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Mechanisms of Disease > Lecture 7.1: Cellular Adaptations > Flashcards

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
Q

What is Dysplasia?

A

A term used to describe the presence of abnormal cells within a tissue or organ, often pre-cancerous

26
Q

Are Cell Adaptations reversible?

A

Yes

27
Q

What effect does a harmful agent have on regeneration?

A

It defines whether there will be resolution or scarring

28
Q

Resolution vs Scarring

A

In Resolution: harmful agent removed, limited tissue damage, regeneration

In Scarring: harmful agent persists, extensive tissue damage, permanent cells

29
Q

What is Reconstitution?

A

• Replacement of a lost part of the body
• Requires the coordinated regeneration of several types of cells

30
Q

Reasons for Atrophy (4)

A

• 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
Q

Mechanisms of Atrophy: Increased Protein Degradation

A

Ubiquitin Proteasome Pathway

32
Q

What is Involution?

A

It is physiological atrophy by apoptosis

33
Q

What is Neoplasia?

A

The uncontrolled, abnormal growth of cells or tissues in the body, cancerous

34
Q

Mechanisms of Atrophy: Loss of Endocrine Stimuli

A

• Breast
• Reproductive Organs

35
Q

Mechanisms of Atrophy: Persistent Injury

A

Polymyositis (inflammation of muscle)

36
Q

Mechanisms of Atrophy: Aging

A

Senile Atrophy of Brain and Heart

37
Q

Mechanisms of Atrophy: Pressure

A

• Tissues around an enlarging benign tumour are compressed
• Probably secondary to ischaemia

Mechanisms of Disease (11 decks)

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