1. Phlebotomy Principles Preferably anticubital; definitely avoid underside of wrist. Largest vein smallest needle for what you need to draw Do not draw labs from the same arm as an IV infusion If you must, stop IV, flush line and wait about 5 minutes to draw. Monitor site for hemostasis prior to applying bandaid and leaving. Drawing labs from a central line, waste 5 cc of blood (may reinstill) All specimens labeled at bedside by the person who drew the blood. Label with: –Pt name –Pt ID number –Date –Time –Initials of person who drew blood

2. Hematology CBC –RBC –Hemglobin –Hematocrit WBC with Differential: –Bands –Segmented Neutrophils –Basophils –Eosinophils –Monocytes –Lymphocytes Erythrocyte Sedimentation Rate

3. Lab Test Significance Normal Value Too Hi Too Low Hematocrit(Hct) Prep: none Percentage of RBCs in the plasma Men: 42-49% Women 35-47% Effected by hydration. Lose of plasma relative to RBCs elevated Hct (i.e. burn pts). In euvolemic pt, increased Hct indicates true increase in RBCs Decreased Hct can be caused by overhydration or a true decrease in RBCs. Hct immediately after blood lose will be normal (equal loss of RBCs and Plasma). Within a few hours plasma vol normal but  RBCs causes  Hct Hemoglobin(Hgb) Prep: none Amount of “heme” pigment in the RBCs. Normally Hct is 3 times Hgb. Vital in assessing types of anemia. Hgb is vehicle for transporting oxygen. Men: 14-16.5 g/100 ml Women: 12-15 g/100 ml Hyperchromic (too much Hgb pigment) Hypochromic (too little hgb pigment) is seen in diseases with abnormal types of Hgb that are fragile (sickle cell. Hypochromic, microcytic cells are seen in iron deficiency anemia

4. Lab Test Significance Normal Value Too Hi Too Low Red Blood Cell Count (RBC) Prep: none Number of Red Blood Cells per cubic millimeter of blood. The hormone, erythropoietin, secreted from the kidneys stimulates RBC production by red bone marrow. Tissue hypoxia causes increased release of erythropoietin. “Anemia” is a nonspecific term for decreased RBCs. Dx Anemais Men: 4.5-5.3 million/mm 3 Women: 4.1-5.1 million/mm 3 Pregnancy: 5-5 – 6 million/mm 3 In congenital heart disease, and chronic lung disease the body increases RBCs to attempt to compensate for hypoxia. Also occurs in persons who live at high altitudes. Increased RBCs called Polycythemia or Erythrocytosis Decreased RBC count can be due to 1) abnormal loss of erythrocytes (bleeding) 2) abnormal destruction of erythrocytes (look for increased bilirubin) 3) lack of needed elements or hormones for erythrocyte production (renal failure) 4) Bone marrow suppression. White Blood Cell Count (WBC) Prep: none Total number of White Blood Cells in a cubic millimeter of blood. 4,800-11,000 /mm If elevated - infection Severe bacterial infections will cause an elevation in WBC count due to a rise in neutrophils. Leukopenia: Chemotherapy, radiation therapy, leukemia and aplastic anemia. In addition, many common medications.

5. Decreased RBCs Hemolysis Decreased RBCs related to Anemia Renal Failure Bone Marrow Suppression

6. Lab Test Significance Normal Value Too Hi Too Low Bands (Stabs or Young Neutrophils) Prep: none Immature neutrophils increase (shift to the left) with overwhelming bacterial infection. 0-5% Increase when body if fighting overwhelming bacterial infection, increases number of immature neutrophils Shift to right – excessively high segmented neutrophils sometimes seen in anemias, liver disease, or long- term infections. Segmented Neutrophils (Segs or Polys) Prep: none Body’s first defense against bacterial infection and severe stress. Mature neutrophils are segs. 45-75%Neutrophilia Shift to right – excessively high segmented neutrophils sometimes seen in anemias, liver disease, or long-term infections.Neutropenia Reduced when there is a shift to the left and more immature neutrophils. Neutropenic precautions. Eosinophils Prep: none Function not clearly understood, but are associated with antigen- antibody response. 0-8%Eosinophilia Most common cause for elevation is allergic reaction (asthma, hay fever) or hypersensitivity to medication. Also, parasitic infestation (round worms will cause it). Incresed levels of adrenal steroids will decrease eosinophil count (i.e. patients with COPD on corticosteroids)

