Inflammation and Defense Mechanisms/Immunology Flashcards

1
Q

T/F: The protective inflammation response can potentially be harmful.

A

True.
Can injure normal tissue if stay too long

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2
Q

What cells are present with inflammatory present?

A

WBC and plasma proteins

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3
Q

What is the goal for inflammatory reaction?

A

To bring WBC and plasma proteins to site of infection/tissue damage

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4
Q

What is inflammation induced by?

A

damaged host cells, cytokines, and others

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5
Q

T/F: Inflammation is uncontrolled and self-limited.

A

False. Inflammation is controlled and self-limited

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6
Q

What is the cardinal signs and their corresponding names?

A

pain-dolar
redness-rumor
swelling-edema
heat-calor
loss of function

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7
Q

What are the triggering factors to inflammation?

A

infection, trauma, or surgery

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8
Q

What does the local reaction stimulate?

A

neutrophils and macrophages

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9
Q

What is released after neutrophils and macrophages?

A

the mediators: inflammatory cytokines

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10
Q

What is usually associated with release of the mediators?

A

secondary system reactions such as fever, complement activation, and vasodilation

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11
Q

Is periodontitis acute or chronic?

A

chronic

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12
Q

What usually occurs with acute inflammation?

A

the body will react to the foreign insult by fever, diarrhea, or sneezing to get rid of

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13
Q

Why should the bodies response to acute inflammation not be stopped?

A

if it can’t remove particle or heal, it could cause a chronic problem

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14
Q

In which inflammation, is the response causing damage to tissue?

A

chronic inflammation such as any periodontal disease

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15
Q

What cells (the good ones) are involved in inflammation? What is their purpose?

A

neutrophils, macrophages, lymphocytes, plasma cells

function: try to clear infection and heal body

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16
Q

Which cell type is first line of defense in inflammation?

A

neutrophils

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17
Q

What is the daily production of neutrophils and were is it mostly found?

A

production: 10^11 cells per day
90% in bone marrow

18
Q

What is the half life of neutrophils in circulation and in tissues?

A

t1/2 in circulation: 6-9 hrs
t1/2 in tissues: 1-4 days

19
Q

What are the chemotactic factors the cause the response for neutrophils?

A

IL-8 from injured cells
LTB-4 through inflammatory cascade
C5A from complement
FMLP from bacteria

20
Q

Describe the process of neutrophils:

A
  • neutrophils migrate through endothelium and are in the site of injury in tissue within 6 hrs.
  • they peek at 24-48 hours.
  • collegenase and elastase allow endothelial to become permeable and are released at connective tissue and basil membrane
  • once at wound site, engulf bacteria via phagocytosis and enzymatic and oxygen radical mechanism
  • also secrete IFN- gamma (interferon gamma) to activate macrophages
  • macrophages then secrete the pro-cytokines to cause vasodilation and the cycle continues
21
Q

How do byproducts and lipopolysaccharides allow neutrophils to pass through endothelial cell?

A

by releasing IL-8 to allow for it to become more permeable

22
Q

How do other toxins allow neutrophils to pass through endothelial cell?

A

by releasing IL-1, TNF, and PGE2 which causes vasodilation causing more blood to bring neutrophil in

23
Q

How does the inflammatory cascade work?

A

when neutrophils get in, it releases interferon gamma which causes macrophages to come. when macrophages come they also release IL-1, TNF, and PGE2 to cause more vasodilation and bring more neutrophils in

24
Q

What are macrophages goals in inflammation?

A

1) phagocytose antigens
2) release IL-1, TNF, and PGE2 to fight infection and allow more blood flow for reentry of neutrophils

25
Q

What are the pro-inflammatory cytokines?

A

IL-1, TNF, and PGE2

26
Q

What’s the main goal of the pro-inflammatory cytokines?

A

fever & leukocytosis, complement activation (increase permeability), increase serum glucocorticoids and decrease serum iron

27
Q

How do the endothelial cells become activated and why is this important?

A

inflammatory cytokines: IL-1 and TNF activate endothelial cell allowing for hyper adhesive for leukocytes to attach

28
Q

What cells are part of lymphocyte inflammation?

A

T cells and B cells

29
Q

How do T cells work?

A

1) CD4 (T-helper cell) humoral response to activate B cells to become plasma cells and secrete specific antibody

2) CD8 cell mediated response to kill any cell infected with the specific antigen

30
Q

What is the main cell type found in established lesion of periodontitis?

A

plasma cell

31
Q

What is the function of plasma cells?

A

help form an antibody so antigen is removed

32
Q

T/F: if neutrophils aren’t present, inflammatory process will not be affected.

A

False.
if no neutrophils, lower amount of macrophages, slower time of healing

33
Q

What are the protective layers in order from outside to inside?

A

sulcus, epithelium, connective tissue

34
Q

How is the sulcus good at protecting?

A

the gingival sulcular fluid

35
Q

If there is inflammation, will there be more or less gingival sulcular fluid?

A

more gingival sulcular fluid to flush out bacteria

36
Q

What is one of the most important things in getting rid of inflammation?

A

get rid of etiology first and then treat symptoms. If calculus persists, inflammation becomes long standing and chronic so treatment should be calculus removal and NOT anti-inflammatory medicine

37
Q

In chronic inflammation, how are neutrophils bad?

A

the neutrophils release collagenase and elastase which are what allow endothelium to become more permeable so it can also let in bacteria

sum: removes protective layer and allows for bacteria to be let in

38
Q

In chronic inflammation, how are macrophages bad?

A

macrophages cause release of the pro-cytokines: IL-1, TNF, and PGE2 which are osteoclast activators and can promote bone resorption

39
Q

in chronic inflammation, how are B cells bad?

A

it is a major secretor of IL-1 during periodontal disease and can result in bone resorption

40
Q

Why does bone loss occur in periodontitis?

A

Because of the pro-inflammatory cytokines! They are osteoclast activators so they eat away bone. In inflammation, there are MANY pro-inflammatory cytokines