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MNT II > Liver, Gallbladder, and Pancreas > Flashcards

Liver, Gallbladder, and Pancreas Flashcards

1
Q

Liver

A

Largest gland in the body and is essential for life although survival is possible with 10-20% function. Plays major role in macronutrient and micronutrient digestion, metabolism, and storage. Metabolizes steroids, detoxifies drugs, alcohol, and ammonia.

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2
Q

Alcoholic Liver Disease

A

Damage to the liver and it’s function due to alcohol excess and abuse.

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3
Q

End-Stage Alcoholic Liver Disease Characteristics

A

Malnutrition, portal hypertension with varices, ascites, hyponatremia, hepatic encephalopathy, fat malabsorption, osteopenia, thrombocytopenia with anemia, and glucose alterations.

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4
Q

Non-Alcoholic Fatty Liver Disease (NAFLD)

A

Inflammation of the liver caused an accumulation of fat deposits in the liver tissue. Associated with obesity, diabetes, dyslipidemia, and insulin resistance. Causes may include drugs and inborn errors of metabolism. May progress to NASH.

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5
Q

NAFLD Can Lead To…

A

Fibrosis, cirrhosis, NASH, and hepatocellular carcinoma.

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6
Q

Non-Alcoholic Steatohepatitis (NASH)

A

Accumulation of fibrous tissue in the liver. Chronic liver disease and cirrhosis may develop in these patients.

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7
Q

NASH Medical Treatment

A

Gradual weight loss, insulin sensitizing drugs like metformin, and treatment of dyslipidemia.

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8
Q

Cholestatic Liver Diseases

A

Primary Biliary Cirrhosis (PBC)

Sclerosing Cholangitis

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9
Q

Primary Biliary Cirrhosis (PBC)

A

An immune-mediated chronic cirrhosis of the liver due to obstruction or infection of the small and intermediate-sized intrahepatic bile ducts. 90% of patients are women.

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10
Q

Sclerosing Cholangitis Definition

A

Fibrosing inflammation of segments of extrahepatic bile ducts that may be an immune disorder.

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11
Q

Sclerosing Cholangitis Characteristics

A

50-75% of pts also have inflammatory bowel disease.
60-70% of pts are men.
Increased risk of fat soluble vitamin deficiencies due to steatorrhea.
Hepatic osteodystrophy due to vitamin D and Ca malabsorption resulting in secondary hyperparathyroidism and osteomalacia or rickets.
Treated with immunosuppressants.

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12
Q

Hemochromatosis

A

Inherited disease of iron overload. Stores 20-40 g of iron in the liver compared to 0.3-0.8 g in normal persons. Causes hepatomegaly, esophageal varices, and glucose intolerance. Treated with phlebotomy.

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13
Q

Wilson’s Disease

A

Autosomal recessive disorder associated with impaired biliary copper excretion. Copper accumulates in the liver, brain, cornea, and kidneys. May present with neurological signs like Kayser-Fleischer rings, low serum ceruloplasmin, and psychiatric symptoms. Always presents before age 40. Treated with copper-chelating agents, zinc supplementation, and a low copper diet.

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14
Q

a1-Antitrypsin Deficiency

A

Causes cholestasis or cirrhosis and can cause liver and lung cancer. Liver transplant is the only treatment.

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15
Q

Liver Test Panel

A 
Aspartate Transaminase (AST)
Alanine Aminotransferase (ALT)
Alkaline Phosphatase (ALP)
Total bilirubin
Direct bilirubin
PT/PTT
Ceruloplasmin
Total protein
Albumin
Viral serologies
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16
Q

AST and ALT

A

High AST (200 u/l) and ALT (300 u/l) are indicative of liver disease in presence of jaundice or non-specific symptoms of acute illness.

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17
Q

ALP

A

Usually normal in acute and chronic liver disease. High levels are usually indicative of obstruction of biliary drainage.

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18
Q

Bilirubin

A

Results from the breakdown of hemoglobin in the RBCs and removal from the body by the liver which excretes in the bile.
Rises when the liver is unable to excrete bilirubin or when there is excessive destruction of RBCs.

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19
Q

Ceruloplasmin

A

Normal value is 25-63 mg/dL. Copper bound to ceruloplasmin constitutes the largest amount of ceruloplasmin in circulation. In Wilson’s disease ceruloplasmin mobilization from the liver is drastically reduced because of low production of ceruloplasmin.

