Dyspepsia 1

DR. ADORATA COMAN

Dyspepsia

� That means symptoms localized in upper abdomen, caused by superior digestive tract. We must take in count another causes: structural, organical, biochemically or bacteriological.

- Its incidence: 30 – 38% on general population

- 50% of gastro-enterology "diseases"

- main age: 25 – 50years male : female = 1:2

� Depends of alcohol intake and smoking.

� An important economical cost.

Dyspepsia

We define "dyspepsia" like an association of heterogenousdisturbances, but, in fact and practice, there are some types ofdyspepsia:

1. Like gastro – oesophagial reflux;

2. Dysmotility like;

3. Ulcer like;

4. Biliary tract disturbances like;

5. Flatulence.

Classifications (By A.M. Caballero Plasencia and co. (1990)): I. Organic dyspepsia: about 50 – 60%

II. Functional dyspepsia: 1) irritative acidity - bilio – pancreatic secretion

2) nervous

3) motility

4) esential

Dyspepsia - organic disorders:1) gastro–duodenal – ulcer – 20 – 28%

– cancer, gallblader stones

– hyatal hernia and reflux oesophagitis

– acute gastritis

– mesenterical ischaemic diseases

– chronic inflammatory disease of the bowel

2) systemical diseases – chronic renal failure, panarteritis nodosa, systemic lupus dis.

3) urinary tract dis. → stones, infections

4) vertebral column dis. – morbpott, artrosis

5) genitally diseases

6) metabolic diseases – diabetes, hydro – electrolites disturbances

7) endocrinological dis. – thyroid or parathyroid disturbances

8) cardio–vascular dis. – cardiac failure, pericarditis

9) other

Dyspepsia - functional disorders:

1) irritative – gastric hyposecretion/hyper

– reflux gastro–oesophageal

Duodeno–gastric – anti–inflammatory drugs

2) nervous → stress, anxiety, depression

3) motility → specific disorders: – oesophageal diffuse

– gastroparesis

– pilore, cardial spasm

4) idiopathic 15%.

Dyspepsia - treatment

– antispastic drugs: papaverinederivates, mebeverine,

- 5HT receptor agonists, trimebutine,

– prokinetics – domperidone, eritromicyne,

-metoclopramide – central and peripheral effects: increase gastric dopa agents (d2) clearing

– colecistokinine.

Treatment for non-ulcer dyspepsia:

1) external factors: no alcohol, diet

2) psychological therapy

3) hypersecretion: inh. H2, IPP, other antisecretoryagents

4) motility troubles: prokinetics

– motilium

– prepulside (cisaprid)

5) Helicobacter pylori:

Pathological enthity on oesophagus

(oesophagial syndrom)

1. Reflux oesophagitis (GERD)

– dysphagia = difficulty in swallowing

– heart burn = burning retrosternaly

+ odynophagia = pain on swallowing

+ vomiting (regurgitation without nausea)

+ hypersialic secretion

Pathological enthity on oesophagus

2. Oesophagus dyverticulitis

– pharynx – oesophagus diverticul – quintously cough

– sense of strange body

– odynophagia

– regurgitation

– thoracic dyverticul due to traction – larynx compression

– epiphrenic dyverticul – mediastinal compression

+ hiccup

Pathological enthity on oesophagus

3. Oesophagial cancer

– odynophagia (pain)

– contiously evolutive dysphagia

+ regurgitation

+ vomiting

+ general signs of malignancy

4. Oesophagial peptic ulcer

– dysphagia + odynophagia

– acid regurgitation (on clinostatism)

+ belching

Dysphagia

Muscle disorders: Organic lessions:

– fluctuating in time – evolutive dysphagia

– both solids + liquids (first solids, then liquids)

– steady

Causes: diffuse spasm of oesophagus Causes: oesophagus disorder

– achalasia – neighbouring disorder

(mediastinal)

– neurological diseases – general disorders

(e.g. atherosclerosis (colagenosis)

diabetes mellitus

colagenosis

endocrinopathies)

Acute oesophagitis� Def.: acute inflammation of oesoph., mucosis secondary to

infection, chemical, mechanical agents postcaustic (75% –caustic/corosive agents).

