KULIAH GANGGUAN HEMOSTASIS

PERDARAHAN
SURADI MARYONO SpPD- KHOM
FK . UNS
SURAKARTA

HEMOSTASIS DAN GANGGUAN

HEMOSTASIS
HEMOSTASIS :
HAEMA = DARAH. STASIS =NORMAL/STABIL/BERHENTI
MEMPERTAHANKAN SISTEM HEMATOLOGI TETAP NORMAL

* GANGGUAN

HEMOSTASIS :
- PERDARAHAN
- TROMBOSIS .

PERDARAHAN :
- HILANGNYA DARAH DARI SISTEM SIRKULASI
- PERDARAHAN ADA 2 MACAM :
- KEDALAM : BILA DARAH KELUAR DARI PEMBULUH
DAR TUBUH, TTP MASIH ADA DIRUANG TUBUH .
- KELUAR

: DARAH MELEWATI LOBANG TUBUH: VAGINA,

MULUD, ANUS , KULIT.

- EXSANGUINASI , PERDARAHAN KOMPLIT.

- DISSANGUINASI , PERDARAHAN MASIV.
- VOLUME PERDARAHA 10-15% VOLUME DARAH TUBUH, PD
ORANG SEHAT TDK ADA GEJALA KLINIS ( DONOR DARAH 810%).]

The American College of Surgeons: ADVANCED TRAUMA LIFE SUPPORT

(ATLS ), PERDARAHAN ADA 4 KLAS:
KLAS I
TANDA

: - PERDARAHAN SAMPAI 15% VOL. DARAH TUBUH. TDK TJD PERUBAHAN

VITAL , TAK PERLU TERAPI.

KLAS II : - 15-30 % , TERDAPAT GEJALA : TAKHIKARDIA , PENYEMPITAN JARAK
SISTOLIK DAN DIASTOLIK. TJD VASOKONTRIKSI PERIFER, KULIT PUCAT
DAN DINGIN. RESUSTISASI DNG CAIRAN : KRISTALOID ( LARUTAN
NACL, RINGER LAKTAT), TRANSFUSI DARAH BELUM PERLU.
KLAS III : - 30-40% VOLUME SIRKULASI. TEK DRAH MULAI TURUN, FREKUENSI
DETAK
JANTUNG TERUS MENINGKAT , PERFUSI PERIFER DAN STATUS MENTAL
MEMBURUK . PERLU CAIRAN KRISTALOID DAN TRANSFUSI BIASANYA
DIPERLUKAN.
Class IV : - INVOLVES LOSS OF >40% OF CIRCULATING BLOOD VOLUME.
THE LIMIT OF THE BODY'S COMPENSATION , AGGRESSIVE RESUSCITATION
IS
REQUIRED TO PREVENT DEATH.
INDIVIDUALS IN EXCELLENT PHYSICAL AND CARDIOVASCULAR , MAY HAVE
MORE
EFFECTIVE COMPENSATORY MECHANISMS BEFORE CARDIOVASCULAR
COLLAPSE.
- WHILE HAVING POOR PERIPHERAL PERFUSION (SHOCK).
- ELDERLY PATIENTS / WITH CHRONIC MEDICAL CONDITIONS MAY HAVE LESS
TOLERANCE TO BLOOD LOSS, LESS ABILITY TO COMPENSATE,
CARE MUST BE TAKEN IN THE ASSESSMENT OF THESE PATIENTS.

I. PERDARAHAN:
PROSES HEMOSTASIS ADA 3 TAHAP
1. HEMOSTASIS PRIMER : PBL DARAH, TROMBOSIT,
ENDOTEL, AGREGASI DAN PELEPASAN FAKTOR
TROMBOSIT. 3-5 MENIT BERHENTI DNG PMBTKN
PLATELET PLAG ( SUMBAT TROMBOSIT)
2. KOAGULASI, 3-10 MENIT TERBENTUK FIBRIN
MEMPERKUAT SUMBAT TROMBOSIT. SEKUNDER
3. FIBRINOLISIS, SBG TAHAP AKHIR, WAKTU 24 -72 JAM ,
FIBRIN LARUT, LUKA SEMBUH.
TERTIER

The human hemostatic system can be defined as consisting of multiple independent yet integrally related cellular
and protein components that function to maintain blood fluidity under normal conditions and to promote localized,
temporary thrombus formation at sites of vascular injury. The six major components of this hemostatic
system are vascular endothelium, platelets, plasma coagulation proteins or "factors," natural
anticoagulant proteins, fibrinolytic proteins, and antifibrinolytic proteins. In the presence of an intact
endothelium, there is no "clot" formation taking place inside the blood vessels, even though a low, basal physiologic
level of coagulation factor activation is occurring continuously. This highly regulated hemostatic system maintains a
delicate balance between a prohemorrhagic state and a prothrombotic state. This balance is maintained by the
concomitant actions of platelets, coagulation factors, and fibrinolytic inhibitors (on one side of the "hemostatic
scale"), and of natural anticoagulants and fibrinolytic proteins (on the other side of the scale). (7)

