Stool (Textbook) Flashcards
Normal Fecal Specimens
Contains:
- Bacteria
- Cellulose
- Undigested foodstuffs
- GI secretions
- Bile pigments
- Cells from the intestinal walls
- Electrolytes
- Water
Breakdown and Reabsorption Sites
Although digestion of ingested proteins, carbohydrates, and fats takes place throughout the alimentary tract
Small intestine is the primary site for the final breakdown and reabsorption of these compounds, using digestive enzymes secreted by the pancreas include trypsin, chymotrypsin, amino peptidase, and lipase. Bile salts provided by the liver aid in the digestion of fats.
Diarrhea Classification
Based on four factors:
- Illness duration
- Mechanism
- Severity
- Stool characteristics
Diarrhea lasting <4 weeks is defined as acute, and diarrhea persisting for >4 weeks is termed chronic diarrhea.
Diarrhea Mechanisms and Differentiation
The major mechanisms of diarrhea are:
- Secretory
- Osmotic
- Intestinal hypermotility
The laboratory tests used to differentiate these mechanisms are:
- Fecal electrolytes (fecal sodium, fecal potassium)
- Fecal osmolality
- Stool pH
Fecal Osmolarity and Calculation
- Total fecal osmolarity is close to the serum osmolality (290 mOsm/kg)
- Fecal sodium is 30 mmol/L
- Fecal potassium is 75 mmol/L
The fecal sodium and fecal potassium results are used to calculate the fecal osmotic gap.
Osmotic gap = 290 – [2 (fecal sodium + fecal potassium)]
Fecal Osmolarity Values
Osmotic diarrhea is >50 mOsm/kg
Secretory diarrhea is <50 mOsm/kg
Fecal pH
A fecal fluid pH of <5.6 indicates a malabsorption of sugars, causing an osmotic diarrhea.
Causes of Secretory Diarrhea
Caused by increased secretion of water.
- Bacterial
- Viral
- Protozoan infections
All produce increased secretion of water and electrolytes, which override the reabsorptive ability of the large intestine, leading to secretory diarrhea.
Other causes include: drugs, stimulant laxatives, hormones, inflammatory bowel disease (Crohn disease, ulcerative colitis, lymphocytic colitis, diverticulitis), endocrine disorders (hyperthyroidism, Zollinger-Ellison syndrome, VIPoma), neoplasms, and collagen vascular disease.
Osmotic Diarrhea Causes
Caused by poor absorption (maldigestion/malabsorbtion) that exerts osmotic pressure across the intestinal mucosa, presenting increased fecal material to the large intestine, resulting in water and electrolyte retention in the large intestine (osmotic diarrhea), which in turn results in excessive watery stool.
Causes:
- Disaccharidase deficiency (lactose intolerance)
- Malabsorption (celiac sprue)
- Poorly absorbed sugars (lactose, sorbitol, mannitol)
- Laxatives
- Magnesium-containing antacids
- Amebiasis
- Antibiotic administration
Altered Motility Diarrhea
Conditions of enhanced motility (hypermotility) or slow motility (constipation). Both can be seen in irritable bowel syndrome (IBS), a functional disorder in which the nerves and muscles of the bowel are extra sensitive
Hypermotility: excessive movement of intestinal contents through GI tract, normal absorption of intestinal contents/nutrients cannot occur. It can be caused by enteritis, the use of parasympathetic drugs, or with complications of malabsorption.
Rapid vs Slow Dumping
Rapid gastric emptying (RGE): hypermotility of the stomach and the shortened gastric emptying half-time, causing the small intestine to fill too quickly with undigested food; hallmark of early dumping syndrome (EDS). Symptoms begin 10 to 30 minutes following meal ingestion.
Late dumping: occurs 2 to 3 hours after a meal and is characterized by weakness, sweating, and dizziness.
Hypoglycemia is often a complication of dumping syndrome
Normal Excretion
Healthy people have a gastric emptying half-time range of 35 - 100 minutes, controlled by fundic tone, duodenal feedback, and GI hormones
Emptying time of <35 minutes is considered RGE.
Steatorrhea
Fecal Fat
Absence of bile salts that assist pancreatic lipase in the breakdown and subsequent reabsorption of dietary fat (primarily triglycerides) produces an increase steatorrhea that exceeds 6g per day
Cystic fibrosis, chronic pancreatitis, and carcinoma, are also associated with steatorrhea.
