Innate Immunity: the inflammatory response Flashcards

1
Q

is innate immunity specific or not nonspecific

A
  • NON SPECIFIC (does not matter what the pathogen is)
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2
Q

What line of defense does it contain?

A
  • first and second ONLY
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3
Q

what is included in the first line of defense?

A
  • physical barriers
  • chemical barriers
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4
Q

what are physical barriers?

A
  • skin
  • mucous membrane
  • sections of the skin (ear wax, tears, sweat)
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5
Q

what are chemical barriers? (first line)

A
  • stomach acid
  • lysozymes in the eye
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6
Q

what cells are in the second line of defense? (inflammation)

A
  • mast cells
  • neutrophils
  • macrophages
  • NK cells
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7
Q

what are the function of mast cells & what does it cause?

A
  • degranulate and release histamine = causing vasodilation & increased capillary permeability
  • also helps w/ communication
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8
Q

what is the function of neutrophils

A
  • phagocyte, first on site, most abundant
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9
Q

what are the function of macrophages?

A
  • antigen presentation, phagocytosis, and immunomodulation (helps body stay homeostatic)
  • turn into monocyte
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10
Q

what is the function of inflammation?

A
  • prevent infection and damage from microorganisms (activate plasma proteins & dilute toxins)
  • limit and control tissue damage ( stop it from spreading)
  • stimulate the adaptive immune response
  • promote healing
  • rapid and non-specific
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11
Q

what are the general causes of inflammation?

A
  • infection, cell damage, ischemia, nutrient deprivation, temperature extremes, radiation
  • or body recognized a threat of one of those things
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12
Q

what are the 5 signs of inflammation?

A
  • pain
  • heat
  • redness
  • swelling
  • loss of function
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13
Q

what role do plasma proteins system play in inflammation

A
  • they are involved in 3 separate but interconnected systems
    1. complement system = blood clotting
    2. clotting system = plasma proteins = fibrous
    3. the kinin system = vasodilation
  • end product of each sequence is a biologic effect that contributes to inflammation
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14
Q

what is the bradykinin system?

A
  • protein that lowers blood pressure by widening blood vessels
  • produced by the kinin system
  • lowers BP by widening blood vessels and allows for water to leak into the surrounding tissue causing inflammation & pain
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15
Q

what are the plasma proteins involved with inflammation?

A
  1. interleukins
  2. interferon
  3. chemokines
  4. cytokines
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16
Q

what does interleukins (plasma proteins) do?

A
  • produced primarily by macrophages and lymphocytes in response to a pathogen or stimuli by inflammation
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17
Q

what are interferon?

A
  • protects against viral infections
  • produced and released virally by infected host cells in response to viral double stranded RNA
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18
Q

what do the plasma protein chemokines do?

A
  • induce WBC chemotaxis = the movement of WBC to site of injury
  • produced by macrophages, fibroblast, endothelial cells
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19
Q

what does the complement system do for the process of inflammation?

A
  • destroys the pathogens directly, activates or stimulates other components of inflammation
  • also does opsonization and chemotaxis
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20
Q

what does the coagulation system do for the process of inflammation?

A
  • forms a fibrinous meshwork at n injured or inflamed site (blood clot)
  • fibrin is the main insoluble protein
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21
Q

what does the Kinkin system do for the process of inflammation?

A
  • functions to activate and assist inflammatory cells
  • has bradykinin: causes dilation of BV, pain. smooth muscle contraction, vascular permeability
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22
Q

what are the main cells involved in inflammation?

A
  • phagocytes: neutrophils, macrophages, eosinophils
  • mast cells
  • platelets (clotting)
  • endothelial cells (lining of BV)
23
Q

what is the function of the neutrophils?

A
  • high count = new infection
  • predominate in early inflammatory responses
  • 6 to 12 hours first on site
  • ingest bacteria, dead cells, cellular debris
  • cells short lived and become purulent exudate
24
Q

what do monocytes become & when do they arrive @ site of infection ?

A
  • they become macrophages
  • arrive at inflammatory site within 3 - 7 days (along w/ all immune cells)
25
Q

what do mast cells do?

A
  • important cellular activator of inflammation
  • granulated filled with histamine that gets released when they degranulate
26
Q

what’s the function of eosinophils?

