Drug Information and Courses from MediaLab, Inc.

A urine specimen that has remained at room temperature for an extended period of time may produce a false-positive protein result on a reagent strip. A false positive may also occur in the presence of bacterial contamination, alkaline medication, or quaternary ammonium compounds such as disinfectants or drugs, and with skin cleansers containing chlorhexidine.

No blood is found in the urine of healthy individuals although samples from menstruating females, frequently, but not always, test positive for blood. Hematuria is associated with renal or genital urinary disorders in which the bleeding is the result of irritation to the involved organs or trauma. Examples include renal calculi, pyelonephritis, glomerulonephritis, tumors, trauma or exposure to toxic chemicals or drugs and/or strenuous exercise. Hemoglobinuria may be due to the lysis of red cells within the urinary tract. If it is caused by intravascular hemolysis, the hemoglobin is then filtered through the glomeruli. In the normal individual, the hemoglobin molecule attaches to haptoglobin and in this way bypasses the kidney filtration system. When the hemoglobin/haptoglobin system is overwhelmed, as in cases of hemolytic anemia, severe burns, transfusion reaction, infection or strenuous exercise, hemoglobin passes into the urine.

False negative results may occur in the presence of significant levels of protein or glucose and in urines with high specific gravity which may crenate the white blood cells causing them to be come unable to release esterases. Some drugs such as Cephalexin (Kelfex®), Cephalothin Keflin®) or high concentrations of oxalic acid may also cause decreased test results. Tetracycline may cause decreased activity, and high levels of the drug may cause a false negative reaction. Large amounts of ascorbate may cause false negative results.

False positive results can occur in screening procedures for bilirubin due to color interference from large amounts of blood in the urine, very concentrated urine or drugs that discolor the urine such as Pyridium. Because of this it is important to verify positive bilirubin results with a confirmatory test such as the Ictotest®.

In follow-up to the observations of the ESBL screening test, the following antibiotic susceptibility profile was later reported: Ampicillin = R; Cefazolin = R; Cefoxitin 1 = S; Ciprofloxacin 0.25 = S; Gentamicin 1 = S; Ceftazidime 32 = R; Imipenem The susceptibility of the 2nd generation drug cefoxitin, with resistance of the 1st generation cefazolin and the 3rd generation ceftazidime, is another way in addition to the screening test in which ESBL activity may be detected. It is recommended that clinical microbiologists check the antibiotic susceptibility profiles for possible ESBL activity of clinically significant isolates of K. pneumoniae and E. coli.Most automated systems have built in methods for automatically detecting an ESBL isolate, or provide an "alert" that such a strain may be present.

The federal drug testing custody and control form (CCF) must be used to document every urine collection required by the Department of Transportation drug testing program. At the present time, these include the: Federal Motor Carrier Safety Administration (FMCSA) Federal Aviation Administration (FAA) Research and Special Programs Administration (Pipeline) (RSPA) Federal Transit Administration (FTA) Federal Railroad Administration (FRA) United States Coast Guard (USCG)

It should also be understood that a Federally Regulated CCF need not be used in every situation involving a company regulated by the Department of Transportation. For example, if an interstate truck driver slips and falls while standing on the loading dock of a trucking terminal, and the trucking company for which the driver works requires a post-accident drug screen, a Non-Federally Regulated CCF would be appropriate for this collection. The driver was not involved in a safety sensitive assignment. On the other hand, if the driver had an accident while driving, then a Federally Regulated CCF must be used since the driver was in a safety sensitive position when the accident occurred.

