Cell Injury & Cell Death Flashcards
Necrosis
Cell death due to injury
-Initiated by pathologic stimuli from outside the cell and results in the dissolution or removal of that cell
Apoptosis
Cell death due to physiological turn over of cells
- Involves activation of a coordinated internal cellular program that are mediated by defined cellular proteins
- A specific, energy dependent, programed cell death
- Helps to maintain homeostasis
Calcium Influx
Hallmark of irreversible cell injury or cell death
Morphologic Characteristics
- excessive cell swelling
- dramatic changes to cellular organelles
Adaptation
Allows cells to survive in the short term
Homeostasis
(LOSS OF) forms the basis of most disease states
Cellular Adaptions
- Hyperplasia
- Hypertrophy
- Metaplasia
- Dysplasia
Atrophy
the shrinkage of tissue or organ size due to a reduction in cell size
Hypertrophy
An increase in cell size in response to stress
Hyperplasia
An increase in cell number and is distinct from hypertrophy
Non-dividing cells
(CARDIAC MYOCYTES) cannot divide, so adapt through hypertrophy
Dividing cells
(EPITHELIAL CELLS) may undergo hyperplasia as well as hypertrophy under stress
Metaplasia
The reversible process whereby one mature cell type is replaced by another less mature cell type
Dysplasia
Disordered growth and maturation of the cellular components of a tissue
Accumulate Substances
Under stress, cells tend to do this in response to metabolic derangments
Hallmarks of cell injury
-Accumulating substances leading to cell injury or cell death
Mechanisms of Cellular injury
Pathologic stimuli
- Intrinsic (genetic) or extrinsic (acquired)
- Provide etiology (cause) of disease
- Elicit cellular responses - pathogenesis of disease
Severity & Duration
(of pathologic stress) determine outcome of cell injury
Causes of Necrosis
- Trauma
- Intoxication
- Deficiency
Mechanisms of Cellular Injury
-Hypoxic Cell Injury: Impaired energy production
-Free Radical Injury: Form damaging reactive oxygen species (ROS)
-Impaired Calcium Homeostasis: Compromise cell membrane
CALCIUM INFLUX=Cell death
Reactive Oxygen Species (ROS)
Protection: superoxide disumtase (SOD) converts superoxide into hydrogen peroxide
-Catalase converts hydrogen peroxide into water and oxygen
Excess ROS
Form when oxygen is limited
- Damage the cell (lipids, proteins, etc.)
- Leaking Membranes
- Calcium Influx
- Cell death
Ischemia
Lack of blood flow (oxygen)
Coagulative Necrosis
- Basic cell outline is preserved
- Acidosis denatures proteins
- Protenin denaturation causes coagulation
Liquifactive Necrosis
- Results from autolysis or heterolysis
- Involves digestion of cell remains
- Typical abscess formation
Caseous Necrosis
A combination of coagulative & liquefactive necrosis
-The necrotic debris is not digested completely by hydrolases, so tissues appear soft and granular (cheesy)
Fat Necrosis
Focal areas of fat destruction.
This destruction of lipids is associated with abnormal release of pancreatic enzymes (lipase)
Gangrene
Cell death resulting from severe hypoxia - most commonly caused by ischemia
Dry Gangrene
Coagulative necrosis as a result of ischemia
Wet Gangrene
Tissue is infected with bacteria and phagocyte cells are recruited, releasing enzymes that lead to a liquifactive process
Gas Gangrene
Infection caused by Clostridium spp., anaerobic bacteria that produces toxins that damage the connective tissue and cause gas
Apoptotic Bodies
Defined fragmented DNA
-formation of distinct structures
Phagocytosis
Process of removing dead cells
-NO inflammatory response
Autodigestion
Necrosis involves activation of enzymes that digest cellular components
-This may stimulate an inflammatory response
Substances that Accumulate (as a consequence of ADAPTATION)
-Lipids: Especially heart & liver
-Glycogen: In liver and skeletal muscle
-Pigments
- Melanin: formed by melanocytes in skin
- Hemosiderin: formed by hemoglobin, iron
- Billirubin: in liver
-Lipofuscin: fine granular golden-brown pigment formed from phosphilipids & proteins derived from degenerating membranes
-Minerals: Calcium —- Calcification
Hyaline change: Non specific indicator, formed from protein
Karyolysis
Irreversible cell death characterized by lysing of nucleus, due to action of DNAse and RNAse
Karyorrhexis
Irreversible cell death characterized by fragmentation of the nucleus
Pyknosis
Irreversible cell death characterized by condensation of the nucleus and clumping of chromatin
Hypoxic Cell Injury
- Reduction of oxygen - Ischemia
- Impair energy production
- body switches from aerobic to anaerobic processes
- Anaerobic metabolism = lactic acid production =lactic acidemia - Loss of ability to fuel the cells and maintain the integrity of those pumps on the surface
Oxygen Free Radicals
Reactive Oxygen Species (ROS)
- Unpaired electrons on the molecular oxygen = highly reactive
- Interact with lipids & proteins in the cell = compromised integrity of cell
- Damage cell – leaking membranes - calcium able to enter the cell
Superoxide Dysmutase (SOD)
An enzyme that maintains homeostasis within the cell in the presence of oxygen free radicals
- A form of molecular oxygen that has been radicalized
- Converts to hydrogen peroxide
Catalase
An enzyme that takes the hydrogen peroxide created by superoxide dysmutase and converts to water and oxygen
=Happy cells
