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Life Protection > Chronic Inflammation > Flashcards

Chronic Inflammation Flashcards

1
Q

What is chronic inflammation?

A

Long lasting inflammatory response (weeks, months)

may be after acute inflammation

slow insidious onset (not preceded by acute)

attempts to repair damaged tissue via scarring and fibrosis

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2
Q

Aetiology of chronic inflammation

A

Fails to eliminate agent causing inflammation eg Mycobacterium tuberculosis

Exposure to low level irritants or foreign materials that cant be decimated by enzymatic breakdown or phagocytosis

An autoimmune disorder in which the immune system recognizes the normal component of the body as a foreign antigen, (Rheumatoid Arthritis, Systemic Lupus Erythematosus)

A defect in the cells responsible for mediating inflammation leading to persistent or recurrent inflammation (Auto-inflammatory disorders)

Recurrent episodes of acute inflammation. However, in some cases, chronic inflammation is an independent response and not a sequel to acute inflammation

Biochemical inducers of oxidative stress and mitochondrial dysfunction - increased production of free radical molecules, advanced glycation end products (AGEs), uric acid (urate)crystals, oxidized lipoproteins, homocysteine etc.

Chronic inflammation underlies many disorders: cancer cancer, atherosclerosis, Alzheimer, type 2 diabetes

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3
Q

Outcomes of chronic inflammation

A

Injury -> acute inflammatory response -> vascular changes, neutrophil receuitment and cytokine production -> should resolve issue

  • could lead to fibrosis after healing
  • or if acute inflammation is progressive leads to chronic
  • or injury that triggers chronic inflammation
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4
Q

Causes of chronic inflammation

A

Failure to close acute inflammatory reactions
(persistent infections eg bacteria, viruses, fungi, parasites)

Misdirected inflammatory reaction
=> harmless environmental substances (allergies)
=> self antigens (autoimmune diseases)

Chronic inflammation underying many disorders eg cancer, atherosclerosis, Alzheimer’s type 2 diabetes
-> directed against endogenous substances: crystals => cholesterol (atherosclerosis), urate (gout

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5
Q

Chronic vs acute inflammation

A

Longer duration
More immune cells - adaptive immune responses
- macrophages, lymphocytes, T cells and B cells

Altered tissue structure/function- eg

  • destruction and scarring (necrosis, fibrosis, scarring- deposition of collagen)
  • Angiogenesis
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6
Q

Cells in chronic inflammation

A

Macrophages- act as sentinels

=> derive from monocytes (circulation); inflammation
=> tissue resident macrophages: Kupffer cells (liver), microglia (brain), alveolar macrophages (lungs); different origin – foetal liver, yolk sac

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7
Q

Lymphocytes in chronic inflammation

A
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8
Q

Bidirectional signalling in chronic inflammation

A

T cell differentiates by receiving signals from APC via MHC and TCR + cytokines = Th1 cell

Signals come from APC and activated macrophage

Th1 then activates B cells and cytotoxic T cells to propagate inflammation

BIDIRECTIONAL bc signals from Th1 -> releases IFN-y to activate macrophage (+ CD40 and CD4 provide signals)

Macrophage can receive INF-y signalling from Th1 and NK cells

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9
Q

Where are mast cells found?

A

Connective tissue close to vessels

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10
Q

Where is MBP found?

A

Major basic protein in eosinophils- destroys parasites/tissues
in IgE mediated allergic reactions

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11
Q

Neutrophils in chronic inflammation

A

some types of chronic inflammation: suppurative inflammation (abscess, osteomyelitis); lung disease smoking/irritants

recruited by chemokines (IL-8) from macrophages/T cells

neutrophil-rich infiltrate called ‘acute on chronic inflammation’

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12
Q

Interferon gamma (IFN-y)

A

Produced by T cells, NK cells

Activates macrophages (increased MURDER activity)

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13
Q

Soluble mediators in chronic inflammation

A 
Cytokines
IFN-y
TNF- alpha
IL-17
IL-12
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14
Q

Types of chronic inflammation

A
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15
Q

Non-specific chronic inflammation

A

Often develops when acute inflammation fails to eradicate causative agent

Tissue destruction: e.g. gastric / duodenal peptic ulcers

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16
Q

Ulcer / ulceration:

A

=> local defect/excavation of the surface of an organ or tissue

=> caused by sloughing/shedding of inflamed necrotic tissue

=> oral mucosa, stomach, intestines, genitourinary tract
- peptic ulcer stomach/duodenum: acute and chronic inflammation coexist

=> skin and subcutaneous tissue of lower limbs (old people with circulation problems => ischemic necrosis)

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17
Q

Helicobacter pylori-associated gastritis

A
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18
Q

Peptic ulcer (gastric/duodenal)

A

Bc of H. pylori or NSAIDs

Acute inflammation phase: neutrophil infiltration in ulcer margins & base
Chronic inflammation phase:

=> granulation tissue formation in ulcer margins & base followed by

=> fibrous scarring, infiltration with lymphocytes, macrophages, plasma cells

19
Q

Chronic inflammation in autoimmune disease

A
20
Q

Rheumatoid arthritis

A

Progressive damage to cartilage in joints

=> joint synovium expanded by inflammatory cell infiltrate and fibrin deposition (pannus)

