ASSESSMENT AND MANAGEMENT

OF PATIENTS WITH HEPATO BILARY

DISORDERS

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 Introduction
• The hepato biliary system is an accessory
system of the GI conations the liver, gall
bladder and pancreas
• The liver, the largest gland of the body,
It is a chemical factory that manufactures,
• Stores,
• Alters, and
• Excretes a large number of substances
involved in metabolism.

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Diseases of the Liver

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 Physiology of liver

The Role of the Liver in digestive processes

The location of the liver is essential in this function

because
•It receives nutrient-rich blood directly from the
gastrointestinal (GI) tract and
•Then either stores or transforms these nutrients into
chemicals that are used elsewhere in the body for
metabolic needs.

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 Gastrointestinal Physiology
Functions of liver
• Storage, metabolism & release of nutrients & some
vitamins.
• Detoxification and elimination of toxins, drugs &
metabolites.
• Synthesis of biologically important protein such as
albumin, clotting factors, apolipoproteins.
• Synthesis & secretion of bile important for lipid
digestion & absorption.
• Role in immune function & clearance of intestinally
absorbed bacteria. 6
Gastrointestinal Physiology
Bile pigments (Bilirubin):

End product of Hgb degradation in the monocyte-

macrophage system in the spleen, bone marrow, and liver.

Bilirubin is transported in the blood bound with albumin,

otherwise free bilirubin is toxic.

Bilirubin is taken by the liver in its free form and

conjugated with glucuronic acid to form a non-toxic water
soluble bilirubin glucuronide that is finally secreted to the
bile canaliculi & excreted.
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Gastrointestinal Physiology

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 Liver Anatomy

• Liver is the largest

gland of the body.

• The liver is divided into

right and left lobes by
the external marking of
the falciform ligament.

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• The blood that perfuses the liver comes
from two sources.
– Approximately 70% of the blood supply
comes from the portal vein, which
drains the GI tract and
– Rich in nutrients but lacks oxygen.
– The remainder of the blood supply enters
by way of the hepatic artery and rich in
oxygen.

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 Portal v. 70%

Hepatic a. 30%

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 Assessment and Diagnostic Findings

• The liver and spleen are often moderately enlarged

for a few days after onset; otherwise, apart from
jaundice, there are few physical signs.

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 P/E: Percussion
• Liver Span

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 P/E: Palpation
• Palpation: On inspiration, the liver is palpable about
3 cm below the right costal margin in the mid-
clavicular line.

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Hooking Technique

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 Liver Function Test
• More than 70% of the parenchyma of the liver
may be damaged before liver function test results
become abnormal.
• Function is generally measured in terms of:
a) serum enzyme activity (ie, alkaline
phosphatase, lactic dehydrogenase, serum
aminotransferases)
b) serum concentrations of proteins (albumin and
globulins), bilirubin, ammonia, clotting factors,
and lipids.
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 LFT
• Serum aminotransferases (also called transaminases)
are sensitive indicators of injury to the liver cells and
are useful in detecting acute liver disease such as
hepatitis.
Alanine aminotransferase (ALT) (formerly called
serum glutamic-pyruvic transaminase [SGPT]),
Aspartate aminotransferase (AST) (formerly called
serum glutamic-oxaloacetic transaminase
[SGOT]), and
Gamma glutamyl transferase (GGT) (also called
G-glutamyl transpeptidase)
• The most frequently used tests of liver damage. 19
 Cont…d

1. Liver enzymes: Damage to hepatocytes causes release of

intracellular enzymes like ALT and AST. Normal levels
range between 0 and 35 U/L. In acute hepatitis, they
often rise to 20 fold or more.
2. Serum bilirubin: normal levels range between 0.3 and 1
mg/dl. When levels go above 2.5 -3.0 mg/dl jaundice
appears (called icteric hepatitis)
3. Alkaline phosphatase may be increased by about 3 fold
except in cholestatic hepatitis, in which the increment is
very much higher.