This program is intended to provide guidance and training to those individuals who will be conducting Department of Transportation (DOT) regulated urine specimen collections. While this program is more than just an overview, obvious restraints prohibit an in-depth discussion of every procedure or problem that might be encountered.This program only serves as a training program. It does not represent final authority. Every effort has been taken to keep this course up-to-date with current regulations. However, if anything you see in this program conflicts with the federal regulations (49 CFR 40), the federal regulations prevail and must be followed.Training to qualify as a drug screen collector must include the flawless completion of five mock collections. These mock collections must include the following scenarios and must be performed in the presence of a qualified collector: Two uneventful collections. One collection in which the quantity of specimen is not sufficient. One collection in which the temperature of the specimen is out of range. One collection in which the donor refuses to sign either the donor certification on the pink copy of the CCF or refuses to initial the security strips.

All collection sites must meet the following security requirements: Must be able to prevent unauthorized access to the site during collection. Ensure that the donor does not have access to items that could be used to adulterate or dilute the specimen (e.g. soap, water, cleaning agents, etc.) Secure faucets, toilet tank tops, and other appropriate areas with tamper-evident tape if necessary. Ensure that the donor is at all times under the supervision of the collector or other collection site personnel. Provide for the secure handling and storage of specimens. (Specimens should be stored at 4-6º C. The refrigerator used should not be readily accessible to the general public and should be used only for the storage of urine drug screens and other clinical specimens. The refrigerator should be marked with a biohazard sign. No food or drink should ever be placed in the refrigerator.)

Refusal to Complete Donor Certification on Pink Copy of CCF or Initial Security Strips.If the donor refuses to complete the donor certification on the pink copy of the CCF, or refuses to initial the security strips after they have been affixed to the specimen vials, this is not considered a refusal to test. Do not debate with the donor. It is the responsibility of the collector to note the fact in the "Remarks" section of the CCF. Failure to do so may result in a Fatal Flaw. The MRO may not release the results of the drug screen unless the collector has noted in the "Remarks" section why the donor certification was not completed.Refusal to Provide ID or Social Security NumberIf the donor refuses to provide the collector with an ID or Social Security Number, this is not considered a refusal to test. The collector must make a notation of the fact in the "Remarks" section of the CCF. Failure to do so may result in a Fatal Flaw. After making the notation, the collector continues with the collection.

Scenario 1:A donor was asked to wash her hands prior to picking out the drug screen collection kit. The collector noticed that the donor was washing only one hand.Collector's Response:The collector would tell the donor that washing only one hand was an indication of possible interference with the testing process and that it could be interpreted as a refusal to test.Scenario 2:The donor is asked to remove his hat before going into the restroom. As he reluctantly did so, it was noticed that he was trying to conceal that a container was hidden inside the hat.Collector's Response:The collector must tell the donor that a directly observed collection will be conducted and explain the reason why.

The prothrombin time is a screening test that helps to assess the functionality of both the extrinsic and common pathways. The effectiveness and presence of factors I, II, V, VII, and X are assayed in this diagnostic test, as they are all found in the aforementioned pathways. The results of the prothrombin time are used in conjunction with other diagnostic tests, as well as the clinical picture of the patient, to determine any hemostatic abnormalities which may be present. In addition to being an integral part of the coagulation disorder assessment process, the PT is also used to determine therapeutic effectiveness of oral anticoagulants, by monitoring drugs such as Warfarin, Coumarin, and Dicoumarol. Prothrombin time test results are reported as the number of seconds needed for a clot to form in the patient specimen using the laboratory's instrument/reagent system, and as the International Normalized Ratio (INR).

A platelet function assay (PFA) is a screening test for the evaluation of platelets/primary hemostasis. Common clinical applications include the following: Preoperative evaluation of platelet function Determining the presence of drug-induced platelet dysfunction Determining platelet functionality in high-risk pregnancy Evaluation of patients with suspected inherited or acquired platelet disorders such as von Willebrand disease Evaluation of a bleeding patientA PFA instrument is able to differentiate between drug-induced platelet defects and other platelet defects. PFA tests are superior to the bleeding time test. The bleeding time is often not reproducible and, in spite of attempts at standardization, remains prone to variations in test results between persons performing the test. It is also relatively insensitive to platelet function. The bleeding time cannot be used to identify patients who may have recently ingested aspirin or non-steroidal anti-inflammatory drugs or patients who may have a platelet defect attributable to these drugs. The bleeding time is used to assess platelet function, but may be affected by platelet quantity. NOTE: Aspirin, and some other drugs, may falsely prolong bleeding times. Patients must be asked about aspirin use, and be aspirin free for 7-10 days prior to testing, for valid results.

