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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
Q

Describe portal vein thrombosis

A

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
Q

Describe peliosis hepatis

A

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
Q

How is Hep 1 transmitted

A

fecal oral

blood not so much - the viremia is super transient

28
Q

Describe Hep A course

A

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
Q

Describe Hep B transmittions.

A

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
Q

Describe Heb B clinical course

A

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
Q

Describe Heb D characteristics and transmission

A

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
Q

Describe Heb D clinical course

A

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
Q

Describe Heb C transmission

A

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
Q

Describe Heb C clinical course

A

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
Q

Describe Hep E transmision

A

RNA birus spread fecal oral

36
Q

DEscribe Hep E clinical course

A

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
Q

Which hepatitis viruses do we have vaccines for?

A

Hep A
Hep B (and thus indirectly against Hep D)
Hep E, but not commercially available

38
Q

Serology for Hep A?

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
Q

Serology for Hep B?

A

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
Q

What will be high in acute infection of HBV?

A

HbsAg and IgM anti-HBcore

41
Q

What will indicate recovery and immunity?

A

IgG anti-core

42
Q

What is the “core window”

A

the only positive thing will be the IgM anticore

the surface antigen and antisurface antigen cancel each other out

43
Q

What serology would indicate chronic carrier state for HBV?

A

positive HBsAg and negative for IgM anti-HBcore

and no other antibodies

44
Q

Serlogy for hep C?

A

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
Q

Serology for hep D?

A

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
Q

Serology for Hep E?

A

IgM antiHEV and HEV RNA

47
Q

List the tests used to screen blood to avoid transufsion transmitted hepatitis.

A

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
Q

Describe how perinatally acquired HBV is prevented.

A

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
Q

Describe the possible clinical presenations of acute viral hepatitis?

A

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
Q

When is an acute viral hepatitis defined as a chonic viral hepatitis/

A

persistent chronic inflammatory destruction of live parenchyma - hepatitis lasting more than 6 months is defined as chronic hepatitis

Hep B, C and D

51
Q

Describe the pathologic findings seen in acute viral hepatitis

A

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
Q

Is actue viral hepatitis frequently biopsied?

A

No

53
Q

Describe the pathologic findings that can be present in a patient with chronic viral hepatitis with ongoing necroinflammatory changes

A

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
Q

Why is it sometimes necessry fo rperform liver biopsy in these patients?

A

you need to do a biopsy to see how bad the cirrhosis is

55
Q

Describe the pathologic clues that can be seen on liver biopsy that would suggest that someone may have chronic HBV infection.

A

groudn glass hepatocyte

56
Q

Also describe the pathologic clues that would usggest chronic HCV infections.

A

mild steatosis

57
Q

Describe some of the causes of acute massive hepatic necrosis.

A

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
Q

If these patients survive, do they always get cirrhosis?

A

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
Q

Define autoimmune hepatitis/

A

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
Q

Describe the key antibodies used in diagnosis of autoimmune hepatitis

A

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
Q

What feature seen on liver biopsy may suggest a diagnosis of autoimmune hepatitis?

A

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
Q

Contrast the treatment of AIH with that of chronic viral hepatitis

A

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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