Inflammation

Question 1

innate immunity

Answer 1

non-specific immunity –> natural barriers and inflammation

inflammatory response

Question 2

adaptive immunity

Answer 2

targets specific microbes (antigens) that have breached surface barriers

develops after exposure to specific antigen

full immune response

Question 3

purpose of inflammation

Answer 3

minimize the effects of injury by rapidly diluting, destroying, or neutralizing the harmful agent

allows new tissue to be generated

protective effect

Question 4

causes of inflammation

Answer 4

direct physical damage
ischemia/infarction
allergic reaction
extremes of heat or cold
infection

Question 5

inflammation process

Answer 5

cell injury –> damaged cell releases inflammatory mediators into ISF and blood)

1. acute inflammation (local response) –> vascular stage; cellular stage
2. systemic response (fever,, malaise, headache, anorexia)

Question 6

leukocytes

Answer 6

neutrophils
basophils
eosinophils

Question 7

lymphocytes

Answer 7

T-lympho (cell-mediated)

B-lympho (anti-bodies)

monocytes (phagocytosis; travel in BVs)

macrophages (mature monocyte; phagocytosis; remove debris)

Question 8

5 cardinal signs of inflammation

Answer 8

redness
warmth
swelling
loss of function
pain

Question 9

vascular response

Answer 9

1. vasodilation

2. increased capillary permeability

Question 10

vasodilation importance

Answer 10

hyperemia = increase in blood flow to the injured tissue (getting more WBC to injured area to help with resolution)

vasodilation –> redness and warmth

Question 11

capillary permeability importance

Answer 11

more permeability = need to get WBC from capillary into injured tissue; fluid into ISF can also dilute toxin

plasma proteins enter interstitial space –> fluid in IS space increases –> swelling; loss of function

Question 12

mediators: later stages of inflammation

Answer 12

mast cells activate membrane phospholipids –> arachidonic acid

AA –> leukotrienes (lipooxygenase) or prostaglandins/thromboxanes (cyclooxygenase)

L = increased capillary permeability

PG = vasodilation and increased capillary permeability

Question 13

cellular response

Answer 13

changes in endothelium; WBCs move into area of injury or infection

Question 14

stages of cellular response

Answer 14

1. margination and adhesion of WBCs to endothelium (vessel wall near injured tissue)
2. diapedesis (migrate through endothelium; go through capillary bed)
3. chemotaxis –> neutrophils attracted to area of inflammation
4. phagocytosis (removal of debris/antigen)

Question 15

cause of fever

Answer 15

pyrogens (interleukin-1)

act on hypothalamus

Question 16

purpose

Answer 16

body temp higher –> impairs growth of bacteria, viruses, and pathogens

Question 17

patterns

Answer 17

varying depending on what is causing the fever (can give clues to what is causing it)

intermittent, remittent, sustained, recurrent

Question 18

course of a fever

Answer 18

1. release of pyrogens in circulation
2. hypothalamic control reset –> high
3. body response = increase body temp (shiver, vasoconstriction, increased HR/BMR, curl up body)
4. body reaches new temperature (feel warm)
5. remove pyrogens –> resets hypothalamus to normal
6. body response –> increase heat LOSS (sweating, vasodilation, lethargy, extend body)

Question 19

complications of inflammation

Answer 19

1. infection

2. skeletal muscle spasm

Question 20

chronic inflammation common characteristics

Answer 20

Less swelling and exudate

Presence of more macrophages, fibroblasts, lymphocytes

Continued tissue destruction

More fibrous scar tissue

Granuloma may develop around foreign object

Question 21

ASA and NSAIDS

Answer 21

inhibit cyclooxygenase –> less production of PG –> limiting cap. permeability –> decreased swelling and vasodilation

local effects –> reduces warmth and redness in inflammed tissue

systemic effects –> decrease fever and reduce pain

Question 22

acetaminophen

Answer 22

systematic effects

reduces PGs –> fever and pain management

Question 23

glucocorticoids

Answer 23

inhibit arachidonic acid –> decrease in leukotrienes AND PG (decreased vasodilation and cap. permeability)

prolonged use: decrease bone density; decrease WBC activity (prone to infection)