Cirrhosis of the Liver
Dr Ibraheem bashayreh, RN, PhD
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 Glisson’s 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 (Laennec’s) cirrhosis
– Postnecrotic cirrhosis
– Biliary cirrhosis
– Cardiac cirrhosis
Etiology and Pathophysiology
• Alcoholic (Laennec’s) 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 rightsided 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
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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
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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
patient’s breath
• From accumulation of digested byproducts
Development of Ascites
Fig. 42-6
Diagnostic Studies
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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
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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
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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 FOWLER’s
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