Diseases of Gastrointestinal Tract Questions And Answers
Question 1. Write Short notes on Stomatitis.
Or
Write Notes On Stomatitis.
Answer. Stomatitis is the inflammation of the mouth and is caused by bacterial, viral, and fungal infections in persons with poor oral hygiene or with blood dyscrasias.
Causes of Stomatitis
- Local Causes of Stomatitis
- Poor oral hygiene
- Excessive use of tobacco
- Alcohol and spices
- Use of broad-spectrum antibiotics
- Drugs such as iodine or gold.
- General Causes of Stomatitis
The main general causes are infectious diseases. There are various types of infective stomatitis:- Bacterial, e.g. streptococcal stomatitis and Vincent’s stomatitis
- Viral, e.g. herpes simplex and herpes zoster
- Fungal, e.g. candidiasis and actinomycosis
- Recurrent aphthous stomatitis
- Mucocutaneous diseases, e.g. Lichen planus, pemphigus vulgaris, lupus erythematous, etc.
- Miscellaneous, e.g. diabetes, uremia, and drug toxicity.
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Clinical Features of Stomatitis
- Lip, tongue, and gums are inflamed, swollen, and painful.
- The tongue is furred and a foul smell is present.
- Sometimes ulceration of the mucus membrane is present when a person is suffering from infectious stomatitis.
- The patient feels pain and difficulty in opening the mouth.
- There was an *excoriation and redness of the mucus membrane of the oral cavity.
General Medicine BDS 3rd Year Question and Answers
Treatment of Stomatitis
- If the drug is the causative factor discontinuation of the drug is done.
- It allergen is the causative factor remove allergen.
- Antihistaminic drugs such as cetirizine are to be given to the patient.
- Topical corticosteroid application should be done.
- Triamcinolone acetate is effective.
- Tetracycline mouthwash should be given which should be used four times a day for 5 to 7 days.
- Nutritional supplements are to be given such as vitamin B12, iron, and folic acid.
Question 2. Write Short notes on Chronic Gastritis.
Answer. When the acute gastritis remains for a longer time and is not treated, it becomes chronic and is known as chronic gastritis.
Etiology of Chronic Gastritis
- Repeated injury to gastric mucosa by tea, coffee, alcohol, spices
- Infection from the throat, teeth, gums, and sinuses
- NSAIDs
- Autoimmune pathology
- Very hot beverage
- Gastrectomy.
Types of Gastritis
- Superficial
- Atrophic
- Hypertrophic
- Infectious
- Eosinophilic.
There are mainly two types of chronic gastritis:
- Type A gastritis
- Type B gastritis.
Type A Gastritis (less common)
- It involves the body of the stomach and spars antrum.
- It is caused by autoimmune disorders like type I diabetes mellitus, Sjögren’s syndrome, Graves disease, Hashimoto disease, myasthenia gravis, etc.
- It is caused due to autoimmune activity against parietal cells.
- Parietal cell antibodies can be detected in serum.
- In severe cases, parietal cell atrophy leads to a deficiency of intrinsic factors which leads to pernicious anemia.
- The disease is asymptomatic and the long-term complication is gastric carcinoma.
Treatment of Type A Gastritis
- In severe cases, corticosteroids are administered.
- In mild cases, parenteral iron should be administered.
Type B Gastritis
- This is a more common form of gastritis and involves the antrum of the stomach.
- The usual cause is gramnegative bacteria H. pylori.
- The condition is the precursor of peptic ulcer.
- There is the possibility of gastric carcinoma.
Diagnosis of Type B Gastritis
- Gastric acid study, i.e. achlorhydria
- Hemoglobin decreases
- Serum gastrin increases.
Management of Type B Gastritis
- Anti H. pylori treatment
- Triple drug therapy: Proton pump inhibitor or ranitidine 400 mg BD + Bismuth subcitrate + Amoxicillin 1 gm or clarithromycin 500 mg or metronidazole 500 mg BD
- Quadruple therapy: Omeprazole 10 mg BD + Tetracycline 500 mg QID + Bismuth subcitrate QID + Metronidazole 500 mg TDS.
