GI Flashcards
What is the schilling test
Schilling test – is the definitive test for the diagnosis of PA
●The test measures the amount of an oral dose of radioactively labeled vitamin B12 that is absorbed in the gut and excreted in the urine.
GIST:
●Oral radioactive B12 is followed by an injection of unlabeled vitamin B12 to saturate all vitamin B12 receptors in the tissue and plasma. Thus any amount absorbed in the gut will be in excess, and will be filtered in the kidneys to appear in the urine.
● If there is no radioactivity in the urine, this means that there is either Malabsorption or Pernicious Anaemia due to lack of Intrinsic Factor
●The test is repeated, but this time the radioactively labeled B12 is accompanied by a dose of IF.
● If absorption is now normal, this means that the patient has PA
What is the pentagastrin test
Patient fasting
●Pass radio-opaque naso-gastric tube
Aspirate:
●Resting juice
●Basal juice (60 min)
Inject sub-cutan pentagastrin 6 g/kg bdy wt
Aspirate:
●Post-pentagastrin secretion (4 x15 min)
What are the reference ranges for the pentagastrin test
Resting juice: <50ml
●Basal juice: <5 mmol/h (HCl)
●Post-pentagastrin secretion (MAO/PAO)
♂: < 45mmol/h
♀: <35 mmol/h
What is achlorhydia
Inability to secrete gastric acid so that the pH of gastric juice produced in response to the pentagastrin test ≥ 7
(normal gastric acid pH: 1.5-3.5)
Hypochlorhydria and Achlorhydria may be found in:
●Pernicious anaemia (Addisonian Auto-immune gastritis)
●Gastric carcinoma
Acid output is increased in
Duodenal ulcer and Zollinger-Ellison syndrome
Acid output is decreased in what conditions
Gastric ulcer
Gastric carcinoma
What is peptic ulcer
●An ulcer in or adjacent to an acid producing area of the gut (Stomach, Meckel’s diverticulum)
Causes:
●Decreased () mucosal resistance (Cells + mucus)
●Increased () Acid + pepsin
●NB: effective management of PU leads to 50% reduction in acid output (pre: intra-treatment)
What is the Hollander’s test
Patient fasting
●Pass radio-opaque naso-gastric tube
Aspirate:
●Resting juice
●Basal juice (60 min)
Inject sub-cutan insulin 0.2 u/kg bdy wt
Aspirate:
●Post-insulin secretion (8 x 15 min)
What’s the blood glucose during Hollander’s test
Fasting blood glucose is measured before the injection of insulin
●Blood glucose is measured at 15, 30, 45 and 60 minutes after the injection of insulin
What are the reference ranges in the insulin hypoglycemia test
Hypoglycaemia: plasma glucose< 2.2 mmol/L in at least one of the blood specimens
●[H+] > 20 mmol/L above basal⇒ Incomplete vagotomy
●Output in any 4 consecutive 15 min specimens≥ 10 mmol⇒ Incomplete vagotomy
What is plasma gastrin
Reflects the rate of gastrin production by the pyloric antrum
●[Plasma gastrin] is in the fasting state when gastric acidity is high
●[Plasma gastrin] is after meals when gastric acidity is low (as a result of dilution & buffering of gastric acid)
In diseases causing hyperacidity (e.g. DU) [plasma gastrin] is except in Zollinger-Ellison syndrome
●In hypochlorhydria or achlorhydria (e.g. pernicious anaemia) [plasma gastrin] is except in a situation where atrophic gastritis has destroyed gastrin producing cells
What is Zollinger Ellison’s syndrome
0.1% of all patients with PUD
●Severe, multiple recurrent peptic ulcers
●Autonomous gastrin production
●♂: 60-65%, ♀: 30-35%
●Excessive production of acid by the stomach
●Non- islet cell tumour of the pancreas
●May occur as part of the MEN syndromes (20%)
60% of the gastrinomas are malignant with metastasis in local lymph nodes and liver
Symptoms / signs:
●Abdominal pain & dyspepsia
●Chronic diarrhoea & malabsorption as a result of inactivation of pancreatic enzymes by H+
resting and basal juice in the pentagastrin test
●Overnight aspiration (resting juice)> 1L
containing ≥ 100 mmol/L HCl
●Diagnosis confirmed by finding [plasma gastrin] in the fasting patient
(100->1000 pg/ml)
●BAO/MAO> 0.6
What is acute pancreatitis
Acute inflammation of the pancreas
Two forms:
●Oedematous: (mortality: 5-10%)
●Haemorrhagic /(Necrotizing) with severe tissue necrosis: (mortality: 20-50%)
Associations:
●50+ years
●Biliary tract disease (e.g. cholelithiasis)
●Alcoholism
On elimination of the causative factor, normal exocrine and endocrine functions are restored
Gall stones present in about 50% of all cases
●About 5% of patients with gall stones develop acute pancreatitis
●Vascular and infective causes also known
●25% of all cases are not secondary to any known cause (idiopathic)
What is plasma amylase
Activity usually in acute pancreatitis
●Values >5x the upper reference value (180 Somogyi u/dL) found in >50% of cases and usually occurs on the 1st or 2nd day of illness
●Smaller increases in most acute abdominal conditions
●In acute pancreatitis plasma -amylase activity returns to normal within 3-5 days
What is urine amylase
Rises with plasma -amylase but offers no advantage over measurement of plasma - amylase
Limitations:
●Renal decompensation in the elderly
●Macroamylasaemia (presence of aggregates of -amylase with immunoglobulins in plasma which are unable to pass through the kidney filter)
What are some lips and trypsin activities
Levels of lipase and trypsin are increased in acute pancreatitis and in other conditions where plasma - amylase activity is increased
●They are more difficult to measure than - amylase
●Serum lipase is more sensitive and specific for pancreatitis and may eventually replace amylase measurements
●Lipase is only slowly cleared from plasma so remains elevated for a longer period than plasma amylase
