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INTERPRETATION OF LAB TESTS

INTERPRETATION OF LAB TESTS. Barb Bancroft, RN, MSN www.barbbancroft.com BBancr9271@aol.com. Rule number one …. Know your own lab’s normal values Various methods of testing and various “normal ranges”…. Serum protein electrophoresis. List the plasma proteins 1) albumin

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INTERPRETATION OF LAB TESTS

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  1. INTERPRETATION OF LAB TESTS Barb Bancroft, RN, MSN www.barbbancroft.com BBancr9271@aol.com

  2. Rule number one … • Know your own lab’s normal values • Various methods of testing and various “normal ranges”…

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

  4. Yes. • The removal of fibrinogen = serum. • So, the serum proteins are albumin and the “globulins”. • Fibrinogen—(1.5-4.0 g/dL or 150 to 400 mg/dL) • hyperfibrinogenemia (greater than 400 g/dL) increases the risk of clotting • What conditions increase the risk of clotting? Obesity, venous stasis, hip and pelvic surgery, immobility, age

  5. What else? • Endogenous estrogen? • Estrogen excess increases fibrinogen • Combined oral contraceptives? The “old days” vs. today’s COCs… • HT? (hormone therapy) • Dose dependent…age dependent… • Aging and fibrinogen—increases by 1% per year after age 30

  6. What else? • Smoking increases fibrinogen • So how about smoking and estrogen, eg, oral contraceptives or HT in the PMF? • Use the patch! Or an IUD…

  7. Biological Rhythms and clotting • Liver produces clotting factors overnight • Clotting factors are highest in the a.m. • DVT (venous clot or red clot) is formed; breaks off in early a.m. and travels to lungs—Pulmonary embolism at 7:30 a.m. • MI (arterial clot or white clot)—inflammation (inflammatory mediators are highest in the a.m.) triggers plaque rupture; platelets are stickiest in the early a.m. due to highest blood sugar; platelet plug forms, triggers clotting cascade; takes 2 hours to form; MI at 9 a.m. • ASA inhibits platelet aggregation • Coumadin/Heparin inhibit clotting factors

  8. Total Serum Proteins • Albumin • Globulins • (Albumin comprises 2/3 of the total serum proteins; globulins 1/3) • A direct albumin level can be used to determine nutritional status and/or the prognosis in liver disease

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

  10. Serum electrophoresis albumin globulins β α1 α2 Γ

  11. Albumin • Functions—holds water in the vascular space • Binds drugs (protein-bound vs. “free” drug) • Hypoalbuminemia (less than 3.0 g/dL or 30 g/L)—what are the causes? • Liver disease—decreased synthesis due to liver disease or due to an OLD liver…(1% rule) • Or leaky kidneys…

  12. Patient with ascites? • SAAG—serum ascites/albumin gradient; • SAAG=albuminserum / albuminascites • ratio greater than 1.1 is 97% predictive of portal hypertension as the cause of ascites • SAAG less than 1.1 is nonportal hypertension—nephrotic syndrome, infection (TB, fungal, CMV), pancreatic ascites, ovarian cancer, peritoneal carcinomatosis

  13. Kidney disease • Nephritis—1-2+ protein in the urine • Nephrosis—3-4+ protein in the urine • Protein in the urine is usually albumin—macroalbuminuria with 1+-4+ • “Early” and reversible kidney disease in the diabetic or hypertensive patients is manifested by spilling “microalbuminuria” • TREAT with “PRILS”-ACE INHIBITORS

  14. “Prils”—The ACE inhibitors • Captopril (Capoten) • Enalapril (Vasotec) • Lisinopril (Prinivil, Zestril) • Perindopril (Aceon) • Moxepril (Univasc) • Benazepril (Lotensin) • Quinapril (Accupril) • Trandolapril (Mavik) • Ramipril (Altace) • Etc…

  15. “Angie” and the healthy kidney… • Afferent arteriole (vasodilated via (prostaglandins) • Blood entering glomerulus • Glomerulus→filter • Efferent arteriole (vasoconstricted via (angiotensin 2) • Blood exiting glomerulus PG filter AT2 Toilet

  16. “Angie, the “prils” and the Diabetic/hypertensive Kidney…hyperglycemia/HTN • Afferent arteriole (  vasodilation by (  prostaglandins) • Blood entering glomerulus • Glomerulus→filter • Efferent arteriole (  vasoconstriction via (  angiotensin 2) • Blood exiting glomerulus Microalbuminuria**

  17. The elderly • The 1% rule • The process of senescence begins at ___? • 1% decline in function per year in organ systems such as the liver • Serum albumin in the elderly • Decreased binding sites for drugs—increased bioavailability of drugs and drug toxicity

  18. The globulins… The alpha 1 globulins— • High-density lipoprotein—the good guy • 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

