Clinical Chemistry Dr Basma Al Sudani Lecture 1 Laboratory Tests involved in the diagnosis and treatment of disease Purposes reliable for proper decision making measures chemical changes in the body ID: 935054
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Slide1
DRUG LAB INTERACTION
Diploma
(Clinical Chemistry)
Dr
.
Basma
Al-
Sudani
Lecture 1
Slide2Laboratory Tests
involved in the diagnosis and
treatment of disease
Purposes:
reliable for proper decision making
measures chemical changes in the body
detection of any dysfunctions in the body
monitor drug therapy
Slide3Features that describe the following
aspects of the Drug laboratory effects
:
nature of effect
route of administration
direction and strength of effect
level of documentation
sex of patient
age of patient
onset of effect after starting the medication
duration of effect after stopping the medication
clinical significance of effect
Slide4CLASSIFICATION
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
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
Slide6Laboratory 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
Slide7FALSE POSITIVE
-indicates a given condition is present when it is not
FALSE NEGATIVE
-it appears negative when it should not
Slide8QUANTIATIVE TEST
Test with normal values reported in ranges
QUALITATIVE TEST
Test with positive or negative outcomes
SEMIQUANTITATIVE TEST
Those with varying degrees of positivity
Slide9The quality of Quantitative assay is measured in terms of accuracy.
ACCURACY
-
Extent to which mean measurement is close to the true value
PRECISION
-
Refers to the reproducibility of the assay
Slide10DRUG LABORATORY TEST INTERACTION
SERUM BILIRUBIN
Slide11Bilirubin
Is a bile pigment.
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.
Slide12Bilirubin
It is extracted and
biotransformed
mainly in the liver, and excreted
in bile and urine.
Slide13Formation of
Bilirubin
Hemoglobin from senescent or
hemolyzed
red cells is broken down, releasing
heme
.
Heme
is then degraded in humans by the enzyme
heme
oxygenase
(HO), which is the rate-limiting step in the formation of
bilirubin
.
HO converts
heme to biliverdin IX.
Slide14Formation of
Bilirubin
4.Biliverdin is a hydrophilic compound that is reduced by
biliverdin
reductase
into the hydrophobic compound
bilirubin
Slide15Formation 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.
Slide16Formation of
Bilirubin
Primary site of synthesis:
-SPLEEN
Secondary site of synthesis:
- LIVER & BONE MARROW
Slide17Two Types of
Bilirubin
Prehepatic
Posthepatic
Slide18TYPES
SYNONYMS
CHARACTERISTICS
Prehepatic
Unconjuganted
Free
Indirect-reacting
Does not cross
glomerular
filtrate
Harmful
to neonatal nervous system
Formed in
reticuloendothelial
system (peripheral) requires organic solvent for
diazo
rx
Slide19TYPES
SYNONYMS
CHARACTERISTICS
Posthepatic
Conjuganted
Glucoronide
Direct-reacting
Freely
crosses
glomerular
filtrate
Formed by enzymatic activity, in liver
Gives
diazo
rx
in
aqueos
medium
Slide20Unconjugated
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 tissues
Diffuses – yellow colour
Doesn’t diffuse
Van den bergh
Indirect +
Direct +
Slide21Serum Bilirubin
A break down product of
porphyrin
ring of
heme
– containing proteins , found in blood in 2 fractions – conjugated/
unconjugated
Slide22Serum 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
Slide23Serum
Bilirubin
(direct and total )
Direct or conjugated
bilirubin
is frequently the result of obstructive jaundice, either from
extrahepatic
or
intrahepatic
origin.
Slide24Serum
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
Slide25Serum
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
Slide26How Do I Prepare for the
Bilirubin
Blood Test
you will need to fast (not eat or drink anything other than water) for four hours before you have the test performed.
Drink a normal amount of water before going to the laboratory or collection site.
You may have to stop taking certain medications before the test is performed, but only if your doctor tells you to do this
Slide27How 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
Slide28Procedure
Collect 5 to 10 ml of venous blood in a red-top tube
Hold the medication that would increase or decrease serum
bilirubin
for 24 hrs.
