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Y1 TP2 Pathological Processes (topic 3 Onwards) > 7. Cellular Adaptations > Flashcards

7. Cellular Adaptations Flashcards

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
Q

Hypertrophy

A

• Hypertrophy – cells increase in size

26
Q

Atrophy

A

• Atrophy – cells become smaller

27
Q

Metaplasia

A

• Metaplasia – cells are replaced by cells of a different type

28
Q

Hyperplasia - features

A

• 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
Q

Hyperplasia - physiological examples

A

○ Proliferative endometrium under influence of oestrogen

○ Bone marrow produces erythrocytes in response to hypoxia (high altitude training)

30
Q

Hyperplasia - physiological examples pathological

A

○ Exczema – proliferation of skin cells

○ Thyroid goitre in iodine deficiency – thyroid becomes much bigger

31
Q

Hypertrophy features

A
  • 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
Q
  • physiological examples hypertrophy
A

○ Atheltes body builders – skeletal muscle

○ Pregnant uterus (hypertrophy +hyperplasia)

33
Q

Pathological examples- hypertrophy

A

○ 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
Q

Compensatory hypertrophy

A

• One kidney does more work to make up for removed kidney

35
Q

Atrophy - features

A
  • 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
Q

Atrophy physiological example

A
  • Ovarian atrophy in post menopausal women

* Decrease in size of uterus after parturition

37
Q

Atrophy example pathological

A

• 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
Q

Atrophy of extracellular matrix -bone

A
  • In bed ridden patients or astronauts as they don’t use bone much
    • Osteroporosis
39
Q

Apoptosis - features

A
  • Enzymes
    • Growth factor withdrawal
    • Engulf
    • This can be reversible up to a certain point
40
Q

Metaplasia- features

A
  • 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
Q

Metaplasia examples

A
  • 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
Q

Myeloid metaplasia

A

• Myeloid metaplasia – bone marrow is destroyed but spleen undergoes metaplasia to become bone marrow

43
Q

Myosotis ossificans

A

• Myositis ossificans, metaplasia of fibroblasts in muscle that becoem osteoblasts that produce bone

44
Q

Does metaplasia predispose to cancer?

A

• 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
Q

Aplasia

A

—> organ fails to form
• Complete failure of a specific tissue or organ to develop
• An embryonic developmental disorder

46
Q

Aphasia - examples

A
  • 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
Q

Hypoplasia

A

—> 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
Q

Hypoplasia - excemples

A
  • Renal
    • Breast
    • Testicular in Klinefelter’s syndrome
    • Chambers of the heart
49
Q

Involution

A

—> Overlaps with atrophy = Normal programmed shrinkage of an organ
• Uterus after childbirth, thymus in early life, proand mesonephros

50
Q

Reconstitution

A

—> 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
Q

Atresia

A

—> no lumen, lumen is not continus

  • ‘No orifice’
  • Congenital imperforation of an opening
  • Examples: Pulmonary valve Anus Vagina Small bowel
52
Q

Dysplasia

A

—> Abnormal maturation of cells within a tissue – go from a normal tissue to an abnormal tissue

  • Potentially reversible
  • Often pre-cancerous condition
53
Q

Dysplasia - example

A

e.g. cervix – smear test
• Dysplaisia in hpv develops abnormal looking cells
Look for how many and what kind of abnormal cells are observed

Y1 TP2 Pathological Processes (topic 3 Onwards) (9 decks)

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