Week 2 - Hepatic Flashcards
What are the main functions of the liver?
Glucose metabolism / Blood sugar balance
- Excess energy gets stored as glycogen in liver
- When needed, liver converts glycogen to glucose
Breakdown of Old Erythrocytes
- Excretion of Bilirubin
- Helps production of bile
Storage of micronutrients
- Minerals: Copper, Zinc, Mg, Iron
- Vitamins: A, D, E, K, B12
Detoxification:
- Drugs/Alcohol/ Environmental Toxins
- Fatty acids
- Steroid hormones
- Ammonia into Urea
Protein Synthesis:
- Albumin = Keeps fluid where it should be
- Many clotting factors = prevents bleeding
- Impaired liver = Increased risk for bleeding
In regards to protein synthesis, what can you expect from an impaired liver?
- Increased ammonia in the blood (ammonia is a toxic byproduct of protein metabolism)
- Edema d/t lack of albumin
- Neuropathy; impaired cognitive ability d/t ammonia buildup
laboratory Tests for Liver Function
Serum Aminotransferases
Serum protein studies:
- Albumin
Serum ammonia:
- Impaired liver = higher ammonia
Prothrombin Time:
- Impaired liver = higher prothrombin tim
Diagnostic Studies
Ultrasound
Magnetic Resonance Imagery (MRI)
Endoscopy
Liver Biopsy
- Lay on left side for procedure
- Lay on Right side for recovery
Assessment /findings for liver function
Pallor or Jaundice
Muscle Atrophy - Impaired protein synthesis
Edema - Low Albumin
Skin excoriation - Indicative of liver disease; because Bile salts under skin are irritative
Bruising/Bleeding - d/t decreased production of clotting factors
Liver Dysfunction Etiology
Alcoholism - Puts extra strain on liver
Infection -
Anorexia
Metabolic Disorder
Nutritional Deficiencies
What is Bilirubin?
Produced in the liver, spleen and bone marrow
- Results from the breakdown of hemoglobin; a byproduct of hemolysis
- Liver removes bilirubin from blood and excretes bilirubin in bile
What are the two types of bilirubin?
Conjugated / Direct
- Circulates in the blood
- Direct byproduct of hemolysis
“This bilirubin is ready to be added/turned into bile, and thus ready to be excreted from the body”.
Unconjugated / Indirect:
- Binds with protein in the blood
- Converted by liver for excretion
” This is a byproduct of red blood cells being broken down. It still needs to be processed by the liver before it can be excreted properly”
Liver Conditions: Jaundice / Icterus
What is it?
Not a diagnosis, it is a symptom of liver dysfunction
Result from high serum concentration of bilirubin
Describe the three types of Jaundice
Hemolytic (External Issue):
- Excessive destruction of RBCs
- Elevated serum Unconjugated bilirubin
Hepatocellular (Internal issue; with the liver itself) :
- Liver disease
- Elevated serum conjugated and unconjugated bilirubin
Obstructive (External Issue):
- Caused by blockage of bile from liver to intestinal tract
- Elevated serum conjugated bilirubin
- (Bilirubin needs to bind to bile in order to be excreted, but the bile is backed up so it can’t leave the body)
Describe Hemolytic Liver Dysfunction
Hemolytic (External Issue):
- Excessive destruction of RBCs
- Elevated serum Unconjugated bilirubin
“The body’s breaking down RBCs too fast, so the plasma gets flooded with bilirubin. Even if the liver is functioning normally is can’t excrete the bilirubin fast enough.
- Increased risk of stones in gallbladder (“Increased bilirubin = increased bilirubin gallstones”)
Describe Hepatocellular Liver Dysfunction
What is it?
S/S?
