DRUG LAB INTERACTION

Laboratory Tests
• involved in the diagnosis and
treatment of disease
Purposes:
1. reliable for proper decision making
2. measures chemical changes in the body
3. detection of any dysfunctions in the body
4. monitor drug therapy
 Features that describe the following
aspects of the Drug laboratory effects:
o nature of effect
o route of administration
o direction and strength of effect
o level of documentation
o sex of patient
o age of patient
o onset of effect after starting the medication
o duration of effect after stopping the medication
o clinical significance of effect
o CLASSIFICATION
Screening Test
- Used in patient with no signs and symptoms of a disease
eg. Serum cholesterol for assessing cardiovascular
disease risk
Diagnostic Test
- Done in patient with signs and symptoms of disease or with
an abnormal screening test
MONITORING DRUG THERAPY
o Laboratory Test Results:
– Assess the therapeutic and adverse effects
of a drug
– Determine the proper drug dose
– Assess the need for additional or alternate
drug therapy
– Prevent test misinterpretation resulting
from drug interference
 Laboratory Test Results
• NORMAL VALUES
– Usually determined range by applying
statistical methods to result from a
representative sample of general population
• NORMAL LAB TEST RESULT
– Fall within a predetermined range of values
• ABNORMAL LAB TEST RESULT
– Fall outside a predetermined range of values
oFALSE POSITIVE
-indicates a given condition is present when it is not

oFALSE NEGATIVE
-it appears negative when it should not
oQUANTIATIVE TEST
– Test with normal values reported in ranges
oQUALITATIVE TEST
– Test with positive or negative outcomes
oSEMIQUANTITATIVE TEST
– Those with varying degrees of positivity
The quality of Quantitative assay is measured in terms of
accuracy.
oACCURACY
-Extent to which mean measurement is close to the true
value
oPRECISION
-Refers to the reproducibility of the assay
DRUG LABORATORY TEST
INTERACTION

1. SERUM BILIRUBIN
 H H H H

Bilirubin
O CH CH2 CH O
N N N N
24 23 22 21
18 17 13 12 8 7 3 2
H3C H3C
H2C CH CH2 CH2 CH3 CH3 CH CH2

•Is a bile pigment.

HOOC H2C CH2 COOH

Bilirubin

• Results from the degradation of heme, one of the

breakdown products of red blood cells
•It is thought to be a toxin because it is associated
with neonatal jaundice, possibly leading to irreversible
brain damage due to neurotoxicity.
 H H H H

Bilirubin
O CH CH2 CH O
N N N N
24 23 22 21
18 17 13 12 8 7 3 2
H3C H3C
H2C CH CH2 CH2 CH3 CH3 CH CH2

•It is extracted and biotransformed HOOC H2C CH2 COOH

Bilirubin

mainly in the liver, and excreted

in bile and urine.
 Formation of Bilirubin
1. Hemoglobin from senescent or hemolyzed red cells
is broken down, releasing heme.
2. Heme is then degraded in humans by the enzyme
heme oxygenase (HO), which is the rate-limiting step
in the formation of bilirubin.
3. HO converts heme to biliverdin IX.
Formation of Bilirubin
4.Biliverdin is a hydrophilic
compound that is reduced by
biliverdin reductase into the
hydrophobic compound
bilirubin
 Formation of Bilirubin
5. HO catalyses an oxidase reaction opening the heme
ring to convert one of the bridge carbons to carbon
monoxide. This step releases iron from the now linear
tetrapyrrole yielding biliverdin.
6. Biliverdin reductase reduces the double bond on
nitrogen inside one of four of the pyrrole rings leading
to the formation of bilirubin.
Formation of Bilirubin
Primary site of synthesis:
-SPLEEN

Secondary site of synthesis:

- LIVER & BONE MARROW
 Two Types of Bilirubin

o Prehepatic
o Posthepatic
 TYPES SYNONYMS CHARACTERISTICS
Prehepatic Unconjuganted Does not cross glomerular
filtrate
Free Harmful to neonatal nervous
system

Indirect-reacting Formed in reticuloendothelial

system (peripheral) requires
organic solvent for diazo rx
 TYPES SYNONYMS CHARACTERISTICS
Posthepatic Conjuganted Freely crosses glomerular
filtrate
Glucoronide Formed by enzymatic activity,
in liver

