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120 Cards in this Set

  • Front
  • Back
what to assess with jaundice
urine / stool color changes
abdominal swelling
pain at RUQ
yellow sclera
pruritis
light/clay colored stools
fever / chills
increased indirect bilirubin
increased direct bilirubin
when is it suspected that jaundice is OBSTRUCTIVE?
when DIRECT bili is increased
elevated level of bilirubin in urine is caused by...
increased level of DIRECT bili because DIRECT bili is H20 soluble
the organ that CONJUGATES bilirubin
LIVER
causes of JAUNDICE
gallstones
tumors
intrahepatic jaundice - caused by drug reactions
hepatitis
hemolytic reactions -RBCs
transfusion reactions
the ratio that diagnoses type of liver dysfunction
AST/ALT ratio
if ALT is increased, what pathophysiology is suspected?
damage to liver cells
if AST is increased, diseases are suspected?
if AST is 10x more elevated, GALLSTONES

if AST is 20x more elevated, HEPATITIS
skin care approaches to jaundice: (2)
corticosteroids to relieve itching

Bile sequestering agents
when doing Diagnostic tests for liver disease, what are nursing interventions to prep the client?
Keep PT NPO because food increases pain
give IV hydration
give pain management
LIVER functions
glucose metabolism
ammonia conversion
protein metabolism
vit and iron storage
drug metabolism
bile formation
bilirubin excretion
liver function studies (6) LABS
AST/ALT/GGT/GGTP/LDH
serum protein
pigment studies (direct/indirect bili), urine bili and urobilinogen
prothrombin time PTT
alk.phos
ammonia
cholesterol
diagnostic studies for liver function
liver biopsy
U/S
CT
MRI
most common cause of hepatic dysfunction
MALNUTRITION r/t alcoholism
other causes of hepatic dysfunction other than ETOH
infection
anoxia
metabolic disorders
nutritional deficiencies
hypersensitivity states
clinical manifestations of hepatic dysfunction
jaundice
portal hypertension
hepatic encephalopathy or coma
nutritional deficiencies
types of jaundice
hemolytic
hepatocellular
obstructive
hereditary hyperbilirubinemia
yello or green tinged body tissues, sclera and skin due to increased bili levels
jaundice
the jaundice types that are most associated with liver disease
hepatocellular and obstructive jaundice types
s/s of hepatocellular jaundice
pT appears mildly or severely ill
s/s of hepatocellular jaundice
pt appears mild to severely ill
lack of appetite, nausea, wt loss
malaise, fatigue, weakness
headache, chills and fever if infectious in origin
s/s of obstructive jaundice
dark orange brown urine and light clay colored stools
dyspepsia and intolerance of fats, impaired digestion
obstructed blood flow through the liver resulting in increased pressure throughout the portal venous system
portal hypertension
portal HTN results in ...
ascites
esophageal varices
ascites is caused by ...
portan HTN
vasodilation of splanchnic circulation (blood flow to organs)
decreased metabolism of aldosterone
decreased synthesis of albumin
movement of albumin into the peritoneal cavity
assessment of ascites
record abd girth and daily wt
look for striae, distended veins and umbilical hernia
assess for fluid via percussion
monitor F/E imbalances
treatment of ascites
low Na diet
diuretics
bed rest
paracentesis
admin of salt-poor albumin
TIPS shunt
position of paracentesis
sitting
first line of therapy for patients with ascites from cirrhosis
Aldactone
a life threatening complication of liver disease. may result from the accumulation of ammonia and other toxic metabolites in the blood
hepatic encephalopathy and coma
assissment of hepatic encephalopathy
EEG
LOC
potential seizures

