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
Filtration

CHO Metabolism Lipid (Fat) Metabolism

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

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

1
 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.

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

Assessment of Abnormal Lab Findings in

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

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

Diagnostic Studies for Liver Diagnostic Studies of Liver - continued

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

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)

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

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

4
 Hepatitis D
• Transmission: Same as for HBV. Causes infection as a
complication of Hep B, infection only together with HBV.
Incomplete RNA virus
• Incubation: Not firmly est in humans. HBV infection
must precede HDV. Chronic carriers of HBV are at risk
throughout their carrier state.
• Dx: Anti-HDV IgM -current infection
• Anti-HDV IgG-past infection
• Prognosis: May be acute or short lived or become
chronic.
• Prevention: Same as for HBV.HBV vaccine for all at risk
will also prevent HDV infection.
Hepatitis - Isolation Precautions
• Isolation Precautions:
• Private room only necessary for pt with poor hygiene
• Gown if direct soiling possible
• Gloves if direct body fluid contact
• Linen: other places double bag
• Specimens: Label enteric precautions/blood & body fluid
precaution

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
present
• 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
(hyperbili)

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

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

6
 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

7
 Assessment-
food pref -see if excessive fat & CHO are
in diet
• Ask whether any foods are
not tolerated. Ask whether
the following GI symptoms
occur in R/T intake of fatty
foods:
• Flatulence
• Dyspepsia (indigestion)
• Eructation (belching)
• anorexia
• Nausea/vomiting
• Abdominal pain or
discomfort or heaviness
Dx Tests
• May >serum levels of
alkaline phosphatase,
AST, SGOT, LDH =abn
liver function
• Direct (conjugated) &
Indirect (unconjugated)
serum bilirubin levels > if
obst process is present
• >WBC=inflammation
• Pancreatic involvement-
serum & urine amylase
levels>
Dx Tests-Continued
Endoscopic Rerograph
Cholangiopancreatography
• Used both radiography &
• Oral Cholescintigraphy
• Dx acute cholecystitis &
early biliary duct obs
(PIPIDA SCAN) IV injection endoscope advanced
o an agent, gamma camera
takes serial images over an
hour to record the agents
progress through the liver,
biliary ducts, GB, and
duodenum. Lacks resolution calculi& stenosis
needed to detect stones
• Ask whether pain occurs
after pt has eaten a high
fat or high volume meal
or after assuming a
recumbent position.
• Abd Palpatation:
• GB tender on palpation
• Guarding & ridigity,
rebound tenderness
(Blumberg’s sign)
indicate peritoneal
irritation
• Cholecystitis
suspected-Oral
cholecystogramOCG
(not done if serum
bilirubin >1.8mg/dl) or
GB radiographic series
to confirm presence of
biliary tract disease.
• HIDA scan-detects abn
hepatobiliary function
• Upper GI series to R/O
other cause of abd
pain-Gastritis & Peptic
ulcer disease
endoscopy to examine
the pancreatic ducts &
hepatobiliary tree.
Procedure-side view
thru pt mouth until
reaches ampulla of vater.
Contrast media then
injected. Can help dx
pancreatic & biliary duct
disease, locate cysts,
Physical Clinical S/S
• if GB is inflamed. Deep
inspiration can be very
• Vague abd pain-may limited. Test used also
radiate to rt shoulder. for dx Ca GB &
When RUQ pain & cholecystitis.
tenderness suggest acute
• Pain triggered by high
cholecystitis look for fat, high volume meal,
Murphy’s sign - pt is or from recumbant
asked to inhale when position
examiner’s fingers are
hooked under the liver • Anorexia, rebound
tenderness (Blumbergs
border at bottom of rib
cage. Inspiration causes sign), fever, Jaundice
the GV to descend onto the • Clay colored stools,
fingers, producing pain steatorrhea (fatty
stools)
Dx Tests-continued
Oral Cholecystography
• Oral Cholecystography • Procedure-24hr pre test,
Uses an iodine based pt takes dye in tab from
with water. Films taken to
dye, visualized the GB &
ductal system. Liver asses GB ability to
concentrate dye. Pt eats
extracts the dye from the fatty meal. Dr takes more
bld & excretes it into bile.
films to assess GB
If GB does NOT show on contractile ability. *Before
film, stones may have test check for allergies.
obstructed it. Withhold food & fluids
before test.
Nsg Dx
• High risk for altered GI tissue perfusion F/T risk of
obstruction by gallstones
• High risk for fluid volume deficit R/T hypovolemia from
severe vomiting
• Sleep pattern distrubance R/T acute pain
• Anxiety R/T pain & possible surgery
• Altered nutrition: More than body requirements R/T
excessive dietary fat intake
8
 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
• Initally pain is a steady
• Familial (or due to dietary
habits-excessive dietary CHO epigastric area, same as
intake)
• Obese-impaired fat
metabolism
• Diets-<cal, liquid protein-
cause liberation of CHO from
tissues which are excreted as
crystals in bile
• Pregnant-delay GB empty
Chron’s disease
• Type 1 DM
S/S
mild ache in mid
choleystitis
• Biliary colic-cystic duct of
GB obstructed. Intense
pain as spasm tries to
push stone thru duct-so
severe accom by
tachycardia, pallor,
diaphoresis, extreme
exhaustion
Some asymptomatic, most c/o spastic or steady pain
• Pain may last several hr,
stems from GB distention (in
case of cystic duct stones) or
from spasm of sphincter of
Oddi or ductal muscles.
• Pain begins in
midepigastrium, radiates
RUQ, Rt shoulder & back.
• N/V may accom pain
• After attack, area over GB
may be tender 24-72 hr
• Fever & chills may
result from inflamm
• May cause infection
• if stone in bile duct will
cause jaundice: before
frank jaundice sets in
may notice lt stools,dark
urine
• Attacks usually due to
fat intolerance:
Inflammed GB contracts
to release bile for fat
digestion, possibly
precipitates pain.

