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Immunology + Pathology > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

What does neoplasm mean

A

‘new growth’

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2
Q

What is a tumour

A

Neoplasm
Abnormal mass of tissue
Growth is unco-ordinated and exceeds that of normal tissues
Persists after removal of the stimuli that initiated the change

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3
Q

In what tissue do neoplasms usually occur

A

Epithelial – lining/covering/glandular tissue ​

Connective tissue​

Other tissues

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4
Q

What are the types of tumours

A

Benign
Malignant

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5
Q

What are the differences between the growth of benign and malugnant tumours

A

BENIGN
-expansion
-may be encapsulated
-localised
-slow

MALIGNANT
-Invasion/Infiltration
-No capsule
-matastasis (outwith normal area)
-rapid variable

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6
Q

What are the clinical effects of benign tumours

A

Lump/pressure/obstruction depending on site and size
+/- hormone secretion
Treates by local excision

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7
Q

What are the possible clinical effects of a malignant tumour

A

-Local pressure, infiltration and destruction, distant metastasis
-+/- hormone secretion
-local excision and chemotherapy or radiation if metastasis presents

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8
Q

What are the epithelium origins of both benign and malignant epithelial tumours

A

BENIGN
squamous epithelium - papilloma
Glandular epithelium - adenoma

MALIGNANT
squamous epithelium - squamous cell carcinoma
Glandular epithelium - adenocarcinoma

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9
Q

How do we name tissues originating in the connective tissue

A

Smooth = Leiomyoma - Leiomyosarcoma

Fibrous = Fibroma - Fibrosarcoma​

Bone = Osteoma - Osteosarcoma​

Cartilage = Chondroma - Chondrosarcoma​

Fat = Lipoma - Liposarcoma​

Blood vessel = Angioma - Angiosarcoma

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10
Q

What causes papilloma

A

Variety of HPV (16, 18)

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11
Q

What coes carcinoma indicate

A

Epithelial tumour

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12
Q

Where do lymphoma and leukaemia originate

A

Lymphoid and haemopoietic

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13
Q

What tumours are found in melanocytes

A

naevus (mole)
melanoma

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14
Q

What tumours could be found within germ cells

A

Benign teratoma
Malignant teratoma

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15
Q

What is a carcinogen

A

Any substance or agent with the potential to cause cancer

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16
Q

What are some chemical carcinogens

A

Smoking polycyclic hydrocarbons including tars
Diet, drugs, alcohol
Asbestos

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17
Q

What are the two stages of chemical carcinogenesis

A
  1. Initiation – permanent DNA damage (mutations)​
  2. Promotion – agent promotes proliferation
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18
Q

What is the latent period

A

Time from promotion to clinical tumour

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19
Q

What is involved in the initiation step of carcinogenesis

A

When a carcinogen induces a genetic change resulting in a neoplastic potential

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20
Q

What is promotion and progression of carcinogenesis

A

Promotion: Another factor stimulates the initiated cell for division. (clonal proliferation). Does not act on non-initiated cells.​

Progression; Additional mutations resulting in malignancy

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21
Q

What are examples of physical carcinogenesis

A

Ionising radiation​

damages DNA, causing mutations​

radioactive metals and gases ​

radium - bone and bone marrow tumours

Ultraviolet light

Damages DNA
skin cancer

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22
Q

What makes a tissue sensitive to radiation

A

The speed at which cells are renewed (more rapid, more sensitive)

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23
Q

List the tissues from most to least sensitive to radiation

A

embryonic tissues​

haematopoietic organs (spleen, bone marrow)

gonads ​

epidermis​

intestinal mucous membranes (variable) ​

connective tissue​

muscle tissue and nerve tissue

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24
Q

What are the classifications of viruses

A

DNA viruses ​
-more common​
-viral DNA inserted into host DNA​

RNA viruses​
-reverse transcribed and then inserted​

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25
Q

What viruses causes tumours

A

Epstein-Barr virus - Burkitt’s lymphoma
nasopharyngeal carcinoma

Hepatitis B/C - hepatocellular carcinoma

Human papillomavirus - cervical and oropharyngeal carcinoma

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26
Q

What is the epidemiology of cancer

A

20% of deaths​

2nd most frequent cause of death​

30% of population will develop cancer​

highest in elderly​

type​
90% carcinoma​
10% lymphoma or sarcoma (more in young)

27
Q

What is the most common form of cancer

A

Carcinoma

28
Q

What is the aetiology of oral cancer

A

multifactorial
tobacco - smoking or smokeless tobacco​
betel quid (chewing habits)​
alcohol​
diet and nutrition​
oral hygiene​
viruses HPV EBV HHV-8​
Immunodeficiency​
Socioeconomic factors​
GORD

29
Q

What is leukoplakia

A

White patch that cannot be rubbed off or attributed to any other cause (oral cancer)

30
Q

Why is it important to identify dysplasia and get it checked

A

Tissue that shows dysplasia:
HAS THE POTENTIAL TO BECOME MALIGNANT​

Abnormality confined to epithelium; underlying tissue not affected.

