ACCESSORY ORGANS  OF THE DIGESTIVE  SYSTEM
REVIEW OF  ANATOMY  AND  PHYSIOLOGY ACCESSORY ORGANS OF THE DIGESTIVE SYSTEM: Liver Gall bladder and ductal system Pancreas
This is an in-situ photograph of the chest and abdominal contents. As can be seen, the liver is the largest parenchymal organ, lying just below the diaphragm. The right lobe (at the left in the photograph) is larger than the left lobe. The falciform ligament is the rough dividing line between the two lobes.
REVIEW OF  ANATOMY  AND  PHYSIOLOGY LIVER Liver lobules Hepatic sinusoids (capillaries) lined with Kupffer cells Portal circulation – brings blood to the liver from : stomach, spleen, pancreas & intestines
REVIEW OF  ANATOMY  AND  PHYSIOLOGY FUNCTIONS OF THE LIVER: Carbohydrate metabolism  Glycogenesis Glycogenolysis  Gluconeogenesis Fat metabolism - ketogenesis Protein metabolism  anabolism  deamination  urea formation Secretion of bile Detoxification Metabolism of vitamins A,D,K,B &  Clotting factors, esp prothrombin
REVIEW OF  ANATOMY  AND  PHYSIOLOGY FUNCTIONS OF THE BILIARY SYSTEM: Gallbladder – concentrate & store bile Ductal system – route for bile to reach the intestines Bile is formed in the liver & excreted into the  hepatic duct Cystic duct drains the gallbladder Hepatic duct joins he  cystic duct  to form  common bile duct . Sphincter of Oddi  : relaxed, bile enters duodenum; contracted, bile stored in the gall bladder;  controlled by  cholecystokinin  from duodenal mucosa
REVIEW OF  ANATOMY  AND  PHYSIOLOGY PACREAS: Head, Body Tail Pancreatic duct FUNCTIONS OF THE PANCREAS: Exocrine :  trypsinogen, chymotrypsin, amylase, lipase Endocrine :  islets of Langerhans: insulin and glucagon
CASE STUDY Sirius, 54 y.o., was brought by his family because of vomiting of blood. He’s drowsy, with VS of : 36 o , 110, 28, 80/60. He’s a chronic alcoholic; jaundiced & with big abdomen
CASE STUDY What other assessment findings would you expect? What are your plans?
NURSING ASSESSMENT MANIFESTATIONS OF LIVER DISORDERS Jaundice Hemorrhage / bleeding problems Pruritus and itching Ascites Generalized Edema Intolerance of Sedation
MANIFESTATIONS OF LIVER DISORDERS JAUNDICE CAUSES: Prehepatic – hemolysis Intrahepatic – liver parenchymal dse Poshepatic – obstruction of bile ducts
MANIFESTATIONS OF LIVER DISORDERS HEMORRHAGE Due to inadequate prothrombin & other clotting factors Management :  Bile salts p.o.,  Vit K, p.o. & parenteral,  use of small needle with injection,  use of soft toothbrush,  check urine and stool for blood.
MANIFESTATIONS OF LIVER DISORDERS PRURITUS & ITCHING Caused by bile pigment deposited to skin Management:  bathing with tepid water & use of oil-based lotion  cholestyramine –  binds with bile salts and facilitates excretion withfeces Use soft linen Short fingernails
MANIFESTATIONS OF LIVER DISORDERS ASCITES Causes :  portal hypertension  decreased plasma colloid osmotic pressure hyperaldosteronism
MANIFESTATIONS OF LIVER DISORDERS ASCITES Management :  daily weight & abdominal girth  low Na diet, fluid restriction, diuretics  relieve symptoms from pressure of ascites : high fowler’s turning & positioning  IV albumin,  Paracentesis Peritoneovenous Shunt
MANIFESTATIONS OF LIVER DISORDERS GENERALIZED EDEMA Insufficient albumin INTOLERANCE OF SEDATION Most sedatives are metabolized in the liver except  phenobarbital
DISEASES OF THE LIVER HEPATITIS CIRRHOSIS CANCER OF THE LIVER
HEPATITIS TYPES:  Viral Hepatitis  Toxic Hepatitis  – exposure to hepatotoxin : carbon tetrachloride. Morphine, barbiturates
HEPATITIS Hepatitis A  Infectious Fecal-oral route Hepatitis B Serum hepatitis Blood & body fluid transmission
HEPATITIS DIAGNOSIS: Screening test for Hepatitis Liver function tests: SGOT Alkaline Phosphatase SGPT Imaging: Ultrasound
Grossly, there are areas of necrosis and collapse of liver lobules seen here as ill-defined areas that are pale yellow. Such necrosis occurs with hepatitis.
