Exam # 2 Review Questions Liver Flashcards
- How much liver function is required to sustain life?
10-20% of liver function is required to sustain life
- How does the role of the liver in carbohydrate metabolism challenge nutritional care in the MNT of liver disease?
The liver is involved in gluconeogenesis, glyconeogenesis, and glycogenolysis
- How does the role of the liver detoxifying drugs and alcohol challenge medical care of the patient with liver disease?
As the liver detoxifies drugs and alcohol, it can’t metabolize fat causing fatty liver.
- Which type of viral hepatitis rarely develops into chronic hepatitis?
Hepatitis A; cause feces, contaminated drinking water, food
- Which type of viral hepatitis is currently receiving attention as the most important cause of chronic liver disease?
Hepatitis C (Hepatitis Chronic…); often transmitted through blood; most common and serious
- Define Fulminant hepatitis
D: no - preexisting liver disease; develop hepatic encephalopathy (8 wks onset); etiology - virus, chemical toxicity, medications, reye syndrome S: alt. consciousness, neuromuscular disturbance
- Identify the most common cause of hepatic steatosis and other common causes
lipid accumulation of x > 5% of the liver mobilization of fatty acids from adipose tissue, uncontrolled diabetes, obese, increased synthesis of FA and TAG, decreased FA oxidation (trapping of triglycerides in the liver)
- How can hepatic steatosis be corrected
1) Eliminate alcohol 2) Lose weight 3) Control diabetes
- Differentiate between steatosis, steatohepatitis, NASH, and NAFLD
1) Steatosis - Fatty liver 2) Steatohepatitis - fatty and inflammed; harder to cure 3) Non-alcoholic steatohepatitis (T2D, Drugs, and Obesity)
- Why is the onset of cirrhosis silent?
You only need 10-20% of liver function; most common cause is alcohol (acetaldehyde)
- What is often the first sign of cirrhosis?
1) Jaundice (over production of bilirubin, impaired uptake/excretion) 2) Bruising 3) increased sensitivity to meds, 4) increased ascites, fluid retention
- What lab value would you expect with to be elevated in a patient exhibiting jaundice?
Elevated bilirubin
- Why is jaundice in newborns a common finding? How is it treated? What are the potential complications if not treated?
1) Baby breaks down extra RBCs; liver can’t handle it 2) Light therapy 3) can cause deafness, brain damage, and behavioral problems 4) Potential complications: deafness, brain damage, and behavioral problems
- Describe the relationship between portal hypertension, ascites, and esophageal varices.
1) Portal hypertension - scarred liver tissue restricts the flow of blood (backs up into the portal vein) (leads to ascites and esophageal varices) 2) Ascites - fluid retention in the abdominal cavity, aldosterone implicated, spirolactone and diuretics treat ascites 3) Esophageal Varices - norm deaal blood flow through the liver blocked develop collaterals to divert blood flow to esophageal ( common cause of death in cirrhosis) S: vomit red blood, or produce melena.
- ID other contributing factors to the development of ascites
Portal HTN and decreased albumin production
- What are the major causes of hepatic encephalopathy?
D: impaired mental ability; neuromuscular disturbances, alt consciousness; occurs in 50-80% of patients w/ chronic hepatic failure. Protein intake factor in only 7-9% of cases. Causes: ammonia, increased AA and decreased BCAAs
- What lab value would you expect to be elevated in a patient who exhibited hepatic encephalopathy?
Increased ammonia, decreased BCAAs, and increased AAs ; (Increased A’s, decreased B’s)
- What are the symptoms of hepatic encephalopathy?
Changes in consciousness, fluctuating neurologic signs, asterixes (flapping tremor); Fector hepaticus (breath smells sweet or musty), alterations in judgement, personality or mood
- Identify the mode of action for two medications use in the medical treatment of hepatic encephalopathy?
1) Lactulose” laxative” - acidifies colonic contents retaining ammonia as an ion and acts as a laxative to remove ammonia 2) Rifaximin “ref. bacteria to a minimum…” - antibiotic, decreased bacteria that produces ammonia
- Define wilson’s disease and primary biliary cirrhosis
1) Wilson’s - inherited , too much copper deposited in the brain, cornea ( Kayser - Fleischer ring), and kidneys. leads to cirrhosis and neurological damage treated with low copper diet and copper binding agents 2 - Primary biliary cirrhosis - chronic liver disease with a slow progressive destruction of bile ducts in the liver, 90% women. Leads to cirrhosis, portal hypertension, transplantation, or death.
20 a. What is the standard protocol for alcohol patients?
The usage of a banana bag. (100 mg thiamin, 1 mg folic acid, and a multivitamin)
20 b. ID the four signs of poor hepatic disease prognosis
1) hepatic encephalopathy, esophageal varices, Wernicke - korsakoff syndrome, or hepatorenal syndrome
20 c. Hepatorenal syndrome
poor renal function in liver disease patients; occurs in 1 to 10 patients.
20 d. Liver cancer
most often occurs a secondary cancer (metastasis) ; cancer that does occur in the liver happens as a result of cirrhosis; carriers of hepatitis B/C are at increased risk. certain parasites, toxins, and drugs increase the risk.
20 e. Biliary Atresia
D: congenital condition born w/ absence or inadequate size of bile ducts flow is blocked from the liver to the gallbladder, waste products cannot be removed. T: Kasai procedure (connect liver to small intestine)
20 f. Chronic active hepatitis
normal liver tissue replaced with scar tissue (cirrhosis)
20 g. Wernicke- Korsakoff syndrome
D: CNS damage, thiamin deficiency, common w/ alcohol syndrome (alcohol blocks active transport of thiamin, CNS cells are sensitive to loss s: vision changes, loss of muscle coordination, mem loss, inability to form new memories, confabulation, hallucinations
- define galactosemia and reye’s syndrome what is the current recommendation related to Reye’s syndrome and aspirin?
1) Galactosemia - lack enzyme to convert galactose to glucose; galactose builds up and cirrhoses the liver. 2) Reye’s syndrome - acute disorder in which fat accumulates in the liver and child goes into a deep coma 3) give no aspirin to children under the age of 19
- Identify general MNT goals/treatment for ESLD
D: End stage liver disease liver function less than 20% S: alt. motor functions, confusion C: ammonia accumulation altered neurotransmitters G: 1) prevent/correct weight loss 2) control edema and ascites 3) fluid retention for hyponatremia 4) mineral/vitamin supplementation (b Vitamins and thiamin) 5) monitor CHO intake 6) monitor blood glucose
- Why do we recommend small, frequent feedings and bedtime snacks?
To prevent hypoglycemia. Overnight fasting leads to lipolysis, hepatic ketogenesis, and gluconeogenesis. Avoid fasting!
What is a common concern for malnutrition amongst alcoholics?
Alcohol replaces calories, and frequently leads to B vitamin deficiency and thiamin depletion
- Identify the short and long term nutritional complications of immunosuppressive therapy post liver transplant
Short-term - promote healing and recovery; long term prevent/treat obesity; hyperlipidemia, hypertension, and diabetes mellitus
- Define hemochromatosis. What is the risk to the liver? How is it treated?
D: iron overload, excessive iron absorption 3x the normal amount (genetic or alcoholism) G: hepcidin (regulates iron homeostasis in the liver by facilitating iron transport) S: liver cirrhosis, hepatocellular carcinoma T: phlebotomy (remove blood once a week 500 ml / 250 mg iron until ferritin below 50, then once every 2-3 months to maintain levels MNT: no alcohol, iron supplements, iron fortified cereal products, vitamin c supplements, moderate intake of iron containing foods.
