Hepatic Disorders Flashcards
Liver
Largest internal organ in the body; essential for life
Metabolic functions include: carbohydrate, protein and fat metabolism; detoxification of the blood; steroid metabolism
Bile Synthesis functions include: bile production, excretion and storage
Mononuclear phagocyte system functions include: breakdown of old RBC’s, WBC’s, bacteria, etc. Breakdown of Hgb to bilirubin and biliverdin
11 primary functions of the liver
Bile production (helps small intestine break down and absorb fats, cholesterol and vit)
Absorbs and metabolizes bilirubin (formed by breakdown of hgb, stored in liver and then used to make more RBCs)
Assists in creating blood clotting factors (coagulants) - need bile
Fat metabolism
Carb metabolism
Vit and mineral storage
Protein metabolism
Filters blood (hormones, alcohol, drug)
Immunological functions (Kupffer cells)
Production of Albumin (transports fatty acids and steroids, prevents leaky BVs)
Synthesis of angiotensinogen (maintains BP)
Cirrhosis
characterized by scar tissue - cells are nodules causing scaring
Liver cells attempt to regenerate (Regenerative process is disorganized)
- Abnormal blood vessel and bile duct formation
- Overgrowth of new fibrous connective tissue distorts liver’s normal structure, impedes blood flow.
- Irregular regeneration and disorganized regeneration, poor cellular nutrition and hypoxia d/t inadequate blood flow and scar tissue result in decreased liver functioning.
Cirrhosis is the final stage of chronic liver disease.
Patho of cirrhosis
Factors that can lead to cirrhosis
- Chronic alcohol use disorder
- Nonalcohol fatty liver disease (NAFLD)
- Cases of nutrition-related cirrhosis have resulted from extreme dieting, malabsorption, and obesity.
- Patients with Hepatitis b and C
- Environmental factors, as well as a genetic predisposition
- Biliary cirrhosis
- Cardiac cirrhosis
Chronic alcoholic disorder with cirrhosis
Excessive alcohol ingestion is the single most common cause of cirrhosis.
Alcohol has a direct hepatotoxic effect.
Some controversy continues as to whether the cause of cirrhosis is alcohol or the protein malnutrition that frequently coexists with chronic ingestion of alcohol
Biliary cirrhosis
Associated with chronic biliary obstruction
Diffuse fibrosis of liver with jaundice
Cardiac cirrhosis
From longstanding severe right-sided heart failure
Common Assessment findings for hepatic disorder
- GI issues (clay stool)
- Anorexia
- N V
- Constipation
- Jaundice (increased bili)
- Scleral Icterus (yellowing of eyes)
- pruritis
- Fatigue (protein metabolism affected)
- anemia
- Varices
- Petechiae, bleeding
- Peripheral, pulmonary edema
- confusion, coma
- ascites
- protruding abdo
Liver function labs
increased liver enzymes: ALT, AST, LDH, Alk Phos, GGT
decreased serum albumin levels (normal 3.5 – 5.0 G/dl)
increased prothombin time ( normal 11-15 sec.)
Unconjugated bilirubin (fat soluble, indirect)- too much bilirubin in the blood.
Conjugated bilirubin (water soluble, direct)- impaired excretion
Collaborative care of cirrhosis
Rest
Avoidance of alcohol, Aspirin, acetaminophen, and NSAIDs
Management of ascites
Prevention and management of esophageal variceal bleeding
Management of encephalopathy
Cirrhosis manifestations
jaundice
skin lesions
- spider angioma occurs on the nose, cheeks, upper trunk, neck and shoulders (increased corticosteroid use as well)
- palmar erythema - a red area tha blanches with pressure appears on the palms of the hands
- both of these are caused by low levels of circulating estrogen as a result of the liver’s inability to metabolize steroid hormones
Hematological problems
- thrombocytopenia: decreased thrombopoietin (plts)
- leukopenia (decreased WBCs)
- anemia
- all these are from backup of blood from portal vein to spleen
- decreased prothrombin - clotting problems (bleeding of gums, nosebleed, petechiae, easy bleeding)
Endocrine Disorders
- gynecomastia: increased breast gland size (increased estrogen)
- hypogonadism: decrease in male testosterone can cause muscle wasting and infertility
Peripheral Neuropathy
- found in alcoholic cirrhosis probably caused by deficiency in thiamine, folic acid and Vit B12 (weakness, numbness and nerve pain - hand in feet)
Portal hypertension (blocks)
- blocks and gets backed up
- causes esophageal varices
Esophageal Varices
result of portal HTN - trying to offset circulation block, very fragile, do not tolerate high pressure, oozy
- dx: GI assessment (risk of bleeding, what does vomit and stool look like?), VS (decreased BP, increased HR), hypovolemic shock, gastroscopy, ultrasound
greatest risk = bleeding
tx: IV fluids, transfusion of RBCs, plts etc., ligation (stop bleeding)
Supportive measures for acute bleed
Fresh-frozen plasma
Packed RBCs
Vitamin K
Proton pump inhibitors
Octreotide
Octaplex (in severe cases)
Peripheral edema and ascites
edema is caused by decreased colloidal oncotic pressure due to impaired synthesis of albumin and portal HTN
- manifests: pedal, peripheral
ascites: accumulation of serious fluid in perineal or abdo cavity d/t increased portal pressure (proteins shift d/t increased pressure which doesn’t actually happen) - third spacing - can be taken out by paracentesis
- manifestations: abdo distension (edema moves to lower back), weight gain, stridor, signs of hypovolemia, decreased u/o, signs of dehydration, hypokalemia
Care of peripheral edema and ascites
Focused on sodium restriction, diuretics, and fluid removal
Diuretics
Paracentesis
- Removes fluid from abdominal cavity
- Temporary measure
- Continuous reinfusion of ascitic fluid from the abdomen to the vena cava
- Not first-line therapy
- Relief provided is only temporary.
