Accessory Concept

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    August 16, 2010 ACCESSORY

    Biliary tract and exocrine pancreas

    y Accessory organs andits locations

    y Liver largest organ

    y Gallbladder R side

    y Pancreas L side; headis nearS.I.; tailisnearspleeny Ampulla of Vater connection of the CBD

    and pancreaticduct

    y CBDcanaffect pancreas, gallbladder

    Biliary tract

    1. Commonbile duct

    y Cystic, hepaticduct

    2. Cysticduct

    y From gallbladderto the CBD

    3. Gallbladder

    y Saclike organlocated under the R side ofliver

    y Stimulated to contract by CCK and motilin

    BILE fat emulsifierand helps with absorption;composed of (50% bile salts, H2O and electrolytes,bilirubin, lecithin, cholesterol)

    Flow of Bile:

    liver Hepaticduct R orL Common hepaticduct

    gallbladder cysticduct sphincterof Oddi

    Exocrine Pancreas

    y Glandlocatedbehind the stomach on L sideofabdomen

    y Pancreatic enzymes

    y AMYLASE breaks down CHOy TRYPSIN breaks down CHON

    y LIPASE breaks down FATS

    SECRETIN secretion ofalkaline fluids; inhibitsaction of gastrin; decrease gastricacid secretionandmotility

    Chyme induodenum

    S cells produce secretin

    Absorbedinintestine

    Pancreas

    Secrete alkaline rich fluid

    Pancreatic enzymes do not work in an acidicenvironmentthe need foranalkaline rich fluid.

    CCK stimulates gallbladderand pancreas

    (CCK) Cholecystokininand Acetylcholine

    yC and A acinarcells enzyme releasey Feedback mechanism inhibits secretion ofmore pancreatic enzymes

    ALTERATIONS:

    y Cholelithiasis

    y Cholecyctitis

    y Choledolithiasis

    y Pancreatitis

    CHOLELITHIASIS (gall stones)

    y Formation of stones in gallbladder

    y Lith stones

    y Chole gallbladdery RF: (4Fs)

    y F female

    y F fat

    y F forty (increasedcholesterol)

    y F fertile

    Gall stones are crystalline structures formedbyconcentration (hardening) oraccretion (adherence ofparticles, accumulation) ofnormal orabnormalbileconstituents (80% are cholesterol)

    Theories of gallstone formation

    1. Bile changes incomposition

    2. Gallbladderstasis bile stasis (gallbladderonlycontracts with the presence of food)

    3. Infection predisposes a person to stone formation

    4. Genetics anddemography Caucasian

    Cholesterol needs to combine with bile salts andlecithinin orderto dissolve in water

    Pathophysiology:

    Unconjugatedbile precipitate

    Formation of PIGMENT stones (frbilirubin orsalts; isdifferent

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    Malabsorptiondisorder

    Malabsorption of bilesalts

    Decreased bilesynthesis

    Supersaturation ofbile with cholesterol

    obesity, increased age

    increased hepaticsecretion ofcholesterol

    estrogen therapy

    (multiple)pregnancy

    gallbladder sludge

    clofibrate meds (todec. cholesterol)

    dec. serumcholesterol

    inc. cholesterolexcretion into the bile

    rapid weightloss

    liver excretescholesterol

    Supersaturation ofbile with cholesterol

    cholesterol-saturated gall stones

    irritates gallbladder

    CHOLELITHIASIS

    obstruction of thepassage of bile

    contraction ofthe gallbladder

    RUQ painreferred to the

    shoulder

    vagalstimulaiton

    N/V

    Abd. guarding,facial grimace

    gallbladderdistention andinflammation

    markedtenderness in the

    RUQ on deepinspiration

    prevents fullinspiratoryexcursion

    dec. bile in theduodenum

    malabsorption ofvit ADEK (fatsoluble vits)

    S/Sx: A blurrevision

    D dec. Caformation

    E dec.antioxidant

    K bledding

    hemorrhag

    retention in the

    gallbladder

    bile absorbed inthe circulation

    jaundice

    continuous bile retention inthe gallbladder

    abscess, necrosis,perforation

    seeping into the peritonealcavity

    peritonitis (end complicationof cholelithiasis)

    bile salts inthe skin

    pruritus

    dec. in GIT

    inc. in KIDNEY

    feces: clay colored;urine: very dark

    Ultrasound,

    cholecystogra

    -phy, ERCP

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    Assessment:1. Biliarycolic pain, pain occurs 3-6 hours afterheavymeals

    2. Anorexia, N/V

    3. Sensation of fullness, intolerance to fatty food

    4. Steatorrhea, jaundice, bleeding tendencies, claycolored stool

    Diagnostic tests:

    1. ULTRASOUND

    y Most sensitive/ accurate

    y X eat (it willdistend gallbladder)y I: jaundice, allergic to contrast medium

    2. ERCP (endoscopic retrogradecholangiopancreatography)

    y Contrast mediumy Direct visualization of hepatobiliary system

    performed with a flexible endoscopey Multiple positions requiredduring procedure

    to pass the endoscope

    PriorNursing responsibilities in ERCP:

    1. Explain procedure

    2. Assess allergy to seafood/iodine

    3. NPO 4 hours

    4. Explain to patient he willbe sedated (informed

    consent)

    5. Remove dentures to prevent aspiration

    Post op Nursing responsibilities in ERCP: ( VS,monitorgag reflex)

    3. MRI

    y Remove magnetic things

    y Assess claustrophobia

    4. PTC (percutaneous transhepaticcholangiography)

    y Cholangio-CBDy Injection ofdye (biliary tract)y Hepaticducts withinliver, CBD, cysticduct

    and gallbladderare outlines

    y NPO

    y Allergy

    y Informedconsent(sedated)

    y Hct, prothrombin time, prone to bleeding?

    y Administerantibiotic (prophylaxis)

    5. Oral cholecystography

    y To detect gall stone andassess ability of gallbladderto fill /concentrate its contents,contaract and empty

    y Eg ofcontrast agentL IOPANIOC ACIDy Post: instruct client to eat in orderto contract

    gallbladderthus excreting bile

    Health promotion

    y low fat diet

    y idealbody weight

    y limit numberof pregnanciesy TPN for1 month

    Nursing management

    y Pain medsy Comfort measures

    y Diet modifications

    y Weight loss

    y IVF

    y Refer forS ofdehydration

    Medical management (palliative forsymptoms)

    1. Meds

    y Analgesics

    y Antacids H2 blockers orPPI

    y Antiemetics

    y Antibioticsy Nitroglycerin

    2. F&E

    y IVF

    Management

    1. Gallstone dissolution

    y Cholesteroldissolving agents (CDA)

    y CDCA

    y UDCAy MOA: dec. cholesterol synthesis inbile

    y For6-12 months

    Nonsurgical management

    1. Endoscopy

    Endoscope Duodenum CBD

    Passage of stone Enlarges it Ampulla of Vater

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    2. Extracorporeal shock wave lithotripsy

    y I : symptomaticcholelithiasis with >4stonesy Stone yellow)y Painand tenderness in RUQ

    y Increasedabdominal girthy Tachycardia

    y Bil eorbloodleaking from wound

    y Drop inBP

    JP Drain

    y The original suctiondrain.

    y The drainitselfis inside the body. It is madeof Teflonand has multiple drainage holes.

    y The drainis connected to clearplastic tubing

    which is usually sutured to the skinat the

    point it leaves the skin. The tubing connects

    to abulbreservoir. The bulb, when

    squeezed empty, applies constant suction to

    the drainand pulls the fluid out of the body.

    The drainis removed when the excess fluid

    has stoppeddraining from the body.

    y A JP drain maybe used, forexample,forabdominal orthoracicdrainage. JP

    stands forJackson-Pratt.

    T tube:

    y keep the duct patent until edema subsides

    y allows bile to drain out of the patient's bodyinto a small pouch, knownas abile bag

    y The amount of bile, which varies in colorfrom deep gold to dark green, can then bemeasured.

    y If a T-tube is put in place, it may remainattached to abile bag fora week or possibly

    longer.y When the bile bag is removed the T-tube willbe t ied or capped. It will remain in place forseveral months so that it can be used forspecial testing.

    Nursing responsibilities forPatients with T tube:1. Semi fowlers position

    2. Characteristic ofdrainage (volume 350-400ml); forfoul odorand purulent drainage

    3. Report suddenincrease inbile output

    4. monitorforinflammationand protect skin from

    irritation

    5. drainage system below the gallbladder

    6. JP drain willbe removedafter7-14 days

    7. T tube removedafter6 weeks

    Stool with bile- yellow > indicatorT tube canberemoved

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    Clamp tube before a mealand observe forabdominaldiscomfort anddistention, N, chills orfever

    Unclamp tube if N/V occurs

    CHOLECYSTITIS

    y Inflammation of gallbladder

    y 3 types:1. Acalculous Cholecystitis (RF: 4Fs,sedentary)no stones2. Chronic Cholecystitis (less pain, noincrease in WBC)3. Acute inflammation

    Assessment:

    y (+) Murphys signy N/V

    y Fevery Mildjaundice

    y Guarding, rigid, rebound tenderness

    Medical management

    1. antibiotics

    Surgical management

    1. Cholecystectomy

    2. cholecystostomy surgicaldrainage of gallbladder

    Nursing management:

    1. diet (low fat)

    2. antibiotics, analgesics, antispasmodics

    CHOLEDOCHOLITHIASIS

    y Stones in CBDy JAUNDICE (intermittent orrecurrent)

    Surgical management:

    y Cholecystectomyy ERCP with endoscopic papillotomyand

    stone extractiony Choledocolithotomy

    PANCREATITIS

    y Inflammation of pancreas

    y Associated with escape of pancreaticenzymes into surrounding tissue

    y Classifications: acute andchronicpancreatitis

    Acute pancreatitis

    y Acute inflammatory process of the pancreasresulting inauto digestion of the pancreas byits own enzymes

    y Life threateningy Etiand RF: biliary tract obstruction,alcoholism, trauma

    y Painaggravatedby supine positionandafterheavy meals

    alcohol intake

    stimualte HCLand secretin

    roduction

    pancreaticenzymes

    stimulation

    causeobstruction inthe sphincter

    of pancreaticduct

    gallstones

    enter CBD

    lodge at ampullaof vater

    biliary tractobstruction

    inactive enzyme backflow

    activation of enzymes

    auto digestion

    production and releaseof pancreatic enzyme

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    production and release ofpancreatic enzyme

    (inc. serumlipase) fatty

    acids arereleased

    combines withionized Ca+

    hypocalcemia

    (inc. serumtrypsin)

    release oftrypsin

    polypeptideformation

    thrombosis

    gangrene

    inc. serumamylase)release ofelastase

    blood vesseland duct

    destruction

    necrosis

    hemorrhage

    release ofkallikrein

    release ofvasoactivepeptides

    vasodilation

    inc. vascularpermeability

    edema

    irritation ofinflamedpancreas

    abdominalpain,

    tenderness,back pain

    vagalstimulation

    N/V

    leukocytes clusteraround necroticareas (inc. WBC)

    bacterialproliferation in

    area

    suppuration (pus)and lesionformation

    destruction ofpancreatic islets

    hyperglycemia

    abscess pseudocyst (pus)

    impedes bileflow through

    CBD

    JAUNDICE

    hypovolemia

    hypoTN,cyanosis,

    coldclammy

    skin

    dec. inbowelsounds

    exudates withpancreaticenzymes

    frperitoneal

    cavity viatransdiaphrag

    matic lympchannels

    atelactasis,pneumonia

    S ofpancreatitis)

    rigid,

    boardlikeabdomen

    CULLEN'SSIGN (bluisdiscoloratioof umbilicu

    TURNER'SSIGN (bluisdiscoloratio

    of flank -BACK)

    Abdominal

    guarding,facial grimace,

    pain

    aggravatedby

    supine

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    Assessment

    PAIN - sudden onset of mid epigastric pain orLUQ radiating at the back after heavymeals/supine position

    Diagnostic test

    y Historyand PE

    y ERCP

    y CT scan

    y Abdominal Xray

    y Lab exam (alkaline phosphotase,bilirubin, BUN, glucose)

    y 48-72 hours elevated AMYLASE

    y 5-14 days elevated LIPASE

    y (morphine-spasm of sphincter+pancreatitits)

    Medical management (palliative)

    y Pain mgt (Demerol, meperidine CNSdepression)

    y Fluidvolume status, electrolyte balance

    y Nutritional status (TPN, NGT forsuctioning)

    y Decreased Endocrine function

    y Treat complications (respiratory care) oxygen, turning, position

    y NPO, semifowlers with flexed knees(chest knee)

    Surgical management

    1. laparotomy with sump drainage

    2. debridement with surgicaldrainage orretroperitonealdrainage

    3. subtotal pancreatectomy

    4. Whipples surgery (remove distal 3rd

    ofstomach, part ofduodenum, CBD, gallbladder,head of pancreas); complication: hemorrhage

    Nursing management

    y NPO and hydration, NGT suction (Xacidic environment), TPN

    y Supplemental preparations

    y Pain meds, antacids, H2 receptorantagonists (decrease acidity)andanticholinergics

    y No alcohol

    y Bedrest to decrease metabolicdemand

    y Positioning

    y Deep breathingandcoughing exercises

    y Low fat and high calorie diet

    Chronic Pancreatitis

    y Continuous prolongedinflammationandfibrosing process of the pancreas

    y Formation of scartissue

    y Etiology

    Alcoholism (70-80%)

