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NP - Liver Disease Lecture
Terms in this set (46)
General on Liver Disease
One of the largest organs
3 lb in weight
First stop for nutrient rich blood from intestines
Functions of the Liver (12)
1. Synthesizes bile (so influences the nutritional status of ppl)
2. Aids in metabolism of protein, CHO, fat and vitamins
3. Protects body through modification of toxic substances. Liver is the junkyard of the body. (EtOH and drugs)
4. Converts galactose and fructose into glucose for usable energy
5. Helps with blood sugar contol by releasing glycogen when needed. If sugar levels low. "LIVER DUMPING"
6. Transamination, or formation of non-essential AA
7. Deamination: Assembles AA and enables use of AA as energy or stored as fat
8. Storing vitamins and minerals as needed
9. Produces proteins like albumin, prealbumin, transferrin
10. Detoxifies ammonia into urea. (otherwise altered mental status.
11. Synthesizes glycogen, gluconeogenesis
12. Activation of vitamin D
Anatomy of Liver
1. Located in the upper rt quadrant of abdoment.
2. Follows curve of diaphragm
3. Brownish red but can be yellowish brown because of too much fat
Metabolic Functions of the Liver (8)
1. Carbohydrate Metabolism
2. Lipid Metabolism
3. Protein Metabolism
4. Enzyme Metabolism
5. Vitamin Metabolism
6. Bile Acid Metabolism
7. Heme Metabolism
Carbohydrate Metabolism in the Liver
3. Oxidation via TCA cycle
Lipid Metabolism and the Liver
5. Esterification of FA
6. FA oxidation
7. Uptake/formation/breakdown of phoshotides
8. Syntheiss/degradation/esterification/excretion of cholesterol
9. Formation of lipoproteins
Protein Metabolism and the Liver
1. Synthesis of serum proteins
2. Sysnthesis of prothrombin
3. Globin of hemoglobin
5. Nucleoproteins and serum mucoprotein
6. Degradation of some proteins to peptides and AA
7. Synthesis of urea
Enzyme Metabolism and the Liver
1. Synthesis of alkaline phosphatase
2. Mono-amine oxidases (MAOs)
3. Acetylcholine esterase
5. Cholesterol esterases
7. Beta glucoronidase
8. Glutamic oxalacetic transaminase (SGOT-AST)
9. Glutamic pyruvic transaminase (SPGT-ALT)
Vitamin Metabolism and the Liver
1. Formation of acetyl CoA from pantothenic acid
2. Hydroxylation of vitamin D to 25-OH D3
3. Formation of 5-methyl tetrahydrofolic acid (THFA)
4. Methylation of niacinamide
5. Phosphorylation of pyroxine
6. Dephosphorylation of thiamin
7. Formation of coenzyme B12
Bile Metabolism and the Liver
1. Transformation of cholesterol to 7-hydroxycholesterol to cholic acid and chenodeoxycholic acid
Heme Metabolism and the Liver
1. Heme is oxidized to biliverdin, which is then reduced to bilirubin
2. Bilirubin is transported to the liver where it is converted to bilirubin diglucuronide to be excreted with the bile pigments
Other Functions of the Liver
1. Conjugation, detoxification and degradation
2. Reticuloendothelial system (RED) activity
3. Water movement regulation
4. Fetal hematopoiesis
Bile Definition and Functions (2)
1. Complex aqeous soln secreted by the liver
2. Emulsifying agent. Decreases surface area of fat allowing surface tension to break up fat globules
3. Aid in the absorption of FA, monoglycerides, cholesterol and other lipids by forming micelles that are soluble in chyme. Allows lipids to be absorbed.Otherwise couldn't absorbed.
Enterohepatic Circulation and Bile
95% of bile salts are reabsorbed in blood from the small intestine. Happens 2 to 3 times per meal. Will happen 18 times before excreted in feces.
1. In small intestine bile emusifies fats
2. In colon, bile is trapped by fiber and lost in feces or it is reabsorbed into the blood
3. Liver cholesterol used to generate bile
4. Gall bladder stores the bile until needed in the intestine then cycle starts again.
Bile Compostion (4)
1. Water is 97%
2. Bile salts
3. Bile pigments
4. Inorganic Salts
Bile saltes are formed from...
Bile Pigments are made of....
Inorganic salts present in bile (2)
1. Means yellowish tint to the body tissues, including the yellowness of skin and deep tissues. Skin and eyes can become yellow.
2. Caused by large quantitites of bilirubin in extracellular fluid that are caused by liver and gallbladder disorders. Above 2.2 mg/dL. Usual is around 1.1 mg/dL
Inflammation of the liver.
Can be type A, B, C, D, and E and most are viral or caused by toxins, obstruction, parasites or drug use
Type A Hepatitis
2. Contracted through contaminated water (mostly 3rd world), food and sewage
3. "Food service hepatitis"
4. Oral/fecal routes and then cooking with unclean hands
Proper Meds and rest will clear up
Type B and C Hepatitis
2. Contaminated needles, blood transfusion, open wounds or cuts, sexual contact
Tougher to handle.... interferon is helping Hepatitis C.
