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Principles 2018 > Pathology part 4 > Flashcards

Pathology part 4 Flashcards

1
Q

Define cancer?

A

Uncontrolled cell proliferation and growth that can invade other tissues

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2
Q

What is a tumour?

A

Swelling
Benign or malignant
Inflammatory or foreign body

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3
Q

Define neoplasm

A

New growth not in response to stimulus

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4
Q

What can neoplasm be?

A

Benign, premalignant or malignant

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5
Q

What is neoplasm not

A

Clinician code for cancer

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6
Q

Where can neoplasm be

A

Anywhere apart from lease of eye

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7
Q

Define malignant

A

Metastatic potential

Goes beyond basement membrane of epithelium

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8
Q

Define metastases

A

Spread to other sites

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9
Q

what are the precursor legions of malignancy?

A

Dysplasia
Metaplasia
Even hyperplasia

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10
Q

What happens to bronchial epithelium in reaction to thermal/chemical injury?

A

Metaplasia to squamous epithelium from columnar

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11
Q

What kind of metaplasia occurs in the bladder?

A

Transitional epithelium to squamous as a result of inflammation from catheters

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12
Q

How can hyperplasia become autonomous?

A

No longer require stimulus

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13
Q

Why are obese people at risk of hyperplasia?

A

Steroid hormone structure is closely shared by cholesterol

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14
Q

Define dyplasia

A

Disordered growth not in response to stimulus

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15
Q

What is invasion?

A

Growth beyond the basement membrane

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16
Q

How is dysplasia graded?

A

High grade most abnormal and closer to cancer

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17
Q

What is CIS?

A

Carcinoma in situ
Dysplasia affecting the whole of the epithelium- applies to non-glandular epithelium

Last stage before becoming invasive

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18
Q

What causes cancer?

A 
Genes
Smoking 
Alcohol 
UV radiation 
Other radiation
Drugs
Infections
Obesity
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19
Q

What is a weinberg hallmark?

A

Specific genes/proteins with specific functions that enable cellular progression to malignancy

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20
Q

What is the double hit hypothesis?

A

one working gene is enough. Two faulty copies to have a functional problem. Those who have inherited one faulty copy already are at increased risk

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21
Q

How many carcinogens does smoke contain?

A

> 40

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22
Q

Where is aflatoxin found? What does it cause?

A

fungus on peanuts

p53 mutation

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23
Q

Where is beta-napththhylamine found?

A

Chemical dyes

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24
Q

Where are nitrosamines found?

A

Food preservative

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25
Q

What can arsenic cause?

A

Skin cancer

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26
Q

What are initiators?

A

long lasting genetic damage. Not sufficient to cause cancer. Must be followed by a promoter

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27
Q

What are promoters?

A

require initiators to have caused damage. Time period can vary after initiation

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28
Q

Which cancers is smoking associated with?

A

Lung cancer- small cell
Head and neck cancers
Bladder cancer
Cervical cancer- with HPV

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29
Q

What are polycyclic aromatic hydrocarbons?

A

Potent carcinogen

Can be present in animal fat from meat

Smoked meat and fish

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30
Q

Which cancers are aflatoxin associated with?

A

Liver cancer

31
Q

Where are aflatoxin cancers common?

A

China

32
Q

Which cancers are beta naphythylines associated with?

A

Bladder cancer
Conjugated in the liver with glucuronic acid and therefore not toxic for long
Human urine contains glucuronidase - bummer

33
Q

What does radiation cause?

A

Formation of pyrimidine dimers in DNA

Nucleotide excision repair (NER) is eventually overwhelmed

34
Q

What is xeroderma pigmentosa?

A

Genetic defect in NER and suffer from numerous skin cancers

35
Q

Which scans can increase cancer risk?

A

CT scans

36
Q

What is the process by which viruses cause cancer?

A

Microbial carcinogenesis

37
Q

What is the oncogene product of one of the HPV viruses?

A

E7

38
Q

What is the role of E6 oncogene?

A

Increases destruction of p53

39
Q

What is the role of E7 oncogene?

A

prevents retinoblastoma (RB) protein from acting

40
Q

What is the role of retinoblastoma?

