Disorders of the liver Flashcards
What are the functions of the liver
o Accessory digestive gland, produces bile (alkaline compound that aids in digestion of fat + absorption of vit K)
o Plays major role in carbohydrate metabolism and has numerous function
• Gluconeogenesis: synthesis of glucose from certain AAs (lactate, glycerol)
• Formation of glucose from protein + fat
• Glucogenolysis: breakdown of glycogen into glucose
• Glucogenesis: formation of glycogen from glucose
o Lipid metabolism
• Cholesterol synthesis
• Lipogenesis: production of triglycerides
o Produces coagulation factors
• Fibrinogen, prothrombin, protein C, protein S, antithrombin, clotting factors 5,7,8,9,10,11
o 1st trimester of the fetus:
• Liver is main site of RBC production
• By 32 wks: bone marrow has taken over to create RBCs
o Breakdown of insulin + other hormones
o Converts ammonia to urea (excreted by kidneys)
o Stores Vit A, Vit D, Vit b12, Vit K, Iron
o Detoxification of various metabolites
o Plasma protein synthesis
o The production of biochemicals necessary for digestion
o Regulation of glycogen storage
o Decomposition of red blood cells
o Hormone production
Glucogenolysis:
breakdown of glycogen into glucose
Glucogenesis:
formation of glycogen from glucose
What is viral hepatitis
liver inflammation d/t viral infection. Can be either acute, recent infection, rapid onset OR chronic. It is a systemmic viral disease primarily affecting liver. Types include: Hep A, B, C, D, E (and G but not common)
How are liver cells damages in viral hepatitis?
Liver cells can be damaged in TWO WAYS d/t:
• Direct action of virus
• Cell-mediated immune responses to virus
Cell injury leads to inflammation + necrosis of liver:
• Hepatocytes + liver appear swollen
• Diffuse necrosis present
• Severe inflammation: BILIARY may develop, causing backup of bile into blood
• Hepatic cells may regenerate or fibrous scar tissue forms in liver
• Scar tissue often obstructs blood + bile flow leading to further damage (interferes with unique organization of liver lobule, ischemia)
• Chronic inflammation in Hep B, C, D: persistent inflammation, necrosis of liver for MORE THAN 6 MONTHS
• Eventually causes permanent liver damage + cirrhosis
• Increased incidence of hepatocellular cancer assoc with chronic hepatitis
What is Hepatitis A
Hepatitis A: caused by small RNA virus (HAV)
o Hepatitis A can be found in the feces, bile, and sera of infected individuals
o Usually transmitted by the fecal-oral route (contaminated water, shell fish)
o Short incubation period (2-6 weeks)
o Causes acute, self-limiting infection; does NOT have carrier/chronic state
o Fecal shedding of virus occurs before onset of signs
• IgM HAV appear (1st group), IgG HAV (2nd group) (remain in serum for years, providing immunity against infection)
What are risk factors for Hep A
o Risk factors (spread by fecal oral route)
• Crowded, unsanitary conditions
• Food and water contamination
• Daycare centers
• Sexual transmission (in homosexual pop)
What is hepatitis B
Double stranded DNA virus; contains 3 antigens that each stimulates antibody production in the body
o Long incubation period: avg 2 mo
o Large amts of HBV surface antigen produces by infected liver cells early in course of infection
• Antigen in serum - High risk of continued active infection + damage to liver
o Common: carrier state – asymptomatic, but contagious
o Window/prolonged lag time occurs before serum markers, symptoms become present
• Virus cannot be detected but can be transmitted
• Long incubation period – harder to track sources and transmission
How is Hep B transmitted?
o Transmitted through contact with infected blood, body fluids, or contaminated needles • Body piercing • Tattooing • Blood Transfusion • Sexual transmission • Mother to fetus • Vertical transmission: breast feeding? • Maternal transmission can occur if the mother is infected during the third trimester
Hepatitis C
Single stranded RNA virus.
- Can exist in carrier state and be chronic (50%- 80% of hepatitis C cases result in chronic hepatitis)
- MOST COMMON hepatitis transmitted via blood transfusions
What are the causes of Hepatitis C
Causes:
• Blood transfusion
• Sharing of needles
• Mother to baby (Maternal transmission to fetus occurs in 5-10% of cases
• Body piercing/tattoos
• Unprotected sex w/ multiple partners
o Primary mode of transmission is IV drug use through sharing of needles
o Secondary risk is through high-risk sexual behavior.
