Bookmark and Share

Front Back
•The branch of medicine that deals with the essential nature of disease, especially the structural and functional changes in cells, tissues, and organs that are caused by disease
The 2 ways Cells Respond to Stress
and Injurious Stimuli?
1.) Adaptation

2.) Cell injury
 •Cell death
- Necrosis
- Apoptosis
achieving a new steady state and preserving viability and function
change in phenotype
•Hyperplasia –
increased cell number
•Atrophy –
decreased cell and organ size
Cell injury results......
when cells can no longer adapt, are exposed to damaging agents, or suffer from an intrinsic abnormality
•Reversible cell injury –
injury is mild, or damaging stimulus is removed
Causes of Cell Injury?
1. Oxygen deprivation
2. Chemical agents
3. Infectious agents
4. Immunologic reactions
5. Genetic defects
6. Nutritional imbalances
7. Physical agents
8. Aging
lysosomal digestion of a cell’s own components following nutrient deprivation...subcellular response to injury
Hypertrophy of Smooth ER
compensatory mechanism to toxins metabolized in SER....subcellular response to injury
Mitochondrial alterations –
changes in number, size, and shape....subcellular response to injury
Cytoskeletal alterations
abnormal assembly and functions of filaments, or abnormal accumulation of filaments....subcellular response to injury
Cell injury results from....
functional and biochemical abnormalities in one or more of several essential cellular components
Mechanisms of Cell Injury?
1. Depletion of ATP
2. Damage to mitochondria
3. Influx of calcium
4. Oxidative stress
5. Defects in membrane permeability 6. Damage to DNA and proteins
Injurious stimuli
(e.g., oxygen or nutrient deprivation, reactive oxygen species, toxins)
Hallmarks of reversible cell injury
1. swelling and fatty change
2. severe disturbances in mitochondrial and membrane functions
Reversible cell injury
•cellular swelling and fatty change
•plasma membrane blebbing
•clumping of chromatin
•Breakdown of plasma and organellar membranes
•Leakage and enzymatic digestion of cell contents
•nuclear chromatin condensation
•formation of apoptotic bodies
fragmentation (“nuclear dust”)
dissolution of nuclear structure as a result of enzymatic digestion
Patterns of tissue necrosis?
1. Coagulative necrosis
2. Gangrenous necrosis
3. Liquefactive necrosis
4. Caseous necrosis
5. Fat necrosis
6. Fibrinoid necrosis
Coagulative necrosis
•cells are dead, but basic tissue architecture is preserved for several days
•characteristic of infarcts in solid tissues except the brain
Gangrenous necrosis
•term usually applied to coagulative necrosis of lower leg
Liquefactive necrosis
•seen in focal bacterial or fungal infections
•inflammatory cells and leukocytes digest tissue
Caseous necrosis
•caseous means cheese-like
•most often in foci of tuberculosis infection
Fat necrosis
•focal areas of fat destruction often resulting from acute pancreatitis
Fibrinoid necrosis
•usually seen in immune reactions involving blood vessels
Apoptosis (programmed cell death)
a highly regulated process of cell death mediated by suicide genes, which activate enzymes that degrade the cell’s own DNA and proteins
Physiologic apoptosis
•a normal process that is important for embryonic development, and removal of cells no longer needed in adult tissues
•Pathologic apoptosis –
eliminates cells genetically altered or injured beyond repair without eliciting a severe host reaction
Causes of Pathologic Apoptosis
1. DNA Mutations
2. Accumulations of misfolded proteins
3. Cell injury in certain infections
4. Pathologic atrophy in parenchymal organs after duct obstruction
Intracellular Accumulations
Abnormal deposits in cells and tissues are the result of excessive intake or defective transport or catabolism
Fatty liver
Alcohol abuse and diabetes associated with obesity are the most common causes of fatty change (steatosis) in the liver
Accumulation of coal particles in the lung
•Accumulation of blood-derived brown pigment called hemosiderin
•Occurs in tissues when there is excess of iron
Hereditary Hemochromatosis
•Autosomal recessive mutation in HFE gene
•yellow-brown pigment
•free radical peroxidation of membrane lipids
•accumulates in many tissues
•normally in lysosomes
•“wear-and-tear pigment”
•Dystrophic calcification
- depositition of calcium at sites of cell injury and necrosis

 - normal calcium metabolism
•Metastatic calcification
- depositition of calcium in normal tissue
- derangement in calcium metabolism
- usually caused by hypercalcemia as a consequence of excessive parathyroid hormone
Causes of Cellular Aging
1. Accumulation of DNA damage
2. Replicative senescense
3. Accumulation of metabolic damage
x of y cards Next >|