Download - NCM Lecture (Liver and Gallbladder)
ACCESSORY ORGANS
OF
THE DIGESTIVE SYSTEM
REVIEW OF ANATOMY AND PHYSIOLOGY
ACCESSORY ORGANS OF THE DIGESTIVE SYSTEM:
LiverGall bladder and ductal systemPancreas
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
LIVERLiver lobulesHepatic sinusoids (capillaries) lined with
Kupffer cellsPortal 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 PHYSIOLOGYFUNCTIONS OF THE BILIARY SYSTEM:1. Gallbladder – concentrate & store bile2. Ductal system – route for bile to reach the
intestines1. Bile is formed in the liver & excreted into the
hepatic duct2. Cystic duct drains the gallbladder3. Hepatic duct joins he cystic duct to form
common bile duct.4. Sphincter of Oddi : relaxed, bile enters
duodenum; contracted, bile stored in the gall bladder; controlled by cholecystokinin from duodenal mucosa
REVIEW OF ANATOMY AND PHYSIOLOGYPACREAS:Head,BodyTailPancreatic ductFUNCTIONS OF THE PANCREAS:Exocrine : trypsinogen, chymotrypsin,
amylase, lipaseEndocrine : islets of Langerhans: insulin and
glucagon
CASE STUDYSirius, 54 y.o., was brought by his family
because of vomiting of blood.
He’s drowsy, with VS of : 36o, 110, 28, 80/60.
He’s a chronic alcoholic; jaundiced & with big abdomen
CASE STUDYWhat other assessment findings would
you expect?
What are your plans?
NURSING ASSESSMENTMANIFESTATIONS OF LIVER
DISORDERSJaundiceHemorrhage / bleeding problemsPruritus and itchingAscitesGeneralized Edema Intolerance of Sedation
MANIFESTATIONS OF LIVER DISORDERS
JAUNDICE
CAUSES:Prehepatic – hemolysis Intrahepatic – liver parenchymal dsePoshepatic – obstruction of bile ducts
MANIFESTATIONS OF LIVER DISORDERS
HEMORRHAGEDue to inadequate prothrombin & other
clotting factorsManagement :
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 & ITCHINGCaused by bile pigment deposited to
skinManagement:
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
ASCITESCauses :
portal hypertension decreased plasma colloid osmotic pressure hyperaldosteronism
MANIFESTATIONS OF LIVER DISORDERS
ASCITESManagement :
daily weight & abdominal girth low Na diet, fluid restriction, diuretics relieve symptoms from pressure of ascites :
high fowler’s turning & positioning IV albumin, ParacentesisPeritoneovenous Shunt
MANIFESTATIONS OF LIVER DISORDERS
GENERALIZED EDEMA Insufficient albumin
INTOLERANCE OF SEDATIONMost sedatives are metabolized in the
liver except phenobarbital
DISEASES OF THELIVER
HEPATITIS
CIRRHOSIS
CANCER OF THE LIVER
HEPATITISTYPES:
Viral Hepatitis
Toxic Hepatitis – exposure to hepatotoxin : carbon tetrachloride. Morphine, barbiturates
HEPATITIS
Hepatitis A InfectiousFecal-oral route
Hepatitis BSerum hepatitisBlood & body fluid transmission
HEPATITIS
DIAGNOSIS:
Screening test for Hepatitis
Liver function tests:SGOTAlkaline PhosphataseSGPT
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.
HEPATITISPLANNING & 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
HEPATITISPLANNING & IMPLEMENTATION1. 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
HEPATITISPLANNING & IMPLEMENTATION
3. Nutrition : Well- balanced, high P,
high C
4. Providing comfort measures
5. Administer medications : Antivirals Liver supplements
CIRRHOSISEND RESULT OF HEPATO-CELLULAR INJURY
Parenchymal cell death Regeneration & scarring Diminished blood flow fibrosis Fatty degeneration Portal vein obstructionTYPES:1. Postnecrotic – post Hep B; macronodular2. Portal (Laenec’s) – alcoholism;
micronodular3. Biliary – obstruction4. Cardiac – from portal hypertension
CIRRHOSISASSESSMENT:
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.
