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Medsci 203 > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

List the four cardinal signs of inflammation

A
  1. redness
  2. heat
  3. swelling
  4. pain
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2
Q

Inflammation delivers _____ and _____ to injured sites

A

nutrients and oxygen

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3
Q

List two functions of exudate

A
  1. carries toxins from an affected area via lymphatic drainage to local lymph nodes (where they may stimulate immune responses)
  2. carries antibodies and other substances into the affected area to neutralise harmful agents
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4
Q

Inflammation limits the spread of _____ _____ via structures such as fibrin mesh and abscess walls

A

harmful agents

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5
Q

Inflammation provides _____ to digest inflammatory exudates following the “crisis”

A

hydrolases

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6
Q

Inflammation initiates ____

A

repair

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7
Q

What three “go signals” that induce inflammation are released by tissue damage?

A
  1. Neurons - bioactive peptides
  2. Broken cells - intracellular molecules aka damage/danger-associated molecular patterns (DAMPs)
  3. Microbial products (e.g endotoxin/LPS)
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8
Q

What are bioactive peptides released in response to?

A

Pain

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9
Q

What do DAMPs signal and who are they sensed by?

A

DAMPs signal cell damage and are sensed by pattern-recognition receptors (PRRs)

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10
Q

What are microbial products such as endotoxin/LPS recognised as?

A

Pathogen-associated molecular patterns (PAMPs) by pattern-recognition receptor (PRRs)

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11
Q

PRRs may be _____ (complement) or ___-_____ (toll-like receptors, TLRs)

A

soluble or cell-bound

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12
Q

The cells that rapidly respond to initial “go signals” of inflammation following tissue damage are:

A

mast cells/basophils and macrophages

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13
Q

Mast cells are full of granules and initiate inflammation by releasing mediators such as: (4)

A
  1. histamine
  2. proteases (tryptases)
  3. lipid-derived signals
  4. cytokines (e.g TNF)
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14
Q

What changes do the signals released from degranulating mast cells cause? (2)

A

Rapid microvascular change and redness-heat-swelling-pain response

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15
Q

_____ is the mechanism that leads to redness and heat

A

vasodilation

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16
Q

Excess blood flow is known as:

A

hyperaemia

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17
Q

Most blood vessels are lined by ______ endothelium

A

continuous endothelium

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18
Q

Endothelial cells are closely connected by ___ junctions and ____ junctions

A

tight junctions and adherens junctions

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19
Q

Vascular permeability (leakiness) ocurs when:

A

Vascular permeability (leakiness) ocurs when endothelial cells retract to create gaps.

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20
Q

Describe venular endothelial cell reactions to mild injuries, such as an insect bite - is this reversible?

A

Inflammatory signals cause venular endothelial cells to rapidly and reversibly retract, creating 0.1-0.4um gaps between the cells through which protein-rich fluid (inflammatory exudate) can pass

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21
Q

Describe what happens to endothelial cells during severe injuries

A
  • Endothelial cell damage
  • Detachment from the basement membrane
  • Persistent increases in vascular permeability
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22
Q

Describe the two types of persistance increases of vascular permeability during severe injury and give examples of each

A
  1. Delayed - e.g sunburn, bacterial toxins - leakage from capillaries and venules
  2. Immediate - e.g burns, trauma - leakage from all types of vessels until the vessel is blocked with a clot or repaired
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23
Q

Normally, fluid is forced out of capillaries at the _____ end via ______ pressure and re-enters them at the ___ end.

A

Normally, fluid is forced out of capillaries at the arteriolar end via hydrostatic pressure and re-enters them at the venular end.

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24
Q

During inflammation, increased hydrostatic pressure in the capillaries and increased water-binding capacity of proteins in exudates leads to _____________

A

Retention of fluid in the extravascular space between cells (interstitium)

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25
Q

Accumulated fluid generates _____, also known as _____

A

swelling, oedema

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26
Q

_____ of tissue, together with _______ mediators, causes pain

A

Stretching of tissue, chemical mediators

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27
Q

Signals that control blood vessel function during inflammation may be secreted locally by ____ or derived from ______ _______

A

cells, plasma proteins

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28
Q

Signals that control blood vessel function during inflammation induce some or all of the following actions: (5)

A
  1. Vasopermeability - generating exudate
  2. Vasodilation
  3. Neutrophil adhesion to endothelium
  4. Bronchoconstriction
  5. Pain + itching
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29
Q

Vasodilation occurs via synthesis of these lipid mediators (3)

A
  1. Prostacyclin I2
  2. Platelet-activating factor (PAF)
  3. Nitric oxide
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30
Q

What is an example of a vasoactive amine? Where can it be found?