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

9

Cholelithiasis - Rx
• Extracorporeal Shock
Wave Lithotripsy
shock waves
shatter gallstones.
3 or
fewer CHO stones,
function GB, no Hx of
liver or pancreatic
disease, no pacemaker
or pregnant.
Once
shattered, travel thru
biliary ductal system to
be excreted via
intestines
Surgical Management -
Traditional Cholecystectomy
• Pre-op
• Focus to prevent resp
complicatoins. Instruct
Deep breath, cough, turn.
Use splint. Pt reluctant
due to hight incision Rt
subcostal area & surgical
manip near diaphragm.
Incentive spirometer.
OOB evening of or 1st
day post op
Traditional Cholecystectomy -
Post op continued Nsg Care T-Tube
• consistency, odor of
• Pain-controlled with IM
Demerol or PCA pump.
*Morphine not given due to
resp complications R/T abd
incision.
• N/V-antiemetics
• Drain-surgeon removed dsg
& drain by 24-48 hr
• T-Tube-may remain in place
6 wk or longer
• Nsg Care T-Tube
Assess amt color,
• Percutaneous
Transhepatic Biliary
Catheter Insertion
Catheter decompresses
obstructed extrahepatic
ducts so bile can flow.
Common for inoperable
hepatic, pancreatic or
bile duct CA. Non
surgical option for poor
surgical risks for Rx of
biliary obst. due to
gallstones
• Post op
• Avoid kinking the tube
• Normally drains 300-500cc
brown green bile 1st 24 hr
• Drainage gradually <to 200-
400cc/d
• Clamp tube 1-2hr before meals
& unclamp 1-2 hrs after eating.
• Pt may experience abd pain,
nausea, amber urine, clay
stools-unclamp
drainage q4h then q8h.
Initial post-op bloody
drainage, changes to
green-brown bile. Bile
output 400cc/day with
gradual >in amt.
Report bile drainage
>500-1000cc/day.
*Collect & admin excess
bile output to pt by NGT
or give synthetic bile salts
(Decholin)
Surgical Management Traditional
Cholecystectomy Usual surgical Rx for pt with
acute & chronic cholecystitis
• Cholecystectomy: excises
GB & ligates the cystic
duct. Body adapts by > bile
flow into duodenum. Druing
surgery may explore
common bile duct for
additional stones or
perfrom a cholangiogram to
ID any retained stones.
Ductal manipulation leads
to inflammation. MD will
insert a T tube after
exploring the common.
Traditional Cholecystectomy -
Post op continued
• Report an output >500cc in 24
hr to MD. May need to receive
T-tube at level of abd to avoid
excessive drainage. Excessive
drainage may indicate
obstruction-excessive bile
drainage can be returned to pt
via NGT or in fruit juice
• Within 7 days after surgery, MD
removes tube after evaluating
results of
Traditional Cholecystectomy
post op continued
• Report sudden > in bile
output after a normally <
amount (9-10days post).
• Inspect skin around T-tube
site. Change dsg daily, keep
dsg dry.
• Maintain in Semi-Fowlers
position-keep drainage
system below level of GB.
Never irrigate, aspirate, or
clamp without MD order
• Raise drainage bag to
• bile duct. Permits bile
drainage during healing
• Operative Procedure:
Removes GB &
explores CBD, T-tube
inserted to ensure
patency of the duct.
Penrose/JP(Jackson
Pratt drain) inserted in
GB bed to prevent fluid
accumulation. Drainage
serosanguinous & bile
stained in first 24 hr
post op
• T-tube cholangiogram. If
stones are located during
this test, they can be
removed without further
surgery.
• Weeks or even years
after surgery, pt may still
develop signs of GB pain,
frequently due to retained
or newly formed stones.
• level of abd (4-5days
post) Assess for
feelings of fullness,
nausea, or pain.
• Clamp T-tube for 1-2 hr
before & after meals,
assess tolerance for
food
• Observe stools for
return of brown color 7-
