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Transition block 1 > Pathology - neoplasia > Flashcards

Pathology - neoplasia Flashcards

1
Q

What is neoplasia?

A
  • New growth
  • Not in response to a stimulus
  • Can be benign, pre-malignant or malignant
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2
Q

What are some examples (pathology terms) of pre-cursor lesions?

A

Dysplasia, metaplasia and even hyperplasia

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3
Q

What is metaplasia and what can it lead to?

A
  • Reversible change from one mature cell type to another mature cell type
  • Metaplastic tissue is an at risk site for the development of cancer
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4
Q

What is a common metaplastic response to a noxious stimulus?

A
  • Squamous metaplasia
  • Squamous epithelium covers the skin and is very resistant to noxious stimuli so squamous metaplasia is therefore commonly encountered in response to injury e.g. the lung bronchial epithelium is not good with thermal injury so turns to squamous epithelium
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5
Q

When might squamous metaplasia occur in the bladder?

A

Usually transitional epithelium in the bladder, catheter (for example) creates inflammation so causes squamous metaplasia to occur

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6
Q

What is dysplasia?

A
  • Disordered growth
  • Growth is not in response to a stimulus
  • No invasion i.e. growth beyond BM
  • Often graded - low grade most normal, high grade most abnormal and closest to becoming cancer
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7
Q

What is carcinoma in situ?

A
  • Dysplasia affecting the whole of the epithelium
  • Last stage before becoming invasive
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8
Q

What are Weinberg’s hallmarks of cancer?

A
  1. Increased growth signals
  2. Remove growth suppression
  3. Achieve apoptosis
  4. Achieve immortality
  5. Become invasive
  6. Make your own blood supply (angiogenesis)
  7. Loss of DNA repair
  8. Avoid immune detection
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9
Q

What are some examples of autosomal dominant genes that cause cancer?

A
  • RB mutation - retinoblastoma in children
  • APC gene - familial adenomatous polyposis (FAP)
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10
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 are at an increased risk
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11
Q

What do initiators do?

A

Long lasting genetic damage, no sufficient to cause cancer, must be followed by a promotor

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12
Q

What do promoters do?

A

Require initiators to have caused damage, time period can vary after initiation

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13
Q

What cancer types is smoking associated with?

A

Lung cancer (SCLC), head and neck cancers, bladder cancers and cervical cancer

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14
Q

What type of cancer are aflatoxins associated with and where can they be found?

A
  • Liver cancers
  • Found in fungus on peanuts
  • Associated with p53 mutations
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15
Q

What type of cancer are beta naphthylines associated with and where can they be found?

A
  • Bladder cancers
  • Found in dye
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16
Q

What is xeroderma pigmentosa caused by?

A

Genetic defect in NER (nucleotide excision repair) and patients suffer from numerous skin cancers

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17
Q

What type of cancers do radiation increase the risk of?

A

Leukaemias and thyroid cancers

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18
Q

What tumours are associated with EBV?

A

Burkitt lymphoma, B-cell lymphomas, Hodgkin lymphomas, nasopharyngeal carcinoma

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19
Q

Why can obesity cause cancer?

A
  • Hyperplasia in endometrium
  • Cholesterol analogous to oestrogen
  • Increases risk of renal cell carcinoma
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20
Q

What are the 3 types of growth receptor involved in cancer growth?

A
  1. Receptors with intrinsic tyrosine kinase activity
  2. 7 transmembrane G protein-coupled receptors
  3. Receptors without intrinsic tyrosine kinase activity
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21
Q

What is Myc protein?

A

A nuclear transcription factor that promotes growth - DNA replication etc.

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22
Q

What types of cancer is a Myc protein mutation seen in?

A
  • Common in lymphoma, neuroblastoma, SCLC
  • Burkitt lymphoma t(8;14) - Myc translocation
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23
Q

What is the most commonly mutated kinase in cancer?

A
  • PI3K
  • Targeted in haematological malignancies
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24
Q

What do tumour suppressors do and how do they play a role in cancer?

A
  • Stop growth of cells e.g. p53
  • Cells with malignant ambitions must remove them to survive and proliferate
25
Q

What is p53 and what is its function?

A
  • Tumour suppressor gene - most commonly mutated protein across all cancers
  • Causes cell cycle arrest - senses DNA anomaly at G1 and pauses cell cycle.
  • If the DNA is repaired it restarts the cell cycle, if not it initiates apoptosis
  • It also increases levels of p21 which is a CDK inhibitor
26
Q

VHL is another tumour suppressor, what is its role in cancer?

A
  • Von-Hippel Lindau
  • Causes renal cancers when defective
  • Loss of VHL increases level of angiogenic growth factors
27
Q

What does PTEN do?

A
  • Increases transcription of p27 which blocks CDKs and cell cycle progression - without PTEN and therefore p27, cells can proliferate uncontrollably
  • Inhibits PI3K pathway
28
Q

How do cancer cells acquire unlimited replicative potential?

