Cirrhosis of the Liver

Lukman Hakim Zain

Div Gastroenterohepatologi
Ept IPD FKUSU/RSHAM
 ANATOMY & PHYSIOLOGY
LIVER
a. Weighing between 1,200 and 1,600 g, the liver is the largest
glandular organ in the body. It is located in the right upper
abdominal quadrant, under the right diaphragm.
b. The liver is divided into four lobes: left, right, caudate and
quadrate. The lobes are further subdivided into smaller units
known as lobules.
c. The liver contains several cell types including hepatocytes
(ie. Liver cells) and Kupffer cells (i.e. phagocytic cells that
engulf bacteria).
d. Bile is continuously formed by hepatocytes (about 1L/day).
Bile comprises water, electrolytes , lecithin,fatty acids,
cholesterol, bilirubin and bile salts.
e. The Liver is surrounded by a tough fibroelastic capsule
called Glissons capsule.
FUNCTIONS OF THE LIVER
Regulating blood glucose level by making glycogen,
which is stored in hepatocytes.
Synthesizing blood glucose from amino acids of
lactate through gluconeogenesis.
Converting ammonia produced from gluconeogenetic
by-products and bacteria to urea
Synthesizing plasma proteins such as albumin,
globulins, clotting factors, and lipoproteins.
Breaking down fatty acids into ketone bodies
Storing vitamins and trace metals
Affecting drug metabolism and detoxification
Secreting bile
Liver cirrhosis
 Description

A chronic, progressive disease of the liver

Extensive parenchymal cell
degeneration
Destruction of parenchymal cells
 Description

Regenerative process is disorganized,

resulting in abnormal blood vessel and
bile duct relationships from fibrosis
 Description
Normal lobular structure distorted by
fibrotic connective tissue

Lobules are irregular in size and shape

with impaired vascular flow

Insidious, prolonged course

Etiology and Pathophysiology

Cell necrosis occurs

Destroyed liver cells are replaced by
scar tissue
Normal architecture becomes nodular
Etiology and Pathophysiology
Four types of cirrhosis:
Alcoholic (Laennecs) cirrhosis
Postnecrotic cirrhosis
Biliary cirrhosis
Cardiac cirrhosis
Etiology and Pathophysiology
Alcoholic (Laennecs) Cirrhosis
Associated with alcohol abuse
Preceded by a theoretically reversible
fatty infiltration of the liver cells
Widespread scar formation
 Etiology and Pathophysiology
Postnecrotic Cirrhosis
Complication of toxic or viral hepatitis
Accounts for 20% of the cases of
cirrhosis
Broad bands of scar tissue form within
the liver
Etiology and Pathophysiology
Biliary Cirrhosis
Associated with chronic biliary
obstruction and infection
Accounts for 15% of all cases of
cirrhosis
 Etiology and Pathophysiology

Cardiac Cirrhosis
Results from longstanding severe right-
sided heart failure
Manifestations of Liver Cirrhosis

Fig. 42-5
 Clinical Manifestations
Early Manifestations
Onset usually insidious
GI disturbances:
Anorexia
Dyspepsia
Flatulence
N-V, change in bowel habits
 Clinical Manifestations
Early Manifestations

Abdominal pain
Fever
Lassitude (laziness)
Weight loss
Enlarged liver or spleen
 Clinical Manifestations
Late Manifestations

Two causative mechanisms

Hepatocellular failure
Portal hypertension
 Clinical Manifestations
Jaundice

Occurs because of insufficient

conjugation of bilirubin by the liver cells,
and local obstruction of biliary ducts by
scarring and regenerating tissue
 Clinical Manifestations
Jaundice

Intermittent jaundice is characteristic of

biliary cirrhosis
Late stages of cirrhosis the patient will
usually be jaundiced
 Clinical Manifestations
Skin

Spider angiomas (telangiectasia, spider

nevi)
Palmar erythema
 Clinical Manifestations
Endocrine Disturbances

Steroid hormones of the adrenal cortex

(aldosterone), testes, and ovaries are
metabolized and inactivated by the
normal liver
 Clinical Manifestations
Endocrine Disturbances

Alteration in hair distribution

Decreased amount of pubic hair
Axillary and pectoral alopecia
 Clinical Manifestations
Hematologic Disorders

Bleeding tendencies as a result of

decreased production of hepatic clotting
factors (II, VII, IX, and X)
 Clinical Manifestations
Hematologic Disorders

