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intro to biomedical sciences IBMS > acute and chronic inflammation part 1 > Flashcards

acute and chronic inflammation part 1 Flashcards

A broad understanding of inflammation in terms of historical discovery and identification, functions and context within the body, types of inflammation, contributing components. The mechanisms of acute inflammation.

1
Q

what is inflammation

A

is a protective response to tissue insult or injury aimed at eliminating the cause of injury, remove damaged celled and initiate repair

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2
Q

what are the 5 carinal signs of inflammation

A 
calor/warmth
rubor/ redness/ erythema  
tumor/ swelling/ oedema 
dolor/ pain
functino laesa/ lack of function
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3
Q

what did john hunter propose

A

that inflammation wasn’t a disease but a response to tissue injury

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4
Q

when did john hunter propose this idea

A

late 18th century

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5
Q

who introduced the idea of functino laesa

A

ruodolf virchow- the father of pathology

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6
Q

which cells are involved in an inflammatory response

A

Circulating plasma proteins and cells of the immune system.
Vasculature and it’s endothelium
Liver production of proteins of complement, clotting and acute phase.

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7
Q

what are souces of mediators

A

nitric acid
histamines
cytokines

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8
Q

what do PMN leukocytes do

A

elimination of microbes and dead tissue

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9
Q

what do extra cellular proteins matrix do

A

repair

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10
Q

when is an inflammatory reaction triggered

A

induced by chemical mediators that are produced by host cells in response to injurious stimuli

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11
Q

what are the steps for an inflammatory response

A 
RECOGNITION- of injurious 
RECUIRTMENT- of leukocyte
REMOVAL- of the agent causing the injury
REGULATION- of the response
RESOLUTION- of the response and repair
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12
Q

examples of the injurious stimuli which can trigger inflammatory reactions

A

infectious agents- bacteria, yeast, virus
foreign bodies
immune reactions eg immune complex like antigen- antibody complex
physical
irration
thermal injury

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13
Q

what do we call the immune complex if it is self

A

auto immune complex

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14
Q

what can happen if the noxious stimulus cannot be removed and or the acute inflammatory response is not resolved

A

can lead to state of chronic inflammation

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15
Q

when can inflammation cause damage

A

Very strong inflammatory reaction (e.g. severe infection).
Prolonged reaction (agent resists eradication)
Response is inappropriate (e.g.self or harmless environmental antigen)

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16
Q

what does thermal injury lead to sometimes

A

tissue necrosis

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17
Q

what is the onset of acute inflammation

A

fast min hours

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18
Q

what is the duration of acute inflammation

A

short few mins- few days

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19
Q

what are the infiltrating cells in acute inflammation

A

PMNS and macrophage

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20
Q

what type of injury is caused in acute

A

self limiting

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21
Q

what are the local systemic signs of acute inflmmation

A

prominent

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22
Q

what is the onset of chronic inflammation

A

slow, days

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23
Q

what is the duration of chronic inflammation

A

variable

possible months and years

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24
Q

what are the infiltrating cells in chronic inflammation

A

macrophage and lymphocyte due to the fact adaptive immune system to contribute

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25
Q

what type of injury is caused in chronic

A

severe gets progressively worse

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26
Q

what might differ between acute and chronic inflammation macrophages

A

might be activated differently and might be activated differently

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27
Q

what is the local and systemic signs of chronic

A

less prominent can be subtle

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28
Q

what are the two major groups of activities in acute inflammation

A

vascular changes

cellular events

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29
Q

what does acute inflammation do

A

delivers leukocytes and plasma proteins to the injury site

leukocytes clean infection and dead cells

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30
Q

what is included in vascular changes

A

vasodilation
vascular permeability
endothelial cell activity

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31
Q

what is included in cellular events

A

leukocyte recruitment

activation og leukocyte infiltrating tissue

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32
Q

describe recognition of injurious stimulus

A

Phagocytes, Dentritic Cs and epithelial cells express PRR (Pattern Recognition Receptors) to recognise and bind to distinct molecular patterns not seen in healthy vertebrate cells.

33
Q

describe the pathway of initiation of inflammation with macrophages

A

engulf invading pathogens which triggers them to release pro inflammatory cytokines

34
Q

give examples of pro inflammatory cytokines

A

TNF-α, IL-1β, IL-6) and chemokine (CXCL8 aka IL-8

35
Q

what is a cytokine

A

secreted in response to a stimulus, affect the behaviour of cells (autocrine, paracrine, endocrine)

36
Q

what is a chemokine

A

a chemoattractant protein that stimulates the migration of cells (phagocytes and lymphocytes).

