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Liver Disorders

Performs >300 functions, can be serious

• Liver structure/function: Largest internal organ Portal

Liver, Biliary and Pancreatic vein, & hepatic artery supply blood to liver Portal: 75%
of blood bringing nutrients from GI
Disease oxygenated blood
tract Hepatic: 25% as
Can function with
damage to 90% of its mass, liver removal or total
Liver Disorders - Hepatitis destruction can cause death within 10 hr Damaged liver
Biliary disorders -Cholecystitis, can regenerate in 3 weeks, normal function in 4 months
• Functions: Bile production & secretion
Pancreatitis Metabolism CHO, Protein,Fat
Vitamin & mineral storage
Detoxification Blood storage

CHO Metabolism Lipid (Fat) Metabolism

• Major functions of liver in R/T to glucose metabolism are: • The major functions of the liver in R/T fat metabolism
• 1. Glycogenesis-the conversion of glucose to blycogen are:
• 2. Glycogenolysis-the breakdown of glycogen to blucose • 1. Oxidation of fatty acids for energy
• 3. Storage of glycogen • 2. Formation of most lipoproteins
• 4. Conversion of galactose & fructose to glucose • 3. Synthesis of cholesterol & phospholipids
• 5. Gluconeogenesis-conversion of amino acids to • 4. Synthesis of fat from proteins & carbohydrates
• *When glucose is Not needed, body stores it as • *Liver provides energy from fats by splitting them into
blycogen. Later, if glucose is needed, liver can break glycerol and fatty acids, followed by the oxidation of the
down glycogen to release glucose. fatty acids, leading to the release of > amounts of

Protein Metabolism Liver Disorders - Assessment

• Primary functions of liver in R/T protein metabolism are:

• 1. Deamination (removal by hydrolysis of the NH2 radical • Liver paplable Rt Upper Quadrant-firm sharp ridge
from an amino compound) of amino acids with smooth surface.
Size estimated by percussing upper & lower
• 2. Formation of urea for the removal of ammonia from
borders. Dull sound. If enlarged, degree to which
the body extends below Right costal margin.
• 3. Formation of plasma proteins Cirrhosis-small/hard;
• 4. Biotransformation of hormones, drugs, & other Hepatitis-soft edge easily moved
substances • Various S/S:
Jaundice: occurs when serum bilirubin levels
exceed 2mg/dl Yellow tinge stems from bilirubin
deposits in bodies tissues
Dark amber urine Fatigue Ascites
Peripheral edema Weight loss Anorexia
Nausea Vomiting

Assessment of Abnormal Lab Findings in Liver Disease
Direct Bilirubin: Adult 0-0.2 mg/dL
Serum Enzymes
Indirect Bilirubin: Adult <1.1 mg/dL
Abnormal Finding
Significance Total Bilirubin: Adult 0.3-1mg/dL
• 1. >serum asparate • 1. Hepatic cell
aminotransferase (AST) destruction, hepatitis • Bilirubin: the orange-yellow pigment of bile, formed
(formally SGOT) by breakdown of Hgb in RBC after termination of their
(most specific indicator)
• 2. >serum alanine normal lifespan. (RBC breakdown too fast)
aminotransferase (ALT)
(formally SGPT) • 2. Hepatic cell • Production In reticuloendothelial cells, primarily
• 3. > lactate dehydrogenase destruction, hepatitis Kupffer’s cells, of liver & in reticulo-endothelial cells
(LDH) of spleen, bone marrow, & lymph nodes. Most
• 4. > serum alkaline • 3. Hepatic cell destruction bilirubin formed from Hgb as reticuloendothelial cells
phosphatase break down erythrocytes that reached the end of120
day life span. Remainder of bilirubin formation is from
• 4. Obstructive jaundice, enzymes that contain heme & from destruction of
hepatic metastasis damaged, abnormal erythrocytes that have a short
life span.

Water insoluble indirect unconjugated Bilirubin -continued
Water soluble direct conjugated
• Transport: Once bilirubin is produced,it is transported in
plasma to liver. Bilirubin is bound to molecules of albumin • Conjugated bilirubin is water soluble, yellow green
pigment that crosses cell membrane & enter bile
& is indirect or unconjugated. Water- canaliculi. As it mixed with fluid, conjugated bilirubin
insoluble unconjugated bilirubin normally travels in the becomes a component of bile
bloodstream to liver, where it is converted to water- • Purpose of Testing Bilirubin:
soluble, conjugated form & excreted into bile. Small amt. Total bilirubin used to evaluate liver function,
diagnose or monitor the progression of jaundice,
of unconjugated bilirubin remains in plasma circulation, the determine whether an infant needs treatment of jaundice
rest acted on by liver to convert it to direct, conjugated to >bili in CNS Indirect &
bilirubin. Direct bilirubin help identify the underlying cause of
hyperbilirubinemia Ex: Direct bilirubin
• Conjugation: Within the liver cells, indirect bilirubin is 1st is water soluble & can be excreted in urine (dark brown),
separated form albumin,then acted on by enzyme suggests disease affecting defect or excretion such as
glucuronyl transferase, is conjugated with glucuronic acid, gallstones, tumor blocking common bile duct
& transformed into direct, conjugated bilirubin

Assessment of Abnormal Lab Findings in

Liver Disease - Bilirubin > Bilirubin Findings
Abnormal Findings Significance
• 1. Hepatic cell disease • >Direct Bilirubin-
• 1. >serum total bilirubin
• >Total serum bilirubin continue Biliary
• 2. Hepatitis, liver Hepatocellular damage atresia Gallstone
• 2. > serum direct conjugated
bilirubin metastasis Cancer of liver Obstruction Acute pancreatitis
in biliary tree Neonatal • >Indirect Bilirubin
• 3. > serum indirect • 3. Cirrhosis (physiologic) jaundice Hemolytic anemias
• unconjugated bilirubin Hemolytic Malaria
disease Hodgkin’s disease
• 4. > urine bilirubin
• 4. Hepatocellular
• >Direct Bilirubin Neonatal (physiologic)
obstruction, viral or toxic jaundice Rh
liver disease Hepatocellular necrosis
Infection in liver Cancer of or ABO incompatible
• 5. > urine urobilinogen liver, biliary duct, Blood transfusion
• 5. Hepatic dysfunction reaction
• 6. < fecal urobilinogen • Cirrhosis
• 6. Obstructive liver disease

