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GASTROENTEROLOGY TOPICS
By Dr. Henry Klotz
Auburn Community Hospital
Gastroenterology
HEPATITIS B: SEROLOGICAL MARKERS
HBsAg HBsAb Anti-HBC HBeAg HBeAb HBV DNA
HEPATITIS B SURFACE ANTIGEN
HEPATITIS B SURFACE ANTIGEN
Marker for hepatitis B virus
Most commonly used test to detect hepatitis B
Protein found on capsule of hepatitis B virus
INFECTION TIMELINE 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
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
HEPATITIS WINDOW PHASE 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
SURFACE ANTIGEN & ANTIBODY 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.
E ANTIGEN – E ANTIBODY 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.
WHO DEVELOPS CHRONIC HEP B 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.
FACTS ABOUT HEPATITIS B 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%
HEPATITIS B VACCINE Made synthetically- contains no blood
products. Therefore: YOU CANNOT GET HEPATITIS
B FROM THE VACCINATION. Three doses are given: 0, 1 month, 6
months.
HEPATITIS B VACCINE- FOR WHOM? All infants at birth. All children until 18 who have not been
vaccinated. High risk groups
VACCINATION FACTS 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.
VACCINATION FACTS 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.
SURFACE ANTIBODY POSITIVE ?? HBsAg Negative
HBsAb Positive
Anti-HBc Negative
----------------------------
Immune due to
vaccination
HBsAg Negative
HBsAb Positive
Anti-HBc Positive
---------------------------
Immune due to
recovery from
Hepatitis B
vaccination
ACUTE OR CHRONIC HEP B HBsAg Positive
HBsAb Negative
Anti-HBc Positive
IgM Anti-HBc Positive
IgG Anti-HBc Negative
Acute Hep B Infection
HBsAg Positive
HBsAb Negative
Anti-HBc Positive
IgM Anti-HBc
Negative
IgG Anti-HBc Positive
Chronic Hep B
Infection
HEPATITIS B TREATMENT 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.
MAJOR DIFFERENCES HEPATITIS B & HEPATITIS C1. Fewer patients with hepatitis C get acute
symptoms with initial infection as compared to hepatitis B
2. Sexual transmission is very common with hepatitis B; much less common with hepatitis C.
3. Only 5% of hepatitis B goes on to become chronic while 80% of hepatitis C becomes chronic.
4. There is a vaccine to prevent hepatitis B there is no vaccine to prevent hepatitis C.
5. There is no treatment to cure hepatitis B. Treatments do exist to cure most cases of hepatitis C.
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.
WHO SHOULD GET SCREENED FOR HEPATITIS C? Anyone who have ever used intravenous
drugs or snorted drugs. Received a blood transfusion before 1992. Baby boomers= were born between 1945-
1965. 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.
TESTING FOR 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.
HEPATITIS C GENOTYPE 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).
HEPATITIS C
ELEVATED ALK PHOSPHATASE 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.
PRIMARY BILIARY CIRRHOSIS (PBC) 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
COPD AND LFT ELEVATION 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 DEFICIENCY 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.
GALLBLADDER DISEASE
TEST FOR THE GALLBLADDER
• 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
TESTING FOR STRUCTURE
Does It Run?
What is inside?
TESTING FOR FUNCTION
Does It Run?
Yes!
How much bile leaves the gallbladder when it contracts (squeezes) and empties. Normal more than 35%
Gallbladder Ejection Fraction
MICROSCOPIC COLITIS 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.
MICROSCOPIC COLITIS 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.
MICROSCOPIC COLITIS What is interesting is that there is a
higher-than-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.
MICROSCOPIC COLITIS 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
FATTY LIVER 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.
FATTY LIVER 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.
NAFLD - FATTY LIVER 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.
CLOSTRIDIUM DIFFICILE 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%.
CLOSTRIDIUM DIFFICILE 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.
CLOSTRIDIUM DIFFICILE 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.
CLOSTRIDIUM DIFFICILE Most common antibiotics causing C. diff Clindamycin Ampicillin Amoxicillin Cephalosporins Fluoroquinolones
C DIFF TREATMENT Flagyl (PO or IV) Vancomycin- only PO or rectally (Pulsed
therapy) Fidaxomicin (Dificid 200 mg po bid X 10
days). Probiotics Fecal transplant Colectomy
EOSINOPHILIC ESOPHAGITIS 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)
EOSINOPHILIC ESOPHAGITIS
EOSINOPHILIC ESOPHAGITIS
EOSINOPHILIC ESOPHAGITIS 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.
EOSINOPHILIC ESOPHAGITIS
PANCREATIC CYSTS
PANCREATIC CYSTS The common use of ultrasounds and CT
scans have led to the finding of pancreatic cysts.
Overview of detection, diagnosis, treatment and terminology.
PANCREATIC CYSTS 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.
EOSINOPHILIC ESOPHAGITIS
EOSINOPHILIC ESOPHAGITIS
EOSINOPHILIC ESOPHAGITIS Flovent inhaler 220 mcg. Swallowed
NOT inhaled. 2 puffs twice daily. Budesonide viscous suspension
(Pulmicort respules) Prednisone for severe cases
PANCREATIC CYSTS
PANCREATIC CYSTS 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.
PANCREATIC CYSTS 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.
PANCREATIC CYSTS 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.
ANAL FISSURE 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.
ANAL FISSURE
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, low-quality evidence) or internal anal sphincterotomy (strong recommendation, high-quality evidence)
