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TUMOR PATHOLOGY Flashcards

1
Q

neoplasia

A

abnormal tissue growth and it persists even after a stimuli

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2
Q

hyperplasia

A

increase in the number of cells

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3
Q

hypertrophy

A

increase in the size of the cell

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4
Q

difference between a malignant and a benign

A

malignant is invasive while benign is non invasive

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5
Q

benign neoplasm

A

slow growing encapsulated and smooth well circumscribed.

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6
Q

atrophy

A

decrease in the organ due to the reduction of the size and or the number of cells
could be physiological or pathological .

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7
Q

arrangement of a tissue

A

the epithelium
mucosa + connective tissue
glands

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8
Q

metaplasia

A

complete change of the form of a cell that is from stratified to squamous

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9
Q

which tumor is inflammtory

A

malignant

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10
Q

characteristics of benign neoplasm

A

may compress organs
in some cases may cause pain if they are in the brain or if they compress a nerve.

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11
Q

examples of benign tumors

A

osteoma
shwannoma
angioma
fibroma
adenoma
papilloma

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12
Q

adenocarcinoma

A

invasive cancer of the glandular tissue

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13
Q

type of malignant cancer

A

Breast adenocarcinoma​

Prostate adenocarcinoma​

Lung adenocarcinoma​

Lung squamous cell carcinoma​

Colorectal adenocarcinoma​

Melanoma​

Lymphoma​
leukamia
sarcoma

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14
Q

all neoplasms are tumors

A

true

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15
Q

carcinoma and sarcoma

A

types of malignant tumors

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16
Q

apoptosis

A

regulated cell death

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17
Q

oncogenes

A

from mutated proto-oncogenes that can now cause cancer

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18
Q

physical characteristics of cancer cells

A

1.hyperchromatic that is more DNA inside
2.coarse chromatin because they are ready to divide
3.pleomorphic - they are not of the same size
4.disorganised structure.
5.highly mitotic and abnormal forms.
6.bigger nucleus

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19
Q

behaviour of cancer cells

A

have unregulated growth
loss of cohesion
there is immaturity
immortality

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20
Q

replicative immortality

A

fully functioning telomerase that keeps on adding the telomeres .
they replicate and never die

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21
Q

activation of invasion and metastasis

A

ability to invade the connective tissue and cause metastasis

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22
Q

ability of cancer cells to gain oxygen and nutrients

A

through angiogenesis
angiogenesis growth factors are switched on while inhibitors are switched off.

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23
Q

ability to resist cell death

A

apoptosis caspaces are altered

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24
Q

cancer cells effect on cellular energetics

A

they use glycolytic metabolism
there is intake of alot of nutrients with production of less ATP.

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25
Q

Ability to increase in number

A

proliferative growth factors that alters the cell cycle
the growth receptors are also altered

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26
Q

ability to evade growth suppressors

A

that is tumor suppressor genes
alteration of p53

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27
Q

some tumor cells mediate a tumor associated inflammatory response

A

yes or no

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28
Q

carcinogenic and necrosis

A

there is release of cellular contents into the interstitium
this causes an inflammatory response

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29
Q

metastasis

A

spread of cancer cells through loss of cell to cell adhesion ,
loss of cell to ECM adhesion molecules

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30
Q

metastasis methods

A

Local spread​

Lymphatic spread​

Haematogenous spread​

Trans-coelomic spread​

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31
Q

metastasis through the lymph nodes

A

invasion of the connective tissue
entry to lymphatics
travel through lymphatics
exit of the lymphatics
entry to the lymph node
growth in the lymph node

32
Q

trans - coelomic spread

A

-spread through the body cavity
in the peritoneal ; gastric , colonic , ovarian
-pleural that is the lung

33
Q

local effects of cancer

A

pain
haemorrhage
loss of function

34
Q

local effect on the brain

A

confusion
coma
seizure

35
Q

local effect of tumor on the lungs

A

dyspnoea
haemoptysis

36
Q

local effects of tumors on the liver

A

jaundice blockage of the gall bladder.
coagulopathy that is because of the blockage of the proteins that are used in coagulation.

37
Q

local effects of cancer in the colon

A

diarrhoea
constipation
haemorrhage

38
Q

local effect of the tumors on bone

A

anaemia
pain
fracture

39
Q

systemic effects of cancer

A

cachexia
DVT
paraneoplastic syndrome

40
Q

cachexia characteristics

A

weakness and wasting due to chronic illness
loss of muscle is greater and faster than fat loss.

