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