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I&I > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Features of acute inflammation?

A
  • Initial RAPID response to tissue injury, mins-hrs to develop, lasts short while hrs-days
  • INNATE response
  • NON-SPECIFIC
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2
Q

Features of chronic inflammation?

A

-Long LASTING weeks-months
may follow acute or slow insidious onset
-↑tissue DESTRUCTION
-Attempts to repair damaged tissue –>fibrosis

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3
Q

Causes of acute inflammation?

A

-Infections
-Tissue damage∵
Physical agents= frost bites, burns, ionising UV
Chemical agents= chemical burns, irritants
Mechanical injury + ischaemia= trauma, tissue crush, reduced blood flow
-Foreign bodies

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4
Q

Causes of chronic inflammation?

A
  • Failure to close inflammatory reactions= constant infections
  • Misdirected inflammatory reaction= harmless environmental substances (allergies) + self antigens (autoimmune diseases)
  • Cancer, atherosclerosis, Alzheimer, Type 2= directed against endogenous substances: crystals -> cholesterol, urate (gout)
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5
Q

Why acute inflammation?

A 
Alert body
↓ spread of infection + damage
Protect injured site from infection
Eliminate dead cells/tissue
Create conditions needed for healing
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6
Q

If acute didn’t exist?

A

No control of infections, impaired wound healing, tissue wouldn’t be repaired

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7
Q

5 R’s of acute?

A 
Recognition of injury
Recruitment of leukocytes
Removal of agent
Regulation (closure of response)
Resolution/repair
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8
Q

Signs of acute?

A 
Red∵ ↑blood flow-hyperaemia 
Swell∵ fluid accumulation ∵ ↑ vessel permeability
Heat∵ ↑blood flow + metabolic activity
Pain∵ ⇶pain mediators, ↑p on nerve ends
Loss of function∵ ↑ swelling + pain
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9
Q

What are systemic changes of acute?

A

Fever
Neutrophilia
Acute phase reactants

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10
Q

Why fever?

A

endogenous pyrogens - IL-1, TNF-α

exogenous pyrogens - microbial components

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11
Q

Why neutrophilia?

A

G-CSF stimulates bone marrow⇶immature neutrophils to replenish dead

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12
Q

Why acute phase reactants?

A

IL-6, IL-1, TNF-α induces liver to produce:
C-reactive protein CRP
fibrinogen
complement
serum amyloid A protein SAP
↑ fibrinogen–> stacking of🔴(rouleaux)–> 🏃sedimentation rate

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13
Q

Form of Systemic Inflammatory Response Syndrome SIRS?

A

Sepsis

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14
Q

Vascular events of acute?

A

Vasodilation in small vessels
↑blood flow
↑vessel permeabilty (microvessels)

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15
Q

Overall effect of vascular events of acute?

A

ⓦ+plasma🐟 exit vessels ➩ site

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16
Q

How vasodilation happens?

A

Injured cells, macrophages, mast cells ⇶ HISTAMINE, serotonin

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17
Q

Why ↑blood flow ➩ site?

A

So influx of ⓦ, fluid, O2, nutrients

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18
Q

How vessels ↑ permeabilty?

A
  • Contraction of endothelial cells∵histamine,serotonin –>leakage of fluid + cells in site
  • endothelial cell activation–> ↑adhesion ∞
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19
Q

What’s inflammatory exudate?

A

H2O, salts, plasma🐟(fibrinogen), inflammatory cells, 🔴 get out of vessels + enter tissues/ serous cavities ∵ ↑ vessel permeabilty

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20
Q

What’s transudate

A
  • fluid leaks∵ altered osmotic/hydrostatic p

- normal vessel permeability

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21
Q

Cellular events of acute?

A

Migration + accumulation of cells
Removal of pathogens/dead cells
Migration + accumulation of monocytes

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22
Q

How cells migrate + accumulate?

