Disorders of the Liver and Pancreas Heptobilary Flashcards
Liver
“Metabolic factory” of the body
- Largest internal organ in the body; essential for life
- Functions in the manufacture, storage, transformation, and excretion of many substances involved in metabolism, production of plasma proteins and clotting factors, Breakdown of old and damaged erythrocytes, Bile production
-Receives blood from hepatic portal vein
Transport of nutrients from intestine to liver
-Hepatocytes store nutrients
Play role in carbohydrate, protein, fat metabolism
Pancreas
Exocrine (contributes to digestion) and endocrine functions (insulin, glycagon, somatostatin, and pancreatic polypeptide)
Secretes digestive enzymes, electrolytes Trypsin Chymotrypsin Carboxypeptidase Ribonuclease Pancreatic amylase Bicarbonate ions
Pancreatic duct joins bile duct to enter duodenum
slide 6 has manifesations of liver disease
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Prehepatic jaundice
Result of excessive destruction of red blood cells
Characteristic of hemolytic anemias or transfusion reactions
Unconjugated bilirubin level elevated
Intrahepatic jaundice
Occurs with disease or damage to hepatocytes
Hepatitis or cirrhosis
Both unconjugated and conjugated bilirubin levels may be elevated.
Posthepatic jaundice
Caused by obstruction of bile flow into gallbladder or duodenum
Tumor, cholelithiasis
Increased conjugated bilirubin level
Light-colored stool caused by absence of bile
Bilirubin Measurement in Jaundice
Direct or conjugated bilirubin can be measured in the blood.
Total bilirubin is measured in blood.
Indirect or unconjugated bilirubin = total bilirubin minus direct bilirubin
Cirrhosis
Progressive destruction of the liver – leads to cellular death when 80 – 90% f the liver has been destroyed
Damaged liver regenerate as fibrotic areas instead of functional cells, causing lymph damage and alterations in live restructure, function and blood circulation
Extensive diffuse fibrosis
Interferes with blood supply
Bile may back up.
Loss of lobular organization
Degenerative changes may be asymptomatic until disease is well advanced.
Liver biopsy and serologic test to determine cause and extent of damage
Causes of cirrhosis
-Alcoholic liver disease (15%)
-Biliary cirrhosis
Associated with immune disorders
-Postnecrotic cirrhosis
Linked with chronic hepatitis (26% Hep C, 15% Hep B) or long-term exposure to toxic materials
-Metabolic
Usually caused by genetic metabolic storage disorders
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Functional Losses with Cirrhosis
Decreased removal and conjugation of bilirubin
Decreased production of bile
Impaired digestion and absorption of nutrients
Decreased production of blood-clotting factors (Prothrombin/Fibrogen) & plasma Proteins (albumin)
Impaired glucose and glycogen metabolism
Impaired conversion of ammonia to urea
Inadequate storage of iron and vitamin B12
Congestion in intestinal walls and stomach
Impairing digestion and absorption
Development of esophageal varices **next slide
Hemorrhage
Development of ascites, an accumulation of fluid in the peritoneal cavity **following 2 slides
Causes abdominal distention and pressure
Decreased inactivation of hormones and drugs- Drug dosages must be carefully monitored to avoid toxicity.
Decreased removal of toxic substances (ammonia & drugs)
Reduction of bile entering the intestine- Impairs digestion and absorption
Backup of bile in the liver- Leads to obstructive jaundice
Blockage of blood flow through the liver- Leads to portal hypertension
Congestion in the spleen- Increases hemolysis
Cirrhosis: Subjective Data
- Personality changes, forgetfulness, disorientation
- Fatigue, drowsiness, mild tremors, or flue-like sx
- Gynecomastia, ab distention & measure abd girth
Initial manifestations often mild and vague
of cirrhosis
Fatigue, anorexia, weight loss, anemia, diarrhea
Dull aching pain may be present in upper right abdominal quadrant.
