Lecture 7.1: Cellular Adaptations Flashcards

1
Q

Types of Cell Adaptation (5)

A

1) Regeneration
2) Hyperplasia
3) Hypertrophy
4) Atrophy
5) Metaplasia

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2
Q

What does size of cell population depend on?

A

• Rate of Cell Proliferation
• Cell Differentiation
• Cell Death by Apoptosis

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3
Q

What is Cell Proliferation controlled by?

A

• Signals from microenvironment which stimulate/ inhibit cell proliferation
• Hormones
• Local mediators
• Direct cell-cell or cell-stroma contact

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4
Q

Autocrine Cell Signalling

A

The same secreting and responding cell

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5
Q

Paracrine Cell Signalling

A

Secreting cell and responding cell are different, but co-located

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6
Q

Endocrine Cell Signalling

A

Endocrine organs synthesise hormones conveyed through blood stream-target organs distant from site of synthesis

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7
Q

Final Outcomes of Signalling Biochemistry (4)

A

• Survive (resist apoptosis)
• Divide (enter cell cycle)
• Differentiate (take on specialised form and function)
• Die (undergo apoptosis)

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8
Q

Epidermal Growth Factor [EGF]: What is it? What produces it? Receptor?

A

• Mitogenic for epithelial cells, hepatocytes and fibroblasts
• Produced by keratinocytes, macrophages and inflammatory cells
• Binds to epidermal growth factor receptor (EGFR)

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9
Q

Vascular Endothelial Growth Factor [VEGF]: What is it? What produces it?

A

• Potent inducer of blood vessel development (vasculogenesis)
• Role in growth of new blood vessels (angiogenesis) in tumours
• Role in chronic inflammation and wound healing
• Tumour cells, Macrophages, Platelets, Keratinocytes, Renal Mesangial

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10
Q

Platelet-Derived Growth Factor [PDGF]: What is it? What produces it?

A

• Causes migration & proliferation of fibroblasts, smooth muscle cells &
monocytes
• Stored in platelet alpha granules and released on platelet activation
• Produced by macrophages, endothelial cells, smooth muscle cells and
tumour cells

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11
Q

Granulocyte Colony Stimulating Factor [GCSF]

A

• Treatment to stimulate poorly functioning bone marrow
• Glycoprotein that stimulates the bone marrow to produce granulocytes and
stem cells and release them into the bloodstream

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12
Q

What is the most important checkpoint in the cell cycle?

A

• The Restriction (R) Point
• It is towards the end of G1, is the most critical checkpoint
• Is most commonly altered checkpoint in cancer cells

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13
Q

What is Control of the Cell Cycle managed by?

A

• Tightly regulated by proteins called cyclins and associated enzymes called
cyclin-dependent kinases (CDKs)
• CDKs become active by binding to and complexing with cyclins

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14
Q

How do CDKs drive the Cell Cycle?

A

• Activated CDKs drive the cell cycle
• They phosphorylate proteins critical for cell cycle transitions
• E.g. retinoblastoma susceptibility protein
• Activity of cyclin-CDK complexes is tightly regulated by CDK inhibitors
• Some growth factors shut off production of these inhibitors

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15
Q

What are Labile Cells? Examples?

A

• Cells that continuously multiply and divide throughout life
• Skin Epidermis
• Gut Epithelium
• Bone Marrow

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16
Q

What are Stable Cells? Examples?

A

• Cells that multiply only when needed
• Spend most of the time in the quiescent G0 phase of the cell cycle
• But can be stimulated to enter the cell cycle when needed
• Liver Hepatocytes
• Bone Osteoblasts
• Proximal Tubules of the Kidney
• Endocrine Glands

17
Q

What are Permanent Cells? Examples?

A

• Cells that are unable to replicate in postnatal life
• Cannot mount an effective proliferative response to significant cell loss
• Nervous Cells
• Cardiac Muscle Cells
• Skeletal Muscle Cells

18
Q

What is Regeneration?

A

Regeneration is the natural process of replacing or restoring damaged or missing cells, tissues and organs by by identical cells to maintain tissue or organ size

19
Q

What is Hyperplasia?

A

An increase in the number of cells in an organ or tissue, these cells are also enlarged

20
Q

What is Hypertrophy?

A

A considerable increase in the size of an organ or tissue, caused by enlargement of its cellular components not hyperplasia

21
Q

What is Atrophy?

A

A decrease in the size of a tissue or organ due to cellular shrinkage

22
Q

What is Metaplasia?

A

The replacement of one differentiated somatic cell type with another differentiated somatic cell type in the same tissue, it is a reversible change

23
Q

What is Aplasia?

A

The lack of development of a tissue/limb/organ during embryonic life

24
Q

What is Hypoplasia?

A

A condition of arrested development in which an organ or part remains below the normal size or in an immature state

25
What is Dysplasia?
A term used to describe the presence of abnormal cells within a tissue or organ, often pre-cancerous
26
Are Cell Adaptations reversible?
Yes
27
What effect does a harmful agent have on regeneration?
It defines whether there will be resolution or scarring
28
Resolution vs Scarring
In Resolution: harmful agent removed, limited tissue damage, regeneration In Scarring: harmful agent persists, extensive tissue damage, permanent cells
29
What is Reconstitution?
• Replacement of a lost part of the body • Requires the coordinated regeneration of several types of cells
30
Reasons for Atrophy (4)
• Reduced functional demand and workload/Disuse Atrophy • Loss of innervation/Denervation atrophy • Inadequate blood supply/Avasular Atrophy • Inadequate nutrition: wasting of muscles with malnutrition = sarcopaenia
31
Mechanisms of Atrophy: Increased Protein Degradation
Ubiquitin Proteasome Pathway
32
What is Involution?
It is physiological atrophy by apoptosis
33
What is Neoplasia?
The uncontrolled, abnormal growth of cells or tissues in the body, cancerous
34
Mechanisms of Atrophy: Loss of Endocrine Stimuli
• Breast • Reproductive Organs
35
Mechanisms of Atrophy: Persistent Injury
Polymyositis (inflammation of muscle)
36
Mechanisms of Atrophy: Aging
Senile Atrophy of Brain and Heart
37
Mechanisms of Atrophy: Pressure
• Tissues around an enlarging benign tumour are compressed • Probably secondary to ischaemia