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Peptic Ulcer Disease


My question involves the most serious consequences of untreated or insufficiently treated PUD, but I will post general notes here for my own reference. Enjoy! (??? means I doubt the factoid due to weak source, but I'm listing it anyway for discussion)

FACTOIDS:
--some experts have recommended a large-scale public health effort to eradicate H. pylori
--researchers are working on a vaccine
--cure of active peptic ulcer disease increased life expectancy by 2.3 years in people ages 40 to 44 years.
--impact of cure decreased with advancing age: for pts 70-74, life expectancy increased by only 121 days.
--ulcer = mucosal erosions equal to or greater than 0.5 cm
--~80% of ulcers are associated with Helicobacter pylori
--only 20% of H. pylori cases go to a doctor
--more peptic ulcers arise in the duodenum than in the stomach
--~4% of stomach ulcers are caused by a malignant tumor
--duodenal ulcers are generally benign
--timing of symptoms in relation to meal may differentiate between gastric and duodenal ulcers: gastric ulcer gives epigastric pain during or after the meal, duodenal ulcers manifest before the meal — when acid (production stimulated by hunger) is passed into the duodenum
--ulcers in lower esophagus can be caused by GERD
--most often localized on the lesser curvature of the stomach
--prevalence in the west of Helicobacter pylori infections roughly matches age (i.e., 20% at age 20, 30% at age 30, 80% at age 80 etc)
--prevalence is higher in third world countries
--Transmission: food, groundwater, human saliva (such as from kissing or sharing food utensils.) (Mayo clinic disputes kissing assertion)

RISK FACTORS:
--H. pylori (see section on microbe)
--NSAIDs: block the function of cyclooxygenase 1 (cox-1), which is essential for the production of prostaglandins which stimulate mucus production. Newer NSAIDs (celecoxib, rofecoxib) only inhibit cox-2, less essential in the gastric mucosa, roughly halving the risk of NSAID-related gastric ulceration. (If prescribing NSAIDS test for H. pylori first and eradicate if needed).
--age (over 45 very likely to have H. pylori)
--glucocorticoids (e.g. dexamethasone and prednisolone), lead to atrophy of all epithelial tissues, role in ulcerogenesis is relatively small.
--smoking --> atherosclerosis, vascular spasms, --> vascular insufficiency --> ulcers through ischemia
--anticoagulant use
--laxatives (overuse) is also known to cause peptic ulcers.
--genetics (debatable)
--type O blood (debatable)
--Gastrinomas (Zollinger Ellison syndrome), rare gastrin-secreting tumors, cause multiple and difficult to heal ulcers.

STRESS as a risk factor: (debatable, research goes both ways)
-----no direct proof that psychological stress causes ulcers, lots of theories and debate:
-----mechanical ventilation, burns & head trauma pts have move ulcers
-----Thai hospital study shows chronic stress was strongly associated withincreased risk, and combination of chronic stress and irregular mealtimes was a significant risk factor (PMID 12948263).
----mice showed that both long-term water-immersion-restraint stress and H. pylori infection were independently associated with the development of peptic ulcers (PMID 12465722).
----stress can cause the production of excess stomach acid

S/Sx:
--Abdominal pain, classically epigastric with severity relating to mealtimes
--Nausea, and lots of vomiting ("coffee grounds")
--Loss of appetite and weight loss
--halitosis
--duodenal ulcers are classically relieved by food, while gastric ulcers are exacerbated by it
--Bloating and abdominal fullness, belching
--Waterbrash (rush of saliva after regurgitation to dilute acid in esophagus)
--Hematemesis (vomiting of blood); this can occur due to bleeding directly from a gastric ulcer, or from damage to the esophagus from severe/continuing vomiting.
--Melena (tarry, foul-smelling feces due to oxidized iron from hemoglobin)
--gastroesophageal reflux disease (GERD)(history of heartburn)
--In patients over 45 with more than 2 weeks of the above symptoms, the odds for peptic ulceration are high enough to warrant rapid investigation by EGD
--tobacco smoking, blood group, spices used to be considered risk factors but haven't proven to have a big impact on occurencee

