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LIVER Flashcards

1
Q

What is hepatic steatosis? Steatohepatitis? What are the major causes?

A

hepatic steatosis: fatty changes in the liver

steatohepatitis: fatty liver with inflammatory changes

from alcohol consumption –> alcoholic steatohepatitis

microvesicular (small droplet) or macrovesicular (large droplet)

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2
Q

What is this section? What is A-D?

A

normal liver histology

A: bile duct

B: hepatic artery

C: hepatic vein

D: central vein

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3
Q

What type of cell death is caused by hepatic artery thrombosis?

A

necrosis

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4
Q

What type of cell death is caused by hepatic ischemic injury?

A

necrosis

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5
Q

What type of cell death is caused by viral hepatitis?

A

apoptosis

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6
Q

What is the time course of acute liver failure?

A

failure within 6 months

  • fulminant liver failure < 2 weeks from onset*
  • sub-fulminant liver within 3 months*
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7
Q

What are common causes of acute liver failure?

A

drugs (acetaminophen)

toxin ingestion

viruses

autoimmune hepatitis

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8
Q

What does this histology section suggest?

A

acetaminophen toxicity in hepatic tissue

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9
Q

What are major causes of chronic liver failure?

A

alcohol, non-alcoholic steatohepatitis, viruses, autoimmune hepatitis, biliary disease, genetic metabolic diseases

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10
Q

What does this histology section suggest?

A

cirrhosis

trichrome stain

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11
Q

What does this histology section suggest?

A

steatohepatitis

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12
Q

What does this histology section represent?

A

mallory bodies in alcoholic hepatitis

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13
Q

What are the three ways that fatty acids can get into the liver?

A

1) peripheral adipose tissue breakdown (FFAs enter from systemic circulation)
2) dietary intake (portal circulation)
3) de novo synthesis in hepatocytes from acetyl-CoAs

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14
Q

What are major causes of macrovesicular fatty changes in liver?

A

nutritional: obesity, parenteral nutritions, intestional bypass surgery
metabolic: diabetes, hyperlipidemia, Wilson’s disease

drug-related: alcohol, corticosteroids

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15
Q

What are major causes of microvesicular fatty changes in the liver?

A

acute fatty liver of pregnancy, Reye’s syndrome, tetracycline toxicity

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16
Q

What is cryptogenic cirrhosis?

A

cirrhosis that cannot be explained by HBV, HCV, alcoholism, genetic diseases, etc.

major cause: non-alcoholic steatohepatitis

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17
Q

What level of alcohol consumption increases risk of cirrhosis?

A

40-60 g daily

steady daily drinking more harmful, but regular binge drinking also bad

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18
Q

How is ethanol oxidized for elimination?

A

ethanol –(ADH)–> acetaldehyde –(ALDH2)–> acetate

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19
Q

What are the three major pathways of ethanol metabolism?

A

1) oxidation of ethanol by alcohol dehydrogenase
2) microsomal ethanol oxidizing system (via a CYP)
3) catalase mediated (via catalase)

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20
Q

What is the effect of genetic variation in alcohol dehydrogenase?

A

more common in Chinese/Japanese populations

ethanol is converted rapidly to acetaldehyde but is not quickly metabolized to acetate

leads to flushing, palpitations, sweating

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21
Q

What are the major metabolic effects of alcohol?

A

increased lipoprotein synthesis

increased serum triglycerides

increased liver triglycerides

increased blood and tissue acetaldehyde

increased testosterone breakdown

increased drug metabolism

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22
Q

What are the three stages of alcoholic liver disease?

A

1) hepatic steatosis
2) alcoholic steatohepatitis
c) cirrhosis

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23
Q

What are mallory bodies?

A

bodies composed of intermediate filaments plus ubiquitin that are common in centrizonal areas of alcoholic hepatitis

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24
Q

What is the mechanism of fibrosis in alcoholic steatohepatitis?

A

stellate cell activation

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25
Q

What is the continuum of fibrosis in alcoholic injury?

A

1) pericellular fibrosis (around hepatocytes and central veins)
2) perivenous fibrosis
3) portal fibrosis
4) septal fibrosis

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26
Q

What type of cancer is associated with alcoholic cirrhosis?

A

hepatocellular carcinoma

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27
Q

How do liver cells die?

A

necrosis, apoptosis

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28
Q

Can you distinguish alcoholic from nonalcoholic steatohepatitis by a liver biopsy?

A

nope

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29
Q

How does obesity/metabolic syndrome cause liver injury?

A

buildup of triglycerides in hepatocytes, plus esterification of fatty acids and/or reactive oxygen specias causes inflammation which leads to steatohepatitis

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30
Q

How is ethanol metabolized?

A

ethanol –> acetaldehyde –> acetate

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31
Q

What is total body iron in normal individuals?

A

3-5 g

35% stored in ferritin, 65% in hemoglobin

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32
Q

What is the form of iron in the body in iron overload conditions (ex. hemochromatosis)?

A

iron deposits in various tissues (liver, heart, pancreas), stored as ferritin or aggregated ferritin (hemosiderin)

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33
Q

How is iron absorption regulated?

A

absorbed in intestinal mucosal cells, physiologically regulated

only about 10% of daily iron is absorbed to maintain iron balance and make up for daily iron loss

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34
Q

How is iron excreted from the body?

A

via desquamated/dead cells

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35
Q

What is the major iron storage compound in the body? Where in the body is it stored?

A

ferritin

stored in liver (Kupffer cells, hepatic parenchymal cells), reticuloendothelial system, bone marrow, muscle

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36
Q

What does a serum ferritin level of < 10 ug/L indicative of?

