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71 Cards in this Set

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A&P of the Liver
 Liver: Largest organ
 Dual Blood Supply
 Stores 200-400ml blood
 Contains 50,000-100,000 lobules
 Kupffer cells: Phagocytes
 Metabolic Factory & Waste Disposal
 Storage Plant
Primary Liver Functions
 Vascular
Blood supply
•hepatic portal vein (75% blood)
–nutrients and toxins absorbed across the intestinal epithelium
–breakdown product of blood cells from spleen
–endocrine secretion of pancreas
•hepatic artery (25 % blood) –Oxygen
–mixes with venous blood
• Blood Storage
• Blood Filtration

 Secretory
• Bile Salt Production
• Conjugation & Secretion of Bilirubin
• Removal of Unused Cholesterol


 Metabolic
• Carbohydrates
• Fats
• Proteins
• Clotting Components
• Rids clotting factors
• Detoxification

 Storage
• Blood, Glucose, Fat, Vitamins, Minerals
Primary Liver Functions
 Vascular
Blood Storage
• Blood Filtration
Primary Liver Functions
 Secretory
• Bile Salt Production
• Conjugation & Secretion of Bilirubin
• Removal of Unused Cholesterol
Primary Liver Functions
 Metabolic
• Carbohydrates
• Fats
• Proteins
• Clotting Components
• Rids clotting factors
• Detoxification
Primary liver Functions
 Storage
• Blood, Glucose, Fat, Vitamins, Minerals
Diagnostic Tests of Liver Function
 Cholesterol
 Albumin
 Immunoglobins
 PT,PTT
 Serum Ammonia
 Bilirubin


o Serum Enzymes
• AST
• ALT
• GGT
• LDH
Diagnostic Tests of Liver Function
 Albumin
 Albumin
Normal levels: 3.5-5.0 g/dl
A component of total protein and is the most abundant protein in blood plasma. It keeps fluid inside your blood vessels. If levels of albumin are low, there is the possibility of primary liver disease, kidney disease, tissue damage or inflammation, and malnutrition (note: this is probably not a complete list).
Diagnostic tests of liver functions
o Serum Enzymes
ALT-what is ALT, describe what it does in the body.
• ALT Alanine aminotransferase

Alanine aminotransferase (ALT), formerly called serum glutamate pyruvate transaminase, or SGPT, is an enzyme necessary for energy production. It is present in a number of tissues, including the liver, heart, and skeletal muscles, but is found in the highest concentration in the liver. Because of this, it is used in conjunction with other liver enzymes to detect liver disease, especially hepatitis or cirrhosis without jaundice. Additionally, in conjunction with the aspartate aminotransferase test (AST), it helps to distinguish between heart damage and liver tissue damage

Serum increasse in body
ALT elevations are not specific for primary hepatocellular disease. Bile duct obstruction (e.g., pancreatitis) causes ALT elevation within 3 to 4 days, and the elevation persists for at least several days. It is probable that retained bile salts physically damage the cell membranes of surrounding hepatocytes and result in enzyme leakage.

ALT is simply a screening test for hepatocellular damage.

Outcome:

(a) If values decrease by 50% every 1-2 days, prognosis is good.

(b) Continuing elevations suggest persistent hepatocellular disease (consider further tests: e.g., serum bile acids assay, liver biopsy).
Diagnostic Tests of Liver Function
 Cholesterol
 Cholesterol
Norms: less than 200
blood lipid synthesized by the liver...used to form bile salts..
Person has to be NPO for 12 hours before the test, then collect 3-5ml of venous blood
Diagnostic tests of liver functions
o Serum Enzymes
GGT
• GGT Gamma-glutamyl transferase
0-45unit/l average
Gamma-glutamyl transferase (GGT), sometimes called gamma-glutamyl transpeptidase (GGPT), is an enzyme that is compared with ALP levels to distinguish between skeletal disease and liver disease. Because GGT is not increased in bone disorders, as is ALP, a normal GGT with an elevated ALP would indicate bone disease. Conversely, because the GGT is more specifically related to the liver, an elevated GGT with an elevated ALP would strengthen the diagnosis of liver or bile-duct disease. The GGT has also been used as an indicator of heavy and chronic alcohol use, but its value in these situations has been questioned recently. It is also commonly elevated in patients with infectious mononucleosis.
Diagnostic Tests of Liver Function
 PT,PTT
 PT,PTT 1.5-2.5 x control
PT involves the interactions of fibrinogen and prothrombin, which are synthesized by the liver
PT is relatively insensitive for detecting mild hepatocellular dysfunction. Because the biologic half-lives of the involved clotting factors are short (hours to a few days), the PT has a high prognostic value in acute liver injury. In acute viral or toxic hepatitis, PT > 5 sec above control is an early indicator of fulminant hepatic failure.
Diagnostic Tests of Liver Function
 Immunoglobins
 Immunoglobins
Increases in
o Liver disease
o Cirrhosis of the liver (most cases)
Serum immunoglobulins rise in most cases of chronic liver disease when the reticuloendothelial system is defective or bypassed by portal venous shunts.
Serum globulin levels rise slightly in acute hepatitis and more markedly in chronic active hepatitis, particularly of the autoimmune variety. The pattern of immunoglobulin increase adds little: IgM is quite elevated in primary biliary cirrhosis, IgA in alcoholic liver disease, and IgG in chronic active hepatitis.
Diagnostic tests of liver functions
o Serum Enzymes
LDH
• LDH 70-250 unit/l

LDH (lactate dehydrogenase) is an enzyme found in the kidneys, liver, heart, muscle, brain, lungs and red blood cells. An increased level may be indicative of disease in one of those areas. When matched with elevated liver or kidney enzymes, an elevated LDH confirms disease in one of those organs.