Assessment of Abnormal Lab Findings in Assessment of Abnormal Lab Findings in
Liver Disease - Serum Proteins Liver disease - Other Tests
Abnormal Findings Significance Abnormal Findings Significance
• 1. > serum total protein • 1. Acute liver disease • 1. > serum ammonia • 1. Advanced liver disease
• 2. < serum total protein • 2. Chronic liver disease or portal-systemic
• 3. < serum albumin encephalopathy (PSE)
• 3. Severe liver disease • 2. Prolonged prothrombin time
• 4. > serum globulin
• 4. Immune response to (PT)
liver disease • 2. Hepatatic cell damage
& synthesis of
Monitor S/S of bleeding

Diagnostic Studies for Liver Diagnostic Studies of Liver - continued

• Endoscopic Retrograde Cholangiopancreatography
• Liver function studies: One of several tests used to (ERCP) - identifies the cause of jaundice
evaluate various function of the liver such as • Procedure (1)Dr advances a small side viewing
metabolism, storage, filtration, and excretion. endoscope through the pt mouth, esophagus, stomach,
& duodenum until he identifies the ampulla of
Vater(hepatopancreatic ampulla-the dilation formed by
• Kinds of liver function tests include: SGOT, SGPT, the junction of the pancreatic & bile ducts as they open
Alkaline Phosphatase (ALP), serum bilirubin, into the lumen of the duodenum). (2) Contrast medium
prothrombin time is injected (3) Because the dye used contains
iodine obtain allergy history (4) For 48 hours after
• Over 70% of parenchyma (the functional tissue of an monitor temp, serum amylase levels. If nausea, vomiting
organ as distinguished from supporting or connective or abd pain, suspect chemical pancreatitis & call MD
tissue) may be damaged before the Liver Function
Test are abnormal

Diagnostic Studies - Liver Biopsy - Hepatitis-liver inflammation stems from

dx diffuse & local liver disease virus or hepatoxic agent
• Best known and most prevalent hepatitis types
• Prior to test: 1) Check coagulation studies result from: Hepatitis A virus (HAV)
(2) Pt typed and cross-matched Hepatitis B virus (HBV)
(3) Check consent Hepatitis non-A non-B (NANB)
(4) Withhold food&fluids for 6 hours prior virus
During Test: Hold breath after a full expiration during
• Most common type: HAV or infectious hepatitis
needle insert(to prevent pleural cavity/diaphram puncture)
• Most severe course: HBV
Post Procedure (1) Lie on right or serum hepatitis Also
side for 1st 2 hr & maintain strict bedrest for 24 hr. Place highly contagious, can be acquired through exposure to
pillow under costal margin (2) Monitor V/S q1-2hr asymptomatic carriers
at 10-20 min intervals for hemorrhage/hypovolemia or peritonitis
signs (abd distension, rigidity, pain, rebound tenderness, < or
• Post transfusion hepatitis: NANB (hepatitis C)
absent bowel sounds, N/V,tachycardia,chills, fever, breathes
rapid&shallow, anxious) (3) Examine biopsy site at least once an
hour for bleeding (Vit K can be given)

Hepatitis Passive & Active
Hepatitis - Pathophysiology
• Active Immunity:
• Passive Immunization: Hepatitis B vaccine may – Patho: Similar in all forms Virus
Standard Immune provide active immun invades portal tracts, periportal space,
globulin may contain before exposure to hep lobules or liver
antibodies against B virus. Killed virus Causes inflammation & destruction of
hepatitis B. However, vaccine for all high risk
another preparation parerchymal cells
categories as
called hepatitis B healthcare workers, Necrosis, degeneration, autolysis of individual
immune globulin dialysis pt & family, hepatocytes
contains much higher repeat transfusions, Infiltration of liver by leukocytes Liver
levels of antibody. spouses/sig others of enzymes releases, Liver function
Vaccine given in 3 HBsAG-positive decreases
doses within 6 months. persons, sex
promiscuous, prison
workers, handler

Hepatitis A Virus (HAV) Serologic Markers

Most Common -Most Contagious in early stages • Hepatitis A: Dx established by the presence of Hep
often before Dx is made A virus Antibodies in the body (anti-HAV) ongoing
inflammation by the liver evidenced by the presence
• Transmission: Oral/anal RNA virus of immunoglobulin m (IgM) antibodies which persist
Food, water, shellfish from contaminated water 4-6 wk. IgG antibodies indicate previous infection,
Fecal to oral route, poor sanitation & contaminated persist in serum & provide permanent immunity to
water. Many outbreaks traced to infected food handlers. HAV
Private • Hepatitis B: Hep B double shelled DNA virus with
room, stool & urine isolated. inner core & outer shell, look for presence of antigens
Incubation: 2-6 wk Average 4 wk located on shell or surface of virus as the most
• Dx: Anti-HAV IgM+ in acute hepatitis significant serologic marker. HBsAg-
IgG+ after infection presence establishes the dx & infectious state of Hep
• Prognosis: Good, generally full recovery; no chronic B. Carrier State/Chronic Hep-If
carrier state HBsAG longer than 6 mo.
• Prevention: Hygiene. Immune globulin (passive)-given Normally HBsAG <& disappear & antibodies Anti-
to persons who have been in direct contact with HBsAB appear =HepB recoveryImmunity
Hep A pt