A

iron deficiency

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37
Q

What is a ferritin level of > 300 ug/L (in men) or > 200 ug/L (in women) indicative of? What is the major risk of an iron level > 1000 ug/L?

A

indicative of iron overload (hemochromatosis)

> 1000 puts patients at risk of cirrhosis

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38
Q

What is hemochromatosis?

A

a group of disorders where there is a progressive increase in total body iron stores + a deposition of iron in the parenchymal cells of the liver, heart, pancreas, and other organs

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39
Q

What genetic mutation is associated with primary (hereditary) hemochromatosis?

A

hemochromatosis (HFE) gene C282Y mutation

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40
Q

What is the triad of symptoms associated with hemochromatosis?

A

diabetes mellitus (pancreas)

hyperpigmentation (bronzing of skin)

cirrhosis of liver (secondary to iron overload)

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41
Q

How is hemochromatosis diagnosed?

A

increased total body iron stores (esp in parenchymal cells) in absence of other known causes of iron overload

can also identify the HFE C282Y mutation

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42
Q

What is hepcidin? How does it function?

A

a peptide hormone produced by the liver that regulates body iron metabolism

it controls extracellular iron concentrations by binding to and degrading cellular iron exporter ferroportin

hepcidin levels inversely related to iron absorption –> low hepcidin means iron absorption cannot be stopped

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43
Q

What is the mechanism of tissue injury in iron overload?

A

excess iron deposited in lysosomes as hemosiderin –> leads to increased acid hydrolase activity and lysosomal fragility –> release of lysosomal enzymes –> cell death –> fibrosis

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44
Q

What tests are used to diagnose hemochromatosis?

A

invasive: liver biopsy and measurement of iron concentration (most reliable, but not often feasible)

non-invasive: serum iron concentration high, elevated transferrin saturation, elevated seurm ferritin, screen for HFE mutations

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45
Q

How is hemochromatosis managed?

A

goal = keep transferrin saturation below 55%

weekly phlebotomy to remove iron, medicinal leeches, desferrioxamine B (chelating agent) injected twice daily

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46
Q

What is PiMM vs. PiZZ?

A

variations of alpha-1 antitrypsin genes

PiMM is normal PiZZ is abnormal

homozygous PiZZ leads to risk of developping liver disease and emphysema

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47
Q

What is the function of wild type alpha-1 antitrypsin? How is it produced and circulated?

A

a serum protease inhibitor that inhibits elastase, trypsin, chymotrypsin, thrombin, and bacterial proteases to prevent lung damage

produced by the liver and then secreted into the blood where it travels to the lung

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48
Q

What is the mechanism of damage associated with mutant alpha-1 antitrypsin?

A

1) mutant protein cannot be secreted from hepatocytes, so it accumulates and leads to hepatitis and cirrhosis
2) protein cannot reach lungs, leading to emphysema from failure to prevent lung damage

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49
Q

What is the pathophysiology of Wilson’s disease?

A

excessive accumulation of copper in tissues due to increased absorption or decreased elimination in feces

very low ceruloplasmin levels

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50
Q

What is the genetic cause of Wilson’s disease?

A

genetic defect in ATP7B, which encodes a copper-transporting ATPase 2

normally transports copper into bile and plasma and attaches copper to ceruloplasmin

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51
Q

What are the clinical manifestations of Wilson’s disease?

A

liver: cirrhosis, chronic inflammation
brain: degeneration and cavitation of putamen, globus pallidus, caudate nuclei, thalamus, brain stem
eye: Kayser-Fleisher rings

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52
Q

What are the treatments for Wilson’s disease?

A

oral chelation therapy with D-penicillamine or trientine

zinc administration (blocks copper absorption

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53
Q

What type of virus is Hep A? How is it transmitted?

A

RNA

food-borne, water-borne, shellfish, possible sexual transmission, fecal-oral

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54
Q

What type of virus is Hep E? How is it transmitted?

A

RNA

fecal-oral, possible sexual transmission, water-borne epidemics

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55
Q

What type of virus is Hep B? How is it transmitted?

A

DNA

sexual, transfusion, needle stick, drug abuse, etc.

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56
Q

What type of virus is Hep C? How is it transmitted?

A

RNA

sexual, transfusion, needle-stick, drug abuse, etc.

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57
Q

What type of virus is Hep D? How is it transmitted?

A

RNA (needs HepB antigen to infect)

sexual, transfusion, needle-stick, drug abuse, etc.

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58
Q

What serotypes of hepatitis are likely to cause chronic changes?

A

Hep C most likely, also Hep B (and subsequently Hep D)

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59
Q

What types of hepatitis can cause hepatocellular carcinomas?

A

Hep B and Hep C (when chronic)

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60
Q

What is the hepatitis B virion?

A

dane particle (encodes a bunch of proteins that cause disease)

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61
Q

What antibodies are associated with HBsAg? HBcAg? HBeAg?

A

HBs: IgM and IgG anti-HBsAg

HBc: IgM and IgG anti-HBcAg

HBe: anti-HBeAg

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62
Q

What Hep C genotype is associated with hepatic steatosis?

A

genotype 3

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63
Q

What are the lab characteristics of chronic Hep C?

A

elevated ALT, AST, and HCV RNA in serum

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64
Q

How is Hep A replicated?

A

replicates in intestinal mucosa first, then liver parenchymal cells

increase in IgM at onset that lasts for months, increase in IgG at onset that lasts for life

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65
Q

What is the pathology of acute viral hepatitis?

A

lobular disarray –> smudging of cellular outlines

ballooning and acidophilic hyaline bodies

focal hepatic necrosis

lymphocytic parenchymal and portal inflammation

cholestasis

kupffer cell and macrophage hypertrophy/hyperplasia

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66
Q

What is the clinical presentation of acute viral hepatitis?

