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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
Hep B
partially dsDNA (all others hep viruses are RNA viruses) freq of chronic liver disease 10%
26
fecal oral hep virus transmission
Hep A, E: and NEVER go on to chronic liver disease (acute) | (BCD parenteral)
27
Parenteral hep virus transmission
B: 10% go on to chronic liver disease C: 80% D: 5% *look at rest of table 10/26 9am
28
Hep C virus infection
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
HCV Risk factors
``` IV drug abuse multiple sexual partners recent surgery needle stick injury HCV infected person contact employment in med/dental fields ```
30
Acute infections of HCV
always asymptomatic!!! - 15-20% clear virus after infec - rare:fulminant hepatitis 80% w/ chronic hep go to stable disease, 20% go to cirrhosis
31
Chronic hepatitis histology
spotty | can see lymphoid aggregate
32
Hep B virus infection
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
Hep B acute hepatitis
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
Hep B w/ recovery
incubation: 8 weeks Sx: jaundice, pain, fatigue HBeAg, HBV-DNA, HBsAg signify active disease/viral rep IgM to IgG Ab confer immunity
35
Hep B chronic carrier
incubation, infection | HBeAg, HBV-DNA, HBsAg remain present due to ineffective immune response against virus
36
Hep B histology
ground glass hepatocytes (Hep B virions) Sanded nucleus (O shape)
37
Hep D virus
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
Hep A
fecal oral causes acute hepatitis only (weeks to months) jaundice, pain, fatigue
39
Hep E
acute hep only fecal oral higher mortality in pregnant women
40
Autoimmune liver disease
Autoimmune Hepatitis Primary Biliary Cirrhosis Primary Sclerosing Cholangitis
41
Autoimmune Hepatitis
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
Primary Biliary Cirrhosis
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
PSC
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
Drug induced liver injury
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
Acetaminophen
Major cause of ACUTE liver failure that leads to liver transplant in United States Intrinsic hepatotoxin Centrilobular necrosis (zone 3)
46
Metabolic liver diseases
Steatosis/Steatohepatitis: Alcohol-related Non Alcoholic Hereditary Hemochromatosis Wilson Disease Alpha-1-antitrypsin deficiency
47
Steatosis
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
Steatohepatitis
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
Alcohol steatosis
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
Non-alcholic steatosis/ steatohepatitis
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
Hereditary hemochromatosis
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
Wilson Disease
``` 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
Alpha-1-Antitrypsin deficiency
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
Abnorm of blood flow
``` Problems with blood entering liver (obstruction) intrahepatic causes (not getting thru liver-- often cirrhosis) post hepatic obstruction (hepatic v thrombosis) ```
55
Malignant liver masses in adults
heptaocellular carcinoma | cholangiocarcinoma
56
Benign liver masses in adults
Hemangioma Focal Nodular Hyperplasia Hepatocellular Adenoma
57
Hepatocellular carcinoma
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
Cholangiocarcinoma
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
Hemangioma
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
Focal nodular hyperplasia
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
Hepatocellular adenoma
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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