Proses_Radang_.pdf

7/23/2019 Proses_Radang_.pdf

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Kuliah Blok Infeksi

Proses Peradangan dan Infeksi Lokal

Brian Wasita

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•Inflammation

An important physiological reaction whichoccurs 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)

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The outcome of inflammation

(Kumar et at, 2005)

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(Lister et at, 2007)

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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)

(Kahn MA and Solomon LW, 2007)

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Systemic Manifestation of Inflammation

Clinical manifestation

1. Fever (IL-1, IL-6, TNF-α)2. Chills

3. Malaise4. Somnolent

5. Anorexia6. Increased pulse and blood pressure

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(Kumar et at, 2005)



Laboratory findings

1.Leukocytosis (IL-1, TNF-α)2.Leukopenia (ex:thypoid fever, viral

infection)3.Increased acute phase protein (ex: CRP)

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Kumar et at, 2005



Acute Inflammation Chronic Inflammation

DurationShort duration (minutes,

several hours, a few days)

Longer duration (weeks,

months)

Main characteristics

Edema

Emigration of leukocytes

(especially neutrophils)

The presence of

lymphocytes andmacrophages

Proliferation of blood

vessels

Fibrosis

Tissue necrosis

(Kumar et at, 2005)

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Acute Inflammation due to frostbite

Chronic inflammation due

to Rheumatoid arthritis

Figures source: Wikipedia

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Acute Inflammation

Three major events

1.Changed in vascular caliber that leads inan increase in blood flow.

2.Increased vascular permeability that causevascular leakage.

3.Leukocyte extravasation and phagocytosis

(Kumar et at, 2005)1

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2

Ch d i l lib d l



Changed in vascular caliber and vascular

leakage

(Kumar et at, 2005)

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Leukocyte extravasation

Step:

1.Margination, rolling, and adhesion2.Diapedesis

3.Migration in interstitial tissue toward chemotactic stimulus

(Kumar et at, 2005)

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Endothelial/Leukocyte Adhesion Molecules in Leukocyte

extravasation


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Phagositosis


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Chemical mediators of Inflammation


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Arachidonic Acid Pathway



Arachidonic Acid Pathway

AA is 20-carbon polyunsaturated fatty acid

Source: dietary diet or by conversion from linoleic acidRelease from membrane phospholipids by: mechanical,chemical, physical

stimuli or by other mediatos

(Kumar et at, 2005)

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(Kumar et at, 2005)

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Cytokines in inflammation



Cytokines in inflammation

Cytokines:

Protein produce by many type of cells (especially activated lymphocytes and

macrophages) that modulate the function of other cell types.


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(Kumar et at, 2005)

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Leukocyte induce tissue injuryLeukocyte release product into extracellular sapce which can caused endothelial

injury and tissue damage.

The product released by leukocyte:

lysosomal enzyme, oxygen derived active metabolites, and product of archidonic

acid metabolism (prostaglandins and leukotrienes)


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Treatment of Inflammation

1.Eliminate the source of inflammation

2.Inhibit mediator of inflammationa.Glucocorticoids (steroid)

•Down regulate specific target gene (COX-2,gene pro-inflammation(Ristimäki,2004) )

•Up-regulate genes that encode potent anti

inflammatory protein ex: lipocortin 1

b. NSAID

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Chronic inflammation• Prolonged duration of inflammation in which active

inflammation, tissue destruction, and tissue

repairing are proceeding simultaneouslyCauses:

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)(Kumar et at, 2005)2

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Hi t l i l f t



Histological features

1. Infiltration of mononuclear cells (macrophages, lymphocytes, and

plasma cells).

2.Tissue destruction.3.Connective tissue replacement of damaged tissue, angiogenesis, and

fibrosis.

Kumar et at, 2005

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Cells in chronic inflammation

1. Macrophage (Kupffer cells in liver,

alveolar macrophages in lungs)2. Lymphocytes (T and B)

3. Mast cells4. Eosinophils

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Kumar et at, 2005



Morphologic variation in acute and chronic

inflammation

1. Serous inflammation

2. Fibrinous inflammation3. Supurative inflammation

4. Ulcers


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Specific pattern of chronic inflammation

Granulomatous inflammation

Predominant cell type is an activated macrophage with a modified epithelial-like

appearance.

(ex: tuberculosis, sarcoidosis, leprosy, syphilis)

Granuloma:

A focal area of granulomatous inflammation, consists of a microscopic aggregationof macrophages that are transformed into eptithelium-like cells surrounded by a colar

of mononuclear leukocytes principally lymphocytes and occasionally plasma cells.

Kumar et at, 2005

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Tuberculous granuloma

(Kumar et at, 2005)

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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.

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Skin abscess Acute appendicitis



Inflammatory response for infection

1. Suppurative (Polymorphonuclear) Inflammation

The reaction to acute tissue damage

Characteristic •Increased vascular permeability

• Leukocytic infiltration, predominantly of neutrophils

•Pus formation

Infectious agent •extracellular Gram-positive cocci and Gram-negativerods.

(Kumar et al, 2005)

2 Mononuclear and granulomatous inflammation



2.Mononuclear and granulomatous inflammation

Characteristic Mononuclear

•Diffuse infiltrate of predominantly mononuclear cells

•Plasma cells : primary syphilis

•Lymphocytes : HBV, viral infection

Granulomatous:

Giant celss: TBC

Infectious agent •Viruses, intracellular bacteria, spirochetes, intracellular

parasites or helminths.

(Kumar et al, 2005)

3 Cytopathic cytoproliferative Inflammation



3. Cytopathic-cytoproliferative Inflammation

Characteristic Depent on the type of virus

•Inclusion bodies : CMV or adenovirus

•Polykaryons: measles virus or herpes virus

•Blisters : herpes virus

•Unusual individual and aggregate morphologic lession

(veneral warts) : HPV

Infectious agent •Virus : CMV, measles virus, herpes viruses, HPV,poxviruses

Virus-mediated damage to individual host cells in the

absence of host inflammatory response

(Kumar et al, 2005)

4 Necrotizing Inflammation



4. Necrotizing Inflammation

Characteristic Rapid and severe tissue damage with only few/no

involvement of inflammatory cells.

Infectious agent Clostridium perfringens, Entamoeba hystolitica, herpes

virus, HBV

(Department of Pathology University of Pittsburgh School of

Medicine)

(Kumar et al, 2005)

5 Chronic inflammation and scarring



5. Chronic inflammation and scarring

Characteristic Rarely appear in pure form, they frequently overlap

In cutaneous leishmaniasis:

Central part: ulcerated area filled with neutrophils

Peripheral area: a mixed infiltrate of lymphocytes and

mononuclear cells

Infectious agent Schistosoma, Leishmania, CMV

Final common pathway of many infection

(Kumar et al, 2005)



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: AcuteInflammation/ 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. Ristimäki 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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Proses_Radang_.pdf