| What is liver cirrhosis? | It is irreversible chronic injury to liver parenchyma, final common pathway of chronic liver injuries, we see hepatocyte necrosis, collapse of reticulin network, CT deposition, distortion of vascular bed, nodular regeneration of liver parenchyma, extensive fibrosis w/formation of regenerative nodules |
| How is the pathogenesis of portal HTN? | Liver cirrhosis causes disturbed liver architecture, active hepatic vasoconstriction (both will increase resistance to portal flow) and increased splanchnic flow (which will increase the portal flow itself) which will lead to portal HTN
Resistance x Flow = Pressure (both increase in cirrhosis) |
| What are the causes of liver cirrhosis? | Alcohol, viral hepatitis, autoimmune hepatitis, drugs, metabolic disease, biliary cirrhosis, chronic hepatic congestion, cryptongenic (idiopathic) |
| How is the natural history of liver cirrhosis? | Chronic liver disease, leads to compensated cirrhosis (where we see median survival of 9 years), this may or may not progress into decompensated liver cirrhosis (this transition is where we get complications and median survival is 1.6 years) and eventually death |
| What is the Child-Pugh score for cirrhosis? | Assessment of cirrhosis |
| What are results of Child-Pugh score? | If score 5-6 pts (grade A cirrhosis - 2-year survival is 85%)
If score 7-9 pts (grade B cirrhosis - 2-year survival is 60%)
If score 10-15 pts (grade C cirrhosis - 2-year survival is 35%) |
| What is model of end stage liver disease (MELD) score? | Mathematical survival mode, estimates risk of 4 months mortality, based on bilirubin, creatinine and INR |
| What are the PE findings in case of liver cirrhosis? | Stigmata of chronic liver disease, small liver span, splenomegaly, signs of decompensation.
We see High BP/HR/Temp, asterixis, hepatomegaly, splenomegaly, ascites, spider angiomata, Kayser-Fleischer rings, Xanthomas, Gynecomastia, hyperpigmenation, edema, altered mental status. |
| What are the hx findings to look for in liver cirrhosis? | pain, fever, confusion, weight loss, sex, drugs, alcohol, medications, pruritis, malaise, dark urine, increased abdominal girth, edema, autoimmune, HIV, prior biliary surgery, family hx of liver disease |
| What are labs done evaluating jaundiced pt? | AST-ALT-ALP, Bi (total/indirect), Albumin, INR, glucose, electrolytes, acetaminophen level (maybe acute toxicity), CBC, ammonia, viral serology, ANA-AMA-ASMA, Igs, ceruloplasmin, iron profile, blood culture. |
| How is portal HTN assessed? | Using HVPG (hepatic venous pressure gradient) which is the difference between pressure of hepatic vein and inferior vena cava when pt is lying down.
We get development of varices and ascites in case HVPF>10 mmHg, Variceal bleed if HVPG>12. |
| What are esophageal varices? | Develop in 50-60% of cirrhotic pt, bleeding accounts to 1/5 - 1/3 of all cirrhosis death, MR (40-70%, 50% within 6 weeks)
In portal HTN we might get spontaneous portosystemic collaterals, which are serpentine venous channels crossing through several levels from lamina propria to deep submucosa of esophagus. |
| What are the determinants of variceal bleed? | Varix size, cherry red spots and red wale markings, HVPG>12 mmHg |
| What are goals of therapy of varices? | Primary prophylaxis (identify pt at high risk of bleed), control of acute bleed, secondary prophylaxis (prevent repeat of bleed) and bridge to definitive therapy. |
| What are the treatment options of varices? | Resuscitation and hemodynamic stabilization, combination of pharmacology and endoscopic rx, TIPS and shunts surgery in refractory cases.
Pharmacology tx (somatostatin/octreotide: immediately started to reduce portal pressure, improve dx and Rx success; Vasopressin/Terlipressin: potent vasoconstrictors to decrease splanchnic arterial pressure, used under close monitor)
Endoscopic tx (Sclerotherapy [obliterating varicoseal veins by adding sclerosing agents controls hemorrhage 60-100% of cases, complications include chest pain, fever, dysphagia, pleural effusion, esophageal ulcers]
Band ligation [placement of elastic band over the varix causing vein strangulation controls bleed 90% w/risk of 30% for rebleeding, fewer complications than sclerotherapy |
| Give the algorithm of management of varices? | . |
| What is ascites? | Most frequent complication of liver cirrhosis, 50% of compensated cirrhotic pt develop it and are followed for 10 years, where 50% of pt w/ascites will die w/in 2 years if not transplanted.
