Week 4: Gallbladder, Pancreas, and Liver Flashcards
What is cholelithiasis?
stones in the gallbladder
Etiology of cholelithiasis?
unkown
Risk factors for cholelithiasis
female, estrogen, obesity, sedentary, diet and family hx
What is bile’s function?
help digest lipids and transport waste products
Components of bile?
bilirubin, cholesterol, bile salts, water, protein and calcium
Pathogenesis of cholelithiasis?
bile stasis—->super saturation with cholesterol—-> precipitation—> stones remain in the gallbladder or migrate through the ducts
Cholelithiasis manifestations?
sometimes silent, biliary colic ( steady severe pain, RUQ may radiate to R shoulder)
Obstructed bile flow manifestation?
jaundice, dark foamy urine, clay stools, steatorrhea (oily stool), puritis, intolerance of fatty foods, and bleeding tendencies
Cause for Jaundice symptoms with an obstructed bile flow?
bile cannot flow into duodenum leading to a high bilirubin
Cause for dark amber urine with an obstructed bile flow?
soluble bilirubin in the urine
Cause for clay colored stools with an obstructed bile flow?
bilirubin does not reach small intestine to be converted into urbilinogen
Cause for steatorrhea (oily stools) with an obstructed bile flow?
no bile salts in duodenum preventing fat digestion
Cause for puritis with an obstructed bile flow
deposit of bile salts into skin tissue
Cause for intolerance to fatty foods due to an obstructed bile flow
No bile in small intestine to help with fat digestion
Cause for bleeding tendencies with an obstructed bile flow
decreased absorption of vitamin K
What is cholecystitis?
Inflammation of gallbladder
Reasons for cholecystitis
GALLSTONES, prolonged immobility or fasting, bacterial infection, receiving TPN, DM
What happens to the gallbladder during cholecystitis?
edematous, hyperemic, distended abdomen, and over time scarring and decreased function will occur
S/S of cholecystitis
Cholic pain, fever, N/V, restlessness, diaphoresis
Lab values associated with cholecystitis
increased bilirubin, liver enzymes and WBC
If obstruction is low enough increases amylase
Pharmacotherapy for gallbladder problems?
analgesic (ketorolac), antiemetic, anticholinergics, and bile acids (rarely used)
What is pancreatits?
inflammation of the pancreas
Risk factors for pancreatitis
middle age, African Americans
Etiology of pancreatits
biliary tract disease (women), ETOH abuse (men)
S/S of pancreatits
LUQ or epigastric pain, sudden onset that may radiate towards their back, N/V, fever. cyanosis or green coloring on the abdomen
Labs associated with pancreatitis
increases amylase, lipase, glucose and WBC
Complications of acute pancreatitis
pseudocyst, abcess, pulmonary complications, hypotension, tetany bc of hypoCa, increased risk for clotting
What is a pseudocyst?
a fluid filled cavity that surrounds the outside of the pancreas
S/S of a pseudocyst
similar to pancreatitis, but also a palpable epigastric mass
What is a pancreatic abscess?
a large fluid filled cavity inside the pancreas that may result in extensive necrosis in the pancreas
What is chronic pancreatitis
inflammation in the pancreas that persists over weeks-months
Main etiology for chronic pancreatitis
ETHOH abuse (~50% of alcoholics)
What happens to the pancreas during chronic pancreatitis?
destruction of tissue (necrosis), scar tissue (fibrosis), loss of pancreatic enzyme and insulin
S/S of chronic pancreatitis
signs of dysfunction after acute attack, chronic pain, DM, malabsorption of fat, and weight loss
Drug therapy for pancreatits
morphine (pain), dicyclomine (antispasmodic), antacids and H2-receptor antagonists (decrease secretion of pancreatic enzyme),PANCRELIPASE (replacement therapy for pancreatic enzyme), and insulin (if DM occurs)
What is the major functions of the liver?
- metabolism and storage of FAT, CHO, vitamins and minerals,
- blood volume reservoir
- blood filter
- blood clotting factors
- drug metabolism and detoxification
What is portal circulation?
when the stomach, intestine, spleen and pancreas bring blood to the liver
Where does the blood enter the liver?
portal vein
What is the first pass effect?
When a drug’s bioavailability decreases due to being metabolized in the liver before it can be systemically circulated
What are Liver Function Test (LFT)
liver enzymes (AST, ALT, Alk Phos), Bilirubin (conjugated and unconjugated) serum Ammonia, protein, albumin and prothrombin time
Normal lab value for ALT
5-35
Normal lab value for AST
0-35
Normal lab value for Alk Phos
29-90
Normal lab value for total bilirubin
0.1-1.2
Normal lab value for conjugated (direct) bilirubin
0.1-0.3
Normal lab value for unconjugated (indirect) bilirubin
0.1-1.0
Normal lab value for serum Ammonia
15-45
Normal lab value for serum protein
6.0-8.3
Normal lab value for serum albumin
3.5-5.0
Normal lab value for prothrombin time
10-13
What causes jaundice?
an increase level of bilirubin in the blood. Usually visible when total bilirubin is 2.0-2.5
Reasons for elevated indirect or unconjugated bilirubin
bilirubin overproduction OR impaired liver function
What are the 3 classes of jaundice?
hemolytic, hepatocellular, and obstructive
Reason for elevated direct or conjugated bilirubin
liver is working but cannot get bilirubin out (e.g obstruction due to gallstones)
What causes hemolytic jaundice?
increased breakdown of RBC, causing an increase in bilibrubin
What causes hepatocellular jaundice?
liver isn’t working, so bilirubin is not filtered out of the blood
What causes obstructive jaundice?
decreased or obstructive flow of bile, typically from a gallstone
Strains of hepatitis?
