Hereditary Mixed Polyposis Syndrome

What is hereditary mixed polyposis syndrome?

Hereditary mixed polyposis syndrome (HMPS) is a hereditary condition that is associated with an increased risk of developing polyps in the digestive tract, most commonly in the colon and/or rectum. A polyp is a growth of normal tissue that forms a lump. As the name suggests, a variety of polyps may occur. People with HMPS are thought to have an increased risk of developing colorectal cancer, since some of these polyps may turn into cancer over time, unless they are removed.

The same types of polyps that develop in HMPS can also develop in individuals without HMPS. Compared to the general population, people with HMPS typically have higher numbers of polyps, develop them at younger ages, and often develop them more quickly. Examples of the types of polyps that can be seen in HMPS include:

Adenomas, or adenomatous polyps – these have a potential to turn into cancer, unless they are removed
Hyperplastic polyps – these typically do not have a risk of turning into cancer
Hamartomatous or Juvenile polyps – these may have a risk of turning into cancer; the term “juvenile” does not refer to the age of the individual
Serrated polyps – these may have a risk of turning into cancer

What causes HMPS?

HMPS is a genetic condition that predisposes a person to an increased risk of developing cancer and polyps. This means that the condition can be passed from generation to generation in a family. For most families with HMPS, a specific gene mutation causing the syndrome cannot be identified, although some families will have an inherited mutation in the GREM1 gene, but this is rare.

How is HMPS inherited?

Normally, every cell has 2 copies of each gene: 1 inherited from the mother and 1 inherited from the father. Rarely, a family with HMPS will be found to carry a mutation in the GREM1 gene. In these families, genetic testing can help identify which individuals are at risk for developing polyps and cancer, and which individuals are not. For HMPS families without an identifiable genetic mutation, all individuals should undergo screening to test for possible polyps and/or cancer.

Although most families with HMPS do not have a specific gene mutation that can be identified, HMPS is believed to follow an autosomal dominant inheritance pattern, in which a mutation (alteration) needs to happen in only 1 copy of the gene for the person to have an increased risk of getting that disease. This means that a parent with a gene mutation may pass along a copy of their normal gene or a copy of the gene with the mutation. Therefore, a child who has a parent with a mutation has a 50% chance of inheriting that mutation. A brother, sister, or parent of a person who has a mutation also has a 50% chance of having the same mutation.

Options exist for people interested in having a child when a prospective parent carries a GREM1 gene mutation that increases the risk for this hereditary cancer syndrome. Preimplantation genetic diagnosis (PGD) is a medical procedure done in conjunction with in-vitro fertilization (IVF). It allows people who carry a specific known genetic mutation to have children who do not carry the mutation. A woman’s eggs are removed and fertilized in a laboratory. When the embryos reach a certain size, 1 cell is removed and is tested for the hereditary condition in question. The parents can then choose to transfer embryos which do not have the mutation. PGD has been in use for over 2 decades, and has been used for several hereditary cancer predisposition syndromes. However, this is a complex procedure with financial, physical, and emotional factors to consider before starting. For more information, talk with an assisted reproduction specialist at a fertility clinic.

How common is HMPS?

HMPS is considered to be rare.

How is HMPS diagnosed?

There are no specific diagnostic criteria for HMPS. HMPS is suspected in individuals and families with a history of multiple colon polyps of different types. It is also important to consider the possibility of 1 of the other hereditary polyposis syndromes, such as familial adenomatous polyposis (FAP), Peutz-Jeghers syndrome, and juvenile polyposis syndrome. There is currently no blood test that can help diagnose HMPS.

What are the estimated cancer risks associated with HMPS?
People with HMPS are considered to be at increased risk for developing colorectal cancer, but the amount of risk is not currently known.

What are the screening options for HMPS?

A colonoscopy is a test that allows a doctor to view the entire large intestine. Individuals with GREM1 mutations should begin having screening colonoscopies at age 25 to 30 or earlier if someone in the family had a diagnosis of polyps and/or colorectal cancer before the age of 30. Individuals with GREM1 mutations who are found to have polyps at their initial colonoscopy should continue having colonoscopies every 1 to2 years. Individuals with GREM1mutations who do not have polyps at their initial colonoscopy should continue having colonoscopies every 2 to 3 years.

