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

Secretion of bile Detoxification Metabolism of vitamins A,D,K,B & Clotting factors, esp prothrombin

anabolism deamination urea formation

REVIEW OF ANATOMY AND PHYSIOLOGY

FUNCTIONS OF THE BILIARY SYSTEM: 1. Gallbladder concentrate & store bile 2. Ductal system route for bile to reach the intestines
1.
2. 3.

4.

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. drowsy, with VS of : 36o, 110, 28, 80/60. a chronic alcoholic; jaundiced & with big abdomen

Hes

Hes

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 fowlers 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 illdefined 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: 1. Postnecrotic post Hep B; macronodular 2. Portal (Laenecs) alcoholism; micronodular 3. Biliary obstruction 4. 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.

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:

LABS:

JAUNDICE ICTERIC SCLERAE PRURITUS SPIDER ANGIOMA PALMAR ERYTHEMA MUSCLE ATROPHY PROLONGED EASY BRUISING

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:
1. 2.

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: 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 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: 1. Iced normal saline lavage 2. Blood transfusions 3. Vitamin K 4. Sengstaken Blakemore - 3 lumen

Keep scissors at bedside Label each lumen

5. 6. 7. 8.

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

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 Fs : 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

PATHOPHYSIOLOGY
Bile acids and lecithin decrease in bile

The capacity to dissolve cholesterol is reduced

GALLSTONES
Excess cholesterol precipitate as crystals

CHOLELITHIASIS
ASSESSMENT: 1. Biliary colic:

RUQ pain, usually postprandially Referred pain: R subscapular (BOAS SIGN) Epigastric pain Nausea & vomiting Jaundice Clay-colored stools Hyperbilirubinemia Elevated alkaline phosphatase

2.

Evidence of choledocholithiasis:

DIAGNOSIS : Ultrasound

CHOLELITHIASIS
PLANNING & IMPLEMENTATION: MEDICAL INTERVENTION 1. Low fat diet 2. Prevent dehydration 3. 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

CHOLELITHIASIS
SURGICAL INTERVENTION
1. 2. 3. 4.

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
Instruct

optimal health
client over pre-operative plan

GALLBLADDER SURGERY
POST-OP NURSING CARE: Prevent complications Providing biliary drainage Preventing distention Manage pain Fowlers position Maintain nutrition Discharge planning & homecare d/c after 7-10 days

GALLBLADDER SURGERY
COMPLICATIONS: 1. Bleeding 2. Cardiorespiratory 3. Thrombophlebitis 4. Wound Evisceration and Dehiscence

GALLBLADDER SURGERY
POST-OP NURSING CARE: Prevent complications Providing biliary drainage Preventing distention Manage pain Fowlers position Maintain nutrition Discharge planning & homecare d/c after 7-10 days

GALLBLADDER SURGERY
BILIARY 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 SURGERY
POST-OP NURSING CARE: Prevent complications Providing biliary drainage Preventing distention Manage pain Fowlers 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 3rd day peristalsis and release of flatus

GALLBLADDER SURGERY
POST-OP NURSING CARE: Prevent complications Providing biliary drainage Preventing distention Manage pain Fowlers 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 MURPHYS SIGN

CHOLECYSTITIS
LABS: 1. Increased WBC 2. Increased serum amylase DIAGNOSIS: Utltrasound COMPLICATIONS: 1. Abscess 2. Perforation 3. choledocholithiasis

CHOLECYSTITIS
MANAGEMENT IVF Antibiotic NG tube decompression Cholecystectomy

DISEASES OF THE PANCREAS

PANCREATITIS
ACUTE

CHRONIC

CANCER

OF THE PANCREAS

PANCREATITIS
INFLAMMATION EDEMA OBSTRUCTION OF PANCREATIC DUCT RUPTURE & RELEASE OF DIGESTIVE ENZYMES AUTOLYSIS OF PANCREATIC TISSUE

NECROSIS

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
NO

OF PAIN:

Demerol

MORPHINE!

DIET
Avoid

caffeine and alcohol Small frequent feeding of BLAND, easy digestable food
PANCREATIC
Viokase/

EXTRACTS

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

a. b. c. d.