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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Chronic hepatitis diagnosis

Chronic hepatitis diagnosis is clinic, biological, but mostly histological. Chronic hepatitis can often be asymptomatic, or the clinical features are completely nonspecific, and therefore they are sometimes discovered by routine bilogical investigations.
Almost a half of patients suffering from acute hepatitis are discovered by periodical analyses or by a routine ultrasonography, which will show splenomegaly. When presuming the existence of chronic hepatitis, one should start with an exact etiological history, a correct clinical examination, a biological evaluation of the hepatic disease (the four biological syndromes: cytolytic, hepatoprive, inflammatory and billiar), an abdominal ultrasonography to evaluate the spleen dimension and the possible signs of portal hypertension.

The staging of chronic hepatitis is made compulsory by a hepatic biopsy (HBP). The biopsy will allow the correct histological framing, and also a quite exact prognosis, and sometimes will bring important etiological data, and it will allow in the same time a therapeutical decision. Non invasive markers which measures fibrosis were recently introduced. They use biological tests or hepatic elastography.

The histological staging of chronic hepatitis requires a compulsory hepatic puncture. This is a technique with low invasivity and a minimal risk. Lately HPB has been done by ultrasonographic control. THe bioptic fragment, after fixing and coloration with HE or special colorations, will be interpretated by an experimented pathologist. Whis will describe the lesions, a histological classification in chronic persistent hepatitis, in chronic active hepatitis, and the chronic lobular hepatitis, and then will use a quantifying score of lesions. At this moment, there are more histological framing scores.

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The recto colonic neoplasm diagnosis

The rectocolonic neoplasm diagnosis is made by the following diagnostic procedures:

• rigid rectoscopy
• flexible rectosigmoidoscopy
• colonoscopy
• irigography
• hemoccult test

Rigid rectoscopy requires a rigid metallic rectoscope and allows the examination of approx. 20-25 cm of the rectosigmoid. The device is not expensive, the technique is easy and it allows the diagnosis of rectal cancer. In addition to the anal examination and anoscopy (which diagnose the pathology of the anal channel and rectal ampoule), it may correctly evaluate the distal region of digestive tube.

Flexible rectosigmoidoscopy uses the flexible sigmoidoscope for the diagnosis. It allows the exact evaluation of the left colon (most often up to the splenic angle of colon), where 70-80% of colon neoplasms are only two enemas and the discomfort of the patient is not very high.

Barium enema evidences the colon by retrograde fulgilling of colon with barium. The double contrast technique is useful. It does not allow biopsy from suspect lesions and it does not allow therapeutic measures. The technique is the most widespread method of colon evaluation, but gas a diagnostic sensibility clearly inferior to the colonoscopy.

In the future it is anticipated the using of CT spiral (virtual colonoscopy) to reconstruct the colon and to diagnose the neoplasia or big polyps). Also in some dedicated centers, the abdominal ultrasound examination and especially hydrosonography may sometimes diagnose the colon neoplasm. Echoendoscopy allows the evaluation of the extension in layers of the neoplasm.

The Hemoccult test allows the determination of occult hemorrhages in the stool. It is rather a screening test, in general population; it helps to discover suspect persons that will be afterwards examinated endoscopically. The Hemoccult test is recommended every year, generally after 50 years of age. The Hemoccult test II, more modern, does not require special preparation and has a superior sensibility.

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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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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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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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Gastro-duodenal ulcer Etiopathogenesis, Physiopathology, Diagnosis

Definition of gastric-duodenal ulcer
Gastric ulcer and duodenal ulcer represent limited interruptions, unique or multiple of the gastro-duodenal  wall continuity, accompanied by a fibrous reaction, penetrating through the mucosa, submucosa and even to the serosa.

Peptic ulcer epidemiology
The clinical prevalence is 5-10% of the population. The real prevalence, based on necroptic studies, is 20-30% in men and 10-20% in women. Nowadays there is an important decreasing tendency of the disease prevalence. 
Gastro-duodenal ulcer etiopathogenesis
Approximately 10% of the adult population suffers or have suffered from gastro-duodenal ulcer. Helicobacter Pylori-this germ affecting over 2 billions of people! The infection is produced via faecal-oral or possibly oral-oral.
The Helicobacter Pylori acute infection manifests it self like an acute gastroduodenitis, with self-limited evolution. There remains a chronic gastritis, which will be involved in the  ulcer genesis. In case of antral gastritis(inflammation), this will lead to the increase of gastrin secretion and implicitly to acid hypersecretion. As a response to the acid secretory excess, which will get into the duoden, a gastric metaplasia will appear into the duodenum, a compulsory stage in the duodenal ulcerogenesis. In case of gastric body gastritis, this will lower the mucosal resistance to the aggressive factors, thus generating gastric ulcer. The prevalence of  Helicobacter Pylori infection in duodenal ulcer is 90-95% and approximately 70-80% in the gastric ulcer.

Gastric and duodenal ulcer physiopathology
A. Aggressive factors.
They are increased in the peptic ulcer genesis. There are three important aggressive factors.

1. The Helicobacter Pylori infection
The most probable mechanism of transmission is faecal-oral, the source of infection in the underdeveloped countries being the water. Its location in the stomach is between the apical membrane and the mucus layer, thus it is well adapted to the acid stomach environment. Its pathogenetic factors are the enzymes and cytotoxines secreted:urease(eliminating ammonia, which creates an alkaline pH, phospholipase and protease(digest the mucus and gastric and duodenal apical mucosa), the vacuolising cytotoxin.
Ulcerogenesis induced by Helicobacter Pylori is by direct action on the gastroduodenal mucosa and indirectly by increasing the clorhidropeptic secretion. The direct mechanism is determined by the  inflammatory process initiated by Helicobacter Pylori toxins, which induces an acute gastritis that becomes chronic subsequently. Helicobacter Pylori does not grow on the duodenal mucosa, but only on the islands of gastric metaplasia in the duoden; these appear as a protection mucosal reaction to the increasing acid secretion. The indirect mechanism of Helicobacter Pylori is realized by the urease secretion which creates an alkaline environment around the gastrin secretory cells, thus stimulating the gastrin secretion and so the hypersecretion.
 
