Diet Information and Courses from MediaLab, Inc.
These are the MediaLab courses that cover Diet and links to relevant pages within the course.
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| A patient that is on a vegetarian diet will most likely have an acid urine pH. | View Page |
| pH Value Due to the wide range in urine pH values in healthy individuals, pH results must be evaluated in conjunction with the patient's medical condition. Factors to be considered include: respiratory or metabolic acidosis respiratory or metabolic alkalosis renal function crystal or calculi formation urinary tract status diet | View Page |
| Acid and alkaline urine pH Reasons for acidic urine pH include: a high-meat diet, respiratory/metabolic acidosis, and hypochloridemia. A urine with a high concentration of glucose may also have a lower pH. An alkaline pH may be the result of a vegetarian diet, respiratory/metabolic alkalosis, or a bacterial infection caused by urease-producing bacteria. Urine that contains bacteria can become more alkaline if the specimen remains at room temperature for an extended period of time. A pH can be falsely interpreted as more acidic than it actually is if improper technique is used and excess urine is allowed to pool on the reagent strip. The reagents from the protein pad, that includes an acid buffer, can run over into the pH pad if the strip has these two tests located next to each other. | View Page |
| Match the following factors with the expected pH: | View Page |
| Three Kinds of Ketones When the body breaks down fat for energy, three intermediate products are formed. These products, collectively referred to as ketones, are acetone, acetoacetic acid, and beta-hydroxybutyric acid. Normally, the body gets the energy it needs from carbohydrates in the diet. However, stored fat is broken down and ketones are produced and appear in the urine if the diet does not contain enough carbohydrate to supply the body with glucose for energy or if the body cannot use glucose properly. | View Page |
| False Negative Results False negative results may occur in urine specimens that did not remain in the bladder a sufficient length of time for the bacteria to reduce a measurable quantity of nitrate to nitrite. Other reasons for false negative results include high specific gravity, ascorbic acid levels above 25mg/dL or low pH (<6). Less frequently, the cause may be due to a lack of sufficient nitrate in the diet (green vegetables) or further reduction of nitrite to nitrogen when large numbers of bacteria are present. In patients receiving antibiotics, the metabolism of the bacteria may be inhibited which would also produce a false negative reaction. | View Page |
| Increased excretion of creatinine would be expected in which of the following groups: | View Page |
| Other Causes of Ketonuria Ketonuria can also be found in conditions associated with a decreased intake of carbohydrates (starvation), digestive disturbances, dietary imbalance (high fat/low carbohydrate diet), eclampsia, prolonged vomiting and diarrhea, glycogen storage diseases, vigorous exercise, fever, and following administration of anesthesia. Ketone bodies are mildly toxic to the body, tending to interfere with the excretion of uric acid, produce mild depression of the central nervous system, and cause acidosis. | View Page |
| Lp(a) Lipoprotein (a) is a modified version of LDL containing a unique protein, apolipoprotein (a). It was discovered in 1963 and is well-associated with vascular disease. Do not confuse apolipoprotein (a) with apolipoprotein A that is found on high density lipoprotein particles. Lipoprotein (a) is abbreviated as Lp(a). Lp(a) is an LDL particle whose ApoB molecule has formed a disulfide bond with another protein called Apo(a), see figure. Apo(a) is a protein very similar in structure to plasminogen. Numerous retrospective case control studies and prospective studies have shown Lp(a) to be an independent risk factor for vascular disease. This means that Lp(a) levels alone (not in conjunction with LDL, or patient risk factors) can predict cardiovascular risk. Lp(a) has been called the most atherogenic lipoprotein. Serum concentrations of Lp(a) are related to genetic factors; drugs and diet changes do not typically lower Lp(a) as they do LDL. | View Page |
| Adult Treatment Panel How do physicians interpret risk marker results? Assuming the laboratory offers, and physicians order, cardiovascular risk marker tests, how are these results used? The National Cholesterol Education Program periodically assembles scientists and physicians to create lipid treatment guidelines for patients. These panels are referred to as the Adult Treatment Panel (ATP). The third assembly of the ATP did not give specific guidelines regarding risk marker use in patients but they did acknowledge their potential utility. The general consensus is that novel cardiovascular risk markers should be used in selected patients, such as those who already have significant risk factors (hypertension, smoking, obesity, etc.) or in patients who have family histories of cardiovascular disease. The value in using risk markers is that they will not only uncover cardiovascular risk but they can also be used to motivate patients to alter lifestyle and diet. It is expected that as these emerging cardiovascular risk markers continue to be validated in clinical studies, they will become very useful and perhaps even be part of a new standard of care for patients.If risk marker levels can be correlated to treatment strategies, physicians will find them especially useful in tracking patient success. | View Page |
| Coagulation Disorders - Acquired A lack of Vitamin K can cause a loss of functionality in Vitamin K dependant coagulation factors, specifically, factors II, VII, IX and X.
