INTERPRETATION OF LAB TESTS

Barb Bancroft, RN, MSN www.barbbancroft.com BBancr9271@aol.com

Rule number one

Know your own labs normal values Various methods of testing and various normal ranges

Serum protein electrophoresis

List the plasma proteins 1) albumin 2) globulins 3) fibrinogen Is there a difference between serum proteins and plasma proteins?

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 mg/dL) increases the risk of clotting What conditions increase the risk of clotting?

Estrogen excess increases fibrinogen COCs? HT? (hormone therapy) Endogenous estrogen?

 Smoking increases fibrinogen So how about smoking and estrogen, eg, oral contraceptives or HT in the PMF? Aging and fibrinogenincreases by 1% per year after age 30

Biological Rhythms and clotting

Liver produces clotting factors and inflammatory mediators primarily at night; kicks them out in the a.m. Adrenal gland produces cortisol and epinephrine in a.m. increasing blood sugar and making platelets sticky 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

DIC (Disseminated Intravascular Coagulation)

Overutilization of platelets and clotting factors Microvascular clots formed shutting down organ systemskidneys, lungs, brain Platelet counts falling; clotting factors decreasing After fibrin clots are formed, fibrinolysis occurs FSPs (fibrin split products), FDPs (fibrin degradation products), D-dimers What triggers DIC?

Total Serum Proteins

Albumin Globulins (Albumin comprises 2/3 of the total serum proteins; globulins 1/3) Total serum protein (TSP) 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

Serum Protein Electrophoresisbased on molecular weight and overall charge (positive or negative)

Well in the gel Electrical current running through gel

Serum electrophoresis

albumin globulins

Albumin
Functionsholds water in the vascular space Binds drugs (protein-bound vs. free drug) Hypoalbuminemia (less than 3.0 g/dL)--what are the causes? Liver diseasedecreased synthesis Or leaky kidneys

Kidney disease
Nephritis1-2+ protein in the urine Nephrosis3-4+ 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

PrilsThe ACE inhibitors

(Brazilian pit viper)
Captopril (Capoten) Enalapril (Vasotec) Lisinopril (Prinivil, Zestril) Perindopril (Aceon) Moxepril (Univasc) Benazepril (Lotensin) Quinapril (Accupril) Trandolapril (Mavik) Ramipril (Altace) Etc

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

Angie, the prils and the Diabetic/hypertensive Kidneyhyperglycemia/HTN

Afferent arteriole ( vasodilation by ( prostaglandins) Blood entering glomerulus Glomerulus filter Efferent arteriole ( vasoconstriction via ( angiotensin 2) Blood exiting glomerulus

Microalbuminuria**

The elderly
The 1% rule The process of senescence begins at ___? 1% decline in function per year in organ systems such as the liver (major exceptions are clotting factors and the size of the prostate) Serum albumin in the elderly Decreased binding sites for drugsincreased bioavailability of drugs and drug toxicity

The globulins
The alpha 1 globulins 1) alpha one antitrypsin 2) High-density lipoproteinthe good guy 3) HDLs clear excess cholesterol from the blood; HDLs 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 4) For every 5 mg/dL (0.13 mmol/L) decrease in HDL below the mean, the risk of CHD increases by 25%

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

What else boosts HDLs?

Exercise Estrogen Ethanol

So, whats my motto?

Run a mile, drink a beer, pop a Premarin Have a nice glass of wine with almondcrusted salmon with my Mom OR

Increasing HDLs
Decrease carbohydrate intake (modified Atkins diet) Say YES to drugs Niacin/Niaspan boosts HDL the mostup to 25% Drugs the statin sisters (mostly lower LDL)-(simvastatin/Zocor, rosuvastatin/Crestor)**, atorvastatin (Lipitor), fluvastatin/Lescol, pravastatin/(Pravachol) Metformin (Glucophage) increases HDLs The glitazones increase HDLs

Alpha-2 globulins
Transport proteinstransferrin (iron), Thyroid binding globulin (TBG), ceruloplasmin (copper)