A

Neutrophils arrive 1st via complex process to exit from vessels

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23
Q

How dead cells + pathogens removed

A

Neutrophils phagocytose–> live briefly –> die–> pus

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24
Q

How monocytes migrate + accumulate?

A

Monocytes (in blood) differentiate→ macrophages(at tissue)–>phagocytosis–>clearance of site + tissue repair factors TGF-β

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25
Q

Neutrophil recruitment?

A

Adherence to endothelial lumen surface, migrates via vessel wall

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26
Q

Steps of neutrophil recruitment?

A
  • Margination + rolling
  • Integrin activation by chemokines
  • Firm adhesion to endothelium
  • Transmigration via endothelium ➩tissue
  • Chemotaxis to site
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27
Q

Function of adhesion ∞ + eg

A

Involved in neutrophil recruitment
Selectins
Integrins
Ig superfamily cell adhesion molecules CAM

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28
Q

What are Selectins + diff types?

A

Expressed by activated endothelium, mediate rolling of neutrophils
P,E,L

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29
Q

What’s P-selectin?

A

in pre-formed granules

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30
Q

What’s E-selectin?

A

induced by IL-1 + TNF-α (cytokines produced by macrophages, mast cells, endothelial cells at site)

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31
Q

What’s L-selectin?

A

expressed by ⓦ, ligands on endothelium

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32
Q

What are ligands?

A

carbs PSGL-1, sialyl-Lewis

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33
Q

How do selectins work?

A

Endothelial selectins bind to ligands on neutrophis–> low affinity interaction–> disrupted by flowing blood –> repetitive binding + detaching –> slow rolling

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34
Q

What are Integrins?

A

(LFA-1) expressed by rolling neutrophils - low affinity state ∴ can’t bind to ligands

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35
Q

How do integrins have high affinity state?

A

Activated endothelial cells produce chemokines –> bind to receptors on neutrophils –> integrin activation –>

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36
Q

How do integrins work?

A

bind to ligands on endothelium∴ adhesion of neutrophils to endothelium

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37
Q

What are the integrin ligands?

A

induced by IL-1 and TNF-α (cytokines produced by macrophages, mast cells, endothelial cells at site)
ICAM-1 (intracellular)
VCAM-1 (vascular)

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38
Q

How neutrophils transmigrate?

A

via interendothelial spaces –> pass via vessel wall + enter tissue –> chemotaxis via tissue towards site

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39
Q

What guides migration via tissues?

A

Gradient of chemoattractants

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40
Q

What are chemoattractants?

A

Produced at site, diffuses ➩ adjacent tissues + form gradient

  • 🐛 components (peptides containing N-formyl-methionine-leucine-phenylalanine; lipids)
  • chemokines IL-8
  • complement components C5a
  • leukotriene B₄ (LTB₄)
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41
Q

Time of neutrophils at site?

A

short lived 6-24hrs

dies in tissue 24-48hrs

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42
Q

Time of monocytes at site?

A

lives longer 24-48hrs, profilerate

at tissue → macrophage

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43
Q

Pathogen destruction mechanisms?

A

⇶granule content
Phagocytosis
Generation of reactive O2/N species
Formation of Neutrophil Extracellular Traps NETs (netosis)

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44
Q

What’s NETs?

A

mesh of chromatin - traps microbes, contains anti-microbial ∞

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45
Q

Types of neutrophil granules?

A

Specific (small) : lysozyme, collagenase, gelatinase, lactoferrin, alkaline phosphatase
Azurophil (large) : myeloperoxidase, lysozyme, defensins, acid hydrolases, proteases (elastase, cathepsin G, collagenases, proteinase 3)

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46
Q

How to terminate acute?

A

Anti-microbial mechanisms via inflammatory mediators

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47
Q

Inflammatory mediators :(

A

Non specific ∴ normal tissues damaged

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48
Q

Termination of acute?

