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GI Exam 2 > Liver Pathology > Flashcards

Liver Pathology Flashcards

1
Q

biggest cause of chronic liver disease? Second most?

A

hep C

alcoholic liver disease

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2
Q

Obstruction outside liver bile ducts - which test high?

A

AP - alkaline phosphatase

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3
Q

**What is normal total bilirubin level in blood?

**At what level do we get jaundice?

A

0.1-1.2 mg/dL

> 2 mg/dL = jaundice

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4
Q

How do we measure conjugated and unconjugated bilirubin?

A

there is a direct test for conjugated

unconjugated is indirectly measured by measuring total bilirubin and subtracting conjugated

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5
Q

What does cholestasis mean?

A

slow flow of bile

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6
Q

Cellular process of conjugating bilirubin - steps, enzymes, locations

A

1) UC-Bilirubin-Albumin complex taken up by hepatocyte from circulation
2) Glutathione S transferase enzyme needs to work on UC-bilirubin-albumin to get into ER
3) In ER UGT1A1 conjugates the bilirubin to ONE or TWO sugars = now C-bilirubin is water soluble
4) ready to be excreted as bile! enzyme in canicular membrane Via MRP2 or MRP3

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7
Q

**What enzyme conjugates the bilirubin? where does this occur?

A
  • UGT1A1 -uridine diposhphate glyconisyl transferase (glucuronyl transferase?)
  • in the Endoplasmic reticulum
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8
Q

What are causes of unconjugated hyperbilibubinemias?

A
  • RBC overproduction
  • reduced uptake at liver cell
  • defective conjugation
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9
Q

What are causes of conjugated bilirubinemias?

A
  • defective excretion - cant get out of hepatocyte

- defective secretion - cant get into bile duct system

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10
Q

Which hereditary hyperbilirubinemia is autosomal dominant??

A

ONLY one is Crigler Najjar syndrome type 2

(decreased UGT1A1 activity

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11
Q

Gilbert syndrome

1) What is the issue here?
2) What inheritance pattern?
3) Liver pathology?
4) What is the clinical course?
5) When do issues present? TX?

A

1) unconjugated hyperbilirubinemia
- decreased UGT1A1 activity - due to promoter mutation

2) AUTOSOMAL RECESSIVE (FYI: ALL HEREDITARY UNCONJUGATED AND CONJUGATED HYPER-BILIRUBINEMIAS ARE AUTOSOMAL RECESSIVE EXCEPT CRIGLER NAJJAR TYPE 2 IS AUTOSOMAL DOMINANT)
3) NO LIVER PATHOLGY
4) innocuous
5) jaundice when stressed or fasting - NO TX - normal life

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12
Q

Crigler Najjar Syndrome type 1

1) What is the defect here? Bilirubin levels?
2) What is the inheritance?
3) Liver pathology?
4) Clinical course?
5) TX?

A

1) unconjugated hyperbilirubinemia
-type1=ABSENT UGT1A1 activity
= BILIRUBIN GOES UP TO 8-11mg/dL)**

2)type1 = autosomal RECESSIVE
(FYI: ALL HEREDITARY UNCONJUGATED AND CONJUGATED HYPER-BILIRUBINEMIAS ARE AUTOSOMAL RECESSIVE EXCEPT CRIGLER NAJJAR TYPE 2 IS AUTOSOMAL DOMINANT)

3) NO LIVER PATHOLOGY
4) type1 = fatal in neonates w/ kernicterus(yellow basal ganglia)
5) NEED phototherapy and a transplant

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13
Q

What are the unconjugated hereditary hyperbilirubinemias?

A
  • Crigler-Najjar synd type 1 and 2

- Gilbert sydrome

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14
Q

What are the conjugated hereditary hyperbilirubinemias?

A
  • Dublin-johnson syndrome

- rotor syndrome

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15
Q

Dublin Johnson Syndrome

1) What is the defect here?
2) What is the inheritance?
3) Liver pathology?
4) Clinical course?
5) Diagnosis? TX?

