TOPIC 8 - cirrhosis, liver disease, and hepatitis Flashcards
cirrhosis
extensive irreversible scarring of the liver, usually caused by a chronic reaction to hepatic inflammation and necrosis.
typically has a progressive, slow, destructive course resulting in end-stage liver disease.
characterized by widespread fibrotic scarring that changes the liver. Inflammation results in the destruction of hepatocytes and leads to nodular tissue and the liver becomes hard and shrinks in size leading to a decrease in liver function.
risk factors for cirrhosis
ETOH, viral hep (or chronic hep B and C), autoimmune hepatitis, fatty liver disease, drugs and chemical toxins, gallbladder disease, metabolic causes, genetic causes, cardiovascular disease
assessment and manifestations related to cirrhosis
Fatigue
Jaundice
Peripheral edema
Ascites
Skin lesions
Hematologic disorders
Endocrine disturbances
Peripheral neuropathies
labs related to cirrhosis
elevated AST, ALT, LDH, PT, INR, bilirubin
decreased K, protein, albumin
diagnostics for cirrhosis
gold standard = biopsy (identify liver cell changes)
– high risk for bleeding
xrays may show hepato or splenomegaly or massive ascites
ultrasound detects ascites, hepato or splenomegaly and the presence of biliary stones or duct obstruction
EGD directly visualizes the upper GI tract to detect bleeding, esophageal varices, stomach ulcers, or duodenal ulcers
nursing interventions for cirrhosis
monitor fluids, electrolytes, admin albumin and diuretics, skin care, Na restriction of 2g/day
pre and post op responsibilities for paracentesis
pre op :
Ensure permit is signed
Base line vital signs
Patient teaching
Have to empty their bladder
Ensure their IV is patent
post op :
Monitor vital signs
Lie down on side without wound for 2 hours
Monitor for leakage from site
Don’t get up until the nurse tells you to
Check for new orders for fluids
chronic liver complications
portal hypertension, ascites, peripheral edema, esophageal varices, coagulopathy, hepatic, encephalopathy, hepatorenal syndrome, biliary obstruction jaundice
complications of cirrhosis
Portal Hypertension
Bleeding
Jaundice
Hepatic encephalopathy
Hepatorenal syndrome
Ascites
Esophageal varices
biliary obstruction leads to
decreased production of bile and prevents absorption of vitamin K = bleeding and bruising
what can cause esophageal varices
portal hypertension
can be life threatening from severe blood loss that leads to hypovolemia
what causes neurologic toxic manifestations in hepatic encephalopathy
ammonia crossing the blood brain barrier
other characteristics of hepatic encephalopathy
asterixis (tremors in arms and hands)
fetor hepaticus (musty sweet breath from accumulation of digestive by-products that the liver cannot degrade)
incubation period of hepatitis A
15-50 days
incubation period of hepatitis B
45-180 days
incubation period of hepatitis C
14-180 days
transmission route of hepatitis A
fecal oral
transmission route of hepatitis B
Blood & mucous membranes
Perinatal
High risk sexual contact
transmission route of hepatitis C
same as hep B
those at risk for hepatitis A
Crowded conditions, poor personal hygiene, poor sanitation, contaminated food/milk/water/shellfish, sexual contact with an infected person, IV drug users, receiving food from someone handling/preparing food
those at risk for hepatitis B
Contaminated needles, syringes, blood, sexual contact with an infected person, tattoos/ body piercings with contaminated needle, asymptomatic person, blood and blood products
those at risk for hepatitis C
same as hep B
most infectious when (hep A)
During the first 2 weeks prior to onset of symptoms and 1-2 weeks after the onset of symptoms
most infectious when (hep B)
Before & after symptoms appear. Infectious 4-6 months, carriers can be infectious for life
most infectious when (hep C)
1-2 weeks before symptoms appear, during course of disease, 75-85% of people will develop chronic hepatitis c and be infectious during their life
assessment of Hep B and C
Anorexia
N/V