A

neutrophils die
inflammatory mediators degraded
regulatory mechanisms - anti-inflammatory
repair mechanisms - tissue regeneration/connective tissue

49
Q

Outcomes of acute

A

Resolution-affected tissue restored to normal
Repair-lost tissue replaced by connective tissue,fibrosis
Chronic-if acute unresolved

50
Q

How resolution happens?

A

damaging agent removed
injured tissue replaced by same cell type∴ no change in tissue structure/function
restoration of normal tissue structure only if residual tissue’s structurally intact

51
Q

How repair happens?

A

scarring alters tissue function

macrophages⇶ TGF-β -promotes fibrosis

52
Q

How chronic happens after acute?

A

Abscess formed by mass of necrotic tissue caused by pyrongenic 🐛.. if not drained/reabsorbed→

53
Q

What type of tissues have high regeneration ability + eg?

A

Labile tissues- ÷ continuously

epithelial cells eg 🏼, airways, gut, blood cells

54
Q

What type of tissues have intermediate regeneration ability + eg?

A

Stable tissues
normal state: quiescent cells (G0/G1) injury –> ÷
eg liver, kidney, pancreas. endothelial cells, fibroblasts

55
Q

What type of tissues have no/little regeneration ability + eg?

A

Permanant tissues

eg neurons, myocardium, skeletal muscle

56
Q

Factors that favour tissue regeneration?

A

minimal cell death + destruction
good regeneration ability of tissue
🏃‍♂️ removal of debris + clearance of infection
removal of foreign matierial - sutures, bone frag
immboilisation of wound edges - sutures

57
Q

Factors that prevent tissue regeneration?

A 
extensive injury + haemorrhage
infection
old age
diabetes
poor health/nutrition - 🐟, vit C deficiency
💊 - corticosteroids
poor vascular supply
foreign bodies 
dehiscence - p/torsion/movement on wound edges
58
Q

Cells involved in chronic?

A 
Macrophages
Lymphocytes - T + B
Eosinophils
Mast cells
Neutrophils
59
Q

Role of macrophage?

A

-act as sentinels present in:
kupuffer cells (liver), microglia (brain), alveolar macrophages (lungs)
-produce growth factors–> tissue repair
-take up dead microbes,cells –> elimination
-activate T cells
-⇶ inflammatory cytokines - TNF-α , IL-1, chemokines

60
Q

Role of lymphocytes

A
  • granulomatous inflammation, autoimmunity, allergy
  • T produce cytokines –> recruit + activate macrophages
  • B –> plasma cells –> produce antibodies
61
Q

How are lymphocytes activated?

A

microbes, dead cells

62
Q

How are lymphocytes recruited?

A

from macrophages TNF-α , IL-1

63
Q

What’s tertiary lymphoid tissue /TLO + eg?

A

clusters of lymphocytes, macrophages, plasma cells similar to lymphoid tissue in lymph nodes eg rheumatoid arthritis

64
Q

Role of eosinophils?

A

parasite infections, Ig-E mediated allergies

MBP Major Basic 🐟 destroys parasites/tissues

65
Q

Where are mast cells found?

A

connective tissue close to vessels - in acute + chronic

66
Q

What type of chronic inflammation are neutrophils present in?

A

suppurative inflammation -abscess, osteomyelitis

lung disease -🚬/irritants

67
Q

How are neutrophils recruited?

A

macrophages, T cells⇶ chemokines IL-8

68
Q

What does ‘acute on chronic inflammation’ mean?

A

neutrophil-rich infiltrate

69
Q

Role of cytokines?

A

soluble mediator for cell-cell communication used in acute +/or chronic

70
Q

How are cytokines produced?

A

macrophages, lymphocytes, dendritic cells

endothelial, epithelial cells, connective tissue

71
Q

What are the soluble mediators for chronic?

A

cytokines : IFN-γ Interferon-gamma, TNF-α, IL-17, IL-12

72
Q

Role of IFN-γ?

A

activates macrophages–> ↑microbicidal activity

73
Q

How’s IFN-γ produced?

A

T cells + NK cells

74
Q

Types of chronic inflammation?

