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1. Oleh:
Yudha Anggit J, S.Kep, M.Kes
PATOLOGI ANATOMI &
PATOLOGI KLINIK
Radang, Pemulihan
Jaringan & Sistem
Hemopoetik
“Wahai Tuhanku, tambahkanlah pengetahuan
kepadaku dan anugerahkanlah pemahaman
kepadaku…amin”

2. Radang (Inflamasi)
 Definisi= Respon dari jaringan hidup terhadap
cedera, yang menimbulkan eksudat (cairan kaya
protein (kecuali eksudat bening/serous) yg
keluar dari vaskuler).
 Manifestasi= - Lokal
- Umum
* transudat= cairan keluar melalui suatu membran baik
dari vaskuler maupun jaringan, cenderung sangat cair
dan kurang bahan padatnya.

3. Manifestasi Lokal:
1. Makroskopik: panas (kalor), nyeri (dolor), bengkak
(tumor), kemerahan (rubor) & berkurangnya fungsi
(functio laesa)
 5 “tanda radang yg utama” dirintis oleh Celsus.
2. Mikroskopik: konstriksi arteriolar sementara -
vasodilatasi - permeabilitas dinding vaskuler  -
eksudat - hemokonsentrasi - marjinasi leukosit -
emigrasi leukosit & diapedesis eritrosit - kemotaksis
leukosit PMN - fagositosis - timbul makrofag /
histiosit fagositik

4. Extravasation of leukocyte
Margination, rolling, adhesion, diapedesis, chemotaxis
& phagocyitosis

5. 3. Komponen dasar
Manifestasi Lokal :
Vaskular: Terjadi peningkatan aliran darah yg
relatif statik pada daerah radang  rubor &
kalor
Selular
1) Vaskular
2) Selular
3) Eksudat
Dari darah: - Leukosit PMN (Polimorfonuklear)
- Limfosit (T & B)  imun selular &
humoral
- Monosit
Dari jaringan: - Histiosit / Makrofag jaringan
- Fibroblas
- Sel datia

6. * Leukosit PMN= Neutrofil (sel pertama & terbanyak pada
radang akut; 60% dari seluruh leukosit), Eosinofil (kebanyakan
berkaitan dgn infeksi parasit dan alergi; 3% dari leukosit) &
Basofil & sel mast (kebanyakan pada penyakit yg diperantarai
sistem imun; 1% dari leukosit)
* Limfosit (30% dari leukosit)= tidak mencapai daerah radang
pada stadium dini, tapi penting pada radang kronik
* Monosit (6% dari leukosit)= merupakan sel fagosit jumlahnya
sedikit, respon kemotaksis lemah
* Histiosit= morfologi mirip monosit, aktif dalam fagositosis
* Fibroblas= sel fibrosa muda pada stadium peyembuhan
* Sel datia= sel besar berinti banyak berupa fusi dari histiosit,
banyak macamnya namun yg sering adalah sel datia benda
asing (inti tersusun sentral) & sel datia Langhans (inti tersusun
perifer membentuk susunan "tapal kuda")

7. Silsilah Sel Darah
(Stem Cell Differentiation and Hematopoesis)

9. Jenis Radang dgn sel-sel khasnya:
1. Akut: Leukosit PMN, kecuali tifoid.
2. Subakut: Leukosit PMN, Sel plasma & Limfosit.
3. Kronik: Limfosit, Sel plasma & Fibroblas.
* Pada semua jenis radang ditemukan monosit
dan makrofag, walau bervariasi.
*Comparison between acute and chronic inflammation:
Acute Chronic
Causative
agent
Pathogens, injured tissues
Persistent acute inflammation due to non-degradable
pathogens, persistent foreign bodies, or autoimmune
reactions
Major cells
involved
Neutrophils
Mononuclear cells (monocytes, macrophages, lymphocytes,
plasma cells), fibroblasts
Primary
mediators
Vasoactive amines, eicosanoids
INF-γ and other cytokines, growth factors, reactive oxygen
species, hydrolytic enzymes
Onset Immediate Delayed
Duration Few days Up to many months, or years
Outcomes
Healing, abscess formation,
chronic inflammation
Tissue destruction, fibrosis