Beta globulinsthe bad guys

LDLs (low density lipoproteins)directly deposit into the walls of the arteries via the process of oxidation, forming atherosclerotic plaques The higher the LDLs, the greater the risk for plaque formation and atherosclerosis

 New guidelineswith CAD or a risk equivalent (diabetes), the LDL should be 70 mg/dL For the rest of us with other risk factors 100 mg/dL (<2.85 mmol/L) Unless youre perfect--130 mg/dL (<3.37 mmol/L)

Risk factors for increased LDLs

Family history Diet high in trans fats and saturated fats Smoking High iron levels (increases oxidation) High insulin levels Couch potato Fat around the middle

LDL reduction
Estrogen?? Exercise? Eat right? Foods; fiber; almonds; plant stanols Nix red meat, sat fats and trans fats

Say YES to statinsthe statin sisters Say yes to the statin sisterslova (Mevacor), atorva (Lipitor), prava (Pravachol), simva (Zocor), fluva (Lescol), rosuva (Crestor) Statins are anti-inflammatory, anti-lipid, decrease plaque formation, stabilize plaques, prevent plaque rupture

VLDL (very low density lipoproteins)--triglycerides

If the fasting triglyceride level is 500 mg/dL, the postprandial TGs are 1000 mg/dL Reduce refined sugars and alcohol The role of niacin, and the fibrates, Lopid or Tricor; bile acid sequestrants (Questran, Wellchol) Ideal is less than 150 mg/dL (1.70 mmol/L) Borderline high is 150-199 (1.70-2.25 mmol/L)

Total cholesterolscreening purposes onlybest 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) 2) Hypothyroidism (TSH) (0.4-4.2 U/mL or mU/L) for 21-54 yo; 0.5-8.9 U/mL or mU/L for 55-87)

WBC and DIFFERENTIAL

5 types of mature WBCs and one immature WBC circulate in the cold, cruel world known as peripheral blood Normal range 5,000 to 10,000 (350012000)

The List
Segs (poly, PMN, segmented neutrophil)(57-63%) of the total white count; acute inflammation, bacteria (1.517.07) Bands (0-4%) (0.00-.51)precursor to the seg THE SEGS + BANDS as a % of the TOTAL WBC is the ANC (Absolute Neutrophil Count) Lymphocytes (30%)-first responder to viruses; cells of the immune system (0.65-2.8) Monocytes (4%)cells of chronic inflammation (0.000.51) 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)

The granulocytes
All of the cells with the last name phil are called granulocytes The neutrophils are most important acute inflammation, acute necrosis phagocytic The eosinophils are increased in allergic responses and with parasitic infections (Carlotta) Basophilsallergies and anaphylaxis

5 types of WBCs
Segs(phagocyte) its 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)

How do segs grow up?

Stem cells Myeloblast (BM) Promyeloctye (BM) Myelocyte (BM) Metamyelocyte (juvenile) (BM) Band neutrophil (BM and PB) Segmented neutrophil (BM and PB)

 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 necrosisMI, gangrene of the bowel, acute appendicitis

Shift to the left

During the time of acute need, the bone marrow is functioning overtimemassive 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 segs and bands and maybe even a metamyelocyte or two shift toward immaturity Shift-to-the-leftincreased number of bands What is the usual number of bands? 0-4% Bands and SIRSthe systemic inflammatory response syndrome

Clinical conditions with an increased WBC and shift-to-the-left

GABHS Pyelonephritis Acute appendicitis Bacterial meningitis

Drugs and neutropenia

Chemotherapy (all patients) 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

The Absolute Neutrophil Count (ANC)

% segs + %bands x total WBC 57% segs (5.7) + 3% (0.3) bands x 10,000 = 6,000 (6.0) Neutropenia is defined as an ANC less than 1000 (1.0)various degrees of neutropeniafrom bad to worse to worser Neulasta (G-CSF)(Granulocyte Colony Stimulating Factor)

SEGSnormal function
Margination, pavementing, migration, engulfment, and degranulation (releasing enzymes) Yum.