LDH can be quite high with malignancies involving the liver.
Diagnostic Tests of Liver Function
 Serum Ammonia
 Bilirubin
 Serum Ammonia
level: 15-45 mcg/dl
Serum ammonia levels are elevated, as the liver fails to effectively convert ammonia to urea for renal excretion.
 Bilirubin
Hyperbilirubinemia results from increased bilirubin production, decreased liver uptake or conjugation, or decreased biliary excretion.

Increased bilirubin production (eg, from hemolysis) or decreased liver uptake or conjugation (eg, Gilbert's disease) causes unconjugated (or free) bilirubin in serum to increase. Decreased bile formation and excretion (cholestasis) elevates conjugated bilirubin in serum, and the latter appears in urine.
Diagnostic tests of liver functions
o Serum Enzymes
• AST
o Serum Enzymes
• AST Aspartate aminotransferase

Aspartate aminotransferase (AST), formerly called serum glutamic-oxaloacetic transaminase, or SGOT, is another enzyme necessary for energy production. It, too, may be elevated in liver and heart disease. In liver disease, the AST increase is usually less than the ALT increase. However, in liver disease caused by alcohol use, the AST increase may be two or three times greater than the ALT increase.
Diagnostic Tests
 Radiological tests
• Ultrasound

• CT Scan
Diagnostic Tests
 Radiological tests
• Ultrasound
Findings obtained by US are morphologic and independent of function. US is the most important investigative tool in screening for biliary tract abnormalities and mass lesions in the liver. US is better at detecting focal lesions (> 1 cm in diameter) than diffuse disease (eg, fatty liver, cirrhosis). In general, cysts are echo-free; solid lesions (eg, tumors, abscesses) tend to be echogenic. The ability to localize focal lesions permits US-guided aspiration and biopsy.

• CT Scan
CT is sensitive to variations in density of differing hepatic lesions. The addition of an IV contrast agent helps differentiate more subtle differences between soft tissues and define the vascular system and the biliary tract. CT shows liver structures more consistently than US; neither obesity nor intestinal gas obscures them. CT is especially useful for visualizing space-occupying lesions (eg, metastases) in the liver and masses in the pancreas. CT can detect fatty liver and the increased hepatic density associated with iron overload. CT is expensive and necessitates radiation exposure; both factors lessen its routine use compared with US.
Diagnostic Tests
 Liver Biopsy
 Liver Biopsy
Percutaneous liver biopsy provides valuable diagnostic information with relatively small risk and little patient discomfort. Performed with the patient under local anesthesia, this bedside procedure entails aspiration or cutting. The needle is inserted through an anesthetized intercostal space anterior to the midaxillary line, just below the point of maximal dullness on expiration. The patient lies still and maintains expiration. The liver is rapidly entered with either suction applied (Jamshidi) or a cutting sheath advanced (Trucut). The result is a procedure that takes 1 to 2 sec and yields a liver specimen 1 mm in diameter and 2 cm long. Occasionally, a second pass is necessary; if a second or third attempt is unsuccessful, then needle biopsy should be guided by ultrasound (US) or CT. US-guided biopsies using a biopsy gun, whose spring mechanism fires a modified Trucut needle, are less painful and provide a high yield. US guidance is particularly useful for sampling focal lesions or avoiding vascular lesions (eg, hemangiomas).

At biopsy, the liver's texture can be ascertained on needle insertion: a hard, gritty feel suggests cirrhosis. The biopsy is examined routinely for histopathology. Cytology, frozen section, and culture may be useful in selected cases. In suspected Wilson's disease, copper content should be measured. Gross inspection provides information: fragmentation suggests cirrhosis; a fatty liver is pale yellow and floats in formaldehyde; carcinoma is whitish.

Fine-needle biopsy under US guidance detects metastatic carcinoma in at least 66% of cases and may establish the diagnosis despite negative scanning techniques; cytologic examination of the biopsy fluid yields positive findings in an additional 10% of cases. Results are less valuable in lymphoma and correlate poorly with the clinical impression of hepatic involvement. Biopsy is especially valuable in detecting TB or other granulomatous infiltrations and can clarify graft problems (ischemic injury, rejection, biliary tract disease, viral hepatitis) after liver transplantation.
Diagnostic Tests
 Paracentesis
 Peritoneal Lavage
 Paracentesis
Insertion of a needle into the abdominal cavity to remove fluid for examination
Purpose: To investigate the cause of ascites.
Abnormal in Cirrhosis, pancreatitis, rupture of gall bladder, spleen, or liver, etc.
 Peritoneal Lavage
Types of Cirrhosis
o Biliary -- 15%
o Cardiac -- Rare
o Post-Necrotic -- 2%


 Laennec's -- 75% of cases in U.S.
 Alcoholism is 8th leading cause of death among adult Americans. 3rd leading cause of death in males 29-59 years.
Laennec's Cirrhosis
Laennec's Cirrhosis
 Predisposing Factors-alcohol
 Effects on total body systems
 Nursing management-Assess history, physical assessment-symptoms-related to mal-nurtrition, portal hypertension, hypoalbuminemia, and hyperaldosteronism.
Assess Early signs and symptoms or later signs, assess psychological symptoms.
Nursing interventions for cirrhosis: rest, positioning, Oxygen, nutrition, skin care, potential for injury, management of pain. Monitor for infection, administer antacids or histamine antagonists, inability to detoxify drugs, monitor alcohol withdrawal, monitor for complications.
 Patient teaching
 Medical Treatment
Laennec's Cirrhosis
 Effects on entire body:
• Endocrine
Loss of libido, Gynecomastia in males, Impotence, Infertility, Amenorrhea,
Potential complication: diabetes

• Immune System
Leukocytopenia
Increased susceptibility to infections.
• Hepatic
Atrophic, nodular liver
Splenomegaly-enlarged spleen
Potential complication: liver cancer

