GI Accessory Organ Pathophys Flashcards
Liver Disorders/Enzymes
Liver structure/function
- largest structure in the body
- dual blood supply (hepatic artery is 20% of supply w/ oxygenated blood; portal vein is 80% of blood & is nutrient rich)
- 2 lobes divided by the coronary ligament
- contains R & L hepatic duct which join to form the common hepatic duct which joins with the cystic duct (GB) to form the common bile duct
Liver Disorders/Enzymes
role/function of hepatocytes
- remove and excrete waste/hormones/drugs/toxins (alter them to help urinary excretion) & processes nutrients
- synthesize plasma proteins (clotting factors)
- produces immune factors (phagocytes in liver produce acute reactants)
- produce bile acids for fat absorption
- excrete bilirubin
- stores vitamins, minerals, sugars
Liver Disorders/Enzymes
pathophys of bilirubin
- catabolism of hgb –> heme –> biliverdin –> unconjugated bilirubin –> bound to albumin or unbound
- unconjugated bili: lipid souble, not excreted by renal system
- unbound bili: taken up by hepatocytes –> conjugated bili/water soluble –> becomes part of bile
- normal total serum bili: 0.2-1.2 mg/dL
Liver Disorders/Enzymes
flow of bile
- R or L hepatic duct –> common hepatic duct
- 50% into cystic duct for storage in GB
- 50% into common bile duct –> emptying into duodenum via sphincter of Oddi
Liver Disorders/Enzymes
pathophys of biliary obstruction
- blockage of bile flow into SI (inability of bilirubin to reach intestinal tract giving stool a pale color)
- can occur anywhere along path from liver to intestines (most common = gallstones)
- can lead to jaundice (consequence of bile stasis and buildup on conjugated bili in blood; total serum bili > 3 mg/dL)
- can lead to bili excretion in urine (normally none in urine)
Liver Disorders/Enzymes
jaundice classifications
- prehepatic: overproduction or impaired uptake by liver leading to unconjugated hyperbilirubinemia
- hepatic: reduced conjugation (unconjugated hyperbilirubinemia)
- posthepatic: reducted excretion (conjugated hyperbilirubinemia)
Liver Disorders/Enzymes
Hyperbilirubinemia evaluation
- determine if it is conjugated (direct) or unconjugated (indirect)
- unconjugated: results from overproduction, impairment of uptake, or impaired conjugation, evaluate for hemolytic anemia
Liver Disorders/Enzymes
describe 4 liver enzymes
- alanine aminotransaminase (ALT): liver specific (40 IU/mL)
- aspartate aminotransaminase (AST): found in liver, cardiac, and muscle tissue (40 IU/mL)
- Alkaline Phosphatase (ALK): found in liver, bone, and intestinal tissue (120 IU/mL)
- Gamma-Glutamyl transpeptidase (GGTP): found in liver (50 IU/mL)
Liver Disorders/Enzymes
how to use liver enzymes to differentiate hepatocellular injury and cholestasis
- hepatocellular injury: elevated AST/ALT
- Cholestasis: elevated ALK +/- high total bili
Hepatitis
4 phases of classic presentations
- viral replication (pt is asx but pos serology and enzyme markers)
- prodromal (anorexia, n/v/d, malaise, urticaria, pruritis, altered taste, arthralgia, fatigue, cigarette smoke aversion)
- icteric (dark urine, pale stools, GI sx persist, malaise, RUQ pain, hepatomegaly)
- convalescent (sx and incterus resolve, normal LFTs)
Hepatitis
potential clinical outcomes of HBV
- resolution (90%)
- fulminant (< 1%)
- HBsurfaceAg > 6 mo (9%); can lead to resolution, asx carrier, chronic persistent hepatitis, chronic active hepatitis
Hepatitis
what do each of these mean for HBV infection?