Direct-reacting Gives diazo rx in aqueos

medium
 Unconjugated Conjugated
In water insoluble soluble
In alcohol soluble soluble
normal 0.2-0.9mg/dl 0.1-0.4mg/dl
In bile Absent Present
In urine Always absent Normally absent
Absorption gut Absorbed Not absorbed
Diffusion into Diffuses – yellow Doesn’t diffuse
tissues colour
Van den bergh Indirect + Direct +
 Serum Bilirubin

o A break down product of porphyrin ring of

heme – containing proteins , found in blood in 2
fractions – conjugated/unconjugated
 Serum Bilirubin ( indirect )
•Protein bound and is associated with the increased destruction
of RBCs
•Indirect bilirubin= total- directbilirubin
•Reference Values
Adult and Children:
- 0.1-1.0 mg/dL,
1.7-17.1µ mol/L
 Serum Bilirubin
(direct and total )
oDirect or conjugated bilirubin is frequently the
result of obstructive jaundice, either from
extrahepatic or intrahepatic origin.
 Serum Bilirubin
(direct and total )
•Reference Values:
ADULT:
Total: 0.1-1.2 mg/ Dl, 1.7-20.5µ mol/L
Direct: 0.1-0.3 mg/dl, 1.7-5.1µmol/L
 Serum Bilirubin
(direct and total )
•Reference Values:
CHILDREN:
Newborn: Total: 1-12mg/dl, 17.1-20.5 µmol/L (SI)
Child: 0.2-0.8 mg/dl
 How Do I Prepare for the Bilirubin Blood Test
o you will need to fast (not eat or drink anything other
than water) for four hours before you have the test
performed.
o Drink a normal amount of water before going to the
laboratory or collection site.
o You may have to stop taking certain medications before
the test is performed, but only if your doctor tells you to
do this
 How the test is Performed
• A blood sample is
needed.
• This may be taken
from a vein. The
test is called
a venipuncture.
And heelstick. Venipuncture heelstick
 Procedure
o Collect 5 to 10 ml of venous blood in a red-top tube
o Hold the medication that would increase or decrease
serum bilirubin for 24 hrs.
o Do not eat or drink (NPO) except for water
Take note:
If a hematoma develops at the venipuncture or heelstick
site, apply warm soaks.
o
 Caution
• Whenever blood is drawn for liver function tests,
avoid self contamination to prevent possible
infection
• Protect drug specimen from light
• Blood should be sent to the laboratory
immediately
 Clinical Implications
• DECREASED LEVEL: • INCREASED LEVEL:
- Iron deficiency anemia -Obstructive jaundice
Drug influence: caused by stones or
 aspirin, penicillin, neoplasms
prednisone,asthma -Hepatitis -Liver cirrhosis
medication(theophylline) -Metistatic cancer
-Wilson’s disease
 Clinical
Drug Influence:
Implications
 hydralazine, allopurinol,
probenicid,diuretics(Furosemide),antibiotic(Penicillin G)

•
Interfering Factors:
High fat dinner
• Carrots and yam
• Hemolysisof blood specimen
• Blood specimen exposed to sunlight certain drugs
 Aspirin
Is a weak organic acid that is
unique among the NSAIDs in
that it irreversibly acetylates
(and thus, inactivates)
cyclogenase.
 Aspirin
o TYPE OF DRUG INTERACTION:
- Drug- laboratory interaction
o MECHANISM OF INTERACTION:
-Decrease serum bilirubin level
-Reduction of the level of platelet TXA2, resulting in the
inhibition of platelet aggregation and prolonged bleeding.
 Aspirin
-inhibits thromboxane A2 synthesis from arachidonic acid
in platelets by irreversible acetylataion of a serine,
resulting in a blockade of arachidonate to the active site
and thus, inhibition of COX1
o EFFECT:
-Iron deficiency anemia (false negative value)
o MANAGEMENT:
-Avoid taking aspirin prior to laboratory test.
 Hydralazine
-this drug cause direct
vasodilation, acting primarily
on arteries and arterioles.
 Hydralazine
o TYPE OF DRUG INTERACTION:
- Drug-laboratory interaction with serum
bilirubin
o MECHANISM OF INTERACTION:
-increase the bilirubin serum level
 Hydralazine
o EFFECT:
- Changes in the liver function test (false positive
value)
o MANAGEMENT:
-Complete chemical and biochemical recovery
occurs after discontinuation.
 Allopurinol
-purine analog.
-the primary metabolite is
alloxanthine, which is also
xanthine oxidase inhibitor.
-its active metabolite are
excreted in the feces and
urine.
 Allopurinol
o TYPE OF DRUG INTERACTION:
- Drug-laboratory interaction with serum
bilirubin.