In both cases, 14 days course is preferred.
- Parenteral vitamin B12 is administered.
Question 3. Describe the management of Acute Diarrhea.
Answer.
General Management of Acute Diarrhea
- Rest, maintenance of fluid, and electrolyte balance.
- ORS should be given to all children as early as possible.
- Patients with constant vomiting or moderate to severe dehydration require IV fluid.
- Ringer lactate is ideal, normal saline may be given.
Treatment of Antimicrobial/ antidiarrheal
- Ciprofloxacin 500 mg BD for three days or nalidixic acid 1 gm 6 hourly for 5 to 7 days.
- It may be combined with the tinidazole 300 mg BD for 6 days
General Medicine BDS 3rd Year Question and Answers
Antimotility Agent of Diarrhea
This should be used in children before 5 years of age.
- Loperamide or diphenoxylate atropine.
- Codeine could be used.
- Sodium and water-conserving agent, i.e. racecadotril is the newer drug safely given in children and adults.
It reduces the loss of sodium and water in the stool.
Causes Of Acute Diarrhea.
- Acute Diarrhea
- infective diarrhoea
- Bacterial: The bacteria which cause acute diarrhea are
- Shigella, Salmonella, E.coli, etc.
- Viral: The viruses which result in diarrhea are
- parvovirus, Hawaii, etc.
- Protozoal: The protozoans are Ehistolytica, giardia, etc.
- Toxic and systemic causes
- Some drugs result in acute diarrhea, i.e. broad-spectrum antibiotics.
- Noninfective diarrhoea
- Crohn’s disease
- Irritable bowel syndrome
- Acute psychological stress
- Drugs such as amoxicillin, antacids, cholinergic, etc.
- infective diarrhoea
- Chronic diarrhea
- Ulcerative colitis
- HIV associated enteritis
- Whipple’s disease
- Pancreatic insufficiency
- ZollingerEllison syndrome
- Medullary carcinoma of the thyroid
- Irritable bowel syndrome.
Question 4. Outline The Management Of Amoebic Liver Abscess.
Answer.
Investigation of Amoebic liver abscess
- TLC and DLC: Leukocytosis is present.
- Stool study shows cyst.
- Sigmoidoscopy: Ulcers are seen.
- USG.
- Aspiration study.
- Immunofluorescence test for autoantibodies
Management Of amoebic liver abscess/Hepatic Amoebiasis
- Early cases are responding well with metronidazole 800 mg TID for 5 days or tinidazole 2 gm daily for three days.
- Luminal amoebicide: Diloxanide furoate 500 mg 8 hourly for 10 days should be given to determine the luminal cyst.
- If the abscess is large and does not respond to chemotherapy repeated aspiration under ultrasonic guidance is required.
- Rupture of the abscess into the peritoneal cavity requires immediate aspiration or surgical drainage.
Question 5. Write a Short Note On Malabsorption Syndrome.
Or
What Is Malabsorption Syndrome, Causes Of Malabsorption, Clinical Features And Its Management?
Answer. Malabsorption syndrome comprises a large number of pathological conditions in which there is a disturbance of processes by which nutrients are transferred from the lumen of the intestine into circulation.
Etiology of Malabsorption
- Stomach:
- Precipitate emptying after postgastrectomy dumping.
- Lack of intrinsic factor.
- Excess acid secretion in ZollingerEllison syndrome.
- Pancreatic: Inadequate enzyme and bicarbonate secretion.
- Biliary: Due to defective micelle formation.
- Endocrine diseases
- Parasitic or drug.
Various diseases along with their etiologies can cause malabsorption as: - Disorders of intraluminal digestion
- Pancreatic enzyme deficiency in chronic pancreatitis, cystic fibrosis, and pancreatic carcinoma
- Disturbances of gastric function after gastroenterostomy and partial gastrectomy
- Deficiency of bile acids in Crohn’s disease, resection of terminal ileum, stagnant loop syndrome, or blind loop syndrome.
