Acute hepatocellular injury /medicine / haneen ayad +++ sajad al-asady al-nahrain collage of medicine / baghdad _ iraq

3.  Symptoms:
1. Malaise
2. Fatigue
3. Anorexia
4. Nausea
5. dark urine
6. abdominal pain
7. Headache
8. Fever
9. myalgia, and
10. arthralgia.
 Signs:
1. Jaundice
2. scleral icterus
3. Hepatomegaly
4. tender liver
5. splenomegaly, and
6. rash.

5. A serum bilirubin level in the range of 2.5 to 3.0 mg/dl usually produces
detectable scleral icterus.
The serum bilirubin concentration is determined by the rates of bilirubin
production (resulting from the catabolism of hemoglobin and other heme-
containing enzymes) and elimination (including excretion into bile and the renal
excretion of conjugated bilirubin).
As a result, hemolysis and changes in renal function can considerably alter the
serum bilirubin concentration.

7. 1. Exposure to toxins is a common cause of acute liver injury. Such
toxins include ethanol, acetaminophen, halogenated hydrocarbons, an
d the toxin from the mushroom Amanita phalloides
2. Infections can also cause acute
liver injury. The most common infections are those caused by hepati
tis
viruses A, B, C, D, and E, but parasites, bacteria, and fungi also can
cause infectious hepatitis.
3. Hepatic injury can also stem from ischemia;
this is usually a result of severe systemic hypotension or congestive
heart failure.
4. metabolic disorders such as Wilson's disease and Reye's syndrome

11. 1. HBsAg is present in the settings of acute infection, chronic infection,
and the carrier state.
2. IgG classes of Anti HBs and anti HBc appear and the HBsAg level
declines, indicating a state of immunity after resolution of the acute
infection.
3. IgM anti HBc or IgM anti HAV is usually present only during acute
infection,
4. Anti HBs appears alone, without anti HBc, in response to hepatitis B
vaccine.

12.  a. HBsAg−, anti-HBs+, anti-HBc+ 1. Acute hepatitis B
 b. HBsAg−, anti-HBs+, anti-HBc− 2. Acute hepatitis A
 c. HBsAg+, IgManti-HBc+ 3. Prior HBV infection, now immune
 d. HBsAg+, IgManti-HBc− 4. Prior HAV infection, now immune
 e. Anti-HAV(total)+, IgManti-HAV− 5. Hepatitis B chronic carrier
 f. Anti-HAV(total)+, IgManti-HAV+ 6. Received hepatitis B vaccine

13.  a. HBsAg−, anti-HBs+, anti-HBc+ 1. Acute hepatitis B
 b. HBsAg−, anti-HBs+, anti-HBc− 2. Acute hepatitis A
 c. HBsAg+, IgManti-HBc+ 3. Prior HBV infection, now immune
 d. HBsAg+, IgManti-HBc− 4. Prior HAV infection, now immune
 e. Anti-HAV(total)+, IgManti-HAV− 5. Hepatitis B chronic carrier
 f. Anti-HAV(total)+, IgManti-HAV+ 6. Received hepatitis B vaccine

14.  a. HBsAg−, anti-HBs+, anti-HBc+ 1. Acute hepatitis B
 b. HBsAg−, anti-HBs+, anti-HBc− 2. Acute hepatitis A
 c. HBsAg+, IgManti-HBc+ 3. Prior HBV infection, now immune
 d. HBsAg+, IgManti-HBc− 4. Prior HAV infection, now immune
 e. Anti-HAV(total)+, IgManti-HAV− 5. Hepatitis B chronic carrier
 f. Anti-HAV(total)+, IgManti-HAV+ 6. Received hepatitis B vaccine

15.  a. HBsAg−, anti-HBs+, anti-HBc+ 1. Acute hepatitis B
 b. HBsAg−, anti-HBs+, anti-HBc− 2. Acute hepatitis A
 c. HBsAg+, IgManti-HBc+ 3. Prior HBV infection, now immune
 d. HBsAg+, IgManti-HBc− 4. Prior HAV infection, now immune
 e. Anti-HAV(total)+, IgManti-HAV− 5. Hepatitis B chronic carrier
 f. Anti-HAV(total)+, IgManti-HAV+ 6. Received hepatitis B vaccine

16.  a. HBsAg−, anti-HBs+, anti-HBc+ 1. Acute hepatitis B
 b. HBsAg−, anti-HBs+, anti-HBc− 2. Acute hepatitis A
 c. HBsAg+, IgManti-HBc+ 3. Prior HBV infection, now immune
 d. HBsAg+, IgManti-HBc− 4. Prior HAV infection, now immune
 e. Anti-HAV(total)+, IgManti-HAV− 5. Hepatitis B chronic carrier
 f. Anti-HAV(total)+, IgManti-HAV+ 6. Received hepatitis B vaccine

17.  a. HBsAg−, anti-HBs+, anti-HBc+ 1. Acute hepatitis B
 b. HBsAg−, anti-HBs+, anti-HBc− 2. Acute hepatitis A
 c. HBsAg+, IgManti-HBc+ 3. Prior HBV infection, now immune
 d. HBsAg+, IgManti-HBc− 4. Prior HAV infection, now immune
 e. Anti-HAV(total)+, IgManti-HAV− 5. Hepatitis B chronic carrier
 f. Anti-HAV(total)+, IgManti-HAV+ 6. Received hepatitis B vaccine

18.  a. HBsAg−, anti-HBs+, anti-HBc+ 1. Acute hepatitis B
 b. HBsAg−, anti-HBs+, anti-HBc− 2. Acute hepatitis A
 c. HBsAg+, IgManti-HBc+ 3. Prior HBV infection, now immune
 d. HBsAg+, IgManti-HBc− 4. Prior HAV infection, now immune
 e. Anti-HAV(total)+, IgManti-HAV− 5. Hepatitis B chronic carrier
 f. Anti-HAV(total)+, IgManti-HAV+ 6. Received hepatitis B vaccine

20.  the serum AST level is usually
higher than the serum ALT level.
 the serum level of glutamyltranspeptidase is often elevated b
ecause of
induction of this enzyme by chronic ethanol ingestion.

22. Ischemic liver injury, or shock liver, usually occurs in the setting
of a recognized circulatory disturbance, such as hypotension or acute
myocardial infarction.
1. A rapid and dramatic rise in the AST and ALT
levels is seen, with an equally rapid decline. The aminotransferase
level can rise into the thousands, approaching levels seen with acute
viral hepatitis.
2. A slow, steady increase in the serum bilirubin
concentration subsequently occurs and peaks several days later.
3. A liver biopsy is not needed for diagnosis, but, when specimens
are obtained, they show centrilobular necrosis.

24.  Fulminant hepatic failure is defined as progression to signs of liver failure,
including hepatic encephalopathy, within 12 weeks of the onset of symptoms.
 Such a picture occurring 12 to 24 weeks from the onset of symptoms is
considered sub fulminant hepatic failure.
 Fulminant hepatic failure may be caused by viral , toxic, ischemic, or other
causes of hepatocellular injury.
 The mortality rate for these entities is extremely high.
 Intensive support is indicated in affected patients, and liver transplantation
should be considered if spontaneous recovery does not occur .

25.  A 37-year-old housewife reports 3 weeks of general fatigue, several days of
dark urine, and 1 day of scleral icterus. She denies vomiting, but complains
of mild, continuous pain in the right upper quadrant, and intermittent
nausea.
Physical examination reveals the patient to be jaundiced but comfortable.
She shows no signs of malnutrition and has no spider angiomas or palmar
erythema.
The liver is tender and measures 15 cm by percussion in the midclavicular
line; it is palpable 4 cm below the costal margin on inspiration.
The spleen is not palpable, and the examination findings are otherwise
unremarkable.

27. 1. Very high aminotransferase levels (>1,000 IU/L) usually indicate an acute
hepatocellular injury.
2. Moderately high levels (two to five times normal) can be seen
in chronic diseases such as chronic viral hepatitis.
3. An AST/ALT ratio that exceeds 1 suggests the
presence of alcoholic liver disease.
4. Alkaline phosphatase and bilirubin
levels that are elevated out of proportion to the aminotransferase
concentrations suggest a biliary obstructive process

28. Normal range:
• AST <50 U/L
• ALT <50 U/L
• Total bilirubin <1 mg/dl
• ALP <130 U/L

29. Normal range:
• AST <50 U/L
• ALT <50 U/L
• Total bilirubin <1 mg/dl
• ALP <130 U/L

30. Normal range:
• AST <50 U/L
• ALT <50 U/L
• Total bilirubin <1 mg/dl
• ALP <130 U/L

31. Normal range:
• AST <50 U/L
• ALT <50 U/L
• Total bilirubin <1 mg/dl
• ALP <130 U/L

32. Normal range:
• AST <50 U/L
• ALT <50 U/L
• Total bilirubin <1 mg/dl
• ALP <130 U/L

34. patient presenting with liver disease should be asked about :
1. travel history
2. parenteral risk factors, including transfusions, IV drug use
3. sexual contacts
4. professional exposure (health care workers hepatitis B and C)
5. medications
6. alcohol intake
7. childhood liver disease
8. and family history

36. The selection of tests should be guided by the nature of the clinical history.
(a) IgM anti HAV to check for acute hepatitis A
(b) IgM anti HBc to check for acute hepatitis B
(c) Anti HCV to check for acute hepatitis C

38. 1. Sexual or household contacts of people with hepatitis A should be
passively immunized with immunoglobulin.
2. Sexual or household contacts of people with hepatitis B should be
immunized with hepatitis B vaccine.
3. They should exercise careful standard precautions to avoid fecal oral
transmission.
4. They should avoid parenteral contact (the sharing of razors, toothbrushes,
and the like).
5. Sexual contact should be minimized during the acute stage of the illness.
After clinical recovery, it is important to determine whether the HBsAg has
disappeared and anti HBs has appeared. Failure to clear HBsAg suggests
development of a chronic hepatitis B carrier state.

40. Repeat testing for anti HCV in 6 months is appropriate because this test may not be positive in
the acute setting.

42.  A low serum ceruloplasmin level and a high urinary copper excretion are
highly suggestive of Wilson's disease.
 A high serum ferritin level and high transferrin saturation are highly
suggestive of hemochromatosis.
 The definitive test for both of these disorders is a liver biopsy.
 Genetic testing for familial hemochromatosis is now available.

44. Liver biopsy is not usually needed for diagnosis or prognosis in patients with acute liver
diseases.
Exceptions might include establishing the diagnosis of:
 drug induced or toxic hepatitis
 ischemic liver injury
 granulomatous disease

46. Most patients with acute hepatitis do not require hospital admission.
However , those who exhibit evidence of severe liver injury, such as hepatic
encephalopathy, a bilirubin level above 15 mg/dl, or an increasing prothrombin
time, and those with severe anorexia or nausea, should be hospitalized.