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Yr 2 - EMS > Cell Injury and Cell Death > Flashcards

Cell Injury and Cell Death Flashcards

1
Q

What is atrophy vs hypertrophy?

A

Muscle atrophy is a decrease in muscle mass; muscle hypertrophy is an increase in muscle mass due to an increase in muscle cell size

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2
Q

What is oncosis?

A

Pre lethal changes preceding cell death (generally regarded as a severe injury to cell membrane integrity or other vital functions)

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3
Q

What is ‘reversible cellular injury’?

A

This occurs if extreme stress persists and the cell is unable to adapt to overcome the stress. This type of injury results in cellular and morphological changes, that can still be reversed if the stress is eventually removed.

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4
Q

What are the hallmarks of reversibly injured cells?

A
  1. ATP depletions (due to decreased levels of oxidative phosphorylation) 2. Oxygen and oxygen derived free radicals 3. Loss of intercellular calcium hemostasis 4. Defects in membrane permeability 5. Cell swelling
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5
Q

What is cellular swelling?

A

An enlargement of an acutely injured cell, caused by changes in ion concentration and water influx

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6
Q

Describe the steps leading to cellular swelling in reversible cellular injury.

A
  1. Decreased ATP due to decreased levels of oxidative phosphorylation
  2. Decreased Na+/K+ pump as this is ATP dependent
  3. Increased Na in the cell
  4. Increased water in the cell (osmosis)
  5. Cellular swelling

It is the first change to occur during cell injury.

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7
Q

What are the components of Na+ regulation?

A
  1. Plasma Membrane 2. Plasma Membrane Na+ pump. 3. ATP concentration.
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8
Q

The plasma membrane is slightly ‘leaky’ to Na+. What does this allow?

A

This allows minimal amounts of Na+ to gradually move into the cell

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9
Q

How is this gradual influx of Na+ compensated for? What does this ensure?

A

There is a perpetually active Na+/K+-/ATPase pump, that pumps Na+ out of the cell constantly, in exchange for pumping K+ into the cell. This K+ is able to leave the cell freely. This ensures that Na+ does not buildup within the cell

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10
Q

In cellular injury, what 3 things may interrupt the Na+ movement in and out of a cell? What is the end result of all 3 of these processes?

A
  1. The plasma membrane may be damaged, increasing its leakiness to Na+, and thus overriding the capacity of the Na+/K+-ATPase pump to keep Na+ at low levels.
  2. The Na+K+-ATPase pump may be directly damaged, and thus Na+ is able to slowly build up within the cell without being removed.
  3. Interfering with the synthesis of ATP, the fuel source for the Na+/K+-ATPase pump.

End result –> osmotic pressure builds within the cell due to increased ions, and water and fluids move into the cell, resulting in the cell becoming swelled.

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11
Q

How does ATP depletion lead to cellular swelling?

A
  1. Decreased ATP
  2. Decreased activity of Na/K pump
  3. Increased Na in cell
  4. Increased water in cell (osmosis)
  5. Cell swelling
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12
Q

Characteristics seen in reversible cell injury?

A
  1. Pallor (paleness)
  2. Appears enlarged
  3. Hydropic change
  4. Cell swelling
  5. Vacuolar degeneration
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13
Q

What is vacuolar degeneration? How does fluid building up in the cell lead to this?

A
  • Cell becomes distended and cellular organelles appear to become more spaced out within the cell.
  • Most of the extra fluid actually builds within the ER, causing the ER to appear much more distended.
  • As time goes on, regions of the ER burst and become encapsulated in clear vacuoles containing chunks of the ER –> This is known as vacuolar degeneration.
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14
Q

Characteristics of irreversible cell injury?

A

Mitochondrial swelling, lysosomes swells, damage to membrane, leakages of enzymes

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15
Q

Diagram of irreversible cell injury

A
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16
Q

Which 3 types of membrane damage can lead to irreversible cell injury?

A
  1. Lysosome membrane damage
  2. Cell membrane damage
  3. Mitochondria membrane damage
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17
Q

What is a lysosome?

A
  • A membrane-bound cell organelle that contains digestive enzymes
  • They break down excess or worn-out cell parts. They may be used to destroy invading viruses and bacteria.
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18
Q

How can membrane damage to the lysosome lead to irreversible cell injury?

A

Leakage of lysosomal enzymes into the cytosol –> this leads to enzyme degradation of the cell

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19
Q

How does damage to the cell membrane affect Ca? How does this lead to irreversible cell injury?

