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MBCHB 1 > TUMOR PATHOLOGY > Flashcards

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
Ability to increase in number
proliferative growth factors that alters the cell cycle the growth receptors are also altered
26
ability to evade growth suppressors
that is tumor suppressor genes alteration of p53
27
some tumor cells mediate a tumor associated inflammatory response
yes or no
28
carcinogenic and necrosis
there is release of cellular contents into the interstitium this causes an inflammatory response
29
metastasis
spread of cancer cells through loss of cell to cell adhesion , loss of cell to ECM adhesion molecules
30
metastasis methods
Local spread​ Lymphatic spread​ Haematogenous spread​ Trans-coelomic spread​
31
metastasis through the lymph nodes
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
trans - coelomic spread
-spread through the body cavity in the peritoneal ; gastric , colonic , ovarian -pleural that is the lung
33
local effects of cancer
pain haemorrhage loss of function
34
local effect on the brain
confusion coma seizure
35
local effect of tumor on the lungs
dyspnoea haemoptysis
36
local effects of tumors on the liver
jaundice blockage of the gall bladder. coagulopathy that is because of the blockage of the proteins that are used in coagulation.
37
local effects of cancer in the colon
diarrhoea constipation haemorrhage
38
local effect of the tumors on bone
anaemia pain fracture
39
systemic effects of cancer
cachexia DVT paraneoplastic syndrome
40
cachexia characteristics
weakness and wasting due to chronic illness loss of muscle is greater and faster than fat loss.
41
paraneoplastic syndrome
abnormal production of hormones the hormones have systemic effects.
42
examples of hormone production that is altered by cancer
PTH ACTH ADH
43
DVT
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
what is pre cancer
dysplasia that is disordered cell growth and doesnt involve spread
45
what is neoplasma
Abnormal growth of cells, uncoordinated with normal tissue and continuing even after cessation of stimulus​
46
wilson and junger principles of screening
look at the photo
47
molecules involved in signal trasduction in a cell
the receptor for growth factor the growth factors as ligands the amplification system that is the messenger molecule and other molecules involved.
48
example of a signal transduction molecule
BRAF
49
cell cycle inhibitors
p53 retinoblastoma
50
factors that cause inhibition of a molecule
change in the structure change in the molecule that is attached
51
retinoblasma
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
longest phase of the cell cycle
G1 phase
53
how does growth factor cause progression past the G1 phase restrictor
the growth factors eg amino acid levels and glucose levels.
54
role of the growth factors
they ellicit a pathway that cause the amplification of molecules leading to phosphorylation of the RB molecule.
55
cells that have inactive growth factor receptors that come together to form the active receptor when the growth factor binds​
HER2
56
molecule responsible for damaged DNA repair
p53
57
rationale of p53
1.blocks the formation of phosphorylated Retinoblastoma 2.damaged DNA repair.
58
location of action of p53
both G1 and G2M
59
mismatch repair genes
they help recognise and replace DNA bases and induces p53 to stop the cell cycle .
60
oncogene
A mutated gene that can cause cancer​
61
mutation of malignant melanoma
BRAF
62
sources of mutation
smoking sunlight inheritance de novo mutations
63
sources of DNA damage
radiation chemotherapy
64
example of a cancer caused by MLH1
colon cancer
65
how does smoking cause cancer
Numerous chemicals in cigarette smoke  metabolised to carcinogens in liver  released into circulation  damage DNA  numerous mutations  eg mutations in p53
66
sunlight UV radiation and cancer
the UV radiation causes gene mutations in the p53 gene which causes increased risk in cancer.
67
human papilloma virus and cancer
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
c myc protein
Increases proteins which push the cell towards cell division Proteins produced which promote cell division
69
cymc and cancer
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
cancers formed by translocation of the cymc sequence
lymphoma
71
name of the cymc translocation
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
how do environmental factors contribute to cancer
they cause the cell to be abnormal therefore increasing susceptibility to cancer.
73
how does alcohol cause cancer
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
Human papilloma virus
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
epstein barr virus
virus that infects B cells causes B cells to proliferate

MBCHB 1 (62 decks)

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