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ESA 2- Mechanisms of Disease > Cellular Adaptations > Flashcards

Cellular Adaptations Flashcards

1
Q

What does the size of cell populations in adults depend?

A

The rate of cell proliferation, cell differentiation and cell death by apoptosis

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2
Q

What are increased cell numbers seen with?

A

Increased cell proliferation or decreased cell death

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3
Q

What may cell proliferation occur as the result of?

A

Physiological or pathological conditions

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4
Q

Give an example of where excessive physiological stimulation can become pathological

A

Prostatic hyperplasia

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5
Q

What do proto-oncogenes do?

A

Regulate normal cell proliferation

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6
Q

How do cells in a multicellular organisms communicate?

A

Through chemical signals

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7
Q

How is cell proliferation largely controlled?

A

Largely by signals (soluble or contact dependant) from the microenvironment which either stimulate or inhibit cell proliferation

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8
Q

What are the potential final outcomes of signalling biochemistry?

A

Divide
Differentiate
Survive
Die

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9
Q

How do cells divide?

A

They enter the cell cycle

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10
Q

What happens when cells differentiate?

A

They take on a specialised form and function

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11
Q

How do cells die when signalled?

A

They undergo apoptosis

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12
Q

What are the types of cell signalling?

A

Autocrine
Paracrine
Endocrine

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13
Q

What is autocrine signalling?

A

Cells respond to the signalling molecules that they themselves produce

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14
Q

What is intracrine signalling?

A

A type of autocrine signalling whereby the cell synthesises a factor which has an effect by binding to intracellular receptors within the cell.
The factor is therefore not secreted by the cell

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15
Q

What is paracrine signalling?

A

A cell produced the signalling molecule, which acts of adjacent cells

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16
Q

Where are the effector cells in paracrine signalling?

A

Close to the secreting cell

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17
Q

Are the cells affecting by paracrine signalling the same as the one secreting?

A

No, they are often of a different type

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18
Q

What is endocrine signalling?

A

Hormones are synthesised by cells in an endocrine organ, and then conveyed in the blood stream to target cells to effect physiological activity

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19
Q

What happens when a signalling molecule binds to a receptor?

A

It causes a series of events, which results in modulation of gene expression

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20
Q

Where are the receptors to signalling molecules located?

A

Usually in the cell membrane, but can also be in the cytoplasm or nucleus

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21
Q

Give an example of a type of receptor located in the nucleus?

A

Steroid hormone receptors

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22
Q

What can cell to cell signalling be via?

A

Local mediators
Direct cell-cell or cell-stroma contract
Hormones

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23
Q

What is particularly important amongst local mediators for cell proliferations?

A

Growth factors

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24
Q

What are growth factors?

A

Polypeptides that act on specific cell surface receptors

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25
Q

What codes for growth factors?

A

Proto-oncogenes

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26
Q

How do growth factors differ from hormones?

A

Hormones from endocrine organs travel via the blood stream to reach their target cells, whereas growth factors act only over a short distance, or on the secreting cell itself

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27
Q

Do growth factors act on many cell types, or restricted targets?

A

There are many different types of growth factors, some which act on many cell types and some on restricted targets

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28
Q

What do growth factors do?

A

Stimulate cell proliferation or inhibition

May also affect cell locomotion, contractility, differentiation viability, activation and angiogenesis

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29
Q

How do growth factors exert their effects?

A

They bind to specific receptors and stimulate transcription of genes that regulate the entry of the cell into the cell cycle and the cell’s passage through it

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30
Q

Give 4 examples of growth factors

A

Epidermal growth factor
Vascular endothelial growth factor
Platelet-derived growth factor
Granulocyte colony-stimulating factor

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31
Q

What does epidermal growth factor (EGF) do?

A

Mitogenic for epithelial cells, hepatocytes and fibroblasts.

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32
Q

What produces EGF?

A

Keratinocytes, macrophages and inflammatory cells

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33
Q

What does EGF bind to?

A

Epidermal growth factor receptor (EGFR)

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34
Q

What does vascular endothelial growth factor (VEGF) do?

A

It is a potent inducer of blood vessel development (vasculogenesis), and has a role in growth of new blood vessels (angiogenesis) in tumours, chronic inflammation and wound healing

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35
Q

Where is platelet-derived growth factor (PDGF) stored?

A

In platelet α granules

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36
Q

When is PDGF released?

A

On platelet activation

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37
Q

Other than platelets, what produced PDGF?

A

Macrophages, endothelial cells, smooth muscle cells and tumour cells

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38
Q

What doe PDGF do?

A

Causes migration and proliferation of fibroblasts, smooth muscle cells and monocytes

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39
Q

What does granulocyte colony-stimualting factor (G-CSF) do?

