I. Answers A, C, and E are true statements, whereas B and D are false.
II. Answers A, B, D, and E are true statements, whereas C is false.
III. Answers B, D and E are true statements, whereas A and C are false.
IV. Answers A and C are false statements, whereas B, D and E are true.
V. Answers A, B, C and D are true statements, whereas E is false.
VI. Answers A, B, and C are true statements, whereas D and E are false.
1. The gastric acid secretion rate is (0.35 * 150) = 52.5 mmol per hour. This is obviously higher than normal, but an unspecific result.
2. The patient has lost 52.5 mmol of hydrochloric acid, and is now in an acute metabolic alkalosis comparable to the postprandial alkaline tide after a meal.
3. The alkalosis is normalised by two means. The fall in H+ of the ECF means a smaller respiratory drive, and the hypoventilation immediately accumulate CO2, whereby PaCO2 rises and pH of the extracellular space begins to fall. The final compensation of the alkalosis is renal. The fall in H+ of the tubular cells implies a smaller tubular H+ secretion and thus a smaller bicarbonate reabsorption. Hereby, the bicarbonate excess is excreted over hours.
4. The Zollinger-Ellison syndrome is caused by gastrin-secreting tumours mainly localised in the pancreas, so a direct way to the diagnosis is simply to measure the concentration of gastrin in the plasma.
1. The high serum [gastrin] increases the density of gastric glands, parietal cells and the HCl secretion drastically. When the excessive amount of HCl and pepsin enters the duodenum, they work together to damage the duodenal mucosa.
2. The patient suffers from the effects of a gastrin secreting tumour ( a so-called gastrinoma). No hyperplasia of G cells was found in the antral mucosa. The most frequent location of gastrinomas is in the pancreas (Zollinger-Ellisons syndrome).
3. The presence of peptides and amino acids from a meal in the stomach, would stimulate gastrin secretion, if hyperplastic antral G cells were present - and thus be the cause of the high serum [gastrin].
Our male patient seems to have a gastrin producing tumour in the pancreas.
4. The extremely acid chyme enters the duodenum of the patient and denature pancreatic lipase, which is extremely pH sensitive. Therefore, lipids are not broken down and absorbed. The result is steatorrhoe (fatty stools), and increased intestinal secretion. The high serum [gastrin] increases intestinal secretion of fluid and ions, which further augments the diarrhoea.
5. Omeprazole is bound irreversibly to the parietal proton pump whereby the effect is longlasting. New proton pump molecules must be synthesized before HCl is produced again.
6. One mol of glucose corresponds to the energy of (180 g* 15.4 kJ/g) = 2797 kJ. 30 mmol of glucose equals (30* 2797/1000) = 84 kJ/mol of H+.
1.The haematological diagnosis is microcytic anaemia probably caused by iron deficiency.
2.The patchy granulomas of the colon are often also present in the terminal ileum in this condition. The diagnosis is ileitis terminalis or Crohns disease.
3.Primary treatment seldomly includes surgery. Usually, the patient benefit from low-fat diet and 30 mg prednisolone daily.
4.The fatty stools (steatorrhoe) indicates inefficient reuptake of bile acids in the terminal ileum. The patient excrete large amounts of bile acids, fat, proteins and water with faeces. This is why the patient is emaciated and tired. The bile acids bind Ca2+, so the patient develops hypocalcaemia and osteomalacia. The bile acids spoil the mucosa of the colon making segmental surgery necessary. The patient ends up with a short bowel. Frequent fistulas through the bowel wall and to the skin also reduce the life quality of the patient. Later lack of vitamin B12 will cause a perniciosiform anaemia.
5.Ulcerative colitis and coeliac disease. steatorrhoe typically points to ileal involvement. Frequent bloody diarrhoeas indicate colic involvement as in ulcerative colitis.
Gluten-sensitive enteropathy or coeliac disease describes a condition where the duodenal and jejunal mucosa is more or less destroyed by hypersensitivity towards gluten. Desquamation of the mucosa can descend along the small intestine and include the terminal ileum. Symptoms and signs include stomatitis with ulcers, diarrhoea, steatorrhoea, abdominal pain, osteomalacia and malnutrition with oedema. The differential diagnosis is sometimes difficult.