- Disorders of transport in the intestinal mucosal cell
- With histologically abnormal mucosa (infiltration, inflammation, or infection of mucosa) in coeliac disease, tropical sprue, lymphoma, Whipple’s disease, giardiasis and radiation enteritis
- With histologically normal mucosa (genetic diseases) in lactase deficiency, pernicious anemia
- Disorders of transport from mucosal cells in abdominal lymphoma, tuberculosis, telangiectasia of mesenteric lymphatics, beta hypoproteinemia,
- Impaired nutrient uptake in lymphatic obstruction, cardiac heart failure, and pericarditis
- Miscellaneous: Diabetes mellitus, hyperthyroidism, hyperparathyroidism
Clinical Features of intestinal mucosal cell
- *Steatorrhea is presenting symptoms.
- Diarrhea or abdominal discomfort.
- Nutritional deficiencies, i.e. deficiency of vitamins A, D, B12, and K
- General features like anemia, sore mouth, loss of weight, fatigue, and lethargy.
- Bone pain may be present.
- Skin changes like pellagra are present
- The patient also suffers from peripheral neuropathy, irritability, and lack of confidence.
Investigations of intestinal mucosal cell
Tests are carried out to detect nutritional deficiencies.
These tests indicate the malabsorption of a particular nutrient and not its cause.
- Fecal fat stimulation: It confirms steatorrhea and fat malabsorption.
Sudan III stain may show an increase in stool fat. Quantitative estimation of fat in the stool is more reliable and sensitive.
A 72hour stool collection while the patient is on a defined diet is used for fat estimation.
Excretion of more than l0 g fat per day suggests fat malabsorption. - Schilling test: This is useful in the diagnosis of cobalamin (B12) malabsorption and its causes like pernicious anemia, chronic pancreatitis, achlorhydria, and bacterial
overgrowth. In this test, radiolabelled cobalamin (l mg 68°C) should be given orally and its excretion in urine is measured. 1 mg cobalamin is administered intramuscularly to saturate hepatic binding sites so that all radiolabelled cobalamin is excreted in the urine.
The test is abnormal if less than l0% of the radiolabelled cobalamin is excreted in the urine in 24 hours.
This will help in differentiating the various defects responsible for the malabsorption of cobalamin. - D-xylose test: It detects carbohydrate malabsorption. 25 g of Dxylose is given orally and its excretion is measured in urine.
Excretion of less than 4.5 g in 5 hours is suggestive of malabsorption. - Upper gastrointestinal endoscopy and biopsy of small intestinal mucosa: It is essential for the diagnosis of conditions like tropical sprue, celiac sprue, Whipple’s disease, and Crohn’s
disease. - Barium meal contrast radiography: Radiological assessment of the small intestine with barium contrast is helpful in the evaluation of structural abnormalities in Crohn’s disease,
diverticulae and strictures. - Pancreatic exocrine functions: They should be carried out in patients with steatorrhea.
- Serological studies: In some of the conditions such as celiac sprue and pernicious anemia autoantibodies are detected.
- Small intestinal biopsy (duodenal or jejunal): It is carried out for conformational diagnosis.
Management of intestinal mucosal cell
- Diet: A high-protein and low-fat diet is taken.
- Digestants: Pancreatic enzyme preparations are administered after meals.
- Treatment of anemia: All three hematinics vitamins B12, folic acid, and iron given.
- Vitamin supplements: Vitamin B complex and vitamin D are given.
- Treatment of diarrhea: Codeine and loperamide are administered.
- Steroids: Prolonged therapy with prednisolone is given.
- Elimination of bacterial overgrowth: Tetracycline 250 mg TDS for one week.
Question 6. Write a Short Note On Bacillary Dysentery.
Answer. Bacillary dysentery is mainly caused by Shigella.
Etiology of bacillary dysentery.
- It occurs because of contaminated food or files.
- It is caused by unwashed hands after defecation.
- It is also caused due to wars and natural calamities which
- causes poor sanitation and crowding.
Clinical Features of bacillary dysentery
- Diarrhea, colicky abdominal pain, and tenesmus, i.e. spasmodic contraction of the anal or bladder sphincter with pain.
