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Medical Nutrition Therapy II > Chapter 16 (Diseases of the liver, gallbladder, and exocrine pancreas) > Flashcards

Chapter 16 (Diseases of the liver, gallbladder, and exocrine pancreas) Flashcards

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USMLE® Step 1 flashcards
1
Q

Which organ is the first stop for all nutrients?

A
  • the liver
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2
Q

what is the largest gland in the body?

A
  • the liver
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3
Q

How many lobes does the liver have and what are each lobe made up of?

A
  • four lobes; two functional (right and left)

- each lobe is made up of thousands of lobules around a central vein

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4
Q

True or false: Cells of the liver are resilient and regenerate?

A
  • True
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5
Q

What organ is the primary blood reservoir and central to metabolism?

A
  • the liver
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6
Q

How much blood does the liver store at any given time?

A
  • 200 - 400 mL
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7
Q

The liver receives nutrients from the digestive tract and processes them for distribution throughout the body through what?

A
  • the hepatic portal vein

- which the hepatic vein returns blood to the heart from the liver

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8
Q

what supplies oxygen rich blood from the heart to the liver?

A
  • hepatic artery
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9
Q

What does the liver regulate?

A
  • glucose and cholesterol
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10
Q

what does the liver store?

A
  • vitamins
  • glycogen
  • copper
  • iron
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11
Q

The liver metabolites and is the detoxifier/clearance of what?

A
  • drugs
  • hormones
  • toxins
  • ammonia
  • bilirubin
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12
Q

the liver synthesize and secretes what?

A
  • albumin
  • other transport proteins
  • lipoproteins
  • clotting factors
  • cholesterol
  • bile
  • glucose
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13
Q

what is the two major functions of the liver?

A
  • bile secretion

- enterohepatic circulation of bile (recirculation of bile salts)

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14
Q

what are the two functions of bile?

A
  • emulsify

- absorption - formation of micelles

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15
Q

What does the liver reuse 95% and 5% newly synthesized in the enterohepatic circulation?

A
  • bile salt
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16
Q

How much bile salt does the liver make a day in the enterohepatic circulation?

A
  • 600 - 1000 mL
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17
Q

How much bile salt do we lose in our feces through the enterohepatic circulation?

A
  • 5%
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18
Q

What are some of the pertinent laboratory values for the liver?

A
  • liver function tests (LFTs)
  • non-invasive screening for liver function
  • allow recognition of type of liver disease
  • assessment of severity and predict outcomes
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19
Q

What is looked at when doing a liver function test?

A
  • 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)
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20
Q

What is Jaundice?

A
  • yellowish tint to body tissues; skin, eyes
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21
Q

what is the yellowish tint to body tissues caused by?

A
  • large quantities of bilirubin in extracellular fluid
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22
Q

what is the normal plasma concentration of bilirubin and at what level does the skin start to appear yellowish?

A
  • < 1.1 mg/dL
  • can rise to >5 mg/dL
  • skin appears yellowish at 2.4 - 3 mg/dL
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23
Q

what are the 3 main causes of jaundice?

A
  • Hemolytic (increased destruction of RBCs
  • Hepatic (decreased uptake of bilirubin, decreased liver function)
  • Obstructive (obstruction of bile ducts or liver cells)
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24
Q

What are the pathophysiology of the liver?

A
  • metabolic alterations
  • decreased intake
  • altered absorption
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25
Q

what pathophysiology is common to the hepatobiliary tract?

A
  • Jaundice
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26
Q

What causes metabolic alterations in the liver?

A
  • decreased glycogen stores
  • insulin resistance common in end stage (cirrhosis)
  • altered vitamin and mineral metabolism and storage
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27
Q

what decreases nutrient intake in the liver?

A
  • anorexia (no appetite)
  • early satiety (fullness quickly; fluid full)
  • ascites
  • restrictive diets
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28
Q

what would cause altered absorption in the liver?

