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Yr 2 - IBMS > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What is Inflammation?

A

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

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2
Q

How can Inflammation Damage Healthy Tissue?

A

strong inflammatory reaction, prolonged reaction, when response is inappropriate

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3
Q

5 SIGNS OF INFLAMMATION (CDFRT) - call doctor for reaction time

A

Calor - heat
Dolor - pain
Function Laesa - loss of fucntion
Rubor - redness/erythema
Tumor - swelling/oedema

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4
Q

What are the 5 R’s

A

Recognition of Injurious Stimulus
Recruitment of Leukocytes
Removal of Agent causing Injury
Regulation of Response
Resolution of Response and Repair

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5
Q

PRR

How is injurious Stimulus Recognised? (Recognition)

A

phagocytes, dendritic cells, epithelial cells express PRR

  • recognise and bind to specific molecular patterns
  • fast response

the specificity of the PRR’s are genome encoded

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6
Q

John Hunter (1800’s) said inflammation is not a disease, but a response to tissue damage

A
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7
Q

How does Circulatory Plasma Proteins and Vasculature have a part in Inflammatory Response? (Recognition)

A

CPP = clotting systems, complement, cells of immune system

V = blood system and its endothelium

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8
Q

What can a LOT of tissue trauma lead to?

A

Necrosis, Apoptosis, Ischemia, Chemical Insults

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9
Q

What is Tissue Necrosis?

A

Loss of membrane integrity and release of cellular content into extracellular space

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10
Q

How can Inflammation be Triggered? (4)

A

Infectious agents
foreign bodies
immune reactions
trauma - physical, thermal, irradiation

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11
Q

What is Cell Apoptosis, how does it Happen?

A

programmed cell death

= DNA is packaged and content released into membrane bound parcels and then engulfed by phagocytes
- induced by nK cells and cytotoxic T cells

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12
Q

What is Ischemia?

A

loss of oxygen - leads to necrotic cell death

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13
Q

What happens if the Stimulus isn’t Removed? Or if Acute Response Cannot be Resolved.

A

the injury persists
chronic inflammation

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14
Q

Two Types of Inflammation

A

Acute and Chronic

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15
Q

Describe Acute Inflammation. Onset, Duration, Infiltrating Cells, Injury and Local/Systemic Signs

A

Onset - quick
Duration - short
Infiltrating Cells - PMNS and macrophages
Injury = mild and self-limiting
Local/Systemic Signs = clear and prominent

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16
Q

Describe Chronic Inflammation. Onset, Duration, Infiltrating Cells, Injury and Local/Systemic Signs

A

Onset - slow
Duration - months-years
Infiltrating Cells = macrophage and lymphocytes
Injury = Severe and gets worse
Local/Systemic Signs - subtle and less prominent

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17
Q

What are the Vascular Changes? (Recognition)

A

Vasodilation, Permeability, Endothelial Cell Activation

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18
Q

What are the Cellular Events? (Recognition)

A

Leukocyte recruitment of PMN’s
Leukocytes infiltrate tissues

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19
Q

What is the Most Important PRR and Where is it Found?

What Structures can they be?

A

TLR - Toll Like Receptors
on extracellular surfaces or facing inwards on endosome

Heterodimeric or Homodimeric

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20
Q

TLR-1,2,4,5,6 are on Extracellular Surfaces, What are their Functions? (Recognition)

A

TLR-1 - hetero - recognise triacyl lipopeptides
TLR-2 - hetero - recognise di/triacyl lipopeptides and lipopolysaccharide
TL-4 - recognise lipopolysaccharide
TLR-5 - recognise flagellin
TLR-6 - hetero - recongise diacyl lipopeptides

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21
Q

TLR-3,7,9 are on Endosomal Surfaces, What are their Functions? (Recognition)

A

3 - detect double stranded RNA
7 - detect single stranded RNA
9 - bind to unmethylated CpG DNA (cytosine-guanine nucleotide)

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22
Q

What are Lectin Like Receptors? (Recognition)

A

a type of PRR
- binds to pathogen derived sugars

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23
Q

What is the Cytosol?

A

the matrix of the cytoplasm

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24
Q

What is a NLR and it’s function? (Recognition)

A

Nod-Like Receptor

recognises lipids, bacterial peptiglycans and components of dead cells

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25
Q

What is a RIG-I and it’s Function? (Recognition)

A

Retonoic Acid-Inducible Gene I

recognise the 5-triphosphate from viral RNA in the cytoplasm
- eukaryotic gets modified so it doesn’t get recognised

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26
Q

What is a NLRP3 inflammasome? (Recognition)

A

recognises dead cell components, crystal and some pathogenic bacterial components by activating zymogen form of caspase form

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27
Q

What does Caspase do when Activated? (Recognition)

A

activates a protease
cuts, cleaves and activates precursor form of IL-1-beta
this is secreted = acute inflammation

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28
Q

What are the Key Cells of Recognition? (8) TLRLMNNN

A

PMNS, macrophages, lymphocytes, TLR, Lectin Like Receptors, NLR, RIG-I and NLRP3 Inflammasome

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29
Q

What is Vasodilation? (5)

A

widening of blood vessels
more blood flow
less pressure
less speed
area = warm and red

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30
Q

What Happens with Vascular Permeability?