41
Q

paraneoplastic syndrome

A

abnormal production of hormones the hormones have systemic effects.

42
Q

examples of hormone production that is altered by cancer

A

PTH
ACTH
ADH

43
Q

DVT

A

deep vein thrombosis
tumor pressing on the blood vessel makes the diameter smaller and the flow of blood is altered making the blood more stickier.

44
Q

what is pre cancer

A

dysplasia
that is disordered cell growth and doesnt involve spread

45
Q

what is neoplasma

A

Abnormal growth of cells, uncoordinated with normal tissue and continuing even after cessation of stimulus​

46
Q

wilson and junger principles of screening

A

look at the photo

47
Q

molecules involved in signal trasduction in a cell

A

the receptor for growth factor
the growth factors as ligands
the amplification system that is the messenger molecule and other molecules involved.

48
Q

example of a signal transduction molecule

A

BRAF

49
Q

cell cycle inhibitors

A

p53
retinoblastoma

50
Q

factors that cause inhibition of a molecule

A

change in the structure
change in the molecule that is attached

51
Q

retinoblasma

A

normal molecule that causes inhibition past the checkpoint
addition of a phosphate group by CDKs causes a change that inhibits Rb form being an inhibitor.

52
Q

longest phase of the cell cycle

A

G1 phase

53
Q

how does growth factor cause progression past the G1 phase restrictor

A

the growth factors eg amino acid levels and glucose levels.

54
Q

role of the growth factors

A

they ellicit a pathway that cause the amplification of molecules leading to phosphorylation of the RB molecule.

55
Q

cells that have inactive growth factor receptors that come together to form the active receptor when the growth factor binds​

A

HER2

56
Q

molecule responsible for damaged DNA repair

A

p53

57
Q

rationale of p53

A

1.blocks the formation of phosphorylated Retinoblastoma
2.damaged DNA repair.

58
Q

location of action of p53

A

both G1 and G2M

59
Q

mismatch repair genes

A

they help recognise and replace DNA bases and induces p53 to stop the cell cycle .

60
Q

oncogene

A

A mutated gene that can cause cancer​

61
Q

mutation of malignant melanoma

A

BRAF

62
Q

sources of mutation

A

smoking
sunlight
inheritance
de novo mutations

63
Q

sources of DNA damage

A

radiation
chemotherapy

64
Q

example of a cancer caused by MLH1

A

colon cancer

65
Q

how does smoking cause cancer

A

Numerous chemicals in cigarette smoke  metabolised to carcinogens in liver  released into circulation  damage DNA  numerous mutations  eg mutations in p53

66
Q

sunlight UV radiation and cancer

A

the UV radiation causes gene mutations in the p53 gene which causes increased risk in cancer.

67
Q

human papilloma virus and cancer

A

produces the E6 protein that binds and inactivates p53 which causes increased risk of uncontrolled cell division.
Infection of cervix  produces E6 protein which binds and inactivates p53. [Also produces E7 protein which binds and inactivates retinoblastoma gene product.] Increased risk of subsequent uncontrolled cell division  precancer  cancer

68
Q

c myc protein

A

Increases proteins which push the cell towards cell division
Proteins produced which promote cell division

69
Q

cymc and cancer

A

if cymc breaks off and joins an immunoglobulin regulatory sequence the cells are pushed forward in the cell cycle and the cells are stopped form dying and this promotes cancer.

70
Q

cancers formed by translocation of the cymc sequence

A

lymphoma

71
Q

name of the cymc translocation

A

This translocation is called t(8;14) [note that the left over bit of chromosome 8 joins the other left over bit of chromosome 14 as well.

72
Q

how do environmental factors contribute to cancer

A

they cause the cell to be abnormal therefore increasing susceptibility to cancer.

73
Q

how does alcohol cause cancer

A

large amounts of acetylaldehyde which goes to the systemic circulation and causes double stranded breaks of DNA in many genes which causes an increased risk of cancer.
they also cause damage of numerous genes such as p53

74
Q

Human papilloma virus

A

Infection of cervix  produces E6 protein which binds and inactivates p53. Also produces E7 protein which binds and inactivates retinoblastoma gene product. Increased risk of subsequent uncontrolled cell division  precancer  cancer

75
Q

epstein barr virus

A

virus that infects B cells
causes B cells to proliferate

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