Viral Hepatitis

systemic, viral infectnecrosis & inflam of liver cells

* clinical, biochemical, & cellular
A adult pop. < 25% of kids -antibodies to HAV
HAV antibody ^ w/ age, & ppl 50 + -prior exposure.
Hepatitis A Virus infectious hepatitis
gCxRNA virus (Enterovirus) fecaloral route,
- In BM b4 start of sx & during 1
st
few days of illness.
shellfish from sewage-contaminated waters.
g incubation period 15 & 50 days -mean :28 -30 days
Can last 4- 8 wks longer & more sev 40+
most recover & rarely progresses to acute liver necrosis
or fulminant hepatitis cirrhosis of liver or death.
carrier & chronic hepatitis
virus-briefly in serum,when jaundice occurs noninfect
Clinical Manifestations
g jaundice anicteric asx
sx mild, *F-like URInfect, low-F*. A*( early sx)
g cx release of toxin by damaged liver or failure of
damaged liver cells to detoxify an abn product.
g Later, jaundice & dark urine
Indigestionvague epigastric distress, *N, burn,&
flatulence. strong aversion to taste of cigs or presence
of cig smoke & other strong odors.
g sx clear jaundice reaches its peak10 days after
sx mild in kids; adults more severe, & longer.
Assessment & Diagnostic Findings
g liver & spleen mod enlg few days after onset;
Hepatitis A antigen in BM 7 -10 days B4 illness & 2-3
wks after sx.
HAV antibodies serum, not until sx
immunoglob anal antibodyacute or past infect .
Prevention
g vaccine Havrix & Vagta
Protection w/in several wks after 1
st
dose
g Immune globulin may suppress sx disease
]Caution w. previous angioedema, hives, or other allergic
reactions immune globulin
Epinephrine allergic reaction.
Medical Management
Bed rest acute stage & diet restriction of phys activity.
During A* , freq small feedings, supl IV fluids with
glucose.
Gradual but progressive ambulation hasten recovery,
Nursing Management
Home unless sev. Teach +/R for contracting HAV
Hepatitis B Virus blood (percutaneous & permucosal
routes)
blood, saliva, semen, & vag secretions
transmit mucous memb &opening skin or infect moms
long incubation period
reproduces in liver & in serum long time transmis
g contract HBV infectdevelop antibodies & recover
spontaneously in 6 mos. Mortality: up to 10%.
g HBV progress to carrier state or develop chr hepatitis
w/ persistent HBV infect & hepatocell injury & inflam.
g major cx of - cirrhosis & hepatocellular carcinoma.
old ^/R-sev liver cell necrosis or fulminant hepatic fail
Elim alterations to liver fx meds, OH
Clinical Manifestations incubation 1 -6 mos
F* & resp sx-rare
arthralgias & rashes. + appetite, dyspepsia, abd pain,
aching, malaise, & weak.
may(not)-Jaundice light-colored stools & dark urine
liver- tender & enlg 12-14 cm vertically.
spleen is enlg & may b palpable
posterior cervical lymph nodes may b enlg
Assessment & Diagnostic Findings
HBV is a DNA virus antigenic particles:
- HBcAgB core antigen (in inner core)
- HBsAgB surface antigen (on viral surface, a marker
of active replication & infect )
- HBeAgan independent protein circulating in blood
- HBxAggene product of X gene of HBV DNA
Ea. antigen elicit its specific antibody & marker in diff
stages
- anti-HBcantibody to core antigen of HBV; acute
phase may indicate continuing HBV in liver
-anti-HBsantibody to surface determinants on HBV;
late convalescence; indicates recovery & development of
immunity
-anti-HBeantibody to hepatitis B e-antigen; + infect
-anti-HBxAgantibody to hepatitis B x-antigen; ongoing
replication of HBV
Active Immunization: Hepatitis B Vaccine
Recommend ^/R HBV HCV & chr liver diseases
g A yeast-recombinant hepatitis B vaccine (Recombivax
HB) active immunity
booster hemodialysis & some immunocompromised
3 deltiod IM doses; 2
nd
& 3
rd
1 & 6 months
Antibody response - anti-HBs levels 1- 3 mos after
Passive Immunity: Hepatitis B Immune Globulin
(HBIG) passive immunity to hep B & for exposed to
HBV who have never had hep. B & hep B vaccine.
