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What organ makes bile?
Liver
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Mode of Transmission of Hep A
fecal-oral route, contaminated drinking water and food
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Mode of Transmission of Hep B and C
bodily fluids (sex, blood, saliva)
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MNT for Acute hepatitis
No specific MNT, just symptom management
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Causes of chronic hepatitis
viral infection (HBV, HBC), autoimmune disease, hepatoxic agents (drugs, chemicals, alcohol), metabolic disorders (wilson's disease, hemochromatosis)
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MNT for Chronic hepatitis
Monitor for poor intake and weight loss (may experience anorexia and nausea but malnutrition is not common)
Avoid alcohol and inquire about supplement use (herbal and others)
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Nutritional Needs for Chronic hepatitis
Energy: 30-35 kcal/kg
Protein: 1-1.2 g/kg
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What biologically causes Alcoholic Liver Disease?
Acetaldehyde damages the mitochondria and alters hepatocyte function
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Stage 1 of ALD?
Hepatic steatosis or Fatty Liver
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Stage 2 of ALD?
Alcoholic Hepatitis--widespread inflammation of hepatocytes
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Clinical manifestations for Alcoholic Hepatitis
Hepatomegaly, increased serum bilirubin, transaminases in blood (AST, ALT--should be in liver not blood), altered serum albumin
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MNT for Alcoholic Hepatitis
Alcohol cessation
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Nutritional Needs for Alcoholic Hepatitis
Energy: >35 kcal/kg
Protein: 1-1.2 g/kg
MV with minerals and additional thiamin and folate supplement
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Stage 3 of ALD?
Alcoholic Cirrhosis
final stage, irreversible (only cure is liver transplant)
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Accumulation of fat in the hepatocytes due to increased uptake of lipids by the liver, increased hepatic lipogensis, and or decreased fat oxidation
Caused by: obesity, type 2 diabetes, hypertriglyceridemia, medications, parenteral nutrition
Non-Alcoholic Fatty Liver Disease (NAFLD)
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MNT For NAFLD
If obese: gradual weight loss, restrict calories to lose 10% of body weight, increase PA
If diabetes: MNT to improve glucose control/health diet
If Hypertriglyceridemia: reduce intake of concentrated sweets/refined CHO, limit alcohol, low saturated fat/trans fat diet, weight loss and exercise
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Damage of the hepatocytes caused by reflux or retention of bile acids due to blockage of the bile ducts
Cholestatic Liver Disease
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Progressive destruction of the intrahepatic bile ducts (mostly women), can lead to cirrhosis
primary biliary cirrhosis (PBC)
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Fibrosing inflammation of the extra hepatic bile ducts and possibly the intrahepatic bile ducts (mostly men), can cause cancer of bile ducts, can lead to cirrhosis
Possibly due to autoimmune injury to the bile ducts
Primary Sclerosing Cholangitis (PSC)
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MNT for Cholestatic Liver Disease
If fat malabsorption: water soluble form of fat soluble vitamins supplements, Ca supplement, fat restriction (40 g/day-- Do NOT recommend MCT oil), monitor for weight loss
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Increased deposition of iron in the tissue due to increased absorption from the GIT and increased storage--deposits in hear, liver, pancreas and joints
Hemochromatosis
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MNT for Hemocromatosis
- Well-balanced diet without exceeding DRI for iron
- Reduce intake of heme iron sources like meat
- Avoid iron supplements
- Avoid highly fortified foods, alcohol (increased iron absorption), vitamin C supplements
- STRICT low iron diet DOESNT work
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impaired biliary copper excretion: copper accumulates in the liver, brain, cornea, kidneys
Wilson's Disease
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MNT for Wilson's Disease
- Avoid high copper foods (lamb, pork, duck, salmon, organ meat, shellfish, nuts, seeds, chocolate, soy protein, milk dried beans, bran cereals, mushrooms)
- Avoid alcohol
*Low copper diet (<2 mg/day) is no longer required but may help in the initial phase of treatment
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Hepatitis that comes on really fast and is a result of acute, severe liver injury that destroys the majority of the hepatocytes and results in liver failure
Fulminant Hepatitis
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MNT for Fulminant Hepatitis
- Usually requires nasogastric tube feed
- MNT for hepatic encephalopathy: increased intracranial pressure and/or ascites-->possible sodium and fluid restriction (concentrated tube feed with fluid restriction)
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Nutritional Requirements for Fulminant Hepatitis
Energy: 30-35 kcals/kg
*not super high because patients are not moving/unconscious
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<30% of liver function, caused by injury to the liver cells, characterized by fibrosis and disruption of the tissue and vasculature architecture. Altered structure causes increases intrahepatic vascular resistance, portal hypertension and ascites
End Stage Liver Disease: Cirrhosis
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Hyperbilirubinemia, yellowing of the skin and sclera of eyes, occurs in liver disease due to cholestatic liver disease
Jaundice
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Abnormally high blood pressure in the portal venom system due to the obstruction of blood flow through liver
Portal Hypertension
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The opening and dilation of pre existing blood vessels which connect the portal venous system to the superior and inferior vena cava that is used to bypass the obstructed liver
Collateral Circulation used with portal hypertension
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Shunt that diverts blood away from blocked liver and to heart--Treatment option for portal HTN
Protacaval shunt
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Fragile, enlarged collateral veins caused by portal HTN
Esophageal varices
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Treatment for esophageal varices
- Beta blockers: to decrease blood pressure
- Sclerotherapy: agents to clot blood
- Balloon tamponade: puts pressure on the wound to help clot
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MNT for Esophageal varices
- No oral or nasoenteric enteral nutrition during acute bleeding episodes
- After bleeding resolves: clears to full liquids to
- mechanical soft
- Chew foods very well and don't want rough food rupturing vein
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Accumulation of fluid, serum proteins, and electrolytes in the peritoneal cavity
Ascites
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MNT For Ascites
- 2 g Na Restriction
- Possible fluid restriction if hypervolemia and significant hyponatremia: 1.5 L/day (watch for dehydration)
- Adequate protein to replace losses from frequent paracentesis (draining of fluid into bag)
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How do diuretics work to help ascites?