A
  • reduced bile synthesis or release
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29
Q

What is hepatitis?

A
  • inflammation of the liver

- can be acute or chronic

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30
Q

What causes hepatitis?

A
  • virus
  • bacteria
  • toxins
  • obstruction
  • parasites
  • drugs
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31
Q

What can develop from hepatitis?

A
  • cirrhosis (end stage)

- liver cancer

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32
Q

How is hepatitis A (HAV) contracted?

A
  • transmitted almost exclusively by fecal-oral route
  • contaminated drinking water, food, sewage
  • treatable, short term
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33
Q

How is hepatitis B (HBV) or serum hepatitis contracted?

A
  • transmitted via blood, blood products, semen, and saliva

- short term illness

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34
Q

How is hepatitis C (HCV) contracted?

A
  • exposure to blood/body fluids from an infected person

- more serious

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35
Q

Hepatitis C is associated with the development of what?

A
  • chronic liver disease
  • cirrhosis
  • need for liver transplant
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36
Q

What are the clinical manifestations of hepatitis?

A
  • jaundice, dark urine, anorexia, fatigue, headache, nausea, vomiting, fever
  • hepatomegaly (lg. liver), and splenomegaly (lg. spleen)
  • bilirubin, alkaline phosphatase, serum AST elevated
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37
Q

what are the nutritional implications of hepatitis?

A
  • weight loss

- nutritional deficiency

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38
Q

What are the nutrition assessment for hepatitis?

A
  • weight and weight history
  • food intake
  • lifestyle factors
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39
Q

what would be the nutrition diagnosis for hepatitis?

A
  • inadequate oral food and beverage intake
  • inadequate protein and calorie intake
  • food-medication interaction
  • impaired nutrient utilization
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40
Q

what are the nutrition interventions for hepatitis?

A
  • 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
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41
Q

what define alcoholism?

A
  • chronic consumption of >80g of ethanol/day (40g for men; 20g for women per day)
  • dependency may be evident as tolerance or withdraw symptoms
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42
Q

Ethanol rapidly and completely absorbed even with what?

A
  • malabsorption
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43
Q

Can ethanol be stored?

A
  • no d/t oxidation
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44
Q

what is an alcoholic liver disease referred to?

A
  • fatty liver (steatosis)
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45
Q

What is present in 90% of chronic alcohol abusers?

A
  • steatosis (fatty liver)
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46
Q

What causes steatosis (fatty liver)?

A
  • excess acetyl CoA converted to fatty acids
  • hypertriglyceridemia
  • fat deposition in hepatocytes
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47
Q

Fatty liver (steatosis) can also develop in absence of alcohol, including in persons who have had what?

A
  • bariatric surgery
  • those with cystic fibrosis
  • associated with obesity and metabolic symptoms (NASH)
  • increased visceral fat are more susceptible
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48
Q

what is malnutrition in alcoholics is caused by what?

A
  • displacement of nutrients from not eating
  • maldigestion or malabsorption of nutrients d/t GI complications
  • weight gain and obesity
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49
Q

What is the formula to calculate kcal derived from ethanol?

A
  • (0.8 x proof x ounces = kcal)
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50
Q

Which organs are contributing to the GI complications for the malnutrition in the alcoholic?

A
  • esophagus
  • stomach
  • intestine
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51
Q

what causes malnutrition in the alcoholic d/t the esophagus, GI complications?

A
  • heartburn
  • reduced LES pressure
  • esophagitis
  • stricture
  • tears from vomiting
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52
Q

What cause malnutrition in the alcoholic d/t the stomach, GI complications?

A
  • gastritis
  • duodenitis
  • atrophy of mucosal barrier
  • hemorrhage
  • PUD
  • pernicious
  • anemia
  • stomach cancer
53
Q

What causes malnutrition in the alcoholic d/t the intestine, GI complications?

