Lecture 17: Liver Disease Flashcards
largest gland in body is:
the liver
hepatocytes form ___% of liver mass, and are crucial for:
80; metabolism of aa and ammonia, detox, biochem oxidation rxns
____% of liver cells need to be injured before signs of dysfunction occurs
80-90
liver receives blood from ___ and ___
hepatic artery (bring in oxygen supply); hepatic portal vein (venous blood drains from GI tract to liver for nutr processing/storage)
blood leaves liver from:
hepatic vein (back to heart to reoxygenate)
yellow/green fluid composed of cholesterol, bile acid, bilirubin, water, K, Na, bicarbonate, copper, other metals
bile
bile is produced in ___ stored in ____ and is an ___ agent
liver; gallbladder; emulsifying
acute liver failure caused by __________
acute hepatitis, shock liver, fulminant liver disease, acute on chronic liver failure
what is fulminant liver disease?
someone healthy develops liver failure within 2-8 weeks of liver insult
chronic liver failure usually driven by ____ which causes ____
inflammation; fatty liver/steatosis, fibrosis, cirrhosis, hepatocellular carcinoma
what is diff between compensated and decompensated liver disease?
comp: pt has cirrhosis but doesn’t show external s/s of liver disease
decomp: person has s/s related to their liver disease
categories of causes of liver disease?
toxins, metabolic, infections, immune-mediated, other
obesity can cause NALFD which is:
non-alcoholic fatty liver disease
primary causes of liver diseases:
alcohol, obesity, viral (hep a b c)
clinical manifestations of liver disease:
jaundice, bruising, muscle wasting, altered hair distribution, encephalopathy, cirrhosis, hepatorenal syndrome, tea coloured urine, esophogeal varices, spider angloma, etc.
liver function tests/liver panel includes these enzymes, these proteins, these clotting studies, ammonia, and bilirubin
enzymes: ALP, ALT, AST, GGT, LDH; proteins: albumin, total protein, clotting: PTT, INR
is total (unconjugated) or direct (conjugated) bilirubin more often measured?
total
bilirubin is breakdown product of ____
heme
jaundice of eyes called:
icteric sclerae
prob of itchiness (pruritis)?
might create open wounds, probs with wound healing and blood clotting
why jaundice happen?
^ bilirubin cause ^ RBC destruction which causes ^ bilirubin uptake but decrease liver fxn which ends up in bile duct obstruction
primary symptoms/complications of portal hypertension (blood flow forced backward, veins enlarge):
ascites, esophageal varices, hepatic encephalopathy
accumulation of fluid in peritoneal cavity where fluid leaks from ___ to abdominal space, leading to decrease in _____
capillaries; albumin
how to remove ascites?
abdominal paricentesis (there will be protein in the fluid)
low pressure veins in esophagus and upper stomach that become distended cuz ^ pressure due to portal HTN
esophageal varices
if non-bleeding esophageal varices, can use _____ tubes; if actively bleeding, hold EN for ____ h post-banding
nasoenteric; 48-72
critically ill pt should use ____ tube
sengstaken - blakemore
pathogenesis of hepatic encephalopathy?
ammonia bypasses liver metabolism and accumulates, metabolized at extrahepatic sites to glutamine which ^ oxidative stress, crossing blood brain barrier and accumulate in brain (toxic)
is plasma ammonia level good indicator of NH3 levels and HE?
nope
primary treatment for HE:
lactulose (potent and effective laxative , osmotic diarrhea), antibiotics (v colonic concentration of bacteria producing NH3)
3 major cause malnutrition in cirrhosis?
1) factors resulting in decreased po intake, 2) physio aberrations resulting impaired digestion/absorption 3) impaired nutr metabolism
anorexia is caused by ___ deficiency
zinc
etiology of sarcopenia/muscle wasting in cirrhosis:
anabolic resistance, accelerated lipolysis, accelerated aa oxidation, increased autophagy mediated proteolysis in muscle, hyperammonemia
goals of Nutrition therapy for sarcopenia?
promote/maintain N balance, promote liver regeneration, prevent metabolic abnormality exacerbations, treat malnutrition
strategies to improve PO intake in liver disease:
small frequent meals, nutr dense foods, ONS, EN may be warranted
should protein be restricted in HE?
no because ^ skel muscle breakdown releases more N containing AA that can further ^ NH3 production
protein recommendations for HE:
1-1.5 g/kg/d *not below 0.8
altered aa metabolism in liver failure can result in ^ circ levels of ____ amino acids and v in plasma ____ amino acids
aromatic; branched chain
^ aaa can worsen HE as cross blood brain barrier cuz act as _____
false neurotransmitters
benefits of BCAA?
anabolic
alcoholic liver disease is spectrum of these 3 disorders:
fatty liver, hepatitis, cirrhosis
hepatotoxic alcohol threshold where ALD likely develop:
men 4 drinks a day, women 2 drinks a day
vit/min deficiencies in alcoholism:
folic acid, thiamine, vit e, niacin, vit c, d, k, a, zn, fe, ca, k, mg
essential coenzyme in CHO metabolism
thiamine
thiamin deficiency causes:
wernicke’s encephalopathy (hypothermia, confusion, ataxia, ocular probs), korsakoff’s syndrome (memory probs)
hepatic manifestation of metabolic syndrome/insulin resistance
NAFLD
NAFLD may progress to ___ cuz of fat accumulation associated with liver cell inflamm and scar
NASH (non alcoholic steatohepatitis)
risk factors for developing NASH:
adipose tissue inflamm, gut microbiota, oxidative stress, hepatocyte apoptosis, hepatic inflamm
nutr consideration for NAFLD?
diet/physical activity, 10% wt loss, supplement vit E
liver disease pt have high ___ use
complementary / alternative medicine
