cirrhosis of the liver dr ibraheem bashayreh, rn, phd

Cirrhosis of the LiverCirrhosis of the Liver

Dr Ibraheem bashayreh, RN, PhD Dr Ibraheem bashayreh, RN, PhD

ANATOMY & PHYSIOLOGYANATOMY & PHYSIOLOGYLIVERa. 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.

LIVERa. 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 LIVERFUNCTIONS 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

• 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

DescriptionDescription

• A chronic, progressive disease of the liver

– Extensive parenchymal cell degeneration

– Destruction of parenchymal cells

• A chronic, progressive disease of the liver

– Extensive parenchymal cell degeneration

– Destruction of parenchymal cells


• Regenerative process is disorganized, resulting in abnormal blood vessel and bile duct relationships from fibrosis

• Regenerative process is disorganized, resulting in abnormal blood vessel and bile duct relationships from fibrosis


• Normal lobular structure distorted by fibrotic connective tissue

• Lobules are irregular in size and shape with impaired vascular flow

• Insidious, prolonged course

• Normal lobular structure distorted by fibrotic connective tissue

• Lobules are irregular in size and shape with impaired vascular flow

• Insidious, prolonged course

Etiology and PathophysiologyEtiology and Pathophysiology

• Cell necrosis occurs

• Destroyed liver cells are replaced by scar tissue

• Normal architecture becomes nodular

• Cell necrosis occurs

• Destroyed liver cells are replaced by scar tissue

• Normal architecture becomes nodular


• Four types of cirrhosis:

– Alcoholic (Laennec’s) cirrhosis

– Postnecrotic cirrhosis

– Biliary cirrhosis

– Cardiac cirrhosis

• Four types of cirrhosis:

– Alcoholic (Laennec’s) cirrhosis

– Postnecrotic cirrhosis

– Biliary cirrhosis

– Cardiac cirrhosis


• Alcoholic (Laennec’s) Cirrhosis

– Associated with alcohol abuse

– Preceded by a theoretically reversible fatty infiltration of the liver cells

– Widespread scar formation

• Alcoholic (Laennec’s) Cirrhosis

– Associated with alcohol abuse

– Preceded by a theoretically reversible fatty infiltration of the liver cells

– Widespread scar formation


• 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

• 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


• Biliary Cirrhosis – Associated with chronic biliary

obstruction and infection

– Accounts for 15% of all cases of cirrhosis

• Biliary Cirrhosis – Associated with chronic biliary

obstruction and infection

– Accounts for 15% of all cases of cirrhosis


• Cardiac Cirrhosis – Results from longstanding severe

right-sided heart failure

• Cardiac Cirrhosis – Results from longstanding severe

right-sided heart failure

Manifestations of Liver CirrhosisManifestations of Liver Cirrhosis

Fig. 42-5

Clinical ManifestationsEarly Manifestations


• Onset usually insidious

• GI disturbances:

– Anorexia

– Dyspepsia

– Flatulence

– N-V, change in bowel habits

• Onset usually insidious

• GI disturbances:

– Anorexia

– Dyspepsia

– Flatulence

– N-V, change in bowel habits



• Abdominal pain

• Fever

• Lassitude (laziness)

• Weight loss

• Enlarged liver or spleen

• Abdominal pain

• Fever

• Lassitude (laziness)

• Weight loss

• Enlarged liver or spleen

Clinical ManifestationsLate Manifestations

Clinical ManifestationsLate Manifestations

• Two causative mechanisms

– Hepatocellular failure

– Portal hypertension

• Two causative mechanisms

– Hepatocellular failure

– Portal hypertension

Clinical ManifestationsJaundice


• Occurs because of insufficient conjugation of bilirubin by the liver cells, and local obstruction of biliary ducts by scarring and regenerating tissue

• Occurs because of insufficient conjugation of bilirubin by the liver cells, and local obstruction of biliary ducts by scarring and regenerating tissue



• Intermittent jaundice is characteristic of biliary cirrhosis

• Late stages of cirrhosis the patient will usually be jaundiced

• Intermittent jaundice is characteristic of biliary cirrhosis

• Late stages of cirrhosis the patient will usually be jaundiced

Clinical ManifestationsSkin

Clinical ManifestationsSkin

• Spider angiomas (telangiectasia, spider nevi)

