Nutrition Liver Disease (14)
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- the largest solid organ in the body (1,200-1,500g) with a right lobe that's larger than the left lobe
- it has a dual blood supply (the portal vein carries nutrient rich, O2 poor blood to liver while the hepatic artery carries nutrient poor, O2 rich blood to liver)
- blood flow fluctuates during different times of day & depends on food intake
- liver cells are constantly turning over, with a hepatocyte's lifespan being ~120 days
Normal Functions of the Liver
- 1. clearance, detoxification, & excretion
- 2. synthesis
- 3. storage
- 4. endocrine/exocrine
- *its multiple functions describe why it's so large
- its endocrine functions consist of maintaining blood component concentrations while its exocrine functions consist of transporting secretions through bile duct to the duodenum
What kinds of compounds undergo clearance, detoxification, or excretion by way of the liver?
- a variety of molecules such as drugs, hormones, alcohol, bilirubin, or ammonia
- such substances are often detoxified followed by their derivatives either returning to circulation or excreted into bile
What are some compounds MADE in the liver & where are they exported to?
- a lot of synthesis occurs in the liver
- it makes amino acids, transaminases, & alkaline phosphatase for local use inside the liver
- urea, plasma proteins (albumin*), & lipoproteins are made for release into circulation
- bile acids, cholesterol, & phospholipids are synthesized for release into BILE
What compounds are STORED in the liver?
- Glycogen: provides the body with glucose (except muscle)
- Vitamin B12
- Fat Soluble Vitamins A, D, E, and K
- Ferritin: iron containing protein that releases it when needed (so the liver stores iron)
Glucose Regulation in the Liver
- the production & breakdown of glucose/glycogen all happens within the liver
- glycolysis: metabolized into energy
- glycogenesis: incorporated into glycogen
- glycogenolysis: glycogen breakdown
- gluconeogenesis: synthesis from non-carbohydrate carbon substrates
- *when liver disease occurs oftentimes so does glucose DYSregulation in the form of HYPOglycemia
Fat Metabolism in the Liver
- lipogenesis and lipolysis
- FA esterification & oxidation
- cholesterol & bile acid synthesis / degradation / esterification
- lipoprotein formation
What does having high levels of TAGs often contribute to?
- Nonalcoholic Fatty Liver Disease (NAFLD)
- the #1 cause of liver disease in the US as a result of obesity
What proteins are produced in the liver?
- Glycoproteins (eg. transferrin)
- Acute Phase Proteins (eg. ceruloplasmin)
- Clotting Factors
Where does urea formation originate?
- the liver
- it is excreted via the kidney
- urea is formed because humans cannot easily/quickly remove ammonia (the breakdown product of protein) & must convert it to another less toxic substance
How does liver disease often progress regardless of its cause?
- inflammation → fibrosis → scarring → cirrhosis
- it takes many years for the liver to develop dysfunction because it can regenerate itself up to a certain point
- liver disease has different causes however it always progresses the same way
- chronic scarring & fibrosis of the liver
- blood trying to flow through a cirrhosed liver is met with LOTS of resistance
- it's IRREVERSIBLE & causes many life-threatening sequelae (pathological conditions)
- eg. hypoalbuminemia & longer clotting times (prothrombin, ProTime/INR) as a result of the liver losing its ability to synthesize proteins
How is liver dysfunction measured?
- LFTs: liver function tests
- LFTs measure the level of liver enzymes (AST & ALT, transaminases) in the blood
- normally such enzymes should only be found in liver cells, however with liver dysfunctions & hepatocyte death, liver enzyme levels may be high in the blood
- normally in 20-40 range
How is liver FUNCTION measured?
- by measuring albumin & clotting factors (via ProTime INR), proteins produced BY the liver
- normal levels indicate the liver is still functional
- LFTs measure dysfunction, not function; it's important to see what state the liver is in after measuring serum transaminases
What are some causes of liver disease?
- Infections (hepatitis, cytomegalovirus)
- Toxins (alcohol, acetaminophen OD)
- Metabolic factors
- Immunological factors
- Altered circulation
- Biliary obstruction
- A: causes 20-40% of viral hepatitis in US; spread by fecal-oral route
- B: spread via sexual transmission, perinatal, & blood
- C: blood borne transmission [IV drug] treated with antiretroviral therapy
Which Hepatitis LACKS a preventative vaccine?
