Transcript Hepatitis B surface Antibody

By Dr. Henry Klotz
Auburn Community Hospital
Gastroenterology
 HBsAg
 HBsAb
 Anti-HBC
 HBeAg
 HBeAb
 HBV
DNA
 Marker
 Most
for hepatitis B virus
commonly used test to detect hepatitis B
 Protein
found on capsule of hepatitis B virus
 Hepatitis
B exposure
 1-10 weeks: Hepatitis B surface antigen
(HBsAg) appears
 Liver enzyme elevation & symptoms appear
 4-6 months: HBsAg is undetectable
 Persistence of HBsAg > 6 months is indicative
of chronic infection
 Hepatitis
B Surface Antibody (HBsAb)
 Detection indicates:


Recovery from acute hepatitis B
Immunity from future hepatitis B
 Appears
several weeks to months after HBsAg
disappears
 Last a lifetime, giving lifelong immunity to
hepatitis B
 HBsAg-------WINDOW ----------HBsAb
 Window
of acute hepatitis B filled by
Anti-HBC
 The only serological marker at this time is
the IgM version of the hepatitis B antibody
against the hepatitis B core antigen (found
only in liver cells, not blood, so cannot be
tested for)


IgM– immediately post acute infection x 6 months
IgG- appear 6 months after an infection
 Generally
you should not see surface
antigen and surface antibody together.
 In 20% of HBsAg you will also see HBsAb.
 These antibodies for all intents and
purposes do nothing in the sense that they
do not neutralize hepatitis B surface
antigen.
 These people are still considered carriers
of hepatitis B.
 HBeAg-
marker of hepatitis B replication
and infectivity.
 Associated with high levels of DNA
 Therefore the person is more infectious.
 The sero-conversion from HBeAg to HBeAb
occurs even before the surface antigen
converts to surface antibody.
 In patients with chronic hepatitis B this
sero-conversion may never occur.
 Under
1 year of age = 90%
 Ages 1 to 5 = 50%
 Adults – Less than 5%
 Clearance of hepatitis B surface antigen is
½% per year.
 That means 1 in 200 will clear Hepatitis
spontaneously on a yearly basis.
 How
long does hepatitis B survive outside
the body? Seven days
 What is the incubation period of hepatitis
B? On average of 90 days. (60 to 150 days)
 How long do symptoms last? Usually Several
weeks but they can last several months.
 What is the fatality rate of acute hepatitis
B? ½ to 1%
 Made
synthetically- contains no blood
products.
 Therefore: YOU CANNOT GET HEPATITIS B
FROM THE VACCINATION.
 Three doses are given: 0, 1 month, 6 months.
 All
infants at birth.
 All children until 18 who have not been
vaccinated.
 High risk groups
 Can
hepatitis B vaccine be given to
pregnant women or lactating women? Yes,
because it contains no live virus.
 Can
hepatitis B vaccine be given after an
acute exposure? Yes, it can be effective
especially if given with HBIG.
Is there any harm in vaccinating people who
have had hepatitis B? No, they are already
immune but will not be harmed.
 After receiving vaccination for hepatitis B
should the patient be routinely tested to see if
they developed antibodies? No, only Infants of
HBsAg positive mothers, dialysis patients, HIV
and other immunocompromised patients,
healthcare workers and others in high-risk
situations and sexual partners of patients with
chronic hepatitis B . This should be done 1 to
2 months after completion of the vaccinations.


HBsAg Negative

HBsAg Negative

HBsAb Positive

HBsAb Positive

Anti-HBc Negative

Anti-HBc Positive
----------------------------
---------------------------
Immune due to
Immune due to recovery
vaccination
from Hepatitis B
vaccination

HBsAg Positive

HBsAg Positive

HBsAb Negative

HBsAb Negative

Anti-HBc Positive

Anti-HBc Positive

IgM Anti-HBc Positive

IgM Anti-HBc Negative

IgG Anti-HBc Negative

IgG Anti-HBc Positive

Acute Hep B Infection

Chronic Hep B
Infection
 No
cure.
 Medications are used to inhibit viral
replication, decrease liver inflammation
and slow progression to cirrhosis.
 When to use medication?
 When liver inflammation is detected as
measured by either liver biopsy, high levels
of hepatitis B DNA and high levels of ALT.
1.
2.
3.
4.
5.
Fewer patients with hepatitis C get acute
symptoms with initial infection as compared
to hepatitis B
Sexual transmission is very common with
hepatitis B; much less common with hepatitis
C.
Only 5% of hepatitis B goes on to become
chronic while 80% of hepatitis C becomes
chronic.
There is a vaccine to prevent hepatitis B
there is no vaccine to prevent hepatitis C.
There is no treatment to cure hepatitis B.
Treatments do exist to cure most cases of
hepatitis C.
 Most
patients are unaware they have
hepatitis C because they did not have
acute hepatitis symptoms of jaundice or
acute illness lasting weeks to months as
can be seen with hepatitis B.
 The screening test for hepatitis C is the
antibody to hepatitis C.
 Anyone
who have ever used intravenous
drugs or snorted drugs.
 Received a blood transfusion before 1992.
 Baby boomers= were born between 19451965. This group has a disproportional high
number of hepatitis C positive individuals.
 Baby boomers= 80% of chronic hepatitis C.
 HIV-infected individuals – they have many
of the same risk factors.
 Incarcerated individuals =16 to 41% have
evidence of hepatitis C.
The recommended screening test is hepatitis C
antibody. If this is positive then the hepatitis C
virus is tested for. This is known as the viral
load or hepatitis C RNA PCR level.
 80% of people who have acute hepatitis C will
become chronic carriers.
 The hepatitis C antibody test will be positive in
everyone who has ever had hepatitis C
INCLUDING the 20% that have cleared the
hepatitis C virus from their bodies and for all
intents and purposes are cured.