A

1) conjugated hyperbilirubinemia
- impaired bilary excretion of bilirubin glucuronides due to mutation in canalicular multidrug resistance protein 2 (MRP2) - cant move conjugated into canalicular system!

2) autosomal recessive
3) pigmented cytoplasmic globules* = BLACK LIVER* Due to epinephrine metabolic products
4) innocuous -

5) asymptomatic- no TX- may have jaundice during pregnancy
use labs = normal urinary copropoyphyrins with increased ISOMER 1 (ISOMER 3 is higher in Rotor)

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16
Q

What is the inheritance of all conjugated hereditary hyperbilirubinemia?

A

autosomal recessive (Dublin Johnson and Rotor syndrome)

FYI ALL HEREDITARY UNCONJUGATED AND CONJUGATED HYPER-BILIRUBINEMIAS ARE AUTOSOMAL RECESSIVE EXCEPT CRIGLER NAJJAR TYPE 2 IS AUTOSOMAL DOMINANT W/ VARIABLE PENETRANCE

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17
Q

Rotor Sydnrome

1) What is the defect here?
2) What is the inheritance?
3) Liver pathology?
4) Clinical course?
5) Diagnosis? TX?

A

1) conjugated hyperbilirubinemia
- decreased hepatic uptake and storage?
- decreased bilary excretion?

2) autosomal recessive
3) No liver pathology
4) innocuous

5) Asymptomatic jaundice - NO TX
- increased total coproporphyrin excretion with ISOMER 1 in normal range and ISOMER 3 IS HIGHER - with DUBIN ISOMER 1 IS HIGH!)

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18
Q

Only hereditary hyperbilirubinemia that shows pathology in the liver?

A

Dubin Johnson -pigmented cytoplasmic globules

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19
Q

Crigler Najjar Syndrome Type2

1) What is the defect here?
2) What is the inheritance?
3) Liver pathology?
4) Clinical course?
5) TX?

A

1) unconjugated hyperbilirubinemia
- DEC UGT1A1 activity

2) autosomal DOMINANT WITH VARIABLE PENETRANCE**
(FYI: ALL HEREDITARY UNCONJUGATED AND CONJUGATED HYPER-BILIRUBINEMIAS ARE AUTOSOMAL RECESSIVE EXCEPT CRIGLER NAJJAR TYPE 2 IS AUTOSOMAL DOMINANT)

2) NO LIVER PATHOLOGY
4) mild with occasional kernicterus
5) Phenobarbital reduces level!***

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20
Q

Progressive familial intrahepatic cholestasis (PFIC)

1) What is the general issue here?
2) Are these diseases worse/milder than hereditary hyperbilirubinemias?
3) When present with signs?
4) inheritance?
5) What happens to person?

A

1) hereditary defects in bilary epithelial transporters = slowing of bile flow!
2) WORSE - usually progress to cirrhosis in adolescence = need liver transplant
3) during childhood
4) autosomal recessive
5) cholestasis; fat malabsorption; fat sol vit deficiency; osteopenia; liver failure

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21
Q

Most common issue that leads to liver transplant with PFICs?

A

Biliary atresia in infant

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22
Q

What compounds does normal bile contain?

A
  • cholic, chenodeoxycholic acid taurine/glycine salts
  • cholesterol
  • lecithin (phosphatidylcholine = for protection!)
  • bilirubin
  • bicarb
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23
Q

Where is the location of disease on cellular level for PFIC 1, 2, and 3?

A
  • 1 = on cholangiocytes and hepatocytes ON APICAL MEMBRANE

- 2 and 3 = on hepatocyte on APICAL (CANALICULAR) MEMBRANE

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24
Q

Which PFIC is due to a canalicular ATPase problem?

A

PFIC1 - energy breakdown pumps

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25
Q

Transport of what is messed up in PFIC2?

A

bile salts

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26
Q

Transport of what is messed up in PFIC3?

A

phosphatidylcholine

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27
Q

PFIC-1 (Byler Disease)

-What is the issue?