Hepatitis B
Transmission: Worldwide, esp in drug addicts,
homosexuals, expose to blood & blood products.
Hepatitis C Virus (HCV)
Parenteral, sex contact, fecal-oral route.
• Incubation: 6wk - 6mo (Average 12-14wk) • Transmission:Blood/bld product, Sexual contact.
DNA virus Major cause post-transfusion.
• Dx: HBsAg in serum indicates current or chronic RNA virus
infection HBeAG (a marker for > Infectivity) • Incubation: 5-10 wk. Average40-60 days)
AntiHBc (a marker for infection at some time) • Dx: Anti-HCV(a marker for infectoin with HCV virus)
AntiHBe(a marker for < infection) Recombinant immunoglot assay
AntiHBs (a marker for immunity and the antibody • Prognosis:Chronic carrier rate high. Generally full
produced in response to the HBV vaccine) recovery.
• Prognosis: Good, generally full recovery except for • Prevention: Risk factors similar to Hepatitis B Screen
chronic carriers. Mortality rate 10-20% donated blood, avoid bld to bld exposure.
• Prevent: HBVvaccine(active) Immune Immune globulin (passive)
globulin(passive) Condom use, screen donated blood. • *There is NOT an HCV vaccine.
Healthcare workers protective equipment-needle safety,
gloves, gowns

Hepatitis D Hepatitis - Isolation Precautions
• Transmission: Same as for HBV. Causes infection as a • Isolation Precautions:
complication of Hep B, infection only together with HBV. • Private room only necessary for pt with poor hygiene
Incomplete RNA virus
• Incubation: Not firmly est in humans. HBV infection • Gown if direct soiling possible
must precede HDV. Chronic carriers of HBV are at risk • Gloves if direct body fluid contact
throughout their carrier state. • Linen: other places double bag
• Dx: Anti-HDV IgM -current infection • Specimens: Label enteric precautions/blood & body fluid
• Anti-HDV IgG-past infection precaution
• Prognosis: May be acute or short lived or become
• Prevention: Same as for HBV.HBV vaccine for all at risk
will also prevent HDV infection.

Hepatitis-Clinical Findings
Hepatitis: Assessment (1) Preicteric State (Intestinal Phase)
May not have any s/s during incubation period Define icteric-pertaining to or resembling jaundice
• Health History: - • Nonspecific flu like symptoms -Malaise ( body weak)
Suspected exposure to contaminated food, water, -Fatigue -Headache -Myalgias - (diffuse muscle pain
equipment, or hepatitis carriers - accompanied by malaise) -Anorexia, NVD Distaste for
Recent needle sticks - *Recent Ear piercing, body dietary protein, fatty foods not tolerated well. -Abd pain
piercing, tattooing - Recent 2dary to Glissans cap stretching via > liver
travel to areas with poor sanitation -Recent blood • HAV: occurs more abruptly; higher elevations in
transfusions - temp
Occupation, socioeconomic status, health habits-living • HBV: occurs more slower & longer incubation period -
conditions (close quarters) - Precicteric stage characterized by immune injuries:
Medication history (1)Urticaria (reaction skin eruption, hives, itch)
• Physical Exam: l)Jaundice-intrahepatic obstruction due (2)polyarthritis(inflam joints) (3) arthralgias (joint pain)
to edema of livers bile channels • NANB: milder acute stage but > to chronic active hep, or
2) Right upper quadrant abdominal fulminant hep. *Many cases of HAV may not progress
pain beyond this stage, easily overlooked

Hepatitis Clinical Findings

2) Icteric Stage Occurs few days to a week Hepatitis Clinical Findings
following onset of preicteric. (3) Posticteric Stage: Convalescent
• Jaundice: When bilirubin reaches 3-4mg/dl
• Lasts a few weeks, symptoms rapidly resolve
• Cholestasis: light colored stools, high fat content
(term refers to an interruption in flow of bile, indicated • Rising levels of serum antibodies occur in most pt
< or absent bile in stool) • Pt may feel ok, tests may not return to normal for 2-6
• Liver enlarge & tender Liver enzymes > markers months
• Jaundice (a)2dary to > unconjugated bilirubin, liver
unable to conjugate
(b) Breakdown if RBC> due to shorter life span
causing an >of hgb RBC breakdown too fast due to
a shorter life span of RBC. Orange-yellow pigment of
bile(bilirubin) is formed by the >hgb when the RBC
breaksdown, deposited in the skin & excreted in urine
when present in the blood in excessive amounts

Diagnostic Tests: Serologic Markers Liver Enzymes
• Serum Enzymes: ALT, • Serum Albumin:
AST, LDH: highly elevated in Remains normal except
• Hepatitis A: Anti-HAV • Hepatitis B: viral hepatitis than in other liver
antibodies in serum: disorders due to liver cell in a prolonged course or
HbsAG outer surface chronic active hepatitis
IgM is 1st to appear inflammation & necrosis
coat of antigen
IgG follows closely *IgM • Serum Bilirubin: Rises in
HBcAG inner core jaundiced pt
anti-HAV indicates acute
or very recent infection antigen • Serum PT/PTT: Will be
HbeAg “e” antigen prolonged moderately or • CBC:
• *Dx of Acute HAV also severly Leukopenia (<WBCs)
indicates low infectivity • Hepatitis C: Anti- mild anemia during icteric
• IgG anti-HAV: evidence HCV: may not appear stage due to mild
of previous infection & can until late in course of hemolytic anemia
no longer transmit infection, possibly up to 1
year after

Hepatitis - Nursing Care

Hepatitis - Treatment Encouraging adequate rest ( >metabolic needs),
providing proper nutrition, preventing disease spread
• Once contracted only symptomatic treatment given: • Upright position may < liver flow
-Prophylactic therapy may help prevent once • Provide most of calories in am when appetite is best.
expose High calorie needs for wound healing.
- Immune globulin gives temporary immunity to HAV High protein <fats tolerated easier.
Should be given 6wk after direct exposure. Give to family • Mild antiemetic such as benedryl may help control
-HBIG provides passive nausea
immunity to hepatitis B This is costly and reserved for
postexposure prophylaxis • No ETOH during and up to 6 months following-lytes
-HBV provides active and permanent • Any hepatitoxic meds that can exacerbate liver cell
immunity injury should be D/C if not essential: Tylenol, ASA,
(Heptavax-B) Librium/Valium, Dilantin, Haldol, Aldomet , Antithyroid
drugs, Oral contraceptives

