NUR 300 Exam 4 UPDATED ACTUAL
Questions and CORRECT Answers
Differentiate between compensated and uncompensated cirrhosis. Describe the complications of
each. - CORRECT ANSWER Compensated will likely not have any complications but can
easily become uncompensated.
Decompansated includes portal HTN, esophageal varcies, peripheral edema, ascites, hepatic
encephalopthy, hepatoreneal syndrome.
Define portal hypertension - CORRECT ANSWER Portal circulation is how all blood goes
through the liver via the portal vein. If the liver is not functioning correctly, the blood backs up
and causes increased venous pressure in portal circulation, which can weaken the veins. This
leads to splenomegaly, large collateral veins, esophageal varices, and eventually HTN overall.
Describe esophageal varices and why they are the most life-threatening complication. -
CORRECT ANSWER These are complexes of tortuous veins at the lower end of the
esophagus. They contain little elastic tissue and are fragile. If they bleed, it is very dangerous
because it can affect and compromise the airway. It is also very difficult to stop them from
bleeding.
What is ascites? How are hydrostatic and oncotic pressure affected? - CORRECT
ANSWER It is the accumulation of protein-rich useless fluid in the abdomen. An increased
hydrostatic pressure and a decreased oncotic pressure leads to it. Water continues to follow the
protein. This can affect respiratory function so you may need to do paracentesis.
What is hepatic encephalopathy? What can contribute to this? - CORRECT
ANSWER Hepatic encephalopathy is altered neurologic status resulting from toxin
buildup, particularly ammonia. Contributing factors include constipation, blood in GI tract,
azotemia, dietary protein restriction. It can come in stages. Ammonia can cross the BBB
Describe hepatorenal syndrome. What solves it? - CORRECT ANSWER It is a seirous
complication of cirrhosis that causes renal failure. However, there is no structural problem with
the kidney. If you get a new liver, the problem resolves. May need dialysis before the transplant
though.
,What drugs are associated with cirrhosis? - CORRECT ANSWER Propranolol to control
portal HTN
Lactulose
Vitamin K (clotting)
H2 receptor decrease gastric aciditiy
Diuretics for ascites and edema
And rifaximin removes bacteria from the intestinal tract and decreases ammonia production
Lactulose's MOA and major adverse effects - CORRECT ANSWER MOA is osmotic
action in GI tract, shifts water from blood into GI tract and causes diarrhea. This enhances
removal of ammonia from the blood. Major adverse effects: dehydration.
Cholelithiasis risk factors - CORRECT ANSWER Women, young, estrogen, lifestyle,
family history
What is bile - CORRECT ANSWER Bile is produced in the liver and stored in the
galbladder. Helps digest lipids and transport waste products. Components are bilirubin,
cholesterol, bile salts, water, protein and calcium.
What is the pathogenesis of cholelithiasis? - CORRECT ANSWER Bile stasis leads to
super saturation with cholesterol and then precipitation.
Clinical manifestations of cholelithiasis? - CORRECT ANSWER Sometimes silent but
sometimes biliary colic: steady, severe pain, RUQ may radiate to right shoulder. Occurs 3-6
hours after high fat meal. Tachy, diaphoresis, pain.
What are the symptoms of obstructed bile flow? - CORRECT ANSWER Jaundice, dark
amber urine, clay colored stools, steatorrhea, puritis, intolerance to fatty foods, bleeding
tendencies.
, Cholecystitis etiology - CORRECT ANSWER Usually obstruction from gallstones or
biliary sludge. Other causes are prolonged immobility/fasting, bacterial infection, or parenteral
nutrition, or diabetes mellitus.
The reason not eating causes it is because your body is producing bile but it's not going
anywhere because there is no food to digest. This leads to inflammation of the galbladder which
can decrease functioning.
What are the CMs of cholecystitis? - CORRECT ANSWER Similar to cholelithiasis.
Fever, N/V, restless, diaphoresis. Increased bilirubin, lizer enzymes, and WBCs. May see an
increase in amylase if also blocked at the pancreas. Think similar to cholelithiasis but also fever
and increased WBCs related to -itis.
What kind of drugs would you give to someone with galbladder problems? - CORRECT
ANSWER An analgesic, antiemetics, antiholingerics, and maybe bile acids
Describe the risk factors and etiology of pancreatitis. - CORRECT ANSWER Age (middle
age) and race (a.a. are 3x more likely). Etiology: biliary tract or ETOH abuse.
Describe the pathogenesis of pancreatitis. - CORRECT ANSWER Pancreatic cells are
injured, pancreatic enzymes are activated, and there is autodigestion. THe result is mild to severe
pancreatitis.
Describe the clinical manifestations of acute pancreatitis. - CORRECT ANSWER LUQ or
epigastric pain that can radiate to the back and has sudden onset. It can be accompanied by N/V,
abdominal distention, hypo BS, fever, hypotension, tachycardia, and jaundice. Amylase, lipase,
glucose, and WBC will all be elevated.
You may also see Turner's or Cullen's sign which will look like an old bruise.
Name the complications of acute pancreatitis. - CORRECT ANSWER Pseudocyst,
abscess, pulmonary complications, hypotension, tetany from hypocalcemia, and increased risk
for clotting.
