PDAT GI LIVER CIRROHOSIS

LECTURE 2

what is the core idea of liver cirrohosis? 

you have damage or scarring done to the liver which causes hepatocytes to be destroyed which leads to blood flow being unable to happen in the liver so you have a build up of pressure causing the liver to stop working

what are the 2 things that happen when someone has liver cirrohosis that messes with the function of the liver?

destruction of hepatocytes and the development of fibrosis and nodules

what happens as a result of liver architecture being destroyed?

loss of liver function and back up of blood which causes hypertension and resistance to blood flow into the liver

why is hypertension and resistance to blood flow a consequence of liver cirrohosis?

fibrosis and nodules block blood flow through the liver so pressure builds up behind the liver

why is cirrohosis both a plumbing problem and a functional problem?

it is a plumbing problem because of the blocked blood flow and it is a functional problem because of the destruction of hepatocytes 

why do varices form in cirrohosis?

blood cant pass through the liver so it finds alternate pathways (other veins) which causes the veins to enlarge and become fragile and even burst

why are varices at high risk of bleeding?

they are thin and fragile veins that are under high pressure so they can easily burst

what is the first line treatment for varices? why?

non selective beta blockers are the first line treatment because they hit both B1 and B2 receptors

why is it important that non selective beta blockers hit b2 receptors?

this is important because B2 receptors are the ones on blood vessels that can constrict down which results in blood flow to the portal vein eventually reducing blood pressure 

what are the non selective beta blockers?

propanolol, nadolol, and carvedilol

why are non selective beta blockers used as prevention of varices?

since they block the b2 receptors which reduce blood flow and pressure to the portal vein they can reduce the possibility of a variceal bleed by half 

why dont beta 1 selective blockers work for varices?

they dont cause spalchnic vasoconstriction so theres no reduction in portal blod flow

what is the formal phrase and definition of the type of vasoconstriction that non selective beta blockers do?

splanchnic vasoconstriction which is when there is a reduction in portal blood flow

what is the most common complication of cirrohosis?

ascites

how do ascites form in liver cirrohosis?

people with bad livers dont make albumin so no fluid goes into the blood vessels so the body thinks it has low fluid volume so it will activate the RAAS system which retains sodium and water and pressure goes to the periotoneum

what are the 3 main drivers of ascites?

portal hypertension, low albumin, and sodium/water retention

why do we have low albumin in ascites?

people with bad livers dont make albumin

why does low albumin cause fluid build up?

albumin normally pulls fluid into blood vessels

why does the body retain sodium and water in cirrohosis?

vasodilation makes the body think volume is low

what are the symptoms of ascites?

increased abdominal girth, weight gain, abdominal pressure, shortness of breath and difficulty walking

how many pounds of fluid are usually in the abdomen when someone has ascites?

20 pounds

how do we diagnose someone with ascites?

pull 30-50 ml of fluid and check the fluid for infection and the cause of the ascites

what essentially leads to ascites?

sodium and water retention

what is SAAG in ascites? what is it used for?

measures albumin content of ascites and compare it to blood. we can use it to see if a patient has portal hypertension/liver cirrohosis

what SAAG value indicates that someone has ascites?

greater than or equal to 1.1 g that is portal hypertension

what does a high SAAG vs a low SAAG indicate?

a high saag indicates liver problems and a low one indicates a different issue

what is a treatment for ascites?

therapeutic paracentesis which is taking out 8-10 ounces all at once 

how are the signs and symptoms of cirrohosis usually described?

they are insidious meaning we dont even know they are happening.

is cirrohosis well compensated or decompensated? what does this mean?

it is well compensated. this means it shows up without signs and symptoms

when someone does have cirrohosis what do the symptoms look like when they actually do come?

malaise (general uncomfort), fatigue, and poor appetite

what is the outcome of liver cirrohosis when it has progressed too far?

enstage liver disease

what makes liver cirrohosis compensated vs decompensated?

compensated means it can be tolerated there are no signs and symptoms. decompensated means that hospitalization usually occurs and someone is having complications due to the cirrohosis

is enstage liver disease compensated or decompensated?

it is decompensated because this is usually when complications are seen

what are common complications in enstage renal disease?

jaundice, ascites, encephalopathy (confusion), and/or variceal bleeding

why do people get jaundice in enstage renal disease?

people get jaundice because the liver usually clears bilirubin but in enstage renal disease the liver cant so bilirubin builds up in the skin

what is the description of jaundice?

yellow skin or eyes

what are skin signs of enstage renal disease?

caput medusa, spider angioma, and palmar erythema

how do people get capot medusa in enstage liver disease?

capot medusa comes from swollen blood vessels due to blood being unable to flow through the liver 

what is spider angioma in enstage liver disease? how does it happen?

spider angioma is burst blood vessels it happens because blood cant flow through the liver 

what does spider angioma look like?

red spots on body

what does palmar erythema look like?

red palms

what does palmar erythema come from?

vasodilation due to blood not being able to flow through the liver and building up in blood vessels

what lab values do we use for enstage renal disease?

elevated INR, decreased thromopoetin, low albumin

what does INR measure? why is it used as a lab value for ESLD?