7. Lab Test Significance Normal Value Too Hi Too Low Basophils Prep: none Clinical significance not known 0-3% Do know that leukemia and other pathologic alterations in bone marrow production may increase basophils. Corticosteroids, allergic reacions and acute infections may decrease basophil count. Lymphocytes Prep: none Principle component of body’s immune system. Only small portion of these circulate in the blood stream. Most are T lymphocytes. 90% of leukemias (acute or chronic) are lymphocytic. 25-35%Lympocytosis A common reason is lymphocytic leukemia. Lymphocytes also increase in many viral infections including mumps, hepatitis, pertusis, infectious mononucleosis. Also sometimes with some tumors and often with tuberculosis. Lymphocytopenia HIV and AIDs are the most common cause of reduced lympocytes (T- lymphocytes in particular). Adrenocorti- costeroids and other immunosuppressive medication. Autoimmune disease such as systemic lupus erythematosus. Monocytes Prep: none Monocytes are present in tissue as macrophages. Act as phagocytes in some chronic inflammatory diseases 4-6%  PAD. Some protozoan infections (i.e. malaria), and rickettsial infection (i.e. rocky mountain fever) increase monocytes. Chronic ulcerative colitis also. Depleted in overwhelming bacterial infection.

8. Lab Test Significance Normal Value Too Hi Too Low Erythrocyte Sedimentation Rate (Sed Rate) Prep: Fasting not necessary but a fatty meal may cause plasma alteration. Measures the speed at which RBCs settle in a tube of anticoagulated blood. Increased plasma globulins or fibrinogen increase sticking together and settling. If they are macrocytic the settle faster; microcytic slower. Non-specific for chronic inflammation, or chronic infection. Men: 0-17 mm/hr Women: 1-25 mm/hr Pregnancy: 44-114 mm/hr May be normal as in pregnancy. However an increase in sed rate typically reflect an inflammation or tissue injury. Sed rate > 100 mm/hr (in nonpregant persons) is most likely caused by infection, malignant tumors, collagen vascular disease. Also elevated in Rheumatoid Arthritis, Pelvic Inflammatory Disease, AIDs and Temporal Arteritis. Low sed rate is not usually clinically significant. May be associated with sickle cell anemia, hypoalbuminemia or a deficiency in Factor V.

9. Coagulation Studies Activated Partial Thromboplastin Time Prothrombin Time INR Platlet Count Bleeding Time Fibrin Split Products

10. Coagulation Studies Lab Test Significance Normal Value Too Hi Too Low Activated Partial Thromboplastin Time (aPTT) Prep: Draw blood 1 hour prior to intermittent heparin dose. Transport to lab immediately. Usually used to monitor heparin therapy effects. Evaluates how well the coagulation cascade is functioning. 20-36 seconds Heparin Therapy desired value: 1.5 – 2.5 times normal Increased likelihood of bleeding. Usually due to too much heparin, decrease dosage. Protamine sulfate is antidote if patient too anticoagulated from heparin (risk of clots though). In persons not taking heparin signifies bleeding disorder such as hemophilia A (facot VIII) or B (Christmas disease – factor IX) Subtherapeutic heparin therapy, increase dosage. Not clinically significant except for reflectign hypercoagulability.

