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INFLAMASI

Isa Ma’rufi
Fakultas Kesehatan Masyarakat
Universitas Jember
Inflamasi

respon fisiologis tubuh terhadap suatu injuri


dan gangguan oleh faktor eksternal.
Inflamasi

mekanisme proteksi yang terbatas


terhadap trauma atau invasi mikroba
dengan reaksi yang menghancurkan,
mengurangi, mengurung (sekuestrasi),
atau membatasi bahan yang berbahaya
dan merusak jaringan.
Inflamasi diperlukan
• Menahan & memisahkan jejas
• Menghancurkan mikroorganisme
• Menginaktifkan toksin
• Mencapai penyembuhan dan perbaikan
Efek Negatif Inflamasi
• Reaksi hipersensitivitas
• Kerusakan organ progresif
• Pembentukan jaringan parut
• Mengancam jiwa
Inflamasi
• benda asing yang masuk tubuh
• invasi mikrorganisme
• trauma
• bahan kimia yang berbahaya
• faktor fisik
• alergi.
Jalur peradangan
• Vasodilatasi pembuluh darah
• Permeabilitas vaskuler meningkat
• Kerusakan dan kebocoran vaskuler
• Cairan dan sel meningkat
• radang
Symptoms
• Redness (rubor) (kemerahan)
• Heat (calor) (panas)
• Swelling (tumor) (pembengkakan).
• Pain (dolor) (rasa sakit)
• Functio laesa (perubahan fungsi)
2 MACAM INFLAMASI
• INFLAMASI AKUT
• INFLAMASI KRONIK
INFLAMASI AKUT
• Inflamasi akut adalah respon yang cepat
dan segera terhadap cedera yang
didesain untuk mengirimkan leukosit ke
daerah cedera.
• ditandai dengan perubahan vaskular,
eksudasi cairan dan protein plasma serta
akumulasi neutrofil yang menonjol.
FAKTOR INFLAMASI AKUT
Vasodilatation: Events in Acute Inflammation
• Histamine
• Prostaglandins
• Nitric oxide

Increased vascular permeability:


• Histamine
• Anaphylatoxins C3a and C5a
• Kinins
• Leukotrienes C, D, and E
Chemotaxis:
• PAF
• Complement fragment C5a
• Substance P
• Lipoxygenase products,
lipoxins & leukotrines (LTB4)
• Chemokines

Tissue Damage
• Lysosomal products
• Oxygen-derived radicals
• Nitric Oxyde
Table 3–2. Mediators of Acute Inflammation.

Mediator Vasodilation Immediate Sustained Chemotaxis Opsonin Pain


Histamine + +++ – – – –

Serotonin (5–HT) + + – – – –

Bradykinin + + – – – ++

Complement 3a – + – – – –

Complement 3b – – – – +++ –

Complement 5a – + – +++ – –

Prostaglandins +++ + + – –

Leukotrienes – +++ + +++ – –

Lysosomal proteases – – ++1 – – –

Oxygen radicals – – ++1 – – –


Summary of Mediators of Acute Inflammation
ACTION
Mediator Source Vascular Leakage Chemotaxis Other
Histamine and
Mast cells, platelets + -
serotonin
Bradykinin Plasma substrate + - Pain
C3a Plasma protein via liver + - Opsonic fragment (C3b)
Leukocyte adhesion,
C5a Macrophages + +
activation
Mast cells, from
Potentiate other
Prostaglandins membrane - Vasodilatation, pain, fever
mediators
phospholipids
Leukocyte adhesion,
Leukotriene B4 Leukocytes - +
activation
Leukotrienes Bronchoconstriction,
Leukocytes, mast cells + -
C4 D4 E4 vasoconstriction
Platelet
Bronchoconstriction,
Activating Factor Leukocytes, mast cells + +
leukocyte priming
(PAF)
Acute-phase reactions,
IL-1 and TNF Macrophages, other - +
endothelial activation
Chemokines Leukocytes, others - + Leukocyte activation

