Pathology - Cell Injury, Adaptation, & Death

Front 1

Pathogenesis

Back 1

the pathogenesis of a disease is the sequence of events at the organ, cellular, ultrastructural, and molecular levels by which the disease develops

Front 2

Pathognomonic

Back 2

A particular abnormality that is found only in one condition.

Hint 2

"Hearing the fetal heart tone is pathognomonic of pregnancy."

Front 3

Symptoms

Back 3

what the patients sees or feels

Front 4

Signs

Back 4

evidence of disease discovered by the physician or dentist - abnormalities on physical exam

Front 5

Findings

Back 5

physical, lab, or x-ray results

Front 6

Biopsy

Back 6

When tissues are removed from a live patient and sent to the pathologist for diagnosis.

Hint 6

"Bios" means life.

Front 7

Autopsy/Necroscopy

Back 7

When tissue is removed from a dead patient and examined by the pathologist.

Front 8

Common causes of cell injury

Back 8

-O2 deprivation
-physical agents
-chemical agents
-immune rxns
-genetic defects
-infectious agents
-nutritional imbalances
-aging

Front 9

Ischemia

Back 9

loss of arterial blood flow, "holding back the blood," includes no oxygen (hypoxia) AND no substrates for glycolysis.
*the most common cause of cell injury*

Front 10

Hypoxia

Back 10

Insufficient oxygen. Cell loses the ability to carry on sufficient aerobic oxidative respiration --> reduced ATP generation.

Front 11

Reperfusion injury

Back 11

When the restoration of oxygen to a cell that was ischemic or hypoxic for a while causes more injury to the cell.
-extra Ca influx
-increase in inflammatory cells --> release free radicals
-damaged mitochondria --> free radicals

Front 12

Free radicals

Back 12

Unstable compounds with unpaired electrons, i.e. H., HO., O2., hydrogen peroxide, superoxide

Front 13

Atrophy

Back 13

Cells get smaller in size (not number) to survive.
Causes: decreased use, decreased blood supply, decreased nutrition, hormones.

Front 14

Hypertrophy

Back 14

Cells get larger in size (not number) in response to demand.
Causes: increased workload, hormones.

Front 15

Hyperplasia

Back 15

Cells increase in number (not size).
Causes: hormones, GFs, etc.

Front 16

Metaplasia

Back 16

Environmental stress causes one mature cell type to replace another.

Hint 16

Smoking affects the epithelial cells of the larynx and trachea this way.

Front 17

Dysplasia

Back 17

Disorderly proliferation.

Front 18

Involution

Back 18

Decrease in cell number (not size) due to apoptosis.

Front 19

Cell Adaptations

Back 19

Adaptations that occur after prolonged exposure to adverse stimuli or exaggerated normal stimuli, which can include: atrophy, hypertrophy, involution, hyperplasia, metaplasia, dysplasia, or some combination.

Front 20

Subcellular responses to cell injury

Back 20

-lysosomal catabolism
-induction of sER
-alterations in mitochondria
-changes in the cytoskeleton
-induction of stress proteins (heat shock proteins)

Front 21

Heterophagy

Back 21

A type of lysosomal catabolism in which the secondary lysosome/phagolysosome contains engulfed material from outside the cell.

Hint 21

"Hetero" means other.

Front 22

Autophagy

Back 22

A type of lysosomal catabolism in which an autophagic vacuole surrounds damaged organelles from within it's own cell.

Hint 22

"Auto" means self.

Front 23

Lipofuscin granules

Back 23

A secondary lysosome/phagolysosome that contains undigested particles composed of oxidized lipids; it is often pigmented. Accumulates in aging tissues or can be a sign of chronic tissue damage.

Front 24

First site of cell injury

Back 24

mitochondria

Front 25

Dystrophic calcification

Back 25

Pathologic calcification with no calcium derangement; usually occurs in dead or dying tissues.

Front 26

Metastatic calcification

Back 26

Pathologic calcification that almost always reflects some derangement in calcium metabolism. Hypercalcemia causes calcium deposits in normal tissue.

Front 27

Cell swelling

Back 27

The first observable change when a cell is damaged. Reversible injury that reflects damage to water transport, mitochondrial damage, hydropic degeneration.

Front 28

Autolysis

Back 28

Enzymes from the cell itself digest the cell contents.

Front 29

Heterolysis

Back 29

Enzymes from arriving inflammatory cells digest the cell contents.

Front 30

Pyknosis

Back 30

Condensation of the nucleus (nuclei shrink).
Indicates cell is dead.

Front 31

Karyorrhexis

Back 31

Fragmentation of the nucleus ("nuclear dust").
Indicates cell is dead.

Front 32

Karyolysis

Back 32

Dissolution of nuclear structure (as a result of enzymatic digestion).
Indicates cell is dead.

Front 33

How you know WHETHER the cell is dead or alive.

Back 33

Nuclear changes.

Front 34

How you know HOW the cell has died.

Back 34

Cytoplasmic changes.

Front 35

Necrosis

Back 35

Accidental cell death!
Localized death of cells or tissues in a living organism. Produces an inflammatory response.
-Caused by exogenous injury and usually involves groups of cells
-cells are swollen, show nuclear changes, and have ruptured cell membranes

Front 36

Apoptosis

Back 36

Cell suicide!
Programmed death of single cells within a living organism. Does not produce an inflammatory response.
-generally energy dependent
-cell fragments ("apoptotic bodies")to be taken up by macrophages/adjacent parenchymal cells.

Front 37

Coagulative necrosis

Back 37

-outline of cell preserved for days
-death is sudden: denatures structural proteins and destructive enzymes
-hypoxic death (except in CNS)

Front 38

Liquefactive necrosis

Back 38

-cells dissolve by enzymes: autolysis or heterolysis
-infiltrations of PMNs and dead cell components --> abscess!
-seen in bacterial and fungal infections
(ex. pneumonia)

Front 39

Caseous necrosis

Back 39

-combination of coagulative and liquefactive necrosis
-gross appearance is white and cheesy
-GRANULOMA: cells surrounded by lymphocytes and macrophages
-typical of Mycobacterium tuberculosis (TB!), sarcoidosis, foreign body rxns, deep fungal infections

Front 40

Gummatous necrosis

Back 40

Specific to SYPHILIS! (spirochete)

Front 41

Hemorrhagic necrosis

Back 41

-dead tissues contain many RBCs
-Usually due to blockage of a vein while the arterial supply continues to deliver blood.

Front 42

Enzymatic fat necrosis

Back 42

-lipases digest fat cells
-triglycerides released from the cell bind with calcium to form soaps (saponification!)
-most strongly asso. with damage to the PANCREAS, which has many digestive enzymes and is surrounded by fat.