 Subtypes
based on the RNA
 6 major genotypes
 In the US we generally only find types 1,2,3.
 Previously, interferon (by SQ injection) and
ribavirin were used = many side effects.
 Today, genotype 1 is treated with Harvoni,
one tablet a day or Viekira Pak multiple
tablets daily (including ribavirin).
 Genotype 2 and 3= Sovaldi (sofosbuvir) and
ribavirin.
 Over 95% cure rate ( 8-24 week treatment).
50
year old woman presents
complaining of fatigue and
pruritus for 6 months.
Routine labs show normal
CBC and normal LFT’s except
for an elevated alkaline
phosphatase of 260.
 Middle-aged
women
 Elevated alkaline phosphatase !!!
 Symptom: itching
 End stage- jaundice
 Physical exam: Xanthomas/xanthalasmas
 Hypercholesterolemia with low risk CAD
 Antimitochondrial antibody (AMA) !!!
 liver biopsy with granulomas
 Ursodeoxycholic acid improves survival.
 End stage-liver transplant
A
45 year old male with dyspnea on exertion
for the last several months. He reports he
has always believed he has had some form of
asthma or chronic lung infection. Otherwise
healthy. No FH of lung disease. Not a smoker.
He does not drink alcohol and takes no
medication. On physical exam you note mild
expiratory wheezes and clubbing but note no
other abnormal findings. Chest X-ray hyperlucency. Blood work - moderate
elevation of liver transaminases.
Alpha-1 Antitrypsin is synthesized in the
liver.
 It’s a protein that inhibits several enzymes
including elastase, collagenase, and trypsin.
 These enzymes can damage the lungs if
Alpha-1 Antitrypsin is produced in too low
quantities due to a genetic defect.
 In the liver of these people there is a
buildup of this mutated protein which is
cytotoxic to hepatocytes and leads to
cirrhosis.

• Ultrasound (Sonogram)
• A test of anatomy and structure
• Checks for gallstones and the gallbladder wall
• HIDA Scan
• A test of gallbladder function
• Checks for bile flow
TEST FOR THE GALLBLADDER
TESTING FOR STRUCTURE
TESTING FOR FUNCTION
How much bile leaves the
gallbladder when it contracts
(squeezes) and empties.
Normal more than 35%
Gallbladder Ejection
Fraction
 Microscopic
colitis refers to finding certain
inflammatory changes in the ascending or
right colon that appear normal to visual
inspection.
 Many cases of irritable bowel syndrome have
been found in actuality to be microscopic
colitis.
 Clinically patients have chronic non-bloody
watery diarrhea.
There are two types of microscopic colitis.
Collagenous colitis and lymphocytic colitis.
 In collagenous colitis there is a thick layer of
collagen under the superficial mucosa.
 In lymphocytic colitis there are increased
number of lymphocytes that damage the surface
epithelial layer.
 The main goal of the colon is water
reabsorption. If a reabsorption does not occur
too much water will reach the rectum leading to
diarrhea.
 In both of these types of microscopic colitis
there is damage to the mucosa in the colon
leading to less water reabsorption permitting
more water to be eliminated causing diarrhea.

 What
is interesting is that there is a higherthan-expected correlation between
microscopic colitis and celiac disease. So
patients that are put on a gluten-free diet
and do not improve may in fact also have
microscopic colitis which would need to be
treated as well.
 Caused by NSAIDs, especially use greater
than six months, proton pump inhibitors as
well as ranitidine and selective serotonin
reuptake inhibitors.
 Treatment:
 Budesonide
(Entocort, Uceris)
 Steroid
 High
first pass metabolism (80-90%)
 Rapidly biotransformed to metabolites that
have minimal steroid activity
 Taper down from 9 mg daily to 6 mg to 3 mg
 Common
finding on abdominal ultrasound or
CT.
 For years it was viewed as totally benign.
 Now recognized as a serious condition.
 The most common cause of liver disease in
the western world.
 Within 10 years it is projected to be the main
cause of liver transplantation in the world.
 Defined
as NAFLD: non-alcoholic fatty liver
disease.
 It is a spectrum of progressive liver disease.
 Earliest and most benign change is simple
steatosis.
 Progresses to NASH: non-alcoholic
steatohepatitis. ( IN 1/3 OF NAFLD).
 Progresses to fibrosis.
 Progresses to cirrhosis.
 The
hepatic component of metabolic
syndrome- both have insulin resistance.
 Associated with obesity, type 2 diabetes and
cardiovascular disease.
 Weight reduction and increased physical
activity can reverse all stages except
cirrhosis.
 Bacteria
that is an anaerobic spore that
produces toxin.
 3-20% of people are colonized by C. diff but
are asymptomatic.
 When “good” intestinal bacteria are
decreased by antibiotics, C diff proliferates.
 The colitis the toxin causes can be mild to
life threatening.
 In 2011, 500,000 got C diff colitis and 29,00
died from it= 6%.
80% of deaths from C diff occurs in people
over 65 years old.
 11 % of people over 65 who get C diff die
within one month.
 20% of people who respond to treatment
relapse and get C diff again.
 40-60% of relapsers will get C diff a third
time.