A

Stimulates the bone marrow to produce granulocytes, particularly neutrophils, and release them into the blood

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40
Q

What is G-CSF used as?

A

A treatment to stimulate poorly functioning bone marrow, e.g. during chemotherapy

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41
Q

What happens when a cell receives instruction to divide?

A

The cell enters the cell cycle

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42
Q

What is the sequence of the cell cycle?

A

G1 → S → G2 → M

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43
Q

What happens after cell cycle completion?

A

The cell either re-starts to process from G1, or exists (G0) until further growth signals occur

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44
Q

What can happen to cells in G0?

A

They can undergo terminal differentiation

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45
Q

What is the result if cells undergo terminal differentiation?

A

There is a permanent exit from the cell cycle

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46
Q

How does increased growth of tissue occur?

A

Either by shortening the cell cycle, or by conversion of quiescent cells to proliferating cells by making them enter the cell cycle

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47
Q

What can be seen of the cell cycle under the light microscope?

A

Only M (mitosis) phase is distinctive

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48
Q

What does the M phase of the cell cycle consist of?

A

Mitosis and cytokinesis

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49
Q

What is mitosis?

A

Cellular division

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50
Q

What is cytokinesis?

A

Cell division to yield two daughter cells

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51
Q

What is the part of cell cycle that isn’t M called?

A

Interphase

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52
Q

What does interphase encompasses?

A

G1, S, and G2

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53
Q

What is G1?

A

Gap 1- pre synthetic, where the cell grows

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54
Q

What is S?

A

DNA synthesis

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55
Q

What is G2?

A

Gap 2, premitotic where the cell prepares to divide

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56
Q

Cumulatively, what does interphase include?

A

DNA replication and protein synthesis for growth in cell size

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57
Q

What is cell cycle progression controlled by?

A

Key ‘checkpoints’ which sense damage to DNA and ensure cells with damaged DNA do not replicate

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58
Q

What is the most critical cell cycle checkpoint?

A

Restriction (R) point

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59
Q

When is R?

A

Towards the end of G1

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60
Q

What happens to cells that pass the R checkpoint?

A

The majority of them will complete the full cell cycle

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61
Q

What happens if R checkpoint activation occurs?

A

The p53 protein suspends the cell cycle and triggers DNA repair mechanisms, or, if the DNA cannot be repaired, apoptosis.

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62
Q

Where are the other cell cycle checkpoints?

A

At the G1/S transition, and G2/M transition

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63
Q

What is checked for at the G1/S checkpoint?

A

DNA damage before DNA replication

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64
Q

What is checked for at the G2/M checkpoint?

A

DNA damage after DNA replication

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65
Q

What are defective cell cycle checkpoints a major cause for?

A

Genetic instability in cancer cells

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66
Q

What is progression through the cell cycle tightly regulated by?

A

Proteins called cyclins and associated enzymes called cyclin-dependent kinases (CDKs)

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67
Q

Which stage of the cell cycle is particularly tightly regulated?

A

The G1/S transition

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68
Q

How do CDKs become active?

A

By binding to and complexing with cyclins

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69
Q

How do activated CDKs drive the cell cycle?

A

By phosphorylating proteins that are critical for progression of the cell to the next stage of the cell cycle

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70
Q

What is the activity of cyclin-CDK complexes tightly regulated by?

A

CDK inhibitors

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71
Q

How do growth factors work, with regard to CDKs?

A

Some by stimulating the production of cyclins

Some by shutting off production of CDK inhibitors

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72
Q

How are cells classified based on their ability to multiply?

A

Labile
Stable
Permanet

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73
Q

What are labile cells?

A

Cells that continue to multiply through their life

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74
Q

What are stable cells?

A

Cells that can multiply in a regenerative burst, but are usually quiescent

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75
Q

What are permanent cells?

A

Cells that cannot proliferate

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76
Q

How has the classification of cells depending on how they divide been modified?

A

Following our understanding that many terminally differentiated cells can’t divide, and following the discovery that cells in a tissue are very often replaced by cells derived from stem cels and not mature differentiated cells

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77
Q

Are stem cells present in adult tissues?

A

Yes, many of them

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78
Q

What are stem cells?

A

Cells with prolonged proliferative activity which show asymmetric replication

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79
Q

What happens in asymmetric replication?

A

One of the daughter cells remains as a stem cell while the other differentiated into a mature, non-dividing cell

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80
Q

How are embryonic stem cells different to normal adult stem cells?

A

In that they are pluripotent and can give rise to any of the tissues in the human body. Adult stem cells can usually only give rise to one type of adult cell- their lineage is specific

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81
Q

How has the classification of cells by their ability to divide developed?