COMMON: Hep A, B and C (HAV, HAB, and HAC) RARE: Epstein-Barr and cytomegalovirus
S/S of hepatitis in the prodromal phase?
2wks after exposure–> fatigue, anorexia, malaise, N/V, hyperalgesia (extreme response to pain), cough, low grade fever, and HIGHLY transmissible
S/S of hepatitis in icteric phase?
jaundice, dark urine, clay colored stools, enlarged liver, tenderness on palpation, fatigue, and increasing abdominal pain
S/S of hepatitis in the recovery phase
resolution of jaundice, symptoms begin to diminish, but liver may remain enlarged/tender
Complications associated with hepatitis
chronic hepatitis, liver cirrhosis, liver cancer, and acute liver failure
How can HepA be transmitted?
fecal-oral, parental, sexual. Typically caused my unsanitary food service workers
HepA S/S
acute onset w/ fever, mild severity, does NOT lead to chronic hepatitis
Ways to prevent HepA
hand hygiene and HepA vaccine
Ways HepB can be transmitted
parental, sexual. Common with IV drug use and unprotected sex
S/S of HepB
insidious onset, severe disease that may develop into chronic hepatitis
How to prevent Hep B
HBV vaccine, safe sex, and hand hygiene
How can HepC be transmitted
parental and sexual. Extremely common with IV drug use and unsafe sex bc NO vaccine
S/S of HepC
insidious onset, mild-severe symptoms, ~80% develop into chronic
How to prevent HepC
NO vaccine, blood screenings, hygeine
Complication of HepC
hepatocellular carcinoma (will need a transplant)
Dose and timing of HepA vaccine?
2 doses 6 months apart
Who is recommended to receive the HepA vaccine?
all children starting at 6 months and special high risk populations
Dose and timing of HepB vaccine?
3 doses 4 months apart
Who is recommended to receive the HepB vaccine?
All infants beginning as newborns
Who will receive drug treatment for HepB
high risk patients, elevated AST levels, hepatic inflammation and those with advanced fibrosis
Disadvantages of pharm for HepB
prolonged therapy, costs, s/e and high relapse rate
What is liver cirrhosis (scarring)
irreversible, inflammatory, fibrotic liver disease that changes structurally due to injury (typically alcohol or virus)
What does chaotic fibrosis lead to?
obstructive biliary channels and blood flow, causing the pt to be jaundice and have portal hypertension
What are common causes for cirrhosis of the liver?
Hep B&C, excessive alcohol intake, idiopathic, and non-alcoholic fatty liver disease (NASH or NALFD)
What are the stages of alcoholism and liver disease?
alcoholic fatty liver, alcoholic steatohepatitis, and alcoholic cirrhosis
What stages of alcoholism and liver disease is the damage reversible?
alcoholic fatty liver
What stages associated with alcoholism and liver disease is the damage irreversible?
alcoholic steatohepatitis and alcoholic cirrhosis
What are early manifestations of cirrhosis?
N/V, anorexia, flatulence, change in bowel habits, fever, weight loss, and palpable liver
What are late manifestations of cirrhosis?
jaundice, peripheral edema, decreased albumin and PT, ascites, skin lesions, hematologic problems (anemia, bleeding), endocrine problems, varicies, and encephalopathy
What is portal hypertension?
the build of pressure at the portal vein caused by resistance of blood flow from intestines, stomach, and pancreas. Damage done is irreversible
What is hepatic encephalopathy?
when the liver is failing to rid the body of toxins and those toxins build up in the brain causing mental status changes (typically ammonia).
What is acute liver failure?
NOT cirrhosis!! necrotic and inflammed hepatocytes, typically caused from a tylenol overdose or after a viral hepatitis
Why would someone with liver failure take lactulose?
because it decreases ammonia levels which decreases the odds of hepatic encephalopathy
MOA of lactulose
converts ammonia to ammonium
What considerations need to be made when giving lactulose?
make sure that the pt is not experiencing hypokalemia, as it has similar s/e to hepatic encephalopathy
MOA for rifaximin
inhibits bacteria RNA synthesis by binding to bacterial DNA
s/e of rifaximin
peripheral edema, nausea, ascites, fatigue, pruritis, rash, abd pain, and anemia
What complication is associated with rifaximin?
C. diff
Indications for taking rifaximin
to prevent hepatic encephalopathy