o MECHANISM OF INTERACTION:
-increases the bilirubin serum level.
 Allopurinol
o EFFECT:
- Obstructive jaundice caused by stones or neoplasms,
hepatitis, cirrhosis of the liver, infectious mononucleosis.

o MANAGEMENT:
-close monitoring of serum bilirubin levels is important
-avoid taking allupurinol prior to laboratory test
REFERENCES:

• http://www.healthline.com/health/bilirubin-blood
• http://labtestsonline.org/understanding/analytes/bilirubin/tab/sample
• http://www.authorstream.com/Presentation/drraghu74-1306242-bilirubi
n-metabolism-corr/
• ww.powershow.com/view/efd1d-
OTY3M/Bilirubin_powerpoint_ppt_presentation
• Remington 21st edition
• Laboratory and Diagnostic Test with Nursing Implications (4 th edition)
• Lippincott’s Pharmacology
• A manual of Laboratory and Diagnostic Test (7 th edition)
DRUG LABORATORY TEST
INTERACTION

2. GLUCOSE LEVEL
 What is Glucose?
oTHE PRINCIPAL FUEL FOR ALL BODY ACTIVITIES.
oPRINCIPAL AND ALMOST
EXCLUSIVELYCARBOHYDRATE CIRCULATING IN
BLOOD.
oMost important simple sugar in human
metabolism.
 Formation of Glucose
oGlycogenesis(glucose-glycogen)
oGlycogenolysis(glycogen –glucose)
oGluconeogenesis(monocarbohydrate like
glycerol-glucose)
oGlycolysis(glucose –lactate and pyruvate)
 Definition of Terms
oLiver –THE CLEARING HOUSE FOR GLUCOSE
METABOLISM; IT CONVERTS EXCESS GLUCOSE TO
STORAGE FORMS FOR LATER USE
o Glycogen – primary storage form of glucose
oElevated level- caused by the disorders of the pituitary
gland and certain brain lesions.
oHyperglycemia –may cause shock and severe
hemmorhaage
oDepressed level(hypoglycemia)-is characterized of
hyperinsulinism due either to endogenous pancreatic
lesions or to exogenous over dosage.
oDiabetes mellitus
A disorder of carbohydrate metabolism
characterized by state of hyperglycemia due to
insulin deficiency.
o Glucose Tolerance Test(GTT)
Analyzing blood glucose at timed intervals
following ingestion of a standard glucose dose;
oral glucose tolerance test(OGTT)
o Hyperglycemia
Blood glucose concentration above normal
o Hypoglycemia
Blood glucose concentration below normal
o Glycogen oGlycogenolysis
Storage form of glucose Conversion of stored
found in high glycogen to glucose
concentration in the
liver oGlycosuria
o Glycolysis Glucose in the
Energy production as a urine;glucosuria
result of metabolic
breakdown of glucose
o Glucagon oFalse negative
Pancreatic hormone that Result that appears negative
increases blood glucose when it should no
concentration by promoting the oRenal threshold
conversion of glycogen to glucose Blood concentration above
oFalse positive which a substance not
normally excreted by the
Result that indicates that a kidneys appears in the urine.
given condition is present oGluconeogenesis
when it is not. Formation of glucose
 2 Types of Disorders of
Glucose Metabolism
oHyperglycemia
oHypoglycemia
 Diseases or disorders
associated hyperglycemia
Harmful to the body when it is so high that the
increased extracellular osmotic pressure causes
cellular dehydration; coma can be produces by
severe dehydration of brain cells. And also
acidosis.(uncontrolled diabetes mellitus)
 Diseases or disorders
associated hypoglycemia
The clinical symptoms of hypoglycemia resemble
those of celebral anoxia, which may include one or
more of the following.
faintness,weakness,dizziness,tremors,anxiety,hunger,
palpitation of the heart or “cold or sweat” there may
even be mental confusion and motor incoordination
 Critical Glucose Values
-blood glucose level falls -blood glucose over
below 50mg/dl(hypoglycemic) 400mg/dl
Symptoms : Symptoms :
Fainting Confusion Dry skin
Weakness Lethargy Nausea
Confusion Extreme thirst Coma
Lack of coordination Weak pulse
 Glucose Test

