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CSI- Winter > Hepatitis/Alcoholic Liver Disease > Flashcards

Hepatitis/Alcoholic Liver Disease Flashcards

1
Q

Pathological features of hepatitis

A
  • inflammation of the liver
  • Hepatocellular necrosis (focal or extensive)
  • Inflammatory cell infiltration of the liver (Portal areas vs parenchyma)
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2
Q

Acute hepatitis

A

-condition lasting less than 6 months
1. Complete resolution of liver damage with return to normal function and structure
OR
2. Rapid progression of the acute injury toward extensive necrosis and a fatal outcome

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3
Q

Chronic hepatitis

A
  • sustained inflammatory process lasting longer than 6 months
  • Difficult to differentiate from acute hepatitis on clinical or histologic criteria alone
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4
Q

Common causes of acute hepatitis

A
  • Viral hepatitis (A through E)
  • Drugs (prescription, OTC and illicit)
  • Alcohol
  • Toxins
  • Autoimmune
  • Wilson Disease
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5
Q

Wilson Disease

A
  • Autosomal recessive disorder
  • Results in accumulation of copper in various tissues (liver, brain, and corneas)

-Neuropsychiatric s/s along with liver disease is present

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6
Q

How to diagnose Wilson Disease

A

Low serum ceruloplasmin with high urinary and hepatic copper levels

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7
Q

Treatment for Wilson Disease

A
  • Indefinite
  • Copper chelation
  • Zinc supplementation
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8
Q

Acute hepatitis can be caused by direct toxin induced necrosis via

A

Acetaminophen or Amanita phalloides toxin (fungus/mushroom)

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9
Q

Acute hepatitis can be caused my host immune-mediated damage

A

-viral

Hep A, B, C, D, E viruses

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10
Q

Most common cause of acute hepatitis in the US?

A

Hep A virus

-Hep B is 2nd most common
Most extensively characterized

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11
Q

Most prevalent hepatitis virus world wide?

A

Hep C

  • But is an infrequent cause of symptomatic acute hepatitis
  • Accounts for most cases of acute hepatitis previously designated as non-A, non-B
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12
Q

Hep B antigens

A

HBsAg (surface)
HBeAg (Be Ag)
HBcAg (core)

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13
Q

Hep Be Ag is found….

A

Hepatitis Be antigen (HBeAg) is found in the EARLY phase of hepatitis B infection, then a bit later the hepatitis Bs antigen becomes detectable

-Serum levels of both antigens rise rapidly during the period of viral replication.

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14
Q

In HBV carriers and patients with chronic hepatitis B, positive HBeAg results usually indicate

A

presence of ACTIVE HBV replication and high infectivity

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15
Q

In HBV carriers and pts with chronic hep B, a negative HBeAg result indicates

A

very minimal or lack of HBV replication

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16
Q

What type of virus is Hep D?

A
  • Hepatitis D is an incomplete RNA virus
  • Requires HBV (HBsAg) for transmission**
  • Thus only causes hepatitis in people with HBV
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17
Q

Hepatitis E is typically found in endemic areas and is most commonly associated with __________

A

poor sanitation

-Shares many similarities with hepatitis A

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18
Q

SEE SCREEN SHOT OF COMPARISON CHART

A

of all hepatitis viruses

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19
Q

Acute viral hepatitis usually starts with

A
  • a prodromal phase (several days)
  • Typically constitutional and GI symptoms
  • Jaundice with bilirubinuria and acholic stools follow (pts usually feel better by now)
  • Hepatomegaly is present
  • Splenomegaly is present in 20% of patients

Many patients are asymptomatic or have symptoms without jaundice and thus do not seek medical attention

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20
Q

5-10% of hepatitis-B and C cases will have _________

A
  • arthritis and urticaria

- Resembling serum sickness (due to immune complex deposition)