Prednisone and the neutrophil

Inhibits migration and degranulation, hence its antiinflammatory properties Prednisone also increases blood sugar due to glycogenolysis (metformin can be used to inhibit glycogenolysis) High blood sugars inhibit the function of segs Diabetes Blood glucose greater than 180 mg/dL (9.99 mmol/L) inhibits seg 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 segsis fever good for you? YES!

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

Inflammationlab tests
C-reactive protein -- < 1 mg/dL or < 10 mg/L; the CRP is an acute phase reacting protein; 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-CRPlow 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 Inflammatory mediators, IL-6 and TNF- 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 YIKESso 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)

What can reduce hs-CRP?

Exercise Loss of abdominal fat Statins glitazonesrosi- and pioAspirin Omega-3 fatty acids Nuts The Mediterranean diet is anti-inflammatory

Inflammationthe sed rate

Sed raterate of the settling of RBCs in anticoagulated blood; low sensitivity and specificity; many factors can influence the sed rate Newborn1-2mm/hr Neonates and children3-13 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 yearsthe maximum normal ESR at a given age is: Males age in years/2; Females age in years + 10/2

Monocyte/Macrophage
Monocyte in blood, macrophage in tissue (Kupffer cell in liver, microglial cell in brain) 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

Chronic inflammation--TB
Many chronic inflammatory conditions have the last name osis Tuberculosis, sarcoidosis, histoplasmosis, amyloidosis red snappersthe tubercle bacillis Macrophages circling and containing the bacillis and keeping it in check or dormant Granulomashistologic appearance of macrophages circling the wagons so to speak

Macrophages and Vitamin D

If you have consumption, go up on the mountain

The macrophagethe link between inflammation and immunity

The macrophage is the antigen processing and presenting cell It engulfs the pathogen Chews it up Processes it and presents it to the helper T cell (T4 cell) of the immune system

Antigen processing and IL-1 release

CD4

IL-1 release TNF-a IFN-

T4 cell CD4

IL-2

ON

macrophage With CD4 receptor

T4 or helper T cell

What else does IL-1 do?

Increases temperature set point by increasing the production and release of prostaglandins in the hypothalamus

IL-1 release
Increases serotonin release from brainstemvomiting Increases serotonin release from the duodenumnausea Duodenumthe organ of nausea

IL-1 release
Increases melatonin production and makes you sleepy

IL-1 release
Lowers pain thresholdeverything hurts Your hair hurts Your teeth hurt Your skin hurts Youre miserable

Cells of the immune system-lymphocytes

3 types of lymphocytes
B lymphocytes (16%)bone-marrow derived T lymphocytes (80%)thymus-derived NK cells (4%)Natural Killer cells

Cell-mediated immunityT cells

Viruses Fungus Parasites Protozoa Cancer Transplants

T lymphocytes (thymus-derived)
First responders to viral infections Release interferon alpha to inhibit viral attachment to surrounding cells T cells change their appearance and become atypical lymphocytes (reactive) 12-16% with CMV, 5-6% with hepatitis, greater than 20% with EBV

Who belongs to the herpes family?

HSV-1 HSV-2 VZV CMV EBV HHV-6, 7 KSHV

B lymphocytes
B cell---plasma cell---antibody production (immunoglobulins)--immunophoresis

Y
IgM, IgG, IgA, IgD, IgE

Gamma globulins
Immunoglobulins Antibodies Immunophoresis IgM, IgG, IgA, IgD, IgE
+ -

Plasma cells produce antibodies

IgMfirst antibody formed to an infection acute titersHSV-IgM (acute phase of infection) IgGsecond antibody formed to an infection; lasts forever; crosses placenta; convalescent titersHSV-IgG (reactivation of earlier infection) Another example: CMV infection in transplant patientsprimary (IgM) or reactivation (IgG)?

Plasma cells produce antibodies

IgAbarrier antibody; saliva, tears, urine, breast milk

IgD--??

 IgEantibody of allergies Drills a hole in the mast cell releases primary granules full of histamine

What to do?
Get rid of your pet? Dont sleep with the enemy? Give em a bath once a week?