INR tells you how long it takes blood to clot. we use it as a lab value because when the liver is damaged it cant make enough clotting factors so blood takes long to clot

does an elevated or low INR indicate liver disease? why?

elevated INR means liver disease because this means blood takes longer to clot

why is decrease thrombopoetin a sign of enstage liver disease? what does thrombopoetin do?

this is because the liver produces thrombopoetin. thrombopoetin is a hormone that produces platelets

in enstage liver disease should we expect high or low platelet counts? why?

low because thrombopoetin is unable to produce them

what is splenomegaly and how does splenomegaly happen in enstage liver disease?

enlarged spleen due to blood not being able to flow through the liver so blood backs up into the spleen

why does enstage liver disease patients with splenomegaly have low platelets?

get low platelets because when the spleen gets too big it holds onto platelets

why is there low albumin in enstage liver disease?

the liver produces albumin so if its damaged it cant be produced

why is albumin important? why is it bad when it runs low?

albumin keeps fluid inside of blood vessels. when it runs low theres no way to keep fluid inside of blood vessels so it leaks out causing ascites

what does the portal vein do?

collects blood from the GI tract and sends it to the liver

when HVPG is greater than what value does it mean someone has portal hypertension?

HVPG (hepatic venous pressure gradient) >5 mmHG is portal hypertension

a build up of blood in which veins causes caput medusa?

in the paraumbilical veins

a build up of blood in which veins causes varices?

build up of blood in intrinsic veins of esophagus

when the pressure gradient is at which value is someone at risk for varices?

10

when the pressure gradient is which value is someone at risk for hemmorage/bleeding?

when the gradient is at 12

what are things to monitor for when giving a patient a beta blocker? why?

monitor heart rate (bradycardia) and blood pressure because it can drop heart rate and blood pressure 

what is the goal of using beta blockers to prevent varices?

titrate to maximum dose tolerared by blood pressure and heart rare

what are signs and symptoms of acute variceal bleeding?

weakness/fatigue/dizziness, blood in the vomit, and dark tarry stools

what are the treatment strategies for variceal bleeding?

pharmacologic therapy and medical procedures such as band ligation, sclerotherapy, and balloon tamponade

what is band ligation?

grab a blood vessel squeeze it with a band the the bleeding should stop

what is sclerotherapy?

an injection is put into a vein to scar it shut

what is the moa of octreotide?

it is a selective splanchnic vasoconstrictor which reduces portal pressure

when should octreotide be started?

start immediately and continue for 72 hours

what are things to monitor for when giving octreotide?

monitor for hypo or hyperglycemia and bradycardia

how is octreotide administered?

via IV

what treatment would we use to reduce mortality in variceal bleed?

we would use the antibiotic ceftriaxone for 5 to 7 days

what is a secondary prevention strategy to prevent vascites?

intrahepatic shunt (tips)

what is a intrahepatic shunt?

it is a shunt that goes through the liver connect portal vein to hepatic vein to relieve pressure

what is first line treatment to prevent bleeds in varices?

non selective beta blocker

what is the 2nd line treatment to prevent varices?

band ligation

what is the first line treatment for an acute bleed in varices?

octreotide with an antibiotic and band ligation

what is the 2nd line treatment for an acute bleed in varices?

tips (shunt)

what is the first line treatment to prevent a rebleed in varices?

non selective beta blocker with band ligation

what is second line treatment to prevent a rebleed in varices?

tips (shunt) or transplant

what is non pharmacologic treatment that all patients with ascites should do? why?

all patients with ascites should restrict sodium intake to <2 grams/day. without sodium restruction diuretics will fail.

what are non pharmacologic treatments that select patients with a serum Na less than 125?

restrict fluid intake to 1 to 1.5 L/day

what is the pharmacologic treatment for ascites?

loop diuretics (spirinolactone)

what is the MOA of spirinolactone?

it inhibits aldosterone

what type of diuretic is spirinolactone? why is this important for monitoring?

potassium sparing diureric. this is important for monitoring because we must monitor potassium levels for hyperkalemia

what are side effects of spirinolactone?

elevated potassium, hyponatremia, and gynecomastia

what is the consequence of having elevated potassium in spirinolactone?

arrthymias

what is spirinolactone usually given with for ascites? why?

you will use spirinolactone and furosemide together in the beginnning to keep potassium in balance

what type of loop diuretic is furosemide?

potassium wasting diuretic

what is the ratio for dosing furosemide with spirinolactone?

often a ratio of 100 mg spirinolactone to each 40 mg of furosemide. initial furosomedie dose is 40 mg/day

what is a potassium sparing diuretic other than spirinolactone we can use? when would we use it in ascites?

potassium sparing diuretic. good for patient with tender breast

what is the dosing for amiloride when converting from spirinolactone?

10 mg amiloride may be used to replace 100 mg of spirinolactone

does amiloride inhibit aldosterone?

no it doesnt

what are lab values we should monitor when giving a patient a diuretic?

serum creatinine and serum electrolytes

how much weight do we want a patient on a diuretic to lose if they do not have edema?

decrease weight by 0.5 kg/day

what is the weight loss goal for a patient on a diuretic if they have peripheral edema?

decrease weight by 1 kg/day if peripheral edema

why is spirinolactone first line for ascites?

it blocks aldosterone which is the main driver for sodium retentoin

why is furosemide added to spirinolactone?

to balance potassium and increase fluid removal

why does sodium restriction matter in ascites?

if sodium intake is high the body will keep retaining water and diuretcis wont work

how does spontaneous bacterial peritonitis occur?

bacterial overgrowth in gut due to poor immune system and the bacteria escapes the gut and enters the ascites fluid

why do we treat SBP even if cultures are negative?

high neutrophils indicate infection even if bacteria arent detected

what is the presentation of spontaneous bacterial peritonsis?

sometimes people are asymptomatic, fever, abdominal pain, and change in mental status

what is used to diagnose SBP? what does it indicate?

we use PMN to diagnose, it indicates the amount of neutrophils present

why is neutrophil count used for SBP diagnosis?

neutrophils fight off infection so if there is a high amount theres probably an infection present