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Semester II - GHD > Chronic Inflammation > Flashcards

Chronic Inflammation Flashcards

1
Q

What’s Chronic Inflammation?

A

Inflammation of prolonged duration in which active inflammation, tissue destruction and attempts at repair are proceeding simultaneously

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2
Q

What are the predominant cell types in chronic inflammation?

A
  1. Lymphocytes
  2. Plasma cells
  3. Macrophages
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3
Q

Does chronic inflammation always proceed acute inflammation?

A

No

  • May follow acute inflammation which it does not resolve but it can begin insidiously
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4
Q

What are the 3 causes of primary chronic inflammation?

A
  1. Resistance of infective agent to phagocytosis
  2. Endogenous materials
    - Necrotic adipose tissue, bone, uric acid, keratin (epithelial/’sebaceous’ cyst), hair (pilar cysts)
  3. Exogenous materials
    - Silica (dust + pulmonary lung fibrosis), suture material (foreign nature of material can illicit an immune response), prosthesis, splinter
  4. Autoimmune diseases
    - Lichen planus (oral)
    - Non-organic specific e.g. Rheumatoid arthritis
    - Contact hypersensitivity
  5. Specific diseases of unknown aetiology
    - Chronic inflammatory bowel disease e.g. ulcerated colitis
    - Primary granulomatous diseases e.g. Crohn’s disease
    • Progression from acute inflammation
  • Osteomyelitis
  • *Recurrent episodes of acute inflammation
  • Chronic cholecystitis
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5
Q

What are the effects of Chronic inflammation?

A
  1. Infiltration with mononuclear cells
    - Macrophages etc
  2. Tissue destruction
  3. Attempts at healing
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6
Q

What’s an ulcer?

A

A loss of an epithelial lining so the underlying tissue is exposed - granulation tissue is produced and that’s why it can appear raised

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7
Q

What’s the microscopic appearance in acute inflammation?

A
  • Cellular infiltrate
  • Multinucleate giant cells
  • Production of new fibrous tissue
  • Continuing destruction
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8
Q

Is chronic inflammation a self perpetuating cycle of destruction?

A

Yes

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9
Q

What’s the dominant immune cell in chronic inflammation?

A

Macrophages

  • Circulate as monocytes
  • Emigrate into the extravascular tissue early in acute inflammation
  • Macrophage activation is mediated by cytokines (IFN-gamma, endotoxins and chemical mediators)
  • Activation leads to an increase in cell size, lysosomal enzymes, more active metabolism and greater phagocytosis

HOWEVER
- Biological active produces secreted by macrophages lead to tissue injury and fibrosis (i.e. chronic inflammation)

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10
Q

What biological produces of activated macrophages cause 1. tissue injury and 2. fibrosis

A

1.

  • Proteases
  • Coagulation factors
  • AA metabolites
  • Nitric Oxide

2.

  • Growth factors (PDGF, TGFbeta)
  • Fibrogenic cytokines
  • Remodelling collagenesis
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11
Q

What are the other cells in chronic inflammation?

A
  1. Lymphocytes
    - T cells = produce cytokines to attract, hold and activate macrophages
    - B cells = antibody production - activate macrophages via secretion of TNF, IL-1 and chemokines – persistent in inflammatory response
  2. Plasma cells = differentiated B cell which produce antibodies
  3. Eosinophils = Mediated by Immunoglobulin E and parasitic infections
    - release TGF, VEGF, PDGF
  4. Mast cells = widely distributed and release histamine and products of arachidonic acid oxidation (prostaglandins=inflammation)
  5. Neutrophils = particularly if persisting microbes
    - type of phagocyte
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12
Q

What’s necrotic tissue?

A

Tissue which is undergoing unplanned cell death - stimulated by chronic inflammation and this then stimulates necrosis - positive feedback cycle

  • perpetuates inflammatory cascade by the activation of:
    1. Kinin (vasodilation)
    2. Coagulation
    3. Complement
    4. Fibrinolytic system
    5. Mediators released from leukocytes
    6. Uric acid released from dying cells
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13
Q

What’s Granulomatous inflammation?

A
  • Distinctive pattern of chronic inflammation
  • Characterised by focal accumulation of activated amcrophges which often develop epithelial-like patterns (look like epithelial cells)
  • Immunologically mediated, infectious and non0infectious conditions
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14
Q

What are the characteristics of Granulomas?

A
  • Large vesicular nuclei, folded nuclear membrane, plentiful eosinophilic granular cytoplasm and indistinct cell borders
  • Hypoxic centre
  • Little phagocytic activity and more secretory function
  • Can contain giant cells and surrounded by lymphocytes
  • Typically, the offending pathogen will be at the centre of the granuloma
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15
Q

What are Giant cells?

A
  • Accumulated of macrophages
  • Form when foreign particles are too large to be ingested by just 1 macrophage - fuse together
  • Large cytoplasm with multiple nuclei
  • Not always granuloma for giant cells to be present
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16
Q

What are Langhans’ giant cells?

A

Typically found in TB patients

  • The peripheral rim of nuclei
  • Large eosinophilic cytoplasm
17
Q

What are Immune granulomas?

A
  • Insoluble particles such as microbes induce cell mediated immune responses
  • Macrophages engulf material, process and present it to T-Helper cells
  • T-Helper cells produce IL-2 which activates other T-cells and INF-gamma which activates macrophages = multinucleate giant cells
18
Q

Give some examples of non-infective granulomas

A
  1. Rheumatoid disease - systemic
  2. Crohn’s disease - can present orally with inflammation of lips/tongue/cheeks
    - Dentists can be the 1st to identify Crohn’s
19
Q

What’s Pyogenic Granulomata?

A

Technically it should be called Lobular Capillary Haemangioma - growth of blood vessels (capillaries)

  • Not granulomatous
  • Not purulent
  • Caused by irritation, trauma, hormones and poor hygiene - harmless swelling
  • Bleeds readily due to being made of blood vessels
  • CAN BE CAUSED BY A DENTURE
20
Q

What are the 3 factors in Chronic inflammation healing and repair?

A
  1. Organisation: of specialised tissue
  2. Formation of granulation tissue
  3. Wound healing
21
Q

What happens during the organisation in chronic inflammation healing and repair?

A
  • Dead tissue is removed by phagocytosis via macrophages/phagocytes
22
Q

What’s granulation tissue?

A

Collection of fibroblasts and collagen deposits, macrophages

  • Agiogenesis occurs
23
Q

What are the products of granulation tissue?

A 
Fibrous tissue (scar)
- small firm blemish on skin
24
Q

What are the problems associated with granulation tissue?

A

Peritonitis (inflammation of lining of stomach)

  • adhesion between loops of bowel following Peritonitis cna prevent the bowl from contracting properly
  • Unsightly scar formation
  • When granulation tissue replaces heart muscle it cannot contract so it impairs heart function
25
Q

What are the sequences involved in wound healing?

A
  1. Injury, blood clot, acute inflammation and fibrin
  2. Granulation tissue growth and angiogenesis
  3. Phagocytosis of fibrin
  4. Myofibroblasts move in and lay down collagen
  5. Contraction of scar
  6. Re-epithelialisation
26
Q

What are the main differences between acute and chronic inflammation?

A

Acute: Rapid onset - Chronic: slower onset and prolonged

Acute: Calor, dolor, rubor, tumour - Chronic: few signs… granulation tissue, scarring

Acute: acute inflammatory cells/neutrophils - Chronic: lymphocytes, macrophages etc

Acute: Vascular damage - Chronic: Neo-vascularisation (new blood vessel formation)

Semester II - GHD (20 decks)

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