A
  • they are mildly phagocytic cells
  • defense against parasites and they regulate vascular mediators
27
Q

what do platelets do?

A
  • part of coagulation cascade
  • promote wound healing
28
Q

what do natural killer cells do?

A
  • recognizing and eliminating cells infected with viruses and some function in eliminating cancer cells
29
Q

what are 3 cellular components in inflammation

A
  • histamine
  • leukotrienes
  • prostaglandins
30
Q

what does histamine do?

A
  • vasoactive molecule released from mast cells in degranulation
  • vasodilation = increased blood flow into microcirculation
  • causes retraction of endothelial cells lining the capillaries = increased vascular permeability
31
Q

what do leukotrienes do in inflammation?

A
  • they are a lipid mediator
  • inflammation mediator synthesizes by mast cells
  • have a histamine like reaction
  • produces a slower, longer acting response
32
Q

what is the function of prostaglandins in inflammation?

A
  • lipids with hormone like properties
  • inflammation mediator made by mast cells
  • causes: increased vascular permeability, neutrophil chemotaxis, pain, fever
33
Q

what are the 3 main events in inflammation?

A
  1. increased vascular permeability
  2. emigration of leukocytes
  3. phagocytosis
34
Q

what happens in the first step of inflammation? (increased vascular permeability)

A
  1. vasodilation due to chemical mediators (histamine)
  2. endothelial cell retraction
  3. increased capillary permeability
  4. movement of fluid capillaries into tissues
35
Q

what happens in step two of inflammation? (emigration of leukocytes)

A
  1. chemotaxis: directional migration of WBC along concentration gradient of chemotactic factors
  2. mechanisms for accumulating neutrophils and monocytes at the site of injury
  3. blood flow thru capillaries slows as fluid is lost and viscosity increases (makes thicker blood, slows process) = neutrophils roll / stick to endothelium = migration
    - neutrophils and monocytes migrate through the capillary wall and site of injury
36
Q

what is diapedeses?

A
  • cells leaving
37
Q

what happens in step three of inflammation? (phagocytosis)

A
  • Performed by phagocytes
    Neutrophils (early) and macrophages (later)
    Eosinophils (mild)
  • Recognition & adherence = to eat (thx complement system bc opsonization)
  • Engulfment (endocytosis)
  • Fusion with lysosome
  • Destruction = mini particles after the body takes away as waste
38
Q

what is a phagocyte

A

process of a cell ingesting and disposing of foreign material (antigens)

39
Q

what are the 2 types of inflammation?

A
  • acute & chronic
40
Q

what makes inflammation acute?

A
  • short in duration
  • lasting less than two weeks
41
Q

what makes chronic inflammation?

A
  • last 2+ weeks
  • proceeded by an unsuccessful acute response
  • Dense infiltration of lymphocytes & macrophages (if unable to remove [pathogen, granuloma formed)
42
Q

what are the systemic manifestations of inflammation?

43
Q

what is fever caused by?

A
  • by exogenous (outside) & endogenous (inside) pyrogens
44
Q

where does fever act on?

A
  • directly on hypothalamus
45
Q

what is Neutrophilic leukocytosis:

A
  • increased number of neutrophils
46
Q

what does increase of plasma proteins being synthesized do

A
  • means muscle catabolism meaning the PT will feel weak due to muscle breakdown
47
Q

what are the pros and cons of fever?

A
  • Pro: microorganism can be killed by higher temp
  • Con: may make the host more susceptible to microorganisms
48
Q

whats the treatment for fever?

A
  • Consider clinical picture or what’s happening in the PT body
  • Antipyretics (Tylenol or ASA = fever reducers)
  • Block prostaglandins
49
Q

what are the local manifestation of inflammation? classic symptoms

A
  • redness
  • heat
  • swelling
  • pain
  • loss of function
50
Q

what is serous exudate?

A
  • serous = watery
  • exudate = fluid leaves the site of infection
  • watery exudate that indicates possible early inflammation
51
Q

what’s fibrinous exudate?

A
  • cloudily / thick
  • thick, cloudily exudate, stands of fibrin
52
Q

purulent exudate?

A
  • indicates bacterial infection
  • yellow, thick, gross
  • pus: poaque, indicates bacterial infection
53
Q

what causes abscess formation?

A
  • walled off lesion usually w/ purulent exudate
  • BV are walled off