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Dental Hygiene: Periodontics I > Quiz 6 > Flashcards

Quiz 6 Flashcards

(61 cards)

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1
Q

Antigen

A

molecule that triggers the immune response

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2
Q

Innate Immunity

A

present at birth; always present
not antigen specific
immediate response to infection
1st line of defense

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3
Q

Adaptive Immunity

A

develops throughout life after initial exposure to antigen
antigen specific
lag time between infection and response
2nd line of defense

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4
Q

Which type of immunity involves memory and may develop lifelong immunity?

A

Adaptive
-immunological specificity
-immunological memory

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5
Q

Innate immunity cells

A

neutrophils
monocytes
macrophages
eosinophils
mast cells
NKT-lymphocytes

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6
Q

Adaptive immunity cells

A

T-lymphocytes
B-lymphocytes

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7
Q

What is the bodies response to infection called?

A

Host response

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8
Q

Primary function

A

to defend life of host by identifying foreign substances in body and defending against them by
-developing immune cells that target invaders
-producing biochemical substances to amplify immune response and counteract invaders

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9
Q

Dysfunction Immune/Loss of Immune Response

A

loss of immune function
can be deadly
ex/ HIV

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10
Q

Overactive Immune Response

A

can harm body that its trying to protect
ex/ rheumatic heart disease

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11
Q

Neutrophils

A

1st cells deployed, most abundant

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12
Q

Eosinophils

A

parasitic infections, collaborate w/ mast cells and basophils to regulate allergic response

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13
Q

Periodontal pathogens are most effectively destroyed by…

A

PMNs

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14
Q

Basophils

A

allergic response, coordinates physiological activity
*largest by least common granulocyte

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15
Q

Mast cells

A

release key inflammatory mediators for allergic response, protect against pathogens

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16
Q

Agranulocytes

A

no granules, lymphocytes, monocytes/macrophages

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17
Q

PML (polymorphonuclear leukocytes)

A

multilobulated nucleus, does not include mast cells

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18
Q

Monocytes

A

single irregular nucleus, no granules, located in bloodstream*

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19
Q

Plasma B cells

A

make antibodies

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20
Q

Memory B cells

A

remembers previous exposure and evoke more rapid enhanced response

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21
Q

Fragment Antigen Binding (Fab)

A

antigen binding region, binds to microbe and helps to kill it

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22
Q

Fragment Constant (Fc)

A

region at tail end that binds to immune cell and proteins of complement system
*binds to B cell

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23
Q

Major classes of immunoglobulins/antibodies

A

IgG
IgM
IgA
IgE
IgD

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24
Q

IgG

A

most abundant, opsonizer (enhances phagocytosis, only one that can pass through placental barrier

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25
IgM
first to respond, largest, pentamer structure (10 binding sites), most efficient in clumping of particles (agglutination)
26
IgA
principle defense at mucosal barriers, main one in secretions (SALIVA), poor activator of complement system, J chain
27
IgE
host allergic response, parasites, binds to mast cells and basophils
28
IgD
least abundant and least understood
29
T-cells
cell mediated immunity produces cytokines
30
T-helper (CD4)
most important, regulates differentiation and maturation of B cells so antibodies are produces, activates cytoxic T cells, induces macrophages
31
T-cytotoxic (CD8)
neutralizes virally infected cells and tumor cells (direct or indirect) -impaired function feature of many chronic autoimmune diseases
32
NKT
naturally kill target, releases massive quantity of inflammatory mediators and other cytokines
33
NK vs NKT
NK are a separate and distinct category, they mature and develop in circulation, do not require reactivation
34
Macrophages
largest, highly pagocytic, agranulocyte, located in tissues, important role in chronic perio/inflammation
35
NK lymphocytes
large granular larger than B or T cells both types of immunity attribute preprogrammed natural killer *DO NOT REQUIRE PREACTIVATION
36
4 functions of complement system
1. destruction of pathogens 2. opsonization of pathogens 3. Recruitment of phagocytes 4. Immune clearance
37
Destruction of pathogens
membrane attack complex- protein unit capable of puncturing cell membrane *known as lysis
38
Opsonization of pathogens
coats surfaces of bacteria to allow phagocytes to bind and destroy it
39
Recruitment of phagocytes
additional phagocytes called to infection site
40
Immune clearance
immunce complexes removed from circulation "housekeeping"
41
Attraction of leukocytes to infection site
1. migration 2. chemotaxis 3. Phagocytosis
42
Transendothelial migration
tissue resident leukocytes release cytokines and chemokines into CT to recruit more leukocytes from bloodstream *leukocytes squeeze between cells of blood vessel wall to exit bloodstream extravasation- cell squeezing
43
Chemotaxis
leukocytes enter CT and drawn to invading pathogens via cytokines and chemokines swarm like migration pattern of neutrophils- neutrophilic swaming
44
Phagocytosis process
1. bacteria attached to membrane (pseudopodia) 2. ingested, forms phagosome 3. phagosome fuses w/ lysosome 4. lysosomal enzymes digest material 5. digested products released from cell
45
How does phagocytosis result in local tissue destruction?
released enzymes during the process cause damage to local tissues the same way they destroy bacteria tissue
46
Characteristics of inflammation
dilation of blood vessels increased permeability of blood capillaries increased blood flow leukocyte migration into tissues
47
Mast cells release...
cytokines, which in turn dilate capillaries and increase vascular permeability (inflammation)
48
Inflammatory biochemical mediators
biologically active proteins secreted by cells that activate body's inflammatory response
49
Chemokines (subgroup of cytokines)
attract immune cells to site of infection or injury and regulates chemotaxis
50
Inflammatory mediators involved with periodontitis
cytokines, prostaglandins, matrix metalloproteinases (MMP)
51
Cytokines
name for any protein that is secreted by cells and affects nearby cells, signals immune system to send more phagocytes to infection site
52
Cytokines involved in periodontits
Interleukin 1 (IL-1) Interleukin 6 (IL-6) Interleukin 8 (IL-8) Tumor necrosis factor alpha (TNF-a)
53
Prostanglandins
Powerful: D, E, F, G, H, I PGE: Important role in bone destruction* -macrophages is major source of PGE
54
Overproduction of MMPs
breakdown of connective tissue of periodontium
55
Effects of MMPs
without collagen, degradation of gingiva -> recession PDL-> pocket formation Alveolar bone -> tooth mobility
56
Acute inflammation
increased movement of plasma and leukocytes from blood to injured tissues heat, redness, swelling, pain, loss of function
57
Chronic inflammation
accumulation of macrophages, exaggerated inflammatory response
58
C-reactive protein
journal of Periodontology 2001 inflammatory effects from oral disease cause oral bacterial byproducts to enter bloodstream. These byproducts trigger liver to make CRP, inflames arteries and promotes blood clot formation
59
Remission
signs/symptoms disappear partially or completely- chronic inflammation
60
Exacerbation
sign/symptoms may recur in all of their severity in active period of disease
61
Goals of inflammatory response
1. prevent initial infection/remove damaged tissue 2. prevent spread of infection/repair damaged tissue 3. recruit effector cells if immune cells of innate system cannot control infection or repair tissues 4. mobilize effect cells (T & B lymphocytes)

Dental Hygiene: Periodontics I (9 decks)

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