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Semester 2 Pathological Processes > L12: Cellular adaptation > Flashcards

L12: Cellular adaptation Flashcards

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?

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?

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?

A

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

22
Q

What are the main types of cell adaptation?

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?

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?

A

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

25
Q

When does hyperplasia happen physiologically?

A

Proliferation of endometirum under influence of oestrogen

Proliferation of erythrocytes in response to hypoxia

26
Q

When does hyperplasia happen pathologically?

A

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
Q

What is hypertrophy? Why does it happen?

A

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
Q

What type of tissue does hypertrophy normally occur in?

A

Mostly in permanent tissue as they have little or no replicative potential
Labile and stable tissue usually occurs alongside hyperplasia

29
Q

When does hypertrophy occur physiologically?

A

Skeletal muscle

Smooth muscle of uterus-> enlarges approximately 70 fold

30
Q

When does hypertrophy occur pathologically?

A

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
Q

What is compensatory hypertrophy?

A

When one thing enlarges due to removal of the other one e.g. kidney removal causes other kidney to enlarge

32
Q

How do athletes adapt using hypertrophy? What happens when they stop? How is it different to pathological hypertrophy?

A

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
Q

What is atrophy? When does it happen?

A

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
Q

Is tissue atrophy only a result of cell atrophy?

A

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
Q

When is atrophy used physiologially?

A

Ovarian atrophy post-menopausal women

Decrease in uterus size after parturition

36
Q

When is atrophy used pathologically?

A
  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
Q

Whats is metaplasia? Why does it happen?

A
  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
Q

What types of tissues can undergo metaplasia?

A

Labile or stable cells

39
Q

Give examples of when metaplasia can be useful?

A

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
Q

Give examples of when metaplasia occurs but is of no use?

A

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
Q

Does metaplasia predispose to cancer?

A

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
Q

What is aplasia?

A

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
Q

What is hypoplasia?

A

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
Q

What is involution?

A

Overlaps with atrophy
Normal programmed shrinkage of an organ
Uterus after childbirth, thymus in early-life, pro- and mesonephros

45
Q

What is reconstitution?

A

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
Q

What is dysplasia?

A

Abnormal maturation of cells within a tissue
Potentially irreversible
Often pre-cancerous condition

47
Q

What is atresia?

A

No orifice
Congenital imperforation of an opening
Examples: anus, vagina, pulmonary valve, small bowel

Semester 2 Pathological Processes (16 decks)

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