A

malaise, fatiguability, nausea, fever, muscle joint pains, jaundice phase

ALT and AST increased

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67
Q

What is the clinical course of acute hep A and hep E?

A

rarely becomes fulminant hepatitis, no chronicity

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68
Q

What is the chronic carrier state of acute viral hepaitis?

A

persistence of Hep B as an asymptomatic carrier

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69
Q

What is the progression of chronic hep B?

A

asymptomatic carrier –> chronic hepatitis –> cirrhosis of liver –> hepatocellular carcinoma

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70
Q

What phase of infection is suggested by IgM anti-HAV? IgG?

A

IgM: acute hep A

IgG: recovered, immunity

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71
Q

What is the significance of anti-HbsAg? Absent antibody in the presence of hep B infection?

A

anti-HbsAg: total recovery, immune to HBV

absent: acute disease/chronic carrier

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72
Q

What is the significance of IgM anti-HBcAg? IgG?

A

IgM: acute HBV

IgG: past exposure, cured or carrier

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73
Q

What are major causes of chronic hepatitis?

A

hep B, hep C, autoimmune hepatitis, drug-induced hepatitis, metabolic disorders

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74
Q

What type of hepatitis is suggested by ground glass cells in liver?

A

hepatitis B infection

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75
Q

What type of hepatitis is suggested by lymphoid follicles in portal areas, fatty change and bile duct damage?

A

hep c infection

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76
Q

What type of hepatitis is suggested by cholestasis, eosinophilic infiltration, bile duct damage, granulomas?

A

drug-induced hepatitis

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77
Q

What type of hepatitis is suggested by prominent plasma cell infiltrate?

A

autoimmune hepatitis

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78
Q

What does this section suggest?

A

iron accumulation

  • brown pigment on left = iron*
  • blue pigment on right = hemosiderin stain*
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79
Q

What do these sections suggest?

A

alpha-1 antitrypsin mutation

  • top image = round inclusions of mutated protein*
  • bottom image = prominent round deposits, cirrhotic scars*
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80
Q

What does this section suggest?

A

Wilson disease

glycogenated nuclei, steatosis

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81
Q

What does the section on the right suggest?

A

chronic portal inflammation associated with chronic viral hepatitis

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82
Q

What diagnosis does this section suggest?

A

chronic hep B

ground-glass hepatocytes

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83
Q

What does this section suggest?

A

cirrhosis (nodular)

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84
Q

What is the dietary composition of fat? How much of it is absorbed?

A

diet: triacylglycerol, cholesterol esters, phospholipids, unsaturated fatty acids, fat soluble vitamins

almost all (98%) is absorbed

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85
Q

What is the structure of a triglyceride?

A

glycerol backbone + three fatty acids

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86
Q

What is a saturated vs. unsaturated fatty acid?

A

saturated = no double bonds

unsaturated = 1+ double bonds

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87
Q

Lingual and gastric lipases hydrolyze __________ from triacylglycerol, generating ____________

A

one fatty acid; diacylglycerol and one free fatty acid

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88
Q

Pancreatic lipases hydrolyze __________ from triglyceride to generate ______________.

A

2 faty acids; 2-monoacylglyerol plus 2 free fatty acids

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89
Q

How does bile get into the intestine?

A

liver makes bile –> stored in gallbladder until a meal –> gallbladder contracts causing bile to enter the duodenum through the sphincter of Oddi

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90
Q

How do bile salts act on fats?

A

promote formation of mixed micelles to the brush border of the intestinal mucosal cells

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91
Q

What happens to fat after it reaches enterocytes?

A

taken up into enterocytes by passive diffusion –> long-chain fatty acids resynthesize triglycerides –> packaged with ApoB48 + cholesterol esters + phospholipids into chylomicrons and transfered to lymphatics via exocytosis

short and medium chain fatty acids are absorbed directly into portal circulation

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92
Q

Describe enterohepatic circulation of bile acids.

A

bile salts transfer lipids to enterocytes and then remain in intestinal lumen –> some get passively reabsorbed, most are taken up in the ileum (via a transporter), some are lost to fecal excretion (5%)

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93
Q

Where are bile salts reabsorbed?

A

small intestine (ileum)

colon

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94
Q

How is bile acid synthesis regulated?

A

bile acids bind to a nuclear receptor (FXR) in intestine in liver –> triggers cascade that suppresses an enzyme that makes bile acids (CYP7a1) and releases FGF19 (suppresses bile acid synthesis)

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95
Q

Which one of the following statements is true? Digestion of triglycerides by pancreatic lipase:

a) produces 2-monoacylglycerol (MAG) and free fatty acids
b) yields products which are less soluble in water than the triglycerides
c) requires fatty acyl-CoA before lipase can attack the triglycerides
d) produces only glycerol and short-chain fatty acids
e) is followed by simple diffusion of the digestion products and released into the portal circulation

A

a) produces 2-monoacylglycerol (MAG) and free fatty acids

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96
Q

Which one of the following statements is true? Bile salts act to:

a) emulsify dietary lipids and form chylomicrons
b) aid in the absorption of short-chain fatty acids
c) prevent resynthesis of triglycerides in the enterocyte
d) convert VLDL particles to LDL particles
e) emulsify triglycerides and form mixed micelles

A

e) emulsify triglycerides and form mixed micelles

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97
Q

Which of the following is not true of bile?

a) the major organic molecules in bile are bile acids, cholesterol, and phospholipids
b) hepatic bile is more concentrated than gallbladder bile
c) excretion in bile is a major source of elimination of cholesterol from the body
d) cholecystokinin stimulates the release of bile into the duodenum after a fatty meal
e) an excess of biliary cholesterol relative to bile acids and phospholipids promotes gallstone formation

A

b) hepatic bile is more concentrated than gallbladder bile

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98
Q

Which of the following is true of enterohepatic circulation of bile salts?

a) the enterohepatic circulation allows the return of bile acids to the liver through the systemic circulation
b) about 95% of bile salts are absorbed in the colonvia passive uptake
c) bile acids returning to the liver stimulate synthesis of new bile acids from cholesterol
d) uptake of bile acids in intestinal cells stimulate release of FGF19
e) the bile acid pool recirculates about once daily

A

d) uptake of bile acids in intestinal cells stimulate release of FGF19

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99
Q

What does the gallbladder do to bile?

