Hepatic And Biliary System

Question 1

80 percent of blood supply to the liver

Answer 1

portal vein

Question 2

20 percent of blood supply to the liver

Answer 2

hepatic artery

Question 3

hepatic artery

Answer 3

brings oxygen rich blood

Question 4

portal vein

Answer 4

brings oxygen poor blood from GI containing nutrients and toxins, and blood cells an breakdown products from the spleen

Question 5

sinusoids

Answer 5

transport connection of the liver from portal vein and hepatic artery to thin-walled central veins

Question 6

blood flow of liver

Answer 6

portal vein + hepatic artery > sinusoids > central veins > hepatic veins > inferior vena cava

Question 7

hepatocytes

Answer 7

polygonal shape; large centrally located nucleus, often binucleate cells are present, glycogen granules and lipids present

Question 8

bile canaliculus

Answer 8

channel between two adjacent hepatocytes

Question 9

lobular model

Answer 9

plates of hepatocytes and sinusoids are arranged in a radial pattern around a central vein

Question 10

hepatocyte integrity - serum measurement

Answer 10

Aspartate aminotransferase (AST) and Alanine aminotransferase (ALT)

Question 11

biliary excretory function - serum measurements

Answer 11

bilirubin, alkaline phosphatase, and gamma-glutamyl transpeptidase (GGT)

Question 12

hepatocyte synthetic function - serum measurements

Answer 12

serum albumin and coagulation factors

Question 13

Bile functions

Answer 13

emulsification of dietary fat and elimination of bilirubin

Question 14

liver functions

Answer 14

process nutrients, storage, removal of toxins, syntesis of bile

Question 15

jaundice

Answer 15

serum levels of bilirubin above 2 mg/dL - yellowing of skin and sclera

Question 16

cholestasis

Answer 16

systemic retention of not only bilirubin but also other solutes eliminated in bile (due to impaired bile flow)

Question 17

bilirubin

Answer 17

end product of heme degradation

Question 18

pathogenesis of jaundice

Answer 18

excess bilirubin production, reduced hepatic uptake, impaired conjugation, decreased hepatocellular excretion, or impaired secretion

Question 19

gilbert’s syndrome

Answer 19

increased unconjugated bilirubin (causes jaundice)

Question 20

uridine diphosphate gluconosyltransferase

UGT

Answer 20

help conjugate bilirubin with glucuronic acid at sinusoidal membrane of liver (which is needed to excrete bilirubin)

Question 21

Dubin-Johnson syndrome

Answer 21

increased conjugated bilirubin due to deficiency of bilirubin canalicular transport protein

Question 22

cholestasis

Answer 22

obstruction of bile flow

Question 23

bilirubin metabolism

Answer 23

uptake from circulation > intracellular storage > conjugation with glucuronic acid > biliary excretion

Question 24

kernicterus

Answer 24

brain damage caused by excessive jaundice - high levels of unconjugated bilirubin accumulates in basal ganglia in new born can cause cerebral palsy

Question 25

phototherapy/bilirubin

Answer 25

converts bilirubin into water soluble isomers

Question 26

liver failure

Answer 26

loss of 80% of hepatic functional capacity

Question 27

acute liver failure

Answer 27

sudden and massive hepatic destruction | EX: acetaminophen overdose

Question 28

chronic liver failure

Answer 28

12th most common cause of mortality, progressive liver injury for years

Question 29

cirrhosis

Answer 29

end-stage process - marked by diffuse transformation of the entire liver into regenerating parenchymal nodules surrounded by dense bands of scar and variable degrees of vascular shunting

Question 30

space of Disse

Answer 30

between endothelial cells of sinusoids and hepatocytes....

Question 31

stellate cells

Answer 31

activated in liver fibrosis to produce a dense layer of matrix material that is deposited in the space of Disse

Question 32

Kuppfer cells

Answer 32

activated in liver fibrosis and produce cytokines that contribute to fibrosis and hepatocyte dysfunction and death

Question 33

portal hypertension

Answer 33

increased resistance to portal blood flow. clinical consequences (1) ascites (2) portosystemic venous shunts (3) congestive splenomegaly (4) hepatic encephalopathy

Question 34

ascites

Answer 34

accumulation of excess fluid in the peritoneal cavity

Question 35

portosystemic shunts

Answer 35

reversed flow from portal to systemic circulation by dilation of collateral vessels and development of venous bypass due to rise in portal system pressure.

Question 36

hepatic encephalopathy

Answer 36

cerebral edema and impaired neuronal function due to elevated ammonia levels in blood and the central nervous system

Question 37

caput medusa

Answer 37

abdominal wall collaterals appear as dilated subcutaneous veins extending from the umbilicus toward the rib margins (outcome of portosystemic shunts of portal hypertension)

Question 38

hemorrhoids

Answer 38

veins around and within the rectum (outcome of portosystemic shunts of portal hypertension)

Question 39

esophageal varices

Answer 39

can cause massive hematemesis and death (outcome of portosystemic shunts of portal hypertension)

Question 40

cellular level of cirrhosis

Answer 40

myofibroblasts (activated stellate cells), dense extracellular matrix, loss of fenestration, loss of microvilli, activation of kuptfer cells

Question 41

3 forms of alcoholic liver injury

Answer 41

1. hepatocellular steatosis (fatty change) 2. alcoholic hepatitis 3. steatofibrosis (including cirrhosis)

Question 42

reversible alcoholic liver injury

Answer 42

steatosis and hepatitis

Question 43

irreversible alcoholic liver injury

Answer 43

cirrhosis

Question 44

hepatic steatosis

Answer 44

"fatty liver" accumulation of lipid droplets which distend the hepatocyte and push the nucleus aside. Liver becomes large, soft, yellow and greasy (reversible with abstention from further alcohol)

Question 45

pathogenesis of hepatic steatosis

Answer 45

changes in lipid metabolism and cell injury by reactive oxygen species

Question 46

morphology of hepatic steatosis

Answer 46

fat droplets most prominent where is begins (around the Central Vein) and extends outwards

Question 47

Alcoholic hepatitis morphology

Answer 47

hepatocyte swelling and necrosis, mallory-denk bodies, and neutrophilic reactions

Question 48

mallory-denk bodies

Answer 48

clumped, amorphous, eosinophilic material in ballooned hepatocytes - made up of tangled intermediate filaments such as keratin 8 and 18 in complex with ubiquitin

Question 49

alcoholic steatofibrosis

Answer 49

chicken wire fence pattern of fibrosis

Question 50

micronodular (Laennec) cirrhosis

Answer 50

first described for end-stage alcoholic liver disease, | diffuse nodules on surface, green tint, and microscopically fatty accumulation is "burned out"

Question 51

greenish tint of micronodular cirrhosis

Answer 51

cholestasis

Question 52

Hepatits A transmission

Answer 52

contaminated water and food

Question 53

HAV virus category

Answer 53

non-enveloped, positive strand RNA picornavirus

Question 54

Hep A immunology

Answer 54

IgM appear with onset, followed by IgG anti HAV, creating lifelong immunity

Question 55

HBV virus category

Answer 55

hepadnaveridae DNA virus

Question 56

Hepatitis B transmission

Answer 56

unprotected sex/childbirth transmission

Question 57

Hep B immunology

Answer 57

vaccination induces effective immunity with protective anti HBs antibody response

Question 58

Hep B outcomes

Answer 58

(1) acute hepatitis followed by recovery and clearance, (2) acute hepatic failure, (3) non-progressive chronic hepatitis, (4) chronic ending in cirrhosis, (5) carrier state, (6) hepatocellular carcinoma