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Test Normal Clinical functions
Pigment Studies
Serum bilirubin, 0–0.3 mg/dL (0–5.1 µmol/L) These studies
direct measure the ability
Unconjugated < 1.1 mg/dL (< 19 µmol/L) of the liver to
bilirubin conjugate and
Serum bilirubin, 0.3–1.2 mg/dL (1.7–20.5 excrete bilirubin.
total µmol/L)
Urine bilirubin 0(0)
Urine 0.05–2.5 mg/24 h (0.09–4.23
urobilinogen µmol/24 h)
Fecal 40–200 mg/24 h (0.068–0.34
urobilinogen mmol/24 h)
(infrequently
used) 21
Protein Studies
Total serum 7.0–7.5 g/dL Proteins are manufactured by the liver.
protein (70–75 g/L) Their levels may be affected in a
Serum 4.0–5.5 g/dL variety of liver impairments.
albumin (40–55 g/L) Albumin: Cirrhosis
Serum 1.7–3.3 g/dL Chronic hepatitis
globulin (17–33 g/L) Edema, ascites
Globulin: Cirrhosis
Liver disease
Chronic obstructive jaundice
Viral hepatitis
Albumin/glo A > G or 1.5:1– A/G ratio is reversed in chronic liver
bulin (A/G) 2.5:1 disease
ratio (decreased albumin and increased
globulin)
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Test Normal Clinical functions
Serum Aminotransferase or Transaminase Studies
AST (SGOT) 10–40 units (4.8–19 The studies are based on release
U/L) of enzymes from damaged liver
ALT (SGPT) 5–35 units (2.4–17 U/L) cells. These enzymes are elevated
in liver cell damage.
Serum 20–120 µg/dL (11.1– Liver converts ammonia to urea.
Ammonia 67.0 µmol/L) Ammonia level rises in liver
150–250 mg/dL (3.90– failure.
6.50 mmol/L)

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 Management of
Patients with Hepatic
Disorders

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 Definitions for Hepatitises
 Acute: Short term and/or severe.
 Chronic: Lingering or lasting - may or may not be severe
 Fulminant: Developing quickly and lasting a short time,
high mortality rate.
 Cirrhosis: Hardening: may be the result of infection or
toxins (e.g. alcohol)
 Jaundice: Yellowing of the skin, eyes, etc due to raised
levels of bilirubin in the blood due to liver damage.
 Hepatocellular carcinoma： is closely associated with
hepatitis B, and at least in some regions of the world with
hepatitis C virus.
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 Types of hepatitis
• Two types of hepatitis, which are defined
based on duration:
– Acute hepatitis: lasts for about 6 months or less.
– Chronic hepatitis: for over 6 months

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 Hepatic Dysfunction
Results from damage to the liver’s
parenchymal cells, either directly from
primary liver diseases or
Indirectly from obstruction of bile flow or
derangements of hepatic circulation.
May be:
 Acute or
Chronic (more common)-cirrhosis of
the liver
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 Causes of HD:
1. Infectious
 viral (Hepatitis A,B,C,D,E,G)
 bacterial ,protozoa and fungal
2. Non infectious
 Alcohol
 Toxins
 Autoimmune
 Metabolic disorders

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 The most common and significant
symptoms of liver disease

Jaundice

Portal hypertension, ascites, and varices

Hepatic encephalopathy or coma

Nutritional deficiencies

Hematologic problems

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 Brain storming

1.What do we mean by jaundice?

2.How many types of jaundice do you know?

3.Which type do you think is/are associated with

liver disease?

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 I JAUNDICE
Yellow or green tinged body tissues including
the sclera, and skin due to increased serum
bilirubin levels (>2.5 mg/dl)
Is a cardinal symptom of liver or gallbladder
disease and RBC disorders
It may result from impairment of
Hepatic uptake,
Conjugation of bilirubin, or
Excretion of bilirubin into the biliary system.