• Gastrointestinal
Nausea and Vomiting, diarrhea, Abdominal pain
anorexia, ascites, clay colored stools, peptic ulcers, GI bleeding, Hemorrhoids

• Neurologic
Hepatic encephalopathy
(agitation-lethargy-stupor-coma), Paresthesias, Sensory disturbances, Asterixis (liver flap), Tremor, delirium

• Cardiovascular
increases portal pressure,
bounding pulse, Pulmonary hypertension, Dysrhythmias

• Hematologic
decreased clotting factors,
Thrombocytopenia, anemia,
Potential Complication: disseminated intravascular coagulation

• Integumentary
Jaundice, Purpura, Palmar erythema, Spider nevi,
Superficial veins dilate on abdomen and chest, Nail changes, Clubbing, Loss of Axillary and pubic hair
Complications of Cirrhosis
o Portal Hypertension
o Hepatorenal Syndrome
o Esophageal Varices
o Ascites
(GI Bleeding)
o Nutritional Hepatic Deficiencies

oEncephalopathy

oLiver Abscess

oSkin Disorders
Portal Hypertension Protocol
 Daily Weight
 Low Salt Diet/Fluid Restrictions
 Low Protein Diet
 Spironolactone (Aldactone)
 Albumin
Esophageal Varices
treatment
 Fluid/Blood Replacement
 Gastric Lavage
 Fresh Frozen Plasma, Platelets
 Vitamin K, Pitressin, Propranolol
 Sclerotherapy
 Esophageal Tamponade (Sengstaken¬Blakemore Tube)
Ascites
o Where does it come from?


o How do you treat it?
Ascites
o Where does it come from?

Cause:
Disease in the peritoneal cavity:

1. Malignant conditions (cancer) -- peritoneal carcinomatosis, hepatocellular carcinoma ("liver cancer"), cancer metastasized to the liver.

2. Mesothelioma
Infections -- bacterial peritonitis, fungal peritonitis, Tuberculosis peritonitis, HIV-associated peritonitis

3. Others -- vasculitis, granulomatous peritonitis, familial Mediterranean fever, and eosinophilic peritonitis


Portal hypertension
1. Liver diseases -- cirrhosis, Alcoholic Hepatitis, massive hepatic metastases, fulminant hepatic (liver) failure, fatty liver of pregnancy, hepatic fibrosis

2. Hepatic (liver) congestion -- congestive Heart Failure, Budd-Chiari syndrome, tricuspid insufficiency, constrictive Pericarditis, and veno-occlusive disease
Portal vein occlusion

Low protein (albumin) conditions
1. Severe Malnutrition with anasarca, protein-losing enteropathy (body loses protein from the gastrointestinal tract), and 2. Nephrotic Syndrome (a kidney condition)

Miscellaneous
1. Pancreatic ascites, ovarian disease, Myxedema (thyroid disease), chylous ascites, bile ascites, urine ascites, nephrogenic ascites


o How do you treat it?
Large volume paracentesis (fluid removal) may be performed for symptomatic relief. Fluid should be removed slowly to prevent secondary circulatory hypovolemia.
Identify and treat the underlying cause. See individual disease sections for specific treatments.
Diuretic induced diuresis.
Hepatic Encephalopathy

Treatments to decrease intestinal ammonia production
Hepatic Encephalopathy.
Hepatic encephalopathy is a syndrome observed in patients with cirrhosis. Hepatic encephalopathy is defined as a spectrum of neuropsychiatric abnormalities in patients with liver dysfunction, after exclusion of other known brain disease. It is characterized by personality changes, intellectual impairment, and a depressed level of consciousness.

Diet
 Cathartics
o Lactulose (Cephulac)
 Antibiotics
o Neomycin
 Comfort Measures if end-stage Cirrhosis & Hepatic Failure
 Or if precipitated by GI bleed, Stop bleeding
Hepatorenal Syndrome
Hepatorenal syndrome (HRS) is the development of renal failure in patients with advanced chronic liver disease, occasionally fulminant hepatitis, who have portal hypertension and ascites.

oD/C Nephrotoxic Drugs
 Treat Electrolyte abnormalities
 Treat symptomatically
 Hard to distinguish between this and Hepatic Encephalopathy
 Primary cause of death in end-stage cirrhosis
Skin Problems With Cirrhosis
o Pruritis
o Jaundice
o Spider Angiomas & Nevi-Spider angioma is so named because of its appearance: a central, red, elevated area with surrounding broken blood vessels radiating outward like a spider's legs.
o Palmar Erythema (Palmar erythema is reddening of the palms )
o Clubbing of Fingers
Nutritional Deficiencies-what diet does a person have to have when they have Cirrhosis
 Protein Restrictions
 Sodium Restrictions
 Fluid Excess: Edema, Ascites
 Fluid Restriction
 Vitamin & Mineral Supplements
 High Calorie, Moderate Fat Needed
Nursing Diagnosis for Hepatic Failure
 Nutrition, Imbalanced: Less than Required
 Activity Intolerance
 Disturbed Thought Processes
 Self-Care Deficit
 Potential Fluid Volume Excess
 Risk for Injury: Trauma (Bleeding)
 Impaired Skin Integrity
 Risk for Infection
Common Hepatic Medications
Pitressin (Vasopressin)

Lactulose (Chronulac)

Neomycin

Aldactone
(Spironolactone)

VitaminK (Aquamephyton)

Albumin

CJ Pepcid (Or other H2
blocker)