What substance is the index of severity of acute pancreatitis
Methaem-albuminaemia
Develops sometimes in acute pancreatitis:
●Proteolytic breakdown of haemoglobin
●Haem /methaem formed
●Haem metabolized to bilirubin
●Methaem combines with plasma albumin to form methaem-albumin
Usually only a trace of methaem-albumin is detectable in the plasma of healthy individuals
What is this
Methaem-albuminemia
What is chronic pancreatitis
Persistence of pain or symptoms after acute episode with:
Structural and functional impairment:
●Impairment of pancreatic exocrine function (e.g. release of lipase)
●Impairment of pancreatic endocrine function (e.g. release of insulin)
Pentagastrin stimulates …………. secretion
HCl
What is Zollinger-Ellison syndrome
The Zollinger-Ellison (Z-E) syndrome results from a tumor (gastrinoma) of the pancreatic islet cells. Its characteristics include (1)fulminant peptic ulcers, (2) massive gastric hyper- secretion, (3) hypergastrinemia, (4) diarrhea, and (5) steator- rhea. About half of all gastrinomas are multiple, and about two thirds are malignant. One fourth of all gastrinomas are part of the multiple endocrine neoplasia syndrome, type 1 (MEN I), with associated tumors, or hype~plasiai,n pancreatic islets and parathyroid and pituitary glands. In individuals with Z-E syn- drome, fasting gastrin concentrations usually are increased substantially, ranging from 2 to 2000 times normal. Fasting plasma gastrin is usually greatly increased, also ranging from 2 to 2000 times normal. Concentrations more than 10 times the upper limit of normal, in the presence of gastric acid hypersecretion, are virtually diagnostic of gastrinoma. The fasting plasma gastrin concentration at presentation in spo- radic 2-E syndrome correlates with the size and site of the tumor and the presence of hepatic metastases and therefore has prognostic value.
Because management of the patient with Z-E syndrome usually requires surgical intervention, it is important to distin- guish hypergastrinemia caused by gastrinomafrom other condi- tions that may lead to similar increases in plasma gastrin. For example, increased concentration of plasma gastrin occurs in (1) hypochlorhydria or achlorhydria,(2) patients being treated with acid-suppressing drugs (e.g., histamine Hz-receptor antagonists or PPIs), (3) H. pylon infection, (4) pernicious anemia, and (5) patients with chronic atrophic gastritis associ- ated with parietal cell antibodies.Surgical resection or diseases of the kidneys or small intestine also can cause hypergastrine- mia, possibly because these are important sites of gastrin degradation or excretion.
Increased basal gastrin concentrations may be classified as “appropriate” or “inappropriate” according to their association with decreased or increased gastric acid secretion. For example, in patients with very low or absent acid secretion and a func- tionally intact gastric antrum, an increase in plasma gastrin is physiologically appropriate and is expected.
Acid output is increased in what conditions
Zollinger Ellison syndrome
Duodenal ulcer
Acid output is decreased in what conditions
Gastric ulcer
Gastric carcinoma
What is peptic ulcer disease
Spiral-shaped organisms have been observed in the stomach for many years hut it was only in 1985 that the association was made between Helicobacter pylori (known then as Campylo- bacter pylori) and peptic ulcer disease. Most estimates suggest that the bacterium is present in the mucous layer of the stomach in half of the population of the world. In Europe 30% to 50% of adults, and in the United States at least 20% of the adult population, are infected with the organism. Colonization with H. pylori causes a chronic inflammatory reaction in the gastric mucosa even when direct endoscopic observation appears normal. Carriers of the organism are at increased risk of gastric cancer (twofold to tenfold) and peptic ulcer (threefold to tenfold). About 90% of gastric cancer patients are infected with H, pylon, compared with 40% to 60% of age-matched controls and there is a significant correlation between infec- tion rates and gastric cancer incidence and mortality. However, although a large proportion of gastric cancer can be attributed to infection with H. pylori, only in a minority of infected subjects will the inflammatory reaction progress to gastric cancer and the current consensus is that asymptomaticsubjects should not be screened for H. pylori infection.”
At least 95% of patients with duodenal ulcer disease are infected with H, pyloli, and eradication of H. pylori is the recommended treatment for patients with duodenal or gastric ulcer who are H. pylori- positive. Effective combined antibiotic and acid suppression regimens (using PPls) are available with eradication rates of about 90%.
The reason for a gastric mucosal infection causing duodenal ulceration is complex but involves a number of pathways leading to increased acid production. Before the role of H. pylori in the development of peptic ulcer disease was under- stood, vagotomy (surgical sectioning, or cutting, of the vagus nerve) was the main form of treatment used to reduce gastric acid output, thereby leading to an environment more condu- cive to healing of the ulcer.
H . pylori produces urease, and hydrolysis of endogenous urea to bicarbonate and ammonia may create a more hospitable microenvironment for its survival in the stomach. The ability of the organism to rapidly hydrolyze urea is the basis of the urea breath tests and of the direct urease tests on gastric biopsy samples. Mammalian cells do not produce urease.
