PATOGENESIS TERJADINYA RENJATAN PADA DHF

SECONDARY HETEROLOGOUS DENGUE INFECTION

VIRUS REPLICATION + ANAMNESTIC ANTIBODY RESPONSE

VIRUS ANTIBODY COMPLEX


COMPLEMENT ACTIVATION
 complement 
ANAPHYLATOXIN (C3a, C5a)
 Histamin level 
VASCULAR PERMEABILITY in 24-hours urine

 > 30% in shock cases LEAKAGE OF PLASMA Ht 
 24 – 48 hours  Na + 
HYPOVOLEMIA fluid in the serous cavitis

SHOCK
 
ANOXIA    ACIDOSIS
Sumber: Suvatte, 1977
HIPOTESIS TERJADINYA TROMBOSITOPENI
PADA INFEKSI VIRUS DENGUE SEKUNDER

KETERANGAN:
0 : antibodi IgG terhadap virus
dengue
C : aktivasi sistem komplemen
oleh kompleks IgG-virus
dengue
 : virus dengue
 : trombosit yang bersirkulasi

Sumber: Funahara dkk., 1983

 PATOGENESIS PENDARAHAN PADA DHF
SECONDARY HETEROLOGOUS DENGUE INFECTION
 
VIRUS REPLICATION ---- + ---- ANAMNESTIC ANTIBODY RESPONSE

VIRUS ANTIBODY COMPLEX
 
PLATELET AGGREGATION COAGULATION ACTIVATION
COMPLEMENT
ACTIVATION
PLATELET REMOVAL PLATELET FACTOR III
BY RES RELEASE
PLASMIN
THROMBOCYTOPENIA ACTIVATED HAGEMAN
FACTOR ANAPHYLATOXIN

Impaired CONSUMPTIVE KININ SYSTEM

Platelet COAGULOPATHY
Function KININ
CLOTTING  VASCULAR
FACTORS PERMEABILITY 
FDP 

EXCESSIVE HAEMORRHAGE
Sumber: Suvatte, 1977
HIPOTESIS POTOGENESIS DHF/DSS

Sumber: Halstead