What are complications of Hep B and C
o Complications
• Chronic hepatitis with cirrhosis
• End Stage Liver Failure
• Hepatocellular Carcinoma
What is hepatitis D?
An incomplete RNA virus that requires presence of HBV to replicate + produce active infection
o Increases severity of HBV infection o Same transmission route as HBV o Depends on HBV for replication o Transmitted by blood o High incidence of infection in IV drug users
Hepatitis E
Hep E is a single stranded RNA virus (SPREAD BY Fecal-oral transmission)
o Developing countries (Asia, Africa) – high mortality rate in pregnant women
o Similar to Hepatitis A in course
• Lacks chronic, carrier state
Overview of viral hepatitis
There is currently no method to destroy hepatitis in body
o Gamma-globulin helpful when given earlier in course of infection
o Rest, diet high in protein, carbs, vitamins (most useful)
o HBV, HCV may be treated with interferon + epivere to decrease viral replication (Effective in 30-40% of individuals)
o Slow-acting interferon + antiviral drug (vibovaren?) reduced rate of viral replication in 80% of HCV pts
o Gradual destruction of liver occurs leading to cirrhosis, hepatocellular cancer
What are the stages of acute hepatisis
- Prodromal (preicteric) phase (onset my be insidious). Begins 2 weeks after exposure (nonspecific symptoms: fatige, malaise, anorexia & nausea, chills, muscle aches, elevated serum levels of liver enzymes. And sometimes: fever, headache and mild URQ discomfort
- Icteric phase (jaudice stage). Lasts 2-6 weeks.
• Marks onset of jaundice – serum bilirubin levels rise
• Yellowing of skin + sclera
• Biliary obstruction increases stool light in color (steatorrhea), urine becomes darker, skin becomes puridic
• Liver becomes tender + enlarged mild, aching pain
• Severe cases: blood clotting time may be prolonged (d/t Impaired synthesis of blood clotting factors)
• This stage lasts longer in HBV! - Recovery phase (posticteric). Marked by an improvement of symptoms and reduction in signs.
- Average acute stage of HAV 8-10 wks (but HBV is prolonged over 16 weeks)
What is liver cirrhosis
Extensive diffuse fibrosis, loss of lobular organization in liver.
It is an irreversible inflammatory disease that disrupts liver function and structure
• Decreased hepatic function due to nodular and fibrotic tissue synthesis (fibrosis)
o Initially, liver enlarged but becomes small, shrunken with extensive fibrosis
o Asymptomatic degenerative changes until disease is well advanced
Pathophysiology of liver cirrhosis
o Pathophysiology:
• Loss of liver cell fxn: Interference of blood + bile flow in liver
• Obstruction of bile ducts + blood flow by fibrosis tissue
• Reduction of bile entering intestine
• Backup of bile in liver
• Blockage of blood flow to liver
• Congestion in spleen
• Congestion in intestinal walls + stomach
Types of liver cirrhosis
- Alcoholic
- Non-alcoholic Fatty Liver
- Biliary (bile canaliculi)
- Metabolic
Name some of the clinical manifestations of Cirrhosis
-Portal Hypertension
• Hepatic Necrosis
• Esophageal Varices: large, distended veins
• Esophageal veins have several points of anastomosis (collateral channels that join with gastric veins)
• Increase pressure of blood extends into esophageal veins leading to large, distended veins
• Located near mucosal surface of esophagus
• Veins easily torn by food passing
• Possible hemorrhage
• Splenomegaly
• Ascites
What is the stool and urine like in a PT with cirrhosis?
light colored stools (d/t decreased bile in GI tract) and dark urine (d/t increase urobilinogen)
Why do some PTs with cirrhosis develop hepatic encephalopathy?
Due to the build up of ammonia
What are complications of end stage liver disease (when liver is unable to perform)
- Reduced Clotting
- Impaired Ammonia Metabolism
- Impaired Bilirubin Metabolism
- Hypoglycemia
- Increased Aldosterone Production
What is the treatment of cirrhosis
-Supportive treatment
• Avoiding fatigue and avoiding exposure to infection
-Dietary restrictions: restrict protein, Na+ intake
• Encourage high carb, vit supplements
-Diuretics
• Serum electrolytes may have to be balanced
• Lasiks: reduce body fluid
-Paracentesis: remove excess fluid; peritoneal cavity punctured by needle to remove peritoneal fluid
• Albumin transfusion to prevent 3rd spacing of fluid
- Antibiotics: Neomyocin – reduce intestinal flora + control serum ammonia levels
- Ruptured Esophageal varices need emergency Tx