A

Rb usually binds E2F. When free of Rb, E2F promotes transcription of DNA polymerase etc.

41
Q

What cancers is EBV implicated in?

A

Burkitt-lymphoma
B-cell lymphoma
Hodgkin lymphoma
Nasopharyngeal carcinoma

42
Q

How does chronic inflammation cause lymphomas?

A

constant lymphocyte reproduction may lead to errors in production

43
Q

What causes increased risk of hyperplasia in the endometrium

A

Obesity

CHolesterol analagous to oestrogen

44
Q

What meat container carcinogens?

A

BBQ meat

45
Q

What are sustained growth signals?

A

Signal cells to get big, grow and not stop

Avoid normal homeostatic controls

46
Q

What are the three categories of growth receptors?

A
  1. Receptors with intrinsic tyrosine kinase activity
  2. 7 transmembrane G protein-coupled receptors
  3. Receptors without intrinsic tyrosine kinase activity
47
Q

What does the EGFR overecpression cause?

A

carcinomas

48
Q

What is the BRAF mutation?

A

Mutation of RAF

Melanoma
COlorectal

49
Q

What is the RAS mutation responsible for?

A

lung
Pancreas
Colorectal
Thyroid

50
Q

What is Myc?

A

Nuclear transcription factor that promotes growth

51
Q

What is mutation of Myc common in?

A

Lymphoma, neuroblastoma, small cell cancer of the lung

52
Q

What is PI3K mutated in?

A

Haematological malignancies

53
Q

What are APC mutations?

A

One of the most common in colorectal cancer

-can occur as a germline mutation causing an inherited condition FAP and gardeners

54
Q

What is the role of tumour supressors?

A

Stop growth

Cells with malignant ambitions must remove them

55
Q

What is the most commonly mutated protein across all cancers?

A

p53

56
Q

What is the roll of p53?

A

Cell cycle arrest- senses DNA abnormalities at G1 and pauses cell cycle, increases levels of p21 which is a CDK inhibitor

inhibits phosphorylation of Rb

Induces apoptosis if DNA not repaired via BAX pathway

57
Q

What is CDK activated by?

A

Cyclins

58
Q

What is VHL?

A

Von-Hippel Lindau

Loss of VHL increases level of angiogenic growth factors

59
Q

What is the role of PTEN?

A

Increases transcription of p27

60
Q

What is the role of p27

A

Blocks CDKs and cell cycle progression

61
Q

What does CDK so?

A

Inhibits PI3K/AKT pathway we saw earlier

62
Q

What happens in malignancy to allow unlimited replication?

A

Mutation that reactivates telomerase

63
Q

What is Bcl-2

A

anti-apoptotic molecule

binds Bax/Bak to stop holes being punched in mitochondria

64
Q

What is VEGF?

A

Vascular endothelial growth factor

Up-regulated in some malignancies

65
Q

Describe BRCA?

A

Complex genes and proteins
Breast, ovarian, pancreatic tumours
Role in DNA repair and cell cycle arrest at G1/S phase

66
Q

What are mismatch repair proteins?

A

Family of proteins responsible for identifying faults in the code – mismatched sequences

67
Q

When are MRPs abnormal?

A

Lynch syndrome

commonly develop colorectal carcinomas

68
Q

How can we find faulty protein expression?

A

Immunohistochemistry

69
Q

What do we look for in immunohistochemistry?

A

frequency of mismatched sequences by analysing microsatellites – segments of repeated DNA code specific to an individual
If the microsatellites are full of errors this is called microsatellite instability and indicates the proteins aren’t working

70
Q

What is PD-L1?

A

Programmed death ligand 1

Inhibits T-cell proliferation

Tumour express this to avoid immune system

71
Q

How do cancers chew up surrounding tissues?

A

Increase expression of matrix metalloproteinases (MMP)

Cells can then chew there way through surrounding tissues and blood vessels

72
Q

Is cancer clonal?

A

No
Single parent yes
Identical children no

73
Q

What is the most important concept in treatment resistance?

A

Sub-clones- chemotherapy and targeted therapy may work against certain but not all clones

Principles 2018 (34 decks)

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