1 www.digestivediseases.blogpost.com
Showing posts with label disease. Show all posts
Showing posts with label disease. Show all posts

Spokane Digestive Disease Center

Spokane Digestive Disease Center, Sddc North ASC is committed to providing outstanding patient care in the Spokane area, but before you commit to Spokane Digestive Disease Center, Sddc North ASC for a procedure make sure you compare and shop for the medical procedures you require. It may save you hundreds of dollars. To compare Spokane Digestive Disease Center, Sddc North ASC to other healthcare providers in the Spokane, WA area simply click on the procedure name below to see the other facilities and prices in your area.

Specializing In Upper Endoscopy, Modern Medical Technology, Colonoscopy and Colon Cancer Screening, Capsule Endoscopy, Practice Limited to Gastroenterology and Endoscopic Procedures, Complete Gi Care, Exceptional Staff of Professional & Ancillary Personnel, Complete Care, Board Certified by The American Board of Internal Medicine & The Subspecialty Board of Gastroenterol, Ambulatory Surgery Center.

Facility Overview

Featured Medical Procedure Costs
Procedure                  Performed Last Year     Average List Price
Colonoscopy                   2500+                           $2,550.00
Upper GI Endoscopy       2500+                           $2,850.00

Contact:
46 E Rowan Ave, Spokane, WA 99207
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GERD Surgery: Fundoplication [VIDEO]

Fundoplication surgery may be used to treat gastroesophageal reflux disease (GERD) symptoms that have not been well controlled by medicines. In fundoplication surgery, the upper curve of the stomach Click here to see an illustration. (the fundus) is wrapped around the esophagus and sewn into place to strengthen the valve between the esophagus and stomach (lower esophageal sphincter).

This 3D medical animation on GERD Surgery shows how the upper portion of the stomach is wrapped around the lower esophagus to strengthen the cardiac sphincter of the stomach. This helps prevent GERD (gastroesophageal reflux disease), or heartburn. Hiatal hernia repair is also depicted. This involves pulling a portion of the stomach that has protruded from the diaphragm back into place.

 
Source: http://www.nucleusinc.com/medical-animation

Surgery may be an option when:
  • Treatment with medicines does not completely relieve a person's symptoms, and the remaining symptoms are proved to be caused by reflux of stomach juices.
  • A person does not want or, because of side effects, a person is not able to take medicines over an extended period of time to control his or her GERD symptoms.
  • Along with reflux a person has symptoms such as asthma, hoarseness, or cough that do not adequately improve when treated with medicines.
Read more:

Gastroesophageal Reflux Disease  www.digestivediseases.com
GERD includes all the symptoms that result from ferux

of gastric content into the esophagus

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Treatment of Celiac Disease

Treatment of Celiac Disease


Celiac Disease (CD) is a life-long digestive disorder found in individuals who are genetically susceptible. Damage to the small intestine is caused by an immunologically toxic reaction to the ingestion of gluten. This does not allow food to be properly absorbed. Even small amounts of gluten in foods may affect those with celiac disease and cause health problems. Damage can occur to the small bowel even in the absence of symptoms.
This is a simple overview of the Gluten-Free (GF) diet. Not all areas of the diet are as clear-cut as portrayed by this Guide. This is intended to be used as a safe and temporary survival tool until the newly diagnosed celiac obtains additional information. Understanding these dietary requirements will enable the newly diagnosed to read labels of food products and determine if a product is GF.
Gluten is the generic name for certain types of proteins contained in the common cereal grains wheat, barley, rye and their derivatives.

ALLOWED Grains/Flours

Rice, corn (maize), soy, potato, tapioca, beans, garfava, sorghum, quinoa, millet, buckwheat, arrowroot, amaranth, teff, Montina®, flax, and nut flours.

NOT ALLOWED in any form

Wheat (enkorn, durum, faro, graham, kamut, semolina, spelt), rye, barley and triticale.
Frequently overlooked foods that may contain gluten and need to be verified:
Breading, Coating mixes, Panko Brown rice syrup
Croutons Energy Bars
Flour or cereal products Imitation bacon
Imitation seafood Marinades
Pastas Processed Luncheon Meats
Sauces, gravies Self-basting poultry
Soy Sauce or soy sauce solids Soup bases
Stuffings, Dressing Thickeners (Roux)
Communion wafers Herbal supplements
Nutritional supplements Vitamins & mineral supplements
Prespcription Drugs Over-the-counter medications