fetor hepaticus - A peculiar odor of the breath in individuals with severe liver disease caused by volatile aromatic substances that accumulate in the blood and urine.
is a tremor of the wrist when the wrist is extended (dorsiflexion) --- It can be a sign of hepatic encephalopathy, damage to brain cells due to the inability of the liver to metabolize ammonia to urea. The cause is thought to be related to abnormal ammonia metabolism. most often in drowsy or stuporous patients with metabolic encephalopathies, especially in decompensated cirrhosis or acute hepatic failure.
asterixis
med to reduce serum ammonia levels
lactulose
medical management of hepatic encephalopathy
eliminate cause
lactulose
IV glucose to minimize protein catabolism
protein restriction diet
reduction of ammonia from GI tract via gastric suction, enemas, oral antibiotics
discontinue sedatives, analgesics and tranquilizers
monior for complications and infections
occurs with 1/3 of patients with cirrhosis and varices
bleeding esophageal varices
in esophageal varices, when is mortality high?
first episode: 30-50%
clinical manifestations of bleeding esophageal varices
hematemesis
melena
general deterioration
schock
how often should PTs with cirrhosis undergo screening endoscopy? and why do they do it?
every 2 years; to detect any bleeding esophageal varices
tx of bleeding varices
treatment of shock
O2 admin
IV fluids, lytes, vol.expanders
blood and blood products
vasopressin, somatostatin, OCTREOTIDE
nitro
propranolol and nadolol (beta blockers)
refers to the use of mercury-weighted balloons instilled into the esophagus or stomach, and inflated to stop refractory bleeding from vascular structures -- including esophageal varices and gastric varices -- in the upper gastrointestinal tract.
balloon tamponade
tx that exert pressure directly to bleeding sites in the esophagus and stomach
balloon tamponade (eg. sengstaken-blakemore tube)
nsg interventions : bleeding esophageal varices
monitor for hepatic ecephalopathy
monitor for DT R/T ETOH withdrawal
monitor tx via tube care and GI suction
oral care
reduce stress/PT teaching
a systemic viral infection with necrosis and inflammation of liver cells with symptoms of cellular and biochemical changes
viral hepatitis
Hep transmitted via fecal oral transmission

incubation: 15-50 days

lasting 4-8 weeks

dark urine, indigestion, liver swelling
A
do liver cells regenerate?
yes, within 3-4 months, however if damage is extensive, no regeneration occurs
transmitted via blood, sex, semen and body fluids

incubation: 1-6 mos

major cause of cirrhosis and LIVER CA
Hepatitis B
meds for chronic hep B
interferon
antivirals: lamivudine (Epivir) and adefovir (Hepsera)
aka post transmission hepatitis and the MOST COMMON

via needle sticks and sex

causes 1/3 of liver ca and most common cause of liver transplants
Hep C
`meds for hep C
interferon
ribavirin (Rebetol)
3 stages of viral hepatitis
prodromal
icteric
posticteric (recovery)
who are at risk for hep D?
only persons with hep B
transmission is via blood / sex but more likely progresses to fulminant liver failure and cirrhosis
hep D
transmitted by fecal-oral route with incubation of 15-65 days
hep E
which is transmitted via poor hygiene/sanitation
hep A
T or F. Pt may remain aymptomatic with Hep C
true
non-viral hepatitis causes
drugs
toxics
scarring, fibrosis, resulting in disrupted hepatic blood flow
cirrhosis
3 types of cirrhosis
alcoholic
postnecrotic
biliary
tx for hep A
no tx

immunoglobulin for high-risk individuals (nurses, military)
tx for hep B
no treatment

prevention,
antiemetics, analgesics prn
s/s of hepatic cirrhosis
edema,
ascites,
portal HTN,
hemorrhoids
varicose veins
esophageal varices
anemia
mental retardation
cirrhosis via scarring at portal areas, chronic alcoholism
alcoholic cirrhosis
obstruction of bile canaliculi, necrosis, fibrosis, gallstones, pancreatitis, can be autoimmune
Biliary cirrhosis
chronic disease; can be caused by dialysis, Wilson's disease