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20
Q

Screening for Liver Disease

A

Asymptomatic high risk individuals should be screened for chronic hepatitis. ALT is the most cost-effective screening test for metabolic or drug-induced liver injury. AST should also be measured with hx of alcohol abuse (in alcoholic hepatitis AST is > ALT). Individuals at high risk for viral hepatitis should be screened using specific viral serologies in addition to ALT.

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21
Q

Predictors of Liver Disease Prognosis

A

Prothrombin time: the most important predictor of prognosis; prolonged PTT indicative of poor prognosis.
Albumin: serum albumin <2.5 g/dL indicates high risk of death.

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22
Q

Clinical Manifestations of Cirrhosis

A 
Encephalopathy
Esophageal varices
Portal hypertension
Hepatorenal syndrome
Tea-colored urine
Clay-colored urine
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23
Q

Esophageal Varcies

A

Abnormal, enlarged veins in the lower part of the esophagus. Endoscopic tube used to tamponade bleeding vessels. Repeated therapy may cause esophageal strictures and dysphagia. Cannot feed enterally during acute bleeding episodes. May require PN.

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24
Q

Causes of Malnutrition in Liver Disease

A 
Anorexia
Early satiety or dysgeusia
N&V
Maldigestion or malabsorption
Restricted diets
Altered metabolism
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25
Q

Dysgeusia

A

Altered taste.

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26
Q

End-Stage Liver Disease and Hepatic Encephalopathy

A
  1. Consider major causes of encephalopathy
  2. Treat underlying cause
  3. Treat with medications (lactulose and neomycin)
  4. Ensure adequate diet is consumed
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27
Q

Major Causes of Encephalopathy

A 
GI bleeding
Fluid and electrolyte abnormalities
Uremia
Use of sedatives
Hypo- or hyperglycemia
Alcohol withdrawal
Constipation
Acidosis
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28
Q

Lactulose

A

A nonabsorbable disaccharide used to treat encephalopathy. Acidifies colonic contents and acts as a laxative to excrete ammonia.

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29
Q

Neomycin

A

Nonabsorbable antibiotic used to treat encephalopathy by decreasing colonic ammonia production.

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30
Q

Hepatic Encephalopathy

A

A disorder of mental activity, neuromuscular function and consciousness that occurs as a result of either chronic or acute liver failure. This complex neuropsychiatric syndrome is primarily caused by metabolic abnormalities. The syndrome may occur spontaneously or be induced by some precipitating factor and may be reversible by improvement in liver function, correction of precipitating factors, or the administration of therapy. However, HE can eventually lead to coma, and may be fatal especially in acute liver function.

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31
Q

Prevalence of HE

A

Occurs in 50-70% of pts with chronic hepatic failure.
Caused by protein in only 5%.
95% of persons with cirrhosis tolerate mixed protein diets of up to 1.5 g/kg of protein.

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32
Q

MNT for HE

A

It the pt is protein sensitive, start with 0.5-0.7 g/kg of protein and increase level to tolerance, up to 1.5 g/kg in protein-calorie malnutrition. Provide adequate calories to prevent catabolism of endogenous protein stores.

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33
Q

Stages of HE

A

Stage 1- Milk confusion, agitation and irritability.
Stage 2- Lethargy, disorientation, inappropriate behavior, and drowsiness.
Stage 3- Somnolent but arousable, confused, and aggressive behavior.
Stage 4- Coma.

34
Q

MNT in ESLD

A

Energy needs are highly variable; 30% of pts are hypometabolic and 20% are hypermetabolic. Use indirect calorimetry when available. Vitamin and mineral supplements.

35
Q

ESLD MNT- Energy Needs

A

25-35 kcal/kg dry weight.

Ascites, infection, and malabsorption will increase needs.

36
Q

ESLD MNT- Fat

A

25-40%
May try MCT if steatorrhea is present; with severe cases, try fat restriction and discontinue if diarrhea does not improve.

37
Q

ESLD MNT- Protein Needs

A

1-1.5 g/kg dry weight depending on degree of malnutrition, malabsorption, and metabolic stress. Protein should only be restricted in pts with fulminant hepatic failure. May try BCAA formulas for >grade 2 encephalopathy.

38
Q

ESLD MNT- CHO

A

High intake of both complex and simple carbohydrates.