Macrophages,
+ + Vasodilatation, cytotoxicity
endothelium
Suppurative or purulent inflammation is
characterized by the production of large amounts
of pus or purulent exudate consisting of
neutrophils, necrotic cells, and edema fluid.
FIBRINOUS INFLAMMATION
With more severe injuries and the resulting greater
vascular permeability, larger molecules such as
fibrinogen pass the vascular barrier, and fibrin is
formed and deposited in the extracellular space
An ulcer is a local defect, or excavation, of the
surface of an organ or tissue that is produced by
the sloughing (shedding) of inflammatory necrotic
tissue
INFLAMASI KRONIK
• Radang kronis dapat diartikan sebagai
inflamasi yang berdurasi panjang
(berminggu-minggu hingga bertahun-
tahun) dan terjadi proses secara simultan
dari inflamasi aktif, cedera jaringan, dan
penyembuhan.
• Inflamasi kronis menyusul respons akut berupa
influks monosit, eosinofil.
• Bila keadaan menjadi terkontrol, neutrofil
dikerahkan lagi dan berdegenerasi. Selanjutnya
akan dikerahkan sel mononuklear.
• Pada stadium ini, dikerahkan monosit, makrofag,
limfosit dan sel plasma yang memberikan
gambaran patologik dari inflamasi kronis .
• Inflamasi kronis dapat bermula dari
inflamasi akut bila agen perusak menetap,
tetapi yang lebih sering terjadi adalah
bahwa respons inflamasi itu adalah
respons inflamasi kronis sejak awal.
Penyebab Inflamasi Kronis
• infeksi persisten oleh mikroorganisme
intrasel tertentu (seperti basil tuberkel,
Treponema palidum, dan jamur-jamur
tertentu),
• kontak lama dengan bahan yang tidak
dapat hancur (misalnya silika)
• penyakit autoimun.
Maturation of Mononuclear Phagocytes
• inflamasi akut :perubahan atau kerusakan
vaskuler luas dan infiltrasi neutrofil.

• inflamasi kronis: menunjukkan ciri infiltrasi


jaringan dengan sel mononuklear seperti
makrofag, limfosit, dan sel plasma disertai
dengan destruksi jaringan.
• Makrofag merupakan pemain kunci dari
respons inflamasi kronis.

• Makrofag: banyak melepaskan produk


bioaktif atau mediator.
• aktivitas makrofag secara terus menerus
dapat berakibat kerusakan jaringan
berkelanjutan.
Effects of Macrophage Activation
Sel yg berperan:
• Infiltration with mast cells, lymphocytes and plasma cells
• Lymphocytes
– Mobilization in both antibody – mediated
• Mast Cells
– Widely distributed in connective tissues and participate in both acute
and persistent inflammatory reactions
– Binds the Fc portion of the IgE antibody
• Plasma Cells
– Produce antibody directed either against persistent antigen in the
inflammatory site or against altered tissue components
• Eosinophils
– parasitic infections
– Mediated by IgE
– Eotaxin – a chemokine that has the ability to prime eosinophils for
chemotaxis
Lung Granuloma From
Tuberculosis (Tubercle)
Scar Formation From a Granuloma
Table 5–1. Differences between Acute and Chronic Inflammation.

Acute Chronic

Duration Short (days) Long (weeks to months)

Onset Acute Insidious

Specificity Nonspecific Specific (where immune response is activated)

Inflammatory cells Neutrophils, macrophages Lymphocytes, plasma cells, macrophages,


fibroblasts
Vascular changes Active vasodilation, increased permeability New vessel formation (granulation tissue)

Fluid exudation and edema + –

Cardinal clinical signs + –


(redness, heat, swelling, pain)

Tissue necrosis + (ongoing)


– (Usually)
+ (Suppurative and necrotizing inflammation)

Fibrosis (collagen deposition) – +

Operative host responses Plasma factors: complement, immunoglobulins, properdin, etc; Immune response, phagocytosis, repair
neutrophils, nonimmune phagocytosis

Systemic manifestations Fever, often high Low–grade fever, weight loss, anemia

Changes in peripheral blood Neutrophil leukocytosis; lymphocytosis (in viral infections) Frequently none; variable leukocyte changes,
increased plasma immunoglobulin
MEDIATOR INFLAMASI
Mast Cells & Allergy
Functions of nitric oxide (NO) in blood vessels and macrophages, produced by
two NO synthase enzymes. NO causes vasodilation, and NO free radicals are
toxic to microbial and mammalian cells. NOS: nitric oxide synthase.
Complement Activation Pathways
The activation and functions of the complement system. Activation of
complement by different pathways leads to cleavage of C3. The functions of
the complement system are mediated by breakdown products of C3 and other
complement proteins, and by the membrane attack complex (MAC)
Production of microbicidal reactive oxygen
intermediates within phagocytic vesicles.
Basophils & Mast Cells

Histamine
• SEKIAN, TERIMA KASIH……..