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Basic Pathology > Innate Immunity and Inflammation > Flashcards

Innate Immunity and Inflammation Flashcards

1
Q

immune response

A

coordinated reaction to an antigen or pathogen

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2
Q

pathogen

A

a microorganism that can cause disease;

virus, fungus, bacteria, protozoa, helminths

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3
Q

antigen

A

any substance that elicits an immune response (exogenous or endogenous); proteins, carbohydrates, nucleic acids

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4
Q

antigen examples

A
  • surface proteins on a pathogen
  • noninfectious environmental agents (pollens, foods, bee venom)
  • clinical products (drugs, vaccines, transplanted tissues)
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5
Q

immune system functions

A
  • prevents infection and cell injury
  • distinguish self from non-self
  • destroy infected and malignant cells
  • initiates repair
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6
Q

normal immune responses

A
  • pruritus (itching)
  • malaise (general feeling of unwellness)
  • anorexia (loss of apetite)
  • limited collateral damage of normal tissue
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7
Q

abnormal immune responses

A
  • immune deficiencies, acquired or congenital; (not enough of a response)
  • hypersensitivities (allergies), autoimmune diseases; (exaggerated or over-active immune response)
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8
Q

first line of defense

A

prevent injury/infection; barriers

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9
Q

second line of defense

A

inflammation

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10
Q

third line of defense

A

adaptive immune response

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11
Q

innate immunity

A
  • present at birth
  • immediate
  • non-specific
  • activates inflammation and the adaptive immune response
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12
Q

innate immunity: physical barriers

A
  • prevent entry
  • tight junctions- epithelial tissue throughout the body
  • temperature- cool skin limits bacteria growth
  • epithelial turnover- cornea turns over every 7 days
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13
Q

innate immunity: mechanical barriers

A
  • blinking
  • coughing/sneezing
  • mucociliary escalator
  • swallowing
  • GI tract peristalsis
  • vomiting
  • defecation
  • urination
  • ejaculation
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14
Q

innate immunity: biochemical barriers

A

secretions and synthesized materials:

  • tears (antibacterial)
  • gastric juices (pH)
  • mucus (antibacterial)
  • sweat (pH, antibacterial)
  • sebum (antibacterial)
  • earwax (antibacterial)
  • saliva (digestive enzymes)

normal bacterial flora:

  • commensal
  • 1-3% of human body mass
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15
Q

inflammation

A
  • part of the innate immune system
  • responds rapidly, non-specifically, repeatably
  • vascular and cellular responses
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16
Q

inflammation causes the following to occur

A
  • activation of immune system components
  • mast cell degranulation
  • cellular injury
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17
Q

inflammation goals

A
  • limit infection and further damage
  • control bleeding
  • interact with adaptive immune system
  • prepare the area of injury for healing
  • limit and control the inflammatory process
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18
Q

tissue name + “-itis”

A

inflammation of that tissue

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19
Q

systemic manifestations of inflammation

A
  • fever
  • increased pulse
  • increased blood pressure
  • leukocytosis
  • increased plasma synthesis
  • cytokine effects
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20
Q

fever

A

pyrogens (endogenous or exogenous) act on hypothalamus to increase body temp

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21
Q

leukocytosis

A

increasing the number of circulating WBCs

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22
Q

increased plasma protein synthesis

A

complement, coagulation, and kinin cascades; helps w/ scabbing

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23
Q

cytokine effects

A

malaise and lethargy

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24
Q

cardinal signals of inflammation

A
  • calor/heat
  • rubor/redness
  • tumor/swelling
  • dolor/pain
  • functio idesa/loss of function (secondary)
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25
Q

calor/heat

A

blood at body core temp enters site

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26
Q

rubor/redness

A

influx of RBCs to the area

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27
Q

tumor/swelling

A

fluid entering tissues

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28
Q

dolor/pain

A

inflammatory mediators sensitize nerve endings

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29
Q

vascular response

A

deliver fluid to area of injury:

  • contains WBCs and other immune components
  • dilutes bacteria, etc., at injury site
  • provides nutrients and oxygen for immune cells and wound repair
30
Q

vascular response- how?

A

1) brief vasoconstriction
2) mast cells release histamine
3) vasodilation
4) increased capillary permeability
5) exudation (leakage/build up) of fluid and cells (cellular emigration)

31
Q

serous exudate

A

water exudate; indicates early inflammation; common w/ friction like a blister;
ex: central serous chorioretinopathy

32
Q

fibrinous exudate

A

thick, clotted exudate; indicates more advanced inflammation; can lead to dysfunctional wound healing and scarring;
ex: pseudomembrane

33
Q

purulent exudate

A

pus; indicates a bacterial infection;

ex: bacterial conjunctivitis

34
Q

hemorrhagic exudate

A

exudate contains blood; indicates vascular disease;

ex: diabetic retinopathy

35
Q

cellular mediators of inflammation

A
  • mast cells
  • natural killer cells
  • platelets
  • granulocytes (“phils”)
  • monocytes
  • dendritic cells
  • lymphocytes