39
Q

ESLD MNT- Electrolytes

A

Restrict sodium with edema or ascites. 1500-2000 mg/day.

40
Q

ESLD MNT- Fluid

A

Restrict fluid if hyponatremia is present 1000-1500 mL/day.

41
Q

Ascites

A

Accumulation of fluid in the abdominal cavity caused by portal hypertension, hypoalbuminemia, lymphatic obstruction, and renal retention of sodium and fluid. Medical treatment is paracentesis and diuretics.

42
Q

Ascites MNT

A

Restrict sodium to 2g or less. More severe restrictions may be unpalatable. Supplement protein if frequent paracentesis.

43
Q

Hyponatremia

A

Decreased ability to excrete water because of persistent release of antidiuretic hormone, sodium loss via paracentesis, excessive diuretic use, or sodium restriction.

44
Q

MNT for Hyponatremia

A

Fluid intake restricted to 10-1.5 L/day. Moderate sodium intake.

45
Q

Steatorrhea

A

Replace LCT with MCT oils. May trial low fat diet, but do not restrict unnecessarily; if steatorrhea doesn’t improve, discontinue restriction.

46
Q

Liver Transplantation Diet

A

Nutrition support is needed before and after transplant. Long-term preventive nutrition to optimize health and to avoid or minimize: excessive wt gain, hyperlipidemia, hyperglycemia, hypoglycemia, hypertension, and osteopenia.

47
Q

Potentially Hepatotoxic CAM Products in Liver Tx

A

Black cohash
Germander
Ephedra
Kava

48
Q

Functions of the Gallbladder

A

Concentrate, store, and excrete bile that is produced by the liver.

49
Q

Bile

A

Primary constituents are cholesterol, bilirubin (from hemoglobin) and bile salts.

50
Q

Bile Salts

A

Essential for digestion and absorption of fats, fat soluble vitamins, and some minerals.

51
Q

Cholelithiasis

A

Involves the presence of gallstones, which are concentrations that form in the biliary tract, usually in the gallbladder. Calculi form in the gallbladder.

52
Q

Choledocholithiasis

A

The presence of one or more gallstones in the common biliary duct (CBD). Rapid weight loss (gastric bypass, fasting, VLC diets) associated with biliary sludge and gallstones.

53
Q

Implications of Choledocholithiasis

A 
Blockage can cause:
Impaired lipid absorption
Light colored stools
Secondary biliary cirrhosis
Obstruction of the distal CBD can lead to pancreatitis if pancreatic duct is blocked.
54
Q

Choledocholithiasis Risk Factors

A 
Female gender
Pregnancy
Older age
Family hx
Obesity
Truncal body fat distribution
Diabetes
Certain drugs like lipid lowering meds, oral contraceptives, and estrogens.
55
Q

Medical Management of Choledocholithiasis

A

Surgical removal of the gallbladder via open lap or laparoscopic procedure. Chemical dissolution or shock wave lithotripsy may be tried. Stones in the bile ducts may be removed via endoscopic retrograde cholangiopancreatography techniques. (ERCP).

56
Q

Cholelithiasis

A

Correct risk factors like obesity and VLC diets if possible. After cholecystectomy, diet can be advanced to regular diet as tolerated. Liver secretes bile directly into small intestine; the intestine adapts.

57
Q

Cholecystitis MNT

A

Low fat diet to prevent gallbladder contractions.

58
Q

Acute Cholecystitis MNT

A

NPO initially. Use PN if prolonges. Then initiate low fat diet with either hydrolyzed low fat enteral feeding or oral diet with 30-45 g/day of fat. May need water-soluble forms of fat-soluble vitamins if malabsorption is suspected

59
Q

Chronic Cholecystitis MNT

A

Long-term low fat diet with fat being 25-30% of total calories. May need water-soluble forms of fat-soluble vitamins if malabsorption is suspected.

60
Q

Endocrine Functions of the Pancreas

A

Secretes glucagon, insulin, and somatostatin into bloodstream for regulation of glucose.

61
Q

Exocrine Functions of the Pancrea

A

Secretes enzymes directly into GI tract to digest protein, fat, and CHO.

62
Q

Pancreatitis

A

Inflammation of the pancreas that can be mild or severe. Significant morbidity and mortality.

