Chapter 16 (Diseases of the liver, gallbladder, and exocrine pancreas) Flashcards
Which organ is the first stop for all nutrients?
- the liver
what is the largest gland in the body?
- the liver
How many lobes does the liver have and what are each lobe made up of?
- four lobes; two functional (right and left)
- each lobe is made up of thousands of lobules around a central vein
True or false: Cells of the liver are resilient and regenerate?
- True
What organ is the primary blood reservoir and central to metabolism?
- the liver
How much blood does the liver store at any given time?
- 200 - 400 mL
The liver receives nutrients from the digestive tract and processes them for distribution throughout the body through what?
- the hepatic portal vein
- which the hepatic vein returns blood to the heart from the liver
what supplies oxygen rich blood from the heart to the liver?
- hepatic artery
What does the liver regulate?
- glucose and cholesterol
what does the liver store?
- vitamins
- glycogen
- copper
- iron
The liver metabolites and is the detoxifier/clearance of what?
- drugs
- hormones
- toxins
- ammonia
- bilirubin
the liver synthesize and secretes what?
- albumin
- other transport proteins
- lipoproteins
- clotting factors
- cholesterol
- bile
- glucose
what is the two major functions of the liver?
- bile secretion
- enterohepatic circulation of bile (recirculation of bile salts)
what are the two functions of bile?
- emulsify
- absorption - formation of micelles
What does the liver reuse 95% and 5% newly synthesized in the enterohepatic circulation?
- bile salt
How much bile salt does the liver make a day in the enterohepatic circulation?
- 600 - 1000 mL
How much bile salt do we lose in our feces through the enterohepatic circulation?
- 5%
What are some of the pertinent laboratory values for the liver?
- liver function tests (LFTs)
- non-invasive screening for liver function
- allow recognition of type of liver disease
- assessment of severity and predict outcomes
What is looked at when doing a liver function test?
- alanine transaminase (ALT) elevated d/t liver damage
- aspartate aminotransferase (AST) elevated d/t liver damage
- bilirubin (yellow compound)
- albumin (might be low)
- prothrombin time (blood clotting)
What is Jaundice?
- yellowish tint to body tissues; skin, eyes
what is the yellowish tint to body tissues caused by?
- large quantities of bilirubin in extracellular fluid
what is the normal plasma concentration of bilirubin and at what level does the skin start to appear yellowish?
- < 1.1 mg/dL
- can rise to >5 mg/dL
- skin appears yellowish at 2.4 - 3 mg/dL
what are the 3 main causes of jaundice?
- Hemolytic (increased destruction of RBCs
- Hepatic (decreased uptake of bilirubin, decreased liver function)
- Obstructive (obstruction of bile ducts or liver cells)
What are the pathophysiology of the liver?
- metabolic alterations
- decreased intake
- altered absorption
what pathophysiology is common to the hepatobiliary tract?
- Jaundice
What causes metabolic alterations in the liver?
- decreased glycogen stores
- insulin resistance common in end stage (cirrhosis)
- altered vitamin and mineral metabolism and storage
what decreases nutrient intake in the liver?
- anorexia (no appetite)
- early satiety (fullness quickly; fluid full)
- ascites
- restrictive diets
what would cause altered absorption in the liver?
- reduced bile synthesis or release
What is hepatitis?
- inflammation of the liver
- can be acute or chronic
What causes hepatitis?
- virus
- bacteria
- toxins
- obstruction
- parasites
- drugs
What can develop from hepatitis?
- cirrhosis (end stage)
- liver cancer
How is hepatitis A (HAV) contracted?
- transmitted almost exclusively by fecal-oral route
- contaminated drinking water, food, sewage
- treatable, short term
How is hepatitis B (HBV) or serum hepatitis contracted?
- transmitted via blood, blood products, semen, and saliva
- short term illness
How is hepatitis C (HCV) contracted?
- exposure to blood/body fluids from an infected person
- more serious
Hepatitis C is associated with the development of what?
- chronic liver disease
- cirrhosis
- need for liver transplant
What are the clinical manifestations of hepatitis?
- jaundice, dark urine, anorexia, fatigue, headache, nausea, vomiting, fever
- hepatomegaly (lg. liver), and splenomegaly (lg. spleen)
- bilirubin, alkaline phosphatase, serum AST elevated
what are the nutritional implications of hepatitis?
- weight loss
- nutritional deficiency
What are the nutrition assessment for hepatitis?
- weight and weight history
- food intake
- lifestyle factors
what would be the nutrition diagnosis for hepatitis?
- inadequate oral food and beverage intake
- inadequate protein and calorie intake
- food-medication interaction
- impaired nutrient utilization
what are the nutrition interventions for hepatitis?