- Fever, dehydration, and weakness with tenderness over the colon.
- Arthritis may be seen.
Management of bacillary dysentery
- Oral rehydration therapy is given.
- IV replacement of water and electrolyte loss is necessary.
- Ciprofloxacin 500 mg 12 hourly for two days is given.
- Antidiarrheal medication is given.
Question 7. Differentiate Between Gastric Ulcer And Duodenal Ulcer.
Answer.
Question 8. Discuss Causes Of Acute Gastritis.
Answer. The causes of acute gastritis are:
- NSAIDs and analgesics: They not only cause gastric erosion by predisposing to peptic ulcer.
- Antimitotic drugs
- Renal failure
- H.pylori initial infection
- Other infections, i.e. streptococcal, viral, fungal, etc.
- Iron therapy
- Stress and burns
- Postoperative.
Question 9. Enumerate The Causes Of Upper Gi Hemorrhage.
Answer. The causes of upper GI hemorrhage are:
Esophageal causes
- Esophageal varices
- Esophagitis
- Esophageal ulcers
- Esophageal cancers.
Gastric causes
- Gastric ulcer
- Gastric cancer
- Gastritis
- Gastric varices.
Duodenal ulcer
- Duodenal ulcer
- Vascular malformations
- *Hematobilia
- Bleeding from the pancreatic duct
Question 10. Outline the treatment of acute gastroenteritis.
Answer. Inflammation of the stomach and intestinal tract that causes vomiting, diarrhea, or both.
Treatment acute gastroenteritis
- Rehydration with liquid is the keyword to avoid dehydration and electrolytic imbalance.
- Antidiarrheal treatment is given, i.e.
- Antimicrobial agent
- Ciprofloxacin 500 mg BD for three days or nalidixic acid 1 gm 6 hourly for 5 to 7 days. It may be combined with the tinidazole 300 mg BD for 6 days.
- Antimotility agent
This should be used in children before 5 years of age.- Loperamide or diphenoxylate atropine.
- Codeine could be used.
- Sodium and water-conserving agents, i.e.
Racecadotril is the newer drug safely given to children and adults. It reduces the loss of sodium and water in the stool.
- Antimicrobial agent
General Management Acute Gastroenteritis
- Rest, maintenance of fluid, and electrolyte balance.
- ORS should be given to all children as early as possible.
- Patients with constant vomiting or moderate to severe dehydration require IV fluid.
- Ringer lactate is ideal, normal saline may be given.
Question 11. Write a short note on dysphagia.
Or
Write a short answer on dysphagia.
Answer. Dysphagia is defined as difficulty in swallowing.
Causes of Dysphagia.
- Disease pertaining to the esophagus and its surrounding structures.
- Stomatitis
- Pharyngitis
- Glossitis
- PulmmerVinson syndrome
- Esophagitis
- Carcinoma of esophagus
- Pressure by a mediastinal tumor on the esophagus
- Achalasia (Failure of reflex) of the lower end of the esophagus.
- Dysphagia in neurological disorders
- Postdiphtheric paralysis
- Myasthenia gravis
- Motor neuron disease
- Scleroderma or other related collagen disorders
- Acute bulbar paralysis.
Clinical Features of Dysphagia
- Presence of anemia
- Koilonychia
- Glaze tongue
- Malnutrition
- Nasal regurgitation
- Bulbar palsy
- Severe weight loss
- Malignancy
- Chest pain
- Hoarseness of voice
Treatment of Dysphagia
Dysphagia is a symptom complex of a number of diseases hence treatment has to be planned depending on the etiological factors.
Question 12. Write a short note on gastroesophageal reflux disease.
Answer. A chronic condition in which the lower esophageal sphincter allows gastric acids to reflux into the esophagus, causing heartburn, acid indigestion, and possible injury to the esophageal lining.
Mechanism
Etiology of gastroesophageal reflux disease
- Relaxed or hypotonic sphincter: It is due to diabetes mellitus, hiatus hernia, and fatty meal.