They dehydrate the blood and so the water in the abdomen moves into the blood in an effort to rehydrate it
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Syndrome characterized by impaired mentation, neuromuscular disturbances and altered consciousness
Hepatic Encephalopathy (HE)
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MNT for Acute HE
- **unnecessary protein restriction should be avoided
- 1.2 g/kg should be tolerated--if not effective use a temporary protein restriction of 0.6-0.8 g/kg then in crease to 1.2 (DONT GO LOWER THAN 0.6)
- If needing tube feed: pick appropriate tube feed for protein needs
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MNT for Chronic HE
- Protein: 0.6-0.8
- High fiber
- High dairy--casein is lower in AAA and higher in BCAA than meat
- Vegetable proteins are high in BCAA--vegetarian diet?
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Energy Requirements for ESLD
Well-Compensated Patients: 25-35 kcal/kg
Malnourished Patients: 30-40 kcal/kg
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Protein Requirements for ESLD
1.0-1.5 g/kg
If HE: 1.2 g/kg
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Carbohydrate Requirements for ESLD
Monitor for hyperglycemia--may need insulin and consistent CHO diet
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Fat Requirements for ESLD
- 30% of total calories
- Monitor for steatorrhea= restrict LCT= 40 g/day
- (LCT= long chain triglycerides?)
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Fluid Requirements for ESLD
If hypervolemia and significant hyponatremia (serum < 125): restriction of 1.5 L/day (monitor intake and output records, weight, serum Na and osmolality)
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Electrolyte Requirements for ESLD
- Sodium: if ascites, edema= 2 g Na restriction
- Monitor electrolytes when on diuretics
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Vitamin Requirements for ESLD
- MVI, fat soluble vitamins in water soluble form (if fat malabsorption)
- Alcoholic liver disease: increased thiamin and folate and vitamin K
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Beriberi and wernike corsicoff syndrom (permanent dementia)
Thiamin Deficiency
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Mineral Requirements for ESLD Exceptions
Provide DRI for minerals except:
- No Cu and Mn supplements (can have food) in cholestatatic liver disease
- No Fe supplements in hemohromatosis
- No Cu supplements in Wilson's disease
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Mineral Requirements for ESLD
- GI bleeding: may need increased Fe
- Alcoholism: may need increase Zn and Mg
- Diuretics: may need increase K, Mg, Ca, and Zn
- Steatorrhea: may need increased Ca, Mg, Zn
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General Recommendations for ESLD
- Eat small, frequent meals
- If poor appetite: oral nutrition supplements, may require tube feedings
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Immediate Post-Transplant Requirements (Liver Transplant)
Energy: MSJE= REE x 1.3-1.5 (combined AF and SF) OR 30-35 kcal/kg
- Protein: 1.5-2.0 g/kg
- MVI with minerals
- Ca supplementation: 800-1200 mg/day
- Usually require tube feeding initially
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DNI with Corticosteriods
- Na Retention and edema
- Hyperglycemia
- Hyperlipidemia
- Increased Appetite and protein wasting
- Decreased absorption of Ca and P
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DNI with Cyclosporine
- Na Retention
- Hyperkalemia
- Hyperlipidemia
- HTN
- Decreased Mg
- Hyperglycemia
- N/V
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DNI with Azthioprine
- Mouth sores
- Esophagitis
- N/V/D
- anorexia
- decreased taste
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DNI with Tacrolimus
- Hyperglycemia
- Hyperkalemia
- N/V
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Long-Term Post-Transplant Goals (after 2 months/healing/rest of life)
- Goal: maintain healthy body weight (ppl on steroids are hungry)
- Prevent: diabetes, HTN, hyperlipidemia, osteopenia, food-borne illness
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Long-Term Post-Transplant MNT (after 2 months/healing/rest of life)
- Protein: 1 g/kg (increased DRI, med can cause muscle wasting)
- Healthy Diet: low in SFA/trans fat, reduced simple CHO, 2 g Na
- Educate on: healthy eating, methods to avoid food-borne illness
- MVI with minerals, Ca supplements (800-1500 mg, only if corticosteroids)
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What causes Non-Alcoholic Fatty Liver Disease
Obesity, type 2 DM, hypertriglyceridemia, medications, parenteral nutrition (can cause cirrhosis if living on it)
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How does altered structure of tissue and vasculature fuck up your liver?
Altered structure causes--> increased intrahepatic vascular resistance-->portal hypertension and ascites
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What causes ascites?
Portan hypertension, decreased production of albumin (oncotic pressure fucked)
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Immunosuppressive Medication that causes Na retention and edema, hyperglycemia, hyperlipidemia, increased appetite, protein wasting, decreased absorption of Ca and P
Corticosteriods
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Immunosuppressive Medication that causes Na retention, hyperkalemia, hyperlipidemia, HTN, decreased Mg, hyperglycemia, N/V
Cyclosporine
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Immunosuppressive Medication that causes mouth sores, esophagitis, N/V/D, anorexia, decrease tastes
Azatioprine
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Immunosuppressive medication that causes hyperglycemia and hyperkalemia N/V
Tacrolimus
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