A

concentrates and acidifies it

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100
Q

What is the difference between absorption of short/medium chain and long chain fatty acids?

A

short/medium: transported directly in enterocytes

long: re-esterified to triglycerides and transported in chylomicrons

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101
Q

What are the primary bile acids in humans? How are they synthesized?

A

cholic acid, chenodeoxycholic acid

synthesized from cholesterol with CYP7A1

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102
Q

What are intrahepatic causes of cholestasis? Extrahepatic causes?

A

intrahepatic: impaired flow of bile acids out of hepatocytes into bile canaliculi
extrahepatic: blockage of extrahepatic bile ducts

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103
Q

What are the consequences of cholestatic liver disease?

A

liver toxicity (excess bile acids in hepatocytes)

itching (from bile acids) and jaundice (bilirubin)

fat malabsorption

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104
Q

Where does the common hepatic duct arise?

A

from the confluence of left and right hepatic ducts

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105
Q

What are cholangioles?

A

terminal bile ducts that pass through portal tracts to become interlobular ducts

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106
Q

How is the common bile duct formed?

A

common hepatic duct + cystic duct from gallbladder join together

107
Q

What is the function of the choledochoduodenal junction?

A

regulates flow of bile and pancreatic enzymes and filling of gallbladder

108
Q

What is the ampulla of vater?

A

the location where the common bile duct and pancreatic duct join at the duodenum

109
Q

What is the extrahepatic phase of bilirubin formation?

A

aged RBCs are broken down and heme is catabolized to unconjugated bilirubin –> unconjugated bilirubin binds to albumin and travels to liver

110
Q

What is the hepatic phase of bilirubin formation?

A

unconjugated bilirubin is conjugated (by UGT1A1) and becomes water soluble

111
Q

How is bilirubin excreted?

A

conjugated bilirubin is water soluble and diffuses through cytoplasm to bile canaliculi and excreted into bile by an energy-dependent mechanism

112
Q

What is the mechanism of prehepatic jaundice?

A

excess production of unconjugated bilirubin –> hemolysis, hemolytic anemia, ineffective erythropoiesis

113
Q

What is the mechanism of hepatic jaundice?

A

liver conditionsthat lead to buildup of bilirubin

114
Q

What is Gilbert syndrome?

A

a genetic defect in the promoter region of the gene encoding UDP-glucuronosyltransferase 1 (enzyme that conjugates bilirubin) leading to impaired clearance of unconjugated bilirubin

115
Q

What is Crigler-Najjar syndrome?

A

mutations in the UDP glucuronosyltransferase 1 gene leading to severe unconjugated hyperbilirubinemia

milder if heterozygous

116
Q

What is the mechanism of posthepatic jaundice?

A

cholestasis due to extrahepatic biliary tree problems

117
Q

What is the clinical presentation of cholestasis?

A

1) impaired bile formation/flow
2) conjugated hyperbilirubinemia
3) increased serum bile acids
4) increased serum lipids
5) increased serum alk phos levels (disproportionate to serum transaminase levels)

118
Q

What is the mechanism of pruritis associated with cholestasis?

A

retention of pruritogens, bile acids in the skin

119
Q

What is primary biliary cholangitis? Who does it typically affect?

A

chronic cholestatic disease of unknown etiology

mostly occurs in white, middle aged females

120
Q

What is the pathophysiology of primary biliary cholangitis?

A

unknown etiology, involves immunologic-autoimmune components

includes antibodies to anti-mitochondrial antibodies (AMA)

121
Q

What are the clinical features of primary biliary cholangitis?

A

pruritis (itching), fatigability, jaundice, xanthomas (cholesterol tumors), osteoporosis, osteomalacia

122
Q

What are the laboratory findings of primary biliary cholangitis?

A
  • elevated alk phos
  • antimitochondrial antibodies (AMA)
  • antibodies against 2-oxo acid dehydrogenase complex
123
Q

What pathological findings are associated with primary biliary cholangitis?

A
  • chronic, non-suppurative destructive cholangitis (septal and interlobular bile ducts)
  • epithelioid granulomas with cytotoxic T cells and inflammation in portal tracts
  • loss of ducts
  • progression to biliary cirrhosis
  • increased risk of liver cancer
124
Q

What is primary sclerosing cholangitis?

A

chronic liver disease with persistently elevated serum alk phos

125
Q

What gastric condition is associated with primary sclerosing cholangitis?

A

inflammatory bowel disease (specifically ulcerative colitis)

126
Q

What are the findings of primary sclerosing cholangitis on cholangiopgraphy?

A

stricture, beading, irregularities of the intrahepatic and extrahepatic biliary system

127
Q

What are the liver biopsy findings associated with primary sclerosing cholangitis?

A

imflammation, cholangitis, fibrosis, obliteration of intralobular and septal bile ducts, ductopenia, biliary cirrhosis

128
Q

What complications are associated with primary sclerosing cholangitis?

A

cholestasis, cholangiocarcinoma, colorectal cancer, colitis, hepatocellular carcinoma

129
Q

What are the basic morphologic patterns of extrahepatic biliary atresia?