A

We now consider the classification in relation to tissues (a group of similar specialised cells with a specific function)

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82
Q

What can cell populations be classified as?

A

Permanent cell populations
Labile cell populations
Stable cell populations

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83
Q

What has happened in permanent cell populations?

A

The terminally differentiated cells within some tissues have left the cell cycle and cannot replicate

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84
Q

Give 3 examples of permanent cell populations?

A

Cardiac muscle
Skeletal muscle
Neural tissue

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85
Q

Can stem cells be present within permanent cell populations?

A

Yes, but they cannot mount an effective proliferative response against significant cell loss

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86
Q

What happens if neurones are destroyed?

A

The tissue space is filled by glial cells

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87
Q

How does skeletal muscle have a very limited regenerative capacity?

A

Through stem cells attached to the endomysial sheath

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88
Q

How does damage to the heart heal?

A

With a scar

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89
Q

Why does damage to the heart heal with a scar?

A

Because no stem cells are present in the heart

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90
Q

Give two examples of labile cell populations

A

Bone marrow

Epithelium

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91
Q

What do labile cell populations such as in bone marrow and epithelium consist of?

A

Mature differentiated cells that cannot replicate

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92
Q

Why is tissue such as bone marrow and epithelium considered proliferative?

A

As the cells in them are short lived, and are continually being replaced by cells derived from stem cells

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93
Q

What can stable cell populations be said to be?

A

An intermediate between permanent and labile tissues

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94
Q

Give two examples of stable cell populations

A

Liver

Kidney

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95
Q

What cells are involved in proliferation in stable cell populations?

A

Mature cells as well as stem cells

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96
Q

Give 5 examples of cells that are usually non-replicating, but can be induced to enter to cell cycle and replicate if necessary

A 
Liver hepatocytes
 Bone osteoblasts
 Fibroblasts
 Smooth muscle cells
 Vascular endothelial cells
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97
Q

What is required to induce a usually non-replicating cell to enter the cell cycle?

A

A large number of genes

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98
Q

What genes arerequired to induce a usually non-replicating cell to enter the cell cycle?

A

Proto-oncognes

Genes required for ribosome synthesis and protein translation

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99
Q

Are stem cells present in stable cell populations?

A

Yes

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100
Q

What state are the stem cells in stable cell populations in?

A

Usually quiescent, or proliferate very slowly, however they can proliferate persistently when required

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101
Q

What is the regenerative capacity of bone?

A

Very good

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102
Q

What is the regenerative capacity of tendons?

A

Poor

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103
Q

Why do tendons heal very slowly?

A

As they have few cells and few blood vessels

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104
Q

What is the result of tendons healing very slowly?

A

Secondary rupture at a site of previous injury is not uncommon

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105
Q

What is the regenerative capacity of articular cartilage?

A

Poor

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106
Q

What is the regenerative capacity of adipocytes?

A

Nil

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107
Q

How are new fat cells formed?

A

By undifferentiated but committed cells that lie among the adipocytes

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108
Q

What is the regenerative capacity of epithelia?

A

Very good

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109
Q

What exceptions are there to epithelia having a very good regenerative capacity?

A

Lens of the eye

Renal podocytes

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110
Q

Where will surface epithelia regenerate?

A

Over denuded areas

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111
Q

What is the regenerative capacity of the liver?

A

Very good

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112
Q

How is the regeneration capacity of the liver shown in transplant patient?

A

Transplanted livers adjust their size to the size of the recipient

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113
Q

What is the regenerative capacity of mesothelia?

A

Good

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114
Q

What is the regenerative capacity of melanocytes?

A

They tend to regenerate too little or too much

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115
Q

What colour are scars in pigmented skin?

A

Usually pale

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116
Q

What is the regenerative capacity of smooth muscle?

A

Very good

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117
Q

What is the regenerative capacity of striated muscle?

A

Limited

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118
Q

What is the regenerative capacity of peripheral nerves?

A

Regenerate in a predictable way

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119
Q

How quickly do sprouting axons grow?

A

1-3mm/day

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120
Q

What happens if the gap regenerating axons have to cross is too wide?

A

They form a disordered tangle, which can result in a painful amputation neuroma

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121
Q

What is the regenerative capacity of neurone?

A

None (in humans)

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122
Q

When do neurones cease to multiply?

A

Before birth

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123
Q

How can lost neurones be replaced?

A

They can’t

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124
Q

How do people with hemiplegia secondary to strokes recover?

A

Because of the ability of the CNS to establish alternative pathways

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125
Q

What is the ability of the CNS to establish alternative pathways called?

A

Plasticity

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126
Q

How can cells respond to challenges that are not severe enough to cause injury?