Genetic mutations in HIV are well known and are very likely, considering the presence of two RNA molecules per virus. Either or both RNA molecules can mutate. These mutations potentially lead to drug resistance or encourage the virus to evade the body's immune response. Mutations have created three major groups of HIV - M, N, and O. M is found in 99% of all the HIV cases in the world. N and O are primarily found in West African countries. N, though, infects only a very small number of individuals. The M group has subgroups lettered A to J. Subgroup B predominates in North America.

Genetic mutations in HIV are well known and are very likely, considering the presence of two RNA molecules per virus. Either or both RNA molecules can mutate. These mutations potentially lead to drug resistance or encourage the virus to evade the body's immune response. Mutations have created three major groups of HIV - M, N, and O. M is found in 99% of all the HIV cases in the world. N and O are primarily found in West African countries. N, though, infects only a very small number of individuals. The M group has subgroups lettered A to J. Subgroup B predominates in North America.

This slide shows a marrow aspiration smear with numerous ring sideroblasts. Normal red cell precursors have only one or at most two granules of iron in their cytoplasm. These abnormal red cell precursors have numerous iron containing granules in their cytoplasm indicating abnormal iron incorporation. This iron is actually incorporated into mitochondria. Ring sideroblasts can be seen in idiopathic sideroblastic anemia, and in sideroblastic anemia induced by drugs, lead poisoning, and alcohol abuse.

ABO antibodies are not usually produced by an infant until 3 to 6 months of age. Antibodies found in the sera of newborns are almost always IgG, passively acquired from the mother. Thus, serum testing of newborns is not performed. Anti-A and anti-B titers are highest at ages 5-10 years and then they gradually decrease. Thus, in elderly patients, ABO antibodies may be difficult to detect. In patients with hypogammaglobulinemia, some leukemias, lymphomas or patients who are taking immunosuppressive drugs, the expected antibodies may be weak or even absent, reflecting the low levels of gamma globulin in the patient’s serum. As previously mentioned, these and other ABO typing discrepancies must be resolved before true ABO type can be determined.

Specialists in cytogenetics detect chromosome abnormalities and genetic disorders. Cytogenetics counseling may only be performed by an individual licenses in the cytogenetics specialty at the director level. Specialists in molecular genetics analyze DNA and RNA to find disease-related genotypes, mutations, and phenotypes in order to detect or predict disease and identify carriers. Specialists in histocompatibility test to determine tissue compatibility, prevent infections, and investigate and post-transplant problems. Techniques include blood typing, HLA typing, HLA antibody screening, disease markers, flow cytometry, crossmatching, HLA antibody identification, lymphocyte immunophenotyping, immunosuppressive drug assays, allogenic, isogeneic and autologous bone marrow processing and storage, mixed lymphocyte culture, stem cell culture, cell mediated assays, and assays for the presence of cytokines. Specialists in andrology and embryology examine gametes and embryos, including production, morphology, number, and motility, to address issues of fertility and infertility.

Offering or taking a bribe, kickback, bonus, commission, or inducement is against the rules of the Board and against the law. Many companies give away small promotional items, such as pens or note pads, to promote their products. This is legal, but be cautious about accepting more valuable items. This could be seen as a bribe. All of the following are serious violations of Board, state, and federal rules:Participating in any commissions, bonuses, kickbacks, inducements, or split-fee arrangements from physicians, health care providers, suppliers, hospitals, nursing homes, other clinical laboratories, pharmacies, and other facilities.Exploiting or influencing a patient for financial gain, including promoting, selling, or withholding services, drugs, or referrals.