A

1) obstruction of common bile duct with patent hepatic ducts
2) obstruction of hepatic ducts with patent porta hepatis ducts
3) obstruction of bile ducts at the porta hepatis

130
Q

What are the 5 “F”s associated with cholelithiasis?

A

female, fat, fair (white), fertile, fifty

131
Q

What are the major types of gallstones?

A

pure cholesterol stones: solitary, round/oval, radiating crystalline structure

pigment stones: predominantly calcium bilirubinate, trace cholesterol

mixed stones

132
Q

What are the three steps of cholesterol gallstone formation?

A

1) cholesterol in bile in an unstable state, making it susceptible to precipitation
2) cholesterol must be nucleated (either alone - homogenous, or with other substances - heterogenous)
3) nucleated structure grows into a stone

133
Q

What causes cholecystitis?

A

obstruction of the cystic duct, often by a gallstone

leads to distended, tense, and discolored duct and possible perforation

134
Q

What are the complications of calculous cholecystitis?

A

pancreatitis, hydrops/emphyema, porcelain gallbladder, perforation, bile peritonitis, fistulas

135
Q

What is the most common type of carcinoma of the gallbladder?

A

adenocarcinoma

136
Q

A patient dies shortly after a diagnosis of primary sclerosing cholangitis. What was the neoplasm?

A

cholangiocarcinoma

137
Q

What are possible causes of extra-hepatic cholestasis?

A

primary sclerosing cholangitis, stones, carcinoma, congenital (atresia), trauma/stricture

138
Q

What does this histology suggest?

A

primary biliary cholangitis

139
Q

What does this histology show?

A

primary sclerosing cholangitis

bile ductules with onion-skin concentric fibrosis

140
Q

What populations are at risk of hep A? How do they contract it?

A

more common in underdeveloped areas without access to vaccines

fecal/oral is main route of transmission; associated with poor hygiene, IV drug use, etc.

141
Q

What is the pathogenesis of hepatitis A infection?

A

HAV enters via small intestine –> travels to liver where it replicates –> travels through biliary system to small intestine –> sheds in feces to infect more people

142
Q

What are the signs/symptoms of hep A?

A

jaundice, fever, fatigue, abdominal pain, nausea, vomiting, arthralgias

can also be asymptomatic

143
Q

How is hep A diagnosed?

A

HAV IgM detection for active infection

no viral load test

IgG detection defines immunity

144
Q

Is there a vaccine for hep A?

A

yes

145
Q

Who is at risk of catching hep B? how is it transmitted?

A

prevalant globally, blood-borne virus and sexually transmitted

146
Q

What are the major virulent proteins produced by hep B?

A

1) sAg –> marker of carrier status
2) polymerase (reverse transcriptase)
3) core Ag –> nucleocapsid
4) protein X –> gene activation

147
Q

What is the pathogenesis of hep B?

A

exists mainly in hepatocyte nuclei

148
Q

What are the symptoms of hep B?

A

determined by age of acquisition

can be asymptomatic or present with jaundice, fatigue, abdomoinal discomfort, etc.

149
Q

What are the main serologies associated with hep B?

A

sAg and total antibodies (IgG and IgM)

viral load can also be measured

150
Q

What serologies are associated with resolved hep B infection?

A

clearance of sAg while Ab is still present in the serum

151
Q

What is the treatment for hep B?

A

usually not needed, only recommended if viral load is high and there is advanced fibrosis

treat with: reverse transcriptase inhibitors (low cure rate)

152
Q

What is the risk of maternal-to-child transmission in hep B?

A

correlated to viral load, risk with c-section or vaginal delivery

153
Q

What cancer screenings are needed for hep B?

A

hepatocellular carcinoma

monitor semi-annually with CT or MRI and alpha-fetal protein

154
Q

How is hep C transmitted?

A

IV, intranasal drug use, tattoos, etc.

155
Q

What is the pathogenesis of hep c?

A

mostly in hepatocytes, but can have extra-hepatic reservoirs

liver damage is due to viral cytotoxicity and immune mechanisms

most patients will have chronic disease

156
Q

What is the treatment for hep C infection?

A

most patients spontaneously resolve

in patients that do not resolve, use oral anti-viral cocktail with a high cure rate (but very expensive)

157
Q

Is there a vaccine for Hep C?

A

no

158
Q

What cancer screenings are required after hep c diagnosis?

A

hepatocellular carcinoma screening semi-annually

159
Q

How is hep D transmitted?

A

parenteral transmission (IV drug use, sex)

co-infection with hep B

160
Q

What is the serological difference between Hep D co-infection and superinfection?

A

co-infection: HDV IgM and viral load with typical acute HBV serologies

super-infection: HDV IgM/IgG and a viral load with markers of crhonic HBV

161
Q

How is Hep D treated?

A

treat hep B –> hep D cannot survive without hep B

162
Q

Is there a hep D vaccine?

A

no, but the hep B vaccine acts as a de facto hep D prevention mechanism

163
Q

How is hep E transmitted?

A

fecal oral transmission, under cooked food, poor sanitation

mostly occurs in central america, africa, and asia

164
Q

How is hep E diagnosed?

A

elevated liver injury tests with symptoms

sometimes IgM and viral load can be measured

165
Q

What are three risk factors for hepatitis A?

A

poor sanitation, IV drug use, homelessness

166
Q

How do you determine the status of a suspected HBV patient?

A

serologies are the first-order tests

cAb (IgM/total) and sAg (and sAb)

viral load is measured to determine infectivity

167
Q

Why is treatment not given to all chronic HBV patients?

