Hepatic and Biliary Flashcards
Exam 3
How many hepatic veins are there? What do they drain into?
3 - right, middle, and left
Drain into vena cava
The right and left lobes of the liver are separated by the ____________
Falciform Ligament
There are __ total segments of the liver
8 - divided by blood supply and bile drainage
Bile ducts travel along _______, and bile drains through the _______ into _____ and _______
portal veins
hepatic duct
gall bladder and common bile duct
Bile enters the duodenum via the ______
Ampulla of Vater
The liver receives how much of CO?
25% - 1.25-1.5 L/min
- highest proportionate COP of all organs
The portal vein arises from what?
The splanchnic vein and superior mesenteric vein
Why is portal vein blood partially deoxygenated?
Perfuses GI organs, pancreas & spleen
The portal vein provides ___% of HBF, while the hepatic artery provides __%
75%, 25%
What percentage of oxygen delivered to the liver is via the portal vein vs the hepatic artery?
50% each
The hepatic artery branches off the _____
aorta
The hepatic artery _______ in response to low portal venous flow
dilates
What is the most common cause of portal HTN?
Cirrhosis
Portal HTN can result in _____ and ______
↑Portal venous pressure → blood backsupinto systemic circulation
- esophageal and gastric varices
What is a normal HVPG, portal HTN, and variceal rupture?
Normal 1-5 mmHg
HVPG > 10 mmHg
HVPG > 12 mmHg
What are the risk factors of liver disease (9)?
Family hx, ETOH, lifestyle, DM, obesity, illicit Drug use, mult sexual partners, tattoos, transfusion
What are the signs of liver disease on physical exam (7)?
Pruritis, jaundice, ascites, asterixis (flapping tremor), hepatomegaly, splenomegaly, spider nevi
What are the 7 liver labs?
- BMP, CBC
- PT/INR
- Aspartate aminotransferase (AST)
- Alanine aminotransferase (ALT)
- most liver-specific enzymes
- Bilirubin
- Alkaline Phosphatase
- ɣ-glutamyl-transferase (GGT)
Which imaging can detect portal blood flow?
Doppler US
What are the 3 groups of hepatobiliary disease?
- Hepatocellular injury
- Reduced synthetic function
- Cholestasis
Which labs will be increased in hepatocellular injury?
↑AST/ALT (hepatocyte enzymes)
- Acute Liver Failure (ALF): elevated 25x
- Alcoholic Liver Dz (ALD): AST:ALT ratio usually at least 2:1
- NAFLD: ratio usually 1:1
Which lab values will be altered in reduced synthetic function?
↓Albumin, ↑PT/INR
Which lab values will be altered in cholestasis?
↑AlkPhosphatase,↑GGT,↑bilirubin
Which lab values will be altered in bilirubin overload (hemolysis)?
Increased unconjugated and conjugated bilirubin
_______ secrete bile through bile ducts into the CHD
Hepatocytes
Which organ stores bile? What vessel secretes bile directly into the duodenum?
GB stores bile to deliver during meals, CBD secretes bile directly into duodenum
What are the risk factors of cholelithiasis “gallstones”?
Obesity, ↑cholesterol, DM, pregnancy, female, family hx
What are the S/S of cholelithiasis “gallstones”?
80% asymptomatic
- RUQ pain, referred to shoulders
- N/V, indigestion
- fever (acute obstruction)
What is the treatment of gallstones?
IVF, abx, pain mgmt, and lap cholecystectomy
What is choledocolithiasis?
Stone obstructing CBD→ biliary colic
What are the initial vs cholangitis s/s of choledocolithiasis?
- Initial sx: N/V, cramping, RUQ pain
- Cholangitis sx: fever, rigors, jaundice
What is the treatment for choledocolithiasis?
Endoscopic removal of stone via ERCP
How does an Endoscopic Retrograde Cholangiopancreatography (ERCP) work?
- Endoscopist threads guidewire through Sphincter of Oddi, into Ampulla of Vaterto retrieve stone from pancreatic duct or CBD
- GA, usually prone w/left tilt (head to R, tape ETT to left)
How is an oddi spasm treated during ERCP?
1 mg of glucagon
______ is the end product of heme-breakdown
Bilirubin
What is the difference between conjugated vs unconjugated bilirubin?
