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Cell Injury: Cell death
Compare and contrast necrosis and apoptosis
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Providing suitable examples from recent
literature, critically discuss the advantages and disadvantages given to a human by programmed cell
death
Necrosis
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Premature cell death as a result of pathologic response
Trauma, infection, chemical, hypoxia, ischemia
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Aging: cellular senescence > impaired replication and repair capabilities > increase cell death
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This is the case in heart cells
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20-30 mins after ischemia cell death
occurs
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Apoptosis is not associated with ATP loss
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(phospholipid mass)
Phospholipid precipitates are phagocytosed or broken down into fatty acids
Fatty acids become calcified creating calcium soap and dead cells maybe become calcified
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Nuclear condensation and dissolution
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Sodium pump damages>influx of water causing swelling>anaerobic glycolysis>lower ph=lower
enzyme activity>influx of calcium damaging cellular components>ribosome detachments >
polysomes to monosomes > reduced protein synthesis > lysosome and membrane
disruption>necrosis
Ischemia and toxins: cytosolic calcium increase, initially calcium is released from intracellular
stores
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It activates a number of enzymes
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Proteases: break down membrane and cytoskeletal
proteins
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ATPases increasing ATP depletion
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Outline of dead cells remains, firm tissue
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Injury denatures proteins AND enzymes therefore proteolysis of dead cells cannot occur
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Typical of infarcts (except the brain)
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Liquefactive

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Occurs in tissue rich in fluid (brain)
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of leukocytes to one area > damaging
enzymes causing liquidation of tissue
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If a result of acute inflammation usually pus
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Atheroma > thrombosis > ischaemia > necrosis
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The addition of bacterial infection > liquefactive necrosis
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Example: lungs: haemorrhagic infarction, wedge shaped, went to pleural surface, therefore have
effusion and exudates; neutrophils in it; have pleuritic chest pain (knife-like pain on inspiration)
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Caseous
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Cheese-like
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Collection of lysed cells, looks granular
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Cell outlines cannot be seen
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Either have mycobacterial infection (any infections, including atypical, or systemic fungal
infection); these are the ONLY things that will produce caseation in a granuloma
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Fat necrosis
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Focal area fat destruction
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Pancreatic enzymes leak from acinar cell (pancreatic cell) > liquefy membranes of fat cells in
peritenum + lipases split triglyceride esters in fat cells > fatty acids released + calcium > chalky
white appearance (fat saponification)
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Fibrinoid necrosis
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Ab and Ag deposited in artery wall > immune complex + fibrin > amorphous appearance
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: In the chronic stage, fibrinoid necrosis of the vessels causes thrombosis and
tissue infarction
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Often associated with hep C
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Programmes cell death
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The cell fragments and breaks apart
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Dead cell is cleared before contents leak out therefore different to necrosis
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Programmed cell destruction during embryogenesis
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g
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Cell loss in cells that continually proliferate so as to regulate numbers: intestinal crypt epithelia
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E
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Immune cells
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Cytotoxic t cell induced death against viruses and tumours
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DNA can be repaired by p53 protein
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Kills cell infected with viruses
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Causes cervical cancer
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If damaged cancer
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mitochondrial
membrane increased permeability=leakage of these proteins>apoptosis
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Apoptosis is considered a vital component of various processes including normal cell turnover,
proper development and hormone-dependent atrophy, embryonic development and chemicalinduced cell death
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Apoptosis also occurs as a defence mechanism such as in immune reactions or when cells are
damaged by disease or noxious agents
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Disadvantages:
There aren't any apparent disadvantages of the phenomenon of apoptosis but errors in the
processes can lead to critical situations
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Inappropriate apoptosis (either too little or too much) is a factor in many human conditions
including neurodegenerative diseases, ischemic damage, autoimmune disorders and many types
of cancer
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ncbi
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nih
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com/podcast/apoptosis-necrosis-and-calcification-usmle-step-1mp3s-notes



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