There are no specific screening guidelines developed for HMPS individuals who lack a GREM1 mutation, although regular screening colonoscopies are appropriate. Many doctors would suggest beginning screening 5 to 10 years earlier than the youngest age at which polyps or colorectal cancer were identified in a family member. If polyps are found, screening may need to be done every 1 to 2 years. Learn more about what to expect during a colonoscopy.

Screening options may change over time as new technologies are developed and more is learned about HMPS. It is important to talk with your doctor about appropriate screening tests.

Toxic Megacolon


  • Extension of inflammation into smooth muscle layer causing paralysis
  • Damage to myenteric plexus and electrolyte abnormalities are not consistently found


  • Inflammatory bowel disease (ulcerative colitis> Crohn’s disease)
  • Infectious colitis: bacterial (C. difficile, Salmonella, Shigella, Campylobacter), viral (cytomegalovirus), parasitic (E. histolytica)
  • Volvulus, diverticulitis, ischemic colitis, obstructing colon cancer are rare causes

Clinical Features

  • Infectious colitis usually present for > 1 wk before colonic dilatation
  • Diarrhea ± blood (but improvement of diarrhea may portend onset of megacolon)
  • Abdominal distention, tenderness,± local/general peritoneal signs (suggest perforation)
  • Triggers: hypokalemia, constipating agents (opioids, antidepressants, loperamide, anticholinergics), barium enema, colonoscopy

Diagnostic Criteria

  • Must have both colitis and systemic manifestations for diagnosis
  • Radiologic evidence of dilated colon
  • Three of: fever, HR >120, WBC >10.5, anemia
  • One of: fluid and electrolyte disturbances, hypotension, altered LOC


  • CBC (leukocytosis with left shift, anemia from bloody diarrhea), electrolytes, elevated CRP, ESR
  • Metabolic alkalosis (volume contraction and hypokalemia) and hypoalbuminemia are late findings
  • AXR: dilated colon >6 em (right> transverse> left), loss of haustra
  • CT: useful to assess underlying disease


  • NPO, NG tube, stop constipating agents, correct fluid and electrolyte abnormalities, transfusion
  • Serial AXRs
  • Broad-spectrum antibiotics (reduce sepsis, anticipate perforation)
  • Aggressive treatment of underlying disease (e.g. steroids in IBD, metronidazole for C. difficile)

Indications for surgery (50% improve on medical management):

  • Worsening or persisting toxicity or dilation after 48-72 h
  • Severe hemorrhage, perforation
  • High lactate and WBC especially for C. difficile
  • Procedure: subtotal colectomy+ end ileostomy (may be temporary, with 2nd operation for re-anastomosis later)


  • Average 25-30% mortality

Hemoptysis or bloody sputum

Hemoptysis or bloody sputum should be diagnosed early in an impeccable manner and in depth diagnosis plays a major role in treating hemoptysis or bloody sputum. In this section of the article you will read about the treatment for hemoptysis or bloody sputum, recovery, prevention, prognosis and yoga poses for hemoptysis or bloody sputum.

Treatment for Hemoptysis or Bloody Sputum

  • Mild cases of hemoptysis or bloody sputum should be examined carefully to find the underlying problem that can become life threatening of left untreated. Doctors are clueless whether the mild problem would snowball into a major one in the near future.
  • Massive case of hemoptysis or bloody sputum can result in death due to the lack of oxygen in the body and abundance of carbon dioxide. Doctors try to control the bleeding or aim to localize the source to save life of the patient. Surgical resection combined with laser therapy could deliver sterling results to the victims of hemoptysis or bloody sputum.
    Antibiotics are administered to the patient suffering from mild or even massive cases of hemoptysis or bloody sputum. Bronchogenic carcinoma is treated based on the extent of the infection.
  • Chronic hemoptysis or bloody sputum can be treated sometime by the use of antibiotics in an impeccable manner. If the patient is suffering from other types of diseases, the doctors may administer aggressive treatment.
  • Embolization to rectify the anomalies of bronchial artery is one of the popular techniques that incorporate the injection of the liquid substance in the body to inhibit the blood supply. The injection plays an important role in saving the life of the patient but can also cause complications in hemoptysis or bloody sputum.
  • Surgical resection leads to the elimination of the tissues that can cause instances of hemoptysis or bloody sputum. It is considered as an important treatment for the hemoptysis or bloody sputum which is caused due to aspergilloma.
  • Laser therapy is used to eliminate tumors accompanied by lesions. It is also used to expand the respiratory tract. The advantages and the disadvantages of the different techniques are based on the skill sets of the medical specialists. Physician along with surgeon and radiologist conduct the operation.

