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

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Hepatitis B, causes, symptoms, diagnosis [VIDEO]

This education video explains what hepatitis B is. It discusses its causes, symptoms, diagnosis, treatment, and prevention.

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Gallbladder cancer treatment

Nowadays there is almost a consensus that asymptomatic gallstones be only watched and not surgically solved. Reminding that only 1 - 2% of the asymptomatic cases  become symptomatic annually the expectative appears to be the most logical and economical solution. If the symptoms appears to be the most logical and economical solution. If the symptoms appear, a therapy will be initiated.

The symptomatic gallstones will be treated. Most often this treatment is surgical and more rarely treated by nonsurgical techniques. Since the laparoscopic colecistectomy was introduced, the trust of patient into the intervention has increased. It involves a safe intervention, a short hospitalization and minimal postoperatory inconvenient (when the surgeons are well trained in this technique). The uncomplicated cholelithiasis cases are usually treated by this technique, but also the acute cholecistitis or vesicular hydrops. In the scleroatrophic lithiasic cholecistitis or when there is a suspicion of common bile duct lithiasis, the classic technique of open colecistectomy is preffered. In case of common bile ductolithiasis suspicion the exploration of common bile duct is mandatory.

The nonsurgical techniques of treatment of gallstones are the medicamentous litholisis and the extracorporeal lithotripsy.

Medical therapy (gallstone dissolution) is effective in the cholesterol calculi, preferably small, those fill in less than a half of the vesicular volume and when the gallbladder has a permeable infundibulo - cystic zone. The therapy consists in the administration of ursodeoxycholic acid (10 mg / kg body / day) - Ursofalk or its combining with chenodeoxycholic acid (10 - 15mg / kg body / day) - Litofalk for 3 - 12 months, up to the complete solubilisation of calculi. The overseeing of the results is made by ultrasonography.

Extracorporeal lithotripsy consists of fragmenting the cholesterol calculi by extracorporeal shock waves; it addresses to the unique or less numerous calculi, preferable under 15mm. The fragments resulted from lithotripsy will then be solved by administrating billiary acids up to the complete disappearance of all calculi fragments from the bladder. Both nonsurgical techniques are relatively-expensive.

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Colon Cancer Treatment

The treatment of colon neoplasia is surgical. The intervention should be done as soon as possible, its type depending on the tumor location. The preoperatory evaluation will include the evaluation of lymph node extension and of metastases (pulmonary, hepatic or peritoneal). The postsurgical chemotherapy is indicated to patients in stages Dukes B2 and C. Schemes including 5 fluoro-uralic, asociated with folinic acid are used. considering the increasing survival postchemotherapy, it is indicated that, after surgery, the patient is sent to continue the treatment to the oncologist.

                                                          Fig.1 Colon Cancer
Radiotherapy is addressed especially to the rectal cancer, which, by its position in the small pelvis, cannot always be correctly eliminated.

The prophylaxis of colonic cancer represents an actual requirement of the medicine, regarding the place ranked by this neoplasia in the world.
- primary prophylaxis consists in measures of nourishment education, over a big number of years  trying to educate the population to consume mostly vegetables, a fibers - rich diet (whole meal, cereals), calcium and to reduce the fats, the protein excess (especially red meat).
- seccondary prophylaxis consists the removal of causes that might lead to a colonic neoplasm, especially the discovering of polyps and endoscopic polypectomia. The discovering of polyps in general population is quite difficult because of the immense number of endoscopic explorations that should be done. Therefore, tests type Hemoccult are recommended followed by colonoscopy in the persons found positive. The prophylactic colonoscopy must be also performed in persons with high risk of cancer: inflammatory bowel diseases, descendents of persons with colon cancer, colonic polyps history.

The molecular screening will represent in the future the ideal method of secondary prophylaxis, by noticing the genetic mutations predisposing to colon cancer.
After the surgical resection of a colon neoplasm, CEA may be used to show the possible local recurrences. The ultrasonography and CT for possible hepatic metastases are also useful.

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Ulcerative Colitis, Physiopathology, Diagnosis, Treatment

Definition
It represents an intestinal inflammatory disease, characterized by recurrent attacks of diarrhea with mucus and blood, alternating with periods of silence.

Clinical features of ulcerative colitis
Digestive manifestations consist in episodes of diarrhea with blood, mucus and pus. The diarrheic episodes consist usually 3-10 stools/day, and in the severe cases there may only appear emissions of blood, mucus and pus. Abdomen on being palpated is painful in the hypogastric area or along the course of the colon.

Extradigestive manifestation are: anemia, fever or low-grade fever in the episode, weight loss, and fatigue. Sometimes arthritis, erythema nodosum, uveitis may appear.

Physiopathology
In the physiopathology of inflammatory bowel disease, more factors are incriminated:
a) Environment factors: the normal intestinal microflora
b) Immunologic factors: defects of local immunity of the mucosa.
c) Genetic factors.

Paraclinical findings
Laboratory data: iron-deficiency anemia,with hypochromia and low sideremia, hypoalbuminemia, inflammatory syndrome (ESR increased,sometimes leukocytosis, reactive C protein increased).
Stool examination is useful in order to exclude an infectious disease such as bacterial dysentery.
Endoscopic data.Typically for ulcerative colitis is the permanent involvement of rectum (recto-colitis), the continuous character of endoscopical lesions. The endoscopy shows the typical aspect of the episode: the mucosa “cries blood”. The mucosa is frail, with superficial ulcerations, diffuse erythema, loss of typical vascular pattern, covered with mucus and pus. The pseudopolyps may be present.
The biopsy proving an inflammatory infiltrate with polimorphonuclear cells at the level of mucosa,  the presence of cryptic abcesses, exulcerations.

