August 16, 2010 ACCESSORY Biliary tract and exocrine pancreas

Pancreatic enzymes do not work in an acidic environment the need for an alkaline rich fluid. CCK ± stimulates gallbladder and pancreas

y y y y y y

Accessory organs and its locations Liver ± largest organ Gallbladder ± R side Pancreas ± L side; head is near S.I.; tail is near spleen Ampulla of Vater ± connection of the CBD and pancreatic duct CBD can affect pancreas, gallbladder

(CCK) Cholecystokinin and Acetylcholine
y y

C and A acinar cells enzyme release Feedback mechanism ± inhibits secretion of more pancreatic enzymes

y y y y

Biliary tract 1. Common bile duct

Cholelithiasis Cholecyctitis Choledolithiasis Pancreatitis

Cystic, hepatic duct CHOLELITHIASIS (gall stones)
y y y y y y y y

2. Cystic duct

From gallbladder to the CBD

3. Gallbladder
y y

Saclike organ located under the R side of liver Stimulated to contract by CCK and motilin

Formation of stones in gallbladder Lith ± stones Chole ± gallbladder RF: (4Fs) F female F fat F forty (increased cholesterol) F fertile

BILE ± fat emulsifier and helps with absorption; composed of (50% bile salts, H2O and electrolytes, bilirubin, lecithin, cholesterol) Flow of Bile: liver Hepatic duct R or L cystic duct Common hepatic duct sphincter of Oddi

Gall stones are crystalline structures formed by concentration (hardening) or accretion (adherence of particles, accumulation) of normal or abnormal bile constituents (80% are cholesterol) Theories of gallstone formation 1. Bile ± changes in composition 2. Gallbladder stasis bile stasis (gallbladder only contracts with the presence of food) 3. Infection predisposes a person to stone formation 4. Genetics and demography ± Caucasian Cholesterol ± needs to combine with bile salts and lecithin in order to dissolve in water Pathophysiology: Unconjugated bile precipitate


Exocrine Pancreas
y y y y y

Gland located behind the stomach on L side of abdomen Pancreatic enzymes AMYLASE ± breaks down CHO TRYPSIN ± breaks down CHON LIPASE ± breaks down FATS

SECRETIN ± secretion of alkaline fluids; inhibits action of gastrin; decrease gastric acid secretion and motility Chyme in duodenum S cells produce secretin Absorbed in intestine Pancreas Secrete alkaline rich fluid

Formation of PIGMENT stones (fr bilirubin or salts; is different


urine: very dark CHOLELITHIASIS 2 . ERCP bile salts in the skin dec. necrosis. hemorrhage dec. antioxidants gallbladder sludge N/V clofibrate meds (to dec. cholesterol) K bledding. increased age increased hepatic secretion of cholesterol Malabsorption of bile salts estrogen therapy RUQ pain referred to the shoulder (multiple) pregnancy Abd.Malabsorption disorder obesity. in KIDNEY pruritus feces: clay colored. guarding. serum cholesterol rapid weight loss continuous bile retention in the gallbladder inc. in GIT inc. bile in the duodenum Decreased bile synthesis marked tenderness in the RUQ on deep inspiration malabsorption of vit ADEK (fat soluble vits) Supersaturation of bile with cholesterol prevents full inspiratory excursion S/Sx: A blurred vision D dec. Ca formation E dec. cholesterol excretion into the bile liver excretes cholesterol retention in the gallbladder abscess. facial grimace vagal stimulaiton contraction of the gallbladder obstruction of the passage of bile gallbladder distention and inflammation dec. cholecystogra -phy. perforation Supersaturation of bile with cholesterol bile absorbed in the circulation seeping into the peritoneal cavity cholesterolsaturated gall stones jaundice peritonitis (end complication of cholelithiasis) irritates gallbladder Ultrasound.

