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Principles > Disorders of Growth > Flashcards

Disorders of Growth Flashcards

1
Q

What is differentiation?

A

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

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2
Q

What is hyperplasia?

A

An increase in cell number

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3
Q

Is hyperplasia always pathological?

A

No, can be physiological

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4
Q

What is hypertrophy?

A

An increase in cell size

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5
Q

Where does hypertrophy tend to occur?

A

In muscle: skeletal and cardiac

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6
Q

What is atrophy?

A

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

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7
Q

What are some of the causes of atrophy?

A

Ageing

Lack of use/stimulation

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8
Q

What is hypoplasia?

A

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

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9
Q

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

A

Hypoplasia

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10
Q

What is metaplasia?

A

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

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11
Q

Give a clinical example of metaplasia.

A

Barrett’s oesophagus

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12
Q

What is dysplasia?

A

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

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13
Q

Which - metaplasia or dysplasia - is pre-malignant?

A

Dysplasia

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14
Q

What are the three cell types?

A

Labile cells
Stable cells
Permanent cells

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15
Q

What are labile cells?

A

Cells that are continuously dividing e.g. surface epithelium

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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

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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

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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

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19
Q

What is apoptosis?

A

Programmed cell death

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20
Q

Is apoptosis always pathological?

A

No

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21
Q

What are some inducers of apoptosis?

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

Name some disorders in which there is increased apoptosis.

A

Neurodegenerative disorders
AIDS
Reperfusion injury

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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

Principles (8 decks)

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