HEPATITIS PLANNING & IMPLEMENTATION 1.  Prevent spread of the disease. Hepatitis A  Transmission : fecal-oral route Incubation period : 2-7 wks (virus in the blood & feces) Most infective 2 wks before onset of s/sx Enteric precautions Gloves when handling stools Handwashing
HEPATITIS PLANNING & IMPLEMENTATION 1.  Prevent spread of the disease. Hepatitis B Transmission : Blood & body fluid  Exposed individuals :  Hep B immunoglobulin, provides passive immunity High Risk Individuals : Hep B vaccine Those who handle blood Homosexual males IV drug users Hemodialysis patients 2.  Obtain rest to promote liver regeneration
HEPATITIS PLANNING & IMPLEMENTATION 3.  Nutrition : Well- balanced, high P,    high C 4.  Providing comfort measures 5.  Administer medications : Antivirals Liver supplements
CIRRHOSIS END RESULT OF HEPATO-CELLULAR INJURY Parenchymal cell death Regeneration & scarring Diminished blood flow  fibrosis Fatty degeneration Portal vein obstruction TYPES: Postnecrotic – post Hep B; macronodular Portal (Laenec’s) – alcoholism; micronodular Biliary – obstruction Cardiac – from portal hypertension
CIRRHOSIS ASSESSMENT: Gastrointestinal System   DUE TO METABOLIC CHANGES IN THE LIVER (P,C,F ) Anorexia Nausea & vomiting Weight loss Flatulence Fatigue  ABDOMINAL PAIN HEPATOMEGALY ASCITES
Ongoing liver damage with liver cell necrosis followed by fibrosis and hepatocyte regeneration results in cirrhosis. This produces a nodular, firm liver. The nodules seen here are larger than 3 mm and, hence, this is an example of "macronodular" cirrhosis.
Mallory's hyaline is seen here, but there are also neutrophils, necrosis of hepatocytes, collagen deposition, and fatty change. These findings are typical for acute alcoholic hepatitis. Such inflammation can occur in a person with a history of alcoholism who goes on a drinking "binge" and consumes large quantities of alcohol over a short time.
CIRRHOSIS ASSESSMENT: Endocrine System THE LIVER IS UNABLE TO METABOLIZE HORMONES OF THE ADRENAL CORTEX, OVARIES, ESTROGEN AND TESTES AMENORRHEA GYNECOMASTIA LOSS OF PUBIC HAIR IMPOTENCE Hepato-Renal Syndrome RENAL FAILURE WITHOUT DISEASE
CIRRHOSIS ASSESSMENT: Other: JAUNDICE ICTERIC SCLERAE PRURITUS SPIDER ANGIOMA PALMAR ERYTHEMA MUSCLE ATROPHY PROLONGED  EASY BRUISING LABS: LIVER FXN TESTS S. BILIRUBIN PROLONGED Prothrombin time DECREASED Serum Albumin DECREASED Hgb & Hct
CIRRHOSIS -  management Sufficient rest & comfort Measures to relieve pruritus Nutrition: high calorie, low to moderate P, high C, low fat,Vit A, B comp, C, D and K Monitor, prevent bleeding. Diuretics if with ascites Client teaching : avoid hepatotoxic drugs : opiates & sedatives, avoid alcohol
CIRRHOSIS COMPLICATONS: HEPATIC COMA PORTAL HPN  ESOPHAGEAL VARICES
Submucosal veins in the esophagus become dilated. These are known as esophageal varices. Varices are seen here in the lower esophagus as linear blue dilated veins. There is hemorrhage around one of them. Such varices are easily eroded, leading to massive gastrointestinal hemorrhage.