Thiamine

Inderal
Sclerotherapy
Laennec's Cirrhosis/ alcoholic cirrhosis
 Nursing Management
(lesson objective)
 Nursing Management:
• Nursing Diagnosis-
Excess Fluid volume, Disturbed thought process (accumululated nitrogenous waste products and other metabolites affect mental status)
Ineffective protection (Impaired coagulation, esophageal varices,--significant risk for hemorrhage)
Impaired skin integrity
Imbalanced nutrition-less than body requirements
• Assessment-monitor v.s. report tachycardia or hypotension, Assess neurologic status, level of consciousness and mental state, Assess urine specific gravity, assess for jugular vein distention, measure abdominal girth, assess weight, check for peripheral edema. Monitor I&O.
• Planning-Avoid factors that may precipitate hepatic encephalopathy, avoid hepatoxic meds and CNS depressant drugs, plan for consistent nursing care assignments. Plan to report abnormal coagulation studies and platelet counts. Plan to prevent skin breakdown,
• Interventions-administer meds or enemas as ordered to reduce
nitrogenous products. Monitor bowel function and provide measures to promote regular elimination.
Use measures to prevent dry skin, apply an emollient or lubricant as needed to keep the skin moist, avoid soap or preparations with alcohol. Turn every 2 hours. Administer prescribed antihistamnine. Low sodium diet, small meals and frequent snacks, etc.
• Evaluation-Skin intact, pt is not scratching, no signs of hemorrhage or bleeding, fluid volume decreased, pt alert and oriented, pt eats 90% of meals and 80% of snacks.
Acetaminophen Overdose & Hepatic Failure
 Cause may be either OD of Tylenol or Impaired Liver Function
 Antidote: Mucomyst (N-Acetylcysteine)
STAT!
 Per NG tube or-oral
 Smells like rotten eggs!
 NEW! Acetadote LV. as 21 hour infusion
Hepatitis
o Comparison of types:
 Alcoholic-Alcoholic hepatitis is a syndrome of progressive inflammatory liver injury associated with long-term heavy intake of ethanol. The pathogenesis is not completely understood.

Patients who are severely affected present with subacute onset of fever, hepatomegaly, leukocytosis, marked impairment of liver function (eg, jaundice, coagulopathy), and manifestations of portal hypertension (eg, ascites, hepatic encephalopathy, variceal hemorrhage). However, milder forms of alcoholic hepatitis often do not cause any symptoms.
Alcoholic hepatitis usually persists and progresses to cirrhosis if heavy alcohol use continues. If alcohol use ceases, alcoholic hepatitis resolves slowly over weeks to months, sometimes without permanent sequelae but often with residual cirrhosis.


 Toxic
Inflammation of the liver due to an adverse reaction with a drug
Drugs that can be associated with drug-induced hepatitis include acetaminophen, vitamin A, and PTU (a drug treatment for tuberculosis).

 Hepatobiliary
 Viral
• A-fecal-oral route
B-parenterally and sexually, most often by mucous membrane exposure or percutaneous exposure to infectious body fluids. Saliva, serum, and semen all have been determined to be infectious.
C-parenterally, perinatally, and sexually. HCV is transmitted most reliably through transfusion of infected blood or blood products, transplantation of organs from infected donors, and sharing contaminated needles among intravenous drug users.
D-requires the presence of HBV to replicate
Modes of transmission for HDV are similar to those for HBV, although perinatal transmission rarely occurs and has not been documented in the United States.
E- fecal-oral route, with fecally contaminated water providing the most common means of transmission.


o Manifestations:
• Preicteric Phase-Patients experience anorexia, nausea, vomiting, alterations in taste, arthralgias, malaise, fatigue, urticaria, and pruritus. Some even develop an aversion to cigarette smoke.
When seen by a health care provider during this phase, patients are often diagnosed as having gastroenteritis or a viral syndrome.

• Icteric Phase-Patients may note darkening of the urine, followed by pale-colored stools.
In addition to the predominant gastrointestinal symptoms and malaise, patients become icteric and may develop right upper quadrant pain with hepatomegaly.

• Posticteric Phase-Symptoms and icterus resolve.
Liver enzymes return to normal
Hepatitis
o Fulminant Hepatitis
o Chronic Hepatitis
o Laboratory & Diagnostic Tests:
o Pharmacology
• Pre-Exposure
Prophylaxis
• Post-Exposure
Prophylaxis

• CDC
Recommendations
Hepatitis

 Nursing Diagnosis & Care
(objective)
 Nursing Diagnosis & Care
• Risk for Infection (Transmission)
Interventions: Use standard precautions. Practice meticulous handwashing. The hepatitis viruses are spread by direct contact with feces or blood and body fluids. For clients with HAV or HEV, use standard precautions and contact isolation if fecal incontinence is present. the fecal-oral route is the primary mode of transmission of these viruses.
Encourage prophylactic treatment of all members of household and intimate sexual partners
• Activity Intolerance
Interventions: encourage planned rest periods throughout the day. Adequate rest is necessary for optimal immune function. Assist to identify essential activities and those that can be deferred or delegated to others. Identifying essential and nonessential activities promotes client's sense of control. Suggest using level of fatigue to determine activity level.
• Imbalanced Nutrition: Less than body requirements
Interventions:
Help plan a diet of appealing foods that provides a high kilocaloric intake of approximately 16 carbohydrate kolocalories per kilogram of ideal body weight.
Encourage planning of food intake according to symptoms of the disease. Discuss eating smaller meals and using between meal snacks to maintain nutrient and calorie intake. clients with acute hepatitis often are more anorexic and nauseated in the afternoon and evening; planning majority of calorie intake in the morning helps maintain adequate intake.
Encourage nutritional supplement drinks

• Disturbed Body Image

• Impaired Physical Mobility
• Deficient Knowledge (Of disease process)
• Pain
• Risk for Imbalanced Fluid Volume
Hepatitis



 Patient and Family Teaching:
Hepatitis



 Patient and Family Teaching:
• Handwashing, don't share eating utensils, avoiding food handling or preparation activities by the client with hepatitis A;
• Personal Hygiene
• Sexual contact-abstain during acute infection and using barrier protection if a carrier or for chronic infection
• Food/Water Contamination
• Hepatotoxic Drugs-avoid such as alcohol, acetaminophen, and selectd other drugs.

