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32 Cards in this Set
- Front
- Back
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Once the adaptive capacity of the cell is surpassed what happens? |
cell injury |
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Which happens first morphological changes or biochemical events and what is the significance? |
Biochemical events happen first, morphological changes next - a specific cell showing morphological changes consistent with moderate cell injury may already be dead |
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Describe the spectrum of cell injury |
Normal Cell Homeostasis (Normal) >>Reversible Cell Injury (Cloudy swelling, fatty change) >>Irreversible Cell Injury (Oncosis Apoptosis) |
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The severity and result of cell injury depends on what 5 things |
Intensity of exposure |
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Cellular adaptations/changes which may be physiological or pathological can include (5 things)
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Hypertrophy |
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T/F? Atrophy / Decreased cell size is always pathological
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F Can be physiological (normal) or pathological (abnormal) |
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What 3 important ways do cells respond to injury
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Adaptation |
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What are the 5 possible causes of cell injury |
Hypoxia (circulatory disturbance/ischemia, decreased oxygen carrying capacity, interference with the respiratory chain |
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What are the two most important things for normal cell function
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Intact membranes and energy supply |
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Which two things are likely to cause cell injury and why?
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Membrane damage |
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What is the fundamental role of cell membranes
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Act as a selective barrier for the cell and maintain correct internal osmolality, which depends on energy dependent ionic pumps |
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A damaged membrane leads to what
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Influx of Na+, Ca2+, water into cells and cell organelles resulting in swelling , cell function is inhibited Also disruption of protein synthesis rER Disruption of energy production by mitochondria |
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How does membrane damage occur
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Most agents damage membranes via free radicals |
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What are free radicals and where do they come from
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Free radicals are highly reactive small molecules, with an unpaired electron, usually charged oxygen molecules. Often free radicals are released when agents of disease contact cellular components, eg ionising radiation, toxins Free radicals are also produced by normal endogenous processes, but are mopped up by antioxidants (selenium, vitamin E, superoxide dismutase, glutathione etc). Free radicals are also used by the immune system to kill foreign or infected cells - 'oxidative burst' of phagocytosis. |
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How do free radicals cause cell injury |
Free radicals ae released faster than the cell can neutralise them, and cause peroxidation of membrane lipids. The free radical reacts with the membrane lipid to form lipid peroxides and in a chain reaction of lipid peroxidation, significant membrane damage can result, increasing permeability. Free radicals also cause damage to proteins and nucleic acids. |
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What is enzyme induction |
Enzyme induction involves the smooth ER enzymes. The smooth ER metabolises metabolites and toxins and released free radicals in the process, if the cell I chronically exposed to a toxin, the smooth ER proliferates to increase its ability to deal with toxins. A sudden large dose of the drug can lead to a massive free radical release - and more damage is done by this than the toxin would have caused. This happens mostly in the liver |
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What agents of disease directly damage cell membranes? |
Irradiation, toxin, complement, vitamin E and selenium deficiency |
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Important free radicals are
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superoxide anion & hydroxyl radical |
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describe lipid peroxidation |
free radicals are able to combine with unsaturated lipids in cell membranes to form organic free radicals which combine with oxygen to form lipid hydroperoxyl radical which forms another lipid radical plus lipid peroxides. These lipid peroxides are unstable and form aldehydes and additional organic free radicals. The whole process is self-sustaining and can cause widespread membrane damage as well as damage to DNA, enzymes and structural proteins |
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membrane dysfunction can lead to what problems in the cell |
protein synthesis disruption due to ER damage; membrane permeability disruption; and mitochondrial respiration disruption due to membrane damage and influx of calcium. |
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the earliest and most significant manifestation of energy depletion is
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swelling of the cell and its organelles due to failure of the energy-dependent Na-K-ATPase ion pump; Na+ floods in taking water with it which causes swelling, and K+ rushes out which may upset cardiac conduction. Mitochondria and rER are most affected by the swelling so that (of most immediate concern) the energy shortage is accentuated and (later) protein synthesis is disrupted. |
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What causes energy (ATP) depletion?
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A deficiency of ATP could theoretically occur with a disruption anywhere in energy metabolism. However, the most common situation in which ATP production is impaired is hypoxia (oxygen shortage) and hence failure of aerobic respiration. Without oxygen, electrons cannot be transported which inhibits ATP production by oxidative phosphorylation; ATP production by the TCA cycle then slows as well. In a desperate bid to maintain ATP supply, glycolysis is stimulated but this has the undesirable effects of converting pyruvate into lactic acid, lowering the pH and further embarrassing ATP production. |
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What can lead to hypoxia |
Oxygen not reaching the blood e.g. tracheal obstruction or filling of alveoli with fluid or inflammatory exudate. Oxygenated blood not reaching the tissues e.g. infarction, constant pressure on a tissue from a tumour; hypovolaemic shock. "Respiratory poisons" acting at specific sites in the respiratory pathway. In these cases oxygen available within the cell cannot be utilised. Apart from cyanide toxicity associated with certain poisonous plants, this type of poisoning is probably rare in animals not involved in espionage.
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Which cells are most susceptible to hypoxia
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Cells with a high metabolic rate (neurons, myocardial fibres, renal epithelium)
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What cell injury changes can be see with the light microscope?
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Cellular swelling Altered cytoplasm staining characteristics Loss of fine detail Cytoplasmic vacuolation / vacuolar degeneration which can be Hydropic degeneration - organelle swelling Phagolysosome formation Loss of cytoplasmic organelles Accumulation of lipid droplets (fatty change / fatty degeneration)
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What ultra-structural changes does cell injury cause
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Loss of cell membrane surface specialisations ie microvilli and cillia Breakdown of intercellular attachments Cytoplasmic blebbing Mitochondrial swelling + deposits ER dilation + detachment of ribosomes Myelin figure formation Lysosomal swelling |
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Define pyknosis
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Nucleus condensing |
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Define karyorrhexis |
Nucleus fragmenting
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What morphological changes are associated with reversible cell injury / sublethal injury
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Cloudy swelling - hydropic degeneration Fatty degeneration / fatty change Vacuolar degeneration |
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Is this liver change reversible or irreversible?
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Reversible - normal, mild vacuolation of liver cells |
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Is this liver change reversible or irreversible?
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Marked hepatic lipidosis = reversible
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Define steatosis |
(fatty change, fatty degeneration or adipose degeneration) is the process describing the abnormal retention of lipids within a cell. |
