The behaviour of Tumours Flashcards

1
Q

whats the difference between benign and malignant

A
Benign 
-	Slow growing 
-	Well circumscribed borders, encapsulated, spherical and oval 
-	Well differentiated 
-	Low mitotic rate
-	Non invasive (basement membrane is not breached) 
-	No metastasis 
-	Uniethal 
-	No necrosis 
Malignat 
-	Rapidly growing 
-	Non encapsulated and irregular shapes
-	Poorly differentiated
-	High mitotic rate
-	Invasive – basement membrane is breached
-	May metastasise
-	Lethal 
-	Necrosis; reduces apoptosis
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2
Q

Describe Knudsons two hit hypothesis

A
  • He observed that in inherited retinoblastoma compared to sporadic disease
  • Occurred at an earlier age, children often had tumours in both eyes
  • Suggested susceptibility he suggested multiple hits necessary to cause cancer
  • A mutation in both alleles of a tumour suppressor gene is required as a single functional tumour suppressor gene is usually sufficient for normal function
    This can occur in two ways
  • In sporadic cancer – 2 acquired mutations, 1st hit occurs mutation in one allele and 2nd hit occurs in 2nd allele – tumour grows at a later age as it takes time for both hits to occur
  • In hereditary cancer – mutation in one allele already and only 1 hit needed for both alleles to be mutated this is a tumour that occurs at an earlier age
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3
Q

describe the histology of cancer cells

A
  • Lots of cells undergoing cell division
  • Centre of tumour can be necrotic
  • Shedding or loss of tumour cells from outside
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4
Q

what are the 4 reasons why patients die from cancer

A
  • metastasis
  • immunosuppression - Lymphomas and leukaemias
  • organ failure - - Tumours cause organs to fail
  • haemorrhage - - Infiltration of bone marrows
  • secondary malignancies
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5
Q

describe how metastasis kills a patient

A
  • Spreads around the body to many organs. Metastatic diseae occupies vital sites
  • Metastatic burden +1kg = death (intracranial tumours is around 100g whether benign or metastatic before death)
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6
Q

what does tumour growth rate depend upon

A
- doubling time of tumour cells
•	Doubling time – mitotic rate of tumour
•	Lengthens as tumour grows
•	30 doublings = 1 g (months to years)
•	10 more doublings = 1 kg

fraction of tumours are in the replicative pool
• May only be 20% even in rapidly growing tumours
• Tumour stem cells

rate at which tumours are
shed or lost - apoptosis and maturation

extent of differentiation of the tumour

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7
Q

desire be how metastasis occurs

A
  1. Undergo Epithelial to Mesenchymal Transitioning
  2. Breakdown of basement membrane
  3. Local invasion of ECM
  4. Tumour cells travel to vascular/lymphatic system and undergo intravasation
  5. They circulate through the body via lymph/vascular systems and undergo extravasation at a new site
  6. Undergo Mesenchymal to Epithelial Transitioning
  7. Micrometastasis forms (only a few cells)
  8. If micrometastasis cells survive in new environment they form a macrometastasis
  9. Tumour has spread from one place to another
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8
Q

what do the lymph nodes do

A
  • Drain excess interstitial fluid form the body
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9
Q

how are lymph nodes linked to cancer

A
  • Lymph nodes draining a cancerous organ are likely to drain fluid containing cancerous cells
  • Biopsy the sentinel node of a cancer when staging the cancer
  • Lymph nodes are surgically removed
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10
Q

What are the two ways that the metastatic cells can move through the body system:

A
  • haematogenous dissemination

- lymphatic dissemination

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11
Q

where does colon cancer, breast cancer and prostate cancer metasise to

A
  • advanved colon carcinoma in the liver
  • breast cancer often metastasises to the brain
  • metastatic prostate cancer at sites of a new or reactive bone formation site
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12
Q

what is an important component of the TNM staging system

A

number od nodes

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13
Q

significance of nodal metastasis in therapeutics

A
  • Overall risk of recurrence
  • Extent of nodal involvement
  • Histological grade and other considerations
  • Adjuvant therapy
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14
Q

significance of nodal metastasis

Example: breast cancer.

