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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
What is a RIG-I and it's Function? (Recognition)
Retonoic Acid-Inducible Gene I recognise the 5-triphosphate from viral RNA in the cytoplasm - eukaryotic gets modified so it doesn't get recognised
26
What is a NLRP3 inflammasome? (Recognition)
recognises dead cell components, crystal and some pathogenic bacterial components by activating zymogen form of caspase form
27
What does Caspase do when Activated? (Recognition)
activates a protease cuts, cleaves and activates precursor form of IL-1-beta this is secreted = acute inflammation
28
What are the Key Cells of Recognition? (8) TLRLMNNN
PMNS, macrophages, lymphocytes, TLR, Lectin Like Receptors, NLR, RIG-I and NLRP3 Inflammasome
29
What is Vasodilation? (5)
widening of blood vessels more blood flow less pressure less speed area = warm and red
30
What Happens with Vascular Permeability?
- Endothelium is leaky and gaps between cells increase - plasma fluid and proteins enter and leave tissues area = swollen, oedema
31
What Fluid leaves the Cells when there is Vascular Permeability? What is the Function of this Fluid?
Serum Exudate - GCF is an exudate - to deliver components to the necessary site
32
What is Endothelial Cell Activation? (5)
- 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
33
How is Vascular Dilation induced?
by cytokines IL-1, TNF, Histamines and Kinins
34
STEPS OF RECRUITING LEUKOCYTES (5)
- margination - rolling - stable adhesion - transmigration - chemotaxis
35
How does Margination work? (Recruiting Leukocytes)
- vasodilation - slower blood flow - WBC accumulate on periphery of inside of vessels
36
What Travels Faster in the Blood Vessels, WBC or RBC?
RBC - they are smaller
37
What is Rolling? (Recruiting Leukocytes) (5)
- 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
38
What is Stable Adhesion (Recruiting Leukocytes) (4) What Molecule Helps the Leukocyte pass through?
- 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
39
What is Transmigration? (Recruiting Leukocytes)
- leukocytes secrete enzymes e.g. collagenases - create hole in basement membrane - enzyme passes through - exit blood vessel - enter tissue
40
What is Chemotaxis? (Recruiting Leukocytes)
leukocyte follows chemical gradient
41
What is Arachidonic Acid?
intracellular pro-inflammatory mediators with a short half-life
42
What can Arachidonic Acid be Metabolised into? (2)
cylooxygenase and 5-lipoxygenase
43
Cycloxygenase is metabolised from Arachidonic Acid, What can it Create? (2)
prostaglandins and thromboxane
44
What are Prostaglandins made from and their function? (3)
made from cycloxygenase - increase sensitivity to pain - clotting
45
What Medicines are Prostaglandins inhibited by? (3)
aspirin, ibuprofen and neproxin
46
5-Lipooxygenase is Metabolised from Arachidonic Acid, What can it Create?
Leukotrienes and Lypoxins
47
Leukotrienes is made from 5-Lipooxygenase, What is its Function?
Chemoxtaxis and Vascular Permeability
48
How do you Remove the Agent Causing Injury? (4)
- Phagocytosis - Secrete Microbial Substances into Extracellular Space - Pro-Inflam Cytokines - Release Extracellular Traps
49
What are the steps of Phagocytosis? (Removal) (7)
- 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
Recognition from Phagocytosis may also be via Opsonins, What are these? (Removal)
complement components such as antibodies - increase the efficiency of recognition
51
What Cells Partake in Phagocytosis? (Removal)
macrophage, neutrophils and dendritic cells
52
What is Respiratory Burst in Phagocytosis? (Removal)
the rapid production of reactive oxygen species
53
How does Respiratory Burst Work during Phagocytosis? (3)
- NADPH converted into O2 by phagocyte oxidase - oxygen into hydrogen peroxide or hyperchlorid by MPO myeloperoxidase - super oxide + nitric oxide = peroxynitrite
54
What is the Effect of Respiratory Burst? (Removal)
toxic products - cause damage to DNA, membranes and proteins
55
What Microbicidal Substances are released into the Extracellular Space? (Removal) (7)
Antimicrobial peptides, reactive oxygen, nitrogen species, lysosomal enzymes, chemokine, cytokines, NETosis
56
The Function of Microbicidal Substances (Removal) one side effect also.
Toxic to kill and destroy pathogens but can cause bystander damage to host cells
57
What do Neutrophils contain that cause Damage? (Removal)
azurophilic granules store microbicidal substances - blue in colour
58
How can Neutrophils cause Damage? (Removal)
azurophilic granules store microbicidal substances - blue in colour
59
What are the Neutrophilic Enzymes? (3) (Removal)
neutrophil elastase, proteinase 3, cathepsin g = Proteolytic enzymes to engulf materials
60
Function of Pro-Inflam Cytokines. (Removal)
amplify the response
61
Define NETosis (Removal)
the release of extracellular traps by neutrophils
62
What is the Function of Netosis? (Removal)
bind debris, clear up and get rid of pathogen
63
What are the 'nets' made from in Netosis? (Removal)
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
How are NET's formed? (Removal) (4)
- 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
For DNA to escape the nucleus during NETosis, PAD4 is necessary, what is this and its function? (Removal)
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
Orally, where can large quantities of NET's be found? (Removal)
in the gingival crevicular fluid of periodontitis
67
What are the 2 Key Regulators of the Regulation of the Response?