-used to aid in diagnosing and managing

diabetes, or in managing hypoglycemia.
MECHANISM REGULATING BLOOD GLUCOSE LEVELS:
oInsulin
-lowers blood glucose
-cellular membrane to glucose and transportation of
glucose into cells.
oGlucagon
-increase blood glucose concentration
-stimulates glycogenolysis
 Laboratory Tests
oGLUCOSE FASTING BLOOD SUGAR(FBS)
oGLUCOSE POSTPRANDIAL(FEASTING BLOOD
SUGAR)-(Two hour postprandial blood
sugar,PPBS)
oGLUCOSE TOLERANCE TEST-ORAL(GTT)(SERUM)
 FASTING BLOOD GLUCOSE
operformed when on a blood sample taken
when the patient has not eaten for specified
period of time.
ousually obtained before breakfast after the
patient has gone without food since the previous
evening’s meal
 FASTING BLOOD GLUCOSE
oThis test is commonly used to screen for diabetus
mellitus ,in which absent or deficient insulin
allows persistently high blood glucose levels
oPURPOSE of the test;
-to screenfor diabetes mellitus
-to monitor drugs or diet therapy in the payient
with diabetes mellitus
 FASTING BLOOD GLUCOSE
PRECAUTIONS:
-patients with hyperglycemia,thalasemia or chronic renal failure
and those undergoing dialysis may have increased levels.
(referance value)
ADULT
Serum plasma(70-110mg/dl)
Whole blood(60-100mg/dl)
Elderly (70-120mg/dl)
 FASTING BLOOD GLUCOSE
CHILD
Newborn (30-80mg/dl)
Child (60-100mg/dl)
Panic value(LT40mg/dl and GT700mg/dl)
PROCEDURE:
-collect 5 to 10 ml of venue blood and after the blood
-NPO except water for 12 hours before the test
-give insulin as ordered and after the blood sample taken.
 Factors Affecting Laboratory Results
*DRUGS
-cortisone
-thiazide
-loop diuretics(increase blood sugar)
*Trauma
*the clinical test for determining glycosuria maybe falsely
positive if the client is taking excessive amounts of aspirin,
vit c, and certain antibiotics(cephalosporin)
 Drug Influence
DECREASED:
Insulin excess
ELEVATED:
ACTH
Cortisone
Diuretics
Furosemide
Ethacrynic acid
Anesthesia drugs
DRUG LABORATORY TEST: FUROSEMIDE(LASIX)
LABORATORY TEST: FASTING BLOOD GLUCOSE(FBG)
MECHANISM OF ACTION(INTERACTION)
Inhibition of the Na/k/cl transporter in the
ascending limb of henle’s loop resulting in low
level of k that can interfere on glucose metabolism.
Hypokalemia decreases the amount of insulin
produce in the body
CONSEQUENCE(EFFECT)
Hyperglycemia(false positive result)
MANAGEMENT
Potassium sparing diuretics substitution
DRUG LABORATORY TEST:INSULIN EXCESS
LABORATORY TEST: FASTING BLOOD GLUCOSE(FBG)
MECHANISM OF ACTION(INTERACTION)
Insulin allows glucose to enter and be converted to free
fatty acids.
Insulin facilitates the conversion of glucose to glycogen
and it decreases the rate of gluconeogenesis in the liver
therefore excess insulin that declines glucose level in
the blood
CONSEQUENCE(EFFECT)
Hypoglycemia(false negative result)
MANAGEMENT
Reducing the dose of insulin
 Glucose Postprandial
oMeasuring of glucose two hours after the patient has
eaten
oMost reliable if the patient is tested following a standard
glucose dose(50-110g) rather than a random meal
oIt is a valuable screening tool for detecting diabetes
mellitus
 Glucose Postprandial
oThe test is performed when the patient demonstrates
symptoms of diabetes(polydipsia and polyuria) or when
results of the fasting plasma glucose test suggest diabetes.
oPURPOSE of the test;
-to screenfor diabetes mellitus
-to monitor drugs or diet therapy in the payient with diabetes
mellitus
 Glucose Postprandial
RESULTS:
High postprandial glucose levels-
pancreatitis,cushing’ssyndrome,acromegaly,
pheochromocytoma,hyperlipoproteinemia, etc.
Low postprandial glucose levels-
hyperinsulinism,insulinoma,von gierke’s
disease,hypoglycemia,etc.
 Glucose Postprandial
ADULT PROCEDURE:
Serum plasma(LT140 Collect venous blood 2 hours
mg/dl/2h) after the client finishes eating
Whole blood(LT mg/dl/2h) breakfast or lunch