A

-Progressive familial intrahepatic cholestasis (PFIC)

  • canalicular ATPase
  • ATP8B1
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28
Q

PFIC-2

-what is the issue here?

A

-Progressive familial intrahepatic cholestasis (PFIC)

  • Bile salt export pump broken
  • ABCB11
  • MDR2???????? NOT ON SLIDE?
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29
Q

PFIC-3

-what is the issue here?

A

-Progressive familial intrahepatic cholestasis (PFIC)

  • phosphatidylcholine transfer
  • MDR3- if missing/broken=EPITHELIAL DAMAGE
  • ABCB4
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30
Q

MDR2 transports?

A

bile salts PFIC2

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31
Q

MDR3 transports?

A

phospholipids PFIC3

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32
Q

Rossette formation around areas of bile in hepatocytes on biopsy?- what disease pathology?

A

PFIC!

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33
Q

causes of jaundice and cholestasis is?

A

PREHEPATIC:(hemolytic anemia) related to anything that causes RBC breakdown (erythroblastosis, immune hemolysis, congenital RBC disease (sickle cell, thalessemia, sherocytosis)
-Impaired uptake: hepatocellular injury, drugs, newborn
HEPATIC DAMAGE (VIRUS AND ALCOHOL!)
ANY KIND OF OBSTRUCTION TO THE DUCTS

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34
Q

Drugs that cause hepatocellular damage?

A

chlorpromazine

erythromycin

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35
Q

top 2 causes of hepatocellular damage?

A

1- virus

2- alcohol

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36
Q

Hepatic disorders that cause duct obstruction:

A

1) diffuse infiltrative
- granulomatous disorders (TB)
- malignancy
2) inflammation of bile ducts
- drugs
- primary bilary cirrhosis
3) others
- estrogens
- steroids

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37
Q

top two causes of posthepatic dysfunction?

A
  • gallstones

- head of pancreas cancer

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38
Q

symptoms of cholestasis?

A
  • pruritus
  • jaundice
  • CLAY COLORED POOP
  • dark urine
  • bleeding diathesis
  • xanthomas
  • osteoporosis
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39
Q

Lab results for cholestasis?

A 
incleased AP
increased GGT
increased 5 nucleotidase
hyperbilirubinemia >1.2
hyperlipidemia (xanthomas)
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40
Q

Pathology of choestasis on microscopy?

A
  • bile canaliculi are filled with bile (stained orange/yellow)
  • hepatocytes are swollen and filled with bile (yellow/orange)
  • kupffer cells in sinusoids are filled with bile (Same)
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41
Q

Ductular reaction seen with which condition?

A

cholestasis - ducts proliferate

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42
Q

Feathery degeneration see with which condition?

A

cholestasis - the cells are swollen, injured and filled with bile - also leaking AST and ALT

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43
Q

What happens as the cholestasis condition progresses?

A

get secondary bilary cirrhosis - fibrosis!!!!

need fibrosis to get cirrhosis!!

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44
Q

top two causes of liver cirrhosis?

A

alcohol

viral hep

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45
Q

What factor will drive fibrosis?

A

TGF-beta

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46
Q

Which cells proliferate in liver fibrosis?

A

stellate cells

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47
Q

Whcih cells are secreting al the factors that cause proliferation and fibrosis that leads to cirrhosis?

A

kupffer cells

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48
Q

Macronodular cirrhosis is seen in which kind of patients?

A

LARGER PIECES OF TISSUE
hep B
hep C
Wilsons disease

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49
Q

What are the two types of cirrhosis and describe each:

A

1) compensated: can live with but can progress to decompensated
2) decompensated: this is the problematic one where: portal hypertension; hepatorenal syndrome; liver failure; hepatic encephalopathy

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50
Q

Micronodular cirrhosis is seen in in which kind of patients?

A

SMALLER PIECES OF TISSUE

Alcoholic!