11. Lab Test Significance Normal Value Too Hi Too Low Prothrombin Time (PT) Prep: None Obtain baseline prior to coumadin therapy. Diets high in green leafy vegtables (vit K) will decrease PT Male Adults: 9.6 -11.8 seconds Female Adults: 9.5 – 11.3 seconds Coumadin Therapy: 1.5 – 2 times lab control. Increased likelihood of bleeding. Too high may need to administer IM injection of vitamin K > 30 seconds places client at significant risk of bleeding. Increased likelihood of bleeding. Too high may need to administer IM injection of vitamin K Typically not significant unless on coumadin. Subtherapuetic coumadin dosing, increase dosage or pt at risk for clot. INR Prep: None A calculated adjustment to standardize PT results based on the type of thromboplastin reagent used (varying sensitivities) 2.0 – 3.0 for standard coumadin therapy 3.0 - 4.5 for high dose coumadin therapy Increased likelihood of bleeding. Too high may need to administer IM injection of vitamin K Subtherapuetic coumadin dosing, increase dosage or pt at risk for clot.

12. Lab Test Significance Normal Value Too Hi Too Low Bleeding time Prep: Do not administer heparin for at least 3 hours prior. The time required for the interaction of all steps in the clotting cascade to clot blood. Use BP cuff up to 40 mm Hg and filter paper. 2– 9 minutes Evaluation of bleeding disorders such as DIC, or hemophilia. Test will be falsely prolonged by any anticoagulant therapy, agitation of vial or exposure of blood tube to high temp. None. Platlet Count Prep: none Platlets are vitally important in hemostatic plug formation, coagulation factor activation. Bleeding precautions for thrombocytopenia patients. 150,000-400,000 cells/mm 150,000-400,000 cells/mm 3 Living at high altitudes, chronic cold weather and exercise increase platlet count. Increased risk of clots. Thrombocytopenia. Increased risk of bleeding. Seen in DIC, various bleeding disorders. Some medications may cause thrombocytopenia (i.e. heparin, chemotherapy). Fibrin Degredation (Split) Product (FDP or FSP) Resulst from breakdown of fibrin clots by the action of the enzyme plasmin. Used to diagnose DIC < 2.5 mcg/ml Suggestive of DIC None

13. LFTs AlbuminSGOTSGPT Alkaline phosphatase AmmoniaBilirubin

14. LFTsTestSignificance Normal Value Too High Too Low Serum Alkaline phosphatase (ALP) Prep: fasting for 12 hours prior; avoid hepatotoxic meds 12 hours prior or the results may be elevated. Mostly in liver and bone. Also intestines and placenta. Increased during new bone formation – therefore children have higher levels 100-115 U/L Children 1-2 times adult levels Not specific test. If the alkaline phosphatase is elevated, biliary tract damage and inflammation should be considered. May be renal or GI too. May also elevate during periods of bone growth (pagets disease) In child prior to puberty indicates lack of normal bone formation. Serum Ammonia level Prep: fast, except for water, and avoid smoking for 8 to 10 hours prior. The liver normally convert NH3 (ammonia), a byproduct of protein metabolism into urea to be excreted by kidneys. 35 - 65 mg/dL In severe liver failure BUN decreases as ammonia levels increase. Elevated ammonia levels will cause s/s of hepatic encephalopathy. None

15. Hepatic Encephalopathy Hepatic encephalopathy is a potentially-reversible neuropsychiatric abnormality in the setting of acute or chronic liver failure due to elevated ammonia levels –Dx by exclusion of other neurological, psychiatric, infectious, and metabolic etiologies Manifestations –earliest manifestations: "day-night reversal” individuals tend to sleep during the day and stay awake at night. –impairment in spatial perception: poor ability to copy or draw various simple images, e.g., cube, star, clock. –changed level of consciousness –asterixis is the hallmark of hepatic encephalopathy: Detected by having the patient hold out his outstretched arms and hands while cocking his wrists back. In the presence of asterixis, there is a non-synchronized, intermittent flapping motion at the wrists Treatment –Treat cause –Antibiotics may be given to kill bacteria present in the bowel, thereby decreasing bacterial conversion of protein to ammonia –Lactulose: osmotic diarrhoea, thus lessening the time available for intestinal bacteria to metabolise protein into ammonia within the bowel.