• Palmar erythema

• Spider angiomas (telangiectasia, spider nevi)

• Palmar erythema

Clinical Manifestations Endocrine DisturbancesClinical Manifestations Endocrine Disturbances

• Steroid hormones of the adrenal cortex (aldosterone), testes, and ovaries are metabolized and inactivated by the normal liver

• Steroid hormones of the adrenal cortex (aldosterone), testes, and ovaries are metabolized and inactivated by the normal liver

Clinical Manifestations Endocrine DisturbancesClinical Manifestations Endocrine Disturbances

• Alteration in hair distribution

– Decreased amount of pubic hair

– Axillary and pectoral alopecia

• 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)

• Bleeding tendencies as a result of decreased production of hepatic clotting factors (II, VII, IX, and X)



• Anemia, leukopenia, and thrombocytopenia are believed to be result of hypersplenism

• Anemia, leukopenia, and thrombocytopenia are believed to be result of hypersplenism

Clinical Manifestations Peripheral Neuropathy

Clinical Manifestations Peripheral Neuropathy

• Dietary deficiencies of thiamine, folic acid, and vitamin B12

• Dietary deficiencies of thiamine, folic acid, and vitamin B12

ComplicationsComplications

• 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

• 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

• Characterized by:

– Increased venous pressure in portal circulation

– Splenomegaly

– Esophageal varices

– Systemic hypertension



• Primary mechanism is the increased resistance to blood flow through the liver

• Primary mechanism is the increased resistance to blood flow through the liver


Splenomegaly


Splenomegaly

• Back pressure caused by portal hypertension chronic passive congestion as a result of increased pressure in the splenic vein

• 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

• Increased blood flow through the portal system results in dilation and enlargement of the plexus veins of the esophagus and produces varices



• Varices have fragile vessel walls which bleed easily

• Varices have fragile vessel walls which bleed easily


Internal Hemorrhoids


Internal Hemorrhoids

• Occurs because of the dilation of the mesenteric veins and rectal veins

• Occurs because of the dilation of the mesenteric veins and rectal veins


Caput Medusae


Caput Medusae

• Collateral circulation involves the superficial veins of the abdominal wall leading to the development of dilated veins around the umbilicus

• 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

• Ascites:- - Intraperitoneal accumulation of

watery fluid containing small amounts of protein



• Factors involved in the pathogenesis of ascites:

- Hypoalbuminemia Levels of aldosterone Portal hypertension

• 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

• Liver damage causes blood to enter systemic circulation without liver detoxification



• Main pathogenic toxin is NH3 although other etiological factors have been identified

• Frequently a terminal complication

• Main pathogenic toxin is NH3 although other etiological factors have been identified

• Frequently a terminal complication

Complications Fetor HepaticusComplications Fetor Hepaticus

• Musty, sweetish odor detected on the patient’s breath

• From accumulation of digested by-products

• Musty, sweetish odor detected on the patient’s breath

• From accumulation of digested by-products

Development of AscitesDevelopment of Ascites

Fig. 42-6

Diagnostic StudiesDiagnostic Studies

• Liver function tests

• Liver biopsy

• Liver scan

• Liver ultrasound

• Liver function tests

• Liver biopsy

• Liver scan

• Liver ultrasound

Diagnostic StudiesDiagnostic Studies

• Esophagogastroduodenoscopy

• Prothrombin time

• Testing of stool for occult blood

• Esophagogastroduodenoscopy

• Prothrombin time

• Testing of stool for occult blood

Collaborative CareCollaborative Care

• Rest

• Avoidance of alcohol and anticoagulants

• Management of ascites

• Rest

• Avoidance of alcohol and anticoagulants

• Management of ascites

Collaborative CareCollaborative Care

• Prevention and management of esophageal variceal bleeding

• Management of encephalopathy

• Prevention and management of esophageal variceal bleeding

• Management of encephalopathy

Collaborative Care Ascites


• High carbohydrate, low protein, low Na+ diet

• Diuretics

• Paracentesis

• High carbohydrate, low protein, low Na+ diet

• Diuretics

• Paracentesis



• Peritoneovenous shunt

– Provides for continuous reinfusion of ascitic fluid from the abdomen to the vena cava

