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MCD Cell Pathology > 3 Cancer > Flashcards

3 Cancer Flashcards

1
Q

*Q: Define cancer.

A

A: a disease caused by an uncontrolled division of abnormal cells in a part of the body

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2
Q

*Q: Define neoplasia. Can be?

A

A: the presence or formation of new, abnormal growth of tissue = uncoordinated and persists after the cessation of the stimuli that initiated the change

benign or malignant

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3
Q

*Q: Define metastasis.

A

A: the development of secondary malignant growths at a distance from a primary site of cancer

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4
Q

*Q: Define carcinogen. Name 6 classes.

A

A: a substance capable of causing cancer in living tissue (causes genetic damage)

chemicals
viruses
ionising/non ionising radiation
hormones
bacteria/fungi/parasites
miscellaneous
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5
Q

*Q: What is the aim of cancer screening?

A

A: Detect cancer either at pre-invasive stage/early

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6
Q

*Q: What will make a cancer screening programme successful? (4)

A

A:Reliable prediction of tumour behaviour

Treatment available

Target population has enough people to justify expense

Cost-effective and reliable screening tool

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7
Q

Q: Most common cancers in men? Women?

A

A: Prostate W: breast

Lung

Colon/Rectum

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8
Q

*Q: How does cancer link to age? (2)

A

A: Incidence of cancer worldwide increasing as people are living for longer

in general, higher incidence >55 yrs (to get cancer, need to develop DNA defects which takes time)

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9
Q

*Q: How does cancer link to geography? (2)

A

A: diff places have diff levels of cancer incidence

stomach cancer is higher in japan than US
colon cancer is lower in japan that US
-both due to diets

melanoma higher in NZ and australia than scandinavia
-people that live there are white and not used to it

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10
Q

*Q: How does cancer link to genetics? (3 mechanisms for hereditary genetics and examples).

A

A: Autosomal dominant - inherited cancer syndrome where a single mutant gene is responsible eg retinoblastoma, FAP

Autosomal Recessive - inherited defective DNA repair mechanisms eg xeroderma

Unknown/(mixed multiple factors) - Familial Cancer Syndromes eg BRCA, breast

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11
Q

*Q: What can X ray radiation increase the chances of?

A

A: leukaemia and solid tumours

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12
Q

*Q: What are the 4 classes of regulatory genes? (targets for DNA damage)

A

A: Oncogenes - growth promoting genes

Tumour Suppressor Genes - growth inhibiting genes

Apoptosis - genes regulating programmed cell death

DNA Repair Genes - prevent mutations in normal cycle

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13
Q

*Q: What are the clinical effects of a tumour? (4)

A

A: benign and malignant can both affect

  • Anxiety about lumps and bumps
  • Related to location - pressure, ulceration, infection, bleeding
  • Metabolic cancer cachexia (reduced fat and muscle bulk, increased basal metabolic rate) mediated by tumour necrosis factor (TNF)
  • Paraneoplastic syndromes which are seen as bizarre but have an underlying cancer cause eg suddenly high calcium levels or increased clotting risk
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14
Q

*Q: What allows Grading of cancer? What does staging give you? (2) What is it based on? (3) Uses? (3) Is staging or grading more useful?

A

A: Histological - low or high grade- Based on the degree of differentiation -> allows grading

STAGING 1. gives prognosis to patient 2. defines therapy needed

size, spread to regional lymph nodes, metastases presence

combines clinical, radiological and pathological findings

staging

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15
Q

Q: How do you diagnose/test for cancer presence? (2) Confirmation? (2) Metastasise? (3)

A

A: Tumour markers and blood serology used to test for the presence of cancer

Biopsy or Fine Needle Aspiration (FNA) is used to extract a bit of tissue or fluid to test to confirm the presence of cancer

To see if the cancer has metastasised imagine will be used:
CT
MRI
PET

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16
Q

*Q: What are the 2 basic components of tumours?

A

A: parenchyma= proliferating neoplastic cells (the functional tissue of an organ)

stroma= the supportive tissue of an epithelial organ, tumour, gonad, etc., consisting of connective tissues and blood vessels (holds it together)

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17
Q

*Q: Describe the name of a benign tumour.

A

A: suffix: oma

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18
Q

*Q: Describe the name of a malignant tumour. (2)

A

A: carcinoma for perenchymal tumours

sarcoma for stromal tumours

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19
Q

Q: Describe the name of a tumour from:

glandular tissue.
ovaries.
epidermis.
mucous membrane.

A

A: adenoma (glandular tissue)

cystadenoma (ovaries)
papilloma (epidermis)
polyp (mucous membrane)

20
Q

Q: Describe the name of a tumour from stromal tissue:

fat.
fibrous/ connective tissue.
blood vessels.
smooth muscle.
bone.
cartilage.
A

A: lipoma (fat tissue)

fibroma (fibrous or connective tissue)
angioma (blood vessels)
leiomyoma (smooth muscle)
osteoma (bone)
chondroma (cartilage)
21
Q

*Q: How do benign and malignant tumours differ in terms of differentiation/anaplasia?

A

A: - Malignant tumours show anaplasia (very disorganised and doesn’t resemble tissue it came from/ complete lack of differentiation)
- Benign tumour cells are relatively well differentiated (can recognise which tissue it came from)

22
Q

*Q: How do benign and malignant tumours differ in terms of growth rate?

