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INTERPRETATION OF LAB TESTS with a Pharmaceutical Focus

INTERPRETATION OF LAB TESTS with a Pharmaceutical Focus. Barb Bancroft, RN, MSN, PNP Chicago, IL www.barbbancroft.com BBancr9271@aol.com AUGUST 5, 2010. Rule number one …. Know your own lab’s normal values

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INTERPRETATION OF LAB TESTS with a Pharmaceutical Focus

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  1. INTERPRETATION OF LAB TESTS with a Pharmaceutical Focus Barb Bancroft, RN, MSN, PNP Chicago, IL www.barbbancroft.com BBancr9271@aol.com AUGUST 5, 2010

  2. Rule number one … • Know your own lab’s normal values • The reference values are affected by many variables, including patient population and laboratory methods used

  3. Rule #2--READ the package insert for suggested testing intervals • This is specifically a CYA (Cover your “donkey”) procedure for prescribing purposes • Every drug and every pharmaceutical company has different testing intervals—it would be wise to know them • Examples: Amiodarone (Cordarone)—liver function tests (LFTs) at baseline and every six months (if the LFTs are greater than 3x the ULN, or doubles in a patient with elevated baseline LFTs, decrease the dose or d/c the drug)

  4. Another example: • Spironolactone (Aldactone) and eplerenone (Inspra)—check potassium and renal function (serum creatinine) at baseline, three and seven days after initiation, monthly for three months, then quarterly; restart monitoring cycle if ACE or ARB is added or their dose is increased; • Do not start if serum creatinine is greater than 2.5 mg/dL (221 mmol/L) in men or greater than 2 mg/dL (176.8 mmol/L) in women (for spironolactone ≥ 200 mmol/L per Canadian Cardiovascular Society) • Reduce dose or d/c if serum potassium > 5.5 mEq/L (same as mmol/L in Canada)

  5. Is genotyping necessary with certain drugs? • Carbamazepine—baseline HLA-B*1502 testing in Asians—severe skin reactions can occur • High prevalence (15%) in Hong Kong, Thailand, Malaysia, and parts of the Philippines, followed by Taiwan (10%), North China (4%), and Japan and Korea (1%). In South Asians, including Indians, risk is 2-4% (Novartis Pharmaceuticals Corporation—Product information. February 2009)

  6. Serum protein electrophoresis • List the plasma proteins 1) albumin 2) globulins 3) fibrinogen • Is there a difference between plasma proteins and serum proteins?

  7. Yes. The removal of fibrinogen • So, the serum proteins are albumin and the “globulins”. • Fibrinogen—(1.4-4.0 mg/dL or 140 to 400g/L) • Hyperfibrinogenemia (greater than 4.0 g/dL or 400 g/dL) increases the risk of clotting

  8. What conditions increase the risk of clotting? • Venous catheters • Heart failure/Atrial fibrillation • Immobilization • Trauma • Surgery • Pregnancy and postpartum • Prolonged travel (economy class syndrome—air travel) • Heparin-induced thrombocytopenia • Estrogen therapy (?)

  9. What about the estrogen controversy? • Estrogen excess increases fibrinogen • COC’s? The “old days” vs. today • HT? (hormone therapy—E + P—po, not patch or gel or any other topical route) • How about your own ovaries, ie, endogenous estrogen?

  10. What else increases fibrinogen? • Smoking increases fibrinogen • So how about smoking and estrogen, eg, oral contraceptives or HT in the PMF? (use patch) • Smoking accelerates aging • Aging and fibrinogen—increases by 1% per year after age 30 • How many 30 –year-olds are on warfarin/Coumadin?

  11. Biological rhythms and clotting • DVT (venous clot or redclot) may take a few hours or a few weeks to form depending on the circumstances; attached to the deep veins of the legs and pelvis; breaks off in early a.m. due to standing up and moving around; takes 30 minutes to travel to the lungs—Up at 7 a.m.? Pulmonary embolism at 7:30 a.m. • Coumadin/Heparin inhibit clotting factors (red clots) • If the pulmonary embolism is huge, tissue plasminogen activator (Activase/alteplase or reteplase/Retavase; streptokinase) may be infused • Incidence varies based on AGE(0.2 cases/100,000 in kids under 15 ; 700 cases per 100,000 in patients over 85

