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Semester 2 Pathological Processes > L12: Cellular adaptation > Flashcards

L12: Cellular adaptation Flashcards

(47 cards)

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1
Q

What does the size of a cell population depend on?

A

Rate of proliferation
Rate of differentiation
Rate of cell death by apoptosis

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2
Q

How does the cell population increase?

A

↑ rate of cell proliferation +/- ↓ cell death
Can be physiological or pathological
Excess physiologcial–> pathological

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3
Q

What controls cell proliferation?

A

Proto-oncogenes and tumour supressor genes
Chemical mediators–> microenvironment–> stimulate or inhibit cell proliferation
Signalling molecules–> bind to receptor leading to modulation of gene expression: cell membrane, cytoplasm and nucleus

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4
Q

What is the cell cycle?

A

Cycle the cells go through to divide

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5
Q

What are the different stages of the cell cycle? What happens in each stage?

A

G1–> growth stage one–> cell contents duplicate
S–> synthesis–> DNA replicates
G2–> growth stage two–> double checks for errors
M–> mitosis and cytokinesis–> nucleus divides into two, pulling sister chromosome to opposite sides of the cell
–>cytokinesis–> cells divides into two cells

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6
Q

What happens after cytokinesis?

A

Cell either re-enters the cell cycle at G1 and makes 2 new cells
Cells go into G0 phase until further growth signals occur or undergo terminal differentiation to permanently exit the cell cycle

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7
Q

How does increased growth of a tissue occur?

A

Shortening of the cell cycle

Conversion of quiescent cells to proliferating cells

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8
Q

Collectively what are the stages between mitosis called?

A

Interphase

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9
Q

Which stage can most clearly be seen under the light microscope?

A

Mitosis

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10
Q

What are the different steps to mitosis?

A

Prophase–> centrioles move to opposite poles of the cell, nuclear envelop disintegrates, chromosomes condense
Metaphase–> chromosome line up along the metaphase plate, spindle fibres attach
Anaphase–> spindle fibres contract pulling chromosome apart
Telophase–> nuclear envelop begins to reform, chromosomes decondense

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11
Q

What controls the cell progression through the cycle?

A

Three checkpoint: Restriction (R) point, G1/S checkpoint and G2/M checkpoint
Check for damage and repair damage before progression

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12
Q

Which checkpoint is the most critical checkpoint? Why?

A

The restriction point
Point of ‘no return’
Towards the end of G1
Activation activates p53 proteins which delays cell cycle and triggers DNA repair mechanism or apoptosis

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13
Q

What triggers activation of p53?

A

Stresses

  • -> oxidative stress
  • -> nutrient deprivation
  • -> hypoxia
  • -> DNA damage
  • -> Oncogene expression
  • -> Ribosomal dysfunction
  • -> Telomere attrition
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14
Q

What are the 3 consequences of p53 activation?

A

Arrests cell temporarily–> activated p21 prevents phosphorylation of cyclins–> Cell cycle arrest –> Allow DNA repair
Arrest cells permanently–> nothing happens to them
Triggers apoptosis

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15
Q

What is the function of the G1/S checkpoint and G2/M checkpoint?

A

G1/S–> checks for DNA damage before replication

G2/M–> checks for DNA damage after replication

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16
Q

What regulates progression through the G1/S checkpoint?

A

Cyclin and cyclin dependent kinases (CDKs)

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17
Q

How do cyclins and CDKs work?

A

Cyclins bind to the CDK activating them
Cyclin-CDK complexes are then able to phosphorylate proteins downstream activating or inhibiting them
Activated proteins, such as TFs, can lead to DNA replication
Different cyclins are present at different stages of the cell cycle

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18
Q

What control the activity of the CDKs?

A

Activity tightly regulated
Activated by cyclins
Inhibited by cyclin dependent kinase inhibitors

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19
Q

How does the G1/S checkpoint work?

Study These Flashcards
A

1- Retinoblastoma protein (Rb) is bound to a TF inhibiting it
2- Cyclin D binds to CDK4 forming cyclin D/CDK4 complex
3- Cyclin D/ CDK4 complex phosphorylates the Rb inactivating it
4- Release TF which binds to the DNA and transcribes it

20
Q

In summary what are the main tumour supressor genes?

Study These Flashcards
A

Inhibit cell cycle
p53–> arrest cell cycle if cell damaged to allow repair or apoptosis
Rb–> Brakes on G1/S checkpoint
CDK inhibitors

21
Q

In summary what are the main oncogenes?

Study These Flashcards
A

Promote cell cycle
Cyclins/CDK complex
Growth factors
ras, myc, erbB2, Bcl2

22
Q

What are the main types of cell adaptation?

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A

Hyperplasia- Increase in cell number above normal
Hypertrophy- Increase in cell size
Atrophy- Decrease in cells size
Metaplasia- Change from one cell type to another

23
Q

What is hyperplasia? Why does it happen?

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A

Increase in tissue or organ size due to increased cell numbers
Response to increased
- functional demand or
- hormonal stimulation or
- compensatory (increase in tissue mass after damage)
Remains under physiological control
Can occur because of pathology but proliferation is still normal
Repeated cell divisions at risk of mutations and neoplasia

24
Q

What types of tissues can hyperplasia occur in?

