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DEMS Pt 1 > Viral and Non Viral Liver Disease > Flashcards

Viral and Non Viral Liver Disease Flashcards

1
Q

Define acute liver disease including etiologies and histology

A

Less that 6 months of symptomatic liver disease with elevated ALT and AST as well as hepatic damage evident..
Etiology: Acute viral, drugs, autoimmune, idiopathic
Histology: Lobular disarray, wide spread inflammation and hepatocyte injury, numerous necrotic hepatocytes
NO FIBROSIS

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2
Q

Define chronic liver disease including etiologies and histology

A

Greater than 6 months of symptomatic liver disease with injury or inflammation
Etiology: Viral, autoimmune, drugs (not technically chronic but produce chronic appearance), idiopathic, many causes of acute disease can lead to chronic
Histology: Less prominent inflammation, patchy, mostly portal tract based, less lobular disarray, rare necrotic hepatocytes
Increasing fibrosis over time

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3
Q

Name five common histological patterns of liver injury

A 
Degeneration
Cytoplasmic accumulations
Hepatocyte death
Inflammation
Regeneration
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4
Q

What is the appearance and common diagnosis in liver degeneration?

A

Degeneration appears as ballooning degeneration in which the hepatocytes swell and the organelles are clumped together with keratin and pushed to the side. Reversible
ddx: Steatohepatitis

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5
Q

What is the appearance and common diagnosis of cytoplasmic accumulations?

A 
Accumulations can be:
Fat - steatosis
Bile - Cholestasis
Iron - hemosiderosis
Copper - Wilson's disease, severe cholestasis
Viral particles - viral hepatitis
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6
Q

What is the appearance and common diagnosis of hepatocyte death?

A

Necrosis - coagulative necrosis
Apoptosis - eosinophilia of the cytoplasm, small dark nucleus (single cells are called “Acidophils”)
Location of cell death in the liver narrows differential:
Acidophils in the interface zone: Autoimmune or Viral
Acidophils and necrosis in the confluence zone: Ischemia

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7
Q

What is the appearance and common diagnosis of liver inflammation?

A

Types of infiltrate are not specific for a diagnosis, but may help to limit the ddx:
Neutrophils - commonly Steatohepatitis
Eosinophils - commonly adverse drug reactions
Plasma cells - associated with autoimmune hepatitis
Lymphocytes - nonspecific, common to viral but many others
Location of inflammation is helpful, too:
Portal based inflammation: biliary disease
Interface inflammation: viral and autoimmune
Zone 3 inflammation: Autoimmune or acute cellular rejection (transplants, also immune moderated)

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8
Q

For Hep C, list the type of virus, mode of transmission, risk of chronicity, pathology, and serology

A

Type of virus: ssRNA, genetically unstable so it can evade ab that are produced
Transmission: Blood and bodily fluid (parenteral, mother to child, IV drug use, sexual contact)
Chronicity: 80% of HVC carriers will develop chronic disease, and can present as fulminant liver failure
Histology: Non-specific, necroinflammatory activity and fibrosis in interface and lobular regions, Lymphocytes
Serology: HVC RNA indicates ongoing infection

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9
Q

For Hep B, list the type of virus, mode of transmission, risk of chronicity, pathology, and serology

A

Type of Virus: dsDNA
Transmission: Blood and bodily fluids (parenteral, mother to child, IV drug use, sexual contact) Developing countries
May be asymptomatic, acute, chronic, or fulminant hepatitis
Chronicity: 5% develop chronic hepatitis
Pathology: Ground Glass cytoplasmic accumulations
Serology:
HBsAG: Hep B surface AG = infection is current
HBsAB: Hep B surface AB = prior infection or immunized
HBeAG: Hep B envelope AG= surrogate marker for heavy viral load
HBeAB: Hep B envelope AB= previous severe infection
HBc IgM: Hep B core IgM = acute immune response
HBc IgG: Hep B core IgG = chronic immune response

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10
Q

For Hep D, list the type of virus, mode of transmission, risk of chronicity, pathology, and serology

A

Type of Virus: circular RNA
Transmission: Parenteral, but can only infect along with HBV (usually via IV drug use)
Chronicity: ~70% for confection (HBV)
Potentiates HBV infection by increasing risk of fulminant hepatitis, increasing rate at which it progresses to end stage liver disease

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11
Q

For Hep A and E, list the type of virus, mode of transmission, risk of chronicity, pathology, and serology

A

Type: ssRNA
Mode of Transmission: Fecal-oral route
Chronicity: Does not produce chronic hepatitis, ACUTE ONLY!!
Serology: detection of serum IgM (both) or IgG (HEV)

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12
Q

What are the general rules and exceptions for the Hepatitis viruses concerning type of virus, mode of transmission, risk of chronicity, pathology, and serology?