ADA 3 KOMPONEN PENTING:

1. EKSTRAVASKULER:
- BESAR JARINGAN
- JENIS JARINGAN
- BESAR TEK. JAR.(USIA MUDA > TUA)
2. VASKULER:
* LAPISAN ENDOTEL DAN OTOT POLOS
LAP. ENDOTEL BERPERAN SINTESIS:
- TISSUE FACTORS, PROSTASIKLIN, FAKTOR VON WILLEBRAND,
AKTIVATOR PLASMINOGEN, ANTI TROMBIN III DAN
TROMBOMODULIN.
* JAR. IKAT SUBENDOTEL:
- MEMBRANA BASALIS, KOLAGEN, ELASTIN DAN FIBRONEKTIN
3. INTRAVASKULER :
TROMBOSIT, PROKOAGULAN, AKTIVATOR DAN INHIBITOR :
KOAGULASI DAN FIBRINOLISIS.

FIGURE 1. Coagulation cascade. a=activated factor; Ca=calcium; L=phospholipid.

Reprinted with permission from Davie EW, Fujikawa K, Kisiel W. The coagulation
cascade: initiation, maintenance, and regulation. Biochemistry. 1991;30:10363-10370.

Gambar 1. Sistem koagulasi, inhibitor dan fibrinolisis (Dikutip dari

Folkman dkk).

MEKANISME PEMBEKUAN

PENYEBAB PERDARAHAN :
1. KELAIANAN PEMBULUH DARAH :
* KELAINAN STRUKTUR PBL DARAH
* AKIBAT INFEKSI/ IMUN.
** DIDAPAT:
- PURPURA SIMPLEK RINGAN , USIA SUBUR GANGGUAN FRAGILITAS PBL
DARAH KULIT

- PURPURA SENILIS MANULA , OK. ATROFI JAR. KOLAGEN.

- AKIBAT INEKSI: DHF, DEMAM TIFOID, ENDOKARDITIS BAKTERIEL,
SEPSIS.
- AKIBAT OBAT2-AN : PINISILIN, ISONIACIDE, ASPIRIN, TIAZID,
OKSITETRASIKLIN

** DITURUNKAN : HEMORHAGIS TELEANGIECTASIS.

2. FIBRINOLISIS BERLEBIHAN

3. KELAINAN TROMBOSIT : KUANTITATIF DAN KUALITATIF.

* KUANTITATIF :
TROMBOSITOPENIA
- GANGGUAN PRODUKSI (MEGAKARIOSIT TURUN , MEGAKARIOSIT NORMAL)
- DISTRUKSI PERIFER BERLEBIHAN ITP.
- PRIMER (IDIOPATIK)
- SEKUNDER : SLE, LMH, CLL.
- DISTRIBUSI ABNORMAL (POOLING). SPLENOMEGALI

* KUALITATIF:
GANGGUAN FUNGSI TROMBOSIT
- DIDAPAT : GAGAL GINJAL, OBAT-OBATAN, HIPERGAMAGLOBULINEMIA.
- DITURUNKAN: VON WILLEBRAND DISASE, SINDROMA BERNARD SOULIER,
STORAGE POOL DISEASE, GLANZMANN THROMBOCYTOPENIA
(DEFF. GP.IIb-IIIa)

Signaling mechanisms linking platelet receptors to integrin activation. GPVI ligation activates the
ITAM-signaling pathway, whereas stimulation of G proteincoupled receptors triggers pathways
involving Gq, Gi/z, and G12/13, adenylyl cyclase. DAG indicates diacyl glycerol; IP3, inositol-1,4,5trisphosphate; PI-3-K/phosphoinositide-3-kinase /; PIP2, phosphatidylinositol-4,5bisphosphate; PIP3, phosphatidylinositol-3,4,5-trisphos-phate; PKC, protein kinase C;
PLC2/3, phospholipase C-2/3; RhoGEF, Rho-specific guanine nucleotide exchange

4. DEFEK MEKANISME PEMBEKUAN DARAH :

a. KONGENITAL. :
- HEMOFILIA A (KLASIK) : OK. GANGGUAN SINTESIS/AKTIFITAS
F. VIII. (F.VIIIc , F.VIII vw, F.VIII R.Ag).
- HEMOFILIA B. (CHRISTMAS DISEASE) : OK. DEFF. F.IX
- PENYAKIT VON WILLEBRANT : OK. DEFF. F.VIII vw.
b. AKUISITA :
- DEFISIENSI VIT. K
VIT.K :
- LARUT DLM LEMAK
- SUMBER , SAYURAN HIJAU
- DLM TUBUH JUGA DISINTESA OLEH BAKTERI USUS
- DIBUTUHKAN HATI UTK SINTESA FAKTOR-2 PEMBEKUAN (
F: II,VII,IX ,X) GANGGUAN HATI PROD. VIT TURUN
PERDARAHAN.

TROMBOSITOPENIA: