ASSESSMENT OF CLIENT WITH HEPATIC, BILIARY TRACT AND PANCREATIC DISORDER history Chief complaint: Abdominal pia Urine changes ‘anorexls Jaundice Nausea and vomiting Bleeding tendencies Weight oss Asetes Stoo changes Edema ofthe limbs Food intolerance Fatigue, Fever ‘Altered level of consciousness PAST MEDICALHISTORY “Niajor nesses or hospitalization Recent skinfmucous membrane disruption “Ear piercing, tattooing blood transfusion, dental procedures *Medleations Hepatotonc drugs (Acetamenophen, INH, sulfonamides, thiazide, diuretics, Arson, methotrexate *FaMy HISTORY -Cance of liver, hepatits, alcoholism, obesity “PSYCHOSOCIAL History and LIFSTYLE “Occupation an work envionment ose contact with hazardous waste or polluted water. ‘Travelin hepatitis pancreatic endemic area Consumption of raw/teamed shelich fom polled water. Contact with hepatitis infected animal or people Habits Food preference Mes! preparation Use of alcoho! “PHYSICAL EXAMINATION General appearance and heath status jaundice, obvioul lor impaired) Nutetiona status [Assess abdomen ~ examine palnful area lat LABORATORY AND DIAGNOSTIC TESTS FOR LIVER FUNCTIONS Fat metabolism ‘Serum total cholesterol and cholestrol esters ‘decreased inhepatoceluar damage ‘creased Inlay obstruction ‘Normal range: 40 ~ 220 mg/d Serum phospholipids “decrease in hepatocellular damage increased in ilar obstruction Normal range: 150-250 mg/d *Protein metabolism Total serum protein decreased in hepatocellular damage Iramunogiobuins aA. Ip@~ increased in iver cierhosis eG —inerensedin chronic active hepatitis billary lerhoss lah increased in hepatitis A Bun ‘Decreased in severe hepatocellular disease obstruction of portal enous flow Protime, PTT, APTT Ineressedin hepatocellular damage increase rik f bleeding ) Blood Ammonia levelsIncreased in hepatocellular damage (causes hepatic encephalopathy) NV: 75 ue/dl *Bieubin metabolism Total serum bitrubin Increased in hepatocellular damage (causes jaundice) NV:0.1-1 met Conjugated or Direct bitrubin Increased in ily obstruction Unconjugated or indie bilirubin Increased in hemolysis of RBC and hepatocellular damage Urine Birubin (fam test) Increased conjugated birubin in urine — hepatocellular/abstructve biliary disease (Unconjugated biirubin snot excreted in urine because itis not water-soluble) Utine Urobitinogen Decreased in obstructive bilary disease Increased in hepatocellular damage NV:0.2~1.2 units Fecal Urobiinogen stereobitn) Increased in hemolysis of RBC [Absence of fecal urobilinogen: obstructive biary disease (causes acholic stool which 'spaleferay/ctay ~colored stool ‘Serum enzymes: increased in hepatocellular demoge AST/SGOT ALT/SGPT ‘the most specific indicator o ver function ion 666T ( Gammaclutamyttranspeptidase) Inereased in ver cirrhosis in alcohol-induced ‘Aaline phosphatase Slight to moderate elevation Hepatocellular disease Severe elevation Obstructive biliary disease Uttrasound ofthe liver Preparation NPO8~12 hours Laxative, the night before the procedure ‘Adequate hydration Biopsy ofthe liver Preparation Secure written consent NPO2~4 hours Vitamin K injection Monitor Pro time jnital VS Position patent t left side instruet client to exhale deeply, hold breath for 5~ 10 seconds during needie Insertion to prevent trauma ta diaphragm, Care after ver biopsy ‘Tur client to right side for 4 hours to apply pressure and prevent bleeding Bed rest for 28 hours Monitor VS every 30min. to every hou for the ist 24 hours Paracentess (Peritoneal 2p) Preparation: Secure written consent Checkinitial vs ‘Askeclient to empty te bladder to prevent puncture ‘Check serum protein studies. levels are low, procedure may be postponed by the physician.Place client in siting / upright position Care after Paracentesis Assess: V5 (asess BP for hypotension) Urine ouput Rigidity ofthe abdomen Signs and symptoms of bleeding, peritonitis, hypowolemic shock These ate the potential complications of paracentesis Endoscopic retrograde Cholangiopancreatography (ERCP) Direct visualization with radiographic examination of the lve, gallbladder and ‘the pancreas. Contrast mediums introduced via an upper GI endoscopy, 2s X-raysare taken simultaneously. Preparation before ERCP Secure writen consent NPO 10-12 hours Check for allergy to ldine / seafoods Take intial VS ‘Atropine $04, vallum as ordered Local anesthete spray into the throat Place inet side Care ater ERCP: 'NPO after gag reflex returns “Turn to side to prevent aspiration ‘Monitor signs and symptoms of sepss, perforation, pancreatitis HEPATO-BILIARY AND PANCREATIC SYSTEM. 