Study These Flashcards
A

Liable (multiply continusously throughout life) or stable tissue (multiply upon stimulation)

25
When does hyperplasia happen physiologically?
Proliferation of endometirum under influence of oestrogen | Proliferation of erythrocytes in response to hypoxia
26
When does hyperplasia happen pathologically?
Neoplasia--> not under physiological control Secondary to excessive hormone stimulation or growth factors, at risk of mutation Epidermal thickening in chronic eczema Enlargement of thryoid gland in response to iodine deficiency (thyroid goitre)
27
What is hypertrophy? Why does it happen?
Increase in tissue or organ size due to an increase in the size of the cells Response to increased functional demand or hormonal stimulation More cytoplasm and structural components are produced so workload is shared between a greater mass of cellular components
28
What type of tissue does hypertrophy normally occur in?
Mostly in permanent tissue as they have little or no replicative potential Labile and stable tissue usually occurs alongside hyperplasia
29
When does hypertrophy occur physiologically?
Skeletal muscle | Smooth muscle of uterus-> enlarges approximately 70 fold
30
When does hypertrophy occur pathologically?
Ventricle cardiac muscle--> response to hypertension or valvular disease Smooth muscle hypertrophy above intestinal stenosis--> push intestinal contents along Bladder smooth muscle--> obstruction due to prostate gland enlargement
31
What is compensatory hypertrophy?
When one thing enlarges due to removal of the other one e.g. kidney removal causes other kidney to enlarge
32
How do athletes adapt using hypertrophy? What happens when they stop? How is it different to pathological hypertrophy?
Increase cardiac muscle size Able to pump more oxygen and blood around the body When they stop--> decreases in size Has to be done slowly Coronary supply also increases to heart in athletes In pathological hypertrophy it doesn't--> anoxia--> ischaemia--> Fibrosis
33
What is atrophy? When does it happen?
Shrinkage of a tissue due to an acquired decrease in size and/or number of cells Reduced supply of GF and/or nutrients Shrinks to size at which survival is still possible Reduces structural component of the cell May eventually result in cell death
34
Is tissue atrophy only a result of cell atrophy?
Organ/ tissue atrophy is typically due to combination of cellular atrophy and apoptisis It is reversible but only up to a point In organs undergoing atrophy parenchymal cells will disappear before stromal cells and atrophic organs therefore contain a lot of connective tissue (not random deletion by apoptossis)
35
When is atrophy used physiologially?
Ovarian atrophy post-menopausal women | Decrease in uterus size after parturition
36
When is atrophy used pathologically?
1. Atrophy of disuse--> reduced functional demand/workload--> muscle atrophy after disuse (reversible) 2. Loss of innervation--> denervation atrophy--> wasted hand muscles after median nerve damage 3. Inadequate blood supply--> thinning of skin on legs with peripheral vascular disease 4. Inadequate nutrition--> wasting of muscle with malnutrition 5. Loss of endocrine stimulation--> breast, reproductive organs 6. Persistent injury--> polymyositis (inflammation of muscle) 7. Aging--> senile atrophy--> brain, heart 8. Pressure--> tissue around an enlarging benign tumour (probably secondary to ischaemia) 9. Occlusion of secretory duct--> paranchymal cells undergo apoptosis 10. Toxic agents and drugs--> bone marrow and testes 11. X-rays--> direct cellular damage or microcirculatory damage Immunological mechanisms--> antibodies against cells
37
Whats is metaplasia? Why does it happen?
1. Reversible change of one adult differentiated cell type to another 2. Stems cells within the tissue are reprogrammed and switch to producing a different type of progeny 3. Considered abnormal regeneration 4. Only in epithelial cells and varieties of connective tissue 5. Expression of new genetic programme to produce a cell more suited to an altered environment 6. Metaplasia cells are fully differentiated and the process is reversible 7. Only in cells that can regenerate 8. Does not happen across germ layers
38
What types of tissues can undergo metaplasia?
Labile or stable cells
39
Give examples of when metaplasia can be useful?
When bone marrow is destroyed Splenic tissue undergoes metaplasia to bone marrow Columnar epithelium lining ducts of salivary glands, pancreas, bile ducts or renal pelvis can change to stratified squamous epithelium after chronic irritation by stones--> useful as more resistant to mechanical abrasion
40
Give examples of when metaplasia occurs but is of no use?
Bronchial pseudostratified ciliated epithelium converted to stratified squamous epithelium as a result of smoking Irritate epithelium Changes--> mucous builds up causes you to cough Oesophageal reflux--> oesophageal stratified squamous epithelium changes to gastric or intestinal type epithelium with persistent acid reflux Connective tissue--> bone marrow Skeletal muscle--> fibroblast converted to osteoblasts--> premature return to activity before healing has occurred
41
Does metaplasia predispose to cancer?
Epithelial metaplasia can lead to dysplasia and cancer --> Squamous metaplasia and lung squamous cell carcinoma --> Barrett's epithelium and oesophageal adenocarcinoma --> Intestinal metaplasia of stomach and gastric adenocarcinoma But the reasons behind are not understood
42
What is aplasia?
Complete failure of tissue or organs to develop Embryonic development disorder e.g. thymic aplasia- infections and auto-immune problems - aplasia of kidney Also describes organs who's cells have stopped proliferating
43
What is hypoplasia?
Underdevelopment or incomplete development of tissue or organ at embryonic stage, inadequate number of cells Congenital condition so not opposite if hyperplasia (Atropy--> bit wastes away) Examples: renal, breast, testicular in Klinefelter's syndrome, chambers of the heart
44
What is involution?
Overlaps with atrophy Normal programmed shrinkage of an organ Uterus after childbirth, thymus in early-life, pro- and mesonephros
45
What is reconstitution?
Replacement of a lost body part rather than a small group of cells Coordinated regeneration of several cells required Examples: -Lizards tail regrowth -Deer antlers (17.5mm/day) Most mammals reconstitution is minimal--> cant even replace root of hair--> scars are hairless
46
What is dysplasia?
Abnormal maturation of cells within a tissue Potentially irreversible Often pre-cancerous condition
47
What is atresia?
No orifice Congenital imperforation of an opening Examples: anus, vagina, pulmonary valve, small bowel

Semester 2 Pathological Processes (16 decks)

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