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Flashcards in Disorders of Growth Deck (55)
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1
Q

What is differentiation?

A

The process by which a less specialized cell becomes a more specialized cell type

2
Q

What is hyperplasia?

A

An increase in cell number

3
Q

Is hyperplasia always pathological?

A

No, can be physiological

4
Q

What is hypertrophy?

A

An increase in cell size

5
Q

Where does hypertrophy tend to occur?

A

In muscle: skeletal and cardiac

6
Q

What is atrophy?

A

Reduction in cell size and number in an organ that was normal size

7
Q

What are some of the causes of atrophy?

A

Ageing

Lack of use/stimulation

8
Q

What is hypoplasia?

A

Reduced size of an organ - never fully developed to normal size

9
Q

Which of the following - hyperplasia, hypertrophy, atrophy and hypoplasia - is not potentially reversible?

A

Hypoplasia

10
Q

What is metaplasia?

A

The replacement of one differentiated cell type with another mature differentiated cell type

11
Q

Give a clinical example of metaplasia.

A

Barrett’s oesophagus

12
Q

What is dysplasia?

A

Abnormality of development - alteration in size, shape, and organization of adult cells

13
Q

Which - metaplasia or dysplasia - is pre-malignant?

A

Dysplasia

14
Q

What are the three cell types?

A

Labile cells
Stable cells
Permanent cells

15
Q

What are labile cells?

A

Cells that are continuously dividing e.g. surface epithelium

16
Q

What are stable cells?

A

Cells with a low level of replicative activity
May divide rapidly when needed - many cells wait in stage G0 of cell cycle for recruitment
e.g. hepatocytes, fibroblasts, endothelium

17
Q

What are permanent cells?

A

Non dividing cells that are unable to re-enter the cell cycle
e.g. neurones, skeletal and cardiac muscle cells

18
Q

Why is regulation of the cell cycle important?

A

There are many things that could go wrong (e.g. incorrect DNA replication, too much recruitment of cells from G0) that could result in increased proliferation or mutation, leading to disease

19
Q

What is apoptosis?

A

Programmed cell death

20
Q

Is apoptosis always pathological?

A

No

21
Q

What are some inducers of apoptosis?

A
Withdrawal of growth factors
Viruses
Free radicals
Ionising radiation
DNA damage
Fas ligand/CD95 interaction
22
Q

Name some disorders in which there is increased apoptosis.

A

Neurodegenerative disorders
AIDS
Reperfusion injury

23
Q

Name some disorders in which there is reduced apoptosis.

A

Neoplasia

Auto-immune disease

24
Q

What is the Fas ligand/CD95?

A

A type-II transmembrane protein that belongs to the tumor necrosis factor (TNF) family
Its binding with its receptor induces apoptosis

25
Q

What is the p53 gene?

A

A tumour suppressor gene which regulates the cell cycle

26
Q

What is the Bcl-2 family?

A

A family of regulator proteins which regulate cell death, by either inducing or inhibiting apoptosis

27
Q

What is thought to be the major cause of replicative senescence?

A

Progressive telomere shortening

28
Q

Why do telomeres get shorter with each DNA replication?

A

DNA polymerase cannot replicate DNA at the very ends of chromosomes - the telomeres

29
Q

In which cells is telomerase - the enzyme responsible for maintenance of telomere length - present in?

A

Germ cells
Stem cells
Cancer cells

30
Q

What happens to somatic cells when their telomeres become too short?

A

Growth is arrested - the cells are irreversibly arrested in G0/G1 and lose the ability to respond to growth factors

31
Q

What is a neoplasm?

A

An abnormal mass of tissue
Growth exceeds and is uncoordinated with that of the normal tissues
Continues after cessation of the stimuli that evoked the change

32
Q

What are the characteristics of benign neoplasms?

A
They resemble normal tissue and are well differentiated
They grow by expansion and do not invade other tissues
They are encapsulated
No necrosis
Normal N:C ratio
Few mitotic figures
Minimal pleomorphism
Do not metastasise
33
Q

What are the characteristics of malignant neoplasms?

A
Invasive growth pattern
Not encapsulated
Necrosis common
N:C ratio increased
Pleomorphic
Mitotic figures more frequent/abnormal
May metastasise
34
Q

What name is given to a malignant tumour derived from squamous epithelium?

A

Squamous carcinoma

35
Q

What name is given to a malignant tumour derived from glandular epithelium?

A

Adenocarcinoma

36
Q

What are the components of a neoplasm?

A
Neoplastic cells
Blood vessels
Inflammatory cells - macrophages, lymphocytes, pleomorphs
Fibroblasts
Stroma
37
Q

What is the key difference between dysplastic cells and cancer cells?

A

Dysplastic cells are not invasive

38
Q

What is the definition of metastasis?

A

Tumour implants that are discontinuous with the primary lesion - “secondary” tumours

39
Q

What are some common sites for metastatic disease?

A
Regional lymph nodes
Liver
Lung 
Bone
Brain
Adrenal gland
Skin
40
Q

Which tumours tend to spread through the lymphatic route?

A

Carcinoma

41
Q

Which tumours tend to spread through the haematogenous route?

A

Sarcoma

42
Q

Which organs are very effective at arresting circulating cancer cells?

A

Lung and liver

43
Q

Does metastatic spread correlate with blood supply?

A

No

44
Q

Which cancers are at risk of direct implantation in terms of lymphatic spread?

A

Mesothelioma

Chondrosarcoma

45
Q

What are some of the key elements that allow cancer development?

A
As the tumour progresses:
Escape from senescence
Evasion of apoptosis
Limitless replication potential
Angiogenesis
Invasion & metastasis
46
Q

Why might cancer cells exhibit genomic instability?

A

They have defective DNA repair mechanisms - tumours are more likely to express various mutations

47
Q

What are the basic two steps of tumour development?

A

Initiation - electrophilic molecules, DNA damage

Promotion - stimulation of proliferation

48
Q

How do DNA viruses initiate carcinogenesis?

A

Do not contain oncogenes - they encode proteins that bind to and inactivate host proteins

49
Q

How do RNA viruses initiate carcinogenesis?

A

Contain specific viral oncogenes which are highly homologous to human genes

50
Q

What are some of the classical oncogenes?

A
PDGF
EGFR
ras
src
myc
Bcl2
51
Q

What are the four ways in which proto-oncogenes can be activated?

A

Amplification
Translocation
Point mutation (think ras)
Insertional mutagenesis

52
Q

What type of virus is the human papilloma virus?

A

DNA virus

53
Q

How might p53 or other tumour suppressor genes be inactivated?

A

Point mutation
Deletion
Degradation
Other structural changes

54
Q

What are some of the characteristics of classical oncogenes?

A

Stimulate cell proliferation
Inhibit cell death
Are dominant

55
Q

What are some of the characteristics of tumour suppressors?

A

Inhibit cell proliferation
Stimulate cell death
Are recessive