For More Information about Celiac Disease see this

For More Information about Celiac Disease see this

American Celiac Disease Alliance
2504 Duxbury Place
Alexandria, VA 22308
Phone: 703–622–3331
Email: info@americanceliac.org
Internet: www.americanceliac.orgleaving site icon
American Dietetic Association
120 South Riverside Plaza, Suite 2000
Chicago, IL 60606–6995
Email: hotline@eatright.org
Internet: www.eatright.orgleaving site icon
Celiac Disease Foundation
13251 Ventura Boulevard, #1
Studio City, CA 91604
Phone: 818–990–2354
Fax: 818–990–2379
Email: cdf@celiac.org
Internet: www.celiac.orgleaving site icon
Celiac Sprue Association/USA Inc.
P.O. Box 31700
Omaha, NE 68131–0700
Phone: 1–877–CSA–4CSA (272–4272)
Fax: 402–643–4108
Email: celiacs@csaceliacs.org
Internet: www.csaceliacs.orgleaving site icon
Children's Digestive Health and Nutrition Foundation
P.O. Box 6
Flourtown, PA 19031
Phone: 215–233–0808
Fax: 215–233–3918
Email: mstallings@naspghan.org
Internet: www.cdhnf.orgleaving site icon
www.celiachealth.orgleaving site icon
Gluten Intolerance Group of North America
31214 124th Avenue SE
Auburn, WA 98092–3667
Phone: 253–833–6655
Fax: 253–833–6675
Email: info@gluten.net
Internet: www.gluten.netleaving site icon
National Foundation for Celiac Awareness
224 South Maple Street
Ambler, PA 19002–0544
Phone: 215–325–1306
Email: info@celiaccentral.org
Internet: www.celiaccentral.orgleaving site icon
North American Society for Pediatric Gastroenterology, Hepatology and Nutrition
P.O. Box 6
Flourtown, PA 19031
Phone: 215–233–0808
Fax: 215–233–3918
Email: naspghan@naspghan.org
Internet: www.naspghan.orgleaving site icon
www.cdhnf.orgleaving site icon

Crohn’s Disease Is Associated with Restless Legs Syndrome

Researchers investigating a link between restless legs syndrome (RLS) and Crohn’s disease (CD) uncovered results that demonstrate RLS occurs frequently in people with CD and appears to be a possible extraintestinal manifestation of CD. This research appeared in the February 2010 issue of Inflammatory Bowel Disease.

CD is an ongoing disorder that causes inflammation of the digestive tract, also referred to as the gastrointestinal (GI) tract. CD can affect any area of the GI tract, from the mouth to the anus, but it most commonly affects the lower part of the small intestine, called the ileum.

CD has a variety of possible extraintestinal manifestations: arthritis, skin problems, kidney stones, gallstones, and liver diseases. This study is the first to show central nervous system (CNS) manifestations of CD.

A total of 272 patients with CD participated in the study, and researchers found a 43 percent incidence rate and 30 percent prevalence rate of RLS in patients with CD, compared with a 9 percent prevalence rate in the control group. RLS symptoms occurred during or after the onset of CD symptoms in the majority of patients, suggesting a link between CD and RLS.

For more information and to obtain copies, visit www.digestive.niddk.nih.gov.

Pathogenesis of alcoholic liver disease

Metabolism of alcohol in the liver takes place in three ways, result being the same, and in the liver takes place in three ways, result being the same, and acetaldehyde is metabolized with high hepato toxicity. Those three ways are:
1. alcoholdehydrogenasis path is the major way of metabolizing alcohol.
2. microsomal oxidation system - P450, interfere in oxidation of alcohol when its concentration is more than 50 mg/dl.
3. catalyze way, which has a seconday role.

Acetaldehyde is later oxidated up to acetate, but in alcoholics, the capacity of mitochondrion to oxidate acetaldehyde is reduced. Their accumulation leads to the promotion of lipid peroxidates and the formation of complex proteins. Besides the toxic effect of the acetaldehyde, alcohol has its role in developing cirrhosis. It has been proven that adipocytes involved in fibrogenesis are active after chronic consumption of alcohol.

Morphologic aspects in alcoholic liver: there are three typer of hepatic histologic lesions in consumers of alcohol.
1. Alcoholic fatty liver is a genign reversible form produced by accumulation of some drops of lipids in hepatocyte.
2. Alcoholic hepatic comprise of degeneration and necrosis of the hepatocyte, acute infiltration of neutrophyles sometimes pericellular, sinusoidal line and venular line fibrosis, as well characteristic Mallory corpuscles (alcoholic hialin). Alcoholic hepatitis may be reversible, but the lesions are much more severe being the most important precursors of cirrhosis.
3. Alcoholic cirrhosis comprise of fibrosis in all hepatic tissue, from the portal space up to centrolobular vein, and nodule of regeneration.
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Alcoholic liver causes

Alcoholic liver causes or alcoholic liver disease is represented by a nonspecific total morphological lesion associated with clinical / paraclinical manifestation, among which some are induced by the abuse of alcohol.
Prevalence: alcoholic liver varies from country to country depending on the tradition, religion and especially on the cost of the alcoholic drinks in comparison with the income.

