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Y3 Illness N Wellbejng 2 > 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
How abundant is cytosolic calcium usually
Normally low
26
How is increased intra-cellular calcium caused by hypoxia/toxins
- 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+
27
Why is increased calcium harmful to cells
- Increase in Ca2+ activates harmful intracellular enzymes - ATPases / phospholipases / endonucleases - Leads to decrease in ATP / cell membrane / DNA damage
28
What are free radicals
Single unpaired electron
29
What are reactive oxygen species
oxygen-derived free radical that is highly reactive
30
How do free radicals come about How abundant are they What do cells have to counteract the free radicals
- 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
31
What can increased pathological ROS production result in
Oxidative stress
32
What 4 things can cause oxidative stress
- lonising radiation / chemicals - Ischaemia-reperfusion injury - Metals (iron / copper) or chemicals (CCI4) - Nitric oxide - inflammation
33
What are the cellular effects of free radical damage
Damage cell membrane/ lipids / nucleic acid breaks / protein oxidation & fragmentation
34
What is common in most forms of cellular injury
Early loss of selective membrane permeability, especially in oxygen deprivation
35
3 examples of direct damage to the membrane of the cell
Bacterial Viral Immune proteins
36
3 examples of indirect damage to the membrane of the cell
Increase in ca2+ Decrease in ATP ROS formation
37
What affect does membrane damage have on cells
Increase permeability
38
What is lysosomal membrane damage
Intra-cellular lysosomes release digestive enzymes Leads to auto digestion of the cell
39
What can DNA damage often lead to
Apoptosis
40
When there is an excess of misfolded proteins, what is caused
ER stress
41
What is ER stress
When the protein folding demand is higher than the protein folding capacity
42
What 2 things can ER stress lead to
Failure of adaptation Apoptosis
43
Why is it difficult to assign a dominant mechanism to a specific injury
All mechanisms are generally inter-related
44
What is a reversible cell injury
Mechanisms that can be offset if insult to cell is mild/transient
45
What are morphological features of reversible cell injury
Functional / structural alterations occurring in mild and/or early injury that reverse upon removal of the damaging stimulus.
46
What are the 2 microscopic features of reversible cell injury
cellular swelling Fatty change
47
What are the 4 ultra structural features of reversible cell injury
- Plasma membrane blebbing - Mitochondrial swelling - ER dilation - Chromatin clumping
48
What are the 2 main forms of cell death
Apoptosis Necrosis
49
What is the difference between apoptosis and necrosis generally
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
Difference between cell size in necrosis and apoptosis
Necrosis- increased cell size (cell swollen) Apoptosis- reduced cell size (cell shrunken)
51
Difference between nucleus in necrosis and apoptosis
Necrosis- fragmentation Apoptosis- fragmentation and condensation
52
Difference between plasma membrane in necrosis and apoptosis
Necrosis- disrupted (spilling of contents) Apoptosis- intact
53
Difference between nearby inflammation in necrosis and apoptosis
Necrosis - almost always Apoptosis - never
54
Difference between physiological/pathological in necrosis and apoptosis
Necrosis- pathpological Apoptosis- physiological but may be pathological
55
What is coagulative necrosis
necrosis in tissue with connective tissue Connective tissue allows the shape/structure to be preserved
56
What is colliquative necrosis
Tissue with minimal connective tissue This causes the tissue to liquify
57
What is caseous necrosis
‘Cheese’-like necrotic debris held within a defined border
58
What is gangrene necrosis
Coagulative necrosis of a limb (dry) With infection (wet)
59
What is fat necrosis
focal necrosis in fat due to action of lipases (also trauma)
60
What is fibrinoid necrosis what does it cause
Occurs when there is damage to blood vessel walls Causes pink material to be deposited in the vessel walls (fibrin-like)
61
What is apoptosis
Programmed cell death (cellular suicide)
62
3 features of apoptosis
Tightly regulated Removed unwanted cells without damaging surrounding tissues Can be physiological or pathological
63
Physiological examples of apoptosis
-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
What is embryogenesis
Removal of unwanted/excessive cells during development
65
What is involution of hormone-dependent tissues
apoptosis on hormone withdrawal
66
Pathological examples of apoptosis
* DNA damage * Accumulation of misfolded proteins * Infections * Pathological atrophy
67
Why is apoptosis important in DNA damage
- Radiation / drugs, direct or indirect via free radicals - Important as prevents propagation of cells with DNA damage resulting in carcinogens
68
What are the 2 main pathways for apoptosis
Mitochondrial (intrinsic) pathway Death receptor (extrinsic) pathway
69
What happens in the mitochondrial (intrinsic) pathway
- Loss of survival signals, DNA damage etc. - Leakage of pro-apoptotic proteins (mitochondria) - Activates caspases
70
What happens in the death receptor (extrinsic) pathway
- Binding of ligand to a cell surface receptor - Activates caspases
71
What is common in both the pathways of apoptosis? What does this lead to?
Caspase activation Fragmentation of DNA / nuclei Formation of "Apoptotic body" - cell fragments for phagocyte absorption
72
6 morphological features of apoptosis
* Cell shrinkage * Chromatin condensation * Cytoplasmic blebs * Apopototic bodies (AB) * Phagocytosis of Abs * No surrounding damage
73
What the main differences between necrosis and apoptosis
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
How does cell death lead to clinical diagnosis in myocardial infarction
Necrosis occurs Myocardial enzymes released into blood Troponin detected in blood
75
How does cell death lead to clinical diagnosis in pancreatitis
-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
How can apoptosis directly help with clinical diagnosis
Can be seen microscopically in specific conditions e.g liver disease/GVHD
77
What is cellular adaption
Reversible changes in the size, number, phenotype, metabolic activity, or functions of cells in response to changes in their environment
78
What is hypertrophy
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
An example of hypertrophy being physiological
bodybuilding - increases muscle fibre size - results of increasing load stress
80
An example of pathological hypertrophy
Cardiac hypertrophy Increase in myocyte size Result of circulatory stress and hypertension
81
What is hyperplasia
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
Example of physiological hyperplasia
Hormonal (e.g. breast in pregnancy)
83
Example of pathological hyperplasia
Benign prostatic hyperplasia
84
Although hyperplasia is not the same as neoplasia, what can happen give example
Neoplastic change can occur in hyperplastic tissues E.g. endometrial hyperplasia
85
What is atrophy
Reduced size of an organ or tissue resulting from a decrease in cell size and number
86
Example of physiological atrophy
- embryology, postpartum uterus
87
Examples of pathological atrophy
- Decreased workload - Denervation - Diminished blood supply - Inadequate nutrition - Loss of endocrine stimulation - Pressure
88
What is metaplasia
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
Examples of metaplasia
* 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 Illness N Wellbejng 2 (31 decks)

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