Anemia, leukopenia, and

thrombocytopenia are believed to be
result of hypersplenism
 Clinical Manifestations
Peripheral Neuropathy

Dietary deficiencies of thiamine, folic

acid, and vitamin B12
 Complications

Portal hypertension and esophageal varices

Peripheral edema and ascites
Hepatic encephalopathy
Fetor hepaticus: is bad breath with a 'dead
mouse' or sweet faecal smell. ... It may be
caused by severe hepatocellular damage
 Complications
Portal Hypertension

Characterized by:
Increased venous pressure in portal
circulation
Splenomegaly
Esophageal varices
Systemic hypertension
 Complications
Portal Hypertension

Primary mechanism is the increased

resistance to blood flow through the liver
 Complications
Portal Hypertension
Splenomegaly

Back pressure caused by portal

hypertension chronic passive congestion
as a result of increased pressure in the
splenic vein
 Complications
Portal Hypertension
Esophageal Varices

Increased blood flow through the

portal system results in dilation
and enlargement of the plexus
veins of the esophagus and
produces varices
 Complications
Portal Hypertension
Esophageal Varices

Varices have fragile vessel walls

which bleed easily
 Complications
Portal Hypertension
Internal Hemorrhoids

Occurs because of the dilation of

the mesenteric veins and rectal
veins
 Complications
Portal Hypertension
Caput Medusae

Collateral circulation involves the

superficial veins of the abdominal wall
leading to the development of dilated
veins around the umbilicus
 Complications
Peripheral Edema and Ascites

Ascites:
- Intraperitoneal accumulation of
watery fluid containing small
amounts of protein
 Complications
Peripheral Edema and Ascites

Factors involved in the pathogenesis of

ascites:
- Hypoalbuminemia
- Levels of aldosterone
- Portal hypertension
 Complications
Hepatic Encephalopathy

Liver damage causes blood to enter

systemic circulation without liver
detoxification
 Complications
Hepatic Encephalopathy

Main pathogenic toxin is NH3 although

other etiological factors have been
identified
Frequently a terminal complication
 Complications
Fetor Hepaticus

Musty, sweetish odor detected on the

patients breath
From accumulation of digested by-
products
Development of Ascites

Fig. 42-6
 Diagnostic Studies

Liver function tests

Liver biopsy
Liver scan
Liver ultrasound
 Diagnostic Studies

Esophagogastroduodenoscopy
Prothrombin time
Testing of stool for occult blood
 Collaborative Care

Rest
Avoidance of alcohol and anticoagulants
Management of ascites
 Collaborative Care

Prevention and management of

esophageal variceal bleeding
Management of encephalopathy
 Collaborative Care
Ascites

High carbohydrate, low protein, low Na+

diet
Diuretics
Paracentesis
 Collaborative Care
Ascites

Peritoneovenous shunt
Provides for continuous reinfusion of
ascitic fluid from the abdomen to the
vena cava
Peritoneovenous Shunt

Fig. 42-8
 Collaborative Care
Esophageal Varices

Avoid alcohol, aspirin, and irritating

foods
If bleeding occurs, stabilize patient and
manage the airway, administer
vasopressin (Pitressin)
 Collaborative Care
Esophageal Varices

Endoscopic sclerotherapy or ligation

Balloon tamponade
Surgical shunting procedures (e.g.,
portacaval shunt, TIPS)
Sengstaken-Blakemore Tube

Fig. 42-9
Portosystemic Shunts

Fig. 42-11
 Collaborative Care
Hepatic Encephalopathy
Goal: reduce NH3 formation
Protein restriction (0-40g/day)
Sterilization of GI tract with antibiotics
(e.g., neomycin)
lactulose (Cephulac) traps NH3 in gut
levodopa
 Drug Therapy

There is no specific drug therapy for

cirrhosis
Drugs are used to treat symptoms and
complications of advanced liver disease
 Nutritional Therapy
Diet for patient without complications:
High in calories
CHO
Moderate to low fat
Amount of protein varies with degree
of liver damage
 Nutritional Therapy

Patient with hepatic encephalopathy

Very low to no-protein diet
Low sodium diet for patient with ascites
and edema
 Nursing Management
Nursing Assessment

Past health history

Medications
Chronic alcoholism
Weight loss
 Nursing Management
Nursing Diagnoses

Imbalanced nutrition: less than body

requirements
Impaired skin integrity
Ineffective breathing pattern
Risk for injury
 Nursing Management
Planning

