-Hepatitis B virus (HBV) is an enveloped DNA virus belonging to the family hepadnavirus.

-It comprises of a partial double-stranded DNA genome surrounded by HBcAg and carrying viral DNA polymerase (reverse transcriptase) and HBeAg and wrapped in a lipid bilayer membrane containing HBsAg.

-It is the smallest known human DNA virus with respect to genome size.

-It is found in blood, saliva, and semen.

-It is transmitted through blood and blood-derived products, sexual contact, sharing needles and syringes, injecting drugs, and mother-to-child.

-The incubation period may be as brief as 30 days or as long as 180 days (mean approximately 60-90 days).

Symptoms & Signs:

Pathogenesis involves immune-mediated serum sickness-like rash and arthritis leading to constitutional symptoms – anorexia, nausea,  jaundice, fatigue, loss of appetite, fullness in the right upper abdominal quadrant

Diagnosis:

-The laboratory diagnosis of acute hepatitis B infection is best made by demonstrating the presence of HBsAg and IgM antibody to HBcAg in serum, since this antibody disappears within 6 months of the acute infection

-Appearance of antibody to HBsAg signals elimination of infection

-Window period has neither HBsAg nor antibody to HBsAg but antibody to HBcAg (IgM) is present

-In patients who subsequently recover, HBsAg usually becomes undetectable after four to six months. Persistence of HBsAg for more than six months implies chronic infection.

–Chronic infection associated with HBsAg persistence and no development of antibody to HBsAg. IgG antibody to HBcAg present

-In immunity due to vaccination, antibody to HBsAg is seen.

Treatment:

-No specific treatment for acute infection

-Antiviral agents for chronic HBV include pegylated interferon  or nucleotide analogs (entecavir and tenofovir).

Prevention:

-HBsAg is given as a subunit vaccine in three doses (0, 1, and 6 months) to provide long-term protection by producing IgG.

-It is recommended for use in children starting at age 0 to 2 months and in adults given in 3 doses at 0, 1 and 6 months.

Prognosis:

– About 90% of the patients resolve the infection after acute disease that may be asymptomatic.

-The likelihood of liver failure from acute HBV is less than 1 percent.

-Less than 10% of the patients develop chronic infection.

Q: What is the serologic hallmark of HBV infection? Hepatitis B surface antigen (HBsAg)

Q: Why is Hepatitis B core antigen (HBcAg) not detectable in serum? It is an intracellular antigen that is expressed in infected hepatocytes.

Hepatitis A virus (HAV) is a RNA hepatovirus (in the picornavirus family)

– It is a naked capsid (unenveloped), linear single-stranded, positive-sense RNA virus with a cubic (icosahedral) symmetry

-it replicates in the cytoplasm of the intestinal mucosa by using viral RNA polymerase.

-The virus is transmitted by the fecal-oral route

-More than 90% of adult population is seropositive in developing countries

-The incubation period averages 30 days. it is followed by viremia and spread to the liver and cause lymphoid cell infiltration, necrosis of liver parenchymal cells, and proliferation of Kupffer cells.

-There is no chronic carrier state.

-Risk factors: crowding, poor sanitation,in men who have sex with men, in illicit drug users, and in travelers from the developed countries visiting developing areas of the world.

Symptoms & Signs:

-Contagion is greatest 10 to 14 days before the symptoms appear

-When symptomatic, there is usually fever,malaise, myalgia, arthralgia, easy fatigability, upper respiratory symptoms, a distaste for smoking, anorexia, nausea, right upper quadrant abdominal pain, and jaundice.

-Hepatomegaly, liver tenderness, splenomegaly

-Dark urine and clay-colored stools may be noticed by the patient 1 to 5 days before the onset of clinical jaundice.

Diagnosis:

-Initial immune response is the development of HAV-specific IgM antibody followed by appearance of IgG after a few weeks. So, the best method for documentation of acute HAV infection is the demonstration of high titers of virus-specific IgM antibody during the acute phase of illness.

-Reverse transcriptase polymerase chain reaction (RT-PCR) can also be used to detect HAV.

-Serum aminotransferases such as ALT and AST as well as bilirubin levels are elevated.

Treatment:

-There is no specific treatment for HAV.

-Supportive measures include adequate nutrition and rest.

-Immune serum globulin (ISG) provides temporary protection if given before or during the incubation period of the disease.

Prevention: an effective inactivated HAV vaccine given in 2 doses 6-12 months apart is recommended for use in children at age 1 and in adults.

-Hepatitis A vaccine prevents postexposure infection

Prognosis:

– Almost all cases (99%) of HAV are self-limiting.