Unconjugated “indirect”bilirubin is PB to albumin, transported to liver, conjugated into to its H20-soluble “direct” state, excreted into bile
What is the patho of unconjugated vs conjugated hyperbilirubinemia?
- Unconjugated (indirect) hyperbilirubinemia: imbalance btw bilirubin synthesis & conjugation
- Conjugated (direct) hyperbilirubinemia:caused by anobstruction, causing reflux of conjugated bilirubin into the circulation
What are the causes of unconjugated vs conjugated hyperbilirubinemia?
Unconjugated: physiologic jaundice of newborn, jaundice of prematurity, hgb disorders (sickle cell), hemolysis, hereditary defects in conjugation, drug-induced, sepsis
Conjugated: intrahepatic cholestasis, hepatocellular injury, benign post-op jaundice, Dubin-Johnson syndrome, Rotor syndrome, obstructive jaundice, and biliary atresia
What are the 5 most common types of viral hepatitis? Which are more chronic?
A-E
B and C
___ is most common viral hepatitis requiring liver transplant in US
HCV
What is the treatment for viral hepatitis?
12 week course Sofosbuvir/Velpatasvir
What happens if viral hepatitis goes untreated?
cirrhosis, then hepatocellular carcinoma
Differentiate between type B vs C viral hepatitis
B and C - transmitted percutaneously and sexually
B incubation 60-110 days, C is 35-70 days
Type C is worse for adults - chronic liver disease 75% of patients
Type B worse for children - chronic liver disease in 80-90%
What is the most common cause of cirrhosis?
Alcoholic liver disease
What is the treatment for ALD?
- Treatment centered around abstinence
- Management sx of liver failure
- Platelet count <50,000 requires blood transfusion
- Liver transplant an option if criteria is met (abstinence for 1 year)
What are the s/s of ALD (9)?
- Malnutrition
- Muscle wasting
- Parotid gland hypertrophy
- Jaundice
- thrombocytopenia
- Ascites
- Hepatosplenomegaly
- Pedal edema
- Sx of ETOH withdrawal may occur 24-72h after stopping
What are the differing lab values in patients with ALD?
- ↑Mean corpuscular volume (MCV)
- ↑Liver enzymes
- ↑ɣ-glutamyl-transferase (GGT)
- ↑Bilirubin
- Blood ethanol (acuteintox)
How is non-alcoholic fatty liver disease diagnosed?
- hepatocytes contain>5% fat
- Imaging and histology
- Liver biopsy= gold standard in distinguishing NAFLD from other liver dx
What are the causes of non-alcoholic fatty liver disease?
Obesity, Insulin resistance, DM2, Metabolic syndrome
How does non-alcoholic fatty liver disease progress?
- Progresses to NASH, cirrhosis, hepatocellular carcinoma
- NAFLD & NASH have become additional leading causes of liver transplant in US
What is the treatment for non-alcoholic fatty liver disease?
diet and exercise, liver transplant indicated for advanced fibrosis, cirrhosis, related complications
What is the prevalence of NAFLD?
1/4 regardless of weight
6/10 diabetics
9/10 obese people
Which progresses faster? alcoholic or non-alcoholic fatty liver disease?
Alcoholic
Autoimmune hepatitis effects women _____ than men
more
What are the expected lab values of autoimmune hepatitis?
- +autoantibodies & hypergammaglobulinemia
- AST/ALT may be 10-20x norm in acute AIH
What is the treatment for autoimmune hepatitis?
steroids, azathioprine (immunosuppressant)
- Liver transplant indicated when tx fails or acute liver failure ensues
What is the most common cause of drug-induced liver injury?
Acetaminophen OD - normally reversible after drug is removed
What are the 3 specific disorders of inborn errors of metabolism?
- Wilsons Disease
- Alpha-1 Antitrypsin Deficiency
- Hemochromatosis
Inborn Errors of Metabolism occur in 1:_____ births
2500
_______ are a group of rare, genetically inherited disorders that lead to a defect in the enzymes that breakdown and store protein, carbohydrates &fatty acids
Inborn errors of metabolism
Wilsons Disease is also known as _______ and is characterized by impaired ______ metabolism
hepatolenticular degeneration
copper
Copper buildup leads to oxidative stress in the ______, _______, and _______
liver,basal ganglia, and cornea
What are the s/s of Wilsons disease? Lab values?