Radiological examination. The barium enemawill show, in chronic stages, a granular aspect of the affected mucosa, the pseudopolyps, and the loss of normal colonic haustrations, with a tubular aspect of the colon.

Transabdominal ultrasonography  showing the thickness of colonic wall in the acute phase of the colonic extension. The colonic mucosa is thickened more than 5 mm (mostly 7-10 mm).

Positive diagnosis: diarrhea with blood, mucus and pus, the endoscopically, followed by the biopic confirmation.

Clinical forms

• Fulminant
• Chronic intermittent
• Chronic continuous

The assessment of severity is made by number of stools and intensity of clinical signs. Therefore, there are moderate, mild and severe forms:

• the mild form presents up to 4 stools/day, with only little blood and mucus, general state is good, without fever or denutrition, the anemia is discrete;
• the moderate form with 4-6 stools/day, anemia, low-grade fever
• the severe form with more than 6 stools/day, fever over 38 grade Celsius, anemia, hypoalbuminemia, big amount of blood in the stools, general feeling of illness.

 Based on the location of ulcerative colitis there are three forms:

• proctitis or proctosigmoiditis (rectal or rectosigmoidian location)
• left colitis (involvement up to the splenic angle)
• pancolitis (involvement of the whole colon).

Differential diagnosis:

• colon neoplasia - the endoscopic examination will certify the diagnosis
• bacterial dysentery or other infections causes: Salmonella, Shigella, Campilobacter jejuni, Clostridium difficile - the stool examination will prove the germ
• ischemic colitis - endoscopic and bioptic diagnosis
• irradiation colitis - history of therapeutic abdominal diagnosis
• collagen colitis or lymphocytar colitis-with a normal endoscopic; the biopsy will reveal the presence of submucosal collagenous bands or a rich lymphocytary infiltrate.
• Chron’s  disease -characterized by discontinuity of lesions, endoscopically deep ulcerations, sometimes linear.

Evolution
The evolution is cyclic- acute episodes of variable duration, usually weeks or months, followed by remission.

Complications

• the toxic megacolon
• intestinal stenosis
• massive bleeding with severe anemia
• colon cancer
• extradigetive severe manifestations. 

Treatment ulcerative colitis
a. Hygienic and dietary

The diet during the episode will be sparing the digestive function, by avoiding milk and dairy meals  (cream, fermented chesse), raw vegetables and fruit, concentrated sweets.

b.Medication - it depends on the episode severity.
In the severe episode, parenteral nutrition must be used, with liquidian and electrolytes correction, corticotherapy pev. -100-200 mg hydrocortisone hemisuccinate/day and in toxico-septic forms, antibiotherapy, especially against anaerobic germs (Metronidazole). In refractory fulminant Ulcerative colitis, cyclosporine has effectively induced remission, obviating immediate surgery. Because cyclosporine is such a potent immunosuppressive agent, the psysician must be absolutely certain that an infection is not contributing to the colitis. Infliximab is a monoclonal antibody against tumor necrosis factor (TNF)-alpha, a proinflammatory cytokine that occurs early in the inflammatory cascade. Infliximab has only recently been approved for use in ulcerative colitis. The drug is given as an intravenous infusion, typically in an induction regimen of 2 infusions over 2 weeks. In several reports, refractory ulcerative colitis responded to infliximab, and emergency colectomy was avoided.
In moderate forms of ulcerative colitis (4-6 stools/day) the treatment is using prednisone 60mg/day; the doses sre tapered with approx. 10 mg/week, so that after approx. 4-6 weeks the necessary dose to suppress the disease activity is 10 mg/day; the treatment is continued, even if remission is evident, for more than 6 months. The alternative is treatment with Salazopirine 4-6g/day or, more modern, 5-aminosalicylic acid (Mesalazine) 3-4g/day.
In distal forms (rectosigmoidian) a local treatment with suppositories, foam or Salazopirine or 5-aminosalicyclic enemas may be  used, or topic corticoids (Budesonide).
In mild forms, a treatment with mesalazine 2-3g/day or Salazopirine 3-4g/day is administered.
In continuous chronic forms, the treatment is indefinite.
In discontinuous chronic forms, the acute episode is treated with higher doses, and with endoscopic and histological remission, it keeps up with Salazopirine 4-6 g/day or Salofalk 3-4 g/day.

c. Surgical treatment in case of toxic megacolon, when there is a perforation or an uncontrolled bleeding a total colectomy or proctocolectomy has to be done

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The malabsorption syndrome, Treatment, Diagnosis, Evolution

Definition of the malabsorption syndrome
The malabsorption syndrome represents a pathological situation characterized by a disorder of absorption, at small bowel level, of different nutritive compounds.
Malabsorption may be of pancreatic, hepatic or intestinal origin. Malabsorption syndrome may be caused by digestion disorder, with the secondary disorder of absorption(by hepatic, pancreatic causes) or may by ower directly to absorption disorder at the enteral level (in intestinal diseases).
In malabsorption, the most typical sign is steatorrhea, defined as a more than 5g fats/24 hours loss by stool.