 When
C diff faces unfavorable conditions it
forms spores.
 These spores are resistant to alcohol or
detergent. They require 3-5 minutes of
bleach to kill them.
 Spores can exist for 5 months on any surface.
 Only 10 spores are needed to cause
symptomatic infection.
 Most
common antibiotics causing C. diff
 Clindamycin
 Ampicillin
 Amoxicillin
 Cephalosporins
 Fluoroquinolones
 Flagyl
(PO or IV)
 Vancomycin- only PO or rectally (Pulsed
therapy)
 Fidaxomicin (Dificid 200 mg po bid X 10
days).
 Probiotics
 Fecal transplant
 Colectomy
 Difficulty
swallowing (dysphagia)
 Food impaction
 Chest pain that is often centrally located and
does not respond to antacids
 Persistent heartburn
 Upper abdominal pain
 No response to gastroesophageal reflux
disease (GERD) medication
 Backflow of undigested food (regurgitation)
 Eosinophils
form a lining under the mucosa.
 Eosinophils produce a protein that causes
inflammation, and formation of excessive
fibrous tissue in the lining of the esophagus.
 Allergic reaction is mainly to food.
 Eosinophilic esophagitis is a chronic immune
system disease.
 Associated food allergies, environmental
allergies, asthma, atopic dermatitis or
chronic respiratory disease.
 The
common use of ultrasounds and CT
scans have led to the finding of pancreatic
cysts.
 Overview of detection, diagnosis, treatment
and terminology.
3-13% of people have pancreatic cysts.
 Most are benign but once detected a work up is
warranted.
 Obtain fluid to verify the cyst is not malignant.
 If the cyst is proven to be benign we have to
know what type of cyst it is to know what
follow-up to give.
 The easiest and safest way of getting fluid is to
do an endoscopic ultrasound with fine needle
aspiration. ERCP can sometimes be useful.
 CT guided fine needle aspiration is possible but
since the pancreas is the most posterior organ in
the abdominal cavity it can be difficult to reach
the cyst with greater risk of complications.

 Flovent
inhaler 220 mcg. Swallowed NOT
inhaled. 2 puffs twice daily.
 Budesonide viscous suspension (Pulmicort
respules)
 Prednisone for severe cases
 Mucinous
cystic neoplasm (MCN). In one
major study about 75% were adenomatous
and the other 25% had some level of cancer
in them. Adenomatous are precancerous
lesions. Because of the high malignant
potential of this type of cyst surgical
resection is recommended.
 Serous
cystadenoma-These occur in 30% of
cystic pancreatic lesions.
 These are considered benign with less than a
3% chance of malignant transformation.
 They do not require surgery or surveillance.
 However, the cyst can become very large to
the point of becoming symptomatic and then
may require surgery for that reason.
 The
third type of pancreatic cyst is the
intraductal papillary mucinous
neoplasm(IPMN). These are almost always
affect the pancreatic ducts and can either be
benign or malignant. Even if malignant they
carry a better prognosis than pancreatic
adenocarcinoma.
 An
anal fissure is a narrow tear that extends
from the muscles that control the anus (anal
sphincter) up into the anal canal. These tears
usually develop when anal tissue is damaged
during a hard bowel movement or when
higher-than-normal tension develops in the
anal sphincters.
 Symptoms of an anal fissure include a sharp,
stinging, or burning pain during a bowel
movement. The pain, which can be severe,
may last a few hours. You may also notice
spots of bright red blood on toilet tissue.
This blood is separate from the stool.

Acute anal fissure - Providers should use nonoperative treatments
(eg, sitz baths, psyllium fiber, and bulking agents) as the first
step in therapy (strong recommendation, moderate-quality
evidence)

Chronic anal fissure - Providers should treat chronic anal fissure
with topical pharmacologic agents (eg, calcium channel blockers
or nitrates) (strong recommendation, moderate-quality
evidence).
Rectiv- 0.4% nitroglycerin
Diltiazem 2% cream



Chronic anal fissure - Providers should refer patients who do not
respond to conservative or pharmacologic treatment for local
injections of botulinum toxin (strong recommendation, lowquality evidence) or internal anal sphincterotomy (strong
recommendation, high-quality evidence)