A

The preformed histamine stored in granules of mast cells/basophils and platelets.

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31
Q

What are tryptases and what are their functions?

A

Tryptases are mast-cell derived serine proteases - they cleave protease-activated receptors (PARs) on other mast cells, endothelium and neutrophils, which induces inflammation

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32
Q

What is the membrane phospholipid phosphatidylcholine cleaved into?

A

lysophosphatidylcholine (LysoPC) and arachidonic acid

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33
Q

How are membrane phospholipids such as phosphatidylcholine cleaved?

A

Via intracellular Ca2+ and cytosolic phospholipase A2 (cPLA2)

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34
Q

LysoPC is converted into _____ in activated inflammatory cells, endothelial cells and injured tissue cells.

A

platelet-activating factor (PAF)

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35
Q

What is the function of platelet activating factor (PAF)? (2)

A
  1. Aggregation and activation of platelets

2. Leukocyte adhesion, chemotaxis and activation

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36
Q

What can arachidonic acid transform into? (2)

A

Rapid response, short half-life, short-range derivatives:

  1. Cyclooxygenases COX1, COX2
  2. 5-Lipoxygenase
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37
Q

What is the function of COX1 and COX2?

A

Generate prostaglandins, including thromboxanes and prostacyclins

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38
Q

What are COX1 and COX2 inhibited by?

A

Non-steroidal anti-inflammatory drugs (NSAIDs)

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39
Q

What is the function of 5-lipoxygenase?

A

To generate leukotrienes such as LTB4, LTD4 and LTE4

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40
Q

What is the function of LTB4?

A

Recruits neutrophils

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41
Q

What is the function of cysteinyl LTs such as cysLTC4, LTD4, and LTE4

A

Induction of vascular permeability, mucus production and bronchoconstriction

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42
Q

TXA2, PCI2 and PGE2 are all agents of the class ________

A

prostaglandin

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43
Q

LTB4, LTC4, LTD4 and LTE4 are all agents of the class _______

A

leukotriene

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44
Q

TXA2 activity results in:

A

vasoconstriction, platelet aggregation

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45
Q

PCI2 activity results in:

A

vasodilation, platelet disaggregation

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46
Q

PGE2 activity results in:

A

vasodilation, pain

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47
Q

prostaglandins that result in vasodilation are:

A

PCI2, PGE2

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48
Q

LTB4 activity results in:

A

neutrophil chemotaxis and activation

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49
Q

cysLTC4, D4, E4 activity results in:

A

vasopermeability, mucus, bronchoconstriction

50
Q

What four cascades are activated by proteolytic events and lead to rapid development of inflammation with potent vasoactive effects?

A
  1. Coagulation cascade
  2. Fibrinolytic system
  3. Kinin
  4. Complement cascade
51
Q

What are the two activators of the coagulation cascade?

A

TF (haemostasis), FXII (thrombosis)

52
Q

The coagulation cascade is induced following damage to the ________ ___________

A

vascular endothelium

53
Q

______ ______ is released from apoptotic endothelial cells and from exposed basement membranes

A

tissue factor (TF)

54
Q

TF leads to activation of ________

A

thrombin

55
Q

thrombin cleaves: (2)

A
  1. Soluble fibrinogen into fibrin

2. Protease-activated receptors (PARs)

56
Q

What is the function of fibrin?

A

Fibrin traps platelets and cells to form clots, with arrest of bleeding (haemostasis)

57
Q

Released fibrinopeptides are ___-inflammatory

A

pro-inflammatory

58
Q

Protease-activated receptors (PARs) induce _____ _______, PAF release with ______, and leukocyte adhesion

A

Protease-activated receptors (PARs) induce vascular permeability, PAF release with vasodilation, and leukocyte adhesion

59
Q

Hageman factor (factor XII, FXII) activates ____ to propagate thrombi

A

thrombin

60
Q

What is thrombosis?

A

The formation of a blood clot within a blood vessel, which may occlude it and cause dangerous ishaemic events.

61
Q

FXII is activated by ________ from activated platelets.

A

polyphosphates

62
Q

Inhibition of FXII would counteract _____ but not haemostasis

A

thrombosis

63
Q

What does the fibrinolytic system generate?