Specific indications postexposure vaccine with HBIG
(1) exposure needlestick or splashes w. mucous memb
(2) sex w. positive for HBAg
(3) babies born to HBV-moms given HBIG w.in 12 hrs
HBIG plasma - high titers of anti-HBs.
active & passive immunization w. exposed HBV
Medical Management
Goals + infectivity & liver inflam & + sx.
alpha-interferon inject
s/eF*,chills, A* , *N, myalgias, & fatigue
. Delayed s/emore serious+ dose or dc
B] suppress, thyroid dysfx, alopecia, & bacterial infect
g antiviral agents, lamivudine (Epivir) & adefovir
(Hepsera), oral nucleoside analogues, seroconversion
rates, loss of detectable virus, liver fx, & + progres to
cirrhosis w/ lamivudine. decompensat cirrhosis wait 4
liver transplant
Adefovir effective in ppl resistant to lamivudine.
Bed rest until sx of hepatitis have subsided.
Activities -restricted hepatic enlrg & ^ bilirubin &
liver enzymes have disappeared Gradually ^ activity
Adequate nutrition Proteins restricted- impaired liver
to metabolize protein byproducts
control dyspeptic sx & general malaise antacids &
antiemetics meds w. V*
- V*persistshosp & fluid therapy ^/R HIV
Nursing Management
Prolonged recovery from complete sx up to 3-4 mos +
gradual resume of physical encr after jaundice
Teaching Self-Care prolonged recov period home care.
rest & nutrition make arrangement receive
hepatitis B vaccine or hepatitis B immune globulin
Hepatitis C Virus blood transfusions & sex, needles
+ underlying cx 1/3 of hepatocellular carcinoma, & most
common reason for liver transplant
incubation period variable-15 -160 d.
^/R-chronic liver diseasecirrhosis or liver cancer
Small OH progression
benefit from rest, diet, or vitamin supplements.
g antiviral agents, interferon (Intron-A) & ribavirin
(Rebetol) HCV & in tx relapses.
Hemolytic anemia, freq s/e severe d/c
Ribavirin caution -childbear
Molecule polyethylene glycol moiety (PEG) is added to
interferon keep it in body longerextends dose- 1/wk
Pegylated interferon (Pegasys) virologic response rate

Hepatic Cirrhosis
replacement of normal liver tissue w/ diffuse fibrosis that
disrupts structure & fx of liver.
Alcoholic cirrhosis scar tissue surrounds portal
Postnecroticbroad bands of scar tissue. late result of
prev acute viral hepatitis.
Biliary scarring in liver around bile ducts.
Cxchronic biliary obstruct & infect (cholangitis)
scarportal & periportal spaces, where bile canaliculi of
each lobule communicate to form liver bile ductssites of
inflam, & bile ducts occluded w/ thick bile & pus
liver form new bile channels overgrowth of
disconnected, newly formed bile ducts & surrounded by
scar tissue.
SX intermittent jaundice & F* initial liver enlg , hard,
& irregular atrophies.
Pathophysiology Course- 30 or more years.
+protein intakeliver destruct cirrhosis, ^OHfatty liver
chem(carbon tetrachloride, chlorinated naphthalene,
arsenic, or phosphorus) or infectious schistosomiasis.
OHic cirrhosis necrosis- destroyed liver cells
gradually replaced by scar tissueexceeds liver fx
Clinical Manifestations
Coampensated cirrhosis, w/ less severe, vague sx,
decompensated cirrhosis failure of liver to synthesize
proteins, clotting fx, & other substances & sx of portal
^BP, ascites, varices, & hepatic encephalopathy
Liver Enlargement
Earlyliver lrg & cells-loaded w/ fat. firm & sharp edge.
abd pain recent, rapid enlg of liver tension on
fibrous covering of liver (Glisson's capsule).
Later liver +- scar tissue contracts liver. - liver edge, if
palpable, is nodular.
Portal Obstruction & Ascites
Cx chr failure of liver fx & obstruct of portal circulation.
most of blood from digestive organs is collected in
portal veins & carried to liver
cirrhotic liver free blood passage blood backs up
into spleen & GI tract, chr passive congestion
Indigestion & alt bowel fx result.
protein e ^^ in peritoneal cavity ascites
percussion shifting dullness or fluid wave
Infect & Peritonitis
w/ cirrhosis & ascites in absence of an intra-abdominal
source of infect or an abscessspontaneous bacterial
peritonitis (SBP).
