Injuries to Cells Flashcards
Cell response to noxious stimuli
Normal cell limited to small range of function and structure
Stress leads to cell adaptation
If cell can’t adapt then it becomes injured
Cell adaptation
Hyperplasia
Hypertrophy
Metaplasia
Atrophy
Hyperplasia
Increase in cell NUMBER
Results in larger organ
Can occur alongside hypertrophy
- Physiological e.g. menstrual cycle
- Pathological e.g. endometrial hyperplasia if hormone stimulus persists
Hypertrophy
Increase in cell SIZE
Results in larger organ
- Physiological e.g. body builders
- Pathological e.g. heart in hypertension
Metaplasia
One adult cell type REPLACED by another
Occurs as second cell can take on stressors more easily
- e.g. chronic gastro-oesophageal reflux
Reversible
Atrophy
SHRINKAGE in size of cell by loss of cell substance
Occurs because of:
- decreased workload
- reduced blood supply
- inadequate nutrition
- loss of hormonal stimulation
- ageing
Causes of cell injury
Hypoxia - low O2 supply
Ischaemia - loss of blood supply, therefore O2 and nutrients
Chemical exposure - e.g. cigarette smoke, alcohol, paracetamol
Infection
Radiation
Lack of nutrients
Ageing
Immunologic reactions - body’s immune system does not recognise own cells and so attacks them
Morphology of reversible cellular injury
Cellular swelling
Fatty change - deposits of fat within cells
Cell death
Necrosis
- damage to membranes allows enzymes to digest the cell
- local inflammation
- always pathological
Apoptosis
- programmed cell death
- irreparable damage to cells DNA or deprived of growth factors
- can be pathological or physiological
- cell membrane still intact
- bits of cell break off
- dead cell removed by phagocytosis
Physiological apoptosis
Embryogenesis
Involution of hormone dependent tissues upon hormone deprivation
Elimination of cells which have served purpose
Elimination of potentially harmful self-reactive lymphocytes
Apoptosis in pathological conditions
DNA damage
Accumulation of misfolded proteins
Certain infections
Pathological atrophy in parenchymal organs after duct obstruction
Cell death induced by cytotoxic T cells
Mechanisms of apoptosis
Results from activation of enzymes called caspases
- mitochondrial pathway = intrinsic
- fas receptor pathway = extrinsic
Types of necrosis
Coagulative
Liquefactive
Caseous
Fat
Mechanisms of cell injury
Depletion of ATP
Mitochondrial damage
Influx of calcium
Oxidative stress
Damage to cell membrane
DNA damage
Intracellular accumulation of abnormal material
Fat in hepatocytes (liver cells) due to alcohol misuse
Cholesterol in smooth muscle cells in atherosclerosis
Protein in Alzheimer’s and Parkinson’s disease
Neoplasia
Mild DNA damage –> gene mutation
Mutations accumulate and lead to abnormal cells and eventually into cancer
