Biliary System Part 1

Front 1

6 general liver functions:

Back 1

Excretory/detoxification (in bile); Metabolism; Synthesis; Storage

Front 2

General examples of substances stored in liver

Back 2

vitamin K, iron, copper, fat soluble vitamins, glycogen

Front 3

Examples of substances synthesized in liver

Back 3

albumin, alpha I antitrypsin; proteins of coagulation cascade (fibrinogen, prothrombin, VIII,IX, X, XI, and Xli), bile

Front 4

Liver failure becomes apparent when _______ of liver is destroyed or dysfunctional

Back 4

80%

Front 5

Liver injury results in release of these two major indicators of liver function.

Back 5

Ast (aspartate amlno-transterase) andALT (Alanlne amlno-transferase)

Front 6

7 general signs of liver failure:

Back 6

Jaundice, Hypoalbumenernia, Hepatorenal syndrome, Portal hypertension, Encephalopathy, Endocrine abnormalities, coagulopathy

Front 7

Encephalopathy I liver failure is due to the failure of the liver to remover _________ from the blood.

Back 7

ammonia

Front 8

5 general microscopic/macroscopic responses of liver cells to injury

Back 8

Inflammation, Degeneration, necrosis, fibrosis, cirrhosis

Front 9

2 major functions of hepatic bile

Back 9

elimination of bilirubrin and cholesterol; emulsify dietary fat in the gut

Front 10

_______ occurs if blood bilirubin levels are greater than _______mg/dl.

Back 10

Jaundice, 1.2

Front 11

Jaundice becomes clinically apparent If serum bilirubin Is over _________

Back 11

2.0-3.0 mg/dl.

Front 12

Jaundice is best recognized in the __________.

Back 12

sclera

Front 13

Unconjugated bilirubin: Water insoluble; Tightly bound to albumin; Cannot be excreted In urine

Back 13

Conjugated bilirubin; Water soluble; Non-toxic; Loosely bound to albumin; Can be excreted In urine

Front 14

Which type of bilirubin is tightly bound to albumin?

Back 14

Unconjugated bilirubin:

Front 15

Which type of bilirubin is water soluble?

Back 15

Conjugated bilirubin

Front 16

Which type of bilirubin can be excreted in urine?

Back 16

conjugated

Front 17

Conjugation of bilirubin takes place where?

Back 17

Liver --No Eric, it is not the breast

Front 18

Prehepatic Jaundice is associated with the buildup of ________ bilirubin and the ________of red blood cells.

Back 18

Unconjugated, hemolysis

Front 19

A manifestation of Gilbert's disease is:

Back 19

Prehepatic Jaundice

Front 20

Hepatic Jaundice is seen under what general conditions?

Back 20

viral or drug-induced hepatitis, alcoholic hepatitis, tumors, and cirrhosis

Front 21

T/F Hepatic Jaundice is associated with a buildup of conjugated bilirubin only.

Back 21

False: It is mixed conjugated and unconjugated

Front 22

Conjugated hyperbilirubinemia is manifest in what condition?

Back 22

post-hepatic jaundice

Front 23

post-hepatic jaundice is seen in _________ disorders such as gallstones, tumors of bile ducts, pancreas, or duodenum

Back 23

obstructive

Front 24

_________ is the accumulation of unconjugated bilirubin (usually> 20 mg/dl) in the brain causing severe neurologic damage

Back 24

Kernicterus

Front 25

Kernicterus can be seen in this condition that affects infants:

Back 25

hemolytic disease of the newborn (erythroblastosis fetalis)

Front 26

Jaundice resulting from Predominantly unconjugated hyperbilirubinemia has two general causes: 1. overproduction --> hemolytic anemia or

Back 26

2. Impaired/decreased conjugation • Gilbert’s syndrome; 5-7% of population; benign; no functional derangement; Mild elevation of serum unconjugated bilirubin; • Crigler-Najjar Syndrome;Type I fatal, complete lack of enzyme for conjugation; Type 2 non-fatal, partial defect In conjugation; very yellow skin

Front 27

Jaundice resulting from Predominantly conjugated hyperbilirubinemia: Impaired hepatic excretion; • Dubin-Johnson syndrome (hereditary enzyme defect) • Benign; episodic jaundice; black liver grossly • Rotor syndrome (hereditary enzyme defect) • Asymptomatic; liver non-pigmented

Back 27

Jaundice resulting from Predominantly conjugated hyperbilirubinemia: Cholestasis— results from hepatocellular dysfunction or obstruction (gallstones, strictures, neoplasms) Signs and symptoms: pruritis; skin xanthomas; elevated serum alkaline phosphatase Micro: Accumulation of pigment within the parenchyma; bile duct proliferation; portal tract fibrosis; “wispy hepatocytes” due to bile accumulation within the cell

Front 28

Additional causes of jaundice:

Back 28

antifungals, high amounts of beta-carotene, medications

Front 29

3 morphologic changes from liver failure:

Back 29

A. chronic liver disease --> cirrhosis; B. Hepatic dysfunction without necrosis (Reye’s, acute fatty liver of pregnancy); C. Massive acute hepatic necrosis (viral or drug hepatitis; direct toxic damage ----acetaminophen overdose, mushroom or carbon tetrachloride)

Front 30

Elevated ammonia levels in the blood from liver failure that lead to disturbances in consciousness ranging from behavioral abnormalities to coma is called:

Back 30

hepatic encephalopathy

Front 31

Hepatorenal syndrome:

Back 31

liver fails--> kidneys fail drop in urine output, increase in urea nitrogen/creatine levels (in end-stage liver disease)

Front 32

______ is synonymous with end-stage liver disease

Back 32

Cirrhosis

Front 33

T/F Cirrhosis is among the top ten causes of death I western society.