One of the most common findings with portal hypertension is splenomegaly, as seen here. The spleen is enlarged from the normal 300 grams or less to between 500 and 1000 gm. Another finding here is the irregular pale tan plaques of collagen over the purple capsule known as "sugar icing" or "hyaline perisplenitis" which follows the splenomegaly and/or multiple episodes of peritonitis that are a common accompaniment to cirrhosis of the liver.
HEPATIC COMA DEGENERATIVE DISEASE OF THE BRAIN FROM LIVER FAILURE DUE TO  INABILITY  OF THE LIVER TO  CONVERT AMMONIA TO UREA CHANGES IN PERSONALITY AND BEHAVIOR LETHARGY CONFUSION TREMORS STUPOR DIZZINESS COMA FETOR HEPATICUS – FRUITY ODOR BREATH SPIDER TELANGIECTASIA ELEVATED SERUM AMMONIA LEVELS
HEPATIC COMA MANAGEMENT: Neuro monitoring Diet : Restrict P, high C, with Vit K Administer:  enema,  cathartics  LACTULOSE – conversion of ammonia to nonabsorbable ammonium  intestinal antibiotics – NEOMYCIN Management for cirrhosis
ESOPHAGEAL VARICES DILATION OF THE VEINS OF THE ESOPHAGUS FROM PORTAL HYPERTENSION PORTAL HYPERTENSION – resistance to normal venous drainage of the liver into the portal vein MANAGEMENT: Iced normal saline lavage Blood transfusions Vitamin K Sengstaken Blakemore - 3 lumen Keep scissors at bedside Label each lumen IV vasopressin Surgery – shunting of blood to decompress varices Sclerotherapy Percutaneous embolization
CANCER OF THE LIVER Primary Secondary – liver is the most common site of CA mets
Here is an hepatocellular carcinoma. Such liver cancers arise in the setting of cirrhosis. Worldwide, viral hepatitis is the most common cause, but in the U.S., chronic alcoholism is the most common cause.   The neoplasm is large and bulky and has a greenish cast because it contains bile. To the right of the main mass are smaller satellite nodules.
CANCER OF THE LIVER S/SX : Anorexia Weight loss Weakness abdominal fullness and bloating Abdominal pain MANAGEMENT – Total Hepatic Lobectomy RESECTION IS UP TO 90% OF THE ORGAN
 
DISEASES OF THE GALLBLADDER CHOLELITHIASIS  CHOLECYSTITIS
CHOLELITHIASIS FORMATION OF GALLSTONES RISK FACTORS :  4 F’s : female, fat,  forty, fertile Multiparous Oral contraceptives Cirrhosis Obesity Hyperlipidemia Total parenteral nutrition Bile stasis
CHOLELITHIASIS PRECIPITANTS: Alteration in the concentration of lecithin, cholesterol, and bile salts Metabolic changes Cholecystitis Biliary stasis
PATHOPHYSIOLOGY Bile acids and lecithin decrease in bile The capacity to dissolve cholesterol is reduced Excess cholesterol precipitate as crystals GALLSTONES
CHOLELITHIASIS ASSESSMENT: Biliary colic:  RUQ pain, usually postprandially Referred pain: R subscapular  (BOA’S SIGN) Epigastric pain  Nausea & vomiting Evidence of choledocholithiasis: Jaundice Clay-colored stools  Hyperbilirubinemia Elevated alkaline phosphatase DIAGNOSIS : Ultrasound
CHOLELITHIASIS PLANNING & IMPLEMENTATION: MEDICAL INTERVENTION Low fat diet Prevent dehydration Medications: Smooth Muscle relaxants: reduce spasm of the duct & permit bile passage Papaverine Nitroglycerine NO Morphine! Bile acids – Chenodeoxycholic acid (CHENIX) and Ursodeoxycholic acid (ACTIGALL) :for clients who are poor risk for surgery; Toxic to the liver
CHOLELITHIASIS SURGICAL INTERVENTION Cholecystostomy – draining of the gallbladder Cholecystectomy – removal of the gallbladder Choledocholithotomy – removal of stones from the common bile duct Intraoperative Cholangiogram – dye in the bile duct thru the cystic duct, if with choledocholithiasis
GALLBLADDER SURGERY PRE-OP NURSING CARE: Assure optimal health Instruct client over pre-operative plan
GALLBLADDER SURGERY POST-OP NURSING CARE: Prevent complications Providing biliary drainage Preventing distention Manage pain – Fowler’s position Maintain nutrition Discharge planning & homecare – d/c after 7-10 days
GALLBLADDER SURGERY COMPLICATIONS: Bleeding  Cardiorespiratory Thrombophlebitis Wound Evisceration and Dehiscence
GALLBLADDER SURGERY POST-OP NURSING CARE: Prevent complications Providing biliary drainage Preventing distention Manage pain – Fowler’s position Maintain nutrition Discharge planning & homecare – d/c after 7-10 days
GALLBLADDER SURGERY BILIARY DRAINAGE: Bloody drainage – normal during 1 st  2 hrs Greenish brown drainage - after 2 hrs 400 ml in 1 st  24 hrs, 200 ml/24 hrs thereafter Placed above the bile duct to collect overflow drainage
GALLBLADDER SURGERY BILIARY DRAINAGE: T tube stays for 6 wks to 6 mos before it is removed Color to urine & stool should be observed after removal of the tube Chills and fever is normal with clamping of T tube during healing period.