This is an internal issue; liver disease, cirrhosis
- Elevated serum conjugated and unconjugated bilirubin; liver is impaired in both processing and excreting
s/s Hepatocellular Jaundice:
- Loss of appetite
- Nausea
- Weight loss
- Malaise (discomfort/illness)
- Fatigue
- Weakness
“Liver is having trouble processing the unconjugated bilirubin; the liver also has trouble excreting the conjugated bilirubin into the bile ducts. This results in an increase of both”
Describe Obstructive Liver Dysfunction
What is it?
s/s?
Caused by blockage of bile from the liver to the intestinal tract
- Elevated serum conjugated bilirubin
S/S:
- Dark orange-brown urine
- Light clay-colored stool
- Dyspepsia
- Intolerance of fats
(Surface level) How to distinguish Hepatitis and Cirrhosis
Hepatitis: -itis = inflammation of liver
Cirrhosis: Think “cirr” = scarring
Both can lead to:
Abnormal liver function
Liver failure
Liver Cancer
May require transplant
What is Hepatitis?
Hepatitis - An infection that causes necrosis and inflammation of liver cells with characteristic symptoms and cellular
“If it ends in a vowel, it comes from the bowel”
What are the phases of hepatitis?
Pre-Ecteris:
1to3 weeks before jaundice appears
- fatigue
- anorexia
- taste and smell changes
- mild-flu like symptoms
- abdominal discomfort
Icteric:
lasts 2-6 weeks
- appearance of jaundice
- RUQ discomfort d/t enlarged liver
- Dark urine
- Clay colored stool
Post Icteric:
Lasts 2-12 weeks
- Recovery
- Clinival manifestations disappear
- Jaundice subsides
Hepatitis A:
Self limited, no chronic infection
Transmission: Fecal-Oral (Poor hygiene hand-to-mouth contact, close contact)
s/s:
- Mild flu-like symptoms
- Fever
- Anorexia
- Later = jaundice + dark urine
- Indigestion
- Enlarged liver + spleen
Hepatitis A: Treatment and Interventions
Treatment:
- Hep A is self limited
- Bed rest during acute stage
- Nutritional support
Prevention:
- Handwashing
- Safe water
- Proper sewage disposal
Hepatitis B / HBV:
How is it transmitted?
Incubation period?
Complication?
S/S:
May become chronic, not self limited
Transmission: Blood, saliva, semen and vaginal (sexually transmitted)
Incubation: 1-6 months
Long Term Complications:
- Cirrhosis
- Liver cancer; major cause worldwide
- May become chronic
S/S: Similar to Hep A
- Mild flu-like symptoms
- Fever
- Anorexia
- Later = Jaundice, dark urine
- Enlarged liver + spleen
Hepatitis B: Treatment and Intervention
Treatment:
- Meds: Alpha interferon, antiviral agents
Interventions:
- Vaccine
- Screening of blood / blood products
- Standard precaution/infection control measures
- Bed rest
Hepatitis C:
How is it transmitted?
Complication?
Symptoms for assessment?
Frequently becomes chronic, not self limited
Transmission: Blood and sexual contact
- Most common blood borne infection
Incubation: Variable
Long term complications:
- Causes 1/3 of liver cancer
- Most common reason for liver transplant
- Frequently becomes chronic
s/s: similar to A-B-D; mild
- Mild flu-like symptoms
- Fever
- Anorexia
- Later = jaundice
- Indigestion
- Enlarged liver, spleen
Hepatitis C: Treatment and Intervention
Treatment: Curable for most patients
- Direct Acting Antiviral (DAA)
Interventions:
- Prevention
- Screening of blood
- Alcohol & meds that affect liver should be avoided
Hepatitis D (HDV)
Only people with Hep B are at risk for Hepatitis D
Transmission: Blood and sexual contact
s/s: similar to He[ A-B-C
- Mild flu-like symptoms
- Fever
- Anorexia
- Later = Jaundice and dark urine
- Indigestion
- Enlarged liver + spleen
Hepatitis D: Treatment
Similar to other forms of Hepatitis
Meds: Interferon alfa
What is Hepatitis D likely to develop into?