bleeding tendencies. CBD. Explain procedure 2. contaract and empty Eg of contrast agentL IOPANIOC ACID Post: instruct client to eat in order to contract gall bladder thus excreting bile Health promotion y y y y Most sensitive/ accurate X eat (it will distend gallbladder) I: jaundice. Biliary colic pain. prothrombin time. Sensation of fullness. MRI y y 1. cholesterol synthesis in bile For 6-12 months 4. clay colored stool Diagnostic tests: 1. intolerance to fatty food 4. Remove dentures to prevent aspiration Analgesics Antacids H2 blockers or PPI Antiemetics Antibiotics Nitroglycerin 2. Explain to patient he will be sedated (informed consent) 5. Endoscopy Endoscope Passage of stone Duodenum Enlarges it CBD Ampulla of Vater Cholangio-CBD Injection of dye (biliary tract) Hepatic ducts within liver. Anorexia. prone to bleeding? Administer antibiotic (prophylaxis) 3 . monitor gag reflex) 3. PTC (percutaneous transhepatic cholangiography) y y y y y y y y Nonsurgical management 1. ERCP (endoscopic retrograde cholangiopancreatography) y y y Contrast medium Direct visualization of hepatobiliary system performed with a flexible endoscope Multiple positions required during procedure to pass the endoscope Pain meds Comfort measures Diet modifications Weight loss IVF Refer for S of dehydration Medical management (palliative ± for symptoms) 1. Oral cholecystography y y y To detect gall stone and assess ability of gall bladder to fill /concentrate its contents. F&E y IVF Management Post op Nursing responsibilities in ERCP: ( VS. Assess allergy to seafood/iodine 3. ULTRASOUND y y y 5. N/V 3. allergic to contrast medium low fat diet ideal body weight limit number of pregnancies TPN for 1 month Nursing management y y y y y y 2. pain occurs 3-6 hours after heavy meals 2.Assessment: 1. cystic duct and gallbladder are outlines NPO Allergy Informed consent(sedated) Hct. Meds y y y y y Prior Nursing responsibilities in ERCP: 1. jaundice. NPO 4 hours 4. Gallstone dissolution y y y y y Remove magnetic things Assess claustrophobia Cholesterol dissolving agents (CDA) CDCA UDCA MOA: dec. Steatorrhea.

acute Cholecystitis Adv: minimal trauma to abdominal wall CI: choledocholithiasis (CBD) Infuse CO2 into abdominal Shoulder pain (normal) ± ambulate Complications: ’ Pneumonia/atelactasis ’ DVT ’ Pulmonary embolism ’ Biliary tract injury ’ Hemorrhage y A JP drain may be used. can then be measured. skin preparation. NGT 7. drainage system ± below the gallbladder 6. antibiotic Laparoscopic cholecystectomy y y y y y y y The drain is connected to clear plastic tubing which is usually sutured to the skin at the point it leaves the skin. stones of CBD ± supine JP Drain y y The original suction drain. JP drain will be removed after 7-14 days 7. When the bile bag is removed the T-tube will be tied or capped. The drain is removed when the excess fluid has stopped draining from the body. JP stands for Jackson-Pratt. which varies in color from deep gold to dark green. Surgical management Preop: consent. when squeezed empty. Extracorporeal shock wave lithotripsy y y y y y y y Bil eor blood leaking from wound Drop in BP I : symptomatic cholelithiasis with >4stones Stone<3cm diameter No history of liver or pancreatic disease CI : recent acute Cholecystitis. assess CVD status and manifestations of shock or hemorrhage Complications ’ Hemorrhage (general) ’ Pneumonia (general) ’ Thrombophlebitis (general) ’ Urinary retention (general) ’ Bile leakage to abdominal cavity (specific to cholecystectomy) y y keep the duct patent until edema subsides allows bile to drain out of the patient's body into a small pouch. fluid balance and hydration 5. known as a bile bag The amount of bile. respi status (deep breathing) 2.2. T tube: y y y Open cholecystectomy y y y Consists of excising gallbladder from post liver wall and ligating cystic duct. monitor drainage from biliary tubes and incision site 3. for example. vein and artery Post op: 1.yellow > indicator T tube can be removed 4 . applies constant suction to the drain and pulls the fluid out of the body. The bulb. it may remain attached to a bile bag for a week or possibly longer. Report sudden increase in bile output 4. cholangitis. The drain itself is inside the body. The tubing connects to a bulb reservoir. If a T-tube is put in place. for foul odor and purulent drainage 3. monitor for inflammation and protect skin from irritation 5. for abdominal or thoracic drainage. pancreatitis Positions: stones of gallbladder ± prone. prevent infection 6. Characteristic of drainage (volume 350-400ml). T tube removed after 6 weeks S of bile leakage y y y y Bile (green > yellow) Pain and tenderness in RUQ Increased abdominal girth Tachycardia Stool with bile. Semi fowler¶s position 2. analgesics ± meperidine 4. It is made of Teflon and has multiple drainage holes. Nursing responsibilities for Patients with T tube: 1. NPO before midnight. It will remain in place for several months so that it can be used for special testing. enema. I: symptomatic gallbladder disease.