  12. Coagulation profile • Platelet counts and platelet aggregation/clumping (how well platelets aggregate as measured by the bleeding time—3 to 6 minutes) • PT (prothrombin time)—11.3 to 13.3 seconds • INR is used to measure PT in patients on Coumadin (2-3) • aPTT—22.1 to 34 seconds (stable aPTT on heparin is 60 to 84 seconds)

  13. Quantitative and qualitative platelet dysfunction • Platelet counts and bleeding times—quantitative and qualitative measurements • WHAT IS PLATELET TYPE BLEEDING? • Normal platelet count--150,000 to 450,000; • Platelet counts above 100,000 do well w/ hemostasis; • 50,000 to 100000 may show increased bruising; • platelet counts less than 50,000 need monitoring; • spontaneous hemorrhage under 10,000

  14. Platelet-type bleeding • Acute DIC -- Severe thrombocytopenia due to meningococcemia

  15. Platelet type bleeding –thrombocytopenia; chronic DIC • Secondary to malignancy

  16. The most common drugs that cause thrombocytopenia • heparin • sulfa drugs, piperacillin, linezolid, rifampin • quinine and quinidine • cimetidine (Tagamet) • valproic acid(Depakene, Depakote)—check platelet count and coagulation tests baseline, periodically, and prior to planned surgery • Don’t forget ETOH abuse also causes thrombocytopenia

  17. ASA , NSAIDS and clopidogrel (Plavix) cause qualitative platelet dysfunction • Cause a qualitative dysfunction NOT quantitative (numbers are normal, bleeding time is prolonged) • ASA and NSAIDs inhibit the enzyme cyclooxygenase (COX), which in turn prevents the formation of thromboxane A2 and prostaglandins • Clopidogrel (Plavix) blocks platelet aggregation by inhibiting the ADP receptor

  18. Glycoprotein IIb/IIIa receptor inhibitors • Abciximab (ReoPro) • Eptifibatide (Integrillin) • Tirofiban (Aggrastat) • gpIIb/IIIa is a molecule necessary for platelet aggregation

  19. Aspirin’s effect on platelets is irreversible and lasts 7 to 10 days; d/c aspirin 7 days prior to major surgery • d/c NSAIDs (short-acting) 24 hours prior to surgery; long-acting 7 days prior to surgery

  20. Alternative therapies and platelet aggregation • If it starts with a G it inhibits platelet aggregation—gingko, garlic, glucosamine, ginseng, ginger, grapeseed extract • SJW does too as does feverfew (used for migraines) • Fish oil can decrease the ability of platelets to aggregate especially if the patient is taking other G’s + ASA and/or NSAIDS and/or Plavix • d/c feverfew, garlic, ginger, and ginseng 7 days prior to surgery; gingko 36 hours prior to surgery

  21. Arterial clots • Liver produces clotting factors (II, VII, IX, X), cholesterol, glucose, and inflammatory mediators overnight • Spits them all out in the a.m. • MI (arterial clot or white clot)—inflammation is the operative word • inflammatory mediators are highest in the morning; triggers an unstable plaque in one of the coronary arteries to rupture; platelets are stickiest in the early a.m. due to the highest blood sugar of the day; platelet plug forms, triggers clotting cascade; takes 2-3 hours to form; up at 7? MI between 9 and 10 a.m. • ASA inhibits platelet aggregation and decreases inflammation • Chest pain? Chew a 325 mg ASA

  22. Serum Proteins • Albumin • Globulin’s ‘ • Add the two together and you have the total serum protein test or TSP • Albumin comprises 2/3 of the total serum proteins; globulins 1/3—this is called the A/G ratio • Generally used as screening tests altho’ the albumin level can be used to determine nutritional status and/ or prognosis in liver disease • A better test that gives you more bang for your buck is the serum protein electrophoresis

  23. Serum Protein Electrophoresis—based on molecular weight and overall charge (positive or negative) + - Well in the gel Electrical current running through gel