Back 33

TRUE

Front 34

Causes of cirrhosis include:

Back 34

60% from alcohol abuse; 10% viral; 10% blllary tract; diseases/obstructive disorders; 20% autoimmune, drug Induced, hereditary, and cryptogenic (indeterminate cause)

Front 35

Cirrhosis may take one to ___ years to develop.

Back 35

20

Front 36

What is the major pathologic process that accompanies cirrhosis?

Back 36

progressive fibrosis (regenerative firm nodular surface)

Front 37

Pathologic process of necrosis:

Back 37

Necrosis of liver cells; Fibrosis; (fibrous band scars inhibit regeneration); Parenchymal nodules (regeneration of encircled hepatocytes); Disruption of entire liver architecture— irregularly shaped, shrunken, firm, nodular

Front 38

________ occurs with changes within the liver itself.; ________ occurs with changes within the biliary tree.

Back 38

portal cirrhosis; biliary cirrhosis

Front 39

The presence of fibrosis and nodularity impedes blood flow in the liver and is one of the major causes of _____ ____________.

Back 39

portal hypertension

Front 40

T/F Patients with cirrhosis have an increased risk of death from the following:; a. progressive liver failure b. complications of portal hypertension c. hepatocellular carcinoma

Back 40

A. True; B. True; C. True

Front 41

T/F portal hypertension leads to:; A. ascites; B. Spleenomegaly; C. formation of anastamoses (shunts) between the portal and systemic circulation; D. Hepatic encephalopathy E. Undeniable urge to smoke barkies

Back 41

A. True; B. True C. True D. True E. False (except for individuals from low educational and rural backgrounds)

Front 42

Esophageal varices are a result of:

Back 42

formation of anastamoses (shunts) between the portal and systemic circulation (a result of portal hypertension)

Front 43

Inflammatory Disorders of the liver:

Back 43

• Viral hepatitis • Fulminant hepatitis • Autoimmune hepatitis • Liver abscesses

Front 44

Morphologic changes seen with viral hepatitis; • Ballooning degeneration of hepatocytes; • Necrosis of hepatocytes (councilman bodies) are shrunken eosinophilic apoptotic anuclear fragments of hepatocytes)

Back 44

Morphologic changes seen with viral hepatitis; • Bridging necrosis of lobules • Inflammation of portal tracts; macrophages; Kupffer cells proliferate

Front 45

Morphologic changes seen with viral hepatitis • Hepatitis B— ground glass hepatocytes— due to accumulation of HBsAg; sanded nuclei due to abundant HBcAg

Back 45

Morphologic changes seen with viral hepatitis • Hepatitis C-fatty change of hepatocytes; lymphoid aggregates • “Piecemeal necrosis”—periportal necrosis In chronic hepatitis

Front 46

With viral hepatitis, what is the timeline established for acute vs. chronic infection?

Back 46

acute = resolves within 6 months; chronic = > 6 months

Front 47

__ ________hepatitis carriers in US; 1 in __ patients is a carrier

Back 47

4 million; 70

Front 48

What may be one of the first signs of hepatitis?

Back 48

Dark urine

Front 49

characteristics of fulminant hepatitis include:

Back 49

severe acute iiver damage, encephalopathy, coaguiopathy with high risk of death approaching 80%

Front 50

fulminant hepatitis develops within _____ weeks of the onset of liver disease.

Back 50

8

Front 51

Symptoms of Hepatitis:(not always evident)

Back 51

Jaundice of skin and eyes; Dark urine ;Fatigue;Nausea;Abdominal pain;Vomiting

Front 52

Hepatits A: • Transmission by fecal-oral route • Virus In blood, saliva, feces 2-3 weeks before any clinical (flu-like) symptoms • 30-40% of U.S. shows evidence of infection • Blood donations not screened for Hepatitis A

Back 52

Hepatits A: • Mild—often undiagnosed • incubation avg. 25 days, infectious for 4-6 weeks • Usual outcome: no chronic liver disease, no carrier state, immunity

Front 53

Hepatitis B •Transmitted by blood or body fluids (semen, saliva) • Increased risk: multiple sexual partners, iv drug use 50-100 times more infectious than HIV • Incubation time avg.—-75 days • Can remain infective on operatory surfaces up to 7 days, cold sterilization ineffective

Back 53

Hepatitis B • U.S. prevalence—O.5%; approx 1.5 million carriers • Can develop into chronic disease in 2- 10%. -->cirrhosis and liver cancer • Virus does not kill cells directly but activates immune cells --> inflammation and liver damage

Front 54

Hepatitis B • Can acquire infection from needle sticks, contaminated surfaces, splashes to eye or oral mucosa, percutaneously through cuts or breaks in skin, contact with infected saliva • Dentists considered a high risk category • Infection prevalence among general dentists 7-9%; oral surgeons—21% •9 documented cases of transmission from dental provider to patient over past 30 years

Back 54

Hepatitis B • Only DNA virus among the hepatitis viruses thus far • Vaccine has been available since 1982. Highest rate of sero-conversion in the youngest age groups • Vaccine Is 95% effective in preventing chronic infections • 116 countries now have Hep. B vaccine as part of their routine immunizations