Growth disorders 1

Question 1

Define Agenesis

Answer 1

No primordium i.e. there is no development of a structure

Is a congenital problem

Question 2

Define Aplasia

Answer 2

A structures rudiment is present i.e. starts developing, then stops
Is a congenital problem

Question 3

Define Hypoplasia

Answer 3

Lack of development to full size

Is a congenital problem

Question 4

Are atrophy, hypertrophy and hyperplasia quantitative or qualitative adaptive responses?

Answer 4

Quantitative - there is a change in size or number of cells

Question 5

Define atrophy

Answer 5

A structure was a normal size, but is now reduced in either size or number or cells

Question 6

Define hypertrophy

Answer 6

Was normal, is now reversibly increased in size because of an increase in SIZE of component cells

Question 7

Define hyperplasia

Answer 7

Was normal, is now reversibly increased in size because of an increase in NUMBER of cells

Question 8

Which stage of the cell cycle is altered in hypertrophy?

Answer 8

Cells remain in the RNA/protein synthesis stage, inhibiting DNA synthesis and causing cell enlargement without division

Question 9

Which stage of the cell cycle is altered in hyperplasia?

Answer 9

More cells pass through mitosis because of a block in the pathway to G0

Question 10

What are some consequences of starvation?

Answer 10

Generalised atrophy, with replicating cells the most affected aka liver, spleen and skeletal muscles.

Question 11

What are some causes of localised atrophy?

Answer 11

Ischaemia, pressure, disuse, denervation, reduced blood supply

Question 12

Give an example of localised atrophy?

Answer 12

If a salivary gland duct stone forms (usually because of stasis), back pressure builds up in the duct and moves back into the mucous producing cells. This causes irreversible damage, and atrophies these cells

Question 13

Give an example of physiological hyperplasia

Answer 13

Lymph nodes will enlarge and become painful in response to infection because they develop germinal centres, which cause cellular dividing

Question 14

How can thyroid hyperplasia be both physiological and pathological?

Answer 14

Physiological - higher concentrations of thyroxin can increase the number of follicular epithelial cells. This is usually in response to puberty or pregnancy
Pathological - Grave’s disease causes an excess of hormones produces by the thyroid, necessitating hyperplasia

Question 15

What happens in cardiac cells that undergo hypertrophy to meet demand?

Answer 15

There’s an increase in synthesis of RNA, mitochondria, myofilament proteins etc. However, this can only occur up to a certain point, which is limited by blood supply, oxidative capacity of mitochondria etc. There is degenerative change after this point

Question 16

Can compensatory hypertrophy occur?

Answer 16

Yes, usually in response to atrophy i.e. one kidney may atrophy and in response the other will undergo hypertrophy

Question 17

Define metaplasia and describe the pathway by which it may occur

Answer 17

Metaplasia is a reversible condition in which there is a change of one type of differentiated cell to another type of differentiated cell
This usually arises via a proliferation of stem cells with transformation along a different pathway

Question 18

Give an example of metaplasia in the oesophagus

Answer 18

This is called Barrett’s oesophagus and occurs in response to acid reflux. The epithelium changes from squamous to glandular to that the skin can cope with the acid. This does cause a higher susceptibility to adenocarcinoma

Question 19

What is the significance of metaplasia?

Answer 19

Metaplasia and neoplasia may result from the same causative agent. Metaplastic tissues provide a fertile ground for neoplasia to develop, and neoplasia can become malignant.
Metaplasia also occurs in malignancy

Question 20

What are the four mechanisms of atrophy?

Answer 20

1. Decrease in anabolism
2. Increase in catabolism
3. Reduction in cell replication
4. Increased apoptosis

Question 21

What induces metaplasia?

Answer 21

Changes i signals generated by a mixture of cytokines, growth factors and extracellular matrix changes