GALLBLADDER SURGERY POST-OP NURSING CARE: Prevent complications Providing biliary drainage Preventing distention Manage pain – Fowler’s position Nutrition - when biliary drainage is reestablished: Fat –restricted diet Discharge planning & homecare – d/c after 7-10 days
GALLBLADDER SURGERY PREVENTING DISTENTION: NGT until peristalsis returns Rectal tube – expulsion of flatus Enema – 3 rd  day – peristalsis and release of flatus
GALLBLADDER SURGERY POST-OP NURSING CARE: Prevent complications Providing biliary drainage Preventing distention Manage pain – Fowler’s position Nutrition - when biliary drainage is reestablished: Fat –restricted diet Discharge planning & homecare – d/c after 7-10 days
CHOLECYSTITIS CAUSES: Infection: Strep, Staph, E. coli, Typhoid Gall stones Sludge Biliary stasis S/SX: Intolerance to fatty foods Unrelenting RUQ pain & tenderness Referred pain : right subscapular, epigastric Nausea & vomiting MURPHY’S SIGN
CHOLECYSTITIS LABS: Increased WBC Increased serum amylase DIAGNOSIS: Utltrasound COMPLICATIONS: Abscess Perforation choledocholithiasis
CHOLECYSTITIS MANAGEMENT IVF Antibiotic NG tube decompression Cholecystectomy
 
DISEASES OF THE PANCREAS PANCREATITIS  ACUTE  CHRONIC CANCER OF THE PANCREAS
INFLAMMATION EDEMA OBSTRUCTION OF PANCREATIC DUCT RUPTURE & RELEASE OF DIGESTIVE ENZYMES AUTOLYSIS OF PANCREATIC TISSUE NECROSIS PANCREATITIS
ACUTE PANCREATITIS PREDISPOSING FACTORS: Binge alcohol drinking Biliary tract disease Duodenal obstruction Infection Trauma Nutritional deficiency
CHRONIC PANCREATITIS PREDISPOSING FACTORS: Alcohol ingestion Gallbladder disease Autoimmune factors
PANCREATITIS RELIEF OF PAIN: Demerol NO MORPHINE! DIET Avoid caffeine and alcohol Small frequent feeding of BLAND, easy digestable food PANCREATIC EXTRACTS Viokase/ Cotazym – facilitate digestion of fat-soluble vitamins
CANCER OF THE PANCREAS S/SX: Anorexia Weight loss Weakness Nausea Late signs: pain, jaundice ascites, palpable mass SURGERY: Whipples Procedure:  removal of the head of the pancreas, distal stomach, CBD & duodenum
Which laboratory value would the nurse expect to find in a client as a result of liver failure? Decreased serum creatinine Decreased sodium Increased ammonia Increased calcium
God Bless

Liver Powerpoint

  • 1.
    ACCESSORY ORGANS OF THE DIGESTIVE SYSTEM
  • 2.
    REVIEW OF ANATOMY AND PHYSIOLOGY ACCESSORY ORGANS OF THE DIGESTIVE SYSTEM: Liver Gall bladder and ductal system Pancreas
  • 3.
    This is anin-situ photograph of the chest and abdominal contents. As can be seen, the liver is the largest parenchymal organ, lying just below the diaphragm. The right lobe (at the left in the photograph) is larger than the left lobe. The falciform ligament is the rough dividing line between the two lobes.
