NORMAL GASTRIC ANATOMY AND PHYSIOLOGY

Published in Clinical Pathology
Friday, 08 September 2017 01:21
Anatomically, stomach is divided into four parts: cardia, fundus, body, and pyloric part. Cardia is the upper part surrounding the entrance of the esophagus and is lined by the mucus-secreting epithelium. The epithelium of the fundus and the body of the stomach is composed of different cell types including: (i) mucus-secreting cells which protect gastric mucosa from self-digestion by forming an overlying thick layer of mucus, (ii) parietal cells which secrete hydrochloric acid and intrinsic factor, and (iii) peptic cells or chief cells which secrete the proteolytic enzyme pepsinogen. Pyloric part is divided into pyloric antrum and pyloric canal. It is lined by mucus-secreting cells and gastrin-secreting neuroendocrine cells (G cells) (Figure 859.1).
 
Figure 859.1 Parts of stomach and their lining cells
Figure 859.1 Parts of stomach and their lining cells 
 
In the stomach, ingested food is mechanically and chemically broken down to form semi-digested liquid called chyme. Following relaxation of pyloric sphincter, chyme passes into the duodenum.
 
There are three phases of gastric acid secretion: cephalic, gastric, and intestinal.
 
  • Cephalic or neurogenic phase: This phase is initiated by the sight, smell, taste, or thought of food that causes stimulation of vagal nuclei in the brain. Vagus nerve directly stimulates parietal cells to secrete acid; in addition, it also stimulates antral G cells to secrete gastrin in blood (which is also a potent stimulus for gastric acid secretion) (Figure 859.2). Cephalic phase is abolished by vagotomy.
  • Gastric phase: Entry of swallowed food into the stomach causes gastric distension and induces gastric phase. Distension of antrum and increase in pH due to neutralization of acid by food stimulate antral G cells to secrete gastrin into the circulation. Gastrin, in turn, causes release of hydrochloric acid from parietal cells.
  • Intestinal phase: Entry of digested proteins into the duodenum causes an increase in acid output from the stomach. It is thought that certain hormones and absorbed amino acids stimulate parietal cells to secrete acid.
 
The secretion from the stomach is called as gastric juice. The chief constituents of the gastric juice are:
 
  • Hydrochloric acid (HCl): This is secreted by the parietal cells of the fundus and the body of the stomach. HCl provides the high acidic pH necessary for activation of pepsinogen to pepsin. Gastric acid secretion is stimulated by histamine, acetylcholine, and gastrin (Figure 859.2). HCl kills most microorganisms entering the stomach and also denatures proteins (breaks hydrogen bonds making polypeptide chains to unfold). Its secretion is inhibited by somatostatin (secreted by D cells in pancreas and by mucosa of intestine), gastric inhibitory peptide (secreted by K cells in duodenum and jejunum), prostaglandin, and secretin (secreted by S cells in duodenum).
  • Pepsin: Pepsin is secreted by chief cells in stomach. Pepsin causes partial digestion of proteins leading to the formation of large polypeptide molecules (optimal function at pH 1.0 to 3.0). Its secretion is enhanced by vagal stimulation.
  • Mucus
  • Intrinsic factor (IF): IF is necessary for absorption of vitamin B12 in the terminal ileum. It is secreted by parietal cells of stomach.
 
Figure 859.2 Stimulation of gastric acid secretion
Figure 859.2 Stimulation of gastric acid secretion. Three receptors on parietal cells stimulate acid secretion: histamine (H2) receptor, acetylcholine or cholinergic receptor, and gastrin/CCK-B receptor. Histamine is released by enterochromaffin-like cells in lamina propria. Acetylcholine is released from nerve endings. Gastrin is released from G cells in antrum (in response to amino acids in food, antral distention, and gastrin-releasing peptide). After binding to receptors, H+ is secreted in exchange for K+ by proton pump

CONTRAINDICATIONS TO GASTRIC ANALYSIS

Published in Clinical Pathology
Thursday, 07 September 2017 23:53
  • Gastric intubation for gastric analysis is contraindicated in esophageal stricture or varices, active nasopharyngeal disease, diverticula, malignancy, recent history of severe gastric hemorrhage, hypertension, aortic aneurysm, cardiac arrhythmias, congestive cardiac failure, or non-cooperative patient.
  • Pyloric stenosis: Obstruction of gastric outlet can elevate gastric acid output due to raised gastrin (following antral distension).
  • Pentagastrin stimulation is contraindicated in cases with allergy to pentagastrin, and recent severe gastric hemorrhge due to peptic ulcer disease.
 
