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AGPC 4!!!!!! > Lecture 5: Hepatitis > Flashcards

Lecture 5: Hepatitis Flashcards

1
Q

Liver blood flow

A

Liver has double circulation with high o2 concentration – metabolic workshop, digests all nutrients, destroy toxin and metabolizes substances

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2
Q

Hepatocytes

A

metabolize proteins, lipids, carbs, produce bile, produce clotting factors and neutralize toxins. They are functional liver cells. When injured by inflammation or toxins they produce Transaminase – ALT, AST.

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3
Q

Bile

A

metabolizes lipids. Without then the lipids are not emulsified.

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4
Q

Cholangiocytes

A

cells of the inner membrane of the bile duct. If duct is obstructed, the cholangiocytes will produce alkaline phosphatase, another enzyme.

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5
Q

Unconjugated bilirubin

A

Liver metabolizes bilirubin. Bilirubin is produced by old red blood cells. 120 days is the lifespan of a RBC. Hemoglobin –> Haem –> Unconjugated bilirubin inside the spleen. This is indirect bilirubin, it is insoluble. Cannot be excreted by the body. Indirect and insoluble, cannot be excreted. –> Travels to the liver where it is conjugated and made soluble. Liver can get overwheled by too much hemolysis and the unconjugated bilirubin will back into the blood. Hemolysis –> Unconjugated hyperbilirubinemia (indirected hyperbilirubinemia)

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6
Q

Conjugated bilirubin

A

Travels to the liver where it is conjugated and made soluble. This is called direct bilirubin because it can be directly excreted by the body. This is excreted with bile into the stool. Which is why the stool is brown because of bilirubin. Due to direct bilirubin. Urine is yellow due to bilirubin when the kidneys excrete it

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7
Q

Bile duct obstruction (stones, tumors of the pancreatic head) cannot be drained, will

A

spill back conjugated

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8
Q

Hemolysis the problem is this type of bilirubinemia b/c liver is overwhelmed by the amount of bilirubin.

A

unconjugated

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9
Q

In obstruction of common bile duct via stone or tumor the problem is w drainage of this type of bilirubin

A

conjugated, because liver can conjugate but cannot excrete –> hyperbilirubinemia conjugated/direct.

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10
Q

LFTs for Injury

A

AST, ALT, Alkaline phosphatase. ALT and AST produced by hepatocytes, any injury regardless of etiology which cannot be determined which specific cause, will be a group of etiologies will indicate injury to hepatocytes. Alk phos is obstruction of bile flow/cholagiocytes

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11
Q

LFT Function

A

Albumin, PT/INR, Bilirubin

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12
Q

Hepatocellular

A

Injury to hepatocytes
ALT (Alanine aminotransferase)
AST (Aspartate aminotransferase)

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13
Q

Cholestatic

A

Obstruction of the bile flow (stasis of the bile)

Alkaline phosphatase

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14
Q

Hepatocellular caused by

A 
Injury to hepatocytes
Viral hepatitis
Drugs affecting hepatocytes 
Alcohol liver disease 
Non-alcohol liver disease
Autoimmune hepatitis  
Hereditary diseases (hereditary hemochromatosis, Wilson disease)
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15
Q

Cholestatic causes

A

Obstruction of the bile flow
Gall stones in common bile duct
Pancreatic/ hepatic mass
Drugs affecting bile flow

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16
Q

Drugs affecting the liver

A

Tylenol > 7.5 grams per day. TB drugs. Antiseizure drugs. Antifungals. Most commonly: acetaminophen, augmentin

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17
Q

ALT AST much higher than AP means what, and vice versa

A

Usually AST ALT <40.