A

Type of Virus: All ssRNA except HBV (dsDNA)
Transmission: All parenteral except A&E (fecal-oral)
Chronicity: Low except C (80%) and A&E (ZERO)

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13
Q

What do grade and stage mean in hepatitis?

A

Grade = amount of inflammation and injury (0-4)
Grade 0 = no inflammation
Grade 4 = Bridging necrosis with severe inflammation

Stage = amount of fibrous tissue deposition (0-4)
Stage 0 = No fibrosis
Stage 4 = Cirrhosis

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14
Q

What is the importance of hepatocellular carcinoma in chronic liver disease and how is the prognosis determined?

A

HCC is the most common primary malignant tumor of the liver and occurs almost exclusively in people who have chronic liver damage/cirrhotic livers. Highest risk causes of liver damage include: HCV, HBV, NASH and alcoholic liver disease.
Prognosis of HCC is determined by size, presence of vascular invasion, locality, and invasion of adjacent structures.

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15
Q

What is primary biliary cirrhosis, where does it occur, and what tests are useful in diagnosis?

A

Primary Biliary Cirrhosis is an autoimmune disease that destroys the INTRAhepatic bile ducts by inflammation. Onset is insidious with pruritus and jaundice. Usually seen in middle-aged women and is associated with underlying autoimmune disease.
LFT: Elevated ALT, GGT, Bilirubin (like PSC)
Serology: Anti-mitochondrial Antibodies (AMA) and elevated IgM. (unlike PSC)
Pathology: acute and chronic changes to liver
Acute: Lymphocytes and Plasma cells in portal region, associated cholestasis, FLORID DUCT
Chronically: bile duct loss, ductular reaction (new improper ducts), periportal copper accumulation

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16
Q

What is Primary Sclerosing Cholangitis, where does it occur, and what tests are useful in diagnosis?

A

PSC is characterized by patchy inflammation and obliterative fibrosis of EXTRAhepatic bile ducts and intrahepatic ducts. Often asymptomatic, but leads to progressive fatigue, jaundice and pruritus. More common in males and associated with IBD, esp. UC.
LFT: Elevated ALT, GGT, Bilrubin (like PBC)
Serology: none (unlike PBC)
ERCP or MRCP: “Beads on a string” appearance of sequential dilations and constrictions - diagnostic
Histology: Periductular lymphocytic inflammation around large bile ducts, progressive fibrosis (onion skin pattern)

17
Q

Describe autoimmune hepatitis including presentation, tests, pathology/histology, and treatment

A

Autoimmune hepatitis is characterized by inflammation and damage associated with plasma cell infiltrates.
Often presents acutely before settling into a chronic type hepatitis, and is more common in women.
LFT: elevated AST, ALT, normal ALP
Serology: Usually 1 of ANA, ASMA, Anti-LKMB, Increased IgG, but negative AMA (Indicates PBC??)
Path/Histo: Active disease shows inflammation/necrosis at interface and centrolobular regions, zones of confluent necrosis with plasma cells. Still non-specific and may be indistinguishable from acute hepatitis.
Treatment: Steroids (note this is the opposite of viral hepatitis)

18
Q

Describe drug related hepatitis including causes, type of hepatitis, and most common form (with antidote)

A

Drug related hepatitis may result from prescription meds, OTC, or herbal supplements. Injuries may be dose-related (intrinsic) or unpredictable (idiosyncratic).
Type of hepatitis: Nearly any, necrosis, cholestasis, biliary injury, autoimmune-type, steatosis, steatohepatitis, acute or chronic.
Acetaminophen is the most common cause. Causes confluent coagulative necrosis beginning centrolobular (Zone 3) spreading to pan-lobular depending on dose.
N-acetylcysteine is the antidote for toxic overdose.