  • 4.
    REVIEW OF ANATOMY AND PHYSIOLOGY LIVER Liver lobules Hepatic sinusoids (capillaries) lined with Kupffer cells Portal circulation – brings blood to the liver from : stomach, spleen, pancreas & intestines
  • 5.
    REVIEW OF ANATOMY AND PHYSIOLOGY FUNCTIONS OF THE LIVER: Carbohydrate metabolism Glycogenesis Glycogenolysis Gluconeogenesis Fat metabolism - ketogenesis Protein metabolism anabolism deamination urea formation Secretion of bile Detoxification Metabolism of vitamins A,D,K,B & Clotting factors, esp prothrombin
  • 6.
    REVIEW OF ANATOMY AND PHYSIOLOGY FUNCTIONS OF THE BILIARY SYSTEM: Gallbladder – concentrate & store bile Ductal system – route for bile to reach the intestines Bile is formed in the liver & excreted into the hepatic duct Cystic duct drains the gallbladder Hepatic duct joins he cystic duct to form common bile duct . Sphincter of Oddi : relaxed, bile enters duodenum; contracted, bile stored in the gall bladder; controlled by cholecystokinin from duodenal mucosa
  • 7.
    REVIEW OF ANATOMY AND PHYSIOLOGY PACREAS: Head, Body Tail Pancreatic duct FUNCTIONS OF THE PANCREAS: Exocrine : trypsinogen, chymotrypsin, amylase, lipase Endocrine : islets of Langerhans: insulin and glucagon
  • 8.
    CASE STUDY Sirius,54 y.o., was brought by his family because of vomiting of blood. He’s drowsy, with VS of : 36 o , 110, 28, 80/60. He’s a chronic alcoholic; jaundiced & with big abdomen
  • 9.
    CASE STUDY Whatother assessment findings would you expect? What are your plans?
  • 10.
    NURSING ASSESSMENT MANIFESTATIONSOF LIVER DISORDERS Jaundice Hemorrhage / bleeding problems Pruritus and itching Ascites Generalized Edema Intolerance of Sedation
  • 11.
    MANIFESTATIONS OF LIVERDISORDERS JAUNDICE CAUSES: Prehepatic – hemolysis Intrahepatic – liver parenchymal dse Poshepatic – obstruction of bile ducts
  • 12.
    MANIFESTATIONS OF LIVERDISORDERS HEMORRHAGE Due to inadequate prothrombin & other clotting factors Management : Bile salts p.o., Vit K, p.o. & parenteral, use of small needle with injection, use of soft toothbrush, check urine and stool for blood.
  • 13.
    MANIFESTATIONS OF LIVERDISORDERS PRURITUS & ITCHING Caused by bile pigment deposited to skin Management: bathing with tepid water & use of oil-based lotion cholestyramine – binds with bile salts and facilitates excretion withfeces Use soft linen Short fingernails
  • 14.
    MANIFESTATIONS OF LIVERDISORDERS ASCITES Causes : portal hypertension decreased plasma colloid osmotic pressure hyperaldosteronism
  • 15.
    MANIFESTATIONS OF LIVERDISORDERS ASCITES Management : daily weight & abdominal girth low Na diet, fluid restriction, diuretics relieve symptoms from pressure of ascites : high fowler’s turning & positioning IV albumin, Paracentesis Peritoneovenous Shunt
  • 16.
    MANIFESTATIONS OF LIVERDISORDERS GENERALIZED EDEMA Insufficient albumin INTOLERANCE OF SEDATION Most sedatives are metabolized in the liver except phenobarbital
  • 17.
    DISEASES OF THELIVER HEPATITIS CIRRHOSIS CANCER OF THE LIVER
  • 18.
    HEPATITIS TYPES: Viral Hepatitis Toxic Hepatitis – exposure to hepatotoxin : carbon tetrachloride. Morphine, barbiturates
  • 19.
    HEPATITIS Hepatitis A Infectious Fecal-oral route Hepatitis B Serum hepatitis Blood & body fluid transmission
  • 20.
    HEPATITIS DIAGNOSIS: Screeningtest for Hepatitis Liver function tests: SGOT Alkaline Phosphatase SGPT Imaging: Ultrasound
  • 21.