A
  • Endothelium is leaky and gaps between cells increase
  • plasma fluid and proteins enter and leave tissues
    area = swollen, oedema
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31
Q

What Fluid leaves the Cells when there is Vascular Permeability? What is the Function of this Fluid?

A

Serum Exudate - GCF is an exudate

  • to deliver components to the necessary site
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32
Q

What is Endothelial Cell Activation? (5)

A
  • selectin (adhesion molecules) receptors are expressed on cell surface
  • leukocytes with wbc bind via their ligand - (sialyl-lewis-x-modified glycoprotein) to receptor
    = white blood cells bind to inside of tissue wall
  • leukocytes pass through endothelial layer
  • enter tissues
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33
Q

How is Vascular Dilation induced?

A

by cytokines IL-1, TNF, Histamines and Kinins

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34
Q

STEPS OF RECRUITING LEUKOCYTES (5)

A
  • margination
  • rolling
  • stable adhesion
  • transmigration
  • chemotaxis
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35
Q

How does Margination work? (Recruiting Leukocytes)

A
  • vasodilation
  • slower blood flow
  • WBC accumulate on periphery of inside of vessels
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36
Q

What Travels Faster in the Blood Vessels, WBC or RBC?

A

RBC - they are smaller

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37
Q

What is Rolling? (Recruiting Leukocytes) (5)

A
  • pro-inflam cytokines and histamine activate endothelial cells close to site of inflammation
  • adhesion molecules selectins
  • interact with molecule on WBC = sialyl-lewis x-modified glycoprotein
    = weak interactions
  • repeatedly broken and remade as leukocyte rolls along blood vessel wall
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38
Q

What is Stable Adhesion (Recruiting Leukocytes) (4) What Molecule Helps the Leukocyte pass through?

A
  • when leukocytes are activated, there are changes in the integrins
    = the change = higher affinity binding site to cell adhesion molecules
  • cell stop rolling and come to a stop
  • PECAM-1 helps leukocyte pass through vascular endothelial layer
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39
Q

What is Transmigration? (Recruiting Leukocytes)

A
  • leukocytes secrete enzymes e.g. collagenases
  • create hole in basement membrane
  • enzyme passes through
  • exit blood vessel
  • enter tissue
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40
Q

What is Chemotaxis? (Recruiting Leukocytes)

A

leukocyte follows chemical gradient

41
Q

What is Arachidonic Acid?

A

intracellular pro-inflammatory mediators with a short half-life

42
Q

What can Arachidonic Acid be Metabolised into? (2)

A

cylooxygenase and 5-lipoxygenase

43
Q

Cycloxygenase is metabolised from Arachidonic Acid, What can it Create? (2)

A

prostaglandins and thromboxane

44
Q

What are Prostaglandins made from and their function? (3)

A

made from cycloxygenase

  • increase sensitivity to pain
  • clotting
45
Q

What Medicines are Prostaglandins inhibited by? (3)

A

aspirin, ibuprofen and neproxin

46
Q

5-Lipooxygenase is Metabolised from Arachidonic Acid, What can it Create?

A

Leukotrienes and Lypoxins

47
Q

Leukotrienes is made from 5-Lipooxygenase, What is its Function?

A

Chemoxtaxis and Vascular Permeability

48
Q

How do you Remove the Agent Causing Injury? (4)

A
  • Phagocytosis
  • Secrete Microbial Substances into Extracellular Space
  • Pro-Inflam Cytokines
  • Release Extracellular Traps
49
Q

What are the steps of Phagocytosis? (Removal) (7)

A
  • Recognition by phagocytic receptor
  • Engulf pathogen and other inflam materials
  • plasma membrane invaginate
  • Fuse with lysosome
  • in the same vesicular space
  • degradation
  • respiratory burst
50
Q

Recognition from Phagocytosis may also be via Opsonins, What are these? (Removal)

A

complement components such as antibodies
- increase the efficiency of recognition

51
Q

What Cells Partake in Phagocytosis? (Removal)

A

macrophage, neutrophils and dendritic cells

52
Q

What is Respiratory Burst in Phagocytosis? (Removal)

A

the rapid production of reactive oxygen species

53
Q

How does Respiratory Burst Work during Phagocytosis? (3)

A
  • NADPH converted into O2 by phagocyte oxidase
  • oxygen into hydrogen peroxide or hyperchlorid by MPO myeloperoxidase
  • super oxide + nitric oxide = peroxynitrite
54
Q

What is the Effect of Respiratory Burst? (Removal)

A

toxic products - cause damage to DNA, membranes and proteins

55
Q

What Microbicidal Substances are released into the Extracellular Space? (Removal) (7)

A

Antimicrobial peptides, reactive oxygen, nitrogen species, lysosomal enzymes, chemokine, cytokines, NETosis

56
Q

The Function of Microbicidal Substances (Removal) one side effect also.