Bacteremia intestinal flora
sx- Dxparacentesis
+ Antibx tx & prevention of recurrent episodes of SBP.
- hepatorenal synd functional renal fail -unresponsive to
admin of e or diuret - (sev comp)
lack patho in kidney, dehyd or obstruct of
urinary tract or any other renal disorder.
Gastrointestinal Varicesobstruction to blood flow
through liver fibrotic & form blood vessels in GI
blood shunts from portal vessels into blood vessels w/
lower pressures distended abd vesselsvisable (caput
medusae), & distended vessels throughout GI tract.
Esophagus, stomach, & lower rectum
distended blood vessels form varices or hemorrhoids,
cant tol high pressure & vol of blood rupture &
bleed.
g assessobserv-occult & frank bleeding from GI tract.
Edema Late sxchronic liver failure.
g + plasma albumin dependent edema not Facial
^ aldosterone Na & H20 reten & K excretion.
Vitamin Deficiency & Anemia
Inadeq form, use, & storage of vit(A, C, & K)
g hemorrhagic phenomena K defic.
g Chr gastritis & GI fx, w/ poor diet intake & liver
fxanemia assoc w/ cirrhosis.
Mental Deterioration & cog fx w/ impending hepatic
encephalopathy & hepatic coma.
g nuero assess behavior, cog abilities, orient & speech.
Assessment & Diagnostic Findings
g Sev parenchymal liver dysfx+albumin & ^ globulin
g Enzyme tests liver cell damage
^: ALP, AST, ALT, & GGT, & + cholinesterase
g Bilirubin tests: bile excretion or retention
^ bilirubin cirrhosis & other liver disorders.
g PT time prolonged.
g US diff. in density of parenchymal cells & scar tissue.
g CT, MRI, & radioisotope liver scans liver size &
hepatic blood flow & obstruction.
g DXliver biopsy.
g blood gas V/Q imbal & hypoxia.
Medical Management
+ antacids or H
2
antag + gastric distress & GI bleeding.
+ Vit & nutritional supps healing of damaged liver
cells & nutritional status.
+ K-sparing diuretics(Aldactone) or (Dyrenium)
+ ascites, + F/E
- colchicine, (anti-inflam gout) survival in w/ OHic
liver disease or mild-mod cirrhosis
g end-stage liver disease (ESLD) w/ cirrhosis herb
milk thistle (Silybum marianum) to tx jaundice
g Primary biliary cirrhosis tx w/ ursodeoxycholic acid
to liver .
Acute Pancreatitis
mild, self-limited sev, rapidly fatal- respond to tx
Mild acute edema & inflam of pancreas.
Min organ dysfx, & return to NRM fx w/in 6 mos
pat is acutely ill & @/r +vol shock, F/E disturb& sepsis
enzymatic digestion of gland acute pancreatitis.
Enzymes damage local blood vessels bleeding &
thrombosistissue necrotic into retroperitoneal tissues.
Local compl pancreatic cysts or abscesses & acute fluid
collections in or near pancreas.
Sev acute systemic compl w/organ fail, pulm insuff w/
hypoxia, shock, renal fail, & GI bleed
Pathophysiology
g cxSelf-digestion of pancreas by own enzymes trypsin
biliary tract disease; gallstones pancreatitis
Gallstones enter common bile ductobstruct flow of
pancr. juice or causing a reflux of bile from bile duct into
pancr. duct activating powerful enzymes w/in pancreas.
inactive until pancreatic secretions reach duodenum.
g Activation of enzymes vasodilation, ^ vascular perm,
necrosis, erosion, & hemorrhage
undx- chr pancreatitis B4 1
st
epis of acute pancreatitis.
cx bacterial or viral infect , compl. of mumps virus.
Spasm & edema of ampulla of Vater from duodenitis,
Blunt abd trauma, peptic ulcer, ischemic vascular,
^lipidemia, Ca, & use of corticost, thiazide diuret,
contraceptives- ^/R-pancreatitis.
may develop after surgery on or near pancreas or after
instrumentation of pancreatic duct.
