Chapter 4

Question 1

causes of cell injury

Answer 1

• hypoxia
• physical, thermal, chemical
• microorganisms
• inflammation/immune reactions
• nutritional imbalance
• genetic defects
• trauma
• aging

Question 2

most common cell injury?

Answer 2

hypoxia, due to ischemia (insufficient blood supply)

Question 3

loss of oxygen leads to decrease in..

Answer 3

ATP, failure of Na/K pump, sodium moves into cell, water follows and cell swells/potentially dies

Question 4

glycolysis without oxygen = ?

Answer 4

lactate (lactic acid), more acidic, alters cell proteins

Question 5

steatosis

Answer 5

increase in lipid/fat, deposited between or into cells

Question 6

hydropic changes

Answer 6

cell swelling
- loss of ATP
- failure of pump
- sodium remains in cells
- water moves into cells

Question 7

atrophy

Answer 7

without size, shrinkage, decrease in cell size due to physiological (aging) or pathological (decreased blood supply, nutrition, lack of neural/hormone support)

Question 8

hypertrophy

Answer 8

increase in cell size

Question 9

hypertrophy is due to..

Answer 9

• hormonal stimulation
• increased functional demand

Question 10

hypertrophy results in..

Answer 10

• increased protein synthesis within cell
• decreased protein breakdown

Question 11

hyperplasia

Answer 11

increase in cell number

Question 12

hyperplasia due to..

Answer 12

• hormonal stimulation
• increased functional demand
• chronic stress

Question 13

hyperplasia results in..

Answer 13

increased cell division if the cell can divide

Question 14

metaplasia

Answer 14

replacement of one cell type with another

Question 15

metaplasia is most common in..

Answer 15

epithelium
- reversible if stressed removed
- smokers

Question 16

dysplasia

Answer 16

change in cell, abnormal cell division
- premalignant -> precancerous
- often not reversible

Question 17

apoptosis

Answer 17

DNA degrades, cell shrinks, programmed cell death
- removes cells that are “warn out”
- removes unwanted tissue
- physiological or pathological

Question 18

necrosis

Answer 18

pathologic cell death, explosion, leads to inflammation of other cells because of contents leaked
- damage nearby cells
- inflammation results

Question 19

different types of necrosis

Answer 19

• coagulation necrosis (observed with infarcts)
• liquefaction necrosis
• caseous necrosis - cheese, observed with tuberculosis
• gangrenous necrosis (gangrene)

Question 20

infarcts

Answer 20

lack of blood flow/oxygen leads to cell death

Question 21

inflammation

Answer 21

cell response to injury

Question 22

function of inflammation

Answer 22

• limit extent of injury
• remove necrotic debris
• prepare for healing process

Question 23

types of inflammation

Answer 23

• acute: short, resolve
• chronic: issue, months/years (obesity)

Question 24

vascular sequence in acute inflammation

Answer 24

• blood vessels vasodilate
• increase blood flow to injured area
• increased vascular permeability (WBC and plasma leave)
• mast cells release histamine

Question 25

exudate

Answer 25

fluid that leaks out of blood vessels

Question 26

inflammation hallmarks

Answer 26

- swelling (increased leakiness) - redness (more blood flow) - warmth (more blood flow)

Question 27

mediators of inflammation

Answer 27

- prostaglandins: increase vasodilation - leukotrienes

Question 28

inhibitor of mediators

Answer 28

NSAID - nonsteroidal antiinflammatory drug

Question 29

cellular phase sequence of events in acute inflammation

Answer 29

- leukocytes move from blood to injury site - neutrophils mediate inflammation

Question 30

puss

Answer 30

dead neutrophils

Question 31

phagocytosis

Answer 31

cell eating

Question 32

cellular phase steps

Answer 32

- margination - emigration/diapedesis - squeeze through blood vessel - chemotaxis - bacteria releases chemical for neutrophil to follow

Question 33

chemical mediators of inflammation

Answer 33

cytokines: messenger between WBC

Question 34

chronic inflammation

Answer 34

weeks to years, may result from acute inflammation that persists or non-acute cause present at low level for a long time

Question 35

characteristics of chronic inflammation

Answer 35

- edema and hyperemia less pronounced - few or no neutrophils present - fibrosis (scar tissue)

Question 36

clinical appearance or acute and chronic inflammation

Answer 36

- abscess: collection of puss in the center - cellulitis: inflammation of dermis, deep skin infection - ulcer: type of lesion, cut in the membrane of the cell, stomach

Question 37

regeneration

Answer 37

nearly complete restoration

Question 38

fibrous connective tissue repair

Answer 38

scarring, does not restore original function

Question 39

type of repair depends on type of cells forming tissue

Answer 39

continuously dividing vs. non dividing

Question 40

would healing stages

Answer 40

- inflammation - proliferative - remodeling

Question 41

proliferation

Answer 41

- create new - collagen (laid by fibroblasts) and extra cellular matrix (in between connective tissue) - granulation tissue (epithelial cells migrate to site, "soft scab", vascularized, made up of macrophages and fibroblasts)

Question 42

remodeling

Answer 42

- maturation of scar (turns white) - laying new collagen - can continue for year + - loss of blood vessels (not needed when collagen arrives)

Question 43

repair hindering

Answer 43

- continuation of inflammation (poor immune system) - advancing age (bed sores) - poor nutrition (lack of vitamin C for collagen, vitamin A for epithelial cells, protein to make collagen and WBC) - diabetes (cardiovascular and circulation and WBC lack) - steroid therapy (decreased immune system and inflammation so healing takes longer)