A

Increased Ca into the cell:

  1. Ca activates proteases and other enzymes –> enzymatic degradation of cell
  2. Ca activates caspaces –> triggers apoptosis
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20
Q

What are 2 features that characterise irreversibility from reversible injury?

A
  1. Irreversible mitochondrial damage
    * results in ATP depletion and lack of oxidative phosphorylation
  2. Profound disturbances in membrane function,
    * especially those that affect internal ionic concentrations, and lysosomal enzyme activity
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21
Q

Examples of causes of cell injury?

A

Hypoxia/Ischemia

Excess Heat or Cold

Radiation

Chemicals. drugs and toxins

Infectious Agents

Immunologic/Autoimmune

Inflammation

Nutrition

Genetics

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22
Q

These causes of cell injury may be caused by one of more of the following mechanisms of cell injury:

A
  1. Depletion of ATP
  2. Mitochondrial Damage
  3. Influx of Ca2+ and loss of Calcium Homeostasis
  4. Accumulation of Oxygen Derived Free Radicals (Oxidative Stress)
  5. Defects in Membrane Permeability
  6. Damage to DNA and Proteins
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23
Q

How can membrane damage to mitochondria lead to irreversible cell injury?

A

Cyt C leakage –> activates caspaces –> triggers apoptosis

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24
Q

Cyt C:

  • Location?
  • Role in apoptosis?
A
  • The cytochrome complex is a small hemeprotein found loosely associated with the inner membrane of mitochondria.
  • Plays a major role in cell apoptosis by activating caspaces
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25
Q

What is apoptosis?

A

Programmed individual cell death seen in physiological growth control and in disease

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26
Q

What is necrosis?

A
  • Death of tissue
  • Includes inflammation and repair
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27
Q

Difference between necrosis and apoptosis?

A

Necrosis - uncontrolled cell death

Apoptosis - programmed cell suicide

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28
Q

Difference in size of between necrosis and apoptosis. How many cells are affected?

A

Necrosis:

  • Cellular swelling
  • Many cells affected

Apoptosis:

  • Cellular shrinking
  • One cell affected
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29
Q

What are the cell contents ingestd by in necrosis vs apoptosis? What inlammatory response does this result in?

A

Necrosis:

  • Cell contents ingested by macrophages
  • Significant inflammation

Apoptosis:

  • Cell contents ingested by neighbouring cells
  • No inflammatory response
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30
Q

What happens to membrane of cell in necrosis vs apoptosis? What does this lead to?

A

Necrosis:

  • Loss of membrane integrity
  • Cell lysis occurs

Apoptosis:

  • Membrane blebbing but integrity maintained
  • Apoptotic bodies form –> these are small membrane-surrounded fragments are cleared by phagocytosis without triggering an inflammatory response
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31
Q

What is autophagy?

A

consumption of the body’s own tissue as a metabolic process occurring in starvation and certain diseases.

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32
Q

Does necrosis lead to an inflammatory response?

A

Yes

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33
Q

Does apoptosis lead to an inflammatory response?

A

No

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34
Q

Does autophagy lead to an inflammatory response?

A

No

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35
Q

Does necrosis lead to cell swelling?

A

Yes - and intracellular membrane dilatation

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36
Q

Process of apoptosis?

A
  • Cell shrinkage
  • DNA fragmentation
  • Caspases activation
  • Apoptotic bodies formation
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37
Q

What happens in autophagy?

A
  • Increased quantity of autophagosomes formation
  • Atg proteins participation
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38
Q

Necrosis vs apoptosis diagram

A
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39
Q

What is apoptosis? Is it natural?

A

Apoptosis, or programmed cell death, is a form of cell death that is generally triggered by normal, healthy processes in the body

Yes, is natural

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40
Q

What is necrosis? Is it natural?

A

Necrosis is the premature death of cells and living tissue.

Caused by factors external to the cell or tissue, such as infection, toxins, or trauma.

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41
Q

Is apoptosis always detrimental? Is necrosis?

A

Apoptosis: Usually beneficial. Only abnormal when cellular processes that keep the body in balance cause too many cell deaths or too few.

Necrosis: Always detrimental

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42
Q

Process of apoptosis?

A
  1. Membrane blebbing (bubble like spots on membrane)
  2. Shrinkage of cell
  3. Nuclear collapse (i.e. degradation of genetic and protein)
  4. Apoptopic body formation
  5. Attracts macrophages to find and engulf the dead cells and their fractions
  6. Macrophages release cytokines that inhibit inflammatory responses
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43
Q

Process of necrosis?

