INDEX

Sr.# Description page#

1 Cirrhosis of Liver 3
2 Introduction 4
3 Definition 5
4 Incidence 5
5 Types of cirrhosis 11
6 Pathophysiology 13
7 Clinical manifestations 15
8 Management Medical 23
9 Surgical management 25
10 References 26
Subject: Pathophysiology
Topic: Cirrhosis of liver
Submitted to: Madam abida aslam
Submitted by: Shazia parveen
Submission date: 26_07_2021
Post RN BSN(2nd semester)
College of Nursing,
King Edward Medical University, Lahore.
 Cirrhosis of Live

Introduction
The term cirrhosis was first used by Rene
Laennec to describe the abnormal liver color of
individuals with alcohol induced liver disease.
Derived from Greek word Kirrhos means
Yellowish brown color.

Cirrhosis is a chronic progressive disease of the

liver characterized by extensive degeneration
and destruction of the liver parenchymal cells.
The liver cells attempt to regenerate, but the
regenerative process is disorganized, resulting in
abnormal blood vessels and bile duct
architecture.
The liver slowly deteriorates and malfunctions
due to chronic injury.
Scar tissue replaces healthy liver tissue, partially
blocking the flow of blood through the liver.
Scarring also impairs the liver's ability to:
control infections
remove bacteria and toxins from the blood
process nutrients, hormones, and drugs
make proteins that regulate blood clotting
produce bile to help absorb fats—including
cholesterol—and fat-soluble vitamins

Definition
cirrhosis is defined as a diffuse process
characterized by fibrosis and the conversion of
normal liver architecture into structural
abnormal nodules

Incidence
The overall incidence of cirrhosis in the US is
approximately 360 per 100,000 population
It is the 10th leading cause of death in the US,
with mortality rate of 9.2 deaths per 100,000
populations. Of those deaths, 45% were alcohol
related. Men are more likely than women to
have alcoholic cirrhosis.
Worldwide, post necrotic cirrhosis is the most
common in women. Mortality is higher from all
types of cirrhosis in men and non whites.

Etiology:
 Not clearly defined
 Alcohol.
Heavy alcohol for several years can cause
chronic injury to the liver and damages.

For women, consuming two to three drinks—

including beer and wine per day and for men,
three to four drinks per day, can lead to liver
damage and cirrhosis.
A common problem in alcoholic is protein
malnutrition.

 Obesity:

 WHO ,2008, estimated that more than 200

million men and close to 300 million women
 were obese, obesity is a common cause of
chronic liver disease , 17% of liver cirrhosis
is attributable to excess body weight. 4.
Chronic hepatitis C. Chronic hepatitis C
causes inflammation and damage to the liver
over time that can lead to cirrhosis and
approximately 20% patient will develop
cirrhosis.
 Chronic hepatitis B and D.

Hepatitis B and D is virus that infects the

liver and can lead to cirrhosis, but it occurs
only in people who already have hepatitis B.
 approximate 10%- 20% will develop
cirrhosis.
 Nonalcoholic fatty liver disease (NAFLD).
This is associated with obesity, diabetes,
protein malnutrition, coronary artery
disease, and corticosteroid medications.
Autoimmune hepatitis. It is caused by the
body's immune system attacking liver cells
and causing inflammation, damage, and
eventually cirrhosis.
 Genetic factors -About 70 percent of those
with autoimmune hepatitis are female.
Diseases that damage or destroy bile ducts.
Several different diseases (cholangitis) can
damage or destroy the ducts that carry bile
from the liver, causing bile to back up in the
liver and leading to cirrhosis.

 Inherited diseases. Cystic fibrosis, alpha-1

antitrypsin deficiency, hemochromatosis,
 Wilson disease, galactosemia, and glycogen
storage diseases are inherited diseases that
interfere the liver function properly,
cirrhosis can result.
 Drugs, toxins, and infections. drug
reactions (Acetaminophen, isonazide ,
methotrexate) prolonged exposure to toxic
chemicals, parasitic infections, and repeated
bouts of heart failure with liver congestion.
 Types of cirrhosis

