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Sem 2 - Pathological Processes > Cellular Adaptations > Flashcards

Cellular Adaptations Flashcards

1
Q

What determines the size of a cell population?

A
  • Depends on the rate of cell proliferation, cell differentiation and cell death by apoptosis.
  • Increased numbers of cells are seen with increased proliferation or decreased cell death.
  • Cell proliferation occurs in physiological and pathological conditions.
  • Excessive physiological stimulation can become pathological e.g. prostatic hypertrophy.
  • Proto-oncogenes regulation normmal cell proliferation.
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2
Q

How is cell proliferation controlled?

A
  • Largely by chemical signals from the microenvironment which wither stimulates or inhibit cell proliferation
  • When a signalling molecule binds to a receptor it results in the modulation of gene expression
  • Receptor usually in cell membrane but can be in the cytoplasm or nucleus (e.g. storoid receptors)
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3
Q

What can the chemical signal make the cell do?

A
  • Survive - resist apoptosis
  • Divide - enter the cell cycle
  • Differentiate - take on specialised form and finction
  • Die - undergo apoptosis
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4
Q

How can a cell population increase it’s number?

A

Increased growth occurs by:

  • Shortening the cell cyle
  • Conversion of quiescent cells to proliferating cells by making them enter the cell cycle.
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5
Q

Can you see the cell cycle by light microscopy?

A

You can only see mitosis

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6
Q

Can cells with damaged DNA replicate?

A

No!

There are three checkpoints to confirm its not mutated.

Restiction (in G1) , between G1 and S and between G2 and M

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7
Q

What is the restiction (R) point?

A
  • Most critical checkpoint
  • Majority of cell that complete cell cycle - point of no retun
  • 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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8
Q

How is the cell cycle controlled?

A
  • Cyclins and cyclin dependant kinases (CDKs)
  • CDKs become active by binding with cyclins
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9
Q

How many times can cells divide (not stem cells)?

A

Leonard Hayflick discovered Hayflick numbers / limits in 1961. This number vaires according to species (to do with size). It is the amount of times cell can divide.

Humans = 61.3

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10
Q

How can cels adapt?

A
  • Hyperplasia – cells increase in number above normal
  • Hypertrophy – cells increase in size
  • Atrophy – cells become smaller
  • Metaplasia – cells are replaced by cells of a different
    type
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11
Q

Are cellular adaptations reversible?

A

Yes

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12
Q

What is hyperplasia?

A

Increase in tissue or organ size due to increase cell numbers.

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13
Q

In which types of tissues does hyperplasia occur?

A
  • Labile or stable conditions
  • Caused by increased functional demand or hormonal stimulation.
  • Remains under physiological control and is reversible (cf neoplasia)
  • Can occur secondary to a pathological cuase but the proliferation itself is a normal response. (cf neoplasia when the proliferation itself it not normal)
  • Repreated cell divisions exposes the cell to the risk of mutations and neoplasia.
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14
Q

What physological examples are there of hyperplasia?

A
  • Proliferative endometrium under the infuence of oestrogen
  • Bone marrow produces erythrocytes in response to hypoxia
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15
Q

What pathological examples are there of hyperplasia?

A
  • Eczema
  • Thyroid goitre in iodine deficiency
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16
Q

What is hypertrophy?

A

Increase in tissue or organ size due to increased cell size.

17
Q

In what types of tissue does hypertrophy occur?

A
  • Labile, stable but especially permanent tissues.
  • Like hyperplasia, caused by increased functional demaind or hormonal stimulation.
  • Cells contain more structural components - workload is shared by a greater mass of cellular compoments
  • In labile and stable tissues hypertrophy usually occurs along with hyperplasia.
18
Q

What physiological examples are there of physiological hypertrophy?

A
  • Skeletal muscle
  • Pregnant uterus (hypertrophy and hyperplasia)
19
Q

What pathological examples are there of hypertrophy?

A
  • Bowel - muscles undergo hypertrophy to push contents out.
  • Bladder
  • Ventricular hypertrophy of the heart
20
Q

Why don’t atheletes get cardiac muscle hypertrophy?

A

Pathological cardiac hypertrophy - increase in amount of capillaries but not enough for size. Anopthia so get areas of fibrosis secondary to ischaemia. This can affect AP passage so arrythmias.

But, atheltes have hypertrophic heart and is fit because he can rest after it has been beating lots. But, if problems with bowels ect.. then no time off.

