7. Cellular Adaptations Flashcards

(53 cards)

1
Q

How is cell proliferation controlled

A

—-> Largely by chemical signals from the microenvironment which either stimulate or inhibit cell proliferation by binding to receptors

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2
Q

How do cells survive

A

• Cell needs prosurvive signals
○ Survive – resist apoptosis
○ An no division
○ Always need the pro survival signals to maintain cell life

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3
Q

Cell death

A

Apoptosis

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4
Q

Stages of cell cycle

A

G1
S
G2
M – mitosis

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5
Q

Mitosis

Stages

A
  • Prophase
    • Metaphase
    • Anaphase
    • Telophase
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6
Q

G0 phase

A

• Terminal differentiation
• Permamnt exit from cell cycle
• Where quiscent cells are that have stopped dividing
○ Some cells can move in and out of G0 phase

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7
Q

Increased growth occurs by:

A
  • Shortening the cell cycle = go through cycle faster

* Conversion of quiescent cells to proliferating cells by making them enter the cell cycle.

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8
Q

3 Cell cycle checkpoints

A

• G1 – detect nutrients for ccell cycle like growth factos
G2 – check forcorrectly replicated DNA
Metaphase to anaphase – check spindle is connected to chromosome

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9
Q

Restriction (R) checkpoint

A

Majority of cells that pass R point will complete cell cycle - point of no return

This checkpoint is most commonly altered in cancer cells
• Mutate genes to inactivate checkpoint and go through without control

Chrcpoint activation delays cell cycle, triggers DNA repair, apoptosis via p53

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10
Q

CDK activation

A
  • Cyclin and CDK bind together
    • When they come togeter they are partially active then fully active
    • Once active it can phosphorylate other targets
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11
Q

Control CDK cyclin interactions

A
  • The regulation of Cdk activity by phosphorylation

* The inhibition of a cyclin–Cdk complex by a CKI – inhibitor proteins bind to and inactivate proteins

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12
Q

Leonard Hayflick - Hayflick numbers/limits (1961)

A
  • Limit to how much the cells can divide
    • Nnumber of cell divisions human cell can go through
    • Humans = 40-60 divisions normally until it stops
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13
Q

Why does cell division eventually stop

A

• As with each division you lose some part of the telomeres
• When the telomeres become too short = cells become senscent
○ Somatic cells don’t have enough telomerase - loose ability to express telomerase to maintain telomeres ends

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14
Q

➢ How to cancer cells survive?

A
  • Cell override the stopping and can continue to divide
    • Cancer cells use and reexpress telomerase which maintains the telomere sites
    • Normlly telomerase is expressed at low levels in somatic cells
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15
Q

Proliferation:

A

• increase in numbers of cells

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16
Q

Growth:

A
• increase in size of the cell 
		○ Multiplicative growth 
		○ Ausectic growth 
		○ Accretionary growth 
		○ Combined pattern of growth
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17
Q

Differentiation:

A

• acquiring a specific morphology and function

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18
Q

Factors impacting size of a cell population

A

Depends on
• rate of cell proliferation
• cell differentiation
• cell death by apoptosis

•  Increased numbers are seen with increased proliferation or decreased cell death
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19
Q

Regeneration:

A

• the ability to replace cells or tissues, destroyed by injury or disease (identical functionality)

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20
Q

3 types of cells

A

Labile
Stable
Permanent

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21
Q

Table cells

A

•Labile cells: high regenerative ability and turnover (e.g. intestinal epithelium)

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22
Q

Stable cells

A

• Stable cells: good regenerative ability and low turnover (e.g. hepatocytes) - can return to G1 and start regenerating

23
Q

Permanent cells

A

• Permanent cells: no regenerative ability (e.g. neurones, cardiac, skeletal muscle cells)