The etiopathogenesis of the malabsorption syndrome
Different disease of the digestive tract may provoke disorders of digestion of alimentary principles and/ or disorders of absorption.
The protein digestion is modified in the pancreatic failure (decreasing of trypsin and chymotrypsin), in accelerated transit speed (enzymatic contact time reduced). The deficitary absorption of aminoacids appears in different intestinal diseases.
Glucide malabsorption is generated by maldigestion , especially in the disaccharidase deficit (lactase, maltase, sucrase) or in the chronic pancreatic insufficiency (deficit of pancreatic amylase). The chronic intestinal sufferance will generate disorders in the monosaccharide absorption.
Lipid malabsorption is generated by lipid maldigestion (gastric resection with Billroth II anastomosis), where billiary salts and lipase get into contact with food nonphysiologically; the Zollinger-Ellison syndrome, where excessive gastric acidity inactivates the pancreatic lipase; the insufficiency of pancreatic lipase in the chronic pancreatitis; the lack of lipid mycellisation by decreasing the billiary acids-pool in chronic hepatic diseases; intestinal bacterial overpopulation or reabsorption failure in the terminal ileon inflammation).
Etiology of the malabsorption syndrome
Causes of maldigestion:
a. Gastric causes:

• gastrectomia Billroth II
• gastroenteroanastomosis
• Zollinger - Ellison syndrome;

b. Billiary causes:

• chronic hepatic diseases
• chronic billiary obstruction

c. Pancreatic causes:

• chronic pancreatitis
• pancreatic cystic fibrosis

d. Intestinal causes:

• disaccharidases deficit (lactase, maltase, sucrase, trehalase)
• afferent loop syndrome (by bacterial overpopulation).

Causes of intestinal malabsorption
a. Abnormal intestinal epithelium absorption:

• celiac disease
• Whipple disease
• intestinal amiloidosis
• chronic intestinal ischemia
• Crohn’s disease of the intestine
• tropical sprue
• intestinal tuberculosis

B. Syndrome of short intestine

• after surgery
• enterocolic fistulas
• surgical intestinal by-pass

c. Abnormal intestinal transport:

• intestinal lymphoma
• idiopathic intestinal lymphangectasia
• congenital cystic pneumatosis

d. Increased intestinal transit speed:

• hypertiroidia
• chronic diarrhea

Clinical forms of malabsorption syndrome

• malabsorption syndrome  maldigestion
• malabsorption syndrome by disorders of intestinal absorption (malabsorption)
• mixt malabsorption syndrome- when digestive disorders sre associated with those of absorption.

Clinical features

• chronic diarrhea weight loss up to generalized malnutrition
• steatorrhea (soft stools, light colored, smelling, adherent)
• the abdominal distension
• bloating
• flatulence
• abdominal discomfort
• weight loss
• the Bichat-bulk disappears
• muscle atrophy
• tegument changing
• together with paleness, rough and dried skin,sometimes with pelagroid pigmentation
• the tongue mucosa is red; lacking its small glands (glossitis), cheilosis
• the nails decolorize and break easily
• axilar and pubian hair reduces, in the latest stages, alopecia
• the disorders in calcium absorption may generate osteomalacia bones pain and tetania
• the deficiency of K vitamin generates tendency to bleeding
• ascites
• anemia
• endocrine disorders: hypofisary failure (with troubles in children growth), corticosuprarenalian failure (Addison disease), gonadic failure (impotence and sterility).

Diagnosis of malabsorption syndrome

• steatorrhea is a cardinal sign. Represent the elimination of more than 5g lipids/24 hours.
• the coloring of a stool probe with Sudan III and numbering of fat corpuscles
• creatorrhea = the proteic loss by stool

The etiology of malabsorption syndrome requires the evaluation:
a. Gastric:

• barium examination, for the diagnosis of  gastrocolic fistula, gastroenteroanastomosis, gastrectomy with Billroth II anastomoses
• gastroscopy: multiple ulcers in Zollinger Ellison syndrome
• dosing gastrinemia possibly gastric chemism  stimulated with Pentagastrine

b. Billiar:

• the biologic diagnosis of billiary obstruction, possibly completed with pancreatic computed tomography and endoscopic retrograde colangiopancreatography (ERCP)

c. Pancreatic:

• pancreatic enzymes (amylase, lipase) may be increased
• the imagistic modified aspect of pancreas or evalution by ERCP of pancreatic ductal aspect
• altered pancreartic functional tests (PABA or Fluorescein diluarat)
• more recently, determination of  I (first) faecal elastase mey demonstrate incipient stages of  pancreatic failure
• determining VIP level (vasoactive intestinal polypeptide) may establish the diagnosis of VIP-oma or pancreatic cholera (severe, watery diarrhea), with hypokaliemia

d. Intestinal:

• barium examination,with intestinal following up or enema-may evaluate the intestinal aspect and motility
• duodenoscopy with duodenal biopsy ( celiac disease) or endoscopy may visualize the mucosal aspect (biopsy).
• D-xilosis test
• Schilling test-evaluates the absorption of B12 vitamin
• small bowel biopsy of jejunal area may show the villous atrophies in celiac disease
• colonoscopy  may show changing of rectocolitis, Crohn’s disease may be diagnosed
• the lactose tolerance test (LTT) which may show a lactase deficit

Differential diagnosis

• The malabsorption syndrome differential diagnosis may be done with different causes of chronic diarrhea, which have not attained malabsorption. In these cases, the weight loss and the modifying of biologic sanguine parameters (proteinemia, albuminemia) do not appear.
• The colon neoplasm is accompanied by weight loss, diarrhea, iron-deficiency anemia and it must be differentiated from malabsorption syndrome.
• In case of hepatic metastase, jaundice may be signaled and a tumoral liver may be palpated.
• The neoplasm syndromes of different causes evolve with excessive weight loss, hypoproteinemia and hypoalbuminemia, but without diarrhea.

