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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Disaccharidase deficiency syndromes

Definition

Its cause is the lack or insufficiency in the secretion of  disaccharidases at the enteral level.
The deficit of disaccharidase may be:

• congenital (the congenital lactase deficiency :the newborn does not tolerate the milk immediately after birth; congenital deficiency; maltase or trehalase).
• asquired during life-time; it may be transient or definitive (the most frequent is the lactase deficit, with the milk intolerance of the adult

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Digestive System Diseases

Digestive diseases are relatively frequent in the developed countries and its frequency increases with age. Its present trend is to increase.

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.

Gastroenterology

• Gastroesophageal reflux disease
• Motor esophageal disorders - achalasia
• Esophagus neoplasm
• Chronic gastritis
• Gastroduodenal ulcer
• Functional dyspepsia
• Stomach Gastric cancer
• Inflammatory bowel disease
• Irritable bowel syndrome
• Colorectal cancer
• Celiac disease
• Disaccharidase deficiency  syndromes
• The malabsorbtion syndrome
• Chronic pancreatitis
• Cholelithiasis

Hepatology

• Chronic viral hepatitis
• Autoimmune hepatitis
• Nonalcoholic steatohepatitis
• Alcoholic liver
• Liver cirrhosis
• Hepatic diseases with immunological mechanism
• Hereditary metabolic disorders
• Liver transplantation

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Digestive System Diagram

There are a couple of distinct sorts of diagrams of the digestive method such a I need to show you. In this beforehand diagram you’ll see the basic serious parts of the digestive system. They include:

• mouth
• esophagus
• stomach
• pancreas
• gall bladder
• liver
• lowly intestine
• large intestine
• rectum

Digestion actually starts in the mouth. Your saliva glands give digestive enzymes such a embark on the digestive process. Each action sends signals to the imminent side of the body to prepare them for the job ahead.

This second diagram of the digestive approach shows you all the many spots of the person overly can develop problems as a result of shoddy digestive health.
When you experience predicament somewhere else, it can often be traced back to an improper function of the digestive tract. This diagram may be exhausted to permit you determine a possible hint at for some of the symptoms you may be experiencing.

This final diagram is to illustrate the various diseases of the digestive method itself. Did you repeatedly presuppose there got so many possibilities?

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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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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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