I. Alcoholic (historically called Laennec’s

cirrhosis) cirrhosis:
also called micro nodular or portal cirrhosis
and usually associated with alcohol abuse.
The first change in the liver from excessive
intake is an accumulation of fat in the liver
 cells; uncomplicated fatty changes in the liver
are potentially reversible if the person stops
drinking alcohol.
If the alcohol abuse continues, widespread
scar formation occurs throughout the liver.
II. Post necrotic cirrhosis ( macro nodular):most
common worldwide , massive loss of liver
cells with irregular patterns of regenerating
cells due to complication of viral, toxic or
idiopathic (autoimmune) hepatitis.
III. Billiary cirrhosis: is associated with chronic
billiary obstruction and infection. There is
diffuse fibrosis of the liver with jaundice.
Cardiac cirrhosis: chronic liver disease
results from long-standing, severe right side
heart failure with corpulmonale, constrictive
pericarditis, and tricuspid insufficiency.
Pathophysiology: Liver insult due to
alcohol ingestion, viral hepatitis, exposure to
toxin Hepatocyte damage Liver inflammation -
↑WBCs, nausea, vomiting, pain, fever, anorexia,
fatigue Alteration in blood and lymph flow
Liver necrosis →liver fibrosis and scarring →
portal hypertension
Ascities, edema,
Spleenomegaly ( thrombocytopenia, leucopenia)
Varices (esophageal varices, hemorrhoids,
anemia)
↓ billirubin metabolism – hyperbilirubinemia,
jaundice
↓ bile in gastrointestinal tract – light colored
stool
↑ urobilinogen – Dark Urine
↓ vit K absorption- bleeding tendency
↓ metabolism of protein, carbohydrate, fats→
hypoglycemia,
↓ plasma protein- ascites and edema
↓androgen and estrogen detoxification(↓
hormone metabolism)- ↑ estrogen and
androgens hormone – Gynecomastia, loss of
body hair, menstrual dysfunction, spider
angioma, palmer erythema, testicular atrophy
↓ Aldesterone metabolism so ↑ levels – sodium
and water retention-- edema
Biochemical alteration - ↑ AST, ALT levels, ↑
bilirubin, low serum albumin, prolong
prothombin time, elevated alkaline phosphatase.
Liver failure
Hepatic encephalopathy
Hepatic coma
Death
Clinical manifestations
Early manifestations
No symptoms
GI disturbances: anorexia, dyspepsia, flatulence,
weakness, fatigue, nausea, vomiting, weight
loss, abdominal pain, bloating, diarrhea,
constipation
Abdominal pain, dull and heavy feeling
Fever, lassitude, weight loss, enlargement of
liver and spleen.

Later manifestations:
Results from liver failure and portal
hypertension
Jaundice
Peripheral edema
Ascites
Others: Skin lesion, hematological disorders,
endocrine disturbances, and peripheral
neuropathy
Advanced stage: small and nodular liver

Jaundice

It results from the functional derangement of

liver cells and compression of bile duct by
connective tissue overgrowth
Jaundice occurs as a result of decreased ability
to conjugate and excrete bilirubin
If obstruction of the biliary tract occurs,
obstructive jaundice may also occur and usually
accompanied by pruritus

Skin lesion
Spider angioma ( telangiectasia or spidernavi)
are small dilated blood vessels with a bright red
center point and spider like branches occurs in
nose, cheeks, upper trunk, neck and shoulders.
Palmer erythema, a red area that blanches with
pressure, is located on the palm of the hand.
Both lesions are due to increase estrogen in
blood as a result of the damaged liver’s inability
to metabolized steroid hormone.

Hematologic problem
Thrombocytopenia, leucopenia, anemia, due to
spleenomegaly (back flow of blood from portal
vein into the spleen.)
Anemia due to inadequate RBC production and
survival, and due to poor diet, poor absorption
and bleeding from varices.
Coagulation problems result from the liver’s
inability to produce prothrombin and blood
clotting and manifested by hemorrhagic
phenomena or bleeding tendencies e.g.
epistaxis, purpura, gingival bleeding, heavy
menstrual flow.

Endocrine problem
In men: Gynecomastia, loss of axillary and
pubic hair, testicular atrophy and impotence
with loss of libido due to increased estrogen
level.
In younger female, amenorrhea may occur and
in older, bleeding may occur.
↑aldosterone hormone may cause sodium water
retention and potassium loss.
Peripheral neuropathy: probably due to
dietary deficiency of thiamine, folic acid and
cobalamin.