  24. Serum electrophoresis albumin globulins β α1 α2 Γ

  25. The globulins… The alpha 1 globulins—there are a few alpha-1 globulins; however, we’ll only discuss the most clinically important for today’s lecture and for YOUR health • High-density lipoprotein—the good guy • What do they do? HDL’s clear excess cholesterol from the blood; HDL’s are also potent “anti-oxidants” and prevent LDL from oxidizing; the HDLs are also potent “anti-inflammatory” lipoproteins; keep levels above 40 mg/dL (1.04 mmol/L) and above 60 mg/dL (≥ 1.55 mmol/L) would be ideal • For every 5 mg/dL (0.13 mmol/L) decrease in HDL below the mean, the risk of CHD increases by 25%

  26. So if HDLs are good for you, how can we boost HDLs without drugs? • Eat right— garlic (crush it, let it sit for 10 minutes, eat it raw or lightly sauteé it for less than 6 minutes), beans, omega-3 fatty acids, fiber, almonds (and other nuts), plant stanols (Take Control, Benechol, Smart Balance, Yoplait Yogurt, Minute Maid Heart Wise OJ) • Decrease saturated and trans fats

  27. Exercise What else boosts HDLs?

  28. What else boosts HDLs? • Estrogen • Premenopausal women have fabulously high HDLs—one of the major reasons the heart is protected prior to menopause

  29. Booze to boost HDLs… a little dab‘ll do ya’… • This is a yes… • 5 oz of wine of any color—This amount→ • Guys, you can have 2 glasses • How much of the hard stuff? 1-2 ounces for women; 2-3 ounces for men • How about a brewski? 12 ounces for women, 24 ounces for men

  30. So, what’s my motto? • Bike a mile, guzzle a brewski, and pop a Premarin…OR… • Have a delicious glass of Chardonnay with a lovely salmon dinner with my Mom… • OR…

  31. Increasing HDLs with pharmacologic agents Say YES to drugs… • Niacin/Niaspan boosts HDL the most—up to 25% • Drugs— the “statin” sisters (prescribed to lower LDL)– rosuvastatin/Crestor) gives you the most bang for your buck in raising HDLs (boosts HDLs by 12-14% vs. ~6% for the other statins) • Metformin (Glucophage) increases HDLs • Pioglitazone (Actos) increases HDLs

  32. Other drugs that influence HDL levels • Increase HDL--glucocorticoids, cyclosporine, tacrolimus • Decrease HDL—androgens/testosterone, progestins, thiazide diuretics, beta-blockers, valproate and related drugs, isotretinoin

  33. Beta globulins—the bad guys • LDLs (low density lipoproteins)—directly deposit into the walls of the arteries via the process of oxidation • The higher the LDLs, the greater the risk for atherosclerosis • Familial hypercholesterolemia—heterozygous vs. homozygous (Quebec)

  34. Guidelines for LDLs • A patient with CAD or a risk equivalent (diabetes), the LDL should be ~70 mg/dL (2.2 mmol/L or even lower, perhaps 1.8 mmol/L) • For the rest of us with other risk factors—100 mg/dL (<2.85 mmol/L) • Unless you’re perfect…--130 mg/dL (<3.37 mmol/L) • Size of the LDL particles…small and dense vs. large and loose (diabetics tend to have small and dense due to high triglycerides)

  35. Risk factors for increased LDLs • Diet high in trans and saturated fats • Smoking • High iron levels • High insulin levels • Couch potato • Fat around the middle

  36. LDL reduction • Exercise? Eat right? • Foods; fiber; almonds; plant stanols • Reduce red meat, sat fats and trans fats

  37. How about drugs to reduce LDL? Say YES to the “statin” sisters… • Say yes to the “statin” sisters—lova (Mevacor), atorva (Lipitor), prava (Pravachol), simva (Zocor), fluva (Lescol), rosuva (Crestor), and the newest statin “sister” is pitavastatin (Livalo) • Statin dose chosen should reduce the LDL by 30-40%

  38. Statin doses • Instead of starting with the lowest doses, begin with a dose that drops the LDL-C by 30-40% • Rosuvastatin/Crestor—5-10 mg = 39-45% LDL reduction • Fluvastatin/Lescol—40-80 mg = 25-31% reduction • Atorvastatin/Lipitor – 10 mg = 39% reduction • Pravastatin/Pravachol – 40 mg = 34% reduction • Simvastatin/Zocor – 20-40 mg = 35-41% reduction • Lovastatin/Mevacor – 40 mg = 31% reduction

  39. Drugs that influence LDL-cholesterol • Increase LDLs: Progestins, androgens, cyclosporines, tacrolimus, thiazide diuretics, setraline, atypical antipsychotics • Decrease LDLs: estrogens/estradiol