HBV is spread in the community through: Sexual contact Drug abusers sharing contaminated needles An infant's exposure to its mother's body fluids

Therapeutic drug monitoring and pharmacogenomics are both pharmacy-related areas within the clinical laboratory. Although each is considered a sub-discipline within laboratory medicine, the two fields overlap significantly. In this course, we will provide an overview of each of these laboratory sub-disciplines and discuss the utility, rationale, and practice of each one.

The liver plays a major role in converting lipophilic nonpolar molecules (drug molecules) to more polar, water-soluble forms through a series of enzymatic reactions. Drug molecules can be modified by either phase I or phase ll reactions. Phase I reactions alter chemical structure by oxidation, reduction, or hydrolysis. Phase ll reactions conjugate drugs to create products that are water-soluble.

In addition to protein availability, other factors may affect drug absorption and distribution in the body as a whole or at specific sites within the body. The following table highlights some of these other factors. Factor Discussion Regional blood flow Reduced area blood flow can be seen in diabetics and enhanced blood flow can be seen in tumors. Lipid solubility of the drug The more lipophilic a drug is, the more likely it will enter the central nervous system. The integrity of the GI tract In a diseased gut, an orally-administered drug may not be absorbed as expected. Age Drug kinetics and dispositions change throughout life. In general, metabolism of drugs is reduced in the elderly. Genetics Mutations or deletions in drug metabolizing enzymes can greatly affect a drug's disposition.

Most drugs are not given as a single dose but are part of a regimen. It is the physician's responsibility to prescribe a drug so that the concentration of that drug reaches a safe and effective level. The dosing-goal for the prescribing clinician, if multiple doses of a drug will be given, is for both the peak and the trough drug levels to be consistently within the therapeutic range. If a drug is given at intervals that are the same as its half-life, it will take about 5 half-lives to reach steady state.

TDM provides a quantitative measure of the circulating concentration of a drug. The physician determines if the dosage of the drug needs to be adjusted based on this information.If a drug concentration is determined to be outside the therapeutic range, it may be for one of the reasons listed in the table below. Reason Discussion Noncompliance Patients may (intentionally or unintentionally) not take the drug. TDM can thus help monitor compliance. Dosing errors The dose may have been erroneous or inappropriate given the patient's condition. Malabsorption The TDM result will reveal if the drug cannot be absorbed well through the gut and an alternative route of administration will be needed. Drug interactions Many drugs interfere with the absorption or metabolism of other drugs. These interactions will be revealed by TDM. Kidney or liver disease Any pathology that affects elimination will cause an elevation in a drug level that will be unmasked by TDM. Altered protein binding Changes in serum proteins can lead to big changes in the amount of free drug in serum. Variations in the genetics of drug-metabolizing enzymes can also affect drug concentrations in the body. This is the field of pharmacogenomics that will be discussed later in the course.

Four major classes of drugs are frequently monitored by TDM: Antibiotics Anticonvulsants Immunosuppressants Cardiac medicationsThere are other drugs that are monitored by TDM that are not included in any of the above classifications, but the majority of TDM testing is performed for drugs that are included in one of these four categories.

Drug-binding proteins in serum can fluctuate in disease states. For example, if albumin levels fall, as can occur in liver failure or nephrotic syndrome, less albumin will be available for drug binding; a subsequent dose may produce a toxic concentration of free drug.The image on the right illustrates the loss of equilibrium between a protein-bound drug and a free drug when drug-binding proteins are diminished.Doses of drugs that are highly protein-bound may need to be adjusted in patients with lower drug-binding protein levels. Examples of some common drugs that are highly protein-bound include thyroxine, warfarin, diazepam, heparin, imipramine and phenytoin. �

When a drug enters the body, it reaches a peak concentration that starts to fall as the drug is eliminated. The figure on the right shows a typical kinetic with a drug given intravenously (IV).

