Exam 2: Liver, Gallbladder, Pancreas
What are the characteristics of compensated cirrhosis? - Answer Patient still has
problems, but in general, they are doing ok/look healthy.
--LFT's are normal.
What are the characteristics of decompensated cirrhosis? - Answer -portal HTN
-esophageal varices
-peripheral edema
-ascites
-hepatic encephalopathy
-hepatorenal syndrome
Why do people with liver cirrhosis get portal hypertension? - Answer Nutshell
Cause: Increased venous pressure in portal circulation
The diseased and scarred liver prevents normal blood flow from the GI tract.
Over time, the blood flow starts to back up at the portal vein, which increases the
pressure.
To compensate, the body starts developing collateral circulation to get around these
backed up areas.
----but they're very weak and are prone to rupture
CM of portal hypertension - Answer -splenomegaly
-ascites
-large collateral veins, which leads to esophageal variceal development
-systemic HTN
What is collateral circulation? - Answer The development of new, smaller branches of
arteries that grow in response to a vessel that has slowly become occluded or nearly
occluded over time.
What is the problem with collateral circulation? - Answer -the vessels are very weak
-it is easy for them to get large and rupture.
R/t portal HTN, what is the most common place for varices to form? - Answer -lower
esophagus
-upper stomach
-rectum
caput medusa - Answer Dilated veins around the umbilicus, associated with cirrhosis of
the liver.
, What are esophageal varices? - Answer Complex of torturous veins at the lower end of
the esophagus (or anywhere where collateral and systemic circulation communicate)
What is the problem with esophageal varices? - Answer They contain little elastic tissue,
so they are fragile and are at risk for bleeding, which can be life-threatening.
Patho of ascites - Answer Incvreased pressure in the portal vein leads to an increase in
hydrostatic pressure (water pushing pressure)
As a result, fluid is forced out of capillaries, and because it is protein-rich, even more
water follows.
Additionally, because the liver function is impaired, more albumin is not made to
compensate, which further exacerbates the issue.
What is ascites? - Answer An accumulation of protein-rich fluid in the
abdomen/peritoneum.
What is the major complication associated with ascites? - Answer If the ascites gets bad
enough, then the fluid compression can lead to respiratory dysfunction.
What is hepatic encephalopathy? - Answer Altered neurologic status resulting from the
toxin build-up, particularly ammonia.
Where is ammonia produced in the body? - Answer Ammonia is a byproduct of protein
breakdown by bacteria in the intestinal tract.
What factors can contribute to the development of hepatic encephalopathy? - Answer -
constipation
-blood in GI tract (blood = protein, so bacteria break it down)
-Azotemia (renal failure)
-^protein consumption
How is hepatic encephalopathy classified? - Answer Stage 1
-mild changes in mental status & sleep-wake cycle.
Stage 2
-Liver flap, barely trembles
Stage 3 (protect airway)
-visible liver flap all the time
-mental status more declined
-very lethargic
Stage 4
-comatose
What are the characteristics of compensated cirrhosis? - Answer Patient still has
problems, but in general, they are doing ok/look healthy.
--LFT's are normal.
What are the characteristics of decompensated cirrhosis? - Answer -portal HTN
-esophageal varices
-peripheral edema
-ascites
-hepatic encephalopathy
-hepatorenal syndrome
Why do people with liver cirrhosis get portal hypertension? - Answer Nutshell
Cause: Increased venous pressure in portal circulation
The diseased and scarred liver prevents normal blood flow from the GI tract.
Over time, the blood flow starts to back up at the portal vein, which increases the
pressure.
To compensate, the body starts developing collateral circulation to get around these
backed up areas.
----but they're very weak and are prone to rupture
CM of portal hypertension - Answer -splenomegaly
-ascites
-large collateral veins, which leads to esophageal variceal development
-systemic HTN
What is collateral circulation? - Answer The development of new, smaller branches of
arteries that grow in response to a vessel that has slowly become occluded or nearly
occluded over time.
What is the problem with collateral circulation? - Answer -the vessels are very weak
-it is easy for them to get large and rupture.
R/t portal HTN, what is the most common place for varices to form? - Answer -lower
esophagus
-upper stomach
-rectum
caput medusa - Answer Dilated veins around the umbilicus, associated with cirrhosis of
the liver.
, What are esophageal varices? - Answer Complex of torturous veins at the lower end of
the esophagus (or anywhere where collateral and systemic circulation communicate)
What is the problem with esophageal varices? - Answer They contain little elastic tissue,
so they are fragile and are at risk for bleeding, which can be life-threatening.
Patho of ascites - Answer Incvreased pressure in the portal vein leads to an increase in
hydrostatic pressure (water pushing pressure)
As a result, fluid is forced out of capillaries, and because it is protein-rich, even more
water follows.
Additionally, because the liver function is impaired, more albumin is not made to
compensate, which further exacerbates the issue.
What is ascites? - Answer An accumulation of protein-rich fluid in the
abdomen/peritoneum.
What is the major complication associated with ascites? - Answer If the ascites gets bad
enough, then the fluid compression can lead to respiratory dysfunction.
What is hepatic encephalopathy? - Answer Altered neurologic status resulting from the
toxin build-up, particularly ammonia.
Where is ammonia produced in the body? - Answer Ammonia is a byproduct of protein
breakdown by bacteria in the intestinal tract.
What factors can contribute to the development of hepatic encephalopathy? - Answer -
constipation
-blood in GI tract (blood = protein, so bacteria break it down)
-Azotemia (renal failure)
-^protein consumption
How is hepatic encephalopathy classified? - Answer Stage 1
-mild changes in mental status & sleep-wake cycle.
Stage 2
-Liver flap, barely trembles
Stage 3 (protect airway)
-visible liver flap all the time
-mental status more declined
-very lethargic
Stage 4
-comatose