rebound tenderness stimualte HCL and secretin roduction cause obstruction in the sphincter of pancreatic duct gallstones enter CBD pancreatic enzymes stimulation Medical management 1. trauma Pain aggravated by supine position and after heavy meals alcohol intake Assessment: y y y y y (+) Murphy¶s sign N/V Fever Mild jaundice Guarding. antispasmodics CHOLEDOCHOLITHIASIS y y lodge at ampulla of vater biliary tract obstruction inactive enzyme back flow Stones in CBD JAUNDICE (intermittent or recurrent) activation of enzymes Surgical management: y y y Cholecystectomy ERCP with endoscopic papillotomy and stone extraction Choledocolithotomy auto digestion PANCREATITIS y y y production and release of pancreatic enzyme Inflammation of pancreas Associated with escape of pancreatic enzymes into surrounding tissue Classifications: acute and chronic pancreatitis 5 .Clamp tube before a meal and observe for abdominal discomfort and distention. Acute inflammation Acute inflammatory process of the pancreas resulting in auto digestion of the pancreas by its own enzymes Life threatening Eti and RF: biliary tract obstruction. cholecystostomy ± surgical drainage of gallbladder Nursing management: 1. Cholecystectomy 2. chills or fever Acute pancreatitis Unclamp tube if N/V occurs y CHOLECYSTITIS y y y y y Inflammation of gallbladder 3 types: 1. N. rigid. antibiotics Surgical management 1. diet (low fat) 2. analgesics. no increase in WBC) 3. sedentary) no stones 2. antibiotics. alcoholism. Chronic Cholecystitis (less pain. Acalculous Cholecystitis (RF: 4Fs.

cyanosis. tenderness. WBC) combines with ionized Ca+ release of vasoactive peptides destruction of pancreatic islets bacterial proliferation in area thrombosis hypocalcemia gangrene necrosis vasodilation hemorrhage inc. facial grimace. in bowel sounds exudates with pancreatic enzymes frperitoneal cavity via transdiaphrag matic lymp channels atelactasis. pain aggravated by supine position and vagal stimulation N/V hypovolemia hypoTN. serum lipase) fatty acids are released (inc. serum amylase) release of elastase blood vessel and duct destruction release of kallikrein leukocytes cluster around necrotic areas (inc. serum trypsin) release of trypsin polypeptide formation inc. cold clammy skin dec. pneumonia S of pancreatitis) rigid. boardlike abdomen CULLEN'S SIGN (bluish discoloration of umbilicus) TURNER'S SIGN (bluish discoloration of flank BACK) 6 .production and release of pancreatic enzyme (inc. vascular permeability suppuration (pus) and lesion formation hyperglycemia edema irritation of inflamed pancreas abdominal pain. back pain abscess pseudocyst (pus) impedes bile flow through CBD JAUNDICE Abdominal guarding.

