MoD 7 Cell Adaptations Flashcards Preview

Amars Semester Two cards > MoD 7 Cell Adaptations > Flashcards

Flashcards in MoD 7 Cell Adaptations Deck (26)
1

How is cell signalling controlled?

Via chemicals that either stimulate or inhibit it.
The signalling molecule bind and it alts gene expression.

2

Name 3 method of cell signalling

Autocrine
Paracrine
Endocrine

3

What are growth factors?

Local mediators involved in cell proliferation
Coded for by proto oncogenes
They stimulate the transcription of genes that regulate the entry into the cell cycle and the safe passage through it.
Eg VEGF, EGF, PDGF, Granulocytes colony stimulating factor (used in chemo as it stimulates neutrophil production).

4

What is G0 of the cell cycle and once a cell enters it, can it come out of it?

It is a stage in the cell cycle where there is nothing occurring. Stabile cells/tissues enter G0 however if there is a large enough stimulus, the tissue can be persuaded to enter G1 of the cell cycle and proliferate.

5

Describe the key points of the cell cycle

Interphase is divided into G1/G2 and G0. Interphase exists either side of mitosis.
G1- cell grows, checkpoint and check for DNA damage (R point-below)
G2- cell prepares to divide. Checkpoint, DNA replicated?

The 'R' point - occurs at the end of G1
- most cells that pass G1 will compete the cell cycle.
- this checkpoint is most commonly altered in cancers.
- activation of this causes DNA repair or apoptosis (P53).

6

How is progression through the cell cycle controlled?

Via Cyclin dependent kinases (CDKs)
- complex with cyclins to become activated.
- acrivated CDKs phosphorylate proteins and drive the cell cycle
- CDKs are regulated by CDK inhibitors.

7

What is 'Hayflicks number' and its value?

The number of times a cell may regenerate.
It's value is approximately 61.3

8

Discuss hyperplasia

Increase in tissue size due to increase in cell numbers of the tissue. Occurs in stabile or labile tissue.
-result of increased functional demand
-this is reversible and under physiological control.
- neoplasia is a risk that hyper plastic tissues face due to the consistent cell divisions so there is increased risk of DNA mutation.
- can be physiological
- more RBC due to hypoxia. Endometrium thickening due to oestrogen.
- can be pathological
- enlarged thyroid/epidermal thickening.

9

What cells are more likely to see hypertrophy?

Permanent tissue cells.

10

With respect to cell size or numbers, what is hypertrophy?

Increase in tissue size to increase in cell size.

11

Describe the sequence of events leading to myocardial exhaustion in a patient with ventricular cardiac hypertrophy

VCH usually due to a stenotic valve so the ventricle hypertrophies. As the muscle is bigger, it needs more blood so new capillaries grow to serve the bigger muscle. However these capillaries are not enough to meet the demand and there are areas of ANOXIA. This decreases the efficiency of the heart so it keeps hypertrophying...anoxic tissue again...repeated cycle until the heart cannot continue -> exhaustion.

12

What is compensatory hypertrophy?

Eg if a kidney is removed, the other kidney grows in size to deal with the additional metabolic placed onto it.

13

What is atrophy?

Decrease in tissue size due to decrease in cell size and/or number.

14

With respect to atrophy, what is a 'residual body'

Anything a cell doesn't need becomes an aggregate and is known as the residual body. It can be seen to be the dustbin of the cell.
Parenchymal cells are lost first followed by stromal cells.

15

Describe one organ that undergoes physiological atrophy.

Post menopause, with the lack of oestrogen (causes thickening) the uterus undergoes atrophy.

16

Give three mechanisms of atrophy

Denervation atrophy - need to have a nervous supply to the muscles otherwise the can atrophy.

Functional demand atrophy - use it or lose it

Inadequate blood supply - eg thinning of the skin of the legs in PVD

17

Name the two mechanisms of atrophy

Cell death - apoptosis. If these cells are on the external surface then they are lost from the body. If not, they are removed via phagocytosis.

Cell shrinkage - harder as most of the cell components are needed for survival. Non-essential components can be lost.
- auto digestion can occur which digests as much as possible leaving residual bodies, which are then tagged for destruction by ubiquitin.

18

Define metaplasia.

REVERSIBLE change from one cell type to another.
Stem cells are effectively reprogrammed to produce different progeny. This is achieved via activation or inactivation of certain genes.

19

Why do cells under go metaplasia ?

Metaplasia occurs due to signals from molecules such as cytokines and growth factors. This is as a result of stimuli that cause proliferation, eg cigarette smoke.

20

What is the point of metaplasia ?

The new epithelium is more suited to its environment.
Eg in Barrets oesophagus. The stratified squamous cell epithelium lining of the oesophagus metaplases to simple columnar with goblet secreting mucus cells, as a result of the constant acidic environment.
This can progress to to dysplasia and then neoplasia.

21

Define aplasia.

Complete failure of a tissue or organ to develop. This is an embryonic development failure.

22

Define Involution

Normal programmed shrinkage of an organ or tissue.
Eg, the uterus and delivery of a baby.

23

Define Hypoplasia.

Congenital under development of an organ or tissue.
NOT the opposite of hyperplasia and Hypoplasia is an embryonic defect.
Eg renal hypoplasia

24

Define atresia.

A body orifice is abnormally closed or absent.
Eg vaginal atresia, tricuspid atresia.

25

Define dysplasia.

Abnormal maturation of cells within a tissue. This can be reversed.
It is often pre cancerous.

26

What are the outcomes of cell signalling? (4)

Death- undergo apoptosis
Survival- resist apoptosis
Divide- enter cell cycle
Differentiate- take on special form and function