ALT X 5 and alk phos x 2 then it is probably alcohol, or hepatitis, or fatty liver etc (hepatic)
Alk phos x 5 but alt x 2 –> cholestasis = stone, tumor –> next step: US

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18
Q

ALT > AST

A

in all hepatocellular conditions except conditions caused by alcohol

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19
Q

AST> ALT

A

in condition caused by alcohol (AST: ALT= 2:1)

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20
Q

AST > ALT (2:1) with AST in 100-200 u/L

A

Alcoholic liver disease

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21
Q

ALT > AST, with ALT in 1000 u/l

A

Acute viral hepatitis (A,B), acute drug induced injury, (acetaminophen >7.5 g/d). Work up: Hepatitis A, B panel, acetaminophen level

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22
Q

ALT > AST, with ALT in 100s u/l

A

Chronic viral hepatitis (B,C), drug-related injury (TB medications, antiepileptic, methotrexate, statins, amiodarone, acetaminophen, amoxicillin-clavulanate), non-alcoholic fatty liver disease, congestive liver disease, autoimmune hepatitis

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23
Q

ALT > AST, with ALT in 100s u/l – work up

A

Hepatitis B,C panel, autoantibodies (ANA), review medication history (obesity, T2DM, hyperlipidemia)

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24
Q

Why when AST ALT is lower in chronic

A

When liver is replaced by fibrous tissue there are no functional hepatocytes so nothing is producing ALT AST

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25
Q

Alkaline phosphatase (<120 u/L)

A

Marker of cholestatic injury (intrahepatic and extrahepatic)
Maybe slightly elevated in hepatocellular injury
Requires evaluation of biliary tree (US-initial test, MRCP is more accurate)

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26
Q

Elevated AP w/ ductal dilation

A 
extrahepatic cholestasis. Choledocholithiasis (sharp pain)
Pancreatic cancer  (painless or dull pain)
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27
Q

Elevated AP w/ out ductal dilation

A

intrahepatic cholestasis. Metastatic disease (colon, prostate) Hepatocellular carcinoma

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28
Q

PT/INR (11-15 sec/1.0)

A

Most sensitive marker of synthetic function of the liver Most sensitive marker of acute liver injury. Marker of prognosis. Increase in PT/INR= decrease in the synthetic liver capacity. Albumin, Bilirubin, PT/INR = Liver Function
PT includes factor 7 half life of 6 hours only and is reflected in prolonged PT – more sensitive to acute changes than the PTT for liver injury but both will be abnormal. ACUTE changes reflected in PT. Not PTT.

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29
Q

Albumin (3.5-5.3 g/dl)

A

Marker of synthetic function of the liver. Decrease in albumin = decrease in the synthetic liver capacity. Albumin is not specific for the liver( decrease in albumin in nephrotic syndrome or malnutrition) Maybe normal in acute injury. Albumin half life is 20 days. Synthetic liver function, does not indicate acute changes. Nephrotic syndrome lose the protein in urine where albumin will also be depleted but not due to liver, same with malnutrition.

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30
Q

Total bilirubin (0.5 -1.0 mg/dL)

A

Marker of synthetic function

Indicator of severity of disease

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31
Q

Jaundice if bili >

A

2

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32
Q

Elevated bilirubin : caused by

A

hemolytic and obstructive

33
Q

Hemolytic

A

increased destruction of red blood cells, overwhelmed liver is unable to conjugate all unconjugated bilirubin (increase in indirect/unconjugated bilirubin)

34
Q

Obstructive

A

obstruction of the bile ducts or damage to the hepatocytes so that the usual amount of conjugated bilirubin cannot be excreted into GI tract (increase in direct bilirubin)

35
Q

Elevated total bilirubin w/ normal direct bilirubin etiology

A

hemolysis need reticulocyte count, anemia, normal liver enzymes, (-) urine bilirubin

36
Q

Elevated total bilirubin w/ elevated direct bilirubin etiology

A

Liver disease (cholestatic or hepatocellular). Abnormal liver enzymes, (+) urine bilirubin

37
Q

Hepatocellular disease labs

A

AST/ALT very high, AP normal to high, total and direct bili normal to high, INR and Albumin usually normal unless severe cirrhosis