A

By adaptations that are not truly pathologic, although they may open the door to disease

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127
Q

What is cell adaptation?

A

The state between a normal unstressed cell, and an overstressed cell

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128
Q

Is cell adaptation reversible?

A

Normally

129
Q

What are the important types of cell adaptation?

A 
Regeneration
 Hyperplasia
 Hypertrophy
 Atrophy
 Metaplasia
130
Q

What is regeneration?

A

The replacement of cell losses by identical cells in order to maintain the size of a tissue or organ

131
Q

Give an example of when is regeneration a normal process

A

Replacement of red and white blood cells by the bone marrow

132
Q

When can regeneration occur after injury by a harmful agent?

A

If the harmful agent is removed, and there is limited tissue damage

133
Q

When is resolution of injury not possible?

A

If the harmful agent persists
If there is extensive tissue damage
If the damage occurs to a permanent tissue

134
Q

What happens when regeneration is not possible?

A

The tissue will heal with a scar

135
Q

Give two examples of where regeneration is seen?

A

In the liver after a partial hepatectomy

In the replacement of the epidermis by keratinocytes following a skin burn

136
Q

Are regenerated cells as good as the original cells?

A

Usually, but not always and not immediately

137
Q

How long does it take regenerated cells to reach morphological and functional maturity?

A

Weeks, months or years

138
Q

Give an example of when can the time that regenerated cells take to be the same as normal cells be an advantage

A

In the influenza virus- the virus kills the epithelial cells of the upper respiratory tract, but spares the regenerating cells that follow as they do not yet have receptors for the influenza virus

139
Q

How many times can cells regenerate?

A

Many- how many times has been found to be species dependant, and depend on the maximum life-span of the species

140
Q

What does a longer species life span mean for regeneration?

A

The more cell divisions can occur

141
Q

What is the number of cell divisions possible called?

A

The Hayflick number

142
Q

What is the mean Hayflick number in humans?

A

61.3

143
Q

What is the Hayflick number in humans related to?

A

The shortening of telomeres

144
Q

What factors induce cells to regenerate?

A

Growth factors in the microenvironment

Cell-to-cell communication

145
Q

How is reconstitution different to regeneration?

A

It is the replacement of a lost part of the body

146
Q

What does reconstitution require?

A

Coordinated regeneration of several types of cell

147
Q

Can mammals reconstitute a body part?

A

No, their ability to do so is minimal, with a few exceptions

148
Q

What are the exceptions to mammals inability to undergo reconstitution?

A

Small blood vessels (capillaries, small arteries and veins) are able to reconstitute
Children less than 4.5 years old have been reported to reconstitute the tip of a finger, if it is cleanly severed and the amputation is beyond the distal phalangeal joint
Rabbits and cats can repair holes punched in their ears up to a point

149
Q

What is hyperplasia?

A

When there is an increase in tissue or organ size due to increased cell numbers

150
Q

What is hyperplasia a response to?

A

Increased functional demand and/or external stimulation

151
Q

Where can hyperplasia occur?

A

Only in labile or stabile cell populations

152
Q

What does hyperplasia remain under?

A

Physiological control

153
Q

Is hyperplasia reversible?

A

Yes

154
Q

How does hyperplasia differ from regeneration?

A

They are biologically similar, but differs in that it leads to an increase in the size of the tissue or organ

155
Q

What are the types of physiological hyperplasia?

A

Hormonal or compensatory

156
Q

What is the result of hormonal hyperplasia?

A

An increase in functional capacity

157
Q

What is the result of compensatory hyperplasia?

A

There is an increase in tissue mass after damage

158
Q

What can hyperplasia occur secondary to?

A

A pathological cause

159
Q

What is the cellular proliferation a normal response to when hyperplasia is secondary to a pathology cause?

A

Another abnormal condition

160
Q

How does pathological hyperplasia usually occur?

A

Secondary to excessive hormonal stimulation or growth factor production

161
Q

What is a risk in hyperplastic tissue?

A

Neoplasia

162
Q

Why is neoplasia a risk in hyperplastic tissue?

A

As the repeated cell divisions that occur in hyperplasia expose the cell to the risk of mutations (which commonly occur during DNA replication)

163
Q

Give 2 examples of physiological hyperplasia?

A

Increased bone marrow production of erythrocytes in response to low oxygen
Proliferation of the endometrium under the influence of oestrogen

164
Q

Give 2 examples of pathological hyperplasia

A

Epidermal thickening in chronic eczema or psoriasis

Enlargement of thyroid gland in response to iodine deficiency

165
Q

What is hypertrophy?

A

An increase in tissue or organ size due to an increase in cell size, without an increase in cell numbers

166
Q

How do cells become bigger in hypertrophy?