- spare liver and provide nutrients for regeneration
- adequate rest, fluids, avoidance of alcohol
- increase dietary intake (30-35 kcal/kg body weight, >/= 3000 kcal)
- small, frequent meals d/t satiety
- adequate protein (1.0-1.2 g/kg body weight)
- may need to restrict fat, if not well tolerated
- replace K and Na if vomiting and diarrhea
what define alcoholism?
- chronic consumption of >80g of ethanol/day (40g for men; 20g for women per day)
- dependency may be evident as tolerance or withdraw symptoms
Ethanol rapidly and completely absorbed even with what?
- malabsorption
Can ethanol be stored?
- no d/t oxidation
what is an alcoholic liver disease referred to?
- fatty liver (steatosis)
What is present in 90% of chronic alcohol abusers?
- steatosis (fatty liver)
What causes steatosis (fatty liver)?
- excess acetyl CoA converted to fatty acids
- hypertriglyceridemia
- fat deposition in hepatocytes
Fatty liver (steatosis) can also develop in absence of alcohol, including in persons who have had what?
- bariatric surgery
- those with cystic fibrosis
- associated with obesity and metabolic symptoms (NASH)
- increased visceral fat are more susceptible
what is malnutrition in alcoholics is caused by what?
- displacement of nutrients from not eating
- maldigestion or malabsorption of nutrients d/t GI complications
- weight gain and obesity
What is the formula to calculate kcal derived from ethanol?
- (0.8 x proof x ounces = kcal)
Which organs are contributing to the GI complications for the malnutrition in the alcoholic?
- esophagus
- stomach
- intestine
what causes malnutrition in the alcoholic d/t the esophagus, GI complications?
- heartburn
- reduced LES pressure
- esophagitis
- stricture
- tears from vomiting
What cause malnutrition in the alcoholic d/t the stomach, GI complications?
- gastritis
- duodenitis
- atrophy of mucosal barrier
- hemorrhage
- PUD
- pernicious
- anemia
- stomach cancer
What causes malnutrition in the alcoholic d/t the intestine, GI complications?
- damage to villi and increased motility leads to malabsorption
- diarrhea
What is PEM (protein energy malabsorption) d/t in an alcoholic liver disease malnutrition?
- poor dietary intake
- malabsorption
- hyper catabolic state (using all of body’s reserves for reg. function)
- altered energy storage
- biochemical changes (seen by labs)
Which vitamin and mineral deficiencies contribute to an alcoholic liver disease?
- folate
- thiamin (berry berry; common)
- B6
- vitamin C and D (common in smokers)
- vitamin K
- vitamin A
- iron
- calcium
- potassium
- recommend multivitamin 2x RDA
Alcoholism malnutrition is a major cause of ?
- liver damage and resulting dysfunction
What is cirrhosis?
- chronic liver disease in which healthy tissue is replace by scar tissue, blocking the low of blood, resulting in loss of liver function
what are the most common causes of cirrhosis?
- chronic alcoholism and HCV
what is the first stage of cirrhosis?
- steatosis (fatty liver)
What are the general symptoms in cirrhosis clinical manifestations ?
- fatigue
- weakness
- nausea
- poor appetite
- malaise (general feel of discomfort)
- vit. and mineral deficiencies
What are the liver specific symptoms in cirrhosis clinical manifestations?
- jaundice
- dark urine
- light stools
- steatorrhea
- itching
- abdominal pain
- bloating
- vit. and mineral deficiencies
What are the major clinical complications of cirrhosis?
- portal hypertension
- hepatic encephalopathy
- ascites (swelling of belly)
- hepatorenal syndrome
- esophageal varices (swollen/large veins)
What is portal hypertension/ascites?
- elevated blood pressure in the portal vein
What are the symptoms of portal hypertension?
- ascites (swelling of belly d/t fluid)
- GI bleeding from varies
- encephalopathy
what is ascites?
- accumulation of fluid in peritoneal cavity
- hepatic fibrosis
- reduced osmotic pressure
- increased attention of sodium
What are the medical treatments for portal hypertension/ascites/
- sodium restriction and/or diuretics (to get of excess fluid)
- paracentesis (w/draw fluid w/catheter) results in protein loss)
what are the surgical procedures for ascites?
- TIPS (transjugular intrahepatic portosystemic shunt)
- DSRS (distal spleno-renal shunt)
what does TIPS, transjugular intrahepatic portosystemic shunt do for ascites?
- reroutes blood flow to the liver and reduces pressure in all auxiliary veins
what does DSRS, distal splenorenal shunt, do for ascites?
- the distal splenic vein is attached to the left renal vein reducing portal hypertension
What are the nutrition therapy for ascites?
- encourage oral protein / supplements (ex. protein bars)
- restrict salt to 2g/d (RDA 1500mg)
- restrict fluid to 1500cc if serum sodium low (<120mEq/L)
- adequate kcal d/t poor appetite, early satiety
- diuretics (only is kidney is functioning)
What is encephalopathy?