Hepatitis - Complications if liver function tests

persist longer than 6 months, likely that one of the forms
of chronic hepatitis has developed
Hepatitis-Complications continued
• (3) Fulminant Hepatitis: • Therapeutic trial of
• (1) Relapsing Hepatitis Rare disorder of rapidly • (5) Chronic Active corticosteroids are used
Symptoms may occur Hepatitis: Symptoms Prognosis unfavorable
• deteriorating hepatic persist >3months
within 6 mo. Generally function can occur within (6) Post Necrotic
milder, healing occurs Common in: - Cirrhosis: follows acute
few days/weeks after Young or elderly
w/o dev chronic liver or chronic hepatitis
acute onset -Immunocompromised pt Characteristics: (a)large
disorder -Hemodialysis or multiple
• (4) Chronic Persistant: areas of
• (2) PostHepatitic Benign follow HBV transfusions Symptoms: collapse(b)broad scars
Syndrom Oder adults. (a)ascites (b) (c)large regenerating
recovery. HBsAg present
Fatigue, & malaise for edema(c)hepatic coma nodules in liver
in serum, asymptomatic These are indicative of
months follow recovery carrier. Major source of Symptoms: none to
despite normal liver extensive liver disease severe encephalopathy
virus for infection.
function tests. Self limit (abnormal structure/ fx
Prognosis excellent brain tissues)
without Rx

Biliary Disorders - Gallbladder Disease Cholecystitis (inflam of gallbladder) Acute
Cholecystitis Chronic Choleystitis
• Inflam follow by fibrosis
• Gallbladder lies on the livers right underside. It holds • Inflammation present
up to 500cc of bile. • Most common occurs as a
Liver normally produces 1-2L of bile each result of cholelithiasis
• Most common occurs as result
day, flows through the cystic duct into gallbladder for
of cholelithiasis
storage. Once there bile grows concentrated. Food
(gallstones) but can occur
ingestion stimulates secretion of the flow of bile into from bacteria invasion or biliary
the duodenum Disorders of • Bile obstruction common;
spasm called acalculous
gallbladder and pancreas initially occur as single may result in cholangitis
choleycystitis (absence of (inflam of bile ducts) &
organ process. However, the inflammatory response gallstones) pancreatitis
may extend to other organs. The anatomic proximity
of the liver, gallbladder, and pancreas, as well as • Bile obstruction not common
possibility of impeded flow of bile from liver through • Jaundice very common
biliary (gallbladder) ductal system, contributes to
potential complications.
• Jaundice not common

Cholecystitis Jaundice
Acute Chronic Most commonly seen in Chronic
• Insuff empty of bile by
GB & GB muscle wall • Extrahepatic • Obstructive Jaundice
• GB inflam-trapped bile reabsorbed disease persist. Cause obstructive jaundice Normal flow of bile
acts as chem irritant to GB wall. This by or lead to formation (common bile duct) into
inflam, irritant, impaired circ cause Bile flow impeded by
ischemia results in tissue slough
of gallstones. GB edema of ducts or duodenum is blocked.
w/necrosis & gangrene. Perforation of becomes fibrotic, Bilirubin
GB wall leads to abscess contracted, < gallstones. unable to reach large
forms/peritonitis. Painful episodes motility, Deficient intestine where its
occur due to organ/ bile duct absorption. Pancreatitis Liver involved - converted to
spasticity-this prevents adequate bile & cholangitis may dev, urobilinogen-this gives
release for fat digestion intrahepatic
due to bile backup. Bile feces its brown color.
obstruction (common As a result,-clay
bile duct) leads to colored stools seen.
jaundice-most Urine dark &
common in chronic. foamy as kidneys try to
excrete excess bilirubin

Etiology of Cholecystitis Incidence of

(inflam of gallbladder) Biliary Tract Disease & Cholecystitis
• *Formation of • Any condition that affects • Sedentary lifestyle • Diabetes-Type I
gallbladder the regular filling or • Family tendency to biliary
calculi(stones) emptying of gallbladder • Pregnancy-delay GB
disease (or due to dietary
or causes “gallbladder emptying
• Surgical trauma habits-excessive dietary
• prolonged anesthesia shock” (in blood flow to CHO intake) • Chron’s disease
gallbladder) • Obesity-impaired fat • Incidence higher in
• Adhesion formation
• Anatomic problems- metabolism women than men
• Edemas twisting or kinking of
• Neoplasma • Diets-<cal, liquid protein-
gallbladder neck or cystic cause liberation of CHO
• Long term dietary duct & pancreatic from tissues which is
fasting enzyme reflux into excreted as crystals in
• prolonged dehydration gallbladder bile
• Gallbladder trauma
• Prolonged immobility

food pref -see if excessive fat & CHO are Physical Clinical S/S
in diet • if GB is inflamed. Deep
• Ask whether pain occurs
after pt has eaten a high inspiration can be very
• Ask whether any foods are • Vague abd pain-may limited. Test used also
not tolerated. Ask whether fat or high volume meal radiate to rt shoulder. for dx Ca GB &
the following GI symptoms or after assuming a When RUQ pain & cholecystitis.
occur in R/T intake of fatty recumbent position. tenderness suggest acute
• Abd Palpatation: • Pain triggered by high
foods: cholecystitis look for fat, high volume meal,
• Flatulence • GB tender on palpation Murphy’s sign - pt is or from recumbant
• Dyspepsia (indigestion) • Guarding & ridigity, asked to inhale when position
rebound tenderness examiner’s fingers are
• Eructation (belching) hooked under the liver • Anorexia, rebound
(Blumberg’s sign) tenderness (Blumbergs
• anorexia indicate peritoneal border at bottom of rib
cage. Inspiration causes sign), fever, Jaundice
• Nausea/vomiting irritation
the GV to descend onto the • Clay colored stools,
• Abdominal pain or
fingers, producing pain steatorrhea (fatty
discomfort or heaviness