A

• A modified radical mastectomy removes the entire breast — including the breast tissue, skin, areola and nipple — and most of the underarm (axillary) lymph nodes which most common site for metastasis. Prevents the cancer from spreading

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15
Q

How do you tell whether a lymph node is infected or not

A

• Sentinel node biopsy - radioactive tracer and a blue dye are administered near site of tumour. Histological analysis of lymph nodes (sentinel nodes) taking up tracer and dye establish whether cancer is present.

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16
Q

what is the difference between staging and grading

A

staging is more of a prognostic measure then grades

17
Q

what is the grade of a tumour

A
  • Grade is how well diffenriated the cells in a tumour our and the measure of mitotic activity, graded 1-4, 1 is a low grade tumour with well differentiated cells whereas 4 is a high grade tumour with poor differentiated cells
18
Q

what is the stage of the tumour

A
  1. Size of the tumour
  2. Extent of growth (or spread)
    - Cancer stage refers to the size and extent (reach) of the (primary) tumour
    - Whether or not cancer cells have spread in the body
19
Q

what factors is the stage of the tumour based on

A
  • Location of the primary tumour
  • Tumour size regional lymph node involvement
  • Number of tumours present
20
Q

describe TNM staging

A

T – size of the cancer and how far it has spread into nearby tissue
N – refers to whether the cancer has spread to the lymph nodes – it can be between 0 (no lymph nodes containing cancer cells) and 3 (several lymph nodes containing cancer cells)
M – refers to whether

21
Q

how do you work out TNM staging of the tumour

A

CT scans
biopsies of sentimental lymph nodes/metastatic sites
PET scans

22
Q

describe stage 1-4

A
  • Within different cancers the criteria of staging is slightly different
  • E.g. size of tumour or number of lymph nodes involved
23
Q

what is paraneoplastic syndrome

A

A clinical syndrome not caused by the direct effect of a cancer mass they accompany malignant disease
Vary in functional impact and clinical presentations

24
Q

How do you clasffy paraneoplastic

A
  • Endocrine
  • Neurological
  • Musculoskeletal/Dermatological
  • Haematological
25
Q

What causes paraneoplastic tumours

A
  • Arise from tumors secretion of susbtances which interfere with normal metabolic pathways:
  • Hormones
  • Peptides
  • Cytokines
26
Q

How are tumours graded

A
  • Grade 1 - cancer cells look similar to the original normal cells and are growing slowly
  • Grade 2 - cancer cells look unlike normal cells and are growing faster than normal
  • Grade 3 - cancer cells look very abnormal and growing very quickly
  • Grade 4 (Anaplastic) – no differentiation at all
27
Q

describe endocrine paraneoplastic syndrome

A

Cushing’s syndrome
- ACTH secreting tumour leads to excess cortisol release from adrenal glands
Hypoglycaemia
- C-peptide production, insulin secretion leading to hypoglycaemic states
Carcinoid syndrome
- Secretion of serotonin/bradykinin from intestinal tumours leading to flushing diarrhoea and bronchoconstriction
Thrombocytosis
- Increase in cytokines such as IL-6 casues increase In haemotologic paraneoplastic syndromes which casues thrombocytosis
Autoimmune response
- Increase in antigen and causes increase in B cells, causes increase in antibody secretion and causes increase in autoimmune response

28
Q

where do tumours come from

A

epithelium - carcinomas
mesenchyma cell - sacromas
blood cells
teratomas

29
Q

describe epithelium

A
  • Tissues lining organs
  • 85% of tumours are mesenchymal
  • These tissues are exposed to carcinogens
  • Their normal function involves a lot of proliferation
30
Q

describe mesnchyma cells

A

• Connective tissue, blood vessels, muscle, bone, cartilage, fat

31
Q

describe blood cells

A
  • Leukaemias originate from white blood cells in bone marrow

* Lymphomas originate from lymphocytes in lymph nodes

32
Q

describe teratomas

A
  • Cells from more than one germ layer
  • Many cell types found in the tumors
  • From gonadal cells