16. TestSignificance Normal Value Too High Too Low Albumin(Alb) Major protein present within the blood. Synthesized by the liver. 3.4-5 g/dL 3.4-5 g/dL Hyperalbuminemia Increased in dehydration due to hemoconcetration. Also, may increase in metastatic carcinomas or diarrhea. Liver failure, alcoholism, and acute infections can cause low albumin (hypoalbuminemia). Malnutrition, in the absence of liver failure, can also cause low albumin. Aspartate transaminase (AST or SGOT) It is less specific for liver disease. May be elevated in other conditions such as an MI. 0-45 U/L Enzyme elevation reflects damage to the hepatic (i.e. hepatitis) or cardiac cells (myocardial infarction), but non-specific. No Clinical Signficance. Alanine transaminase (ALT or SGPT) Found in various bodily tissues, but is most commonly the liver 0- 50 U/L Usually liver or cardiac cause: viral hepatitis, congestive heart failure, liver damage, biliary duct problems, infectious mononucleosis. No clinical significance.

17. Lab TestSignificanceNormal ValueToo HiToo Low Total Bilirubin Prep: fast rro 4 hours prior; eat diet low in yellow foods (i.e. carrots, yams, yellow beans) for 3-4 days prior. RBCs normal life span 120 days. RBC breakdown (normal or abnormal releases bilirubin). Removed from blood by liver, spleen and bone marrow. 0.3 to 1.5 mg/dLIncrease with any type of jaundice. Discoloration of skin and the sclera of the eye occurs when bilirubin accumulates in the blood at a level greater than approximately 2.5 mg/dL. No significance Direct (conjugated) Bilirubin Conjugated bilirubin excreted in GI tract. Tells you whether the problem is occuring before or after the liver. 0 - 0.3 mg/dLElevated direct (or conjugated) bilirubin (post hepatic problem – i.e. obstruction – gall stone) No significance Indirect (unconjugated) Bilirubin Unconjugated circulates in blood stream excreted by kidneys (urobilogen).Tells you whether the problem is occuring before or after the liver. 0.1 - 1.0 mg/dlElevated indirect (or unconjugated) bilirubin (Intra or pre- hepatic problem – i.e. hemolysis, or hepatic failure) No significance

18. Bilirubin Increased by –Increased RBC distruction i.e. hemolytic transfusion reaction –Liver dysfunction failure and inability to conjugate HepatitisCirrhosis Liver Cancer –Inability to excrete conjugated bilirubin Common bile duct obstruction (i.e. gal stone)

19. Hepatitis Testing Antibody test i.e.. Anti-HBs or Anti- HVC Antigentesti.e.. (HBsAg)

22. Pancreatic Function Serum Amylase Serum Lipase Urine Amylase

23. Pancreatic Function Lab Test Significance Normal Value Too Hi Too Low Serum Amylase Prep: list meds since numerous meds can effect level. Results invalid if pt had chole- cystography with contrast within 72 hours This enzymes is produced by the pancreas and salivary glands – digests carbohydrates. Excreted by kidneys. 25-151 units/L Greatly increased along with lipase in acute pancreatitis. Rises 3 – 6 hours after onset of pain. Isolated  Causes: Pancreatic neoplasm Perforated peptic ulcer Intestinal Obstruction Intestinal infarction Acute Cholecystitis Appendicitis Ruptured Ectopic Pregnancy Peritonitis No significance. Serum Lipase Prep: ERCP may  Pancreatic enzyme converts fats and triglycerides into fatty acids and glycerol. 10-140 units/L Elevated in pancreatic disorders along with amylase. More diagnostic then amylase which  from other causes. No significance.

24. Pancreatic Function Lab Test Significance Normal Value Too Hi Too Low Urine Amylase Prep: may be a 2 hour specimen, but typically a 24 hour urine. If the serum amylase is elevated the body tries to excrete it renally. 4-400 units/L Acute pancreatitis. Levels will remain elevated for up to 2 weeks after acute episode even after serum amylase has begun to return to normal. Continued elevation suggests formation of pancreatic pseudocyst. No significance