    Idiopathiccause

    Hereditary

    Biliary tract obstruction

    Pathophysiology:etiologicagent

    Inflammatory process

    Attack ofacute pancreatitis

    Continuous and prolongedinflammatory process

    Scarring andcalcification of pancreatic tissue

    Irreversible damage of endocrine and exocrinefunctions

    S/SX

    Types:

    1. chronic obstructive pancreatitis

    2. chroniccalcifying pancreatitis (akaalcoholinduced pancreatitis) most common,inflammationand sclerosis, mainlyat the headof pancreas and pancreaticduct

    Assessment:DM manifestations, steatorrhea

    Diagnostic test

    y Historyand PE

    y ERCP

    y CT scan

    y Abdominal Xrayy Lab exam (alkaline phosphotase,

    bilirubin, BUN, glucose)

    y 48-72 hours elevated AMYLASE

    y 5-14 days elevated LIPASE

    y (morphine-spasm of sphincter+pancreatitits)

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    Medical management (palliative)

    y Pain mgt (Demerol, meperidine CNSdepression)

    y Fluidvolume status, electrolyte balance

    y Nutritional status (TPN, NGT forsuctioning)

    y Decreased Endocrine function

    y Treat complications (respiratory care) oxygen, turning, position

    y NPO, semifowlers with flexed knees(chest knee)

    y Pancreatic enzyme replacement egpancrelipase (cotazyme). Pancreatin(viokase); take with meals, wipe mouth

    enzymes are irritating to the skin(prevent stomatitis)

    y Bile salts (synthetic)

    Surgical management

    1. Whipples procedure

    2. Total pancreatectomy

    3. cholecystojenostomy

    4. Total pancreaticoduodenectomy withsplenectomy

    5. Biliary stents

    Nursing management

    1. Medications

    2. Assess respiratory function, CV status(hemorrhage), PQRST (pain)

    3. NPO 3-7 days, gastric secretion

    4. Physical movement and mental stimulation

    5. Position forcomfort

    6. IV fluidreplacement and electrolytes

    Management ofclients with hepaticdisorders

    Anatomyand physiology:LIVER

    y RUQ

    y R and L lobe

    y Calciforum divides the lobe

    y 3-4 hours

    y Hepaticcells functional

    y Sinusoid

    y Bile at canaliculus

    y Portalandarterial Circulation

    y Dualcirculationy Arterialcirculation from hepaticartery

    (O2 blood 300-400mL ofblood) fromportalvein GIT

    y Portalveinis connected to liver(1000-1400ml ofblood)

    y Kuppercells pick up organisms fromblood which came from GIT notalways sterile

    y Specialcharacteristics:REGENERATIVE LIVER CELLS

    FUNCTIONS:

    1.Bile secretion/production (choleresis) 600-1200mL/day

    Enterohepaticcirculation recycling ofbile salts,18 times

    Hepatic secretion

    Hepaticresecretion intestinalabsorption

    2. Metabolism ofbilirubin (metabolism -converting substance to be excreted)

    Hmg 120 days

    Heme globin

    Noniron pool biliverdin amino acid pool

    Bilirubin

    Plasma + albumin(oncotic pressure)

    Unconjugatedbilirubin (X secreted easily)

    Liver:

    glucorganic

    acid

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    Unconjugatedbilirubin (X secreted easily)

    Conjugatedbilirubin

    Becomes constituent ofbile

    S.I.

    STERCOBILIN: feces UROBILINOGEN:urine

    3.Vascularand hematologic functions

    y Store blood

    y Kuppercells

    y Prothrombin, fibrinogen, factors I, II, VII,IX, X synthesis

    y Vitamin K absorption

    4.Fat metabolism

    y Fats: synthesized from CHON and Fats

    Absorbedbylacteals inthe intestinalvillilymphatics

    (triglycerides)

    (hydrolyzed)

    LIVER (releasedin the bloodstream)

    Lipoproteins

    Storage ofadipose tissue

    5. CHON metabolism

    LIVER producesCHON albumin

    Deamilation AA oncotic pressure

    Ammonia

    Removes ammonia urea

    LIVER formation plasma CHONs

    6. CHO metabolism

    LIVER stores glycogen(glucose bufferfunction)