Advanced cirrhosis
Ascites and peripheral edema
Increased bruising
Esophageal varices (May rupture, leading to hemorrhage, circulatory shock)
Jaundice, encephalopathy
Cirrhosis: Treatment
Avoidance of alcohol or specific cause
Avoid fatigue
Avoid exposure to infection
Supportive or symptomatic treatment
Dietary restrictions (high carbohydrate intake and vitamin supplements, restrict protein, fat, & Na++)
Balancing serum electrolytes (possibly diuretics)
Paracentesis
Antibiotics to reduce intestinal flora (neomycin)
Cirrhosis: Treatment
-Esophageal and gastric varice:
Long-term management
Shunting procedures
Monitor for hypovolemia & bleeding
- Drug therapy Vitamin K blood clotting
- Emergency treatment if esophageal varices rupture
- Liver transplantation (suitable living donor = liver tissue is able to grow in both donner and recipient providing a complete functional liver for both)
Hepatitis
Inflammation of the liver results in degeneration and necrosis.
Mild inflammation impairs hepatocyte function.
More severe inflammation and necrosis may lead to obstruction of blood & bile flow
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Alcoholic (Fatty liver) Idiopathic (Fatty liver) Viral hepatitis (Local infection) Infection elsewhere in body(infectious mononucleosis or amebiasis) Chemical or drug toxicity
Viral Hepatitis
Cell injury results in inflammation and necrosis in the liver.
-Degrees of inflammation and damage vary.
Liver is edematous and tender.
Causative viruses
Hepatitis A virus (HAV) Hepatitis B virus (HBV) Hepatitis C virus (HCV) Hepatitis D virus (HDV) Hepatitis E virus (HEV)
*Hepatitis A (HAV)
know mainly abc and how they are transmitted
o Small RNA virus
o Infectious hepatitis
o Transmitted by fecal-oral route in areas of inadequate sanitation or hygiene
–Often from contaminated water or shellfish
o Sexual transmission has occurred during anal intercourse.
o Acute but self-limiting infection
o No carrier or chronic state
o Fecal shedding of virus before onset of signs
o Vaccine available for travelers, food care workers, and health care workers
*Hepatitis B (HBV)
o Partially double-stranded DNA virus
o Over 50% of HIV-positive patients are positive for HBV.
o 50% of patients are asymptomatic but contagious because of carrier state.
o Chronic inflammation can occur.
o Transmission primarily by infected blood
o Sexual transmission has been noted.
o Tattooing and body piercing may transmit the virus.
o Vaccine available, routinely given to children
*Hepatitis C (HCV)
Single-stranded RNA virus
Most common type transmitted by blood transfusion
May exist in a carrier state
About 50% of patients enter the chronic state.
Increases risk of hepatocellular carcinoma
Treated with interferon injections
Hepatitis D (HDV)
o Also called delta virus
o Incomplete RNA virus
Requires HBV to replicate and produce active infection
o HDV infection increases severity of HBV infection
Transmitted by blood
Hepatitis E (HEV)
Single-stranded RNA virus
Transmitted by oral-fecal route
No chronic or carrier state
FIRST STAGE
Viral Hepatitis: Manifestations
Preicteric stage
Fatigue and malaise Anorexia and nausea General muscle aching Sometimes fever, H/A, mild URQ discomfort LFT elevated (AST & ALT)
SECOND STAGE
Viral Hepatitis: Manifestations
Icteric stage *longest for Hep B
Onset of jaundice
Stools light in color, urine becomes darker, skin puritic
Liver tender and enlarged (hepatomegaly) = mild aching pain
Severe cases blood clotting times prolonged
THIRD STAGE
Viral Hepatitis: Manifestations
Posticteric stage—recovery stage
Reductions in signs
Weakness persists for weeks
Hep A 8-10w; Hep B 16w
Viral Hepatitis: Treatment
• No method of destroying hepatitis viruses in the body
• Only body defense is formation of antibodies via vaccination
• Supportive measures (Rest, diet high in protein, carbohydrate, and vitamins)
• Chronic hepatitis can be treated with INTERFERON.
o Decreases viral replication
o Effective in only 30% to 40% of individuals
o Drug combination (slow-acting interferon plus antiviral drug) more effective
Gallbladder Disorders
• Cholelithiasis
o Formation of gallstones
o Solid material (calculi) that form in bile
• Cholecystitis
o Inflammation of gallbladder and cystic duct
• Cholangitis
o Inflammation usually related to infection of bile ducts
• Choledocholithiasis
o Obstruction of the biliary tract by gallstones
Gallbladder Disorders (Cont.)
