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GI Week 6 > Liver Pathology 1 > Flashcards

Liver Pathology 1 Flashcards

1
Q

Define jaundice

A

yellow discoloration of the skin due to retention of bilirubin

clinically evident as total serum bilirubin approach 2-3 mg/dl

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2
Q

Define icterus

A

yellow discoloration of the sclera due to retention of bilirubin

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3
Q

Define cholestasis

A

impaired secretion of bile (lots of different causes)

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4
Q

List the steps involved in bilirubin metabolism

A

reticuloendothelial cells convert heme to bilirubin

bilirubin transported to the liver and complexed to albumin (unconjugated bilirubin)

bilirubin is then conjugated with glucuronic acid in the liver cells (conjugated bilirubin)

conjugated bilirubin is excreted in bile (make stool brown)

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5
Q

Where does most bilirubin come from?

A

85% from breakdown of sensecent RBCs

15% from hepatic heme or marrow RBC precursors

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6
Q

WHat cells convert heme to biliruine?

A

reticuloendothelial cells

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7
Q

What will complex biliruin on its way to the liver?

A

albumin

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8
Q

What is used to conjugate the bilirubin?

A

UDP transferase puts on glucuronic acid

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9
Q

List some causes of unconjugated hyperiblirubinemia.

A

increased production of bilirubin: hemolysis in general

impaired hepatic bilirubine uptake

impaired bilirubin conjugated

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10
Q

List some causes of conjugated hyperbilirubinemia .

A

Extrahepatic cholestasis (biliary obstruction)

Intrahepatic cholestasis

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11
Q

Which form of bilirubin is toxic to tissues?

A

unconjugated (water insoluble, bound to albumin, toxic to tissues, not excreted in urine)

note that conjugated bilirubin is water soluble, not tighyly bound to albumin, not toxic to tissues, and excreted in urine when present in serum at high levels (bilirubinuria)

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12
Q

Describe causes and significance of increased unconjugated bilirubin in the neonate?

A

neonatal jaundice (physiologic jaundice of the newborn) is a normal finding because they have neonatal alterations in bilirubin metabolism (increased bilirubin production, decreased bilirubin conjugation and clearance)

cause a mild unconjugated hyperbilirubinemia

not a clinical problem unless it gets high (over 20) at which time you can get neurotoxicity presenting as acute bilirubin encephalopathy and long-term kernicterus

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13
Q

What organ system is affected if bilirubin levels are too high?

A

CNS

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14
Q

What is the treatment for this?

A

phototherapy with blue light

the light converts the bilirubin into water soluble isomers so that it can be excreted

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15
Q

Define Gilbert’s syndrome and the typical lab findings.

A

super common autosomal recessive condition

decreased ducuronyltransferase activity (30% of normal)

so they get increased unconjugated bilirubin after fasting.

totally benign

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16
Q

Describe the mophrologic fingings of hepatocellular cholestasis.

A

intrahepatic/extrahepatic

you’ll get bile within hepatocytes, canalicular bile stasis, feathery degeneration of hepatocytes

in extrahepatic you’ll also have bile lakes, bile witin the distended bile ducts, portal tract edema, bile cduct proliferation within the portal tracts. Maybe promotes ascending hcolangitis.

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17
Q

Describe the morpholoic findings of canalicular cholestasis.

A

You get bile plugs in the canaliculi

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18
Q

Describe the morphologic findings of acute cholangitis.

A

neutrophil infiltrate into the bile ducts

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19
Q

Describe chronic passive congestion

A

you get centrilobular congestion - bldod builds up

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20
Q

Describe centrilobular hemorrhagic necrossi

A

you get centrilobular congestion with necrosis in the middle

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21
Q

Describe cardiac sclerosis.

A

if you have long standing of this, you can get cardiac sclerosis

basically a fibrosin reaction following long standing congestion and centrilobular hecrosis

cuase: right sided heart failure, hepatic vein thrombosis, left sided heart failure and shock

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22
Q

Describe hepatic infarct

A

these rarely occur since the liver has double blood supply, but it can be seen with arterial occlusion due to vasculitis, embolism or tumor

the area of the lobule most susceptible is the centrilobular region (periportal areas will be spared)

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23
Q

Describe Bud Chiari Syndrome.

A

thrombosis of two or more hepatic vein branches (outflow blockage)

you get hepatomegaly (congestion), congestion and abdominal pain

usually caused by conditions that make clots more likely to form, but sometimes idiopathic

diagnose with imaging - US

you get cnetrilobular hemorrhagic necrosis aroud the area

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24
Q

Describe sinusoidal obstruction syndrome.

A

hepatoveno-occlusive disease

you get obstructive nonthrombotic lessions of the central hepatic veins

usually from radiation or hepatoxoins - often in bone marrow transplants, chemo

you get marked narrowing and olibteration of the central veins by subendothelial swelling and fibrosis

get painful hepatomegaly, sudden weight loss, increased bilirubin

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25
Describe portal vein thrombosis
you have a blockage of inflow - either do to intrahepatic disease or extrahepatic disease intrahepatic: cirrhosis is primary cuase, or invasion of portal vein by hepatocellular carcinoima extrahepatic: intra-abdominal sepsis with septic thrombophlevitis of the portal veins, inherited or acquired hypercoagulable disorders, trauma, pancreatitis or pancreatic cnacer ascites DOESN"T occur, but portal hypertension does
26
Describe peliosis hepatis
basically primary hepatic sinusoidal dilatation with potential for rupture and formation of blood filled spaces (can be macroscopic) seen in a variety of disorders: anabolic steroids, oral contraceptives and danazol, AIDS infection with bartonella henselae, or nearby malignancy or tumor usually asymptomatic but can cause intrabdominal hemorrhage or hepatic failure (resolves after correcting cause)
27
How is Hep 1 transmitted
fecal oral blood not so much - the viremia is super transient
28
Describe Hep A course
usually asymptomatic some present clinically with acute hepatitis, and only 0.1% will develop fulminant hepatitis (but those people may die) note that HAV does NOT cause chronic hepatitic or a chronic carrier state (it's a vowel)
29
Describe Hep B transmittions.
double stranded DNA virus with DNA polymerase. icosahedral. has an envelope with surface antigen. Core with C antigen. long incubation period of 4-26 weeks injury due to cellular immune response (CD8 T cells) and lysis of hepatocytes virus is present in blood and body fluis, so you get this through parenteral transmission, sexual/close contact and perinatal
30
Describe Heb B clinical course
most will be asymptomatic 30% will develop acute clinicla hepatitis and will receive care 90% of those will resolve completely only 0.1-0.5% will devlop acute liver failure and may die (from the overwhelming immune response) About 5% of the exposed adults will devleop chronic hepatitis. some will eventually rcover, some will have non-progressive disease, some will have progressive disease to cirrhosis, and some will dvelop hepatocellualr cancer young people infected that don't develop an immune response will become a carrier state
31
Describe Heb D characteristics and transmission
It's Defective! You need to have Hep B as well Can either get it in a chronic hep B infection (superinfection) or as an acute co-infection note that Hep B and D i more severe than B alone - increased mortality and propensity to be chronic D is restricted to IV drug users in the US (but not the case worldwide)
32
Describe Heb D clinical course
you get an acute hepatitis - can't differentiate hep B from HepB/D acute infection usually transient and self limited, but there can be increased severity, liver failure and proression to chronic liver failure (doesn't differ much from hep B) superinfection can convert someone with mild chroni c HBV into acute liver failure or to have liver failure occur in a healthy carrier of hep B. ALso can lead to chronic hepatitis.
33
Describe Heb C transmission
HCV is spread parenterally (blood, IV drug use), by sexual or close contact, rarely perinatally (32% unknown source). Incubation period is 4-26 weeks.
34
Describe Heb C clinical course
acute liver failure is rare - only in 0.2%. so most people with C dont even know they have it 20% will resolve but 80% will develop chronic hep C without even knoing they have it of those 20-30% will devlop cirrhosis so hep C causes 50% of liver disease in the US some can get extrahepatic autoimmune manifestations like cryoglobulinemia
35
Describe Hep E transmision
RNA birus spread fecal oral
36
DEscribe Hep E clinical course
very rare in the US usually self limited, but .5-3% with acute liver failure NOTE - pregnant women have a high mortality of 20%!!! Does NOT cause chronic or carrier states (vowel)
37
Which hepatitis viruses do we have vaccines for?
Hep A Hep B (and thus indirectly against Hep D) Hep E, but not commercially available
38
Serology for Hep A?
infected patients will devlop antibody to the virus IgM HAV will show up first IgG HAV will persist and provide immunity so diagnosis of acute hepatitis A is made in patients with clinical features of acute hepatitis and positive test ofr IgM anti-HAV
39
Serology for Hep B?
HBsAG is surface antigen - indicates ongoing HBV infection (acute or chronic) BV DNA and E antigen indicate active viral replication - infectivity and markers for progression to chronic heaptisi IgM anti-core is most important - detected at onset of acute hep B and then eventually replaced by IgG anti-core. If you have IgM anti-core = acute or recent hepatitis B infection IgG anticore indicate past exposure but do NOT give immunity ANti-surface antigen DOES indicate recovery and immunity Anti-e antigen indicates infeciton is resolving even thought surface antigen may still be present