-Hepatitis A does not cause chronic liver disease

-IgG-specific antibody is protective

Q: What is the major mode of spread of HAV? by fecal–oral exposure

Q: Why demonstration of IgG antibody is not indicative of recent HAV infection? Because it persists indefinitely

Q: Why do acute hepatitis patients produce dark-colored urine and clay-colored stool? Dark-colored urine is due to excessive bilirubin in urine and clay colored stool is due to lack of drainage of bile salts in the stool through the biliary system due to liver infection.

Q: Why is administration of ISG not indicated when a patient develops clinical symptoms of HAV? Because the patient starts producing antibodies by the time of clinical symptoms.

Hidradenitis suppurativa is a refractory, chronic inflammatory follicular disorder in the apocrine gland bearing areas of the axillary, inguinal, and inframammary areas,  involving the skin and subcutaneous tissue

-HS is not a primary infectious process but rather inflammatory.

-It is more common in women.

-Areas commonly affected: Axillae, inguinal areas, breasts, inframammary areas,inner thighs, buttocks, perianal, perineal regions

-HS is most common in the axilla and inguinal area

-Perineal disease is more common in males, whereas axillary disease is more common in females.

-Risk factors: Obesity, smoking, and tight-fitting clothing.

Symptoms & Signs

Patients typically report a gradual onset of persistent or recurrent boil-like lesions in the axillae and/or inguinal area.

Diagnosis:

The diagnosis is made clinically

Stage one: Single or multiple abscesses or nodules

Stage two: Nonconfluent, recurrent abscesses, or nodules with sinus tracts and scars.

Stage three: Similar to stage two, but lesions are diffuse and affect an entire region.

Treatment:

General measures: Smoking cessation, weight loss if overweight, and avoidance of tight-fitting clothes

Stage one: Topical clindamycin, oral antibiotics

Stage two: Stage one therapies, intralesional corticosteroids, oral retinoids (acitretin, isotretinoin, alitretinoin);Hormones (Cyproterone acetate, oral contraceptives), incision and drainage, surgical procedures

Stage three: infliximab, Adalimumab, Extensive excision of the affected area, laser therapy

Prognosis:

HS can end as large abscesses and fistulas. Other complications include strictures, contractures, depression, suicide, arthritis, squamous cell carcinoma

Q: What is the most common presentation of HS? painful, tender, firm, nodular lesions in axillae

Q: Who is the typical patient of HS? Obese, postpubertal female.

Q: What is the most common site of HS? Axilla

-Pilonidal disease occurs when hair becomes entrapped within a cyst in the sacrococcygeal region

-It is a common condition of the skin and subcutaneous tissue at or near the upper part of the natal cleft of the buttocks.

-It  almost always occur in the midline but can have sinus tracts extending off the midline.

-It is typically chronic with recurrent drainage and inflammation,

-It is more common in teenage and young adult males.

-It is three times more common in men than in women.

-Risk factors: Deep natal cleft, obesity, increased hair density between the buttocks

Symptoms & Signs:

red, fluctuant, tender abscess in the gluteal cleft

Diagnosis:

History and Clinical examination is sufficient to diagnose this condition

Treatment: incision and drainage; Wound care

Prognosis: Excellent 

Q: What is the most common site of PD? Natal Cleft

Q: Describe the typical patient with PD? Teenager or young adult male

Previous recommendation/black box warnings indicated that metformin should not be given to men with a serum creatinine greater than 1.5 mg/dL or women with a serum creatinine greater than 1.4 mg/Dl. The main concern here was the increased risk of developing lactic acidosis in patients with high serum levels of metformin due to decreased metformin excretion with decreased renal function. Current guidelines, based on the creatinine clearance (CC) rather than serum creatinine alone, are more liberal, reflecting greater clinical experience with the use of metformin in treating type 2 DM. They include normal use of metformin in patients with CC > 60 ml/min, and cautious use between CC of 45-60. At a creatine clearance of 30-45, patients doing well on metformin can continue taking it, but the dose should generally be reduced by one half. At this CC, patients should not be newly started on metformin. Metformin should not be used in patients with a creatinine clearance < 30 ml/min.

Perianal or perirectal Abscess

Perianal abscesses are typically polymicrobial with both aerobic and anaerobic bacteria.

-They spread through the external sphincter below the level of the puborectalis and become ischiorectal abscesses.

-Anorectal abscesses are more common in early middle-aged males.

Symptoms & Signs: Severe pain in the anal or rectal area, fever, malaise, purulent rectal discharge ischiorectal abscess:  Swelling in the ischiorectal fossa on digital rectal examination

Diagnosis:

-Diagnosis can usually be made with physical exam alone;  CT or MRI help to delineate the anatomy of the abscess

–Erythema, fluctuance, and swelling in the perianal region on external examination

-Digital rectal exam will reveal a painful swelling laterally in the ischiorectal fossa. Treatment: Perianal abscesses are treated with local incision and drainage, while ischiorectal abscesses require drainage in the operating room.

