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Systemic Inflammation and Healing Responses

The document summarizes the acute phase response to inflammation and chronic inflammation patterns. The acute phase response is characterized by decreased appetite, altered sleep, fever, leukocytosis, and changes in plasma protein levels mediated by cytokines like TNF, IL-1, IL-6. Chronic inflammation patterns include eosinophilic, lymphocytic, macrophage, and granulomatous responses. Wound healing involves neovascularization, granulation tissue formation, remodeling, and can result in complications like inadequate scar formation, excessive scar formation, exuberant granulation tissue, or contraction.
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100% found this document useful (1 vote)
136 views3 pages

Systemic Inflammation and Healing Responses

The document summarizes the acute phase response to inflammation and chronic inflammation patterns. The acute phase response is characterized by decreased appetite, altered sleep, fever, leukocytosis, and changes in plasma protein levels mediated by cytokines like TNF, IL-1, IL-6. Chronic inflammation patterns include eosinophilic, lymphocytic, macrophage, and granulomatous responses. Wound healing involves neovascularization, granulation tissue formation, remodeling, and can result in complications like inadequate scar formation, excessive scar formation, exuberant granulation tissue, or contraction.
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SYSTEMIC EFFECTS OF INFLAMMATION

THE ACUTE PHASE RESPONSE


Characterized by: Mediators Notes
1. Decreased appetite
2. Altered sleep pattern
3. Fever TNF, IL-1, IL-6

4. Leukocytosis TNF, IL-1 Neutrophilia – bacterial infection


Lymphocytosis – viral infection (some)
Eosinophilia – parasites; allergic reactions
Leukemoid reaction – extreme elevations

5. Changes in Plasma IL-1, IL-6 Acute-phase proteins (↑ synthesis & plasma levels)
Protein Level  C-reactive proteins
Greatest increase
 Serum amyloid A
 Complement proteins
↑ Inflammation
 Coagulation proteins
 A1-antitrypsin
 Cysteine proteinase inhibitor ↓ Inflammation
 Ceruloplasmin
Negative acute-phase proteins (↓ synthesis & plasma levels)
 Albumin
 Transthyretin
CHRONIC INFLAMMATION PATTERNS
PATTERN NOTES
1. Eosinophilic response Parasites, allergic rxns
2. Lymphocytic & plasma response Viral infections, hypersensitivity, neoplasms
3. Macrophage response
4. Granulomatous response
- Mediated by lymphokines from activated T-cells

o Hypersensitivity type
- “Immune granuloma”
- Lymphocyte-mediated (T-cell mediated rxn)
- Response to [poorly degradable] antigens
- Giant cell: Langhans giant cell in TB
o Non-hypersensitivity type
- “Foreign body granuloma”
- Response to poorly digestible materials
- Giant cell: Bag of beans / M&M appearance

Healing by Repair (Scar formation) Wound Healing


o Neovascularization Primary Intention/union Secondary Intention/union
o Angiogenesis – VEGF; from existing - Minimal tissue loss - Larger defect (ulcer-type wound)
blood vessels - No infection - Infection: Inflammation & necrosis
o Granulation tissue formation - Good approximation of edges - Not good approximation of edges
o Remodeling of connective tissue - Regeneration and maturation - No re-epithelialization (capacity to
o WBCs & edema of epithelium re-epithelialize exceeded)
- Granulation tissue w/in wound - Much more granulation tissue w/
site wound contraction
- Scarring w/ loss of dermal - Myofibroblast predominant after
appendages several days
Pathologic Aspects of Repair
1. Inadequate formation of granulation tissue 3. Exuberant granulation (proud flesh)
or formation of scar can lead to two types  Desmoids or aggressive fibromatoses – proliferation of
of complications: fibroblasts and other repair elements; interface between benign
 Wound dehiscence and low-grade malignant tumors
 Ulceration 4. Contraction
2. Excessive formation of the components of  particularly prone to develop on the palms, soles, and the
the repair process can give rise to: anterior aspects of of the thorax (after serious burns)
 Keloid – CT extend beyond initial
wound
 Hypertrophic scar – does not extend
beyond initial wound

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