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![Liver “The liver ranks first in size, number and complexity](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-1.jpg)
Liver
“The liver ranks first in size, number and complexity
of functions. It is involved in almost every aspect of metabolism.”
Need only 10-20% functioning tissue to sustain life
Hepatocytes: enormous capacity for regeneration
Divide in 24 hours (So regeneration is 1° nutritional priority)
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![](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-2.jpg)
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![Cystic duct Common bile duct](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-3.jpg)
Cystic duct
Common bile duct
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![Functions A. Metabolism of CHO, Prot, Fat, and EtOH 1.](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-4.jpg)
Functions
A. Metabolism of CHO, Prot, Fat, and EtOH
1. CHO: glycogenesis, glycogenolysis,
gluconeogenesis, synthesis of various compounds from CHO intermediates
2. Prot: transamination (to produce NEAAs), deamination of AAs, urea synthesis, synthesis of other N-containing compounds
3. Fat: FA synthesis, formation of TG (lipogenesis), esterification of cholesterol, synthesis of lipoproteins, FA oxidation (beta-oxidation)
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![B. Detoxification of drugs and other toxic substances C. Vitamin](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-5.jpg)
B. Detoxification of drugs and other toxic substances
C. Vitamin and Mineral-related
functions
1. Vitamin A: Storage of vit. A, retinol binding protein; conversion of carotene to retinol/retinyl esters
2. Vitamins D, E & K: storage (K in small amts); involved in one of the activation steps of vit. D (D3 ? 25-OH- D3)
3. Iron and Copper storage
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![D. Blood Reservoir: Acts as a flood chamber between intestinal](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-6.jpg)
D. Blood Reservoir: Acts as a flood chamber between intestinal and
general circulation. Can expand/contract.
1. Normally maintains about 650 ml blood
2. In heart failure, can expand to hold more blood
3. In case of blood loss, can compress and push more blood into circulation
E. Formation of bile (conjugates bilirubin)
F. During stress: synthesizes stress factors (and mobilizes glu from glycogen)
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![“True tests of liver function” Indicators of liver injury Biochemical Markers of Liver Disease](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-7.jpg)
“True tests of liver function”
Indicators of liver injury
Biochemical Markers of Liver
Disease
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![Disorders of the Liver A. Fatty liver– (hepatic steatosis) Accumulation](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-8.jpg)
Disorders of the Liver
A. Fatty liver– (hepatic steatosis)
Accumulation of fat
in hepatocytes
Early stage of liver ds.
Causes: PEM or alcohol abuse
Also: long-term TPN, obesity, small bowel bypass surgery, exposure to toxic substances/drug therapies.
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![1. Alcohol – induced fatty liver: a. Liver cells preferentially](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-9.jpg)
1. Alcohol – induced fatty liver:
a. Liver cells preferentially use FAs
for energy
b. Also package TG ? tissues
c. EtOH present: takes priority (toxin)
d. FAs/ TG accumulate
e. Causes liver to enlarge
f. Biochemical signs:
2. Long-term TPN
a. Constant TPN infusion can cause chronically high insulin levels
b.
c.
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![B. Hepatitis – Inflammation of hepatocytes 2° virus, obstruction, parasite,](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-10.jpg)
B. Hepatitis – Inflammation of hepatocytes 2° virus, obstruction, parasite, drug
or other toxin (including EtOH), causing cell injury
1. Hepatitis A:
a. Symptoms:
b. Often mild, but may have recurrent relapses
2. Hepatitis B,C can ?
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![3. Nutrition Therapy a. Abstinence from alcohol b. Good nutrition](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-11.jpg)
3. Nutrition Therapy
a. Abstinence from alcohol
b. Good nutrition status:
c. Malnourished:
d. Persistent anorexia/nausea:
e. Persistent vomiting:
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![C. Cirrhosis – advanced stage of liver disease scar tissue replaces hepatocytes](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-12.jpg)
C. Cirrhosis – advanced stage of liver disease
scar tissue replaces hepatocytes
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![Consequences of Cirrhosis: 1. Portal Hypertension: elevated BP in the](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-13.jpg)
Consequences of Cirrhosis:
1. Portal Hypertension: elevated BP in the portal
vein 2°obstructed blood flow through the liver.
2. Esophageal Varicies: distended collateral blood vessels that protrude into the esophagus
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![3. Ascites – edema characterized by the accumulation of fluid,](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-14.jpg)
3. Ascites – edema characterized by the accumulation of fluid, electrolytes
and serum proteins in the abdominal cavity
a. Portal HTN forces plasma out of liver’s capillaries into abdominal cavity
b. Kidneys sense decreased blood flow ?
