Session 7-Cellular Adaptations Flashcards

1
Q

How is cell proliferation controlled?

A
  • chemical signals

- when signalling molecule binds to receptor -> modulation of gene expression

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2
Q

What can the chemical signals make the cell do?

A

1) survive - resist apoptosis
2) divide - enter cell cycle
3) differentiate - take on specialised form and function
4) die - undergo apoptosis

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3
Q

How can a cell population increases its numbers?

A
  • shortening cell cycle

- conversion of quiescent cells to proliferating cells by making them enter the cell cycle

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4
Q

Can cells with damaged DNA replicate?

A

No - if damaged DNA cannot be fixed, cell goes into apoptosis

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5
Q

What is the restriction (R) point?

A

Point near the end of G1 - if cells pass R point, they will complete the cell cycle (point of no return)

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6
Q

Which is the most commonly altered checkpoint in cancer cells?

A

R point - checkpoint activation delays cell cycle and triggers DNA repair mechanisms or apoptosis via p53

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7
Q

How is the cell cycle controlled?

A

cyclins or cyclin dependent kinases (CDKs)

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8
Q

How do CDKs become active?

A

Binding with cyclins

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9
Q

How can cells adapt?

A

1) hyperplasia
2) hypertrophy
3) atrophy
4) metaplasia

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10
Q

What is the least reversible cellular adaptation?

A

Atrophy

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11
Q

What is hyperplasia?

A

Increase in tissue or organ size due to increased cell numbers

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12
Q

In which types of tissues does hyperplasia occur?

A

Labile or stable tissues

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13
Q

What causes hyperplasia?

A

Increased functional demand or hormonal stimulation

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14
Q

True or false: hyperplasia remains under physiological control and is reversible

A

TRUE

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15
Q

What does repeated cell division expose the cell to?

A

Risk of mutations and neoplasia

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16
Q

What are some examples of physiological hyperplasia?

A

1) proliferative endometrium under the influence of oestrogen
2) bone marrow produces erythrocytes in response to hypoxia

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17
Q

What are some examples of pathological hyperplasia?

A

1) eczema

2) thyroid goitre

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18
Q

What is hypertrophy?

A

Increase in tissue or organ size due to increased cell size

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19
Q

In which types of tissue does hypertrophy occur?

A

Labile, stable but especially permanent tissues

20
Q

How is workload shared by a greater mass of cellular components in hypertrophic cells?

A

Cells contain more structural components

21
Q

What are some examples of physiological hypertrophy?

A

1) skeletal muscle in body builders

2) pregnant uterus (hypertrophy and hyperplasia)

22
Q

What are some examples of pathological hypertrophy?

A

1) hypertension -> ventricular hypertrophy
2) enlarged prostate
3) proximal tissue to stricture in bowel hypertrophies to push food through

23
Q

Why do patients with systemic hypertension/valvular disease have greater cardiac hypertrophy than athletes?

A

Patients’ heart never rests so more hypertrophy than athletes

24
Q

How can systemic hypertension lead to fibrosis?

A

Cardiac muscle hypertrophies and heart responds by growing more capillaries but never enough to compensate so heart is hypoxic -> fibrosis -> problems with electrical conduction in heart

25
Q

What is compensatory hypertrophy?

A

For eg when one kidney is removed, the other compensates by hypertrophying

26
Q

What is atrophy?

A

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

27
Q

What is happening in the cell in atrophy?

A

1) shrinkage in the size of the cell to a size at which survival is still possible
2) reduced structural components of cell

28
Q

Is tissue atrophy only a result of cell atrophy?

A

Combination of cellular atrophy and apoptosis

29
Q

What is an example of physiological atrophy?

A

Ovarian atrophy in post menopausal women

30
Q

What are some examples of pathological atrophy?

A

1) reduced functional demand/workload = atrophy of disuse - muscle atrophy
2) loss of innervation = denervation atrophy - wasted hand muscles after median nerve damage
3) inadequate blood supply - thinning of skin with peripheral vascular disease
4) inadequate nutrition - wasting of muscles with malnutrition
5) loss of endocrine stimuli - breast
6) persistent injury
7) ageing = senile atrophy
8) pressure - tumour

31
Q

What is metaplasia?

A

Reversible change of one differentiated cell type to another

32
Q

What causes metaplasia?

A

Altered stem cell differentiation

33
Q

What is metaplasia sometimes a prelude to?

A

Dysplasia and cancer

34
Q

In which cell types does metaplasia occur?

A

Labile or stable cells

35
Q

What are some examples of metaplasia?

A

1) bronchial pseudostratified ciliated epithelium -> stratified squamous epithelium due to cigarette smoke
2) stratified squamous epithelium -> gastric glandular epithelium with persistent acid reflux (Barrett’s oesophagus)

36
Q

What can happen if a young person returns to exercise sooner than they should following a skeletal muscle injury?

A

Fibroblasts undergo metaplasia and can form bone

37
Q

What is aplasia?

A

Complete failure of a specific tissue or organ to develop - embryonic developmental disorder

OR

Organ whose cells have ceased to proliferate eg aplasia of bone marrow in aplastic anaemia

38
Q

What is hypoplasia?

A

Underdevelopment or incomplete development of tissue or organ at embryonic stage, inadequate number of cells

39
Q

Why is hypoplasia not the opposite of hyperplasia?

A

Hypoplasia is a congenital condition

40
Q

What is involution?

A

Overlaps with atrophy - normal programmed shrinkage of an organ

41
Q

Give examples of involution

A

Uterus after childbirth

Thymus in early life

42
Q

What is reconstitution?

A

Replacement of lost part of the body

43
Q

Can reconstitution occur in humans?

A

Yes if a child under 4 1/2 years cleanly cuts off the tip of their finger, it can grow back!!!

44
Q

What is atresia?

A

‘No orifice’

Congenital imperforation of an opening eg anus, vagina, small bowel

45
Q

What is dysplasia?

A

Abnormal maturation of cells within a tissue, potentially reversible and often a pre-cancerous condition