DTC330: Liver, GB, Exocrine Pancreas

Whipple procedure

surgical removal of head of pancreas, gallbladder, duodenum, and part of the stomach

acinar cells

exocrine tissue of pancreas

secrete digestive juices into duodenum

islets of Langerhans

endocrine tissue of pancreas

secrete insulin, glucagon, and somatostatin directly into the blood

alpha endocrine cells

25% of islet of Langerhans

secrete glucagon

beta endocrine cells

60% of islet of Langerhans

create and secrete insulin

delta endocrine cells

10% of islet of Langerhans

secrete somatostatin

trypsin & chymotrypsin

hydrolysis of interior peptide bonds --> protein & polypeptides

carboxypeptidase

hydrolysis of terminal peptide bonds --> amino acids & polypeptides

ribonuclease

hydrolysis of RNA --> forms mononucleotides

elastase

hydrolysis of fibrous protein --> peptides and amino acids

lipase

hydrolysis of fat --> single monoglycerides, fatty acids, glycerol

cholesterol esterase

hydrolysis of cholesterol --> cholesterol and fatty acids

alpha-amylase

hydrolysis of starch and dextrin --> dextrin and maltose

islet of Langerhans

make up only 1-2% of cells in the pancreas

pathophysiology of acute pancreatitis

phase I: proteolytic enzymes are activated prematurely, causing damage to acinar cells. Enzymes enter the bloodstream and serum lipase & amylase go up

phase II: immune cells & cytokines direct immune response

phase III: increase vascular permeability --> hemorrhage, edema, pancreatic necrosis

pertinent lab values for pancreatitis

serum lipase & amylase (3x normal value), pro-calcitonin, CRP, interleukin-6 can indicate severity, triglycerides, BUN, creat, lytes, fecal fat test

significance of feeding below ligament of Treitz

feedings better tolerated, reduced GRV

*if at least 60% of goal isn't achieved in 72 hours, advance tube

fecal fat test

measures amount of fat in stool after 3 days of ingesting 100g fat/day

normal: 2-7 grams in 24 hours

pathophysiology of chronic pancreatitis

-local and systemic inflammation leads to pancreatic fibrosis

-stones or strictures may develop in main pancreatic duct or smaller side branches

-loss of pancreatic cell mass leads to diabetes (T3cDM) & EPI

nutrition therapy for acute pancreatitis

-feed as soon as nausea & vomiting subside

-low-fat are better tolerated

-EN should start within 24-72 hours (polymeric formula)

nutrition therapy for chronic pancreatitis

-35kcal/kg --> elevated resting energy expenditure

-1.2-1.5g/kg protein

-smaller, more frequent meals with moderate fat

-pancreatic enzymes taken with meals (50-75K IU lipase/meal, 25-50K IU lipase/snack)

functions of the gallbladder

1. remove water and lytes from bile

2. store bile

3. control delivery of bile salts to duodenum

cholelithiasis

gallstones; when bile is supersaturated with cholesterol, it crystallizes and forms stones

1. cholesterol stones (80% of cases)

2. pigment

3. mixed stones

cholecystitis

inflammation of the gallbladder

-usually due to obstruction, infection, or ischemia

-can be chronic or acute

cholangitis

inflammation of bile ducts

-usually due to obstruction of CBD

-can lead to infection and sepsis

*life-threatening

nutrition therapy for cholelitiasis

BEFORE SURGERY:

-low-fat diet (<30% vs. 50g/day)

-modest protein

-small, frequent meals

-NPO x12 hours pre-op

ACUTE ATTACK:

-keep GB inactive --> NPO until symptoms lessen

-advance diet (low-fat liquids)

etiology of cholelithiasis

factors that increase risk: obesity, diabetes, IBD, cystic fibrosis, rapid weight loss, fat-restricted diets, bariatric surgery, statins,

-prolonged PN and short bowel syndrome can lead to biliary stasis which can cause stones

jaundice

yellowing of skin and sclera from excess serum bilirubin

normal: <1.2mg/dL

jaundice starts: 2.5-3.0mg/dL

paracentesis

abdominocentesis

leads to protein loss

TIPS procedure

Transjugular Intrahepatic Portosystemic Shunt

surgical procedure for ascites; re-routes blood flow to the liver and reduces pressure in auxilliary veins

chronic alcoholism: kcal

30-35 kcal/kg/day

chronic alcoholism: carbs

HIGH; 6-8 g/kg

chronic alcoholism: protein

1.5-2.0 g/kg

alcoholic liver disease

spectrum of 3 disorders;

