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Y3 IWB > PATHOLOGY- Essentials of general pathology- cell injury and cell death > Flashcards

PATHOLOGY- Essentials of general pathology- cell injury and cell death Flashcards

1
Q

What are the 3 responses to cellular stress

A

Adaptation
Reversible cell injury
Irreversible cell injury/death

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2
Q

What are some causes of cell injury and death

A
  1. Oxygen deprivation/deficiency (hypoxia)
  2. Physical/environmental
  3. Chemical agents/toxins/drugs
  4. Infectious agents
  5. Immunologic reactions
  6. Genetic derangements
  7. Nutritional imbalances
  8. Ageing
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3
Q

Cellular response to injury depends on what 3 things

A

Type
Duration
Severity of the insult

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4
Q

What happens when an injurious agent causes cell injury

A

Simultaneously triggers multiple interconnected mechanisms

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5
Q

Cell injury can result due to which 5 cellular processes being disrupted

A
  1. ATP production (via effects on mitochondrial aerobic respiration)
  2. Mitochondrial integrity (independent of ATP)
  3. Plasma membrane integrity
  4. Protein synthesis, folding, degradation and re-folding
  5. Genetic (DNA) integrity
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6
Q

How many mechanisms is there responsible for cell injury

A

6

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7
Q

What are the 6 mechanisms of cell injury

A
  1. ATP depletion
  2. Mitochondrial damage
  3. Increased intra-cellular calcium
  4. ROS/ free radical damage
  5. Membrane damage
  6. DNA damage and protein mis-folding
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8
Q

What 3 energy dependent functions is ATP required for

A
  • Membrane transport
  • Maintenance of ionic gradients (e.g. Na, K, and Ca2+)
  • Protein, DNA & RNA synthesis
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9
Q

What does the efficient production of ATP require

A

Oxygen

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10
Q

ATP depletion can occur due to what 2 things

A

Hypoxia/toxins
Mitochondrial damage

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11
Q

What % reduction in ATP levels can cause critical cellular damage

A

5%-10%

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12
Q

What negative affect does ATP depletion have on pumps, what does this lead to?

A

Failure of Na* / K+ ATPase pumps
Failure of ionic gradients

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13
Q

What affect can ATP depletion have on Na

A
  • failure of Na+/K+ ATPase pumps
  • failure of ionic gradients (increase influx of Ca++, H2O and Na+ and increased effluent of K+)
    -ER swelling, cellular swelling, loss of microvilli
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14
Q

What does hypoxia (insufficient oxygen) cause

A

Anaerobic respiration

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15
Q

What affect does ATP depletion have on anaerobic glycolysis

A
  • anaerobic glycolysis increases
  • glycogen decreases as its converted to lactic acid through glycolysis
  • increase is lactic acid causes lower pH
  • drop in pH causes acidosis
  • results in clumping of nuclear chromatin
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16
Q

What other effects does ATP depletion have

A
  • Enzyme failure
  • Disruption of protein synthesis / folding
  • Irreversible damage to membranes
  • Formation of reactive oxygen species (ROS)
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17
Q

What are the 2 types of damage to the mitochondria

A

Direct
Indirect

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18
Q

3 examples that cause direct damage to the mitochondria

A

hypoxia, toxins, radiation

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19
Q

3 examples that cause indirect damage to the mitochondria

A

Increase in Ca?+ / oxidative stress / phospholipid breakdown

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20
Q

What type of damage to the mitochondria is reversible

A

Early damage

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21
Q

What is the MPTP

A

Membrane permeability transition pore

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22
Q

What is created when there is sustained damage to the mitochondria

A

MPTP

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23
Q

Why is MPTP an issue

A
  • MPTP impairs oxidative phosphorylation which lowers ATP
  • Reactive oxygen species formation increases
  • leads to multiple cellular abnormalities
  • leading to necrosis
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24
Q

What can specific damage of the mitochondria lead to

A

Leakage of mitochondrial proteins leading to apoptosis

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25
Q

How abundant is cytosolic calcium usually

A

Normally low

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26
Q

How is increased intra-cellular calcium caused by hypoxia/toxins

A
  • Hypoxia/toxins lead to pump failure
  • increase in Ca2+ causes release of Ca2+ from motichondria/ER
  • increase in Ca2+ causes increase in membrane permeability, causing further increase in Ca2+
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27
Q

Why is increased calcium harmful to cells

A
  • Increase in Ca2+ activates harmful intracellular enzymes
  • ATPases / phospholipases / endonucleases
  • Leads to decrease in ATP / cell membrane / DNA damage
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28
Q

