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Med Surg Test 4 Study Guide
Med Surg Test 4 Study Guide
Chapter 49
Assessment and Management of Patients With Hepatic Disorders
Has 4 lobes
Each lobe has thousands of lobules
Blood Supply comes from PORTAL vein & HEPATIC artery and come together to mix
into the SINOSOID
Hepatic duct leads the liver & combines w/ cystic duct from GB & together they form
COMMON BILE DUCT
Liver Functions
Glucose metabolism
Ammonia conversion
Protein metabolism
Fat metabolism
Vitamin and iron storage
Bile formation (creates bile)
Bilirubin excretion (rids of bilirubin)
Drug metabolism
Gero considerations
Size change but not the function changes
Decrease clearance of hepatitis B surface antigen
Decrease drug metabolism and clearance
Decrease intestinal and portal vein blood flow
Decrease GB contraction after a meal
Decrease rate of replacement and/or repair of liver cells after injury
Decrease size & weight of liver
Increased prevalence of gallstones (due to increase in cholesterol secretion in bile)
Rapid progression of Hep C and lower response rate
More severe complications of biliary tract disease
Hepatic Dysfunction
Acute or chronic CIRRHOSIS of the liver (caused by damage of prmkinale cells, primary
liver disease, obstruction of bile flow, or hepatic circulation) 80% with cirrhosis
compensate for 10 years until dx
Most common cause is MALNUTRTION r/t alcoholism (respond by replacing glycogen
with lipids leaves scar tissue)
Infection (bacterial or viral)
Anoxia
Metabolic disorders
Nutritional deficiencies
Hypersensitivity states
Medications
Portal Hypertension
Obstructed blood flow through the liver results in increased pressure throughout the
portal venous system
Results in:
o Ascites (50% mortality rate)
o Esophageal varices
Notes:
-Liver is damaged and can’t metabolize aldosterone
-which leads body to retain sodium and water, increased intravascular fluid and
lymphatic flow will cause liver to not be able to synthesis albumin,
-Can cause severe intravascular dehydration or depletion
Treatment of Ascites
Low sodium diet
Diuretics
o Spironolactone: (used for ascites) blocks aldosterone, potassium sparing, can be
used with other diuretics
Bed rest (short term)
Paracentesis (needle through abdomen and ultrasound to look, pull off 5-6 liters of fluid,
may need transfusion of albumin after
Administration of salt poor albumin
Transjugular intrahepatic portosystemic shunt (TIPS)
Always need IV accesses and fluids hanging
Endoscopic Sclerotherapy
*Fine needle injects vasoconstriction meds like epinephrine
Esophageal Banding
Done with endoscopy
Suction and then pull forward to band it
Hepatitis
Viral hepatitis: a systemic viral infection that causes necrosis and inflammation of liver
cells with characteristics symptoms and cellular and biochemical changes within the
liver.
o A & E: fecal oral route (excreted in ones feces and picked up by another person
orally) 25% of cases
o B & C: blood borne (high risk for health care workers)
o D: only people with hepatitis B are at risk
o Hepatitis G & GB virus-C
Nonviral hepatitis: toxic and drug induced
Refer to table 49-4
Hepatitis A
Spread by poor hand hygiene, fecal-oral
There is a vaccine to prevent
Incubation: 2-6 wks
Illness may last 4-8 wks
Mortality rate is .5% for those younger than age 40 years and 1-2% for those older than
age 40 years
Manifestation s/s:
o Mild flulike symptoms
o Low grade fever
o Anorexia
o Later jaundice and dark urine
o Indigestion and epigastric distress
o Enlargement of liver and spleen
Hepatitis B
Transmitted through blood, saliva, semen, and vaginal secretions, sexually transmitted to
infant at the time of birth
A major worldwide cause of cirrhosis and liver cancer (healthcare workers get
vaccinated)
Risk factors: refer to chart 49-8
o Close contact with carrier of hep b virus
o Frequent exposure to blood products
o Health care workers
o Hemodialysis
o IV injection drug use
o Male homosexual and bisexual activity
o Mother to child transmission
o Multiple sex partners
o Recipient of blood or blood products
o recent STI
o tattooing
o travel with unsanitary conditions
Long incubation and variable, similar to hep A
Management of Hepatitis B
Medications for chronic hepatitis type B: alpha interferon and antiviral agents, entecavir,
tenofovir
Bed rest and nutritional support
Vaccine: for persons at high risk, routine vaccination of infants
o Passive immunization for those exposed
o Standard precautions and infection control measures to keep from spreading
o Screening of blood and blood products prior to being transfused
o Treatment for 16-24 weeks
Hepatitis C
Transmitted by blood and sexual contact, including needle sticks and sharing of needles
The most common bloodborne infection
A cause of 1/3rd of cases of liver cancer and the most common reason for liver transplant
Risk factors: refer to chart 49-9
o Children born to women infected with hep c
o Health care workers/ needle stick
o Multiple sex partners
o Past or current IV drug use
o Recipient of blood or blood products
Incubation period is a variable
Symptoms are usually mild or absent (goes undiagnosed for awhile)
Chronic carrier state frequently occurs
Management of Hepatitis C
Antiviral medications: interferon, ribavirin vs simprevir + ledipasiver-sofobuvir and
ombitasvir-paritaprevir-ritonavir packaged with dasabuvir is more commonly tolerated
Have to be on meds for a long time
Measures to reduce spread of infection as with hepatitis B
(get pt to avoid alcohol) Alcohol potentiate disease, medications that effect the lvier
should be avoided
Prevention: public health programs to decrease needle sharing among drug users
Screening of blood supply
Safety needles for health care workers
Hepatitis D and E
Hepatitis D
Only persons with hepatitis B are at risk
Blood and sexual contact transmission
Likely to develop fulminant liver failure or chronic active hepatitis and cirrhosis
**Treatment for D is interferon for a year
**Only persons with HEP B are at risk for HEP D
Hepatitis E
Transmitted by fecal-oral route
Incubation period, 15 to 65 days
Resembles hepatitis A, self-limiting, abrupt onset, not chronic
G and GB-C
5% from virus
50% have had transfusions in the past
not understood well
*MARS or ELAD device: those patients need to have plan to get off the machine and
only for weeks at a time
Hepatic Cirrhosis
Types
o Alcoholic (develops scar tissue around portal area) MOST COMMON
o Post necrotic (broad bands of scar tissue are intertwined within the liver, late
result of viral hepatitis)
o Biliary (scaring around the bile ducts results from chronic biliary obstruction and
infection (cholangitis) Less Common
*Imaging MRI, CT, dx with liver biopsy
Manifestations s/s:
o Liver enlargement
o Portal obstruction
o Ascites
o Infection
o Peritonitis
o GI varices
o Edema
o Vitamin deficiency
o Anemia
o Mental deterioration
o Refer to chart 49-10
Imbalanced nutrition
I&O
Encourage small frequent meals
High calorie diet/ sodium restriction
Protein modified or restricted if patient is at risk for encephalopathy
Supplemental vitamins, minerals, B complex, provide water soluble forms of fat soluble
vitamins if patient has steatorrhea
Consider patient preferences for nutrition
Other interventions
Impaired skin integrity
o Frequent position changes
o Gentle skin care
o Reduce scratching related to pruritus
Risk for injury
o Prevent falls, trauma related to risk for bleeding
Liver Transplant
MELD Score
Liver Abscess
Amebic (result of visiting developing countries, tropics, entaneaba histolytic) or pyogenic
(common in developed counties, polymycrobial substances, E.coli)
S/s: sepsis, dull pain, enlarged liver, ect
Seen with ultrasound or CT scan
Blood cultures and aspirate
IV antibiotics, open surgery if needed, supportive care (IV and ABX)
Chapter 50
Assessment and Management of Patients With Biliary Disorders
Review of A&P
Gallbladder (hollow organ liver underneath the liver)
o Bile
Pancreas
o Insulin
o Glucagon
o Somatostatin
Notes she said:
Gallbladder:
- is a hollow organ underneath the liver
-About 7 and a half to 10 centimeters long and holds 30-50 milliliters of bile
-Connected to the common bile duct by the cystic duct.
-When the sphincter of Oddi is closed bile enters the gallbladder
-Water in bile made from the hepatocytes is absorbed through the walls of the gallbladder so it is
5-10x more concentrated than it’s original form.