25. Renal Function Blood Urea Nitrogen (BUN) Creatinine Creatinine Clearance Serum Uric Acid Urine Uric Acid

26. Lab Test Significance Normal Value Too Hi Too Low Blood Urea Nitrogen No special prep of pt. Urea, a waste product of protein metabolism, is formed by the liver and carried in the blood to be excreted by the kidneys. 8-25 mg/dL Diseased or damaged kidneys can result in  BUN for failure to excrete. Also, decreased perfusion to kidneys or lack of volume flow (dehydration). Also, increased protein intact or GI bleed. Over hydration. Increase in ADH will dilute plasma and decrease BUN artificially. Severe liver failure can reduce metabolism of protein and urea formation, but other nitrogenous waste (i.e. ammonia will increase) Serum Creatinine Minimize intake of ascorbic acid, barbiturates or cephalo- sporins antibiotics which may elevate lab. Waste product of creatinine phosphate, a high-energy compound found in skeletal muscle. Men: 0.6 – 1.5 mg/dL Women: 0.6-1.1 mg/dL Elevated creatinine is caused by damaged nephrons. More diagnostic then BUN Creatinine > 1.5 mg = > 50% nephron function loss. Creatinine > 4.8 = as high as 75% nephron function loss. Decreased level may indicate atrophy of muscle tissue. BUN :Creatinine Ratio should be 10:1

27. Lab Test Significance Normal Value Too Hi Too Low Creatinine Clearance Test Prep: 2, 12 or 24 hour urine collection; discard first void; sometime during collection a serum creatinine is collected. Creatinine Clearance Test is used as an indicator of glomerular filtration rate. Compares serum creatinine with the amount of creatinine excreted in a specified period of time. Better indicator of renal function than BUN or creatinine alone. Men: 95-135 ml/min Women: 85-125 ml/min No significance Decreased creatinine clearance indicates decreased glomerular function. Used to evaluation progression (continued deterioration) of renal disease. A creatinine clearance of at least 10 ml/min is needed to sustain life or dialysis is necessary.

28. Lab Test Significance Normal Value Too Hi Too Low Serum Uric Acid Prep: overnight fast; dietary history regarding foods high in purines. Uric acid is an end product of purine metabolism. Purines are in the nucleoproteins of all cells are obtained from various dietary sources and the breakdown of body proteins. Foods high in purines: LiverSardinesAnchoviesSweetbreadsKidneysSpinachMushroomsAsparagusLentils Men <40: 3.6-8.5 mg/dL Women: 2.3-6.6 mg/dL Hyperuricemia Renal impairment most common cause (decreased excretion). Also preeclampsia, neoplasms, chemotherapy or radiation therapy, chronic malnutrition or diet high in purines. Hypervolemia – diluted (i.e.. Iv fluids or SIADH) None Urine Uric Acid Prep: 24 hour urine collection 250-750 mg/24 specimen

29. Cardiac Biomarkers CKCK-MBLDHMyoglobin Troponin I Troponin T B-Type Natriuretic Peptide C-Reactive Protein

30. Cardiac Biomarkers Lab Test Significance Normal Value Too Hi Too Low Creatinine Kinase (CK or CPK) Prep: If test is being done to evaluate skeletal muscle avoid strenuous exercise prior; avoid ETOH 24 hrs prior; no IM injections Is an enzyme found in cardiac, and skeletal muscle and the brain. Elevation reflects tissue catabolism from cell trauma. Serial testing q 10 hours times 3 typically 26-174 units/L Isoenzymes: CK-MB 0-5% CK-MM 95-100% CK-BB 0% Elevation of total CK must be fractioned down into Isoenzymes. Elevation reflects brain, muscle or cardiac damage. IM injections or strenuous exercise may increase MM. None Lactate Dehydrogenase (LDH1-5) LDH1 and LDH 2 are the isoenzymes more specific to cardiac muscle. Serial testing q 10 hours times 3 100-200 U/L LDH flip strongly suggestive of an MI When LDH1 is higher than LDH2. None