19
Q

Name the four major metabolic liver diseases

A

Steatoheptitis (Alcoholic and Non-alcoholic/NASH)
Hereditary hemochromatosis
Wilson’s disease
a-1-antitrypsin deficiency

20
Q

Describe alcoholic steatohepatitis

A

Defined by clinical history of alcohol use
LFT: AST:ALT ratio >2, normal ALP, elevated GGP
Path/Histo: Mallory bodies (rope like structures of intermediate filaments) and neutrophils

21
Q

Describe non-alcoholic steatohepatitis (NASH)

A

Usually seen in patients with diabetes, metabolic syndrome, obesity, and adverse drug reactions.
LFT: mostly normal
Path/Histo: may have Mallory bodies and neutrophils, but less likely than alcoholic SH.
Leads to fibrosis and possible cirrhosis, starting in the interlobular (zone 3) regions and shows a chicken wire pattern

22
Q

Describe hereditary herochromatosis

A

Genetic mutation that causes abnormal regulation of iron uptake in the duodenum and leads to iron depositions in tissues. More common in men because women can shed iron through the menstrual cycle. Results in progressive cytoplasmic iron deposition in periportal regions first. Differentiated from secondary hemosiderosis by type of liver cell affected:
Hereditary = mostly hepatocytes
Secondary = Mostly Kupffer cells
Clinical manifestation in middle age as a triad:
Liver disease
Diabetes
Heart Failure

23
Q

Describe Wilson’s disease

A

An autosomal recessive disease of copper metabolism. Mutations in ATP7B cause a copper transporter involved with biliary secretion to malfunction.
Presentation: low serum ceruloplasmin levels, neurological symptoms, Kayser-Fleisher rings (around irises)
Histology: patch accumulation of copper in hepatocytes with steatosis and/or acute/chronic hepatitis changes

24
Q

Describe a-1-antitrypsin deficiency

A

An autosomal recessive disorder in which there is decreased production of a protease inhibitor.
PiMM > PiMZ > PiZZ = 10% of normal
Protease inhibitor normally prevents the actions of proteases released by neutrophils to limit tissue damage.
Most patients present with pulmonary emphysema, only a small portion have liver disease.
Histology: cytoplasmic accumulations of hyaline globules PAS positive, pink/purple staining, which are abnormally folded a-1-antitrypsin. Progressive fibrosis.

25
Q

Name the five common tumors of the liver and state whether each is benign or malignant

A 
Hepatocellular carcinoma (Malignant)
Cholangiocarcinoma (Malignant)
Hemangioma (Benign)
Focal Nodular Hyperplasia (Benign)
Hepatocellular Adenoma (Benign, low risk of malignant transformation ~5%)
26
Q

What are the etiology, gross findings, and histology of Hepatocellular Carcinoma?

A

Etiology:
associated with cirrhosis and chronic hepatitis

Gross Findings:
Mass in cirrhotic liver
Invades portal veins and hepatic arteries
Tumor may be green/yellow

Histology:
Thickened Trabeculae (hepatic plate)
Endothelialization of sinusoids
Unpaired arteries from neovascularization
No true portal triads
27
Q

What are the etiology, gross findings, and histology of Cholangiocarcinoma?

A

Etiology:
Intra- or Extra-hepatic
PSC is a risk factor
Often present at an advanced stage (25% 1 yr, 13% 2yr survival)

Gross Findings:
Dense fibrotic mass in hilar region (entrance of triad)
Infiltrative edges
Tan/white color

Histology:
Gland forming, invasive tumor
Abundant desmoplastic response

28
Q

What are the etiology, gross findings, and histology of Hemangioma?

A 
Etiology:
Most common primary hepatic tumor
Most common in women
Neoplasm of dilated vascular space
Presents with RUQ pain, early satiety, N/V

Gross Findings:
Well circumscribed mass in non-cirrhotic liver
Spongy, hemorrhagic surface with thrombosis and infarction

Histology:
Dilated, thin walled vessels
Infarction
Thrombosis

29
Q

What are the etiology, gross findings, and histology of Focal Nodular Hyperplasia?

A 
Etiology:
2nd most common primary liver mass
Associated with hemangiomas
Hyperplastic parenchyma dus to vascular anomaly
Asymptomatic

Gross Findings:
Central stellate scar

Histology:
Central Stellate Scar
Malformed or aberrant vascular structures
Ductular reaction without true portal areas

30
Q

What are the etiology, gross findings, and histology of Hepatocellular adenoma?

A 
Etiology:
Associated with oral contraceptives
Most common in women in childbearing ages
RUQ pain or asymptomatic
Can rupture and hemorrhage

Gross Findings:
Well circumscribed mass in non-cirrhotic liver
Soft, fleshy, cut surface

Histology:
Proliferation of benign hepatocytes
Normal hepatocyte plate thickness
Many unpaired arteries
No bile ducts or portal areas in hyper plastic region
Difficult to distinguish from well differentiated HCC

DEMS Pt 1 (35 decks)

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