Cell adaptation and injury

Question 1

Hyperplasia

Answer 1

increase in number of cells in a tissue or organ

Question 2

Hypertrophy

Answer 2

increase in size of individual cells due to increase in structural components of cells

Question 3

Atrophy

Answer 3

decrease in cell size due to decreased stimulation

Question 4

Metaplasia

Answer 4

one adult cell type is replaced by another adult cell type

Question 5

Amyloid

Answer 5

protein accumulation in extracellular compartment, branching fibrils, when stained with Congo red appears pink under LM/ apple green under polarized light

Question 6

Hyaline change

Answer 6

descriptive term for deposition that causes glassy or amorphous appearance. ex amyloid, russel bodies

Question 7

Lipofuscin

Answer 7

Pigment accumulation due to “wear and tear” common in cardiac myocytes, localizes to perinuclear area

Question 8

Hemosiderin

Answer 8

Pigment accumulation, iron-containing breakdown product of blood. Stains blue with Prussian blue due to iron content

Question 9

Bilirubin

Answer 9

Pigment accumulation, product of breakdown of blood that does NOT contain iron

Question 10

Necrosis

Answer 10

Pathologic, causes inflammation, membrane disruption occurs, cells swell

Question 11

Apoptosis

Answer 11

Pathologic or physiologic, no inflammation, membranes intact, cells shrink

Question 12

Intrinsic pathway of apoptosis

Answer 12

• Bcl-2 family of proteins- balance between pro- and anti- apoptotic. If pro-apoptotic are favored, cytochrome c is released from mitochondria
• cytochrome c stimulates initiator caspases

Question 13

Extrinsic pathway of apoptosis

Answer 13

• Fas ligand binds to Fas receptor

- receptor-ligand binding activates initiator caspases

Question 14

Common execution phase of apoptosis

Answer 14

• initiator caspases activate executioner caspases

- executioner caspases activate endonucleases, proteases, etc

Question 15

Necroptosis, pyroptosis

Answer 15

Similar to apoptosis in that there is a specific stimulus that initiates, but similar to necrosis in that the result involves disruption of membranes and inflammation

Question 16

Mechanisms of cell injury: depletion of ATP

Answer 16

failure of ion pumps, protein synthesis, protein folding. increased glycolysis–> decreased pH, decreased enzyme activity

Question 17

Mechanisms of cell injury: mitochondrial damage

Answer 17

mitochondrial permeability transition pore associated with necrosis due to loss of membrane potential, inability to generate ATP
release of cytochrome c associated with initiating apoptosis

Question 18

Mechanisms of cell injury: Loss of Ca homeostasis

Answer 18

formation of mitochondrial permeability transition pore, ATP depletion, activation of Ca-dependent cellular enzymes including proteases, phosphlipases, endonucleases, caspase

Question 19

Mechanisms of cell injury: oxidative stress

Answer 19

lipid peroxidation of membranes, oxidative modification of proteins, lesions in DNA

Question 20

Sources of reactive oxygen species

Answer 20

mitochondrial oxidative phosphorylation, radiant energy, leukocytes, metals, nitric oxide

Question 21

Removal of free radicals

Answer 21

antioxidant scavangers, transport proteins that bind reactive metals, enzymes like superoxide dismutase, catalase, glutathione peroxidase

Question 22

Mechanisms of cell injury: defects in membrane permeability

Answer 22

Loss of ion potentials, loss of osmotic balance, loss of proteins and other metabolites, lytic enzymes release from lysosomes

Question 23

Morphologic changes in apoptosis

Answer 23

formation of apoptotic bodies, cleavage of DNA

Question 24

Morphologic changes in necrosis

Answer 24

Neutrophil infiltration

Question 25

Morphologic changes in reversible cell injury

Answer 25

Loss of microvilli, blebbing, mitochondrial swelling, dilation of endoplasmic reticulum, fatty change

Question 26

Morphologic changes in irreversible cell injury

Answer 26

Marked mitochondrial swelling, membrane discontinuity, myelin figures, nuclear pyknosis, karyolysis, loss of nuclei

Question 27

Pyknosis

Answer 27

Condensation of chromatin in nucleus

Question 28

Karyolysis

Answer 28

Dissolution of chromatin

Question 29

Karyorrhexis

Answer 29

Destructive fragmentation of nucleus of a dying cell

Question 30

Coagulative necrosis

Answer 30

Common in solid organs, characterized by infiltration of neutrophils and cells that are still distinguishable/ identifiable- architecture of dead tissue is preserved

Question 31

Liquefactive necrosis

Answer 31

Common in CNS, results in a transformation of the tissue into a liquid viscous mass, associated with focal bacterial or fungal infections, the affected cell is completely digested by hydrolytic enzymes, resulting in a soft, circumscribed lesion consisting of pus and the fluid remains of necrotic tissue. Dead leukocytes will remain as a creamy yellow pus

Question 32

Caseous necrosis

Answer 32

Common in TB, fungal infections in lung; no histological architecture is preserved, characterized by acellular pink areas of necrosis surrounded by a granulomatous inflammatory process.

Question 33

Fat necrosis

Answer 33

Unique to pancreas, release of digestive enzymes due to trauma, etc causes saponification of adipocytes

Question 34

Dystrophic calcification

Answer 34

calcification occurring in degenerated or necrotic tissue, occurs as a reaction to tissue damage, can occur even if the amount of calcium in the blood is not elevated. calcium salt deposits aggregate, first in the mitochondria, and progressively throughout the cell. These calcifications are an indication of previous microscopic cell injury. It occurs in areas of cell necrosis in which activated phosphatases bind calcium ions to phospholipids in the membrane.