10 days post op
• Diet -Early post op if
bile flow < give low fat
diet. Usually no special
diet.
10
 Laparoscopic Laser Cholecystectomy
Another Surgical Management for acute & chronic
cholecystitis - Less invasive than traditional
• Not used for pt with
(1)extensive abd
symptoms in past
• (2)Severe acute
cholecystitis
• (3)Palpable gallbladder
• Pre-op: (a)Out pt or
overnight (b) NPO
• Operative: 10mm midline
puncture at umbilicus
Abd cavity insufflated
with carbon dioxide to a
Foods to avoid pt with
Cholecystitis/Cholelitiasis
• Dairy
• Whole milk
Ice cream
Butter Cream
Cheese
• Fried Fatty Foods
• Rich pastries Gravies
Nuts Chocolate
Egg Yolks
Avocado
Pancreas functions
• Exocrine: Enzymes
produced empty directly
into duodenum
• Function: Facilitate
digestion thru secretion of
enzymes into proximal
duodenum
• pressure of 15-20mm
Hg. Trocar catheter
inserted, a laparoscope
is introduced, attached
to video camera, & abd
organs viewed on
monitor. 3 small
punctures to introduce
laproscopic forceps.
Laser used to dissect
GB away from liver bed
& close off cystic artery
& duct. GB extracted
thru midline puncture.
• Gas Forming
• Cabbage Onions
Broccoli
Cauliflower
Sauerkraut Radishes
Cucumbers
Beans
• Endocrine: hormones
produced directly enter
blood steam
• Function: Capable of
neutralizing highly acid
gastric juices that enter
duodenum. Secretions
into pancreatic duct, joins
common bile duct, enters
duodenum at Ampulla of
Vater.
Laparoscopic Laser
Cholecystectomy
• Post op “Free air pain”- from
CO2 retention in the abdomen.
To prevent this, Nurse teaches
pt that early ambulation
promote absorption of CO2.
Pt returns to usual
activities 3-7 days after
Pancreas
• Location: Between
stomach & small
intestine. Triangular
gland, its tail next to
spleen, head next to
duodenum.
• Primary enzyme
producing organ of
digestive system
Produces 1-1.5L of
pancreatic juice every
day.
Pancreas
Exocrine & Endocrine Function
• Exocrine function:
Secretions include: (1)
Amylase-aids digestion of
CHO (2) Trypsin-aids
digestin of protein (3)
lipase-aids digestion of
fats
• Diet Based on pt
tolerance to fats. Special
diet may not be needed.
Low fat if poor tolerance
to fats,may need for 6
• months, add fatty foods
as tolerated
• Pancreatic Juice is clear
with high bicarbonate
content. Secretions
controlled by vagus nerve
& effect of intestinal
hormones secretin &
cholecystokinin
• Pancreatic secretions
contolled by hormones
from GI tract
• Endocrine Function:
Isles of Langerhans:
endocrine part of
pancreas. Cells in
pancreatic tissue alpha,
beta, delta cells (1)
Alpha-produce glucagon
(2) Beta produce insulin
(3) Delta secrete
somatostatin
11
 Pancreas
Endocrine Function
• Insulin: Major function-
(1)<blood glucose. Stored
as glycogen or used for
energy (2) Promotes
storage of fat in adipose
tissue & synthesis of
protein in various body
tissues (3) Rate of
production regulated by
level of glucose in blood
• Glucagon:> bld gucose
by converting glycogen to
glucose in lever.
Somatostatin:
Hypoglycemic effect-
interferes w/release of
growth hormone from
pituitary & glucagon of
pancreas CHO
Metabolism: Cho
converted primarily to
glucose. Controls level
bld glucose synthesize
Pancreas
• Disorders of the Pancreas:
Pancreas has exocrine and endocrine
functions. The exocrine glands called acini aid digestion
by secreting 500-1000 ml of pancreatic juice daily.
Contains mainly water, bicarb,
enzymes, potassium, sodium, chloride, and calcium.
• Pancreas Digestive Functions
Secretes (1)Digestive Enzymes
(a) Amylase (b) Lipase
© Trypsinogen
(2) Bicarbonate Juice

