-
The Liver:
Where does 80% of the circulation come from?
Where does 20% of the circulation come from?
80% of circulation comes from portal vein (brings in nutrients)
20% of circulation comes from hepatic artery
Capable of regeneration
-
The Liver functions:
What does it metabolize?
What does it produce & excrete, and store?
*What does it convert?
Steroid, CHO, protein & fat metabolism.
Detoxification
Bile production and excretion
Storage
Phagocyte system
Converts ammonia to urea
Metabolize & eliminate bilirubin
-
What are some Dx studies for the liver?
Serum protein studies -albumin
Direct & indirect serum bilirubin, urine bilirubin & urobilinogen
CBC with platelets
Coagulation studies
Prothrombin
-
Hepatic Dysfunction
What is the most common cause?
What else may be the cause of dysfunction (disorders/deficiencies)?
malnutrition RT alcoholism
Acute or chronic cirrhosis of liver
Hepatitis
Viral
Anoxia
Metabolic disorders
Nutritional deficiencies
-
What are some "manifestations"? (PCs)
Jaundice (yellow discoloration of the skin d/t build up of bilirubin)
Portal HTN (increased pressure in the capillaries) results in ascites, and varices
Hepatic encephalopathy (build up of toxins in the brain d/t dysfunction of the liver to clear toxins leading to toxic circulation) or coma
Nutritional deficiencies (malnourished d/t liver's impairment of processing nutrients)
-
What is "jaundice"?
Which are associated w/ liver disease?
Yellow- or green-tinged sclera and skin caused by increased serum bilirubin levels
Hemolytic, *hepatocellular, *obstructive
Hereditary hyperbilirubinemia
Hepatocellular and obstructive jaundice are most associated with liver d
-
What are some s/sx associated w/ "hepatocellular"?
Mild or severely ill
Lack of appetite, N/V, weight loss
Malaise, fatigue, weakness
Headache, chills, fever, infection
-
What are some s/sx associated w/ "obstructive"?
stool color?
Dark, orange-brown urine, clay-colored stools
Dyspepsia and intolerance of fats, impaired digestion
Pruritus
-
What is "portal HTN"?
What does it cause and what may it lead to?
Obstructed blood flow through the liver results in increased pressure throughout the portal venous system
Cirrhosis slows the normal blood flow through the liver, thus increasing pressure in the vein that brings blood from the intestines and spleen to the liver.
Affects veins in esophagus causing esophageal varices (enlarged veins), rectum and abdomen
Causes fluids to be pushed out of capillaries leading to third spacing (ascites)
-
Ascites: Fluid in Peritoneal Cavity
What are some causes?
Portal HTN resulting in increased capillary pressure and obstruction of venous blood flow
Vasodilatation of the major abdominal organs
Changes in the ability to metabolize aldosterone, increasing fluid retention
Decreased synthesis of albumin, decreasing serum osmotic pressure
Movement of albumin into the peritoneal cavity
-
What are the Tx for Ascites?
Low-sodium diet
Diuretics
Bed rest
Paracentesis
Administration of salt-poor albumin
- Transjugular intrahepatic portosystemic
- shunt (TIPS)
-
Which is the drug of choice for Ascites?
Spironolatone (Aldactone)
-
Bleeding of Esophageal Varices (enlarged veins)
When does this usually occur?
Occurs in about 1/3 of patients with cirrhosis and varices
First bleeding episode has a mortality rate of 30% - 50%
Manifestations: hematemesis, melena, general deterioration, and shock
Pts w/ cirrhosis should undergo screening endoscopy q2 years
-
Tx of bleeding varices.
How should you treat a Pt w/ bleeding varices (similar as you would treat someone w/...)?
Treat for shock; administer oxygen
IV fluids, electrolytes, volume expanders, blood and blood products
- Vasopressin, somatostatin, octreotide to
- decease bleeding
Nitroglycerin in combination with vasopressin to reduce coronary vasoconstriction
Propranolol and nadolol to decrease portal pressure; used in combination with other treatment
-
What is Hepatitis?
How are they transmitted?
- Viral hepatitis: a systemic viral infection that causes necrosis and inflammation of
- liver cells with characteristic sx and cellular and biochemical changes.
A and E: fecal–oral route; contaminated food (E is not chronic)
B and C: bloodborne
D: only people with hepatitis B are at risk
Hepatitis G and GB virus-C
-
Hep A.
How's it spread?
What is the incubation period?
Mortality rate & Manifestations?
Spread by poor hand hygiene; fecal–oral
Incubation: 15 to 50 days
Illness may last 4 to 8 weeks
Mortality rate is 0.5% for those younger than age 40 years and 1% to 2% for those >40 yo
- Manifestations: mild flu-like sx, low-grade fever, anorexia, later jaundice and dark
- urine, indigestion and epigastric distress, enlargement of liver and spleen
-
How can you prevent/manage Hep A?
Is there a vaccine?
Good handwashing, clean water, & proper sewage disposal
Vaccine available.
Immunoglobulinn for contacts to provide passive immunity
Bed rest during acute stage
Nutritional support
-
Hep B.
How is Hep B transmitted?
What are the tx for Hep B (pharm)?
Is there a vaccine?
What type of precautions?
Bloodborne (like Hep C)
interferon & antiviral agents: lamivudine (Epivir), adefovir (Hepsera)
Vaccine available
Precautions: standard & infection control measures
-
Hep C.
How is it transmitted?
*Most common bloodborne infection; causes 1/3 of cases of liver cancer and the most common reason for
liver transplant
How do you manage Hep C (pharm tx)?
Bloodborne
Antiviral medications: interferon, ribavirin (Rebetol)
-
Splenomegaly.
What is the cause?
What happens to RBCs & WBCs as a result?
What might this lead to?
Caused by Portal HTN.
Blood is shunted into splenic vein.
Increased removal & destruction of RBCs & WBCs, & platelets.
- May lead to anemia, leukopenia, &
- thrombocytopenia
|
|
