Lecture 5: Chronic Inflammation and wound healing Flashcards

1
Q

what are the major players in chronic inflammation

A

Macrophages, lymphocytes, plasma cells, fibroblasts

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2
Q

What are the 4 outcomes of progression to acute inflammation to chronic inflammation

A
  1. Abscess formation
  2. Progression to chronic/granulomatous inflammation
  3. Healing with increased cellularity
  4. Healing by fibrosis
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3
Q

What type of inflammatory response involves fibrin

A

Acute

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4
Q

What type of inflammatory response involves fibrous

A

Chronic

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5
Q

What is granulomatous inflammation and granulomatous formation

A

Type of chronic inflammation in which cells of monocyte-macrophage system predominant and take form of macrophages, epithelioid macrophages, and multinucleated giant cells

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6
Q

What are the 3 distinct morphological areas of a granuloma

A
  1. Innermost- macrophages, multinucleated giant cells +/- cellular necrosis
  2. Middle: macrophages, epithelioid macrophages, and multinucleated giant cells
  3. Outermost: lymphocytes, plasma cells, fibroblasts with fibrous capsule
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7
Q

What is chronic active inflammation and provide an example

A

Same cellular components as chronic inflammation but also contains acute inflammatory response with neutrophils, fibrin, and plasma proteins

Ex: FIP

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8
Q

What is the cause of FIP

A

Mutated feline enteric coronavirus

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9
Q

What does FIP grossly look like

A

Multifocal gray-tan slightly raised foci (pyogranulomatous) that follow vascular structures and tend to coat serosal surfaces with thick effusion

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10
Q

What does the histopathology of FIP look like

A

Pryogranulomatous vasculitis

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11
Q

What is the pathogenesis of FIP

A
  1. Ingestion of feline enteric coronavirus (fecal-oral)
  2. Replication in enterocytes and Peyers patches
  3. Replication and mutation in macrophages and blood monocytes
  4. Virus infected macrophages disseminated to other organs
  5. Host immune response—> pyogranulomatous vasculitis
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12
Q

What are the 4 phases of wound healing and describe each phase

A
  1. Hemostasis: vasoconstriction, blood vessel relaxation, platelet aggregation at exposed collagen
  2. Acute inflammation
  3. Prolioferation: rebuild with granulation tissue, angiogenesis, and epitheliazation
  4. Maturation: synthesis changes from type III collagen to type I, blood vessels regress and decrease, collagen synthesis stops, result: scar formation
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