Sx: range from asymptomatic to sudden-onset liver failure along with neurologic & psychiatricmanifestations
Tx: Copper-chelation therapy & oral zinc to bind copper in the GI tract
How is Wilsons disease diagnosed?
Lab tests (serum ceruloplasmin,aminotransferases,urine copper level)
- Possible liver biopsy for copper level
_______ is a genetic disorder resulting in a defectiveα-1 antitrypsin protein
Alpha-1 Antitrypsin Deficiency
α-1 antitrypsin proteins protect the _____ and _____ from _______
liver & lungs from neutrophil elastase
__________ is the #1 genetic cause of liver transplant in children
α-1 antitrypsin deficiency
How is α-1 antitrypsin deficiency diagnosed?
confirmed w/α-1 antitrypsin phenotyping
How is α-1 antitrypsin deficiency treated?
pooledα-1 antitrypsin is effective for pulmonary sx; however, it doesn’t help with liver disease
- Liver transplant is the only curative treatment for liver disease inα-1 antitrypsin deficiency
________ is the excessive intestinal absorption of iron
Hemochromatosis
- Excess iron accumulates in organs and causes damage to the tissues
What causes Hemochromatosis? How is it diagnosed?
Maybe genetic or caused by repetitive blood transfusions or iron infusions
Dx: genetic mutation testing
What are the expected lab values for patients with Hemochromatosis?
Labs reveal elevated AST/ALT, transferrin saturation, and ferritin
Liver bx may quantify iron levels in the liver and assess the level of damage
What is the treatment for Hemochromatosis?
Tx: weekly phlebotomy, iron-chelating drugs, liver transplant
What is a common comorbidity of patients with Hemochromatosis?
cardiomyopathies
_______ is an autoimmune, chronic inflammation of the larger bile ducts, resulting in fibrosis in the biliary tree?
Primary Sclerosing Cholangitis (PSC)
How does PSC progress?
Fibrosis in biliarytree→strictures (beads on string appearance)→ cirrhosis, ESLD
Males are ____ likely to have PSC than women
more, onset 40s
What are the s/s of PSC?
Fatigue, itching, deficiency of fat-soluble vitamins (A,D,E,K), cirrhosis
How is PSC diagnosed?
- Dx: MRCP or ERCP showing biliary strictures w/ dilated bile ducts
- Liver biopsy reinforces dx, but isn’t always performed
What are the expected lab values of patients with PSC?
Labs:↑alkaline phosphatase andɣ-glutamyl-transferase, +auto-antibodies
What is the treatment for patients with PSC?
- No drug treatments are proven to be effective
- Liver transplant is only long term treatment
- Re-occurrence is common after transplant d/t autoimmune nature
_________ is the autoimmune, destruction of bile ducts withperiportal inflammation & cholestasis
Primary Biliary Cholangitis (PBC)
Primary Biliary Cholangitis (PBC) is also known as
biliary cirrhosis
What are the s/s of PBC?
jaundice, fatigue,& itching
PBC can lead to…
liver scarring, fibrosis, cirrhosis
What causes PBC? What population typically has it?
- Females > Males; often dx’d in middle-ages
- Thought to be c/b exposure to environmental toxins in genetically susceptible individuals
What are the expected lab values of patients with PBC?
Labs: ↑Alk Phos,↑GGT, + Antimitochondrial antibodies
How is PBC diagnosed?
- Imaging: CT,MRI, & MRCP to r/o bile duct obstructions
- Liver biopsy reveals bile duct destruction andinfiltration w/lymphocytes
What is the treatment for PBC?
No cure, but exogenous bile acids slow progression
Acute liver injury occurs within _____ after insult. 50% of cases are caused by ______
6 months
drug-induced - acetaminophen
What are other causes of acute liver failure?
Viral hepatitis, autoimmune, hypoxia, ALF of pregnancy, HELLP
What are the s/s of acute liver failure?
Jaundice, nausea, RUQ pain, cerebral edema, encephalopathy, multi-organ failure, death
Massive hepatocyte necrosis→ cellular swelling &mbrndisruption
What is the tx of acute liver failure?
