Acute inflammation involves increased blood flow and permeability of blood vessels, allowing neutrophils to adhere to vessel walls, transmigrate into tissues, and phagocytose pathogens through adhesion, engulfment, and degradation. This triggers neutrophils to release inflammatory products, while defects can increase infection risk. The key events are vasodilation, increased permeability, neutrophil adhesion and migration to injured sites, phagocytosis, and release of leukocyte products.

1. RADANG AKUT
Mahmud Ghaznawie
Dept Pathology

2. RADANG AKUT
• Perubahan vaskuler
a. Perubahan aliran dan ukuran
pembuluh darah
b. Peningkatan permeabilitas vaskuler
• Peristiwa seluler: ekstravasasi leukosit
dan fagositosis
a. Adhesi dan transmigrasi
b. Kemotaksis dan aktivasi leukosit
Outline

3. c. Fagositosis (pengenalan, perlekatan,
pelahapan dan degradasi)
d. Pengeluaran produk leukosit
e. Defek fungsi leukosit

4. Jejas pada sel

5. RADANG AKUT
• Merupakan respon langsung dan
dini terhadap jejas
• Ditandai perubahan sirkulasi mikro,
eksudasi cairan dan transmigrasi
leukosit dari pembuluh darah ke
tempat jejas

8. CARDINAL SIGN
• Rubor
• Calor
• Tumor
• Dolor
• Functio laesa

9. ISTILAH-ISTILAH
• Eksudasi
• Eksudat
• Transudat
• Edema
• Pus

10. PERUBAHAN VASKULER
• Perubahan kaliber pembuluh darah
dan aliran darah
a. Vasodilatasi
b. Perlambatan sirkulasi
c. Stasis
• Peningkatan permiabilitas vaskuler
(vascular leakage)

12. Mekanisme
terjadinya
vascular leakage
Kontraksi endotel
(histamin,bradikinin,
lekotrin)
Reorganisasi
sitoskeleton
(sitokin)
Jejas langsung
Leakage diperantarai
leukosit
Leakage dari endotel
regeneratif

13. PERISTIWA SEL DARAH PUTIH
• Marginasi, rolling, adhesi
• Transmigrasi (diapedesis)
• Migrasi menuju stimulus
kemotaktik

14. Peristiwa sel darah putih

15. Adhesi leukosit
pada endotel

16. Interaksi endotel neutrofil

17. TRANSMIGRASI
• Terjadi sepanjang interseluler junction
• Tergantung umur lesi dan tipe stimulus
• Neutrofil (6-24 jam)
• Monosit (24-48 jam)
• Pseudomonas (neutrofil ~ 2-4 hari)
• Virus ~ limfosit
• Hipersensitivitas ~ eosinofil

18. Reaksi radang akut

19. Peristiwa Sel Darah Putih

20. Ikatan ligan-reseptor
Ikatan ligan-reseptor

21. FAGOSITOSIS
• Pengenalan dan perlekatan
• Pelahapan
• Pembunuhan atau degradasi

22. Fagositosis
Fc
C3
NADPH
NADP+
Oksidase aktif
SITOPLASMA VAKUOLA FAGOSITIK
Oksidase sitoplasmik
Oksidase membran
Granula spesifik

23. PENGELUARAN PRODUK
LEUKOSIT
• Terdiri dari : E. lisosom,
metabolit aktif O2, prostalglandin
dan lekotrin.

24. DEFEK FUNGSI LEUKOSIT
• Lebih rentan terhadap infeksi
• Genetik :
a. LAD tipe1,2 (defisiensi molekul
adhesi)
b. CGD (defisiensi NADPH oksidase)
c. Chediak-Higashi S. (neutrofenia,
defektif degranulasi, perlambatan
pembunuhan bakteri)

25. • Didapat :
a. Kemotaksis : febris, diabetes ,
sepsis, immunodefisiensi
b. Adhesi : hemodialisis, DM
c. Fagositosis, aktivitas mikrobisidal :
leukemia, anemia, sepsis, diabetes,
neonatus, malnutrisi

26. MANIFESTASI KLINIK
(SISTEMIK)
• Febris : pirogen dan prostalglandin
• Perubahan hitung sel darah putih perifer
- Neutrofil leukositosis
- Neutropenia, limfositosis
• Perubahan protein plasma
C-reactive protein, antitrypsin, fibrinogen,
haptoglobin, ceruloplasmin

27. RINGKASAN
Reaksi radang akut :
• Aliran darah meningkat (dilatasi
arteriol)
• Permeabilitas meningkat
(interendotel junction melebar, jejas
langsung endotel)

28. • Neutrofil (adhesi, transmigrasi,
migrasi ke tempat jejas)
• Fagositosis
• Produk leukosit

29. Acute Inflammation. A capillary
surrounded by PMN leucocyte in are of
inflammation.

30. Purulent exudate in some alveoli of the lung
(left). Alveoli to the right are dilated as
compensatory measure for the obstruction of
alveoli on the left.

31. Alveolar exudate. Leucocytes in the alveoli together
with strands of fibrin. Venules in the alveolar walls
are dilated as part of the inflammatory response.

32. Fibrinous exudate. Pink staining threads of
fibrin with leucocytes in alveoli. The vessels
are dilated.

33. Pus. Section of skin showing an accumulation of the pus
(pustule) in the epidermis. This is often seen in impetigo
which superficial infection caused by coccal bacteria.

34. Purulent exudate. The edge of an ulcer in the
colon. Damaged colonic epithelium is seen on
the left and purulent exudate in the base of the
ulcer on the right.

35. Fibrinopurulent
exudate. The wall
of an ulcer showing
fibrinopurulent
exudate on the
surface (top) and
newly formed
vessels (granulation
tissue) deeper down.

36. Acute inflammation.
Section of heart muscle
an visceral pericardium
showing pink layer of
fibrin on the surface.
Inflammatory cells and
dilated vessels are
present in the
underlying connective
tissue.

37. Acute inflammation. Visceral pericardium.
Movement of the heart in pericardial sac causes
strands of fibrin to project into the lumen of the
pericardial sac.

38. Plasma cells and mast cells

39. Mast cells with fibroblast on the right.
The mast cell granules have stain bright
red with solachrome cyanin.

40. Mast cell granules also stain bright blue with
toluidine blue.

41. Eosinofil leucocyte.