• Disease Course
• Treatment
• Laboratory tests-ALT, AST, etc
• Donating Blood -never again
• Determining Carrier State
• Modes of Transmission
Gallbladder Disorders
 Cholelithiasis
Cholelithiasis is the presence of gallstones in the gallbladder.....Symptoms:
 Cholelithiasis symptoms:
• Epigastric Pain
• Heartburn
• RUQ abd. Pain (may radiate to right subscapular area)
• Jaundice, clay-colored stools
• Intolerance of fatty foods
Gallbladder Disorders
 Cholecystitis

Cholecystitis is inflammation of the gallbladder from obstruction of the cystic duct....Symptoms:
 Cholecystitis
Epigastric Pain
• Heartburn
• RUQ abd. Pain (may radiate to right subscapular area)
• Jaundice, clay-colored stools
• Intolerance of fatty foods
• Fever, >WBC
• Abd. Guarding with rebound tenderness & rigidity
• >Bilirubin, Alkaline Phosphatase, & Amylase
Gallbladder Disorders
 Risk Factors For Gallstone Formation
Gallbladder Disorders
 Risk Factors For Gallstone Formation
• Family history Cirrhosis
• Hyperlipidemia Obesity
• Rapid Weight Loss Diabetes
• Females Pregnancy
• Oral Contraceptives

Aging
• Native American

Caucasian
• Mexican American Biliary Duct D/O
Gallbladder Disorders

 Laboratory Tests:
 Laboratory Tests:
• CBC-May indicate infection and inflammation if WBC elevated.
• Amylase, Lipase-identify possible pancreatitis related to common duct obstruction.
• Serum Bilirubin-Elevated direct (conjugated) bilirubin may indicate obstructed bile flow in the biliary duct system.
• Others as per individual needs
Gallbladder Disorders

 Diagnostic Tests:
 Diagnostic Tests:
• X-rays of abdomen-may show gallstones with a high calcium content
• Oral Cholecystogram-is performed using a dye administered orally to assess teh gallbladders ability to concentrate and excrete bile.
• Cholangiograms
• Ultrasonography-noninvasive exam that can accurately diagnose cholelithiasis. It also can be used to assess emptying of the gallbladder.
Gallbladder Disorders Treatment
o Pharmacology Drugs that dissolve gallstones-Ursodiol (actigall) and chenodiol (chenix) reduce cholesterol content of gallstones, leading to their gradual dissolution. Cholestyramine (Questran) binds with bile salts to promote excretion in the feces.

o Diet Therapy-Food intake may be eliminated during an acute attack of cholecystitis and a nasogastric tube inserted to relieve nausea and vomiting. Dietary fat intake may be limited, especially if the client is obese. If bile flow is obstructed, fat soluble vitamins (A, D, E, and K) and bile salts may need to be administered.
 Surgery
• Open Cholecystectomy-A t-tube is inserted to maintain patency of the duct and promote bile passage while edema decreases. Excess bile is collected in a drainage bag secured below the surgical site. If it is suspected that a stone has been retained following surgery, a postoperative cholangiogram via the T-tube or direct visualization of the duct with an endoscope may be performed.
• Laparoscopic Cholecystectomy-Removal of the gallbladder is the treatment of choice for symptomatic cholelithiasis or cholecystitis. this minimally invasive procedure has a low risk of complications and generally requires a hospital stay of less than 24 hours.
• T -tube placement-Placed in the common bile duct.
Nursing care of the client with a t-tube:
Ensure that the t-tube is properly connected to a sterile container; keep the tube below the level of the surgical wound. This position promotes the flow of bile and prevents backflow or seepage of caustic bile onto the skin. the tube itself decreases biliary tree pressure.


 ESWL - Extracorporeal Shock Wave Lithotripsy-ultrasound is used to align the stones with the source of shock waves and the computerized lithotripter. Positioning is of prime importance throughout the procedure, which usually takes an hour. Mild sedation may be given during the procedure.
 Percutaneous choleycystostomy-ultrasound guided drainage of the gallbladder, may be done in high-risk clients to postpone or even eliminate the need for surgery
Gallbladder Disorders Nursing Diagnosis & Care
 Pain
Discuss the relationship between fat intake and the pain. teach ways to reduce fat intake. Fat entering the duodenum initiates gallbladder contractions, causing pain when gallstones are present in the ducts.
Withold oral food and fluids during episodes of acute pain. Insert a nasogastric tube and connect to low suction if ordered. Emptying the stomach reduces the amount of chyme entering the duodenum and the stimulus for gallbladder contractions, thus reducing pain.
For severe pain, administer meperidine or other narcotic analgesia as ordered. Research indicates that morphine is no more likely to cause spasms of the sphincter of Oddi than meperidine.
Place in Fowlers position
Monitor vital signs every 4 hours.
 Impaired Gas Exchange
 Risk for Infection
 Imbalanced Nutrition: Less than body requirements
Assess nutritional status, including diet history, height and weight, and skinfold measurements. Even overweight clients have vitamin deficiencies.
Evaluate lab: bilirubin, albumin, glucose, and cholesterol-report abnormal.
Refer to a dietitian for counseling to promote healthy weight loss and reduce pain episodes. A low-carbohydrate, low fat, higher protein diet reduces symptoms of cholecystitis. Administer vitamin supplements as ordered.
 Risk for Imbalanced Fluid Volume
 Deficient Knowledge (Disease process)
Gallbladder Disorders Patient & Family Teaching
o Non-Surgical Interventions
o Preoperative Teaching
o Postoperative Teaching
(objective)
Gallbladder Disorders Patient & Family Teaching
o Non-Surgical Interventions-Drugs that dissolve gallstones-Ursodiol (actigall) and chenodiol (chenix) reduce cholesterol content of gallstones, leading to their gradual dissolution. Cholestyramine (Questran) binds with bile salts to promote excretion in the feces.
o Preoperative Teaching-
Postoperative expectations-pain management, deep breathing and mobilization
o Postoperative Teaching-Explain that early mobilization promotes lung ventilation and circulation, reducing the potential for postoperative complications. Provide and reinforce teaching: pain management, incision care, activity level, postoperative follow-up appointments. With early discharge, the client and family assume responsibility for the majority of postoperative care.
Pancreatic Disorders
o Pancreatitis:
Pancreatic Disorders
o Pancreatitis: Inflammation of Pancreas
• Acute: Self-destruction of Pancreas by its own enzymes through autodigestion.
• Chronic: Progressive Disease, normal pancreatic tissue is replaced by connective tissue
Manifestations
o Pancreatitis:
Acute:
• Sudden Onset
• Severe Pain!
• N&V, < bowel sounds
• Distended!Tender Abd.
• Dehydration,
Hypotension
• Shock, Tachycardia
• Grey Turner's Sign
• Cullen's Sign