Dx Tests-continued
Dx Tests
Oral Cholecystography
• May >serum levels of • Cholecystitis • Oral Cholecystography • Procedure-24hr pre test,
alkaline phosphatase, suspected-Oral Uses an iodine based pt takes dye in tab from
AST, SGOT, LDH =abn cholecystogramOCG with water. Films taken to
(not done if serum dye, visualized the GB &
liver function ductal system. Liver asses GB ability to
• Direct (conjugated) & bilirubin >1.8mg/dl) or concentrate dye. Pt eats
GB radiographic series extracts the dye from the fatty meal. Dr takes more
Indirect (unconjugated) bld & excretes it into bile.
serum bilirubin levels > if to confirm presence of films to assess GB
obst process is present biliary tract disease. If GB does NOT show on contractile ability. *Before
• HIDA scan-detects abn film, stones may have test check for allergies.
• >WBC=inflammation
hepatobiliary function obstructed it. Withhold food & fluids
• Pancreatic involvement- before test.
serum & urine amylase • Upper GI series to R/O
levels> other cause of abd
pain-Gastritis & Peptic
ulcer disease

Dx Tests-Continued
Endoscopic Rerograph Nsg Dx
• Used both radiography & • High risk for altered GI tissue perfusion F/T risk of
endoscopy to examine obstruction by gallstones
• Oral Cholescintigraphy
the pancreatic ducts &
• Dx acute cholecystitis & hepatobiliary tree. • High risk for fluid volume deficit R/T hypovolemia from
early biliary duct obs Procedure-side view severe vomiting
(PIPIDA SCAN) IV injection endoscope advanced • Sleep pattern distrubance R/T acute pain
o an agent, gamma camera thru pt mouth until • Anxiety R/T pain & possible surgery
takes serial images over an reaches ampulla of vater.
Contrast media then • Altered nutrition: More than body requirements R/T
hour to record the agents excessive dietary fat intake
injected. Can help dx
progress through the liver,
pancreatic & biliary duct
biliary ducts, GB, and disease, locate cysts,
duodenum. Lacks resolution calculi& stenosis
needed to detect stones

Cholelithiases-leading biliary tract disease Cholelithiasis
goes by the name gallstones
• Presence of 1 or more gallstones • Incidence: • Other predisposing factors:
• Patho: Supersaturatonof bile with CHO Five “F”S profile: Obesity
Excessive bile salt losses female, fat, forty, fertile &
<GB emptying rates flatulent DM
<in bile concentraton Beyond age 50 sex
Stone’s may lie dormant in gallbladder or distribution evens out. Vagotomy
more to other areas of the biliary tree as GB empties &
refills with bile Pregnancy predisposes
due to >abdominal
pressure that can lead to
bile flow stasis

Cholelithiasis Cholelithiasis - Assessment

Etiology S/S Some asymptomatic, most c/o spastic or steady pain
• Initally pain is a steady • Fever & chills may
mild ache in mid result from inflamm
• Familial (or due to dietary • Pain may last several hr,
habits-excessive dietary CHO epigastric area, same as • May cause infection
choleystitis stems from GB distention (in
intake) • if stone in bile duct will
case of cystic duct stones) or
• Obese-impaired fat cause jaundice: before
from spasm of sphincter of frank jaundice sets in
metabolism • Biliary colic-cystic duct of
Oddi or ductal muscles. may notice lt stools,dark
• Diets-<cal, liquid protein- GB obstructed. Intense
pain as spasm tries to • Pain begins in urine
cause liberation of CHO from
tissues which are excreted as push stone thru duct-so midepigastrium, radiates • Attacks usually due to
crystals in bile severe accom by RUQ, Rt shoulder & back. fat intolerance:
tachycardia, pallor, • N/V may accom pain Inflammed GB contracts
• Pregnant-delay GB empty diaphoresis, extreme to release bile for fat
Chron’s disease exhaustion • After attack, area over GB digestion, possibly
• Type 1 DM may be tender 24-72 hr precipitates pain.

Cholelitiasis - Rx Cholelithiasis
• or poor surgical risks. • Modify diet reduce fat
• Pain-Diet: low fat, intake
Can take up to 2 yrs to • Medical Management
replace fat soluble
dissolve gallstones b) • Initially includes pain relief &
ADEK vit if obst bile
Actigall-can take 4mo- dietary control • Dx:
flow. Admin of bile salts
2yr © • MD won’t order such opiate- • Cholangiogam,
to facilitate digestion &
vit absorp Questran derived analgesics as ultrasound WBC>15,000
Questran(Cholestyrami morphine, except for Demerol suggests more serious
• Meds: Demerol ne) binds with bile salts in (used cautiously) complications
Bentyl -to <spasms intestine, to remove
Bile Acid Therapy- excess bile salts in feces Morphine can cause
dissolve gallstones to < itching caused by spasm of spincter of Oddi
(a) Chenodiol-<CHO excessive accumulation
stones, good on small of bile salts on skin Atorpine sulfate & pro-
stones, used on elderly banthine: relieve spasms by
mild/asmptomatic relaxing smooth ductal

Surgical Management Traditional
Cholelithiasis - Rx Cholecystectomy Usual surgical Rx for pt with
acute & chronic cholecystitis
• Percutaneous • bile duct. Permits bile
• Extracorporeal Shock
Transhepatic Biliary • Cholecystectomy: excises drainage during healing
Wave Lithotripsy
shock waves Catheter Insertion GB & ligates the cystic • Operative Procedure:
shatter gallstones. Catheter decompresses duct. Body adapts by > bile Removes GB &
3 or obstructed extrahepatic flow into duodenum. Druing explores CBD, T-tube
fewer CHO stones, ducts so bile can flow. surgery may explore inserted to ensure
function GB, no Hx of Common for inoperable common bile duct for patency of the duct.
liver or pancreatic hepatic, pancreatic or additional stones or Penrose/JP(Jackson
disease, no pacemaker bile duct CA. Non perfrom a cholangiogram to Pratt drain) inserted in
or pregnant. surgical option for poor ID any retained stones. GB bed to prevent fluid
Once surgical risks for Rx of Ductal manipulation leads accumulation. Drainage
shattered, travel thru biliary obst. due to to inflammation. MD will serosanguinous & bile
biliary ductal system to gallstones insert a T tube after stained in first 24 hr
be excreted via exploring the common. post op

