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Pathological Processes > Cellular adaptations > Flashcards

Cellular adaptations Flashcards

1
Q

Increased growth occurs by:

A

Shortening the cell cycle

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

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2
Q

G1 checkpoint

A

Enter S
Is cell big enough?
Is environment favourable?
Is DNA damaged?

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3
Q

G2 checkpoint

A

Enter M
Is all DNA replicated?
Is cell big enough?

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4
Q

What is the restriction (R) point?

A
  • Majority of cells that pass R point will complete cell cycle
  • Most commonly altered checkpoint in cancer cells
  • Checkpoint activation delays cell cycle and triggers DNA repair mechanisms or apoptosis via p53
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5
Q

How is the cell cycle controlled?

A

Cyclin dependent kinases (CDK) become active by binding to cyclins

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6
Q

Human Hayflick limit

A

61.3

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7
Q

How can cells adapt?

A

Hyperplasia - increase in number
Hypertrophy - increase in size
Atrophy - cells become smaller in size or number
Metaplasia - cells are replaced by cells of a different type

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8
Q

In which types of tissue does hyperplasia occur?

A
  • Labile or stable
  • Caused by increased functional demand or hormonal stimulation
  • Reversible and under physiological control
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9
Q

Examples of physiological hyperplasia

A
  • Proliferative endometrium under influence of oestrogen

- Bone marrow produces erythrocytes in response to hypoxia

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10
Q

Exampes of pathological hyperplasia

A
  • Eczma

- Thyroid goitre in iodine deficiency

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11
Q

In which type of tissue

A
  • Labile and stable
  • Caused by increased functional demand or hormonal stimulation
  • Cells contain more structural components
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12
Q

Compensatory hypertrophy

A

Increase in size of an organ or tissue when called upon to do additional work or to perform the work of destroyed tissue or of a paired organ.

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13
Q

Examples of physiological atrophy

A
  • Ovarian atrophy in post menopausal women

- Uterus after child birth

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14
Q

Examples of pathological atrphy

A
  • Atrophy of disuse
  • Denervation atrophy
  • Inadequate blood supply
  • Inadequate nutrition
  • Loss of endocrine stimuli
  • Persistent injury (polymyositis)
  • Senile atrophy
  • Pressure (sometimes secondary to ischaemia in tumoirs)
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15
Q

What is metaplasia?

A
  • Labile and stable tissues
  • Due to altered stem cell differentiation
  • May be adaptive, cells that can withstand stress better
  • Metaplastic cells are fully differentiated and the process is reversible
  • Sometimes a prelude to dysplasia and cancer
  • No metaplasia across germ cells
  • Expression of a new genetic programme
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16
Q

Examples of metaplasia

A
  • Bronchial pseudostratified ciliated epithelium –> stratified squamous epithelium due to effect of cigarette smoke
  • Stratified squamous epithelium –> gastric glandular epithelium with persistent acid reflux (Berrett’s oesophagus)
  • If there is damage to bone marrow the spleen can take over blood cell production
17
Q

Metaplasia predisposition to cancer

A
  • Barrett’s epithelium and oesophageal adenocarcinoma

- Intestinal metaplasia of the stomach and gastric adenocarcinoma

18
Q

What is aplasia?

A
  • Complete failure of a specific tissue or organ to develop

- e.g. Thymic aplasia (infections and autoimmune problems), aplasia of a kidney

19
Q

What is hypoplasia?

A
  • Underdevelopment of incomplete development of tissue or organ at embryonic stage
  • e.g. testicular in Klinefelter’s syndrome
20
Q

What is involution?

A
  • Normal programmed shrinkage of an organ

- e.g. uterus after childbirth, thymus in early life

21
Q

What is reconstitution?

A
  • Replacement of a lost part of the body

- e.g. reports of finger growing back in child under 4

22
Q

What is atresia?

A

Congenital imperforation of an opening

23
Q

What is dysplasia?

A
  • Abnormal maturation of cells within a tissue
  • Potentially reversible
  • Often pre-cancerous condition

Pathological Processes (6 decks)

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