A
  1. Membrane disruption
  2. Respiratory poisons and hypoxia which cause ATP depletion
  3. Metabolic collapse
  4. Cell swelling and rupture leading to inflammation.
  5. Necrotic cells are not targeted by macrophages for cleaning of their cellular debris, so the effects of the cell rupture can spread quickly and throughout the body for long periods of time.
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44
Q

How is an inflammatory response inhibited in apoptosis?

A

Macrophages release cytokines that inhibit inflammatory responses

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45
Q

Does necrosis require energy input? Does apoptosis?

A

Apoptosis is energy-dependent, meaning it requires input from a cell for cell death to occur.

Necrosis does not require any energy input from a cell, as external factors or localised infections are what trigger necrosis.

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46
Q

What are caspases?

A

A family of protease enzymes that trigger apoptosis

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47
Q

Do cells and organelles swell in necrosis? In apoptosis?

A

Cells and organelles swell in necrosis

Cells shrink in apoptosis

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48
Q

Is control of intracellular environment controlled in apoptosis? In necrosis?

A

Necrosis: control is lost, cells rupture and spill contents

Apoptosis: control is maintained, cytoplasm packaged as ‘apoptotic bodies’

49
Q

What is coagulative necrosis?

A
  • A type of accidental cell death typically caused by ischemia or infarction
  • The architectures of dead tissue is preserved for at least a couple of days.

E.g. Myocardial infarction

50
Q

What is liquefactive necrosis?

A
  • Digestion of dead cells to form a viscous liquid mass.
  • The loss of tissue and cellular profile occurs within hours

E.g. bacterial or fungal infection, CNS hypoxia

51
Q

What is gangrenous necrosis?

A

Referring to a grossly visible pattern of necrosis due to ischemia resulting from obstructive occlusion of vasculature –> putrefaction of the tissue

E.g. limb ischaemia

52
Q

What is caseous necrosis?

A

A unique form of cell death in which the tissue maintains a cheese-like appearance. It is also a distinctive form of coagulative necrosis. The dead tissue appears as a soft and white proteinaceous dead cell mass.

E.g. tuberculosis

53
Q

What is fat necrosis?

A

Fat necrosis is a condition that occurs when a person experiences an injury to an area of fatty tissue –> a lump of dead or damaged (breast) tissue

54
Q

What is fibrinoid necrosis?

A

a specific pattern of irreversible, uncontrolled cell death that occurs when antigen-antibody complexes are deposited in the walls of blood vessels along with fibrin.

55
Q

Do cells retain their outlines in coagulative necrosis?

A

Yes

56
Q

What is the predominant necrotic process in coagulative necrosis?

A

Protein denaturation and there is only a small contribution from enzymatic degradation

–> metabolic activity ceases

57
Q

Where is liquefactive necrosis seen?

A

In the brain –> due to lack of supporting stroma (the supportive tissue of an epithelial organ, tumour, gonad, etc., consisting of connective tissues and blood vessels)

58
Q

What is gangrenous necrosis mainly caused by?

A

Infection/bacteria

59
Q

How does gangrenous necrosis appear?

A

Black

60
Q

What are the 3 types of gangrenous necrosis?

A
  • Wet
  • Dry
  • Gas
61
Q

What is the main cause of caseous necrosis?

A

Tuberculosis

62
Q

Appearance of caseous necrosis?

A

Structureless dead tissue, amorphous pink material in centre with necrotic debri

63
Q

Causes of fat necrosis?

A
  • Enzymes
  • Trauma
64
Q

What 2 conditions is fibrinoid necrosis seen in?

A
  1. Malignant hypertension
  2. Autoimmune diseases
65
Q

What is the most common necrosis?

A

Coagulative necrosis in the myocardium

66
Q

What are the 2 types of cell injury?

A

Reversible and irreversible

67
Q

Diagram of cell injury –> cell death

A
68
Q

What is cell adaptation?

A

It is a reversible functional and structural response of cells to environmental changes or stimulation during which new steady states are achieved, allowing the cell to survive and continue to function.

69
Q

Hypertrophy vs hyperplasia?

A

Hypertrophy refers to an increase in the size of the cell while hyperplasia refers to an increase in the number of cells or fibers.

70
Q

What are the 4 types of cell adaptation?