ELDERLY Food is restricted for 2 hours
after breakfast or lunch
Serum (LT160mg/dl/2h)
before the test, but water is
Blood (LT140mg/dl/2h) not.
 Factors Affecting
Laboratory Results
oSMOKING
oSAME WITH GLUCOSE FASTING BLOOD
SUGAR(DRUG INFLUENCE)
DRUG LABORATORY TEST:
GLUCOCORTICOIDS(CORTISONE)
LABORATORY TEST: GLUCOSE-POSTPRANDIAL
MECHANISM OF ACTION(INTERACTION)
GLUCOCORTICOIDS INCREASE A SERUM GLUCOSE
LEVELS AND THUS STIMULATE INSULIN RELEASE AND
INHIBIT THE UPTAKE OF GLUCOSE.
It also increase the hepatic glucogenesis and
gluconeogenesis
CONSEQUENCE:
Hyperglycemia(false positive result)
MANAGEMENT:
Drugs that affect test results should not be
taken prior taking laboratory tests if possible.
 GLUCOSE TOLERANCE TEST(GTT)
oBlood glucose is then measured at set intervals for two
to three hours following ingestion of glucose
oUrine samples may be collected and tested for glucose
at the same times blood is taken for the GIT
oGlucose is normally reabsorbed from the glomerular
filtrate by the kidney tubules,so the blood glucose level
must be elevated before it exceeds the kidney’s capacity
to reabsorb
 GLUCOSE TOLERANCE TEST(GTT)
oThe blood glucose concentration above which
glucose can be detected in urine is called the
renal threshold for glucose(160-180mg/dl)
oThe presence of glucose in urine may be the
indication of DM.
 GLUCOSE TOLERANCE TEST(GTT)
oIt is the most sensitive method of evaluating borderline cases
of diabetes mellitus. Plasma and urine glucose levels are
monitored for 3 hours after ingestion of a challenge dose of
glucose to assess insulin secretion and the body’s ability to
metabolize glucose.
oPURPOSE of the test;
-to confirm diabetes mellitus in selected patients
-to help diagnose hypoglycemia and malabsorption syndrome.
 GLUCOSE TOLERANCE TEST(GTT)
RESULTS
o Decreased glucose tolerance, in which glucose levels peak
sharply before falling slowly to fasting levels, may confirm
diabetes mellitus or may result from cushing’s disease,
hemochromatosis,pheochromocytoma or cns lesions
o Increased glcose tolerance,may indicate insulinoma
malabsorption syndrome,addisons disease, hypothyroidism,
etc.
 GLUCOSE TOLERANCE TEST(GTT)
PRECAUTIONS:
oExercise or stress may decrease the glucose level.
oSpecify on the laboratory request when the patient last
ate, and when the last pretest dose of insulin or oral
antidiabetes drug was given
oIf the sample is to be drawn by a technician, tell the
patient the exact time the venipuncture must be performed.
 GLUCOSE TOLERANCE TEST(GTT)
Reference Value:
TIME SERUM(MG/DL) BLOOD(MG/DL)
FASTING 70-110 60-110
½ HOUR LT160 LT150
1 HOUR LT170 LT160
2 HOURS LT125 LT115
3 HOURS FASTING LEVEL FASTING LEVEL
URINE:NEGATIVE
 GLUCOSE TOLERANCE TEST(GTT)
PROCEDURE:
•A diet adequate in carbohydrate should be consumed for 2 or 3
days prior to testing
•Client remains NPO for 12 hours before the test, except for water
•No food should be eaten
•Drugs that affect test results should not be taken for 3 days prior
to the GTT, if possible
•Collect 5 ml venous blood. Collect a fasting urine specimen.
 GLUCOSE TOLERANCE TEST(GTT)
•Give 100g glucose (lemon flavored solution or glucola).
Some physicians will give glucose according to body
weight(1.75g/kg) as in pediatrics
•Obtain blood and urine specimen ½,1,2,3 hours after
glucose intake.
 GLUCOSE TOLERANCE TEST(GTT)
•ELEVATED BY:
CORTISONE
ORAL CONTRACEPTIVES
ESTROGENS
DIURETICS
THIAZIDES
SALICYLATES
ASCORBIC ACID
DRUG LABORATORY TEST: ORAL
CONTRACEPTIVES(progesterone and estrogen)
LABORATORY TEST: ORAL GLUCOSE TOLERANCE
TEST
MOA(INTERACTION)
There is a reduction in the rate of absorption of
carbohydrates from the GI tract
CONSEQUENCE(EFFECT)
Hyperglycemia(false positive result)
MANAGEMENT:
Drugs that affect test results should not be
taken prior taking laboratory tests if possible.
REFERENCES:

•Laboratory and diagnostic tests with nursing implications 4 th

edition
•A manual of laboratory and diagnostics tests 7 th edition
•Pharmacologgy 4th edition 2009
•Katzung” Basic and clinical pharmacology 12th edition 2012”
•Nursing the series for clinical excellence
“Deciphering Diagnostic test”
•CLINICAL CHEMISTRY: interpretation and techniques 2 nd edition
DRUG LABORATORY TEST
INTERACTION

3. CREATININE
 CREATININE CLEARANCE TEST
-Compares level of creatinine in the urine with
the creatinine level in the blood helps
provide information on the kidneys
- Creatinine test is used to measure the
amountof creatinine in the blood
 Creatinine
-a chemical waste compound that is produced
during normal skeletal muscle contractions
- normally filtered through the kidneys and
excreted in the urine
- a breakdown product of creatine, which is an
important part of muscle
 Creatinine Clerance
CREATININE CLEARANCE MEASURE NORMAL CREATININE
OF EXTENT OF RENAL FUNCTION
LEVELS IN URINE (based
 above 80- normal
 50- 80- slightly reduced
on a 24hour basis)
 30-50- mild renal failure  male: 14-26 mg/kg
 10-30- moderate renal failure  female: 11-20 mg/kg
 less than 5- 10- severe renal
failure
 Creatinine Clerance
Creatine levels depends:
• glomerular filtration rate
a panic value of 10 mg/dL in non dialysis patients
• reference values for creatinine levels
ADULT MALE
- 0.8- 1.2 mg/dL ( 62- 115 μmol/L)
- they have higher values than females because
they have larger body mass
 Creatinine Clerance
reference values for creatinine levels
 ADULT FEMALE
- 0.6-0.9 mg/dL ( 53-97 μmol/L)
-increase in pregnancy; results in lower
serum level
 Creatinine Clerance
reference values for creatinine levels
Children: 0.2-1 mg/dL
-age can be a factor in an increase of creatinine
level; values are proportional with that of the body
mass therefore the older the child is the higher
creatinine level (depends on body mass of child)
 Creatinine Clerance
Abnormal results
 high creatinine levels usually indicates renal
disease that has seriously damaged 50% or more of
the nephrons
 low creatinine levels (lower than normal) may
cause dehydration, renal ischemia, renal outflow
obstruction
 Creatinine Clerance
CLINICAL IMPLICATIONS OF CREATININE TEST
 decreased in creatinine clearance is found in any condition
that decreases blood flow such as:
• impaired kidney function
• shock
• hemmorrhage
• COPD
• CHF
 Creatinine Clerance
INCREASED CREATININE CLEARANCE
-High cardiac output
- pregnancy
INCREASED URINE CREATININE
-Gigantism
-hypothyroidism
- diabetes mellitus
- acromegaly
- rhabdomyolosis
 Creatinine Clerance
DECREASED URINE CREATININE
-Hyperthyroidism
- anemia
- muscular dystrophy
ASCORBIC ACID- CREATININE TEST INTERACTION

-Ascorbic acid (Vitamin C)

- a water- soluble vitamin
-It is used for the prevention and treatment of
scurvy.
ASCORBIC ACID- CREATININE TEST INTERACTION

PRESCRIPTION ANALYSIS
 Type of Interaction: Pharmacological
Interference (Alteration of Creatinine level)
 Interactant drug: Ascorbic acid (Vit. C)
 Mechanism of Interaction: false increase in
creatinine level due to reduced glomerular
filtration rate
ASCORBIC ACID- CREATININE TEST INTERACTION

PRESCRIPTION ANALYSIS
 Consequence: Increase level of creatinine in
the blood which leads to wrong diagnosis
 Management: the patient should not take
ascorbic acid when he/she will undergo
creatinine test because it would alter the results
of the test
 CEFOXITIN - CREATININE TEST INTERACTION

-Cefoxitin
- a semi- synthetic, broad spectrum cepha
antibiotic.
- derived from cephamycin C, which is produced
by Streptomyces lactamdurans.
 CEFOXITIN - CREATININE TEST INTERACTION

PRESCRIPTION ANALYSIS
 Type of Interaction: Pharmacological
Interference (Alteration of Creatinine level)
 Interactant drug: Cefoxitin
 Mechanism of Interaction: Cefoxitin increases
renal tubular secretion of creatinine
 CEFOXITIN - CREATININE TEST INTERACTION

