T1L16: How the Cell Responds to Injury Flashcards
Tissue growth [4]
Increase in cell size or number by synthesis of new components
Multiplicative: Increase in cell number by mitotic division
Auxetic: Increase in cell size
Accretionary: Increase in extracellular tissue
Cell turnover [4]
Growth = Increase in cell number – Decrease (cell death)
Fetal development shows rapid growth and constant programmed cell death (apoptosis)
In adults, many tissues loose proliferative ability
Cell turnover permits maintenance of continuously growing tissues (e.g. skin, intestinal mucosa) and regeneration (injury, disease)
Proliferative ability [3]
- LABILE CELLS continuously proliferate, have a short lifespan and a rapid turnover time (blood cells, many epithelial cells)
- STABLE CELLS have good regenerative ability but would normally have a low cell turnover (quiescent tissues or facultative dividers, e.g. hepatocytes)
- PERMANENT CELLS have very little or no regenerative ability (terminal differentiation, e.g. neurons)
Hypertrophy [4]
Increase in cell size owing to increase structural components
Only adaptive response available to permanent cells
Physiological: Muscle training, uterine - hormone stimulation
Pathological: Cardiac - hypertension, bladder - prostatic enlargement
Hyperplasia [3]
Increase in cell number, cells divide (labile or stable)
Physiological: Hormonal or compensatory
Pathological: Excess hormonal stimulation. Endometrial - oestrogen or prostatic - androgens
Atrophy [3]
Reduced cell size or cell number
Physiological: Testicular or ovarian - loss of hormonal stimulation when older
Pathological: Denervation of muscle (poliomyositis), vascular atrophy of brain, malnutrition, disuse atrophy of muscle or bone in immobilisation.
Pressure - mass effect
Metaplasia [3]
Reversible change when 1 differentiated cell is replaced by another, usually in epithelium and adaptive response to a change in environment
Physiological: Metaplasia of cervical - simple columnar epithelium to stratified squamous epithelium
Pathological: Metaplasia from bronchial ciliated columnar epithelium to stratified squamous (acidf reflux response
Cellular injury
Severely stressed so cannot adapt
• Renal tubule cell injury
• Reduced oxidative phosphorylation and ATP depletion
• Cellular swelling - ion concentration and osmotic water influx
Changes in intracellular organelles and cytoskeleton
Mechanism of necrosis [6]
ATP depletion
Mitochondrial damage
Influx of calcium
Accumulation of oxygen radicals
Increased membrane permeability
DNA and protein damage
Macroscopic patterns of necrosis [3]
COAGULATIVE NECROSIS
○ Shape and architecture are preserved for some time
LIQUEFACTIVE NECROSIS
○ Liquified, viscous, soft lesion
○ Brain
○ In bacterial infection
CASEOUS NECROSIS
○ Cheese-like appearance
Usually mycobacterial
Necrosis [7]
Regional Cells swell Nuclei shrink Cell membrane ruptures Cell contents leak Causes inflammatory response Always PATHOLOGICAL
Apoptosis [7]
Local Cell shrink Nuclei fragment Membrane intact but altered Apoptotic bodies No inflammation Often physiological (sometimes pathological)
Autophagy associated cell death [4]
The cell breaks down its own contents as a survival mechanism in nutrient deprivation
Regulated by autophagy genes
Overlap with apoptosis
May be a defense against neoplasia
Apoptosis [4]
Pathway of programmed cell death
Usually tightly controlled
Activation of intracellular enzymes to degrade DNA and proteins
Cell membrane remains intact but attracts phagocytes
Physiological apoptosis [5]
Programmed apoptosis in embryogenesis
Involution of hormone dependent tissues after hormone withdrawal (e.g. menstrual cycle)
High turnover tissues (e.g. intestinal epithelium)
Elimination of self-reactive / autoimmune lymphocytes
Programmed apoptosis of inflammatory cells at the end of the inflammatory response