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Cont…d

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Why sclera tissue of the eye have yellow color
before the skin?
Types of JAUNDICE
Hemolytic
Hepatocellular
Obstructive
• Hepatocellular and obstructive jaundice are
commonly associated with liver disease.
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 I. Hemolytic/ Prehepatic Jaundice
Results from an increased destruction of the
red blood cells
Although functioning normally, liver cannot
excrete the bilirubin as quickly as it is formed.
Flood the plasma with unconjugated bilirubin
so rapidly
Causes
Hemolytic transfusion reactions
Sickle cell crisis
Hemolytic anemia
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Bilirubin Metabolism

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 …hem.j cont
• The bilirubin in the blood is predominantly
unconjugated or free.

• Fecal and urine urobilinogen levels are

increased, but the urine is free of bilirubin.

• Patients with this type of jaundice, unless

their hyperbilirubinemia is extreme, do not
experience symptoms or complications.
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II. Hepatocellular/ hepatic Jaundice

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 Hepato-cellular Jaundice Cont’d…
Causes of cellular damage
Infection by viral hepatitis or other viruses
Medication or chemical toxicity or alcohol
Hepatic carcinoma
Lab Tests:
 ed unconjugated serum bilirubin
 ed AST & ed ALT levels

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 III. Obstructive / Posthepatic Jaundice
Is due to impended or obstructed flow of bile
A. Intrahepatic obstruction
 May involve obstruction of the small bile ducts within
the liver
 Can be caused by
 Pressure on these channels from inflammatory
swelling of the liver
 Inflammatory exudate within the ducts themselves

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 Obstructive Jaundice Cont’d…

B. Extra-hepatic obstruction

 Caused by occlusion of the bile duct by a gallstone,

an inflammatory process, a tumor, or pressure
from an enlarged organ

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 Obstructive Jaundice Cont’d…
Clinical Findings
Bile backed up into the liver substance

Reabsorbed into the blood

Carried throughout the entire body

Staining the skin, mucous membranes, and

sclera
Deep orange and foamy urine
Light or clay-colored stool
The skin may itch intensely
Intolerance to fatty foods 41
 Obstructive Jaundice Cont’d…

Lab tests:
AST, ALT levels generally rise only
moderately,
increased conjugated and unconjugated
bilirubin

no fecal or urinary urobilinogen

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 Portal
Hypertension

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The Portal Venous System

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 Portal hypertension (PHpn)
Normal pressure in the portal vein is 5 to 10
mmHg

Obstructed blood flow via the damaged liver

results in increased blood pressure

PHpn is commonly associated with hepatic

cirrhosis

It can also occur with noncirrhotic liver disease like

thrombosis, or clotting in the portal vein

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PP Alcoho Abuse, Infection, Drugs, Bilary Obstruction

Destruction of Hepatocytes

Replacement of destroyed liver cells gradually by scar tissue

The amount of scar tissue exceeds that of the functioning liver tissue

Fibrosis/Scar Jaundice

DHN
Impaired blood and lymph flow
 ed pressure in the venous & sinusoidal channels BP
Fatty infiltration—fibrosis/scar

Ascites
Hepatomegally Portal
Splenomegaly Hypertension 46
Esophageal varices
 PHpn C/Ms
GI bleeding/ Varices

Spleenomegally

Ascites

Hepatic encephalopathy

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 Ascites
Ascites is the accumulation of fluid in the
peritoneal cavity
Risk factors
 Cirrhosis—for 80% of cases
 Renal factors: stimulation of RAA system
 Other conditions like
 Congestive heart failure

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 PP Portal Hypertension/Resistance
to Blood Flow

Leakage of plasma Vasocongestion

into liver lymphatics within intestinal
vasculature
Production of liver
Transudation of plasma
lymph with high
into the abdominal
protein
cavity
Leakage of lymph
into abdominal
Ascites
cavity with
osmotic
gradient Leakage of plasma
between out of vascular
lymph & ECF
space
Intravascular oncotic pressure

Albumin production

Hepatocyte Dysfunction 49
 Clinical Manifestations
 ed abdominal girth
Bulging of flanks
Shifting dullness
Fluid wave/trill
Everted umbilicus (severe)
Rapid weight gain
SOB
Visible striae and distended veins over the
abdominal wall
Signs of dehydration
Decreased urine output
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Assessing for abdominal fluid wave

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 Management of Ascites

Dietary Modification
Diuretics
Bed rest
Paracentesis
Insertion of a peritoneovenous shunt

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 Esophageal Varices

 A complex of longitudinal tortuous and extremely

dilated sub-mucosal veins at the lower end of the
esophagus, enlarged and swollen as the result of
portal hypertension

 The vessels are especially susceptible to

hemorrhage.

