deck_659289 Flashcards

1
Q

How is cellular proliferation controlled?

A

– Hormones– Local mediators– Direct cell-cell or cell-stroma contact

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2
Q

What is autocrine signalling?

A

The cell secretes the growth factors which stimulate itself

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3
Q

What type of signalling is paracrine signalling?

A

The secreting cell and responding cell are different

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4
Q

Describe epidermal growth factor

A

– Mitogenic for epithelial cells, hepatocytes and fibroblasts– Produced by keratinocytes, macrophages and inflammatory cells– Binds to epidermal growth factor receptor (EGFR)

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5
Q

Describe Vascular endothelial growth factor and what it is involved in

A

Potent inducer of blood vessel development (vasculogenesis) and role in growth of new blood vessels (angiogenesis) in tumours, chronic inflammation and wound healing

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6
Q

Describe Platelet-derived growth factor

A

– Stored in platelet alpha granules and released on platelet activation– Also produced by macrophages, endothelial cells, smooth muscle cells and tumour cells– Causes migration and proliferation of fibroblasts, smooth muscle cells and monocytes

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7
Q

What are the final outcomes of signalling?

A

Survive (resist apoptosis)Divide (enter cell cycle)Differentiate Die (apoptosis)

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8
Q

By what methods does increased growth occur by?

A

By shortening the cell cycle and by conversion of quiescent cells to proliferating cells (convert G0 cells to G1 cells)

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9
Q

Define mitosis

A

nuclear division

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10
Q

Define cytokinesis

A

Cell division

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11
Q

Name the different phases in cell division

A

G1SG2MG0

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12
Q

What occurs in G1?

A

Gap oneIs pre synthetic and when the cell grows

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13
Q

What occurs in S phase?

A

DNA synthesis

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14
Q

What occurs in G2?

A

Gap 2Premitotic timeThe cell is preparing to divide

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15
Q

What is interphase made up of?

A

G1, S and G2

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16
Q

How is the cell cycle controlled?

A

Checkpoints which occur though the cycle

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17
Q

What are the checkpoints in the cell cycle?

A

G1 = after G1, before S phaseG2 = after G2, before M phaseRestriction point

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18
Q

Describe the R point

A

After this point, cells are not responsive to growth factors so division will take place. – Is the most commonly altered checkpoint in cycle in cancer cells

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19
Q

What does activation of R checkpoint do?

A

Delays cell cycle and triggers DNA repair mechanisms or apoptosis via p53

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20
Q

What regulates the progression through the cell cycle?

A

Cyclins and CDKs (cyclin dependent kinases)

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21
Q

How do cyclins and CDKs regulate the cell cycle?

A

Cyclins bind with CDKs to form an active complex. Activated CDKs phosphorylate proteins which are critical in cell cycle transitionsThis activity is tightly regulated

22
Q

How is cyclin production stimulated?

A

Growth factors

23
Q

What do stem cells power?

A

Proliferative capacity which replenishes the loss of differentiated cells.

24
Q

Describe the stem cells present in labile cell populations

A

Divide persistently to replenish losses

25
Q

Describe the stem cells present in stable cell populations

A

Stem cells normally quiescent or proliferate very slowly, but proliferate persistently when required

26
Q

Describe the stem cells present in permanent cell populations

A

Stem cells present, but cannot mount an effective proliferative response to significant cell loss.

27
Q

Give some examples of labile cells

A

Surface epithelia e.g. epidermis, gut epitheliumBone marrow

28
Q

Give some examples of stable cells

A

Liver hepatocytesBone osteoblasts

29
Q

Give some examples of permanent cells

A

Brain neuronesCardiac and skeletal muscle

30
Q

Define cell adaptation and state whether it is reversible or irreversible

A

the state between a normal unstressed cell and an overstressed injured cellIt is reversible

31
Q

Define regeneration

A

Replacement of cell losses by identical cells to maintain tissue or organ size

32
Q

What are the two outcomes of regeneration?

A

RESOLUTION – The harmful agent is removed, tissue damage is limited and regeneration occursSCAR – Harmful damage persists so extensive tissue damage occurs. Sometimes permanent cells.

33
Q

Give some examples of regeneration

A

Hepatocytes can regenerate post lobectomySkin epidermis regenerates after burns

34
Q

Define hyperplasia

A

Increase in tissue or organ size due to increased cell numbers

35
Q

Describe some characteristics of hyperplasia

A

Is under physiological controlOnly occurs in stable or labile populationsCan occur secondary to a pathological cause NB – multiple division expose the cell to increased risj of mutation and neoplasia

36
Q

Give some physiological and pathological examples of hyperplasia

A

PHYSIOLOGICALEndometrium of uterus under influence of oestrogen Bone marrow produces more erythrocytes in response to hypoxiaPATHOLOGICALEczema – thickened epidermisThyroid goitre in iodine deficiency

37
Q

Define hypertrophy

A

Increase in tissue or organ size due to increased cell size

38
Q

Where doe hypertrophy usually occur and what causes it?

A

In permanent cells as they cannot divide– caused by increased functional demand or hormonal stimulation– can occur alongside hyperplasia– cells will contain more structural components

39
Q

Give some physiological and pathological examples of hypertrophy

A

PHYSIOLOGICALSkeletal muscle in body buildersPregnant uterusPATHOLOGICALVentricular hypertrophy due to hypertenstion(RV hypertrophy is due to pulmonary hypertension)Bladder smooth muscle wall hypertrophy(due to obstruction and enlarged prostate gland)

40
Q

Define atrophy

A

Shrinkage of a tissue or organ due to an acquired decrease in size and/or number of cells

41
Q

What is organ or tissue atrophy usually due to?

A

a combination of cellular atrophy and apoptosis

42
Q

Describe atrophy

A

Cellular atrophy = loss of cell sizeCell shrinks to a size at which survival is still possible – there are reduced structural components of the cell. Is an adaptive response which may result in death.

43
Q

Give a physiological example of atrophy

A

Ovarian atrophy in post menopausal women

44
Q

What can pathological atrophy be due to?

A

– Reduced functional demand/workload (muscle atrophy after disuse)– denervation atrophy– Inadequate blood supply (thinning of skin on legs with peripheral vascular disease)– Inadequate nutrition (malnutrition)– Loss of endocrine stimuli (breast, repro organs)– Persistent injury (polymyostisis)– Aging = senile atrophy (brain, heart)– Pressure: tissues around growing benign tumour

45
Q

Define metaplasia

A

Reversible change of one differentiated cell type to another cell type

46
Q

Where can you generally see metaplasia?

A

In epithelial cells

47
Q

Why can metaplasia occur?What can it lead to?

A

It may represent an adaptive substitution of cells that better adapted to a particular environment.Can lead to dysplasia and cancer

48
Q

Give an example of metaplasia

A

SMOKERSBronchial pseudostratified ciliated epithelium –> stratified squamous epithelium due to effect of cigarette smokeBARRETT’S OESOPHAGUSStratified squamous epithelium –> gastric glandular epithelium with persistent acid reflux

49
Q

Define aplasia

A

Complete failure of a specific tissue or organ to developIs an embryonic developmental disordere.g. thymic aplasia –> autoimmune and infections

50
Q

Define hypoplasia

A

Underdevelopment or incomplete development of a tissue or organ at the embryonic stagee.g. kidneys, testes in Kilinefelters syndrome, chambers of the heart

51
Q

Define dysplasia

A

Abnormal maturation of cells within a tissue which is potentially reversible. Often is pre-cancerous