PRESCRIPTION ANALYSIS
 Consequence: increase level of creatinine in
the urine which leads to misdiagnosis
 Management: Creatinine test should be
made at least two hours after administration of
Cefoxitin
IBUPROFEN - CREATININE TEST INTERACTION

-Ibuprofen
-a non-steroidal anti- inflammatory drug (NSAID)
- used to relieve pain and reduced fever and
inflammation
IBUPROFEN - CREATININE TEST INTERACTION

PRESCRIPTION ANALYSIS
 Type of Interaction: Pharmacological
Interference (Alteration of Creatinine level)
 Interactant drug: Ibuprofen
 Mechanism of Interaction: decreased
creatinine clearance by the kidney
IBUPROFEN - CREATININE TEST INTERACTION

PRESCRIPTION ANALYSIS
 Consequence: decreased creatinine level in
the urine which leads to misdiagnosis.
Management: Creatinine test should be made
at least six hours after the administration of
Ibuprofen to avoid wrong diagnosis.
 DIURETICS - CREATININE TEST INTERACTION

-Diuretics
- medicines that aid the elimination of sodium
( salt) and water from the body.
 DIURETICS - CREATININE TEST INTERACTION

PRESCRIPTION ANALYSIS
 Type of Interaction: Pharmacological
Interference (Alteration of Creatinine level)
 Interactant drug: Diuretics (Furosemide, HCTZ)
 Mechanism of Interaction: false increase in
creatinine level due to reduced glomerular
filtration rate.
 DIURETICS - CREATININE TEST INTERACTION

PRESCRIPTION ANALYSIS
 Consequence: Increased creatinine level in
the blood which leads to misdiagnosis.
 Management: avoid diuretic therapy prior to
creatinine test to reduced risk of inaccurate
laboratory test results.
 Summary
• Drugs that may alter the laboratory test results
such as Ibuprofen, ascorbic acid, diuretics, and
cefoxitin should be avoided so that accurate
results will be obtained.
• If these drugs are taken prior to creatinine test
the patient should report it to the physician.
REFERENCES:

• Laboratory and Diagnostic Tests with Nursing Implications, 4 th edition

• A Manual of Laboratory and Diagnostic Tests, 7 th edition
• Lippincott’s pharmacology, 4th edition
• Creatinine Test: By Janis O. FloresThe Gale Group Inc
•Biopharmaceutics by Leon Shargel
• Diciphering Diagnostic Tests by Lippincott
•http://www.nlm.nih.gov/medlineplus/ency/article/003611.htm
• http://www.rnceus.com/renal/renal creat.html
• http://www.rxlist.com
• http://www.mims.com
DRUG LABORATORY TEST
INTERACTION

4. BLOOD UREA NITROGEN

(BUN)
 Blood Urea Nitrogen (BUN)
•urea is formed when protein is broken down in
your body
•it is a waste product produced in the liver and is
excreted in the kidneys*
 Blood Urea Nitrogen (BUN)
Formation of Urea:
After ingestion of protein, hydrolysis of amino acids occurs
in the intestine. The absorbed amino acid are carried to the
liver and other tissues where they may be utilized for the
synthesis of new proteins, converted to other compounds
or utilized for energy. When catabolized, the amino group
ends up in urea, a waste product excreted by the kidney.
 Blood Urea Nitrogen (BUN)
•Determine whether your kidneys are functioning
normally.
•Determine whether your kidney disease is getting
worse.
•Monitor treatment of your kidney disease.
•Determine whether severe dehydration is present.
 Blood Urea Nitrogen (BUN)
Factors that alter BUN
protein breakdown*
hydration status
liver failure*