 Bleeding or hemorrhage from esophageal varices

occurs in approximately one third of patients with
cirrhosis and varices

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 Factors that contribute to hemorrhage
Straining at stool
Sneezing, coughing, or vomiting
Esophagitis
Irritation of vessels by poorly chewed foods or
course foods or irritating fluids
Reflux of stomach contents (especially alcohol)
Liver cirrhosis

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Endoscopic Sclerotherapy

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 Hepatic Cirrhosis

 Characterized by irreversible chronic injury

of the hepatic parenchyma

 Extensive degeneration and destruction of the

liver parenchyma cells and by replacement of liver
tissue by fibrous scar tissue.

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 Types of cirrhosis or scarring of the liver:

A. Alcoholic cirrhosis
Frequently due to chronic alcoholism for
decades, resulting in:
Chronic inflammatory
Toxic effects on the liver
Blocking the normal metabolism of protein, fats,
and carbohydrates
Scar tissue characteristically surrounds the portal
areas
Is the most common type of cirrhosis
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 Types of Cirrhosis Cont’d…
B. Postnecrotic cirrhosis
There are broad bands of scar tissue as a
late result of a previous bout of acute viral
hepatitis (hepatitis B or hepatitis C)
C. Biliary cirrhosis
Scarring occurs in the liver around the bile
ducts
Is the result of chronic biliary obstruction
and infection (cholangitis)
Much less common
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 Clinical manifestation
Early manifestation
 Palpation of liver reveals a firm, lumpy, (nodular),
usually enlarged liver.
 GI disturbance – anorexia, nausea, vomiting…
 Hepatomegally
 Pain
Late manifestation
 Ascites, gastro intestinal bleeding from varices
 Encephalopathy, splenomegally, jaundice, skin
lesion, Anemia
 Sodium and fluid retention

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 Diagnosis
History  Liver scans/biopsy- Detects fatty
Physical infiltrates, fibrosis, destruction of hepatic
tissues, tumors
Exam
 Esophagogastroduodenoscopy (EGD)-
Diagnostic demonstrate presence of esophageal
Studies varices
 Electrolytes: Hypokalemia
 Urine urobilinogen: May/may not be
present.
 Fecal urobilinogen: Decreased.

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 Dx
 Increased Serum bilirubin
 Increased Serum ammonia: because of inability to
convert ammonia to urea.
 Decreased Serum glucose: impaired glycogenesis
 Decreased Serum albumin
 CBC: Hb/Hct and RBCs may be decreased because
of bleeding
 Increased Liver enzymes

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 Medical Management
Symptomatic management
Identifying and treat the cause
Vitamins and nutritional supplements
Potassium-sparing diuretics (spironolactone,
triamterene)--to decrease ascites
Avoidance of alcohol

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 Nursing Diagnoses may include:
Activity intolerance related to fatigue, general debility,
muscle wasting, and discomfort
Imbalanced nutrition, less than body requirements,
related to chronic gastritis, decreased GI motility, and
anorexia
Impaired skin integrity related to compromised
immunologic status, edema, and poor nutrition
Fluid Volume excess related to compromised regulatory
mechanism (e.g., syndrome of inappropriate antidiuretic
hormone [SIADH], decreased plasma proteins,
malnutrition) or excess sodium/fluid intake evidenced by
edema, anasarca, weight gain
Knowledge, deficient regarding condition, prognosis,
treatment, self-care, and discharge
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Thanks for your
time &attention

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