RBCS AND ANEMIAS

Barb Bancroft, RN, MSN, PNP www.barbbancroft.com barb@barbbancroft.com

What do you need to make happy healthy red blood cells? Good Genes Hemoglobinopathies due to genetic disorders How can you tell the type of hemoglobin you have?

Hemoglobin ElectrophoresisHbA, HbS, HbF, HbAS, HbSC, HbThal

+ cathode anode -

Well in the gel Electrical current running through gel

Healthy Kidneys
Erythropoietin production and hypoxia Renal failure and Epogen (Procrit) Epo and the Black Market IL-1 (Interleukin-1) and the suppression of erythropoietinthe anemia of chronic disease

Healthy thyroid-Hypothyroidismlow metabolic rate

Decreased metabolism decreases the production of normal-appearing red blood cells

Iron
FACT: you need iron to grow verticallynot

Irontoo much, too little

Hemochromatosisexcess iron storage and serum ferritin Celiac disease and short stature due to failure to absorb iron Women have 20% less blood than men, hence, lower iron stores and a higher risk of iron deficiency anemia

How much iron do we need a day?

20 mg (1mg from food and 19 from recycled old RBCs) Iron absorption and diet Recycling iron

Kids and iron

Kids and iron deficiency anemia (fast food restaurants dont serve a lot of iron containing foods) You need iron to grow vertically

Iron
Fact: you need iron to grow a baby

Fact: You lose iron when you bleed

You dont have enough RBCs to recycle the iron

 Elderly and iron absorption PMF??iron supplements? Not unless youre symptomatic with iron deficiency

Serum ferritin
Serum ferritin adults M = 20-250 ng/mL or mcg/L F = 10-120 Iron overload > 400 ng/mL in M and > 200 ng/mL in females; consider hemochromatosis Iron deficiency with levels < 10 ng/mL (mcg/L)

B12
2000 to 5000 mcg are stored in the liver Have enough stored for 5 to 7 years if you stopped eating all foods containing B12 today and stopped taking any supplements with B12 Use about 1 mcg per day for maintenance You need B12 in food, a stomach to produce IF to bind to it, a small intestine to absorb it, and a liver to store itso what can go wrong?

B12 deficiency (200-800 pg/mL)

Over 55 years of age Lack of IF (intrinsic factor)autoimmune gastritis, gastrectomy patients No animal protein in dietvegetarians or Tea and Toasters Liver failure Lousy diet (alcoholics) Malabsorption (Crohns disease, celiac disease, gastric by-pass surgery) Drugs that either decrease absorption such as Metformin; PPIs decrease IF

The prazolesProton Pump Inhibitors the over 50 crowdB12 level after 2 years
MOAInhibition of the proton pump at the lumenal surface of the stomachespecially after a
meal PPIs work here H+, Intrinsic Factor-B12 Lumenal surface

Parietal cell Basilar surface H2 receptors H2

H2 blockers work here

B12 deficiency
The number one cause of nutritional DEMENTIA in the U.S. One of the top 3 causes of peripheral neuropathy Anemia B-12 is a co-factor in the production of serotonin How can we replace B12? 4 Sshow much? Can you overdose on B12? No, the one dreaded side effect however is:

Folic acid and Dr. George Herbert

40 days and 40 nights Maintenance of healthy RBCs Maturation of the neural tube (first 28 days) Take folic acid 400 mcg (0.4 mg) BEFORE you get pregnant + eat Green leafys and citrus fruits

Drugs that block folic acid synthesis that are taken longer than 40 days and 40 nights TMP/SFX (Bactrim, Septra) Rheumatrex (Methotrexate) Phenytoin (Dilantin) Oral contraceptives

Supplement with folic acid

Differentiation and Maturation

Stem cell (BM) Erythroblast (BM)(nucleated) Pronormoblast (BM) (nucleated) Normoblast (BM) (nucleated) Reticulocyte (BM and PB)(no nucleus) Erythrocyte (PB) (process takes 7-12 days)

Nucleated RBCs in the peripheral bloodno, no (blast cells) Has this patient had his/her spleen removed? The reticulocyte count0.5-1.5% of total RBC count; takes 7-12 days to make and release a retic from the bone marrow Is this patient reticking?