31. TestIndication Normal Range Myoglobin Cardiac enzymes elevation reflects cardiac damage Normal < 85 ng/ml TroponincTnT Normal < 0.05 ng/ml May be elevated by CRF Troponin I cTnI Normal < 0.05 ng/ml Not elevated by CRF B-Type Natriuretic Peptide (BNP) Used to diagnosis CHF and severity Normal cut off <100 pg/ml C-Reactive Protein A marker for inflammation and risk of atherosclerosis, MI, CVA, PVD, diabetes. Produced by the liver in response to inflammatory process. CRP <1 mg/L lowest risk CRP 1-3 mg/L intermediate risk CRP >3 mg/L highest risk

32. Biomarker Trends OnsetPeakReturn CK 3-6 hr 10-30 min 3-4 days CK MB 4-8 hr 10-30 hr 3 days Myoglobin 2-6 hr 8 hr 12-18 hrs Troponin 3-5 hr 14-21 hr 3 days AST 6 hr 12-14 hr 4 days LDH 24-48 hr 3-6 days 14 days

33. Lipid Profiles Lab Normal Value Comments Total Cholesterol < 200 mg/dl Essential for the production of bile salts and steroid hormones, but excess increase atherosclerotic plaque. O.5-1.0% of the population have hyperlipidemia that is familial. The remainder is caused by DIET, liver disease with biliary obstruction, corticosteroids, hypothyroidism, and pancreatic dysfunction. HDLs are the “good” cholesterol (doesn’t stick in coronaries. HDLs > 45 mg/dl LDLs < 100 mg/dl Triglycerides <150 mg/dl Elevated due to diet, but also can be elevated due to nephrotic syndrome, pancreatic dysfunction, diabetes and hypothyroidism.

34. Glucose Studies Fasting blood sugar Glucose tolerance test Glycosylated hemoglobin (HbA 1c )

35. Lab Test Significance Normal Value Too Hi Too Low Fasting Blood Sugar Prep: No food for at least 8 hours; water ok. Diagnosing diabetes 80-100 mg/dL Prediabetics have FBS of 100-125 mg/dL Stress, infection, corticosteroids, TPN, PPN will increase BS Too much insulin injected. Too little food, too much exercise. Glucose Tolerance Test Prep: eat usual diet for several days prior. Then fasting after 12 mn. Given a glucose drink and BS checked at 1- 2-3 hour intervals Diagnosing diabetes FBS: 80-100 mg/dl 1Hour:120-160mg/dL 2 Hour: 80-140mg/dL 3 Hour: 80-100mg/dL An inadequate return to normal indicative of diabetes.

36. Lab Test Significance Normal Value Too Hi Too Low Glycohemoglo bin (hemoglobin) A1C Prep: none Evaluates long term compliance with diabetic regimen and overall stability of BS in normal range 4-6% nondiabetics <7% ideal range for diabetcis >9% poor diabetic control Poor diabetic control Too much insulin injected. Too little food, too much exercise.

37. Thyroid Studies TSHT3T4

38. Thyroid Labs Lab Normal Value Comments TSH 0.5-6 µU/ml The thyroid gland is under the control of the pituitary gland. When the level of T3 & T4 drops too low, the pituitary gland produces Thyroid Stimulating Hormone (TSH) which stimulates the thyroid gland to produce more hormones. T3 (Serum Triiodothyronine) 80-180 µg/dl T3 & T 4 secreted from thyroid in response to TSH. Low T3 and T4 levels could mean a diseased thyroid gland ~ OR ~ a non- functioning pituitary gland which is not stimulating the thyroid to produce T4. If the T3 and T4 levels are low and TSH is not elevated, the pituitary gland is more likely to be the cause for the hypothyroidism. Hyperthyroidism: Graves' disease (antibody ass autoimmune response) is the most common etiology (70-80% of hyperthyroidism. Other causes include: Toxic thyroid adenoma, Toxic multinodular goitre. T4 (Serum Thyroxine) 4.6-12 µg/dl