Complication Portal
hypertension
The nodules and scar tissue can compress
hepatic veins within the liver.
This causes the blood pressure within the liver
to be high, a condition known as portal
hypertension.
Portal venous pressure is more than 15mmHg or
20 cm of water (normal 5-10mm Hg)
Pressure exceeding greater than 22 mm Hg in
the portal vein or a pressure difference between
the portal vein and the hepatic vein of greater
than 12 mm Hg will result in portal
hypertension. Measuring portal pressure
involves inserting a catheter into the portal vein.
The internal jugular, femoral, or medial
antecubital vessels are the best way to access the
hepatic and portal veins.
Is characterized by ↑venous pressure in the
portal circulation, spleenomegaly, large
collateral vein, ascites, systemic hypertension,
and esophageal varices.
The common area to form collateral channels
are in the lower esophagus( the anastomosis of
the left gastric vein and azygos vein), the
parietal peritoneum, rectum.
High pressures within blood vessels of the liver
occur in 60% of people who have cirrhosis.
Esophageal Varices:
Esophageal Varices are a complex of tortuous
veins at the lower end of the esophageal
enlarged and swollen as a result of portal
hypertension.
10-30% of UGI bleeding due to rupture of
varices.
80% bleeding due to esophageal Varices.
20% due to gastric varices.

Peripheral edema and Ascites:

Edema results from decreased colloidal oncotic
pressure from impaired liver synthesis of
albumin (hypoalbuminia)
Ascites is the accumulation of serous fluid in the
peritoneal cavity.
Protein move from the blood vessels via the
larger pore of sinusoids into the lymph space.
When the lymphatic system is unable to carry
off the excess protein and water, they leak
through the liver capsule into the peritoneal
cavity.

Hepatic encephalopathy/Coma:
Hepatic encephalopathy is a neuropsychiatric
manifestation of liver damage.
It can occur in any condition in which liver
damage causes ammonia to enter the systemic
circulation without liver detoxification.
Liver is unable to convert ammonia to urea. The
ammonia crosses the blood brain barrier and
produces neurologic toxic manifestations.

Asterixis; impaired writing and ability to draw

line figures.
Increased drowsiness; disorientation;
inappropriate behavior; mood swings; agitation
of extremities.

Medical management
Dietary modification: table salt, salted butter,
margarine, ordinary can and frozen foods should
be avoided.The diet should be adequate calories
and protein (gm/day) unless hepatic
encephalopathy is present, in which case protein
is limited.
Restrict fluid

Diuretics: spironolactone, aldosterone blocking

agents.
Vitamins B and fat soluble vitamins (A, D, E,
K).
Corticosteroids drugs to improve liver
function in post necrotic cirrhosis.
Daily weight loss should not exceed 1 to 2 kg
(2.2 to 4.4 lb) in patients with ascites and
peripheral edema or 0.5 to 0.75 kg (1.1 to 1.65
lb) in patients without edema.
Bed Rest: useful therapy
upright position activation of the renin-
angiotensin-aldosterone system and sympathetic
nervous system results in reduced renal
glomerular filtration and sodium excretion and a
decreased response to loop diuretics avoid
Paracentesis: removal of fluid (ascites) from
the peritoneal cavity through a small surgical
incision or puncture made through the
abdominal wall under sterile conditions (upto 5-
6l removal is safe)
Insertion of a peritoneovenous shunt to redirect
ascitic fluid
Transfusion of blood components also may be
required
An indwelling urinary catheter to monitor urine
output
Pharcological therapy:
Vasopressin (↓portal pressure)
Vasopressin +Nitroglycerine (↓ portal pressure)
Somatostatin and octreotide (↓ bleeding)
Balloon Temponade: used for controlling
hemorrhage
Use of double ballon teamponade Isengstaken
Blakemore tube)
Used to to exert pressure on the cardia (upper
orifice of the stomach) and against the bleeding
varices
The balloon in the stomach is inflated with 100
to 200 mL of air.
An x-ray is done to confirm proper positioning
of the gastric balloon
Esophageal banding therapy (variceal band
ligation)
a modified endoscope loaded with an elastic
rubber band is passed through an overtube
directly onto the varix (or varices) to be banded.
After suctioning the bleeding, the rubber band is
slipped over the tissue, causing necrosis,
ulceration, and eventual sloughing of the varix.
Surgical management
Liver transplantation
Removing the liver and replacing it with a
healthy donor organ is another way to treat liver
cancer or liver cirrhosis
About percent of people who undergo liver
transplantation, survive.