COMPLICATIONS
--GI BLEEDING (common complication) --> anemia, blood in vomit or feces
--PENETRATION of muscular wall of stomach or duodenum-->liver or pancreas
--PERFORATION: gastric or duodenal --> surgical emergency!!! ( -->peritonitis) immediate intense spreading pain esp w/ movement, rebound tenderness
--PYLORIC STENOSIS: scarring and swelling due to ulcers causes narrowing in the duodenum and gastric outlet obstruction --> severe vomiting
--CANCER: People with ulcers caused by Helicobacter pylori have 3 to 6 times the chance of developing stomach cancer later in life. There is no increased risk of developing cancer from ulcers that have other causes. 1998 study: Polyps May Disappear After H. Pylori Treatment: Gastric polyps may disappear after treatment for Helicobacter pylori, according to a study. These small growths on the stomach lining can cause stomach pain and bleeding, and may become malignant. Endoscopic removal is recommended, but the new findings indicate that this should be attempted after treatment for H. pylori, which may lead to the disappearance of many of these polyps. Drugs used to eradicate H. pylori caused polyps to disappear in 71% of patients with such polyps within 12 to 15 months. These results strongly suggest that eradication of H. pylori leads to regression and disappearance of hyperplastic gastric polyps. Annals of Internal Medicine November 1, 1998;129:712-715.
--PERNICIOUS ANEMIA: H Pylori May Cause Vitamin B12 Deficiency And Pernicious Anemia: This study detected H. pylori in 56% of 138 patients with pernicious anemia. Upon treatment and eradication of the H. pylori infection, there was significant improvement of B12 status in 40% of the infected patients. The authors conclude that H. Pylori is a causative factor in many cases of B12 deficiency and that detection and eradication of it may correct the deficiency. Arch Intern Med. 2000;160:1349-1353 COMMENT: The B12 deficiency may be caused by H. Pylori if the bacteria damages the parietal cells which produce intrinsic factor which is required to absorb B12.
--MORNING SICKNESS: Infection with Helicobacter pylori, the bacteria that causes stomach ulcers, may also cause a severe form of morning sickness in pregnant women. Researchers at the University of Vienna in Austria found that over 90% of pregnant women with hyperemesis gravidarum -- severe nausea and vomiting often leading to weight loss and electrolyte disturbances -- were infected with H. pylori. The researchers hypothesize that in the early phase of pregnancy, changes in a woman's body fluid concentration affect the acidity (pH) of the stomach, which may in turn activate latent H. pylori residing in the stomach. Obstetrics & Gynecology April 1998;91:615-617 http://www.mercola.com/1998/archive/bacteria_linked_to_severe_morning_sickness.htm
--HEART DISEASE: Without proper treatment (which usually involves antibiotic therapy), H. pylori infx can trigger low-grade inflam which persists for years, placing a subtle but steady strain on cardiovascular system. Most recent studies investigating a link between the bacterium and heart disease have looked at a broad range of H. pylori strains, and have produced conflicting results. Italian researchers sought to discover if infection with one of the most virulent strains of H. pylori (containing the CagA gene) was especially related to incidence of heart disease. The investigators discovered that "a total of 38 of 88 patients and 15 of 88 controls were infected by CagA-positive Helicobacter pylori (43% versus 17%)." In contrast, they found that CagA-negative strains were clearly not related to (incidence of) ischemic heart disease. The study authors caution that, at this point, their research cannot prove that CagA-positive H. pylori causes or contributes to heart disease, only that it is associated with an increased incidence of the disease. But they note that other investigators are examining similar associations between heart disease and chronic infections with organisms such as Chlamydia pneumoniae, cytomegalovirus, and the herpes virus. Circulation May 1998;97 http://www.mercola.com/1998/archive/ulcer_bacteria_linked_to_heart_disease.htm
--LYMPHOMA

HELICOBACTER PYLORI
--gram negative microaerobe with spiral flagelli
--not really resistant to the extremes of acidity found in stomach but knows how to cope
----alkalinizes its own environment, hides in stomach mucus
--major causative factor (60% of gastric and up to 90% of duodenal ulcers)
--settles in the antral mucosa
--causes chronic active gastritis (type B gastritis), resulting in a defect in the regulation of gastrin production by that part of the stomach
--gastrin secretion can either be decreased (most cases) resulting in hypo- or achlorhydria or increased
--gastrin stimulates the production of gastric acid by parietal cells
--in H. pylori colonization responses that decrease gastrin, the increase in acid can contribute to erosion of the mucosa and ulcer formation