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21
Q

Labs with acute hepatitis

A

-Aminotransferases (ALT and AST) are often greater than 20-fold normal and as high as 100-fold normal
-Elevation in bilirubin (>2.5 to 3 mg/dL) results in jaundice and defines icteric hepatitis
-Alkaline Phosphatase is usually 3xs normal
(except in cholestatic hepatitis)
-CBC usually shows mild leukopenia (w/ atypical lymphocytes)

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22
Q

+ HepBcAb IgG means

+HepBsAb means

A

pt had been infected with HBV

pt has mounted an immune response to the virus and is now immune

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23
Q

Serology for acute hepatitis B infection

A

+ HBsAg
- HBsAb
+ HBcAb IgM

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24
Q

Serology for chronic carriers of hep B

A

+ HBcAb IgG
- HBcAb IgM
+ HBsAg (+ HBeAg)
-HBsAb

Chronic active: HBeAg
Chronic passive: HBeAb

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25
Q

Serology of people vaccinated against hep B

A

+ HBsAb only

(Vaccine ONLY contains HBsAg)
-no core Abs and no Ags present (the only way to get these is to be exposed to the actual virus)

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26
Q

Serology for window period of Hep B infection

A

-Window period is the time when HBsAg has disappeared, but HBsAb isn’t detectable yet

+ for HBcAb ONLY

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27
Q

Cholestatic hepatitis

A
  • Self-limited with marked conjugated hyperbilirubinemia, alkaline phosphatase and pruritus
  • Usually associated with hepatitis A
  • Usually associated with hepatitis-A
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28
Q

Fulminant hepatitis

A
  • Due to massive hepatic necrosis

- Occurs in

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29
Q

Chronic hepatitis is typically seen in (which types)

A

hepatitis B, C and D

  • 1-10% in HBV (90% in neonates)
  • 85% in HCV
  • Common in HDV
30
Q

Rare complications

with HBV and HCV

A
  • Cryoglobulinemia (HBV and HCV)
  • Glomerulonephritis (HBV and HCV)
  • Polyarteritis nodosa (HBV)
31
Q

Treatment for Hep A, B, E

A

All cases of hepatitis A, B and E are self-limited
-Unless complicated by fulminant hepatitis

-Antiviral therapy in hepatitis B has not shown clear benefit

32
Q

Treatment for Hep C

A

Early treatment (within 12 wks of diagnosis) with interferon-alpha induces high sustained virologic response rates

33
Q

Treatment in all other cases of hepatitis

A
  • Supportive
  • Rest
  • Maintenance of hydration
  • Adequate dietary intake (low-fat, high carb)
  • Avoid alcohol
  • Treat nausea/vomiting with antiemetics
  • Hospitalization may be required in those with severe dehydration and/or deteriorating liver function
34
Q

Prevention of hepatitis

A
  • Good hygiene is preventative for all cases

- Proper universal precautions for preventing Hepatitis B and C

35
Q

Vaccination available for

A
  • Hepatitis-A, Hepatitis-B and Hepatitis-E
  • Hepatitis-D will be covered by the Hepatitis-B vaccine

**There is no vaccine for Hepatitis-C

36
Q

Post-exposure immunoglobulin is available for

A
  • Hep A and Hep B

- No proven benefit for Hep C

37
Q

There are several important classes of drugs that cause hepatitis

A
  • Analgesics
  • Antibiotics and antivirals
  • Central nervous system agents
  • Herbs
38
Q

Leading cause of acute liver failure in US

A

Acetaminophen overdose

-Mortality rate of close to 30%

39
Q

Analgesics that cause drug/toxin induced hepatitis

A
  • Acetaminophen
  • Nonsteroidal anti-inflammatory drugs (NSAIDs)
  • Salicylates (aspirin) cause dose-dependent hepatocellular injury; usually mild and easily reversible
40
Q