D-Xylose Test
Distinguishing maldigestion and malabsorption
D-Xylose is a sugar that does not need to be digested but does need to be absorbed to be present in the urine
Urobilin
Imparts brown color to feces
Conjugated bilirubin formed in the degradation of hemoglobin passes through the bile duct to the small intestine, where intestinal bacteria convert it to urobilinogen and stercobilinogen, which through intestinal oxidation is converted to urobilin.
Therefore, stools that appear pale (acholic stools) may signify a blockage of the bile duct.
Intestinal Bleeding/Irritation
Blood that originates from the esophagus, stomach, or duodenum takes approximately 3 days to appear in the stool; degradation of hemoglobin produces the characteristic black, tarry stool.
Blood from the lower GI tract requires less time to appear and retains its original red color.
Mucus-coated stools indicate intestinal inflammation or irritation.
Microscopic Examination
Specimens can be examined as wet preparations stained with methylene blue or as dried smears stained with Wright’s or Gram stain.
In patients with pancreatic insufficiency, microscopic examinations for fecal fats are ordered. Increased amounts of striated fibers may also be seen in biliary obstruction and gastrocolic fistulas
Fecal Leukocyte Detection
The presence of lactoferrin, a component of granulocyte secondary granules, indicates an invasive bacterial pathogen.
A lactoferrin latex agglutination test is available for detecting fecal leukocytes
Fecal Muscle Fiber Detection
Slides for muscle fiber detection are prepared by emulsifying a small amount of stool in 10% alcoholic eosin
Undigested fibers have visible striations running both vertically and horizontally. Partially digested fibers exhibit striations in only one direction, and digested fibers have no visible striations.
Fecal Lipids
Lipids included in the microscopic examination of feces are neutral fats (triglycerides), fatty acid salts (soaps), fatty acids, and cholesterol.
More than 60 droplets/high-power field can indicate steatorrhea; however, the split fat stain representing total fat content can provide a better indication (specimen mixed with acetic acid and heated. Stained droplets represent free fatty acids, fatty acids produced by hydrolysis of the soaps and the neutral fats)
Fecal Lipid Implications
An increased amount of total fat on the second slide with normal fat content on the first slide is an indication of malabsorption
Maldigestion is indicated by increased neutral fat on the first slide
Occult Blood
Any bleeding >2.5 mL/150 g of stool is considered pathologically significant, and no visible signs of bleeding may be present with this amount of blood, fecal occult blood testing (FOBT) is necessary.
Home gFOBT Kit
The kits contain guaiac-impregnated filter paper enclosed in a cardboard slide, to which the fecal specimen (front of slide) and hydrogen peroxide are added.
Sealed containers have facilitated colorectal cancer screening by allowing patients at home to place a specimen on a filter paper slide and bring or mail it to the laboratory for testing
gFOBT
Guaiac-based test for occult blood (gFOBT) based on detecting the pseudoperoxidase activity of hemoglobin, it is not too sensitive as blood from dietary sources can be found normally in stool. Uses a different indicator chromogen that urine strip.
Pseudoperoxidase Hemoglobin + H2 O2 + guaiac oxidized guaiac + H2 O (colorless) (Blue color)
igFOBT
The immunochemical fecal occult blood test (iFOBT) is specific for the globin portion of human hemoglobin and uses polyclonal anti-human hemoglobin antibodies
More sensitive to lower GI bleeding and can be used for patients who are taking aspirin and other anti-inflammatory medications.
The iFOBT tests do not detect bleeding from other sources, such as a bleeding ulcer, thus decreasing the chance for false-positive reactions
Porphyrin Based FOBT Flourometric Test
Test for hemoglobin based on the conversion of heme to fluorescent porphyrins, more sensitive to upper GI bleeding
Fecal Fat Testing
- Van de Kamer titration: fecal lipids are converted to fatty acids and titrated to a neutral endpoint with sodium hydroxide, measures about 80% fat concentration
- Gravimetric: measures all fecal fat
- Near-infrared reflectance spectroscopy
- Nuclear magnetic resonance spectroscopy: calculates water, fat, and nitrogen by comparing reflectance to a calibration curve
- Acid steatocrit: rapid test to estimate the amount of fat excretion
Reported as grams of fat or the coefficient of fat retention per 24 hours [(dietary fat – fecal fat) × 100 (dietary fat)]
Fecal Proteolytic Enzyme Testing
- Trypsin
- Chymotrypsin: resistant to intestinal degradation, sensitive indicator of less severe cases of pancreatic insufficiency, measured spectrophotometrically
- Elastase I: produced by the pancreas, isoenzyme of elastase, present in high concentrations in pancreatic secretions and is strongly resistant to degradation.