Fluid volume deficit
Questions and CORRECT Answers
Differentiate between compensated and uncompensated cirrhosis. Describe the complications of
each. - CORRECT ANSWER Compensated will likely not have any complications but can
easily become uncompensated.
Decompansated includes portal HTN, esophageal varcies, peripheral edema, ascites, hepatic
encephalopthy, hepatoreneal syndrome.
Define portal hypertension - CORRECT ANSWER Portal circulation is how all blood goes
through the liver via the portal vein. If the liver is not functioning correctly, the blood backs up
and causes increased venous pressure in portal circulation, which can weaken the veins. This
leads to splenomegaly, large collateral veins, esophageal varices, and eventually HTN overall.
Describe esophageal varices and why they are the most life-threatening complication. -
CORRECT ANSWER These are complexes of tortuous veins at the lower end of the
esophagus. They contain little elastic tissue and are fragile. If they bleed, it is very dangerous
because it can affect and compromise the airway. It is also very difficult to stop them from
bleeding.
What is ascites? How are hydrostatic and oncotic pressure affected? - CORRECT
ANSWER It is the accumulation of protein-rich useless fluid in the abdomen. An increased
hydrostatic pressure and a decreased oncotic pressure leads to it. Water continues to follow the
protein. This can affect respiratory function so you may need to do paracentesis.
What is hepatic encephalopathy? What can contribute to this? - CORRECT
ANSWER Hepatic encephalopathy is altered neurologic status resulting from toxin
buildup, particularly ammonia. Contributing factors include constipation, blood in GI tract,
azotemia, dietary protein restriction. It can come in stages. Ammonia can cross the BBB
Describe hepatorenal syndrome. What solves it? - CORRECT ANSWER It is a seirous
complication of cirrhosis that causes renal failure. However, there is no structural problem with
the kidney. If you get a new liver, the problem resolves. May need dialysis before the transplant
though.
,What drugs are associated with cirrhosis? - CORRECT ANSWER Propranolol to control
portal HTN
Lactulose
Vitamin K (clotting)
H2 receptor decrease gastric aciditiy
Diuretics for ascites and edema
And rifaximin removes bacteria from the intestinal tract and decreases ammonia production
Lactulose's MOA and major adverse effects - CORRECT ANSWER MOA is osmotic
action in GI tract, shifts water from blood into GI tract and causes diarrhea. This enhances
removal of ammonia from the blood. Major adverse effects: dehydration.
Cholelithiasis risk factors - CORRECT ANSWER Women, young, estrogen, lifestyle,
family history
What is bile - CORRECT ANSWER Bile is produced in the liver and stored in the
galbladder. Helps digest lipids and transport waste products. Components are bilirubin,
cholesterol, bile salts, water, protein and calcium.
What is the pathogenesis of cholelithiasis? - CORRECT ANSWER Bile stasis leads to
super saturation with cholesterol and then precipitation.
Clinical manifestations of cholelithiasis? - CORRECT ANSWER Sometimes silent but
sometimes biliary colic: steady, severe pain, RUQ may radiate to right shoulder. Occurs 3-6
hours after high fat meal. Tachy, diaphoresis, pain.
What are the symptoms of obstructed bile flow? - CORRECT ANSWER Jaundice, dark
amber urine, clay colored stools, steatorrhea, puritis, intolerance to fatty foods, bleeding
tendencies.
, Cholecystitis etiology - CORRECT ANSWER Usually obstruction from gallstones or
biliary sludge. Other causes are prolonged immobility/fasting, bacterial infection, or parenteral
nutrition, or diabetes mellitus.
The reason not eating causes it is because your body is producing bile but it's not going
anywhere because there is no food to digest. This leads to inflammation of the galbladder which
can decrease functioning.
What are the CMs of cholecystitis? - CORRECT ANSWER Similar to cholelithiasis.
Fever, N/V, restless, diaphoresis. Increased bilirubin, lizer enzymes, and WBCs. May see an
increase in amylase if also blocked at the pancreas. Think similar to cholelithiasis but also fever
and increased WBCs related to -itis.
What kind of drugs would you give to someone with galbladder problems? - CORRECT
ANSWER An analgesic, antiemetics, antiholingerics, and maybe bile acids
Describe the risk factors and etiology of pancreatitis. - CORRECT ANSWER Age (middle
age) and race (a.a. are 3x more likely). Etiology: biliary tract or ETOH abuse.
Describe the pathogenesis of pancreatitis. - CORRECT ANSWER Pancreatic cells are
injured, pancreatic enzymes are activated, and there is autodigestion. THe result is mild to severe
pancreatitis.
Describe the clinical manifestations of acute pancreatitis. - CORRECT ANSWER LUQ or
epigastric pain that can radiate to the back and has sudden onset. It can be accompanied by N/V,
abdominal distention, hypo BS, fever, hypotension, tachycardia, and jaundice. Amylase, lipase,
glucose, and WBC will all be elevated.
You may also see Turner's or Cullen's sign which will look like an old bruise.
Name the complications of acute pancreatitis. - CORRECT ANSWER Pseudocyst,
abscess, pulmonary complications, hypotension, tetany from hypocalcemia, and increased risk
for clotting.
Fluid volume deficit