- Fulminant liver failure
- Chronic active hepatitis
- Cirrhosis
Which population is at risk for Hepatitis D?
Only persons with Hepatitis B
Hepatitis E (HEV)
Transmission: Fecal / Oral Route
Incubation: 15-65 days
Treatment: Self-limited, i.e. it heals on its own
Cirrhosis
Non-Fibrous connective scar tissue replaces normal liver cells
Obstructive Liver Disorder
Types:
1) Laennec’s (alcoholic)
- Most common
- Excessive alcohol OR malnutrition
2) Post Necrotic:
- Secondary to infection (hepatitis)
3) Biliary:
- Scarring around bile ducts
- Biliary obstruction and/or infection
Cirrhosis:
s/s
Complications
- Jaundice
- Asterixis (hand flapping)
- Anorexia, nausea, vomiting
- Change in mental status
- Difficulty with ADLs, and maintaining a job/social life
- Anatomic distortion
- Fluid volume changes (shock or asites)
Complications:
- Portal hypertension “scarring blocks blood flow of hepatic portal vein”
- Ascites “Poor albumin production = scattered fluids”
- Esophageal / Gastric varices “Blood in liver gets blocked off and rerouted to smaller, weaker veins in esophagus & stomach. Smaller veins swell and can rupture”
Cirrhosis: Interventions
Diet:
- Small, frequent meals = “Smaller meals are less overwhelming on liver & digestive system”
- High calorie diet = “Patients are at risk of anorexia/malnutrition”
- Vitamin & Nutritional supplements (promotes healing of damaged liver cells)
- Avoid high protein diet (but not protein restriction)
Risk for injury:
- Prevent falls (Increased risk for bleeding d/t impaired liver = decreased clotting factors)
- Evaluate any injury d/t potential excessive bleeding
Activity Intolerance:
- Encourage rest
- Position for respiratory
Impaired skin integrity:
- Cholestryamine Resine: Binds to bile salts = decreased itching
Liver Dysfunction: Portal Vein Hypertension
Results in increased pressure throughout the portal venous system
Complications:
- Ascites
- Esophageal Varices
Treatment = Portal systemic Shunt:
- Decrease portal pressure
- Can prevent portal hypertension
- Decreases risk for esophageal varices
Transjugular Intrahepatic Portosystemic Shunt (TIPS)
Creation of an artificial tract from the hepatic vein to the portal
- Helps to relieve portal hypertension
Ascites
Definition: Collection of fluid in the peritoneal cavity
Etiology:
Portal Hypertension
- Increased capillary pressure, obstruction of venous blood flow = fluid gets forced out
Changes in ability to metabolize aldosterone
- Increase fluid retention
- “Kidneys sense low blood volume d/t fluid leaking out from portal hypertension. Renin-Angiotensin system gets signaled to retain sodium and water to ‘correct’ low volume = increased fluid retention.”
Albumin
- Decreased synthesis of albumin = decreased serum osmotic pressure
Ascites: Assessment
Abdominal girth (tape Measure)
Daily weight
Inspect:
- Striae
- Distended veins
- Umbilical hernia
Percussion
Ascites: Treatment
Low sodium diet
Medications:
- Diuretics
- Albumin
Paracentesis: Drawing fluid out of cavity
How is paracentesis conducted?