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51
Q

What are complications of portal-HTN

A
  • gastro-esophageal varices
  • rectal varices (hemorrhoids)
  • caput medusae
  • ascites
  • hypersplenism
52
Q

Lab results of liver cirrhosis?

A
  • dec albumin
  • inc serum bilirubin
  • inc transaminases(ALT and AST)
  • inc GGT (cholestasis)
  • inc Prothrombin time (clotting factors not produced)
53
Q

Spider angiomas on skin - which disease?

A

LIVER CIRRHOSIS

54
Q

definition and hepatic/non-hepatic causes of ascites:

A
  • excess fluid in peritoneal cavity
    1) hepatic=
  • chronic/cirrhotic liver disease
  • subacute liver disease
    2) nonepatic=
  • systemic diseases =
  • ->TB
  • -> pancreatitis
  • ->nephrotic syndrome
  • HEART FAILURE*
  • peritoneal disease
55
Q

What is SAAG?

What are interpretation of SAAG?

A

-SAAG= serium-ascites albumin gradient

  • if SAAG >1.1g/dL = portal hypertensive
  • if SAAG<1.1g/dL = non-portal hypertensive (nephrotic, peritoneal disease, TB…)
  • if above 25 = due to Right heart failure
56
Q
  • Formation of fluid?

- Mesenteric capilary leaks becuase of?

A

-lymph exudate can come straight off of liver
Mesenteric capillaries:
-increased hydrostatis pressure (due to increased portal pressure)
-decreased oncotic pressure of blood drives fluid out (due to decreased albumin production by damaged liver)

Viscious cycle of adrenals thinking there is low volume so Renin angiotensis system is activated… leads to formation of more fluid in abdomen

57
Q

Chronic hepatic failure happens in what case?

This leads to?

A

FIBROSIS and Cirrhosis! ====> HCC!

58
Q

Acute hepatic failure types:

A

1) fulminant: total liver destruction - no liver architecture
- early onset
- no previous hepatic disease
- coagulopathy
- encephalopathy
- multiple organ failure
- HIGH MORTALITY
2) subfulminant: architecture can still be seen but ZONE 2 and 3 are destroyed

59
Q

Clinical features of Hepatic failure:

A
  • 1) encephalopathy-ammonia
  • 2) coagulopathy-clotting factors
  • 3) jaundice-bilirubin back up
    4) hypoglycemia (burn up gylcogen stores and LDH increases)
    5) metabolic acidosis
  • 6) multiple organ failure
  • hypotension
  • pulmonary edema
  • DIC
60
Q

4 forms of hepatic failure

A

Hyperacute
acute
subacute
chronic

61
Q

Hyperacute hepatic failure:

A

happens 7 days or less of the first symptoms such as jaundice of a liver dysfunction

62
Q

Acute hepatic failure:

A

within 4 weeks of the first symptoms of a liver dysfunction

63
Q

Subacute hepatic failure:

A

presents if the interval is 5-12 weeks

64
Q

chronic liver failure:

A
  • occurs in the context of CIRRHOSIS!

- many causes: alcohol, hepB or hepC, autoimmune, hereditary, metabolic causes (iron or copper overload…etc)

65
Q

Hepatorenal syndrome:

A
  • acute renal failure that occurs in the setting of cirrhosis or fulminant liver failure w/ no other previous kidney disease! Sometimes happens with portal HTN
  • altered BV tone and blood flow = altered blood flow to kidneys (Peripherally dilated and renal vasculature is constricted!)
66
Q

Signs and Labs of hepatorenal syndrome:

A
  • LIVER + RENAL FAILURE
  • normal kidney with oliguria or anuria
  • LABS: INC BUN and CREATININE
  • low urinary Na
  • normal urinary sedimentation
  • POOR PROGNOSIS
67
Q

What is hallmark of hepatorenal syndrome?

