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GI- Week 6 > Nelson: Liver > Flashcards

Nelson: Liver Flashcards

1
Q

What is jaundice?

A

Yellow discoloration of the SKIN d/t retention of bilirubin

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2
Q

When is jaundice clinically evident?

A

as total serum bilirubin approaches 2-3 mg/dl

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3
Q

What is icterus?

A

yellow discoloration of the SCLERA d/t retention of bilirubin

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4
Q

What is cholestasis?

A

impaired secretion of BILE

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5
Q

What are the steps involved in bilirubin metabolism?

A

Reticuloendothelial cells convert heme (brkdown of old RBC, hepatic heme, marrow RBC precursors) to bilirubin>
bilirubin is transported to the liver complexed w/ ALBUMIN (unconjugated bilirubin)>
cbilirubin is conjugated w/ glucuronic acid in liver cells (conjugated bilirubin)>
conjugated bilirubin is excreted in BILE (brown stools)

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6
Q

What form of bilirubin is toxic to tissues?

A

Unconjugated (indirect)

  • water soluble
  • bound to albumin
  • not excreted in the urine
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7
Q

Which form of bilirubin is water soluble, not toxic to tissues and is excreted in the urine when present at high serum levels?

A

conjugated bilirubin

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8
Q

What are some of the causes of unconjugated bilirubinemia?

A
  1. Increased bilirubin production
  2. impaired hepatic bilirubin uptake
  3. impaired bilirubin conjugation
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9
Q

What increases bilirubin production?

A
  • Extravascular hemolysis
  • Extravastation of blood into tissues
  • Intravascular hemolysis
  • Dyserythropoiesis
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10
Q

What impairs hepatic bilirubin uptake?

A
  • Heart failure
  • Portosystemic shunts
  • Gilbert’s syndrome
  • Drugs
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11
Q

What impairs bilirubin conjugation?

A
  • Crigler-Najjar syndrome (I or II)
  • Gilbert’s syndrome
  • Neonatal jaundice
  • Hyperthyroidism
  • Ethyinyl estradiol
  • Liver disease
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12
Q

What causes conjugated hyperbilirubinemia?

A
  1. extrahepatic cholestasis (biliary obstruction)

2. interhepatic cholestasis

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13
Q

What causes biliary obstruction?

A
  • Choledocholithiasis
  • Tumors
  • PSC
  • AIDS
  • Pancreatitis
  • Strictures
  • Parasitic infxns
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14
Q

What causes intrahepatic cholestasis?

A
  • Hepatitis (many types)
  • Drugs & toxins
  • Primary biliary cirrhosis
  • Sepsis & hypoperfusion
  • Infiltrative diseases
  • Total parenteral nutrition
  • Following organ transplant
  • Hepatic crisis in sickle cell
  • Pregnancy
  • End-stage liver disease
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15
Q

What causes normal neonatal alterations in bilirubin metabolism?

A
  1. Increased bilirubin production (neonates have relatively more RBCs with a shorter life span)
  2. Decreased bilirubin clearance (due to physiologic decrease in UGT1A1 activity)
  3. Increased enterohepatic circulation*
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16
Q

What are pathological causes of unconjugated hyperbilirubinemia?

A
  • Immune-mediated hemolysis (ABO or Rh(D) incompatibility)
  • Inherited RBC membrane or enzyme defect
  • Sepsis
  • Inherited defects in UGT1A1 activity (e.g. Crigler-Najjar syndrome, Gilbert’s syndrome)
  • Breast milk jaundice*
  • Intestinal obstruction*
  • Breastfeeding failure jaundice*
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17
Q

What are normal TB levels in almost all term and near term newborn inftants?

A

> 1 mg

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18
Q

If an infant has mild unconjugated hyperbilirubinemia w/ peak TB what can you expect the levels to be?

A

— 7 to 9 mg/dl in Caucasian & AA infants

— 10 to 14 mg/dl in Asian infanats

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19
Q

A TB >25-30 mg/dl in an infant is indicative of….

How do you treat it?

A

severe hyperbilirubinemia

Phototherapy

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20
Q

How does severe hyperbilirubinemia affect other organ systems?

A
  1. Bilirubin-induced neurologic dysfunction (BIND)
  2. Acute bilirubin encephalopathy (ABE)
  3. Long-term neurologic sequelae or kernicterus (if inadequately tx)
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21
Q

What is Gilbert’s syndrome?

A

AR, BENIGN disorder

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22
Q

What causes Gilbert’s syndrome?

A

decreased GTF activity (UGT1A1 is 30% of normal)

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23
Q

What lab findings are associated w/ gilbert’s sndrome?