A

The protease plasmin, that degrades fibrin and allows blood flow to occur again

64
Q

What are the functions of plasmin? (4)

A
  1. Degrades fibrin
  2. Cleaves ECM proteins
  3. Activates matrix metalloproteases (MMPs)
  4. Cleaves PARs
65
Q

Cleavage of PARs by plasmine induces the release of _______ signals

A

inflammatory

66
Q

FXII mediates the proteolytic activation of the protease _________

A

kallikrein

67
Q

kallikrein releases the peptide _______

A

bradykinin

68
Q

Bradykinin induces the following four changes:

A
  1. Vascular dilation
  2. Vascular permeability
  3. Neutrophil chemotaxis
  4. Pain
69
Q

The anti-microbial complement pathway is activated by three things:

A
  1. proteaes
  2. antigen-antibody complexes
  3. bacterial products
70
Q

Proteolytic cleavage in the anti-microbial complement pathway produces the following four products:

A

Convetases: C3a, C5a, C3b, C5b

71
Q

What are the functions of convertases C3a and C5a?

A

Mast cell degranulation, vascular permeability, neutrophil chemotaxis

72
Q

What is the function of convertase C4b?

A

Opsonisation - promotes phagocytosis of particles

73
Q

What is the function of convertase C5b?

A

C5b is part o fthe membrane attack complex involved in bacterial cell lysis

74
Q

List 3 examples of cytokines

A
  1. TNF
  2. Interleukins (ILs - 35 different species)
  3. Interferons (IFNs)
75
Q

What are chemokines?

A

Chemoattractants that recruit cells to sites of injury and infection

76
Q

TNF ___-regulates inflammation

A

up-regulates

77
Q

The effects of TNF were first inferred a century ago by a New York physian by the name of __________

A

William Coley

78
Q

Wasting away of fat and muscle is known as

A

Cachexia

79
Q

Why isn’t TNF used as an anticancer agent? (2)

A
  1. Induces unpleasant flu-like symptoms

2. Is ineffective against cancer types common today (carcinomas)

80
Q

At low concentrations, TNF and IL-1 induce ___________ in endothelial cells

A

protein-synthesis

81
Q

Low concentrations of TNF and IL-1 leads to the following three effects 3 in endothelial cells:

A
  1. Vasodilation
  2. Vasopermeability
  3. Expression of endothelial cell adhesion molecules (selectins, ICAM-1, VCAM-1) that recruit inflammatory cells
82
Q

List three types of endothelial cell adhesion molecules:

A
  1. Selectins
  2. ICAM-1
  3. VCAM-1
83
Q

High concentrations of TNF and IL-1 induce: (4)

A
  1. fever
  2. the coagulation cascade
  3. production of fibrotic (scar) tissue
  4. cachexia
84
Q

Injury without infection generates ____ inflammation

A

sterile inflammation

85
Q

Sterile inflammation is initiated by molecules released from dead cells and damaged extracellular matrix known as ________. When there is infection + inflammation, microbes release _____.

A

DAMPs, PAMPs

86
Q

List 5 examples of DAMPs

A
  1. ECM fragments
  2. Intracellular proteins
  3. DNA and RNA
  4. ATP
  5. Crystals
87
Q

What are P2X7 purinergic receptors for?

A

ATP

88
Q

Signalling from TLRs and P2X7Rs activates ____________ such as caspase 1

A

inflammasomes

89
Q

What is the function of caspase 1?

A

Cleavage of pro-IL-1β into active IL-1β

90
Q

IL-1α is an intracellular _____ that is released when cells ____

A

cytokine, lyse

91
Q

IL-1α and IL-1β induce __________________ for leukocytes

A

endothelial cell adhesiveness

92
Q

What is margination?

A

The adherence of neutrophils to the endothelium

93
Q

During margination, neutrophils in _____ leave the ______ stream and concentrate in the ______ zone.

A

venules, axial (central) stream, plasmatic zone

94
Q

Rolling of neutrophils along endothelium is mediated by which molecules?

A

P and E selectins on endothelial cells and glycoproteins with sugar residues (sialyl-Lewis-X) on neutrophils

95
Q

Firm adhesion with flattening occurs when inflammatory mediators up-regulate which molecules on endothelial cells and neutrophils?

A

ICAM-1 and VCAM-1 on endothelial cells

LFA-1 (an integrin) on neutrophils

96
Q

Transmigration is also known as ______

A

Diapedesis

97
Q

What happens during transmigration/diapedesis?

A

Adherent neutrophils push their way between/through endothelial cells, releasing elastase to digest basement membrane so that they can enter the extravascular tissue

98
Q

What is the difference between chemotaxis and necrotaxis?

A

Necrotaxis is the movement of leukocytes in response to chemical signals during sterile inflammation, whereas chemotaxis is in the presence of an infection

99
Q

List 3 kinds of chemotactic signals

A
  1. N-formylated peptides (NFPs)
  2. Chemokines such as LTB4, bradykinin, C3a and C5a
  3. Bacterial products
100
Q

What is the significance of NFPs?

