Chapter 14: The Liver, Biliary System, Flashcards Preview

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Flashcards in Chapter 14: The Liver, Biliary System, Deck (53)
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1

End stage liver damage
Diffuse bands of fibrosis and nodular regeneration destroys normal architecture of liver
Fibrosis is mediated by what?
Increased risk of hepatocellular carcinoma (HCC)
60-70% due to EtOH, or viral hepatitis, biliary disease, hemochromatosis
Portosystemic shunts partially alleviate portal HTN: esophageal varices, caput medusae, hemorrhoids

Cirrhosis
TGF-beta from stellate cells underneath the endothelial cells lining sinusoids mediate fibrosis

2

Results of what cause the following?
Esophageal varices (=> hematemesis)
Peptic ulcer
(BOTH cause Melena)
Splenomegaly
Caput medusae
Ascites
Anorectal varices (=> hemorrhoids)

Effects of portal HTN

3

Results of what cause the following?
Hepatic encephalopathy
Scleral icterus
Jaundice
Fetor Hepaticus (breath smells musty)
Liver flap = asterixis (coarse hand tremor)
bleeding tendency (indecreased clotting factors, increased prothrombin time)
anemia
ankle edema
Spider nevi
Gynecomastia
Testicular atrophy

Effects of liver cell failure
(The last 3 are due to hyperestrogenism since damaged liver no longer breaks down estrogen)

4

What does liver cirrhosis look like on CT? Histology?

CT = nodularity of liver contour secondary to regenerating macronodules
Histology = regenerative nodules and bridging fibrosis

5

Decreased ceruloplasmin is seen in?

Wilson disease

6

Increased alk phos is seen in?

Obstructive hepatobiliary disease, hepatocellular carcinoma, bone disease

7

If ALT > AST?

viral hepatitis

8

If AST >ALT?

Alcoholic hepatitis

9

IF increased amylase?

acute pancreatitis or mumps

10

If increased gamma-glutamyl transpeptidase (GGT)?

Increased in various liver and biliary disease (like ALT)
BUT NOT INCREASED in bone disease
Associated with EtOH use

11

Increase lipase?

Acute pancreatitis (Most Specific)

12

Fulminant liver failure and encephalopathy in children with viral illness (which ones?) who take aspirin
Likely related to mitochondrial damage of hepatocytes
Mech: aspirin metabolites decrease beta-oxidation by reversible inhibition of mitochondrial enzyme
WHEN IS THE ONLY TIME A CHILD SHOULD GET ASPIRIN?

S/S: hypoglycemia, elevated liver enzymes, fatty liver, hepatomegaly and nausea w/vomiting, may progress to coma/death

Reye Syndrome

Viruses: VZV, influenza B

Kawasaki disease

13

Reversible change with moderate alcohol intake
Macrovesicular fatty change that may be reversible with EtOH cessation
Accumulation of fat in hepatocytes

Alcoholic liver disease:
hepatic steatosis or fatty liver

14

Requires sustained, long term EtOH consumption
Chemical injury to hepatocytes due to acetaldehyde
Swollen and necrotic hepatocytes w/neutrophilic infiltration
Mallory bodies (damaged cytokeratin filaments, eosinophilic inclusions)

S/S: painful hepatomegaly and liver enzymes?
Seen with binge drinkers

EtOH hepatitis
Increased AST > ALT (ratio > 1.5)

15

Final and irreversible
long term complication of chronic EtOH induced liver damage
Micronodular
Irregularly shrunken liver with "hobnail" appearance
Sclerosis around central vein (zone 3)
jaundice, hypoalbuminemia

EtOH cirrhosis

16

Metabolic syndrome (insulin resistance, obesity) => fatty infiltration of hepatocytes => cellular ballooning and eventual necrosis
May cause cirrhosis and HCC
Independent of EtOH use, diagnosis of exclusion
Liver enzymes?