A

There is often a mutation that reactivates telomerase - telomerase renews the length of telomeres

29
Q

What is an example of an anti-apoptotic molecule?

A
  • Bcl-2
  • Common in follicular lymphoma, translocation t(14;18), switches on Bcl-2, no cell suicide
30
Q

How do cancer cells cause angiogenesis?

A
  • VEGF - vascular endothelial growth factor
  • Useful target for treatment
31
Q

What does BRCA gene mutation cause?

A
  • Breast, ovarian and pancreatic tumours
  • Complex roles in ER and AR regulation
  • Also has a role in DNA repair and cell cycle arrest at G1/S phase
32
Q

What are mismatch repair proteins and what can a mutation in these cause?

A
  • Family of proteins responsible for identifying faults in the code - mismatched sequences
  • Abnormal in Lynch syndrome, commonly develop colorectal carcinomas
33
Q

What is Lynch syndrome?

A
  • 3% of all colorectal cancers
  • Microsatellite instability
34
Q

What does lineage promiscuity mean?

A
  • Given the faulty repair mechanism and lack of apoptosis each daughter cell develops new mutations with each division and so on
  • Sub-clones and sub-clones
  • Not all sub-clones will possess the ability to become malignant
35
Q

Why are sub-clones important in treatment?

A
  • Important concept in treatment resistance
  • Chemotherapy and targeted therapies may work against certain but not all clones
  • Recurrence occurs when a clone has a survival advantage that means it isn’t effected by a specific treatment
36
Q

What does an encapsulated lesion suggest about its pathology?

A
  • Forming a capsule takes time so suggests that the lesion is slow growing
  • Slow growing lesions are usually benign
37
Q

What is the difference between a homogenos and heterogenous lesion macroscopically?

A
  • Homogenous - cut surface is uniform, one area looks the same as another
  • Heterogenous - different areas, haemorrhage, necrosis
38
Q

What is differentiation?

A

All cells originate from a stem cell, receive various signals to mature into a specific cell type with a specific function

39
Q

What is the difference between a well differentiated and a poorly differentiated cell?

A
  • Well = look more like what they should look like (low grade)
  • Poorly = difficult to tell what the cell of origin is (high grade)
40
Q

What is cancer of the epithelium called?

A

Carcinomas

41
Q

What is cancer of glandular tissue called?

A

Adenoma or adneocarcinoma

42
Q

What is cancer of squamous tissue called?

A

Papilloma vs squamous cell carcinoma

43
Q

What is cancer of bladder tissue called?

A

Transitional cell carcinoma or urothelial cell carcinoma

44
Q

What are malignant lesions of mesenchymal tissue called?

A

Sarcomas e.g. bone, cartilage, fat, smooth muscle, skeletal muscle

45
Q

What is a cancer of fat called if it is benign and malignant respectively?

A
  • Benign = lipoma
  • Malignant = liposarcoma
46
Q

What is a cancer of bone called if it is benign and malignant respectively?

A
  • Benign = osteoma
  • Malignant = osteosarcoma
47
Q

What is a cancer of cartilage called if it is benign and malignant respectively?

A
  • Benign = enchondroma
  • Malignant = chondrosarcoma
48
Q

What is a cancer of skeletal muscle called if it is benign and malignant respectively?

A
  • Benign = rhabdomyoma
  • Malignant = rhabdomyosarcoma
49
Q

What is a cancer of smooth muscle called if it is benign and malignant respectively?

A
  • Benign = leiomyoma
  • Malignant = leiomyosarcoma
50
Q

What is a cancer of nerves called if it is benign and malignant respectively?

A
  • Benign = neurofibroma, schwannoma
  • Malignant = malignant peripheral nerve sheath tumour
51
Q

What is a cancer of blood vessels called if it is benign and malignant respectively?

A
  • Benign = haemoangioma
  • Malignant = angiosarcoma, Kaposi’s sarcoma
52
Q

What is different about blood cancers?

A
  • ALL malignant
  • Different rules because they’re already systemic e.g. leukaemia and lymphoma
53
Q

What genetic techniques are used in investigating cancer?

A

Karyotype, cytogenetics (FISH), molecular genetics

54
Q

What cancers tend to present early?

A
  • Vocal cord - change in voice occurs early
  • Skin cancers - you can see them
  • Breast and testicular cancer - self-examination
55
Q

What can obstruction to the bladder and kidneys cause?

A

Can’t drain urine, backwards pressure, kidney stops function, build up of toxins and abnormal electrolyte balance

56
Q

What is weight loss due to cancer known as and why does it occur?

A
  • Cachexia
  • Tumour uses up a lot of energy and can produce all sorts of molecules that result in increased metabolism throughout the body, mainly TNF
57
Q

What does paraneoplastic mean and what are some paraneoplastic changes?

A
  • Paraneoplastic - not directly related to the tumour
  • Tumours can produce hormones, can result in electrolyte disturbances (high calcium, low sodium), osteoarthropathy, unusual neurological symptoms
58
Q

What are some common paraneoplastic syndromes?

A
  • Skin rash
  • Fever

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