A

Because they contain more structural components

NOT due to swelling

167
Q

Where can hypertrophy occur?

A

In many tissues, but seen especially in permanent cell populations

168
Q

Why is hypertrophy seen particularly in permanent cell populations?

A

As these populations have little or no replicative potential, and so any increase in organ size must occur via hypertrophy

169
Q

What does knowing the regenerating capacity of each cell type enable you to do?

A

Predict the type of response to increased functional demand

170
Q

What is hypertrophy a response to?

A

Increased functional demand and/or hormonal stimulation

171
Q

What are cells undergoing hypertrophy and hyperplasia doing?

A

Synthesising more cytoplasm (i.e. protein)

172
Q

What do hypertrophic cells contain?

A

More structural components

173
Q

What is the result of hypertrophic cells containing more structural components?

A

The cellular workload is shared by a greater mass of cellular components

174
Q

Can hypertrophy occur in cells where division is possible?

A

It can, but often occurs alongside hyperplasia

175
Q

What is true of cases where hyperplasia and hypertrophy occur simultaneously?

A

They are triggered by the same stimulus

176
Q

What does endocrine stimulation usually result in?

A

A combination of hypertrophy and hyperplasia

177
Q

Give 2 examples of physiological hypertrophy

A

Skeletal muscle hypertrophy of a body builder

Smooth muscle hypertrophy of a pregnant uterus

178
Q

How much does the uterus enlarge in pregnancy?

A

~70%

179
Q

What is the enlargement of the uterus in pregnancy under the influence of?

A

Oestrogen

180
Q

Give two examples of pathological hypertrophy

A

Ventricular cardiac muscle hypertrophy
Smooth muscle hypertrophy above an intestinal stenosis
Bladder smooth muscle hypertrophy with bladder obstruction due to an enlarged prostate gland

181
Q

What causes ventricular muscle hypertrophy?

A

Response to systemic hypertension or valvular disease

182
Q

What causes smooth muscle hypertrophy above an intestinal stenosis?

A

The extra work of pushing the intestinal contents through the narrowing

183
Q

Where does hypertrophy of the cardiac muscle occur physiologically?

A

In athletes

184
Q

Why is hypertrophy in the heart in athletes not pathological?

A

Because with exercise, unlike with hypertension or valvular heart disease, the heart is under strain for only a few hours/day, and has the rest of the day to recover

185
Q

What is the problem with a pathologically hypertrophic heart?

A

There is relative anoxia

186
Q

Why is there relative anoxia in a pathologically hypertrophic heart?

A

Because although the number of capillaries in the heart increases, is it not sufficient to satisfy the increased muscle mass

187
Q

What is the result of the cell damage due to anoxia?

A

Fibrosis is often seen in pathologically hypertrophic hearts

188
Q

What is the result of fibrosis in the heart?

A

It decreases the compliance of the cardiac muscle, and therefore its effectiveness

189
Q

What does progressive pathological cardiac hypertrophy eventually lead to?

A

Myocardial exhaustion

190
Q

What is a simple way to study the effect of functional overstrain?

A

To remove one of the two paired organs, e.g. if one kidney is removed, the other enlarges, leading to compensatory hypertrophy

191
Q

What happens when the stimulus for hypertrophy and hyperplasia disappears?

A

The cells and organs become normal size again

192
Q

What happens when there is excessive nutrition?

A

There is an increase in fat and an increase in protein synthesis

193
Q

Why is obesity in children especially problematic?

A

Because once fat cells are made, they are with us for life- fat cells acquired at an early age will be there for life

194
Q

What is atrophy?

A

Shrinkage of a tissue or organ due to an acquired decrease in size and/or number of cells

195
Q

What results in atrophy?

A

A reduced supply of growth factors and/or nutrients

196
Q

How can atrophy be considered?

A

From two perspectives- at the level of the cell, and at the level of the organ/tissue

197
Q

What is cellular atrophy?

A

A decrease in cell size

198
Q

What is organ/tissue atrophy due to?

A

Typically, a combination of cellular atrophy and apoptosis

199
Q

When does organ/tissue atrophy occur?

A

When many cells in the tissue undergo atrophy and apoptosis

200
Q

What does cellular atrophy involve?

A

Shrinkage in the size of the cell to a size at which survival is still possible

201
Q

How does an atrophic cell differ from a normal one?

A

It contains a reduced number of structural components, and has reduced function

202
Q

What is atrophy a form of?

A

Adaptive response which may result in cell death

203
Q

How can atrophy occur?

A

Cell deletion or cell shrinkage

204
Q

What does wether atrophy occurs by cell deletion or cell shrinkage depend on?