Evolution

• malabsorption syndrome evolution is chronic, progressive, when the etiology is not discovered and treated. Denutrition evolves to excessive weight loss, and the uncorrected biological disorders aggravate.

Complication

• hypoalbuminemia with edema and sever ascites
• the decrease of  protrombin index with multiple bleedings
• anemia
• the sever decrease of serum electrolytes: K, Na, Ca, Mg
• the decrease of vitamins

Treatment
The therapeutic attitude in malabsorption syndrome is mostly related to its etiology.
The alimentary diet : in celiac disease( where wheat, barley, oat and rye will be compulsory avoided, but replaced with rice and flour,potatoes) or the lactase defocot(where milk and dairy products will be completely avoided).
In chronic pancreatitis , the diet will completely avoid the alcohol intake and will drastically reduce fats.
On chronic diarrheas, the food rich in hard vegetal fibers will be avoided(radish, cabbage).

Medical therapy
- in  Zollinger - Ellison syndrome the resection of gastrinoma and intense blocking of acid secretion will be done, using H / K ATP-ase pump proton blockers

• Omeprazole 40-160mg/day
• Lansoprazole or Pantoprazole
• Sandostatin 200mg/day subcutaneous

- in chronic pancreatitis – the enzyme substitution

• Creon
• Nutrizym
• Cotazym
• Panzytrat
• Digestal forte

- in intestinal causes of malabsorption of malabsorption, the medical treatment has  to have two compounds the dismicrobism which is treated with intestinal eubiotics: Saprosan 3x1 tb/day
Antinal 4x1 tb/day
Intetrix 4x1 tb/day
and on  the other hand the intestinal protection with products like Smecta 3x1 packet/day
or reduction of transit speed in case of the acute diarrhea with Loperamid (Imodium) 1-2 tb when needed.
in cesa of excessive flatulence - Dimeticone
in Crohn’s disease - Mesalazina
- corticotherapy
- Azathioprine

- in the Verner - Morrison syndrome – octreotide (Sandostatin) 200-300 mg/day

- in the Whipple disease - antibiotics

• Tetracycline 4x250mg/day
• Ampicilline
• Trimetoprim/ Biseptol,10-12 months

- the following deficits must be corrected :

• hypoalbuminemia by administration plasma
• iron- deficiency anemia by administrating iron
• macrocytic anemia by administrating B12 vitamin /folic acid
• the electrolytic deficits (Na, K) will be corrected parenterally and those of Ca  and  Mg usually by oral medication.
• the vitamin deficits (B complex, D and K) will be corrected, as well as the hormonal ones, when they appear.

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Stomach (gastric) cancer

Gastric neoplasia represents the second cause of mortality by cancer  in the world, after the pulmonary one.
Epidemiology
Linked to the alimentary habits (in Japan the frequency is especially high). In Europe, it is more frequent in the northern zones, also relater to the alimentary habits (canning).
This cancer is 2-3 times more frequent in men than in women, and its frequency increases with age (average age at the moment of diagnosis is over 60 years). It rarely appears under 45 years.

Risk factors is gastric cancer

• alimentary habits: the high content in nitrosamine in canned food  by salt and smoke, are favoring factors to the gastric neoplasm; by contrary, the alimentation rich in fruit and vegetables containing C and A vitamins, protects the stomach.
• the genetic factor: the existence of a familial predisposition to this type of neoplasia
• the low socio-economic standard - may be a favoring factor, probably because of the alimentation, infection Helicobacter Pylori etc.
• the Helicobacter Pylori infection. Helicobacter Pylori was recently appointed by WHO as a first range carcinogen, thus assessing its involvement in the etiopathogenesis of this neoplasm. The Helicobacter Pylori intervention is realized by induction of atrophic gastritis with intestinal metaplasia, which represents a potential evolution towards dysplasia and neoplasia. 

Gastric affections predisposing to gastric cancer

• atrophic chronic gastritis: mostly related to the Helicobacter Pylori infection; on this background dysplasic lesions show quite often, evolving from an easy to severe dysplasia (the latter considered in fact an intra-epithelial cancer).
• gastric adenomatous polyps: represent a premalignant stage, especially those with bigger dimensions (over 1 cm, and those over 2 cm have big chances of malignization). Therefore, endoscopic polypectomia of these polyps is indicated at the very moment of their discovery.
• gastric resection in the antecedents (for ulcer) represent a risk factor, generally over 15 years from resection. Usually, an inflammatory stomitis is noticed, as well as lesions of gastritis in the gastric segment left, which may degenerate to malignancy. Therefore, the necessity of endoscopic following of operated stomach after more than 15 years from resection.
• gastritis with giant folds Menetriere has a risk of approx. 15% of malignant transformation.
• gastric ulcer. It is compulsory to take multiple biopsies from each gastric ulcer at every endoscopy and the gastric ulcer healing must be endoscopically checker (with biopsy from the scar). To be mentioned the possibility of some ulcerated cancers, susceptible of scarring under medical treatment.

