- Life processes, interactions, and adaptations
- The movement of materials and energy through living communities
- The successional development of ecosystems
- The abundance and distribution of organisms and biodiversity in the context of the environment.
- Brown: Normal
- Black: Bleeding in upper gastrointestinal tract (proximal to cecum), Drugs (iron salts, bismuth salts, charcoal)
- Red: Bleeeding in large intestine, undigested tomatoes or beets
- Clay-colored (gray-white): Biliary obstruction
- Silvery: Carcinoma of ampulla of Vater
- Watery: Certain strains of Escherichia coli, Rotavirus enteritis, cryptosporidiosis
- Rice water: Cholera
- Unformed with blood and mucus: Amebiasis, inflammatory bowel disease
- Unformed with blood, mucus, and pus: Bacillary dysentery
- Unformed, frothy, foul smelling, which float on water: Steatorrhea.
- Sedimentation techniques: Ova and cysts settle at the bottom. However, excessive fecal debris may make the detection of parasites difficult. Example: Formolethyl acetate sedimentation procedure.
- Floatation techniques: Ova and cysts float on surface. However, some ova and cysts do not float at the top in this procedure. Examples: Saturated salt floatation technique and zinc sulphate concentration technique.
- Occult blood
- Excess fat excretion (malabsorption)
- Reducing sugars
- Fecal osmotic gap
- Fecal pH
- Intestinal diseases: hookworms, amebiasis, typhoid fever, ulcerative colitis, intussusception, adenoma, cancer of colon or rectum.
- Gastric and esophageal diseases: peptic ulcer, gastritis, esophageal varices, hiatus hernia.
- Systemic disorders: bleeding diathesis, uremia.
- Long distance runners.
- Ingestion of peroxidase-containing foods like red meat, fish, poultry, turnips, horseradish, cauliflower, spinach, or cucumber. Diet should be free from peroxidase-containing foods for at least 3 days prior to testing.
- Drugs like aspirin and other anti-inflammatory drugs, which increase blood loss from gastrointestinal tract in normal persons.
- Foods containing large amounts of vitamin C.
- Conversion of all hemoglobin to acid hematin (which has no peroxidase-like activity) during passage through the gastrointestinal tract.
- Deficiency of pancreatic lipase (insufficient lipolysis): chronic pancreatitis, cystic fibrosis.
- Deficiency of bile salts (insufficient emulsification of fat): biliary obstruction, severe liver disease, bile salt deconjugation due to bacterial overgrowth in the small intestine.
- Diseases of small intestine: tropical sprue, celiac disease, Whipple’s disease.
- Microscopic stool examination after staining for fat: A random specimen of stool is collected after putting the patient on a diet of >80 gm fat per day. Stool sample is stained with a fat stain (oil red O, Sudan III, or Sudan IV) and observed under the microscope for fat globules (Figure 845.2). Presence of ≥60 fat droplets/HPF indicates steatorrhea. Ingestion of mineral or castor oil and use of rectal suppositories can cause problems in interpretation.
- Quantitative estimation of fecal fat: The definitive test for diagnosis of fat malabsorption is quantitation of fecal fat. Patient should be on a diet of 70-100 gm of fat per day for 6 days before the test. Feces are collected over 72 hours and stored in a refrigerator during the collection period. Specimen should not be contaminated with urine. Fat quantitation can be done by gravimetric or titrimetric method. In gravimetric method, an accurately weighed sample of feces is emulsified, acidified, and fat is extracted in a solvent; after evaporation of solvent, fat is weighed as a pure compound. Titrimetric analysis is the most widely used method. An accurately weighed stool sample is treated with alcoholic potassium hydroxide to convert fat into soaps. Soaps are then converted to fatty acids by the addition of hydrochloric acid. Fatty acids are extracted in a solvent and the solvent is evaporated. The solution of fat made in neutral alcohol is then titrated against sodium hydroxide. Fatty acids comprise about 80% of fecal fat. Values >7 grams/day are usually abnormal. Values >14 grams/day are specific for diseases causing fat malabsorption.
(Plasma sodium × Urine creatinine)
- Causes of increased specific gravity:
a. Reduced renal perfusion (with preservation of concentrating ability of tubules),
e. Urinary tract obstruction.
- Causes of reduced specific gravity:
a. Diabetes insipidus
b. Chronic renal failure
c. Impaired concentrating ability due to diseases of tubules.
- Pre-renal azotemia: shock, congestive heart failure, salt and water depletion
- Renal azotemia: impairment of renal function
- Post-renal azotemia: obstruction of urinary tract
- Increased rate of production of urea:
• High protein diet
• Increased protein catabolism (trauma, burns, fever)
• Absorption of amino acids and peptides from a large gastrointestinal hemorrhage or tissue hematoma
- Diacetyl monoxime urea method: This is a direct method. Urea reacts with diacetyl monoxime at high temperature in the presence of a strong acid and an oxidizing agent. Reaction of urea and diacetyl monoxime produces a yellow diazine derivative. The intensity of color is measured in a colorimeter or spectrophotometer.
- Urease- Berthelot reaction: This is an indirect method. Enzyme urease splits off ammonia from the urea molecule at 37°C. Ammonia generated is then reacted with alkaline hypochlorite and phenol with a catalyst to produce a stable color (indophenol). Intensity of color produced is then measured in a spectrophotometer at 570 nm.
- It is produced from muscles at a constant rate and its level in blood is not affected by diet, protein catabolism, or other exogenous factors;
- It is not reabsorbed, and very little is secreted by tubules.
Causes of Increased Serum Creatinine Level
- Pre-renal, renal, and post-renal azotemia
- Large amount of dietary meat
- Active acromegaly and gigantism
- Increasing age (reduction in muscle mass)
- Jaffe’s reaction (Alkaline picrate reaction): This is the most widely used method. Creatinine reacts with picrate in an alkaline solution to produce spectrophotometer at 485 nm. Certain substances in plasma (such as glucose, protein, fructose, ascorbic acid, acetoacetate, acetone, and cephalosporins) react with picrate in a similar manner; these are called as non-creatinine chromogens (and can cause false elevation of serum creatinine level). Thus ‘true’ creatinine is less by 0.2 to 0.4 mg/dl when estimated by Jaffe’s reaction.
- Enzymatic methods: These methods use enzymes that cleave creatinine; hydrogen peroxide produced then reacts with phenol and a dye to produce a colored product, which is measured in a spectrophotometer.
- Increased BUN with normal serum creatinine:
• Pre-renal azotemia (reduced renal perfusion)
• High protein diet
• Increased protein catabolism
• Gastrointestinal hemorrhage
- Increase of both BUN and serum creatinine with disproportionately greater increase of BUN:
• Post-renal azotemia (Obstruction to the outflow of urine)
Obstruction to the urine outflow causes diffusion of urinary urea back into the blood from tubules because of backpressure.
Causes of Decreased BUN/Creatinine Ratio (<10:1)
- Acute tubular necrosis
- Low protein diet, starvation
- Severe liver disease
(72 × Serum creatinine in mg/dl)
The agents used for measurement of GFR are:
- Exogenous: Inulin, Radiolabelled ethylenediamine tetraacetic acid (51Cr- EDTA), 125I-iothalamate
- Endogenous: Creatinine, Urea, Cystatin C
- A small amount of creatinine is secreted by renal tubules that increase even further in advanced renal failure.
- Collection of urine is often incomplete.
- Creatinine level is affected by intake of meat and muscle mass.
- Creatinine level is affected by certain drugs like cimetidine, probenecid, and trimethoprim (which block tubular secretion of creatinine).