Overall goals:
Relief of discomfort
Minimal to no complications
Return to as normal a lifestyle as
possible
 Nursing Management
Nursing Implementation

Health Promotion
Treat alcoholism
Identify hepatitis early and treat
Identify biliary disease early and treat
 Nursing Management
Nursing Implementation
Acute Intervention
Rest
Edema and ascites
Paracentesis
Skin care
Dyspnea
Nutrition
 Nursing Management
Nursing Implementation

Acute Intervention
Bleeding problems
Balloon tamponade
Altered body image
Hepatic encephalopathy
 Nursing Management
Nursing Implementation
Ambulatory and Home Care
Symptoms of complications
When to seek medical attention
Remission maintenance
Abstinence from alcohol
 Nursing Management
Evaluation
Maintenance of normal body weight
Maintenance of skin integrity
Effective breathing pattern
No injury
No signs of infection
Gallbladder Disorders
ANATOMY & PHYSIOLOGY
BILIARY SYSTEM
a. Canaliculi the smallest bile ducts located between
liver lobules, receive bile from hepatocytes. The
canaliculi form larger bile ducts, which lead to
hepatic duct.
b. Hepatic duct from the liver joins the cystic duct
from the gallbladder to form the common bile duct,
which empties into the duodenum.
c. Sphincter of Oddi controls the flow of bile into the
intestine.
d. Gallbladder is a hollow pear-shaped organ that is
30-40mm long. Normally holds 30-50mL of bile and
can hold up to 70mL when fully distended.
 BILIARY SYSTEM

Draining bile from hepatocytes to the

gallbladder by way of biliary tree
Storing bile in the gallbladder and
releasing it to the duodenum, which is
mediated by the hormone
cholecystokinin-pancreozymin.
 The Gallbladder

Located below the liver

The cystic duct joins the hepatic duct to
become the bile duct
The common bile duct joins the pancreatic
duct in the sphincter of Oddi in the first part
of the duodenum
Stores and concentrates bile
Contracts during the digestion of fats to
deliver the bile
Cholecystokinin is released by the duodenal
cells, causing the contraction of the
gallbladder and relaxation of the sphincter
of Oddi
 CHOLELITHIASIS
Refers to formation of calculi (ie, gallstones
in the bladder.

Predisposing Factors:
1. Obese
2. Female
3. >40 yrs
4. OC, Estrogen, intake
5. Fair
 CHOLELITHIASIS
Supersaturated bile, Biliary stasis

Stone formation

Blockage of Gallbladder

Inflammation, Mucosal Damage and WBC infiltration

CHOLECYSTITIS
Common locations of gallstones
Gall Stones
 CHOLECYSTITIS

inflammation of gallbladder with gallstone

formation.
PATHOLOGY-SIGNS AND SYMPTOMS
CHOLECYSTITIS/ CHOLELITHIASIS
Signs and Symptoms:
Severe Right abdominal pain radiating to the
back
Fever
Fat intolerance
Anorexia, n/v
Jaundice
Pruritus
Easy bruising
Tea colored urine
Steatorrhea
CHOLECYSTITIS/ CHOLELITHIASIS

Diagnosis:
US detects the presence of gallstone
Serum alkaline phosphatase 50-120 u/L
WBC
Endoscopic retrograde
cholangiopancreatography (ERCP) -
 CHOLECYSTITIS/ CHOLELITHIASIS
Nursing Management:
Administer Rx Medications
Diet increase CHO, moderate CHON,
decrease fats
Meticulous skin care
Instruct patient to AVOID HIGH- fat diet and
GAS-forming foods
Assist in surgical and non-surgical measures
ESWL non-invasive fragmentation of stones
by using repeated shockwaves directed at the
gallstones in the gallbladder or common bile
duct.
CHOLELITHIASIS/CHOLEC
YSTITIS
Surgical procedures- Surgical
Cholecystectomy, Choledochotomy,
Laparoscopic cholecystectomy
 CHOLELITHIASIS/CHOLEC
YSTITIS
Post-operative nursing interventions
1. Monitor for surgical complications
2. Post-operative position after recovery from
anesthesia- LOW FOWLERs
3. Encourage early ambulation
4. Administer medication before coughing and
deep breathing exercises
5. Advise client to splint the abdomen to prevent
discomfort during coughing
6. Administer analgesics, antiemetics, antacids
7. Care of the biliary drainageor T-tube drainage
8. Fat restriction is only limited to 4-6 weeks.
Normal diet is resumed