Gastric analysis is not a commonly performed procedure because of following reasons:
 
  • It is an invasive and cumbersome technique that is traumatic and unpleasant for the patient.
  • Information obtained is not diagnostic in itself.
  • Availability of better tests for diagnosis such as endoscopy and radiology (for suspected peptic ulcer or malignancy); serum gastrin estimation (for ZE syndrome); vitamin assays, Schilling test, and antiparietal cell antibodies (for pernicious anemia); and tests for Helicobacter pylori infection (in duodenal or gastric ulcer).
  • Availability of better medical line of treatment that obviates need for surgery in many patients.

LABORATORY TESTS FOR GASTRIC ANALYSIS

Published in Clinical Pathology
Thursday, 07 September 2017 23:53
  1. Hollander’s test (Insulin hypoglycemia test): In the past, this test was used for confirmation of completeness of vagotomy (done for duodenal ulcer).

    Hypoglycemia is a potent stimulus for gastric acid secretion and is mediated by vagus nerve. This response is abolished by vagotomy.

    In this test, after determining BAO, insulin is administered intravenously (0.15-0.2 units/kg) and acid output is estimated every 15 minutes for 2 hours (8 post-stimulation samples). Vagotomy is considered as complete if, after insulin-induced hypoglycemia (blood glucose < 45 mg/dl), no acid output is observed within 45 minutres.

    The test gives reliable results only if blood glucose level falls below 50 mg/dl at some time following insulin injection. It is best carried out after 3-6 months of vagotomy.

    The test is no longer recommended because of the risk associated with hypoglycemia. Myocardial infarction, shock, and death have also been reported.

  2. Fractional test meal: In the past, test meals (e.g. oat meal gruel, alcohol) were administered orally to stimulate gastric secretion and determine MAO or PAO. Currently, parenteral pentagastrin is the gastric stimulant of choice.

  3. Tubeless gastric analysis: This is an indirect and rapid method for determining output of free hydrochloric acid in gastric juice. In this test, a cationexchange resin tagged to a dye (azure A) is orally administered. In the stomach, the dye is displaced from the resin by the free hydrogen ions of the hydrochloric acid. The displaced azure A is absorbed in the small intestine, enters the bloodstream, and is excreted in urine. Urinary concentration of the dye is measured photometrically or by visual comparison with known color standards. The quantity of the dye excreted is proportional to the gastric acid output. However, if kidney or liver function is impaired, false results may be obtained. The test is no longer in use.

  4. Spot check of gastric pH: According to some investigators, spot determination of pH of fasting gastric juice (obtained by nasogastric intubation) can detect the presence of hypochlorhydria (if pH>5.0 in men or >7.0 in women).

  5. Congo red test during esophagogastroduodenoscopy: This test is done to determine the completeness of vagotomy. Congo red dye is sprayed into the stomach during esophagogastroduodenoscopy; if it turns red, it indicates presence of functional parietal cells in stomach with capacity of producing acid.
 
REFERENCE RANGES
 
  • Volume of gastric juice: 20-100 ml
  • Appearance: Clear
  • pH: 1.5 to 3.5
  • Basal acid output: Up to 5 mEq/hour
  • Peak acid output: 1 to 20 mEq/hour
  • Ratio of basal acid output to peak acid output: <0.20 or < 20%

INDICATIONS FOR GASTRIC ANALYSIS

Published in Clinical Pathology
Thursday, 07 September 2017 23:18
In gastric analysis, amount of acid secreted by the stomach is determined on aspirated gastric juice sample. Gastric acid output is estimated before and after stimulation of parietal cells (i.e. basal and peak acid output). This test was introduced in the past mainly for the evaluation of peptic ulcer disease (to assess the need for operative intervention). However, diminishing frequency of peptic ulcer disease and availability of safe and effective medical treatment have markedly reduced the role of surgery.
 