A
  1. Hyperplasia
  2. Metaplasia
  3. Atrophy
  4. Hypertrophy
71
Q

What are the definitions of:

  1. Hyperplasia
  2. Atrophy
  3. Hypertrophy
  4. Metaplasia
A
  1. Increase in the cell number
  2. Decrease in the size and metabolic activity of cells
  3. Increase in the size and functional activity of cells
  4. Change of phenotype of cells
72
Q

Hypertrophy diagram - myocyte

A
73
Q

In response to increased hemodynamic loads (due to increased BP) , what adaptation happens to the heart muscle?

A

The heart muscle becomes enlarged (as a form of adaptation) This form of adaptation leads to thickening of LV wall.

74
Q

Does a hypertrophied organ have any new cells?

A

No - just larger cells (increased cell and organ size)

75
Q

Hypertrophy can also result from physiological, rather than pathological, states. What is an example of this?

A

The massive physiologic growth of the uterus during pregnancy (hormone-induced)

76
Q

What is the most common epithelial metaplasia? Where does this occur?

A

The most common epithelial metaplasia is columnar to squamous –> occurs in the respiratory tract in response to chronic irritation

77
Q

What is metaplasia?

A

Metaplasia is a process whereby one type of mature tissue is replaced by another type of mature tissue not indigenous to that organ or tissue. Metaplastic transformation likely represents a reactive or reparative response to some chronic injury or irritation.

78
Q

What is atrophy?

A

Decreased cell & organ size as a result of decreased nutrient supply or disuse.

79
Q

Atrophy of disuse?

A

Decreased workload causing atrophy –> When a fractured bone is immobilised in a plaster cast or when a patient is restricted to complete bed rest, skeletal muscle atrophy rapidly ensues

80
Q

What is the end result of progressive cell injury?

A

Cell death

81
Q

What are the 2 main types of cell death?

A

Necrosis and apoptosis

82
Q

What is reversible cell injury characterised by?

A
  • generalized swelling of the cell and its organelles
  • blebbing of the plasma membrane
  • detachment of ribosomes from the Endoplasmic reticulum
  • clumping of nuclear chromatin.
  • if the injurious stimulus is removed –> the cell can repair these derangements and return back to normal
83
Q

If the injury is persistent or excessive, what then happens?

A

Cell death by necrosis:

  • breakdown of plasma membrane, organelles and nucleus
  • leakage of cell contents –> triggering inflammatory response
84
Q

What characterises necrosis?

A

severe mitochondrial damage with depletion of ATP, rupture of lysosomal and plasma membranes

85
Q

What is apoptosis characterised by?

A
  • nuclear dissolution
  • fragmentation of the cell without complete loss of membrane integrity
  • rapid removal of the cellular debris (cellular

contents do not leak out –> no inflammatory response

86
Q

What are the ultrastructural changes of reversible cell injury?

A
  1. Plasma membrane alterations: such as blebbing, blunting, and loss of microvilli
  2. Mitochondrial changes: swelling and the appearance of small amorphous densities
  3. Dilation of the ER, with detachment of polysomes; intracytoplasmic myelin figures may be present
  4. Nuclear alterations, with disaggregation of granular and fibrillar elements
87
Q

Apoptosis vs necrosis diagram

A
88
Q

Are the cell contents ingested by macrophages in necrosis/apoptosis?

A

Necrosis:

  • Cell contents ingested by macrophages
  • Significant inflammation

Apoptosis:

  • Cell contents ingested by neighbouring cells
  • No inflammatory response
89
Q

Does cellular swelling occur in necrosis/apoptosis?

A

Necrosis –> cellular swelling

Apoptosis –> cellular shrinkage

90
Q

Is there loss of membrane integrity in necrosis/apoptosis?

A

Necrosis:

  • Loss of membrane integrity
  • Cell lysis occurs

Apoptosis:

  • Membrane blebbing but integrity maintained
  • Apoptotic bodies form
91
Q

Is there random degradation of DNA in necrosis/apoptosis?

A

Necrosis:

  • Lysosomal leakage
  • Random degradation of DNA

Apoptosis:

  • Mitochondria release pro-apoptotic proteins
  • Chromatin condensation and non-random degradation of DNA
92
Q

What is necrosis?

A

is death of tissue following bioenergetic failure and loss of plasma membrane integrity (uncontrolled cell death).

93
Q

What are the 6 types of necrosis?

A
  1. Coagulative
  2. Liquefactive (colliquative)
  3. Gangrenous
  4. Caseous
  5. Fat necrosis
  6. Fibrinoid necrosis
94
Q

What is the most common form of necrosis?