Antibiotics/Antivirals that induce hepatitis

A
  • Antibiotics are the most frequently incriminated agents causing drug-induced liver injury due to widespread use
  • *Amoxicillin-clavulanic acid is the leading cause of antibiotic-related liver injury and results in cholestatic hepatitis**
  • Nitrofurantoin, isoniazid, trimethoprim-sulfamethoxazole
  • Fluoroquinolones
  • HIV treatment agents have been linked to hepatic injury
41
Q

CNS agents that cause hepatitis

A

-Second only to antimicrobials as a frequent cause of drug-induced liver injury
-Anticonvulsants and anesthetics are two important categories
(Sodium valproate, phenytoin, carbamazepine and lamotrigine)
-Halothane was implicated in liver injury/insult
(Newer halogenated anesthetics like isoflurane and enflurane have a much lower incidence of hepatotoxicity)

42
Q

Herbs that are hepatotoxic

A

-Senecio, Heliotropium, Crotalaria, and comfrey contain alkaloids that cause hepatic veno-occlusive disease

-Hepatotoxicity ranging from mild hepatitis to massive necrosis and fulminant hepatitis has been associated with:
Chaparral, germander, pennyroyal oil, mistletoe, valerian root, comfrey and Ma huang

43
Q

Chronic hepatitis

A
  • A hepatic inflammatory process that does not resolve after 6 months
  • Those with acute viral hepatitis and persistence of serum viral antigens and nucleic acids (beyond a similar period)
44
Q

Most common acute viral hepatitis to lead to chronic hepatitis

A

hep C

hep A and E do NOT CAUSE chronic hepatitis

45
Q

______ is considered the most frequent cause of chronic hepatitis in US and Western Europe.

A

Nonalcoholic steatohepatitis (NASH)

46
Q

Drug that can lead to chronic hepatitis

A

Methyldopa

47
Q

Chronic Hep B

A
  • Occurs in 5-10% of those with acute hepatitis-B
  • High versus low replicative phase
  • 7 drugs currently approved as single agent treatments
48
Q

Chronic Hep C

A
  • Develops in 75-80% of individuals acutely exposed to hepatitis-C
  • More than 20% of these patients may develop cirrhosis in about 30 years
  • Six major genotypes (In US, genotype 1 most common)
  • Determines treatment type and prognosis
  • New class of agents for hepatitis-C
49
Q

Autoimmune liver disease

A
  • Occurs typically in young women

- Significant hepatic inflammation, high numbers of plasma cells and fibrosis

50
Q

Serology for autoimmune liver disease

A
  • Presence of hypergammaglobulinemia
  • antinuclear antibody (ANA) or anti-smooth muscle antibody (Anti-SMA)

-This is the most common classic type or type 1 variant

51
Q

Treatment for autoimmune liver disease

A

Corticosteroids and azathioprine are main stay of treatment

52
Q

Nonalcoholic Fatty Liver Disease encompasses

A
  • Steatosis (fatty liver)
  • Nonalcoholic steatohepatitis (NASH)
  • Cirrhosis (secondary to NASH)

-Most common reason for abnormal liver function tests among adults in the US and Western Europe

53
Q

Nonalcoholic Fatty Liver Disease occurs in

A

Overweight, diabetic and have hyperlipidemia

1/3 of america, 30 million people

54
Q

Diagnosing NAFLD

A

Most accurate means of diagnosis = liver biopsy with histologic examination

55
Q

Treatment of NAFLD

A
  • Weight reduction and exercise are established to improve liver histology in NASH.
  • Trials looking at lipid-lowering agents and drugs to improve insulin resistance are ongoing
  • Efficacy and safety have not been established at this time
56
Q

Alcohol abuse leads to

A

Alcoholic Fatty Liver and Alcoholic Hepatitis (reversible)

Cirrhosis is not reversible

57
Q

MOI of alcohol

A

-Ethanol, Acetaldehyde and Nicotinamide adenine dinucleotide phosphate (NADP) are directly hepatotoxic