Bioavailability refers to the amount of drug that actually reaches the circulation. It is calculated by comparing (in the same subjects) the area under the serum concentration - time curve (AUC) of an equivalent dose of the intravenous form and oral form. This is illustrated in the diagram on the right.For IV drugs, the bioavailability is 100%For oral medications, the bioavailability will be less than 100%, due in part to any of these reasons:* Oral drugs take longer to enter the circulation.* Oral drugs have slower absorption and distribution than IV drugs.* The amount of drug that is absorbed can depend on the status of the GI tract (stomach pH, presence of food, integrity/health of the intestines, speed of the GI tract, etc.)For oral drugs to be effective, bioavailability typically should be greater than 70%.Not all of a drug taken orally is able to have a pharmacologic effect; the dose would need to be higher than an IV dose.Since the absorption of an oral drug is slower than an IV drug and the drug takes longer to enter the circulation, clearing the drug will also most likely take a longer time.

To assess drug concentrations during the trough phase, blood should be drawn immediately before the next dose. To assess peak levels, the time for drawing depends on the route of administration: Oral: One hour after drug is taken (assumes a half-life of > two hours) IV: 15-30 minutes after injection/infusion Intramuscular (IM): 30 minutes - one hour after injection

However, every patient is unique. Changes in the gut (if the drug is taken orally), genetic variations in the liver's metabolizing enzymes, and the status of organs (like the kidneys and liver) all affect how a drug will be handled by an individual. TDM helps to ensure that a dosing regimen is appropriate for a given patient.

TDM is not useful for these drugs or in these specific situations: Intracelluar drugs that need to be converted to active forms (like AZT) Drugs in which the effects last much longer than the serum concentrations of the drugs; examples include antineoplastics (cancer chemotherapies) and warfarin Narcotic pain medications where continued use can lead to tolerance such that the levels needed for pain relief in one person would be toxic to another person

Anticonvulsants typically have narrow therapeutic windows. When levels are too low, the risk for seizure remains present. Drug levels that are too high can depress the central nervous system and may even lead to coma. Examples of anticonvulsants that are monitored by TDM include: Carbamazepine (Tegretol) Valproic acid (Depakene) Phenytoin (Dilantin) Phenobarbital Primidone (Mysoline)

Inotropics (drugs used to increase the pumping ability of the heart) and antiarrhythmics may need TDM. The cardiac glycoside inotropics digoxin and digitoxin have narrow therapeutic windows. Overdose can cause vomiting, diarrhea, confusion, visual disturbances, and cardiac arryhthmias. Examples of cardiac medications that are monitored by TDM include: Digoxin Digitoxin Procainamide N-Acetylprocainamide (NAPA) -the metabolite of procainamide Quinidine

Fluoresence polarization immunoassay (FPIA) is also a homogenous competitive immunoassay. In this system, fluorescein-labeled drug competes with unlabeled drug from the patient's serum sample for binding sites on an antibody reagent. The patient's sample, presumably containing the therapeutic drug that is being monitored, and the fluorescein-labeled drug are added to a chamber containing antibody for that drug. The labeled and unlabeled drug will compete for binding sites on the antibody. The greater the amount of drug in the sample, the fewer the number of binding sites that are available for the labeled analyte, leaving a greater number of small, free fluorescein-labeled molecules in the solution.When the chamber is excited with plane polarized light, fluorescein will absorb the light and emit it at a higher wavelength as fluorescent light. A small, free fluorescein-labeled drug rotates randomly and faster than it would if it were bound to antibody, interrupting the light and leading to less emission of light. The larger antibody-drug-fluorescein complexes rotate slower and emit more light in the measured plane. A lower level of drug in the patient's sample results in greater emission of polarized light because there are more antibody-drug-fluorescein complexes present to produce light in the measured plane. A higher level of drug in the patient's sample results in a lower emission of polarized light. This inverse relationship between the concentration of the drug and the polarization units (signal) is illustrated in the image below.

