Analysis of Urine and other Body Fluids  Gastric secretions

 Colorless, watery, acidic, digestive fluid produced in

GASTRIC JUICE ANALYSIS the stomach
 Pale yellow
Origin and regulation of Gastric secretions  pH is 1-3
 Stomach is ready to receive the food  Secretes 2-3 L/ day
 Food is mixed with acid mucus and pepsin  Chemical composition:
 Stomach adds significant amount of digestive juice - inorganic salts and organic components that
to meal include, mucin, digestive enzymes, hormones
 Can be mediated by cephalic phase
 Food is released in to the duodenum Goblet cells or mucus cells
Anatomical consideration

Histological representation of gastric wall

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).
o Once secreted, pepsinogen is activated by stomach
Physiological view of gastric glands 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).
 Gastric acid secretion is controlled by three mechanisms:
2. Gastric phase  Neurocrine (denoting an endocrine influence on or
-triggered by the presence of food in the stomach by the nerves).
- Accounts for 70-90% of the acid secretion  Endocrine (gastrin)
 Paracrine (histamine)
3.Intestinal phase. In contrast to true endocrines these hormones are not
 Presence of chyme, most probably amino acids in released into the bloodstream but into the surrounding
the intestine triggers approximately 5% of the gastric tissues and act in the immediate vicinity, e.g. intestinal
acid secretion. mucosal hormones.

Hydrochloric Acid (HCl) Production PATHOLOGY

1.Cl- diffuses from the blood into the duct of gastric gland.
2.CO2 diffuse from the blood into the parietal cell.
3. CO2 combines with H2O to form H2CO3.
4. H2CO3 dissociates into bicarbonate and H+
5. H+ combines with Cl- in duct of gastric gland to form HCl-.
6. An ATP pump is necessary to pump the HCl- into the lumen
PEPTIC ULCER is an open sore.
-They are usually found in the lining of the stomach,
esophagus or upper small intestine.
 Gastric Ulcers - Ulcers in the stomach.
 Duodenal Ulcers - Ulcers in the upper area of the
small intestine, the duodenum.