  40. VLDL (very low density lipoproteins)--triglycerides • Dietary causes? Copious amounts of refined sugars, high fructose corn oil, and alcohol (?) • Genetics • Ideal is less than 150 mg/dL (1.70 mmol/L) • Borderline high is 150-199 (1.70-2.25 mmol/L) • TG are a major risk factor for peripheral neuropathy in the diabetic • TG and fatty liver disease

  41. Drugs? Fish oil for TG reduction? • Niacin/Niaspan (see slides at the end of handout for titrating Niacin) • Gemfibrozil (Lopid) • How much fish oil? • For fish oil? READ the label –1000 mg of combined EPA and DHA per day for maintenance; cardiologist may prescribe more

  42. Lovaza—prescription omega-3s • Or the cardiologist may prescribe a form of fish oil which provides ALL YOU NEED in one pill • LOVAZA (old name, Omacor); used for very high triglyceride levels; 4 g/day is the dose

  43. Pharmacological management of hypertriglyceridemia • Triglyceride levels greater than 1000-1500 mg/dL (11.3 to 16.9 mmol) require treatment with fibrates to reduce the risk of acute pancreatitis • “fibrates”--(TriCor, Lipofen, Triglide, and Lipidil in U.S. and Bezalip in Canada) • Lifestyle modifications—weight loss results in a mild-to-moderate decrease (about 22%) and an increase in HDL (about 9%), largely because of an increase in HDL2, about 43%) • The level of small, dense LDL particles may decrease by as much as 40%

  44. Drugs that increase triglycerides • Alcohol • Estrogens • Androgens, testosterone • Glucocorticoids • Cyclosporine • Tacrolimus • Thiazide diurectics • Beta-blockers • Sertraline (Zoloft) possibly • Protease inhibitors • Valproic acid • Isotretinoin • (progestins decrease TGs)

  45. WBC and DIFFERENTIAL • 5 types of mature WBC’s and one immature WBC circulate in the “cold, cruel world” known as peripheral blood • Normal range 5,000 to 10,000 (3500-12000)

  46. The differential… • Neutrophils (polys, PMN, segs)(57-63%) of the total white count; acute inflammation, acute bacterial infections, acute necrosis (1.51-7.07) Bands (0-4%) (0.00-.51)—precursor to the neutrophil • Too many? Neutrophilia. • Too few? Neutropenia (usually preceded by two words— “life threatening…” • Lymphocytes (30%)-first responder to viruses; cells of the immune system (0.65-2.8)

  47. The differential, continued… • Monocytes (4%)—macrophages in tissues; cells of chronic inflammation; antigen processing cell (APC) (0.00-0.51); • Eosinophils (3%)—cells that respond to parasites and allergies (0.00-0.42) (Carlotta) • Basophils (less than 1%)—who cares? Contain histamine (0.00-0.16) (basophilia—CML, PV) • *all the cells with the last name “phil” are collectively called granulocytes—hence, the term agranulocytosis means a decrease of all three; but in clinical practice agranulocytosis means neutropenia

  48. Neutrophils • Phagocytic functions-- their only job in the world is to EAT until they die • Cell of acute inflammation • First responder to bacterial invasion (strep, staph, E. Coli, H. flu, meningococcus, Pseudomonas, C. difficile) • Loves acute necrotic tissue (gangrene, MI, appendicitis) • Fastest dividing cell in adult bone marrow

  49. How do neutrophils grow up (the process of differentiation)? • Stem cells • Myeloblast (BM=bone marrow) • Promyeloctye (BM) • Myelocyte (BM) • Metamyelocyte (juvenile) (BM) • Band neutrophil (BM and PB=peripheral blood) • Segmented neutrophil (BM and PB)

  50. Differentiation and the “shift to the left” • During the time of acute need, the bone marrow is functioning overtime…massive production results in a partial loss of quality control concerning the immaturity of the cells that are released into the peripheral blood • WBC and diff will show an increased number of neutrophils and bands and maybe even a metamyelocyte or two— • shift toward immaturity— “more immature forms” • Shift-to-the-left—increased number of bands • What is the usual number of bands? 0-4% • Bands and SIRS—the systemic inflammatory response syndrome—greater than 10% bands

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