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My DEMS I > Viral and Non-viral Liver Disease > Flashcards

Viral and Non-viral Liver Disease Flashcards

1
Q

Cirrhosis

A

Scarred liver
End point to many chronic liver diseases

Compensated:
Functional
Decompensated:
Failing functions

-diffuse fibrous septation that divides liver parenchyma into nodules

Result of chronic recurring death of hepatocytes, deposition of extracellular matrix, and architectural and vascular reorganization

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2
Q

Liver has high

A

functional reserve and regenerative capacity

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3
Q

Liver functions

A 
Lipid, carb, prot metab
Coagulation factor produc
Detox
stores vit/glycogen
Reticuloendothelial system
Bile processing and secretion
Albumin production
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4
Q

Bile flows in ___ direction of blood in liver

A

opposite

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5
Q

Portal tracts/triads

A

PV
HA
BD

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6
Q

Acute vs chronic injury

A

acute injury usually resolves

Chronic injury–> cirrhosis (scarred down)–> liver failure

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7
Q

Liver failure signs/sx

A

Jaundice (bilirubin buildup in tissues)
Ascites, peripheral edema (from hypoalbuminemia)
smell (sulfur metabolites)
spider angiomata (estrogen problem)
Palmar erythema
Hypogonadism and gynecomastia in men
Coagulapathy
Encephalopathy (derangements in consciousness, accum of ammonia in blood)
Hepatorenal syndrome (vascular perfusion abnormalities)

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8
Q

gross failed liver

A

Massive necrosis (death of most of liver: gray; yellow/green is alive)

**Cirrhosis: nodular, shrunken, scarred liver

Dysfunction without cirrhosis or necrosis (looks normal)

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9
Q

Cirrhotic liver gross

A

septation

parenchymal nodularity

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10
Q

Portal hypertension

A

Increase blood pressure in portal system

Result of vascular reorganization in liver

Increase in sinusoidal pressure (increased vascular resistance)

  • abnormal portal- systemic shunts (large connections) Ex: esophageal varices; hemorrhoids; periumbilical caput medusae
  • hepatic encephalopathy,
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11
Q

Jaundice and cholestasis

A

Bilirubin production > Bilirubin clearance

Excessive extrahepatic bilirubin production
Reduced hepatocyte uptake
Impaired conjugation
Decreased hepatocellular excretion
Impaired bile flow**
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12
Q

Most common chronic liver diseases in US adults

A 
Viral hepatitis C
Alcohol induced liver disease
Non-alc fatty liver disease
Viral hep B
Other
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13
Q

Hepatitis

A

Necroinflammatory injury to hepatocytes
Inflammatory injury and death of hepatocytes

etiologies:
Steatohepatitities:
(Alcohol or not)
Viral
Common cause of chronic liver disease
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14
Q

Hepatitis on histology

A 
swelling/degen
apoptosis/lobular
apo/interface
bridging necrosis
geographic coagulative necrosis

**look @ pics

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15
Q

Inflammation in hepatitis

A

Lymphocytes – many hepatitides; common in viral
Neutrophils – common in steatohepatitis (assoc w/ fat)
Eosinophils – common in drug injury
Plasma cells – common in autoimmune hepatitis

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16
Q

Acute hepatitis

A

New onset (

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17
Q

Chronic hepatitis

A

Long-standing, on-going hepatocyte injury and inflammation (>6 months)

Common causes: chronic viral hepatitis, autoimmune hepatitis, drug injury

Microscopic findings: less prominent inflammation and injury, preponderance of portal tract-based inflammation, fibrosis; looks “less severe” than acute; Spotty

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18
Q

General features of liver injury

A

Cytoplasmic accumulations

Degeneration, necrosis, and apoptosis

Inflammation

Regeneration, fibrosis, and cirrhosis

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19
Q

Cytoplasmic accumulation

A

*may be cause of disease or just seen due to disease

Fat – Steatosis
Bile – Cholestasis
Iron – Hemosiderosis/ genetic hemochromatosis
Copper – Wilson Disease / chronic cholestasis
Viral particles – Viral hepatitis

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20
Q

Histology of viral inclusion

A

“ground glass inclusion”

-cells filled with virions

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21
Q

Regeneration and fibrosis

A
  • cycles of inj/regen
  • activated stellate cells deposit collagen
  • architectural and vascular reorganization
  • leads to cirrhosis
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22
Q

Fibrosis histology

A

type I collagen (blue) (normally just in portal tract)

  • lines wrapping around hepatocytes
  • pericellular fibrosis

Portal fibrosis: larger, rounder portal tracts
Periportal fibrosis: stellate appearance of portal tracts
bridging fibrosis: connections of collagen (portal tract to tract or to central v.)
well defined septa w/ nodules: cirrhosis

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23
Q

what can you use to track chronic hepatitis?