38
Q

Cholestastatic disease

A

AST/ALT normal to high, AP very high, total and direct bili normal to high, INR and Albumin usually normal unless severe cirrhosis

39
Q

Hep A

A

Fecal oral transmission, Traveling to endemic areas (fecal contamination of water, food) Only acute form; self-limiting. Fulminant hepatitis is rare

40
Q

Hep B

A

Blood Unprotected sex Mother-baby transmission, at risk Unprotected sex IVD users, Acute and chronic . Chronic in 90% of infected infants and only 5% of infected adults. Cirrhosis (in 20% of chronically infected 20 years after exposure) Hepatocellular carcinoma (HCC 2% risk per year)

41
Q

Hep C

A

Blood Unprotected sex (very rare) transmission, at risk IVD users Healthcare workers, 85% of infected individuals will have chronic infection. Cirhosis (in 20% of patients 20 years after exposure). Hepatocellular carcinoma (HCC 2% risk per year)

42
Q

Hep D

A

Coexist w B, all the same as B

43
Q

Hep E

A

fecal oral, same as A

44
Q

Clinical manifestations of acute hepatitis (regardless of etiology)

A 
Maybe completely asymptomatic 
in severe cases : Fatigue, Anorexia
Weight loss 
Nausea, +/- vomiting 
Abdominal discomfort 
Low grade fever 
(+/-) arthralgia
Signs: Jaundice, scleral icterus, dark urine, pale stool,  liver tenderness, hepatomegaly
45
Q

Clinical manifestations of chronic hepatitis

A

Asymptomatic (discovered by abnormal liver enzymes/ abnormal US imaging) or Mild symptoms (fatigue, abdominal discomfort “ fullness”, anorexia) or Symptoms of decompensated cirrhosis (ascites…)

46
Q

Cirrhosis leads to reduced albumin which causes

A

decreased oncotic pressure and transudation of fluid –> ascites

47
Q

physical exam for ascites includes what?

A

Bulging flunks (observation), fluid wave (palpation), shifting dullness (percussion)

48
Q

Chronic liver disease stigmata

A

“Spider” angioma, Palmar erythema, Gynecomastia

49
Q

Portal hypertension leads to?

A

distention of abdominal veins aka Caput medusae

50
Q

Hepatic encephalopathy results from ?

A

hyperammonemia

51
Q

Workup for suspected hepatitis includes?

A

Consider travel history, risk factors, alcohol consumption, medications review, history of diabetes, obesity, hyperlipidemia

LFTs and bilirubin (increased direct bilirubin, increased ALT more than AST, minor elevation of Alk phosphatase)

Viral hepatitis serology (A,B,C)

Consider CMV serology (CMV IgM), EB (EB IgM)

52
Q

HBs Ag is?

A

Surface antigen. Rises first and indicates active infection. Triggers production of surface antibodies (Anti HBs)

53
Q

Anti HBs is?

A

Antibodies for surface antigen, indicates resolution of active infection and immunity (and successful vaccination)

54
Q

HBc Ag is?

A

Core antigen. NOT detected in blood. Triggers production of surface antibodies ( IgM Anti-HBc, IgG-Anti HBc)

55
Q

IgM Anti HBc is?

A

Antibodies to core antigen. Indicates acute infection

56
Q

IgG Anti-HBc is?

A

Antibodies to core antigen. Indicates resolution of infection

57
Q

HBe Ag

A

E antigen. Indicates high level of infectivity ( correlates with high viral load)

58
Q

Anti- HBe

A

Antibody to e antigen. Indicates low level of infectivity

59
Q

acute hep B serology?

A

HBs Ag, IgM anti-HBc


60
Q

Resolution of acute Hepatitis B serology?

A

anti-HBs, IgG anti-HBc


61
Q

Chronic Hepatitis B serology?

A

HBs Ag, IgG anti-HBc


62
Q

Interpret: (-) HBsAg, (-) anti-HBc, (-) anti-HBsAg

A

nothing. should be vaccinated.