Surgical Management - Traditional Cholecystectomy -

Traditional Cholecystectomy Post op continued
• Pre-op • Post op • T-tube cholangiogram. If
• Focus to prevent resp • Avoid kinking the tube • Report an output >500cc in 24 stones are located during
complicatoins. Instruct • Normally drains 300-500cc hr to MD. May need to receive this test, they can be
brown green bile 1st 24 hr T-tube at level of abd to avoid removed without further
Deep breath, cough, turn.
• Drainage gradually <to 200- excessive drainage. Excessive surgery.
Use splint. Pt reluctant 400cc/d drainage may indicate
due to hight incision Rt • Clamp tube 1-2hr before meals obstruction-excessive bile • Weeks or even years
subcostal area & surgical & unclamp 1-2 hrs after eating. drainage can be returned to pt after surgery, pt may still
manip near diaphragm. • Pt may experience abd pain, via NGT or in fruit juice develop signs of GB pain,
Incentive spirometer. nausea, amber urine, clay • Within 7 days after surgery, MD frequently due to retained
OOB evening of or 1st stools-unclamp removes tube after evaluating or newly formed stones.
results of
day post op

Traditional Cholecystectomy
Traditional Cholecystectomy -
post op continued
Post op continued Nsg Care T-Tube
• consistency, odor of
• level of abd (4-5days
drainage q4h then q8h.
• Pain-controlled with IM • Report sudden > in bile post) Assess for
Initial post-op bloody
Demerol or PCA pump. output after a normally < feelings of fullness,
drainage, changes to
*Morphine not given due to amount (9-10days post). nausea, or pain.
green-brown bile. Bile
resp complications R/T abd output 400cc/day with • Inspect skin around T-tube • Clamp T-tube for 1-2 hr
incision. gradual >in amt. before & after meals,
site. Change dsg daily, keep
Report bile drainage assess tolerance for
• N/V-antiemetics dsg dry. food
• Drain-surgeon removed dsg *Collect & admin excess • Maintain in Semi-Fowlers • Observe stools for
& drain by 24-48 hr bile output to pt by NGT position-keep drainage return of brown color 7-
• T-Tube-may remain in place or give synthetic bile salts system below level of GB. 10 days post op
6 wk or longer (Decholin) Never irrigate, aspirate, or • Diet -Early post op if
• Nsg Care T-Tube clamp without MD order bile flow < give low fat
• Raise drainage bag to diet. Usually no special
Assess amt color,

Laparoscopic Laser Cholecystectomy Laparoscopic Laser
Another Surgical Management for acute & chronic Cholecystectomy
cholecystitis - Less invasive than traditional
• Not used for pt with • Post op “Free air pain”- from • Diet Based on pt
• pressure of 15-20mm CO2 retention in the abdomen.
(1)extensive abd tolerance to fats. Special
Hg. Trocar catheter To prevent this, Nurse teaches
symptoms in past diet may not be needed.
inserted, a laparoscope pt that early ambulation
• (2)Severe acute is introduced, attached promote absorption of CO2. Low fat if poor tolerance
cholecystitis to video camera, & abd Pt returns to usual to fats,may need for 6
• (3)Palpable gallbladder organs viewed on activities 3-7 days after • months, add fatty foods
• Pre-op: (a)Out pt or monitor. 3 small
as tolerated
overnight (b) NPO punctures to introduce
• Operative: 10mm midline laproscopic forceps.
puncture at umbilicus Laser used to dissect
Abd cavity insufflated GB away from liver bed
with carbon dioxide to a & close off cystic artery
& duct. GB extracted
thru midline puncture.

Foods to avoid pt with

• Dairy • Gas Forming • Location: Between • Pancreatic Juice is clear
• Whole milk • Cabbage Onions stomach & small with high bicarbonate
Ice cream Broccoli intestine. Triangular content. Secretions
Butter Cream Cauliflower gland, its tail next to controlled by vagus nerve
Cheese Sauerkraut Radishes spleen, head next to & effect of intestinal
• Fried Fatty Foods Cucumbers duodenum. hormones secretin &
Beans • Primary enzyme cholecystokinin
• Rich pastries Gravies
Nuts Chocolate producing organ of • Pancreatic secretions
Egg Yolks digestive system contolled by hormones
Avocado Produces 1-1.5L of from GI tract
pancreatic juice every

Pancreas functions Pancreas

Exocrine & Endocrine Function
• Exocrine: Enzymes • Endocrine: hormones • Exocrine function: • Endocrine Function:
produced empty directly produced directly enter Secretions include: (1) Isles of Langerhans:
into duodenum blood steam Amylase-aids digestion of endocrine part of
• Function: Facilitate • Function: Capable of CHO (2) Trypsin-aids pancreas. Cells in
digestion thru secretion of neutralizing highly acid digestin of protein (3) pancreatic tissue alpha,
enzymes into proximal gastric juices that enter lipase-aids digestion of beta, delta cells (1)
duodenum duodenum. Secretions fats Alpha-produce glucagon
into pancreatic duct, joins (2) Beta produce insulin
common bile duct, enters (3) Delta secrete
duodenum at Ampulla of somatostatin

