Liver Cirrhosis Flashcards
What is liver cirrhosis ?
It is a chronic progressive diffuse disease of different etiology with hepatocyte damage with signs of their functional insufficiency, fibrosis and rebuilding of normal liver architecture leading to structural abnormal regenerative nodules(false lobules) formation and portal hypertension formation and in some cases to liver deficiency
Classification of L.C
By etiology
- viral
- nutrition deficiency
- chronic alcoholism
- cholestatic
- as a result of toxic or toxic allergic hepatitis
- constitutional-family
- because of chronic infiltration of liver by some substances with following inflammatory reaction (hemachromatosis, hepatocerebral dystrophy,or Wilson-conovalovs disease
- developing at the phone of chronic infections(TB,syphillis,brucellosis)
- other etiology because of unknown reasons (cryptogenic)
By morphology
Micro nodular
Macro modular
Mixed
Biliary cirrhosis (primary and secondary)
Micronodular cirrhosis is characterised by nodes of regeneration mostly of same size and diameter less than 3mm and partitions of the same width.
Macronodular nodes are large,more than 3mm(to 5cm), partitions don’t have the right form and different width.
According to activity-active,progressive
-nonactive
According to degree of functional lesions-compensated ,subcompensated,decompensated
Classification by C.G.Child (Child Pugh)is used for appraisal of condition severity and risk of surgical operation in liver cirrhosis. It accounts the signs of function of hepatocytes insufficiency availability of ascites, liver encephalopathy and exhaustion. Prognosis of class C is very unfavourable only liver transplantation can save the patient
Index. Class A. Class B. Class C
Bilirubin gr%. <2,0. 2.0-3,0. >3,0
Albumin gr%. >3.5. 3-3,5. <3,0
Ascites. - Moderate. Severe
Encephalopathy. - Moderate. Severe
Exhaustion. - Moderate Severe
Pathogenesis of L.C
Reserved circle in L.C; necrosis-inflammation-neofibrillogenesis-damage of hepatocytes blood supplying-necrosis
The process starts by hepatocyte lesion under the influence of different etiological factors
Parenchyma destruction causes active reaction of C.T(mesenchyma) influencing secondary for damage of infarct hepatocytes and leading to steplike necrosis formation.
Hepatocyte lesion is the main stimuli of liver cells regeneration which can be seen as concentric enlargement of remained parenchymal part. It leads to pseudolobule formation,
Products of hepatocytic disintegration are also one of the reasons of inflammatory reaction. Inflammatory infiltrates spread from portal fields to central parts of lobules and lead to postsinusoidal block development
Inflammatory process in the liver is characterised by high fibroplastic activity helping collagen fibres formation
CT partitions format as result. They join central veins with portal tracts, contain vessel anastomoses according which blood throws down from central veins to liver vein system without lobular parenchyma.
Fibrous tissue also presses mechanically venous vessels in liver tissue.
Such rebuilding of liver vessels causes portal hypertension development.
Portal hypertension is the reason of portocarva shunt,ascites and splenomegaly development.
Bleeding from varicose-widened veins of stomach cardiac part and esophagus can lead to death of the patient
Ascites, etiology and Pathogenesis
Colloid osmotic plasma pressure decreasing as result of hypoalbuminemia
Hyperaldosteronism
Renal blood supplying decreasing and renal function damage
Increased lymphoproduction in liver
Increased secretion of vasopressin, ADH special answer for noncell osmolarity increasing
Clinical picture of L.C
Early symptoms are Meteorism Decrease appetite Nausea Widening of the veins at the lateral parts of abdominal wall and layer around umbilicus(caput medusa) Ascites Weight loss Confusion Dark urine and grey feces Xantholasma Itchy skin
Syndromes are hepatorenal
Pathological hyper generation
Cholestatic
Portal hypertension
Hepatorenal syndrome
Shown by progressive oliguria and azotemia in the absence of structural damage to kidney
It usually occurs in patients with fulminant hepatitis or advanced cirrhosis with ascites
Pathogenesis involves extreme vasodilation of splancnic arterial circulation leading to decreased central arterial volume
Complications of L.C
Bleeding from upper parts of the GIT Liver precoma and coma Secondary infection like pneumonia Hepatorenal syndrome Transformation of cirrhosis to cancer Vein thrombosis Concrements formation in bile tracts (in primary biliary cirrhosis)
What is primary and secondary Biliary cirrhosis?
Primary biliary cirrhosis-autoimmune due to AMA (anti mitochondrial antibodies) ,
T cells attack small bile duct, CD4 and CD8 T lymphocytes directly target biliary epithelial cells, overtime leads to impaired bile formation and bile secretion causing cholestasis.this leads to retained toxic material which damage hepatocytes and liver inflammation.
andisturbance of formation and flow of bile, bile escapes from cells causes destruction of tissues ,bile ducts are slowly destroyed is usually a complication of viral hepatitis, drug intoxication, especially after intake of hormonal contraceptives
Symptoms-fatigue,purity’s,dry mouth and eyes
Physical exam- hepatomegaly, skin hyperpigmentation,jaundice,xanthelesma
Secondary biliary cirrhosis-is a complication of cholelithiasis, tumor of vaters papilla.
Syndromes-jaundice and cholemia
Portal hypertension and hepatocellular failure develop late
On examination there are multiple traces of scratches, xanthelesmas on eyelids,elbows,buttocks,
Bony changes as clubbing of fingers, osteoporosis, stools are acholic, urine is intensive dark
Patients have longstanding fever due to accompanying cholangitis
Ascites is seen later on in the disease
Palpation of the abdomen reveals big,dense, painful liver with an even sharp edge, the spleen is distinctly large and decreased
Auscultation of heart reveals bradycardia
CBC shows hyperbilirubinemia , BP is decreased
Hemochromatosis(bronze diabetes)
Mainly affects men
It is connected with derangement of iron metabolism,its excessive deposition in tissues of the internal organs-skin, liver,pancreas,myocardium with frustration of their functions.