• Peritoneovenous shunt

– Provides for continuous reinfusion of ascitic fluid from the abdomen to the vena cava

Peritoneovenous ShuntPeritoneovenous 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)

• Avoid alcohol, aspirin, and irritating foods

• If bleeding occurs, stabilize patient and manage the airway, administer vasopressin (Pitressin)



• Endoscopic sclerotherapy or ligation

• Balloon tamponade

• Surgical shunting procedures (e.g., portacaval shunt, TIPS)

• Endoscopic sclerotherapy or ligation

• Balloon tamponade

• Surgical shunting procedures (e.g., portacaval shunt, TIPS)

Sengstaken-Blakemore TubeSengstaken-Blakemore Tube

Fig. 42-9

Portosystemic ShuntsPortosystemic Shunts

Fig. 42-11

Collaborative Care Hepatic EncephalopathyCollaborative 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

• 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 TherapyDrug Therapy

• There is no specific drug therapy for cirrhosis

• Drugs are used to treat symptoms and complications of advanced liver disease

• There is no specific drug therapy for cirrhosis

• Drugs are used to treat symptoms and complications of advanced liver disease

Nutritional TherapyNutritional Therapy

• Diet for patient without complications:

– High in calories CHO

– Moderate to low fat

– Amount of protein varies with degree of liver damage

• Diet for patient without complications:

– High in calories CHO

– Moderate to low fat

– Amount of protein varies with degree of liver damage

Nutritional TherapyNutritional Therapy

• Patient with hepatic encephalopathy

– Very low to no-protein diet

• Low sodium diet for patient with ascites and edema

• Patient with hepatic encephalopathy

– Very low to no-protein diet

• Low sodium diet for patient with ascites and edema

Nursing ManagementNursing Assessment

Nursing ManagementNursing Assessment

• Past health history

• Medications

• Chronic alcoholism

• Weight loss

• Past health history

• Medications

• Chronic alcoholism

• Weight loss

Nursing ManagementNursing Diagnoses

Nursing ManagementNursing Diagnoses

• Imbalanced nutrition: less than body requirements

• Impaired skin integrity• Ineffective breathing pattern• Risk for injury

• Imbalanced nutrition: less than body requirements

• Impaired skin integrity• Ineffective breathing pattern• Risk for injury

Nursing ManagementPlanning

Nursing ManagementPlanning

• Overall goals:

– Relief of discomfort

– Minimal to no complications

– Return to as normal a lifestyle as possible

• Overall goals:

– Relief of discomfort

– Minimal to no complications

– Return to as normal a lifestyle as possible

Nursing ManagementNursing ImplementationNursing ManagementNursing Implementation

• Health Promotion

– Treat alcoholism

– Identify hepatitis early and treat

– Identify biliary disease early and treat

• Health Promotion

– Treat alcoholism

– Identify hepatitis early and treat

– Identify biliary disease early and treat


• Acute Intervention– Rest– Edema and ascites– Paracentesis– Skin care– Dyspnea– Nutrition

• Acute Intervention– Rest– Edema and ascites– Paracentesis– Skin care– Dyspnea– Nutrition


• Acute Intervention

– Bleeding problems

– Balloon tamponade

– Altered body image

– Hepatic encephalopathy

• Acute Intervention

– Bleeding problems

– Balloon tamponade

– Altered body image

– Hepatic encephalopathy


• Ambulatory and Home Care

– Symptoms of complications

– When to seek medical attention

– Remission maintenance

– Abstinence from alcohol

• Ambulatory and Home Care

– Symptoms of complications

– When to seek medical attention

– Remission maintenance

– Abstinence from alcohol

Nursing ManagementEvaluation

Nursing ManagementEvaluation

• Maintenance of normal body weight

• Maintenance of skin integrity

• Effective breathing pattern

• No injury

• No signs of infection

• Maintenance of normal body weight

• Maintenance of skin integrity

• Effective breathing pattern

• No injury

• No signs of infection

Gallbladder DisordersGallbladder DisordersGallbladder DisordersGallbladder Disorders

ANATOMY & PHYSIOLOGYANATOMY & PHYSIOLOGY

BILIARY SYSTEMa. 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 SYSTEMa. 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 SYSTEMBILIARY 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.