Pancreas Pancreas
Endocrine Function
• Insulin: Major function- • Glucagon:> bld gucose • Disorders of the Pancreas:
(1)<blood glucose. Stored by converting glycogen to Pancreas has exocrine and endocrine
as glycogen or used for glucose in lever. functions. The exocrine glands called acini aid digestion
energy (2) Promotes Somatostatin: by secreting 500-1000 ml of pancreatic juice daily.
Contains mainly water, bicarb,
storage of fat in adipose Hypoglycemic effect- enzymes, potassium, sodium, chloride, and calcium.
tissue & synthesis of interferes w/release of
• Pancreas Digestive Functions
protein in various body growth hormone from Secretes (1)Digestive Enzymes
tissues (3) Rate of pituitary & glucagon of (a) Amylase (b) Lipase
production regulated by pancreas CHO © Trypsinogen
level of glucose in blood Metabolism: Cho (2) Bicarbonate Juice
converted primarily to
glucose. Controls level
bld glucose synthesize

Pancreatitis Pancreas -Pathophysiology

• Pancreatitis: an inflammatory process brought on by • (1)Normally pancreas secretes proteolytic & lipolytic
premature activation of pancreatic enzymes which enzymes in an inactive form into duodenum. Once in
destroys ductal structures & pancreatic cells, resulting in duodenum they convert into active form with help of
fibrosis & autodigestion. May be acute or chronic but some intestional enzymes
acute does not typically evolve into chronic pancreatitis
unless complications occur. • (2) For some reason these enzymes are activated in
• A pt admitted with acute pancreatitis is acutely ill & pancreas before they reach the intestine. Could be by
needs emergency treatment. Mortality rate is 5% in pt direct toxic injury to pancreatic cells. This cause tissue
with mild form of acute pancreatitis. damage to pancreas. Thrombosis & gangrene. This can
Severe pancreatitis (necrotizing or be localized or confined to one area.
haemorrhapic pancreatitis) often leads to complications • (3) As vicious cycle begins, further tissue damage &
and can be fatal. enzyme activation occur.

Acute Pancreatitis Acute Pancreatitis

• Mild, self-limiting to severe, rapidly fatal • Severe Acute systemic • Acute Pancreatitis
complications: (1) Patho: digestion of
• Mild Acute: Formerly interstitial or edematous Acute resp distress syndrome
pancreatitis(1) Edema & inflammation(2) minimal organ (2) Shock (3)
pancreas by its own
dysfunction (3) Return to normal within 6mo (4) still Diseminated intravascular enzyme, esp trypsin
acutely ill (5) At risk for: shock, F/E disturbance, sepsis coagulopathy (4) Etiology: -
Pleural effusion 80% have biliary tract
• Severe Acute : Formerly necrotizing or hemorrhagic
pancreatitis (1) Widespread, complete enzymatic disease -Long
digestion of gland (2) Tissue becomes necrotic, damage term alcohol use
extends retroperitoneal tissue (3) Complication:
pancreatic cysts, abscesses, acute fluid collects in or
near pancreas

Acute Pancreatitis
Acute Pancreatitis
Clinical Manifestations
Severe abd pain -Major symptom - Clinical Manifestations
• From irritation, edema • (3) May be diffuse, • (3) Fever (4) Jaundice (5)
inflam pancreas to nerve difficult to locate • Ecchymosis may signify internal Mental confusion (6)
endings -Tension on • (4) May be a/w abd bleeding-notify MD stat agitation (7)
pancreatic capsule, obst Tachycar, cyanosis, cold
distentions (5) N/V- not • (1) Grey Turner’s Sign clammy skin (8)
Pancreatic duct relieve pain orSpots- Ecchymosis of flank, Acute renal failure
• (1)Main mid egigastrum (6) No relief w/anacid inidicates retroperitoneal common
bleeding. (2) • (9) Resp distress &
or LUQ & max pain (7) May dev rigid or board
several hr into illness. like abd-can remain soft Cullen’s Sign- hypoxia
Ecchymosis/bluish discoloration (10) Dyspnea
Penetrate& radiates to in absence of peritonitis (11) Tachypnea -abn
around umbilicus due to
back-*reason seek care* (8) May have poor intraperitoneal hemorrhage into rapid resp (12)
(2) Freq acute onset 24- defined palpable abd abd wall. (May be caused by
Abn bld gas values (13)
48 hr after heavy meal or mass (9)< peristalsis Steatorrhea-Stools bulky,
ruptured ectopic pregnancy or pale, foul smell, fatty
alcohol acute paancreatitis)

Pancreatitis Dx eval
Severe Pancreatitis (1) Serum amylase most reliable in 1st 24-48hr after
Clinical Manifestations onset of acute abd pain. Most widely used, but an
• Severe Pancreatitis (1) • (2) Subcutaneous fat absence
• (2) Urinary high level does
amylase • (4)not
WBC R/O disease (
Hypotension necrosis & cerebral Elevate & remain > nl 5000-10,000)
Hypovolemia abnormalities: longer than serum (3-35 • (5) Hyperglycemia
Hypoperfusion Belligerence, confusion, IU) lipase is solely • (6) Abd films-presence of
Hypotension reflects psychosis, & coma pancreatic origin (3) air in duodenal loop (7)
hypovolemia & shock • (3) Transient Serum lipase: specific Ultrasound-detect
caused by loss of lg amts hyperglycemia found in more accurate indicator pancreat edema (8)
of protein rich fluid into 50% pt due to damage of Peaks 24hr, rapid fall to Abn CT scan
tissue & peritoneal cavity islet cells normal by 48-72 hr (56-
Hypoperfusion 190 U/L) Lipase rise after • (9) Hypocalcemia
48 hr, stays up 5-7days
(0-110 units/L)

Pancreatitis-Medical Management
(a)Usually a/w massive fluid isolation. Acute Pancreatitis
(b)Fluid accumulates in bowel 2dary to ileus or in
peripancreatic region due to edema. Major Goals
(c)Fluid• lost
• (1) Replace fluids, correct (d) in emesis
Anticholinergics-< vagal • Relief of pain/discomfort
hypovolemia & restore elect stim, <Gi motility, inhibit
balance Ca+ Mag+ panc enzymes • Improved resp function
(2) Bld transfusions may be • (4) Dialysis- peritoneal
required for severed toxins (5) Narcotics- demerol
• Improved nutritional status
hemorrhagic (3) choice drug-mild pain • Maintenance of skin integrity
Attempts to suppress subsides 3-4d, severe up to
pancreatic exocrine 2wk • Absence of complicaitons
function: (a) NGT suction • *No morphine-spasm of
(b) Histamine H2 receptor sphincter of Oddi could
antagonists-< HCl prod so potentiate further
pancenzymes not activated pancreatic injury (6)
by acid ph © antacids- ABT not necessary in mild-
neutralize gastric secretions mod cases, more severe
cases may be