inflammation and sclerosis. turning. BUN. bilirubin. part of duodenum. subtotal pancreatectomy 4. electrolyte balance Nutritional status (TPN. Whipple¶s surgery (remove distal 3 of stomach.Assessment PAIN . antacids. glucose) 48-72 hours elevated AMYLASE 5-14 days elevated LIPASE (morphine-spasm of sphincter +pancreatitits) Medical management (palliative) y y y y y y Pain mgt (Demerol. debridement with surgical drainage or retroperitoneal drainage 3. laparotomy with sump drainage 2. chronic calcifying pancreatitis (aka alcohol induced pancreatitis) ± most common. mainly at the head of pancreas and pancreatic duct Assessment: DM manifestations. head of pancreas).sudden onset of mid epigastric pain or LUQ radiating at the back after heavy meals/supine position Diagnostic test y y y y y y y y History and PE ERCP CT scan Abdominal Xray Lab exam (alkaline phosphotase. position NPO. steatorrhea Diagnostic test y y y y y y y y History and PE ERCP CT scan Abdominal Xray Lab exam (alkaline phosphotase. glucose) 48-72 hours elevated AMYLASE 5-14 days elevated LIPASE (morphine-spasm of sphincter +pancreatitits) y y Deep breathingand coughing exercises Low fat and high calorie diet Chronic Pancreatitis y y y Continuous prolonged inflammation and fibrosing process of the pancreas Formation of scar tissue Etiology ’ Alcoholism (70-80%) ’ Idiopathic cause ’ Hereditary ’ Biliary tract obstruction Pathophysiology: etiologic agent Inflammatory process Attack of acute pancreatitis Continuous and prolonged inflammatory process Scarring and calcification of pancreatic tissue Irreversible damage of endocrine and exocrine functions S/SX Types: 1. chronic obstructive pancreatitis 2. TPN Supplemental preparations Pain meds. BUN. CBD. bilirubin. H2 receptor antagonists (decrease acidity) and anti cholinergics No alcohol Bed rest to decrease metabolic demand Positioning rd y y y 7 . meperidine ± CNS depression) Fluid volume status. semifowler¶s with flexed knees (chest knee) Surgical management 1. NGT suction (X acidic environment). gallbladder. NGT for suctioning) Decreased Endocrine function Treat complications (respiratory care) ± oxygen. complication: hemorrhage Nursing management y y y NPO and hydration.

Total pancreatectomy 3. gastric secretion 4. CV status (hemorrhage). Biliary stents Nursing management 1. NGT for suctioning) Decreased Endocrine function Treat complications (respiratory care) ± oxygen.Medical management (palliative) y y y y y y y Pain mgt (Demerol. take with meals. IV fluid replacement and electrolytes Management of clients with hepatic disorders Anatomy and physiology:LIVER y y y RUQ R and L lobe Calciforum divides the lobe Heme 3-4 hours Hepatic cells ± functional Sinusoid Bile at canaliculus Portal and arterial Circulation Dual circulation Arterial circulation from hepatic artery (O2 blood 300-400mL of blood) from portal vein GIT Portal vein is connected to liver (10001400ml of blood) Kupper cells ± pick up organisms from blood which came from GIT ± not always sterile Special characteristics: REGENERATIVE LIVER CELLS FUNCTIONS: 1. cholecystojenostomy 4. Physical movement and mental stimulation 5. 18 times Hepatic secretion Hepatic resecretion intestinal absorption 2. semifowler¶s with flexed knees (chest knee) Pancreatic enzyme replacement eg pancrelipase (cotazyme). Bile secretion/production (choleresis) ± 6001200mL/day Enterohepatic circulation ± recycling of bile salts. wipe mouth ± enzymes are irritating to the skin (prevent stomatitis) Bile salts (synthetic) y Surgical management 1. Metabolism of bilirubin ±(metabolism converting substance to be excreted) Hmg 120 days globin biliverdin Bilirubin Plasma + albumin(oncotic pressure) Unconjugated bilirubin (X secreted easily) amino acid pool Non iron pool Liver: glucorganic acid 8 . Total pancreaticoduodenectomy with splenectomy y y y y y y y y y y 5. Pancreatin (viokase). Position for comfort 6. PQRST (pain) 3. turning. Whipple¶s procedure 2. NPO 3-7 days. electrolyte balance Nutritional status (TPN. position NPO. Assess respiratory function. meperidine ± CNS depression) Fluid volume status. Medications 2.