A

The type of tissue involved

205
Q

What happens when cell deletion occurs?

A

Certain cells are picked out and induced to perform apoptosis

206
Q

What happens to cell remnants left after apoptosis?

A

If they are situated on an external surface, they will be lost into the lumen, or from the surface of the body
Otherwise, they will be removed by phagocytosis, either by macrophages or by neighbouring cells

207
Q

What happens in organs undergoing atrophy by cell deletion?

A

Parenchymal cells will disappear before stromal cells

208
Q

What is the result of parenchymal cells disappearing before stromal cells in organs undergoing atrophy?

A

These organs often contain a large amount of connective tissue

209
Q

Why does cell shrinkage have limits?

A

Because most cellular organelles are essential for survival

210
Q

What can be pared down in cell shrinkage?

A

Some non-essential organelles, e.g. fibrillar material can be lost by skeletal muscle

211
Q

How does cell shrinkage occur?

A

By self digestion

212
Q

What happens when cell shrinkage occurs by self-digestion?

A

Residual bodies are seen within cells

213
Q

What are the residual bodies found in cells that have shrunk?

A

Autophagosomes, which contain lipofuscin and the remains of organelles that can’t be further digested

214
Q

How is ubiquitin involved in cell shrinkage?

A

It is involved in the process by binding with proteins that are to be removed and therefore targeting them for destruction

215
Q

Can extracellular matrix be lost in atrophy?

A

Yes

216
Q

What is bone atrophy, or osteoporosis?

A

Loss of bone mass (not bone calcium)

217
Q

What is the major stimulus to bone formation?

A

Mechanical stress

218
Q

Who can bone atrophy be a problem for?

A

Bed-ridden patients Astronauts

219
Q

What is atrophy often linked with?

A

Disease

Senescence

220
Q

Is atrophy reversible?

A

Up to a point, but after years or months it is less so, particularly when parachymal cells are replaced by connective tissue

221
Q

How is atrophy best treated?

A

Removal of the cause

222
Q

Give two examples of physiological atrophy

A

Ovarian atrophy in post-menopausal women

The decrease in size of the uterus after parturiton

223
Q

What can cause pathological atrophy?

A 
Reduced functional demand/workload
 Loss of innervation
 Inadequate blood supply
 Inadequate nutrition
 Loss of endocrine stimulation
 Persistant injury
 Ageing
 Pressure
 Occlusion of a secretory duct
 Toxic agents and drugs
 X-rays
 Immunological mechanisms
224
Q

What is atrophy due to reduced functional demand/workload known as?

A

Atrophy of disuse

225
Q

When may atrophy of disuse occur?

A

Due to immobilisation in a plaster cast

226
Q

Is atrophy due to immobilisation reversible?

A

Yes, with activity

227
Q

How can protein loss be reduced with immobilisation in a plaster cast?

A

By passive mechanical stretching and electrical stimulation

228
Q

Where are the principals preventing protein loss in immobilisation used?

A

Physiotherapy

229
Q

What is atrophy due to loss of innervation called?

A

Denervation atrophy

230
Q

Give an example of denervation atrophy

A

Wasted striated muscle within the hand after median (motor) nerve damage

231
Q

What can sensory nerve denervation cause?

A

Some degree of atrophy within the hands and feet

232
Q

What happens with sensory nerve denervation?

A

The skin becomes thinner (atrophic) and scaly, and the nails become course and brittle

233
Q

Give an example of atrophy caused by inadequate blood supply?

A

Thinning of ski on legs with peripheral vascular disease

234
Q

When does inadequate blood supply result in tissue atrophy?

A

When there is partial but prolonged inadequacy of blood flow

235
Q

Give an example of atrophy caused by inadequate nutrition

A

Wasting of muscles with malnutrition

236
Q

What happens in inadequate nutrition?

A

Adipocytes shrink dramatically

237
Q

Which tissue is least susceptible to starvation induced atrophy in adults?

A

The brain

238
Q

Give two examples of atrophy caused by loss of endocrine stimulation?

A

Occurs in the breast and reproductive organs with withdrawal of hormonal stimulation
Wasting of the adrenal gland with loss of pituitary ACTH following hypophysectomy

239
Q

What is the best way to shut down and atrophy an endocrine gland?

A

Give doses of the glands own hormone

240
Q

Give an example of where persistent injury can cause atrophy?

A

Polymyositis

241
Q

What is polymyositis?

A

Inflammation of the muscle

242
Q

What is atrophy due to ageing called?

A

Senile atrophy

243
Q

Where does senile atrophy usually occur?

A

In permanent tissues

244
Q

Give 6 things affected by senile atrophy

A 
Brain
 Heart
 Liver
 Kidneys
 Spleen
 Immune system
245
Q

What happens to the liver, kidneys and spleen with senile atrophy?

