Inflammatory Process/Acute Inflammation/Chronic Inflammation

Question 1

main goal of inflammatory process

Answer 1

to repair tissue, destruction of healthy tissue occurs in the process

Question 2

exogenous element

Answer 2

physical, chemical and mechanical injuries
pathogenic organisms

Question 3

endogenous elements

Answer 3

genetic
immune dysfunction or deficiency
degenerative

Question 4

two major kinds of inflammation

Answer 4

acute: limited in area and duration, cardinal signs
chronic: long duration or history of repeated insults or injuries

Question 5

what suffix is for inflammation of an area

Answer 5

‘itis’

Question 6

three phases of acute inflammation

Answer 6

1. Initiation (Events 1-5)
2. Amplification (Events 6 & 7)
3. Termination (Event 8)

Question 7

initiation

Answer 7

activated when injury occurs
changes to microcirculation
loss of fluid from blood into tissues
white blood cells move to area

Question 8

amplification

Answer 8

chemical mediators direct more and different types of white blood cells into the injured area
increasing response and neutralizing agents causing the response

Question 9

termination

Answer 9

requires other chemical substances to stop or inhibit inflammatory process
if it continues, more damage will result

Question 10

event 1

Answer 10

vasoconstriction of microcirculation controls bleeding
-chemical mediators released
-lasts a few minutes only

Question 11

event 2

Answer 11

vasodilation
-more blood flows into the area
-chemical mediators are released

Question 12

event 3

Answer 12

blood vessel become permeable
-fluid or exudate leaves vessels
-chemical mediators
-signs of inflammation evident

Question 13

cardinal signs of inflammation

Answer 13

1. heat
2. redness, hyperemia
3. swelling
4. pain
5. loss of function

Question 14

event 4

Answer 14

vascular stasis (slowing of blood)
-margination (WBCs move to vessel’s walls)
-pavementing (WBCs adhere to walls)
-transmigration (WBCs squeeze through vessel walls)
-plasma fluid is lost, blood vessels thicker
-red blood cells to center of vessels

Question 15

event 5

Answer 15

chemotaxis
-cells directed by chemical mediators to move in a specified direction
-WBCs ‘attracted to’ or ‘driven to’ injury

Question 16

event 6

Answer 16

opsonization (cell death)
-opsonins (immunoglobin) found in exudate
-organisms coated with opsonins
-leukocytes prepare foreign organisms for phagocytosis

Question 17

event 7

Answer 17

phagocytosis
-foreign matter eliminated or destroyed by phagocytosis
-if injury is extensive, more chemical mediators

Question 18

event 8

Answer 18

termination of process
-foreign material and debris removed through lymphatic system
-chemical mediators will inhibit or stop further action by inflammatory process and area will complete healing or repair process

Question 19

what do systemic manifestations do and examples

Answer 19

help control the injury
encourage removal of offending agents and debris association with the IP
start repair process
depends on the extent and length of the IP
does not always occur

pyrexia, leukocytosis, lymphadenopathy

Question 20

pyrexia

Answer 20

fever
destroys pathogens by creating a higher temp and mobilize WBC
can be caused by non-infectious agents as well, dehydration and excess thyroid hormone

Question 21

leukocytosis

Answer 21

increase of WBC
neutrophils: respond to bacteria, inflammatory disorders and certain drugs
lymphocytes: respond to viruses
monocytes: predominate in chronic infections

Question 22

lymphadenopathy

Answer 22

swollen lymph nodes

Question 23

outcomes of acute inflammation

Answer 23

no tissue damage: may progress to chronic inflammation or resolves completely
tissue damage: may progress to chronic inflammation, abscess formation, resolution of the inflammatory process, regeneration, repair

Question 24

chronic inflammation

Answer 24

longer than 2 weeks = chronic inflammation
can happen without preceding acute inflammation (Chronic Periodontitis)
large number of mononuclear cells in tissue
TISSUE DESTRUCTION

Question 25

steps of chronic inflammation

Answer 25

1. macrophages driven to area by chemotactic agents from Neutrophil and from chemical mediators
2. macrophages secrete more chemokines to recruit more monocytes from blood vessels where they will become macrophages
3. other chemical mediators released by macrophages stimulate or enhance lymphocyte actions

Question 26

what plays a role in tissue destruction while performing their job

Answer 26

macrophages

Question 27

what causes bone and tissue destruction during chronic periodontitis

Answer 27

lysosomal enzymes that leak out of cells into surrounding tissues can destroy normal cells and collagen fibers in the area and can activate osteoclasts causing bone destruction

Question 28

granulomatous inflammation

Answer 28

a subset of chronic inflammation that form granulomas
contain giant cells (macrophages) and other inflammatory cells
surround a type of foreign matter
forms a wall around the substance to prevent spread

Question 29

abscess formation

Answer 29

when pyogenic or pus-forming microbes and enzymes enter the tissue
attracts leukocytes
if resistant to phagocytosis the tissues in the area are destroyed due to the death of neutrophils and resulting lysosomal enzyme release
resulting debris accumulates as exudate forming an abscess

Question 30

fistula

Answer 30

when enzymes that are released by macrophages bore through the tissues following the path of least resistance allowing the exudate to flow into another area or to find a path to the outside

Question 31

how do teeth become abscessed

Answer 31

death of the pulp and associated tissues
-cellulitis
-ludwigs angina
-bacteremia
-septicemia
-cavernous sinus thrombosis

Question 32

resolution of inflammatory process

Answer 32

if not caused by trauma it goes away
if tissue damage healing can only begin when etiology is removed it can result in regeneration or scarring

Question 33

regeneration and tissues that can and cannot

Answer 33

the body’s attempt to restore itself
epithelium and liver can regenerate
cardiac and nerve cannot

Question 34

fibrous repair

Answer 34

recreates a near-normal architecture but not normal function

Question 35

types of fibrous repair

Answer 35

primary intention: wound margins are clean and held together, migrating epithelial cells have little distance to travel
secondary intention: edges of wound cannot be brought together, begins at base and proceed bottom to top

Question 36

process of fibrous repair

Answer 36

1. initiated almost immediately after injury
2. blood clot forms; fibroblasts and vascular endothelial cells appear
3. angiogenesis: endothelial cells form new blood vessels; fibroblasts form collagen fibers
4. formation of granulation tissue: forms framework, becomes less vascular
5. epithelialization: epithelial cells grow across lower edges of wound forming basement membrane and normal stratified squamous epithelium

Question 37

factors affecting wound healing

Answer 37

type, size, location, vascularity, infection, foreign material, excessive granulation tissue, systemic factors

Question 38

complications of wound healing

Answer 38

inadequate scar formation: inadequate amount of granulation tissue
excessive scar formation: keloid
wound contracture: can cause mobility limitations

Question 39

tooth extraction: bone and soft tissue repair

Answer 39

1. extraction
2. blood clot formation
3. angiogenesis: 10 to 12 days
4. bone formation: osteoblasts
5. alveolar process remodeled
6. replaced with spongy bone: filled in 12 weeks

Question 40

dry socket

Answer 40

initial blood clot is disrupted and bone surface becomes exposed and necrotic
2-4 days after extraction
alveolar osteitis

Question 41

alveolar osteitis

Answer 41

necrotic bone must be resorbed by the body and granulation tissue must form along the walls of the socket instead of within a clot