A

A: - Benign tumour are slower growing than malignant tumours
-malignant tumours have rapid turnover

23
Q

*Q: How do benign and malignant tumours differ in terms of local invasion?

A

A: - Benign tumours don’t tend to infiltrate the basal lamina (can cause pressure effects)-> remain localised
- Malignant tumours infiltrate the basal lamina

24
Q

*Q: How do benign and malignant tumours differ in terms of metastasises?

A

A: - Benign tumours don’t metastasise (v rare)

25
Q

*Q: What are the 4 mechanisms of invasion/metastasis? Which method does breast cancer like? Which is the most common route for sarcoma and carcinomas?

A

A: lymphatic (spread through lymph channels- breast cancer likes this method)- carcinoma initally

haematogenous (through blood stream)- sarcomas and carcinomas later

body cavities (transcoelomic spread)

contiguous (grows continuously and spreads)

26
Q

*Q: What are the 4 factors that affect who gets cancer?

A

A: age
geography
environmental
genetics

27
Q

Q: Which cancers specifically affect young people? (3) Why?

A

A: leukaemias
neuroblastoma
wilms tumour

usually associated with very specific genetic abnormalites

28
Q

*Q: How does cancer link to the environment? (5)

A

A: UV light

diet and weight

smoking, alcohol

viruses eg HPV, HBV, EBV

29
Q

Q: What is carcinogenesis? (3)

A

A: mulistep process from normal cell to cancerours

malignancy is acquired in a step wise fashion

accumulation of successive mutations in DNA (could put up with one but not many)

30
Q

*Q: What are chemical carcinogens? Structure? Act?

A

A: =chemicals that damage DNA

no common structural features

act with or without conversion (conversion could be an enzyme or other metabolic conversation to turn non harmful chemical carcinogenic)

31
Q

Q: Who tends to be affected by oncogenic viruses? Associated with? Examples? (4)

A

A: young people

immunosuppresion

Human Papilloma Virus (HPV) for cervical cancer
Epstein–Barr virus (EBV) for Burkitt lymphoma
HBV for HCV for hepatic cancers

32
Q

Q: What’s the mechanism of oncogenic viruses?

A

A: (oncogenic RNA viral genome transcribed into DNA by E prior to incorp) oncogenic viral DNA directly incorporated int host cell DNA

alters genetics of host (functioning)

33
Q

Q: What type of radiation can cause cancer? (3)

A

A: sun, x rays, nuclear bomb fall out

ionsing= damages DNA

34
Q

Q: What can increased oestrogen exposure cause?

A

A: increased risk of breast cancer

35
Q

Q: What is a naturally occurring carcinogen for liver cancer?

A

A: aspergillus flavus (fungus)

36
Q

Q: Name 3 miscellaneous agents that cause cancer.

A

A: asbestos
vinyl chloride
metals eg nickel

37
Q

*Q: Where are oncogenes derived from? What happens when oncogenes are overactive? Name 3 examples associated with tumours.

A

A: genes regulating normal cell growth (ON SWITCH)// proto-oncogenes

too much cell growth, cancer

  • Myc - burkitt lymphoma
  • N-myc - neuroblastoma
  • CyclinD1 - mantle cell lymphoma
38
Q

*Q: What are tumour suppressor genes? When can it cause cancer? 3 examples.

A

A: OFF SWITCH

doesn’t tell oncogenes to turn off

  • Rb gene for genetically inherited retinoblastoma
  • P53 (housekeeper of genome)
  • BRCA-1 and 2 for breast cancer (are familial)
39
Q

Q: Which 2 clinical effects of a tumour are often the cause of death?

A

A: metabolic cancer cachexia

paraneoplastic syndromes

(loss of homeostatic reserve)

40
Q

Q: How can a benign tumour creating pressure be bad?

A

A: eg in brain or in any other sensitive place

41
Q

Q: Name 2 laboratory methods for cancer diagnosis. Other methods? (3)

A

A: cytology FNA (looking at cells)- freehand or ultrasound guided

histology (take bits of tissue)- biopsy

stains, markers, molecular methods eg microarrays

42
Q

Q: Why has the cervical screening programme been so successful? How successful? Describe the screening programme itself. What does the disease start as?

A

A: found a cure associated with HPV

vaccinated against it now

70% reduction in deaths over 30 yrs programme

-detectable with relatively easy low cost process

disease starts as CIN = cervical dysplasia

43
Q

*Q: Are veins or arteries penetrated more frequently during hemogenous spread of cancer? why? What are the most common sites? (2) why?

A

A: -veins, thickness of walls

-liver and lungs, lymphatic drainage

44
Q

*Q: With the lymphatic spread of cancer, what can be evoked? then?

A

A: immune response -> nodal hyperplasia

45
Q

*Q: Which gene regulates apoptosis? Overexpression? found?

A

A: bcl-2 prevents programmed cell death

overexpression= indolent growth of lymphocytes found in many low grade lymphomas

46
Q

*Q: What are the 5 major classes of chemical carcinogens?

A

A: -hydrocarbons (polycyclic aromatic ones= E action)

  • amines (aromatic ones= other metabolic conversion)
  • nitrosamines
  • azo dyes (other metabolic conversion)
  • alkylating agents (w/o converting)

MCD Cell Pathology (6 decks)

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