A

Their weight is reduced

246
Q

What happens to the immune system with senile atrophy?

A

It becomes less responsive

247
Q

What is the reason for senile atrophy?

A

Seems more complex than the Hayflick number

Could involve the progressive accumulation of somatic mutations, so as the system can no longer function

248
Q

What could the progressive accumulation of somatic mutations occur secondary to?

A

Free radical damage

249
Q

Give two examples of where pressure can cause atrophy

A

Tissues around an enlarging benign tumour, such as the cerebral hemisphere adjacent to a meningioma
Thoracic aortic aneurysms can press against the sternum and erode through it

250
Q

What can be seen when a thoracic aortic aneurysm can eroded through the sternum?

A

A pulsatile mass beneath the skin

251
Q

Why does occlusion of a secretory duct cause atrophy?

A

It causes the parenchymal cells of the gland to undergo apoptosis

252
Q

Give an example of atrophy due to occlusion of a secretory duct

A

In the pancreas ligation of the main duct, or blockage of the main duct by a stone, results in the disappearance of the exocrine glands of the pancreas alone.

253
Q

What is the result of the disappearance of the exocrine glands of the pancreas?

A

The pancreas then appears as a mass of connective tissue contain larger ducts and intact islets of Langerhans

254
Q

What is an exception to occlusion of a secretory duct causing atrophy?

A

The testis after ligation of the vas deferens

255
Q

What is the result of the ligation of the vas deferns not causing atrophy?

A

Vasectomies can be successfully reversed

256
Q

Where can become atrophic due to toxic agents and drugs?

A

Bone marrow

Testes

257
Q

How do x-rays cause atrophy?

A

By direct cellular damage and microcirculatory damage

258
Q

Give an example of where an immunological mechanism causes atrophy?

A

Atrophic gastic mucosa in pernicious anaemia

259
Q

How does atrophic gastric mucosa in pernicious anaemia arise?

A

The body produces autoantibodies against parietal cells. The parietal cells produce intrinsic factor, which is required for absorption of vitamin B12. Lack of vitamin B12 results in anaemia

260
Q

What is metaplasia?

A

Reversible replacement of one adult differentiated cell type by another of a different type

261
Q

What happens in metaplasia?

A

Cells of one phenotype are eliminated, and replaced by cells of a different phenotype

262
Q

How is the phenotype of cells changed in metaplasia?

A

The stem cells within the tissue are reprogrammed and switch to producing a different type of progeny

263
Q

What can metaplasia be considered as?

A

Abnormal regeneration

264
Q

Where does metaplasia occur in adult mammals?

A

Only within varieties of epithelia, and within varieties of connective tissue

265
Q

Why could it be seen as surprising that metaplasia only occurs within epithelia and connective tissue?

A

Because all cells have the same full complement of genetic material, and therefore the potential to form any cell type

266
Q

Is there metaplasia across germ layers?

A

None proven

267
Q

Is there metaplasia from a connective tissue to epithelium?

A

Not proven

268
Q

What cell populations does metaplasia occur in?

A

Only those can replicate- it is not known to occur in adult striated muscle or in neurones

269
Q

What does metaplasia involve?

A

Expression of a new genetic programme- turning on certain genes, and turning certain genes off

270
Q

What does expression of a new genetic programme result in?

A

Cells assuming a different structure and different function

271
Q

What does metaplasia occur secondary to?

A

Signals from molecules such as cytokines and growth factors

272
Q

What is metaplasia often induced by?

A

Stimuli that cause cell proliferation, e.g. chemical or mechanical irritants

273
Q

What is the end result of metaplasia?

A

To change one cell type to another more suited to the altered environment

274
Q

Where is metaplasia most commonly seen?

A

In epithelial tissue

In columnar epithelium

275
Q

Why do columnar epithelium undergo metaplasia?

A

They are fragile, so they turn into more resilient squamous epithelium

276
Q

Where is epithelial metaplasia common?

A

On surface linings

277
Q

Why is epithelial metaplasia common on surface linings?

A

Because they are exposed to insults

278
Q

What may happen to metaplastic epithelium?

A

It may loose functions that the original epithelium performed

279
Q

Give an example of where metaplastic epithelium has lost function?

A

Mucus secretion is lost when columnar epithelium becomes squamous epithelium

280
Q

How does metaplastic epithelium differ from dysplastic epithelium?

A

Metaplastic epithelium is fully differentiated

Dysplastic epithelium has disorganised and abnormal differentiated

281
Q

How is cancerous epithelium different from metaplastic epithelium?