1 Metabolic Function Tests {Decreased total serum cholesterol and serum phospholipids - because the liver ‘unable to metabolire fats, Decreased total serum protein, BUN — because the vers unable to metabolize protein, Low serum protein cautes decreased colloidal orotic pressure tat leads to edema Including ascites. ‘& Prolonged PT, PTT, APTT because the liver is unable to metabolize protein thats required to synthesize cloting factors. This increases risk for bleeding <._Elevated serum ammonia because the lwer is unable to convert ammonia into ures This causes hepatic encephalopathy. Ammonia isnot water soluble, therefore it cannot be excreted from the body unessitis converted into urea, Urea is water-soluble ‘and can really be excreted from the bod. @. Elevated total {fH Blirubin ~ because the wer is unable to metabolize bilirubin. This ‘causes jaundice f. Elevated unconjugated/inicec bilirubin because the lier is unable to conjugate ‘lrubin. This causes further jaundice. ‘2 Elevated urine urobilinogen — because of increased levels in the blood, the kidney fier theurabilinogen 1h levated urine bilirubin —because levels of bilirubin inthe blood is high, the Kidneys filter leubin fom the blood. Bilary obstruction i validated bythe folowing laboratory findings Elevated serum cholesterol and serum phospholipids. Elevated conjugated/ciect bilirubin Elevated urine bilirubin Decreased urine urobilinogen ‘e. Absence of fecal uroblinogen/stercobilin this result to acholic stool 2. Serum enzyme studies “Hepatocellular damage is characterized by elevated ASTISGOT),ALT(SGPT), LDH, serum alkaline phosphatase“Gamma 3. Acute pany lutamtra a is, SDetiace (Gari reais schon NODSY of the Niver ered bye “Post KIRCton bts the proc, ston of the chen in the right side of the abdomen. at ean Intec etal deg Prevent trauma tothe diaphragm, wl Postion thee Prevent bleeding eae levated if ver cis ted serum pec ed by act {nd serum amytace eit Pris “Check initiat ASK the cli Bladder vital signs nt PN eater oe oct open nce fing “Pace he cena upright or “After the | Procedure, hs Hypotension ne [Fever painand gg ene tote Ctnapneaas ra Aen ae Sey er co tet Ase fray ose eh {Ae the procedure, cep he eae Prevent aspirate 7-Uhra sound the ga badder ~ The most definitive test to detect galistones, LIVER CIRRHOSIS |s a chronic and nodular reger tissue, sitting posi Monitor the ct most chara ion. To localize Huds in i fof MYPOvolemc shock and perenne sods Manestation of hypoveenn ston abdomen indicates peritonite the lower abdomen 82 reflex returns, tur client to sides to Progressive disease of the tver cha acterized by diffuse neration. Repeated destruction of hey ‘damage to cells with fibrosis atic cells causes the formation of sexe DIFFERENT TyPES oF F LIVER CIRRHOSI5 Alcoholic cirrhosis and entire lobes. naar crthosis~ develops from chronic biliary obstruction, ble tals and inflammation resuiting in severe obstructive jaundice. 4. Cardiac cirthosis~ is associated with sever enlarged, edematous c and fibrosis, >ngestive heart failure and results in an amore, resulting i Ws alcholabse mst common ose, he causes of ver cioss ar as lows al oh an imino ncn raps basen an congentve het fa Ther factors leads to destruction af hepa Foros nd scarring ofthe ver may eaose Gene ecw wig Increased pressuein te pot ven ssi chanel e) futyvaton thea cian) ‘ ‘These three factors eventually leads to portal hypertension ee ny ae terete dros Pralhpeenson open ea He thin the portal vein that develop as a result of obstruction. pressure wth the Early Manifestations of Liver Cirrhosis: 1.61 disturbances: 1. Anorexia 2. Dyspepsia aFlatulence Nausea and vomiting Changes in howel habits (darthea and constipation) ‘These symptoms occur as a result and proteins. ‘ofthe lve altered metaboliem of carbohydrates, fats 2.Fever 3-Lassitude 4, Slight weight loss 5: Enlargement ofthe liver and spleen {The Iver i palpable in many patients with cerhoss) Late Manifestations of tver cirrhosis 1. Jaundice 2. Skin lesions “Spider angiomas (telangiectasia) Palmar erythema 3. Hematologic problems ‘Thrombocytopenia. -Leukopenia ~ Anemia these re due to splenomegaly, which causes removal of blood cells fom