Prognosis: After drainage of an abscess, most patients are found to have a fistula in ano.

-Delayed treatment can result in tissue necrosis and sepsis.

-Surgical referral after drainage recommended because of the risk of fistula formation.

Anal Fistula

–An anorectal fistula is the chronic manifestation of the acute perirectal process that forms an anal abscess

-The majority of anorectal fistulas originate from an infected anal crypt gland

-Drainage of an anorectal abscess results in cure for about 50% of patients while the remaining 50% develop an anal fistula.

-Causes of fistulas that connect to the rectum include: Crohn disease, Lymphogranuloma venereum, rectal tuberculosis, cancer

Symptoms & Signs: purulent discharge, itching, tenderness, and pain

Diagnosis: Drainage from the internal and/or external openings.

-An indurated tract is often palpable.

-Goodsall’s rule can be used as a guide in determining the location of the internal opening

Imaging studies: Endosonography (EUS), fistulography, CT or MRI show air or contrast material within the fistula.

Treatment: Fistula in ano is treated by surgical excision under anesthesia

Anal fissure is a slit-like linear or rocket-shaped tear,usually <5 mm in the squamous epithelium of the anus distal to the dentate line.

-Usually they arise from trauma during defecation

-They are more common in the third through the fifth decades.

-They most commonly occur in the posterior midline (90%); 10% occur anteriorly

-Chronic fissures are those present for >6 weeks.

-Fissures that occur off the midline should lead to suspect other conditions such as syphilis, tuberculosis, HIV/AIDS, Crohn Disease, anal carcinoma

Symptoms & Signs:

Classic complaint: Severe,relentless, tearing pain during defecation followed by throbbing discomfort; May lead to constipation because of fear of recurrent pain

With chronic fissures, there is fibrosis and a skin tag at the outermost edge (sentinel pile)

Diagnosis:

Visual inspection of the anal verge while gently separating the buttocks

Sentinel pile: A skin tag at the distal end of the fissure

Anal manometry: elevation in anal resting pressure

Treatment:

Most primary acute anal fissures respond to medical management, while chronic fissures more often require surgical intervention

Conservative: Stool softeners, increased dietary fiber, topical anesthetics (lidocaine, prilocaine), glucocorticoids, sitz baths, nifedipine ointment, nitroglycerin ointment, diltiazem ointment, botulinum toxin injected into the internal sphincter

Surgical: anal dilatation and lateral internal sphincterotomy

Prognosis: Most simple anal fissures resolve in 2 to 4 weeks.

Q: What is the most common cause of rectal bleeding in infancy? Anal fissure

Q: What is the most common cause of painful rectal bleeding? Anal fissure

Q: What is the most common side-effect of nitroglycerin ointment? Headache

Q: What is the most common etiology of anal fissure? Anal trauma due to bowel movements

Q: What do you suspect in a child with large, irregular, multiple anal fissures? Sexual abuse

-If you feel you have hemorrhoids and need treatment, please visit Dr.Paul Kattupalli for a personal examination.

-Hemorrhoids are dilated submucosal vessels in the anus

-Hemorrhoids that originate above the dentate line are “internal” and those that originate below are “external.”

–Internal hemorrhoids are arteriovenous communications between terminal branches of the superior rectal artery and rectal veins; they are covered with mucosa and transitional zone epithelium.

-External hemorrhoids arise from the inferior hemorrhoidal veins located below the dentate line; they are covered with squamous epithelium.

-Three main hemorrhoidal complexes traverse the anal canal—the left lateral, the right anterior, and the right posterior. Engorgement and straining lead to prolapse of this tissue into the anal canal.

-Hemorrhoids normally appear at 3 o’clock (when patients are in the lithotomy position), 7 o’clock, and 11 o’clock positions around the anus.

-Staging of hemorrhoids:

Stage I: Enlargement with bleeding

Stage II: Protrusion with spontaneous reduction

Stage III: Protrusion requiring manual reduction

Stage IV: Irreducible protrusion

Risk factors: Straining at stool, constipation, prolonged sitting, pregnancy, obesity, and low-fiber diets

Symptoms & Signs

Hemorrhoids are usually asymptomatic. Painless bright red blood seen either in the toilet or upon wiping when the blood vessel ruptures.Both internal and external hemorrhoids may develop a thrombosis, which causes significant pain.

External hemorrhoids:  mild pain, bright red rectal bleeding. Severe pain suggests thrombosis in the hemorrhoid.

Internal hemorrhoids: bleeding, fullness, discomfort, mucoid discharge,irritation of perianal skin, soiling of underclothes.