- Gallstones vary in size and shape.
- Form in bile ducts, gallbladder, or cystic duct
• May consist of:
o Cholesterol or bile pigment
o Mixed content with calcium salts
• Small stones
o May be silent and excreted in bile
• Larger stones
o Obstruct flow of bile in cystic or common bile ducts; cause severe pain, which is often referred to subscapular area
Risk factors for gallstones
Women twice as likely to develop stones High cholesterol in bile High cholesterol intake Obesity Multiparity Use of oral contraceptives or estrogen supplements Hemolytic anemia Alcoholic cirrhosis Biliary tract infection
4F’s of gallbladder=
Fat, Fertile, Female, Forty
Obstruction of a duct by a large calculi
o Sudden severe waves of pain
Radiating pain right shoulder/neck
o Nausea and vomiting usually present
o Pain continues, and jaundice develops.
Bile backs up into the liver and blood.
Risk of ruptured gallbladder if obstruction persists
Pain decreases if stone moves into duodenum
o Surgical intervention may be necessary.
May be removed using laparoscopic surgery
Low-fat diet necessary following surgery
Inflammation of the pancreas
Results in autodigestion of the tissue
Premature activation of pancreatic proenzymes (trypsin, amylase and lipase) which digests the pancreatic tissues = massive inflammation, bleeding & necrosis
May be acute or chronic
Acute Pancreatitis
Acute form considered a medical emergency
Pancreas lacks a fibrous capsule…
Acute Pancreatitis
Destruction may progress into tissue surrounding the pancreas
Substances released by necrotic tissue lead to widespread inflammation
–Hypovolemia and circulatory collapse may follow.
Chemical peritonitis results in bacterial peritonitis.
Acute Pancreatitis
Septicemia may result.
Adult respiratory distress syndrome and acute renal failure are possible complications.
Causes
Acute Pancreatitis
Gallstones
Alcohol abuse
Sudden onset may follow intake of large meal or large amount of alcohol
Acute Pancreatitis: Manifesations
- -Severe epigastric or abdominal pain radiating to the back (primary symptoms) Pain increases in supine position
- -Signs of shock (Caused by hypovolemia d/t inflammation and hemorrhage – low PB, palor, diaphoresis, rapid & weak pulse)
- -Low-grade fever until infection develops (then temperature may then rise significantly)
- -Abdominal distention and decreased bowel sounds (Decreased peristalsis and paralytic ileus)
Diagnostic tests
Acute Pancreatitis
Serum amylase levels—first rise, then fall after 48 hours
Serum lipid levels are elevated.
Hypocalcemia
Leukocytosis
Treatment
Acute Pancreatitis
Oral intake is stopped.
Treatment of shock and electrolyte imbalances
Analgesics for pain relief – NOT MORPHINE – (causes spasm of the sphincter of Oddi)
LIVER PROBLEM PEOPLE
dont have vit k so they bruise easly
there is so much extra uric acid that its fucks with neuro
jaundice - because the liver is not breaking down billirubin
encephalopathy
splenomegaly
portal hypertension
anemia- because liver cant store WBCs and the bofy can use b12 and iron which wont create WBCS
leukopenia- low blood sells that puts them in a risk of infection
gynemomastia -big titties
pruritus
first place you will see jaundice will be in the eyes
every time you see high levels of bilirubin
think of liver
females should always have hemoglobin levels
between 120-160
hepititis is
really inflammation of the liver
when the liver starts to degenerate
it because fibirous and it wont function as well
for ascities
the diuretics will draw the fluid the from the peri cavity into the vascular system so that they can remove the fluid because thats how diuretics work
hep difference between crhrosis
altered taste ad smakk
fever
malaisa
headache
galbladder mani
- sudden severe waves of pain
- nausea and vomiting
- if pain continues, and jundice develops
- +surgical intervention may be mecessarn
clincal manis caused by bile flow (chart)
- jaundice
- dark urine
- cramping
- steatorrhea
