Robbins Chapter 2 Key Concepts Flashcards
Appearance Hypertrophy
increase in size of the cells and organ size
Cause of hypertrophy
increased workload induced by growth factors in response to mechanical stres
What type of cells does hypertrophy occur
cells that are incapable of cell division
Appearance of Hyperplasia
increase in cell number
Cause of hypertrophy
hormones and growth factors
What types of cells does hyperplasia occur
cells that are able to divide or have abundant stem cell
Appearance of atrophy
decreased size of the cell or organ
Cause of atrophy
decreased nutrient supply or disuse
increased breakdown of cellular organelles
decreases synthesis of cellular building blocks
Appearance of metaplasia
change in phenotype of differentiated cells
Cause of metaplasia
chronic irritation that causes change in cell type to better accommodate the changed phenotype
Results of metaplasia
reduced function and increased risk for malignancy
Reversible cell injury characteristics
cellular swelling fatty change plasma membrane blebbing mitochondrial swelling dilation of ER, eosinophilia
Necrosis characteristics
increased eosinophilia nuclear shrinkage fragmentation dissolution breakdown of plasma membrane myelin figures leakage and enzymatic digestion of cell contents
Patterns of tissue necrosis (6)
coagulative, liquefactive, caseous, gangrenous, fat, fibrinoid
Mechanisms of cell injury (6)
ATP depletion Mitochondrial damage Influx of Ca+ Accumulation of ROS Increased permeability of membrane Accumulation of damaged DNA and misfolded proteins
Cell injury by ATP depletion
failure of energy dependent functions –> reversible injury –> necrosis
Cell injury by Mitochondrial damage
ATP depletion –> failure of energy dependent functions –> necrosis or potentially apoptosis
Cell injury by influx of calcium
activation of enzymes that damage cellular components
can trigger apoptosis
Cell injury by Accumulation of ROS
covalent modification to lipids, proteins, and nucleic acids
Cell injury by increased permeability of membrane
affects plasma membranes, lysosomal membranes, mitochondrial membranes
results in necrosis
Mild Ischemia
reduced oxidative phosphorylation –> reduced ATP –> failure of Na pump –> influx of sodium and water –> cause cell swelling
Severe/prolonged Ischemia
severe swelling of mitochondria –> calcium influx –> rupture of lysosomes and plasma membrane –> death due to necrosis and apoptosis via release of cytochrome c
Reperfusion Injury
oxidative stress –> blood flows to ischemic area –> influx of calcium –> influx of leukocytes –> local activation of classical complement system
Apoptosis definition
regulated cell death that eliminates unwanted or irreparable damaged cells with least host reaction
Characteristics of apoptosis
enzymatic degradation of proteins and DNA DNA damage accumulation of misfolded proteins pro-apoptotic proteins activated anti-apoptotic proteins inhibited
Death Receptor (Extrinsic) Pathway function
elimination of self-reactive lymphocytes and damage by CTLs
How is the Death Receptor (extrinsic) pathway initated
death receptor (TNF receptor family) engagement by ligands
