AUBF: ANALYSIS OF URINE AND OTHER BODY FLUIDS

LECTURE 7: GASTRIC JUICE ANALYSIS

1st SEMESTER | S.Y. 2024-2025

ORIGIN AND REGULATION OF GASTRIC SECRETIONS

✓ Stomach is ready to receive the food
✓ Food is mixed with acid mucus and pepsin
✓ Stomach adds significant amount of digestive juice to meal
✓ Can be mediated by cephalic phase
✓ Food is released into the duodenum

Histological representation of gastric wall

Physiological view of gastric glands

GASTRIC SECRETIONS Goblet cells or mucus cells

✓ Colorless, watery, acidic, digestive fluid produced
in the stomach
✓ Pale yellow
✓ pH is 1-3
✓ Secretes 2-3 L/ day
✓ Chemical composition:
- inorganic salts and organic components that
include, mucin, digestive enzymes, hormones

CABAY, J. B. | BMLS3 | PLT COLLEGE, INC.

PARIETAL CELLS:
✓ secrete HCl into the stomach: HCl important in the activation of pepsinogen and inactivation of
microorganisms.
✓ It secrets intrinsic factor necessary for intestinal absorption of vitamin B12.

CHIEF CELLS:
✓ It secretes pepsinogen (zymogen): Once secreted, pepsinogen is activated by stomach acid into the
active protease pepsin
✓ Secretes Gastric Lipase responsible for the initiation of fat digestion

GASTRIC SECRETION PHASES

Gastric acid secretion can be divided into three phases:
1. Cephalic phase
- Mediated by the CNS and triggered by smelling,
chewing or even the thought of food.
- Mediated by the vagus nerve and accounts for 10-
30% of the acid secreted).
2. Gastric phase
- -triggered by the presence of food in the stomach
- Accounts for 70-90% of the acid secretion
3. 3.Intestinal phase: Presence of chyme, most probably
amino acids in the intestine triggers approximately 5% of
the gastric acid secretion.

HYDROCHLORIC ACID (HCL) PRODUCTION

1. Cl- diffuses from the blood into the duct of
gastric gland. 2.CO2 diffuse from the blood
into the parietal cell.
2. CO2 combines with H2O to form H2CO3.
3. H2CO3 dissociates into bicarbonate and H+
4. H+ combines with Cl- in duct of gastric
gland to form HCl-.
5. An ATP pump is necessary to pump the HCl-
into the lumen
COMPOSITION AND FUNCTION OF GASTRIC SECRETIONS
1. HCl converts pepsinogen to pepsin for chemical digestion
- provides optimal pH environment for pepsin
- destroys some bacteria
- stimulates the small intestinal mucosa to release Secretin and CCK
- promotes the absorption of Ca2+ and Fe2+ in small intestine
2. Pepsinogen (precursor of pepsin): digestion of proteins
3. Mucus
- mixture of mucoproteins and mucopolysaccharides
- forms a protective barrier: Mucus-bicarbonate barrier
4. Intrinsic factor: Combines with vitamin B12 to make it absorbable.
5. Electrolytes: Gastric secretion contains all electrolytes found in the other body fluid.

GASTRIC ACID SECRETION IS CONTROLLED BY THREE MECHANISMS:

a) Neurocrine (denoting an endocrine influence on or by the nerves).
b) Endocrine (gastrin)
c) Paracrine (histamine)
In contrast to true endocrines these hormones are not released into the bloodstream but into the
surrounding tissues and act in the immediate vicinity, e.g. intestinal mucosal hormones.

PATHOLOGY
▪ PEPTIC ULCER is an open sore: They are usually found in the lining of the stomach, esophagus or
upper small intestine.
a) Gastric Ulcers - Ulcers in the stomach
b) Duodenal Ulcers - Ulcers in the upper area of the small intestine, the duodenum.

