Liver Disease Part 1 Flashcards
General Function of the liver is Macronutrient metabolism
More specifically…
______ storage
____________
synthesis of ____________
synthesis of ____, _____, ______, and ______
___________
______ production
glycogen
gluconeogenisis
non-essential amino acids
TG, cholesterol, phospholipids, and lipoproteins
FA beta oxidation
ketone production
Another general function of the liver is storage, activation, and transport for many vitamins and minerals…
Storage of _______ (6 vit/minerals)
Synthesizes transport proteins for ______ (4)
Converts _________ to vitamin ___
converts _____ to its active form; intermediate step in _____ activation
Converts vitamin ___ to _______
fat-soluble vitamins, zinc, iron, copper, manganese, vitamin B12
vitamin A, iron, zinc, copper
beta-carotene, A
folate
Vit D
K
prothrombin
liver also has functions for…
____ formation
converting _____ to ______
synthesis of ______ proteins = ______
synthesis of ____________ factors
filters ______ form the blood
detoxification of ___________
bile
ammonia to urea
plasma proteins=albumin
blood clotting
bacteria
drugs and alcohol
What are the types of viral hepatitis?
hepatitis A (HAV)
hepatitis B (HBV)
hepatitis C (HCV)
how can hep A be transmitted
fecal-oral route
contaminated drinking water
food
How can Hep B and C be transmitted
blood
other body fluids
Symptoms of Acute Viral Hepatitis
malaise, anorexia, nausea, RUQ pain
fever, arthralgia, rash
jaundice
goal of acute viral hepatitis
recovery and regeneration of hepatic cells
MNT for acute viral hepatitis
no specific MNT
symptom management
chronic hepatitis is when there is ≥____ course of hepatitis
can progress and lead to ______
6 month
cirrhosis
chronic hepatitis is from ____ or ____ infections.
this is an ________ disease and may be from __________ agents.
Can also be from metabolic disorders such as ________ or _________
HBV or HCV
autoimmune
hepatotoxic
Wilson’s disease
hemochromatosis
chronic hepatitis may cause symptoms of ________ and _______ and they should be monitored for ______ and ______
anorexia and nausea
poor intake and wt loss
MNT for Chronic hepatitis
______ kcal/kg
_______ g/kg
avoid ______
inquire about ______
35
1.2-1.5
alcohol
supplement use
One of the most common liver diseases in the U.S.
alchoholic liver disease
Alcohol metabolism results in _________ which damages the __________ and alters _________function
acetaldehyde
mitochondria
hepatocyte
ALD stages
Stage 1: Hepatic Steatosis
Stage 2: Alcoholic Hepatitis
Stage 3: Alcoholic Cirrhosis
ALD Stage 1: Hepatic Steatosis
- pathophysiology (whats happening?)
- symptoms?
- reversible?
decreased FA oxidation
increased hepatic lipogenesis
trapping TG in liver
no symptoms
yes with abstinence from alcohol
ALD Stage 2: Alcoholic Hepatitis
Whats happening?
Manifestations?
Symptoms?
widespread inflammation of hepatocytes
- hepatomegaly
- elevated serum bilirubin and transaminases (AST, ALT)
- possible decreased serum albumin
anorexia, RUQ pain, N/V/D, weakness, wt loss, fever
ALD Stage 3: Alcoholic Cirrhosis
liver injury and degeneration
end stage liver disease
irreversible
MNT for Alcoholic Hepatitis
Alcohol cessation may resolve damage
High kcal diet: ____ kcal/kg
______ g/kg protein
supplementation:
_______(3)
35
1.2-1.5
MVI with minerals
Thiamin: 50-100 mg
Folic acid: 1 mg daily
NAFLD is now known as ________
metabolic dysfunction-associated fatty liver disease (MAFLD)
MAFLD is the accumulation of ____ in the ______
Due to _______, _______, and/or _______.
fat
hepatocytes
increases uptake of lipids
increases hepatic lipogenesis
decreases fat oxidation
MAFLD is often benign but _________ can lead to _________
this is cause by ?
steatohepatitis
cirrhosis
obesity
insulin resistance or type 2 DM
dyslipidemia
metabolic syndrome
parenteral nutrition
MNT for MAFLD for Individuals with obesity=> ________, ______, and _______.