A

increased unconjugated bilirubin

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24
Q

Morphological findings show:
bile w/in hepatocytes
canalicular bile stasis
feathery degeneration of hepatocytes

A

intrahepatic cholestasis

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25
Q 
Morphological findings show:
Canalicular bile stasis
Feathery degeneration of hepatocytes
Bile lakes
Bile w/in distended bile ducts
PORTAL TRACT EDEMA
Bile duct proliferation w/in portal tracts
A

Extrahepatic cholestasis

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26
Q

What is acute cholangitis? What is seen morphologically?

A

secondary bacterial infection of the biliary tree

Extrahepatic biliary obstruction → ascending cholangitis

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27
Q

What is chronic passive congestion?

A

centrilobular congestion

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28
Q

WHat is centrilobular hemorrhagic necrosis?

A

centrilobular congestion w/ cenrilobular necrosis

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29
Q

What is cardiac sclerosis?

A

fibrosing rxn following long standing CPC and or centrilobular necrosis

Pathology–centrilobular fibrosis

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30
Q

What are the common causes of CPC, CHN and CS?

A

RHF, LHF, shock, hepatic vein thrombosis>

congestion and hypoperfusion> centrilobular necrosis

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31
Q

What is a hepatic infarct?

A

rare

secondary to double blood supply

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32
Q

What is a hepatic infarct often caused by?

A

vasculitis, embolism, or tumor

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33
Q

What is hepatic vein thrombosis (bud chiari syndrome)?

A

thrombosis of 2+ hepatic vein branches

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34
Q

What is the classical clinical triad for HVT?

A

hepatomegaly
ascites
abd pain

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35
Q

What often causes HVT?

A

conditions htat make clotting more likely

May also have a thrombosis in the IVC

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36
Q

How do you dx HVT?

A

imaging of thrombi

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37
Q

What si the pathology of HVT?

A

centrilobular hemorrhagic necrosis

cardiac sclerosis

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38
Q

What is sinusoidal obstruction syndrome?

A

presence of obstructive, non-thrombotic lesions of small hepatic veins in pts exposed to radiation &/or hepatoxins

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39
Q

What is the pathogenesis of sinusoidal obstruction syndrome?

A

toxic damage to hepatic sinusoidal endothelium, secondary to cytoreductive agents (e.g. chemotherapy)> MARKED NARROWING/OBLITERATION OF CENTRAL VEIN lumens by SUBENDOTHELIAL SWELLING AND FIBROSIS

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40
Q

What is the acute form of sinusoidal obstruction syndrome associated with?

A

painful hepatomegaly
sudden wt gain
increased serum bilirubin

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41
Q

What is the chronic form of sinusoidal obstruction syndrome associated with?

A

Toxic effects of pyrrolizidine alkaloids found in certain herbal teas

sx of budd chiari

42
Q

How do you dx sinusoidal obstruction syndrome?

A

clinical features
imaging
liver biopsy (chronic form)

43
Q

What complications are associated wtih portal vein thrombosis?

A

portal HTN (no ascites b/c obstruction is presinusoidal)

44
Q

What are extrahepatic causes of portal htn?

A
  1. Intraabdominal sepsis
  2. hypercoaguable disorders
  3. trauma
  4. pancreatitis or pancreatic cancer
45
Q

What are intrahepatic causes of PVT?

A
  1. cirrhosis

2. invasion of portal vein by hepatocellular carcinoma

46
Q

What is Peliosis Hepatis?

A

primary hepatic sinusoidal dilation w/ sinusoidal rupture> blood filled spaces

typically resolves after correction of underlying disorder

47
Q

How is hepatitis A transmitted?

A

Fecal- oral (contaminated food & water)

48
Q

How does Hepatits A cause infection?

A

Incubates 2-6 wks>

Virus infects liver cells → hepatocellular injury d/t CD8+ T-cell & lysis of infected hepatocytes

49
Q

How does HAV usually present?

A

majority are asymptomatic
some present w/ acute hepatitis

does NOT cause chronic hepatitis

50
Q

How is HBV transmitted?

A

Parenteral, Sexual/close contact, perinatal

Blood & body fluids (saliva, semen, vaginal secretions)

51
Q

How does HBV cause infection?

A

Incubation period = 4-26 wks

Virus infects liver cells → hepatocellular injury d/t CD8+ T-cell & lysis of infected hepatocytes

52
Q

What percent of HBV pts are asymptomatic? acute? chronic?

A

Majority (70%) of pts asymptomatic
Some (30%) clinical acute hepatitis
90% of infections resolve

5% develop chronic hepatitis

(1) → Non-progressive disease
(2) → Progressive disease→ cirrhosis
(3) → Hepatocellular carcinoma
(4) → Asymptomatic carrier state (esp. if exposed as young

53
Q

How is HCV transmitted?