- Hepatitis C
- in addition, there's an increased prevalence of Hepatitis C in the baby-boomer population b/c it was inappropriately screened in their lifetime
- both A & B HAVE a preventative vaccine
What are the two major ways that ethanol is oxidized to acetaldehyde (aka broken down)?
- 1) the alcohol dehydrogenase (ADH) pathway in the cytosol of liver cells
- 2) the microsomal ethanol oxidizing system (MEOS)
MEOS (microsomal ethanol oxidizing system)
- when ethanol is digested by the CYP2E1 enzyme, a cytochrome P450 isoform, to acetaldehyde in the smooth endoplasmic reticulum
- its activity increases during chronic alcohol consumption, accounting for increased tolerance in heavy drinkers (2 systems to breakdown alcohol)
- it's less efficient (uses more energy) than the standard ADH pathway
With which ethanol oxidation system will acetaminophen poisoning more readily occur?
- MEOS system
- alcohol can create problems by interfering with the cytochrome P450 system, which is also used to process many drugs such as acetaminophen & barbiturates
Alcoholic Liver Disease
- progression: steatosis → hepatitis (inflammation) → cirrhosis
- 15 – 20% of people who chronically abused alcohol develop advanced liver injury due to overuse & chronic inflammation of hepatocytes
- for men this takes 40 – 80 g/day (~4 drinks) for several years, for women 20 – 40 g/day (~2 drinks) for several years
- often there's a genetic component to who develops and who doesn't develop liver disease due to alcohol intake
How much alcohol is usually in a single drink/serving?
- fatty deposits in the liver
- outwardly people are asymptomatic
- may develop with transient or chronic alcohol use, just depends on if there's a lot consumed
- fat deposits in liver can be reversed if drinking stops
- however if alcohol use continues, 20 – 30% of people develop alcoholic hepatitis or cirrhosis
- inflammation of the liver that develops after years of alcohol abuse
- symptoms include fever and tender hepatomegaly (sensed enlargement of the liver)
Non-alcoholic Fatty Liver Disease (NAFLD)
- accumulation of lipid in hepatocytes; the hepatic manifestation of metabolic syndrome
- is possibly a result of insulin resistance & a failure to suppress the lipolysis (breakdown) of adipose tissue
- therefore there is an increased efflux of free FAs from adipose tissue to the liver
What are the effects of insulin resistance on TAG synthesis & FA oxidation?
- Insulin resistance INCREASES TAG synthesis but INHIBITS FA oxidation → leading to TAG accumulation
- when the body senses insulin the response is anabolic, aka to go into storage mode
- insulin inhibits the liberation of fat from adipose tissue b/c it indicates there is an alternative source of available energy
- insulin resistance fails to repress fat breakdown: there is an efflux of free FAs from adipose to the liver where it is stored instead of oxidized
- metabolism derangement also leads to increased synthesis of TAGs
Non-alcoholic Steatohepatitis (NASH)
- an extreme form of NAFLD consisting of both lipid accumulation AND inflammation of the liver
- it's thought to be caused by a “Second Hit”, an event that induces an inflammatory response (eg. viral infection, or the body's own response to NAFLD)
- 2-3% of NAFLD cases will progress to NASH
How is NASH treated?
the same way metabolic disease is treated: weight loss, lifestyle changes, and decreased intake of carbohydrates & fat are encouraged
What are risk factors for NAFLD/NASH?
- anything that is tied to insulin resistance: obesity, type 2 diabetes, & hyperlipidemia (for example)
- being female, rapid weight loss (esp. due to fasting/bypass surgery - possibly overwhelming liberation of FAs from adipose), parenteral nutrition (a hepatotoxic agent), or certain medications
- most commonly overdosed medication
- adults should have no more than 4g/day; 7.5–10g is toxic in adults
- has a short half life (2–4 hrs)
- disease in which the body absorbs & stores too much iron in the liver; it isn't liberated from the liver well either
- iron in ingestion should be minimized to avoid liver damage
- it can be treated with phlebotomy
- an increase in deposition & inability to liberate copper from the liver
- copper intake should be minimized to avoid liver damage
Causes of Liver Disease
- Metabolic Factors: Hemochromatosis, Wilson’s Disease
- Immunological Factors: Autoimmune Hepatitis, Primary Biliary Cirrhosis, Primary Sclerosing Cholangitis
Primary Biliary Cirrhosis & Primary Sclerosing Cholangitis
- irritation & inflammation of the bile ducts of the liver, which blocks the flow of bile
- this obstruction damages liver cells and can lead to cirrhosis
- underlying cause of the inflammation is believed to be autoimmunity
- Biliary Cirrhosis: seen more in women
- Sclerosing Cholangitis: often accompanies ulcerative colitis
- treatment for both is liver transplant
What are some complications of cirrhosis?