A

current therapy is effective at viral suppression, but not immune-activation –> medication will be needed for life and is not curative

168
Q

How do you differentiate between HCV exposure and active disease?

A

exposure: positive Ab test

viral load suggests active disease

169
Q

Who should be tested for HCV infection?

A

all individuals 18+ should have antibody testing once

170
Q

What is the essential HBV component for HDV replication?

A

HDV cannot replicate without sAg from HBV

171
Q

Which population has high risk mortality if exposed to HEV?

A

HEV is generally an acute viral infection

can have high risk mortality in pregnant patients or in solid organ transplants

172
Q

What phase of hep B illness is this:

positive IgM anti-HBc

positive HBeAg

high HBV DNA

increased ALT

A

acute hbv

173
Q

What phase of hep B illness is this:

negative IgM anti-HBc

positive HBeAg

high HBV DNA

normal ALT

A

chronic, immune tolerant HBV

174
Q

What phase of hep B illness is this:

negative IgM anti-HBc

positive HBeAg

high HBV DNA

increased ALT

A

chronic, immune active hbv

175
Q

What phase of hep B illness is this:

negative IgM anti-HBc

negative HBeAg

low HBV DNA

normal ALT

A

chronic hbv, inactive carrier

176
Q

Which serotype of hepatitis does this describe:

acute illness, controlled through sanitation/vaccination

A

HAV

177
Q

Which serotype of hepatitis does this describe:

serologies key to assessment, treatment determined by liver status/risk and viral load

A

HBV

178
Q

Which serotype of hepatitis does this describe:

screen if > 18 and/or pregnant, pan-genotypic, treatment with high cure rate and low-side effects (but expensive)

A

HCV

179
Q

Which serotype of hepatitis does this describe:

requires sAg for viability

A

HDV

180
Q

Which serotype of hepatitis does this describe:

acute illness, high pregnancy fatality rate

A

HEV

181
Q

What enzyme conjugates bilirubin?

A

UGT1A1

182
Q

What vitamin deficiencies are seen in cholestasis? Symptoms?

A

malabsorption of fat soluble vitamins (due to lack of bile flow)

vitamin D –> rickets

vitamin K –> coagulopathy

vitamin A –> night blindness

vitamin E –> neuropathy

183
Q

What are the general mechanisms of neonatal jaundice?

A

increased production of bilirubin

decreased excretion of bilirubin

combination

184
Q

What are causes of neonatal jaundice secondary to increased bilirubin production?

A

fetal-maternal bloodgroup incompatibilities

extravascular blood in body tissues

polycythemia

red blood cell abnormalities

induction of labor

185
Q

What are causes of neonatal jaundice secondary to decreased excretion of bilirubin?

A

breast feeding

increased enterohepatic circulation

inborn errors of metabolism

hormones and drugs

prematurity

hepatic hypoperfusion

cholestatic syndromes

biliary tree obstruction

186
Q

What are causes of neonatal jaundice secondary to increased production and decreased excretion of bilirubin?

A

sepsis

intrauterine infection

congenital cirrhosis

187
Q

When is neonatal jaundice abnormal?

A
  • before 36 h of age
  • persists beyond 10 days of age
  • higher than 12 mg/dL
  • elevation of direct-reacting fraction of bilirubin
188
Q
A
189
Q

What is Gilbert’s syndrome?

A

a rare genetic syndrome due to alteration in promoter for the bilirubine uridine diphosphage glucuronyl transferase (UDP-GT) gene

leads to mild indirect hyperbilirubinemia and a benign clinical course

190
Q

What is Crigler-Najjar syndrome?

A

type 1: severe, complete absence of UDP-GT, high bilirubins, can lead to brain damage (kernicterus)

type 2: partial activity of UDP-GT, less severe, responsive to phenobarbital

191
Q

What is dubin johnson syndrome?

A

genetic deficiency in cMOAT/MRP2 gene, which encodes the transporter of conjugated bilirubin

manifests as mild conjugated hyperbilirubinemia with no evidence of hepatocellular/canalicular injury

192
Q

What is idiopathic neonatal hepatitis?

A

idiopathic liver disease characterized by multi-nucleated giant cells

presents with jaundice and hepatosplenomegaly

diagnosis of exclusion

193
Q

What is gestational alloimmune liver disease/neonatal hemochromatosis?

A

a rare condition associated with extrahepatic siderosis caused by maternal antibodies crossing the placenta and attacking the neonatal liver

poor survival rate, treated by treating the mother

194
Q

What are the neonatal symptoms of alpha 1 antitrypsin deficiency?

A

neonatal cholestasis, juvenile cirrhosis, chronic hepatitis, hepatocellular carcinoma

195
Q

What is galactosemia?

A

a defect in galactose-1-phosphate uridyl transferase that leads to accumulation of toxic metabolites of galactose

clinical manifestations: lethargy, vomiting, acidosis, cataracts, UTI, jaundice, hemolytic anemia

196
Q

What is tyrosinemia?

A

an autosomal recessive deficiency of fumarylacetoacetate hydrolase that leads to build up of tyrosine metabolites

clinical presentation: acute liver dysfunction, jaundice, hepatomegaly, ascites, rickets, predisposition to hepatocellular carcinoma

197
Q

What is the treatment for galactosemia? Tyrosinemia?

A

dietary avoidance

tyrosinemia can also be treated with NTBC to reduce formation of metabolites

198
Q

What is intrahepatic alagille’s syndrome?

A

characterized by reduced interlobular bile ducts with associated multi-system abnormalities

caused by genetic disruptions of chromosome 20 affecting the NOTCH signaling pathway

presents as jaundice and conjugated hyperbilirubinemia

199
Q

What are choledochal cysts?