Acute Pancreatitis Acute Pancreatitis Nursing
Nursing Interventions Interventions - continued
• (1) Relieve • (2)NG suction *Remove • *Between acute attacks: diet
Pain/Discomfort gastric secretions, relive • (4) Improve breathing high in CHO, low fat, low
To < secretions of abd distention *BR to pattern *Semi-Fowlers to < protein. Avoid heavy meals,
pancreatic anzymes <metabolic rate pressure on diaphragm from alcohol
*Demerol(meperidine) <secretions of pancreatic distended abd & to > resp • If pancreas severe damaged
choice med expansion *Freq change of may need to replace
& gastric enzymes
*Avoid Morphine- position to prevent atelextasis pancreatic enzymes to
• (3)Pain> in severity & pooling or resp secretions replace enzyme deficit & aid
cause spasm of
sphincter of Oddi Notify MD *may *Assess Pulmonary by digestion. Pancrelipase
*NPO to < formation & have hemorrhage of monitoring pulse O2, ABGs & symptomatic Rx malabsorp
pancreas * may need C&DB syndrome Tab,cap,packet
secretion of sceretin
*Parental F/E to more analgesics (5)Nutrition Status
restore/maintain fluid *TPN-serum glucose monitor (6)Impared skin
q4-6h*Oral feeds > grad as integrity-turn q2h, Protect
acute S/S < from drainage

Acute Pancreatitis-Monitoring/Managing
Potential Complications Pancreatic enzymes
• (1) F/E Imbalance N/V, • Assess for ascites- • Lipolysis-hallmark of • Ca levels may remain < for 7-
movement of fluid from measure abd girth qd, pancreatic necrosis is 10 days If consistently
vascular compartment to enzymatic fat necrosis of the remain <8 assoc with poor
• Palpate abd for fluid wave,
peritoneal cavity, fever endocrine & exocrine glands prognosis
Wt daily. IV fluids-may
diaphoresis, gastric suction receive bld, albumin of pancreas by enzyme • Enzyme Replacement-
• Assess skin turgor, lipase. Fatty acids are give with meals or snacks to
• (2) Hypovolemia, released & combine with
Moistness of mucous aid in digestion &
membranes, Weight daily, shock, renal failure- ionized Ca to form a soap abdorption of fat & protein
Accurate I&O-urine, NG may be indicated by <BP, like product. Initial rapid Pancreatin
secretions, ect. <urine output lowering of serum CA not Pancrelipase (Cotazym) also
• (3) Pancreat necrosis- readily compensated for by contains CA carbonate to >
• Other factors for F/E parathyroid Body needs
Risk of hemorrhage, septic depleted CA levels
imbalance: >body temp, ionized CA, cannot
shock, multiple organ
wound drainage. usebound CA,hypoca occur
failure. May require debrid,
insert mult drains

Surgical Management Chronic Pancreatitis

• Done in four circumstances: • Pancreas repeatedly destroyed by flare ups of usually
• (1) uncertainty of dx mild attacks. Results in scarring,fibrosis, & damage is
• (2) Rx of pancreatic sepsis irreversible
• (3) Correction of associated biliary tract disease • In chronic as in acute: (a)
dull pain alternates w/severe pain (b) vomiting ©
• (4) Progressive clinical deterioration despite clinical fever (d) when sitting in bed with knees flexed &
intervention. pressing a pillow into abdomen pt may feel some relief
• If biliary pancreatitis: an endoscopic transduodenal (e) generally experiences more pain when lying supine
sphincterotomy may be done to remove a gallstone that (f) weight loss because pt feels more pain after eating
may be dislodged in Ampulla of Vater (g) signs of diabetes due to islet destruction

Chronic Pancreatitis
Diagnosis Treatment of Chronic Pancreatitis
• Dx: pancreatic enzyme • (1) Control pain (a)
analysis may be normal alcohol abstinence (b) • (3) Surgery
• radiographic control of diet © begin Pancreaticojejunosto
because of reduction in
visualization of bile & with non-narc analgesics my: anastomoses duct of
amount of functioning
pancreatic ducts then progress to narc Wirshung to side end of
tissue jejunum, to relieve pain.
• (d) Serum amylase • (2) Treatment of
(a) mild >of WBC count Helps relieve ductal obst
• (f) Urine amylase - endocrine dysfunction: in pt with pancreatic
(b) Ultrasound CT scan
Insulin therapy fibrosis
• © (ERCP) Endoscopic 2hr or 24 hr collection
Treatment of exocrine • Subtotal
Retrograde • (g) GTT may be done to pancreatomy: Resect up
dysfunction: Pancreatic
cholangiopancreatograph eval pancreatic islet cell enzyme therapy to 80%or remove organ
y most useful study to dx, function entirely
provides • Post op Complications:
diabetes & steatorrhea Rx-
insulin & enzymes

Pancreatic Tumors:
Whipple’s Procedure or
Radical Pancreaticoduodenectomy
• Surgery involves • common bile duct, and
resection of proximal stomach to the jejunum is
pancreas (proximal done
pancreatectomy), the • When pancreatitis is
adjoining duodenum confined to head of
(duodenectomy), the pancreas, resection of
distal portion of the distal stomach,
stomach (partial duodenum, common bile
gastrectomy) and the duct, GB and pancreas to
distal segment of the mid body. Islet cells are
common bile duct. excised and transplanted
• Anastomosis of the to prevent DM
pancreatic duct,