It has been said that we live in a new era of "individualized medicine". One of the primary drivers for this idea is the emerging field of pharmacogenomics (PGx). Pharmacogenomics (PGx) is the study of how individual variations in the human genome affect responses to medications. The term "pharmacogenetics" is also used for this discipline (people in the field use both terms); however, the term 'pharmacogenomics' is becoming more popular since we now know the entire human genome. The primary reason that individuals metabolize and respond to drugs differently is the inter-individual differences in receptor proteins and enzymes that metabolize the drugs. Mutations in these receptor proteins and enzymes can give rise to very different responses to drugs. In PGx, these mutations are referred to as variants.

Many CYP450 enzymes have been characterized, and the substrates (drugs) that each can recognize have been worked out to a large extent. These subfamilies of CYP450 enzymes have all been associated with polymorphisms that can affect drug disposition: CYP1A2, CYP2C9, CYP2C19 and CYP2D6.

When discussing PGx, we classify a person according to his/her phenotype (metabolic capacity for a given enzyme).A poor metabolizer (PM) is a person who lacks the functional enzyme and therefore exhibits decreased metabolism of drugs. This person would require lower doses of a drug that is metabolized by that enzyme. A PM who receives a standard dose is more likely to experience unwanted side effects or toxicity. A PM can also experience diminished effects with drugs that need to be metabolized to active compounds by the enzyme in question.An ultrarapid metabolizer (UM) will require a higher dose than usual since he/she will eliminate the drug more quickly. A UM may be resistant to standard treatments, and it may take some time to adjust the dosage before therapy is achieved.An intermediate metabolizer (IM) has one wild-type (normal) copy of the gene and one absent or dysfunctional copy. The IM group is very heterogeneous.A person with normal enzyme activity is referred to as an extensive metabolizer (EM). This person should respond to standard dosages of a drug. Most people are EM's. This is the population in which most dosing regimens have been worked out in clinical trials.

Genotyping can give us a definitive profile of a given CYP450 enzyme's mutations. But since there are dozens of mutations usually associated with each enzyme, a complete characterization of a CYP450 is not always realistic. Without complete sequencing of the entire allele, it may not be possible to entirely rule out a mutation in a patient who shows none of the more common polymorphisms. If we consider the number of possible mutations and the possible presence of inducing/inhibiting substances, phenotyping for drug metabolism may sound more reasonable than genotyping.

By knowing a patient's disposition to specific drugs, the physician should be able to start the patient on an appropriate regimen rather than perfecting treatment based on trial and error. Drugs whose metabolism may prove to be problematic can be avoided, and second-line therapies that are metabolized by different, unaffected enzymes can be chosen. Clinical chemists, pharmacologists, and physicians need to translate knowledge of CYP450 polymorphisms into clinically-validated treatment algorithms. Dosing recommendations for PM, EM, IM and UM patients are beginning to appear in the literature for various classes of drugs, and the FDA is encouraging the incorporation of pharmacogenomic testing in the development process for new drugs.

The genes involved in warfarin metabolism are CYP2C9 and vitamin K epoxide reductase complex subunit 1 (VKOR). Warfarin owes its anticoagulant action to its inhibition of VKOR. This enzyme recycles vitamin K, a critical element for the clotting factors II, VII, IX, and X, as well as for proteins C, S, and Z. There are six CYP2C9 alleles that are known to cause prolonged metabolism of warfarin: CYP2C9 *2, *3, *4, *5, *6, and *11. (Polymorphisms in CYP450 genes are denoted with asterisks.)One-third of the patients that receive warfarin metabolize it differently than expected and experience a higher risk of bleeding.Genetic testing for the two most common polymorphisms (CYP2C9*2 and *3) as well as for VKOR may be able to reduce the variability associated with warfarin dosing response. Labs performing PGx testing can provide general warfarin dosing recommendations based on the patient's genotype analysis. The lab report will indicate whether a patient has a normal, mild, moderate, high, or very high sensitivity to warfarin. For example, a patient who has one CYP2C9 normal wild-type allele (CYP2C9 *1), one polymorphism (CYP2C9*3), and also a VKOR polymorphism is predicted to have a moderate sensitivity to warfarin. This patient should have frequent INR monitoring and possible warfarin dose reduction. It is important to recognize that knowing a genotype does not necessarily guarantee accurate dose prediction; other drugs and/or environmental or disease factors can also alter CYP2C9 activity. Therefore, monitoring the INR is still very important.

