Cellular Injury Flashcards
Cell Injury Causes
- Usually reversible
- Cell injury and death are an ongoing process balanced by cell renewal
- Causes of Cell Injury
- Physical Agents
- Radiation Injury
- Chemical Injury
- Biologic Agents
- Nutritional Imbalances
Cell Injury Physical Agents
- Mechanical Forces
- Body impact with another objects
- Split and tear, fracture bones, injured blood vessels
- Extremes of Temperature
- Heat—vascular injury, accelerates metabolism, disrupt cell membranes
- Cold—increase blood viscosity; induces vasoconstriction.
- Electrical Injuries
- Tissue injury and disruption of neural and cardiac impulses
- The body act as a conductor of the electrical source
Radiation Injury
- Wide spectrum of wave-propagated energy
- From ionizing gamma rays to radio-frequency waves
- A photon—particle of radiation energy
- Ionizing, ultraviolet, Nonionizing Radiation
- ionizing=more damage
Radiation Injury: Ionizing Radiation
Ionizes molecules and atoms in the cells.
Immediately kill cells, interrupt cell replication
E.g. localized irradiation to treat cancer
Ultraviolet Radiation
causes sunburn and increases the risk of skin cancer.
Damages DNA of the cell
Nonionizing Radiation
Includes infrared light, ultrasound, microwaves
Causes vibration and rotation of atoms and molecules, which is converted to thermal energy.
Injury is mainly thermal and involve dermal and subcutaneous tissue injury
Chemical Injury
- Drugs
- Alcohol—gastric mucosa, liver
- Antineoplastic drugs
- Tylenol
- Lead Toxicity
- Sources—flaking paint , root vegetables, water pipes, paint
- Absorbed through the GI tract or lungs into the blood
- Stored in bones and eliminated by the kidneys
- Anemia—cardinal sign—lead competes with enzymes for hgb synthesis- because they compete patient cannot make hgb
- Nervous system—demyelination of cerebral and cerebellar white matter and death of cortical cells—acute encephalopathy
- Mercury Toxicity
- Dental filling—very rear—mercury vapor released into the mouth
- Consumption of long-lived fish, such as tuna and swordfish
Biological agents that cause cell injury
Viruses
Bacteria
Parasites
Nutritional Cell Injury
- Excess
- Obesity and diet high in saturated fat
- Deficiency
- Starvation
- Iron Deficiency Anemia
Mechanisms of cell injury
- Free Radical Formation
- Hypoxia and ATP depletion
- Disruption of Intracellular Calcium Homeostasis
Free Radical Injury
- Free radical—highly reactive chemical species with an unpaired electron in the outer orbit of the molecule.
- Interact with proteins, lipids, and carbohydrates damaging cell membranes and nuclei acids that make up DNA.
- Reactive Oxygen Species (ROS)—oxygen-containing molecules that include free radical produced endogenously by normal metabolic processes or cell activity
- Superoxide
- Hydroxil radical (OH.)
- hydrogen peroxide (H2O2)
Hypoxic Cell Injury
- Deprives the cell of oxygen and interrupts oxidative metabolism and the generation of ATP.
- Causes
- Inadequate amount of oxygen in the air
- Respiratory disease
- Ischemia
- Anemia
- Inability of the cells to use oxygen
- Causes
IMpaired Calcium Homeostasis
- Calcium functions as second messenger and cytosolic signal for many cell responses.
- Normally intracellular calcium is lower than extracellular
- Maintain by membrane-associated calcium/magnesium ATPase exchange system
- Increase calcium activates a number of enzymes:
- Phospholipases—damage the cell membrane
- Proteases—damage the cytoskeleton and membrane proteins
Mechanism of Cell injury: Free radical effects
- oxidation of cellular structures, nuclear and mitochondrial dna
- cell membrane damage
Mechanism of Cell Injury Hypoxia Effects
- accumulation of intracellular fluids, dilation of endoplasmic reticulum
- increased membrane permeability
- decreased mitochondrial function
- decreased glycogen stores
- decreased intracellular PH
- decreased protein sysnthesis
- decreased lipid deposition
apoptosis process
A—shrinking of the cell structure
B and C—condensation and fragmentation of the nuclear chromatin
D and E—separation of nuclear fragments and cytoplasmic organelles into apoptotic bodies
F—engulfment of apoptotic fragments by phagocytic cell
APOPTOSIS DOES NOT TRIGGER INFLAMMATION