Clinical picture of gastric cancer
It may be heterogeneous, depending on how advanced the cancer is. The most frequent symptoms are epigastralgia, freakish appetite leading to total anorexia (sometimes the complete refusal to eat meat), progressive weight loss, and iron deficiency anemia. The epigastric pain may mimic the ulcer symptoms, appearing after meals, often disappearing with gastric protectives. Weight loss may get in the advanced forms to a neoplasic extreme weakness. More rarely, a digestive hemorrhage may appear, endoscopically confirming the diagnosis of gastric cancer. In the advanced forms there might be an epigastric palpable abdominal mass.
Rarely the gastric neoplasia may be discovered starting with an anemic symptoms. Paraneoplasic syndromes may appear migratory phlebitis, acantosis nigricans etc.
Precocious gastric cancer is usually asymptomatic, or there may appear some discrete dyspeptic symptoms. Therefore, it is most often randomly discovered, by occasion of an endoscopy done for an epigastric symptomatology.
Pathological picture in gastric cancer
Histological, the gastric cancer is an adenocarcinoma, with different degrees of differentiation. The less differentiated, the more aggressive it is. There are some neoplasms with histological aspect of “sealed ring”.

Macroscopically: the neoplasm may be protrusive, ulcerated infiltrative. The protrusive aspect, bleeding, is typical to malignity. The ulcerated has irregular margins, infiltrated, rough and must be differentiated via endoscopy from gastric ulcer (b multiple endoscopic biopsies). The infiltrative type of cancer (linitis plastica) realizes a diffuse, extensive infiltration of gastric wall, conferring rigidity to this one, and it must be differentiated by gastric lymphoma.
The transparietal extension of gastric cancer is usually precocious, invading the neighbor organs. The lymphatic extension is also rapid, with the involvement of territories of gastric lymphatic drain and then to a certain distance. The metastases are more often in the liver and lung. Sometimes a carcinomatous peritonitis may appear.

The TNM stadialization (tumor, ganglionar node, and metastasis) allows the establishment of prognosis and of therapeutic approach:
- tumor

• T1 involves the mucosa and submucosa
• T2 penetrates into the muscularis propria
• T3 involving of serosa
• T4 penetrates into the surrounding organs

- lymph nodes:

• N0 lack of ganglionar invasion
• N1 involvement if nodes in the neighborhood
• N2 involvement of distant lymph nodes

- metastases:

• M0 lack of metastases
• M1 distant metastases

The diagnosis of gastric cancer
It most often starts with a dyspeptic syndrome, epigastralgia, progressive weight loss or an anemic unexplained syendoscondrome. The familial aggregation, or already known premalignant lesions may turn the attention to the disease.
Clinical examination usually brings poor arguments, but in the advanced stages an epigastric mass or/and some supraclavicular lymph nodes involvement may be present.
Paraclinical findings of gastric cancer

• biologically, an iron – deficiency anemia is the rule or severe). There are still gastric neoplasias that may evolve without anemia (linitis plastica).
• Gastroscopy is the election diagnostic method. It allows the visualization of the lesion, signals its characteristics (friability, bleeding) and prelevation of multiple biopsies for the compulsory histological diagnosis confirmation.

Acording to endoscopy, the advanced gastric cancer may be: protrusive, ulcerated or infiltrative (sometimes these types may intricate).
The early gastric cancer (superficial – involving only  the mucosa and submucosa) is endoscopically classified.

• Type I – protrusive
• Type II – superficial II a - overplane, II b – plane, III c – depressed
• Type III – excavated

In early gastric cancer the five – years survival after the operation 95%.

• gastric barium-examination is generally a diagnostic surpassed method,generally addressed to the advanced neoplasms or cases with plastic linita(where the diagnostic-help is useful,often superior to the endoscopy.The X-ray examination cannot  diagnose all the early stages of the disease and does not allow biopsy prelevation.Diagnostics endoscopy per primam is preferred to a checking-out of an nuclear radiological examination,due to the risks of radiological diagnosis failure.
• echoendoscopy permits the T and M stadialization
• transabdominal ultrasonography may show hepatic metastases or perigastric adenopaties.Sometimes, a casual abdominal ultrasonography  may discover an epigastricmass “in cockade”, which may suggest a gastric neoplasia (the subsequent endoscopic check-out is compulsory). 

Prognosis of gastric cancer
The gastric cancer prognosis depends on the TNM extensions, histological type (poor oe well-differentiated), and patient’s age.
The survival is very good only in the superficial cancers (95% in 5 years). The radical surgery may be done in only 1/3 of cases, in which the 5 year-survival is approx.25%.
Treatment of gastric cancer
A. Surgical. Surgery is the best and radical therapy in gastric cancer. A gastrectomy with lymphadenectomy is performed.Usualy, a subtotal  gastrectomy or total (with esojejunostomy) is done, depending on the location and extension of the tumor.
B. Endoscopic. The surgically over passed cancers may still benefit from an endoscopic haemostatic treatment with argon Beamer.
A mucosectomia may also be done in the early stages of cancer (“in situ”). It consists into serum injection under the neoplasia lesion thus transforming it into a sessile polyp, which will be polypectomised afterwards. The piece obtained will be examine by a pathologist.
C. Chemotherapy. Post surgical chemotherapy is generally indicated, almost in more advanced cases, and it includes more cures of Adriamycine with 5- Fluorouracil.