• > Amylase (1st 48 hrs)
• >Lipase (after 48 hrs &
for 5-7 days)
• Hyperglycemia
• Hypocalcemia
• >WBC
• Fever
• Cold, clammy skin
Pancreatitis Manifestations
 Chronic:
• Episodic upper abdominal pain (radiates to back)
• N&V, Weight loss
• Flatulence
• Constipation
• Steatorrhea (Fatty, Frothy, Foul-smelling stools)

• Malabsorption
• Diabetes
• >Amylase
• >Bilirubin
• Ascites
• Abdominal mass
• Major cause:
Alcoholism
Pancreatitis Complications
 Acute:
 Acute:
• ARDS
• Hyperglycemia
• Hypocalcemia
• Pancreatic Abscess
• Pancreatic Pseudocyst
• Pancreatic Fistula
Pancreatitis Complications
 Chronic:
 Chronic:
• Chronic insufficiency of pancreatic hormones & enzymes
• Diabetes
• Malabsorption
• Steatorrhea-fatty, frothy, foul smelling stools caused by a decrease in pancreatic enzyme secretion.
• Permanent & progressive destruction of pancreas
Pancreatitis Lab Tests
o Amylase**-normal values 25-125 U/L. rises within 2-12 hours of onset of acute pancreatitis to 2-3 times normal. Returns to normal in 3-4 days.
0 Lipase** -<200 U/L. Levels rise in acute pancreatitis; remains elevated for 7-14 days
o Glucose-70-110 mg/dL-may be transient elevation in acute pancreatitis.
o Bilirubin-0.1-1.0 mg/dL compression of the common duct may increase bilirubin levels in acute pancreatitis.
o Alk. Phos.- 30-90 U/L Compression of the comon duct may increase levels in acute pancreatitis.
o Calcium**-8.9-10.3 mg/dL or 4.5-5.5 mEq/L. Hypocalcemia develops in up to 25% of clients with acute pancreatitis
o WBC-4500-10,000 mm3. Leukocytosis indicates inflammation and is usually present in acute pancreatitis
o CEA-
Pancreatitis Diagnostic Tests
o Ultrasound-can identify gallstones, a pancreatic mass, or a pseudocyst
o CT Scan-may be ordered to identify pancreatic enlargement, fluid collections in or around the pancreas, and perfusion deficits in areas of necrosis.
o Abdominal and Chest X-Rays
o ERCP (Endoscopic Retrograde
Cholangiopancreatography) may be performed to diagnose chronic pancreatitis and to differentiate inflammation and fibrosis from carcinoma.
o Fine needle aspiration biopsy-May be performed to differentiate chronic pancreatitis from cancer of the pancreas; the cells that are aspirated are examined for malignancy.
Pancreatitis Pharmacology
o Demerol
o Antibiotics
o Antacids, H2 blockers
o Proton pump inhibitors
o Antispasmotics
o Enzymes
o Antiemetics
Pancreatitis Nursing Diagnosis
o Pain-
Interventions:Use a standard pain scale, note nonverbal cues of pain: restlessness or remaining rigidly still; tense facial features, clenched fists, rapid, shallow respirations, tachycardia, diaphoresis. Administer analgesics on a regular schedule.
o Risk for Imbalanced Nutrition: Less than body requirements.
Interventions: monitor lab values: albumin, trasferrin, Hgb and HCT-decreased in malnutrition. Decreased pancreatic enzymes affect protein catabolism and absorption; decreased transferrin affects iron absorption. Weigh daily or every other day, maintain stool chart, monitor bowel sounds, administer prescribed IV fluids.
o Risk for Imbalanced Fluid Volume
Interventions: Assess cardiovascular status every four hours or as indicated.
Monitor renal function. Obtain hourly urine output, monitor neurologic function, including mental status, LOC, and behavior.
o Risk for Infection
o Ineffective Breathing Pattern
o Impaired Gas Exchange
o Deficient Knowledge
o Ineffective Protection
Pancreatitis
Patient & Family Teaching
Pancreatitis
Patient & Family Teaching