It has many causes : most imp is cirrhosis, then comes peritoneal malignancy, heart failure and other causes |
| What is abdominal paracentesis? | most rapid and cost-effective method of determining cause of ascites, done on all pt w/new onset of ascites, and pt admitted to hospital w/ascites, CBC, albumin and cultures done routinely.
Contraindicated in case of DIC or fibrinolysis. |
| How is ascites assessed? | Serum Albumin Ascites Gradient (SAAG)
It correlates w/portal HTN, accurate indirect index of portal pressure, not diagnostic of cirrhosis but indicates HTN.
Classifications are high gradient (>1.1 g/dl, indicates cirrhosis, alcoholic hepatitis, cardiac arrest, mixed ascites, portal vein thrombosis, Budd-Chiari syndrome and veno-occlusive disease)
Low gradient (<1.1 g/dl, indicates peritoneal malignancy, TB peritonitis, pancreatic ascites, bowel obstruction, bowel infarction, nephrotic syndrome or serositis) |
| How is refractory ascites? | It occurs for 10% of cirrhotics, 80% of it are diuretics intractable and 20% are diuretics resistant. |
| How is the management of ascites? | TIPS, large volume paracentesis, and Na restriction and diuretics. |
| What is spontaneous bacterial peritonitis? | One of the complications of low protein cirrhotic ascites, spontaneous infection of other form is rare, delay in dx and initiation of therapy carry high mortality.
It occurs by translocation of bacteria across GI epithelium to lymphatics and then to peritoneal cavity (more risk for low prortien ascites <1g/dl)
It presents as fever, jaundice, abdominal pain, confusion (70%), hypotension (25%) and maybe asymptomatic 35% of the time.
Dx by PMN >250 (90% accurate), positive ascitic fluid culture, abscence of surgical source
Most organisms involved are gram - bacilli (E.coli and Kleb - 70%), then comes gram + (Strep viridans - 25%) and then anaerobes (5%) |
| What is the tx of SBP? | Empiric tx of PMN>250, 3rd gen cephalosporin (cefotaxime 2g IV q 8 hrs for at least 5 days), Quinolnes (cipro/ofloxacin 200mg IV q 12 hrs), augmentin, followup paracentesis after 48 hrs of tx to assess response. |
| How is the prophylaxis of SBP? | primary (never had SBP before, low ascites proteins <1g/dl during hospitalization needs 400 mg norfloxacin PO dialy, if we have active GI hemmorhage give 400 mg norfloxacin PO for 7 days or ceftriaxone 1mg IV for 7 days)
Secondary (all pt who had SBP previous, norfloxacin 400 mg PO daily till resolution of ascites/ transplant, or cipro 750 mg PO/week |
| What is hepatorenal syndrome? | Functional renal failure due to cirrhosis in absence of intrinsic kidney disease, type I HRS (acute rapid oligorrhea unresponsive to volume expansion, very poor prognosis w/less than 2 week survival) Type II HRS (slowly progressive, diuretic resistant ascites, median survival 6 months) |
| What is the tx of HRS? | transplant (only curative rx), albumin w/vasoconstrictors, terlipressin (may be useful but has serious side effects), TIPS (bridge to transplant).
It is shown that proven efficacy is for liver transplant only, a bridge/ unknown efficay is for vasoconstrictors + albumin therapy, and ineffective renal vasodilators and hemodialysis |
| What is hepatic encephalopathy? | Combination of acute hepatic failure, chronic hepatic failure or porto-systemic shunting could lead to complex neuropsychiatric syndrome
Precipitated by (uremia, GI bleed, dehydration, constipation, infection, metabolic alkalosis, hypokalemia, excessive dietary protein, sedatives, hypoxia, hypoglycemia, hypothyroid, anemia)
Dx (clinical dx, poor correlation w/ ammonia levels, psychometric testing and EEG (only used in research))
Tx (Identify precipitating factors and correct, protein restriction 30-40 g/day, non absorbable disaccharides, non absorbed oral Abx like neomycin/ rifamixin. |
| how is portal HTN dx? | Good correlation w/ HVPG which is =WHVP-FHPG, if HVPG>5 mmHg --> Portal HTN.
Safest most reproducible method of dx is HVPG, we may get portal pressure measurement as a definitive dx, but they are difficult and have complications (the direct measurement methods) |