Follow-up for Hemoptysis or Bloody Sputum

  • If the infection is severe, patients should regularly follow-up with the doctors. Mild instances of hemoptysis or bloody sputum should be treated with antibiotic or more aggressive technique is required in case of acute infection. If the doctors are able to diagnose the underlying reason behind the disease, it is important to monitor the whole range of symptoms for a couple of years even when the treatment is completed. X-rays of the chest should be performed on a regular basis.

Surgery for Hemoptysis or Bloody Sputum

  • Coughing up of the blood, if severe and life-threatening, may require surgery to remove a lung (pneumonectomy).

Home Remedies for Hemoptysis or Bloody Sputum

  • Cough suppressants are the major home remedies for hemoptysis or bloody sputum. For minor or mild cases of hemoptysis or bloody sputum which is caused by bronchitis, cough suppressants might be carried out with the help of the doctors. It is vital to monitor the blood that occurs in the cough.
  • Amount of blood in the mucus
  • Dizziness is the indication of the blood loss.
  • Fever accompanied by chest pain can also be an important symptom.

Recovery Period/Healing Time for Hemoptysis or Bloody Sputum

  • Recovery period/healing time for hemoptysis or bloody sputum depends on the skill set of the doctors and the mode of the treatment. They can provide the estimated time for recuperation from the disease and also the possibility of recurrence.

Some of the steps that can be taken to prevent hemoptysis or bloody sputum are as follows:

  • Stop Smoking to Prevent Hemoptysis or Bloody Sputum: Smoking should be stopped to control the instances of hemoptysis or bloody sputum. It can create lung infection.
  • Alcohol and Diet Plays Major Role in Preventing Hemoptysis or Bloody Sputum: Alcohol should be shunned to protect the lungs and digestive system from hemoptysis.
    If you drink alcohol, do not exceed the recommended daily limits (three to four units a day for men and two to three units a day for women).
  • Alcohol needs to be consumed in controlled amounts and within the prescribed limit.
  • Balanced diet would go a long way in improving the immune system.

Vaccinations can Play a Crucial Role in Preventing Hemoptysis or Bloody Sputum: If you want advanced protection against hemoptysis, it is important to get the vaccines that would help to combat flu as well as pneumonia. Vaccines can be useful for:

  • Babies along with young children
  • Flu jab can be useful for pregnant females
  • People who are more than 65 years of age
  • People suffering from deficient immune system.
  • Ability to Work (Return to Work Considerations): Patients suffering from bouts of
  • breathlessness can benefit greatly by resting between the tasks during job.

Prognosis/Outlook for Hemoptysis or Bloody Sputum

  • The prognosis/outlook for majority of the victims of hemoptysis or bloody sputum is good. Majority of the patients suffering from hemoptysis or bloody sputum get treated and can recuperate quickly. Less than 2% of the patients suffer from the massive case of hemoptysis or bloody sputum. People having underlying cause as cancer are prone to higher mortality rate. Patients suffering from bleeding also experience lots of problems.
  • The prognosis of the embolization of bronchial artery & surgery rely upon on the magnitude of the underlying illness being administered. Complexity of respiratory failure, infection and bleeding could lead to death.
  • Artery embolization accompanied by the surgery to treat the underlying problem may cause complications such as infection or even excessive bleeding. Respiratory issues might result in death.