a) Gastric ulcer
✓ also known as peptic ulcer
✓ localized area of erosion in the stomach lining
✓ result in:
- abdominal pain
- possible bleeding
- gastrointestinal symptoms
The Causes, Signs and Symptoms
- The most common cause of gastric ulcer is a stomach infection associated with the Helicobacter
pylori (H pylori) bacteria.
- Gastric Ulcer can be constant or sporadic, and the disease course varies among individuals.
- Other risk factors for gastric ulcer include: alcohol, tobacco and prolonged use of medications
such nonsteroidal anti-inflammatory drugs (NSAIDs).
 - Gastric ulcer, pain cannot be relieved by eating foods.
- Hematemesis
- In gastric ulcers, pain occurs 1-2 hours after eating

b) Duodenal ulcer
✓ Peptic ulcer in the duodenum
✓ ➢ localized area of erosion is in the duodenum.
✓ ➢ S/S:
- abdominal pain
- possible bleeding
- gastrointestinal symptoms

The Cause, Signs and Symptoms

✓ The most common cause of duodenal ulcer
✓ is Helicobacter pylori (H pylori) bacteria. Other risk factors include overuse of alcohol, tobacco
and medications such as aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs).
✓ Duodenal ulcer
- it can be relieved by eating
- blood in the stool called melena.
- pain occurs 3-4 hours after eating.

TESTING FOR GU AND DU

✓ Look for the presence of the H. pylori bacteria
✓ Analyze patient’s blood (if anemic) and stool (if with blood).

ENDOSCOPY
✓ Commonly used because biopsies can be taken during the procedure.
✓ can examine the upper digestive system.
✓ Can help to identify the type of ulcer and whether it is malignant.
✓ Can see if the ulcer has perforated the stomach, which can be a very serious complication.
✓ Sometimes, an upper GI series of traditional X-rays is used.

Treatment: Medication is effective for ulcers.

Antibiotics: Treatments of both types of ulcers to Antacids: In cases of hypersecretion of acid
lessen the number of H. pylori bacteria. Example: Zantac to neutralize acidity of the
Examples: amoxicillin, clarithromycin and stomach.
tetracycline.
✓ In gastric ulcers, avoid food which causes hyperacidity and irritation such as spicy foods, milk,
cheese and ice cream, chocolates and coffee.
✓ In duodenal ulcers, no special diet is needed. However, there are findings that alcohol can aggravate
duodenal ulcers.
✓ Surgery is needed if an ulcer is bleeding, cancerous or has caused perforation. If surgery is done
quickly, the prognosis is usually good.

SUMMARY:
1. Gastric ulcers occur in the stomach while duodenal ulcers occur in the duodenum.
2. Gastric ulcers cause pain 1-2 hours after eating. Duodenal ulcers cause pain 3-4 hours later.
3. Gastric ulcer pain cannot be relieved by eating. Abdominal pain in duodenal ulcers can be relieved by
eating.
4. Gastric ulcers cause hematemesis or vomiting of blood duodenal ulcers cause melena or blood in the
stool.
5. 5.A gastric ulcer has a special diet while duodenal ulcers do not.

PEPTIC ULCER DISEASE

✓ Peptic ulcers: Erosions of the mucous membranes of the stomach or duodenum produced by action
of HCl.
✓ Zollinger-Ellison syndrome: Ulcers of the duodenum are produced by excessive gastric acid
secretions.
✓ Helicobacter pylori: Bacterium that resides in GI tract that may produce ulcers.
✓ Acute gastritis: Histamine released by tissue damages gastric mucosa and inflammation stimulates
further acid secretion.

MANAGEMENT OF ULCERS
✓ Proton pump inhibitors (omeprazole)
✓ Antibiotics assist in eradicating H. pylori bacteria
✓ Histamine 2 (H2) receptor antagonists (Ranitidine)
✓ Local antacids
✓ Lifestyle Changes

SPECIMEN COLLECTION: Intubation (nasal or oral): Benign procedure but unpleasant and traumatic for
the patient.
Procedure:
a) Patient in sitting position
b) Bedfast patients lie on his left with elevated head approximately 45º
NASAL INTUBATION
- Less difficult to perform
- Tube (Levin) may or may not be chilled
- Nasal tube should be calibrated with measurements
- Adult: 55cm corresponds to the approximate distance from mouth
to antrum