    Converts galactose and fructose glucose

    Converts CHO triglycerides adipose tissue

    7.storage ofironandvitamin

    Liver stores vits. A, D, B12

    (Apoferritin + iron (extrain serum) =ferritin)

    8.Metabolicdetoxification

    Liver active chemical medium detoxify

    Liver inactivates steroid hormones(testosterone,progesterone,

    corticosteroids, aldosterone)Assessment

    y Hepatotoxic substances with infectiousagents

    y Occupational, recreational and travelhistory

    y History ofalcoholanddrug use

    y Past medical history

    y S and sx that suggest liverdisease

    Lab tests

    Bile formationand secretion

    Test Normalvalue

    1. direct (conjugatedbilirubin

    0.03 mg/Dl

    2. indirect(unconjugatedbilirubin)

    0.1 mg/Dl

    3. total serum bilirubin 0.1-1.2 mg/Dl

    Protein studies

    Test Normalvalue

    1. total serum CHON 7.0-7.5g/Dl2. serum albumin 3.5-5.5 g/Dl

    3. serum globulin 2.5-3.5 g/Dl4. A/G ratio 1.5:1 to 2.5:1 g/Dl

    ALT 2.5(JAUNDICE), definitive, increasedproblem in LIVER

    AST foundinincrease metabolic substances

    Increasedalkaline phosphotase inbile

    obstruction

    Coagulation studies

    Test Normalvalue

    1. PT 11.5-14 sec

    2. PTT 25-40 sec

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    Serum enzymes

    Test Normalvalue

    1. AST 8-20 u/Dl2. ALT 10-35 u/Dl

    3. alkalinephosphotase

    32-92 u/Dl

    4. LDH LDH5.Blood ammonia 150-250 u/Dl

    Diagnostic test

    1. abdominal Xray

    2. liverscan

    y Contrast medium

    y Assess allergy

    y NPO 4 hours

    3. Splenoportogram

    y Determine adequacy of portalcirculation

    y Contrast medium

    4. MRI

    5. CT scan

    6. ERCP

    7. Liverbiopsy

    y Most specific

    y Percutaneous liverbiopsy

    Nursing preop responsibilities (liverbiopsy)

    y PT and PTT (prolong vit K or post ponebiopsy)

    y Consent

    y NPO

    y Baseline VS (bleeding)

    Nursing during responsibilities (liverbiopsy)

    y Expose R hypochondriac

    y Client inhale and exhale thenhold

    breathat the end of expiration (toprevent puncturing the diaphragm)

    Nursing afterresponsibilities (liverbiopsy)

    y R side lying with pillow on puncturedincision site

    y Bedrest 24 hrs

    y No coughing/straining/heavylifting

    y VS

    JAUNDICE

    y Yellow/greenish yellow discoloration ofsclera skinanddeeper tissue

    Types:

    1. Hemolyticjaundice(prehepatic)

    y Causes: BT reactions, immune reaction,membrane defects of erythrocytes , toxicsubstances incirculation

    Inc. breakdown RBC

    Inc. heme production

    Inc. amt of unconjugatedbilirubin

    2. Hepatocellularjaundice (intrahepatic)

    Hepatitis cirrhosis, hepaticcancer

    Alt. ability ofliverto conjugate bilirubin

    Inc. amount of unconjugatedbilirubin

    3. Obstructive jaundice (post hepatic)

    Liver,tumor,hepatitis,cirrhosis

    Swelling orfibrosis oflivercanaliculi &bile ducts

    Bile cant pass through

    Bile absorbedincirculation

    Stones in CBD, Biliarystricture

    CBDis occludedby gallstone

    Bile cant pass through

    Bile absorbedincirculation

    CM

    y Yellow sclera

    y Yellowish orange skin

    y Claycolored feces

    y Teacolored uriney Pruritus

    y Fatigue

    y Anorexia

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    Medical management

    y Determine cause of jaundice healthhx, PE, liver function test, hematologictest

    y Reduce pruritus and maintain skinintegrity oral cholestyramine resin,antihistamines, phenolbarbital

    Nursing management(Assess S of jaundiceformation)

    Interventions

    y Tepidbath

    y Lotion

    y Loos clothing

    y Soft bedding

    y Short nails

    y Keep room cool

    Surgical management

    y Choledochostomy-exploration of theCBD

    HEPATITIS

    y Inflammation of the liver caused byvirus, bacteria, or exposure tomedication orhepatotoxins

    y Goal of therapy: rest the inflamedarea

    Alcoholichepatitis

    Inflammation

    Degeneration

    Necrosis of hepatocytes andinfiltration ofleukocytes

    Mallorybodies

    Manifestations:

    y Anorexia, N/V

    y Ascites

    y Fever

    y Encephalopathy

    y Abdominal pain

    y Splenomegaly

    y Hepatomegaly

    y Jaundice

    y Anemia, leukocytosis, inc. bilirubinlvel

    y Biopsy fatty hepatic tissue

    Nursing management

    y Increased VII, CHO diet

    y Folicacidand thiamine supplement

    y Parenteral fluids

    y Liquid formulas to increase caloric

    intakey No alcohol!