Alcoholic liver causes: excessive alcohol consumption has varied effect on organisms. Due to some unknown cause, 1/3 of chronic consumers of alcohol do not have hepatic consequences.
1. Duration and consumption of alcohol, it is considered that 60-80 ml of absolute alcohol/day for men and 40-50 ml of absolute alcohol women as a toxic dose. The duration of consumption is also important, a consumption of more than 5 years is considered as a risk. Continous consumption is more dangerous than intermittent consumtion. As well, hepatic injury does not depend on the type of drink but in this alcohol content.
2. Gender: females are more susceptible than men are, because at the same quantity of alcohol ingested reach a higher blood concentration. In women, gastric metabolism is reduced comparing to men and cytochrome P450 is less efficient.
3. Genetic factors: although no genetic markers has proved to have a clear association with susceptibility to alcoholism, seems to inherit certain behavior related to the alcohol consumpion.
4. Coinfection with hepatic viruses (B or C) accelerates the severity of the alcoholic liver disease.
5. Nutritional factors: protein caloric malnutrition precedes alcoholism in patients with socio-economic level leading to the appearance of alcoholic liver. It has been proved that healthy diet may protect those who consume alcohol, at least for a period.
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Treatment of gastroesophageal reflux disease

Treatment of gastroesophageal reflux disease
A. Diet
  • dietary restrictions: avoiding bulky meals, avoiding food that decreases LES pressure:coffee, chocolate, carbonated drinks, mint products, fatty foods, alcohol or foods that increase the acid secretion: orange juice, carbonated drinks, white vine, and acid food);
  • avoiding smoking. It is said that smoking increases the acid secretion and lowers the LES pressure;
  • avoiding lying recumbent immediately after eating;
  • weight loss in the obese patients (reducing the abdominal pressure);
  • avoiding medications that decrease the LES pressure: nifedipin (calcium channel blockers), nitrates, aminophylline, caffeine and anticholinergics. These are also studies suggesting that NSAIDS and aspirin are associated with esophageal lesions, being able to induce esophagitis and even esophageal strictures.
B. Medication – involves 2 types of drugs:

1. Antisecretory drugs. This treatment decreases the acid secretion:
Proton pump blockers are the most potent antisecretory drugs:
  • Esomeprazole (Nexium) 40 mg/day.
  • Omeprazole (Losec, Ultop, Antra) 20 mg bid;
  • Pantoprazole (Controloc) 40 mg/day;
  • Lanzoprazole (Lanzap) 30 mg/day;
  • Rabeprazole 20 mg/day;
The duration of treatment is 4-8 weeks, or a few months in resistant cases.
H2 blocking agents:
Ranitidine 150 mg bid;
Famotidine 40 mg/day;
Nizatidine (Axid) 150 mg bid.
H2 blocking agents; they may be used 2-6 weeks or even more in resistant cases.

2. Prokinetic
  • Metoclopramide, 10 mg tid, 30 bid minutes before meals. Its effect  is the increasing of LES tone; it also increases the esophageal clearance and hastens the gastric emptying.
  • Domperidone (Motilium) is effective on the LES and gastrokietic; the effect on the reflux is lower than that of Metoclopramide.
3. Antiacids - medication with direct neutralizing effect: Maalox, Novalox, Rennie, Dicarbocalm, containing magnesium and aluminium salts; the patients se them when the symptoms appear, with a spectacular disappearance of symptoms. They effect is only symptomatic, the esophagitis lesions persisting. An interesting drug of this group is the sodium alginate (Gaviscon, Nicon), which forms a protective layer over the esogastric mucosa.
4. Mucosal protectives. Sucralfate is an aluminium polisulfatate sucrose, which links the billiary acids and pepsin and stimulates the gastric secretion of prostaglandins and epidermic growth factor, thus favoring the epithelium healing. It is sometimes indicated in esophagitis.
The strategy of treatment is to begin, generally, in case of acid reflux, with PPI, in case of failure, a prokinetic is added. If the patients complain of billiary reflux, the therapy will be prokinetic.
C. Endoscopic
  • Esophageal structures. The most preffered treatment in peptic strictures is done endoscopically, by Savary probe dilators or pressure balloons.
  • Superior digestive hemorrhage. The severe cases require endoscopic hemostasis by Adrenaline injections, Argon Beamer photocoagulation or hemoclips application.
  • Barrett’s esophagus. The columnar epithelium patches with different degrees of dysplasia may be destroyed by Argon plasma photocoagulation.
  • Endoscopic fondoplicature – represents a new noninvasive method, in which the gastric fundus is wrapped around the esophagus thus creating a very sharp His angle.
D. Surgical
  In rare cases with severe esophagitis without response to drug therapy, surgery may be needed.
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Gastroesophageal reflux disease, Etiopathogenesis, Symptoms, Diagnosis

