Cellular Responses to Stress and Toxic Insults

Question 1

Increase in SIZE of cells resulting in increased size of organ; cellular adaptation of non-dividing cells (i.e. myocardial fibers).

Answer 1

Hypertrophy

Question 2

Increase in NUMBER of cells; examples: BPH, papilloma virus infection

Answer 2

Hyperplasia

Question 3

Reduction in the size of an organ or tissue due to decrease in cell size and number; example: Alzheimer’s disease

Answer 3

Atrophy

Question 4

A reversible change in which one differentiated cell type is replaced by another cell type; example: Barrett esophagus

Answer 4

Metaplasia

Question 5

The first manifestation of almost all forms of injury to cells; due to influx of ions (and water) due to failure of energy-dependent ion pumps.

Answer 5

Cellular swelling

Question 6

A type of reversible injury, characterized by appearance of lipid vacuoles in the cytoplasm; often seen in cells participating in fat metabolism (liver, heart).

Answer 6

Fatty change (Steatosis)

Question 7

Type of cell death, which results from a pathologic cell injury; undergoes cellular swelling and eventual pyknosis, karyorrhexis, and karyolysis.

Answer 7

Necrosis

Question 8

It is the irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis; there is nuclear shrinkage with increased basophilia.

Answer 8

Pyknosis

Question 9

It is the destructive fragmentation of the nucleus of a dying cell.

Answer 9

Karyorrhexis

Question 10

It is the complete dissolution of the chromatin of a dying cell.

Answer 10

Karyolysis

Question 11

Type of cell death, which is energy-dependent, tightly regulated, and associated with normal cellular functions; often physiologic; the cell undergoes shrinkage and fragmentation.

Answer 11

Apoptosis

Question 12

Pathway of apoptosis triggered by loss of survival signals, DNA damage and accumulation of misfolded proteins; inhibited by anti-apoptotic members of the Bcl family.

Answer 12

Mitochondrial/Intrinsic pathway

Question 13

Initiator caspase for intrinsic pathway of apoptosis.

Answer 13

Caspase 9

Question 14

Pathway of apoptosis responsible for elimination of self-reactive lymphocytes and damage by cytotoxic T lymphocytes; initiated by TNF receptors.

Answer 14

Death receptor/Extrinsic pathway

Question 15

Initiator caspases for extrinsic pathway of apoptosis.

Answer 15

Caspase 8, 10

Question 16

Executioner caspases.

Answer 16

Caspase 3, 6

Question 17

Regulated cell death that results in necrosis (morphologically); caspase-independent; activates RIP1 and RIP3 complexes that lead to increased ROS and decreased mitochondrial ATP production.

Answer 17

Necroptosis

Question 18

Type of apoptosis often seen in microbe-infected cells; caspase 1 releases IL-1, and together with caspase 11, causes cell injury.

Answer 18

Pyroptosis

Question 19

It involves sequestration of cellular organelles into cytoplasmic autophagic vacuoles that fuse with lysosomes and digest enclosed material; used as a survival mechanism under various stress conditions (i.e. nutrient deprivation).

Answer 19

Autophagy

Question 20

Marker for autophagy; involved in formation of autophagosome.

Answer 20

LC3

Question 21

A form of tissue necrosis in which the component cells are dead but the basic tissue architecture is preserved; affected tissues take on a firm texture; often seen in infarcts of all solid organs (heart, spleen, kidney) except the brain.

Answer 21

Coagulative necrosis

Question 22

Characterized by digestion of dead cells, resulting in transformation of the tissue into a liquid viscous mass; often seen in infections (pus) and in hypoxic death of cells within the CNS.

Answer 22

Liquefactive necrosis

Question 23

This term is usually applied to a limb, generally the lower leg, that has lost its blood supply and has undergone coagulative necrosis with superimposed liquefactive necrosis involving multiple tissue layers.

Answer 23

Gangrenous necrosis

Question 24

Friable, white appearance of necrosis; appears as a structureless collection of fragmented or lysed cells and amorphous granular debris enclosed within a distinctive inflammatory border (granuloma); “cheese-like”.

Answer 24

Caseous necrosis

Question 25

Refers to focal areas of fat destruction, typically seen in acute pancreatitis; there is release of activated pancreatic lipases into the substance of the pancreas and the peritoneal cavity; the foci of necrosis contain shadowy outlines of necrotic fat cells with basophilic calcium deposits (saponification), surrounded by an inflammatory reaction.

Answer 25

Fat necrosis

Question 26

A special form of necrosis usually seen in immune reactions involving blood vessels; deposits of immune complexes, together with fibrin that have leaked out of vessels, result in a bright pink and amorphous appearance in H&E stains, called “fibrinoid” (fibrin-like) by pathologists.

Answer 26

Fibrinoid necrosis

Question 27

Abnormal calcium deposition occurring in the absence of calcium metabolic derangements; examples: Psammoma bodies in cancers with papillary architecture and meningioma

Answer 27

Dystrophic calcification

Question 28

Effect of caloric restriction on longevity.

Answer 28

Increased due to decreased IGF-1 signaling

Question 29

Calcium deposition in normal tissues occurring in the presence of hypercalcemia; example: calcinosis

Answer 29

Metastatic calcification

Question 30

Proteins that are produced in response to food deprivation; with actions that lead to prolonged longevity (anti-apoptotic, anti-ROS).

Answer 30

Sirtuins