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Microbiology BDS1 > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

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1
Q

what is acute inflammation?

A

quickly developing response of living tissue to infection/damage, initiation for innate immunity

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2
Q

what are the three main processes involved in acute inflammation?

A

vascular dilation, increased vascular permeability, neutrophil activation and migration

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3
Q

how long does acute inflammation last for?

A

few hours to days

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4
Q

what are the four main causes of acute inflammation?

A

microbial infection, physical agents, irritant and corrosive chemicals, tissue necrosis

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5
Q

what does microbial inflammation result from?

A

microbial recognition

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6
Q

what are the physical agents of acute inflammation?

A

physical trauma, UV radiation, heat, cold

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7
Q

what are the irritant and corrosive chemicals that cause acute inflammation?

A

acids, alkali, oxidising agents, microbial virulence factors

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8
Q

what causes tissue necrosis?

A

lack of oxygen or nutrients, inadequate blood flow

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9
Q

what are the cardinal signs of inflammation?

A

redness, heat, swelling, pain and loss of function

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10
Q

how does an inflamed area redden?

A

dilation of small blood vessels

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11
Q

how does an inflamed area have heat?

A

increased blood flow

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12
Q

how does swelling occur in acute inflammation

A

accumulation of fluid in extra vascular space (oedema)

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13
Q

how does pain occur in inflammation

A

stretching/distortion of tissues due to oedema, chemical mediators induce pain

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14
Q

give an acute inflammation

A

gingivitis

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15
Q

what are the 4(5) steps of inflammation?

A

initiation, progression, amplification, resolution, no resolution?

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16
Q

what is the initiation stage of gingivitis?

A

microbes in dental plaque recognised by gingival epithelial cells via pattern recognition receptors

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17
Q

what is the progression stage of gingivitis

A

containment of microbes by innate immune cells and antimicrobial compounds (AMPs and secretory IgA)

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18
Q

what is the amplification stage of gingivitis

A

recruitment and activation of innate immune cells via chemokine/cytokine activity and vascular dilation

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19
Q

what is the resolution stage of gingivitis?

A

healing and repair

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20
Q

what happens if there is no resolution in gingivitis

A

periodontitis

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21
Q

what are the steps of the amplification stage of inflammation?

A

bacteria trigger macrophages to release cytokines and chemokines - vasodilation and increased vascular permeability cause redness, heat and swelling - inflammatory cells migrate into tissue, releasing inflammatory mediators that cause pain

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22
Q

what are the vascular responses to inflammation?

A

small blood vessels adjacent to site of damage become dilated, endothelial cells swell and retract, exudation, endothelial cells activated to promote immune cells passage to damaged tissues

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23
Q

what does retraction of endothelial cells result in?

A

migration of neutrophils and monocytes/macrophages to damaged tissues

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24
Q

what does exudation mean?

A

the vessels become leaky and allow passage of water, salts and some proteins

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25
Q

what is oedema?

A

defined as an excess of watery fluid collecting in the cavities or tissues of the body, increased blood and lymph flow

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26
Q

what does inflammatory exudate provide to tissues?

A

fluids and salts, glucose and oxygen, complement proteins and antibodies, fibrin

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27
Q

what does increased lymph flow allow?

A

increased influx of inflammatory infiltrate

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28
Q

what are the different types of mediators

A

chemical or protein

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29
Q

what are the main types of chemical mediators?

A

HISTAMINE, BRADYKININ, PROSTAGLANDINS, leukotrienes and serotonin

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30
Q

what are the protein mediators?

A

cytokines and chemokines

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31
Q

what is histamine?

A

breakdown product of histidine

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32
Q

where is histamine stored?

A

in granules of immune cells such as mast cells

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33
Q

what does degranulation do?

A

release histamine

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34
Q

what is the role of histamine?

A

a neurotransmitter causing itching

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35
Q

what does histamine cause?

A

vascular dilation

36
Q

what are prostaglandins produced by?

A

macrophages and neutrophils (with leukotreines)

37
Q

what is a prostaglandin

A

the product of fatty acid metabolism

38
Q

what is the most abundant prostaglandin?

A

prostaglandin E2 (PGE2)

39
Q

what do prostaglandins cause?

A

vascular dilation

40
Q

what are the roles of prostaglandins in acute inflammation

A

regulate cytokine production, regulate cell recruitment, act on nerve fibres causing pain, involved in tissue remodelling

41
Q

what are prostagandins released from cells in response to?

A

numerous stimuli

42
Q

what are prostaglandins regulated by?

A

cyclo-oxygenase II (COX II)

43
Q

how is cyclo-oxygenase II (COX II) activated?

A

through the stimulation of cells by TLR activation

44
Q

what type of mediators regulate blood vessel changes?