2. The clorhydropeptic hypersecretion
Neither gastric ulcer nor duodenal ulcer can appear without acid secretion, with a higher role in duodenal ulcer. The most importante causes of HCl hypersecretion are: the increasing in number of secretory parietal cells by a genetic mechanism or by hypergastrinemia; the vagal hipertony; the hypersensitivity of parietal cells to vagal stimuli; gastric motility disorders(grown up in duodenal ulcer; with a permanent flux of acid into the duoden, and low in gastric ulcer with gastric stasis).
In addition to the increasing of HCl secretion, pepsin.

3. Billiary acids
They represent another aggressive factor, with ulcerogenous effect by the detergent mechanism on the lipids in the mucosal cells.
B.Defensive factors.
They are low in the ulcer disease, especially in gastric ulcer.Didactically, they are topographically grouped in three:

1. Preepithelial, represented by:

• surface mucus,important in gastric and duodenal mucosal defense,forming a viscous “unshaken” insolubre mucus gel layer, opposed to the retro diffusion of H ions, and lubricating the mucosa;
• bicarbonate ions secreted, which create a neutral pH gradient (7) compared to the acid pH (1-2)in the gastric lumen.

2. Epithelial, represented by the integrity of apical membrane of gastroduodenal mucosa.

3. Postepithelial – vascular, the capillaries having a nutritive role (they bring bicarbonate ions and take away H+ ions).
C. Environmental and individual factors:
Environmental factors, which are considered ulcerogeneous, are:
cigarette smoking by lowering the pancreatic alkaline secretion and canceling the inhibiting mechanisms of acid secretion;
drugs with ulcerogenous potential: aspirin and NSAIDS
other factors: stress, chronic alcohol intake and different alimentary diets.
Individual factors are genetic; there is definite proof of familial aggregation and the existence of genetic markers.
Diagnosis of gastro-duodenal ulcer
The clinical diagnosis. The characteristic pain, linked to food intake (“painful hunger” in duodenal ulcer), the apparition of pain mostly in spring and autumn are typical signs that may suggest an ulcer. However, lately, ulcers discovered endoscopically in the absence of typical symptoms have been reported more and more frequently. Other times, the onset may be dramatic, by a superior digestive hemorrhage (hematemesis and/or melena) or an ulcerous perforation.


Pain is the cardinal symptom in ulcer.
Other symptoms :

• vomiting
• abdominal indigestion
• weight loss
• fatigue

Paraclinic diagnosis is established by endoscopy (gastroduodenoscopy). In the same time, endoscopy allows the biopsy in gastric ulcer, which will show the benign or malignant character of the ulcerous crater. It also evaluates the healing of the ulcer, by proving the scar.
The X-ray
Helicobacter Pylori  detection - causal agent in most gastroduodenal ulcers, is a compulsory diagnostic element in the strategy of ulcer evaluation, having as a purpose a subsequent therapeutic attitude. The Helicobacter Pylori detection is made by direct and methods:

• direct methods require endoscopy with obtaining a series of gastric biopsies from which Helicobacter Pylori is histological determined by urease test (based on the changing of a pH indicator color in the presence of Helicobacter Pylori which produces a high quantity of urease), or by culture on special media-in microaerophile medium).
• indirect methods: determination of antibodies anti Helicobacter Pylori in serum or blood or the respiratory tests. The anti Helicobacter Pylori antibodies may be determined also in the saliva and the eradication of Helicobacter Pylori infection may be more recently determined by the bacteria detection in stool.

Differential diagnosis
Based on the clinical symptomatology, the differential diagnosis of gastroduodenal ulcer must be done with other sufferings of the upper abdomen, such as gastric neoplasia, gastric lymphoma (diagnosed compulsory by endoscopy with biopsy), gallstones (diagnosed by ultrasonography), chronic pancreatitis or functional dyspepsia – (“ulcer-like”).
The endoscopic differentiation of a gastric ulcer must be done with an ulcerated neoplasm, which makes the prelevation of biopsies compulsory in every gastric ulcer, at diagnosis and at healing check-out.
Evolution of gastro-duodenal ulcer
The evolution of gastroduodenal ulcer has sensitively improved, thanks to the apparition of  new antisecretory drugs extremely potent (H2 blockers or H+ K+ ATP-ase pump blockers); the evolution is favorable in most cases, the complications have been reduced, and the cases requiring surgery are relatively rare. In addition the introduction of anti-Helicobacter Pylori therapy has brought to a maximal decreasing of ulcerous recurrences.

Complications

• superior digestive hemorrhage (hematemesis and/or melena).
• ulcerous perforation with acute abdomen picture. Penetration is a covered perforation in the neighbor organs.
• pyloric stenosis
• ulcer malignization (possible in gastric ulcer, but never in the duodenal ulcer).

Prognosis
Ulcerous disease prognosis has improved a lot in the last decades, and mostly in the last decade,when, by a correct therapy of Helicobacter Pylori eradication, the risk of ulcerous recurrence has decreased fewer that 10% / year,compared to an annual recurrence of over 70% in the absence of Helicobacter Pylori eradication. The, mortality in ulcerous disease is increased mostly in the patients aged over 75 years with superior digestive hemorrhage.

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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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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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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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Cholelithiasis diagnosis

Image source

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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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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