Chronic Inflammation1

Question 1

Chronic inflammation

Answer 1

Inflammation prolonged duration (week to month to years) which active inflammation, tissue injure, healing process simultaneously

Question 2

Chronic inflammation characterized by:

Answer 2

1. Infiltration with mononuclear cell: macrophage, lymphocyte, plasma cell.
2. Tissue destruction: product of inflammatory cell.
3. Repair: new vessels proliferation (angiogenesis) and fibroses.

Question 3

Acute inflammation may progress to chronic inflammation, this transition occur when acute inflammation cannot resolved , either because

Answer 3

1. Persistence of the injury agent.
2. Interference with normal process healing.

Question 4

Example: peptic ulcer of the duodenum

Answer 4

Initially show acute inflammation, but the recurrent duodenal epithelial injury interrupt this process and result to both chronic and acute inflammation.

Question 5

Mechanism result to chronic inflammation:
1. Persistence / resistance:

Answer 5

Resistance infections: mycobacterium, histoplsama, parasite, Nocardia, blastomyces.
These can avoid or resist phagocytosis (macrophage, neutrophil) or inside these cell and prevent fusion with lysosome.

Question 6

Mechanism result to chronic inflammation:
2. Isolation:

Answer 6

Some microbes (streptococcaus, staphylococcus) are not resistant to phagocytosis, but can able to isolate themselves from innate and adaptive immunity and antimicrobial drug by hiding themselves in pus

Question 7

Mechanism result to chronic inflammation:
3. Unresponsiveness:

Answer 7

Some foreign material are indestructible and are unresponsive to phagocytosis and enzymatic breakdown
Such as: plant material, grass awns, silica dust, asbestos fibers, some suture material, surgical prostheses.

Question 8

Mechanism result to chronic inflammation:
4. Autoimmunity and leukocyte defect:

Answer 8

Alteration in regulation of adaptive immune response to self antigen result to autoimmune disease and chronic inflammation.

Question 9

Mechanism result to chronic inflammation:
5. Unidentified mechanisms:

Answer 9

canine granulomatous meninoencephalitis the cause of chronic inflammation remains unknown.

Question 10

Outcome of acute inflammation:
- two possible:

Answer 10

1. Fully resolve with return of tissue to normal function and structure.
2. Repair by healing.

Question 11

If conditions do not allow for complete resolution of acute inflammatory response three outcomes can result:

Answer 11

1. Progression to chronic / granulomatous inflammation.
2. Healing by fibrosis.
3. Abscess formation.

Question 12

These outcomes are determined by:

Answer 12

1. Severity of tissue damage.
2. Ability of cell to regenerate.
3. Biological characteristics of stimulus that cause injury.

Question 13

Tissue damage or necrosis —> acute inflammation
Four outcome:

Answer 13

1. Minimal tissue damage —> resolution (complete healing function and structure).
2. Damage Neutralized with Tissue Destruction —> organization with granulation tissue —> Healing by repair (fibrosis).
3. Sever neutrophil response —> abscess formation.
4. Persistent damage agent —> organization with continued inflammation—> chronic inflammation

Question 14

Progression To Chronic/Granulomatous Inflammation:
- occur when:

Answer 14

1. inciting stimulus persisting for a long period of time (weeks to months).
2. Extensive tissue damage and necrosis (third-degree burn).
3. shift of cellular inflammatory response from neutrophils to lymphocytes, macrophages and multinucleated giant cells.
4. Extensive tissue reorganization followed by fibrosis.
5. Agents that continuously induce inflammatory mediators, promoting macrophage infiltration, activation of T lymphocytes, NK cells, mast cells, and fibroblast proliferation.

Question 15

Healing by Fibrosis:
- Occurs:

Answer 15

• following tissue injury in which there is necrosis of tissue framework.
• process:
  1. Macrophages remove dead tissue and acute inflammatory exudate.
  2. Space is filled with fibrovacular tissue (granulation tissue).
  3. Granulation tissue is replaced by immature fibrous connective tissue that is poorly collagenized
  4. Then → mature fibrous connective tissue → healing the wound and forms a scar (cicatrix).
  5. Structural integrity is reestablished but functional integrity is dependant on the extent of loss of epithelial cells.

Question 16

Abscess Formation:

Answer 16

• occurs when acute inflammatory response fails to eliminate the inciting stimulus. When enzymes and inflammatory mediators from neutrophils in exudate liquefy the affected tissue and neutrophils to form pus.
• two type: Septic, Aseptic

Question 17

Septic abscess:

Answer 17

• originate from bacterial infection (Staphylococcus and Streptococcus).
• The color depends on produced by bacterium:
• Staphylococcus and Streptococcus = yellow exudate.
• Pseudomonus aeruginosa = green exudate.
• Serratia marcescens = red

Question 18

Aseptic abscess:
- caused by

Answer 18

• incompletely degraded foreign body.
• failure of injected medications to be completely absorbed.

Question 19

Abscess

Answer 19

• After acute inflammatory response begins, septic abscess consist
  of a collection of neutrophils that may not be
  surrounded by a thin vascularized connective tissue wall (pyogenic membrane) at this point antibiotics can penetrate that capsule. وخلص بنحل
• If septic abscess persist the thin connective tissue wall, mature into a fibrous capsule which is thick and impermeable. اذا كان غير نفاذ وقتها بتحول ل chronic