    y Steroids

    Viralhepatitis

    Hepatitis ARNA

    Hepatitis B DNA

    Hepatitis CRNA

    Hepatitis D,E,F,GRNA

    HEPATITIS A (Infectious hepatitis)

    CA Small, undeveloped,RNA contaminatingHAV

    INCUBATIONPERIOD

    15-45 days, mean 30;2-6 weeks

    Ind @risk Young childrenandyoung adults; healthcare personnel

    RF/transmission Fecal-oralroute,contaminated waterormilk; shellfish fromcontaminated water

    Testing (+)acute HAV inbloodInc. IgM and IgGInc. IgM Abin 4-6 wksInc. IgG Ab

    BET Gamma globulins

    Outcome Mild with fullrecoveryFatalityrate less than1%No carrierstae orinc.risk ofchronicityMay progress tofuminant hepatitis

    Prevention: HW, stool precautions, waterprecautions, vaccine

    IgG Patient has immunity

    IgM newly exposed o the disease (hepatitis)

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    HEPATITISB

    CA Double strandedDNAvirus (HBV)

    INCUBATIONPERIOD

    30-180days, mean 60-90; 6-24 weeks

    Ind @risk Drug users, clients onlong term hemodialysisHealth care personnelYoung adults (sexualand percutaneous)Babies and toddlers

    RF/transmission Blood orbloody fluidcontact, infected salivaorsemen,contaminatedneedles,sexualcontact,parenteralperinatal period, orbody fluidcontact at

    birthTesting HbA g-Ab system in

    bloodHbsAgHbsAg 6 weeks(newlyinfected carrierstate)

    Acute HbsHbe Ag

    POET HepaBimmuneglobulinForchronic hep B:interferon, adefovir(Hepsera)and

    lamivudine (Epivir)Outcome Inc. risk for chronic

    hepatitis, fulminanthepatitis, cirrhosis andhepaticcancerMaybe severe, fatalityrate 1-10%Possible carrierstate

    Prevention: HW, screening ofblooddonors,testing of pregnant women, needle precautions,avidintimate sexualcontact if test forHbsAg is(+)

    HEPATITIS C (NANB/POST TRANSFUSIONHEPATITIS)

    CA Single stranded RNAvirus

    INCUBATIONPERIOD

    15-160 days, 505-10 weeks/2-12 wks

    Ind @risk Parenteraldrug useClientsreceivingfrequent bloodtransfusionsHealth care personnel

    RF/transmission Blood orbloody fluidcontact, infected salivaorsemen,contaminatedneedles,sexualcontact,parenteralperinatal period, orbody fluidcontact at

    birthTesting Anti HCV- most

    accurate indetecting

    POET Alpha interferon orpegylatedinterferon +ribavin

    Outcome Frequent occurrenceofchroniccarrierstateandchronicliverdiseases

    Inc. risk of 1rHepatocellularcarcinoma

    Prevention: needle/ blood precautions, HW

    Immunitybyvaccine orhistoryofhepatitis

    HEP C > carcinoma, FH, chronic hepatitis>most fatal

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    HDV (B) (DELTA AGENTS HEPATITIS)

    CA HDV, delta hepatitisagentDefective RNA virus

    INCUBATIONPERIOD

    30-180days, mean 60-90; 7-8 weeks/2-10wks

    Ind @risk Drug users, clients onfrequent BT, clientreceiving hemodialysis

    RF/transmission Blood orbloody fluidcontact, occurs as dualinfection with HBVHDAg earlyincourseofinfectionHDAb laterdiseasestage

    Testing HbA g-Ab system inbloodHbsAg

    HbsAg 6 weeks(newlyinfected carrierstate)

    Acute HbsHbe Ag

    POET interferon

    HEPATITIS E (A) (ENTERICALLYTRANSMITTED OR EPIDEMIC NANBHEPATITIS)

    CA Unenveloped, singlestranded RNA virus

    INCUBATIONPERIOD

    14-60 days, mean 40;2-9 weeks

    Ind @risk Travelers to countrieswith high incidence ifhepatitis EEating/ drinkingfood/watercontaminated withvirus

