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Semester 4 > case 4 - cellular biology > Flashcards

case 4 - cellular biology Flashcards

1
Q

what is atrophy

A

cell shrinking

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2
Q

how may atrophy be achieved

A

by apoptosis, reduced functional activity, loss of inervation, reduced blood supply, diminished nutrition, loss of hormonal or growth factor stimulation

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3
Q

what is hypertrophy

A

increase in size of existing cells

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4
Q

what is hypertrophy accompanied by

A

an increase in functional capacity

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5
Q

what is the change in number of cells called

A

hyperplasia or aplasia

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6
Q

what is hyperplasia

A

increased number of cells caused by an increase in cell division

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7
Q

what is aplasia

A

decreased number of cells

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8
Q

what is metaplasia

A

this is an adaptive response to evironmental stimuli

specialised cell types change their pattern of differentiation to a new mature stable cell type

this allows them to withstand stress better

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9
Q

what is dysplasia

A

the enlargement of tissue by the proliferation of abnormal cells as a developemtal disorder or an early stage in the development of cancer

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10
Q

what is anaplasia

A

loss of intracellular structural differentiation within a cell often with increased capacity for multiplication as in a malignant tumour

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11
Q

what is the steps in cancer

A

metaplasia followed by dysplasia followed by anaplasia

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12
Q

what does interphase commence with

A

G1

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13
Q

what happens in G1

A

normal cell functions and cell growth, duplication of organelles

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14
Q

what happens to the cells in G1

A

they become sensitive to growth factors and anti proliferative factors

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15
Q

what happens once the cells have entered the cell cycle

A

there is no reversal - the point at which the cell enters the cell cycle and no longer be affected by growth/anti proliferative factors

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16
Q

what is this point called

A

the restriction point

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17
Q

what is G0

A

when cells stay in G1 for a long time and possibly never divide again

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18
Q

what happens during S phase

A

synthesis phase - DNA replication

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19
Q

what happens in G2

A

chromosome begins to condense in preparation for the next mitotic division

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20
Q

what do cyclins active

A

CDKs

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21
Q

what are CDKs

A

enzymes that control the progression through the cell cycle - checkpoint control

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22
Q

what do checkpoint controls prevent

A

DNA replication or mitosis of damaged cells and either stop the cell cycle to allow for DNA repair or eliminate irreversibly damaged cells by apoptosis

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23
Q

what do CDKs promote

A

DNA replication and various aspects of the mitosis process and are required for cell cycle progression

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24
Q

what inhibits CDKs

A

CKi’s - in particular p21

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25
Q

where is cyclin B found in high quantities

A

in the late G2 stage, peaking during mitosis

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26
Q

what does cyclin B associated with to activate it

A

CDK1

27
Q

what does this cyclin B/CDK1 complex do

A

phosphorylates proteins to cause mitosis

28
Q

what do MAP do

A

cause spindle formation

29
Q

what does lamin do

A

usually makes a protein meshwork which the nuclear envelope sits on. upon phsophorylation, this meshwork breaks down, leading to the breakdown of the nuclear envelope

30
Q

what does histone cause

A

the condensation of the chromosomes

31
Q

what is Ras normally bound to and what state is it in

A

normally bound to GDP and is usually inactive

32
Q

how does Ras activate

A

by binding to GTP

33
Q

what happens once Ras is in the active form

A

it can initiate signalling cascades to cause:
- inhibition of apoptosis
- cell growth
- protein synthesis

34
Q

what type of gene is ras

A

it is an oncogene - its mutation causes it to remain in the active form, thus causing a significant increase in cell growth and proliferation

35
Q

what pathway must be mutated to cause colorectal cancer

A

wnt pathway

36
Q

what is the intracellular protein complex comprised of that Wnt interacts with

A

GSK-3B
APC (tumour suppressor gene)
B-catenin (oncogene)

37
Q

what happens in the absence of Wnt

A

it is in the unstimulated state. GSK-3B is active, thus phosphorylating B catenin

this causes the proteolytic degradation of B catenin

38
Q

what happens when Wnt signals are present

A

they bind to the receptor, the intracellular protein complex becomes disrupted.

