Exam 1: Liver Flashcards
what is a lobule
functional unit of the liver
what are hepatocytes
liver cells that produce and secrete bile
what does bile do
bile stimulates peristalsis and breaks down fats in the intestine
what are canaliculus
channels between hepatocytes that drain bile into the common bile duct into the duodenum and gal bladder
hepatic artery
carries oxygenated blood into the liver
portal vein
carries unoxygenated blood high in nutrients from GI tract into the liver
what is the portal vein’s main responsibility
provides energy for the liver
NUTRIENTS TO LIVER
where do all visceral veins drain
into the portal vein
sinusoids
venous caps of the liver between hepatocytes which carry blood to hepatic vein
where are kupffer cells found
line sinusoids
what do kupffer cells do
act as macrophages to destroy old WBC’s, RBC’s and bacteria
hepatic vein
carries blood from sinusoids to the inferior vena cava
what is the metabolism of bilirubin chain
old RBCs break down in blood stream->
heme breakdown produces unconjugated bilirubin in blood->
bilirubin circulates through liver and is conjugated in the hepatocytes->
bilirubin leaves liver in bile via the hepatic duct->
excreted into duodenum->
excreted via feces
what does bile contain
h2o, electrolytes, bile acids, cholesterol, bilirubin
where does bile drain into
small intestine (duodenum)
most acids that are secreted into the duodenum are what
reabsorbed back into the blood
400-800ml is produced a day in an adult
bilirubin must be what to exit the blood
Conjugated… water soluble
what is jaundice
symptom of liver disease caused by hyperbilirubinemia (excess bilirubin in blood)
Leads to deposition of bile pigment in skin and sclera
what are the 3 types of jaundice
- hemolytic jaundice
- intrahepatic obstructive jaundice
- extrahepatic obstructive jaundice
hemolytic jaundice
excessive lysis of RBC
liver cannot keep up conjugating which leads to increased unconjugated bilirubin buildup in blood
intrahepatic jaundice
(damage to liver)
hepatocellular damage, so liver cannot conjugate or excrete bilirubin
increased unconjugated bilirubin buildup in blood
extrahepatic obstructive jaundice
(outside liver)
bile duct obstruction (galstone) so bile cannot get through
leads to increased CONJUGATED bilirubin to accumulate in liver and bloodstream
extrahepatic jaundicce can lead to what
intrahepatic obstructive jaundice due to backup
hepatitis
inflammation of liver
can lead to degeneration and scarring, necrosis of hepatocytes
onset of hep A
acute, sudden
onset of hep B
insidious, gradual
source of infection for hep a
contaminated food/water
poor sanitation
source of infection for hep b
blood- needles, sexual contact
mode of transmission hep A
fecal-oral route and blood
mode of transmission hep b
body fluids- blood, semen, saliva
chronic state hep A
none, self-limiting
chronic state hep B
yes- clinical mani for 6+ months
diagnosis of hep ABC
HAV antigen and antibodies
clinical mani of hep A
Fever malaise anorexia nausea jaundice
clinical mani of hep B
anorexia malaise joint aching abdominal pain jaundice may lead to liver failure
onset of hep C
insidious
what are the mani of hep C
fatigue, can progress to permanent liver damage
who is at risk for hep C
those with history of snorting/injecting drugs and receiving blood before 1992
mode of transmission hep C
blood only
biliary atresia definition
CONGENITAL malformation (incorrect development in utero)
absence or obstruction of common bile duct (ends in pouch)
what is the patho of biliary atresia
atresia leads to plugging, inflammation, fibrosis of bile canaliculi
no drainage of bile-> backs up-> damages hepatocytes
diagnosis of biliary atresia
increased serum direct bilirubin
increased serum liver enzymes
clinical mani of biliary atresia
jaundice
hepatomegaly
acholic (clay colored stools)
Cirrhosis of liver
chronic liver disease (failure) marked by degeneration of hepatocytes
(inflammation, fibrosis, and scarring)
etiology of chrrhosis
- alcholism : breaks down to acetaldehyde which damages hepatocytes
- hepatitis
decreased amino acids because hepatocytes cant keep up leads to
wasting of body tissues
decreased albumin synthesis and decreased levels in the blood stream leads to
edema, ascites (enlarged abdomen), and pleural effusion
decreased synthesis of blood clotting compounds (fibrinogen and prothrombin) leads to
bleeding: ecchymosis epistaxis blood in urine and stool gums bleeding petachiae
decreased conversion of glycogen fats and amino acids to glucose leads to
hypoglycemia
weightloss
fatigue
confusion
decreased detox of drugs leads to
drowsiness, coma
decreased conversion of ammonia to urea leads to
(ammonia cant leave body and screws with brain)
hepatic encephalopathy= personality changes, confusion and coma
increased bilirubin leads
jaundice
dark red/brown urine
acholic stools
pruritis
portal hyper tension leads to
blood back up:
ascites, splenomegaly, caput medusa, esophageal varicies
why does esophageal varicies happen with liver failure
increased pressure builds up in esophageal blood vessels so it ruptures easily, massive hemorrhage and you bleed into airway
liver enzymes in chronic liver failure
increased: LDH ALT AST ALP these are released from damaged hepatocytes
what proteins are decreased in liver failure
albumin and pre-albumin
which two products build up in blood in liver failure
ammonia and bilirubin