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![4. Hepatic Encephalopathy/Hepatic Coma a. Hyperammonemia – Healthy liver converts](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-15.jpg)
4. Hepatic Encephalopathy/Hepatic Coma
a. Hyperammonemia –
Healthy liver converts
ammonia ? urea
Other nitrogenous compounds may contribute as well
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![b. Psychomotor abnormalities: c. Fetor hepaticus – sign of impending](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-16.jpg)
b. Psychomotor abnormalities:
c. Fetor hepaticus
– sign of impending
coma
d. Chronic disturbance in consciousness can lead to coma
e. Serum AA patterns change:
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![Nutrition Therapy in Liver Disease Energy ESLD without ascites: Ascites, infection, malabsorption or malnutrition: CHO](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-17.jpg)
Nutrition Therapy in Liver Disease
Energy
ESLD without ascites:
Ascites, infection, malabsorption or
malnutrition:
CHO
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![Lipids Protein Hepatitis/cirrhosis: Repletion: Stress/decompensation/sepsis: Encephalopathy: restriction is controversial](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-18.jpg)
Lipids
Protein
Hepatitis/cirrhosis:
Repletion:
Stress/decompensation/sepsis:
Encephalopathy: restriction is controversial
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![Vitamins and Minerals Steatorrhea: fat-sol vitamins (water-miscible form) B vitamins:](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-19.jpg)
Vitamins and Minerals
Steatorrhea: fat-sol vitamins (water-miscible form)
B vitamins: EtOH liver ds.
(Wernicke’s Encephalopathy)
Ca++, Mg++ and Zn++ (2’steatorrhea)
Fluids and Electrolytes
Sodium and fluid restriction in ascites
Diuretics are often used
Careful:
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![Monitor Wt, abdominal girth, BUN/creat, Na+, albumin, and lytes.](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-20.jpg)
Monitor
Wt, abdominal girth, BUN/creat, Na+, albumin, and lytes.
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![](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-21.jpg)
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![Diseases of the Gallbladder Cholelithiasis (gallstones) US: Choledocholithiasis Cholecystitis](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-22.jpg)
Diseases of the Gallbladder
Cholelithiasis (gallstones)
US:
Choledocholithiasis
Cholecystitis
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![Acute cholecystitis: Chronic cholecystitis Cholecystectomy ADAT to regular diet Liver](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-23.jpg)
Acute cholecystitis:
Chronic cholecystitis
Cholecystectomy
ADAT to regular diet
Liver drains directly into duodenum
Over time:
“simulated pouch” forms in biliary tract
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![](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-24.jpg)
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![Ds. of the Exocrine Pancreas Pancreatitis Exocrine pancreatic secretions: digestive](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-25.jpg)
Ds. of the Exocrine Pancreas
Pancreatitis
Exocrine pancreatic secretions:
digestive enzymes
bicarbonate-rich “juices.”
Disorders of the pancreas can impair digestion and ? malabsorption
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![Acute Pancreatitis Causes: Also hypertriglyceridemia, hypercalcemia, infections. Pancreatic digestive enzymes](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-26.jpg)
Acute Pancreatitis
Causes:
Also hypertriglyceridemia, hypercalcemia, infections.
Pancreatic digestive enzymes are activated
within the pancreas ?
Enzymes into blood:
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![Hallmark symptoms: Severe cases: Complications:](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-27.jpg)
Hallmark symptoms:
Severe cases:
Complications:
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![MNT for Acute Pancreatitis NPO w/IV hydration Poss. N/G suction Mild-to-Moderate cases:](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-28.jpg)
MNT for Acute Pancreatitis
NPO w/IV hydration
Poss. N/G suction
Mild-to-Moderate cases:
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![Severe cases: enteral/TPN: __________ TF to ↓ pancreatic stimulation TPN](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-29.jpg)
Severe cases: enteral/TPN:
__________ TF to ↓ pancreatic stimulation
TPN if:
edema
intestinal fistula
Drugs:
somatostatin inhibits pancratic secretions -- may be added to TPN
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![Chronic Pancreatitis Most commonly 2° Persistent or recurrent episodes ?](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/87879/slide-30.jpg)
Chronic Pancreatitis
Most commonly 2°
Persistent or recurrent episodes ?
Serum amylase
& lipase:
Pancreatic calcification 2° ongoing necrosis