5:1 to 2. recreational and travel history y History of alcohol and drug use y Past medical history y S and sx that suggest liver disease Lab tests Bile formation and secretion Test Normal value 1. A. Vascular and hematologic functions y y y y Store blood Kupper cells Prothrombin. X synthesis Vitamin K absorption steroid hormones (testosterone. total serum bilirubin 0. II. A/G ratio ALT 2.progesterone. CHON metabolism LIVER Deamilation producesCHON AA Ammonia Removes ammonia LIVER urea plasma CHONs albumin Assessment y Hepatotoxic substances with infectious agents y Occupational. factors I. Fat metabolism y Fats: synthesized from CHON and Fats Absorbed by lacteals in the intestinal villi lymphatics (triglycerides) (hydrolyzed) LIVER (released in the bloodstream) Lipoproteins Storage of adipose tissue 5. Metabolic detoxification Liver Liver active chemical medium inactivates detoxify 3. CHO metabolism LIVER stores glycogen (³glucose buffer function´) galactose and fructose glucose Increased alkaline phosphotase in bile obstruction Coagulation studies Test 1. VII. D. increased AST found in increase metabolic substances formation 6. STERCOBILIN: feces UROBILINOGEN:urine 7.5(JAUNDICE).1-1. direct (conjugated 0.1 mg/Dl (unconjugated bilirubin) 3.0-7.5g/Dl 3.03 mg/Dl bilirubin 2.5 g/Dl 1.5:1 g/Dl definitive. corticosteroids.5-5.I.Unconjugated bilirubin (X secreted easily) Conjugated bilirubin Becomes constituent of bile S. serum albumin 3.5-3.2 mg/Dl Protein studies Test 1. problem in LIVER oncotic pressure Normal value 7. indirect 0. fibrinogen. total serum CHON 2. B12 (Apoferritin + iron (extra in serum) =ferritin) 8. IX. PT 2. storage of iron and vitamin Liver stores vits. serum globulin 4.5-14 sec 25-40 sec Converts Converts CHO triglycerides adipose tissue 9 . PTT Normal value 11.5 g/Dl 2. aldosterone) 4.

ALT 3. Liver biopsy y y Most specific Percutaneous liver biopsy Determine adequacy of portal circulation Contrast medium Inc. membrane defects of erythrocytes . CT scan 6. heme production Inc. ERCP 7. Obstructive jaundice (post hepatic) Liver.Serum enzymes Test 1. hepatic cancer Alt. MRI 5. amount of unconjugated bilirubin 3. Hepatocellular jaundice (intrahepatic) Hepatitis cirrhosis. hepatitis. AST 2. abdominal Xray 2. alkaline phosphotase 4. ability of liver to conjugate bilirubin 3. Biliary stricture CBD is occluded by gallstone Bile can¶t pass through Bile absorbed in circulation CM y y y y y y y Yellow sclera Yellowish orange skin Clay colored feces Tea colored urine Pruritus Fatigue Anorexia Nursing preop responsibilities (liver biopsy) y y y y PT and PTT (prolong vit K or post pone biopsy) Consent NPO Baseline VS (bleeding) Nursing during responsibilities (liver biopsy) y Expose R hypochondriac y Client inhale and exhale then hold breath at the end of expiration (to prevent puncturing the diaphragm) Nursing after responsibilities (liver biopsy) y R side lying with pillow on punctured incision site y Bed rest 24 hrs y No coughing/straining/heavy lifting y VS 10 . LDH 5. Blood ammonia Diagnostic test 1. tumor. cirrhosis Swelling or fibrosis of liver canaliculi &bile ducts Bile can¶t pass through Bile absorbed in circulation Stones in CBD. breakdown RBC Inc. amt of unconjugated bilirubin 2. liver scan y y y Contrast medium Assess allergy NPO 4 hours Normal value 8-20 u/Dl 10-35 u/Dl 32-92 u/Dl LDH 150-250 u/Dl JAUNDICE y Yellow/greenish yellow discoloration of sclera skin and deeper tissue Types: 1. Splenoportogram y y 4. Hemolytic jaundice(prehepatic) y Causes: BT reactions. immune reaction. toxic substances in circulation Inc.