21
Q

What is compensatory hypertrophy?

A

If one of a pair gets smaller / stops working the the other will undergo hypertrophy to compensate. e.g. the kidneys

22
Q

What is atrophy?

A

Shrinkage of a tissue or organ due to an acquired decrease in size and / or number of cells.

23
Q

What is happening in the cell in atrophy?

A
  • Shrinkage in the size of the cell to a size at which survivial is still possible.
  • Reduced structural componants of the cell
  • May eventually result in cell death.
24
Q

Is tissue atrophy only a result of cell atrophy?

A
  • Organ / tissue atrophy typically due to combination of cellular atrophy and apoptosis
  • Is reversible but only up to a point.
25
Q

What happens in tissue atrophy?

A

Penrenchymal cells undergo atrophy and eventually die.

26
Q

What examples are there of physiological atrophy?

A

Decrease in size of uterus after giving birth

Ovarian atrophy in post menopausal women.

27
Q

What examples are there of pathological atrophy?

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
  • Inadequate blood supply: thinning of skin on legs with periphiral vascular disease.
  • Inadequate nutrition: wasting of muscles with malnutrition
  • Loss of endocrine stimuli: breast, reporductive organs.
  • Persistant injury: Polymyositis (infalmmtion of muscle)
  • Ageing = senile atrophy brain, heart
  • Pressure: tissues around an enlarging benign tumour (probably secondary to ischaemia.)
28
Q

What is atrophy of extracellular matrix?

A

Osteoporosis….

29
Q

What is metaplasia?

A

Reversible change of one mature cell differentiated cell type to another.

  • Due to altered stem cell differentiation
  • May represent adaptive substitution of cells tht are sensitive to stress by cell types bettwe able to withstand the adverse environment.
  • Metaplstic cells are fully differentiated and the process is reversible
  • Sometimes a prelude to dysplasia and cancer
  • No metaplasia across germ layers
  • Occurs only in labile or stable cell types
  • Involves expression of a new genetic program
30
Q

What examples are there of metaplasia?

A
  • In smokers, bronchial pseudostratifiedciliated epithelium changes to statified squamous epithelium due to effect of cigarette smoke
  • Stratified squamous epithelium changes to gastric glandular epithelium with persistant acid reflex (Barrett’s oesophagus)
  • The spleen can undertake the functions of the bone marrow by endergoing metaplasia.
  • Firoblasts in skeletal msucles udergo metaplasia to osteoblasts -Myositis ossificans. Occurs in children who dont rest after an injury.
31
Q

Does metaplasia predispose to cancer?

A

Yes! Epithelial metaplasia can be a prellude to dysplasia and cancer.

  • Barrett’s epithelium and oesophageal adenocarcinoma
  • Intestinal metaplasia of the stomach and gastric adenocarcinoma
  • Why is not inderstood.
32
Q

What is aplasia?

A
  • Complete failure of a specific tissue or organ to develop
  • An embryonia developmental disorder
  • e.g.
    • Thymic aplasia - infection and autoimmune problems
    • Apasia of a kidney
  • Also used to describe an organ whose cells have ceased to proliferate e.g. aplasia of bone marrow in aplastic anaemia
33
Q

What is hypoplasia?

A
  • Underdevelopment or incomplete development of tissue or organ at embryonic stage, inadequate number of cells.
  • In a spectum with aplasia
  • Not opposite of hyperplasia as it is congenital condition
  • Cf atrophy whick occur when existing part wastes away
  • Examples
    • Renal
    • Breast
    • Testicular in Klinefelter’s syndrome
    • Chambres of the heart
34
Q

What is involution?

A
  • Overlaps with atrophy
  • Normally programmed shrinkage of an organ
  • Uterus after childbirth, thymus in early life, pro- and mesonephros.
35
Q

What is reconstitution?

A

Replacement of a lost part of the body

e.g. Deer and its antlers.

If a small child under about 4 and you loose the tip of your finger, it has been known to growback perfectally.

36
Q

What is atresia?

A
  • ‘no orifice’
  • Congenital imperforation of an opening
  • e.g.
    • Pulmonary valve
    • Anus
    • Vagina
    • Small bowel
37
Q

What is dysplasia?

A
  • Abnormal maturation of celld within a tissue
  • Potentially reverdible
  • Often pre-cancerous conditions.

Sem 2 - Pathological Processes (13 decks)

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