* HBsAg
* HBeAg
* Anti-HBc
* Anti-HBe/Anti-HBc
- HBsAg: HBV surface antigen indicating active infection
- HBeAg: HBV envelope antigen indicating infection is transmissible
- Anti-HBc: anti-core, indicates infection
- Anti-HBe/Anti-HBc: immunity
Hepatitis
clinical outcomes of HCV
- recovery (15-20%)
- chronic infection (80-85%); leading to cirrhosis (can have end stage liver disease and/or hepatocellular carcinoma)
Liver Diseases
progression from normal liver function to cirrhosis
non-alcoholic
- normal liver
- non-alcoholic fatty liver disease (effects: dyslipidemia, insulin resistance, obesity, metabolic syndrome, T2 DM); caused by lipogenesis
- non-alcoholic steatohepatitis caused by further inflammation (effects: lipi peroxidation, mitochondrial dysfunction, oxidative stress, apoptosis, pro-inflammatory cytokine activation)
- cirrhosis: fibrosis of liver (effects: scarring, advanced cell damage)
Liver Diseases
describe caput medusae
- cardinal feature of portal HTN
- occurs due to cutaneous portosystemic collateral formation between distended and engorged paraumbilical veins which radiate from umbilicus
Liver Diseases
pathophys of cirrhosis
- hepatocyte dysfunction: inability of hepatocytes to perform normal tasks
- portosystemic shunting: portal vein blood flow not flowing through liver; blood not presented to hepatocytes for filtering
- portal HTN: obstructed liver blood flow increases pressure and results in blood back up
Liver Diseases
describe use of lactulose as tx of hepatic encephalopathy
- non-absorbable disaccharide syrup
- digested by colonic bacteria (favors formation of non-absorbable ammonium ion NH4+
- favors change in bowel flora to reduce ammonia forming organisms
- can reduce recurrences
Liver Diseases
pathophys of cirrhosis causing ascites
- late stage liver disease
- extensive liver fibrosis blocks blood flow from portal vein
- blood then backs up in portal vein leading to portal HTN
- fluid leaks out of portal vein and into abd
Liver Disease
albumin levels indicating portal HTN in presence of ascites?
if serum albumin minus ascitis fluid albumin > 1.1
Liver Diseases
describe use of liver transplant for cirrhosis
- consider transplant when cirrhosis has caused ascites, hepatic encephalopathy, variceal hemorrhage, or hepatocellular dysfunction
- perform comprehensive PMHx (cardiac, pulm, dental, cancer screening)
- prioritize based on model of end stage liver disease score (MELD-Na)
- exclusion criteria: severe pulmonary PTN, extrahepatic malignancies, severe CV/pulm/PV disease, substance abuse, poorly controlled psych illness, no social support
Liver Diseases
describe components of Child-Pugh scoring for cirrhosis
Bilirubin (total
* < 2 mg/dL: 1 pt
* 2-3 mg/dL: 2 pts
* > 3mg/dL: 3 pts
Albumin
* > 3.5 g/dL: 1pt
* 2.8-3.5 g/dL: 2 pts
* < 2.8 g/dL: 3 pts
INR
* < 1.7: 1 pt
* 1.7-2.3: 2 pts
* > 2.3: 3 pts
Ascites
* absent: 1 pt
* slight: 2 pts
* moderate: 3 pts
Encephalopathy
* absent: 1 pt
* grade 1/2: 2 pts
* grade 3/4: 3 pts
Liver Diseases
describe scoring of Child-Pugh assessment
- class A: 5-6 pts, 100% survival
- class B: 7-9 pts, 80% survival
- class C: 10-15 pts, 45% survival
Gallbladder
anatomy of gallbladder
- small GI accessory organ in RUQ in posterior aspect of R lobe of liver
- part of biliary system
- regions: fundus (widest), body, neck
- cystic duct: carries bile to the common bile duct
Gallbladder
describe bile
- yellow brown/green alkaline fluid formed by the liver (~1 L daily)
- drains into gallbladder for storage
- composed of cholesterol, bilirubin, water, bile salts, phospholipids, proteins, electro, bicarb
- essential for: digesting/emulsifying fats, excreting cholesterol, anti-microbial activity
Gallbladder
describe biliary tree
- series of ducts w/in liver, GB, and pancreas that empty into small intesting
- components: intrahepatic and extrahepatic
- flow: Liver –> common hepatic duct –> GB –> cystic duct –> common bil duct –> addition of pancreatic duct to common bile duct –> sphincter of Oddi –> ampulla of Vater –> duodenum
Gallbladder
physiology of GB
- store, concentrate, and releases bile into duodenum via common bile duct
- signaled by CCK which is relseased by fatty foods/proteins entering the duodenum