Cell Injury And Death Flashcards
What do the degrees of injury depend on?
Type of injury, severity of injury, duration of injury, type of tissue.
What are causes of cell injury?
Environmental- hypoxia, toxins, infection. Non-environmental- genetic, ageing.
What is hypoxia and what are causes?
Hypoxia is oxygen deprivation. There are different causes: hypoxaemic hypoxia- arterial content of oxygen is low, anaemic hypoxia- decreased ability of haemoglobin to carry O2, ischaemic hypoxia- interruption to blood supply, histiotoxic hypoxia- inability to utilise oxygen due to disabled oxidative phosphorylation enzymes.
What are common mechanisms of cell injury?
Depletion of ATP, direct mitochondrial damage, disruption to calcium homeostasis, oxidative stress and direct damage to DNA+ proteins.
Describe ATP depletion.
Cells deprived of oxygen -> reduction in oxidative phosphorylation -> mitochondrial ATP production stops.
What do free radicals damage?
Lipids, proteins and DNA.
Describe free radical lipid damage.
Unsaturated fatty acids get attacked by free radicals, this causes cell membrane and organelle damage. This results in calcium influx, damage to Na/K pump.
Describe free radical lipid damage.
Unsaturated fatty acids get attacked by free radicals, this causes cell membrane and organelle damage. This results in calcium inf
Describe free radical DNA damage.
Free radicals target nuclear and mitochondrial DNA, they cause single and double strand breaks in DNA
How does the body control free radicals?
Anti-oxidants: lipid soluble vitamins, ascorbic acid, glutathione. Transport proteins: iron binds to transferrin, copper binds to ceruloplasmin. Enzymes: Superoxidase dismutases, glutathione peroxidase.
What do heat shock proteins do?
They help repair and re-fold damaged proteins, or they label them for degradation.
What are reversible and irreversible changes in an injured cell?
Reversible: Swelling (due to Na/K+ pump failure), clumped chromatin (due to reduced pH), ribosome dispersion (lack of ATP), cytoplasmic blebs. Irreversible: nuclear changes, lysosome rupture, membrane defects and lysis of endoplasmic reticulum.
What is apoptosis?
Individual programmed cell death. It can be pathological or physiological. Physiological- embryogenesis, involution of hormone dependent tissue. Pathological- cell death in viral infection, cells with damaged DNA.
What are the two pathways of apoptosis?
Intrinsic- mitochondria release cytochrome C which activate capases which induce apoptosis. Extrinsic- death receptors attach to the cell membrane which then activate capases which lead to cell death
What is necrosis?
In a living organism, the morphological changes that occur after a cell has been dead some time.
What are the types of necrosis?
Coagulative, liquefactive, caseous, fat necrosis, fibrinoid necrosis.
What is coagulative necrosis?
Occurs in solid organs, it retains a ghost outline of cells and tissue architecture. Protein desaturation is prominent in the cell injury/death.
What is liquefactive necrosis?
Loose tissue dies, a complete loss of architecture, release of enzymes which break down tissue.
What is caseous necrosis?
Seen in the lung in TB, ‘cheese’ like
What is fat necrosis?
Direct trauma to fatty areas, acute pancreatitis
Apoptosis vs Necrosis
Apoptosis- Single cell death, cell shrinks, plasma membrane is preserved, organelles contract, dead cells taken up by phagocytes.
Necrosis- grouped cell death, cell swells, plasma membrane destroyed, organelles swell and break down, dead cells start inflammatory process.
What molecules are released by injured cells?
Potassium, enzymes and myoglobin
Describe intra-cellular accumulations.
Accumulations can be: normal cell components, abnormal components, pigment.
Example of normal cell component.
Cerebral oedema: hypoxic cell injury, sodium enters cell and water follows causing cell swelling.