Fever
Fatigue Right upper quadrant pain
Dark urine and light stool
Jaundice
Malaise
Easy fatigability
complications of chronic hepatitis
Skin manifestations
Spider angiomas
Palmar erythema
Gynecomastia
Splenomegaly
Hepatomegaly
Cervical lymph node enlargement
HE
Ascites
drug therapy to decrease viral load and slow rate of disease progression in chronic HBV
nucleoside and nucleotide
interferon therapy
drug therapy directed at eradicating the virus and preventing HCV complications
antivirals
if a client reports “no appetite” or “losing taste for food” … suggest :
increasing fluids and intake of juices
initial vs later assessment of liver cancer
initial can be hard to detect:
Hepatomegaly
Splenomegaly
Fatigue
Peripheral edema
Ascites
Portal hypertension
later s/s:
fever, chills, jaundice, anorexia, weight loss, palpable mass, RUQ pain
most common type of liver cancer
hepatocellular carcinoma
common sites for metastasis
Lung
Gallbladder
Peritoneum
Diaphragm
without treatment for liver cancer :
death in 6-12 months from hepatic encephalopathy or massive GI bleed
assessment of chronic pancreatitis
Pancreatic insufficiency
Acute and/or chronic pain – gnawing/heavy, burning/cramping
Malabsorption & weight loss
Constipation,
Mild jaundice & dark urine
Steatorrhea – can be severe with large BMs that are foul-smelling
Abdominal tenderness
Diabetes mellitus
chronic pancreatitis results in
strictures, calcifications, and progressive destruction of the pancreatic tissue
most common causes of chronic pancreatitis
ETOH abuse and cholethiasis
other :
Chronic alcohol use
Obstruction: inflammation of the sphincter Oddi
Tumor
Pseudocysts
Trauma
Systemic diseases (SLE)
Autoimmune pancreatitis
Cystic fibrosis
diagnostics and labs for chronic pancreatitis
elevated Amylase
elevated Lipase
Serum bilirubin
ALP
ESR
ERCP (visualize ducts)
CT
MRI
Abdominal ultrasound
Stool samples for fecal fat
diet for chronic pancreatitis
low fat, bland, small and frequent meals
pancreatic enzyme replacements !! ( bile salts to facilitate absorption of vit ADEK )
manifestations fo chronic pancreatitis
Abdominal pain (acute): heavy, gnawing feeling or sometimes as burning and cramp-like
Malabsorption
Constipation
Mild jaundice with dark urine
Steatorrhea
Diabetes Mellitus
cholecystitis
Inflammation is the major pathophysiologic condition and may be confined to the mucous lining or involve the entire wall of the gallbladder.
During an acute attack of cholecystitis, the gallbladder is edematous and hyperemic, and it may be distended with bile or pus.
common causes of cholecystitis
gallstones or biliary sludge
inflamed bile duct
manifestations of cholecystitis
Severe pain (biliary colic): pain is steady, excruciating, tachycardia, diaphoresis, prostration, may last up to an hour, occurs 3-6 hours after eating fat.
If total obstruction occurs: see S/S of obstructed Bile Flow
Indigestion to severe pain, fever, chills, and jaundice, tenderness in RUQ, which may be referred to the right shoulder and scapula
4 F’s of cholecystitis
fat, fertile, female, fourty
s/s of obstructed bile flow
Obstructive jaundice
Dark amber to brown urine which foams when shaken
Clay-colored stools
Pruritus
Steatorrhea
Fever, chills
diagnostics for gallstones
Ultrasound
Percutaneous transhepatic cholangiography
Elevated WBCs
ERCP
treatment of gallstones
Removal of stone via ERCP
Disintegrate stone: Extracorporeal shock-wave lithotripsy (ESWL): uses a high-energy shock waves to disintegrate stone
Surgical removal of the gallbladder and/or stones
Laparoscopic Cholecystectomy
Cholecystectomy
cholecystitis interventions
NPO, care of NG tube
Comfort care & pain control
Prepare the client for a procedure or surgery
Client education re: diet, medications, post-op recovery
Monitor for signs/symptoms the condition is getting worse
Monitor for infection
Skin care
post op care for cholecystectomy
Opioids via PCA pump
T-tube (and care of)
Antiemetics
Wound care
NPO
Nutrition therapy
Percutaneous trans hepatic biliary catheter T-tube