A
  • damage to villi and increased motility leads to malabsorption
  • diarrhea
54
Q

What is PEM (protein energy malabsorption) d/t in an alcoholic liver disease malnutrition?

A
  • poor dietary intake
  • malabsorption
  • hyper catabolic state (using all of body’s reserves for reg. function)
  • altered energy storage
  • biochemical changes (seen by labs)
55
Q

Which vitamin and mineral deficiencies contribute to an alcoholic liver disease?

A
  • folate
  • thiamin (berry berry; common)
  • B6
  • vitamin C and D (common in smokers)
  • vitamin K
  • vitamin A
  • iron
  • calcium
  • potassium
  • recommend multivitamin 2x RDA
56
Q

Alcoholism malnutrition is a major cause of ?

A
  • liver damage and resulting dysfunction
57
Q

What is cirrhosis?

A
  • chronic liver disease in which healthy tissue is replace by scar tissue, blocking the low of blood, resulting in loss of liver function
58
Q

what are the most common causes of cirrhosis?

A
  • chronic alcoholism and HCV
59
Q

what is the first stage of cirrhosis?

A
  • steatosis (fatty liver)
60
Q

What are the general symptoms in cirrhosis clinical manifestations ?

A
  • fatigue
  • weakness
  • nausea
  • poor appetite
  • malaise (general feel of discomfort)
  • vit. and mineral deficiencies
61
Q

What are the liver specific symptoms in cirrhosis clinical manifestations?

A
  • jaundice
  • dark urine
  • light stools
  • steatorrhea
  • itching
  • abdominal pain
  • bloating
  • vit. and mineral deficiencies
62
Q

What are the major clinical complications of cirrhosis?

A
  • portal hypertension
  • hepatic encephalopathy
  • ascites (swelling of belly)
  • hepatorenal syndrome
  • esophageal varices (swollen/large veins)
63
Q

What is portal hypertension/ascites?

A
  • elevated blood pressure in the portal vein
64
Q

What are the symptoms of portal hypertension?

A
  • ascites (swelling of belly d/t fluid)
  • GI bleeding from varies
  • encephalopathy
65
Q

what is ascites?

A
  • accumulation of fluid in peritoneal cavity
  • hepatic fibrosis
  • reduced osmotic pressure
  • increased attention of sodium
66
Q

What are the medical treatments for portal hypertension/ascites/

A
  • sodium restriction and/or diuretics (to get of excess fluid)
  • paracentesis (w/draw fluid w/catheter) results in protein loss)
67
Q

what are the surgical procedures for ascites?

A
  • TIPS (transjugular intrahepatic portosystemic shunt)

- DSRS (distal spleno-renal shunt)

68
Q

what does TIPS, transjugular intrahepatic portosystemic shunt do for ascites?

A
  • reroutes blood flow to the liver and reduces pressure in all auxiliary veins
69
Q

what does DSRS, distal splenorenal shunt, do for ascites?

A
  • the distal splenic vein is attached to the left renal vein reducing portal hypertension
70
Q

What are the nutrition therapy for ascites?

A
  • 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)
71
Q

What is encephalopathy?

A
  • syndrome of impaired mental status and abnormal neuromuscular function
72
Q

what are the staging scales for encephalopathy?

A
  • west Haven (awake and alert people)

- Glasgow (for people in commas)

73
Q

what is the pathogenesis of encephalopathy?

A
  • unknown

- inability to eliminate products toxic to brain

74
Q

what are the three hypotheses of encephalopathy?

A
  • ammonia (high levels)
  • synergistic neurotoxin
  • false neurotransmitter (high AAA, low BCAA in brain)
75
Q

what are false neurotransmitters?

A
  • altered amino acid metabolism
76
Q

what causes altered amino acid metabolism?

A
  • increases muscle uptake of BCAA’s (valine, leucine, isoleucine)
  • increased aromatic amino acids in plasma and brain (phenylalanine, tyrosine, tryptophan)
  • altered neurotransmitter synthesis
77
Q

what is the treatment for encephalopathy?