A

Parenterally (blood, IV drug use), Sexual/close contact, rarely perinatally

54
Q

What percent of pts develop chronic HCV?

A

20% develop acute hepatitis
80% develop chronic hepatitis
• 20-30% → cirrhosis
• Most pts asymptomatic

55
Q

What is the MCC of chronic liver disease in the US?

A

HCV

Genotype 1a

56
Q

How is HDV transmitted?

A

Individual w/ chronic HBV (superinfection)

Transmitted simultaneously w/ HBV (coinfection)

57
Q

What does HVC need in order to replicate?

A

Only able to replicate in presence of HBV, encapsulated by HBsAg

58
Q

How does an infection w/ HBV and HDV compare to one w/ HBV alone?

A

MORE SEVERE
• Increased mortality from acute hepatitis
• Increased progression to chronic hepatitis (superinfection form only)

59
Q

What populations is HDV commonly found in?

A

See in IV drug users or certain geographical locations (Brazil, Africa, Middle East, S. Italy)

60
Q

Can you distinguish and acute coinfection of HBV and HDV from HBV?

A

No

transiet & self-limited, increased severity, increased risk of liver failure, rate of progression to chronic no different

61
Q

What can an HDV superinfection cause?

A
  • Convert mild chronic HBV hepatitis →acute liver failure (7-10%)
  • Cause acute hepatitis to erupt in a healthy, inactive HBV carrier
  • → chronic hepatitis (80%, compared to 4% with HBV alone)
  • Carrier state also exists
62
Q

How is HEV transmitted?

A

Fecal oral

63
Q

What population can HEV cause mortality in?

A

Generally self-limited, but can cause mortality in pregnant women
Does NOT cause chronic hepatitis or carrier state
Very prevalent in underdeveloped countries
Very rare in US

64
Q

We have vaccines for all forms of hepatitis except?

A

HCV

HEV does have a vaccine but is not available commercially

65
Q

What serological tests are used for HAV?

A

Infected pts develop Ab response
• IgM HAV preceeds IgG HAV
• IgG persists & provides protective immunity

66
Q

How do you dx HAV?

A

pt w/ clinical features of acute hepatitis & positive test for IgM anti-HAV.

67
Q 
Describe the serological tests associated w/ HBV.
HBsAg
HBeAg and HBV DNA
IgM anti-HBc
IgG anti HBc
Anti HBs
Anti HBe
A

HBsAg-ongoing HBV infection
HBeAg and HBV DNA- active viral replication, progression to chronic hepatitis
IgM anti-HBc- acute hepatitis
IgG anti HBc- past exposure to HBV
Anti HBs- recovery and immunity from HBV infection
Anti HBe- infection is resolving

68
Q

How do you dx acute HBV?

A 
Acute Hepatitis B = 
pt w/ clinical features
HBsAg
IgM anti-HBc
both positive

*If pt has + HBsAg, but – IgM anti-HBc → think chronic hepatitis or carrier state

69
Q

How do you dx chronic HBV?

A

clinical features & HBsAg + for > 6 mo.

• Also order HBeAg & HBV DNA to look for active viral replication

70
Q

What serologic tests are used for HCV?

A

Anti-HCV Ab develop 10 wks post infection, do NOT confer recovery or immunity in most pts

71
Q

What is the preferred screening test for HCV?

A

Ab detection using immunoassays = preferred screening test

72
Q

How do you confirm an active HCV infection?

A

Active infection confirmed by measuring viral load by HCV PCR – used to assess response to therapy

73
Q 
Describe the serologic tests associated w/ HDV.
IgM anti-HDV
IgG anti-HDV
Anti-HDV
HDAg and HDV RNA
A

IgM anti-HDV- acute or recent HDV
IgG anti-HDV- previous infection w/ HDV, confers immunity
Anti-HDV- acute or chronic exposure
HDAg and HDV RNA- acute viral replication, ongoing infection

74
Q

What serological marker persists in superinfecions w/ chronic HDV?

A

IgM anti-HDV can also persist

75
Q

How do you dx HDV?

A 
HBsAg positive
Evidence of HDV infection
—	HDAg or HD RNA positive
—	IgM anti-HDV positive
—	anti-HDV positive
76
Q

What marks an HDV coinfection?

A

IgM anti-HBc positive (acute or recent HBV

77
Q

What marks an HDV superinfection?

A

IgM anti-HBc negative (chronic HBV)

78
Q

How do you test for HDV?

A

— pts w/ high risk factors
— Present w/ unusually severe sx
— Acute hepatitis occurring in chronic HBV carrier

79
Q

How do you detect acute HEV infections?