=> ~70% patients have antibodies anti-rheumatoid factor (IgM antibodies anti-Fc portion of IgG)

21
Q

Chronic suppurative inflammation

A
22
Q

Abscess

A

Fibrosis walls off a focus of acute inflammation => localised collection of purulent inflammation

Often pyogenic bacteria

Central area of necrotic leucocytes & tissue cells; zone with neutrophils; fibroblast proliferation and fibrotic area

Often may have to be laid open to heal (incision & drainage)

23
Q

Chronic granulomatous inflammation

A
24
Q

Granuloma causes

A
25
Q

Chronic granulomatous inflammation

A

Mo- macrophages

26
Q

Granuloma - microscopic appearance

A
27
Q

Multinucleated giant cell

A

Macrophage fusion = multinucleate giant cells (many nuclei)
- adjacent macrophage try to phagocytose the same particle
0hard to destroy particles -> silica, mycobacterium, Schistosoma ova

called LANGERHANS GIANT CELLS
horseshoe arrangement of nuclei

28
Q

Granuloma

A
29
Q

What kind of granuloma has a necrotic centre

A

Caseating granuloma

30
Q

What are the 2 outcomes of granulomatous inflammation in TB?

A
31
Q

Tissue repair vs healing

A

Repair => used for parenchymal and connective tissue

Healing => used for surface epithelia

32
Q

Types of tissue repair

A

REGENERATION
=> proliferation of residual healthy cells (e.g. epithelial cells)
=> proliferation and maturation of tissue resident stem cells

REPLACEMENT
Replacement with connective tissue => scar formation

33
Q

Tissue repair

A
34
Q

Macrophages and resolution of inflammation

A

Complex process where apoptosis of neutrophils and their subsequent clearance drive potent anti-inflammatory, tissue-restoring mechanisms.

Critical role of alternatively activated macrophages, which secrete anti-inflammatory and reparative mediators, and orchestrate these reparative processes

35
Q

Healing of tissue

A

Infectious agent or tissue damage causes acute inflammation

Damaged tissue, dead inflammatory cells and dead organisms are phagocytosed and cleared

Healing starts with organisation (ingrowth of capillaries and fibroblasts => form granulation tissue)

Healing ends with resolution (complete restitution to normal) or more commonly repair (scarring)

36
Q

Healing of skin wounds

A

Regeneration of epithelial cells and
Formation of connective tissue scar

Depending on size and nature the wound heals by 1) primary intention or 2) secondary intention

37
Q

Primary intention

A

=> injury limited to epithelial layer
=> repair by regeneration

e.g. clean, uninfected surgical incision closed by surgical sutures

38
Q

Secondary intention

A

=> more extensive tissue loss
=> repair by regeneration & scarring

e.g. large wounds, abscesses, ulcerations, ischaemic necrosis

39
Q

Skin wound healing primary vs secondary intention

A
40
Q

Healing by primary intention: steps

A

Injury/wound => activation of coagulation => clot formation
=> clot fills wound; external surface of clot dehydrates => wound scab

~24h: neutrophils infiltrate wound margins
=> release of proteolytic enzymes => clear debris/microbes

24-48h: migration & proliferation of epithelial cells at wound edges
=> deposit ECM (extracellular matrix) components
=> meet in the midline, beneath wound scab, thin layer to close wound

Day 3: macrophages replace neutrophils
- granulation tissue starts to invade wound space
=> Mϕ clear debris, fibrin; promote angiogenesis, ECM deposition

Day 5: granulation tissue fills wound; neovessels + edema
=> fibroblast proliferation => produce collagen => deposits in wound

2nd week
fibroblast proliferation & collagen deposition continue
vessel regression
reduction of inflammatory infiltrate -> scar ‘blanching’

1 month
scar made of connective tissue, without/very few inflammatory cells
normal epidermis
dermal appendages destroyed by incision lost permanently
wound strength increases in time

=> fresh wound well sutured => 70% strength of normal skin
=> sutures removed (1 week) => 10% strength
=> wound strength (3 months) => 70-80% strength
=> no further improvement in strength

41
Q

Healing by secondary intention

A

Larger wounds (big tissue loss)

  • bigger clot, more exudate, inflammation more intense
  • higher risk for inflammation-mediated tissue injury

Granulation tissue is more extensive -> bigger scar

  • Pale avascular scar (fibroblasts, dense collagen, no inflammatory cells)
  • Dermal appendages destroyed by incision lost permanently
  • Epidermal layer recovers full thickness and structure

Wound contraction - esp for large surface wounds

  • helps close wound and reduces wound surface
  • myofibroblasts- modified fibroblasts with smooth muscle cell features
  • 6 weeks: reduction of ski defects to 5-10% of original wound size
42
Q

Which one is primary vs secondary

A

Left- primary

Right- secondary

43
Q

Abnormal tissue repair

A
44
Q

Keloid

A

Scar grows beyond margins of original would, predisposing in Afro-Caribbean

Life Protection (10 decks)

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