Procedure to remove ascitic fluid
- Needle introduced through the abdominal wall
Effects:
- Relieves discomfort from distention
- Relieves breathing difficulty from fluid pressing up on the diaphragm
Nursing actions:
- Ensure patient voids prior to procedure
- Record amount of fluid drawn
- IV albumin infused back in
- Monitor BP and output
- Monitor for hypovolemic shock
Hypovolemic shock: s/s
Rapid, weak pulse
Tachypneic
Hypotension
Anxiety
Decreased urine output
Pallor
Confusion
Esophageal / Gastric Varices
Etiology:
Cirrhosis causes portal hypertension which increases prsessure on vessels in the esophagus causing the veins to bulge
Esophageal / Gastric Varices: Assessment
Hematemesis - Vomit stained red (E) or black (G)
Melena - Black, tarry stools (G)
Esophageal Varices: Treatment
Balloon Tamponade / Sengstaken-Blakemore tube
- Balloons inflate which apply direct pressure to varices, which compress them and restrict blood flow to site
- Remains inflated for a few hours
Endoscopic sclerotherapy
- Injection of sclerosing agent into the esophageal varices through endoscope
- Promotes clotting and eventual sclerosis (hardening of the tissue)
- Obliterates the varices
Esophageal banding:
- Rubber bang is slipped over an esophageal varix via endoscope
- Necrosis results
- Varix sloughs off
Esophageal varices: Interventions for prevention
- Patients with cirrhosis should undergo endoscopy screening every 2 years
Monitor for associated complications: - Hepatic encephalopathy from blood breakdown in GI tract
- Delirium r/t alcohol withdrawal
How often should patients with cirrhosis undergo screening endoscopy?
Every 2 years
- This is to look for esophageal varices
Ammonia
Where does it come from?
What it its relationship with the liver? With the brain?
Ammonia is a by product of protein breakdown
The liver breaks down ammonia into urea
This is important because ammonia can negatively effect the brain
Hepatic Encephalopathy
What is it?
Assessment/s.s
Brain dysfunction due to (or secondary to) liver dysfunction
- Life threatening complication of liver disease
Etiology: Usually be d/t accumulation of ammonia and other toxic metabolites in blood
Test: Electroencephalogram
s/s:
Neuro: Changes in level of consciousness, asterixis (involuntary flapping movements of hands), potential seizures
- Fetor hepaticus (sweet, fecal odor to breath)
Hepatic Encephalopathy: Stage 1
S/S
NORMAL Level of consciousness (LOC)
NORMAL electroencephalogram (EEG)
Lethargy
Asterixis
Fetor Hepaticus
Euphoria
Reversal of day-night sleep patterns
Can’t draw stick figures
Hepatic Encephalopathy: Stage 2
s/s
Abnormal EEG, and generalized slowing
Disorientation
Increased drowsiness
Inappropriate behavior
Labile mood
Agitation
Asterixis
Hepatic Encephalopathy: Stage 3
s/s
EEG markedly abnormal
Stupor
Difficult to arouse
Sleeps most of the time
Incoherent speech
Deep tendon reflexes
Hepatic Encephalopathy: Stage 4
COMATOSE
May not respond to painful stimuli
ABSENT: Asterixis, Deep tendon reflexes
Flaccid extremities
EEG markedly abnormal
What do we give to treat Hepatic Encephalopathy?
Lactulose
What is the most significant source of bleeding in a patient with cirrhosis?
Esophageal varices
Why do some forms of hepatitis lead to Anorexia?
- The liver plays an important role in nutrient metabolism
- if the liver is impaired, it cannot regulate metabolism properly, leading to: Nausea and reduced hunger signals
- Impaired liver cannot produce adequate bile which = fat malabsorption, nausea, bloating after eating
- Fever, fatigue = reduced appetite
What are the treatment/interventions for: Hepatitis A, B, C, D, E
A:
Treatment - Self limited; bed rest & nutritional support
Prevention - Handwashing, safe water, vaccine
B:
Treatment - Meds (Alpha interferon & antiviral agents)
Prevention - vaccine, standard precaution, blood screening & blood safety
C:
Treatment - Meds (Direct-acting Antivirals = tenofovir, entecavir)
Prevention - via blood safety, avoid needle sticks; no vaccine
D:
Treatment - Treat Hep B infection; no antiviral for Hep B specifically
Prevention - Hep B vaccine
E:
Treatment - Self limited & no chronic form
Prevention - Handwashing, safe water; NO VACCINE FOR HEP E