A

biopsy surveillance (serial liver biopsies)

grade: amount of inflammation and injury

“Stage” = amount of fibrous tissue deposition

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24
Q

viral hepatitides

A

Hepatotropic viruses = hepatocyte is primary target

Hepatitis C
Hepatitis B
Hepatitis D
Hepatitis A
Hepatitis E

Other viruses also uncommonly cause hepatitis

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25
Q

Hep B

A

partially dsDNA (all others hep viruses are RNA viruses)

freq of chronic liver disease 10%

26
Q

fecal oral hep virus transmission

A

Hep A, E: and NEVER go on to chronic liver disease (acute)

(BCD parenteral)

27
Q

Parenteral hep virus transmission

A

B: 10% go on to chronic liver disease
C: 80%
D: 5%

*look at rest of table 10/26 9am

28
Q

Hep C virus infection

A

Major cause of chronic liver disease in the United States

Genetically unstable = multiple genotypes and subtypes
(Anti-HCV antibodies made, but antibodies are not neutralizing)

Transmission mostly by blood and body fluids

Range of clinical outcomes/presentations
(Most common is a chronic hepatitis (~85%))

29
Q

HCV Risk factors

A 
IV drug abuse
multiple sexual partners
recent surgery
needle stick injury
HCV infected person contact
employment in med/dental fields
30
Q

Acute infections of HCV

A

always asymptomatic!!!

  • 15-20% clear virus after infec
  • rare:fulminant hepatitis

80% w/ chronic hep go to stable disease, 20% go to cirrhosis

31
Q

Chronic hepatitis histology

A

spotty

can see lymphoid aggregate

32
Q

Hep B virus infection

A

Major cause of chronic liver disease worldwide

Can integrate into genome

Transmission by blood and body fluids; also vertical transmission is important

Range of clinical outcomes and presentations
(Most recover; only ~5% progress to chronic hepatitis)

33
Q

Hep B acute hepatitis

A

70% subclinical disease
30% icteric disease (sx)

Most adults (>90%) will clear virus on own
5-10% go to chronic hep, then either clear infec, healthy carrier state (most), 12-20% cirrhosis, and some (6-15%) w/ cirrhosis go to hepatocellular carcinoma.
34
Q

Hep B w/ recovery

A

incubation: 8 weeks
Sx: jaundice, pain, fatigue

HBeAg, HBV-DNA, HBsAg signify active disease/viral rep

IgM to IgG Ab confer immunity

35
Q

Hep B chronic carrier

A

incubation, infection

HBeAg, HBV-DNA, HBsAg remain present due to ineffective immune response against virus

36
Q

Hep B histology

A

ground glass hepatocytes (Hep B virions)

Sanded nucleus (O shape)

37
Q

Hep D virus

A

Replication incompetent, completely dependent on HBV coinfection

Potentiates effects of HBV: increased risk of fulminant hepatitis, increased activity, and faster progression to end stage liver disease

Intravenous drug abuse**

38
Q

Hep A

A

fecal oral
causes acute hepatitis only
(weeks to months)
jaundice, pain, fatigue

39
Q

Hep E

A

acute hep only
fecal oral
higher mortality in pregnant women

40
Q

Autoimmune liver disease

A

Autoimmune Hepatitis

Primary Biliary Cirrhosis

Primary Sclerosing Cholangitis

41
Q

Autoimmune Hepatitis

A

Immune-mediated attack directed at hepatocytes

Clinical Presentation:
F> M (78% ))
Often present in association with other autoimmune diseases.
Has a variable course: indolent to severe

Serology:
Autoantibodies (ANA, ASMA (anti smooth muscle ab), Anti-LKMB) (80%)
Elevated IgG

Histology:
Spotty interface hepatitis
Plasma cell rich

42
Q

Primary Biliary Cirrhosis

A

Immune-mediated attack of intrahepatic small caliber bile ducts

Clinical Presentation:
Insidious onset with pruritus often before jaundice
**Middle aged women most commonly affected
Cholestatic liver function testing (elevated ALP, GGT, bilirubin)

Serology:
Anti-mitochondrial antibody (90%)
Elevated IgM

Prognosis:
25% with liver failure at 10 years

*all pts with PBC do NOT necessarily have cirrhosis at that time

Histology: “active stage” bile ducts damaged by lymphocytes; granulomatous duct destruction
Later: absence of bile ducts, minimal inflamm

43
Q

PSC

A

Primary sclerosing cholangitis

Presumed immune-mediated obliterative fibrosis of intrahepatic and extrahepatic bile ducts (LARGE caliber bile ducts)

Clinical Presentation:
Men > women; 70% of patients have ulcerative colitis
Asymptomatic with persistent alkaline phosphatase elevation
Progressive fatigue, pruritus, and jaundice

Diagnosis:
Cholangiography = alternating biliary strictures and dilation
No specific serologic findings!!
-Can also see “onion skin” fibrosis (concentric rings) around bile duct on biopsy

Prognosis:
Variable clinical course; increased risk for cholangiocarcinoma

44
Q

Drug induced liver injury

A

common

Many patterns of injury (mimics other diseases):
Necrosis, cholestasis, bile ducts, autoimmune-like hepatitis, steatosis, steatohepatitis, acute hepatitis, or chronic hepatitis

Intrinsic or idiosyncratic:
Intrinsic (often dose related) (e.g. acetaminophen)
Idiosyncratic (unpredictable)