  • Induction of cytochrome P-450 (CYP2E1) and cytokine pathways (tumor necrosis factor-ά) are critical in initiating and perpetuating hepatic injury
  • And producing lesions of alcoholic hepatitis
58
Q

Risk for hepatotoxic effects from alcohol:

A
  • Men consuming 40-80 grams of ethanol per day for 10-15 years carries substantial risk for alcoholic liver disease
  • Women appear to have a lower threshold of injury
  • Malnutrition and presence of other forms of chronic liver disease may potentiate toxic effects of alcohol in liver
59
Q

Clinical Features of Alcoholic Liver Disease:

A
  • Tender hepatomegaly (incidental finding)

- Aminotransferases are mildly elevated (

60
Q

Clinical features of Alcoholic HEPATITIS

A
  • Range from being asymptomatic to extremely ill with hepatic failure
  • Anorexia, nausea, vomiting, weight loss and abdominal pain are common symptoms
  • Hepatomegaly is present in 80% of cases
  • Splenomegaly is often present
  • Fever is common
  • Jaundice is commonly present – may be prounounced
  • Cutaneous signs may be found: Spider angiomas, palmar erythema, gynecomastia
  • Ascites and encephalopathy may be present (severe disease)
61
Q

Labs during Alcoholic HEPATITIS

A

-White blood cell count may be markedly elevated (PMNs)
-Aminotransferases are only modestly increased (AST>ALT): 200-400 U/L – An important differentiator from other acute hepatitis
Ratio of AST to ALT nearly always exceeds 2:1

  • Prolonged prothrombin time
  • Hypoalbuminemia
  • Hyperglobulinemia
  • Bilirubin may be markedly increased
62
Q

Histological findings of alcoholic hepatitis include

A
  • Mallory bodies
  • Infiltration by polymorphonuclear leukocytes
  • A network of interlobular connective tissues surrounding hepatocytes and central veins
63
Q

Prognosis of Alcoholic fatty liver disease

A

completely resolves with cessation of alcohol intake

64
Q

Alcoholic hepatitis can also resolve, but more commonly ______

A

it progresses:

  • Cirrhosis (may be present at initial time of diagnosis)
  • Hepatic failure and death
-Encephalopathy, Ascites, Hepatorenal syndrome
Gastrointestinal bleeding (from varices)
65
Q

Treatment

A
  • Abstinence – Fatty liver and early stages of alcoholic hepatitis (without extensive fibrosis) are reversible.
  • Supportive care – High calorie diet with vitamin and protein-supplementation is crucial
  • Corticosteroids
66
Q

What has been shown to benefit sever alcoholic hepatitis?

A

Pentoxifylline- diminishes risk for renal failure

An oral TNF-ά antagonist

67
Q

Liver Cirrhosis

A

-From alcohol, Hepatitis-C, Nonalcoholic Fatty Liver Disease

  • Fibrous tissue replaces healthy hepatocytes and liver tissue
  • An irreversible end result of insult and injury to the liver
68
Q

Many patients with cirrhosis are asymptomatic but some have

A

Variceal bleeding, Ascites, Spontaneous bacterial peritonitis and hepatic encephalopathy

69
Q

Other S/S of cirrhosis

A

-Fatigue, weight loss, anorexia, nausea
Increased abdominal girth, abdominal discomfort
-Jaundice, Abnormal liver span or consistency
-Splenomegaly, Ascites
-Lower extremity edema
-Spider angiomas, Palmar erythema, Gynecomastia
-Nail changes (Terry Nails, Muehrcke lines)
-Caput medusae
-Asterixis
-Testicular atrophy

70
Q

Findings of cirrhosis in CT/ultrasound/MRI

A
  • Relative enlargement of left hepatic and caudate lobes (right lobe atrophy)
  • Surface nodularity
  • Features of portal hypertension (Ascites, Intraabdominal varices, splenomegaly)

CSI- Winter (44 decks)

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