- syndrome of impaired mental status and abnormal neuromuscular function
what are the staging scales for encephalopathy?
- west Haven (awake and alert people)
- Glasgow (for people in commas)
what is the pathogenesis of encephalopathy?
- unknown
- inability to eliminate products toxic to brain
what are the three hypotheses of encephalopathy?
- ammonia (high levels)
- synergistic neurotoxin
- false neurotransmitter (high AAA, low BCAA in brain)
what are false neurotransmitters?
- altered amino acid metabolism
what causes altered amino acid metabolism?
- increases muscle uptake of BCAA’s (valine, leucine, isoleucine)
- increased aromatic amino acids in plasma and brain (phenylalanine, tyrosine, tryptophan)
- altered neurotransmitter synthesis
what is the treatment for encephalopathy?
- depends on type, extent of neurological damage, presence of precipitating factors
- reducing circulating ammonia (lactulose and antibiotics)
- dietary protein restriction (0.6-0.8 g/kg; min. 50g/d), plant sources, increase fiber, milk and cheese)
- monitor serum potassium level (sometimes low)
- correct hypoglycemia and vit. deficiencies
what are the nutritional implications for nutrition therapy for cirrhosis?
- early satiety from ascites (small frequent meals)
- impaired nutrient digestion and absorption
- increased energy expenditure
- hypoglycemia d/t hyperinsulinemia
- hyperglycemia
what are the nutrition assessment for cirrhosis?
- food/liquid intake and intolerances
- lifestyle factors including alcohol intake
- lab values related to liver function and vit./mineral status
- current and past medical diagnoses and treatments
what is the nutrition diagnosis for cirrhosis?
- may relate to complications of cirrhosis
what are the nutrition interventions for cirrhosis?
- energy nutrients (protein should not be restricted (0.8g/kg), carbohydrate restrictions in patients w/diabetes
- vit. and minerals (sodium restriction in ascites)
- enteral feeding; soft diet for patients with esophageal varices
- 30-40 kcal/day for liver patients
how would you monitor and evaluate nutrition therapy for cirrhosis?
- tolerance to feedings
- amount nutrients consumed
- weight changes (dry)
- laboratory values
- cognitive status (depends on mental status)
when is liver transplant considered?
- as a last resort
- in cases where effects of disease have higher potential mortality than transplant
what is used to determine eligibility for liver transplants?
- MELD (model for end stage liver disease scoring system
what MELD scoring system show for eligibility for liver transplant?
- predicts three month survival for patients with advanced liver disease
- uses patient’s lab values for serum bilirubin, serum creatine, and prothrombin time
- patients with cirrhosis (higher MELD score associated w/ increased severity of hepatic dysfunction and increased mortality risk
what are the nutritional implications for nutrition therapy for liver transplant?
- malnutrition and ascites
- need for early nutritional support post surgery
- food borne infections (after transplant poor immune system)
what are the nutrition assessment for liver transplant?
- SGA (subjective global assessment)
- anthropometrics
- dietary intake
- GI symptoms
- biochemical labs
- side effects of post transplant meds. (high blood sugar, hyperlipidemia, sodium retention)
what are the nutrition diagnosis for liver transplant?
- related to energy and nutrient intake, utilization, and expenditure
- altered lab values
- food-medication interactions
- weight loss
- knowledge deficits
what are the pre-transplant nutrition intervention for liver transplant?
- 35-45 kcal/kg
- 1.0-1.5 g/kg of protein
- normalize BS, nitrogen balance, maco- and micronutrients
- the more patients are nutritional sustained the better the outcome after surgery
what are the post-transplant nutrition intervention for liver transplant?
- regular diet
- 30-35 kcal/kg
- 1.0-1.5 g/kg of protein
- other nutrients individualized used on immunosuppressant drug regimen
how would you monitor and evaluate liver transplant patients?
- recovery and healing
- dietary intake
- tolerance to the diet
- weight changes
- incidence of food-borne illness
- nutrient related complications
After the liver makes bile and transfers it to the gallbladder, what does the gallbladder do?
- stores, concentrates, and secretes the bile
How does the gallbladder concentrate bile?
- removal of water and electrolytes
How does the gallbladder secrete bile?
- control of delivery of bile slats to duodenum, sodium and potassium salts
what is a common problem of the gallbladder?
- cholelithiasis (gallstones)
what is cholelithiasis?
- formation of stones within the gallbladder or biliary duct
- biliary sludge (mixture of microscopic particulate - cholesterol crystals and calcium salts)
- biliary stasis (intrahepatic impairment of bile flow) common from TPN
How types of gallbladder stones are there?
- three
- cholesterol (most common, 50-80%, major component of bile)
- pigment (10% of cases, too much bilirubin)
- mixed
what are the causes of gallstones?