  1. To determine the cause of recurrent peptic ulcer disease:
    To detect Zollinger-Ellison (ZE) syndrome: ZE syndrome is a rare disorder in which multiple mucosal ulcers develop in the stomach, duodenum, and upper jejunum due to gross hypersecretion of acid in the stomach. The cause of excess secretion of acid is a gastrin-producing tumor of pancreas. Gastric analysis is done to detect markedly increased basal and pentagastrinstimulated gastric acid output for diagnosis of ZE syndrome (and also to determine response to acidsuppressant therapy). However, a more sensitive and specific test for diagnosis of ZE syndrome is measurement of serum gastrin (fasting and secretin-stimulated).
    To decide about completeness of vagotomy following surgery for peptic ulcer disease: See Hollander’s test.
  2. To determine the cause of raised fasting serum gastrin level: Hypergastrinemia can occur in achlorhydria, Zollinger-Ellison syndrome, and antral G cell hyperplasia.
  3. To support the diagnosis of pernicious anemia (PA): Pernicious anemia is caused by defective absorption of vitamin B12 due to failure of synthesis of intrinsic factor secondary to gastric mucosal atrophy. There is also absence of hydrochloric acid in the gastric juice (achlorhydria). Gastric analysis is done for demonstration of achlorhydria if facilities for vitamin assays and Schilling’s test are not available (Achlorhydria by itself is insufficient for diagnosis of PA).
  4. To distinguish between benign and malignant ulcer: Hypersecretion of acid is a feature of duodenal peptic ulcer, while failure of acid secretion (achlorhydria) occurs in gastric carcinoma. However, anacidity occurs only in a small proportion of cases with advanced gastric cancer. Also, not all patients with duodenal ulcer show increased acid output.
  5. To measure the amount of acid secreted in a patient with symptoms of peptic ulcer dyspepsia but normal X-ray findings: Excess acid secretion in such cases is indicative of duodenal ulcer. However, hypersecretion of acid does not always occur in duodenal ulcer.
  6. To decide the type of surgery to be performed in a patient with peptic ulcer: Raised basal as well as peak acid outputs indicate increased parietal cell mass and need for gastrectomy. Raised basal acid output with normal peak output is an indication for vagotomy.

METHOD OF GASTRIC ANALYSIS

Published in Clinical Pathology
Tuesday, 05 September 2017 23:51
To assess gastric acid secretion, acid output from the stomach is measured in a fasting state and after injection of a drug which stimulates gastric acid secretion.
 
Basal acid output (BAO) is the amount of hydrochloric acid (HCl) secreted in the absence of any external stimuli (visual, olfactory, or auditory).
 
Maximum acid output (MAO) is the amount of hydrochloric acid secreted by the stomach following stimulation by pentagastrin. MAO is calculated from the first four 15-minute samples after stimulation.
 
Peak acid output (PAO) is calculated from the two highest consecutive 15-minute samples. It indicates greatest possible acid secretory capacity and is preferred over MAO as it is more reproducible.
 
Acidity is estimated by titration.
 
Collection of Sample
 
All drugs that affect gastric acid secretion (e.g. antacids, anticholinergics, cholinergics, H2-receptor antagonists, antihistamines, tranquilizers, antidepressants, and carbonic anhydrase inhibitors) should be withheld for 24 hours before the test. Proton pump inhibitors should be discontinued 5 days prior to the test. Patient should be relaxed and free from all sources of sensory stimulation.
 
Patient should drink or eat nothing after midnight.
 
Gastric juice can be aspirated through an oral or nasogastric tube (polyvinyl chloride, silicone, or polyurethane) or during endoscopy.
 
Oral or nasogastric tube (Figure 855.1) is commonly used. It is a flexible tube having a small diameter and a bulbous end that is made heavy by a small weight of lead. The end is perforated with small holes to allow entry of gastric juice into the tube. As the end is radiopaque, the tube can be positioned in the most dependent part of the stomach under fluoroscopic or X-ray guidance. The tube is lubricated and can be introduced either through the mouth or the nose. The patient is either sitting or reclining on left side. The tube has three or four markings on its outer surface that correspond with distance of the tip of the tube from the teeth, i.e. 40 cm (tip to cardioesophageal junction), 50 cm (body of stomach), 57 cm (pyloric antrum), and 65 cm (duodenum). The position of the tube can be verified either by fluoroscope or by ‘water recovery test’. In the latter test, 50 ml of water is introduced through the tube and aspirated again; recovery of > 90% of water is indicative of proper placement. The tube is usually positioned in the antrum. A syringe is attached to the outer end of the tube for the aspiration of gastric juice.
 