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Irritable bowel syndrome, Diagnosis, Treatment

Definition of Irritable bowel syndrome
Irritable bowel syndrome represents a functional disease, characterized by transit disorders, generally constipation alternating with diarrhea, diffuse abdominal pain, sometimes mucus emission.
Clinical features

• diffuse abdominal pain, or located along the colon. They may be smothered, but often have a cramp character, duration of seconds to minutes. Other times the patient feels only an abdominal discomfort. The most often symptoms disappear in the relaxing periods, holiday etc.
• transit disorders are frequent, characteristic being the alternation  constipation-diarrhea. The stool emission is often hard, fragmented, covered with mucus.
• mucus emission accompanies the hard stool. Blood does not appear in stool in the irritable bowel syndrome, but the hard, rough stools may create anal fissures that may bleed.
• bloading 

Diagnosis
Manning criteria:

• abdominal pain that disappear after stool emission
• stool becoming more frequent and soft in the presence of pain
• bloating, flatulence
• sensation of incomplete evacuation of the rectum
• elimination of mucus in stools
• imperious character of defecation

Clinical data of the irritable bowel syndrome diagnosis

• elevated ESR
• leukocytosis
• pus, blood or fat in the stools
• more than 200g of stool per day
• persistent diarrhea
• hipokaliemia
• no spastic response to rectal distension during manometry

Paraclinic diagnosis

• anoscopy, rectoscopy, colonoscopy (sometimes barium enema), to evidence the organic pathology of colon;
• gastroscopy, to show the possible gastric lesions;
• abdominal and pelvic ultrasonography, to show the gallbladder, pancreas and genital organs;
• radiologic evaluation of intestine (enteroclysis or barium examination) or enteroscopy for small bowel pathology.

Differential diagnosis

• ano-rectal and colon neoplasm
• inflammatory bowel disease(ulcerative colitis, Crohn’s disease)
• colonic diverticulosis and diverticulitis
• lactase deficit
• functional dyspepsia

Evolution
The irritable colon evolution is favorable, since there are no complications.
In general, the disease evolves for a long time, with periods of silence or with exacerbations, usually related to stress.

Treatment of irritable colon
1. Diet. When the constipation predominates, the diet will be rich in alimentary fibers. If the diet is not sufficient, constipation will be controlled with laxatives type Forlax (that increase the stool volume). The patients should avoid consuming certain food that induces symptoms.
2. Medication. The therapy consists in:
- antidiarrheic drugs - Smecta(smectitis) or Imodium(loperamid)
- antispastic - Spasmomen
                   -Debridat
                   -Dicetel
                   -No-Spa
                   -the medication is given only when needed
- sedatives - Hidroxizin
-Rudotel

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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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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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Gastritis, Treatment and Classification

What is Gastritis

Gastritis can be an acute or chronic gastric disease, characterized by inflammatory lesions produced by various etiologic and pathogenic factors. They may be asymptomatic or with unspecific clinical expression.
Gastropathies represent a group of gastric mucosal lesions, predominant epithelial and/or vascular (by stasis or ischemia) but without or minimal inflammatory component, unlike gastritis.

Gastritis classification

Gastritis classification is as follows:
1. Clinical evolution
A. Acute. Evolves towards healing or chronicity most of them are self-limited and spontaneously recover.
B. Chronic. They are long-term inflammations that may heal after therapy or evolve no matter of the therapy. Read More
2. Endoscopic
A. Endoscopic forms of gastritis:

• eritematous exudative
• maculo-erosive
• papulo-erosive
• atrophic
• hypertrophic
• hemorrhagic 

B. Classification by extension:

• antral-type B-produced by H. Pylori infection
• fundic-Type A-autoimmune (generating Biermer anemia)
• pangastritis.

3. Histologic

A. Acute gastritis - numerous neutrophiles localized intraepithelial, in the lamina propria or aggregated in the glandular lumens (cryptic abcesses).

B. Chronic gastritis - immuno-competent lymphocytes and plasmocytes. It  evolves in some decades to atrophic gastritis. The activity degrees depend on the presence of neutrophiles and the degree of infiltration in the profound layers. Low activity is characterized by presence of neutrophiles only in the lamina propria. In the moderate activity, the neutrophiles are present in high density in the gastric foveoles. The degree of activity is severe when the neutrophiles are present intraepithelial. Chronic gastritis is inactive when  neutrophiles  are absent.

C. Atrophic gastritis represents the final stage of chronic gastritis evolution, and is characterized by the disappearance of the oxintic glandular structure,with a distortion of the reticulin net. The inflammatory process invades the whole wall thickness; the histopathologic examination should mention the presence or absence of intestinal metaplasia.

The System includes an endoscopic section, with three subdivisions: topography, lesion type, endoscopic category of gastritis, and a histological section, including, the etiology, topography and gastritis forms.

