HandlingBased on the symptoms.
- Compensate well: control, rest, diet , enough fat
- The note: Signed or stop it
- Signed complications; ascites low salt diet provided 0.5 g / day, total liquid 1.5 l / hr, diuretic
- With bleeding: resuscitate, lavase ice water, homeostatic, antacid/antagonise B2, sterilises intestine, klisma high, skleroterapi, ligasi endoscopic varises
- Outbreak prevention varises esophagus: farmakoterapi, ligasi varises.
Supporting examination
- The heart biopsy
- Blood routine: low Hb, anemia normokromik normositer, hipokrom mikrositer, hipokrom makrositer.
- Cholesterol blood is always low prognosis is less good
- Growth rate transaminase enzyme (SGOT / SGPT). The increase resulted from leakage of damaged cells. On inactive cirrhosis does not increase
- Albumin decreased
- Checking CHE (kolinesterase) down. Occurs when the increase means improvement occurred
- Check electrolyte level necessary for the use of diuretic and salt restriction. In NA enselopati degree <4> 500 - 1000 indicates a primary liver cancer.
- Radiology: barium swallow to see the varises esophagus.
- Esofagoskopi: see varises esophagus the form of cherry red spot, red whale marking, diffus redness. Possible bleeding
- USG
- Radionukleid IV
- Tomografi computer
- ERCP: to remove the obstructs ekstrahepatik
- Angiografi
- Punksi ascites: microscopic examination, culture fluid, protein content, amilase and lipase.
Etiology
1. Hepatitis virus type B and C
2. Alcohol
3. Metabolic (hemokromatosis idiopathic, Wilson disease, deficiency alpha 1 anti tripsin, galaktosemia, tirosinemia congenital, DM, hoarding collagen disease)
4. Kolestasisi chronicles / bilier cirrhosis secondary intra and extra hepatic
5. Obstructs flow vena hepatic (Peny.vena occlusive, Budd Chiari syndrome, Perikarditis constrictive, heart pains right)
6. Interference immunologist
7. Toksik and drugs (mtx, INH, Metildopa)
8. Pintasusus smooth operation on Obesity
9. Malnutrition
10. Idiopathic
Sign and symptoms
Soebandiri criteria, when there is 5 of 7:
1. Spider nevi
2. Venectasi / vena collateral
3. Ascites (with or without edema feet)
4. Spelomegali
5. Varices esophagus (hemel)
6. Ratio of albumin: globulin inverted
7. Palmar eritema
Based on clinical manifestations:
1. Kompensata (not affect function hepar)
Fever intermittent
Spider nevi
Palmar eritema
Epitaxy's
Edema legs
Dyspepsia's
painful abdomen
Hepatosplenomegali
2. Dekompensata
Ascites
jaundice
physical weakness
Lost BB
Epistaksis
Hipotensi
Atropi gonadal
Patofisiologi
Infection of viral hepatitis type B / C causes liver inflammation. This causes inflammation necrosis covers a wide area (hepatoseluler), going collapse lobulus heart and stimulate the occurrence of this network, along with scar make septa fibrous diffuse and nodule liver cells. Although the etiology is, picture histologist same or nearly the same. And can be formed from cells that reticulum buffer collapse and changed so scar. Some of the cells to grow back and form nodule with different size and this causes distortion hepatic duct branching and disruption of blood flow and cause a porta hypertensive portal. The next stage occurs necrosis in inflammation and cell duktules, sinusoid, reticule endotel, going active fibrogenesis and septa. Collagen network fari reversible change becomes irreversible when the septa have a permanent aselular in the porta and parenkim heart.
Chirrosis hepatics is a chronic liver disease diffuse marked with the establishment of a network tied with nodule. Usually begins with the process of inflammation, liver cell necrosis a broad, ligament formation network and business nodule regeneration. Architectural distortion heart heart will change the macro and micro-circulation is not organized into a network due to the addition bind and nodule it.
Type Chirrosis Hepatics
There are three types chirrosis or scar formation in the liver:
1. Chirrosis portal Laennec (alcoholic, nutritional) where the network is typical girth seam area portal. Cirrhosis is most commonly caused by chronic alcoholism.
2. Chirrosis post necrotic, there is a network band width of the scar as a follow-up of acute viral hepatitis before
3. Chirrosis bilier, where scar formation of the network occurs in the hearts of bile channel. This type usually occurs due to the obstructs bilier and chronic infection (kolangitis); insidens least