Hepatic Encephalopathy
- anomia is made by the breakdown of proteins by bacteria (goes into portal circulation)
- liver usually converts ammonia into urea (ammonia in blood increases when cant do that)
- ammonia can pass through the BBB - neurotoxic
- increased ammonia
= changes in LOC -confusion, stupor, impaired thinking and judgement,
= neuromuscular disturbances, asterixis, hyperreflexia
tx - decreased protein in diet, lactulose, neomycin
Problems increase by = increased protein, infection, hypovolemia, GI bleed
Lactulose
Can be given PO or PR
It is a colonic acidifier that works by decreasing the amount of ammonia in the blood.
Usual dosing varies but is titrated per LOC and to produce 2-3 soft BMs/ 24h. Often this requires Lactulose 15-30mL TID-QID.
Patient/ caregiver teaching:
- Daily adherence to Lactulose regimen
- Monitoring # of BM’s/ day
- Monitoring for GI bleeds (which increases risk for hepatic encephalopathy and might increase dose of Lactulose)
Drugs and liver function
Avoid hepatotoxic drugs like Acetaminophen, ASA
First Pass effect
This affects increases meds and they should be given in decreased doses.
Use caution in administering medications in patients with advanced liver disease.
Hepatitis
Inflammation r/t the liver. D/t viral infection, not always
Common symptoms:
Anorexia, n/v, malaise, fatigue, headache, low-grade fever, RUQ pain, skin rashes, arthralgias +/- jaundice
Hep A
Contracted by consuming food or water contaminated by feces.
Diagnosed by detection of anti-HAV IgM in the serum.
Supportive care as no treatment available (usually doesn’t cause liver failure)
Self-limiting (usually 4-6 wks duration)
Confers lifelong immunity
Hep B
As an RN you must be immunized for it.
Vaccine-preventable infectious disease
Screening tests: HBsAg, Anti-HBs and Anti-HBc
Transmission perinatally, percutaneously, sexually or horizontally (by permucosal exposure to infectious blood, blood products or other body fluids).
All infants born to HB+ mothers must receive 1st dose of vaccine and immunoglobulins within 12h of birth. Breastfeeding is safe if this is done.
Acute and chronic types.
Most patients with HBV chronic infection require long-term treatment.
What if you are exposed? (single dose of hep B immunoglobulin)
Hepatitis B Immune Globulin- confers temporary passive immunity
Hep C
Hepatitis C is contracted by direct contact with contaminated needles and equipment used to inject drugs - fluids, percutaneously.
most common mode of transmission: sharing of contaminated needles
Diagnostic testing:
Antibody testing (anti-HCV)
Acute infection confirmed (if above +) with HCV RNA.
Chronic Hep C is curable with medication therapy (direct-acting antiviral agents or DAAs). ALL patients with chronic Hep C should be treated unless they have severely decompensated cirrhosis.
What does Hep B and C infection can lead to?
severe scarring of the liver and cirrhosis, HCC, and liver failure if left untreated.
Acute liver failure
Definition: Rapid deterioration of liver function resulting in encephalopathy and coagulopathy in a person with no known hx of liver disease.
Fulminant Hepatic Failure: development of encephalopathy within 8 wks of onset of illness
Most common cause: acetaminophen (acetylcysteine protocol for overdose)
Acute liver failure assessment
Clinical Manifestations:
Jaundice
Coagulation abnormalities (bruising, labs)
Encephalopathy (changes in LOC)
Earliest sign: changes in cognitive functioning
Common Complications:
Cerebral edema
Renal Failure
Hypoglycemia (unique)
Metabolic acidosis
Sepsis
Multiorgan failure
Acute liver failure diagnostics
Serum bilirubin levels: elevated
PT: high or prolonged
LFTs (esp ALT – primary (troponin to the heart) and AST): elevated
Glucose: low
CBC: hgb (low), hematogrit (low), platelets (low), RBC (low)
Acetaminophen levels: Screening
Drugs and other toxins: Screening (depending on hx)
Viral hepatitis serology: Especially HAV, HBV and HEV
Plasma Ammonia: encephalopathy (elevated)
Liver biopsy may be performed via transjugular route b/c of coagulopathies or when other liver diseases are suspected. (important for inserting NGs)
CT/ MRI/ Ultrasound – helpful for info re: liver size, contour, presence of ascites, tumours and patency of the blood vessels.
Nursing care of acute liver failure
Transfer to critical care ASAP following diagnosis
Transfer to transplant center for Grade 1 or 2 encephalopathy
Liver transplant is the treatment of choice for Acute Liver Failure
Neurological monitoring very important! AVOID things that could increase ICP or chemically alter mental status.
Protect renal function by:
- Maintain adequate fluid balance (protective)
- Avoid nephrotoxic meds (NSAIDs and immunoglycosides)
- Promptly identify and treat infection
Minimize agitation
Ensure seizure pads on bedrails and pt environment is safe
Provide good skin and oral care
Consider nutritional impact!
BE CAUTIOUS with NG tube insertion and use!!
Liver transplant
Indications:
Localized and/ or recurrent hepatocellular carcinoma (HCC)
Some with end-stage liver disease (depending on cause)
Contraindications:
Widespread malignant disease
Severe extrahepatic disease
Recent hx of other malignancy
Ongoing drug/ alcohol use
Inability to adhere/ comprehend rigorous post-transplant course
Deceased (cadaveric) donor
Living donor (a portion), but significant risk of complications exists
Post transplant complications:
bleeding
infection
rejection
Monitoring for infection is KEY b/c it is the leading cause of morbidity and mortality post-transplant. (low grade) Fever may be the only sign of infection.