24
Q

Hyperplasia

A

• Hyperplasia – cells increase in number above normal

25
Hypertrophy
• Hypertrophy – cells increase in size
26
Atrophy
• Atrophy – cells become smaller
27
Metaplasia
• Metaplasia – cells are replaced by cells of a different type
28
Hyperplasia - features
• Only happens to labile or stable tissues as they can divide • Caused by increased functional demand or hormonal stimulation • Remains under physiological control and is reversible (cf. neoplasia) ○ Under some cases if you keep dividing you increase the risk of accumualting mutation * Can occur secondary to a pathological cause but the proliferation itself is a normal response (cf. neoplasia – the proliferation itself is abnormal) * Repeated cell divisions exposes the cell to the risk of mutations and neoplasia
29
Hyperplasia - physiological examples
○ Proliferative endometrium under influence of oestrogen | ○ Bone marrow produces erythrocytes in response to hypoxia (high altitude training)
30
Hyperplasia - physiological examples pathological
○ Exczema – proliferation of skin cells | ○ Thyroid goitre in iodine deficiency – thyroid becomes much bigger
31
Hypertrophy features
* Labile, stable and especially permanent tissues * Like hyperplasia, caused by increased functional demand or hormonal stimulation * Cells contain more structural components – workload is shared by a greater mass of cellular components * Cells become bigger and add to the functionality * In labile and stable tissues hypertrophy usually occurs along with hyperplasia
32
- physiological examples hypertrophy
○ Atheltes body builders – skeletal muscle | ○ Pregnant uterus (hypertrophy +hyperplasia)
33
Pathological examples- hypertrophy
○ Cardiac muscle in response to pulmonary hypertension ○ Bladder smooth muscle obstructed due to enlarged prostate gland – tissue has to try harder to remove urine ○ Smooth muscle hypertrophy before an intestinal stenosis – intestine becomes bigger to push contents through
34
Compensatory hypertrophy
• One kidney does more work to make up for removed kidney
35
Atrophy - features
* Shrinkage in the size of the cell to a size at which survival is still possible * Reduced structural components of the cell and cell function * May eventually result in cell death * Organ/tissue atrophy typically due to combination of cellular atrophy and apoptosis * Is reversible, but only up to a point
36
Atrophy physiological example
* Ovarian atrophy in post menopausal women | * Decrease in size of uterus after parturition
37
Atrophy example pathological
• Reduced functional demand/workload = atrophy of disuse muscle atrophy after disuse, reversible with activity • Loss of innervation = denervation atrophy: wasted hand muscles after median nerve damage, muscle does not receive right signals • Inadequate blood supply: thinning of skin on legs with peripheral vascular disease • Inadequate nutrition: wasting of muscles with malnutrition • Loss of endocrine stimulation: breast, reproductive organs = less hormones • Persistent injury: polymyositis (inflammation of muscle) • Aging = senile atrophy: brain, heart become smaller Pressure: tissues around an enlarging benign tumour (probably secondary to ischaem
38
Atrophy of extracellular matrix -bone
* In bed ridden patients or astronauts as they don't use bone much * Osteroporosis
39
Apoptosis - features
* Enzymes * Growth factor withdrawal * Engulf * This can be reversible up to a certain point
40
Metaplasia- features
* May represent adaptive substitution of cells that are sensitive to stress by cell types better able to withstand the adverse environment * Metaplastic cells are fully differentiated and the process is reversible (cf. dysplasia and cancer) * Sometimes a prelude to dysplasia and cancer * Occurs only in labile or stable cell types * Involves expression of a new genetic programme
41
Metaplasia examples
* Bronchi in smokers - Bronchial pseudostratified ciliated epithelium is changed to → stratified squamous epithelium due to effect of cigarette smoke, stratifed sqaumous cells are betetr at dealing with smoke but they don't produce mucous * Acid reflux - Stratified squamous epithelium becomes → gastric glandular epithelium with persistent acid reflux (Barrett’s oesophagus)
42
Myeloid metaplasia
• Myeloid metaplasia – bone marrow is destroyed but spleen undergoes metaplasia to become bone marrow
43
Myosotis ossificans
• Myositis ossificans, metaplasia of fibroblasts in muscle that becoem osteoblasts that produce bone
44
Does metaplasia predispose to cancer?
• Epithelial metaplasia can be a prelude to dysplasia and cancer. • Barrett’s epithelium and oesophageal adenocarcinoma • Intestinal metaplasia of the stomach and gastric adenocarcinoma Mechanism is not clear
45
Aplasia
---> organ fails to form • Complete failure of a specific tissue or organ to develop • An embryonic developmental disorder
46
Aphasia - examples
* Thymic aplasia - infections and auto-immune problems * Aplasia of a kidney • Also used to describe an organ whose cells have ceased to proliferate, e.g. aplasia of bone marrow in aplastic anaemia
47
Hypoplasia
---> Underdevelopment or incomplete development of tissue or organ at embryonic stage, inadequate number of cells • Not opposite of hyperplasia as it is a congenital condition
48
Hypoplasia - excemples
* Renal * Breast * Testicular in Klinefelter’s syndrome * Chambers of the heart
49
Involution
---> Overlaps with atrophy = Normal programmed shrinkage of an organ • Uterus after childbirth, thymus in early life, proand mesonephros
50
Reconstitution
---> Replacement of a lost part of the body normally in animals Humans have angiogenesis • Form new capillaries • Basis for wound healing • Important in cancer – angiogeneis helps cancer survive
51
Atresia
---> no lumen, lumen is not continus * ‘No orifice’ * Congenital imperforation of an opening * Examples: Pulmonary valve Anus Vagina Small bowel
52
Dysplasia
---> Abnormal maturation of cells within a tissue – go from a normal tissue to an abnormal tissue * Potentially reversible * Often pre-cancerous condition
53
Dysplasia - example
e.g. cervix – smear test • Dysplaisia in hpv develops abnormal looking cells Look for how many and what kind of abnormal cells are observed