Not all become malignant-may regress.​

Dysplasia (histopathology) is the gold standard for assessing this (at present)​

31
Q

What epithelial tissues does dysplasia affect

A

Squamous eg. oral, cervix - the basis of cervical screening ​

Glandular eg Barrett’s oesophagus, colonic polyps​

Transitional eg bladder

32
Q

What are the accelerator genes in carcinogenesis

A

Oncogenes

33
Q

Which genes act as the brakes

A

Tumour suppressor genes

34
Q

What is an epigenetic mutation

A

No change to the DNA itself
Groups attach to the DNA and influence expression of the genes ex silence or increase activity

35
Q

What do oncogenes do

A

Regulate cell division

36
Q

What are the proteins that oncogenes code for called

A

Oncoproteins

37
Q

What do oncogenes do to accelarate uncontrolled division

A

tight regulation may be lost mutation​
-increases activity of product​

excess normal product​
-duplication of the gene ​
-viral product​

enhanced transcription ​
-translocation​
-chromosome rearrangement

38
Q

What do tumour suppressor genes do

A

Act to inhibit cell division and suppress growth

39
Q

How does TP53 act in response to damages DNA

A

stops the cell cycle to allow DNA repair​

apoptosis (if repair not possible)​

40
Q

What gene is often inactivated in cancer

A

TP53 - mutation/deletion

41
Q

What is the two hit hypothesis

A

Oncogene - 1 cell deleted
Tumour suppressor - both must be deleted
Before the cell begins to become malignant

42
Q

At what point does cell division stop and DNA checked

A

Restriction points

43
Q

How many cases of head and neck cancer show deletion or mutation of the TP53 gene

A

50%

44
Q

What are some inherited cancer syndromes

A

Retinoblastoma
Some colon cancers

45
Q

What causes familial cancer

A

family clusters​

gene(s) and pattern of inheritance not clear

-Breast, ovary, colon

46
Q

What are the modes of spread of cancer

A

local spread​

lymphatic spread​

blood spread (haematogenous)​

transcoelomic spread​

Intraepithelial spread ( Paget’s disease of the breast)

47
Q

What is metastasis

A

spread of the malignant cells to distant organs forming secondary tumours​

48
Q

What are the patterns of spread of sarcomas and carcinomas

A

carcinomas​
-lymphatic​
-blood (often later)​

sarcomas​
-blood (lymphatic spread rare)​

predictable patterns of spread​
-lung to local nodes, liver, bone and brain​
-tongue to neck nodes, later lung and spine​

49
Q

What are the 6 hallmarks of cancer

A

Evading apoptosis
Insensitivity to anti-growth signals
Self-sufficiency in growth signals
Sustained angiogenesis
Tissue invasion & metastasis
Limitless replicative potential

50
Q

What does the grading of a tumour mean

A

Biological nature of the tumour
(hitsopathology)

51
Q

What is the stage of a tumour

A

Extent of spread

52
Q

How can we determine the grade of a tumour

A

Histological assessment of :​

Invasion into underlying tissue​

Cellular atypia : abnormal mitotic activity, nuclear pleomorphism, differentiation, necrosis​

Various methods​
-numerical grades (1,2,3 etc)​
-low, intermediate, high​
-degree of differentiation (squamous cell carcinoma

53
Q

What is staging

A

The extent or severity of a person’s cancer

54
Q

How can staging be determined

A

Physical exams, imaging procedures, laboratory tests, pathology and surgical reports - determine staging​

55
Q

What staging system is used for oral cancer

A

TNM
Tumour size
Lymph node involvement
Presence of metastases

56
Q

What is the immune response to tumours

A

Immune surveillance. ​

Can suppress or enhance carcinogenesis

Elimination - equilibrium - escape

57
Q

How can the immune system recognise tumour cells

A

Products of mutated genes​

Overexpressed proteins (tyrosinase)​

Viral proteins (HPV,EBV)​

Oncofetal antigens (carcinoembryonic antigen)

58
Q

What is the elimination response

A

Cell mediated immune response​

-Cytotoxic T-lymphocytes (CD8+)​
-Natural killer cells. First line of defence against tumour cells.​
-Macrophages. Mechanisms similar to anti-microbial killing.

59
Q

How can tumour cells evade the immune response

A

Cells may acquire molecular changes such as:​
-Alter tumour antigen expression regularly, Lack of T-cell recognition​
-Activation of immunoregulatory pathways leading to T-cell unresponsiveness and apoptosis.​
-Immunosuppressive factors eg. cytokines (TGF-β). Inhibit T-cell response​

60
Q

What is immunotherapy

A

Use the patient’s own immune response to control and destroy malignant cells

61
Q

What are the methods of immunotherapy

A

-Active immunisation.(HPV, Hep B)​
-Reversal of immunosuppression​
-Adopted cell transfer (ACT)
Tumour- infiltrating lymphocytes (TILs)​

CAR T-cell therapy- haematological malignancies​
-Strengthening natural immune responses-research still needed.​

62
Q

What is the equilibrium stage

A

Cancer cells evade detection and lie dormount in the body for a period of time until escape of the immune system due to activation

63
Q

What are the 3 Es

A

Elimination
Equilibrium
Escape

Immunology + Pathology (11 decks)

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