    RF/transmission Fecal-oralroute

    Testing Anti HEVOutcome Mild with fullrecovery

    Fatalityrate less than

    1%No carrierstae orinc.risk ofchronicityMay progress tofuminant hepatitis

    Stages of Hepatitis

    1. Pre-icteric orprodromal stage

    y (Interic=jaundice)

    y CM: fatigue, malaise, fever

    y ranging from severaldays to more thana week, characterizedby theappearance of symptoms like loss ofappetite, fatigue, abdominal pain,

    nauseaandvomiting, fever, diarrhoea,dark urine and pale stools

    2. Icteric stage

    y CM: liveris enlarged

    y jaundice develops at totalbilirubinlevelsexceeding 20 - 40 mg/l

    3. Post icteric (recovery phase)

    y Pain subsides, increased energylevel

    6-8weeks afterexposure, jaundice is subsides

    2-12 weeks afteronsetof jaundice liverfunction

    Management:

    y Bedrest

    y High calorie, low fat diet

    y IVF, TPN

    y Bile acid sequestrants

    y Immunoglobulins andvaccines to family

    y Avoid hepatotoxicdrugs such as(Tylenol); chlorpromazine

    yHCV: INTERFERONy HBV: EPIVIR

    y Lamivudine

    LIVER CIRRHOSIS

    y Chronic, progressive disease oflivercharacterizedbydiffuse degenerationfibrosis (scarring)andnodule formation

    y Cirrhosis is acomplication of manyliverdiseases that is characterizedbyabnormal structure and function of theliver.

    y The diseases that lead to cirrhosis do sobecause theyinjure andkilllivercells,and the inflammationandrepairthat isassociated with the dying livercellscauses scartissue to form. The livercells that do not die multiplyinanattempt to replace the cells that havedied. This results inclusters ofnewly-formedlivercells (regenerative nodules)within the scartissue.

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    y There are manycauses ofcirrhosis;theyinclude chemicals (such as alcohol,fat, andcertain medications), viruses,toxic metals (such as ironandcopperthat accumulate in the liveras aresultof geneticdiseases),andautoimmuneliverdisease in whichthe body's immune system attacks theliver.

    y CM: jaundice (due to the accumulationofbilirubinin the blood), fatigue,weakness, loss ofappetite, itching, easybruising

    CARDIAC CIRRHOSISSevere R sided HF

    Enlarged, edematous, congestedliver

    Liveranoxia

    Livernecrosis and scarring

    Liverdamage

    Decreasedliverfunction

    Chronicalcoholism

    Toxins form alcohol: release ofacetyldehyde

    Damage hepatocytes

    Necrosis of hepatocytes

    Fibrosis

    Livercells regenerate dec. liverfunctionInabnormal pattern

    Livercells loaded with fat

    Enlargement

    Irritates glissoncapsule

    PAIN

    H+ ion >acidity

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    Esophageal varisces

    y Complex torturous collateralveins atlowerend of the esophagus due toprolonged evaluation of pressure

    y Cardinal sign - ESOPHAGEALBLEEDING

    yPainless

    Assessment

    y Hematemesis

    y Melena

    y Anorexia

    y Nausea

    y Splenomegal

    y Caput medusa

    y osplenicdullness

    Diagnostic test

    y Barium swallow (NPO, allergy, inc. fluidintake, laxatives, stool-whitish)

    y Esophagoscopy

    Medical management

    1. Sclerotherapy

    Endoscopy

    Esophagus

    Inject sclerosing

    Inflammationand fibrosis

    Solidifying and stop circulation to the varix

    2. Transjugualrintrahepatic portosystemic shunt(TIPS)

    3. Vasopressin

    y Stop varicealbleeding

    y MOA qportalvenous blood flow byconstricting afferent arterioles

    y SE hypothermia, MI, GI ischemiaand

    acute renal failurey CI patients with recent MI

    4. Balloon tamponade SengstakenBlakemoretube/Minnesota

    y Pressure of the esophagealand gastric

    balloonpstop the bleeding

    y Complications: esophagealrupture,aspiration, pneumonia

    Care of patients with SengstakenBlakemore

    y Semi fowlers

    y Maintain tractiony Scissors at bedside

    y Monitorrespiratory status

    y Label each lumen

    y Maintain prescribedamount of pressurey Mouth andnasalcare every 1-2 hours

    Surgical management

    1. Endoscopicbandligation

    y Device with smallrubberbands (o rings)