    Grossly, there areareas of necrosis and collapse of liver lobules seen here as ill-defined areas that are pale yellow. Such necrosis occurs with hepatitis.
  • 22.
    HEPATITIS PLANNING &IMPLEMENTATION 1. Prevent spread of the disease. Hepatitis A Transmission : fecal-oral route Incubation period : 2-7 wks (virus in the blood & feces) Most infective 2 wks before onset of s/sx Enteric precautions Gloves when handling stools Handwashing
  • 23.
    HEPATITIS PLANNING &IMPLEMENTATION 1. Prevent spread of the disease. Hepatitis B Transmission : Blood & body fluid Exposed individuals : Hep B immunoglobulin, provides passive immunity High Risk Individuals : Hep B vaccine Those who handle blood Homosexual males IV drug users Hemodialysis patients 2. Obtain rest to promote liver regeneration
  • 24.
    HEPATITIS PLANNING &IMPLEMENTATION 3. Nutrition : Well- balanced, high P, high C 4. Providing comfort measures 5. Administer medications : Antivirals Liver supplements
  • 25.
    CIRRHOSIS END RESULTOF HEPATO-CELLULAR INJURY Parenchymal cell death Regeneration & scarring Diminished blood flow fibrosis Fatty degeneration Portal vein obstruction TYPES: Postnecrotic – post Hep B; macronodular Portal (Laenec’s) – alcoholism; micronodular Biliary – obstruction Cardiac – from portal hypertension
  • 26.
    CIRRHOSIS ASSESSMENT: GastrointestinalSystem DUE TO METABOLIC CHANGES IN THE LIVER (P,C,F ) Anorexia Nausea & vomiting Weight loss Flatulence Fatigue ABDOMINAL PAIN HEPATOMEGALY ASCITES
  • 27.
    Ongoing liver damagewith liver cell necrosis followed by fibrosis and hepatocyte regeneration results in cirrhosis. This produces a nodular, firm liver. The nodules seen here are larger than 3 mm and, hence, this is an example of "macronodular" cirrhosis.
  • 28.
    Mallory's hyaline isseen here, but there are also neutrophils, necrosis of hepatocytes, collagen deposition, and fatty change. These findings are typical for acute alcoholic hepatitis. Such inflammation can occur in a person with a history of alcoholism who goes on a drinking "binge" and consumes large quantities of alcohol over a short time.
  • 29.
    CIRRHOSIS ASSESSMENT: EndocrineSystem THE LIVER IS UNABLE TO METABOLIZE HORMONES OF THE ADRENAL CORTEX, OVARIES, ESTROGEN AND TESTES AMENORRHEA GYNECOMASTIA LOSS OF PUBIC HAIR IMPOTENCE Hepato-Renal Syndrome RENAL FAILURE WITHOUT DISEASE
  • 30.
    CIRRHOSIS ASSESSMENT: Other:JAUNDICE ICTERIC SCLERAE PRURITUS SPIDER ANGIOMA PALMAR ERYTHEMA MUSCLE ATROPHY PROLONGED EASY BRUISING LABS: LIVER FXN TESTS S. BILIRUBIN PROLONGED Prothrombin time DECREASED Serum Albumin DECREASED Hgb & Hct
  • 31.
    CIRRHOSIS - management Sufficient rest & comfort Measures to relieve pruritus Nutrition: high calorie, low to moderate P, high C, low fat,Vit A, B comp, C, D and K Monitor, prevent bleeding. Diuretics if with ascites Client teaching : avoid hepatotoxic drugs : opiates & sedatives, avoid alcohol
  • 32.
    CIRRHOSIS COMPLICATONS: HEPATICCOMA PORTAL HPN ESOPHAGEAL VARICES
  • 33.
    Submucosal veins inthe esophagus become dilated. These are known as esophageal varices. Varices are seen here in the lower esophagus as linear blue dilated veins. There is hemorrhage around one of them. Such varices are easily eroded, leading to massive gastrointestinal hemorrhage.
  • 34.
    One of themost common findings with portal hypertension is splenomegaly, as seen here. The spleen is enlarged from the normal 300 grams or less to between 500 and 1000 gm. Another finding here is the irregular pale tan plaques of collagen over the purple capsule known as "sugar icing" or "hyaline perisplenitis" which follows the splenomegaly and/or multiple episodes of peritonitis that are a common accompaniment to cirrhosis of the liver.