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

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.
 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
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 lessen the
number of H. pylori bacteria.
Examples: amoxicillin, clarithromycin and tetracycline.
Antacids: In cases of hypersecretion of acid
Example: Zantac to neutralize acidity of the stomach.
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.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
 Life Style Changes
Specimen Collection
 Intubation (nasal or oral)
- Benign procedure but unpleasant and traumatic for
the patient.
Procedure:
a) Patient in sitting position
b) Bedfast patient 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
 Microscopic Examination
Gastric Intubation  RBC: small amount with no consequence
= Contraindicated in patients with:  WBC: infection/inflammation – gastric mucosa upper
a) Esophageal varices respiratory tract
b) Diverticula  Epithelial Cell: small amount (desquamation from
c) Stenosis various mucosa
d) Malignant neoplasm a) Squamous Cell- mouth, nose, pharynx &
e) Aortic aneurysm esophagus
b) Columnar cells- increased in gastritis
Indications:  Yeast cells- presence in large number in retention of
1.To determine if the patient can secrete any gastric acid gastric juice. Ex. Pyloric obstruction
 Protozoan/Metazoan
Anacidity: failure of pH to fall below 6.0 or 7.0 in the Occurs rarely from reflux of duodenal contents
augmented or maximal histamine, pentagastrin of Histalog Ex. G. lamblia, trophozoite and cyst
test SS larvae
Pernicious Anemia (PA)- treat patient with Vitamin B12. Ascaris ova
Hook Worm ova
2. To measure the amount of acid produced by a patient with  Helicobacter pylori
symptoms of GU, particularly DU or post- operative marginal - Present in 25% adult population
ulcer who has demonstrable lesion by roentgenography. 93% in GU
25% in DU
3. To support a hypersecretory state, characteristic of
- Characteristically found in or under the mucus
Zollinger Ellison Syndrome (ZES) layer on the enterocytes.
4. To determine the completeness of vagotomy
5. Aid in the differential diagnosis of GU from DU H. pylori maybe demonstrated thru:
a) Smear from biopsy specimen & stained with Giemsa
Physical Examination b) Microbial culture
Appearance c) Rapid urease test
Color- pale yellow, translucent Rapid urease test is a rapid diagnostic test for the diagnosis
Viscosity- Slightly viscous of Helicobacter pylori. The basis of the test is the ability of H.
Odor- faintly pungent pylori to secrete the urease enzyme, which catalyzes the
Volume- upto 50mL conversion of urea to ammonia and carbon dioxide.
 12 hours fasting – should be no food particles.
 The presence of food after 12 hours means delayed It involves incubating a gastric biopsy in a urea broth that
emulsification due to pyloric obstruction. contains the pH indicator phenol red. If gastric helicobacters
are present, helicobacter urease breaks down the urea; with
Bile – yellow to green color the release of ammonia, a rise in pH and a color change
- Small amount is normal due to excessive occur.
gagging during intubation.
- Large amount is abnormal due to obstruction of Basal Gastric Secretion
small intestine distal to the Ampulla of Vater. - The acid is secreted in the absence of an external
stimulus.
Mucus – normal gastric secretion from: - Represents the response of the stomach to
a. swallowed saliva – identified by its frothy nature endogenous stimuli (vagus nerve, hormones, gastrin)
b. upper respiratory secretion – highly tenacious & contains which are continually present in the fasting state.
lung particles
c. reflux of duodenal contents – identified by staining  Minimum requirements:
properties. 1. The patients must be in fasting state and free from
the sight or odor of food.
Blood - flecks or streak of blood, minor trauma during 2. All medication influencing gastric secretion must be
intubation, coffee ground appearance blood with acid held for 24 hrs. Ex. Antacids
secretion – longer/duration 3. Away from fear, anger or depression
Sources :
- gastritis One – hour morning aspiration
- ulcers - Standard method of measuring basal secretion
- CA Normal mean basal acid output:
- lesion in the mouth Male: 1.3 – 4.0 mEq/hr
Female & Aged: slightly lower
Maximal Stimulation Test  Hypoglycemia resulting from the administration of
- Output that can’t be increased substantially with insulin, a potent stimulus to gastric acid secretion.
additional stimulation. Stimulus is transmitted by the vagus nerve and
- A dose of pentagastrin is injected and the gastric stimulation can be abolished by vagotomy.
secretion is collected for analysis.  Insulin test is valid only if the blood glucose falls
- Maximal value at 15mins and maintained for 30mins, below 50 mg/dl
falls to basal level at 60mins.
- The maximum acid output is represented by the 15- Technique:
minutes specimen. 1. After 2 hrs overnight fasting, the patient is
Value: ___ mEq/hr intubated, a 2 hrs basal secretion is obtained in
15mins sample.
Basal and Maximal Acid Output in Various Conditions 2. Blood sample for glucose determination are
Number obtained upon completion of basal secretion study
Acid Output at 30, 60, 90mins after insulin injection.
Conditions Sex of
(mEq./hour) 3. Insulin is given at either a fixed dosage of 15-20 units
Patients
or at a calculation dosage of 0.20units/kg body
Basa Maxim weight 50ml syringe.
l al 4. Gastric secretion is collected in 15mins samples for
2hrs after insulin injection.
Male
35 4.2 22.6 5. For each basal and post insulin gastric sample the
Controls Femal
26 1.8 15.2 volume and titrable acidity are determined, the acid
e
output is calculated.
Male
Medical 145 5.3 26.7
Femal Miscellaneous test
students 16 3.3 21.4
e  Mycobacteria culture
- Suspected PTB patients (young children)
Male - Collect gastric secretion immediately upon
Duodenal 256 7.1 35.2
Femal
ulcer 64 4.2 25.7 awakening before increased motor activity of
e
stomach.
Male
Gastric 117 2.9 19.6  Exfoliative cytology
Femal
ulcer 43 1.6 13.1
e - Gastric cytology, gastroscopy and roentgenography
are most useful for investigation of benign and
Male malignant lesions of the stomach.
Gastric 74 1.3 6.7
Femal
carcinoma 32 0.7 3.0 - In the final analysis the most discriminating
e
information is provided by exfoliative cytology or
Male† biopsy.
10 7.9 25.1
Jejunal Femal
4 5.5 16.4
ulcer e Technique in obtaining samples:
4 9.1 36.1
Male‡ a) Sample aspiration of gastric content or juice
b) Abrasive balloons or brushes
Techniques: c) Gastric lavage of saline
1.Basal acid output
Procedure:  Determination of Intrinsic Factor
1) Following an overnight fast, the patient is intubated - Failure to secrete intrinsic factor, gastritis with loss
water maybe taken until 8hrs prior to intubation. parietal cell, antibodies vs intrinsic factor.
2) The residual gastric secretion is aspirated measured Techniques:
qualitatively examined. - In vitro assay using blocking or binding antibodies
3) Continuous aspiration is started manually with a - Measuring absorption of the labeled Vitamin B12 in
syringe. Discard 1st and 2nd samples. vivo
2. Maximal acid output
Procedure:  Determination of Tumor Markers in Gastric
1) administer pentagastrin subcutaneously in a dose of secretion
6ug/kg body weight.
2) Proceed with the collection of gastric secretion Tumor markers and positive rate:
15mm specimen for 1hr. 1. CEA = 31.60%
3) Record the volume and pH 2. CA 19.9 = 62 – 67 %
3. Ferritin = 42 – 60%
Insulin Hypoglycemia Test 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 – Definition of Terms
Ellison syndrome and PA both have elevated gastrin.
Cholecystokinin
Other tests most employed: - is a peptide hormone of the gastrointestinal
1. Gastroscopy or Endoscopy system responsible for stimulating the digestion of
2. Roentgenography
3. Gastric cytology
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.