- hepatic encephalopathy
- portal hypertension
- hepatoadrenal syndrome
What are a lot of the side effects of end-stage liver disease related to?
- increased resistance to blood flow through the liver caused by hepatic fibrosis
- the resistance leads to high pressures in the portal vein & portal system
- thin veins that aren't built to hold excess blood will attempt to accommodate the backup of blood → varices form
- large, dilated veins that occur as a result of portal hypertension
- can be found anywhere in the GI tract but is much more common in the esophagus & stomach
- they can burst (stigmata) causing GI bleeding → a life threatening situation
- small, pinpoint areas of bleeding in the stomach due to varices
- more of a chronic situation of GI bleeding
- still a life threatening situation
- accumulation of fluid in the peritoneal space
- due to elevated hydrostatic pressure from portal hypertension & from decreased plasma oncotic pressure from hypoalbuminemia
- without albumin in circulation/blood vessels, fluid will leak out of plasma into the interstitial space → ascites
- treatment: paracentesis (withdraw the fluid), diuretics, & dietary sodium restriction (2 g/day)
- decreased mental status that can accompany advanced liver disease
- possibly caused by elevated levels of aromatic AAs (eg. ammonia) that could act as NTs
- may present as confusion → drowsiness → somnolence → coma
- sometimes liver formulas are filled w/ more nutritious branched chain amino acids to overcome aromatic AA effect
What is a test for hepatic encephalopathy & therefore liver disease?
- Asterixis Test
- hold arms up in a stop sign motion and look to see if arms shake; a tremor of the hand
- a positive sign of asterixis is a positive sign of hepatic encephalopathy
- simple way to determine if decreased mental status is due to liver disease or something else (eg. substance abuse)
How is hepatic encephalopathy treated?
- 1. Eliminate precipitating factors (eg. excess protein intake, GI bleeding, alcohol)
- 2. Supportive (with severe encephalopathy may not be able to eat, etc.)
- 3. lactulose or neomycin as medical treatments (bind ammonia in gut & causes individuals to have bowl movement to eliminate it)
What percentage of individuals with liver disease will also have malnutrition?
- it's more common in people who have alcoholic liver disease (may be getting their calories from alcohol)
- 12–40% of people w/ non-alcoholic cirrhosis are malnourished
- may cause variceal bleeding, refractory ascites, or spontaneous bacterial peritonitis
What are some causes of malnutrition in liver disease?
- diarrhea (lactulose means pooping a lot, not palatable)
- taste changes
- restrictive diets (may be unpalatable, prevent wanting to eat)
- early satiety (especially with ascites)
- alcohol abuse (may displace food, exacerbate malnutrition)
What metabolic abnormalities might patients with liver disease have?
- after an overnight fast, the metabolism of patients with liver disease is comparable to a patient who's sustained a 72 hour fast without compensatory decrease in BMR
- in this situation BMR would normally DECREASE significantly so as not to lose vital energy stores
- this is similar to what's seen in sepsis or trauma
- the result is increased energy expenditure and a loss of muscle & fat to accommodate the "fast" the body thinks it has gone through
Other Metabolic Abnormalities of Liver Disease
- glucose intolerance (high risk of hypOglycemia b/c glycogenolysis is compromised)
- decreased storage capacity
- Fat malabsorption
- Fat soluble vitamins
- Water soluble vitamin malabsorption
How can a person with liver disease's nutrition be assessed?
- usual methods of assessment such as weight or albumin levels are unreliable
- reliable methods include: tricep skin-fold, midarm muscle mass, & subjective global assessment (presence of edema in lower body, wasting in upper body)
Liver Disease Nutrition Therapy w/ Encephalopathy
- Consider protein restriction
- Once encephalopathy resolves gradually increase protein to normal levels
- Small frequent meals & bedtime snack
- Vitamin & mineral supplementation
- Restrict Na+/fluid if ascites or edema are present
If hepatic is not a problem does protein need to be restricted?
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