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8/8/2019 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)
Recommended