The grading of histological lesions of gastritis in the Sydney System refers to the next six histological characteristics; for each of them there is a grading in moderate, mild and severe:

• acute inflammation-neutrophiles
• chronic inflammation-limphoplasmocytes
• activity-polimorphonuclear infiltrate
• atrophy-loss of specialized glands
• intestinal metaplasia
• Helicobacter Pylori

4.Etiology. The classification of gastritis includes the following possible etiologies:

A. Infectious:

• Bacterial: H. Pylori (mostly), Helicobacter Heilmannii, alpha hemolytic Streptococcus, Staphylococcus etc.
• Viral: Cytomegalovirus, Herpes-virus
• Fungal: Candida
• Parasites: Strongiloides, Toxoplasma.

B. Autoimmune: Atrophic gastritis with Biermer anemia.

C. Drug-induced: NSAIDS(nonsteroid anti-inflammatory)

D. Specific: Crohn’s disease, eosinophilic gastritis, lymphocytar gastritis.

Chronic Gastritis H. Pylori Positive

It is type B gastritis, defined by the inflammation of the gastric mucosa principally antral, induced by Helicobacter pylori.

The pathogenetic mechanism of inducing gastric lesions is related to the peculiarities of the bacteria and to its enzymatic equipment, having a result an immune response of the host (local and systemic) against different proteic structures of the bacteria. The antibodies against the proteins secreted by Helicobacter Pylori with protective role seem to be involved in the gastritis pathogenesis.

The macroscopic aspect is of diffuse or patchy congestion, mostly antral with acute or chronic erosions. In 25% of cases a nodular gastritis appears.

Microscopically, a palimorphonuclear infiltrate may be noticed, together with the gastric cryptic affecting, the apparition of some aggregates of lymphoid follicles, and the reduction of mucus in the epithelial cells. Concerning the evolution, an active chronic gastritis is described(with a rich polimorphonuclear infiltrate), and an inactive chronic gastritis(with prevalence of mononuclear cells).

The clinical features are unspecific and overlap those of the non-ulcer dyspepsia. Epigastric pain, nausea, vomiting may appear. These symptoms disappears only after eradication treatment.

The B type gastritis diagnosis is done endoscopically, showing the antral lesions and also by taking biopsies, showing the Helicobacter Pylori bacteria by different techniques.

The evolution of gastritis may be towards atrophic chronic gastritis and further to intestinal metaplasia, dysplasia and finally gastric cancer or nonHodgkin lymphoma.

The treatment is the eradication of Helicobacter Pylori infection.

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.

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Functional Dyspepsia Diagnosis and Treatment

Definition

Functional dyspepsia is a functional disease(without organic reason), characterized by a symptomatology located in the upper abdomen, its manifestation are epigastric pain, satiety, flatulence or discomfort.

Etiopathogenesis of functional dyspepsia

In cases with quasiulcerous symptomp the role of Helicobacter Pylori or hypersecretory status may be incriminated; in those with flatulence, a disorder in gastric emptying(dismotility)or even disorders of the sensorial digestive perception(the patient perceives as abnormal a usual quantity of gas located in the digestive tube).

Classification of functional dyspepsia

It is done in accordance with the dominant symptoms:

• functional dyspepsia ”ulcer-like”;
• functional dyspepsia type dismotility “dismotility dyspepsia”;
• essential  functional dyspepsia.

In the ulcer-like dyspepsia:

• epigastric pain,
• discomfort,
• frequently painful hungers are prevalent, but the superior digestive endoscopy reveals the absence of ulcer.

In dismotility dyspepsia, the patient complains of  epigastric satiety, a sensation of epigastric “load”, flatulence, eructations, but the digestive investigations will reveal the absence of lesion. Essential functional dyspepsia will contain a mixture of the symptoms above.

Diagnosis

Clinical diagnosis consists of an epigastric symtomatology more or less noisy,but in which loss, digestive hemorrhage or anemia are absent. The prevalent type of symptoms will allow the “framing” into one of dyspepsia forms.

Paraclinic diagnosis consists into a series of explorations, which will demonstrate the absence of organic lesions. Firstly, the abdominal ultrasonography will show a gallbladder without calculi, a normal pancreas, and a liver without changes. The superior digestive endoscopy will show a normal esophagus, stomach and duoden. The barium enemaor colonoscopy will be proved by the absence of organic lesions.

Differential diagnosis in functional dyspepsia must be done with all the organic lesions of the upper abdomen (reflux esophagitis, esophageal neoplasia, achalasia, gastro-duodenal ulcer, gastric neoplasm, gastric lymphoma, acute or chronic pancreatitis, gallstones etc.).

-the irritable colon (characterized by disorders of transit, flatulence, sensation of incomplete  stool, discomfort in the lower abdomen etc.).

Evolution is favorable, with more or less in time, generally according to alimentation, stress etc. The prognosis is favorable.


Treatment of functional dyspepsia

It addresses mainly to the symptoms and it will be administered at their apparition.

Treatment of “ulcer-like” dyspepsia

Antisecretory drugs of the class H2 histaminic blockers:

• Ranitidine 300mg/day
• Famotidine 20-40mg/day,
• or PPI given during the symptomatic periods or PPI (20-40mg)

Eradication of Helicobacter Pylori

In  approximately a half of patients in which the triple the therapy Helicobacter Pylori is eradicated, the symptoms may disappear or reduce, but in the others, the symptoms persist.

Treatment of “dismotility” functional dyspepsia consists generally in prokinetics.