Diverticular Disease


  • Diverticulum -abnormal sac-like protrusion from the wall of a hollow organ
  • Diverticulosis – presence of multiple diverticula
  • Diverticulitis – inflammation of diverticula
  • True (congenital) diverticuli- contain all layers of colonic wall, often right-sided (see Figure 15)
  • False (acquired) diverticuli- contain mucosa and submucosa, often left-sided


  • 95% left-sided in patients of Western contries, 75% right-sided in Asian populations


  • Erosion of the wall by increased intraluminal pressure or inspissated food particles ~ inflammation and focal necrosis ~ micro or macroscopic perforation
  • Usually mild inflammation with perforation walled off by pericolic fat and mesentery; abscess, fistula or obstruction can ensue
  • Poor containment results in free perforation and peritonitis

Clinical Features

  • Depend on severity of inflammation and whether or not complications are present; hence ranges from asymptomatic to generalized peritonitis
  • LLQ pain/tenderness (2/3 of patients) often for several days before admission
  • Constipation, diarrhea, nausea, vomiting, urinary symptoms (with adjacent inflammation)
  • Low-grade fever, mild leukocytosis common,
  • Occult or gross blood in stool rare to coexist with acute diverticulitis

+ Complications (25% of cases):

  • Abscess: palpable tender abdominal mass
  • Fistula: colovesical (most common), coloenteric, colovaginal, colocutaneous
  • Colonic obstruction: due to scarring from repeated inflammation
  • Perforation: generalized peritonitis (feculent vs. purulent)
  • Recurrent attacks rarely lead to peritonitis


+ AXR, upright CXR:

  • localized diverticulitis (ileus, thickened wall, SBO, partial colonic obstruction)
  • free air may be seen in 30% with perforation and generalized peritonitis

+ CT scan (test of choice): very useful for assessment of severity and prognosis

Gastritis Treatment

Description: Gastritis is an inflammatory condition affecting the stomach lining that results in acute or chronic
indigestion, bloating, “gas,” and heartburn. Prevalence: Common. Predominant Age: Any.
Genetics: No genetic pattern.

Causes: Generalized infl ammation of the stomach lining, which, in some cases, may be infectious (Helicobacter
pylori). Risk Factors: Cigarette smoking, alcohol abuse, some medications (nonsteroidal anti-inflammatory drugs
[NSAIDs]), bile reflux, radiation.

Signs and Symptoms
• Nausea, vomiting, dyspepsia, heartburn, and “gas” (symptoms are most common after eating large meals,
consuming certain foods)
• Upper abdominal pain or tenderness
• Hiccups
Differential Diagnosis
• Gastrointestinal reflux
• Ulcer disease (gastric or duodenal)
• Esophageal cancer
• Linitis plastica
Associated Conditions: Bleeding, dysphagia, and gastric or duodenal ulcer.
Workup and Evaluation
Laboratory: No evaluation indicated.
Imaging: No imaging indicated.
Special Tests: Gastroscopy (with or without biopsy) establishes the diagnosis but most often is not necessary.
Diagnostic Procedures: History and physical examination (suspicious), gastroscopy (diagnostic).

General Measures: Dietary changes, elevation of the head of the bed, smoking cessation, alcohol in moderation
only, antacids. (Antacids that coat [liquids] and those that tend to fl oat on the surface of the stomach
contents, such as Gaviscon, give better heartburn relief than other agents.)
Specific Measures: Eliminate medications that contribute to reduced esophageal pressure, such as diazepam and calcium channel blockers, or that may damage the esophagus (nonsteroidal anti-infl ammatory drugs). Use
acid-blocking therapy.
Diet: No specifi c dietary changes indicated.
Activity: No restriction.
Patient Education: Reassurance, diet counseling, behavior modification.

Drug(s) of Choice
Histamine H2 antagonists (cimetidine 800 mg two times daily, ranitidine 400 mg four times daily, famotidine
20 mg two times daily, or nizatidine 150 mg two times daily).
Hydrogen potassium pump blocker (omeprazole 20 to 40 mg daily for 4 to 8 weeks, esomeprazole 20 to 40 mg
daily for 4 to 8 weeks, or pantoprazole 40 mg daily for 8 weeks). Misoprostol (Cytotec, 100 to 200 microg PO
four times daily) if mucosal injury is documented or suspected.
Contraindications: Known or suspected hypersensitivity. Misoprostol is contraindicated during pregnancy and
Precautions: If bismuth is prescribed, warn the patient about black stools. Because of a lack of long-term followup,
hydrogen pump inhibitors may be taken for only 8 to 12 weeks.
Interactions: Multiple drug interactions are possible with agents such as cimetidine; check full prescribing