10. Eksudat: Karena 2 hal yaitu Dilatasi arteriolar &
Peningkatan permeabilitas vaskular
* Perantara kimiawi yg sering:
Amin (histamin aktif / hidroksitriptamin / serotonin 
vasodilatasi &  permeabilitas vaskular);
Kinin (bradikinin & kalidin  vasodilatasi,  permeabilitas
vaskular & nyeri);
Protease (dari neutrofil, beberapa merupakan pirogen 
 permeabilitas vaskular, pelepasan histamin, kemotaktik untuk
monosit, membelah C3 dan C5, mengaktivasi kinin & imobilisasi
neutrofil);
Derivat komplemen (misalnya C3a & C5a  pelepasan
histamin dari sel mast, agen kemotaktik);
Prostaglandin (dilepas neutrofil dan trombosit, midal PGE1 dan
PGE2  vasodilatasi, demam & nyeri, mempotensial aksi kinin
& efek protektif);
Zat anafilaksi reaksi lambat (SRS-A) ( permeabilitas vaskular,
bronkospasme)

11. Name Produced by Description
Bradykinin Kinin system
A vasoactive protein which is able to induce vasodilation, increase vascular
permeability, cause smooth muscle contraction, and induce pain.
C3
Complement
system
Cleaves to produce C3a and C3b. C3a stimulates histamine release by mast
cells, thereby producing vasodilation. C3b is able to bind to bacterial cell
walls and act as an opsonin, which marks the invader as a target for
phagocytosis.
C5a
Complement
system
Stimulates histamine release by mast cells, thereby producing vasodilation. It
is also able to act as a chemoattractant to direct cells via chemotaxis to
the site of inflammation.
Factor XII (Hageman
Factor)
Liver
A protein which circulates inactively, until activated by collagen, platelets, or
exposed basement membranes via conformational change. When
activated, it in turn is able to activate three plasma systems involved in
inflammation: the kinin system, fibrinolysis system, and coagulation
system.
Membrane attack
complex
Complement
system
A complex of the complement proteins C5b, C6, C7, C8, and multiple units of
C9. The combination and activation of this range of complement proteins
forms the membrane attack complex, which is able to insert into
bacterial cell walls and causes cell lysis with ensuing death.
Plasmin
Fibrinolysis
system
Able to break down fibrin clots, cleave complement protein C3, and activate
Factor XII.
Thrombin
Coagulation
system
Cleaves the soluble plasma protein fibrinogen to produce insoluble fibrin,
which aggregates to form a blood clot. Thrombin can also bind to cells
via the PAR1 receptor to trigger several other inflammatory responses,
such as production of chemokines and nitric oxide.
Plasma derived mediators
(Perantara kimiawi dari plasma)

12. Name Type Source Description
Lysosome
granules
Enzymes Granulocytes
These cells contain a large variety of enzymes which perform a
number of functions. Granules can be classified as either
specific or azurophilic depending upon the contents, and
are able to break down a number of substances, some of
which may be plasma-derived proteins which allow these
enzymes to act as inflammatory mediators.
Histamine
Vasoactive
amine
Mast cells, basophils, platelets
Stored in preformed granules, histamine is released in response
to a number of stimuli. It causes arteriole dilation and
increased venous permeability.
IFN-γ Cytokine T-cells, NK cells
Antiviral, immunoregulatory, and anti-tumour properties. This
interferon was originally called macrophage-activating
factor, and is especially important in the maintenance of
chronic inflammation.
IL-8 Chemokine Primarily macrophages
Activation and chemoattraction of neutrophils, with a weak
effect on monocytes and eosinophils.
Leukotriene
B4
Eicosanoid Leukocytes
Able to mediate leukocyte adhesion and activation, allowing
them to bind to the endothelium and migrate across it. In
neutrophils, it is also a potent chemoattractant, and is able
to induce the formation of reactive oxygen species and the
release of lysosome enzymes by these cells.
Nitric oxide Soluble gas
Macrophages, endothelial cells,
some neurons
Potent vasodilator, relaxes smooth muscle, reduces platelet
aggregation, aids in leukocyte recruitment, direct
antimicrobial activity in high concentrations.
Prostaglandins Eicosanoid Mast cells
A group of proteins which can cause vasodilation, fever, and
pain.
TNF-α and IL-
1
Cytokines Primarily macrophages
Both affect a wide variety of cells to induce inflammatory
reactions: fever, production of cytokines, endothelial gene
regulation, chemotaxis, leukocyte adherence, activation of
fibroblasts. Responsible for the systemic effects of
inflammation, such as loss of appetite &  heart rate.
Cell derived mediators