Mortality shock, A*, +BP, or F/E imbal
Attacks may result in complete recovery, w/o
permanent damage, or chronic pancreatitis.
outcomes clinical & labs
Clinical Manifestations
g sev abd pain & tenderness & back pain irritation &
edema of inflamed pancreasstimulate nerve endings.
^ tension on pancreatic capsule & obstruction of
pancreatic ducts midepigast pain -24 -48 hrs after a
heavy meal or OH, & difficult to localize.
g unrelieved by antacids abd distention; a poorly
defined, palpable abd mass; & + peristalsis.
g Abd guarding, board-like abd or soft w/o peritonitis.
g Bruise-flank or umbilicus sev pancreatitis.
*N & V*gastric or bile-stained.
F*, jaundice, confusion, & agitation
+ BP+vol & shock loss of a lot protein-rich fluid
tissues & peritoneal cavity.
^P, cyanosis, & cold, clammy skin.
A.Rnl.F .
Resp distress & hypoxia, diffuse pulm infiltrates, SOB,
^R, & abn ABG.
g Myocardial depression, + Ca, ^BS, DIC
Assessment & Diagnostic Findings
g DX Hx-abd pain, risk fx , psy exam
g Surum amylase & lipase -3x normal limit w.in 24 hrs
amylase returns to normal w/in 48-72hrs
lipase may remain elevated for 5 - 7 days
g Urinary amylase ^ & ^longer than serum amylase
g WBC ^
g ^Ca- severity
g ^BS & glucosuria & ^ bilirubin
g X-ray of abd & chest differentiate pancreatitis from
other disorders & to detect pleural effusions.
g U/S & CT scans^ in diameter of pancreas & to detect
pancreatic cysts, abscesses, or pseudocysts.
g Hct & Hbg bleeding.
g Peritoneal fluid (paracentesis or peritoneal lavage)
^ pancreatic enzymes.
g BM bulky, pale, & foul Fat content 50% & 90%
Med Managementrelieving sx & preventing or tx comp.
g oral intake to inhibit stim of pancreas & its
secretion of enzymes.
g TPN extreme metab stress
enteral route preferred - prevent infect comp,
- tolerate parenteral nutrition.
NG suxN &V + painful abd disten & paralytic
ileus.
gH
2
antag Tagamet &Zantac+pancr. activity by inhib
HCl secretions
g Proton pump inhibProtonix- tol H
2
or ineffect
Pain Management
g analgesia pain relief &+restlessstim panc secretion
g IV opioids morphine Dilaudid
g Antiemetic
Intensive Care
Correction of fluid & blood loss & + albumin maintain
fluid volume & prevent Rnl.F.
monitorhemodynamic & ABG
Antibx infect
Insulin g continuous infusion critically ill
Respiratory Care
Aggressive resp care ^/R - ^ diaphragm, pulm
infiltrates & effusion, & atelectasis.
g Hypoxemia humidify O2 to intubation & mech vent
Biliary Drainage
g biliary drains & stents pancreatic ductendoscopy
+ pain & ^ weight gain.
Surgical Intervention risky g (diagnostic laparotomy)
establish pancr drainage resect or dbride necrosis.
mult. drains & incision left open for irrigation &
repacking q. 2 -3 days to remove necrotic debris
Postacute Management
- Antacids after it resolve.
- Oral feedings low fat & protein gradually.
- Caffeine & OH
Follow-up U/S, x-ray studies, or ERCP resolving
/abscesses /pseudocysts.
ERCP cause & endoscopic sphincterotomy &
removal of gallstones from common bile duct.
Chronic Pancreatitisg imflam disorder
g progressive anat & fx destruction of pancreas.
As cells are replaced by fibrous tissue w/ repeated
attacks of pancreatitis, pressure w/in pancreas mech
obstruct of pancreatic & common bile ducts & duodenum.
atrophy of epithelium of ducts, inflam, & destruction of
secreting cells of pancreas.
g LT OHic ^secretion of protein in pancreatic
secretionsprotein plugs & calculi w/in pancreatic ducts.
Clinical Manifestations
g recurring attacks of sev. upper abd & back pain, w/ V*.
opioids may be ineffect.
Progression pain attacks more sev, freq & longer
cont. sev pain or dull, nagging constant pain.