  19. So if HDLs are good for you, how can we boost HDLs? • Eat right— garlic, beans, omega-3 fatty acids, fiber, almonds (and other nuts), plant stanols (Take Control, Benechol, Smart Balance) • Decrease saturated and trans fats

  20. What else boosts HDLs? • Exercise • Exercise • Ethanol

  21. Drink to boost HDLs… • 5 oz of wine of any color—This amount→ • Guys, you can have 2 glasses • How much of the hard stuff? 1 ounce for women 2 ounces for men • How much beer? 12 ounces for women 24 ounces for men

  22. So, what’s my motto? • Run a mile, drink a beer, eat a bowl of beans and pop a Premarin… • Have a 5-ounce glass of chardonnay with a delicious salmon dinner with my Mom… • OR…

  23. Increasing HDLs • Decrease carbohydrate intake • Say YES to drugs… • Niacin/Niaspan boosts HDL the most—up to 25% • Drugs— the “statin” sisters are prescribed primarily to lower LDL cholesterol but can boost HDL by about 6%; rosuvastatin boosts by 12%)– lovastatin (Mevacor), (simvastatin/Zocor, rosuvastatin/Crestor)**, atorvastatin (Lipitor), fluvastatin/Lescol, pravastatin/(Pravachol) • Metformin (Glucophage) increases HDLs

  24. Alpha-2 globulins • Transport proteins—transferrin (iron), Thyroid binding globulin (TBG), ceruloplasmin (copper)

  25. 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 • Particle size plays a role as well • Small, dense LDLs vs. Large, loose LDLs

  26. LDL guidelines • Guidelines—with CAD or a risk equivalent (stroke, peripheral arterial disease), the LDL should be 70 mg/dL (2.0 mmol/L or even lower to 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)

  27. 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

  28. LDL reduction • If you’re boosting HDLs, you’re reducing LDLs…

  29. Say YES to statins—the “statin” sisters… • The statins inhibit the enzyme in the liver responsible for producing LDL-cholesterol • Since the liver works overtime at night, giving the statin drugs in the evening provides an even greater reduction in LDLs • Statins decrease plaque formation, stabilize plaques, prevent plaque rupture

  30. VLDL (very low density lipoproteins)--triglycerides • What increases TG? High fructose corn syrup, alcohol, pure sugar • Are triglycerides bad for you? Yes, in excess--Increased risk of heart disease, high risk of PN and fatty liver in the diabetic • Ideal is less than 150 mg/dL (1.70 mmol/L) • Borderline high is 150-199 (1.70-2.25 mmol/L)

  31. Marine-based omega-3 fatty acids lower TG • Prescription fish oil is Lovaza • How about non-prescription fish oil? • DHA and EPA should total 1000 mg/day for patients with high triglycerides so READ THE LABEL • May see a Cardiologist prescribe even higher doses of fish oil depending on level of triglycerides

  32. Total cholesterol—screening purposes only—best to do the LIPID PROFILE • Lipid profile after an 8 to 12 hour fast • Patient with triglycerides above 250 mg/dL (2.81 mmol/L) (and an HDL less than 40 mg/dL (1.04 mmol/L)—THINK… 1) Type 2 Diabetes (check the fasting blood sugar (4.1-5.9) or hemoglobin A1C (4-6)) 2) Hypothyroidism (TSH) (0.4-4.2 μU/mL or mU/L) for 21-54 yo; 0.5-8.9 μU/mL or mU/L for 55-87)

  33. 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) (5 to 10 with a range of 3.5-12)

  34. The List… • Neutrophil (segs (57-63%) of the total white count; acute inflammation, acute necrosis, acute bacterial infection(1.51-7.07) Bands (0-4%) (0.00-.51)—precursor to the neutrophil • Lymphocytes (30%)-first responder to viruses; cells of the immune system (0.65-2.8) • Monocytes (4%)—cells of chronic inflammation (0.00-0.51) • Eosinophils (3%)—cells that respond to parasites and allergies (0.00-0.42) • Basophils (less than 1%)—who cares? Contain histamine (0.00-0.16)

  35. The granulocytes… • All of the cells with the last name “phil” are called granulocytes • The neutrophils (segs) are most important—acute inflammation, acute necrosis—phagocytic • The eosinophils are increased in allergic responses and with parasitic infections (Carlotta) • Basophils—allergies and anaphylaxis

  36. 5 types of WBCs • Neutrophils (seg)—(phagocyte)-- only job in the world is to EAT until it dies • Cell of acute inflammation • First responder to bacterial invasion • Loves acute necrotic tissue • 57-63% of total WBC (1.51-7.07)

  37. How do neutrophils grow up? • Stem cells • Myeloblast (BM) • Promyeloctye (BM) • Myelocyte (BM) • Metamyelocyte (juvenile) (BM) • Band neutrophil (BM and PB) • Segmented neutrophil (BM and PB)