39. Urinalysis Routine Urinalysis

40. Lab Test Normal Value Significance Color Clear light yellow Dark yellow, amber too concentrated. Abnormal color may be medication. Pseudomonas bladder infection – green color. Urobilogen causes dark orange – foams when shaken. AppearanceClear Hazy suggests infection pH 5-9 (mean of 6) Acidic: Meat and eggs contribute to acidic metabolic waste. Fruits and vegetables contribute to alkaline urine. Most infections (except E.Coli – most common) cause urine to be alkaline. Cranberry juice makes it acidic. Specific Gravity 1.001-1.035 How dilute or concentrated (reflective of conditions like SIADH or Diabetes Mellitus or Diabetes Insipidus. ProteinNegativeProteinuria Persistent elevated levels (beyond trace) suggestive of renal damage. Heavy exercise may cause transient. SugarNegativeGlycosuria Trace in normal pregnancy. Elevates in later trimester. Otherwise suggest hyperglycemia as in Diabetes Type I or II, may occur with TPN patients. KetoneNegative Increased ketones occur from insufficient glucose available for energy – breaks down fatty acid Diabetes

41. Lab Test Normal Value Significance BilirubinNegative Suggestive of obstructive jaundice. This bilirubin is conjugate (liver functioning) just couldn’t get to GI tract Occult Blood Negative UTI or inflammation in Renal/Urinary system (glomerulornephritis, acute tubular necrosis, malignancy) LeukocytesNegativeUTI NitriteNegativeUTI Urobilogen 0.1-1.0 EU/dL Urobilogen is formed in the intestines from conjugated bilirubin. Some reabsorbed and excreted via kidneys. Will decrease in obstructive jaundice (not making it to intestines. Increased urobilogen occurs with hemolysis. Also, used to detect early liver failure – liver can’t handle reabsorbed urobilogen fast enough. WBCs0-4/hpfUTI RBCs Female 0-5/hpf Male 0-3/hpf UTI or inflammation in Renal/Urinary system (ATN, glomerulonephfritis) Casts0-4/lpf Describes a cylindrically shaped aggregation of some particulate that forms in the distal convoluted tubule or distal nephron via precipitation of a mucoprotein secreted by tubule cells. Elevation indicates renal disease BacteriaNegativeUTI

42. Tuberculosis Tuberculin Skin Test –Intradermally administered, read in 48-72 hours –Read results by looking for induration (raised hardened area) across the forearm (perpendicular to the long axis) in millimeters –Positive = –> 5mm in immunocompromised person –10 mm or more in high risk person –15 mm or more in average person –Never repeat it on someone who has had a previous positive (CXR)

43. Interpreting the Mantoux tuberculin skin test by the Sokol ballpoint pen method involves slowly approaching the site of induration using a ballpoint or felt tip pen from above or below the area until resistance is felt. The procedure is repeated on the opposite side. As shown in (B), the distance between the lines where resistance was noted is measured in millimeters. This measures the degree of induration found 48 to 72 hours after application of the

44. Changes in Urine Color Foods Eating beets can result in reddish-purple urine. Acidic urine will turn red after eating blackberries. Alkaline urine will look reddish after eating rhubarb. Whether your urine is acidic or alkaline is usually determined by other foods you have eaten. Candy or pills with a dye can temporarily turn the urine red. Poison Lead or mercury poisoning can turn the urine reddish. If you suspect you have ingested and have been handling those toxic metals, and your urine is red, you should see your physician.

45. Therapeutic Drug Ranges Medication Therapeutic Range Amitriptyline 120-150 ng/ml Tegretol 5-12 mcg/ml Chloramphenicol 10-20 mgc/ml Digoxin (Lanoxin) 0.5-2 ng/ml Disopyramide (Norpace) 2-5 mcg/ml Gentamicin 5-10 mcg/ml Imiparmine (Tofranil) 150-300 ng/ml Lidocaine (Xylocaine) 1.5-5 mcg/ml Phenobarbital (Luminal) 10-30 mcg/ml

46. Therapeutic Drug Ranges Medication Therapeutic Range Phenytoin (Dilantin) 10-20 mcg/ml Propranolol (Inderal) 50-100 ng/ml Salicylate 100-250 mcg/ml Theophylline (aminophylline, Theo-Dur) 10-20 mcg/ml Tobramycin (Nebcin) 5-10 mcg/ml Valproic Acid (Depakene) 50-100 mcg/ml