� Histology: – acute necrosis – 1–4 days

– granulations tissue – reparatory reaction after necrosis with neoformation vassels – 1 – 2 weeks

– healing with seals – after 3 weeks – 3 months stenosisclinics – hard pain – chest, epigastrum

� Exam: – dysphagia

– necrosis on jugal mucosis and tongue

– dyspnea by laringeal oedema, fever

- Possibly shock, septicemic status.

� Diagnosis: – anamnesis, clinical exam.

– fibro–endoscopy – first → 8 – 72 hours

– early → oedema, shock

– later → stenosis

Acute oesophagitis

Treatment:

– shocking pain status → morphine or derivates

– tampon solution (alcaline)

– antibiotics if necessary risk of mediastinitis.

– after 2 infections, prevention necessary, avoid complication.

– specific feeding – Einhorn tube – 3 weeks – oesophageal

dilatation/surgical,

- gastrostomy, enterostomy, temporary.

Chronic peptic oesophagitis

� Pathogeny: chronic inflammation due to chlorhidropeptic

aggresivity lower oesophagial sphincter has lower pressure

than normal.

Predisposing factors: obesity, gestational, pilor stenosis,

great abdominal tumors, hiatus hernia

� Clinic: – heartburn

– regurgitation with high acidity

– others: iron taste, interscapular pain, bleeding,

cough alcohol intolerance

� Positive diagnosis – oesophagoscopy + X ray

Chronic peptic oesophagitis

� Differential diagnosis: – achalasia

– oes. Cancer

- Ulcer

– ischaemic cardiopathy

– scleroderma complication

� Complications: – bleeding with anaemia

– oesophagial stenosis

– upper respiratory ways perforation – on

� Treatment: – diet (low fat), little intake, not later

– antiacides

– no smoking

– no anticholinergic agents

– others: nitrates, Ca inhibitors, antispastics.

Oesophageal peptic ulcer

Lower oesophageal tract, after 40 years, male : female = 2:1

� Pathology: after g. – oe., reflux on oesophagitis lesions

� Clinics: heartburn, dysphagia, epigastric pain, immediately after meals.

� Diagnosis – X ray, oesophagoscopy

� Differential: – peptic oesophagitis

– gastric ulcer or gastric cancer

� Evolution/complication: – chronic evolution

– healing – rarely

– complications: bleeding, perforations

� Stenosis treatment

– diet

– medication

– surgical selective vagotomy, tumoral oesophagectomy

Mallory–Weiss syndrome

– violent emesis, cough → rises

intraabdominal pressure

– tears on mucosal oesophago –

gastric jonction

– anamnesis

– haemorrhages after effort of

cough retching

– oesophagoscopy

Oesophageal tumors

– non specific symptom –

progressive dysphagia

retrosternal pain

– diagnosis – x ray

– endoscopy + biopsy

– treat. – surgical

Peptic ulcer disease

A common and costly medical problem.

Associated factors:

- age,

- sex,

- race,

- nonsteroidal medication use,

- cigarette smoking,

- family history.

Pathogenesis: Peptic ulcer may be regarded as resulting from an

imbalance of aggressive and defense factors.

Gastric secretion

Normal values: 1,5 – 2 mEq/l

women 2/3 – 3/4 by males

Utility: – for complementary diagnosis of: Ellison – Zollingersyndrom

lack of chloride acide (i.e. Biermer anaemia)

gastric ulcer (lack of acidity with no pick after pentagastrine)

hipersecretion of chloride acid after gastric resection which associate peptic ulcer

– stimulated secretion – by histamine (pentagastrine) s.c. 6µg/kg

– duodenal ulcer – increases x10

– Ellison – Zollinger syndrome – increases X100 – 1000

Biermer anaemia – atrophic gastritis →achlorhidria histamine –refractory, – no basal secretion, – no stimulated secretion

Aggressive factors:

� Hydrochloric acid is the most important, increased acid secretion is found in only to 50% of patients with duodenal ulcers. This suggests that other factors, such as proteolyticenzymes and bile acids are also important in causing peptic ulcer disease.