  • 35.
    HEPATIC COMA DEGENERATIVEDISEASE OF THE BRAIN FROM LIVER FAILURE DUE TO INABILITY OF THE LIVER TO CONVERT AMMONIA TO UREA CHANGES IN PERSONALITY AND BEHAVIOR LETHARGY CONFUSION TREMORS STUPOR DIZZINESS COMA FETOR HEPATICUS – FRUITY ODOR BREATH SPIDER TELANGIECTASIA ELEVATED SERUM AMMONIA LEVELS
  • 36.
    HEPATIC COMA MANAGEMENT:Neuro monitoring Diet : Restrict P, high C, with Vit K Administer: enema, cathartics LACTULOSE – conversion of ammonia to nonabsorbable ammonium intestinal antibiotics – NEOMYCIN Management for cirrhosis
  • 37.
    ESOPHAGEAL VARICES DILATIONOF THE VEINS OF THE ESOPHAGUS FROM PORTAL HYPERTENSION PORTAL HYPERTENSION – resistance to normal venous drainage of the liver into the portal vein MANAGEMENT: Iced normal saline lavage Blood transfusions Vitamin K Sengstaken Blakemore - 3 lumen Keep scissors at bedside Label each lumen IV vasopressin Surgery – shunting of blood to decompress varices Sclerotherapy Percutaneous embolization
  • 38.
    CANCER OF THELIVER Primary Secondary – liver is the most common site of CA mets
  • 39.
    Here is anhepatocellular carcinoma. Such liver cancers arise in the setting of cirrhosis. Worldwide, viral hepatitis is the most common cause, but in the U.S., chronic alcoholism is the most common cause. The neoplasm is large and bulky and has a greenish cast because it contains bile. To the right of the main mass are smaller satellite nodules.
  • 40.
    CANCER OF THELIVER S/SX : Anorexia Weight loss Weakness abdominal fullness and bloating Abdominal pain MANAGEMENT – Total Hepatic Lobectomy RESECTION IS UP TO 90% OF THE ORGAN
  • 41.
  • 42.
    DISEASES OF THEGALLBLADDER CHOLELITHIASIS CHOLECYSTITIS
  • 43.
    CHOLELITHIASIS FORMATION OFGALLSTONES RISK FACTORS : 4 F’s : female, fat, forty, fertile Multiparous Oral contraceptives Cirrhosis Obesity Hyperlipidemia Total parenteral nutrition Bile stasis
  • 44.
    CHOLELITHIASIS PRECIPITANTS: Alterationin the concentration of lecithin, cholesterol, and bile salts Metabolic changes Cholecystitis Biliary stasis
  • 45.
    PATHOPHYSIOLOGY Bile acidsand lecithin decrease in bile The capacity to dissolve cholesterol is reduced Excess cholesterol precipitate as crystals GALLSTONES
  • 46.
    CHOLELITHIASIS ASSESSMENT: Biliarycolic: RUQ pain, usually postprandially Referred pain: R subscapular (BOA’S SIGN) Epigastric pain Nausea & vomiting Evidence of choledocholithiasis: Jaundice Clay-colored stools Hyperbilirubinemia Elevated alkaline phosphatase DIAGNOSIS : Ultrasound
  • 47.
    CHOLELITHIASIS PLANNING &IMPLEMENTATION: MEDICAL INTERVENTION Low fat diet Prevent dehydration Medications: Smooth Muscle relaxants: reduce spasm of the duct & permit bile passage Papaverine Nitroglycerine NO Morphine! Bile acids – Chenodeoxycholic acid (CHENIX) and Ursodeoxycholic acid (ACTIGALL) :for clients who are poor risk for surgery; Toxic to the liver
  • 48.
    CHOLELITHIASIS SURGICAL INTERVENTIONCholecystostomy – draining of the gallbladder Cholecystectomy – removal of the gallbladder Choledocholithotomy – removal of stones from the common bile duct Intraoperative Cholangiogram – dye in the bile duct thru the cystic duct, if with choledocholithiasis
  • 49.
    GALLBLADDER SURGERY PRE-OPNURSING CARE: Assure optimal health Instruct client over pre-operative plan
  • 50.