Overdestruction anemia
High retic countRBCs are being destroyed in the peripheral blood (hemoloysis) and the bone marrow is working overtime to produce more 27-year-old African American female with anemia RBC=3,000,000 (normal range = 4.5-6 million) Retic count 35% (normal range = 0.5-1.5%) What should you think about?

Hemolytic anemias
Hereditary--Sickle cell? Thalassemia? G6PD deficiency Autoimmune hemolytic anemia (lupus) Hemolytic uremic syndrome Coombs testwhat is it used for?

Underproduction anemia
Low retic count Usually due to a deficiency of a nutrient Iron, B12, folic acid Chemotherapy

Some numbers
Total RBC count4.2-5.6 (M) million and 3.85.3 (F) million Hemoglobin adult females (11-15.5 g/dl) (110-155 g/L) males (13-17.3)(130-173 g/L) Hematocrit females39-50 (0.39-0.50) males35-47 (0.35-0.47) Anemia = Hemoglobin of 11 or less

RBC indices(morphology)
MCV 90 (83-97) fL (18-44); micro, normo, macro MCH 29 (27-31) pg (27-35); hypo, normo, poly MCHC34 (32-36) g/dL How do we define anemias? Based on morphologylook at MCV as the most important test

Microcytic anemia
RBC 3,000,000 MCV 65, MCH 22 9/10 with iron deficiency anemia Wheres the bleed? Female? Male? Exercise? NSAIDS? Growing kid? Tea drinking? Not iron deficiency? Think lead poisoning or thalassemia

And dont forget your occult fecal blood testsevery year

Blood in the stool is a primary sign of colon cancer

Macrocytic anemia
RBC 3,000,000 MCV greater than 100 fL MCV between 100 and 120think booze MCV greater than 120think B12 or Folic acid deficiency Whos at risk?

Over 55? Gastrectomy patients Chronic atrophic gastritis Chronic malabsorption (Crohns disease, bariatric surgery, celiac disease) Alcoholics Competition for B12 (tapeworms) Strict vegetarianism drugs

Normocytic anemia
RBCs 3,000,000 MCV normal MCH normal The anemia of chronic diseaseCRF, hypothyroidism, chronic inflammation (TB), cancer (unless a bleed is involved)

Serum Enzymeslab test interpretation

Liver function tests

Cellular integrity (SGOT, SGPT)also known as AST, ALT Bile formation and flow (bilirubin, GGT, alkaline phosphatase)

Hepatocellular enzymes
AST (SGOT) is NON-specificin other words, it is found in many tissues and therefore not specific as a liver enzyme ALT (SGPT) is found almost exclusively in liver cells and is therefore highly specific for the liver If a healthy person demonstrates an elevated ALT, a thorough history is warranted with special questions such as hepatitis exposure, hepatotoxin exposure, and drug effects If enzymes are not terribly elevated (less than 3x normal), recheck the enzyme levels in 2 weeks before doing a multi-million dollar work-up

Hepatotoxin exposure and drug effects

Chemicals (cleaning chemicals such as CCl4 ),
vinyl chloride Vitamin A toxicity Drugsacetaminophen**, statins, ketoconazole, INH, niacin, ACE inhibitors Amiodarone, NSAIDS, Norvir (Rotanovir), ETOH, heparin, valproic acid (Depakote) Herbal productsYerba tea, germander, skull cap, mistletoe (Iscador)

**Acetaminophen (Tylenol)
Acetaminophen is in over 300 OTC products Drippy, coughy, hacky, sneezy, wheezy, headachy, achy, sleepy, ouchy products Prescription productswith the last name cetDarvocet, Percocet When you hear Bayer what do you automatically assume?