- Decreased lower esophageal sphincter pressure: This is due to prolonged gastric tube intubation, scleroderma, and the use of certain drugs such as calcium channel blockers, and nitrates.
- Raised intra-abdominal pressure: It is due to ascites, obesity, and pregnancy.
- Impaired esophageal mucosal function: It is due to the usage of alcohol and smoking.
- Delayed gastric emptying: This is due to pyloric obstruction, fatty foods, and gastroparesis.
- Increased gastric contents: It is due to large meals and ZollingerEllison syndrome.
- Sliding hiatus hernia: Where the esophagogastric junction slides up through the diaphragm resulting in:
-
- Loss of the obliquity of entry of the esophagus into the stomach.
- Loss of the reinforcing effect of intraabdominal pressure on the lower oesophageal sphincter.
These two above-mentioned factors of hiatus hernia facilitate gastroesophageal reflux but do not directly cause it.
- Cardiomyotomy and vagotomy: They decrease the efficiency of the lower esophageal sphincter.
Increased intra-abdominal pressure: Pregnancy, obesity, ascites, weightlifting, and straining increase intra-abdominal pressure. - Reduced tone of lower esophageal sphincter: Cigarette smoking, alcohol, fatty foods, and caffeine act by reducing the lower oesophageal sphincter tone.
- Impaired gastric emptying: Impaired gastric emptying due to obstruction of gastric outlet or use of anticholinergic drugs, fatty foods, and large-volume meals acts by increasing the gastric content available for reflux.
- Systemic sclerosis.
- Drugs that reduce the lower esophageal sphincter tone, e.g. aminophylline, betaagonists, nitrates, calcium channel blockers, etc.
Clinical Features of gastroesophageal reflux
- Typical symptoms: Heartburn and acid regurgitation
- Atypical symptoms: Dysphagia, Globus sensation, noncardiac chest pain, dyspepsia, or abdominal pain.
- Extra-esophageal symptoms: Hoarseness, sore throat, sinusitis, otitis media, chronic cough, laryngitis, dental erosion, and recurrent aspiration.
- Malignancy: Head and neck cancer, esophageal adenocarcinoma
Complications of gastroesophageal reflex
- Esophagitis
- Esophageal strictures
- Esophageal ulcers
- Aspiration pneumonia
- Iron deficiency anemia
- Barretts esophagus
- Carcinoma of esophagus
Investigations of gastroesophageal reflex
- Endoscopy: Enables visualization of esophagitis, strictures, and Barrett’s mucosa which all can be confirmed by biopsy.
- Barium meal can reveal a hiatus hernia.
- Bernstein test is done in patients with high clinical suspicion but with negative endoscopy.
- Resting ECG and stress ECG to rule out ischemic heart disease.
- Esophageal motility studies.
Management of gastroesophageal reflux
1. Conservative measures:
- Abstain from eating within 2 hrs of bedtime
- Elevate the head of the bed by 6 inches
- Sleep in the left lateral decubitus position
- Avoid: Caffeine, nicotine, alcohol, chocolate, mints, carbonated beverages, highfat foods, tomato or citrus-based products
- Avoid if possible medications that can worsen GERD anticholinergic, theophylline, prostaglandin, calcium channel blockers, alendronate
- Weight loss if obese
- Rabeprazole and esomeprazole provide superior gastric acid suppression.
2. Medical treatment of gastroesophageal reflux
- In mild cases liquid antacid is used, i.e. 10 to 15 mL, one to three hours after the meal which provides relief from heartburn.
- In moderate cases, H 2 receptor antagonist, i.e. ranitidine 150 mg BD or QID with meals and before bedtime for 6 weeks.
- In severe cases, proton pump inhibitors are given, i.e. omeprazole 20 to 40 mg/day, pantoprazole 40mg/day, and rabeprazole 10 to 20 mg/day is given.
These should be given for 6 to 8 weeks.
For maintenance therapy treatment should be given for 6 to 8 months. - Metoclopramide or domperidone 10 mg TID increases lower esophageal sphincter tone and promotes gastric emptying.