  38. Neutrophils • Neutrophils (segs) are produced in about 8-10 days; leave the bone marrow and live in the blood for 5-6 hours; migrate into tissues and eat for 36-72 hours; • released rapidly in response to virulent organisms such as strep, staph, E. coli, H. flu, meningococcus, Pseudomonas • Acute necrosis—MI, gangrene of the bowel, acute appendicitis

  39. 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 level of maturity 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 (juvenile) or two— • shift toward immaturity • Shift-to-the-left—increased number of bands • What is the usual number of bands? 0-4%

  40. Clinical conditions with an increased WBC and “shift-to-the-left” • GABHS • Pyelonephritis • Acute appendicitis • Bacterial meningitis

  41. Drugs and neutropenia • Chemotherapy (all patients)—ONCOLOGIC EMERG. • Cimetidine (Tagamet), ranitidine (Zantac) • Carbamazepine (Tegretal); phenytoin • Captopril (Capoten), enalapril (Vasotec), amiodarone, quinidine • Zidovudine (Retrovir) • Clozapine (Clozaril) • Metronidozole (Flagyl) • Gentamicin, clindamycin, imipenem, PCNs, tetracyclines • Azothiaprine (Imuran) • PTU

  42. Neutrophils …normal function • Margination, pavementing, migration, engulfment and degranulation Yum.

  43. Prednisone and the neutrophil • Inhibits migration and degranulation, hence its anti-inflammatory properties • Prednisone also increases blood sugar; high blood sugars can inhibit the function of neutrophils • Diabetes– Blood glucose greater than 180 mg/dL (9.99 mmol/L) inhibits neutrophil migration (normal blood glucose is 74-106 mg/dL or 4.1-5.9 mmol/L) • Elderly with decreased migration of segs, increases infection susceptibility • Fever increases the migration of segs—is fever good for you? YES!

  44. STRESS! • Stress and the WBC • Screaming kids • 24-hours post-op • Last trimester of pregnancy • No bands

  45. Inflammation—C-reactive protein • C-reactive protein -- < 1 mg/dL or < 10 mg/L; • rapid, marked increases occur with inflammation, infection, trauma, tissue necrosis, malignancies, and autoimmune diseases; Increases quickly and dramatically in response to stimuli, and decreases substantially with resolution of the disorder • hs-CRP (vascular inflammation) and coronary artery disease risk level low risk < 1 mg/L; Average 1-3 mg/L; high risk > 3 mg/L (Noncardiovascular causes should be considered if values are > 10 mg/L) PROGNOSTIC INDICATOR (and screening for CV inflammation—next slide)

  46. hs-CRP—low levels of inflammation in the vascular system • High sensitivity assay indicates a high risk of vascular inflammation and subsequent cardiac risk • Use of hs-CRP + lipid values together are more accurate at predicting risk than lipid studies alone • IL-6 and TNF-α are produced within unstable plaques as well as from adipocytes in abdominal fat, which in turn increases hs-CRP production by the liver • The bigger the waistline the greater the hs-CRP • YIKES…so what should your waistline be? • Ridker PM et al. N Engl J of Med 2000; 342:836-43; Ridker PM et al. N Engl J of Med 1997;336:973-9)

  47. What can reduce hs-CRP? • Exercise • Loss of abdominal fat • Statins • Pioglitazone (Actos) • Aspirin • Omega-3 fatty acids • Nuts • The Mediterranean diet is anti-inflammatory

  48. Inflammation—the sed rate • Sed rate—rate of the settling of RBCs in anticoagulated blood; low sensitivity and specificity; many factors can influence the sed rate; used as a screening test and a prognostic indicator • Newborn—1-2mm/hr • Neonates and children—3-13 mm/hr • Post adolescent male (less than 40 years)—1-15 mm/hr • Post-adolescent female (less than 40 years)—1-20 mm/hr • Over forty years—the maximum normal ESR at a given age is: Males age in years/2; Females age in years + 10/2

  49. Monocyte/Macrophage • Monocyte in blood, macrophage in tissue (Kupffer cell in liver, microglial cell in brain, osteoclast in bone, mesangial cell in kidney) • Phagocytes that respond much slower than the seg (2-4 days vs. 5-10 minutes for the seg) • Eats for months • Cell of chronic inflammation

  50. Chronic inflammation--TB • Macrophages circling the “pathogen” is known as a granuloma • Granulomatous diseases are chronic inflammatory diseases with “osis” as a last name…tuberculosis, histoplasmosis, sarcoidosis, amyloidosis • Macrophages secrete numerous cytokines—one is known as TNF-alpha (tumor necrosis factor-alpha) to contain the tubercle bacillis…

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