 Treatment in Hospital & at home
 Prevention of future
attacks
Report symptoms of infection (Fever over 102 or more, pain, rapid pulse, malaise) as pancreatic abscess may develop after initial recovery.
 Diet, Medications-If pancreatic function has been severely impaired, discuss appropriate use of pancreatic enzymes, incluiding timing, dose, potential S.E., and monitoring of effectiveness
A low fat diet is recommended. Provide a list of high-fat foods to avoid. Crash dieting and binge eating should also be avoided as they may sometimes precipitate attacks.
 Alcohol, Smoking
Alcohol can cause stones to form, blocking panreatic ducts and outflow of pancreatic juice.
Smoking and stress stimulate the pancreas adn should be avoided.
 Complications
 S/S to Report to Dr.
Pancreatic Cancer
 Poor Prognosis
 Usually Metastasized at Time of Diagnosis
o Age 50-70
oMen 30% > Women
 65% > African Americans than Caucasians
 Smoking, Chemical Exposure, High-Fat Diet, Pancreatitis, Diabetes
Pancreatic Cancer Manifestations
Pancreatic Cancer Manifestations



 Slow Onset
 Anorexia, Nausea, Weight Loss, Flatulence, Dull Epigastric Pain
 Obstruction of Bile Flow: Jaundice, Clay¬colored stools, dark urine, pruritus


 Pain after eating or while lying supine
 Late signs: Abdominal mass, Ascites
 Often no S/S until far advanced
Pancreatic Cancer Nursing Care/Treatment
Pancreatic Cancer Nursing Care/Treatment



 Resection of Tumor
 Radiation
 Chemotherapy
 Pain Management
 Nutritional Support
 Emotional Support


 Whipple's Procedure:
• Remove head of Pancreas, entire duodenum, distal of stomach, portion of jejunum, & lower 1/2 of common bile duct.
• Drainage tubes, wound care & pain
Medication
Pitressin
(Vasopressin)

Medication
Route
Action
Side- effects/Adverse
Reactions
Nursing Implications
Medication
Pitressin
(Vasopressin)


Route
IV.


Action
Vasoconstrictor,
control GI
bleeding with
esophageal
varices

Side-
effects/Adverse
Reactions

Chest pain, MI,
Water
intoxication,
Fever, Allergic
Reaction

Nursing
Implications

Monitor ECG,
Cardiac status,
Allergic
Reaction
Lactulose
(Chronulac)
Medication
Route
Action
Side- effects/Adverse
Reactions
Nursing Implications
Medication
Lactulose
(Chronulac)

Route
P.O. or
Rectal as
enema

Action
> H20 content
& softens
stools, blocks
diffusion of
ammonia from
colon to blood,
< ammonia
levels

Side-
effects/Adverse
Reactions
Diarrhea, upset
stomach,
nausea,
abdominal pain

Nursing
Implications

Assess mental
status, monitor
# & type of
stools
Monitor
ammonia
levels (lab)
Medication Neomycin (Neo-
Tabs)
Route
Action
Side- effects/Adverse
Reactions
Nursing Implications
Neomycin (Neo-
Tabs)

Route P.O. or Rectal as
enema
Action Bacteriocidal,
Antibiotic, <ammonia-
producing bacteria in the
bowel
Side-effects/Adverse Reactions
Ototoxicity, Neurotoxicity,
Rash

Nursing Implications
Monitor neuro status and for
S/S of allergy
Medication Aldactone
(Spironolactone)
Route
Action
Side- effects/Adverse
Reactions
Nursing Implications
Aldactone
(Spironolactone)

Route
P.O.

Action
Potassium-Sparing Diuretic

Side- effects/Adverse
Reactions
Hyperkalemia, N&V, anorexia,
diarrhea

Nursing Implications
Monitor I&0, Daily weight,
BP, P, K+ level
Medication Vitamin K
(Aquarnephyton)
Route
Action
Side- effects/Adverse
Reactions
Nursing Implications
Vitamin K
(Aquarnephyton)
Route IM or SC (IV route but not recommended)

Action
Fat soluble vitamin, needed
for hepatic production of
several clotting factors

Side- effects/Adverse
Reactions

Hypotension, tachycardia,
flushing, dizziness,
dyspnea

Nursing Implications
Cardiac and Resp.
monitoring, watch for
Anaphylaxis, Shock
Medication Albumin
Route
Action
Side- effects/Adverse
Reactions
Nursing Implications
Medication Albumin
Route IV
Action Plasma Volume
Expander, > plasma colloidal
oncotic pressure, reduces edema, > diuresis

Side- effects/Adverse
Reactions: Circulatory
overload or pulmonary
edema

Nursing Implications
Monitor, BP, I&0, S/S fluid
overload, e-lytes, albumin
level, UOP, decrease in
edema
Drug Name
Vasopressin (Pitressin)
Drug Name
Vasopressin (Pitressin) -- Decreases portal pressure in portal hypertension through vasoconstriction of the splanchnic arterioles thus controlling hemorrhage. A notable undesirable effect is coronary artery constriction, which may dispose patients with coronary artery disease to cardiac ischemia. This can be prevented with concurrent use of nitrates.
Has vasopressor and antidiuretic hormone (ADH) activity. It increases water resorption at distal renal tubular epithelium (ADH effect) and promotes smooth muscle contraction throughout vascular bed of renal tubular epithelium.
Glypressin, triglycyl lysine vasopressin, also can be used in a dose of up to 2 mg IV q6h.

Adult Dose 0.1-0.5 U/min IV and titrate dose prn
After bleeding stops, continue at same dose for 12 h and taper off over 24-48 h

Contraindications Documented hypersensitivity; coronary artery disease

Interactions Lithium, epinephrine, demeclocycline, heparin, and alcohol may decrease effects; chlorpropamide, urea, fludrocortisone, and carbamazepine may potentiate effects
Pregnancy B - Usually safe but benefits must outweigh the risks.

Precautions Caution in cardiovascular disease, seizure disorders, nitrogen retention, asthma, or migraine; excessive doses may result in hyponatremia
Drug Name
Propranolol (Inderal)
Drug Name
Propranolol (Inderal) -- Beta-blocker that lowers heart rate, myocardial contractility, cardiac output, and portal hypertension, thus reducing the risk of bleeding. Additionally, they prevent increases in portal pressure (hepatic venous pressure gradient) during physical exertion.
Both propranolol and nadolol, beta-blockers, are effective in preventing first bleeding and reducing the mortality rate associated with bleeding.