*all originate in the bone marrow

36
Q

cellular mediators activated by:

A
  • plasma protein system products
  • inflammatory cell secretions
  • microbial molecules
  • debris from cellular destruction
37
Q

pattern recognition receptors (PRRs)

A
  • found on surface of resident and circulating immune cells
  • recognize pathogen-associated molecular patterns (PAMPs)
  • also recognize cellular debris
38
Q

mannose

A

large carbohydrate molecule not found on human cells; found on all bacteria cells - tells us that it is non-self

39
Q

neutrophils, eosinophils, and macrophages emigrate toward source

A

1) margination
2) adherence
3) diapedesis
4) chemotaxis

40
Q

phagocytosis

A
  • opsonization, recognition, and adherence
  • engulfment
  • phagosome formation
  • fusion with lysosomal granules (reactive oxygen species, lactoferrin, defensins, lactic acid)
  • destruction of the target
41
Q

mast cells are the key initiator of ___

A

inflammatory and immune response

42
Q

mast cells are located ____

A

in loose connective tissue in high-risk areas of the body- GI tract, lungs, skin, other mucosal tissues

43
Q

mast cells are sensitive and stimulated by ____

A

multiple stimuli:

  • pathogens
  • allergens
  • physical injury
  • chemical agents
44
Q

mast cell degranulation

A

immediate

45
Q

mast cell degranulation products

A
  • histamine

- chemotactic factors

46
Q

histamine

A
  • vasodilator
  • increased glandular production
  • CNS effects (histamine makes you more alert)
47
Q

chemotactic factors

A
  • chemicals that induce movement
  • neutrophil chemotactic factor
  • eosinophil chemotactic factor of anaphylaxis (ECF-A)
48
Q

mast cell synthesis

A

delayed

49
Q

mast cell synthesis products

A
  • leukotrienes

- prostaglandins

50
Q

leukotrienes

A
  • product of the arachidonic acid cascade

- similar effects to histamine in later stages

51
Q

prostaglandins

A
  • induce pain

- pro- and anti- inflammatory properties

52
Q

mast cells in atopic individuals

A
  • more numerous
  • have a higher number of antigen receptors
  • more easily activated
53
Q

natural killer (NK) cells

A
  • recognize and eliminate virus infected cells and cancer cells
  • release perforin (puts holes in cell membrane) and granzyme (induces apoptosis in damaged/defective cells)
54
Q

platelets

A
  • contribute to clot formation
  • multiple triggers
  • degranulate upon activation
  • contribute to wound healing
  • pro- and anti- inflammatory
55
Q

neutrophils

A
  • aka polymorphonuclear neutrophils (PMNs)
  • early responder in inflammation (within hours)
  • ingest bacteria, dead cells, and cellular debris
  • dysfunction increases risk of bacterial infection
56
Q

eosinophils

A
  • mildly phagocytic
  • defend against parasites
  • implicated in allergies and asthma
  • regulate vascular mediators (vasodilation)
57
Q

monocytes/macrophages

A
  • monocytes produced in the bone marrow and are in the blood; once they leave the blood they mature and replicate which turns them into macrophages
  • mature and replicate at inflammatory site (3-7 days)
  • ingest bacteria and cellular debris
  • contribute to activation of adaptive immune system
  • initiate wound healing
58
Q

termination of inflammation

A
  • removal of an offending agent usually ends response

- checks exist to control course of inflammation

59
Q

checks exist to control course of inflammation:

A
  • neutrophil life span is short
  • inflammatory mediators degrade rapidly
  • anti-inflammatory cytokines
60
Q

outcomes of acute inflammation

A

1) complete resolution
2) scarring
3) abscess formation
4) progression to chronic inflammation

61
Q

complete resolution

A

structure and function recoverable; back to normal

62
Q

scarring

A

substantial damage to connective tissue

63
Q

abscess formation

A

pus confined in a closed space; active proteases produce fluid increasing osmotic pressure; usually have to drain

64
Q

progression to chronic inflammation

A

body cannot remove offending agent; persistent bacteria/toxins or autoimmune diseases

65
Q

chronic inflammation

A
  • inflammation lasting 2 weeks or longer

- often related to an unsuccessful acute inflammatory response

66
Q

causes of chronic inflammation

A
  • high lipid and wax content of microorganism
  • ability to survive inside the macrophage
  • toxins
  • chemicals
  • particulate matter
  • physical irritants
67
Q

with chronic inflammation, there is dense infiltration of ___

A

lymphocytes and macrophages

68
Q

with chronic inflammation, there is fibrosis, which is ___

A

thickening and scarring of connective tissue

69
Q

with chronic inflammation, there is angiogenesis, which is ____

A

production of new blood vessels (VEGF)

70
Q

with chronic inflammation, there is granuloma formation, which is ____

A

walling off of offending agent

Basic Pathology (21 decks)

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