PATOLOGI ANATOMI &

PATOLOGI KLINIK

Radang, Pemulihan
Jaringan & Sistem
Hemopoetik
Oleh:
Yudha Anggit J, S.Kep, M.Kes

“Wahai Tuhanku, tambahkanlah pengetahuan

kepadaku dan anugerahkanlah pemahaman
kepadaku…amin”
 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.
 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
 Extravasation of leukocyte

Margination, rolling, adhesion, diapedesis, chemotaxis

& phagocyitosis
3. Komponen dasar 1) Vaskular
Manifestasi Lokal : 2) Selular
3) Eksudat
Vaskular: Terjadi peningkatan aliran darah yg
relatif statik pada daerah radang  rubor &
kalor
Selular
Dari darah: - Leukosit PMN (Polimorfonuklear)
- Limfosit (T & B)  imun selular &
humoral
- Monosit
Dari jaringan: - Histiosit / Makrofag jaringan
- Fibroblas
- Sel datia
* 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")
 Silsilah Sel Darah
(Stem Cell Differentiation and Hematopoesis)
 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
Persistent acute inflammation due to non-degradable
Causative
Pathogens, injured tissues pathogens, persistent foreign bodies, or autoimmune
agent
reactions
Major cells Mononuclear cells (monocytes, macrophages, lymphocytes,
Neutrophils
involved plasma cells), fibroblasts
Primary INF-γ and other cytokines, growth factors, reactive oxygen
Vasoactive amines, eicosanoids
mediators species, hydrolytic enzymes
Onset Immediate Delayed
Duration Few days Up to many months, or years
Healing, abscess formation,
Outcomes Tissue destruction, fibrosis
chronic inflammation
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)
 Plasma derived mediators
(Perantara kimiawi dari plasma)

Name Produced by Description

A vasoactive protein which is able to induce vasodilation, increase vascular

Bradykinin Kinin system
permeability, cause smooth muscle contraction, and induce pain.

Cleaves to produce C3a and C3b. C3a stimulates histamine release by mast
Complement cells, thereby producing vasodilation. C3b is able to bind to bacterial cell
C3
system walls and act as an opsonin, which marks the invader as a target for
phagocytosis.
Stimulates histamine release by mast cells, thereby producing vasodilation. It
Complement
C5a is also able to act as a chemoattractant to direct cells via chemotaxis to
system
the site of inflammation.

A protein which circulates inactively, until activated by collagen, platelets, or

exposed basement membranes via conformational change. When
Factor XII (Hageman
Liver activated, it in turn is able to activate three plasma systems involved in
Factor)
inflammation: the kinin system, fibrinolysis system, and coagulation
system.

A complex of the complement proteins C5b, C6, C7, C8, and multiple units of
Membrane attack Complement C9. The combination and activation of this range of complement proteins
complex system forms the membrane attack complex , which is able to insert into
bacterial cell walls and causes cell lysis with ensuing death.

Fibrinolysis Able to break down fibrin clots, cleave complement protein C3, and activate
Plasmin
system Factor XII.

Cleaves the soluble plasma protein fibrinogen to produce insoluble fibrin,

Coagulation which aggregates to form a blood clot. Thrombin can also bind to cells
Thrombin
system via the PAR1 receptor to trigger several other inflammatory responses,
such as production of chemokines and nitric oxide.
 Cell derived mediators
Name Type Source Description
These cells contain a large variety of enzymes which perform a
number of functions. Granules can be classified as either
Lysosome specific or azurophilic depending upon the contents, and
Enzymes Granulocytes
granules 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.
Stored in preformed granules, histamine is released in response
Vasoactive
Histamine Mast cells, basophils, platelets to a number of stimuli. It causes arteriole dilation and
amine
increased venous permeability.
Antiviral, immunoregulatory, and anti-tumour properties. This
interferon was originally called macrophage-activating
IFN-γ Cytokine T-cells, NK cells
factor, and is especially important in the maintenance of
chronic inflammation.

Activation and chemoattraction of neutrophils, with a weak

IL-8 Chemokine Primarily macrophages
effect on monocytes and eosinophils.

Able to mediate leukocyte adhesion and activation, allowing

them to bind to the endothelium and migrate across it. In
Leukotriene
Eicosanoid Leukocytes neutrophils, it is also a potent chemoattractant, and is able
B4
to induce the formation of reactive oxygen species and the
release of lysosome enzymes by these cells.
Potent vasodilator, relaxes smooth muscle, reduces platelet
Macrophages, endothelial cells,
Nitric oxide Soluble gas aggregation, aids in leukocyte recruitment, direct
some neurons
antimicrobial activity in high concentrations.
A group of proteins which can cause vasodilation, fever, and
Prostaglandins Eicosanoid Mast cells
pain.
Both affect a wide variety of cells to induce inflammatory
reactions: fever, production of cytokines, endothelial gene
TNF-α and IL-
Cytokines Primarily macrophages regulation, chemotaxis, leukocyte adherence, activation of
1
fibroblasts. Responsible for the systemic effects of
inflammation, such as loss of appetite & heart rate.
 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)

 Manifestasi Umum:
- Demam
- Hiperpireksia
- Perubahan dalam darah (leukositosis,
leukopenia, anemia)
- Perubahan pada organ-organ (reaktif lokal
(:makrofag) & umum(:hiperplasi limfe),
degeneratif, septikemia, piemia & bakteriemia)
 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)
 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)
- Umur (~sirkulasi)
- Endokrin
- Suhu
- Ukuran cedera
- Benda asing  debridement
- Sinus & fistula
- Iradiasi
- Saraf sensorik
 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 Besi
Globin Hem
Hemoglobin [4 buah]
Globin Hematin
Biliverdin Besi
Bilirubin
Bilirubin terkonjugasi
Urobilinogen, dst
Urobilin, dst
 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