Non-alcoholic fatty liver disease

Increased ALT > AST (L=lipids)

17

Cirrhosis => portosystemic shunts => decreased NH3 metabolism => neuropsychiatric dysfxn
Spectrum:
Disorientation/mild asterixis to difficult arousal or coma (severe).
Triggers:
Increase NH3 production (due to dietary protein, GI bleed, constipation, infection)
Decreased NH3 removal (due to renal failure, diuretics, post-TIPS)
Treatment?

Hepatic encephalopathy
Treat: lactulose (increases NH4+ generation), low protein diet, and rifaximin kills intestinal bacteria

18

Most common primary malignant tumor of the liver in adults
Associated with Hepatitis B and C, Wilson disease, hemochromatosis, alpha1-antitrypsin deficiency, alcoholic cirrhosis, and carcinogens (aflatoxin from Aspergillus induces p53 mutation)
May lead to Budd-Chiari syndrome
Findings: Jaundice, tender hepatomegaly, ascites, and anorexia, spreads hematogenously
Diagnosis: Increased alpha-fetoprotein, ultrasound or contrast CT

Hepatocellular carcinoma

19

Occlusion of IVC or hepatic veins w/centrilobular congestion and necrosis, leading to congestive liver disease (hepatomegaly, ascites, abdominal pain, and eventual liver failure)
May develop varices and have visible abdominal and back veins. Absence of JVD. Associated with hypercoagulable states, polycythemia vera, pregnancy, and HCC

Budd-Chiari Syndrome

20

Common, benign liver tumor; typically occurs at age 30-50 years. Biopsy contraindicated because risk of hemorrhage

Cavernous hemangioma

21

Rare, benign liver tumor
Subcapsular and grow with estrogen
Associated with oral contraceptive use or anabolic steroid use
Regress upon cessation of drug or could rupture spontaneously and have intraperitoneal bleeding

Hepatic adenoma

22

Malignant tumor of endothelial orgin
Associated with exposure to arsenic, vinyl chloride

Angoisarcoma

23

Result of backup of blood into liver
Commonly caused by R. sided heart failure and Budd-Chiari syndrome
Liver appears mottled
If condition persists: centrilobular congestion and necrosis can result in cardiac cirrhosis

Nutmeg liver

24

Misfolded gene product protein aggregates in hepatocellular ER => cirrhosis with PAS + globules in liver. Codominant trait.
In lung, decrease in this protein => uninhibited elastase in alveoli => decreased elastic tissue => panacinar emphysema

Alpha1-antitrypsin deficiency

25

Earliest sign involves sclera
High serum bilirubin at what level causes symptom?
Occurs 2ndary to increased production of bilirubin or defective metabolism

Jaundice
Bilirubin > 2.5 mg/dL

26

Where and what conjugates bilirubin?
What is urobilinogen all about? What happens to urobilinogen?

The liver
Uridine glucuronyl transferase
Intestinal flora turns Conjugated bilirubin to urobilinogen. Urobilinogen is oxidized to stercobilin (makes stool brown) and urobilin (makes urine yellow)

27

What diseases could cause unconjugated (indirect) hyperbilirubinemia? What would be in the urine?

Hemolytic, physiologic (newborns), Crigler-Najjar, Gilbert syndrome
Increased urine urobilinogen

28

What disease could cause conjugated (direct) hyperbilirubinemia? What would be in the urine?

Biliary tract obstruction: gallstones, pancreatic liver cancer, liver fluke
Biliary tract disease: Primary sclerosing cholangitis, Primary biliary cirrhosis
Excretion defect: Dubin-Johnson syndrome, Rotor syndrome
Decreased urine urobilinogen

29

What diseases could cause mixed (indirect + direct) hyperbilirubinemia? What would be in the urine?

Hepatitis, cirrhosis
Normal or increased urine urobilinogen

30

At birth, immature UDP-glucuronosyltransferase => unconjugated hyperbilirubinemia => jaundice/kernicterus (kernicterus involves severe mental defects etc)

Physiologic neonatal jaundice