DIFFERENTIAL DIAGNOSIS
--Differential diagnosis of epigastric pain:::Peptic ulcer, Gastritis, Gastric carcinoma, GERD, Pancreatitis, Hepatic congestion, acute cholecystitis, Biliary colic, Inferior myocardial infarction, Referred pain (pleurisy, pericarditis, MI)
--chronic ulcer form: round to oval parietal defect ("hole"), 2-4cm diameter, smooth base, perpendicular borders regular with elevated borders & inflam all around
--gastric cancer: the ulcerative form: borders are irregular, surrounding mucosa may present radial folds, as a consequence of the parietal scarring.
--during the active phase, the base of the ulcer shows 4 zones: inflammatory exudate, fibrinoid necrosis, granulation tissue and fibrous tissue. The fibrous base of the ulcer may contain vessels with thickened wall or with thrombosis
--is it malignancy (gastric cancer)? esp in ulcers of the greater (large) curvature of the stomach tho most are also a consequence of chronic H. pylori infection

DIAGNOSIS: GENERAL
--esophagogastroduodenoscopy (EGD), a form of endoscopy, also known as a gastroscopy
--stomach biopsy
--barium contrast xray to see size/shape of ulcers

DIAGNOSIS: CHECK FOR H. PYLORI
UREA
--Urea breath test (noninvasive and does not require EGD)
--Direct detection of urease activity in a biopsy specimen by rapid urease test;
DIRECT BACTERIA ID
--culture from an EGD biopsy specimen; difficult/expensive (most labs not set up to culture H. pylori)
--Histological examination and staining of an EGD biopsy.
ANTIBODIES
--blood levels (does not require EGD)--controversial whether a positive antibody without EGD is enough to warrant eradication therapy
--Stool test for antigens

DIAGNOSIS: TEST FOR PERFORATION BY EXRAY FOR AIR BUBBLE
If a peptic ulcer perforates, air will leak from the inside of the gastrointestinal tract (which always contains some air) to the peritoneal cavity (which normally never contains air). This leads to "free gas" within the peritoneal cavity. If the patient stands erect, as when having a chest X-ray, the gas will float to a position underneath the diaphragm. Therefore, gas in the peritoneal cavity, shown on an erect chest X-ray or supine lateral abdominal X-ray, is an omen of perforated peptic ulcer disease.

TREATMENT - ALLOPATHIC - ACUTE
--cauterize bleeding ulcer
--inject a material that causes a bleeding ulcer to clot
--intravenous fluids and takes nothing by mouth, so the digestive tract can rest
--Since the widespread use of PPI's in the 1990s, surgical procedures (like "highly selective vagotomy") for uncomplicated peptic ulcers became obsolete.
--Perforated peptic ulcer is a surgical emergency and requires surgical repair of the perforation. Most bleeding ulcers require endoscopy urgently to stop bleeding with cautery or injection.

TREATMENT - ALLOPATHIC - CHRONIC
--usually 2 antibiotics plus a PPI and maybe a bismuth compound, if no resolution with this Tx then add more antibiotics
--common antibiotics include: amoxicillin, clarythromycin, tetracycline, metronidazole (side effects: candidiasis)
--avoid NSAIDS
--stress management
--ACID STOPPERS, TWO KINDS: histamine-2 (H2) blockers or proton pump inhibitors
--PROTON PUMP INHIBITORS: (PPIs) reduce gastric acid secretion by up to 99%, followed and has largely superseded another group of pharmaceuticals with similar effects, but different mode-of-action, called H2-receptor antagonists.
--PPIs are the most widely-selling drugs in the world, majority are benzimidazole derivatives; new research indicates that imidazopyridine derivatives may work better
--PPIs irreversibly block the hydrogen/potassium adenosine triphosphatase enzyme system (the H+/K+ ATPase, or more commonly just gastric proton pump) of the gastric parietal cell, the terminal-step in acid production--> significantly more effective than H2 antagonists.
--HISTAMINE BLOCKERS: less used since PPIs were developed
--H2 blockers aka H2 antagonists incl: Cimetidine (Tagamet, Tagamet HB), Famotidine (Pepcid AC, Pepcid Oral), Famotidine Oral Suspension (Pepcid Oral Suspension), Nizatidine capsules (Axid AR, Axid Capsules, Nizatadine Capsules), Ranitidine (Zantac, lots of versions)
--tagamet is OTC now
--side effects of histamine blockers include decreased androgens, men --> erectile disorders, grow tits
--Bismuth compounds (pepto bismol) may actually reduce or even clear organisms.
--instead of NSAIDS use: prostaglandin analogue (Misoprostol)
--In the absence of H. pylori, long-term higher dose PPIs are often used