45
Q

Acetaminophen

A

Major cause of ACUTE liver failure that leads to liver transplant in United States

Intrinsic hepatotoxin

Centrilobular necrosis (zone 3)

46
Q

Metabolic liver diseases

A

Steatosis/Steatohepatitis:
Alcohol-related
Non Alcoholic

Hereditary Hemochromatosis

Wilson Disease

Alpha-1-antitrypsin deficiency

47
Q

Steatosis

A

Accumulation of fat in hepatocytes

Metabolic derangement of hepatocytes

Many causes: metabolic syndrome, alcohol, drug effect, Wilson disease, viral infection

lipid influx> lipid clearance
fat enters via: chylomicrons (diet), from periphery (lipolysis), carbs–> lipogenesis. Removal by beta oxidation (CO2, ketones( or into VLDL

48
Q

Steatohepatitis

A

Hepatocellular injury in association with steatosis:
+/- overt inflammation

Causes: alcohol, metabolic syndrome, drug injury

Not all causes of steatosis also cause steatohepatitis

Often chronic and can lead to fibrosis and cirrhosis

histology
swelling, fat, neutrophils
pericentral/pericellular fibrosis

49
Q

Alcohol steatosis

A

Alcohol steatosis: carb load short circuits feedback control of lipogenesis— so accum of lots of hepatic lipid; also stim of lipolysis from periphery; modification of oxidative state of hepatocyte– Beta oxidation impeded; packaging abnormalities in VLDL
-leads to injury

Histology
see injured hepatocytes, neutrophilic infiltrate, fat
**Mallory bodies (ropy inclusions w/in hepatocytes)

50
Q

Non-alcholic steatosis/ steatohepatitis

A

Fatty liver disease associated with:
Obesity, diabetes type II, hypertriglyceridemia

Increasing prevalence in US

-**lipolysis: increase in delivery from peripheral sources to liver (endocrine abnormalities)
-minor: dietary delivery of fats and certain types of carbs
–>increased hepatic lipid,
changes in B ox, VLDL formation

51
Q

Hereditary hemochromatosis

A

Genetic iron overload disease:
Manifests as liver disease, diabetes, heart failure

AR inheritance
5/1000 (Northern European descent)
-HFE gene mutations (C282Y and H63D)
Abnormal regulation of iron absorption (don’t turn off iron absorption)

histology:
iron deposits in hepatocytes (blue w/ Prussian blue stain)

52
Q

Wilson Disease

A 
Cu overload thru body
-Liver disease, neuropsych problems
-Mut: ATP7B gene
AR inheritance
1/30,000
Transporter involved in bile excretion of Cu (remains in hepatocyte)
53
Q

Alpha-1-Antitrypsin deficiency

A

Genetic decreased production of alpha-1-antitrypsin

Alpha-1-antitrypsin is a protease inhibitor

AR inheritance
PiMM is normal; PiZZ is common disease genotype
Protease inhibitor levels less than 10% normal in PiZZ

In PiZZ…
…most have pulmonary emphysema
…10% develop liver disease

Histology: PASD stain (pink globules) A-1-A

54
Q

Abnorm of blood flow

A 
Problems with blood entering liver (obstruction)
intrahepatic causes (not getting thru liver-- often cirrhosis)
post hepatic obstruction (hepatic v thrombosis)
55
Q

Malignant liver masses in adults

A

heptaocellular carcinoma

cholangiocarcinoma

56
Q

Benign liver masses in adults

A

Hemangioma
Focal Nodular Hyperplasia
Hepatocellular Adenoma

57
Q

Hepatocellular carcinoma

A

Malignant neoplasm of hepatocytes

Most common PRIMARY malignant liver tumor (most common are mets)

Occurs mostly in patients with chronic liver disease (HCV, HBV, alcohol) and cirrhosis

dismal long-term survival

58
Q

Cholangiocarcinoma

A

Malignant neoplasm of bile ducts

May be intrahepatic or extrahepatic

RF: primary sclerosing cholangitis

dismal long-term survival

gross: fibrotic mass
histology: gland forming, malignant, w. abnormal fibrosis or desmoplasia

59
Q

Hemangioma

A

Benign neoplasm of dilated vascular spaces

Most common primary hepatic tumor (~2%)

More common in women (1:4)

Usually small and asymptomatic; Larger ones may require resection

Vague RUQ pain, early satiety, nausea, vomiting

Histology: dilated vascular spaces

60
Q

Focal nodular hyperplasia

A

Benign mass-like proliferation of hepatocytes

Arises due to a local vascular flow anomaly
Old term = “focal cirrhosis”

Second most common primary hepatic mass

More common in F:M 4:1
Usually asymptomatic

Histology: septation, nodularity, **central stellate scar w/ large thickened arteriole

61
Q

Hepatocellular adenoma

A

Benign neoplasm of hepatocytes

mostly in women of child-bearing age

Associated with oral contraceptive use
Usually no underlying chronic liver disease

Asymptomatic or RUQ abdominal pain

Risk is of rupture into abdomen with hemorrhage

***Extremely low risk of malignant transformation

Histology: prolif of hepatocytes

My DEMS I (26 decks)

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