Diagnosis: Perianal inspection, anoscopy; Internal hemorrhoids are not readily palpable and can best be visualized through an anoscope. External hemorrhoids can be seen on external inspection.

Treatment:

Conservative measures: increase fluid intake with meal, eat a high-fiber diet, sitz baths, stool softeners

Medical Treatment: Injection sclerotherapy, rubber band ligation, or application of electrocoagulation (bipolar cautery or infrared photocoagulation), hydrocortisone, Preparation H, Anusol HC, Proctofoam.

Surgical Treatment: excisional hemorrhoidectomy, transhemorrhoidal dearterialization (THD), or stapled hemorrhoidectomy

Endoscopy: Older patients who have not had colorectal cancer screening should undergo colonoscopy or flexible sigmoidoscopy.

Prognosis

Although the most common cause of bright red rectal bleeding is hemorrhoids, tumors must be ruled out as a cause of rectal bleeding in patients >40 years of age.

1. Majority of hemorrhoids are internal or external? Internal
2. Why are uncomplicated internal hemorrhoids painless? due to visceral innervation and lack of sensory innervation.
3. What do you consider in a patient with frequent diarrhea and hemorrhoids? Inflammatory bowel disease
4. What is the most common cause of symptomatic hemorrhoids? Pregnancy
5. What is the best means of definitive therapy for hemorrhoids? Hemorrhoidectomy

Q.What is the objective of sitz baths? to relax anal sphincter

Colon cancer is the third most common cancer in the United States. If you want to schedule a colonoscopy with Dr.Paul Kattupalli, please call our office.

-Polyps are discrete mass lesions that are flat or protrude into the intestinal lumen. They arise from the epithelial cells lining the colon.

-Most commonly sporadic, may be inherited as part of familial polyposis syndrome

Of polyps removed at colonoscopy, over 70% are adenomatous; most of the remainder are serrated; distinguished by histology

-Of polyps removed at colonoscopy, over 70% are adenomatous

-Most colorectal cancers, regardless of etiology, arise from adenomatous polyps.

–Four major pathological groups

• Mucosal adenomatous polyps (tubular, tubulovillous, villous)
• Mucosal serrated polyps (hyperplastic, sessile serrated polyp, traditional serrated adenoma)
• Mucosal nonneoplastic polyps (juvenile polyps, hamartomas, inflammatory polyps)
• Submucosal lesions (lipomas, lymphoid aggregates, carcinoids, pneumatosis cystoides intestinalis)

-Hyperplastic polyps located in the proximal colon (ie, proximal to the splenic flexure) may be associated with an increased risk of neoplasia, particularly those > 1 cm

–Familial adenomatous polyposis of the colon is a rare autosomal dominant disorder associated with a deletion in the long arm of chromosome 5. Thousands of adenomatous polyps appear in the large colon, generally by age 25 years, and colorectal cancer develops in almost all these patients by age 40 years.

–Peutz-Jeghers syndrome (PJS):It is an autosomal dominant syndrome characterized by multiple hamartomatous polyps in the gastrointestinal tract, mucocutaneous pigmentation, and an increased risk of gastrointestinal and non gastrointestinal cancer.

-Pigmentations occur on the lips and perioral region, palms of the hands, buccal mucosa, and soles of the feet.

-The most common sites of gastrointestinal tract malignancy are the colon and pancreas, and the most common site of extraintestinal tract cancer is the breast.

HEREDITARY NONPOLYPOSIS COLORECTAL CANCER:

–The most common genetic colon cancer syndrome is Lynch syndrome, formerly known as HNPCC.

– It is an autosomal dominant condition

Risk factors:

Older age: 85% in those older than age 60 years

Diet: Increased cholesterol is associated with a greater risk of polyps

Excess body weight

Inflammatory bowel disease

Alcohol consumption

Symptoms & Signs: Most patients with adenomatous and serrated polyps are completely asymptomatic. Chronic occult blood loss may lead to iron deficiency anemia. Large polyps may ulcerate, resulting in intermittent hematochezia

Diagnosis:

Laboratory Tests: Fecal occult blood test (FOBT), fecal immunochemical test (FIT), and fecal DNA tests

Imaging Studies:  CT colonography

Endoscopic tests: 1. Colonoscopy, which should be performed in all patients who have positive FOBT, FIT, or fecal DNA tests or iron deficiency anemia.

2. Capsule endoscopy

Treatment: Colonoscopic polypectomy; periodic colonoscopic surveillance

Prognosis:

-Chronic occult blood loss may lead to iron deficiency anemia.

-Untreated patients with polyps larger than 10 mm are at increased risk for colon cancer both at the site of the polyp and at other sites.

Q: What is the best means of detecting and removing adenomatous and serrated polyps? Colonoscopy

Q: FIT or FOBT: Which is more sensitive in the detection of colorectal cancer? FIT