A

Non-specific
Autoimmune
Chronic suppurative
Chronic granulomatous

75
Q

Inflammatory cells of non-specific inflammation?

A

lymphocytes, plasma cells

76
Q

Why does non-specific inflammation happen?

A

when acute FAILS to remove causative agent

77
Q

How does non-specific inflammation happen?

A

caused by Helicobacter pylori or NSAIDs

tissue destruction - gastric/duodenal peptic ulcers

78
Q

Ulceration?

A

loss of dead cells–>local defect/excavation of surface eg oral mucosa, stomach, intestine, GU tract–>granulation tissue fills ulcer–>scar

79
Q

Where’s Helicobacter pylori located?

A

stomach lumen

80
Q

How does chronic gastris happen?

A

-neutrophil infiltration in stomach wall doesnt harm H.pylori
-neutrophils damage epithelial cells
-antibodies against H.pylori ineffective
∴infection persists –>

81
Q

Inflammatory cells of autoimmune inflammation?

A

lymphocytes, macrophages

82
Q

What’s autoimmune inflammation + why does it happen?

A

immune response to self antigens
no acute
progressive, persistent, tissue damage

83
Q

What’s rheumatoid arthritis?

A

Joint synovium expanded by macrophage, lymphocyte infiltrate + fibrin deposition - pannus
Bone + joint destruction
70% patients have IgM antibodies anti-Fc portion of IgG

84
Q

Inflammatory cells of chronic suppurative inflammation?

A

NEUTROPHILS, eosophils

85
Q

What’s chronic suppurative inflammation?

A

persisting pus-forming inflammation

86
Q

How does chronic suppurative inflammation happen?

A

acute purulent inflammation by pyrogenic (pus forming) 🐛 eg Staphilococci –> pus accumulates–> abscess

87
Q

How to remove abscess?

A

surgery- incision + drainage clears pus

88
Q

What’s an abscess + areas?

A

fibrosis walls off of acute–> localised purulent inflammation
central area: necrotic Ⓦ + tissue cells
zone: neutrophils, fibroblast proliferation
fibrotic area

89
Q

What’s chronic granulomatous inflammation + why does it happen?

A

Causative agent not removed –> granuloma formation to isolate + prevent agent spreading

90
Q

What are granulomas made of?

A

macrophages, lymphocytes (T, b), fibroblasts, sometimes necrotic tissue

91
Q

What causes immune granulomas?

A 
Persistent T cell activation ∵
Infection: 
🐛-TB, leprosy, syphilis
Parasitic- Schistosomiasis
Autoimmune diseases:
Crohn's disease 
Rheumatoid arthritis
92
Q

What causes foreign body granulomas?

A

inert materials: talc, sutures, fibres, silica

93
Q

What’s Sarcoidosis?

A

disease which causes granulomas

unknown etiology

94
Q

Inflammatory cells of chronic granulomatous inflammation?

A

epitheliod cells, giant cells, lymphocytes

95
Q

How chronic granulomatous inflammation happens?

A

macrophage responds to agent (INNATE)–> can’t remove it–> ADAPTIVE ∴ T cell activates–> activates macrophages–> change in macrophage appearance:
epitheloid cells-↑ cyroplasm
macrophage fusion- multinucleate giant cells
–>sig tissue destruction

96
Q

How does granuloma look 🔬?

A
  • Centre: cluster of epitheloid cells
  • Infectious agent/ foreign body may be visible
  • Periphery: rim of lymphocytes, fibroblasts, connective tissue
  • Multinucleated giant cells 40-50 μm
  • neutrophils, lymphocytes ~10 μm
  • macrophages ~20 μm
  • Central necrosis area = caseous necrosis seen in TB
97
Q

Why central necrosis area in TB?

A

hypoxia, ROS that damage tissue

mixture of coagulative + liquefactive necrosis

98
Q

What are non-caseating granulomas + where is it seen?

A

no central necrosis area

Crohn’s, sarcoidosis, foreign body granulomas

99
Q

How do multinucleate giant cells arise from macrophages?