A
  • 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
78
Q

what are the nutritional implications for nutrition therapy for cirrhosis?

A
  • early satiety from ascites (small frequent meals)
  • impaired nutrient digestion and absorption
  • increased energy expenditure
  • hypoglycemia d/t hyperinsulinemia
  • hyperglycemia
79
Q

what are the nutrition assessment for cirrhosis?

A
  • 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
80
Q

what is the nutrition diagnosis for cirrhosis?

A
  • may relate to complications of cirrhosis
81
Q

what are the nutrition interventions for cirrhosis?

A
  • 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
82
Q

how would you monitor and evaluate nutrition therapy for cirrhosis?

A
  • tolerance to feedings
  • amount nutrients consumed
  • weight changes (dry)
  • laboratory values
  • cognitive status (depends on mental status)
83
Q

when is liver transplant considered?

A
  • as a last resort

- in cases where effects of disease have higher potential mortality than transplant

84
Q

what is used to determine eligibility for liver transplants?

A
  • MELD (model for end stage liver disease scoring system
85
Q

what MELD scoring system show for eligibility for liver transplant?

A
  • 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
86
Q

what are the nutritional implications for nutrition therapy for liver transplant?

A
  • malnutrition and ascites
  • need for early nutritional support post surgery
  • food borne infections (after transplant poor immune system)
87
Q

what are the nutrition assessment for liver transplant?

A
  • SGA (subjective global assessment)
  • anthropometrics
  • dietary intake
  • GI symptoms
  • biochemical labs
  • side effects of post transplant meds. (high blood sugar, hyperlipidemia, sodium retention)
88
Q

what are the nutrition diagnosis for liver transplant?

A
  • related to energy and nutrient intake, utilization, and expenditure
  • altered lab values
  • food-medication interactions
  • weight loss
  • knowledge deficits
89
Q

what are the pre-transplant nutrition intervention for liver transplant?

A
  • 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
90
Q

what are the post-transplant nutrition intervention for liver transplant?

A
  • regular diet
  • 30-35 kcal/kg
  • 1.0-1.5 g/kg of protein
  • other nutrients individualized used on immunosuppressant drug regimen
91
Q

how would you monitor and evaluate liver transplant patients?

A
  • recovery and healing
  • dietary intake
  • tolerance to the diet
  • weight changes
  • incidence of food-borne illness
  • nutrient related complications
92
Q

After the liver makes bile and transfers it to the gallbladder, what does the gallbladder do?

A
  • stores, concentrates, and secretes the bile
93
Q

How does the gallbladder concentrate bile?

A
  • removal of water and electrolytes
94
Q

How does the gallbladder secrete bile?

A
  • control of delivery of bile slats to duodenum, sodium and potassium salts
95
Q

what is a common problem of the gallbladder?

A
  • cholelithiasis (gallstones)
96
Q

what is cholelithiasis?

A
  • 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
97
Q

How types of gallbladder stones are there?

A
  • three
  • cholesterol (most common, 50-80%, major component of bile)
  • pigment (10% of cases, too much bilirubin)
  • mixed
98
Q

what are the causes of gallstones?

A
  • too much absorption of water from bile
  • too much absorption of bile acids from bile
  • too much cholesterol in bile
  • inflammation of epithelium
99
Q

what is choledcholithiasis?

A
  • 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
100
Q

what is cholecystitis?

A
  • inflammation of the gallbladder
  • develops secondary to obstruction
  • can lead to infection and ischemia (lack of blood flow)
101
Q

what is cholangitis?

A
  • inflammation of the biliary ducts
  • secondary to obstruction of the common bile ducts
  • can to sepsis
102
Q

what are the nutrition implications for nutrition therapy for cholelithiasis?

A
  • indigestion
  • decreased ability to digest fat
  • increased abdominal gas
  • diarrhea post surgery
103
Q

what are the nutrition assessments for cholelithiasis?