Treat the cause, supportive care, liver transplant
What are the expected lab values of acute liver failure?
Rapid increase in AST/ALT, AMS, coagulopathy
_____ is final stage liver disease; characterized by normal _____ being replaced with ____
cirrhosis
Normal liver parenchyma replaced with scar tissue
What are the s/s of cirrhosis?
- Often asymptomatic in early stages
- Sx’s progress to jaundice, ascites, varices, coagulopathy, encephalopathy
What are the most common causes of cirrhosis?
ALD, NAFL, HCV, HBV
What are the expected lab values of patients with cirrhosis?
Elevated labs: AST/ALT, bilirubin, Alk phosphatase, PT/INR
- thrombocytopenia
_______ is the only cure for cirrhosis
transplant
What are the 8 complications from cirrhosis?
Portal HTN, ascites, bacterial peritonitis, varices, hepatic encephalopathy, hepatorenal syndrome, hepatopulmonary syndrome, and portopulmonary HTN
What is the most common complication of cirrhosis? Treatment?
ascities
- ↓Salt diet, albumin replacement
- Transjugular Intrahepatic Portosystemic Shunt (TIPS) - Reduces P-HTN and ascites
_______ is the most lethal complication of varicies; treatment?
Hemorrhage
- Beta blockers help reduce risk
- Prophylactic endoscopic variceal banding & ligation
- Refractory bleeding → balloon tamponade
________ is a complication of cirrhosis in which there is buildup of nitrogenous waste d/t poor liver detoxification
Hepatic Encephalopathy
What are the s/s and tx for Hepatic Encephalopathy?
- Neuropsychiatric symptoms (cognitive impairment → coma)
- Tx: Lactulose, Rifaximin to ↓ammonia-producing bacteria in gut
What is the patho of Hepatorenal Syndrome? Tx?
- Excess production of endogenous vasodilators (NO, PGs)→↓SVR→↓RBF
- Tx: Midodrine, Octreotide, Albumin
_________ is a triad of chronic liver disease, hypoxemia, intrapulmonary vascular dilation
Hepatopulmonary Syndrome
What is the hallmark symptom of Hepatopulmonary Syndrome?
Platypnea (hypoxemia when upright) d/t R to L intrapulmonary shunt
What is the patho and tx for Portopulmonary HTN?
- Pulmonary HTN accompanied by portal HTN
- Systemic vasodilation triggers production of pulmonary vasoconstrictors
- Tx: PD-I’s, NO, prostacyclin analogs, and endothelin receptor antagonists; transplant is only cure
What are the 2 scoring systems for liver disease? What values are they based on?
- Child-Turcotte-Pugh (CTP):points based on bilirubin, albumin, PT, encephalopathy, ascites
- Model for End-Stage Liver Disease (MELD): scorebased on bilirubin, INR, creatinine, sodium
Anesthesia considerations for patients with liver disease?
- ↑Risks aspiration, HoTN, hypoxemia
- Colloids > crystalloids for resuscitation
- Alcoholism increases MAC of volatile anesthetics
- Drugs may have slow onset/prolongedDoA
- Succs and Cisatracurium are ideal (not liver-metabolized)
What is the Transjugular Intrahepatic Portosystemic Shunt (TIPS) procedure?
- “TIPS” procedure to manage portal HTN
- Stent or graft placed btw hepatic vein and portal vein
- Shunts portal flow to systemic circulation
- Reduces the portosystemic pressure gradient
What are the indications and contraindications for TIPS?
Indications:
- Refractory variceal hemorrhage
- Refractory ascites
Contraindications:
- Heart Failure
- Tricuspid regurgitation
- Severe pulmonary HTN
What is a partial hepatectomy?
- Resection to remove neoplasms, leaving adequate tissue for regeneration
- Up to 75% removal is tolerated in pts with normal liver function
What are the anesthetic considerations of a patient undergoing a partial hepatectomy?
- Invasive monitoring - surgeon may clamp IVC or hepatic artery
- Blood products available - postop coagulation disturbances
- Adequate vascular access for blood/pressors - maintain low CVP by fluid restriction to reduce blood loss
What is the intra-op mgmt for liver transplant?
- Maintain hemodynamics (Pressors/Inotropes readily available) - A-line, CVC, PA cath, TEE
- Control coagulation