G RNA HEPATITIS A (Infectious hepatitis) CA Small. hematologic test Reduce pruritus and maintain skin integrity ± oral cholestyramine resin. health care personnel RF/transmission Fecal-oral route.F. bacteria. contaminated water or milk. phenolbarbital Nursing management y y y y y y Increased VII. IgM and IgG Inc. stool precautions.Medical management y Determine cause of jaundice ± health hx. leukocytosis. risk of chronicity May progress to fuminant hepatitis Prevention: HW. RNA contaminating HAV INCUBATION 15-45 days. bilirubin lvel Biopsy fatty hepatic tissue 11 . undeveloped. IgG Ab BET Gamma globulins Outcome Mild with full recovery Fatality rate less than 1% No carrier stae or inc. shellfish from contaminated water Testing (+) acute HAV in blood Inc. vaccine IgG ± Patient has immunity IgM ± newly exposed o the disease (hepatitis) Surgical management y Choledochostomy-exploration CBD of the HEPATITIS y Inflammation of the liver caused by virus. liver function test. N/V Ascites Fever Encephalopathy Abdominal pain Splenomegaly Hepatomegaly Jaundice Anemia. mean 30. IgM Ab in 4-6 wks Inc. PE. or exposure to medication or hepatotoxins Goal of therapy: rest the inflamed area y Alcoholic hepatitis Inflammation Degeneration Necrosis of hepatocytes and infiltration of leukocytes Mallory bodies Manifestations: y y y y y y y y y y Anorexia. water precautions.E. antihistamines. CHO diet Folic acid and thiamine supplement Parenteral fluids Liquid formulas to increase caloric intake No alcohol! Steroids y Nursing management(Assess S of jaundice formation) Interventions y y y y y y Tepid bath Lotion Loos clothing Soft bedding Short nails Keep room cool Viral hepatitis Hepatitis A RNA Hepatitis B DNA Hepatitis C RNA Hepatitis D. PERIOD 2-6 weeks Ind @risk Young children and young adults. inc.

HEPATITIS B Double stranded DNA virus (HBV) INCUBATION 30-180days. needle precautions. risk for chronic Outcome hepatitis.most accurate in detecting POET Alpha ± interferon or pegylated interferon + ribavin Outcome Frequent occurrence of chronic carrier state and chronic liver diseases Inc. cirrhosis and hepatic cancer May be severe. clients on long term hemodialysis Health care personnel Young adults (sexual and percutaneous) Babies and toddlers RF/transmission Blood or bloody fluid contact. or body fluid contact at birth Testing Anti HCV. or body fluid contact at birth Testing HbA g-Ab system in blood HbsAg HbsAg 6 weeks(newly infected ± carrier state) Acute Hbs Hbe Ag POET Hepa B immune globulin For chronic hep B: interferon. testing of pregnant women. parenteral perinatal period. fulminant hepatitis. mean 60PERIOD 90. contaminated needles. sexual contact. parenteral perinatal period. infected saliva or semen. screening of blood donors. adefovir (Hepsera) and lamivudine (Epivir) Inc. FH. 6-24 weeks Ind @risk Drug users. fatality rate 1-10% Possible carrier state Prevention: HW. sexual contact. contaminated needles. 50 PERIOD 5-10 weeks/2-12 wks Ind @risk Parenteral drug use Clientsreceiving frequent blood transfusions Health care personnel RF/transmission Blood or bloody fluid contact. HW Immunity by vaccine or history of hepatitis HEP C > carcinoma. infected saliva or semen. avid intimate sexual contact if test for HbsAg is (+) CA HEPATITIS C (NANB/POST TRANSFUSION HEPATITIS) CA Single stranded RNA virus INCUBATION 15-160 days. risk of 1r Hepatocellular carcinoma Prevention: needle/ blood precautions. chronic hepatitis> most fatal 12 .