Definition of Gastroesophageal reflux disease
Gastroesophageal reflux disease (GERD) includes all the symptoms that result from ferux of gastric content into the  esophagus.
Gastroesophageal reflux (GERD) represents the physiologic phenomenon of gastric content passage into the esophagus, which becomes pathological when the antireflux mechanisms are surpassed.
Reflux esophagitis (RE) consists of esophageal lesions induced by GER, occurring only in certain cases of pathological GER.

Etiopathogenesis (causes)
A. Physiologic causes:
  • Decreasing of the lower esophageal sphincter (LES) pressure. Normally the LES pressure is 20-25 mmHg and it only disappears during swallowing. GER occurs either when LES transiently relaxes because of swallowing, or when the LES basal pressure decreases less than 6 mmHg, thus allowing the castric content to pass into the esophagus. LESpressure can be reduced by drugs (anticholinergic, aminophylline, nitrates, benzodiazepines, calcium channel blockers), food (chocolate, fatty foods, onion, citric, tomato juice mint), coffee, smoking, alcohol.
  • Decreasing of gastric motility with delayed gastric emptying.
  • Disorder of esophageal clearance by refluxed acid gastric content.

B. Mechanical causes:
  • Hiatal hernia – produces a decrease in LES tonus, which allows the reflux.
  • Increasing of intraabdominal pressure: pregnant women, obese, patients with giant abdominal tumors or ascites.
  • The widening of his angle. This angle between the esophagus and stomach is usually very sharp, having the role of a valve at the stomach entrance. In the obese, it enlarges.
  • The relaxation of diaphragmatic crura, the muscular channel through which the esophagus passes from thorax into the abdomen. The relaxation cavity volume increases (emphysema).
  • Sclerodermia. The motor disorders of the esophagus are the result of fibrosis and atrophy of the smooth muscle, the so-called “glass-esophagus”.

The development and severity of reflux esophagitis depend on 3 conditions:
  • the increasing of reflux frequency
  • the increasing of reflux duration
  • the action of aggressive gastric content of the esophageal mucosa

Clinical features (symptoms)

  • Pyrosis is characterized by burning retrosternal discomfort, climbing up the throat. It is aggravated by maneuvers that increase intraabominal pressure (bending forward, load straining, lying recumbent immediately after eating) accompanied sometimes by acid regurgitations as well. If the LES incompetence is severe, solid food can also be regurgitated.
  • Retrosternal pain is often a problem of differential diagnosis with the cardiac pathology. It may appear isolated, without pyrosis, mainly when ingesting irritating food. Odynophagia (painful swallowing) appears during spastic contractions of LES. Dyspagia – difficult swallowing.
  • Respiratory symptoms (stifling, nocturnal dyspneea, asthma crises) or ENT (laryngitis, pharyngeal paralysis, dysphonia) are due to the regurgitation of refluxed acid gastric content and its aspiration.
Paraclinical findings (investigations)
  • Superior digestive andoscopy (esogastrocopy). When confronting with annoying, persistent esophageal symptoms (mainly pain or dysphagia), an esogastroscopy will be done. It will reveal or exclude the possible esophageal lesions (esopagitis, stenosis)., gastroduodenal lesion. Also by means of endoscopy, a discovered lesion may be diopsied.
  • Barium examination it may show the esophageal motor disorders (achalasia, esophageal diffuse spasm), a possible esophageal stenosis, a hiatal hernia.
  • Esophageal pH – metry is very useful to discover the reflux duration.
  • Esophageal manometry allows the subtle discovering of esophageal motor disorders and their possible linking to the clinical symptoms.
Other tests, more rarely used are esophageal scintigraphy or the Berstein test.
Diagnosis of Gastroesophageal reflux disease
Positive diagnosis – is mainly clinical, but most be paraclinical confirmed.

Differential diagnosis
A. With digestive diseases:
  • gastroduodenal ulcer having as typical symptom the epigastric pain;
  • the differenciation between the acid reflux and the alkaline one (mostly after colecistectomy), when the patient complains of bitter taste in the morning.
  • the esophageal diverticula’s, achalasia, esophageal ulcer or cancer.

B. With nondigestive digeases:
  • retrosternal or thoracic pain must be differentiated from a cardiac pain (ECG or the effort test is necessary; in doubtful cases, coronarography is useful)
  • the bronchic asthma crisis may be sometimes induced by the acid reflux, therefore, correlating the crises with pH – metry may be useful for the therapy.
Evolution, complications
The evolution is prolonged with good periods alternating with less good ones, generally because of food intake and life style.