13. Makroskopik lain dari Radang Akut:
- Serosa
- Fibrinosa
- Sero-fibrinosa
- Hemoragik
- Supuratif /purulen (: ulkus, abses, empiema)
- Kataral (sekresi mukoid yg banyak)
- Gangren (~trombosis, devitalisasi)
- Flegmon (~nekrosis edematosa)
- Membranosa
- Selulitis (~sedikit timbul, tepi merah, garis merah di
bawah kulit, nyeri tekan)

14. Manifestasi Umum:
- Demam
- Hiperpireksia
- Perubahan dalam darah (leukositosis,
leukopenia, anemia)
- Perubahan pada organ-organ (reaktif lokal
(:makrofag) & umum(:hiperplasi limfe),
degeneratif, septikemia, piemia & bakteriemia)

15. Perbaikan/Pemulihan Jaringan
(Wound Healing)
 Sifat: Hasil akhir dicapai melalui 1) Regenerasi
sel-sel parenkim organ & 2) Petumbuhan
jaringan ikat penyokong
 Mekanisme=
- Penyatuan primer
- Penyatuan sekunder (dgn granulasi)
- Perbaikan dgn resolusi
- Perbaikan dgn organisasi
- Perbaikan dgn regenerasi (~kecuali sistem
saraf  gliosis & otot  hipertrofi jaringan yg
ada)

16.  Faktor-faktor yg mempengaruhi Perbaikan:
- Jaringan yg terlibat
- Vaskularitas
- Proteksi
- Infeksi
- Gizi (~protein)
- Vitamin (vit. C untuk integritas dinding kapiler &
pematangan kolagen, pada scurvy (avit. C)
kemungkinan tidak ada penyembuhan sama sekali)

17. - Umur (~sirkulasi)
- Endokrin
- Suhu
- Ukuran cedera
- Benda asing  debridement
- Sinus & fistula
- Iradiasi
- Saraf sensorik

18. Sistem Hemopoetik
 Hemoglobin (normal laki dewasa= 13 – 188
g/dL; wanita dewasa= 11,5 – 16,5 g/dL)
Suksinil Ko-A Glisin
Asam aminolevulinat (ALA) [2 buah]
Porfirin
Protoporfirin IX
Hem
Hemoglobin [4 buah]
Hematin
Biliverdin
Bilirubin
Bilirubin terkonjugasi
Urobilinogen, dst
Urobilin, dst
Besi
Globin
Globin
Besi

19.  Beberapa nilai rujukan dewasa normal (satuan
tradisional), plasma:
 Besi= 60 - 190 μg/100ml
 Bilirubin= total (0,3 - 1 mg/100ml); terkonjugasi
(< 0,2 mg/100ml)
 Folat= 5 - 20 ng/ml
 Protein= total (6,2 - 8 g/100ml ); albumin (3,5 -
5,2 g/100ml)
 Vit B12= 160 - 900 pg/ml
 Vit C (asam askorbat)= > 0,3 mg/dL
 Leukosit= 5 – 10 (x 109)/L