Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PoD topics > Outline of disease process > Flashcards

Outline of disease process Flashcards

1
Q

what are 4 main terms used to describe cancer?

A
  • mass
  • neoplasm
  • growth
  • tumour
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is a carcinoma?

A

disorderly growth of epithelial tissue/cells which invade adjacent tissue and spread by the lymphatics and blood vessels to other body parts (malignancy, metastasis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

are most cancers monoclonal? (arise from a single cell?)

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

where do most cancers originate from?

A

epithelial cells (only 20% originate from connective, muscle and nervous tissue)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what cancer type makes up almost a quarter of ALL cancer deaths?

A

lung cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are 6 stages of mitosis?

A
  1. interphase
  2. prophase
  3. metaphase
  4. anaphase
  5. telophase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are properties of cancer cells in terms of:

  1. contact inhibition
  2. growth factor secretion
  3. oncogene expression
  4. tumour suppressor genes
A
  1. LOSS of contact inhibition (don’t stick together well)
  2. INCREASE in growth factor secretion
  3. INCREASE in oncogene expression
  4. LOSS of tumour suppressor genes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are properties of normal cells in terms of:

  1. contact inhibition
  2. growth factor secretion
  3. oncogene expression
  4. tumour suppressor genes
A
  1. contact inhibition
  2. intermittent or co-ordinated growth factor secretion
  3. oncogene expression is rate (proto-oncogenes present instead)
  4. presence of tumour suppressor genes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the 5 stages of carcinogenesis?

A
  1. carcinogen
  2. initiation
  3. promotion
  4. tumour growth
    (pre-clinical cancer, dysplasia)
  5. progression (clinical cancer, when diagnosed), metastasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the 3 cancer initiation causes?

A
  1. chemical
  2. physical
  3. viral
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the 2 cancer promotion factors?

A
  1. growth factors

2. oncogenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are the main chemical carcinogens (cancer initiation)?

A
  1. polycyclic hydrocarbons (in soots and tars)
  2. aflatoxin (liver cancer)
  3. nitrogen mustard (leakemia cancer)
  4. alcohol and smoking (liver, head &neck, GI cancers)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are 2 main physical carcinogens?

A
  1. ionising radiation
    - dose-response relationship
    - radon source
    - risk increased by smoking
    - ventilation reduced risk
  2. mechanism (in the body)
    - chromosome translocation
    - gene amplification
    - oncogene activation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what cancer can herpes virus cause?

A

Burkitt’s lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what cancer can papillomavirus cause?

A

cervical cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what cancer can HTLV1 retrovirus cause?

A

adult T cell leukaemia/lymphoma

17
Q

what cancer can HTLV2 retrovirus cause?

A

hairy cell leukaemia

18
Q

what cancer can hepatitis B cause?

A

liver cancer

19
Q

what do oncogenes do and what are they?

A
  • they’re transforming genes
  • positive regulators of growth
  • represent a gain in function to transformed cells
20
Q

what are growth factors?

A
  • polypeptide molecules
  • regulate cell growth
  • bind to cell membrane receptors
  • stimulate activation of intracellular signal transduction pathways
21
Q

what does autocrine substance mean?

A

cell-produced substance which has an effect on the cell by which it is secreted

22
Q

what does paracrine substance mean?

A

cell-produced substance which has an effect on the adjacent cells

23
Q

what is autocrine stimulation of growth factors and oncogenes?

A
  • cell carries receptor and secretes growth factor

- cell escapes normal control mechanism

24
Q

what is paracrine stimulation of growth factors and oncogenes?

A

Growth factors acting on a cell produced locally by the cell or its immediate neighbours (travels short distances)

25
Q

what is an example of a common tumour suppressor gene?

A

p.53 (most altered gene in tumours)

26
Q

what does p.53 normally do?

A
  • tumour suppressor
  • transcriptional regulator
  • promotes DNA repair
  • apoptosis
  • differentiation
  • induced by DNA damage and hypoxia
27
Q

which stages in the cell cycle does p.53 control?

A

G1/S checkpoint

28
Q

how does the tumour invade? (order of layer it penetrates)

A
  1. invades basement membrane
  2. moves into ECM/connective tissue/ surrounding cells
  3. invades blood vessels
29
Q

what enzymes are involved in invasion and metastasis in ECM? (3)

A
  1. matrix metalloproteinases *MMPs), several subclasses e.g. gelatinases
  2. plasmin; degrades blood plasma proteins e.g. fibrin clots
  3. cathepsin
30
Q

what enzymes are involved in invasion and metastasis in cell adhesion?

A
  1. cahedrins (loss)
  2. integrins
  3. CD44
31
Q

what is angiogenesis?

A

formation of new blood vessels (key factor in maintenance and progression of malignant tumours)

32
Q

what happens to ECM during angiogenesis?

A

ECM is degraded

33
Q

what does angiogenesis allow tumours to do?

A
  • allows easier metastasis

- its own blood supply means no blood flow and nutrients

34
Q

what does VEGF do?

A
  • growth factor
  • stimulates angiogenesis
  • helps tumours grow and develop
35
Q

what does anti-VEGF antibody Avastin do? (therapeutic option)

A
  • binds to VEGF
  • prevents interaction of VEGF with receptors
  • prevents activation of downstream signalling pathways
  • vascular regression occurs
  • tumour remains dormant
36
Q

why does our immune system not recognise “foreign cancer cells”?

A

cancer cells can hide from T cells, because:
- PD1 (programmed death receptor) is present on T lymphocytes
-Ligand PDL-1 is present on tumour cells
Interaction between the two SUPPRESSES T cell action which means lymphocyte cannot identify the foreign body (inhibits immune response)

37
Q

high levels of which two proteins inhibit the immune response?

A

PD1 and PDL1

38
Q

what would happen if PD1 and PDL1 were blocked?

A

immune damage to tumours would occur

PoD topics (34 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions