Dr Ibraheem bashayreh, RN, PhD 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. 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. 2

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 4

Liver cirrhosis

Description Extensive parenchymal cell degeneration 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 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 - 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 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 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 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 72

CHOLELITHIASIS Refers to formation of calculi (ie, gallstones in the bladder. Predisposing Factors: Obese Female >40 yrs OC, Estrogen, intake Fair 74

CHOLELITHIASIS Supersaturated bile, Biliary stasis Stone formation Blockage of Gallbladder Inflammation, Mucosal Damage and WBC infiltration CHOLECYSTITIS 75

Common locations of gallstones

Gall Stones

CHOLECYSTITIS – inflammation of gallbladder with gallstone formation. GALLBLADDER – storage of bile – made up of cholesterol. 79

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 81

CHOLECYSTITIS/ CHOLELITHIASIS Diagnosis: US detects the presence of gallstone Serum alkaline phosphatase – 50-120 u/L WBC Endoscopic retrograde cholangiopancreatography (ERCP) - 82

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. 83

CHOLELITHIASIS/CHOLECYSTITIS Surgical procedures- Surgical Cholecystectomy, Choledochotomy, Laparoscopic cholecystectomy 84

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 87