Alternative Drugs
In patients with H. pylori infection, a combination of bismuth (Pepto-Bismol) and an antibiotic (metronidazole
250 mg every 6 hours, tetracycline 500 every 6 hours, or amoxicillin 500 mg every 8 hours) has been recommended for 2 weeks. A 4-week treatment with clarithromycin (Bixin) and either omeprazole (Prilosec) or ranitidine bismuth citrate (Tritec) may also be used.
• Patient Monitoring: Normal health maintenance. If significant gastric erosion is documented, repeat gastroscopy
after 6 weeks is often recommended.
• Prevention/Avoidance: Reduction of modifi able risk factors (e.g., smoking).
• Possible Complications: Chronic pain, ulcer formation, and perforation.
• Expected Outcome: Generally good symptomatic relief, but long-term therapy is often required.

Hepatitis B Infection

Hepatitis B is an acute infection of the liver parenchymal cells caused by the hepatitis B virus (HBV). The WHO estimates that 400 million people worldwide (6% of the population) are chronic HBV carriers. North America, Western Europe, and Australia are areas of low prevalence, <2%. In the United States an estimated 800,000 to 1.4 million people have chronic HBV infection.


_ The incubation period of HBV infection is 4 to 24 weeks.

_ Patients often present with nonspecific symptoms.

_ Profound malaise

_ Many asymptomatic cases

_ Prodrome

  • 15% to 20% serum sickness (urticaria, rash, arthralgia) during early HBsAg.
  • HBsAg-Ab complex disease (polyarteritis nodosa–arthritis, arteritis, glomerulonephritis).

_ Hepatomegaly (87%) with right upper quadrant (RUQ) tenderness

  • Hepatic punch tenderness
  • Splenomegaly

_ Jaundice, dark urine, with occasional pruritus

_ Variable fever (when present, generally precedes jaundice and rapidly declines following onset of icteric phase).

_ Spider angiomata: rare; resolves during recovery.

_ Rare polyarteritis nodosa, cryoglobulinemia


_ Caused by HBV (42-nm hepadnavirus with an outer surface coat [HBsAg], inner nucleocapsid core [HBcAg; HBeAg]; DNA polymerase; and partially double-stranded DNA genome). There are eight genotypes (A to H) based on nucleotide sequence.

_ Transmission by parenteral route (needle use, tattooing, ear piercing, acupuncture, transfusion of blood and blood products, hemodialysis, sexual contact), perinatal transmission.

_ Recovery

  • Fulminant hepatitis occurring in <1% (especially if coinfected with hepatitis D); 80% fatal.
  • Unusual (5%) prolonged acute disease for 4 to 12 mo, with recovery.
  • Overall fatality increases with age and viral inoculation (e.g., transfusions).

_ Chronic Infection

  • Persistent carrier state without hepatitis (HBsAg positive)
  • Chronic persistent hepatitis (CPH) (clinically well), or chronic active hepatitis (CAH) (HBsAg positive and HBeAg positive).
  • Cirrhosis.
  • Hepatocellular carcinoma (especially after neonatal infection).
  • Chronic infection: more common following low-dose exposure and mild acute hepatitis, with earlier age of infection, in males, and in immunosuppressed patients.
  • One third to one quarter of chronically infected will develop progressive liver disease (cirrhosis, hepatocellular carcinoma).


_ Acute serum specimen for hepatitis B serology (HBsAg, HBsAb, HBcAb, HBeAg, HBeAb), HBDNA by PCR.

_ LFTs.

_ CBC.

_ Liver biopsy: rarely indicated for diagnosis of fulminant viral hepatitis, chronic hepatitis, cirrhosis, carcinoma.


_ In most cases of acute HBV infection no treatment necessary; >90% of adults will spontaneously clear infection.

_ Hospitalization advisable for any patient in danger from dehydration caused by poor oral intake, whose PT is prolonged, who has rising bilirubin level >15 to 20 μg/dl, or who has any clinical evidence of hepatic failure.