GASTRIC INTUBATION: Contraindicated in patients with:

a) Esophageal varices
b) Diverticula
c) Stenosis
d) Malignant neoplasm
e) Aortic aneurysm
Indications:
1. To determine if the patient can secrete any gastric acid
- Anacidity: failure of pH to fall below 6.0 or 7.0 in the augmented or maximal histamine,
pentagastrin of Histology test
- Pernicious Anemia (PA)- treat patient with Vitamin B12.
2. To measure the amount of acid produced by a patient with symptoms of GU, particularly DU or post-
operative marginal ulcer who has demonstrable lesion by roentgenography.
3. To support a hypersecretory state, characteristic of Zollinger Ellison Syndrome (ZES)
4. To determine the completeness of vagotomy
5. Aid in the differential diagnosis of GU from DU

PHYSICAL EXAMINATION
Appearance
- Color- pale yellow, translucent
- Viscosity- Slightly viscous
- Odor- faintly pungent
- Volume- up to 50mL
- 12 hours fasting – should be no food particles.
- The presence of food after 12 hours means delayed emulsification due to pyloric obstruction.

Bile – yellow to green color Mucus – normal gastric Blood - flecks or streak of
- Small amount is normal due secretion from: blood, minor trauma during
to excessive gagging during a) swallowed saliva – intubation, coffee ground
intubation. identified by its frothy appearance blood with acid
- Large amount is abnormal nature secretion – longer/duration
due to obstruction of small Sources:
 intestine distal to the b) upper respiratory secretion ✓ gastritis
Ampulla of Vater. – highly tenacious & ✓ ulcers
contains lung particles ✓ CA
c) reflux of duodenal contents ✓ lesion in the mouth
– identified by staining
properties.

MICROSCOPIC EXAMINATION
▪ RBC: small amount with no consequence
▪ WBC: infection/inflammation – gastric mucosa upper respiratory tract
▪ Epithelial Cell: small amount (desquamation from various mucosa
o Squamous Cell- mouth, nose, pharynx & esophagus
o Columnar cells- increased in gastritis
▪ Yeast cells- presence in large number in retention of gastric juice. Ex. Pyloric obstruction
▪ Protozoan/Metazoan: Occurs rarely from reflux of duodenal contents
Ex. G. lamblia, trophozoite and cyst, SS larvae, Ascaris ova, Hook Worm ova
▪ Helicobacter pylori
o Present in 25% adult population 93% in GU 25% in DU
o Characteristically found in or under the mucus layer on the enterocytes.

H. pylori maybe demonstrated thru:

a) Smear from biopsy specimen & stained with Giemsa
b) Microbial culture
c) Rapid urease test

Rapid urease test is a rapid diagnostic test for the diagnosis of Helicobacter pylori. The basis of the test
is the ability of H. pylori to secrete the urease enzyme, which catalyzes the conversion of urea to
ammonia and carbon dioxide. It involves incubating a gastric biopsy in a urea broth that contains the pH
indicator phenol red. If gastric helicobacters are present, helicobacter urease breaks down the urea; with
the release of ammonia, a rise in pH and a color change occur.

Basal Gastric Secretion

- The acid is secreted in the absence of an external stimulus.
- Represents the response of the stomach to endogenous stimuli (vagus nerve, hormones, gastrin)
which are continually present in the fasting state.
- Minimum requirements:
1. The patients must be in fasting state and free from the sight or odor of food.
2. All medication influencing gastric secretion must be held for 24 hrs. Ex. Antacids
3. Away from fear, anger or depression
One – hour morning aspiration
✓ Standard method of measuring basal secretion
✓ Normal mean basal acid output:
- Male: 1.3 – 4.0 mEq/hr
- Female & Aged: slightly lower

Maximal Stimulation Test

- Output that can’t be increased substantially with additional stimulation.
- A dose of pentagastrin is injected and the gastric secretion is collected for analysis.
- Maximal value at 15mins and maintained for 30mins, falls to basal level at 60mins.
- The maximum acid output is represented by the 15- minutes specimen.
- Value: ___ mEq/hr

Basal and Maximal Acid Output in Various Conditions

Conditions Sex Number Acid Output
of (mEq./hour)
Patients
Basal Maximal
Controls Male 35 4.2 22.6
Female 26 1.8 15.2
Medical Male 145 5.3 26.7
students Female 16 3.3 21.4
Duodenal Male 256 7.1 35.2
ulcer Female 64 4.2 25.7
Gastric Male 117 2.9 19.6
ulcer Female 43 1.6 13.1
Gastric Male 74 1.3 6.7
carcinoma Female 32 0.7 3.0
Jejunal Male† 10 7.9 25.1
ulcer Female 4 5.5 16.4
Male‡ 4 9.1 36.1