A

adjacent macrophages phagocytose same hard to destroy particle eg silica, mycobacterium, Schistosoma ova

100
Q

How do multinucleate giant cells look like?

A

horseshoe nuclei arrangement

40-50 μm

101
Q

Granulomatous inflammation outcomes?

A

agent removed: tissue healing–>fibrosis + Calcium deposition in scarred tissue- x-ray visible

agent persists: 'walled off' by fibrosis tissue, calacium deposition, infection kept in check by T cells + macrophages
compromised immunity (steroids, HIV)--> TB reactivation
102
Q

What’s tissue repair used for?

A

parencymal + connective tissue

103
Q

What’s tissue healing used for?

A

surface epithelia

104
Q

Types of tissue repair?

A

Regeneration + replacement

105
Q

What’s regeneration?

A

proliferation of residual healthy cells

proliferation + maturation of tissue resident stem cells

106
Q

What’s replacement?

A

replaced w connective tissue–> scar

107
Q

How healing starts?

A

Organisation (ingrowth of capillaries + fibroblasts) form granulation tissue

108
Q

How healing ends?

A

Resolution or REPAIR–>scar

109
Q

How can wounds heal?

A

1 or 2ᵒ intention

110
Q

What’s 1ᵒ intention?

A

injury to epithelial layer–>resolution

if wound edges can be apposed

111
Q

What’s 2ᵒ intention?

A

extensive tissue loss–>regeneration+scarring
deep gaping wounds
epithelium regenerates–>normal
adnexal structures–> scar–> restrict function

112
Q

Process of 1ᵒ intention + ⌚?

A

-wound–>activation of coagulation–>clot–>clot surface dehydrates–>wound scab …⌚24hrs…–> neutrophils infiltrate wound margins⇶proteolytic 𝔼–>clear microbe/debris
-24-48hrs : migration + profileration of epithelial cells at wound edges, deposit extracellular matrix components, meet in midline below scab, thin layer to close wound
-Day 3 : macrophages replace neutrophils to clear debris, fibrin, promote angiogenesis, ECM deposition + granulation tissue invades wound space
-Day 5 : granulation tissue fills wound; neovessels + edema –> fibroblast proliferation–> produce collagen–>deposits in wound
-2nd week : fibroblast profileration + collagen deposition continues, vessel regeneration, ↓ inflammatory infiltrate–>scar blanching
-1m : scar made of connective tissue w/o inflammatory cells, normal epidermis, dermal appendages lost permanently ∵ incisions, wound strength ↑:
well sutured=70% strength
sutures removed 1 week=10%
3m=70-80%
then no further improvement

113
Q

Diff between clot vs thrombus?

A

extravascular blood coagulation vs intravascular

114
Q

Process of 2ᵒ intention + ⌚?

A

-Larger wounds ∵ big clot, ↑exudate
-Granulation tissue more extensive–> big scar
pale avascular scar= fibroblasts, dense collagen, no inflammatory cells
dermal appendages lost permanently ∵ incisions
epidermal layer recovers
-Wound contraction
helps close wound + ↓ wound surface
myofibroblasts= modified fibroblasts w smooth muscle cell features
6 weeks : 5-10% of original size + ↓ defects

115
Q

Types of abnormal tissue repair?

A

Wound dehiscence/rupture + ulceration
Hypertrophic scars + keloids
⇧ Wound contraction

116
Q

When does wound dehiscence/rupture+ulceration happen?

A

abdominal surgery–>

inappropriate vascularisation–> (ischemic necrosis)

117
Q

When does hypertrophic scars + keloids happen?

A

excessive collagen deposition–> raised scar–>
scar grows beyond margins–> 🍇
keloid predisposition to Afro-caribbean

118
Q

When does ⇧ wound contraction happen?

A

after severe 🔥
contractures (palms, sores, 𝔸 thorax)
impair joint movements

I&I (4 decks)

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