- Repeated dilatations are used to treat esophageal strictures.
- In anemics oral iron or blood transfusion is given.
3. Surgical treatment of gastroesophageal reflux
- Surgical resection of strictures should be carried out.
- Surgical return of lower esophageal sphincter to the abdomen in a patient with sliding hiatus hernia, construction of an additional valve mechanism is done.
Question 13. Describe the etiology, clinical features, and management of Intestinal Amoebiasis.
Answer.
Etiology of intestinal amoebiasis.
- Amoebiasis is caused by infection by a protozoan parasite known as Entamoeba histolytica.
- A common source of transmission is water especially when it is contaminated by fecal matter or sanitary conditions of the water supply being defective.
- Flies spread infection by feeding on fecal matter or contaminated food.
- Autospread in a patient when cysts are embedded underneath the nails and a person may get infected if he has not properly washed his hands.
Clinical Features of Hepatic Amoebiasis
Symptoms Hepatic Amoebiasis
- The patient has diarrhea and passes 10–15 stools per day.
- Presence of abdominal pain.
- Stools consist of blood and mucus.
- Flatulence is present.
- Fever is present between 38 and 40° with rigors.
Signs Hepatic of Amoebiasis
- Palpation of the abdomen shows diffuse tenderness.
- Chronic cases show a thickened tender sigmoid colon.
- Amoeba is felt as a sausage-shaped mass in the right iliac fossa.
- Tender hepatomegaly is present.
Management of Hepatic Amoebiasis
- Diloxanide florate is given 500 mg TDS × 10 days.
- Metronidazole Or Ornidazole 500 mg TDS × 5 days
- Secnidazole plus 2 gm single dose is given
- Nitazoxanide 500 mg BD is given.
- Dehydroemetine 1.5 mg / kg / day × 5 days IM
Question 14. Write signs and symptoms of malabsorption syndrome.
Answer. Following are the signs and symptoms of malabsorption syndrome:
Symptoms of Hepatic Amoebiasis
- Presence of lassitude and laziness
- Mood fluctuation
- Fatigue and weakness are present
- Pain in the bone is present
- Weight loss is present.
Signs of Hepatic Amoebiasis
- Skin: edema over legs and purpuras
- Eyes: Xerophthalmia and night blindness
- Hematopoietic: Hemorrhagic tendencies are present, anemia
- Gastrointestinal system: Malnutrition is generalized, angular stomatitis, glossitis and diarrhea
- Genitourinary system: Hypotension, amenorrhea, loss of libido, Nocturia
- Skeletal: Muscle wasting, tetany, and presence of paresthesia.
- Nervous system: Peripheral neuropathy.
Question 17. Write acid peptic disease under the following headings:
Etiology
Clinical features
Investigations
Treatment
Answer. Excessive secretion of acid and pepsin or a weakened stomach mucosal defense is responsible for damage to the delicate mucosa and the lining of the stomach, esophagus, and duodenum resulting in ulceration which is known as “Acid Peptic Disease”.
“Acid peptic disease” is a collective term used to include many conditions such as gastroesophageal reflux disease (GERD), gastritis, gastric ulcer, duodenal ulcer, esophageal ulcer, ZollingerEllison Syndrome (ZES) and Meckel’s diverticular ulcer.
Etiology of acid peptic disease
- Helicobacter pylori: H.pylori is responsible for around 60–90% of all gastric and duodenal ulcers.
- NSAIDs: Prostaglandins protect the mucus lining of the stomach. Nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, diclofenac, and naproxen prevent the production of these prostaglandins by blocking the cyclooxygenase enzyme leading to ulceration and bleeding.
- Smoking, alcohol, and tobacco: Cigarettes, alcohol, and tobacco cause an instant and intense acid production which acts as though gasoline is poured over a raging fire.
- Blood group O: People with blood group “O” are reported to have higher risks for the development of stomach ulcers as there is an increased formation of antibodies against the Helicobacter bacteria, which causes an inflammatory reaction and ulceration.