37
Q

describe mast cells

A

located close to body surfaces
release of preformed histamine from granules
anti-parasitic activity and key player in allergic response
express receptor for IgE coated with IgE they are triggered to degranulate when this IgE binds to its ligand

38
Q

describe epithelial cells

A

cells that line our mucosal surfaces
express PRR
maintain homeostasis with commensal bacteria but can respond to pathogens initiating inflammatory responses

39
Q

what do epithelial cells secrete

A

CXCL-8, TNF-α , IL-1β, IL-18 and antimicrobial peptides.

40
Q

what are the different types of cytokine

A

autocrine
paracrine
endocrine

41
Q

what is an autocrine cytokine

A

the cytokine acts back on the one that secretes it

42
Q

what is paracrine cytokine

A

acts on a different cell that one that secreted

43
Q

what is a endocrine cytocine

A

has to enter the blood stream and travel to a different site

44
Q

what type of structures are toll like receptors

A

heterodimeric

homodimeric

45
Q

where are TLR found

A

span the plasma membrane and allow extracellular recognition

or inside the cell and allow for endosomal recognition

46
Q

what does TLR3 detect

A

double stranded RNA- can be involved in viral replication

47
Q

what does TLR7 detect

A

single stranded RNA- not found usually in the endosomnal space

48
Q

what does TLR 9 detect

A

cpG DNA- recognises unmethlyated CpG DNA

49
Q

which TLR are found in the endosomal space

A

TLR3, TLR7, TLR9

50
Q

which TLR are found on the plasma membrane

A

TLR2, TLR6, TLR, 1,TLR5, TLR4,

51
Q

which receptors come together to detect diacyl lipopeptides

A

TLR2, TLR6

52
Q

which TLR come together tot detect triacyl lipopeptides

A

tlr2, tlr1

53
Q

what do TLR2, TLR6 complex detect

A

diacyl lipopeptides

54
Q

what do TLR2, TLR1 complex detect

A

triacyl lipopeptides

55
Q

what does TLR5 detect

A

flagellin

56
Q

what does TLR4 detect

A

LPS

57
Q

what type of receptors provide cytosolic recognition

A

RIG-I and NOD like receptors

58
Q

what does RIG-I bind to

A

viral RNA- unmodified 5 prime

59
Q

what does NLR bind to

A

bacterial lipids eg peptidoglycan

60
Q

how does RIG-I differentiate between viral RNA and self RNA

A

unmodified 5 prime triphosphate on the viral RNA different to messenger RNA

61
Q

What does the NLRP3 inflammasome detect

A

dead cell components( extracellular ATP uric acid)

crystals- uric and gout and some pathogenic bacterial components

62
Q

what is the pathway of the NLRP3

A

forms the NLRP3 inflammasome in the cytoplasm —-> joins on with caspase 1 present in proform ——> activates caspase 1 ——-> zymogen cascade—-> cleaves and activates IL1 beta

63
Q

what are the three stages of recruitment of leukocytes

A

vasodilation
vascular permeability
endothelial cell activation

64
Q

what does vasodilation include

A

widening of blood vessel calibre increases blood flow

leads to erythema and heat

65
Q

what does vascular permeability include

A

permits the extravasation of plasma fluid and proteins to exit and enter the tissues - oedema

66
Q

what does endothelial cell activation include

A

changes to luminal vessel surfaces and reduced blood flow and reduced blood flow speed to allow leukocytes to pass through the endothelial layer, gaming entry to tissues

67
Q

what does vasodilation lead to clinically

A

erythema and heat

68
Q

what does vascular permeability lead to clinically

A

oedema

69
Q

what does endothelial cell contraction can be induced by

A

cytokines IL-1 (interleukin 1) and TNF (tumour necrosis factor)
Histamine and kinins

70
Q

what does damage to the endothelium lead to

A

necrosis of cells due to a burn, UV, toxins, leukocytes induced damage

71
Q

what is margination aided by

A

vessel dilation and reduced blood flow

72
Q

what is margination

A

WBC found at the periphery of the vessel whereas RBC are located in the middle of the vessel

73
Q

what is the rolling stage

A

pro inflammatory cytokines/ histamine will activate endothelial cells—-> express adhesion molecules(selectins) on luminal surfaces

74
Q

what is stable adhesion

A

interactions between integrins (leukocytes) and cell adhesion molecules (endothelium). WBC stops rolling and adheres to the vessel wall

75
Q

what are the stages of recruitment of leukocytes

A 
margination 
rolling 
stable adhesion 
transmigration 
chemotaxis
76
Q

what is transmigration/ (diapedesis)

A

leukocytes squeeze through intercellular endothelial junctions

77
Q

what is chemotaxis

A

movement along a chemical gradient (cytokines/ chemokines, C5a, Arachadonic acid metabolites, bacterial products)

78
Q

what do plasma proteins do

A

mediators of inflammation and clotting factors

intro to biomedical sciences IBMS (35 decks)

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