1. fatty liver (hepatic steatosis)

2. alcoholic hepatitis

3. cirrhosis

NAFLD

Non-Alcoholic Fatty Liver Disease

usually asymptomatic

diagnosis made from history & physical

hepatomegaly common

^GGT, ^AST, ^ALT

NASH

Non-Alcoholic Steatohepatitis

fatty liver causes

alcoholism, T2DM, metabolic syndrome, obestty, PCOS, sleep apnea, dyslipidemia, PN

pancreato-duodenal resection, hypo-pituitarism/gonadism/thyroidism, refeeding syndrome

liver functions

carbohydrate, protein, enzyme, bile acid, vitamin, heme metabolism, storage of glycogen/fats/fatty acids/fat-soluble vitamins, detox, water movement regulation, fetal hematopoiesis

bile

emulsifying agent secreted by the liver that decreases surface tension, allowing intestinal agitation to break up fat globules

contents of bile

cholesterol, bile pigments, bile acids, phospholipids, and bicarbonate

breakdown of RBCs

1. hemoglobin is released and broken into heme + globin

2. heme is converted to biliverdin then transformed into unconjugated bilirubin

3. in the liver, bilirubin is conjugated to soluble glucoronic acid

4. bilirubin is excreted in bile

amount of bile secreted per day

600-100-mL/day produced & secreted

GB can store as much as 12 hours of bile secretion because water/sodium/lytes are constantly absorbed by the mucosa which makes the remaining bile constituents very concentrated

how is bile concentrated

normally 5-fold, but can be 20-fold

AST

aspartate aminotransferase

ALT

alanine aminotransferase

SGOT

serum glutamic oxaloacetic transaminase

LDH

lactate dehydrogenase

clinical significance of ammonia

increased: cirrhosis, liver failure, and with portacaval shunting of blood

doesn't always correlate with hepatic encephalopathy

clinical significance of albumin

decreased: hepatic disease and inflammatory state

usually parallels functional status of parenchymal cells but can be normal with cellular damage

clinical significance of globulin

increased: reflects inflammation

clinical significance of prothrombin time

prolonged: indicates number of seconds for blood to clot

clinical significance of bilirubin

increased: liver & biliary disease

reflects ability of the liver to conjugate and excrete bilirubin

clinical significance of alkaline phosphatase

*MOST SENSITIVE TEST to detect hepatocellular injury from infectious hepatitis

300U/L acute hepatocellular damage

direct bilirubin

conjugated with glucoronic acid, water soluble

increased: intrahepatic disease

indirect bilirubin

unconjugated, water insoluble

increased: hemolysis

hepatic encephalopathy

consequence of liver failure involving impaired mental status and abnormal neuromuscular function

significance of lactulose in HE

stimulates the loss of ammonia from body tissues into gut lumen and prevents the intestine from making additional ammonia

significance of antibiotics in HE

decrease colonic concentration of bacteria that can produce ammonia

HE stage 0

West Haven: no abnormality detected.

Modified: alert, attentive.

HE stage 1

West Haven: trivial lack of awareness, anxiety/dysphoria, short attention span, unable to add

Modified: alert and attentive but with at least one: ataxia, dysarthria, flapping tremor, slow thinking

HE stage 2

West Haven: lethargy, disorientation to time/place, subtle personality change, inappropriate behavior, unable to subtract

Modified: awake but inattentive, disoriented, easy to distract

HE stage 3

West Haven: confusion, gross disorientation

Modified: psychomotor agitation, difficult to understand speech

HE stage 4

coma

nutrition therapy for hepatic encephalopathy

-1.2-1.5g/kg protein (prevent catabolism and the increase in ammonia production)

--> plant proteins better tolerated, have less AAA

-supplement with BCAA

etiology of portal hypertension/ascites

intrahepatic cellular changes due to scar tissue in liver; obstructs normal blood flow and increases pressure in the portal vein --> collateral circulation leads to ascites

ascites

fluid in the abdomen

low serum proteins lower oncotic pressure so fluid shifts from blood into third spaces. blood volume & urine excretion decrease, stimulating RAAS --> fluid and sodium are retained