A
  • RENAL VASOCONSTRICTION

- PERIPHERAL ARTERIAL VASODILATION

68
Q

Type 1 Hepatorenal syndrome:

A
  • rapidly progressive renal failure

- defined by: doubling of initial serum creatinine to a level > 2.5 mg/dL in <2weeks

69
Q

Type 2 Hepatorenal syndrome:

A
  • moderate, steady renal failure

- serum creatinine >1.5mg/dL

70
Q

Hepatopulmonary syndrome:

  • what is the triad here?
  • issues?
  • what is key mediator??
A
  • chronic liver disease, hypoxemia, and intra-pulmonary vascular dilation
  • Ventilation perfusion mismatch= oxygen diffusion limit bc of rapid blood flow through dilated vessels (shunt like) –> blood flows through without getting oxygenated!
  • NO is key mediator!
71
Q

What is Hepatic encephalopathy?
Cause?
prognosis?

A
  • Increased NH3 (AMMONIA) brain diffusion with edema!
  • potentially reversible
  • need to change NH3 into UREA!
72
Q

Clinical features of hepatic encephalopathy

A
  • spatial perception disoriented
  • sleep disturbances
  • personality changes
  • asterixis
  • abnormal EEG

TIME TO WORRY WHEN:

  • lethargy
  • coma
  • decerebrate posture (extended elbows) FYI decorticate is flexed elbows)
73
Q

What is pathogenesis of hepatic encephalopathy?

A

-ammonia NH3 and mercaptons (bacterial breakdown products from intestines) cross BBB = brain swelling and inc intracranial pressure

74
Q

Hep Viruses - which have envelope/capsid which do not?

A

B,C and D are enveloped
A is icosahedral capsid
E is unenveloped

75
Q

Hep Viruses- which are RNA vs DNA?

A

ONLY hepB is dsDNA

A,C,D,E are ssRNA

76
Q

Hep viruses - what is transmission?

A
  • B,C,D are parenteral or close contact
  • A is fecal-oral
  • E is waterborne
77
Q

How to get Hep D?

A

Need to have previous HepB inf or co-infection with hepB and D at same time.

Hep D needs to HepB machinery to replicates

78
Q

Which Hep viruses produce carrier states?

A

Hep B,C and D

79
Q

Hep Virus incubation periods:

A
  • Hep B and C similar with 4 or 2 to 26 weeks respectively

- Hep A, D,E similar with 2 to 6 or 7 or 8 weeks respectively

80
Q

WHich Hep viruses cause chronic hepatitis?

A

Hep B,C and D

81
Q

Which viruses are associated with HCC?

A

Hep B and C

82
Q

Which hep viruses can cause ACUTE ASYMPTOMATIC INFECTION WITH RECOVERY - ONLY SEROLOGIC EVIDENCE:

What is the blood marker for acute serologic evidence?

A

IgM is evidence!!! ACUTE

-Hep A, B most, C, D coinfection, E

83
Q

Which hep viruses can cause ACUTE SYMPTOMATIC HEPATITIS WITH RECOVERY, WITH SOME JAUNDICE/FLU LIKE SYMPTOMS, ALT and AST?

A

-Hep A, B, C, D coinfection and E

ALL OF THEM

84
Q

Which hep viruses cause chronic hepatitis with or without progressing to cirrhosis?

A

infected before but virus is still replicating and destroying liver

Hep B few, C 85%, D superinfection most

85
Q

WHcih hep viruses cause FULMINANT HEP WITH MASSIVE TO SUBMASSIVE HEPATIC NECROSIS?

A

Hep A rare, B rare, C rare, D co and super, E pregnant

86
Q

most common form of viral hepatitis?

A

Hep A!

87
Q

What family virus is Hep A?genetic material? Capsule/membrane?

A

Picorna
ssRNA
icosahedral capsule

88
Q

What family virus is Hep B?

genetic material? Capsule/membrane?

A

Hepadnavirus
dsDNA
enveloped

89
Q

Most common cause of cirrhosis (worldwide) and HCC worldwide?