Adult Dose 20 mg PO bid initially; may titrate upward by increments of 10 mg/d q3-4d according to heart rate (heart rate should be decreased by about 25%, but not <55 bpm)

Contraindications Documented hypersensitivity

Interactions Epinephrine, demeclocycline, and thyroid hormone supplementation may decrease effects
Pregnancy C - Safety for use during pregnancy has not been established.

Precautions May exacerbate or cause gall bladder disease; alters balance in counter-regulatory hormones and may cause hypothyroidism and cardiac conduction defects
Spironolactone
Spironolactone
Spironolactone is a specific pharmacologic antagonist of aldosterone, acting primarily through competitive binding of receptors at the aldosterone-dependent sodium-potassium exchange site in the distal convoluted renal tubule. Spironolactone causes increased amounts of sodium and water to be excreted, while potassium is retained. Spironolactone acts both as a diuretic and as an antihypertensive drug by this mechanism. It may be given alone or with other diuretic agents which act more proximally in the renal tubule.

Spironolactone is indicated in the management of:

Edematous Conditions for Patients With:
• Cirrhosis of the Liver Accompanied by Edema and/or Ascites: Spironolactone levels may be exceptionally high in this condition.
Spironolactone is indicated for maintenance therapy together with bed rest and the restriction of fluid and sodium.

Adverse Reactions:
Digestive: Gastric bleeding, ulceration, gastritis, diarrhea and cramping, nausea, vomiting.
Endocrine: Gynecomastia (see PRECAUTIONS), inability to achieve or maintain erection, irregular menses or amenorrhea, postmenopausal bleeding. Carcinoma of the breast has been reported in patients taking spironolactone but a cause and effect relationship has not been established.
Hematologic: Agranulocytosis.
Hypersensitivity: Fever, urticaria, maculopapular or erythematous cutaneous eruptions, anaphylactic reactions, vasculitis.
Nervous System/Psychiatric: Mental confusion, ataxia, headache, drowsiness, lethargy.
Liver/Biliary: A very few cases of mixed cholestatic/hepatocellular toxicity, with 1 reported fatality, have been reported with spironolactone administration.
Lactulose
Lactulose (beta-galactosidofructose) and lactilol (beta-galactosidosorbitol) are nonabsorbable disaccharides that have been in common clinical use since the early 1970s (the latter is not available in the United States). They are degraded by intestinal bacteria to lactic acid and other organic acids.

Lactulose appears to inhibit intestinal ammonia production by a number of mechanisms. The conversion of Lactulose to lactic acid results in acidification of the gut lumen. This favors conversion of NH4+ to NH3 and the passage of NH3 from tissues into the lumen. Gut acidification inhibits ammoniagenic coliform bacteria, leading to increased levels of nonammoniagenic lactobacilli. Lactulose also works as a cathartic, reducing colonic bacterial load.
used to treat and prevent complications of liver disease (hepatic encephalopathy).

Initial lactulose dosing is 30 mL orally, daily or twice daily. The dose may be increased as tolerated. Patients should be instructed to reduce lactulose dosing in the event of diarrhea, abdominal cramping, or bloating. Patients should take sufficient lactulose as to have 2-4 loose stools per day.

Great care must be taken when prescribing lactulose. Overdosage can result in ileus, severe diarrhea, electrolyte disturbances, and hypovolemia. Hypovolemia may be sufficiently severe as to actually induce a flare of encephalopathy symptoms.
Albumin
Albumin
INDICATIONS AND USAGE
Oncotic Deficit
The common causes of hypoproteinemia are protein-calorie malnutrition, defective absorption in gastrointestinal disorders, faulty albumin synthesis (e.g., in chronic hepatic failure), increased protein catabolism after operation or in sepsis, and abnormal renal losses of albumin in chronic kidney disease. In these situations, the circulating plasma volume is usually maintained by the renal retention of sodium and water, but this is associated with tissue edema and an oncotic deficit. Though relief of the underlying pathology is the definitive therapy for the restoration of the plasma protein level, this process takes time to become effective and the rapid correction of an oncotic deficit by the administration of Albumin, possibly in conjunction with a diuretic, may be indicated.

Acute Liver Failure
In acute liver failure, Albumin may serve the triple purpose of stabilizing the circulation, correcting an oncotic deficit and binding excessive serum bilirubin. The therapeutic approach is guided by the individual circumstances.

Ascites
The use of Albumin for blood volume support may be indicated if circulatory instability follows the withdrawal of large amounts (>1500 mL) of ascitic fluid.


ADVERSE REACTIONS
Though very rare, adverse reactions such as chills, fever, tachycardia, hypotension, urticaria, skin rash and nausea may occur.

The symptoms may disappear if the infusion is slowed or stopped for a short period of time. If necessary, the intravenous administration of 50 to 200 mg of prednisolone may be useful
o Endoscopy (EGD) (Esophagoscopy)
Endoscopic retrograde cholangiopancreatography: ERCP
Besides obtaining excellent images of the biliary tract and pancreas, ERCP allows some visualization of the upper GI tract and the periampullary area. Biopsies and interventional procedures may be performed (eg, sphincterotomy, biliary stone extraction, placement of a biliary stent in a stricture). ERCP is an outpatient procedure that, in experienced hands, has relatively low risk (mainly pancreatitis in 3% after sphincterotomy). It has revolutionized the diagnosis and management of pancreaticobiliary disease. ERCP is especially valuable in assessing the biliary tract in cases of persistent jaundice and in seeking a lesion amenable to intervention (eg, stone, stricture, sphincter of Oddi dysfunction). In jaundice and cholestasis, US to assess duct size should precede ERCP.