Post icteric (recovery phase) y Pain subsides. mean 40. The liver cells that do not die multiply in an attempt to replace the cells that have died. nausea and vomiting. Pre-icteric or prodromal stage 13 .40 mg/l RF/transmission 3. malaise. fatigue. progressive disease of liver characterized by diffuse degeneration fibrosis (scarring) and nodule formation Cirrhosis is a complication of many liver diseases that is characterized by abnormal structure and function of the liver. delta hepatitis agent Defective RNA virus 30-180days. This results in clusters of newlyformed liver cells (regenerative nodules) within the scar tissue. The diseases that lead to cirrhosis do so because they injure and kill liver cells. dark urine and pale stools 2. risk of chronicity May progress to fuminant hepatitis LIVER CIRRHOSIS y Chronic. Icteric stage y y CM: liver is enlarged jaundice develops at total bilirubin levels exceeding 20 . 2-9 weeks Travelers to countries with high incidence if hepatitis E Eating/ drinking food/water contaminated with virus Fecal-oral route Anti HEV Mild with full recovery Fatality rate less than 1% No carrier stae or inc. single stranded RNA virus 14-60 days. diarrhoea. TPN Bile acid sequestrants Immunoglobulins and vaccines to family Avoid hepatotoxic drugs such as (Tylenol). fever ranging from several days to more than a week. jaundice is subsides 2-12 weeks after onset of jaundice ± liver function Management: y y y y y y y y y Bed rest High calorie. and the inflammation and repair that is associated with the dying liver cells causes scar tissue to form.HDV (B) (DELTA AGENTS HEPATITIS) CA HDV. abdominal pain. mean 6090. characterized by the appearance of symptoms like loss of appetite. increased energy level Testing 6-8 weeks after exposure. client receiving hemodialysis Blood or bloody fluid contact. chlorpromazine HCV: INTERFERON HBV: EPIVIR Lamivudine POET HEPATITIS E (A) (ENTERICALLY TRANSMITTED OR EPIDEMIC NANB HEPATITIS) CA INCUBATION PERIOD Ind @risk Unenveloped. 7-8 weeks/2-10wks Drug users. fever. occurs as dual infection with HBV HDAg early in course of infection HDAb ± later disease stage HbA g-Ab system in blood HbsAg HbsAg 6 weeks(newly infected ± carrier state) Acute Hbs Hbe Ag interferon y y y INCUBATION PERIOD Ind @risk (Interic=jaundice) CM: fatigue. clients on frequent BT. low fat diet IVF. RF/transmission Testing Outcome y y Stages of Hepatitis 1.

alkaline phosphotase. ERCP Portal HPN opressure in peritoneal capillaries portosystemic shunting of blood splenomegaly Ascites anemia leukopenia thrombocytope nia bleeding Damage hepatocytes Necrosis of hepatocytes Fibrosis oAST. CM: jaundice (due to the accumulation of bilirubin in the blood). loss of appetite. easy bruising Nursing interventions: y Rest and comfort y Relieve pruritus y Nutritional intake y Prevent infection y Monitor/prevent bleeding y Diuretics as ordered y Health education Portal Hypertension y y Abnormally high BP in the portal venous system or vena cava Normal portal venous BP=5-10mmHg CARDIAC CIRRHOSIS Severe R sided HF Enlarged. ALT. toxic metals (such as iron and copper that accumulate in the liver as a result of genetic diseases). fat. edematous. viruses. congested liver Liver anoxia Liver necrosis and scarring Liver damage Decreased liver function Chronic alcoholism Toxins form alcohol: release of acetyldehyde UZD. liver scan. weakness. CT scan.y y There are many causes of cirrhosis. liver function Portal HPN splenoportogram Enlargement Irritates glisson capsule PAIN hepatic encephalopathy coma death H+ ion >acidity <alkalosis 14 . GGT dev't of collateral channels caput medusae esophageal varisces Obstruction in blood flow hemorrhoids shunting of ammonia and toxins from intestine into general circualtion Liver cells regenerate In abnormal pattern Liver cells loaded with fat dec. and autoimmuneliver disease in which the body's immune system attacks the liver. fatigue. and certain medications). they include chemicals (such as alcohol. MRI. itching.