-Food enters the duodenum the gallbladder contracts and the sphincter of Oddi opens allowing
bile to enter into the intestines (response occurs d/t cholecystokinin CCK released from the
intestinal walls)
-Bile is made up of water electrolytes (sodium, potassium, calcium, chloride and bicarbonate),
lecithin, fatty acids, cholesterol, bilirubin and bile salts
-Bile salts and cholesterol emulsify fats in the distal ileum
-Half of the body’s bilirubin ends up in the bile. It is converted in the intestine to urobilirubin
where it is excreted in feces or urine
If bile flow is impeded and it can’t get to the intestines it in serum levels may rise
Pancreas
Exocrine function – secretion of pancreatic enzymes into the GI tract through the pancreatic duct
-Amylase (breaks down carbs)
-trypsin (digestion of proteins)
-Lipase (breaks down fats)
Endocrine function – Insulin, glucagon and somatostatin into the blood stream, somatostatin
inhibits insulin and glucagon secretion leading to hypoglycemia
Notes:
-Calculous cholecystitis = 90% of all cases the gallbladder can develop edema which
compressed blood vessels which compromises vascular supply.
-Can get Gangrene and perforation may occur
-50% of pts will get secondary infections from organisms that live in the GI tract like
ecoli, kleb and strep
-Acalculous cholecystitis = the other 10% and it comes after major surgical procedures,
severe trauma and burns, cyctis duct obstruction, primary bacterial infections and after
blood transfusion
-Chart 50-1 Cystic fibrosis, DM, frequent change in weight obesity or rapid weight loss, women
-2-3x more prevalent in women than men, they are typically over 40 and obese “3 F’s Female,
Fat and Fourty”
Notes:
-Watch for ROBF – flatus and lack of nausea are more important the BS
-ERAS protocol eliminates NGT unless the patient has N/V
-Emptying an flushing perc chole tubes or post op drains if left
Pancreatitis
Acute: pancreatic duct becomes obstructed, and enzyme back up, causing autodigestion
and inflammation of the pancreas
Chronic: progressive inflammatory disorder with destruction of the pnacrea, cells are
replaced by fibours tissie, pressure within the pancreas increases, obstructing the
pancreatic and common bile ducts
Question: s/s of Chronic Pancreatitis: Recurrent attacks of severe upper abdominal and
back pain accompanied by vomiting
Refer to chart 50-3
Notes:
-Acute can be life threatening
-Chronic can have acute flair ups and by the time it is noticed 90% of the exocrine function has
been lost.
-80% of acute cases are related to cholelithiasis or sustained alcohol use
-Can be mild or severe; mild is typically interstitial edematous pancreatitis vs necrotizing
pancreatitis
-Mild can still be very ill, hypovolemic, can have electrolyte disturbances and develop sepsis
-Severe has the presence of necrotizing pancreases, can be sterile or infected, can involve the
tissue around the pancreas or the parenchyma which is worse
-Spillage of enzymes are toxic and can cause erosion of blood vessels causing thrombosis or
hemorrhage
Management of Pancreatitis
Relieve symptoms and prevent complication
NPO, Enteral feeds distally, NG
H2 antagonist, PPI, Pain medication
IV fluids
Antibiotics only if infection is suspected
Insulin therapy
Notes:
-DHT for feedings past the duodenum into the jejunum is ideal but can be very hard to place (if
surgery is done may get J tube or have DHT placed in OR) NGT to LIWS
-Decrease acid production with PPI
-Opioids for pain, consider PCA
-IVF – think of necrotizing pancreatitis as an internal chemical burns which requires a
tremendous amount of volume replacement
-Antibiotics are often prescribed and rarely needed
-Surgery should be last ditch effort – drains will be placed to irrigate and drain, J tube placement
for distal feeds – necrosectomy can be done via endoscopy, laparoscopically or open ideally you
wait until it is walled off otherwise surgery is difficult
-Management of chronic pancreatitis – monitor nutrition as they are often malnourished
Care
Promote comfort
Prevent complications
Maximize QOL
Choose a center close to home vs farther away
Ulcerogenic Tumors
Tumors involving the islets of Langerhans
Zollinger Ellison Syndrome
o Causes gastric acid production leading to ulcers in the GI tract
o Tumors may be benign or malignant
o Surgical resection is reccomnneded but often not possible because they extend
beyond the pancreas
Notes:
-Causes gastric acid that produces ulcers in the stomach, duodenum and jejunum.
-Can’t even be managed with partial gastric resection
Genetic