- 20% severe painless
Weight loss +intake 2
nd
to A* or fear attack
g Malabsorption late proteins & fats - impaired.
g BM, freq, frothy, & foul- impaired fat
g steatorrhea high fat content
Progression calcification of gland, & Ca stones w/in ducts
Assessment & Diagnostic Findings
ERCP Dx-detail about anat of pancreas & ducts
- tissue 4 anal & diff. from other conditions
(carcinoma)
g MRI g CT scans, & u/sdetect pancreatic cysts.
g glucose tolerance test pancreatic islet cell fx info
needed 4deciding on surgical resection of pancreas.
abn glucose tolerance test diab assoc w/ pancreatitis.
- Acute exacerbations ^ serum amylase levels.
Medical Management Depends on cause
prevent & manage acute attacks, relieving pain &
discomfort, & manage exocrine & endocrine insuffic of
pancreatitis.
Nonsurgical Management
gEndoscopy remove pancreatic duct stones & strictures
manage pain & relieve obstruction
g abd pain & discomfort nonopioid
avoid OH & foods abd pain & discomfort in past.
hazard sev + BS w/ OH is stressed
g Pancreatic enzyme replace w/ malabsorp & steatorrhea.
g proton pump inhib Prilosec, Prevacid w/ enzyme
therapy + gastric acid inactivation of enzymes
Surgical Managementrelieve abd pain & discomfort,
restore drainage of pancreatic secretions, & + freq of
acute attacks of pancreatitis.
g type depends on anatomic & fx abnorm of pancreas
location w/in pancreas, diab, exocrine insuffic,
biliary stenosis, & pseudocysts of pancreas
Cont use of OH? Ability to manage endocrine or
exocrine after surgery.
NOTES from elsewhere
You are assigned to care for a 35-year-old writer who
has been admitted with severe upper abdominal pain
radiating to his back & recurrent vomiting. This is his
second admission for pancreatitis. He admits to
drinking 1 pint of whiskey daily on the weekends &
having several drinks nightly on weekdays. His alcohol
intake has been greater in the past. Laboratory data
include an amylase level of 750 units/L (normal, 25 to
125 units); lipase is 5.6 units/ml (normal, 10 to 140
units); aspartate aminotransferase (AST), 150 units/L (
normal 10-40) & alanine aminotransferase (ALT), 60
units (normal 5-350 WBC 16,000, BUN 34mg/dl, BS 324
mg/dl; serum Ca was 7.2 mg/dl & his K is high. Hgb
dropped from 13.2 to 10.8, serum proteins low &
serum bili is mildly elevated at 2mg/dl.
Do the lab studies support a diagnosis of pancreatitis?
Explain.
levels ^ in blood when pancreas is damaged.
Amylase enzyme - starch to sugar
lipase enzyme- fats to fatty acids & glycerol
Lipase peaks in 24 hrs then +
May have chronic fibrosis from OH (length & degree)
lipase + bc of scarring.
Analyze the lab studies.
g AST-enzyme present in tissues of high metabolic
activity & is released into blood following the injury of
death of cells) - in this case damage to pancreas & liver
possibly.
g ALT ^- obstructive jaundice or biliary disease.
g+ Ca Ca forms complexes w/ fatty acids
musc twitching, tetany, & numb-mouth, irreg
g ^ BS (324) stress & insulin secretion being disrupted
by damaged beta cells in pancreas.
g ^BUN (34) dehydration.
g ^WBC inflam process - clean up crew needed
g ^K cell breakdown & dehyd
g + hgb- retroperitoneal bleeding (abd blood loss) from
autodigestion of pancreas.
g Serum bili mildly ^ obstruct common bile
duct(inflam process & pressure from inflamed pancreas)&
RBC destruct
Pancreatitis patho
Obstruction to the outlow of pancreastic enzymes by bile,
pancreatic duct obstruction itself(edema) or reflux permit
leakage of pancreatic juices containing enzymes into
pancreatic tissue -
g autodigestion pancr enzymes cause destruction of
pancreatic tissue & hemorrhage & tissue necrosis.
OH use^ pancr enzymes constrict of pancr sphincter.
symptoms of pancreatitis
Severe LUQ epigastic pain back
Rigidity &guarding sitting &leaning forward may
help.
- Pain worse -lying down & may pull up L leg- comfort
+/absent bowel sounds + digestion.
N&V buildup of gas & + intestinal activity.