A hypocaloric, lower _____, _________ diet pattern may be beneficial
gradual wt loss
calorie restriction to lose 5-10% of body wt
increased PA
CHO
Mediterranean
MNT for MAFLD
MNT & PA to improve glucose control
Hypertriglyceridemia=>_____, _____, _____, _____
Vitamin ___ supplementation: ____ IU/day
reduce intake of refined CHO
limit alcohol
low saturated fat/trans fat diet
increase intake of omega-3 fatty acids
E
800
cholestatic liver disease
Caused by chronic ______ injury to the _____
These involve ____________ + ______________
Results in _______ and reflux of _____ into the _____=> hepatocyte damage
autoimmune
bile ducts
Primary Biliary Cirrhosis (PBC)
Primary Sclerosing Cholangitis (PSC)
cholestasis
bile acids
liver
progressive destruction of the intrahepatic bile ducts
Primary Biliary Cirrhosis (PBC)
fibrosing inflammation of the extrahepatic & intrahepatic bile ducts
Primary Sclerosing Cholangitis (PSC)
cholestatic liver disease sign and symptoms
jaundice
pruritis
elevated serum bilirubin & alkaline phosphatase levels
fat malabsorption/fat vitamin deficiencies
osteopenia
slow progression to ESLD
MNT for cholestatic liver disease
if fat malabsorption, 40 g/d
fat-soluble vitamin supplement in water soluble form
Ca supplementation
monitor for wt loss
Hemochromatosis is a _______ disorder
recessive genetic disorder
what happens in hemochromatosis
Increased iron absorption from the GIT=> Iron overload=> increased deposition of iron in tissues including the liver
hemochromatosis complications
ESLD
hepatocellular carcinoma
glucose intolerance
arthritis
cardiac involvement
hemochromatosis treatment
phlebotomy to remove Fe from blood & chelating agents
MNT for Hemochromatosis
Regular, well-balanced diet
- Iron-restricted diet usually not indicated
Avoid exceeding the DRI for iron
- Avoid iron supplements and MVI with minerals including iron
- Reduce intake of heme iron sources (Consume more of a plant-based diet)
- Avoid highly fortified foods, vitamin C supplements, & alcohol
Wilson’s Disease is an _______ disorder
results in impaired ________
autosomal recessive
biliary copper excretion
in wilsons disease copper accumulates in the ?
liver
brain
kidneys
cornea
complications of wilson’s disease
chronic hepatitis
ESLD
neurologic symptoms
treatment for wilson’s disease
copper chelating agents
Zn supplementation
MNT for Wilson’s Disease
Low copper diet is no longer required but may be helpful in the initial phase of treatment
Avoid MVI with minerals (if contains copper)
Avoid alcohol - hepatotoxin
high copper foods include
lamb, pork, duck, organ meats
salmon, shellfish
nuts, seeds, chocolate
soy protein & milk
dried beans
bran cereals
mushrooms
Acute liver failure is also called _______
A rare syndrome resulting from acute, severe liver injury that destroys the majority of the hepatocytes=> liver failure
Occurs in the absence of ________
fulminant hepatitis
preexisting liver disease
acute liver failure is…
Rapid clinical deterioration with the onset of ______, ______, and ______
jaundice
coagulopathy
hepatic encephalopathy
causes of acute liver failure
acetaminophen overdose*
viral hepatitis*
autoimmune hepatitis
liver ischemia
Wilson’s disease
toxins
dietary & herbal supplements
Complications of ALF
Hepatic encephalopathy
Coagulopathy
Hypoglycemia
Systemic Inflammatory Response Syndrome (SIRS)
Renal failure
Respiratory failure
Cerebral edema
Coma
Can be fatal without a liver transplant
MNT for ALF
Energy expenditure _______ by up to ___%
________ state
Usually require _______
Increased intracranial pressure &/or ascites=>_____________
increases
30%
Hypercatabolic
enteral nutrition
sodium & possible fluid restriction
End Stage Liver Disease (ESLD) is also known as
cirrhosis
End Stage Liver Disease (ESLD)
Caused by chronic injury to hepatocytes=> ________ and disruption of liver tissue & ________
Altered structure causes=>_________=> _______
Liver becomes ______
reversible?
fibrosis
vascular architecture
increased intrahepatic vascular resistance
portal hypertension
necrotic
Irreversible
Causes of ESLD
Chronic hepatitis (HBV, HCV, autoimmune)
Alcoholic liver disease
Cholestatic liver disease
Metabolic disorders: Hemochromatosis; Wilson’s Disease
Metabolic dysfunction-associated Fatty Liver Disease (MAFLD)
Cryptogenic cirrhosis
ESLD Stages
compensated
decompensated
compensated ESLD
Liver is heavily scarred but still able to perform many of its functions
decompensated ESLD
Extensive scarring
liver is unable to function properly
complications
jaundice is a result of hyper_______.
bilirubinemia
bilirubin is the end product of _______
in liver _______ and then excretion in the ____
Hemoglobin metabolism
conjugation
bile
jaundice occurs due to
obstruction in bile ducts or hepatocyte damage
what is coagulopathy
Decreased production of clotting factors=> increased bleeding risk
Portal Hypertension is ?
Abnormally high blood pressure in the portal venous system due to the obstruction of blood flow through the liver
Portal hypertension results in
ascites
esophageal varices
splenomegaly
With portal hypertension, the ________ is used to bypass the obstructed liver
______ and ______ of preexisting blood vessels which connect ____ of the portal venous system to the ______________
Results in _____ in the GIT that are fragile and easily rupture
Possible treatment=> _______
collateral circulation
Opening & dilation
veins
superior & inferior vena cava
varices
Portacaval shunt
Fragile, dilated collateral veins caused by portal hypertension
esophageal varices
if esophageal varices rupture, results in a _________
GI bleed
treatment for Esophageal varices ?
medications ?
Endoscopic band ligation
B-adrenergic blockers
(e.g., propranolol, metoprolol)
MNT for Esophageal Varices
No oral or nasoenteral nutrition during acute bleeding episodes
After bleeding resolved…
Full liquid diet=>Easy-to-Chew diet
Chew food thoroughly