the circulation ~Anemia is due to inadequate RBC production and survival, poor det, poor absorption of folic acid and bleeding from varies. Endocrine problems: ‘n men: gynecomastia, oss of axillary and pubic har testicular atrophy, decreated libido and impotence. “These are due to increased estrogen levels -in younger women: amenorrhea In oder women: vaginal bleeding Hyperaldesteronism Because the liver fais to metabolize aldosterone adequately “This subsequently causes sodium and water retention and potassium fons. S.Peripheral neuropathy sIsa common findings in alcoholic crthosis “This may be due to thiamine, folie acid and cobalamine deficiencies. ‘COLLABORATIVE MANAGEMENT 1. Promote rest. To reduce metabolic demands onthe liver and masimize liver function, 2. Diet. The diet should be high in calorie (2,000 to 3,000/day and high in erboiydrates to ‘maintain weight. Ample protein to rebuild tssue but not high protein because tis may precipitate hepatic encephalopathy Fat restriction may be necessary during progressive stage ofthe disease, to prevent fatty infiiration ofthe liver. Provide suppiemets of vitamins 18,D,E,K, B-complex and C. 3. ‘Skin are to relieve pruritus “Wash the kin with warm water and mld soap, Change linens and gowns as necessary -Keep the envionment cao. Sweating intensifies prt, -Applyant-pruriic agent inthe skin as prescribed, g calamin lotion, corm starch of ‘oatmeal baths, solutions of bismuth salts aluinum acetate or boric aid. Change postion at regular intervals. ‘Administer oral cholestyramine resin (a bile acid sequestrant which enhances excretion of bile sate via the feces). or phenobarbital as prescribed. 4. Prevent trauma or injury. To prevent bleeding. Monitor the cient for bleeding gums, melena, hematoma, purpura and hematemests -Avoid or minimize parenteral injections Use small guage needle “Apply pressure at jection site for 5 minutes. ‘Avoid vigorous nose blowing, 5. Protect cient from infection ractie asepssloidal osmotic pes Sut and event sting also to manage | ‘hypoalbuminemia, : ister softeners as prescribed) “Hot/spicy, rough foods “Bending, stooping Coughing, sneer flow trough wth pen meh remo tl opantl to reduce poy enw FE Mo) ° ontrothamerthags du tortured sorraee se Menitor val sens une output contac “Rms, ls sa eaonder an ad vatsen peeraeg ped nae MBE Danese gles ey (Metoprolol, Congr Waion, inesn ambonaeSensalen-bemoe bec Minette sereby “Nevo into thestnach dein ees eta Horeca ge ts Sathacal boo sina emote ot eho a release the pressure pes scissors, Airway is always a priority. mati “Sportive measures drngan ct salle neh fing ofr, zen lum and pte ts © Wiamini acumen © ‘MstaminH2}~ receptor locker (eg Cen cnt) © Proton pu tere gente © lacus and neomycin scsi encephalopathy eto breakdows st the intestine ae © _Antbiots to prevent acter infestons. -Sleotherapy. An endoscopes paseo the soph nda sclerosing eget eg inorthate sot) intone thease seer sen nay causing inflaton thevem walsnd re ae " Raperte injections aver a period of weeks may be given until the varies ren ge prominent ee Porn chan Surge cede sa doo duce igs eae tema trypan, anostomosing the ih presse pot nol Systemicvenous syste, The porate shunt ees pot to prevent hepatic blood and release of ammonia inhypertension by sending portal venous blood supply directly into the inferior vena cava, Bypassing the Iver. 10, Reduces arvmonia formation. To prevent hepatic encephalopathy ‘+ Theinterention to reduce ammonia formation are 2 follows ‘4. Chronulac, Duphalac (Lactulose. reduces the pH ofthe colon, decreases production of alkaline ammonia and fcilitates the excretion of ammonia. The expected se effet ofthe drugis 2 4 stools a day its mate than 4 watery stool day, notify the physician. There may be ‘needed to reduce the dose of lactulose. b._ Myeiradin (Neomycin). To reduce colonic bacteria which are responsible for the production of armenia. &Tapwater ornormal saline enema. To remove digested blood from the colon, flowing # pried of blading ito the gastrointestinal tract. Because blood is protein this process increases ammonia it the gut and blood stream. In tur the excessive ammonia disturbs brain function. 11, Avold medications such s narcotics, sedatives, barbiturates, acetaminophen. These 2r€ hepatotoxic medications 112. Avold ASA to prevent bleeding. 43. Most important cient teeching, avoid aleohol