Pancreatitis Pancreas -Pathophysiology

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

12
 Acute Pancreatitis
Clinical Manifestations
Severe abd pain -Major symptom -
• From irritation, edema
inflam pancreas to nerve
endings -Tension on
pancreatic capsule, obst
Pancreatic duct
• (1)Main mid egigastrum
or LUQ & max pain
several hr into illness.
Penetrate& radiates to
back-*reason seek care*
(2) Freq acute onset 24-
48 hr after heavy meal or
alcohol
• (3) May be diffuse,
difficult to locate
• (4) May be a/w abd
distentions (5) N/V- not
relieve pain
(6) No relief w/anacid
(7) May dev rigid or board
like abd-can remain soft
in absence of peritonitis
(8) May have poor
defined palpable abd
mass (9)< peristalsis
Acute Pancreatitis
Clinical Manifestations
• (3) Fever (4) Jaundice (5)
• Ecchymosis may signify internal Mental confusion (6)
bleeding-notify MD stat agitation (7)
Tachycar, cyanosis, cold
• (1) Grey Turner’s Sign clammy skin (8)
orSpots- Ecchymosis of flank, Acute renal failure
inidicates retroperitoneal common
bleeding. (2) • (9) Resp distress &
Cullen’s Sign- hypoxia
Ecchymosis/bluish discoloration (10) Dyspnea
(11) Tachypnea -abn
around umbilicus due to
intraperitoneal hemorrhage into rapid resp (12)
abd wall. (May be caused by
Abn bld gas values (13)
Steatorrhea-Stools bulky,
ruptured ectopic pregnancy or pale, foul smell, fatty
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 (
>10,000
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

13
 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
balance
acute S/S < from drainage

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

Surgical Management Chronic Pancreatitis

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

14
 Chronic Pancreatitis
Diagnosis
• Dx: pancreatic enzyme
analysis may be normal
because of reduction in
amount of functioning
tissue
(a) mild >of WBC count
(b) Ultrasound CT scan
• © (ERCP) Endoscopic
Retrograde
cholangiopancreatograph
y most useful study to dx,
provides
Pancreatic Tumors:
Whipple’s Procedure or
Radical Pancreaticoduodenectomy
• Surgery involves • common bile duct, and
resection of proximal
pancreas (proximal
pancreatectomy), the • When pancreatitis is
adjoining duodenum
(duodenectomy), the
distal portion of the
stomach (partial
gastrectomy) and the
distal segment of the
common bile duct.
• Anastomosis of the
pancreatic duct,
• radiographic
visualization of bile &
pancreatic ducts
• (d) Serum amylase
• (f) Urine amylase -
2hr or 24 hr collection
• (g) GTT may be done to
eval pancreatic islet cell
function
stomach to the jejunum is
done
confined to head of
pancreas, resection of
distal stomach,
duodenum, common bile
duct, GB and pancreas to
mid body. Islet cells are
excised and transplanted
to prevent DM
Treatment of Chronic Pancreatitis
• (1) Control pain (a)
alcohol abstinence (b)
control of diet © begin
with non-narc analgesics
then progress to narc
• (2) Treatment of
endocrine dysfunction:
Insulin therapy
Treatment of exocrine
dysfunction: Pancreatic
enzyme therapy
• (3) Surgery
Pancreaticojejunosto
my: anastomoses duct of
Wirshung to side end of
jejunum, to relieve pain.
Helps relieve ductal obst
in pt with pancreatic
fibrosis
• Subtotal
pancreatomy: Resect up
to 80%or remove organ
entirely
• Post op Complications:
diabetes & steatorrhea Rx-
insulin & enzymes
15