bands of scars are affected
postnecrotic
complications of cirrhosis
decreased sex hormones
aloopecia
menstrual disorders
decreased metabolism of aldosterone leading to edema secondary to H20 and salt retention
decreased metabolism of ammonia resulting to hepatic encephalopathy (decreased coordination, Coma, death)
portal hypertension
hematemesis, anemia
esophageal varices
how to treal esophageal varices
reduce portal hypertension via diuretics and B-blockers
binds to ammonia to prevent coma, death on hepatic encephalopathy patients
lactulose
when NOT to give lactulose? and what is a normal effect on GI system by lactulose?
constipation
diarrhea
the only definitive Dx of cirrhosis
Liver Bx
what to watch out for when doing liver Bx
PT, PTT, INR = RISK OF BLEEDING
is a medical emergency characterized by decreased HnH, slow bleeding, tachycardia, hypotension, esophageal tamponade
ESOPHAGEAL VARICES
labs to help screen for liver cirrhosis
CBC
ammonia
liver U/S
invasive tx of cirrhosis
surgery (Levine shunt)
TIPS shunt
what should RNs do before/after paracentesis
measure abd girth
nsg mgt of liver cirrhosis
daily wt
I/O
fluid restriction
skin integrity
respiratory (SpO2)
bleeding
urine/stool
soft toothbrush
meds for cirrhosis
aldactone
lasix
lactulose
vit. K
antiemetics
things to teach PT about self-mgmt of cirrhosis
avoid canned/frozen foods
limit hi-protein foods
caution with OTC drugs
no alcohol
daily weight
when is patient restricted from protein?
when patient is at risk for ecephalopathy
clinical manifestations of liver ca
pain, dull continous ache RUQ, epigastrium or back

weight loss, weak, anemia

jaundice
is the accumulation of plasma secondary to portal hypertension due to increased aldosterone, increased osmotic pressure, cirrhosis, sodium/H20 retention, 3rd spacing
ascites
tx of increased ammonia levels
get rid of nitrogenous waste
correct F/E imbalance
Lactulose
s/s of increased serum ammonia
ALOC
confused
lethargy
sometimes given to reduce abd bacteria, but be careful, drug is nephrrotoxic
Neomycin
caused by circulatory alterations due to liver cirrhosis
heptorenal syndrome
s/s of hyponatremia
increased BUN/creatinine
decreased sodium
the elderly have decreased liver weight T or F
T
most common cause of parenchymal damage
malnutrition
most common symptoms of liver disease
jaundice, portal htn, nutritional deficiencies, hepatic enceph
jaundice is evident when bili level exceeds _____
2.5 mg/dl
types of jaundice associated with liver disease
hepatocellular and obstructive
complications of prolonged jaundice
gallstones and brain stem damage
jaundice caused by inability of damaged liver cells to clear normal amounts of bili from the blood
hepatocellular
bile is not reabsorbed by intestine and becomes backed up into the liver substance due to tumor, gallstone, inflammatory process, presure from enlarged organ
OBSTRUCTIVE JAUNDICE
possible s/e of diuretic therapy among ascites patients due to dehydration and hypovolemia
ENCEPAHLOPATHY
Why is bed rest (supine) good for ascites pts
because upright position activates RENIN-Angiotensin-aldo system
why is ascites a temporary fix?
because removal of fluid activates Ren-Angio-Aldo system; ascites is back
a shunt vetween the portal circulation and the hepatic vein
TIPS
any patient for liver transplant should be referred for
TIPS
med that decrease ammonia-secreting bacteria in the gut
neomycin sulfate
refer to liver transplant after first episode of....
OVERT HEPATIC ENCEPHALOPATHY
indicates that lactulose is working
2-3 SOFT stools per day; If diarrheic, this may indicate overdose

_______
_______can precipitate hep.encephalopathy therefore prevention should be via lactulose admin
CONSTIPATION
the cause of edema in liver dysfunction ...
HYPOALBUMINEMIA
The cause of bleeding in liver dysfunction
reduced production of blood clotting factors
cause of Wernicke Korsakoff
Thiamine deficiency
why does pruritis develop in liver dysfunction
due to retention of bile salts
landmark signs off Etoh cirrhosis on the skin
liver (reddened palms); spider angioma
the antibody of hep A
HAV
when is portal hypertension suspected?
presence of dilated abdominal veins and hemorrhoids
what to tell pancreatitis patients upon dc
avoid crash dieting
what causes shock on pancreatitis pts
Kinin
primary s/s of pancreatitis
jaundice
priority order for pancreatitis patients upon admission
NG tube with low suction
potential complication for pancreatitis pts
pneumonia
pain medication contraindicated for pancreatitis pts
morphine
what precautions are to be done when caring for hepatitis A pts
contact precautions
how long does fatigue last upon recovery from hep?
2-4 mos
typical diet recommended for hepatitis patients
high carb high protein
first line of defense from hep B
Hep B vaccine
Transmission of Hep C
needlesticks/ blood exposure