A

Toxic to kill and destroy pathogens but can cause bystander damage to host cells

57
Q

What do Neutrophils contain that cause Damage? (Removal)

A

azurophilic granules store microbicidal substances
- blue in colour

58
Q

How can Neutrophils cause Damage? (Removal)

A

azurophilic granules store microbicidal substances
- blue in colour

59
Q

What are the Neutrophilic Enzymes? (3) (Removal)

A

neutrophil elastase, proteinase 3, cathepsin g

= Proteolytic enzymes to engulf materials

60
Q

Function of Pro-Inflam Cytokines. (Removal)

A

amplify the response

61
Q

Define NETosis (Removal)

A

the release of extracellular traps by neutrophils

62
Q

What is the Function of Netosis? (Removal)

A

bind debris, clear up and get rid of pathogen

63
Q

What are the ‘nets’ made from in Netosis? (Removal)

A

dense net of fibres made up of nucleosomal DNA and histone proteins attached to microbicidal molecules

  • contain high concentration of LL37 and Proteinase 3
64
Q

How are NET’s formed? (Removal) (4)

A
  • neutrophil decondenses chromatin
  • nuclear envelope integrity is lost
  • DNA unwound and uncoiled
  • DNA escapes nucleus using PAD4 and content of granules mix (microbicidal substances)
65
Q

For DNA to escape the nucleus during NETosis, PAD4 is necessary, what is this and its function? (Removal)

A

peptidyl arginine deaminase 4

converts arginine and methyl arginine amino acids in the histone proteins into citrulline amino acid

= positive into neutral electrostatic charge

66
Q

Orally, where can large quantities of NET’s be found? (Removal)

A

in the gingival crevicular fluid of periodontitis

67
Q

What are the 2 Key Regulators of the Regulation of the Response?

A

Chemical Mediators
Chemokines

68
Q

What are the Chemical Mediators used in Regulation?

A

Arachidonic Metabolites
Complement Proteins
Coagulation Protiens
Cytokines and Chemokines
Lysosomal Enzymes
Lysosomal Enzymes
NO
ROS
Kinins
Vasoactive Amines

68
Q

What are the Chemical Mediators used in Regulation? (10)

A

Arachidonic Metabolites
Complement Proteins
ROS
Lysosomal Enzymes
Coagulation Proteins
NO
Kinins
Cytokines and Chemokines
Vasoactive Amines

69
Q

Examples and Function of Vasoactive Amines - Chemical Mediator (2) (2) (Regulation)

A
  • Histamines and Seratonins
  • vasodilation and vascular permeability
70
Q

Examples and Function of Arachidonic Metabolites - Chemical Mediator (2) (2) (Regulation)

A
  • Prostaglandins and Leukotrienes
  • Vascular reactions and chemotaxis
71
Q

Examples and Functions of Cytokines and Chemokines - Chemical Mediators (4, 2) (1,2) (Regulation)

A
  • TNF, IL1, IL6, CXCL8
  • leukocyte recruitment and endothelial activation
  • Hepatocytes
  • active liver cells that stimulate synthesis of acute phase proteins
72
Q

Examples and Function of Lysosomal Enzymes - Chemical Mediator (4) (2) (Regulation)

A
  • Neutrophil Elastase, Proteinase 3, Collagenase, Cathepsin C
  • microbicidal and tissue injury
73
Q

Function of NO and ROS - Chemical Mediator (3) (Regulation)

A

(nitrous oxide and reactive oxygen species)
- vasodilation, microbicidal, tissue injury

74
Q

Function of Complement Proteins - Chemical Mediator (3) (Regulation)

A

Leukocyte chemotaxis, oponisation, MAC

75
Q

Function of Coagulation Proteins - Chemical Mediator (3) (Regulation)

A

Triggered by F7

  • endothelial activation
  • leukocyte recruitment
76
Q

Function of Kinins - Chemical Mediator (2,2) (Regulation)

A

Protelytic cleavage - activate precursor
Vascular Reactions and Pain

77
Q

What are Cytokines also called? (Regulation)