Figure 855.1 Oral or nasogastric Ryles tube
Figure 855.1 Oral or nasogastric Ryle’s tube. The tube is marked at 40, 50, 57, and 65 cm with radiopaque lines for accurate placement. The tip is bulbous and contains a small weight of lead to assist the passage during intubation and to know the position under fluoroscopy or X-ray guidance. There are four perforations or eyes to aspirate contents from the stomach through a syringe attached to the base
 
For estimation of BAO, sample is collected in the morning after 12-hour overnight fast. Gastric secretion that has accumulated overnight is aspirated and discarded. This is followed by aspiration of gastric secretions at 15-minute intervals for 1 hour (i.e. total 4 consecutive samples are collected). All the samples are centrifuged to remove any particulate matter. Each 15-minute sample is analyzed for volume, pH, and acidity. The acid output in the four samples is totaled and the result is expressed as concentration of acid in milliequivalents per hour or in mmol per hour.
 
After the collection of gastric juice for determination of BAO, patient is given a subcutaneous or intramuscular injection of pentagastrin (6 μg/kg of body weight), and immediately afterwards, gastric secretions are aspirated at 15-minute intervals for 1 hour (for estimation of MAO or PAO). MAO is calculated from the first four 15-minute samples after stimulation. PAO is calculated from two consecutive 15-minute samples showing highest acidity.
 
Titration
 
Box 855.1 Determination of basal acid output, maximum acid output, and peak acid output
 
  • Basal acid output (BAO)= Total acid content in all four 15-minute basal samples in mEq/L
  • Maximum acid output (MAO) = Total acid content in all four 15-minute post-pentagastrin samples in mEq/L
  • Peak acid output (PAO) = Sum of two consecutive 15-minute post-pentagastrin samples showing highest acidity ×2 (mEq/L)
Gastric acidity is estimated by titration, with the end point being determined either by noting the change in color of the indicator solution or till the desired pH is reached.
 
In titration, a solution of alkali (0.1 N sodium hydroxide) is added from a graduated vessel (burette) to a known volume of acid (i.e. gastric juice) till the end point or equivalence point of reaction is reached. The concentration of acid is then determined from the concentration and volume of alkali required to neutralize the particular volume of gastric juice. Concentration of acid is expressed in terms of milliequivalents per liter or mmol per liter.
 
Free acidity refers to the concentration of HCl present in a free, uncombined form in a solution. The volume of alkali added to the gastric juice till the Topfer’s reagent (an indicator added earlier to the gastric juice) changes color or when the pH (as measured by the pH meter) reaches 3.5 is a measure of free acidity. A screening test can be carried out for the presence of free HCl in the gastric juice. If red color develops after addition of a drop of Topfer’s reagent to an aliquot of gastric juice, free HCl is present and the diagnosis of pernicious anaemia (achlorhydria) can be excluded.
 
Combined acidity refers to the amount of HCl combined with proteins and mucin and also includes small amount of weak acids present in gastric juice.
 
Total acidity is the sum of free and combined acidity. The amount of alkali added to the gastric juice till phenolphthalein indicator (added earlier to the gastric juice) changes color is a measure of total acidity (Box 855.1).
 
Interpretation of Results
 
  1. Volume: Normal total volume is 20-100 ml (usually < 50 ml). Causes of increased volume of gastric juice are—
    • Delayed emptying of stomach: pyloric stenosis
    • Increased gastric secretion: duodenal ulcer, Zollinger-Ellison syndrome.
  2. Color: Normal gastric secretion is colorless, with a faintly pungent odor. Fresh blood (due to trauma, or recent bleeding from ulcer or cancer) is red in color. Old hemorrhage produces a brown, coffee-ground like appearance (due to formation of acid hematin). Bile regurgitation produces a yellow or green color.
  3. pH: Normal pH is 1.5 to 3.5. In pernicious anemia, pH is greater than 7.0 due to absence of HCl.
  4. Basal acid output:
    • Normal: Up to 5 mEq/hour.
    • Duodenal ulcer: 5-15 mEq/hour.
    • Zollinger-Ellison syndrome: >20 mEq/hour.
    Normal BAO is seen in gastric ulcer and in some patients with duodenal ulcer.
  5. Peak acid output:
    • Normal: 1-20 mEq/hour.
    • Duodenal ulcer: 20-60 mEq/hour.
    • Zollinger-Ellison syndrome: > 60 mEq/hour.
    • Achlorhydria: 0 mEq/hour.
    Normal PAO is seen in gastric ulcer and gastric carcinoma. Values up to 60 mEq/hour can occur in some normal individuals and in some patients with Zollinger-Ellison syndrome.
    In pernicious anemia, there is no acid output due to gastric mucosal atrophy. Achlorhydria should be diagnosed only if there is no free HCl even after maximum stimulation.
  6. Ratio of basal acid output to peak acid output (BAO/PAO):
    • Normal: < 0.20 (or < 20%).
    • Gastric or duodenal ulcer: 0.20-0.40 (20-40%).
    • Duodenal ulcer: 0.40-0.60 (40-60%).
    • Zollinger-Ellison syndrome: > 0.60 (> 60%).
    Normal values occur in gastric ulcer or gastric carcinoma.
 