A

anti-IgM HEV & HEV RNA

80
Q

WHat are the tests used to screen blood to avoid transfusion trasnmitted hepatitis?

A
  • HBsAg
  • anti-HBc
  • HBV DNA
  • anti-HCV
  • HCV RNA
81
Q

How is perinatally acquired HBV prevented?

A

Infants of mothers who are positive for hepatitis B surface antigen should receive hepatitis B immune globulin and hepatitis B vaccination within 12 hours of birth, and other infants should receive hepatitis B vaccination before hospital discharge.

82
Q

What is the incubation phase of acute viral hepatitis?

A

variable, dependent on viral type

83
Q

What are the 4 phases of the clincial presentation of acute viral hepatitis?

A
  • Incubation phase: variable, dependent on viral type
  • Preicteric prodrome: nonspecific, constitutional symptoms (malaise, fatigue, nausea, loss of appetite, arthralgias etc.); elevated serum levels of liver enzymes (ALT: alanine aminotransferase; AST: aspartate aminotransferase).
  • Icteric (jaundice) phase: jaundice is not always present (anicteric hepatitis); conjugated hyperbilirubinemia mainly; dark urine (bilirubinuria).
  • Convalescence (recovery) vs. acute liver failure vs. chronic hepatitis (with or without progression to cirrhosis) vs. “healthy” carrier.
84
Q

How do you assess hte degree of liver damage w/ chronic viral hepatitis?

A

liver biopsy

clinical findings are highly variable

85
Q

What are hte pathological findings associated w/ acute viral hepatitis?

A

lobular hepatitis
o Diffuse liver cell degeneration (ballooning degeneration)
o Focal hepatocellular necrosis (“dropout necrosis” – loss of hepatocytes) & apoptosis (councilman bodies)
o Confluent necrosis (seen in severe cases)
o Kupffer cell hyperplasia and hepatocellular regeneration
o Mononuclear inflammation (predominantly lymphocytes) w/in portal tracts and lobules
o “Lobular disarray”

86
Q

Is acute viral hepatitis biopsied?

A

No

87
Q

What defines chronic viral hepatitis?

A

hepatitis lasting more than 6 mos.

88
Q

What pathological findings are associated w/ chronic hepatitis and ongoing necroinflammatory changes?

A

Periportal hepatitis
o Piecemeal necrosis
o Bridging necrosis & progressive fibrosis between periportal tracts → cirrhosis (severe cases)

89
Q

Why is a biopsy required to assess liver damage in chronic viral hepatitis?

A

clinical findings of chronic viral hepatitis are highly variable

90
Q

What is a councilman body?

A

apoptotic body in chronic viral hepatitis

91
Q

Ground glass hepatocytes are associated w/…

A

chronic HBV

92
Q

Spotty, focal pattern of mild periportal hepatitis with mild steatosis is associated w…

A

chronic HCV

93
Q

What are some of the causes of acute massive hepatic necrosis?

A 
o	Acute viral hepatitis 
o	Drug/toxin induced hepatitis (acetaminophen OD = 50%) 
o	Vascular liver diseases 
o	Autoimmune hepatitis 
o	Wilson’s disease
94
Q

If patients w/ acute massive hepatic necrosis survive, do they always get cirrhosis?

A

NO!

Pts suffer from acute liver failure

If pt survives, may not cause cirrhosis (if toxic agengent doesn’t cause fibrosis, liver can regenerate normally)

95
Q

What abs are used to dx type 1 autoimmune hepatitis?

A

Type 1:
anti-nuclear (ANA),
anti-smooth muscle actin (SMA)
anti-soluble liver antigen/liver-pancreas (anti-SLA/LP) antibodies

96
Q

What abs are used to dx type 2 autoimmune hepatitis?

A

Type 2:
anti-liver/kidney microsome-1 (anti-ALKM-1)
&/or
antibodies to a liver cytosol antigen (ALC-1)

97
Q

What features seen on biopsy may suggest a dx of AIH?

A

Chronic hepatitis with increased plasma cells in the periportal lymphocytic inflammatory infiltrate along with lobular inflammation

98
Q

What is the MC AIH and who does it commonly affect?

A

Type I
middle aged females

type II (children and adolescents)

99
Q

How do you tx AIH?

A

immunosuppressive steroids

Differs from chronic viral hepatitis b/c you wouldn’t want to suppress the immune system to fight infxn.

100
Q

What is seen on an acute hepatitis paneL/

A
  • IgM anti-HAV
  • HBsAg
  • IgM anti-HBc
  • Anti-HCV
101
Q

What is seen on a chronic hepatitis panel?

A
  • HBsAg
  • Anti-HBs
  • Anti-HBc
  • Anti-HCV

GI- Week 6 (14 decks)

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