A

It is disorganised, abnormal and irreversible

282
Q

Is metaplasia a good thing?

A

It can sometimes be adaptive and useful

However, can be of no apparent use, and may be detrimental

283
Q

Give two examples of where metaplasia can be adaptive and useful

A

If the bone marrow is destroyed by disease, splenic tissue undergoes metaplasia to bone marrow
The conversion of columnar epithelium lining ducts to stratified squamous epithelium

284
Q

What is it called when splenic tissue undergoes metaplasia to bone marrow?

A

Myeloid metaplasia

285
Q

Which ducts may have columnar epithelium thats converted to stratified squamous epithelium?

A

Salivary glands
Pancreas
Bile ducts
Renal pelvis

286
Q

Why may the lining of ducts change to squamous epithelium?

A

Secondary to chronic irritation to stones

287
Q

What is the advantage of the conversion of columnar epithelial lining to stratified squamous?

A

As stratified squamous is more resistant to mechanical abrasion

288
Q

Give three examples of when metaplasia can be detrimental

A

Transformation of bronchial pseudostratified ciliated columnar epithelium to stratified squamous epithelium
Flat, non- secreting epithelium can be replaced by secretory epithelium or glands such as in the lower oesophagus when the oesophageal stratified squamous epithelium changes to gastric or intestinal type epithelium
When connective tissue changes to bone

289
Q

What does bronchial pseudostratified ciliated columnar epithelium change to stratified squamous epithelium in response to?

A

The effect of cigarette smoke

290
Q

What is the problem with the transformation of bronchial pseudostratified ciliated columnar epithelium to stratified squamous epithelium?

A

The squamous epithelium doesn’t produce cleansing mucus, and lacks cilia to move the mucus along

291
Q

When may oesophageal stratified squamous epithelium change to gastric or intestinal type epithelium?

A

With persistent acid reflux

292
Q

What is persistent acid reflux called?

A

Barrett’s oesophagus

293
Q

When can metaplastic develop?

A

In skeletal muscle following trauma, when fibroblasts within the muscle tissue undergo metaplastic change to osteoblasts

294
Q

What is the development of metaplastic bone called?

A

Traumatic myositis ossificans

295
Q

Where is traumatic myositis ossificans often seem?

A

In young people, usually after premature return to activity before proper healing has occured

296
Q

What often happens to traumatic myositis ossificans?

A

It disappears by metaplasia in the opposite direction

297
Q

What can metaplasia sometimes be a prelude to?

A

Dysplasia and cancer

298
Q

Give two types of epithelial metaplasia that predispose to epithelial cancers

A

Barrett’s epithelium

Intestinal metaplasia of the stomach

299
Q

When odes intestinal metaplasia of the stomach occur?

A

With chronic infection by Helicobacter pylori

300
Q

What is aplasia?

A

The complete failure of a specific tissue or organ develop

301
Q

What kind of disorder is aplasia?

A

Embryonic developmental

302
Q

Give two examples of aplasia

A

Thymic aplasia

Aplasia of a kidney

303
Q

What does thymic aplasia result in?

A

Infections and auto-immune problems

304
Q

Other than an embryonic developmental disorder, what is aplasia also used to describe?

A

An organ whose cells have ceased to proliferate

305
Q

Give an example of aplasia when cells have ceased to proliferate

A

Aplasia of the bone marrow in aplastic anaemia

306
Q

What is involution?

A

The normal programmed shrinkage of an organ

307
Q

What does the term involution overlap with?

A

Atrophy

308
Q

Give 3 examples of involution

A

Uterus after childbirth
Thymus in early life
Temporary foetal organs, usch as the pro- and mesonephros

309
Q

What is hypoplasia?

A

The congenital underdevelopment or incomplete development of a tissue or organ

310
Q

What has happened in hypoplasia?

A

There is an inadequate number of cells within the tissue which is present

311
Q

What kind of disorder is hypoplasia?

A

Embryonic developmental

312
Q

Give 4 examples of hypoplasia

A

Renal hypoplasia
Breast hypolasia
Testicular hypoplasia
Hypoplasia of the chambers of heart

313
Q

Where does testicular hypoplasia occur?

A

Klinefelter’s syndrome

314
Q

Why is hypoplasia not the opposite of hyperplasia?

A

Because it is a congenital condition

315
Q

What is atresia?

A

The congenital imperforation of an opening

316
Q

Give two examples of atresia?

A

Atresia of anus or vagina

317
Q

What is dysplasia?

A

The abnormal mutation of cells within a tissue

318
Q

Is dysplasia reversible?

A

Potentially

319
Q

What is the problem with dysplasia?

A

it is often a precancerous condition

ESA 2- Mechanisms of Disease (11 decks)

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