CIRRHOSISASSESSMENT:
Endocrine SystemTHE LIVER IS UNABLE TO METABOLIZE
HORMONES OF THE ADRENAL CORTEX, OVARIES, ESTROGEN AND TESTES
AMENORRHEA GYNECOMASTIA LOSS OF PUBIC HAIR IMPOTENCE
Hepato-Renal SyndromeRENAL 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 - managementSufficient rest & comfortMeasures to relieve pruritusNutrition: high calorie, low to moderate
P, high C, low fat,Vit A, B comp, C, D and K
Monitor, prevent bleeding.Diuretics if with ascitesClient teaching : avoid hepatotoxic
drugs : opiates & sedatives, avoid alcohol
CIRRHOSIS
COMPLICATONS:
1. HEPATIC COMA
2. 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 COMADEGENERATIVE DISEASE OF THE BRAIN FROM LIVER FAILUREDUE 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:
1. Neuro monitoring
2. Diet : Restrict P, high C, with Vit K
3. Administer: enema, cathartics LACTULOSE – conversion of ammonia to
nonabsorbable ammonium intestinal antibiotics – NEOMYCIN
4. Management for cirrhosis
ESOPHAGEAL VARICESDILATION OF THE VEINS OF THE ESOPHAGUS FROM PORTAL
HYPERTENSION
PORTAL HYPERTENSION – resistance to normal venous drainage of the liver into the portal vein
MANAGEMENT:1. Iced normal saline lavage2. Blood transfusions3. Vitamin K4. Sengstaken Blakemore - 3 lumen
Keep scissors at bedside Label each lumen
5. IV vasopressin6. Surgery – shunting of blood to decompress varices7. Sclerotherapy8. Percutaneous embolization
CANCER OF THE LIVER
Primary
Secondary – liver is the most common site of CA
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
CHOLELITHIASISFORMATION OF GALLSTONES RISK FACTORS : 4 F’s : female, fat, forty, fertile Multiparous Oral contraceptives Cirrhosis Obesity Hyperlipidemia Total parenteral nutrition Bile stasis
CHOLELITHIASIS
PRECIPITANTS:
1. Alteration in the concentration of lecithin, cholesterol, and bile salts
2. Metabolic changes
3. Cholecystitis
4. Biliary stasis
Bile acids and lecithin decrease in bile
The capacity to dissolve cholesterol is reduced
Excess cholesterol precipitate as crystalsGALLSTONES
PATHOPHYSIOLOGY
CHOLELITHIASISASSESSMENT:1. Biliary colic:
RUQ pain, usually postprandially Referred pain: R subscapular
(BOA’S SIGN) Epigastric pain Nausea & vomiting
2. Evidence of choledocholithiasis: Jaundice Clay-colored stools Hyperbilirubinemia Elevated alkaline phosphatase
DIAGNOSIS :Ultrasound
CHOLELITHIASISPLANNING & IMPLEMENTATION:MEDICAL INTERVENTION1. Low fat diet2. Prevent dehydration3. Medications:
1. Smooth Muscle relaxants: reduce spasm of the duct & permit bile passage
Papaverine Nitroglycerine NO Morphine!
2. Bile acids – Chenodeoxycholic acid (CHENIX) and Ursodeoxycholic acid (ACTIGALL) :for clients who are poor risk for surgery; Toxic to the liver
CHOLELITHIASISSURGICAL INTERVENTION
1. Cholecystostomy – draining of the gallbladder
2. Cholecystectomy – removal of the gallbladder
3. Choledocholithotomy – removal of stones from the common bile duct
4. 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 complicationsProviding biliary drainagePreventing distentionManage pain – Fowler’s positionMaintain nutritionDischarge planning & homecare – d/c
after 7-10 days
GALLBLADDER SURGERYCOMPLICATIONS:
1. Bleeding
2. Cardiorespiratory
3. Thrombophlebitis
4. Wound Evisceration and Dehiscence
GALLBLADDER SURGERY
POST-OP NURSING CARE:Prevent complicationsProviding biliary drainagePreventing distentionManage pain – Fowler’s positionMaintain nutritionDischarge planning & homecare – d/c
after 7-10 days
GALLBLADDER SURGERYBILIARY DRAINAGE:
Bloody drainage – normal during 1st 2 hrs
Greenish brown drainage - after 2 hrs
400 ml in 1st 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 SURGERYPOST-OP NURSING CARE:Prevent complicationsProviding biliary drainagePreventing distentionManage pain – Fowler’s positionNutrition - when biliary drainage is
reestablished: Fat –restricted diet
Discharge planning & homecare – d/c after 7-10 days
GALLBLADDER SURGERY
PREVENTING DISTENTION:
NGT until peristalsis returnsRectal tube – expulsion of flatusEnema – 3rd day – peristalsis and
release of flatus
GALLBLADDER SURGERYPOST-OP NURSING CARE:Prevent complicationsProviding biliary drainagePreventing distentionManage pain – Fowler’s positionNutrition - when biliary drainage is
reestablished: Fat –restricted diet
Discharge planning & homecare – d/c after 7-10 days
CHOLECYSTITISCAUSES: Infection: Strep, Staph, E. coli, Typhoid Gall stones Sludge Biliary stasisS/SX: Intolerance to fatty foods Unrelenting RUQ pain & tenderness Referred pain : right subscapular, epigastric Nausea & vomiting MURPHY’S SIGN
CHOLECYSTITISLABS:
1. Increased WBC
2. Increased serum amylase
DIAGNOSIS:
Utltrasound
COMPLICATIONS:
1. Abscess
2. Perforation
3. choledocholithiasis
CHOLECYSTITISMANAGEMENT IVFAntibioticNG tube decompressionCholecystectomy
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 PANCREATITISPREDISPOSING FACTORS:Binge alcohol drinkingBiliary tract diseaseDuodenal obstruction InfectionTraumaNutritional deficiency
CHRONIC PANCREATITIS
PREDISPOSING FACTORS:Alcohol ingestionGallbladder diseaseAutoimmune factors
PANCREATITISRELIEF OF PAIN:
Demerol NO MORPHINE!
DIET Avoid caffeine and alcohol Small frequent feeding of BLAND, easy
digestable foodPANCREATIC 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?
a. Decreased serum creatinine
b. Decreased sodium
c. Increased ammonia
d. Increased calcium