Do not eat or drink (NPO) except for water
Take note:
If
a hematoma develops at the
venipuncture
or
heelstick
site
, apply
warm soaks
.
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
Slide30Clinical Implications
DECREASED LEVEL:
- Iron deficiency
anemia
Drug influence:
aspirin, penicillin,
prednisone,asthma
medication(
theophylline
)
INCREASED LEVEL:
-
Obstructive jaundice caused by stones or
neoplasms
-Hepatitis -Liver cirrhosis
-
Metistatic
cancer
-Wilson’s disease
Slide31Clinical Implications
Drug Influence:
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
Slide32Aspirin
Is a weak organic acid that is unique among the NSAIDs in that it irreversibly acetylates (and thus, inactivates)
cyclogenase
.
Slide33Aspirin
TYPE OF DRUG INTERACTION
:
- Drug- laboratory interaction
MECHANISM OF INTERACTION
:
-Decrease serum
bilirubin
level
-Reduction of the level of platelet TXA2, resulting in the inhibition of platelet aggregation and prolonged bleeding.
Slide34Aspirin
-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
EFFECT:
-Iron deficiency
anemia
(false negative value)
MANAGEMENT:
-Avoid taking aspirin prior to laboratory test.
Slide35Hydralazine
-this drug cause direct
vasodilation
, acting primarily on arteries and arterioles.
Slide36Hydralazine
TYPE OF DRUG INTERACTION:
-
Drug-laboratory interaction with serum
bilirubin
MECHANISM OF INTERACTION:
-
increase the
bilirubin
serum level
Slide37Hydralazine
EFFECT:
-
Changes in the liver function test (false positive value)
MANAGEMENT:
-Complete chemical and biochemical recovery occurs after discontinuation.
Slide38Allopurinol
-
purine
analog.
-the primary metabolite is
alloxanthine
, which is also
xanthine
oxidase
inhibitor.
-its active metabolite are excreted in the feces and urine.
Slide39Allopurinol
TYPE OF DRUG INTERACTION:
-
Drug-laboratory interaction with serum
bilirubin
.
MECHANISM OF INTERACTION:
-
increases the
bilirubin
serum level.
Slide40Allopurinol
EFFECT:
-
Obstructive jaundice caused by stones or
neoplasms
, hepatitis, cirrhosis of the liver, infectious mononucleosis.
MANAGEMENT:
-close monitoring of serum
bilirubin
levels is important
-avoid taking
allupurinol
prior to laboratory test
Slide41DRUG LABORATORY TEST INTERACTION
2. GLUCOSE LEVEL
Slide42What is Glucose?
THE PRINCIPAL FUEL FOR ALL BODY ACTIVITIES.
PRINCIPAL AND ALMOST
EXCLUSIVELYCARBOHYDRATE CIRCULATING IN
BLOOD.
Most important simple sugar in human metabolism.
Slide43Formation of Glucose
Glycogenesis
(glucose-glycogen)
Glycogenolysis
(glycogen –glucose)
Gluconeogenesis
(
monocarbohydrate
like
glycerol-glucose)
Glycolysis
(glucose –lactate and
pyruvate
)
Slide44Definition of Terms
Liver
–THE CLEARING HOUSE FOR GLUCOSE METABOLISM; IT CONVERTS EXCESS GLUCOSE TO STORAGE FORMS FOR LATER USE
Glycogen
– primary storage form of glucose
Elevated level
- caused by the disorders of the pituitary gland and certain brain lesions.
Hyperglycemia
–may cause shock and severe
hemmorhaage
Slide45Depressed
level(
hypoglycemia
)
is
characterized of
hyperinsulinism
due either to endogenous pancreatic lesions or to exogenous over dosage.
Diabetes
mellitus
A
disorder of carbohydrate
metabolism characterized
by state of
hyperglycemia
due to insulin deficiency.