Techniques:
1. Basal acid output
Procedure:
a) Following an overnight fast, the patient is intubated water maybe taken until 8hrs prior to
intubation.
b) The residual gastric secretion is aspirated measured qualitatively examined.
 c) Continuous aspiration is started manually with a syringe. Discard 1st and 2nd samples.
2. Maximal acid output
Procedure:
a) administer pentagastrin subcutaneously in a dose of 6ug/kg body weight.
b) Proceed with the collection of gastric secretion 15mm specimen for 1hr.
c) Record the volume and pH

INSULIN HYPOGLYCEMIA TEST

▪ Hypoglycemia resulting from the administration of insulin, a potent stimulus to gastric acid secretion.
Stimulus is transmitted by the vagus nerve and stimulation can be abolished by vagotomy.
▪ Insulin test is valid only if the blood glucose falls below 50 mg/dl
Technique:
1. After 2 hrs overnight fasting, the patient is intubated, a 2 hrs basal secretion is obtained in 15mins
sample.
2. Blood sample for glucose determination are obtained upon completion of basal secretion study at 30,
60, 90mins after insulin injection.
3. Insulin is given at either a fixed dosage of 15-20 units or at a calculation dosage of 0.20units/kg body
weight 50ml syringe.
4. Gastric secretion is collected in 15mins samples for 2hrs after insulin injection.
5. For each basal and post insulin gastric sample the volume and titrable acidity are determined, the
acid output is calculated.

MISCELLANEOUS TEST
▪ Mycobacteria culture
- Suspected PTB patients (young children)
- Collect gastric secretion immediately upon awakening before increased motor activity of
stomach.
▪ Exfoliative cytology
- Gastric cytology, gastroscopy and roentgenography are most useful for investigation of benign
and malignant lesions of the stomach.
- In the final analysis the most discriminating information is provided by exfoliative cytology or
biopsy.
- Technique in obtaining samples:
a) Sample aspiration of gastric content or juice
b) Abrasive balloons or brushes
c) Gastric lavage of saline
▪ Determination of Intrinsic Factor
- Failure to secrete intrinsic factor, gastritis with loss parietal cell, antibodies vs intrinsic factor.
- Techniques:
 a) In vitro assay using blocking or binding antibodies
b) Measuring absorption of the labeled Vitamin B12 in vivo

DETERMINATION OF TUMOR MARKERS IN GASTRIC SECRETION

Tumor markers and positive rate:
1. CEA = 31.60%
2. CA 19.9 = 62 – 67 %
3. Ferritin = 42 – 60%
4. Tissue polypeptide antigen = 74 – 77 %
Note: sensitivity and conflicting results may be affected by methodology variation and non-
standardization

DETERMINATION OF PLASMA GASTRIN: Not an integral part of gastric analysis, RIA of plasma or
serum gastrin is valuable in Disease of Zollinger – Ellison syndrome and PA both have elevated gastrin.

Other tests most

employed:
1. Gastroscopy or
Endoscopy
2. Roentgenography
3. Gastric cytology

DEFINITION OF
TERMS
▪ Cholecystokinin: is a peptide hormone of the
gastrointestinal system responsible for
stimulating the digestion of fat and protein.
Cholecystokinin, officially called pancreozymin, is synthesized and secreted by enteroendocrine cells
in the duodenum, the first segment of the small intestine.
▪ Pernicious anemia
- is a disease where large, immature, nucleated cells (megaloblasts, which are forerunners of red
blood cells) circulate in the blood, and do not function as blood cells.
- It is a disease caused by impaired uptake of vitamin B-12 due to the lack of intrinsic factor (IF)
in the gastric mucosa.
▪ Intrinsic factor
- also known as gastric intrinsic factor, is a glycoprotein produced by the parietal cells of the
stomach.
- It is necessary for the absorption of vitamin B₁₂ later on in the ileum of the small intestine.
- In humans, the gastric intrinsic factor protein is encoded by the GIF gene.