The complications of reflux disease are:
  • reflux esophagitis, of different degrees, resulting in esophageal peptic ulcer and esophageal stenosis.
  • The Barrett epithelium (endobranchiesophagus) is a columnar epithelial metaplasia of normal squamous mucosa, because of reflux disease healing, after acid exposure, and it represents a premalignant condition to the esophageal cancer.
  • Superior digestive hemorrhage (hematemesis and/or melena) is a rare complication. It generally appears as melena, because the hemorrhages are mild, produced by ulcer or severe esophagitis.
Treatment of Gastroesophageal reflux disease
A. Diet
  • dietary restrictions: avoiding bulky meals, avoiding food that decreases LES pressure:coffee, chocolate, carbonated drinks, mint products, fatty foods, alcohol or foods that increase the acid secretion: orange juice, carbonated drinks, white vine, and acid food);
  • avoiding smoking. It is said that smoking increases the acid secretion and lowers the LES pressure;
  • avoiding lying recumbent immediately after eating;
  • weight loss in the obese patients (reducing the abdominal pressure);
  • avoiding medications that decrease the LES pressure: nifedipin (calcium channel blockers), nitrates, aminophylline, caffeine and anticholinergics. These are also studies suggesting that NSAIDS and aspirin are associated with esophageal lesions, being able to induce esophagitis and even esophageal strictures.
B. Medication – involves 2 types of drugs:

1. Antisecretory drugs. This treatment decreases the acid secretion:
Proton pump blockers are the most potent antisecretory drugs:
  • Esomeprazole (Nexium) 40 mg/day.
  • Omeprazole (Losec, Ultop, Antra) 20 mg bid;
  • Pantoprazole (Controloc) 40 mg/day;
  • Lanzoprazole (Lanzap) 30 mg/day;
  • Rabeprazole 20 mg/day;
The duration of treatment is 4-8 weeks, or a few months in resistant cases.
H2 blocking agents:
  • Ranitidine 150 mg bid;
  • Famotidine 40 mg/day;
  • Nizatidine (Axid) 150 mg bid.
  • H2 blocking agents; they may be used 2-6 weeks or even more in resistant cases.

2. Prokinetic
  • Metoclopramide, 10 mg tid, 30 bid minutes before meals. Its effect  is the increasing of LES tone; it also increases the esophageal clearance and hastens the gastric emptying.
  • Domperidone (Motilium) is effective on the LES and gastrokietic; the effect on the reflux is lower than that of Metoclopramide.
3. Antiacids - medication with direct neutralizing effect: Maalox, Novalox, Rennie, Dicarbocalm, containing magnesium and aluminium salts; the patients se them when the symptoms appear, with a spectacular disappearance of symptoms. They effect is only symptomatic, the esophagitis lesions persisting. An interesting drug of this group is the sodium alginate (Gaviscon, Nicon), which forms a protective layer over the esogastric mucosa.
4. Mucosal protectives. Sucralfate is an aluminium polisulfatate sucrose, which links the billiary acids and pepsin and stimulates the gastric secretion of prostaglandins and epidermic growth factor, thus favoring the epithelium healing. It is sometimes indicated in esophagitis.
The strategy of treatment is to begin, generally, in case of acid reflux, with PPI, in case of failure, a prokinetic is added. If the patients complain of billiary reflux, the therapy will be prokinetic.
C. Endoscopic
  • Esophageal structures. The most preffered treatment in peptic strictures is done endoscopically, by Savary probe dilators or pressure balloons.
  • Superior digestive hemorrhage. The severe cases require endoscopic hemostasis by Adrenaline injections, Argon Beamer photocoagulation or hemoclips application.
  • Barrett’s esophagus. The columnar epithelium patches with different degrees of dysplasia may be destroyed by Argon plasma photocoagulation.
  • Endoscopic fondoplicature – represents a new noninvasive method, in which the gastric fundus is wrapped around the esophagus thus creating a very sharp His angle.
D. Surgical
In rare cases with severe esophagitis without response to drug therapy, surgery may be needed.                                       
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Treatment of ulcerous disease, Helicobacter Pylori infection scheme

