Cellular Response to Stress and Toxic Insults

Question 1

Atrophy:

Answer 1

A reduction in the size of an organ or tissue due to a decrease in cell size and number.

Question 2

Mechanisms of atrophy:

Answer 2

Shrinkage of cells due to increased catabolism of cell organelles, decreased protein synthesis and increased protein degradation in cells.

Question 3

Brown atrophy:

Answer 3

Undigested lipids are stored as residual bodies (lipofuscin granules) when present in sufficient amount impart brown coloration to the tissue.

Question 4

Hypertrophy:

Answer 4

An increase in the SIZE of cells.

Question 5

Hyperplasia:

Answer 5

Increased cell numbers in response to hormones and other growth factors.
- Occurs in tissues whose cells can divide or contain abundant tissue stem cells.

Question 6

Metaplasia:

Answer 6

Transformation or replacement of one adult cell type to another adult cell type.

Question 7

Cell injury:

Answer 7

When cells are stressed so severely that they are no longer able to adapt or when cells are exposed to inherently damaging agents or suffer from intrinsic abnormalities.

Question 8

Karyolysis:

Answer 8

Fading of basophilic chromatin of the nucleus.

Question 9

Pyknosis:

Answer 9

Nuclear shrinkage and increased basophilia.

Question 10

Karyorrhexis:

Answer 10

Break-up and fragmentation of the nucleus. Eventually totally disappears over 2-3 days.

Question 11

Coagulative necrosis:

Answer 11

Preserves basic outline of the coagulated cell due to denaturation of proteins by acidosis, anucleated.
- Usually occurs in conditions of ischemia.

Question 12

Liquefactive necrosis:

Answer 12

Digestion of tissue by hydrolytic enzymes causing it to be completely liquefied.

• Occurs with abscess and fungi of any organ.
• Ischemic brain infarction.

Question 13

Enzymatic fat necrosis:

Answer 13

Activated pancreatic enzymes (lipase) during pancreatitis leak out of acinar cells and liquefy the membranes of fat cells in the peritoneum.

Question 14

Fibrinoid necrosis:

Answer 14

Usually seen in immune reaction involving blood vessels. Complexes of antigens and antibodies are deposited in the walls of arteries.

Question 15

Caseous necrosis:

Answer 15

Composed of fragmented or lysed cells and amorphous granular debris enclosed within distinctive inflammatory debris; surrounded by granulomatous inflammation.
- No cell outline.

Question 16

Gangrenous necrosis:

Answer 16

Usually applied to a limb that has lost its blood supply and has undergone coagulative necrosis involving multiple tissue layers.
- Coagulative necrosis superimposed with bacterial infection causing liquefactive necrosis.

Question 17

Apoptosis:

Answer 17

Cell suicide.

Question 18

Morphological features of apoptosis (4):

Answer 18

1. Cell shrinkage.
2. Chromatin condensation.
3. Formation of cytoplasmic blebs and apoptotic bodies.
4. Phagocytosis of apoptotic cells or cell bodies.

Question 19

Two pathways of caspases activation:

Answer 19

1. Mitochondrial (intrinsic).

2. Death receptor pathways (extrinsic).

Question 20

Free radicals:

Answer 20

Chemical species with a single unpaired electron in an outer orbital.

Question 21

Superoxide dismutases:

Answer 21

SOD

- Responsible for the decay of superoxide.

Question 22

Catalyzes breakdown of H2O2:

Answer 22

Glutathione peroxidases (GSH).

Question 23

Catalase:

Answer 23

Catalyzes the decomposition of hydrogen peroxide.

Question 24

Most common cause of acute cell injury underlying human disease:

Answer 24

Ischemia.

Question 25

Reperfusion injury:

Answer 25

Ischemia - The restoration of blood flow to ischemic but viable tissues results in the death of cells that are not otherwise irreversibly injured.

Question 26

Dystrophic calcification:

Answer 26

• Normal serum calcium.

- Dead and dying tissues.

Question 27

Metastatic calcification:

Answer 27

• Elevated serum calcium in blood.

- Calcification in normal tissues.

Question 28

Fatty changes:

Answer 28

Any abnormal accumulation of triglycerides within parenchymal cells.
- Most often seen in the liver.

Question 29

Most common cause of fatty change in developed nations:

Answer 29

Alcoholism.

Question 30

Endogenous pigment:

Answer 30

Lipofuscin

• Wear and tear pigment.
• Insoluble brownish-yellow granular intracellular material that accumulates in a variety of tissues as a function of age or atrophy.