Turner (flanks) &Cullen (umbilicus) sx
retroperitonea bleeding possibly peritonitis.
Jaundicedinflamed pancreas pressing on bile duct
Clay colored stools + fat absorption enzymes not
getting to duodenum
^BS impaired insulin secret & unable to use glucose.
Tetany + Ca
^/+BPdepending on level of shock, ^P, ^ low-
temp compensatory response to inflam & F/E imbal
Volume deficit + intake & possible 3
rd
space
inflamed pancreas can sequester e to the site, blood loss.
How does acute pancreatic differ from chronic?
Acute varying degrees of edema, hemorrhage &
necrosis, & shock. ^ lab values.
Chronic progressive destructive of pancreas w/ milder
chronic inflam & may not have ^labs
The labs are called to the Dr. New orders are to T & C
for 2 units of PRBCs. Mg level with next blood draw,
BS q 4 hrs. with coverage per protocol, keep an amp of
calcium gluconate at bedside, NG to suction, Consult
with pharmacy & dietician, I O, VS q 4
rationale for these orders? Any other orders you might
anticipate or want to ask the Dr. about?
g + hgb may need blood.
g Mg + is common in OHics abuse. Low
g + calcium w/ + mg levels.
tetany to laryngiospasms .
Emergency Ca gluconate tx.
g Monitor BS & tx w/ insulin
g NG +distention & gas but primarily to + stim of
pancreas release of more enzymes more autodigestion,
necroisis & hemorrhage.
g IV order- TPN or jejunal feedings vit replacement
g Antacids Zantac
g Antichol-Bentyl, Lomine Watch for DTs
Surgery maybe to remove gall bladder if cause
ERCP open blocked bile duct
What do you need to consider if he complains of pain?
Allergies g PCA Morpine best method.
Chronic pancr often can not receive adequate pain control.
positioning, imagery, relaxation, controlling envir stim
g Surgical interv cut nerves to pancreas to + pain.
complications from pancreatitis that may occur?
g Shock & multiple organ failure release of bacterial
endotoxins injury to vessels, kidneys & lungs
g Pleural effusions & respiratory compromise.
g Pancreatic pseudocyst or abscess
What are common patient education needs?
Stop drinking all together if OH induced pancreatitis.
limit drinking for 3 months.
g Previous damage fiborosis cannot be reversed.
+ fat diet if deficient in pancreatic lipase.
pancreatic enzyme replacement 1/3 b4 meals & rest
during meals in cases of chronic pancreatitis.
educ how to take the enzymes.
Hepatitis Etiology & Pathophysiology
inflam of liver 2
nd
to infection, parasitic infestation, OH,
toxins, drugs (INH, acetaminophen)
Afecal-oral; 2nd to sanitation & eating shellfish from
contaminated water
B & C w/ contaminated blood; 2
nd
sex, sharps
R/ Fx Health care -druggies - mult sex.
Hemophiliacs freq transfusions of clotting fx 30% have
unidentifiable sources
Signs & Symptoms May be asymptomatic
Preicteric stage: Flulike symptoms
Icteric stage: N&V, A, malaise, jaundice, presence
hepatitis antigens & antibodies; aspartate
aminotransferase AST, alanine aminotransferase (ALT)
Treatment
Antivirals (interferon)
Vaccines against HAV & HBV b4 exposureactive
immunity
Immune globulins passive immunity post exposure
Nursing Monitor S&S
Calories, protein, fat diet as ordered
Contact precautions for HAV & HEV
educ avoid toxins (Tylen, OH, carbon tetrachloride,
INH)
g Hepatic encephalopathy: precipitating fx g HEPATICS:
Hemorrhage in GIT/ Hyperkalemia Excess protein diet
Paracentesis Acidosis/ Anemia Trauma Infection
Colon surgery Sedatives
g Pancreatitis (acute): GET SMASHED:
Gallstones Ethanol Trauma Steroids Mumps
Autoimmune (PAN) Scorpion stings Hyperlipid-^Ca
ERCP Drugs (including azathioprine and diuretics)
g PANCREAS: PaO2 below 8 Age >55 Neutrophils:
WCC >15 Ca < 2 Renal: Urea >16 Enzymes: LDH >600
