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Cirrhosis of the Liver. Dr Ibraheem bashayreh, RN, PhD . ANATOMY & PHYSIOLOGY. LIVER 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.

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cirrhosis of the liver

Cirrhosis of the Liver

Dr Ibraheem bashayreh, RN, PhD

anatomy physiology
ANATOMY & PHYSIOLOGY

LIVER

  • 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.
  • The liver is divided into four lobes: left, right, caudate and quadrate. The lobes are further subdivided into smaller units known as lobules.
  • The liver contains several cell types including hepatocytes (ie. Liver cells) and Kupffer cells (i.e. phagocytic cells that engulf bacteria).
  • Bile is continuously formed by hepatocytes (about 1L/day). Bile comprises water, electrolytes , lecithin,fatty acids, cholesterol, bilirubin and bile salts.
  • The Liver is surrounded by a tough fibroelastic capsule called Glisson’s capsule.
functions of the liver
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.

Convertingammonia 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

description
Description
  • A chronic, progressive disease of the liver
    • Extensive parenchymal cell degeneration
    • Destruction of parenchymal cells
description8
Description
  • Regenerative process is disorganized, resulting in abnormal blood vessel and bile duct relationships from fibrosis
description9
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
Etiology and Pathophysiology
  • Cell necrosis occurs
  • Destroyed liver cells are replaced by scar tissue
  • Normal architecture becomes nodular
etiology and pathophysiology11
Etiology and Pathophysiology
  • Four types of cirrhosis:
    • Alcoholic (Laennec’s) cirrhosis
    • Postnecrotic cirrhosis
    • Biliary cirrhosis
    • Cardiac cirrhosis
etiology and pathophysiology12
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 pathophysiology13
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 pathophysiology14
Etiology and Pathophysiology
  • Biliary Cirrhosis
    • Associated with chronic biliary obstruction and infection
    • Accounts for 15% of all cases of cirrhosis
etiology and pathophysiology15
Etiology and Pathophysiology
  • Cardiac Cirrhosis
    • Results from longstanding severe right-sided heart failure
clinical manifestations early manifestations
Clinical ManifestationsEarly Manifestations
  • Onset usually insidious
  • GI disturbances:
    • Anorexia
    • Dyspepsia
    • Flatulence
    • N-V, change in bowel habits
clinical manifestations early manifestations18
Clinical ManifestationsEarly Manifestations
  • Abdominal pain
  • Fever
  • Lassitude (laziness)
  • Weight loss
  • Enlarged liver or spleen
clinical manifestations late manifestations
Clinical ManifestationsLate Manifestations
  • Two causative mechanisms
    • Hepatocellular failure
    • Portal hypertension
clinical manifestations jaundice
Clinical ManifestationsJaundice
  • Occurs because of insufficient conjugation of bilirubin by the liver cells, and local obstruction of biliary ducts by scarring and regenerating tissue
clinical manifestations jaundice21
Clinical ManifestationsJaundice
  • Intermittent jaundice is characteristic of biliary cirrhosis
  • Late stages of cirrhosis the patient will usually be jaundiced
clinical manifestations skin
Clinical ManifestationsSkin
  • Spider angiomas (telangiectasia, spider nevi)
  • Palmarerythema
clinical manifestations endocrine disturbances
Clinical ManifestationsEndocrine Disturbances
  • Steroid hormonesof the adrenal cortex (aldosterone), testes, and ovaries are metabolized and inactivated by the normal liver
clinical manifestations endocrine disturbances25
Clinical ManifestationsEndocrine Disturbances
  • Alteration in hair distribution
    • Decreased amount of pubic hair
    • Axillary and pectoral alopecia
clinical manifestations hematologic disorders
Clinical ManifestationsHematologic Disorders
  • Bleeding tendencies as a result of decreased production of hepatic clotting factors (II, VII, IX, and X)
clinical manifestations hematologic disorders27
Clinical ManifestationsHematologic Disorders
  • Anemia, leukopenia, and thrombocytopenia are believed to be result of hypersplenism
clinical manifestations peripheral neuropathy
Clinical ManifestationsPeripheral Neuropathy
  • Dietary deficiencies of thiamine, folic acid, and vitamin B12
complications
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
ComplicationsPortal Hypertension
  • Characterized by:
    • Increased venous pressure in portal circulation
    • Splenomegaly
    • Esophageal varices
    • Systemic hypertension
complications portal hypertension31
ComplicationsPortal Hypertension
  • Primary mechanism is the increased resistance to blood flow through the liver
complications portal hypertension splenomegaly
ComplicationsPortal HypertensionSplenomegaly
  • Back pressure caused by portal hypertension  chronic passive congestion as a result of increased pressure in the splenic vein
complications portal hypertension esophageal varices
ComplicationsPortal HypertensionEsophageal 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 varices34
ComplicationsPortal HypertensionEsophageal Varices
  • Varices have fragile vessel walls which bleed easily
complications portal hypertension internal hemorrhoids
ComplicationsPortal HypertensionInternal Hemorrhoids
  • Occurs because of the dilation of the mesenteric veins and rectal veins
complications portal hypertension caput medusae
ComplicationsPortal HypertensionCaput 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
ComplicationsPeripheral Edema and Ascites
  • Ascites:

- Intraperitoneal accumulation of watery fluid containing small amounts of protein

complications peripheral edema and ascites38
ComplicationsPeripheral Edema and Ascites
  • Factors involved in the pathogenesis of ascites:
    • Hypoalbuminemia
    •  Levels of aldosterone
    •  Portal hypertension
complications hepatic encephalopathy
ComplicationsHepatic Encephalopathy
  • Liver damage causes blood to enter systemic circulation without liver detoxification
complications hepatic encephalopathy41
ComplicationsHepatic Encephalopathy
  • Main pathogenic toxin is NH3 although other etiological factors have been identified
  • Frequently a terminal complication
complications fetor hepaticus
ComplicationsFetor Hepaticus
  • Musty, sweetish odor detected on the patient’s breath
  • From accumulation of digested by-products
diagnostic studies
Diagnostic Studies
  • Liver function tests
  • Liver biopsy
  • Liver scan
  • Liver ultrasound
diagnostic studies45
Diagnostic Studies
  • Esophagogastroduodenoscopy
  • Prothrombin time
  • Testing of stool for occult blood
collaborative care
Collaborative Care
  • Rest
  • Avoidance of alcohol and anticoagulants
  • Management of ascites
collaborative care47
Collaborative Care
  • Prevention and management of esophageal variceal bleeding
  • Management of encephalopathy
collaborative care ascites
Collaborative CareAscites
  • High carbohydrate, low protein, low Na+ diet
  • Diuretics
  • Paracentesis
collaborative care ascites49
Collaborative CareAscites
  • Peritoneovenous shunt
    • Provides for continuous reinfusion of ascitic fluid from the abdomen to the vena cava
collaborative care esophageal varices
Collaborative CareEsophageal Varices
  • Avoid alcohol, aspirin, and irritating foods
  • If bleeding occurs, stabilize patient and manage the airway, administer vasopressin (Pitressin)
collaborative care esophageal varices52
Collaborative CareEsophageal Varices
  • Endoscopic sclerotherapy or ligation
  • Balloon tamponade
  • Surgical shunting procedures (e.g., portacaval shunt, TIPS)
collaborative care hepatic encephalopathy
Collaborative CareHepatic 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
Drug Therapy
  • There is no specific drug therapy for cirrhosis
  • Drugs are used to treat symptoms and complications of advanced liver disease
nutritional therapy
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 therapy59
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
Nursing ManagementNursing Assessment
  • Past health history
  • Medications
  • Chronic alcoholism
  • Weight loss
nursing management nursing diagnoses
Nursing ManagementNursing Diagnoses
  • Imbalanced nutrition: less than body requirements
  • Impaired skin integrity
  • Ineffective breathing pattern
  • Risk for injury
nursing management planning
Nursing ManagementPlanning
  • Overall goals:
    • Relief of discomfort
    • Minimal to no complications
    • Return to as normal a lifestyle as possible
nursing management nursing implementation
Nursing ManagementNursing Implementation
  • Health Promotion
    • Treat alcoholism
    • Identify hepatitis early and treat
    • Identify biliary disease early and treat
nursing management nursing implementation64
Nursing ManagementNursing Implementation
  • Acute Intervention
    • Rest
    • Edema and ascites
    • Paracentesis
    • Skin care
    • Dyspnea
    • Nutrition
nursing management nursing implementation65
Nursing ManagementNursing Implementation
  • Acute Intervention
    • Bleeding problems
    • Balloon tamponade
    • Altered body image
    • Hepatic encephalopathy
nursing management nursing implementation66
Nursing ManagementNursing Implementation
  • Ambulatory and Home Care
    • Symptoms of complications
    • When to seek medical attention
    • Remission maintenance
    • Abstinence from alcohol
nursing management evaluation
Nursing ManagementEvaluation
  • Maintenance of normal body weight
  • Maintenance of skin integrity
  • Effective breathing pattern
  • No injury
  • No signs of infection
anatomy physiology69
ANATOMY & PHYSIOLOGY

BILIARY SYSTEM

  • Canaliculi – the smallest bile ducts located between liver lobules, receive bile from hepatocytes. The canaliculi form larger bile ducts, which lead to hepatic duct.
  • Hepatic duct – from the liver joins the cystic duct from the gallbladder to form the common bile duct, which empties into the duodenum.
  • Sphincter of Oddi – controls the flow of bile into the intestine.
  • 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
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
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
slide72

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
CHOLELITHIASIS
  • Refers to formation of calculi (ie, gallstones in the bladder.
  • Predisposing Factors:
  • Obese
  • Female
  • >40 yrs
  • OC, Estrogen, intake
  • Fair
cholelithiasis75
CHOLELITHIASIS

Supersaturated bile, Biliary stasis

Stone formation

Blockage of Gallbladder

Inflammation, Mucosal Damage and WBC infiltration

CHOLECYSTITIS

cholecystitis
CHOLECYSTITIS

– inflammation of gallbladder with gallstone formation.

cholecystitis cholelithiasis
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 cholelithiasis82
CHOLECYSTITIS/ CHOLELITHIASIS

Diagnosis:

US detects the presence of gallstone

Serum alkaline phosphatase – 50-120 u/L

WBC

Endoscopic retrograde cholangiopancreatography (ERCP) -

cholecystitis cholelithiasis83
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 cholecystitis
CHOLELITHIASIS/CHOLECYSTITIS
  • Surgical procedures- Surgical Cholecystectomy, Choledochotomy,
  • Laparoscopic cholecystectomy
cholelithiasis cholecystitis87
CHOLELITHIASIS/CHOLECYSTITIS

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