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Hepatobiliary System Review

Quick Review for Pathopharm
by

Ben Rieke

on 18 October 2013

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Transcript of Hepatobiliary System Review

The Hepatobiliary Sytem
Starring!
LIVER
GALLBLADDER
Functions of the Liver
There are over 500 functions
Synthesis of bile salts,
bilirubin excretion
, storage of blood, synthesis of bioactive cholesterol, gluconeogenesis, glycogenolysis,
hormone clearance
,
detoxification of thousands of substances
, ketogenesis, lipid storage, lipogenesis, lipoprotein synthesis, mineral storage,
plasma protein synthesis
, transamination of amino acids,
urea synthesis
, synthesis of bioactive vitamin A, and fat soluble vitamin storage
How?
Liver lobule
Arterial blood enters from vascular structures in the liver called sinusoids. The sinusoids are lined with thin epithelium, which allows for easy osmotic permeability.
Rows of hepatocytes border the sinusoids and remove materials from the blood as it flows past
The hepatocytes then release modified excretions back into the blood
Glucose, fats, vitamins, non-toxic metabolites
Venous blood then returns to the hepatic portal vein via the central vein of the liver lobule. Each liver lobule has its own central vein.
Bile is secreted by hepatocytes into biliary canaliculi. Bile is rich in fatty-acid salts made from cholesterol.
Bile drains into the bile ducts, which lead to hepatic duct. This duct then drains into the distally located cystic duct, and on into the gallbladder for storage.
KUPFFER CELLS!
Supported by
THE BILLIARY DUCTS
&
HEPATIC PORTAL SYSTEM
Destroys old cellular components and foreign bodies, like old platelets
The Gallbladder: Form and Function
The gallbladder is sack-like muscular structure attached to the posterior aspect of the liver's right lobe.The gallbladder stores excess bile. It has numerous rugae, like the urinary bladder and stomach, to allow for expansion. Contraction of the gallbladder forces bile into the cystic duct and out to the common bile duct. Cholecystikinin is responsible for triggering this contraction. Bile then enters the small intestine to aid in lipid digestion.
Sphincter of Oddi
Pathologies of the Hepatobiliary System
Liver:
-
Hepatitis
A,B,C,D,E,G
-
Cirrhosis
Portal hypertension
Obstructive Jaundice
Esophageal varices
Ascites
Hepatic encephalopathy
Gallbladder:
-
Cholelithiasis
chronic vs. acute
-Cholecystitis
Hepatitis A (HAV)
Hepatitis B (HBV)
Hepatitis C (HCV)
Hepatitis D (HDV)
Hepatitis E (HEV)
HEPATITIS
Transmitted F->O; incubation period of 15-50 days.
Does not cause chronic infections
like other hepatitis viruses. Most infectious during 2 weeks before onset of symptoms, and is infectious until
1-2 weeks after symptoms appear.
There is a vaccine available for HAV.
Transmitted percutaneously, transmucosally and by sexual contact.
Much more infectious than HIV
, can live on dry surface >7 days. Causes chronic infection; >90% of infants infected develop chronic infection.
No specific treatment is available
- interferons and antiviral medication may help.
A vaccine is available for HBV.
Transmitted percutaneously-
most commonly by needle sharing
. Vary rarely spread sexually. Incubation 14-180 days.
Commonly causes chronic hepatitis
(85% of cases). Tends to be more infective (with more sequelae) with concurrent HIV infection. Treatment similar to HBV.
No vaccine is available for HCV
.
Also called 'delta virus'. Transmitted percutaneously, but is a
concomitant infection of HBV.