    at the end of the endoscope p overthevarix

    2. Portosystemic shunt

    y Anastamosing = high pressure portal

    venous system to the low pressuresystemicvenous system

    Perioperative nursing management

    Preop

    y Explain

    y Tests

    y Consent

    Post op

    y Assess

    y Nutrition

    y IVF

    y Dressing

    y Bloodand urine values

    Nursing management

    y Nutritionalnadneurological status

    y Patient airway

    y Gastriclavage with cool saline

    y Quiet environment

    y s/sx ofbleeding and shock

    y vasopressin

    Health education

    y qesophagealirritation

    y No oinabdominal, thoracicand portalpressure

    y S of hemorrhage

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    Ascites

    y Accumulation of fluidin the peritonealcavity that results from severalPathophysiology

    Assessment/Dx test

    y Percuss abdomen dull

    y Detect fluid wave

    y Paracentesis

    y Abdominal X ray studies

    y Ultrasonography

    y CT scan

    Paracentesis

    y Transabdominalremoval of fluidfromthe peritonealcavity

    Nursing responsibilities (qsalt, qfluidintake,avoid NSAIDS, aspirin)

    Pre op

    y Explain

    y Consent

    y VS,abdominal girth, weight

    y Emptybladder

    y Positionthe patient high fowlers

    Post op

    y Comfortable position

    y Assess: VS, abdominal girth, weight

    status, S of hypovolemiay Dressing

    y Patient education

    Medical management

    y Paracentesis

    y Albumin, IV

    y F&E balance

    y Diet modifications

    y Diuretics

    y Maintain skinintegrity

    y Transjugularintrahepatic portosystemic

    Surgical management

    y LeVeen shunt (peritoneal shunt)

    y a peritoneal-venous shunt usedin thecontrol ofascites

    y It routes excess ascitic fluid out of theperitonealcavityandinto the superiorvenacava or the jugularvein

    Hepatic encephalopathy

    y Portal systemic encephalopathy

    y Accumulation ofammoniaand othermetabolities inblood

    y Altered LOC, impaired thinking,neuromusculardisturbances

    liverdamage/cirrhosis

    presenceof fibroustissue&no

    dules

    ocapillarypressure

    obstructionofvenous

    flow inliver

    splanchnicarterial

    vasodilation

    qbloodvolume

    activationof RAASsystem

    albuminsynthesis

    qoncoticpressure

    esp inpreitoneal

    cavity

    qmetabolismof

    aldosterone

    Na&H2Oretention

    bykidneys

    hypovolemia

    ASCITES

    fluidwave

    downwardprotrudingumbilicus

    weight gain

    oabd. girth dyspnea

    striae&distended

    veins

    abd.distention

    F&Eimbalance

    bulgingflanks

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    Stages of H.E.

    1. Prodromal

    y Not obvious

    y CM: agitation, forgetfulness, restless,inability to concentrate

    2. Impending

    y CM: lethargic, confused, handwritingproblems

    3. Stuporous

    y Severe mentaldeficit, intolerance,hyperreflexia

    4. Coma

    y Comatose

    y (+)babinskireflex

    y Fetorhepaticus (A peculiarodorof thebreath inindividuals with severe liverdisease causedbyvolatile aromaticsubstances that accumulate in the bloodand urine)

    Assessment andDx test

    y EEG

    y Serum ammoniaand CSF

    y Gluatmine levels

    yElectrolyte levely Blood gases

    y Hepatic function test results (egprothrombin, bilirubin, albuminandenzymes)

    Medical management

    y Assess etiology

    y Neomycin (Mycifradin) CI: renalinsufficiency

    y Lactulose

    y Antibiotics (to killbacteriain theintestine)

    y Oral MgSO4/ enemas afterhemorrhagey IV fluids andvitamins

    Nursing management

    y Assess neuro status

    y Restrict CHON, oCHO andvitamin Ksupplements

    y Medications

    y Protect client from injury

    y Bedrest ( to decrease metabolicdemand)

    Livertransplantation

    Livertransplant

    y Forend stage liverdisease

    y Duration: 6-18 hours

    Complications

    y Rejection (occur4-10thday)pjaundice,

    encephalopathy

    y Infection

    y Hemorrhage

    y Atelactasis

    Signs/symptoms of REJECTION

    y Tachycardia

    y Pain on the RUQ orflank

    y ojaundice

    y Fever(early sign)

    Nursing management

    Post op

    y Monitor

    y Drugs to prevent infection:CYCLOSPORINE

    y Discharge instructions (s/sx ofrejection,etc)