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Brian Wasita
Inflammation
An important physiological reaction which
occurs in response to a wide variety of
injurious agents (e.g. bacterial infection or
physical trauma) ultimately aiming to
perform the dual function of limiting damage
and promoting tissue repair
(Scull et al, 2010)
Cardinal sign
1.Rubor (redness)
Due to vessel dilatation and increased blood flow.
2. Calor (heat)
Due to vessel dilatation and increased blood flow.
3.Dolor (pain)
Due to combination of :
Pressure on nervus ending by swelling
Direct effect from mediator inflammation released
in inflammation response.
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4.Tumor (swelling)
Due to accumulation of exudate
5. Functio laesa (loss of function)
Laboratory findings
1.Leukocytosis (IL-1, TNF-)
2.Leukopenia (ex:thypoid fever, viral
infection)
3.Increased acute phase protein (ex: CRP)
Acute Inflammation
Duration
Main characteristics
Chronic Inflammation
Edema
Emigration of leukocytes
(especially neutrophils)
The presence of
lymphocytes and
macrophages
Proliferation of blood
vessels
Fibrosis
Tissue necrosis
Acute Inflammation
Three major events
1.Changed in vascular caliber that leads in
an increase in blood flow.
2.Increased vascular permeability that cause
vascular leakage.
3.Leukocyte extravasation and phagocytosis
Leukocyte extravasation
Step:
(Kumar et at, 2005)
1.Margination, rolling, and adhesion
2.Diapedesis
3.Migration in interstitial tissue toward
1 chemotactic stimulus
4
Phagositosis
1
6
1
7
Cytokines in inflammation
Cytokines:
Protein produce by many type of cells (especially activated lymphocytes and
macrophages) that modulate the function of other cell types.
2
0
2
2
Treatment of Inflammation
1.Eliminate the source of inflammation
2.Inhibit mediator of inflammation
a.Glucocorticoids (steroid)
Down regulate specific target gene (COX-2,
gene pro-inflammation(Ristimki,2004) )
Up-regulate genes that encode potent anti
inflammatory protein ex: lipocortin 1
b. NSAID
2
3
Chronic inflammation
Prolonged duration of inflammation in which active
inflammation, tissue destruction, and tissue
repairing are proceeding simultaneously
Causes:
1.Persistent infections (tubercle bacilli, treponema
pallidum)
2.Prolonged exposure to potentially toxic agents
(exogenous:silica; endogenous: toxic plasma lipid
components)
3.Autoimmunity:rhematoid arthritis,lupus
erythematosus)
2
4
Histological features
1.
2.
3.
4.
Serous inflammation
Fibrinous inflammation
Supurative inflammation
Ulcers
2
8
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Local infection
An infection that is limited to a small area (a certain site
or focus) of the body.
Example: pneumonia, urinary tract or bladder infections,
appendicitis, and skin infections.
Skin abscess
Acute appendicitis
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Characteristic
Infectious agent
Characteristic
Mononuclear
Diffuse infiltrate of predominantly mononuclear cells
Plasma cells : primary syphilis
Lymphocytes : HBV, viral infection
Granulomatous:
Giant celss: TBC
Infectious agent
3.
Cytopathic-cytoproliferative Inflammation
Virus-mediated damage to individual host cells in the
absence of host inflammatory response
Characteristic
Infectious agent
4.
Necrotizing Inflammation
Characteristic
Infectious agent
5.
Characteristic
Infectious agent
References
1. Department of Pathology University of Pittsburgh School of Medicine
http://path.upmc.edu/cases/index.html
2. Kahn MA and Solomon LW: Basic Human Pathology Lecture 5: Acute
Inflammation/ Wound Healing & Repair I,University of Tufts ; 2007
3. Kumar V, Abbas AK,Vausto N, editors. Robbins and Cotran PATHOLOGIC
BASIS OF DISEASE.7thed. Philadelphia: Elseiver Saunders; 2005.
4. Lister MF, Sharkey J , Sawatzky DA , Hodgkiss JP, Davidson DJ, Rossi AG
and Finlayson K. The role of the purinergic P2X7 receptor in inflammation. J
Inflamm (Lond) 2007, March 16; 4:5
5. Ristimki A. Cyclooxygenase 2: from inflammation to carcinogenesis. Novartis
Found Symp. 2004;256:215-21; discussion 221-6, 259-69.
6. Scull CM, Hays WD, Fischer TH. Macrophage pro-inflammatory cytokine
secretion is enhanced following interaction with autologous platelets. J
Inflamm (Lond). 2010 Nov 11;7:53.
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