Cellular Adaptations

Question 1

What determines the size of a cell population?

Answer 1

The size of a cell population depends on proliferation, differentiation and apoptosis of the cells. Increased numbers are seen with increased proliferation/decreased cell death.

Question 2

Proliferation occurs in physiological and pathological conditions and also in cases where excess physiological stimulation turns pathological - give an example.

Answer 2

Prostatic hypertrophy.

Question 3

What regulates and controls normal cell proliferation?

Answer 3

Porto-once genes regulate normal cell proliferation. It’s controlled largely by chemical signs from the microenvironment, which may stimulate or inhibit. A signalling molecule will bind to a receptor to modulate the gene expression. Receptors are usually in the cell membrane, but can be nuclear or cytosolic.

Question 4

Chemical signals can make cells go through many changes in complicated processes with limited outcomes, what are the options?

Answer 4

Survive, die, differentiate (specialised form and function) or divide.

Question 5

What are the different ways to increase the growth of a cell?

Answer 5

Shortening the cell cycle and convert quiescent cells to proliferating - make them enter the cell cycle (G0->G1).

Question 6

When can cells be viewed by light microscopy?

Answer 6

During mitosis and cytokinesis.

Question 7

What is the point of checkpoints on the cell cycle?

Answer 7

Notice any DNA damage for repair or apoptosis before division, so cells with damaged DNA can’t normally replicate.

Question 8

What is the restriction (R) point in the cell cycle?

Answer 8

The most critical checkpoint - most of the cells past the R point will complete the cell cycle. It is the most commonly altered checkpoint in cancers; activation of it delays the cycle and triggers DNA repair mechanisms/apoptosis via p53.

Question 9

What is the cell cycle controlled by?

Answer 9

Cyclins and CDKs (cyclin-dependent kinases), which become active by binding with cyclins. Cyclin binds to a substrate that needs phosphorylation.

Question 10

What is the Hayflick number/limit?

Answer 10

How many times a cell may divide (without telomerase).

Question 11

Cells can adapt in various ways, once they’ve done this, can they go back?

Answer 11

By the majority of methods, cell adaptation is reversible.

Question 12

What is hyperplasia and in which tissues does it occur?

Answer 12

Hyperplasia is an increase in tissue or organ size due to increased cell numbers, in labile or stable tissue.

Question 13

What causes hyperplasia? (And hypertrophy)

Answer 13

Hyperplasia is caused by increased functional demand/hormonal stimulation, which remains under physiological control and is reversible. It may occur secondary to a pathological cause, but the proliferation itself is a normal response. Repeated cell divisions expose the cell to the risks of mutations and neoplasia.

Question 14

Give examples of physiological hyperplasia and that secondary to a pathological cause.

Answer 14

Hypoxia induced bone marrow erythropoiesis and thyroid goitre.

Question 15

What is hypertrophy and in which tissues does it occur? What about compensatory hypertrophy?

Answer 15

Hypertrophy is an increase in tissue or organ size from increased cell size, in labile, stable and especially permanent tissues.
Compensatory hypertrophy is when damage to one of two or a part of organ induces hypertrophy in the rest (e.g. Kidneys).

Question 16

What is the link between hypertrophy and hyperplasia.?

Answer 16

The causes are the same and in labile and stable tissue, they often occur together. For example, a pregnant uterus has both, but right ventricle hypertension will only lead to hypertrophy. Athletes get cardiomyocytes hypertrophy to a degree, but when they rest, more blood vessels can grow in (unlike in the case of hypertension).

Question 17

What is the post of hypertrophy?

Answer 17

The cells contain more structural components, so the work load is shared by a greater mass.

Question 18

What is atrophy?

Answer 18

Shrinkage of tissue or an organ due to an acquired decrease in size and/or number of cells (more associated with pathology). Shrinkage of the size of a cell to a size where survival is still possible - reduced structural components of a cell, may eventually result in cell death. Organ/tissue atrophy is due to a combination of cellular atrophy and apoptosis - it’s reversible up to a point.

Question 19

In cases of tissue atrophy, _____________ is targeted and ___________________ are produced. The residual bodies and ________ cells left behind mean that the tissue looks ___________. An example of physiological atrophy is _________ atrophy in post-______________ women.

Answer 19

Parenchyma
Autophagosomes
Stroma
Fibrotic
Ovarian
Menopausal

Question 20

What are the different types of pathological tissue atrophy? (9)

Answer 20

Atrophy of disease - reduced functional demand/workload; reversible with activity.
Denervation atrophy - loss of innervation leads to muscle wastage. Inadequate blood supply (gradual) e.g. Thinning of the skin on legs with peripheral vascular disease. Inadequate nutrition - wasting of muscles (brain protected-last damaged). Loss of endocrine stimuli - breast, reproductive organs. Persistent injury - polymyositis. Senile atrophy - ageing (brain, heart).
Pressure - tissue around an enlarging benign tumour (ischaemia). Atrophy of ECM e.g. Osteoporosis (pressure and mobility are good stimulants for bone proliferation).

Question 21

What is metaplasia and why does it happen?

Answer 21

The reversible change of one differentiated cell type into another, due to altered stem cell differentiation. It may represent the adaptive substitution of cell types sensitive to stress, so they can better withstand an adverse environment.
Metaplastic cells are fully differentiated.

Question 22

Metaplasia is sometimes a prelude to _________ and cancer. There is no metaplasia across _____ layers. It occurs in ________/stable cell types and involves the expression of a new __________ programme.

Answer 22

Dysplasia
Germ
Labile
Genetic

Question 23

Give some examples of metaplasia and the types of cancer it may precede.

Answer 23

Bronchial pseudostratified ciliated epithelium –> stratified squamous due to cigarette smoke, or a spleen becoming haemopoietic.
Epithelial metaplasia can be a prelude to dysplasia and cancer - Barette’s epithelium and oesophageal carcinoma or intestinal metaplasia of the stomach and gastric adenocarcinoma.

Question 24

What is aplasia? Give an example.

Answer 24

Aplasia is the complete failure of a specific tissue/organ to develop - embryonic developmental disorder e.g. Thymic aplasia leading to infections and autoimmune problems. It also describes an organ whose cells have ceased to proliferate e.g. Aplasia of bone marrow in aplastic anaemia.

Question 25

What is hypoplasia?

Answer 25

Hypoplasia is the under or incomplete development of a tissue or organ at the embryonic stage, resulting in an inadequate number of cells. It is in a spectrum with aplasia, but is not the opposite of hyperplasia as it is congenital.

Question 26

What is involution?

Answer 26

Involution overlaps with atrophy, in that it’s normal programmed shrinkage of an organ, such as the uterus after childbirth or the thymus in adolescence.

Question 27

What is reconstitution?

Answer 27

Reconstitution is the replacement of a lost body part, which is unusual in humans - if under 4.5 years, the tip of the finger may grow back.

Question 28

What is atresia?

Answer 28

Atresia means ‘no orifice’ as is a congenital imperforation of an opening (e.g. Anus or small bowel).

Question 29

What is dysplasia?

Answer 29

Dysplasia is the abnormal maturation of cells within a tissue, which is potentially reversible and often pre-cancerous.