A
  • weight and weight history
  • diet
  • laboratory values
  • medications
104
Q

what are the nutrition diagnosis for cholelithiasis?

A
  • inadequate oral food/beverage intake
  • excessive oral intake
  • altered GI function
  • food-medicine interaction
105
Q

what are the nutrition intervention for cholelithiasis?

A
  • low fat (<30%), modest protein
  • small frequent meals
  • NPO during acute attacks
  • post surgery - moderate fat, plus soluble fiber if diarrhea
106
Q

what do you monitor and evaluate for cholelithiasis?

A
  • adherence and tolerance

- based on signs and symptoms

107
Q

what two major functions does the pancreas have?

A
  • both endocrine and exocrine functions
108
Q

what endocrine function does the pancreas do?

A
  • regulation of glucose homeostasis
109
Q

What exocrine function does the pancreas do?

A
  • secretion of enzymes and other substances directly into the intestinal lumen, for aid in digestion of protein, fats, CHO
  • accessory to GI tract
110
Q

what are some of the digestive enzymes the pancreas secrete?

A
  • trypsin, lipase, amylase
111
Q

what are the pertinent, relevant laboratory values for the pancreas?

A
  • lipase (normal levels: 10 - 140 units/L)

- amylase (normal levels: 23 - 85 units/L)

112
Q

How does lipase, a digestive enzyme, help the pancreas?

A
  • produced and secreted from the pancreas

- hydrolysis to for simple monoglycerides, fatty acids, and glycerol

113
Q

how does amylase, a digestive enzyme, help the pancreas?

A
  • produced and secreted from the pancreas

- hydrolysis to form dextrine and maltose

114
Q

what is a pathophysiology of the exocrine pancreas?

A
  • Pancreatitis (common, high priority)
115
Q

what is pancreatitis?

A
  • inflammation of the pancreas
116
Q

what is the pancreatitis characterized by?

A
  • edema
  • cellular exudate (fluid that is released through the blood vessels)
  • fat necrosis
  • autodigestion
  • hemorrhage of pancreatic tissue
117
Q

what some of the symptoms of acute pancreatitis?

A
  • asymptomatic or

- upper abdominal pain radiating to the back worsening with ingestion of food

118
Q

auto digestion of pancreatic cells in acute pancreatitis are d/t what?

A
  • premature activation of trypsin (enzyme to breakdown protein)
119
Q

what clinical symptom is a definite sign of acute pancreatitis?

A
  • elevated lipase and/or serum amylase
120
Q

medical treatment and outcomes of acute pancreatitis depend on what?

A
  • severity
121
Q

what is chronic pancreatitis?

A
  • chronic, irreversible inflammation
  • chronic abdominal pain
  • diabetes (common)
  • steatorrhea (fat in stool)
122
Q

what does chronic pancreatitis lead to?

A
  • fibrosis with tissue calcification (blocks blood flow)
123
Q

what are the nutrition implications for pancreatitis?

A
  • digestive
  • steatorrhea (malabsorption of fat)
  • decreased vit. B12, D, and E
124
Q

what are the nutrition assessment for pancreatitis?

A
  • height
  • weight and weight history
  • diet
  • anthropometric measures
  • laboratory values
125
Q

what are the nutrition diagnosis for pancreatitis?

A
  • 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
126
Q

what are the nutrition intervention for acute pancreatitis?

A
  • 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)
127
Q

what are the nutrition interventions for chronic pancreatitis?

A
  • 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
128
Q

what would you monitor and evaluate for acute pancreatitis?

A
  • weight
  • improvement in symptoms (nausea, diarrhea)
  • progression to oral feedings
  • lab values (ex. electrolytes)
129
Q

what would you monitor and evaluate for chronic pancreatitis?

A
  • tolerance to diet
  • weight
  • degree of pain
  • fecal consistency

Medical Nutrition Therapy II (2 decks)

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