laxatives. Transjugualr intrahepatic portosystemic shunt (TIPS) 3. pneumonia 15 . GI ischemia and acute renal failure CI patients with recent MI y y y y y Assess Nutrition IVF Dressing Blood and urine values Nursing management y y y y y y Nutritional nad neurological status Patient airway Gastric lavage with cool saline Quiet environment s/sx of bleeding and shock vasopressin Health education y y y qesophageal irritation No o in abdominal.Esophageal varisces y Complex torturous collateral veins at lower end of the esophagus due to prolonged evaluation of pressure y Cardinal sign . stool-whitish) Esophagoscopy Perioperative nursing management Preop y y y Explain Tests Consent Medical management 1. Sclerotherapy Endoscopy Esophagus Post op Inject sclerosing Inflammation and fibrosis Solidifying and stop circulation to the varix 2.ESOPHAGEAL BLEEDING y Painless Assessment y y y y y y y Hematemesis Melena Anorexia Nausea Splenomegal Caput medusa osplenic dullness Care of patients with Sengstaken Blakemore y Semi fowlers y Maintain traction y Scissors at bedside y Monitor respiratory status y Label each lumen y Maintain prescribed amount of pressure y Mouth and nasal care every 1-2 hours Surgical management 1. Endoscopic band ligation y Device with small rubber bands (o rings) at the end of the endoscope p over the varix 2. Balloon tamponade Sengstaken Blakemore tube/Minnesota y y Pressure of the esophageal and gastric balloon pstop the bleeding Complications: esophageal rupture. thoracic and portal pressure S of hemorrhage 4. fluid intake. MI. allergy. inc. Portosystemic shunt y Anastamosing = high pressure portal venous system to the low pressure systemic venous system Diagnostic test y y Barium swallow (NPO. Vasopressin y y y y Stop variceal bleeding MOA qportal venous blood flow by constricting afferent arterioles SE hypothermia. aspiration.

avoid NSAIDS. weight Empty bladder Position the patient ± high fowler¶s Post op y y y y Comfortable position Assess: VS. aspirin) Pre op presence of fibrous tissue&no dules ocapillary pressure albumin synthesis qoncotic pressure esp in preitoneal cavity qmetabolism of aldosterone obstruction of venous flow in liver Na&H2O retention by kidneys y y y y y Explain Consent VS. S of hypovolemia Dressing Patient education splanchnic arterial vasodilation hypovolemia qblood volume Medical management y y y y y y y Paracentesis Albumin.Ascites y Accumulation of fluid in the peritoneal cavity that results from several Pathophysiology liver damage/cirrhosis Paracentesis y Transabdominal removal of fluid from the peritoneal cavity Nursing responsibilities (qsalt. abdominal girth. abdominal girth. girth dyspnea weight gain ASCITES striae& distended veins abd. IV F&E balance Diet modifications Diuretics Maintain skin integrity Transjugular intrahepatic portosystemic activation of RAAS system oabd. impaired thinking. distention Surgical management y y y LeVeen shunt (peritoneal shunt) a peritoneal-venous shunt used in the control of ascites It routes excess ascitic fluid out of the peritoneal cavity and into the superior vena cava or the jugular vein downward protruding umbilicus fluid wave bulging flanks F&E imbalance Hepatic encephalopathy y y Portal systemic encephalopathy Accumulation of ammonia and other metabolities in blood Altered LOC. weight status. neuromuscular disturbances Assessment/Dx test y y y y y y Percuss abdomen ± dull Detect fluid wave Paracentesis Abdominal X ray studies Ultrasonography CT scan y 16 . qfluid intake.

hyperreflexia 4. handwriting problems Complications y y y y Rejection (occur 4-10 day) pjaundice. encephalopathy Infection Hemorrhage Atelactasis th 3. forgetfulness. albumin and enzymes) Post op y y y Monitor Drugs to prevent infection: CYCLOSPORINE Discharge instructions (s/sx of rejection. bilirubin. confused.Stages of H.E. restless. Impending y CM: lethargic. etc) Medical management y Assess etiology y Neomycin (Mycifradin) CI: renal insufficiency y Lactulose y Antibiotics (to kill bacteria in the intestine) y Oral MgSO4/ enemas after hemorrhage y IV fluids and vitamins Nursing management y y y Assess neuro status Restrict CHON. Prodromal y y Not obvious CM: agitation. Stuporous y Severe mental deficit. 1. oCHO and vitamin K supplements Medications 17 . inability to concentrate y y Protect client from injury Bed rest ( to decrease metabolic demand) Liver transplantation Liver transplant y y For end stage liver disease Duration: 6-18 hours 2. Coma y y y Comatose (+) babinski reflex Fetor hepaticus (A peculiar odor of the breath in individuals with severe liver disease caused by volatile aromatic substances that accumulate in the blood and urine) Signs/symptoms of REJECTION y y y y Tachycardia Pain on the RUQ or flank ojaundice Fever (early sign) Nursing management Assessment and Dx test y y y y y y EEG Serum ammonia and CSF Gluatmine levels Electrolyte level Blood gases Hepatic function test results (eg prothrombin. intolerance.

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