Treatment of ulcerous disease

1.The diet
A diet with avoidance of acid, hot or seasoned food might still be recommended. The exclusion of coffee during the acute period may be recommended.
Aspirin intake, as well as NSAIDS and corticoids should be forbidden.
2. Medical therapy
Administration of:
A) Antisecretory drugs
- H2 histaminic receptor blockers:
  • Cimetidine 1000mg/day
  • Ranitidine 300 mg/day
  • Nizatidine(Axid) 300 mg/day
  • Famotidine (Quamatel) 40mg/day
Famotidine will be preferred, given once or twice a day and without drug interferences of Cimetidine(cytochrome P450).
- HK ATP - ase pump blockers:
  • Esomeprazole(Nexium) 40mg/day
  • Omeprazole (Losec, Antra, Ultop) 40 mg/day
  • Pantoprazole(Controloc) 40 mg/day
  • Lanzoprazole(Lanzap) 30mg/day
  • Rabeprazole(Pariet) 20mg/day
The duration of antisecretory therapy will be for 6-8 weeks.
B) Gastric mucosal protectives
  • sucralfate 4g/day (qid)might be associated.
C) Antacids
To neutralize the acid excess and reduce the painful symptoms, symptomatic medication such as Maalox, Almagel, Alfogel etc. are used.
Schemes of treatment in Helicobacter Pylori infection
- The schemes including proton pump blockers (zomeprazole, lanzoprazole or pantoprazole), associated with two antibiotics are indicated, triple or even quadruple schemes are used.
 -The triple therapy includes OAM=Omeprazole(40mg/day)+Amoxicillin(2g/day)+Metronidazole(1500mg/day);
- or the ideal association is OAC=Omeprazole+Amoxicilline+Claritromicine(macrolide in dose of 1000mg/day).
- The quadruple therapy is composed of  Omeprazole+Subcitric bismuth (De-Nol)+Tetracycline+Metronidazole.
The anti HP therapy duration is for 7 day.
Some authors treat a newly discovered Helicobacter Pylori positive ulcer, only with 7 days of anti Helicobacter Pylori therapy. It is still generally preferred that this therapy be followed by one month of antisecretory medication-proton pump inhibitors.
The check-out of Helicobacter Pylori eradication may be done by endoscopy with biopsy (where Helicobacter Pylori may be ditectly pointed out) or by indirect tests (the ideal one being the respiratory test, or possibly the evidence of Helicobacter Pylori in the stool).
3. Endoscopic treatment – endoscopic hemostasis
 Hemostasis by injecting adrenaline 1/10.000 or sclerosant agents (etoxysclerol or even alcohol 90%) determines the stopping of hemorrhage by their vasoconstrictor effect and by compressive mechanic effect, resulted by injection.

Plasma photocoagulation with argon or laser produces a hemostasis by contact coagulation, up to a depth of 3-4 mm. It is used mostly in the diffuse bleedings.
The Rockall Score’is an externally validated mortality risk assessment score for patients admitted with upper gastrointestinal bleeding. It is simple and practical to use, helping identify those at highest risk of dying and needing active intervention. It also identifies those for safe, early discharge (initial score 0, final 2). The Rockall score quantifies the following parameters : age, pulse, systolic blood pressure, co-morbidity and endoscopic findings.
The endoscopic dilatation of pyloric stenosis may be made with small pneumatic balloons or sparking plugs, thus avoiding the trauma of a surgical intervention.
Mucosectomia of gastric ulcerous lesions with dysplasia or even with gastric cancer “in situ” is a method in full expansion, introduced by Japanese endoscopists, which allows the whole excision of premalignant or malignant lesions “in situ”. It has the advantage of avoiding the trauma of surgical intervention, but requires a precise preinterventional staging by echoendoscopy.
4. Surgical treatment
The indications are even more limited: hemorrhages that cannot be stopped endoscopically or pyloric stenosis that cannot be dilated endoscopically. The perforation and penetration are of course absolute indications for surgical intervention.
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Chron's disease, Diagnosis and Treatment

Definition of Crohn's disease

Crohn’s disease is another inflammatory bowel disease. Crohn’s disease involves the terminal ileon only in approximately 30% of cases, in approximately 50%,it is an ileon-colonic disease, and sometimes it affects only the colon. In fact, any segmentbof digestive tube might be affected (including the esophagus, stomach, duoden or appendix but much more rarely).

Etiopathogenesis of Crohn's disease

Bacteria (mycobacterium, pseudomonas), viruses, food allergy, environment factors as well as smoking and industrial toxic agents were implied; genetic factors (familial or ethnic) participate  in the apparition and persistence of the disease. Therefore, the genetic predisposition for Crohn’s disease is big, with an increased risk in Jews. The role of immune factors (umoral and cellular) and stress in the onset of  Crohn’s disease episodes is also known.

Clinical features of Crohn's disease

Clinical picture may be almost absent or absent, but sometimes it suggests the disease.
Typical clinical signs are:
1. digestive
  • diarrhea(without blood)
  • abdominal pain
  • malabsorbtion
  • perianal lesions(fistulas)

2. extradigestive
  • fever or low-grade fever
  • fatigue
  • weight loss
  • arthritis
  • erythema nodosum
  • uveitis

The clinical context  in which we might think of this disease is chronic diarrhea (even if only 2-4 stools/day), low-grade fever, fatigue, perianal fistulas and fissuring.