    GALLBLADDER SURGERY POST-OPNURSING CARE: Prevent complications Providing biliary drainage Preventing distention Manage pain – Fowler’s position Maintain nutrition Discharge planning & homecare – d/c after 7-10 days
  • 51.
    GALLBLADDER SURGERY COMPLICATIONS:Bleeding Cardiorespiratory Thrombophlebitis Wound Evisceration and Dehiscence
  • 52.
    GALLBLADDER SURGERY POST-OPNURSING CARE: Prevent complications Providing biliary drainage Preventing distention Manage pain – Fowler’s position Maintain nutrition Discharge planning & homecare – d/c after 7-10 days
  • 53.
    GALLBLADDER SURGERY BILIARYDRAINAGE: Bloody drainage – normal during 1 st 2 hrs Greenish brown drainage - after 2 hrs 400 ml in 1 st 24 hrs, 200 ml/24 hrs thereafter Placed above the bile duct to collect overflow drainage
  • 54.
    GALLBLADDER SURGERY BILIARYDRAINAGE: T tube stays for 6 wks to 6 mos before it is removed Color to urine & stool should be observed after removal of the tube Chills and fever is normal with clamping of T tube during healing period.
  • 55.
    GALLBLADDER SURGERY POST-OPNURSING CARE: Prevent complications Providing biliary drainage Preventing distention Manage pain – Fowler’s position Nutrition - when biliary drainage is reestablished: Fat –restricted diet Discharge planning & homecare – d/c after 7-10 days
  • 56.
    GALLBLADDER SURGERY PREVENTINGDISTENTION: NGT until peristalsis returns Rectal tube – expulsion of flatus Enema – 3 rd day – peristalsis and release of flatus
  • 57.
    GALLBLADDER SURGERY POST-OPNURSING CARE: Prevent complications Providing biliary drainage Preventing distention Manage pain – Fowler’s position Nutrition - when biliary drainage is reestablished: Fat –restricted diet Discharge planning & homecare – d/c after 7-10 days
  • 58.
    CHOLECYSTITIS CAUSES: Infection:Strep, Staph, E. coli, Typhoid Gall stones Sludge Biliary stasis S/SX: Intolerance to fatty foods Unrelenting RUQ pain & tenderness Referred pain : right subscapular, epigastric Nausea & vomiting MURPHY’S SIGN
  • 59.
    CHOLECYSTITIS LABS: IncreasedWBC Increased serum amylase DIAGNOSIS: Utltrasound COMPLICATIONS: Abscess Perforation choledocholithiasis
  • 60.
    CHOLECYSTITIS MANAGEMENT IVFAntibiotic NG tube decompression Cholecystectomy
  • 61.
  • 62.
    DISEASES OF THEPANCREAS PANCREATITIS ACUTE CHRONIC CANCER OF THE PANCREAS
  • 63.
    INFLAMMATION EDEMA OBSTRUCTIONOF PANCREATIC DUCT RUPTURE & RELEASE OF DIGESTIVE ENZYMES AUTOLYSIS OF PANCREATIC TISSUE NECROSIS PANCREATITIS
  • 64.
    ACUTE PANCREATITIS PREDISPOSINGFACTORS: Binge alcohol drinking Biliary tract disease Duodenal obstruction Infection Trauma Nutritional deficiency
  • 65.
    CHRONIC PANCREATITIS PREDISPOSINGFACTORS: Alcohol ingestion Gallbladder disease Autoimmune factors
  • 66.
    PANCREATITIS RELIEF OFPAIN: Demerol NO MORPHINE! DIET Avoid caffeine and alcohol Small frequent feeding of BLAND, easy digestable food PANCREATIC EXTRACTS Viokase/ Cotazym – facilitate digestion of fat-soluble vitamins
  • 67.
    CANCER OF THEPANCREAS S/SX: Anorexia Weight loss Weakness Nausea Late signs: pain, jaundice ascites, palpable mass SURGERY: Whipples Procedure: removal of the head of the pancreas, distal stomach, CBD & duodenum
  • 68.
    Which laboratory valuewould the nurse expect to find in a client as a result of liver failure? Decreased serum creatinine Decreased sodium Increased ammonia Increased calcium
  • 69.