• Metoclopramide(1 tb 30 minutes before principal meals)
• Domperidone(Motilium 1 tb 30 minutes before principal meals)
• Cisaprid(Coordxinax, Prepulsid 5-10 mg 30 minutes before principal meals). Digestive ferments at meals(Digestal, Mezym, Festal, Kreon etc.) or intestinal gas absorbents, such as dimeticon(Sab-simplex) may also be administered.

Treatment of essential functional dyspepsia, disease with symptoms of the two entities above,will be made with medication addressed to the dominant manifestations(pain or satiety).

In all forms of dyspepsia,if stress plays a role in the apparition of symptoms,an easy sedative treatment should be administered or even psychotherapy(often when the patient find out he has no organic lesions,the psychic effect is positive).

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Esophagus Neoplasm Treatment and Evolution

It represent 15% of digestive cancers. Histological, most of them are epidermoid carcinomas.
It is more frequently met in men (men/ female ratio=3/1), the average age of apparition being 60-65 years.

Some definite etiologic factors (causes) are:

• cigarette smoking
• excess alcohol intake
• alimentary factors : proteic deficiency, low intake of vitamins A, B, C, nitrosamine excess, lack of zinc and molybdenum.
• other conditions: excessively hot liquids intake (tea), ion radiations exposure, infectious agents(Papiloma-virus), genetic factors.

There are also a series of pathological states predisposing to the onset of esophageal cancer:

• ENT cancers
• Barrett’s esophagus
• mega esophagus
• esophageal diverticula’s
• postcaustic stenosis
• peptic stenosis
• Plummer-Vilson syndrome(esophageal iron deficiency dysphagia)

There are aspects that are more pathological:

• they most frequently occur in the lower third (over 50%) and only 20% in the upper third
• macroscopically, the most frequent form is ulcero - vegetant
• microscopically, 90% are epidermoid(squamous) carcinomas. Other rare forms are adenocarcinoma, or very rarely, sarcoma, lymphoma, melanoma.

There are a series of clinic symptoms described, unfortunately they present only in phases when surgical treatment is surpassed: dysphagia, regurgitations, thoracic pains, weight loss, dysphonia.

The diagnosis is mainly endoscopic, with endoscopic biopsies; contrast radiographs may also be useful. Echoendoscopy is useful for the preoperatory staging, CT-scan as well.

Evolution of  esophageal cancer is rapid, with poor prognosis and 5 years-survival of only 5%.

Complications that might appear can worsen the prognosis: eg aspiration pneumonia, eso-bronchic fistula, perforations, hemorrhages.

The treatment has more possibilities:

1. Surgical- the best treatment, perform an esophagectomy with minimum 5 cm above the superior pole of the lesion.
2. Radiation therapy - is a palliation method.
3. Chemotherapy – using Bleomycine,Cisplatine,5-fluorouracil.
4. Endoscopic:

• the mucosal endoscopic resection, mucosectomia – in incipient forms;
• photocoagulation using laser or autofluorescence – also in incipient cancers;
• edoscopic prosthesis – is a palliation method, used to increase life quality and treatment of dysphagia (in advanced cancers).
• endoscopic dilatation has the same purpose, but shorter-term effects.
• rechanneling of esophageal lumen with laser

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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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Achalasia - Symptoms, Diagnosis and Treatment

Definition

The main elements are the LES hipertony, the lack of relaxation of LES with swallowing and the absence of the normal peristaltic in the 2/3 inferior esophagus. Practically there is on relaxation of LES during swallowing.

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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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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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Cholelithiasis treatment

Symptomatic gallstones (cholelithiasis) will be discussed at this traetmen is surgical and, more rarely shown by non-surgical techniques.

Medical Treatment of cholelithiasis

• Ursodeoxycholic acid (10 mg / kg / day)
• Ursofalk or its combination with chenodeoxycholic acid (10-15 mg / kg / day)
• Litofalk is 3-12 months until complete dissolution calculations

Lithotripsy is the fragmentation of Extracoporeal cholesterol stones by shock waves Extracoporeal, estimates that one-way or less, preferably less than 15 mm. Lithotripsy resulting fragments were resolved by the administration of bile acids (ursodeoxycholic acid) until the complete disappearance of all stone fragments into the bladder.

Quick Gallstones Treatment Tips

 

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The Diagnosis Of Celiac Disease

It is largely through two methods of celiac disease treatment:

- serological determination of antibodies to transglutaminase

-Bioptic by endoscopy and biopsy of the dll (ll duodenum)-atrophy of the villi.

Other clinical trials by

-The dedetermination of steatorrhea, which is between 7 and 50 grams of celiac disease severe.

Absorption tests tract (D-test xilosis)

Barium - ray image of the intestine, which will be modified in various ways, generally showing an enlarged rectum

-Malabsorption syndrome are present, either selectively (iron, folic acid, calcium), or global.

The differential diagnosis is done with all cases of diarrhea of other causes:

• lactase deficit
• Crohn’s disease
• intestinal tuberculosis
• chronic pancreatitis

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Celiac Disease Treatment

A. Dietetics

Celiac disease can have a favorable outcome in the case of a gluten-free diet: wheat, barley, oats and rye will be removed from power.

The disease is curable in general after 3-5 years of gluten-free diet deficient, but the favorable clinical response may appear in 3-6 weeks after starting the diet.

B.Medical

- clear when the response to the elimination of gluten from the diet does not appear.

- Low-dose oral corticosteroids (10-20 mg bid) for a period of 4-8 weeks

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