Phenotyping involves measuring the metabolism of a probe drug. For example, with CYP2D6, dextromethorphan or debrisoquine can be given to a patient to see how well the drug is metabolized. Both these drugs are safe and extensively metabolized by CYP2D6. By measuring the parent drug and the metabolite in urine, the metabolic capacity of a CYP450 enzyme can be estimated. Such testing is complex and tedious, however, and has not become routine in clinical laboratories. Therefore, genotyping is likely to be the main tool that is used for assessing the PGx of a patient.

Drugs and toxins including therapeutic drugs and drugs of abuse may be present in the plasma. Other substances too numerous to mention are also present in plasma.

A trough level is drawn immediately before the next dose of the drug is administered.A peak level is drawn 1 to several hours after the drug is administered (depending on the drug).

Physicians need to know the blood concentration of certain drugs in order to select the best dose for their patients.As a phlebotomist, you might be asked to draw peak (highest), and trough (lowest) levels of various therapeutic drugs.

Heinz bodies are 1-3 um particles of denatured hemoglobin settling eccentrically, usually close to the red cell membrane. They are found in erythrocytes in unstable hemoglobin disorders, acute drug induced hemolysis, and following splenectomy. Their formation may be exaggerated by in-vitro incubation of a fresh blood sample with phenylhydrazine. Heinz bodies, as pictured here, are identified using a supra-vital stain, such as new methylene blue or cresyl violet. Bite cells, visible with Wright-Giemsa staining, are visual reminders that the spleen is functional and has pitted the aberrant chunk of hemoglobin from the circulating erythrocyte.

Increased numbers of cuboidal cells are found in renal transplant rejection, acute tubular necrosis (diuretic phase), injuries that interrupt blood flow to the kidney, and acute glomerulonephritis accompanied by tubular damage. Ingestion of various drugs and chemicals may cause significant tubular shedding of these epithelial cells. Cuboidal cells are easily seen in urine in cases of salicylate intoxication.

The characteristics of the more common types of abnormal crystals are summarized in the table below. Crystal Color Significance Leucine Yellow Metabolism Tyrosine Colorless–yellow Liver disease (rare) Cystine Colorless Cystine metabolism Cholesterol Colorless Renal tubular disease Bilirubin Gold-orange Increased bilirubin High doses of ampicillin, sulfonamide drugs or other drugs may also result in urine crystal formation. It is important to check the patient’s current medications when unusual crystals are found in the urine specimen.

TB infection controls include: standardized anti-tuberculosis treatment regimens in the initial phase of therapy; rapid drug susceptibility testing; directly observed therapy in which a health professional watches a patient swallow each dose of medication and records the date that the administration was observed; improved infection control practices.

There are a number of conditions in which hypersegmented neutrophils may be seen, such as megaloblastic anemias that include folic acid deficiency and pernicious anemia. Individuals who are receiving chemotherapy or have long-term chronic infections may also have hypersegmented neutrophils.The cells seen in these conditions would be classified as pathological since the body is responding abnormally as a result of either a deficiency of a component needed for DNA production or because of the toxic effect that chemotherapy drugs have on DNA.

Another example of a May-Hegglin-type body. This smear was from a case of pseudo May-Hegglin caused by drugs. Bizarre appearing platelets can also be seen in cases of pseudo May-Hegglin.