_ IV therapy needed (rarely) for hydration during severe vomiting.

_ Avoid hepatically metabolized drugs.

_ No therapeutic measures are beneficial.

_ Steroids not shown helpful.

_ Treatment for hepatitis B is recommended for patients with acute liver failure (ALF), those with elevated ALT and HBV DNA >10,000 IU/mL, and in patients receiving immunosuppressive therapy.

_ Treatment consists of entecavir or tenofovir.

_ The goal of treatment is a decline in HBV DNA level to <50 IU/mL and normalization of ALT level.

_ If some patients without cirrhosis who can tolerate the side effects of pegylated interferon, it may be used if they have elevated ALT levels and low HBV DNA  levels.

_ Liver transplantation (should be considered for fulminant hepatitis).

Chronic Pancreatitis

Chronic pancreatitis is a recurrent or persistent inflammatory process of the pancreas characterized by chronic pain and by pancreatic exocrine and/or endocrine insufficiency.



  • Persistent or recurrent epigastric and left upper quadrant pain that may radiate to the back
  • Tenderness over the pancreas, muscle guarding
  • Significant weight loss
  • Bulky, foul-smelling stools, greasy in appearance
  • Epigastric mass (10% of patients)
  • Jaundice (5% to 10% of patients)


  • Chronic alcoholism
  • Obstruction (ampullary stenosis, tumor, trauma, pancreas divisum, annular pancreas)
  • Hereditary pancreatitis
  • Severe malnutrition
  • Idiopathic
  • Untreated hyperparathyroidism (hypercalcemia)
  • Mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) gene and the TF genotype
  • Autoimmune pancreatitis (AIP) (5% of chronic pancreatitis cases): presents clinically with jaundice (63% of patients) and abdominal pain (35%). CT may reveal diffusely enlarged pancreas, enhanced peripheral rim of hypoattenuation “halo,” and low-attenuation mass in head of pancreas. Laboratory values reveal elevated serum immunoglobulin (Ig) G4, elevated serum Ig or gamma-globulin level, presence of antilactoferrin antibody (ALA), anticarbonic anhydrase (ACA) II level, anti-smooth-muscle antibody (ASMA), or antinuclear antibody (ANA).
  • Sclerosing pancreatitis: a form of chronic pancreatitis characterized by infrequent attacks of abdominal pain, irregular narrowing of the pancreatic duct, and swelling of the pancreatic parenchyma; patients have high levels of serum immunoglobulins (IgG4). Chronic sclerosing pancreatitis is also known as autoimmune pancreatitis.



  • Pancreatic cancer
  • Peptic ulcer disease
  • Cholelithiasis with biliary obstruction
  • Malabsorption from other etiologies
  • Recurrent acute pancreatitis
  • Renal insufficiency
  • Intestinal ischemia or infarction
  • Other: Crohn’s disease, gastroparesis, inflammatory bowel disease


Medical history with focus on alcohol use, laboratory tests, diagnostic imaging


  • Serum amylase and lipase may be elevated (normal amylase levels, however, do not exclude the diagnosis).
  • Hyperglycemia, glycosuria, hyperbilirubinemia, and elevated serum alkaline phosphatase may also be present.
  • 72-hr fecal fat determination (rarely performed) reveals excess fecal fat. Fecal elastase test requires only 20 g of stool.
  • Secretin stimulation test is the best test for diagnosing pancreatic exocrine insufficiency.
  • Lipid panel: significantly elevated triglycerides can cause pancreatitis.
  • Serum calcium: hyperparathyroidism is a rare cause of chronic pancreatitis.
  • Elevated levels of serum IgG4 are found in sclerosing pancreatitis and AIP.
  • Elevated serum Ig or gamma-globulin level, presence of ALA, ACA II level, ASMA, or ANA in AIP.