• 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 GallbladderThe Gallbladder

Located below the liver The cystic duct joins the hepatic duct to

become the bile ductThe common bile duct joins the pancreatic

duct in the sphincter of Oddi in the first part of the duodenum

Located below the liver The cystic duct joins the hepatic duct to

become the bile ductThe common bile duct joins the pancreatic

duct in the sphincter of Oddi in the first part of the duodenum

Stores and concentrates bileContracts during the digestion of fats to

deliver the bileCholecystokinin is released by the duodenal

cells, causing the contraction of the gallbladder and relaxation of the sphincter of Oddi

Stores and concentrates bileContracts during the digestion of fats to

deliver the bileCholecystokinin is released by the duodenal

cells, causing the contraction of the gallbladder and relaxation of the sphincter of Oddi

CHOLELITHIASISCHOLELITHIASIS

• Refers to formation of calculi (ie, gallstones in the bladder.

• Predisposing Factors:1. Obese2. Female3. >40 yrs4. OC, Estrogen, intake5. Fair

• Refers to formation of calculi (ie, gallstones in the bladder.

• Predisposing Factors:1. Obese2. Female3. >40 yrs4. OC, Estrogen, intake5. Fair

CHOLELITHIASISCHOLELITHIASISSupersaturated bile, Biliary stasis

Stone formation

Blockage of Gallbladder

Inflammation, Mucosal Damage and WBC infiltration

CHOLECYSTITIS

Common locations of gallstonesCommon locations of gallstones

Gall StonesGall Stones

CHOLECYSTITISCHOLECYSTITIS

– inflammation of gallbladder with gallstone formation.

– inflammation of gallbladder with gallstone formation.

PATHOLOGY-SIGNS AND SYMPTOMS

CHOLECYSTITIS/ CHOLELITHIASISCHOLECYSTITIS/ 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

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/ CHOLELITHIASISCHOLECYSTITIS/ CHOLELITHIASIS

Diagnosis:

• US detects the presence of gallstone

• Serum alkaline phosphatase – 50-120 u/L

• WBC

• Endoscopic retrograde cholangiopancreatography (ERCP) -

Diagnosis:

• US detects the presence of gallstone

• Serum alkaline phosphatase – 50-120 u/L

• WBC

• Endoscopic retrograde cholangiopancreatography (ERCP) -

CHOLECYSTITIS/ CHOLELITHIASISCHOLECYSTITIS/ CHOLELITHIASISNursing 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.

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


• Surgical procedures- Surgical Cholecystectomy, Choledochotomy,

• Laparoscopic cholecystectomy

• Surgical procedures- Surgical Cholecystectomy, Choledochotomy,

• Laparoscopic cholecystectomy



Post-operative nursing interventions

1. Monitor for surgical complications2. Post-operative position after recovery from

anesthesia- LOW FOWLER’s3. Encourage early ambulation 4. Administer medication before coughing and

deep breathing exercises5. Advise client to splint the abdomen to prevent

discomfort during coughing6. Administer analgesics, antiemetics, antacids7. Care of the biliary drainageor T-tube drainage8. Fat restriction is only limited to 4-6 weeks.

Normal diet is resumed

Post-operative nursing interventions

1. Monitor for surgical complications2. Post-operative position after recovery from

anesthesia- LOW FOWLER’s3. Encourage early ambulation 4. Administer medication before coughing and

deep breathing exercises5. Advise client to splint the abdomen to prevent

discomfort during coughing6. Administer analgesics, antiemetics, antacids7. Care of the biliary drainageor T-tube drainage8. Fat restriction is only limited to 4-6 weeks.

Normal diet is resumed

cirrhosis of the liver dr ibraheem bashayreh, rn, phd

Documents

liver cirrhosis slide

types of cirrhosis

destroyed liver cells

nodular slide

fibrosis slide

phd slide

anatomy physiology liver

prolonged course slide