A

NFPs are recognised by formylated peptide receptor-1 (FPR 1) and override the effects of all other chemokines in circulation

101
Q

Phagocytes such as neutrophils eliminate damaged tissue and microbes by the coordinated process of ____, _____, and ____

A

phagocytosis, degranulation and respiratory burst

102
Q

What are two types of opsonins?

A

Immunoglobulins, C3b

103
Q

How do phagocytes attach to opsonised particles?

A

Via receptors for immunoglobulins and C3b (the Mac-1 integrin)

104
Q

How do phagocytes attach to non-opsonised particles?

A

Receptors for LPS bind bacteria directly in non-opsonic phagocytosis

105
Q

Describe the mechanism of phagocytosis

A
  1. Pseudopodia extend around bacteria and debris and internalise them in membrane-bound vesicles called phagosomes
  2. Phagosomes fuse with lysosomes (containing hydrolytic enzymes acidified to pH5) to form phagolysosomes.
  3. Lysosomal granules disappear from the cytoplasm - degranulation
  4. Respiratory burst causes pH to rise to 9 and activation of proteases = death of micro-organisms and degradation of debris
106
Q

Describe the process of the respiratory burst

A
  1. Electron transport complex NADPH oxidase (NOX2) assembled on the surface of phagocytic vacuole membranes
  2. O2 reduced to superoxide (O2-•)
  3. Superoxide reduced to peroxide (O2^2-) by myeloperoxidase SOD activity (combines H+ to form H2O2)
  4. pH is raised to 9, activating proteases which degrade cell debris and kill micro-organisms
  5. Superoxide depolarises the vacuole, inducing a K+ influx that releases proteinases
107
Q

Extracellularly, _____ may also catalyse the reaction of H2O2 with chloride to generate ________ to combat bacterial biofilms and fungal hyphae

A

myeloperoxidase, hypochlorous acid

108
Q

List the four outcomes of acute inflammation

A
  1. Systemic responses
  2. Liquefactive necrosis (suppuration)
  3. Regeneration/repair with resolution
  4. Chronic inflammation
109
Q

Fever is caused by pyrogens such as ___, ___, and ___ which affect _____ __________

A

TNF, IL-1 and PGE2, hypothalamic regulation

110
Q

The acute phase reponse of a systemic response is induced by _____. The liver produces plasma proteins such as ______ factors and ____.

A

IL-6, coagulation factors, opsonins

111
Q

What is leukocytosis?

A

An increase in the number of circulating leukocytes, caused by the release of leukocytes from bone marrow

112
Q

Processing of microbial molecules activates ____ immunity

A

adaptive immunity

113
Q

Describe liquefactive necrosis (suppuration) as a result of acute inflammation

A

Infection with pyogenic agents in solid tissues leads to the accumulation of dead neutrophils and tissue cells (pus) - lesions may be localised (abscesses), or spreading (cellulitis)

114
Q

What is the difference between systemic inflammatory response syndrome (SIRS) and sepsis?

A

SIRS - sterile injury, sepsis - infection

115
Q

SIRS and sepsis can be induced by what four factors?

A
  1. DAMPs (NFPs, mitochondrial DNA), pro-inflammatory cytokines (TNF, IL-1) and bacterial toxins into the bloodstream
  2. increase in ratio of pro to anti-coagulants
  3. activation of complement
  4. generation of ROS
116
Q

What occurs as a result of SIRS/sepsis? (5)

A
  1. Widespread vascular dilation and permeability = loss of blood volume
  2. formation of thrombi in small blood vessels (disseminated intravascular coagulation, DIC)
  3. Uncontrolled bleeding due to depletion of clotting factors)
  4. Inadequate organ perfusion, ischaemia
  5. Multi-organ dysfunction or failure (mortality >30%)
117
Q

How can inflammation be turned off? (2)

A
  1. Elimination the stimulatory effects of dead cell and bacterial products
  2. Negative feedback loops involving anti-inflammatory cytokines, lipid mediators, and protease inhibitors
118
Q

During inflammation, the lifetime of neutrophils is extended by three things:

A
  1. cytokines
  2. growth factors
  3. activated endothelium
119
Q

What induces the respiratory burst during phagocytosis?

A

The C3b receptor Mac-1

120
Q

What does the respiratory burst lead to?

A

Generation of ROS, caspase activation and neutrophil apoptosis

121
Q

What cell phagocytoses dead neutrophils?

A

macrophages

122
Q

How does chronic inflammation occur?

A

Chronic inflammation occurs when acute inflammation fails to resolve

Medsci 203 (10 decks)

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