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GI - Y2 > L11 - Development of Neoplasia > Flashcards

L11 - Development of Neoplasia Flashcards

1
Q

What is the effect of NSAIDs on mucosal tissue?

A

NSAIDs (aspirin) deplete mucosal prostaglandins by inhibiting the cyclo-oxygenase (COX) pathway.
Leads to mucosal damage.

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2
Q

Describe intestinal gastric cancer?

A

Differentiated, well formed glandular structure.
Tumours are polyploid or ulcerating lesions with rolled edges.
- more likely to involve distal stomach and occur in patients with atrophic gastritis

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3
Q

Anal fissure

A

Tear in vertical axis of the squamous lining of the anal canal between the anal verge and the dentate line.

Symptoms: pain during / after defecation

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4
Q

Define ‘adenocarcinoma sequence’

A

Step wise pattern of mutational activation of oncogenes (e.g. K-Ras).
And activation of tumour suppressor genes (p53)

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5
Q

Lynch syndrome

A

Hereditary non polyposis colorectal cancer

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6
Q

Cause of Hereditary non-polyposis colorectal cancer

A

Inherited mutations in genes that encode proteins responsible for deletion, excision and repair of errors that occur during DNA replication.

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7
Q

What effect may NSAIDs have on polyps in FAP patients ?

FAP - Familial Adenomatous Polyposis

A

Protective effect - may cause polyp regression.

  • Inhibition of cycloxygenase-2 , COX 2.
  • COX 2 necessary for production of prostaglandin E2.
  • Prostaglandin E2 promotes epithelial proliferation , hence no further proliferation of polyps.
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8
Q

What is the APC gene?

A

APC - Adenomatous polyposis coli

APC - controls Beta-catenin concentrations and interacts with E-Cadherin (involved in cell adhesion)

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9
Q

Wnt signaling pathways

A

Group of signal transduction pathways which begin with proteins that pass signals into a cell through cell surface receptors.

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10
Q

Describe the classic adenocarcinoma sequence?

A
  • both copies of APC gene must be functionally inactivated
  • APC key negative protein regulator of B-catenin, component of Wnt signalling
  • APC protein normally binds to and promotes degradation of B-catenin
  • loss of APC function, B-catenin accumulates, translocates into nucleus
  • forms complex with DNA bind factor TCF
  • activates transcription of genes, MYC cyclin that promotes proliferation
  • further mutations accumulate, mutations in kras that prevent growth and apoptosis.
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11
Q

State briefly factors contributing to cancer development?

A
  1. Inflammatory micro-environment
  2. Insensitivity to growth inhibitors
  3. Self-sufficient growth
  4. Limitless regeneration
  5. Sustained angiogenesis
  6. Evasion of apoptosis
  7. Tissue invasion and metastasis
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12
Q

Describe normal apoptosis

A

Programmed cell death.
Genetically regulated.
Important for development and tissue homeostasis.
No inflammatory response (unlike necrosis)

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13
Q

Briefly overview the cell cycle

A 
G1 - Duplication of cellular contents 
S1 - chromosome duplication 
G2 - cell double checks duplicated chromosomes for errors 
Mitosis 
Cytokinesis
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14
Q

Describe G0 phase?

A

Cell is neither dividing or preparing to divide.

Cells exist in a quiescent stage.

Quiescent - state or period of inactivity or dormancy

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15
Q

Describe the correlation between altered differentiation and prognosis of tumours?

A

Well differentiated tumours - better prognosis

Poorly differentiated tumours - poorer prognosis

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16
Q

Describe invasion and metastasis of a tumour?

A
  1. Proliferation and angiogenesis of tumour
  2. Detachment / invasion into lymphatics, venules or capillaries
  3. Transport
  4. Arrest in organs
  5. Adherence to vessel wall
  6. Establishment of microenvironment
  7. Proliferatory angiogenesis
  8. Metastasis
17
Q

Describe tumour angiogenesis

A

VEGF - vascular endothelial growth factor, regulator of tumour angiogenesis.

  1. Small tumour releases angiogenic factors (VEGF)
  2. Nearby capillaries stimulated to divide and sprout.
18
Q

State briefly the colorectal cancer pathway

A
  1. Normal mucosa
  2. Early adenoma
  3. Late adenoma
  4. Carcinoma
19
Q

Describe development of colorectal cancers?

A
  • usually develop from benign polyps
20
Q

Describe familial adenomatous polyposis?

A
  • 100 to 1000 polyps throughout colon
  • Autosomal dominant
  • mutation in APC gene
21
Q

Describe HNPCC?

A

Hereditary non polyposis colorectal cancer

  • tumour more likely RHS
  • autosomal dominant
  • mutations in DNA mismatch repair genes, MSH2 & MLH1
22
Q

Describe mismatch repair?

A
  1. Error in newly synthesised strand
  2. Binding of mismatch proofreading proteins
    - MSH2, MLH1
  3. DNA scanning detects abnormalities in new DNA strand
  4. Strand removed
  5. Repairs DNA synthesis
23
Q

Briefly describe the colorectal cancer pathway?

A 
Normal mucosa to Early adenoma 
- APC 
- MLH1, MSH2 
Early adenoma to late adenoma 
- k-ras 
Late adenoma to carcinoma 
- p53
24
Q

Describe the function of K-ras gene?

A

Provides instructions for making a protein called k-ras.

Protein relays signals from outside the cell to the cell’s nucleus.
Signals instruct cell to grow and divide, differentiate.

K-ras = GTPase, hence will be turned on and off by GTP & GDP molecules.

Turned on: attaching to GTP
Turned off: bound to GDP

25
Q

How may diet influence risk of developing colorectal cancer?

A
  • leafy green vegetables are protective
  • processed red meat increases risk
  • obesity increases risk
26
Q

Colorectal cancer environmental factors

A 
Diet 
Chronic inflammation 
- ulcerative colitis 
Hormones 
- acromegaly
27
Q

Acromegaly

A

Hormonal disorder. Pituitary gland produces too much GH.

28
Q

Why do some people infected with H. Pylori develop stomach cancer?

A

H.Pylori: Gram -, urease, catalise, oxidase, spiral shaped.
- express virulence factors affecting host signalling pathway.

Superficial gastritis - atrophic gastritis - intestinal metaplasia - dysplasia - gastroadeno carcinoma

29
Q

How has H.Pylori evolved the ability to colonize the highly acidic environment found within the stomach?

A

H.Pylori metabolises urea to ammonia via urease.

Generates neutral environment enveloping the bacterium.

30
Q

Barret oesophagus

A

Healthy oesophageal epithelium replaced with metaplastic columnar cells.

Can occur as result of damage from prolonged exposure of oesophagus to refluxate of gastroesophageal reflux disease GERD.

31
Q

How does GERD lead to Barret oesophagus?

A

Erosion of oesphageal mucosa.
Inflammatory cells infiltrate.
Epithelial necrosis.
Damage believed to promote replacement of healthy oesophageal epithelium with metaplastic columnar cells.

GI - Y2 (18 decks)

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