Pathophysiology Flashcards
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Causes of altered cellular functions
Adaption
Injury
Ageing
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Cellular adaption & types
Changes based on the environment to escape and protect from injury
Atrophy (decreased size)
Hypertrophy (increased size)
Hyperplasia (increase cell number)
Metaplasia (reversible replacement of mature cell to less mature cell)
Dysplasia (irreversible deranged cell growth)
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Cellular Injury & causes
Unable to maintain homeostasis due to stimuli or stress
Hypoxia, nutritional imbalance, chemical agents, physical agents, infection, genetics, ageing
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Hypoxia & causes
Insufficient oxygen supply to tissues in order to maintain homeostasis
- Lack of oxygen entering body (respiratory disease, low atmospheric O2)
- Lack of O2 transport (CVD, anaemia, low Hb, reduced RBC production)
- Ischaemia (lack of/restricted blood flow)
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Mechanisms of cellular injury (list)
ATP depletion
Altered calcium homeostasis
Defects in membrane permeability
Free radicals
ATP Depletion
Mechanism of cellular injury
Loss of O2 reduces ATP synthesis
Failure of Na/K pump = cellular swelling
Anaerobic glycolysis = lactic acidosis
Overall decreased protein synthesis, membrane transport, lipogenesis, loss of membrane integrity
Altered calcium metabolism
Mechanism of cellular injury
Lack of ATP = reduced Ca transport out of cell
High cytosolic Ca = damages plasma membrane, cytoskeleton, activates destructive enzymes, damages mitochrondia
Defects in membrane permeability
Loss of selectivity in transport in all types of injury
* Na, Ca, water influx
Free radicals
Mechanisms of cellular injury
Atoms with unpaired electron
Lipid peroxidation, oxidative stress = alters proteins, DNA, and mitochondria
Esp during reperfusion
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Types of cellular injury
Reversible: cellular swelling (ATP pumps), lipid accumulation (alt liver metabolism) (reversible)
Irreversible: cannot restore homeostasis (DNA & lysosomal leakage, enzyme induced autolysis)
Apoptosis and necrosis
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Apoptosis & types
Programmed cell death, selective self destruction (condensation, blebs, fragmentation)
1. Pathologic = infected cells, damaged DNA, pre-cancerous cells
2: Physiologic = developmental, no inflammation, occurs too great in degenerative conditions (Alzheimer’s)
Necrosis & characteristics
Premature death from injury/noxious stimuli = autolysis, self destruction (ER/Mit swelling, blebs, breakdown, leakage)
- Inflammatory cells (macro, neutro), areas of cell loss
- Clumping of genetic material (karyolysis), cell membrane and organelle disruption
- Lysosome disruption, digestive enzyme leakage, autolysis
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Types of necrosis
- Coagulative: ischaemic injury, protein denaturation (kidneys, heart, adrenals)
- Liquefactive: ischeamic injury to brain (cell dissolusion due to digestive enzymes)
- Caseous: coag+liquefactive (cheese like, TB infection)
- Fat: adipose injury, lipase action (breast, pancreas, abdominal organs)
- Gangrenous: severe hypoxic injury, dry or wet
Ageing & types
Accumulation of changes over time
- Cellular ageing: genetics (DNA repair defects, genetic abnormalities, mutations, alt signalling) & environmental (free radicals, reduced enzymes, abnormal protein accumulation) = atrophy, loss of function and cells
- Tissue ageing: progressive stiffness, rigidity, scarcopenia