Note: Rapid protein catabolism and impairment of

the kidney function will result in an elevated BUN.
 Blood Urea Nitrogen (BUN)
CLINICAL IMPLICATIONS:
– Increased BUN levels
– Decreased BUN levels
 Blood Urea Nitrogen (BUN)
Clinical Implications:
1. High values of BUN (Azotemia)
may indicate:
-Kidey disease -Addison's disease
-diabetes -GIT bleeding
-Hypertension -tissue damage (severe burns)
-Dehydration -Elders may have increased
-high protein levels BUN*(kidneys are unable to
concentrate urine adequately)
 Drug that increase BUN level:
•allopurinol(Alloprin) •carbamazepine (Tegretol)
•vancomycin (Vancocin)
•aminoglycosides(Garamycin)
•propranolol(Inderal)
•furosemide (Lasix)
•rifampin (Rifadin)
•indomethacin (Indocin) •spironolactone (Aldactone)
•methotrexate (MTX) •tetracyclines
•aspirin •thiazide diuretics
•amphotericinB •triamterene (Dyrenium)
 BUN Furosemide Analysis
Drug Laboratory Test: FUROSEMIDE(lasix)
Laboratory Test: Blood Urea Nitrogen Test
MOA: Inhibits the transport of sodium/potassium in the
luminal membrane
Consequence: Increased level of BUN can cause
dehydration, GI bleeding, prerenal failure (low renal blood
supply caused by CHF)
 BUN Furosemide Analysis
Management:
– Report urinary output of the patient
– Check the vital signs
– Determine the hydration status of the patient
– Assess the dietary intake of the patient
 Blood Urea Nitrogen (BUN)
Clinical Implications:
2. Low values of BUN may indicate:
-very low protein diet
-malnutrition
-severe liver damage*
-drinking excessive amounts of liquid
(overhydration)
-low in the 3rd trimester of pregnancy*
 Drug that decrease BUN level:
•Amikacin
•Ascorbic acid
•Capreomycin
•cefotaxime
•Chloramphenicol
•Levodopa
•Phenothiazine
•Streptomycin
 BUN Phenothiazin Analysis
PHENOTHIAZINE
-Prototype: PROMETHAZINE
-Most drugs of this class are H1 antagonists and also possess
considerable anticholinergic activity
-It has prominent sedative effects
-Used primarily for their antiemetic effects
-undergo significant first-pass metabolism
-Metabolized extensively by CYP2D6
 BUN Phenothiazin Analysis
PHENOTHIAZINE
-Major route of metabolism is 7-hydroxylation of tricyclic
system
-because electron-withrawing 2-C1 substituent blocks the
hydroxylation on chlorophenyl ring, the hydroxylation
occurs in 7-position rather than the 2-position
-thus, the frequent major metabolite is the 7-hydroxy
compound
 BUN Phenothiazin Analysis
PHENOTHIAZINE
-7-hydroxy compound is further metabolized by
conjugation with glucoronic acid, and the
conjugate is excreted
 BUN Phenothiazin Analysis
Types of Interaction: Drug-laboratory
Interaction
MOA: Phenothiazine decreases BUN
Consequence: The patient may experience over-
hydration like having irritated cough, dyspnea,
neck-vein engorgement, and chest rales
 BUN Phenothiazin Analysis
Management:
– If BUN becomes abnormal, treatment with Phenothiazine should
be discontinued
– Advise the patient to increase protein-rich food intake and have
low-carbohydrate intake
– A low-protein intake and high-carbohydarte intake can decrease
BUN level
– Consider the liver function of the patient
– BUN is synthesized in the liver which result to decreased levels.
 Blood Urea Nitrogen (BUN)
INTERVENTION:
– Pre Test Patient Care
– Post test Patient after Care
 Renal Function Test
The frist set of laboratory tests performed to determine renal
function are:
– URINALYSIS
– BLOOD UREA NITROGEN
– SERUM CREATININE
These tests are ordered routinely when renal insufficiency is
suspected
If any of these are abnormal, other laboratory and diagnostic
test would be necessary
 Laboratory Test (Renal Function)
Adult: 5-25 mg/ml
Child: 5-20 mg/ml
If the BUN is lightly elevated, it will cause
dehydration by hemoconcentration.
Elevated BUN that remains elevated after
hydration is an indicator of renal disorder
 Laboratory Test (Shock Test)
Adult: 5-25mg/ml
A BUN of 30-40mg/ml could be indicative of
fluid loss and dehydration
BUN greater than 50mg/ml and does not
decrease substantially with the administration of
IV fluids, kidney damage is highly suspected.
 Summary
•BUN is a common renal function test
•AZOTEMIA is excessive retention of nitrogenous waste
products in the blood
•UREA is an end product of protein metabolism w/c is
produced in the liver
•Decreased BUN level occur with significant liver disease
•Increased BUN level may indicate renal disease
REFERENCES:

•Drug interactions and Updates

•CLINICAL CHEMISTRY: Interpretation and Techniques, 2nd Edtion
•Nursing: Deciphering Diagnostic Test
•http://www.scribd.com/doc/153877292/06Mar-Blood-Test-Blood-
Urea-Nitrogen
•http://www.scribd.com/doc/50688505/Blood-Urea-Nitrogen
•http://www.scribd.com/doc/162641483/Laboratory-Tests
•http://www.clinchem.org/content/46/9/1395.long