Hepatitis B can clear up with proper meds and rest
Clinical symptoms of Hepatitis (9)
6. Wt loss
7. Jaundice (more common in A) with dark urine. (Visible yellowing of skin and eyes.
8. Pain in right upper quadrent
9. Hepatomegaly/Splenomegaly (elargement of liver or spleen)
Background on ALcoholism and Alcoholic Liver Dz (ALD)
12th leading cause of death in US
Hispanics 7th leading cause of death
Indian/Alaskan Native males 5th leading cause of death
Etiology of Alcoholic Liver Dz (ALD) (3)
1. Gender... Women more suceptable more than men because metabolize EtOH differently and develop hepatitis or cirrhosis in shorter amt of time. Have greater risk of dying. Increased susceptibility to ethanol activity due to increased concentration of ethanol in blood due to lower BW and lower water concentration. Keep well hydrated
2. Age.. Between 25 to 60, proportion of Body Fat in men doubles and increases 50% in women while the water decreases. EtOH is water soluble and will create a higher blood concentration compared to younger.
3. Race... Toxic effects is poorly understood but increased rate of ALD in minority groups overall
General on ethanol in the body
1. Ethanol is rapidly and completely absorbed in GI tract even malabsorptive states.
2. Ethanol cannot by stored in body
3. Metabolized by oxidative and non-oxidative mechanisms
Ethanol is poison to body. Wants to get rid of it quick
Metabolism of EtOH
Oxidative is primary means of metabolism
1. Absorption starts in the stomach (drugs do too). If drinking on empty stomach will feel effects more.
2. Only 2 to 10 % is eliminated through kidneys and lungs the rest is oxidized through the liver.
3. Alcohol breaks down by alcohol dehydrogenase to actaldehyde and then again with alcohol dehydrogenase to acetate.... CO2 and water and Acetyl CoA... enters TCA cycle
4. Fatty liver can develop after ONE night of heavy drinking
Alcoholics and EtOH Metabolism
Do it differently and use alternative pathways because liver is hurt so much. Scar tissue develops and then body has to find out alternative means to metabolism.
Caused by build up of formaldehyde from ethanol. Enzymes are not enough. If you drink too much, your body cannot keep up and will metabolize alcohol first. Time is best cure
Three stages of ALD (Alcoholic Liver Disease)
1. Hepatic Steatosis (steatohepatitis)
2. Alcoholic Hepatitis
3. Alcoholic Cirrhosis
Stage 1 can sometimes happen AFTER stage 2.
When lipid accumulation in the liver exceeds 5% of liver wt.
Non-alcoholic steatohepatitis is the rest of the people.
Fatty livers in alcoholics
90% of alcoholics have.
1. increased mobilization of FA from adipose tissues
2. incr'ds sythesis of FA
3. decreased FA oxidation
4. increased triglyceride production.
During chronic EtOH consumption there is an increased synthesis and decreased degradation of FA in liver, thus incr ability and availability of FA to cause increased fat deposit in the liver. Fat gets stored there and blocked from leaving. Yellow mustardish liver
Symptoms of Hepatic Statosis
4. Tenderness of liver
6. Decreased albumin and increased LFTs (liver function tests)
Alcoholic Hepatitis Stage
A form of toxic liver injury associated with chronic ethanol consumption. Increased susceptibility to infections, pneumonia, spontaneous bacterial peritonitis, septicemia, sepsis.
Symptoms of Alcoholic Hepatitis
Alcoholic Cirrhosis Stage
Liver damage due to excessive scar tissue that inhibits liver blood flow. Last stage
Liver tries to regenerate but chronic consumption stops and scar tissue forms
Liver failure (25% fxn) is consequence.
Scar Tissue in Liver
Blocks normal perfusion through the liver and decreaseds blood flow leading to decreased delivery of oxygen and nutrients to hepatocytes. Leads to improper regeneration of any new liver cells. Liver failure can be consequence if <25% fxn
Complications of Alcholic Cirrhosis
1. Portal Hypertension
3. Alteration in protein and nitrogen metabolism resulting from hepatic encephalopathy
Complication of alcoholic cirrhosis.
Occurs to roadblocks established by scar tissue
Increased pressure in the liver and in portal vein.
Collateral circulation happens and is diverted to smaller veins and can get overlooks.
VARICES... extremely dilated veins (near stomach, esophagus or around neck)
Complication of alcoholic cirrhosis
Usually late in cirrhosis and not reversible... it will continue to happen.
Accumlation of fluids, proteins and electrolytes within the peritoneal cavity.
This fluid builds up and causes weight gain in peritoneal cavity.
Only way to remove is use of diuretics or pericentesis (shunts in the peritoneal cavity to remove fluid but can remove protein as well)
Can cause development of secondary or portal hypertension or decreased albumin when this happens. End up on fluid restriction and can be difficult to follow
Alteration in protein and nitrogen metabolism resulting from hepatic encephalopathy
Complication of alcoholic cirrhosis
Syndrome of impaired mental status and neuromuscular funciton
Alteration in protein and N metabolism results from
1. Major failure to liver fxn
2. Ammonia build up
3. Inability of liver to eliminate toxins to the brain
4. Decr synthesis of: urea, albumin,
Clinical Manifestions of alteration in protein and N metabolism
1. Changes in mental status and personality
2. May be neuromuscular changes
Nutrition in Hepatitis
Frequent small meals. Alcohol restriciton
Nutrition in Alcoholic Hepatitis
Because of decreased pancreatic enzyme secretion, intestinal transporters, and micelle formation (due to inadequate bile salts), altered absortion of fat soluble vitmains, thiamin and folic acid. B-vitamins and magnesium may be excreted more.
Nutrition and Cirrhosis
35 to 40 kcal/kg per day with protein intake 1.6 kg/day. If encephalopathy, protein restriction. Higher vegetable and dairy recommended. Fat restriction to <30% calories. Sodium restiction to 2 g/day. Use multivitamin and mineral supplement.
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