Involvement of those organs defines bronze diabetes diagnostic triad
-diabetes
-hepatic cirrhosis
-bronze skin colour
It is diagnosed by a blood test-by sharply increased level of serum iron
Wilson-Konovalov disease(hepatolenticular dystrophy)
Related to derangement of copper metabolism with its excessive absorption in the intestine and excessive deposition in the liver, nervous ganglia, in tissues of other organs
Clinically manifested by a combination of symptoms of hepatic cirrhosis and profound damage to nervous system-tremor of extremities, syllable speech, hypertonic of muscles and profound mental disorders.
Diagnosis- biopsy with staining of the material for copper detection, detection of decreased level of copper in the blood and urine
Lab-instrumental diagnosis of L.C
Liver function test Coagulogram Serological test for viral etiology US MRCP
Treatment of L.C
1.Regime
Avoid nervous and physical stress
In high activity and decompensation of liver cirrhosis bed regime is recommended
Exclude all risk factors like alcohol,hepatotoxic drugs , physiotherapeutic procedures should be done
Protein containing food should be limited in encephalopathy,carbohydrates in DM and hyperlipidermia. Incase of edema and ascites, salt should be limited
2.Etiological treatment
Stop alcohol, in virus cirrhosis at the phase of virus replication antiviral therapy is recommended,
3.Hepatocyte metabolism improving
-polyvitamins during 1-2months 2-3 times a day
-lypoic acid 0,025gx4 a day during 2 weeks
-Vitamin group B and their coenzymes
(Flavinate, cocarboxylase)
-preparations of essential phospholipids e.g essentiale , enerliv 1-2 vials iv 10days then 1-2capsules 3/day course 1-2times
Enzyme preparations Creon 1-2tabs 3 times a day during meals
Pathogenetic therapy
Glucocorticoids-for patients with hepatic insufficiency,cholestasis,viral infection especially HCV , pre or hepatic coma, high activity of transaminases>2.5times
Prednisolone 30-60-90mg orally or iv course 3-4weeks then gradually decrease to 4mg a day
Methylprednisolone 4-8mg a day course 3-4weeks then gradually decrease to 4mg a day
Disintoxication therapy
For patients with hepatocellular insufficiency,cholestasis, pre or hepatic coma.
Dextrose solution 5-10%, 200-400ml+vitamin C iv dropper
Ringer solution 100-200ml iv dropper , NaCl 0,9% 200-400ml + vitamin C i/v dropper
albumin 10% 100-200ml i.v dropper
Solution of amino acids (reosorbilakt) 200-400ml i.v dropper
For cholestasis- ursodeoxycholic acid (10-12mg/kg during 1-2months), preparations of calcium and fat soluble vitamin A,E,D,K
Ascites/Edema Sodium/fluid restriction Diuretic spironolactone(veroshpiron 100–200mg) + furosemide (20-160mg). in the morning (under the control of diuresis and electrolyte balance Paracentesis(incase of refractory ascites) For bacterial ascites/peritonitis- cephalosporins 3rd generation e,g ceftazidin 1g 2times a day intramuscularly + synthetic penicillin amoxicillin 500mgx4 a day for 7-10days
Portal hypertension-aim to decrease portal venous pressure
B-blockers e,g propranolol 40-80mg per os x2 a day, nadolol 40-160mg per os once a day
Nitrates e.g isosorbide mononitrate 10-20mg per osx2 a day
Patients who don’t respond to treatment should be considered for trans jugular intrahepatic portosystemic shunting or less frequently a surgical portocaval shunt
Hepatic encephalopathy
Limitation of protein intake up to 40g/day
Decrease of ammonia intake in intestine
Lactulose 60-120ml /day orally
Rifaximim 1200mg/day for 1-2 weeks or ciprofloxacin 500mgx2 a day
Increase deactivation of ammonia in liver and muscle- glutargin 50ml +150ml of 0,9% NaCL x2 a day
Bleeding from varices
Somatostatin 100mg every 2hrs during 2 days i.v
Vasopressin 0,4units/min, then 0,6-0,8 units during 12-24hrs till bleeding is stopped
Ppis or H2 blockers i.v
Balloon tamponade
Endoscopic treatment
Liver transplantation is indicated for end stage liver failure
Encephalopathy in L,C stages , clinical picture
It is buildup of toxins in the brain due to excessive liver damage
Etiology-GIT bleeding
-infection
-taking tranquillisers
-alcohol intake
-massive diuretic therapy etc
Clinical picture-confusion
- drowsiness or lethargy
-anxiety or seizures
-fatigue
- confused speech
- shaky hands
Stages
Stage 0 - no changes,minimal encephalopathy
Stage 1-rhythm disturbance mild confusion,disturbance of sleep (hyper insomnia or insomnia) , slowed ability to perform mental tasks,decrease in attention,mood alteration(depression or euphoria)
Stage 2-lethargy or apathy,moderate disorientation (time or place), personality change, slurred speech,drowsy or lethargy
Stage a3-severe confusion,gross disorientation,disturbance of speech, patient may have fits of rage
Stage 4-coma( unresponsive to verbal or noxious stimuli)
Anastomoses of portal vein
- Esophageal varix- between esophageal branches of azygous vein and left gastric vein
- Caput medusa- between paraumbilical veins and deep and superficial inferior epegastric veins
- Hemorrhoids- between rectal veins
4: Extreperitoneal- between splenic veins and rectal veins