~AST >200~ Albumin < 32 Sugar: Glucose >10 (unless diab)
g LEGAL: Leukocytes > 16.000 Enzyme AST > 250
Glucose > 200 Age > 55 LDH > 350
Cirrhosis
Etiology & Pathophysiology
Fibrous scar tissue & fat accumulate in
liverhepatomegaly & portal ^BP esophageal varices,
hemorrhoids, obstructive jaundice & ascites
Liver fx metabolism ammonia (a metabolized
protein by-product) encephalopathy
Risk Factors
OHics, hepatitis or biliary disease
Industrial chemicals, male gender, 40-60yr old
Signs & Symptoms
Liver enzymes (AST, ALT, LDH, GGT), jaundice,
hepatomegaly
Albumin, bilirubin, globulins, ammonia, PT
Ascites, GI varices, edema 2
nd
to albumin &
aldosterone, retention of Na & H2O
Confusion, agitation, flapping hand tremors (asterixis)
Liver biopsy to confirm diagnosis
Treatment
Vitamins (A, D, E, K, B), zinc, colchicine, K sparing
diur
Lactuloseammonia; albumin
Portal caval shunt, sclerotherapy/ balloon tamponade
varices
Paracentesis for ascites w/ dyspnea
Nursing
Monitor S&S, I&O, abd girth
Liver biopsy: pat hold breath during needle insertion;
keep on right side w/ pillow against insertion site. Assess
for bleeding
Paracentesis: void b4 & maintain an upright position
during procedure; after assess resp status, Sx of shock,
persistent leakage
Balloon tamponade: Provide oral suction, maintain
traction on gastric balloon, - pressure of esopg balloon
Pancreatitis: Inflam of the pancreas activation of
pancr enzymes w.in the pancr self-digesting
Obstruction of pancreatic duct reflux of trypsin
autodigestion inflam
Possible necrosis w/ calcification, perforation, or
hemorrhage
Pancreatic pseudocysts or abscesses may develop
May be idiopathic, acute or chronic & result in DM
Acute suddenly & w/o warning.
Chronic graduallyyears, w/ initial sx-vague
Cause: gallstones & OH. Acute chronic once
pancreatic tissue is destroyed & scarring develops.
^lipidemia, Ca, abd trauma, & bacterial /viral infection.
Signs & Symptoms
Extremely high triglycerides (1000mg/dL)
Abd pain that w/ eating & thorax/back ^ supine
abd distendworse after eat, jaundice N,V, F, &^P
Steatorrhea & glucose intol w/ chronic pancreatitis
Amylase, lipase, Ca
S&S of perforation Rebound tendern, rigid abd, shock
Nursing Focus
is supportive care & the prevention of 2
nd
comp.
Assess labs: ^ levels of amylase & lipase.
Vit A & E, & fat diet as ordered
Provide small freq meals. - BS, Ca Mg Na K & HCO3.
Patient Teaching
Teach Pt to avoid OH & + foods high in fat.
Provide educ prior to dx proceduresabd u/s-gallstones
& a CT -inflam & destruction of the pancreas.
Treatment
NPO, IVF & electrolyte replacement
NGT to GI motility & secretions
Antibx, anticholinergics, pancreatic enzymes (lipase,
trypsin, amylase) w/ meals for chronic
Surgery if 2
nd
to biliary disease
Cholecystitis
Etiology & Pathophysiology
bile flow gallbladder inflam (cholelithiasis),
distention, & autolysis gangrene or perforation
blocked bile flow may obstructive jaundice
Usually 2
nd
to gallstones or other precipitates
Risk Factors
4 Fs: fair, fat, 40, female
Rapid weight, cirrhosis Estrogen therapy
Mult preg DM
Signs & Symptoms
RUQ abd painback, shoulder esp. after fat meal
N&V, T, rebound tender, obstructive jaundicedark urine,
& clay-colored stools
sx bleedfat digestabsorpt of the fat soluble vit K
WBC, bilirubin, alkaline phosphatase
Treatment
Laparoscopic or abd removal of gallbladder
(cholecystectomy)
Incision into common bile duct (choledochostomy)
Dissolution of stones by oral chenodiol or infusion of
solvent into gallbladder
Nursing Monitor S&S
Teach fat diet; IS & coughing (incision near diaphragm)
Preoperative vit K, analgesics
Maintain T-tube drainage if bile duct explored. Tube
removedbrown BMbile flow