� In addition to the standard etiologic factors, Helicobacter pylori, a gram–negative bacteria, is thought to play a role in peptic disease.

Protective factors:

� mucus and

� bicarbonate secretion and

� mucosal blood flow, which are increased by endogenous prostaglandin production. Surface epithelial cells also play an important role in mucosal defense, both by limiting the influx of hydrogen and by restitution, a process in which the migration of epithelial cells over denuded mucosa protects the submucosa from damage.

Peptic ulcer

Clinical presentation

� Pain - is the most complaint in patients with peptic ulcer.

- described as sharp, gnawing, burning, or hunger pain

- usually is well localized in the upper part of the epigastrum, and may radiate to the back, particularly when the ulcer is posterior or penetrating

- often occurs when the stomach is empty, or awakens the patient from sleep an hour or so after midnight.

- is typically improved by ingesting food

- is characteristically intermittent, with periodic exacerbations

� Vomiting can occur in the absence of outlet obstruction. This appears to be more common in patients with channel ulcers and may be related to alterations in atrial motility.

� Complications of peptic ulcer include obstruction, bleeding, and perforation. Occasionally, otherwise asymptomatic patients with duodenal ulcer present anemia, secondary to chronic bleeding.

Diagnosis

� History: medication usage,AINSD.

� Physical examination:

- normal in patient with uncomplicated duodenal ulcer.

- complications: abdominal pain and perithoneal signs suggesting a perforation, or a succussion splash suggesting gastric outlet obstruction.

� Laboratory studies

- blood test for occult blood and haemograms.

- people under 40 years old who have symptoms consistent –with uncomplicated peptic ulcer may be treated with H2–blocker

therapy or antacids as needed, for pain. If the symptoms persist it must be done EDS/Xray.

- serum gastrine levels should be obtained in patients with severe recurrent peptic disease (to exclude gastrinoma).

Diagnosis

� Upper gastrointestinal endoscopy: (sensitivity of 95%). Gastric ulcer should be followed to healing so that nonhealingulcers can be biopsied to exclude malignancy. Is also necessary when evaluating patients with serious complains and normal –appearing X–rays, patients with bleeding, or those who are being considered for peptic ulcer surgery.

� Gastric secretory testing

Acid output is normally greater in men than women anddecreases with age.

Gastric secretory testing is useful when Zollinger–Ellison syndrome is suspected, serum gastrines levels is elevated, or a recurrent ulcer follows ulcer surgery, suggesting an incomplete vagotomy.

Complications

� Hemorrhage (10 to 20%): the blood loss may vary from massive hemorrhage to chronic, occult bleeding, leading to iron deficiency anemia. Once a patient has bleed from a duodenal ulcer, the chance of rebleeding is 30 to 50%.

� Penetration occurs when duodenal ulcers erode through the serosa and adjacent tissue such as the liver or pancreas. It is heralded by increasing pain that radiates into the back and may be intractable.

� Perforation is a catastrophic event, accompanied by acute severe abdominal pain. Surgery remains the treatment of choice.

� Gastric outlet obstruction (pyloric) : "typical" presentation, a patient with long – standing ulcer symptoms develops constant pain and then vomiting. The vomiting may be severe and lead to weight loss, dehydration, and hypokalemic (and ultimately hypochloremic) alkalosis. Obstruction may be caused by edema and inflammation or by scars.

� The ulcer is called refractory if symptoms continue recur after 1 to 2 weeks in a patient receiving a good medical regimen, or if relapses to come longer and more severe and remissions shorter.

Treatment

1. H2 blockers: the H2 receptor antagonists (cimetidine, ranitidine, famotidine, and nizatidine) are potent inhibitors of gastric acid secretion:

- Cimetidine 800 mg at bedtime or 400 mg twice daily;

- Ranitidine 300 mg at bedtime or 150 mg twice/daily;

- Famotidine 40 mg at bedtime or 20 mg twice daily;

Full – dose therapy, administrated for 6 to 8 weeks, with healing rales of about 90%.