Conditions associated with change in gastric acid output are listed in Table 855.1.
 
It is to be noted that values of acid output are not diagnostic by themselves and should be correlated with clinical, radiological, and endoscopic features.
 
Table 855.1 Causes of alterations in gastric acid output
Increased gastric acid output Decreased gastric acid output
• Duodenal ulcer Chronic atrophic gastritis
• Zollinger-Ellison syndrome     1. Pernicious anemia
Hyperplasia of antral G cells     2. Rheumatoid arthritis
Systemic mastocytosis     3. Thyrotoxicosis
• Basophilic leukemia • Gastric ulcer
  • Gastric carcinoma
  • Chronic renal failure
  • Post-vagotomy
  • Post-antrectomy

Bioethics

Published in Bioethics
Monday, 04 September 2017 18:27
Bioethics is the study of the ethical issues emerging from advances in biology and medicine. It is also moral discernment as it relates to medical policy and practice. Bioethicists are concerned with the ethical questions that arise in the relationships among life sciences, biotechnology, medicine, politics, law, and philosophy. It includes the study of values ("the ethics of the ordinary") relating to primary care and other branches of medicine.

Animal Biotechnology

Published in Animal Biotechnology
Monday, 04 September 2017 18:17
Animal biotechnology is a branch of biotechnology in which molecular biology techniques are used to genetically engineer (i.e. modify the genome of) animals in order to improve their suitability for pharmaceutical, agricultural or industrial applications. Animal biotechnology has been used to produce genetically modified animals that synthesize therapeutic proteins, have improved growth rates or are resistant to disease.

Biophysics

Published in Biophysics
Monday, 04 September 2017 18:09
Biophysics or biological physics is an interdisciplinary science that applies the approaches and methods of physics to study biological systems. Biophysics covers all scales of biological organization, from molecular to organismic and populations. Biophysical research shares significant overlap with biochemistry, physical chemistry, nanotechnology, bioengineering, computational biology, biomechanics and systems biology.
 
The term biophysics was originally introduced by Karl Pearson in 1892.

Histopathology

Published in Histopathology
Monday, 04 September 2017 17:55
Histopathology (compound of three Greek words: ἱστός histos "tissue", πάθος pathos "suffering", and -λογία -logia"study of") refers to the microscopic examination of tissue in order to study the manifestations of disease. Specifically, in clinical medicine, histopathology refers to the examination of a biopsy or surgical specimen by a pathologist, after the specimen has been processed and histological sections have been placed onto glass slides. In contrast, cytopathology examines (1) free cells or (2) tissue micro-fragments (as "cell blocks").

Physiology

Published in Physiology
Monday, 04 September 2017 17:39
Physiology (/ˌfɪziˈɒləi/; from Ancient Greek φύσις (physis), meaning 'nature, origin', and -λογία (-logia), meaning 'study of') is the scientific study of normal mechanisms, and their interactions, which works within a living system. A sub-discipline of biology, its focus is in how organisms, organ systems, organs, cells, and biomolecules carry out the chemical or physical functions that exist in a living system. Given the size of the field, it is divided into, among others, animal physiology (including that of humans), plant physiology, cellular physiology, microbial physiology (microbial metabolism), bacterial physiology, and viral physiology.
 
Central to an understanding of physiological functioning is its integrated nature with other disciplines such as chemistry and physics, coordinated homeostatic control mechanisms, and continuous communication between cells.
 
The Nobel Prize in Physiology or Medicine is awarded to those who make significant achievements in this discipline by the Royal Swedish Academy of Sciences. In medicine, a physiologic state is one occurring from normal body function, rather than pathologically, which is centered on the abnormalities that occur in animal diseases, including humans.
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