Can cause infection only when HBV is present. Incubation 2-26 weeks.
HBV-HDV infection increases risk of developing fulminant hepatitis
. HIV-HBV-HDV infection is very serious.
No vaccine is available for HDV
,
but vaccination against HBV sufficiently protects against HDV
Transmitted F->O; common in developing countries,
associated with contaminated water
. Incubation of 15-64 days.
Rare in the USA
. No common tests are available, so blood/biopsies must be sent to gov. labs for confirmation.
No vaccine or treatment is available for HEV at this time.
Symptom Cluster for Hepatitis Infection
Anorexia, N/V/D, malaise, headache, fever, arthralgia, weight loss,
hepatosplenomegaly
,
jaundice
, pruritis,
bilirubinuria
,
clay-colored stool
, abdominal tenderness or pain in the RUQ.
Labs show elevated ALT/AST, elevated serum unconjugated bilirubin, and prolonged PTT
Jaundice and Icterus
Pale, clay-colored stool
Bilirubinuria
CIRRHOSIS
Portal Hypertension
Obstructive Jaundice
Characterized by loss of function, inflammation, and fibrous thickening of the tissue of the liver
May be caused by alcohol abuse, hepatitis, and various other conditions
Hepatic Encephalopathy
Ascites
Esophageal Varicies
Structural changes in the liver from the cirrhotic process compress and destroy the portal and hepatic veins and sinusoids. This causes obstruction of the normal flow of blood through the portal system, resulting in portal hypertension
Characterized by increased venous pressure in the portal circulation, as well as splenomegaly, large collateral veins, ascites, systemic hypertension, and gastric and esophageal varices
Caused by decreased or obstructed flow of bile through the liver or biliary duct system
Bilinogen wastes 'back up' and cannot be eliminated in the feces or urine
A toxic encephalopathic condition characterized by excessive serum ammonia levels. Liver damage causes ammonia to enter the systemic circulation without liver detoxification.
The ammonia crosses the blood-brain barrier and produces neurologic toxic manifestations: insomnia, lack of awareness or concentration, personality changes, confusion, depression, lethargy, drowsiness, disorientation, inappropriate behavior, incomprehensible speech, loss of consciousness, seizure and coma
Accumulation of serous fluid in the peritoneal or abdominal cavity
With portal hypertension, proteins shift from the blood vessels via the larger pores of the capillaries into the lymph space. The lymphatic system cannot accomodate all of this fluid, and so they leak through the liver capsule into the peritoneum. The osmotic pressure of the proteins pulls additional fluid into the peritoneal cavity. May also be caused
by hypoalbuminemia.
Complex of tortuous veins at the lower end of the esophagus, enlarged and swollen as a result of portal hypertension. Gastric varices are located in the upper portion (cardia, fundus) of the stomach
Varices may rupture and bleed in response to ulceration and irritation. Bleeding esophageal varices are the most life-threatening complication of cirrhosis, with massive hemorrhage presenting a medical emergency
Cholelithiasis
Cholecystitis
Develops when the balance that keeps cholesterol, bile salts, and calcium in solution is altered so that precipitation of these substances occurs
Stones may remain in the gallbladder or migrate to the cystic duct or common bile duct. They cause pain as they pass through the ducts, and may lodge in the ducts, producing obstruction. Small stones are more likely to cause obstruction
Commonly associated with obstruction caused by gallstones or biliary sludge. May also be caused by trauma, surgery, and rarely from significant diet change, prolonged immobility, and diabetes
Inflammation may be confined to the mucous lining or involve the entire wall of the gallbladder. During an acute attack of cholecystitis the gallbladder is edematous and hyperemic. Very painful; sharp colicky pain in the RUQ.
REFERENCES
Lewis, S. L., Dirksen, S. R., Heitkemper, M. M., Bucher, L., & Camera, I. M. (2011). Nursing management: Liver, pancreas, and biliary tract problems. Medical-Surgical Nursing: Assessment and Management of Clinical Problems (8th ed., pp. 1058-1101). St. Louis, MO: Elsevier.

Taylor, M. F.The gastrointestinal system. Human Anatomy and Physiology: Part Two (2nd ed., pp. 160-188). Waco, TX: Baylor University Press.
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