Most often associated with a diet lacking in Vitamin K, it may also present in situations of broad spectrum antibiotic use, where normal flora in the gut have been eliminated.
As one might expect, treatment involves a diet rich in Vitamin K containing foods, and judicious use of broad spectrum antibiotics. | View Page |
| Iron Intake and Recycling The typical daily diet of most Americans contains approximately 10 to 15 mg of iron. Sources of dietary iron include heme iron from meats and nonheme iron from whole grains and vegetables. Many processed foods, such as breakfast cereal, are fortified with iron. However, the normal individual absorbs only 5% to 15% of dietary iron, or about 1 to 2 mg daily. Females may absorb slightly more iron than males as they require more iron to replace that lost through menstruation and to meet the increased need for iron in pregnancy.Absorption of iron occurs through the mucosal cells in the duodenum (proximal small intestine). Dietary iron that is not absorbed is excreted in the feces. Intestinal absorption provides the means for regulating the amount of iron in the body.The amount of Iron absorbed is normally low because iron is well conserved within the body. Heme iron from senescent erythrocytes is cycled back into the iron pool and reused for incorporation into developing erythrocytes. Furthermore, iron is normally lost from the body only in very small amounts, primarily through desquamation of mucosal cells in the gastrointestinal tract and losses through body secretions, including urine, sweat and feces. Therefore, under normal conditions, very little dietary iron needs to be absorbed to maintain iron homeostasis.(3) | View Page |
| Serum Iron Serum iron (SI) is a measure of circulating iron bound to transferrin and is reflective of total body iron. SI is elevated in hereditary hemochromatosis (HH) and acute hepatitis. SI is decreased in iron deficiency anemia and chronic inflammation. SI concentrations exhibit diurnal variation, with the lowest values occurring around midnight. In addition, specimens collected from the same individual at the same time of the day may exhibit day to day variations as high as 40%. SI determinations are also affected by diet, menstrual cycle, pregnancy, ingestion of iron supplements, and oral contraceptive use. SI levels alone are considered insensitive indicators of HH. SI is typically measured on automated analyzers using spectrophotometric methods. Iron in the sample is released from transferrin with an acid reagent, reduced to the ferrous state, and reacted with a chromogen such as bathophenanthroline or ferrozine. The intensity of the color change is proportional to the iron concentration. Interference can arise from the use of a hemolyzed sample and contamination of reagents and water with iron. A typical reference interval for SI is 60 - 150 micrograms/dL. SI is usually ordered along with its companion test, the total iron binding capacity (TIBC), or with transferrin (Tf).(2) | View Page |
| This photomicrograph is an acid-fast stained smear prepared from a yeast colony growing on ascospore agar. A helmet-shaped, red-staining, acid fast yeast cell is seen in the center of view at the tip of the arrow, against the background, blue-staining blastoconidia. The presumptive identification of Hansenula anomala was made. Predisposing conditions that may indicate that this isolate is more than a contaminant include: | View Page |
| Oral candidiasis may be directly exasperated by the habitual ingestion of: | View Page |
| A 65 year old Asian female presented to the emergency room exhibiting severe abdominal pain, fever and diarrhea. Examination revealed an enlarged liver that was tender to the touch. Patient history revealed that the woman worked in a fish processing plant for years prior to moving to the United States. Her diet was heavy in raw fish. Stool and duodenal contents were collected and sent to the laboratory for cultures and parasite examination. The cultures were unremarkable. This suspicious form was seen in both specimen types. It measures 27 µm by 14 µm. This patient is most likely suffering from: | View Page |
| A 54 year old Finnish male presented at the local clinic with abdominal pain, weight loss, overall weakness and digestive discomfort. Patient history revealed that the man's diet was rich in raw fish. A complete blood count (CBC) was performed and revealed macrocytic anemia. A stool for parasitic examination was ordered. This suspicious form was seen upon initial screening of the sample. It measures 77 µm by 48 µm. This patient is most likely suffering from an infection with: | View Page |
| TDM and PGx Can we use therapeutic drug monitoring (TDM) to assess PGx?TDM of the drug in question can also tell us a good deal about a drug's metabolism and will also take into account all the other variables at play (co-medications, diet, impaired organ function, etc.) However, unlike genotyping and probe-drug testing, therapeutic drug monitoring must be performed during therapy, not before. So, in fact, TDM is not really used to predict therapy in PGx but serves as a confirmation of PGx findings. TDM and genotyping should be considered complementary and can be used in tandem to, first, predict and then verify appropriate serum drug levels. | View Page |
| 12 hour fast Patients should be on a normal diet, and be normally active for 3 days prior to the test.Patients must fast for 12 hours before beginning the test. | View Page |
| Calcium Oxalate Crystals Calcium oxalate crystals have a characteristic octahedral or envelope shape. Fine focusing will cause the "x" to be refractile. Size may vary from extremely small to quite large. They are associated with diets high in oxalic acid or chemical toxicity. Occasionally calcium oxalate crystals are dumbbell or oval in shape. | View Page |