What are free radicals

A

Single unpaired electron

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29
Q

What are reactive oxygen species

A

oxygen-derived free radical that is highly reactive

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30
Q

How do free radicals come about
How abundant are they
What do cells have to counteract the free radicals

A
  • Normal by-products of cellular respiration (mitochondria)
  • Limited amounts, limited life due to reactivity
  • Mechanisms to counteract - enzymes e.g. SOD (super oxide dismutase) / anti-oxidants
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31
Q

What can increased pathological ROS production result in

A

Oxidative stress

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32
Q

What 4 things can cause oxidative stress

A
  • lonising radiation / chemicals
  • Ischaemia-reperfusion injury
  • Metals (iron / copper) or chemicals (CCI4)
  • Nitric oxide - inflammation
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33
Q

What are the cellular effects of free radical damage

A

Damage cell membrane/ lipids / nucleic acid breaks / protein oxidation & fragmentation

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34
Q

What is common in most forms of cellular injury

A

Early loss of selective membrane permeability, especially in oxygen deprivation

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35
Q

3 examples of direct damage to the membrane of the cell

A

Bacterial
Viral
Immune proteins

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36
Q

3 examples of indirect damage to the membrane of the cell

A

Increase in ca2+
Decrease in ATP
ROS formation

37
Q

What affect does membrane damage have on cells

A

Increase permeability

38
Q

What is lysosomal membrane damage

A

Intra-cellular lysosomes release digestive enzymes
Leads to auto digestion of the cell

39
Q

What can DNA damage often lead to

A

Apoptosis

40
Q

When there is an excess of misfolded proteins, what is caused

A

ER stress

41
Q

What is ER stress

A

When the protein folding demand is higher than the protein folding capacity

42
Q

What 2 things can ER stress lead to

A

Failure of adaptation
Apoptosis

43
Q

Why is it difficult to assign a dominant mechanism to a specific injury

A

All mechanisms are generally inter-related

44
Q

What is a reversible cell injury

A

Mechanisms that can be offset if insult to cell is mild/transient

45
Q

What are morphological features of reversible cell injury

A

Functional / structural alterations occurring in mild and/or early injury that reverse upon removal of the damaging stimulus.

46
Q

What are the 2 microscopic features of reversible cell injury

A

cellular swelling
Fatty change

47
Q

What are the 4 ultra structural features of reversible cell injury

A
  • Plasma membrane blebbing
  • Mitochondrial swelling
  • ER dilation
  • Chromatin clumping
48
Q

What are the 2 main forms of cell death

A

Apoptosis
Necrosis

49
Q

What is the difference between apoptosis and necrosis generally

A

In apoptosis, cell contents contained and not released
In necrosis, the membrane is broken down and there’s leakage of cell contents into tissues (inflammation)

50
Q

Difference between cell size in necrosis and apoptosis

A

Necrosis- increased cell size (cell swollen)
Apoptosis- reduced cell size (cell shrunken)

51
Q

Difference between nucleus in necrosis and apoptosis

A

Necrosis- fragmentation
Apoptosis- fragmentation and condensation

52
Q

Difference between plasma membrane in necrosis and apoptosis

A

Necrosis- disrupted (spilling of contents)
Apoptosis- intact

53
Q

Difference between nearby inflammation in necrosis and apoptosis

A

Necrosis - almost always
Apoptosis - never

54
Q

Difference between physiological/pathological in necrosis and apoptosis

A

Necrosis- pathpological
Apoptosis- physiological but may be pathological

55
Q

What is coagulative necrosis

A

necrosis in tissue with connective tissue
Connective tissue allows the shape/structure to be preserved

56
Q

What is colliquative necrosis

A

Tissue with minimal connective tissue
This causes the tissue to liquify

57
Q

What is caseous necrosis

A

‘Cheese’-like necrotic debris held within a defined border

58
Q

What is gangrene necrosis

A

Coagulative necrosis of a limb (dry)
With infection (wet)

59
Q

What is fat necrosis

A

focal necrosis in fat due to action of lipases (also trauma)

60
Q

What is fibrinoid necrosis
what does it cause

A

Occurs when there is damage to blood vessel walls
Causes pink material to be deposited in the vessel walls (fibrin-like)

61
Q

What is apoptosis

A

Programmed cell death (cellular suicide)

62
Q

3 features of apoptosis

A

Tightly regulated
Removed unwanted cells without damaging surrounding tissues
Can be physiological or pathological

63
Q

Physiological examples of apoptosis

A

-embryogenesis
-involution of hormone-dependent tissues
-control cell turnover in proliferating cells populations
-elimination of potentially harmful self-reactive lymphocytes
-death of host cells after immune response

