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Flashcards in Hepatitis/Alcoholic Liver Disease Deck (70)
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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)
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
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
4
Q
Common causes of acute hepatitis
A
-Viral hepatitis (A through E)
-Drugs (prescription, OTC and illicit)
-Alcohol
-Toxins
-Autoimmune
-Wilson Disease
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
6
Q
How to diagnose Wilson Disease
A
Low serum ceruloplasmin with high urinary and hepatic copper levels
7
Q
Treatment for Wilson Disease
A
-Indefinite
-Copper chelation
-Zinc supplementation
8
Q
Acute hepatitis can be caused by direct toxin induced necrosis via
A
Acetaminophen or Amanita phalloides toxin (fungus/mushroom)
9
Q
Acute hepatitis can be caused my host immune-mediated damage
A
-viral
(Hep A, B, C, D, E viruses)
10
Q
Most common cause of acute hepatitis in the US?
A
Hep A virus

-Hep B is 2nd most common
(Most extensively characterized)
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
12
Q
Hep B antigens
A
HBsAg (surface)
HBeAg (Be Ag)
HBcAg (core)
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.
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
15
Q
In HBV carriers and pts with chronic hep B, a negative HBeAg result indicates
A
very minimal or lack of HBV replication
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
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
18
Q
SEE SCREEN SHOT OF COMPARISON CHART
A
of all hepatitis viruses
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**
20
Q
5-10% of hepatitis-B and C cases will have _________
A
-arthritis and urticaria
-Resembling serum sickness (due to immune complex deposition)
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)
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
23
Q
Serology for acute hepatitis B infection
A
+ HBsAg
- HBsAb
+ HBcAb IgM
24
Q
Serology for chronic carriers of hep B
A
+ HBcAb IgG
- HBcAb IgM
+ HBsAg (+ HBeAg)
-HBsAb

Chronic active: HBeAg
Chronic passive: HBeAb
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)
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
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
28
Q
Fulminant hepatitis
A
-Due to massive hepatic necrosis
-Occurs in
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)