63
Q

Interpret: (-) HBsAg, (+) anti-HBc, (+) anti-HBsAg

A

previous infection that has been resolved. not infected now

64
Q

Interpret: -) HBsAg, (-) anti-HBc, (+) anti-HBsAg

A

pt was successfully vaccinated (core is negative)

65
Q

Interpret: (+) HBsAg, (+) anti-HBc, (+) anti- HBc IgM,

(-) anti-HBsAg

A

acute active infection because + surface antigen, -antibody; Igm+ so acute

66
Q

Interpret: (+) HBsAg, (+) anti-HBc, (-) anti- HBc IgM,

(-) anti-HBsAg

A

infected, chronic because IgM is negative

67
Q

Interpret: (-) anti-HCV

A

no hep c

68
Q

Interpret: (+) anti-HCV , followed by (+) HCV RNA

A

active infection (chronic hep c)

69
Q

Interpret: (+) anti-HCV , followed by (-) HCV RNA

A

resolved spontaneously or treated and cured

70
Q

Treatment of acute viral hepatitis (A and B)

A
  • Supportive (anti-emetics, adequate hydration, adequate nutrition)
  • AVOID alcohol (not limit- avoid)
  • Steroids, high-carbohydrate and low-protein diets are not recommended (small frequent meals)
71
Q

Treatment of chronic hepatitis B

A

Oral direct antiviral therapy monotherapy , 20-25% achieve suppression of viral load

Only patients with significant viral activity (HBeAg and high viral load should be treated

Goal is suppression Hep B replication (low viral load -HBV DNA) and HBeAg seroconversion

Long-term therapy is necessary (4-5 years and more)

72
Q

Treatment of chronic hepatitis C

A

Oral direct antiviral therapy (one pill once a day), >90% patients achieve cure

Goal is to achieve undetectable HCV RNA for at least 6 months after cessation of therapy (= cure)

The treatment and the duration is based on Hepatitis C genotype (genotype 1 accounts for 70%), usually 12-24 weeks

All patients with active HCV infection would benefit, with the exception of those with life expectancy less than 12 months

73
Q

Treatment of compensated cirrhosis

A

Surveillance of HCC every 6-12 months (ultrasound)

Screening for esophageal varices (endoscopy)

Avoidance alcohol (no safe level !)

HAV, HBV, pneumococcal pneumonia, and influenza immunizations

Statins can be safely used

Acetaminophen may be used in persons with cirrhosis in doses of up to 2 g daily

Aspirin and other NSAIDs should be avoided- because can cause kidney damage and also because these pts are predisposed to bleeding
High-caloric small meals

74
Q

Treatment of decompensated cirrhosis

A

Esophageal varices – non-selective beta-blockers ( decrease portal flow)

Ascites – diuretics (Spironolactone) and sodium restriction diet

Hepatic encephalopathy- lactulose (decrease absorption of ammonia)

75
Q

who should we screen for hep c?

A 
Individuals borne 1945-1965 regardless of risk factors 
IV drug users 
HD patients 
HIV infected individuals 
MSM
Abnormal liver enzymes
76
Q

who should we screen for hep b?

A 
All pregnant women (each pregnancy)
IV drug users 
HD patients 
HIV infected individuals 
MSM
Abnormal liver enzymes
77
Q

who should get vaccinated for hep a? (2 doses)

A

Travellers to endemic areas
MSM
Drug users (poor housing conditions, high prevalence of hepatitis C)
Patients with chronic liver disease

78
Q

who should get vaccinated for hep b? (3 doses)

A 
IV drug users 
Multiple sexual partners
MSM
Healthcare/ public safety workers 
Patients with chronic liver conditions 
Patients on HD 
Patients with DM 19-59 y. (sharing needles, finger stick devises, syringes ,needles)

AGPC 4!!!!!! (10 decks)

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