- too much absorption of water from bile
- too much absorption of bile acids from bile
- too much cholesterol in bile
- inflammation of epithelium
what is choledcholithiasis?
- biliary obstruction
- when a gallstone passes from the gallbladder through the cystic duct and lodges in the common bile duct or in the head of the pancreas
- secondary secondary biliary cirrhosis
what is cholecystitis?
- inflammation of the gallbladder
- develops secondary to obstruction
- can lead to infection and ischemia (lack of blood flow)
what is cholangitis?
- inflammation of the biliary ducts
- secondary to obstruction of the common bile ducts
- can to sepsis
what are the nutrition implications for nutrition therapy for cholelithiasis?
- indigestion
- decreased ability to digest fat
- increased abdominal gas
- diarrhea post surgery
what are the nutrition assessments for cholelithiasis?
- weight and weight history
- diet
- laboratory values
- medications
what are the nutrition diagnosis for cholelithiasis?
- inadequate oral food/beverage intake
- excessive oral intake
- altered GI function
- food-medicine interaction
what are the nutrition intervention for cholelithiasis?
- low fat (<30%), modest protein
- small frequent meals
- NPO during acute attacks
- post surgery - moderate fat, plus soluble fiber if diarrhea
what do you monitor and evaluate for cholelithiasis?
- adherence and tolerance
- based on signs and symptoms
what two major functions does the pancreas have?
- both endocrine and exocrine functions
what endocrine function does the pancreas do?
- regulation of glucose homeostasis
What exocrine function does the pancreas do?
- secretion of enzymes and other substances directly into the intestinal lumen, for aid in digestion of protein, fats, CHO
- accessory to GI tract
what are some of the digestive enzymes the pancreas secrete?
- trypsin, lipase, amylase
what are the pertinent, relevant laboratory values for the pancreas?
- lipase (normal levels: 10 - 140 units/L)
- amylase (normal levels: 23 - 85 units/L)
How does lipase, a digestive enzyme, help the pancreas?
- produced and secreted from the pancreas
- hydrolysis to for simple monoglycerides, fatty acids, and glycerol
how does amylase, a digestive enzyme, help the pancreas?
- produced and secreted from the pancreas
- hydrolysis to form dextrine and maltose
what is a pathophysiology of the exocrine pancreas?
- Pancreatitis (common, high priority)
what is pancreatitis?
- inflammation of the pancreas
what is the pancreatitis characterized by?
- edema
- cellular exudate (fluid that is released through the blood vessels)
- fat necrosis
- autodigestion
- hemorrhage of pancreatic tissue
what some of the symptoms of acute pancreatitis?
- asymptomatic or
- upper abdominal pain radiating to the back worsening with ingestion of food
auto digestion of pancreatic cells in acute pancreatitis are d/t what?
- premature activation of trypsin (enzyme to breakdown protein)
what clinical symptom is a definite sign of acute pancreatitis?
- elevated lipase and/or serum amylase
medical treatment and outcomes of acute pancreatitis depend on what?
- severity
what is chronic pancreatitis?
- chronic, irreversible inflammation
- chronic abdominal pain
- diabetes (common)
- steatorrhea (fat in stool)
what does chronic pancreatitis lead to?
- fibrosis with tissue calcification (blocks blood flow)
what are the nutrition implications for pancreatitis?
- digestive
- steatorrhea (malabsorption of fat)
- decreased vit. B12, D, and E
what are the nutrition assessment for pancreatitis?
- height
- weight and weight history
- diet
- anthropometric measures
- laboratory values
what are the nutrition diagnosis for pancreatitis?
- altered GI function
- increased energy expenditure
- inadequate oral intake
- inadequate vit. intake
- impaired nutrient utilization
- altered nutrition-related laboratory values
- increased nutrient (protein/energy) needs
- excessive fat intake
- excessive alcohol intake
- malnutrition
what are the nutrition intervention for acute pancreatitis?
- immediate re-feeding oral intake as tolerated (w/in 48hrs.)
- severe case, early aggressive nutrition support
- enteral route preferred (formula vs. TPN)
- may need jejunal feeds
- semi-elemental diet (partially broken down; less diarrhea)
what are the nutrition interventions for chronic pancreatitis?
- frequent 6 small meals; low to moderate fat
- pancreatic enzymes
- medication to reduce gastric acid secretions
- promote weight gain
- high fiber diet might be bad d/t absorbing enzymes
- neutralize; bicarbonate
what would you monitor and evaluate for acute pancreatitis?
- weight
- improvement in symptoms (nausea, diarrhea)
- progression to oral feedings
- lab values (ex. electrolytes)
what would you monitor and evaluate for chronic pancreatitis?
- tolerance to diet
- weight
- degree of pain
- fecal consistency