 Bayer aspirin is aspirin; Bayer Select Maximum Strength Headache is acetaminophen and caffeine; Bayer Select Pain Relief Formula is ibuprofen

Hepatitis
Hepatitis Arisk factors fecal-oral transmission Salad bars can be particularly dangerous The scallions at Chi-Chis in Pittsburgh (October 2003)

Hepatitis B
Hepatitis Brisk factors Vertical transmission Sexually transmitted IV drug use Blood transfusions

Hepatitis C
Hepatitis Crisk factors Blood transfusions prior to 1992 (July)1 in 3000 prior to 1992 Viet Nam Veterans Sharing needles Multiple sex partners Intranasal cocaine use Body piercing Tattoos

Normal AST/ALT ratio ~ 1

AST 8-20 U/L (0.43-1.28 Kat/Ladult males; 11-26 U/L (0.19-0.44 Kat/Ladult females) ALT 10-40 U/L (0.17-0.68 Kat/Ladult males; 7-35 U/L (0.12-0.60) What is the ratio? Should be ~1 If greater than one consider ETOH AST is especially sensitive to alcohol If alcohol damages liver cells, the AST will increase higher than the ALT Ratio in alcohol induced hepatitis is usually 3:1 to 8:1 Also consider any other cause of a fatty liver (diabetes, obesity)

AST/ALT ratio
If less than 1 consider drugs, viruses, autoimmune hepatitis, hemochromatosis, Wilsons disease, alpha-1 antitrypsin deficiency Always check the TSHmay see mild in liver enzymes with hypothyroidism

Bilirubindirect (conjugated, water soluble) and indirect (unconjugated, fat soluble)

Does bilirubin have any physiologic function? Waste productexcreted in urine and in stool Total bilirubin is 0.3-1.2 mg/dL in adults (521 mmol/L Indirect = <1.1 mg/dL (<19 mol/L) Direct = < 0.2 mg/dL (<3.4 mol/L)

Bilirubin
RBC breakdown by splenic and liver macrophages Bilirubin from RBC breakdown is referred to as unconjugated, fat-soluble Takes 2 steps to find it in the lab, so its called IN-direct

Bilirubin
As it arrives at the liver, it is taken up by the liver cells and is conjugated It is now ready for secretion into the bile ducts and on to the GI tract for excretion A small amount is sent to the kidneys A tiny amount is sent to the blood via the lymphatics (thats why the percentage of direct bilirubin is so low)

Jaundice
Where do you turn yellow first? Two types of jaundice Hemolytic (increased breakdown of RBCs) greater than 80% of total bilirubin is indirect Obstructive (back-up in the biliary system) more than 50% of total bilirubin is direct

Alkaline Phosphatase (ALP)

Think Biliary and Bone Any disturbance in the synthesis, secretion, or excretion of bile leads to the accumulation of bile acids in the liver This in turn increases the synthesis of ALP Sensitive indicator of cholestasis Infiltrative processes such as liver mets

Alkaline Phosphatase (ALP)

ALP is found in osteoblasts Increased with growth spurts1st year and adolescence Pagets disease Osteosarcoma Metastatic disease to bone

Pancreatic enzymes
Amylase and lipase Amylase also found in the parotid gland (mumps) With pancreatitis, amylase rises fast and high (up to 60,000) in the first 12 hours What are the 2 major causes of acute pancreatitis?

Pancreatic enzymes
Other causes of elevations of amylase Perforated peptic ulcer Peritonitis Ruptured ectopic pregnancy Mumps orchitis

Creatine Kinase--CK
High-energy tissues Skeletal muscle (98% CK-3, CK-MM; 2% is CK-MB) Cardiac muscle (40% CK-2, CK-MB; 60% CK-MM) Brain (CK-1, CK-BB)(also large intestine, CK-BB)

LDHLDH1,2,3,4,5
Found in practically every cell The most common enzyme elevated on routine tests Usually an isolated enzyme elevation and not indicative of a problem LDH5 is the most common elevation probably skeletal muscle damage

Troponin T
Structural protein, not serum enzyme Greater than 0.03 mcg/L is the 10% CV cutpoint Cardiac necrosis More cardiac specific than CK-MB, remains elevated for 3-14 days Advantage for delayed diagnosis Rises in 3-12 hours, peaks at 24, down in 3-14 days

Thanks.
Barb Bancroft, RN, MSN, PNP
www.barbbancroft.com BBancr9271@aol.com