2. Antacids – alchalines substances

Important features in the choice of an antacid include:

- neutralizing capacity, magnesium content (which causes loose stool), aluminiumcontent (which is constipating), sodium content, taste and cost.

The usual dose is 20 ml of "concentrated" antacid or 30 ml of regular antacid approximately 6 times a day. Antacids are more effective when taken 1 and 3 hours after meals, but for greater effectiveness absorption should not be taken within 30 minutes of sucralfate or other agents such as antibiotics.

3. Coating agents

Sucralfate (carafate), a sulfated disaccharide, binds to the protein debris in the ulcer crater and blocks penetration of acid and pepsin and also binds bile acids and enhances localized endogenous prostaglandin production. When taken 4 time a day, sucralfate has been shown to be comparable to h2 – blockers.

Treatment

4. Anticholinergics are rarely used. They can be given with antacids or histamine h receptor antagonists to patients whose ulcer is difficult to control; however anticholinergic have been largely replaced by other agents because of lower efficacy or a high incidence of side effects.

5. IPP drugs, Omeprazole, Pantoprazole, Esomeprazole, a proton pump inhibitor, is capable of almost complete elimining gastric acid secretion.

6. Misoprostol (cytotec) is a synthetic prostaglandin (prostaglandin E) that has been shown to be more effective than cimetidine in protecting the gastric mucosa from nonsteroid induced injury.

7. Helicobacter pylori treatment

In patients with recurrent symptoms who are unresponsive to the usual medical referral for upper endoscopy with biopsies to evaluate for the presence of helicobacter indicated.

Biopsy – proved helicobacter may be treated with amoxicilin(250 mg) metronidazol (250 mg tid), claritromycine, tetraciclyne, azytromycine for 2 weeks and pepto – bismol (qid) for a month.

Recurrence of helicobacter is common following treatment.

Acute gastritis

There are acute inflammation of gastric mucosa due to a number of factors of:

� exogenous origin: alcohol, aspirine, cortizon, salicilatcs bases, acids, microbe agents, alergens, thermal agents, x ray.

� endogenous origin: infection (influenza, dyphteria, etc.).

Clinics:- epigastrium pain – chief symptom, continuous – exacerbated by food ingestion

– emesis postprandum (gastric intolerability)

– anorexia, fever

Treatment of – 2 – 3 days exclusively hydric (500 ml) (water, tea) then, 2 – 3 days – vegetable soup, apple, cheese, then 2 – 3 days – bread, boiled meat then – normal diet.

Medication: – IPP, antiacides, antispastic drugs.

– local warm upon epigastrum.

Chronic gastritis

Influenced by various factors external/internal, local or general it appears diffuse chronic lesions with progresive inflammation.

� Factors: 1) traumatics – no hygienic diet, too cold, too hot

- Tachyphagia

- Insufficient masticatio

- Alcohol, smoke

- Drugs – chronic disease (renal failure, infectious diseases)

2) alergical and immunological (i.e. Autoantibody, athrophic g.).

3) hypochromic feriprive anemia

4) duodenal secretion reflux into gastric contents

5) gastric stasis (e.g. – gastritis secondary to pilor stenosis)

6) other – associated with – pernicious anemia

– diabetes mellitus

– tyroiditis, gastric poliposis

Chronic gastritis

� Clinics – asymptomatic – possible

– symptomatic – no characteristics

– epig. pain – no periodicity/continuous

– emesis heartburn, low apetite with signs – epig. sensibility

� Diagnosis: - endoscopy and biopsy. - X ray with barium –relative images due to hypertrophy and atrophy of gastric

mucosa.

� Treatment – to be excluded pathological factors

– diet

– antiacids, gastric protection

– hydro – mineral equilibration,

–– antiacids, IPP, anticholinergic drugs to be associated.