A

female > male, more prevalent in asians

anatomic cyst that presents as abdominal pain, jaundice, palpable RUQ mass

can also present with fever, nausea, vomiting, and pancreatitis

200
Q

What is biliary atresia? What are the two major types?

A

extrahepatic obstruction of the bile ducts that presents with jaundice, pale color stools

two types: splenic malformation (embryonic origin), perinatal viral infection leading to inflammation of bile ducts

201
Q

What is the treatment for biliary atresia?

A

surgical correction to circumvent the biliary tree

may need transplant later on

202
Q

A patient has jaundice, mild RUQ tenderness (without Murphy’s sign), bilirubinemia, elevated alk phos with normal ALT/AST. What is on the differential? How would you distinguish between etiologies?

A

cholestasis

use imaging (ultrasound) to determine if there is biliary obstruction (extrahepatic) or no obstruction (intrahepatic)

203
Q

What is the likely diagnosis for a patient with fatigue, pruritis, abdominal pain, and jaundice with elevated alk phos and GGT? What antibody is likely positive in this patient?

A

primary biliary cholangitis

AMA

204
Q

What is the genetic pattern associated with Gilbert’s disease?

A

TATA box mutation –> 7+ TAs in the TATA box leads to Gilbert’s disease

mutation in promoter region for the gene of interest

205
Q

What genetic mutations cause intrahepatic cholestasis of pregnancy?

A

mutations in the Abcb4 gene (liver transporter)

206
Q

What type of cancer is associated with cirrhosis?

A

hepatocellular carcinoma

207
Q

(micronodular or macronodular) cirrhosis has a greater predisposition to hepatocellular carcinoma

A

macronodular cirrhosis has a greater predisposition to hepatocellular carcinoma

208
Q

What is cirrhosis?

A

a diffuse disease process where fibrous septa and regenerative liver nodules distort the normal lobular architecture

209
Q

What components contribute to fibrosis in cirrhotic livers?

A

increases in all types of collagen (especially type I)

via increased synthesis and decreased degradation

also stellate cell activation

210
Q

_______ cell activation, initiation, and perpetuation contributes to fibrosis in cirrhosis

A

stellate cell activation, initiation, and perpetuation contributes to fibrosis in cirrhosis?

211
Q

What are the characteristics of liver nodules in cirrhosis?

A

hyperplastic, regenerative, and pre-neoplastic

caused by proliferation of surviving hepatocytes

can be micronodular or macronodular

212
Q

What is the difference between the pathology of micronodular and macronodular liver nodules?

A

micronodular: small, uniform, no portal triads
macronodular: large, irregular, coarse, contain portal triads and/or central veins

213
Q

What viruses can cause cirrhosis?

A

hep B and C

214
Q

What toxins can cause cirrhosis?

A

plant, fungal toxins, synthetic chemicals, some drugs

215
Q

What are metabolic causes of cirrhosis?

A

hemochromatosis, wilson’s disease, alpha-1 antitrypsin deficiency

216
Q

What are causes of prehepatic portal hypertension?

A

portal vein thrombosis or compression

217
Q

What are hepatic causes of portal hypertension?

A

cirrhosis, parenchymal disease

218
Q

What are post-hepatic causes of portal hypertension?

A

budd-chiari syndrome, heart failure

219
Q

What complications of portal hypertension are associated with increased collateral circulation?

A

esophageal varices, hemorrhoids, umbilical vein

220
Q

When cancer metastasizes to the liver, where does it come from?

A

frequently from stomach, colon, lung, breast, pancreas

tumors from organs that drain into portal circulation

221
Q

Liver metastases are usually (singluar or multiple)

A

Liver metastases are usually multiple

222
Q

What are the major types of primary liver tumors?

A

hepatocellular carcinoma (most common)

tumors of bile duct epithelium (ex. cholangiocarcinoma)

223
Q

_________ and ________ (drugs) predispose to hepatic adenoma

A

oral contraceptives and contraceptive steroids

224
Q

What are the major characteristics of hepatic adenoma?

A

benign tumor

often asymptomatic

highly vascular, risk of rupture

225
Q

What factors predispose to hepatocelluar carcinoma?

A

alcohol, cirrhosis, aflatoxin B, hep B or C, non-alcoholic fatty liver disease (and obesity)

226
Q

What lab value can be used to assess for hepatocellular carcinoma?

A

increased alpha fetoprotein

227
Q

What is cholangiocarcinoma?

A

adenocarcinoma arising from bile duct epithelium, leads to obstructive symptoms

higher incidence in elderly

228
Q

What are the general mechanisms that lead to cirrhosis and hepatocellular carcinoma?

A

chronic inflammation, fibrosis, reactive oxygen species, oxidative damage

229
Q

What does the thickness of liver cell plates indicate?

A

one cell thick –> normal liver

two cells thick –> regeneration of damaged liver

three + cells thick –> hepatocellular carcinoma

230
Q

The image on the left represents normal liver histology. What is the image on the right?

A

neoplasm –> no normal liver architecture or portal tracts

231
Q

What does the image on the left represent?

A

cholangiocarcinoma

232
Q

What differentiates compensated and decompensated cirrhosis?

A

compensated: asymptomatic for the most part, may have lab anomalies
decompensated: overt clinical complications (ex. jaundice, ascites)

233
Q

What is the pathophysiology of portal hypertension?

A

fibrosis of hepatic sinusoids + inflammation + increased blood volume + clot formation + increased vascular tone

234
Q

How does blood volume contribute to portal hypertension?

A

increase in nitric oxide increases splanchnic arterial flow –> increased cardiac output from decreased peripheral vascular resistance –> overall total body volume overload (into third spaces)

235
Q

What role does vascular tone play in the pathophysiology of portal hypertension?