References
 Brunner And Siddhartha's (2004).Medical-
Surgical Nursing (12th Ed)
 Chintamani .Lewis’s Medical Surgical
Nursing, Mosby .2011
 Cirrhosis of Liver, emedicine, Available
from:
 M. Joycee Black, Hokanson Jane Hawks.
Medical –Surgical Nursing. Clinical
management for positive outcomes. 7th ed.
 MCQ’S PAPER

1. Late-stage chronic liver

disease is called
a) Liver failure
b) Cirrhosis
c) Liver cancer
d) Fatty liver disease

2. What is the most common

type of chronic viral hepatitis
in the U.S.?
a) Hepatitis A
b) Hepatitis B
c) Hepatitis C
d) Hepatitis D and/or E
3. What is/are the most
common cause(s) of chronic
liver disease in the U.S.?
a) Genetics
b) Alcohol abuse
c) Bacteria
d) Viruses

4. A telltale sign of liver disease

is _
a) Hair loss
b) Increased urination
c) Insomnia
d) Jaundice
5. Cirrhosis is most accurately
(definitively) diagnosed by
a) Eye exam
b) Blood test
c) Liver biopsy
d) All of the above

6. Liver disease can also arise

from...
a) Acetaminophen
b) Mushrooms
c) Statins
d) All of the above
7. You are scanning a patient with a
known mass in the left medial
segment of the liver. What
anatomical landmark can you use
to identify the left medial segment
separate from the right anterior
segment of the liver?
a) Left portal vein
b) Ligamentum venosum
c) Middle hepatic vein
d) Ligamentum teres
8. What important functions are
affected by severe, acute, or
chronic liver disease?
a) Blood clotting
b) Elimination of water, salt, drugs. And
toxins from the body
c) Manufacture of blood proteins
d) All of the above
9. lmmunological evidence of munity to
hepatitis B is the
presence of
a) hepatitis B core antibodies
b) hepatitis B core antigen
c) hepatitis B surface antibodies
d) hepatitis B surface antigen
e) any of the above.

10. A known case of cirrhosis suddenly

develop severe jaundice and rapid
deterioration of health. On examination
liver was enlarged and tender. The most
likely investigation is:
a) Alfa feto protein
b) CT abdomen
e) HBs. Ag
d) Alkali ne phosphatase
 Short Questions

Q1
Define cirrhosis?
Ans.
cirrhosis is defined as a diffuse process
characterized by fibrosis and the
conversion of normal liver architecture
into structural abnormal nodules
Q2
Define gland and difference between
endocrine and exocrine?
Ans.
Glands:
It secrets chemical substance called
hormones.
Endocrine.
Secretion directly into blood.
 Exocrine.
Secretion through ducts.
Q3
Describe any four functions of liver?
Ans.
I. It secrets bile and store glycogen.
II. It detoxifies blood from endogenous
exogenous substances e.g toxin, drugs
and alcohol.
III. Storage of vitamin A,D,E,K,B12
IV. It has regeneration power.
 Long essay questions
What is hepatic encephalopathy and what
are the clinical signs and symptoms?
Q What factors may precipitate hepatic
encephalopathy?

Ans.
Hepatic encephalopathy is a
neuropsychiatric syndrome which may
complicate almost all types of liver disease.
It may occur intermittently and be reversible
or may occur acutely, with rapid progression
to coma and death.
Sign and symptoms
I. Flapping tremor of the hands,
II. intellectual deterioration,
III. slurred speech,
IV. confusion,
V. drowsiness
VI. irritability.
factors may precipitate hepatic
encephalopathy
• Factors that may precipitate hepatic
encephalopathy
include:
1. hypokalaemia and/or profound
diuresis
2. diarrhoea and vomiting, because of
the resulting fluid and electrolyte
imbalance, constipation,
3. A large protein meal or
gastrointestinal haemorrhage infection,
especially peritonitis,
4. CNS depressant drugs, such as
opioids or
benzodiazepines.