  • Plain abdominal radiographs may reveal pancreatic calcifications (95% specific for chronic pancreatitis).
  • Ultrasound of abdomen may reveal duct dilation, pseudocyst, calcification, and presence of ascites.
  • Contrast-enhanced CT scan of abdomen is the initial modality of choice. It is useful to detect calcifications, evaluate for ductal dilation, and rule out pancreatic cancer.
  • Endoscopic retrograde cholangiopancreatography (ERCP) had been traditionally used to evaluate for the presence of dilated ducts, strictures, pseudocysts, and intraductal stones. However, for the evaluation of pancreatic parenchyma and duct system newer, less invasive modalities such as magnetic resonance cholangiopancreatography and endoscopic ultrasonography (EUS) are preferred. EUS has a sensitivity of 97% and a specificity of 60% for chronic pancreatitis and a very low complication rate. Fine-needle aspiration biopsy combined with EUS is the preferred modality for evaluation of cystic or mass lesions to determine malignancy.



  • Avoidance of alcohol and tobacco
  • Frequent, small-volume, low-fat meals


  • Avoidance of narcotics if possible (simple analgesics or NSAIDs can be used). describes an approach to the patient with painful chronic pancreatitis.
  • Treatment of steatorrhea with pancreatic supplements (e.g., Pancrease, Creon, Pancrelipase titrated prn based on the amount of steatorrhea and patient’s weight loss). All non–enteric coated enzymes should be used with acid-suppressing medications. Proton pump inhibitors and H2 blockers reduce inactivation of the enzymes from gastric acid.
  • Antioxidants (vitamin A, selenium, vitamin E) may be helpful for pain control in chronic pancreatitis.
  • Percutaneous or via EUS celiac plexus blockade with corticosteroids or neurolysis with ethanol may provide temporary pain relief.
  • Treatment of complications (e.g., type 1 diabetes mellitus).
  • Glucocorticoid therapy in patients with AIP and sclerosing pancreatitis can induce clinical remission and significantly decrease serum concentrations of IgG4, immune complexes, and the IgG4 subclass of immune complexes.



  • Surgical intervention may be necessary to eliminate biliary tract disease and improve flow of bile into the duodenum by eliminating obstruction of pancreatic duct.
  • ERCP with endoscopic sphincterectomy and stone extraction is useful in selected patients.
  • Transduodenal sphincteroplasty or pancreaticojejunostomy in selected patients. Surgery should also be considered in patients with intractable pain.

Hemorrhoids or Piles – Diagnosis & Treatment

A hemorrhoid is a symptomatic dilation of the hemorrhoidal venous plexus resulting in perianal swelling, itching, pain, hematochezia, and fecal soiling.


_ Dilated rectal venous plexus with varying degrees of inflammation.


_ Pregnancy, obesity, chronic cough, constipation, heavy lifting, sedentary work or lifestyle, hepatic disease, colon malignancy, portal hypertension, loss of muscle tone resulting from age, surgery, episiotomy, anal intercourse, or neurologic disease (multiple sclerosis).


  • Rectal bleeding
  • Anal protrusion
  • Anal itching and pain (especially with thrombosis or ulceration)
  • Constipation and straining for bowel movement
  • Rectal incontinence and soiling
  • Hematochezia and stool mucus
  • Anal fissure, infection, or ulceration
  • Hemorrhoidal thrombosis


_ Surgical therapy is appropriate for those patients with debilitating symptoms or for whom medical therapy has failed (15% to 20% of patients). Banding of internal hemorrhoids is better accepted by patients than traditional surgical therapy. Hemorrhoidal banding requires a minimum of equipment and is well suited to the office or outpatient surgical setting. Some aching is generally experienced for several days after hemorrhoid banding procedures. Sitz baths and topical analgesics such as witch hazel are generally sufficient.

_ Increased dietary fiber.

_ Avoid prolonged sitting, straining, or heavy lifting. Encourage physical fitness.


  • Dietary fiber supplements. Stool softeners—docusate sodium (Colace, Dialose, Sof-Lax) 50 to 300 mg PO daily (larger doses are generally divided over the day).
  • Topical analgesic sprays or ointments—benzocaine (Americaine, Hurricaine) 20% spray or gel, dibucaine (Nupercainal) 1% ointment.
  • Antipruritics and anti-inflammatory agents—hydrocortisone (Anusol-HC, Analpram-HC, Cortenema, Cortifoam, Epifoam, Proctofoam-HC), pramoxine 1% (Fleet rectal pads, Analpram-HC), witch hazel 50% (Tucks pads or gel).
  • Astringents—Preparation H.