Chemical Mediators Chemokines
68
What are the Chemical Mediators used in Regulation?
Arachidonic Metabolites Complement Proteins Coagulation Protiens Cytokines and Chemokines Lysosomal Enzymes Lysosomal Enzymes NO ROS Kinins Vasoactive Amines
68
What are the Chemical Mediators used in Regulation? (10)
Arachidonic Metabolites Complement Proteins ROS Lysosomal Enzymes Coagulation Proteins NO Kinins Cytokines and Chemokines Vasoactive Amines
69
Examples and Function of Vasoactive Amines - Chemical Mediator (2) (2) (Regulation)
- Histamines and Seratonins - vasodilation and vascular permeability
70
Examples and Function of Arachidonic Metabolites - Chemical Mediator (2) (2) (Regulation)
- Prostaglandins and Leukotrienes - Vascular reactions and chemotaxis
71
Examples and Functions of Cytokines and Chemokines - Chemical Mediators (4, 2) (1,2) (Regulation)
- TNF, IL1, IL6, CXCL8 - leukocyte recruitment and endothelial activation - Hepatocytes - active liver cells that stimulate synthesis of acute phase proteins
72
Examples and Function of Lysosomal Enzymes - Chemical Mediator (4) (2) (Regulation)
- Neutrophil Elastase, Proteinase 3, Collagenase, Cathepsin C - microbicidal and tissue injury
73
Function of NO and ROS - Chemical Mediator (3) (Regulation)
(nitrous oxide and reactive oxygen species) - vasodilation, microbicidal, tissue injury
74
Function of Complement Proteins - Chemical Mediator (3) (Regulation)
Leukocyte chemotaxis, oponisation, MAC
75
Function of Coagulation Proteins - Chemical Mediator (3) (Regulation)
Triggered by F7 - endothelial activation - leukocyte recruitment
76
Function of Kinins - Chemical Mediator (2,2) (Regulation)
Protelytic cleavage - activate precursor Vascular Reactions and Pain
77
What are Cytokines also called? (Regulation)
Endogenous Pyrogens - made in the body to raise temp
78
What Chemokines are Present in the Liver? (4) (Regulation)
Serum Amyloid Protein Fibrinogen C-reactive protein Mannose Binding Lectin
79
What does C-reactive protein do in the liver? (Regulation) (4)
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
What does MBL do in the Liver? (Regulation)
Peforms opsonin activation, complement activation and lectin pathway - binds carb to lectin = C3 Convertase
81
What is the Function of Chemokines in other parts of the body: liver, bone marrow, hypothalamus, fat muscle cells, dendritic cells
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
How was Resolution of Response Previously Understood to How it is Now?
if signal is removed, duration of response will stop BUT resolution is active and an regulated process
83
What molecules are needed in Resolution?
- 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
After Resolution, Homeostasis can be Returned. Describe Homeostasis.
- few infiltrating homeostasis - cells maintain health and remove debris
85
What Molecules are No Longer Needed During Resolution?
pro-inflam cytokines and chemokines histamines prostaglandins leukotrienes thromboxanes
86
Define Chronic Inflammation
A prolonged duration of the inflammatory response, when regulation and resolution fail.
87
What is the Dominant Cell of Chronic Inflammation?
Macrophages - can be pro or anti inflammatory
88
In Chronic Inflam, Describe the Pro-Inflam Macrophage (5)
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
In Chronic Inflam, Describe the Anti-Inflam Macrophage.
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
What is the Effect of Chronic Inflammation?
- tissue injury - fibrosis - fibroblasts new connective tissue - angiogenesis - new blood vessels
91
What is the Effect of New Tissue During Chronic Inflammation?
non-specialised the function of the tissue can be lost and lead to further damage
92
Describe Characteristics of Chronic Inflam.
- Mononuclear Cells Inflitrate - Tissue Destruction - Granulomatous Tissue - Fibrosis
93
What Oral Infection can have Both Acute and Chronic Inflammation?
Dental Abscess - chronic as fibrous tissue and monocytes cells surround the walls but it is a neutrophil dominated response, making it acute
94
Chronic Inflammation can be Present from the Onset with this Disease.
Rheumatoid Arthiritis
95
Diseases Linked To Periodontitis - an Inflam Disease
Inflammation induced Pregnancy Complication Atherosclerosis Diabetes
96
How is Diabetes Linked to Inflammatory Periodontitis?
- 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
P Gingivalis is a key pathogen, what does it have similar activity to?
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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