Diagnosis of Crohn's disease

The diagnosis is primarily based  on the endoscopy with biopsy. Aphthout lesions  will be discovered, together with deep, linear ulcerations, cobblestone relief of the mucosa, areas of inflammatory stenosis. These lesions may be located in the terminal ileon, colon, but also in the in the esophagus or duodenum. Thus, total colonoscopy with evalution of terminal ileon, but also gastroduodenoscopy is needed. The biopsy is compulsory, revealing the transmural inflammatory and the granulomatous aspect. The presence of profound ulcerations, fibrosis, and fissures is the rule.


X-ray examination is useful when the endoscopy is not accessible barium enema with ileal reflux or enteroclysis (barium administration by duodenal probe) may be used to demonstrate the lesions of terminal ileon or even barium examination, followed-up at 1, 2, 3 and 4 hours. The pathologic aspect:”cobblestone relief” in the terminal ileon, presence of some areas with stenosis (narrowing of the lumen) with  enlargements above, and fistulas.

Abdominal ultrasound examination will reveal the thickening of intestinal wall, thus evaluating the extension of the affected area. The zones of stenosis and dilatation may be evaluated, as well as the presence of some possible complications, such as perforation, fistulas.
The biologic picture in the episode will reveal the inflammatory syndrome with an increasing of ESR, leukocytosis, fibrinogen, RCP. Anemia and hypoalbuminemia may also appear.

The staging of disease

It is done by a few parameters. It quantifies the number of stools, abdominal pain, general well being, complications, use of antidiarrheic drugs, abdominal mass, hematocrit and body weight.
CDAI <150= inactive disease
CDAI 150-219= mild form
CDAI 220-450=moderate form
CDAI >450= severe form

There is an easier classification of Crohn’s disease, elaborated in Vienna –The Vienna classification of Crohn’s disease:ALB (Age, Location, Behavior)

A (Age at diagnostic)
  • A1 <40 years
  • A2 >40 years

L(Location)
  • L1 terminal ileum
  • L2 colon
  • L3 ileum and colon in the same time
  • L4 superior digestive tract

B(Behavior)
  • B1 nonstenosis, nonpenetrating form
  • B2 stenotic form
  • B3 penetrating form.

The differential diagnosis is made with:
  • ulcerative colitis
  • ischemic colitis, irradiation colitis
  • colon neoplasm
  • acute appendicitis

Evolution of Crohn's disease

It is characterized by recurrences. In general, more than 50% of cases relapse after an initial resection. Some studies have shown that the relapses frequency is reversely proportional with the time between diagnosis and first resection

Complications of Crohn’s disease

Complications are a rule in this disease. They are:
  • stenosis
  • fistulas (internal or external)
  • perforation
  • abcess appearance
  • septic state

Treatment of Crohn’s disease

In the acute phase of the disease, it starts with:
Prednisone (or Hydrocortisone hemisuccinate, p.e.v. if needed)  60mg/day,tapering he dose with 10 mg/week, so after 6 weeks the dose will be approx. 15-10 mg/day.The treatment continues with 10 mg/day for 6 months if there is a clinical remission;if needed should be given another 6 months (every 2 days 5-10 mg).
  • Mesalazine 1,5-2 g/day
  • Imuran (Azathioprine) 2-3 mg/kg body/day (for at least 3 months)
  • Metronidazole 500-1000mg/day
  • Budesonide(Budenofalk or Entocort) –the attack dose is 9 mg/day, continuing then with 3 mg/day

The surgical treatment addresses especially to the complications, such as segmental stenosis or perforations or nonresponsive forms to the drug therapy. The interventions may be segmental resections with anastomosis, or, more rarely, the colectomy with ileorectal anastomosis, or proctocolectomy with ileostomy(in the severe and invalidating relapses).
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Cholelithiasis Diagnosis and Treatment

Epidemiology

The gallbladder lithiasis is a quite entity, over 10% of the adult population .

Etiopathogenesis of gallstones

The etiologic factors:
  • genetic predisposition
  • female sex (women/men ration 2-3/1)
  • obesity
  • age
  • hypoproteinemia  
  • the number of birth
  • diabetes mellitus
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Chronic pancreatitis diagnosis and treatment

Definition of chronic pancreatitis

Chronic pancreatitis is a chronic inflammatory disease of the pancreas, with progressive evolution to pancreatic destruction(exocrine and endocrine), evolving towards pancreatic failure.