64
Q

What is embryogenesis

A

Removal of unwanted/excessive cells during development

65
Q

What is involution of hormone-dependent tissues

A

apoptosis on hormone withdrawal

66
Q

Pathological examples of apoptosis

A
  • DNA damage
  • Accumulation of misfolded proteins
  • Infections
  • Pathological atrophy
67
Q

Why is apoptosis important in DNA damage

A
  • Radiation / drugs, direct or indirect via free radicals
  • Important as prevents propagation of cells with DNA damage resulting in carcinogens
68
Q

What are the 2 main pathways for apoptosis

A

Mitochondrial (intrinsic) pathway
Death receptor (extrinsic) pathway

69
Q

What happens in the mitochondrial (intrinsic) pathway

A
  • Loss of survival signals, DNA damage etc.
  • Leakage of pro-apoptotic proteins (mitochondria)
  • Activates caspases
70
Q

What happens in the death receptor (extrinsic) pathway

A
  • Binding of ligand to a cell surface receptor
  • Activates caspases
71
Q

What is common in both the pathways of apoptosis?
What does this lead to?

A

Caspase activation

Fragmentation of DNA / nuclei
Formation of “Apoptotic body” - cell fragments for phagocyte absorption

72
Q

6 morphological features of apoptosis

A
  • Cell shrinkage
  • Chromatin condensation
  • Cytoplasmic blebs
  • Apopototic bodies (AB)
  • Phagocytosis of Abs
  • No surrounding damage
73
Q

What the main differences between necrosis and apoptosis

A

Necrosis
- increased cell size
- nucleus pyknosis (going), karyohexis (going), karyolysis (gone)
-plasma membrane distrupted (spilling of contents)
- almost always has nearby inflammation
-pathological

Apoptosis
- reduced cell size
- nucleus fragmentation/condensation
-plasma membrane intact
- never has nearby inflammation
- physiological but may be pathological

74
Q

How does cell death lead to clinical diagnosis in myocardial infarction

A

Necrosis occurs
Myocardial enzymes released into blood
Troponin detected in blood

75
Q

How does cell death lead to clinical diagnosis in pancreatitis

A

-Necrosis occurs
-Pancreatic enzymes released into blood
-Amylase increases which can be detected
-Lipase increases leading to fat necrosis, this leads to saponification and Ca2+ in the blood decreases

76
Q

How can apoptosis directly help with clinical diagnosis

A

Can be seen microscopically in specific conditions e.g liver disease/GVHD

77
Q

What is cellular adaption

A

Reversible changes in the size, number, phenotype, metabolic activity, or functions of cells in response to changes in their environment

78
Q

What is hypertrophy

A

An increase in the size of cells resulting in an increase of organ size
- No new cells, just larger
- Synthesis of more structural components of the cells

79
Q

An example of hypertrophy being physiological

A

bodybuilding
- increases muscle fibre size
- results of increasing load stress

80
Q

An example of pathological hypertrophy

A

Cardiac hypertrophy
Increase in myocyte size
Result of circulatory stress and hypertension

81
Q

What is hyperplasia

A

An increase in the number of cells in an organ or tissue usually resulting in increased mass of the organ or tissue
- Usually in response to hormones / growth factors in tissues with dividing cells

82
Q

Example of physiological hyperplasia

A

Hormonal (e.g. breast in pregnancy)

83
Q

Example of pathological hyperplasia

A

Benign prostatic hyperplasia

84
Q

Although hyperplasia is not the same as neoplasia, what can happen
give example

A

Neoplastic change can occur in hyperplastic tissues

E.g. endometrial hyperplasia

85
Q

What is atrophy

A

Reduced size of an organ or tissue resulting from a decrease in cell size and number

86
Q

Example of physiological atrophy

A
  • embryology, postpartum uterus
87
Q

Examples of pathological atrophy

A
  • Decreased workload
  • Denervation
  • Diminished blood supply
  • Inadequate nutrition
  • Loss of endocrine stimulation
  • Pressure
88
Q

What is metaplasia

A

Change in which one differentiated cell type is replaced by another cell type
- Adaptive substitution of cells that are sensitive to stress by cell types better able to withstand adverse environment (usually inflammatory)

89
Q

Examples of metaplasia

A
  • Oesophagus
    Acid reflux -> squamous cells -> gastric-like columnar epithelium (Barrett’s)
  • Lungs
    Cigarette smoke -> respiratory-type columnar cells -> squamous cells
  • Cervix
    Vaginal pH decreases -> columnar cells (endocervix) -> squamous cells (ectocervix)

Y3 IWB (31 decks)

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