A

HepB

90
Q

Potential outcomes for HBV infection:

A

**TAKE AWAY: LOTS OF PEOPLE GET INFECTED BUT ONLY FEW PROGRESS & DEVELOP HCC!

1) 2/3 dont even know they got it - recovery
2) 1/3 symptomatic acute hepatitis (jaundice, AST, ALT)– of this 1/3:
a) 90% recover
b) 1% die or confluent hep necrosis
c) 10% chronic hep — of this 10%
- 70-90% are asymptomatic Hb_sAg carrier
- 10-30% chronic hepatitis and cirrhosis –> develop HCC!!!

91
Q

TH2 activated by what cell and what immune response activated?

TH1 activated by what cell and what immune response activated?

A

TH2= Activated by CD4 T-helper;
Activates HUMORAL - B CELLS

TH1=Activated by CD4 T-helpers; 
Activates CELLULAR -T-CELLS (CD8 via MHC class 1)
92
Q

Chronic hepatitis B - Extrahepatic manifestations in

1) Children:
2) Adults

A

1) glomerulonepritis

2) Polyarteritis nodosa

93
Q

1) Co infection regarding hepB/D?

2) Superinfection regarding hepB/D?

A

1) Hep B and D at same time

2) Had HepB before and you get HepD on top of it = BAD NEWS - SUPER = SUPERBAD!

94
Q

Why does HepD need HepB?

A

HepD needs HepBsAg (surface antigen) to replicate

95
Q

Coinfection HepB/D serology presentation?

Most common progression?

A
  • IgM for HepB and D!

- most RECOVER with immunity

96
Q

Superinfection HepB/D - Most common progression?

A
  • Most get chronic hepB/D
  • cirrhosis
  • more die with fulminant (7-10%)
97
Q

most common Hep cause of chronic liver disease? Issue/Progression with this Hep?

A
  • HepC
  • more often goes onto chronic liver disease–>85%! of these 50% get compensated-stable and the other half die. HCC IS RARE
98
Q

Chronic HepC extrahepatic manifestations:

A
  • cryoglobulinemia - protein sludging and precipitating stuff at low temperatures = lesions
  • throiditis
  • glomerulonephritis
  • thrombocytopenia
  • diabetes!
99
Q

Whcih HCV genotype has more severe inflammation?

A

TYPE 2

100
Q

More common to get liver cancer from Hep C factors:

A
  • if have cirrhosis
  • if younger when you got hepC such as with IV abusers
  • male
  • alcohol use ++
101
Q

HepE transmission?

What unique condition make the disease much worse?

A
  • Waterborne!

- if pregnant and get its bad news bears

102
Q

Lobular disarray, Lymphocytic inflammation, ballooning, cholestasis, and/or councilman bodies (apoptotic cells- dark and dense) seen in histology of what disease?

A

acute viral hep

103
Q

Piecemeal necrosis (zone 1 hepatocytes are being destroyed by inflammation) and/or bridging fibrosis is seen in histology of what liver disease?

A

chronic viral hep

104
Q

Ground glass hepatocytes (cells packed with surface antigen) are seen with which type of liver disease?

A

Chronic Hep B

105
Q

Lymphoid aggregates are seen with which type of liver disease?

A

Chronic Hep C

106
Q
  • Primary biliary cirrhosis -
  • what kind of inflammation?
  • what ducts most affected?
A
  • granulomatous inflammation

- small ducts

107
Q
  • Primary sclerosing cholangitis-
  • what ducts more affected?
  • what kind of damage
A
  • large bile ducts!

- fibrosis around the large ducts!

