Chapter 2- Cellular Responses To Stress

Question 1

What is etiology?

Answer 1

The cause of a disease or an initiating event

Question 2

What is pathogenesis?

Answer 2

The mechanism of disease development

Question 3

What is morphological change?

Answer 3

Structural alterations in cells/tissues due to the disease

Question 4

What is clinical significance?

Answer 4

The functional consequences of the morphological change

Question 5

What are some possible causes of cell injury?

Answer 5

Hypoxia
Physical agents
Infectious agents
Immunologic reactions
Genetic derangements
Nutritional imbalances

Question 6

What is adaptation?

Answer 6

Cellular stressors induce a new state causing changes but the cells remain viable

Question 7

What is hypertrophy?

Answer 7

Increased cell size

Increased cell protein production

Question 8

What is hyperplasia?

Answer 8

Increased number of cells

Question 9

What are the different types of hyperplasia and their causes?

Answer 9

Physiologic- hormones or GFs

Pathologic- inappropriate growth

Compensatory- after resection (eg. liver)

Question 10

What is atrophy?

Answer 10

Decreased number or cells and size of cells

Question 11

What is metaplasia?

Answer 11

One cell type is replaced by another

Question 12

What is the difference between a reversible and irreversible injury?

Answer 12

Reversible- changes can be restored if the stimulus is removed

Irreversible- stressor exceeds the cell’s adaptive capacity

Question 13

What are two morphological changes associated with reversible injuries?

Answer 13

1. Cellular swelling due to hypoxia

2. Fatty changes

Question 14

What are the different causes/types of intracellular accumulations?

Answer 14

Inadequate removal of normal substances (transport)

Abnormal endogenous substances (folding)

Defects in metabolism

Abnormal exogenous substances

Steatosis/fatty change (triglyceride accumulation)

Proteins (excess, misfolding, defective transport)

Hyaline change

Glycogen (metabolism abnormality)

Pigments

Question 15

What are the different types of necrosis?

Answer 15

Coagulative
Liquefactive 
Gangrenous
Caseous
Fat
Fibrinoid

Question 16

What are the characteristics of coagulative necrosis?

Answer 16

Cell and tissue framework preserved

Cells are eventually phagocytosed and dissolved by inflammatory cells

Question 17

What type of necrosis is associated with hypoxia cell death?

Answer 17

Coagulative

Question 18

What are the characteristics of liquefactive necrosis?

Answer 18

Autolysis and heterolysis predominate over protein denaturation

Question 19

Where is liquefactive necrosis commonly seen?

Answer 19

The brain

Question 20

What is gangrenous necrosis associated with?

Answer 20

Bacterial infection with coagulative necrosis

Question 21

What are the two types of gangrenous necrosis?

Answer 21

1. Wet

2. Gas (clostridium)

Question 22

What infection is caseous necrosis associated with?

Answer 22

Tb

Question 23

What causes the morphology of fat necrosis?

Answer 23

Lipase releases fatty acids which complex with calcium to form soap

Question 24

What causes fibrinoid necrosis?

Answer 24

Immune complexes deposited in blood vessels cause inflammation and fibrosis

Question 25

What are the differences between apoptosis and necrosis?

Answer 25

Apoptosis- organized/programmes cell death, components released in vesicles (PM intact), no inflammation

Necrosis- PM damage results in the leakage of intracellular enzymes, causing an inflammatory response

Question 26

What are the three things that happen to genetic material during necrosis?

Answer 26

1. Karyolysis- DNA degradation
2. Pyknosis- nuclear shrinkage
3. Karyorrhexis- nucleus is fragmented

Question 27

What are the two pathways of apoptosis and the mechanisms by which they occur?

Answer 27

Intrinsic/mitochondrial- BCL2 proteins activated due to cell injury (mitochondrial leakage), caspase activation

Death receptor- Fas ligand, death receptor complex activates caspases

Question 28

How do caspases exert their effects?

Answer 28

Act of DNase inhibitor, resulting in fragmentation

Question 29

What are some examples of things that lead to apoptosis?

Answer 29

GF deprivation

DNA damage (p53 accumulation stops cycle at G1)

Protein misfolding (unfolded protein response can activate caspases)

TNF family receptors- Fas interactions remove self recognizing lymphs

Cytotoxic lymphs- recognize foreign Ag and secrete porforin

Question 30

What are the most common clinical injuries?

Answer 30

Hypoxia and ischemia

Question 31

What is ischemia-reperfusion injury?

Answer 31

Restoration of blood flow increased cell injury and potentially causes cell death

Question 32

How does ischemia-reperfusion injury occur?

Answer 32

Oxidative stress (free radical accumulation)

Intracellular calcium overload

Inflammation (more cells)

Complement activation (IgM deposition)

Question 33

What is the difference between direct and indirect toxicity?

Answer 33

Direct- chemical directly damages cells

Indirect- chemical is converted to a toxic metabolite that damages cells

Question 34

What is pathologic calcification?

Answer 34

Abnormal tissue deposition of calcium salts

Question 35

What are the two types of pathologic calcification?

Answer 35

1. Dystrophic- in areas of necrosis (eg. atherosclerosis)

2. Metastatic- hypercalcemia causes deposition in normal tissue

Question 36

What can cause metastatic pathologic calcification?

Answer 36

Elevated PTH

Bone destruction

Vitamin D intoxication

Renal failure (secondary hyperparathyroidism)

Question 37

What is cellular senescence?

Answer 37

Limited capacity for replication

Accumulated metabolic and genetic damage