63
Q

Pancreatitis Symptoms

A

Continuous or intermittent pain of varying intensity to severe upper abdominal pain that radiates into the back. Nausea, vomiting, abdominal distention, and steatorrhea. Symptoms may worse with ingestion of food. Elevated serum amylase or lipase (amylase is nonspecific for pancreatitis).

64
Q

Causes of Pancreatitis

A 
Trauma
Certain medications
Hypertriglyceridemia
Hypercalcemia
Some viral infections.
Chronic alcoholism is the most common cause of both acute and chronic pancreatitis. Gallstones is a common cause of acute pancreatitis.
65
Q

Acute Pancreatitis

A

75% alcohol related
15% related to gallstones
10% trauma, hyperlipidemia, hypercalcemia, medications, etc.

66
Q

High Energy Needs for Acute Pancreatitis

A

Metabolic stress state so REE as high as 139% of Harris-Benedict. Sepsis may increase energy needs an additional 15%. Acute pts are more hypermetabolic than chronic pts.

67
Q

Nutritional Alterations in Acute Pancreatitis

A

Glucose intolerance in 40-90% of pts caused by stress response, impaired Beta-cell function, and insulin resistance.

68
Q

Nutritional Alterations in Acute Pancreatitis

A

Changes in fat metabolism in 12-15% of pts, primarily steatorrhea and hypertriglyceridemia.

69
Q

Nutritional Alterations in Acute Pancreatitis

A

Hypocalemia in 25% of pts due to decreased PTH secretion, increased calcitonin, hypomagnesemia, hypoalbuminemia, and saponification of calcium.

70
Q

Nutritional Alterations in Acute Pancreatitis

A

ETOH abuse causes hypomagnesemia, decreased zinc, and thiamine and folate deficiencies.

71
Q

Medical Management of Acute Pancreatitis

A

NPO
Give IV fluids
Administer H2-receptor antagonists and somatostatin

72
Q

Medical Management of Chronic Pancreatitis

A

Manage intestinal pH with antacids, H2 receptor antagonists, and proton pump inhibitors
Administer insulin for glucose intolerance

73
Q

MNT for Acute Pancreatitis

A

NPO
Support with IV fluids
If oral nutrition cannot be initiated in 5-7 days, start nutrition support

74
Q

Enteral Recommendations for Pancreatitis

A

Place nasoenteric tube below the ligament of Treitz. Begin infusion with a standard enteral formula. If there is concern about a particular pt, a low-fat elemental or peptide formula should be used. Monitor pt for intolerance i.e. N&V, abd pain, fever, or increased amylase/lipase.
PN may be initiated if pt does not tolerate EN.

75
Q

Acute Pancreatitis MNT- Energy Needs

A

AP pts are hypermetabolic and catabolic

Harris-Benedict BEE x activity factor x stress factor of 30-50%

76
Q

Acute Pancreatitis MNT: Protein Needs

A

104-2 g/kg body wt

77
Q

Acute Pancreatitis MNT: Fat

A

Up to 2 g/kg body wt per day. Continue to monitor TG

78
Q

Acute Pancreatitis MNT

A 
Once oral diet is started, provide:
Easily digested foods
Low-fat diet
6 small meals
Adequate protein intake
Increased calories
79
Q

Chronic Pancreatitis MNT

A

Provide oral diet as in acute phase. TF can be used when oral is inadequate. Supplement with pancreatic enzymes. Supplement with fat-soluble vitamins and vitamin B12.

80
Q

Pancreatic Enzymes in Chronic Pancreatitis MNT

A

When pancreatic function diminished by about 90%, malabsorption of protein and fat becomes an issue. Avoid alcohol and large meals high in fat. Pancreatic enzyme replacements are given orally with meals at least 30,000 IU lipase at each meal. Level of fat in the diet should be the most pt can tolerate without steatorrhea or pain. May substitute some fat with MCT.

81
Q

Whipple Procedure

A

Pancreaticoduodenectomy is often done for pancreatic carcinoma. Cholecystectomy, vagotomy, or partial gastrectomy may also be done. Pancreatic duct renanastamosed to the jejunum. MNT similar to chronic pancreatitis.

82
Q

MNT in Liver/Biliary Disease

A

Disease of the liver/biliary tract has a profound effect on digestion and absorption. Often leads to malnutrition which exacerbates the disease. Appropriate nutrition care is key in reducing associated morbidity and mortality and improving quality of life.

MNT II (8 decks)

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