- Heredity: Patients suffering from peptic ulcer diseases usually have a family history of the disease, particularly the development of duodenal ulcers which may occur below the age of 20.
- Steroids/other medicines: Drugs like corticosteroids, anticoagulants like warfarin (Coumarin), niacin, some chemotherapy drugs, and spironolactone can aggravate or cause ulcers.
- Diet: A low-fiber diet, caffeinated drinks, and fatty foods are linked to peptic ulcers.
- Other diseases: Chronic liver, lung, and kidney diseases especially tumors of the acid-producing cells all predispose to peptic ulcers. ZollingerEllison syndrome (ZES) is a rare precancerous condition that causes peptic ulcer disease.
Endocrine disorders such as hyperparathyroidism are also implicated in the development of peptic ulcers. - Stress: Stress and neurological problems can also be associated with Cushing’s ulcer and peptic ulcer.
Clinical Features of Hepatic Amoebiasis
- Abdominal Pain: A burning pain in the upper part of the abdomen usually related to mealtimes together with fullness, distension of the abdomen, bloating, with or without nausea, and generalized discomfort also known as “dyspepsia”. The pain is usually so sharply localized that the patient can often indicate the exact place with two or three fingers called the “pointing sign”. Gastric ulcer pain is more after the ingestion of meals while duodenal ulcer pain occurs more due to hunger.
- Nausea, heartburn, vomiting, loss of appetite, and weight loss.
- Gastric outlet obstruction: The ulcer could heal with scarring and result in narrowing of the gastric or intestinal lumen.
This could cause an obstruction to food being passed forward. - Vomiting or passing blood in stool: Signs of bleeding as vomiting of blood or black tarry color of the stool.
- Bleeding and perforation from the ulcer: Bleeding from the site of the ulcer with thinning of the wall may result in perforation.
Investigations of Hepatic Amoebiasis
- Blood tests: Blood tests such as ELISA help in the measurement of antibodies to H. pylori.
Serum gastrin levels should be measured in patients with multiple ulcers to consider gastrin-secreting tumors or Zollinger-Ellison syndrome. Tests for gastric secretion include the “pentagastrin test”, the “chew and spit test” and the “Hollander insulin test”. - Stool Test: The stool test detects the presence of H. pylori in the feces and also establishes whether there is any recurrence after antibiotic therapy.
- Breath test: The urea breath test (UBT) is helpful in the detection of H.pylori.
The patient is made to drink a liquid containing carbonlabeled urea, which is broken down by the bacteria.
The patient is subsequently asked to breathe into a sealed bag, which is tested for the presence of labeled carbon.
A positive test indicates the presence of H pylori infection. - Endoscopy: Endoscopy is considered a more accurate test for the diagnosis of “peptic ulcer diseases” and also helps in taking a biopsy of the affected area. Gastroscopy or esophagogastroduodenoscopy (EGD) is a kind of endoscopy that is carried out on patients to detect peptic ulcers.
- Barium radiography: Xrays are taken of the stomach, esophagus, and duodenum after swallowing barium and the retention of contrast in the ulcer is monitored.
Treatment of Hepatic Amoebiasis
- Eradication of. pylori: The standard protocol to eradicate pylori involves the use of two or three antibiotics, i.e. amoxicillin, tetracycline, clarithromycin, metronidazole, and the use of a proton pump inhibitor, i.e. esomeprazole, omeprazole, lansoprazole, rabeprazole, pantoprazole with or without a bismuth compound for around 2–3 weeks and repeated if there is recurrence.
- Avoid NSAIDs or the concurrent use of a prostaglandin analog (misoprostol) may be prescribed to prevent peptic ulceration due to NSAIDs.
- The use of antacids or H2 receptor antagonists (H2RAs) such as cimetidine, ranitidine, famotidine, and nizatidine helps in the reduction of gastric acid secretion and in turn, increases the gastric pH and reduces the secretion of pepsin.
- Treatment of peptic ulcer complications includes a blood transfusion for hematemesis and melena, the use of antacids and H 2 receptor antagonists for pain, and the treatment of peritonitis in case of perforation of peptic ulcer disease.
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