Cell Injury and Fate Flashcards
2 types of cell injury
Lethal and sub-lethal
Lethal cell injury
produces cell death
sub lethal cell injury
produces injury not amounting to cell death, may be reversible or may progress to cell death
Causes of cell injury
- O2 deprivation
- Chemical agents
- Infectious agent
- Immunological reactions
- Genetic defects
- Nutritional imbalances
- Physical agents(trauma/gunshot wound/radiation)
- Aging
What do the cellular response to injurious stimuli depend on
Type of Injury
Duration
Severity
What do the consequences of an injurious cell depend on
type of cell
cell status
Effects to which two systems cause an immediate effect
cell membrane integrity and ATP generation
why do effects to protein synthesis and genetic apparatus integrity take time for the effects to become apparent
DNA/RNA pathways
what is atrophy
shrinkage of cell/organ and by loss of cell substance
hypertrophy
increase in size of cell and consequently an increase in the size of the organ. Caused by either increased functional demand or specific hormone stimulation
Pathological vs physiological hypertrophy
Physiological (uterus during pregnancy) and pathological ( valve disorders)
Hyperplasia
Increase in number of cells in organ
Physiological hyperplasia
Hormonal or compensatory (e.g. after menstruation when the lining starts to build up again)
Pathological hyperplasia
Due to excessive hormonal or Gf stimulation ( e.g. cancer)
Metaplasia
Reversible change in which one adult cell type is replaced by another. Physiological/pathalogical
Physiological metaplasia
cervix during change between columnar to squamous epithelium in the cervical canal due to changes in the pH of the vagina
Pathological metaplasia
Barretts oseophagus - acid reflux leads to metaplasia changing oesophageal cells from sqaumous to columnar. But can be reversed if you lose weights/use antacids
Dysplasia
Precancerous cells which show genetic and cytological features or malignancy but not invading the underlying tissue
How can you distinguish cancer cells microscopically
see all the nuclei and most ofthe cell is nucleus. so nucleus:cytoplasmic ratio increases
What can you see microscopically in alcoholic fatty changes
fatty change Cellular swelling ( associated with cell and tissue damage)
What can you see in ballooning degeneration
cytoskeleton of hepatocyte is damaged and so rhere is an accumulation of proteins which is causing the cell to swell
what occurs in necrosis
confluent cell death associated with inflammation
coagulative necrosis
structure becomes thick/solid and the nuclei disappear
E.g. myocardial infarction
liquefactive necrosis
where tissue becomes liquefied . Brain is particularly liquefied as not much connective tissue in brain to hold it together.
OCCURS IN BRAIN ONLY
caseous necrosis
a bit cheesy, granulomas visible
Eg, pulmonary tuberculosis
fat necrosis
in acute pancreatitis: if enzymes become activated in pancreas instead of duodenum. FFA will bind to calcium and will precipitate out and so will stain blue in microsopic slide
Eg. Acute pancreatitis
apoptosis
programmed cell death but not associated with inflammation
differentiating apoptosis and necrosis
apoptosis doesn’t have inflammation, can be physiological and active energy-dependent process
causes of apoptosis
embryogenesis, deletion of auto-reactive T cells in thymus, hormone-dependent physiological involution, cell deletion in proliferating populations, a variety of mild injurious stimuli that cause irreparable DNA da,age that,in turn, triggers cell suicide pathways
Necroptosis
Programmed form of cell death associated with inflammation (necrosis)
E.g. associated with viral infections