A

Coagulative necrosis

95
Q

What is coagulative necrosis mostly caused by?

A

Mostly caused by a lack of blood supply and can occur in most organs.

E.g. –> Here, there is a localised wedge-shaped pale area of coagulative necrosis (infarction) in the cortex of the kidney, due to loss of blood supply and resultant tissue anoxia.

96
Q

What is colliquative/liquefactive necrosis? What is the end result?

A

Death of cells in the brain due to a lack of substantial supporting stroma that results in liquefactive necrosis.

The dead cells are broken down to form a liquid mass (liquifies) –> lastly a cyst is formed.

97
Q

What is caseous necrosis? What disease is this commonly seen in?

A

The dead tissue is structureless and the necrotic tissue has a cheese-like (caseous) appearance. Commonly seen in tuberculosis.

Example: This is an extensive caseous necrosis with cheesy tan granulomas in the upper portion of this lung in a patient with TB. The tissue destruction is so extensive that there are areas of cavitation.

98
Q

What is gangrene?

A

A complication of necrosis which occurs when tissues are invaded by bacteria which release proteolytic enzymes. These enzymes degrade the necrotic tissue, releasing foul-smelling gases. The affected tissue becomes green or black.

E.g. Obstruction of the blood supply to the bowel is followed by gangrene.

99
Q

What is fibrinoid necrosis? What is it seen in?

A

Necrosis in the blood vessels - antigen-antibody complexes are deposited in the walls of blood vessels along with fibrin. Seen in autoimmune diseases and malignant HTN.

100
Q

What is fat necrosis? Where is it seen?

A

This is a form of fat destruction seen in trauma/pancreatitis.

101
Q

Mechanism of fat necrosis?

A

Following trauma to adipose (fat) tissue, intracellular fat (triglycerides) is released. Inflammatory response is triggered with polymorphs and macrophages phagocytosing the fat. This eventually proceeds to fibrosis.

102
Q

What is the mechanism behind the Na+/K+ ATPase?

A

Per cycle, it pumps three Na+ ions out and two K+ ions into the cell, coupling the energy derived from the hydrolysis of one ATP molecule.

103
Q

What is the sodium-potassium pump driven by?

A

ATP

104
Q

Why is the sodium-potassium pump affected during cell injury? What does this lead to?

A

Decreased levels of oxidative phosphorylation leads to ATP depletion –> leads to cell swelling as osmotic pressure builds within the cell due to increased ions, and water and fluids move into the cell

105
Q

damage to the membranes of 3 things can cause irreversible cellular injury?

A
  1. Lysosome
  2. Cell membrane
  3. Mitochondria
106
Q

what are caspaces? what do they trigger?

A

proteases that are essential for the initiation and execution of apoptosis - trigger apoptosis

107
Q

What is Cyt C? What does it trigger?

A

The cytochrome complex - activates caspaces which triggers apoptosis

108
Q

What are the detrimental effects of increased Ca into cell?

A
  1. Ca activates proteases and other enzymes –> enzymatic degredation of cell
  2. Ca activates caspaces –> triggers apoptosis
109
Q

What is hydropic change? What is it a sign of?

A

Hydropic change refers to the accumulation of water in the cell - is one of the early signs of cellular degeneration in response to injury.

110
Q

Where does oxidative phosphorylation take place?

A

Mitochondria (damage to mitochondria can result in ATP depletion)

111
Q

Result of damage to the membrane of mitochondria vs damage to mitochondria itself?

A
  • Membrane - leakage of Cyt C –> activates caspaces –> triggers apoptosis
  • Mitochondria itself - lack of oxidative phosphorylation –> ATP depletion
112
Q

Which part of the cell releases pro-apoptotic proteins?

A

Mitochondria

113
Q

How are apoptotic bodies removed?

A

These small membrane-surrounded fragments are cleared by phagocytosis without triggering an inflammatory response

114
Q

Is the membrane more permeable to K+ or Na+?

A

K+

115
Q

How is leakage of cellular contents controlled in apoptosis?

A

Via apoptotic bodies which are then engulfed via phagocytosis

116
Q

How can hypertension lead to necrosis?

A

Fibrinoid necrosis is often a result of very high blood pressure that damages the cells in the blood vessels, eventually leading to cell death

117
Q

What is danger of fibrinoid necrosis?

A

dead blood vessel cells will form fibrin, which is a protein that forms a fibrous material that can block blood flow through the blood vessels

118
Q

Where is Cyt c located?

A

In mitochondria

Yr 2 - EMS (60 decks)

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