the GSK-3B is switched off, thus B catenin is no longer phosphorylated

39
Q

what does this mean

A

that b catenin is no longer targeted for proteolytic degradation. B catenin can now move to the nucleus, where it interacts with transcription factors changing gene expression, and so increasing cell proliferation

40
Q

what does a mutation in the beta catenin gene cause

A

it to remain unphophorylated and stable, thus increasing cell proliferation

41
Q

what stimulates ras to bind to its receptors and what does this activate

A

growth factors stimulate ras, which binds to its receptors, thus activating transcription factors and affecting gene expression, especially cyclin D1

42
Q

what does cyclin D1 activate

A

CDK4

43
Q

what does CDK4 phophorylate

A

Rb into pRb

44
Q

what is Rb normally bound to

A

the E2F family of transcription factors, and inhibits them

45
Q

what happens then when CDK4 phosphorylated Rb

A

pRb now causes the liberation of E2F transcription factors, thus allowing them to enter the nucleus and modulating gene expression, especially of cyclin E

46
Q

what happens to this cyclin E

A

it can now bind to CDK2, thus triggering the S phase of the cell cycle

47
Q

what type of gene is Rb

A

a tumour supressor gene

48
Q

what happens if one copy is mutated

A

it has no effect on the liberation of E2F

49
Q

what happens if both copies of Rb are mutated

A

then E2F is always liberated and the cell continuously enters the cell cycle and the S phase without the importance of checkpoint control

50
Q

what phase do external factors not influence

A

S phase

51
Q

what happens if the S phase doesnt go to plan

A

results in the activation of p53, which will then aim to shut down the cell cycle as a defence mechanism

52
Q

what is p53

A

a transcription factor which is degraded normally, but in response to stimuli it can become active and remains non-degraded

53
Q

what happens to the kinases and ubiquitin ligases

A

these ligases which would normally breakdown p53 are inhibited

54
Q

what does the activation of p53 the result of

A

lack of nucleotides
UV radiation
Ionising radiation
Oncogene signalling
Hypoxia
Blockage of transcription factors

55
Q

what does cell cycle arrest occur by and what does it lead to

A

leads to senescence or return to proliferation and this occurs by up regulation of p21 which is a CKi

56
Q

what does the activation of p53 cause

A

DNA repair
Block of angiogenesis
Apoptosis
P53 drives expression of genes such as puma and noxa.
These activate the BAX intrinsic apoptotic pathway, thus leading to programmed cell death
Bcl-X is a pro-survival protein in colon cancer

57
Q

what is the principle cell type of epithelium of the small intestine

A

the paneth cells

58
Q

where are the paneth cells found

A

below the stem cells in the crypts

59
Q

what is apoptosis

A

This is a programmed sequence of intracellular events leading to the death pf the cell without the release of products harmful to the surrounding cells
intrinsic/extrinsic pathways

60
Q

what is the proteolytic cascade

A
  1. The cell shrinks and condenses
  2. Digestion of the nuclear DNA into small DNA fragments
  3. Cells cytoskeleton disassembles
  4. Blebbing
  5. Cell surface membrane altered to allow phagocytosis
61
Q

what is the extrinsic pathway of apoptosis

A

ligand (TNF alpha or Fas) bind to a receptor on the cell surface membrane of the cell

The activation of the receptor causes a DISC to bind to the internal aspect of the receptor

This causes the activation of enzymes known as caspases (known as paracaspases when inactivated)

Proteolytic cascade occurs

62
Q

what is the intrinsic pathway of apoptosis

A

cell recognises internal damage

BAX (in the cytoplasm) binds to a receptor on the mitochondria

Upon binding, BAX changes shape

Proteins (cytochrome C) in the intramembranous space of the mitochondria leak out into the cytoplasm

Cytochrome c activates the paracaspases into caspases, leading to apoptosis

63
Q

what is necrosis due to

A

trauma
disease
ischaemia

Semester 4 (80 decks)

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