108
Q

Primary Biliary cirrhosis

  • what immune cell issues/
  • which sex more affected?
  • what antibodies?
  • associated with what autoimmune disorders?
  • what genetic component suspected?
A
  • T-cell cytotoxicity
  • 6F to 1M
  • Antimitochondrial antibodies
  • rheumatoid arthritis; glomerulonephritis, lupus…
  • DRW8 tissue type - genetics
109
Q

Primary biliary cirrhosis

-progression and presentation:

A
  • presents with fatigue and ITCHING that progressed over 10-15 years - Granuloatous inflammation!! SMALL DUCTS!
  • progressive jaundice, xanthomas, steatorrhea .. etc
110
Q

Primary biliary cirrhosis - LABS

A
  • inc AMA* (ANTI MITOCHONDRIAL* = AMA?)
  • anti-M2*
  • anti-PDH-E2
  • Inc IgM
  • inc AP/5-NT/GGT - as more small ducts obstructed these values go up
  • inc cholesterol

NEED LIVER BIOPSY

111
Q

Primary biliary cirrhosis STAGES:

A

1) Florid duct lesion - inflammation at protal tracts
- granulomas - epitheliod macrophages destroying ducts
- cholestasis
- ductular proliferation
2) Extension of inflammation outside of portal tract
- fibrosis spreading!
3) Larger areas of fibrosis - ISLANDS FORMING
4) cirrhosis - scarring - ISLAND

112
Q

What does Tx with Ursodeoxycholic acid do for patients with Primary biliary cirrhosis?

A

improves bile flow

113
Q

How long does it take to develop primary biliary cirrhosis?

Leads to:

A

LONG TIME- 10-20 years!

Liver failure
HCC

NEED liver transplant

114
Q

Primary Sclerosing cholangitis:

  • affects what component of liver?
  • sex predominance?
  • age?
  • related condition?
A
  • Fibrous obliterative cholangitis
  • MORE MALES
  • <50yo
  • ulcerative colitis and Crohns
115
Q

Primary sclerosis cholangitis

-presentation/progression:

A
  • majority have no symptoms
  • some have other general symptoms like tired, itching, diarrhea, abdominal pain, jaundice

-some have slow course and some have rapid bile duct obstruction, cirrhosis, and liver failure

116
Q

Primary sclerosing cholangitis - LABS:

A
  • INC AP
  • INC GGT
  • INC 5-NT
  • ERCP
  • INC ALT/AST
  • INC P ANCA***
117
Q

What does endoscopy cholangiography of primary sclerosing cholangitis look like?

A

Beading pattern of ducts

118
Q

Primary sclerosing cholangitis- what does tissue histology look like?

A
  • fibrosis around the ducts - damage due to neutrophils

- fibrious - onion skinning

119
Q

Complications of Primary sclerosing cholangitis?

A
  • *-cholangiocarcinoma
  • chronic cholestasis
  • cholangitis
  • secondary biliary cirrhosis
  • liver failure
120
Q

Autoimmune hepatitis:

what is it?

A
  • inflammation cells are killing hepatocytes

- disease is chronic but resembles acute hepatitis

121
Q

Autoimmune hepatitis - etiology and markers:

A
  • 8F to 1M
  • Autoantibodies: (type1) ANA, (type1)SMA, (type2)antiLKM1 (liver kidney marker)
  • NO VIRAL MARKERS
  • NO AMA
  • inc globulins/IgG
  • HLA DR4
122
Q

What is histology of autoimmune hepatitis?

A
  • lymphocytes and plasma cells destroyin hepatocytes

- start in zone 1 and move from there

123
Q

Autoimmune hepatitis TYPE 1:

  • which markers?
  • age range?
  • prognosis to cirrhosis?
A

SMA and ANA
most common
10yo- elderly
-45% progress to cirrhosis

124
Q

Autoimmune hepatitis TYPE 2:

  • which markers?
  • age range?
  • prognosis to cirrhosis?
A

Anti-LKM1

  • young patients (2-14 yo)
  • *82% progress to cirrhosis
  • poor prognsois
125
Q

Autoimmune hepatitis TYPE 3:

  • which markers?
  • age range?
  • prognosis to cirrhosis?
A
  • Anti SLA/LP
  • 30-50yo
  • 75% progress to cirrhosis
126
Q

Tx for autoimmune hepatitis:

If no Tx outcome?

A

-give immune suppressor - steroids or whatever
-liver transplant
-if no treatment
=cirrhosis
=HCC
=die within 6mo

GI Exam 2 (11 decks)

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