Clinical features

  • abdominal pain, with epigastric or periombilical location, sometimes in the entire upper abdominal region, often appearing after abundant meals.
  • steathorrhea (voluminous, pasty, rancing- smelling)
  • a chronic alcohol abuse
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Gastritis histologic

Chronic gastritis - immuno-competent lymphocytes and plasma cells. It evolves around decades of atrophic gastritis. action rate depends on the presence of neutrophils and the degree of penetration depth and levels. Quiet is characterized by the presence of neutrophils in the lamina propria only. In moderate activity, neutrophils presence of a large gastric foveoles. The degree of activity is a serious, when neutrophils are present in the intraepithelial. Chronic gastritis is activated when neutrophils are absent. No comments

What Is The Plan For Crohn's Disease Diet?

You've probably read about different diets for Crohn's disease on the Internet. But the fact is, it is not scientifically proven inflammatory bowel disease diet. Many experts believe, however, that you can identify certain foods that cause abdominal symptoms, especially during the peak of the disease. Do your "triggers", it is possible that the GI symptoms of gas, bloating, abdominal pain, cramps and diarrhea are more manageable. At the same time, have a time to heal inflammation of the intestine.

Foods that trigger symptoms differ from one person with Crohn's disease. To know what foods to leave out of your diet plan, you will need to determine what foods trigger your account. Many people with Crohn's disease found that the food in the list below worsen symptoms during outbreaks of the disease. It is therefore likely that at least some of these foods trigger the symptoms listed:

  • butter, mayonnaise
  • carbonated beverages
  • coffee, tea, chocolate
  • raw fruits
  • red meat and pork
  • spicy foods
  • whole grains and bran
  • raw vegetables
  • corn husks
  • gas-producing foods
  • nuts and seeds
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Crohn's disease treatment

In the acute phase of the chron's disease, begins:

Prednisone (or hydrocortisone hemisuccinate, PLC, if necessary) 60 mg / day, tapered to 10 mg / week, so after 6 weeks, the dose is approx. 15 to 10 mg / day. The continuous treatment with 10 mg / day for 6 months if clinical remission, and if necessary should be given another six months (mg every 2 days 5-10).

Mesalazine 1.5 to 2 g / day
Imuran (azathioprine) 2-3 mg / kg / day (at least 3 months)
Metronidazole 500-1000mg/day
Budesonide (Entocort Budenofalk o) attack at a dose of 9 mg / day, will be continued, then 3 mg / day
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Crohn’s disease diagnosis

The diagnosis is mainly based on endoscopy and biopsy. Aphthout lesions are found with deep linear ulcers, cobbled streets of the relief of inflammation of the lining of the areas of stenosis. These lesions can be inserted into the terminal ileon, colon, but also in the esophagus or the duodenum. Biopsy is mandatory to reveal transmural inflammation and granulomatous appearance. The presence of deep ulcers, fibrosis and cracks is the norm.



X-ray examination is useful when the endoscopy is not accessible barium enema with ileal reflux or enteroclysis (barium administration by duodenal probe) may be used to demonstrate the lesions of terminal ileon or even barium examination, followed-up at 1, 2, 3 and 4 hours. The pathologic aspect:”cobblestone relief” in the terminal ileon, presence of some areas with stenosis with enlargements above, and fistulas.

Abdominal ultrasound disclosed thickening of the intestinal wall to assess the extent of the affected area. All of stenosis and dilation can be assessed as well as the presence of some of the possible complications such as perforation, fistula.
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Crohn’s disease definition

Crohn's disease is another inflammatory bowel disease. Crohn's disease involves the terminal ileum in 30% of cases, about 50%, is a disease of the ileum, colon, and sometimes affects the colon. In fact, any segmentbof intestine may be affected (including the esophagus, stomach, duodeni or appendix, but much more rarely).



For more informations about Crohn's disease you can check www.digestive-system.com
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Cholelithiasis diagnosis

The clinical diagnosis can be shown when billiary colic or dyspepsia suggests that very often involvementbut billiary gallstones is totally or partially symptoms.

Ultrasonographical paraclinical diagnosis: gallstones appear in a photo hyperreflectogenic and launch the "acoustic shadow".

Symptomatic cholelithiasis, which arises billiary colic (colic billiary is hard or violent pain is part of epigastrum or right upper quadrant of the abdomen, sometimes radiating subscapularis usually continue for more than half an hour). Nausea or vomiting, which appear without colic, which do not cause colic billiary.

The differential diagnosis
  • renal colic
  • chronic pancreatitis pain
  • gallbladder polyp
  • gallbladder neoplasm
  • billiary sludge
  • ulcerous pain

Gallstones, Choleliathesis, Diagnosis to treatment VIDEO

Read more about: Cholelithiasis treatment
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