects upon tumour suppressor or proto-oncogenes (genes that try to suppress cancer development and genes that go on to promote development of cancer.
Usually takes ~5-7 mutations to result in cancer.

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4
Q

What are the 6 enabling characteristics that allow cancer to flourish?

A
  • Evading apoptosis.
  • Self-sufficiency in growth signals.
  • Insensitivity to antigrowth signals.
  • Tissue invasion and metastasis.
  • Limitless replicative potential.
  • Sustained angiogenesis (O2 and nutrients).
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5
Q

What are 2 key pieces of information that we want to make a neoplastic diagnosis?

A
  • What type of tumour is it? (i.e. what is the cell of origin?)
  • Is it benign or malignant?
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6
Q

For benign tumours….
1. Rate of growth is…
2. Manner of growth is…
3. Effects on adjacent tissues.
4. Surgery is…
5. Metastasis?
6. Effect on host.
7. Paraneoplastic effects.

A
  1. Slow.
  2. Expansive, well-defined boundaries.
  3. Often minimal.
  4. Potentially curative.
  5. No.
  6. Often minimal but can be life-threatening if bleeds or in a vital organ.
  7. Possible.
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7
Q

For malignant tumours…
1. Rate of growth is…
2. Manner of growth is…
3. Effects on adjacent tissues.
4. Surgery is…
5. Metastasis?
6. Effect on host.
7. Paraneoplastic effects.

A
  1. Fast.
  2. Invasive, poorly-defined limits.
  3. Often serious.
  4. Only curative if complete resection (clear margins and no metastasis).
  5. Yes.
  6. Often life-threatening.
  7. Possible.
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8
Q

Cytological feature of malignancy.

A

Cellular pleomorphism – increased variation in the size, shape and texture of cells.
Nuclear pleomorphism.
– Size increase.
– Coarse chromatin.
– Increase in nucleoli number.
– Increased nucleolar size.
– Increased mitotic figures
– Abnormal mitotic figures.

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9
Q

Levels of the effects of cancer on the patient.

A
  • Local behaviour.
  • Metastatic behaviour.
  • Paraneoplastic effects.
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10
Q

Local behaviour.

A
  • ## Malignant tumours grow by local invasion and may extend microscopically into surrounding tissues.
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11
Q

Physical clues of local invasion are: -

A

– Diffuse, indistinct boundaries.
– Fixation of the tumour in one or more planes.
– Thickening of adjacent tissue.
– Spontaneous bleeding or ulceration.

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12
Q

How can metastasis of malignant cancers occur?

A

Spread via blood
via lymphatics.
Transcoelomic e.g. across pleura.
Iatrogenic e.g. during FNA.

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13
Q

What us the most common site for development of haematogenous secondary tumours?
Other sites?

A

Lungs.
Largest tumour probably the primary.
Primary lung tumours are rarer.
Other sites include those w/ high blood flow e.g. liver, spleen and kidneys.

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14
Q

What are paraneoplastic effects of cancer?

A

Clinical signs that are the direct result of cancer upon distant organs around the body.
Arise from the production and release of biologically active substances.
Can affect distant organs.
May develop after the diagnosis of cancer OR they may be the first evidence of neoplasia.
Many can be life threatening but many can also be managed to help improve the quality of the patient’s life.

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15
Q

Examples of common categories of paraneoplastic effects.

A

Haematological.
Hyperviscosity.
Hyperhistaminaemia.
Immune-mediated.
Endocrine-related.
Pyrexia.
Cachexia.

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16
Q

Haematological paraneoplastic syndrome.

A

Changes in the counts of RBCs, WBCs and platelets can occur w/ neoplasia.
Anaemia and thrombocytopenia are the most common manifestations.
Many mechanisms for this.

17
Q

Mechanisms for paraneoplastic anaemia

A
  • Myelopthisis
    – invasion of bone marrow by neoplastic cells.
    – a non-regenerative anaemia affecting multiple cell lines.
  • Haemorrhage
    – some neoplasias can bleed e.g. splenic tumours.
    – Typically a regenerative anaemia.
  • IMHA
    – cross-reactivity between cancer cells and RBCs.
    – typically acute, severe and strongly regenerative.
  • Anaemia of chronic disease.
    – many diseases can cause anaemia of chronic disease - due to disordered iron handling?
    – generally mild and non-regenerative.
18
Q

Hyperviscosity syndrome.

A
  • Due to anything that makes the blood more ‘sludgy’.
  • E.g. increased blood cell numbers = erythrocytosis orpolycythemia.
  • Or due to the excessive production of gamma-globulins e.g. multiple myeloma.
19
Q

Hyperhistaminemia.

A
  • Some tumours can release histamine and vasoactive amines e.g. mast cell tumours.
  • Can be responsible for signs local to the tumour such as oedematous swelling, erythema and pruritis.
  • Or far away from the tumour e.g. GI ulcers.
  • Anaphylactic shock is technically possible should there be massive and sudden release of histamine from the tumour – rare!
20
Q

Immune mediated PNS.

A
  • Neoplasia can trigger variety of immune mediated diseases.
  • due to cross-reactivity between cancer cells and healthy cells.
  • e.g. IMHA, IMTP, myasthenia gravis.
21
Q

Endocrine related PNS.

A
  • Endocrine tumours and non-endocrine tumours can produce hormones or hormone-like substances.
  • Clinical signs dept. on the hormone that is being excessively produced:-
    – insulin.
    – parathyroid hormone.
    – thyroxine.
    – sex hormones
    – cortisol.
22
Q

Pyrexia.

A

Mechanism poorly understood.
Thought to be due to production of cytokines by the neoplasm.
Important to rule out and treat other causes of pyrexia that are commonly encountered in patients w/ cancer such as secondary infection.

23
Q

Cachexia.

A

Describes the loss of fat and muscle in patients w/ cancer.
Weight loss can be despite adequate nutritional intake.
Underlying mechanism unknown but thought to be due to production of cytokines by neoplastic cells.