A

Endogenous Pyrogens - made in the body to raise temp

78
Q

What Chemokines are Present in the Liver? (4) (Regulation)

A

Serum Amyloid Protein
Fibrinogen
C-reactive protein
Mannose Binding Lectin

79
Q

What does C-reactive protein do in the liver? (Regulation) (4)

A

a pentraxin - class of PRR that acts an opsonin

  • activates classical complement pathway
  • C1 interacts with pathogen surface = C3 Convertase
  • levels increase with infection
  • used as a marker as it binds directly to bacterial and fungal surfaces
80
Q

What does MBL do in the Liver? (Regulation)

A

Peforms opsonin activation, complement activation and lectin pathway

  • binds carb to lectin = C3 Convertase
81
Q

What is the Function of Chemokines in other parts of the body: liver, bone marrow, hypothalamus, fat muscle cells, dendritic cells

A

Liver
- Serum Amyloid Protein
- Fibrinogen
- C-Reactive Protein = acts as an opsonin and activates classical complement pathway, used as a marker if someone has infection
- MBL - opsonin activation, complement activation and lectin pathway

Bone Marrow Epithelium
- Leucocytosis = increase production and release of neutrophils into bloodstream

Hypothalamus
- increase body temp and antigen processing
- decrease viral and bacterial replication
- increase specific immune response

Fat Muscle Cells
- mobilise protein and energy cells

Dendritic Cells
- TNF-a stimulates migration to lymph nodes and maturation

82
Q

How was Resolution of Response Previously Understood to How it is Now?

A

if signal is removed, duration of response will stop BUT resolution is active and an regulated process

83
Q

What molecules are needed in Resolution?

A
  • immunoresolvants

IL-10
Maresins
Protectins
Resolvins
- inhibit leukocyte infiltration
Lipoxins
- inhibit neutrophil adhesion and chemotaxis to endothelial surfaces
= less recruitment
= prevent continuation of inflam response

84
Q

After Resolution, Homeostasis can be Returned. Describe Homeostasis.

A
  • few infiltrating homeostasis
  • cells maintain health and remove debris
85
Q

What Molecules are No Longer Needed During Resolution?

A

pro-inflam cytokines and chemokines
histamines
prostaglandins
leukotrienes
thromboxanes

86
Q

Define Chronic Inflammation

A

A prolonged duration of the inflammatory response, when regulation and resolution fail.

87
Q

What is the Dominant Cell of Chronic Inflammation?

A

Macrophages
- can be pro or anti inflammatory

88
Q

In Chronic Inflam, Describe the Pro-Inflam Macrophage (5)

A

Classically Activated Macrophage

  • macrophage activated by the cytokins interferon gamma signal produced from the TH1 T-Helper Cell
  • Phagocytosis
  • Secretion of lysosomal enzymes
  • Secrete pro-inflam cytokines
    TNF, IL-1, IL-2, IL-6, IL-23
  • presents antigen to T cells
    = repeats
89
Q

In Chronic Inflam, Describe the Anti-Inflam Macrophage.

A

Alternatively Activated Macrophage

  • macrophage activated from signals from IL-4 or IL-13 from TH2 cells
  • promote repair and anti-inflamm
  • release IL-10 and TGF-β
90
Q

What is the Effect of Chronic Inflammation?

A
  • tissue injury
  • fibrosis - fibroblasts new connective tissue
  • angiogenesis - new blood vessels
91
Q

What is the Effect of New Tissue During Chronic Inflammation?

A

non-specialised

the function of the tissue can be lost and lead to further damage

92
Q

Describe Characteristics of Chronic Inflam.

A
  • Mononuclear Cells Inflitrate
  • Tissue Destruction
  • Granulomatous Tissue
  • Fibrosis
93
Q

What Oral Infection can have Both Acute and Chronic Inflammation?

A

Dental Abscess

  • chronic as fibrous tissue and monocytes cells surround the walls but it is a neutrophil dominated response, making it acute
94
Q

Chronic Inflammation can be Present from the Onset with this Disease.

A

Rheumatoid Arthiritis

95
Q

Diseases Linked To Periodontitis - an Inflam Disease

A

Inflammation induced Pregnancy Complication
Atherosclerosis
Diabetes

96
Q

How is Diabetes Linked to Inflammatory Periodontitis?

A
  • raised inflammation activates and increases the expression of proteins suppressing insulin-signalling pathways
  • raised insulin resistance
    = harder to control blood sugar levels

Diabetes can also affect proteins in our tissue and collagen turnover

97
Q

P Gingivalis is a key pathogen, what does it have similar activity to?

A

PAD 4
- an enzyme that functions in NETosis

research to see if generated autoantigens can trigger autoimmunity

Yr 2 - IBMS (21 decks)

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