PREVENTION:
--drink lots of water
--eat fiber (oatmeal, etc)
--eat regular meals
--get good sleep

TREATMENT: ALTERNATIVE
--all same supports as prevention
--yes, even for people with H. pylori: it's the terrain, not the bug that causes infx
--water consumption: at least 12 glasses of water per day
--avoid all fruit juices, soda, sugar, coffee, sweetened tea
--avoid milk
--avoid alcohol, coffee, fried food
--avoid smoking tobacco (lowers prostaglandin production)
--don't skip breakfast
--eat dinner early (don't go to bed with food in stomach)
--don't drink liquids with meals
--eat in calm/relaxing environment
--increase fiber intake
--fresh raw garlic
--avoid fried foods
--eat cabbage/drink cabbage juice (increases the mucosa lining in the stomach)
--supplement VITAMIN C: high doses of vitamin C inhibit H. pylori growth in culture, inhibitory effects are specific to H. pylori and Campylobacter jejuni, but vitamin C had no effect on other enteric gram-negative bacteria
--vitamin C may protect against gastric cancer. It is estimated that 40% of the US population consumes vitamin supplements, which may account for the lower incidence of gastric cancer in the US compared with Japan, where gastric cancer is the most common cancer. H. pylori is also far less prevalent in the US compared with Japan. Cancer 1997;80:1897-1903
--ulmus fulva (slippery elm) to support recovery of mucus membrane
--zinc: 25 to 50 mg/day (heal mucus membranes)
--vit A (heals mucus membranes)
--probiotics: acidophilus, bifida, the right amount
--exercise: men who walked or ran at least 10 miles a week were 62% less likely than inactive subjects to develop an ulcer. Western Journal of Medicine August 2000;173:101-107.
--Calendula officinalis: Duodenal ulcers and gastroduodenitis complaints faded earlier when Calendula and Symphytum added to antacid treatment, spontaneous pains disappeared in 90 per cent of the patients, gastric acidity did not significantly decrease http://www.ncbi.nlm.nih.gov/pubmed/7336704?dopt=Abstract,
--Calendula again: 19 patients with duodenal ulcer and 19 with gastroduodenitis treated with C. officinalis Symphitum and a laxative mixture of Rhamnus, Citrus and Carum carvi Matev 1981. http://www.ncbi.nlm.nih.gov/pubmed/7336705?dopt=Abstract , obstipation syndrome was treated with a laxative herb combination of Rhamus frangula, Citrus aurantium, Carum carvi, was effective in 100 per cent of the patients, No effect on gastric mucosa was established.
--stress treatment: deep breathing
--alternating hot & cold packs on abdomen

OTHER ALTERNATIVE TX:
--licorice: limited evidence but long used for stomach ease
--Eleutherococcus (Acanthopanax) senticosus = Siberian Ginseng
--Hydrastis canadensis = goldenseal
--Vaccinium macrocarpon = cranberry
--Viscum album (Phoradendron leucarpum, flavescens, serotinum) = Mistletoe, European (American)
--Curcuma longa = turmeric
--Zingiber officinale Roscoe = ginger
--Vaccinium myrtillus = Bilberry
--Panax ginseng C. A. Mey. or quinquefolius L. = Ginseng, Chinese ginseng, American ginseng
--Melaleuca alternifolia = Tea Tree Oil
--Mentha piperita = peppermint
--Silybum marianum Gaertn. = milk thistle
--Hypericum perforatum = Saint John's wort
--Ginkgo biloba
--some sources say avoid mint
--Artemesia = wormwood (kill the bugs)

HISTORY
--1958 John Lykoudis, GP in Greece, treated pts for PUD with antibiotics
--1982 two Australian scientists, J. Robin Warren and Barry J. Marshall asserted that H pylori causes PUD. Paper is poorly received, so Marshall drank a petri dish of the orgs and soon got sick, results published in 1984 Australian Medical Journal
--1997, the US CDC launched a national education campaign to inform health care providers and consumers about the link between H. pylori and ulcers
--2005, the Karolinska Institute in Stockholm awarded the Nobel Prize in Physiology or Medicine to Dr. Marshall and his long-time collaborator Dr. Warren "for their discovery of the bacterium Helicobacter pylori and its role in gastritis and peptic ulcer disease"

Comments

( 1 comment — Leave a comment )
sarahcaron8
May. 7th, 2008 10:04 am (UTC)
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( 1 comment — Leave a comment )

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