40
What will be high in acute infection of HBV?
HbsAg and IgM anti-HBcore
41
What will indicate recovery and immunity?
IgG anti-core
42
What is the "core window"
the only positive thing will be the IgM anticore the surface antigen and antisurface antigen cancel each other out
43
What serology would indicate chronic carrier state for HBV?
positive HBsAg and negative for IgM anti-HBcore and no other antibodies
44
Serlogy for hep C?
anti-HCV show up 10 weeks after infection but they don't confer recover or immunity because the virus has a high mutations rate (so no vaccine) so the presence of antibodies can't tell you anything about acute, chronic or past infection. but ou can use them as a screening test and if positive, you measure the RNA by PCR to see if they actually have a current infection. Also do genotype testing.
45
Serology for hep D?
IgM antiD indicates acute or recent, while IgG antiD indicates previous infeciton and confers immunity HD antigen and RNA indicate active viral replication and ongoign infection coinfection: HBsAG positive and evidence of HDV infection like HDAg or HD RNA or IgM antiD superantigen: IgM antiBc negative, but signs of hep D
46
Serology for Hep E?
IgM antiHEV and HEV RNA
47
List the tests used to screen blood to avoid transufsion transmitted hepatitis.
before 1990, most of this was due to HCV- 10% of patients receiving multiple transfusions would be infected! BUt now we test for it ``` BHsAg antiHBc HBV DNA anti-HCV HCV RNA ```
48
Describe how perinatally acquired HBV is prevented.
infant has a 70-90% chance of aquiring perinatal HBV infeciton more than 90% of them will become inactive or healthy chronic HBV carriers, but 25% of these carriers wille ventually die of cirrhosis or HCcarcinoma Treat with hepatitic B immune globulin and the Hep B vaccine its 85-95% effective if you administer within 2-12 hours after birth!!! So screen all pregnant women for B surface antigen and e antigen
49
Describe the possible clinical presenations of acute viral hepatitis?
pre-icteric prodrom with nonspecific constitutional symptoms like malaise, fatigue and nausea elevated serum levels of liver enzymes (ALT and AST) then an icteric/jaundice phase - although not always present. can have hyperbilirubinemia and bilirubinuria
50
When is an acute viral hepatitis defined as a chonic viral hepatitis/
persistent chronic inflammatory destruction of live parenchyma - hepatitis lasting more than 6 months is defined as chronic hepatitis Hep B, C and D
51
Describe the pathologic findings seen in acute viral hepatitis
you get lobular hepatitis findings which show diffuse liver cell degeneration (ballooning degeneration) with focal necrosis and apoptosis with councilman bodies kupffer cell hyperplasia and hepatocellular regenetation mononuclear inflammation\\lobular disarray
52
Is actue viral hepatitis frequently biopsied?
No
53
Describe the pathologic findings that can be present in a patient with chronic viral hepatitis with ongoing necroinflammatory changes
periporal hepatitis with piecemeal necrosis, brigding necrosis and progressive fibrosis leading ot cirrhosis in severe cases can see ground glass heaptocytes in chronic HBV and focal pattern of periportal hepatisi with mild steatosis in chronic HCV
54
Why is it sometimes necessry fo rperform liver biopsy in these patients?
you need to do a biopsy to see how bad the cirrhosis is
55
Describe the pathologic clues that can be seen on liver biopsy that would suggest that someone may have chronic HBV infection.
groudn glass hepatocyte
56
Also describe the pathologic clues that would usggest chronic HCV infections.
mild steatosis
57
Describe some of the causes of acute massive hepatic necrosis.
when they basically infarct their whole liver because of the immune response, drug or toxins , vascular liver disease, autoimmune hepatitis or wilsons get acute liver failure
58
If these patients survive, do they always get cirrhosis?
not always. the hepatocytes have all infarcted but the extracellular matrix has NOT been remodelled, so the hepatocyes can just regenerate along it normally
59
Define autoimmune hepatitis/
liver injury due to T cell-mediated autoimmune pathogenesis female predominance, negative viral hepatitis markers and serum IgG and gamma blobulin levels will be high (as in any autoimmune issue)
60
Describe the key antibodies used in diagnosis of autoimmune hepatitis
used to lcassify into type ! and 2 type 1 (women): ANA, anti-smooth muscle actin (SMA), anti-sluble liver antiven/liver-pancreas (anti-SLA/LP) type 2 (kids): anti-liver/kidney microsome -1 (antiALMN-1), and/or antibodies to liver cytosol antigen (ALC-1)
61
What feature seen on liver biopsy may suggest a diagnosis of autoimmune hepatitis?
you get increased plasma cells in th eperiportal lymphocytic inflammatory infiltrate along with lobular inflammation (which doesn't really happen in viral - that's just periportal) but always exclude the viral posibilities
62
Contrast the treatment of AIH with that of chronic viral hepatitis
immunosuppressant vs anivirals! therapy is completely different so you need to make sure you know which one it is.

GI Week 6 (14 decks)

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