47. Electrolytes ElectrolyteSymbolFunctions SodiumNa + Distribution of water between extracellular and intracellular fluid Nerve impulses Heart muscle contractibility PotassiumK+K+ Nerve conduction Muscle activity Cardiac muscle function CalciumCa + Bones and teeth Muscular contraction Nerve impulses Coagulation Factor IV MagnesiumMg + Muscular contraction Carbohydrate metabolism Coagulation process ChlorideCl − Distribution of water between cells and plasma Acid/base balance BicarbonateHCO 3 − Maintenance of normal pH Transportation CO 2 from tissue to lungs PhosphorusPGlucose and fat metabolism Energy transfer and storage

48. Lab Test Significance Normal Value Too Hi Too Low Serum Sodium Prep: none A major extracellular catio responsible for serum osmolality 135-145 mEq/L Hypernatremia- consider cause 1) actual gain of sodium (saline IV infusions, sea water ingestion, Cushing’s Syndrome, Hyperaldosteronism - adrenal cortical adenoma also known as Conn's syndrome ) or 2) lose of fluid relative to sodium (dehydration, diabetes insipidous) Hyponatremia – consider cause 1) actual lose of sodium (K-sparing diuretics) or 2) excess of fluid relative to sodium (i.e. Hypotonic IV infusions, SIADH and water intoxication) Serum Chloride Prep: do not allow pt to clench or unclench fist. A component of hydrochloric acid and aids in digestion, osmotic pressure and water balance. 98-107 Eq/L Hyperchloremia - hyperparathyroidism; drug (ammonium chloride), dehydration Hypochloremia – occurs most commonly in prolonged GI suctioning, enteritis, acute intestinal obstruction and continued vomiting (lose of HCl), diarrhea and impaction.

49. Lab Test Significance Normal Value Too Hi Too Low Serum Calcium Prep: fasting sample desirable; excessive milk ingestion, defined as three quarts of milk per day, can cause an increase in plasma calcium. Used in bodily processes such as muscular contraction, cardiac functioning, hormone secretion, and the transmission of nerve impulses. Ionized calcium is essential for blood coagulation. Since calcium is essential for clotting, any condition that decreases the amount of ionized calcium can subsequently lead to coagulation and hemostasis problems. 9.0–10.5 mg/dl The most common cause of increased calcium in the blood is metastatic bone disease. Hodgkin’s disease, multiple myeloma, and leukemia may also cause hypercalcemia. Other disorders or conditions associated with increased calcium levels are hyperparathyroidism, Paget’s disease of bone, prolonged immobilization, and Addison’s disease. Drugs that increase plasma calcium include lithium, vitamin D, thiazide diuretics, thyroid hormone, and hydralazine, an antihypertensive medication. Since much of the plasma calcium is bound to albumin, decreased plasma calcium levels, hypocalcemia, can be related to a lowered plasma albumin level. Other causes hypoparathyroidism and renal failure, Vitamin D deficiencies and malabsorption associated with sprue, celiac disease, and pancreatic dysfunctions. Heparin, magnesium salts, oral contraceptives, aspirin, and corticosteroids and excessive use of laxatives may cause a decrease in plasma calcium

50. Lab Test Significance Normal Value Too Hi Too Low Serum Potassium Prep: do not allow pt to clench or unclench fist. Very suseptible to dietary intake. A major intracellular cation which regulates electrical conduction in muscles, and helps buffer H+ to maintain acid-base balance. 3.5-5.1 mEq/L Hyperkalemia – seen in acidosis (i.e. DKA), renal failure, excessive dietary intake, massive trauma, rhabdomylosis, Addison’s disease, potassium supplements, or potassium sparing diuretics. Hypokalemia – seen in patients on loop diuretics (i.e. lasix and bumex) with inadequate dietary or pharmaceutical supplementation, severe diarrhea or vomiting. Hyper- aldosteronism – retain Na in exchange for K. Alkalosis and Cushing’s. Serum Bicarbonate Prep: ingestion of acid or alkaline susbstance may alter results. Part of the bicarbonate – carbonic acid buffering system responsible for body pH. Produced by kidneys. 22-26 mEq/L