A

SNS alpha1 receptor stimulation leads to increased vascular tone in intrahepatic vessels

236
Q

What symptoms are associated with decompensated cirrhosis?

A

cognitive errors/slow thinking

abdominal fullness, leg swelling, weight gain

fatigue

237
Q

What physical exam findings are associated with decompensated cirrhosis?

A

cognitive errors or asterixis

volume overload (ascites, pitting edema)

malnutrition (muscle wasting)

238
Q

What lab findings are associated with decompensated cirrhosis?

A

low albumin, sodium, platelets, cholesterol, and BUN

high INR, ammonia, and bilirubin

variable liver test findings

239
Q

What is ascites? How is it diagnosed?

A

excessive fluid into the peritoneal cavity

diagnosis: consistent symptoms, fluid wave or shifting dullness on exam, fluid on imaging, paracentesis

240
Q

What is the pathophysiology of ascites?

A

cirrhosis leads to splanchnic vasodilation –> reduces effective arterial circulating volume (including to kidneys) –> to renal vasoconstriction and activation of RAA system, sympathetic nervous system, and vasopressin –> water retention, increased thirst response, vasoconstriction, increased cardiac output

eventually the liver can’t hold all the blood it is getting, so ultrafiltrate of blood weeps into peritoneum

241
Q

What are the treatments for ascites?

A

sodium restriction

diuretics

paracentesis

transjugular intrahepatic portosystemic shunt (TIPS)

liver transplant

242
Q

What is spontaneous bacterial peritonitis?

A

infected ascitic fluid in the peritoneal cavity

243
Q

What are the symptoms of spontaneous bacterial peritonitis?

A

may be asymptomatic or may have confusion and intense abdominal pain with guarding

244
Q

What peracentesis findings are associated with spontaneous bacterial peritonitis?

A

> 250 neutrophils/mm3

245
Q

What is the pathophysiology?

A

occurs only in the setting of ascites

bacteria enters the ascitic fluid through intestinal wall or lymphatics

normal ascitic fluid has anti-infectious properties, but as it gets worse (and if there is malnutrition) infection is more likely

246
Q

What is the treatment for spontaneous bacterial peritonitis?

A

antibiotics with broad spectrum coverage IV for 5 days

247
Q

What is hepatic hydrothorax?

A

abnormal collection of ascitic fluid in the thoracic cavity, often right-sided

248
Q

What are the physical exam findings on hepatic hydrothorax?

A

diminished breath sounds on auscultation, hypoxemia

249
Q

How is hepatic hydrothorax diagnosed?

A

symptoms (dyspnea), physical exam (decreased breath sounds), opacities on chest x-ray, fluid on thoracentesis (used to determine etiology)

250
Q

What is the pathophysiology of hepatic hydrothorax?

A

same pathophysiology of ascites –> ascitic fluid travels from peritoneal space into pleural space through holes in the diaphram (driven by negative intra-thoracic pressure)

251
Q

What are the treatments for hepatic hydrothorax?

A

sodium restriction, diuretics, thoracentesis, transjugular intrahepatic portosystemic shunt, pleurodesis, liver transplantation

252
Q

What is hepatopulmonary syndrome?

A

a secondary lung disorder caused by intrapulmonary shunting due to intrapulmonary vascular dilation and neo-angiogenesis

253
Q

How is hepatopulmonary syndrome diagnosed?

A

symptoms (platypnea), spider angiomata on chest, low PaO2, positive bubble study on echo (vessels dilated enough for bubbles to pass through)

254
Q

What is portopulmonary hypertension?

A

A sub-type of pulmonary arterial hypertension that is caused by excessive vasoconstrictors leading to smooth muscle hyperplasia/hypertrophy, thrombosis, and fibrosis in pulmonary arteries

255
Q

What is hepatorenal sydrome?

A

a syndrome caused by decreased renal perfusion caused by reduced effective circulating volume as a sequelae of portal hypertension

diagnosis of exlusion

256
Q

How is hepatorenal syndrome diagnosed?

A

symptoms: increased weight gain, decreased urine output
exam: ascites, edema
labs: oliguria, increased creatinine, urine studies (pre-renal etiology)

257
Q

What is the treatment for hepatorenal syndrome?

A

vasoconstrictor + vasodilator inhibitor (octeotride), oncotic support

not curative

258
Q

What are esophageal varices?

A

enlarged natural or neo-angiogenic veins that are caused by portal hypertension

caused by hepatofugal flow from the liver that backs up in smaller vessels

259
Q

What are the treatments for esophageal varices?

A

volume control, coagulopathy, control of portal hypertension, octreotide (splanchnic vasoconstriction), acid suppression, antibiotics to prevent infection, TIPS, liver transplant

260
Q

What is hepatic encephalopathy?

A

altered mental status due to toxin build up in the brain

nostly due to ammonia that is unable to be effectively cleared due to liver damage

261
Q

What are the symptoms of hepatic encephalopathy?

A

altered mental status, disorientation, errors in comprehension/memory, decreased bowel movements

262
Q

How do NSbetaB medications work to reduce portal hypertension in patients with varices?

A

they lower cardiac ouptut (beta1 blockade) and constricting the splanchnic nerves (beta2 blockade) that feed the portal system

263
Q

Why does hyper-ammonemia develop in patients with cirrhosis?

A

ammonia is produced throughout the body by host and bacterial processes and is normally metabolized by liver, kidney, and muscle

in cirrhosis, metabolic efficiency is compromised leading to build up of nitrogenous compounds

264
Q

What is the basis for treatments for hepatocellular carcinoma?

A

HCCs are fed by the hepatic artery, which is the main target of treatment

GI (10 decks)

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