4: Cell injury and fate Flashcards
8 causes of stress on the body
Aging
Physical agents (trauma/radiation)
Infectious agents
Genetic defects
Chemical agents (weed killer, drugs)
Oxygen deprivation
Immunological reactions
Nutritional imbalances (e.g obesity, lack of food)
4 most vulnerable parts of the cell
Cell membrane (immediate effects seen)
ATP generation *
Protein Synthesis
Genetic Apparatus
When can morphological changes be seen in a cell
Following cell death, although cell can already be injured
4 types of adaptation
Atrophy
Hypertrophy
Hyperplasia
Metaplasia
Atrophy
Cell shrinks in size
Each cell loses material
Organ gets smaller
Elderly not using muscle - gets smaller
Hypertrophy
Cell size increases
Organ therefore gets bigger
No new cells
e.g pregnancy
Hyperplasia
Increase in NUMBER of cells
Pathological or physiological
Physiological -liver growing after resection
Pathological - cancer
Metaplasia
Cell changes type
Reversible
Barrets oesophagus and bone development
Dysplasia
Pre-cancerous cells showing features of malignancy but has not invaded the underlying tissue
genetic and cytological features of cancer
Large nuceli
incr. nuceli to cytoplasm ratio
incr. number of mitoses
An athlete showed myocardial cells of increased diameter. Cell count was normal. What is the adaptation shown and what could be its cause?
Hypertrophy, due to intense exercise
Cell development after Dysplasia
Neoplasia (malignancy)
Types of cell injury
Reversible
Irreversible
Light microscopic features of reversible cell injury
Fatty change -white spots nothing inside
Cell swelling - white holes some cell space
Light microscopic features of irreversible cell injury
Necrotic changes (4 types)
- unexpected
4 types of necrosis
Coagulative necrosis
Liquefactive necrosis
Caseous necrosis
Fat necrosis
Coagulative necrosis
Structure becomes fixed
e.g myocardial infarction
Liquefactive necrosis
Tissue becomes liquified
e.g liquefactive cerebral infarct- brain doesn’t have much connectuve tissue to keep in place
Caseous necrosis
Tissue looks Cheesy - oozy and structureless
e.g lung from Pulmonary TB
Fat necrosis
Fat becomes liquified
e.g. in acute pancreatitis
Enzymes become activated in pancreas rather than duodenum –> liquifies fat
Apoptosis
Intentional
needs energy
Does not cause inflammation
Can be physiological or pathological
usually a single cell
Uses of apoptosis in the body (5)
Embryogenesis
Deletion of auto-reactive T cells in thymus
Withdrawal of a hormone
Cell deletion in proliferating populations
DNA damage causing cells to be eliminated
Necroptosis
Spectrum of apoptosis and necrosis
energy dependent and has inflammation
-intentional
8 main causes of cell injury
Genetic
Immunological
Nutritional imbalance
Chemical agents
Hypoxia
Ageing
Physical agents
Infectious agents
4 cell mechanisms prone to injury
Cell membrane integrity
ATP generation
protein synthesis
genetic apparatus
- damage to any of these most likely leads to cell death
A woman 30 weeks pregnant, what changes has her uterus undergone
Physiological Hypertrophy
- incr. size of existing muscle
- normal adaptive change