A

protein and chemical mediators (histamine and prostaglandins)

45
Q

what do inflammation processes function to do?

A

provide tissue with necessary tools to eliminate inciting cause and repair any damage

46
Q

what type of cascade are all the four systems of plasma factors?

A

proteolytic cascades, stepwise activation involving formation of enzyme complexes and protein cleavage

47
Q

what are the four enzymatic cascades of plasma factors?

A

complement, the kinin system, the fibrinolytic system, coagulation

48
Q

what is the common activator of the kinin, fibrinolytic and coagulation systems?

A

Hageman factor (coagulation factor 12)

49
Q

how are the four plasma systems interconnected

A

all activated by the same factor, kinin system produce kinins and fibrinolytic systems produce plasmin which both activate the complement systems, plasmin from fibrinolytic system degrades fibrin produced by the coagulation system

50
Q

what is the initiating factor of the classical pathway of complement?

A

antibody attached to microbe

51
Q

what are the 3 pathways of complement?

A

classical, alternative, mannose binding lectin pathway

52
Q

what is the initiating factor of the alternative pathway of complement?

A

microbial cell wall

53
Q

what is the initiating factor of the mannose binding lectin pathway of complement?

A

carbohydrates on pathogen surface

54
Q

what generates kallikrein?

A

the hageman factor

55
Q

how do neutrophils contribute to the kinin-kallikrein system?

A

release kallikreins

56
Q

what does kallikrein do?

A

converts kininogens to kinins (e.g. bradykinin)

57
Q

what are the functions of kinins e.g. bradykinin

A

stimulate complement system, promote localised vasodilation and increased capillary permeability, activate pain receptors, act as chemotaxins

58
Q

what are the three pathways of the coagulation system?

A

intrinsic, extrinsic and common

59
Q

what is the intrinsic pathway of the coagulation system?

A

activated when blood comes into contact with sub-endothelial connective tissues

60
Q

what is the extrinsic pathway of the coagulation system?

A

damaged blood vessel means Human Factor 7 leaves vessel and encounters tissue factor in surrounding tissue

61
Q

what is the common pathway of the coagulation system?

A

production of thrombin which in turn produces fibrin (clot formation)

62
Q

what does the kinin system produce?

A

kinins

63
Q

what does the coagulation produce?

A

fibrin

64
Q

what does the fibrinolytic system produce?

A

plasmin

65
Q

what is the main constituent of clotting?

A

fibrin

66
Q

what does the fibrinolytic system do?

A

involved in the breakdown of clots, prevents clotting, activates complement and indirect role as fibrin degradation products promote vascular permeability

67
Q

what do fibrin degradation products do?

A

promote vascular permeability

68
Q

what is haemostasis?

A

the balance between the coagulation and fibrinolytic system

69
Q

what does haemostasis essentially mean?

A

to stop the flow of blood

70
Q

name some congenital coagulation disorders

A

von willebrand disease, haemophilia A and B

71
Q

what drugs cause acquired coagulation disorders?

A

warfarin and heparin

72
Q

summarise complement

A

three pathways - leads to membrane attack complex formation and anaphylatoxin production

73
Q

summarise the kinin system

A

plasma proteins/enzymes that lead to production of bradykinins

74
Q

summarise coagulation

A

three pathways - formation of a stable blood clot (fibrin)

75
Q

summarise the fibrinolytic system

A

plasmin prevents excessive clotting of blood by degrading fibrin

76
Q

what is disease resolution dependent on?

A

tissue involved, amount of tissue destruction, nature of the harmful agent

77
Q

what is abscess formation (suppuration) an outcome of?

A

acute inflammation

78
Q

what is suppuration?

A

the formation of pus usually arising from an infection with pyogenic bacteria

79
Q

what is pus

A

bacteria with dead and dying neutrophils

80
Q

what surrounds pus once it accumulates?

A

a pyogenic membrane

81
Q

what are the 3 types of dental abscesses?

A

gingival, periodontal and periapical

82
Q

what is a gingival abscess?

A

an abscess formed due to infection or trauma to the surface of gum tissue

83
Q

what is a periodontal abscess?

A

abscess formed due to infection that has moved deeper into the gum areas. this is sometimes called a gum boil

84
Q

what is a periapical abscess?

A

an abscess of a tooth due to infection of the pulp

85
Q

what does the resolution of acute inflammation require?

A

minimal cell death and tissue damage, occurrence in tissues with regenerative capacity, rapid elimination of causative agent, rapid removal of fluid and debris by vascular/lymphatic drainage

86
Q

what is the most common outcome of acute inflammation?

A

resolution

Microbiology BDS1 (20 decks)

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