Slide46Glucose Tolerance Test(GTT
)
Analyzing blood glucose at timed intervals
following ingestion of a standard glucose dose;
oral glucose tolerance test(OGTT)
Hyperglycemia
Blood glucose concentration above normal
Hypoglycemia
Blood glucose concentration below normal
Slide47Glycogen
Storage form of glucose found in high concentration in the liver
Glycolysis
Energy production as a result of metabolic breakdown of glucose
Glycogenolysis
Conversion of stored glycogen to glucose
Glycosuria
Glucose in the
urine;glucosuria
Slide48Glucagon
Pancreatic hormone that increases blood glucose concentration by promoting the conversion of glycogen to glucose
False positive
Result that indicates that a given condition is present when it is not.
False negative
Result that appears negative when it should no
Renal threshold
Blood concentration above which a substance not normally excreted by the kidneys appears in the urine.
Gluconeogenesis
Formation of glucose
Slide492 Types of Disorders of
Glucose Metabolism
Hyperglycemia
Hypoglycemia
Slide50Diseases 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)
Slide51Diseases 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
Slide52Critical Glucose Values
-blood glucose level falls below 50mg/dl(
hypoglycemic
)
Symptoms
:
Fainting
Weakness
Confusion
Lack of coordination
-blood glucose over 400mg/dl
Symptoms :
Confusion Dry skin
Lethargy Nausea
Extreme thirst Coma
Weak pulse
Slide53Glucose Test
-used to aid in diagnosing and managing diabetes, or in managing
hypoglycemia
.
Slide54MECHANISM REGULATING BLOOD GLUCOSE LEVELS:
Insulin
-lowers blood glucose
-cellular membrane to glucose and transportation of glucose into cells.
Glucagon
-increase blood glucose concentration
-stimulates
glycogenolysis
Slide55Laboratory Tests
GLUCOSE FASTING BLOOD SUGAR(FBS)
GLUCOSE POSTPRANDIAL(FEASTING BLOOD
SUGAR)-(Two hour postprandial blood
sugar,PPBS
)
GLUCOSE TOLERANCE TEST-ORAL(GTT)(SERUM)
Slide56FASTING BLOOD GLUCOSE
performed when on a blood sample taken
when the patient has not eaten for specified
period of time.
usually obtained before breakfast after the
patient has gone without food since the previous
evening’s meal
Slide57FASTING BLOOD GLUCOSE
This test is commonly used to screen for
diabetus
mellitus ,in which absent or deficient insulin
allows persistently high blood glucose levels
PURPOSE
of the test;
-to
screenfor
diabetes mellitus
-to monitor drugs or diet therapy in the
payient
with diabetes mellitus
Slide58FASTING 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)
Slide59FASTING 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.
Slide60Factors 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)
Slide61Drug Influence
DECREASED
:
Insulin excess
ELEVATED
:
ACTH
Cortisone
Diuretics
Furosemide
Ethacrynic
acid
Anesthesia
drugs
Levodopa
FUROSEMIDE(LASIX
)
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
Slide63CONSEQUENCE(EFFECT)
Hyperglycemia
(false positive result)
MANAGEMENT
Potassium
sparing diuretics substitution
Slide64INSULIN
EXCESS
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
Slide65CONSEQUENCE(EFFECT)
Hypoglycemia
(false negative result)
MANAGEMENT
Reducing the dose of insulin
Slide66Glucose Postprandial
Measuring of glucose two hours after the patient has eaten
Most reliable if the patient is tested following a standard glucose dose(50-110g) rather than a random meal
It is a valuable screening tool for detecting diabetes mellitus
Slide67Glucose Postprandial
The test is performed when the patient demonstrates symptoms of diabetes(
polydipsia
and
polyuria
) or when results of the fasting plasma glucose test suggest diabetes.
PURPOSE
of the test;
-to
screenfor
diabetes mellitus
-to monitor drugs or diet therapy in the
payient
with diabetes mellitus
Slide68Glucose 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
.
Slide69Glucose Postprandial
ADULT
Serum plasma(LT140 mg/dl/2h)
Whole blood(LT mg/dl/2h)
ELDERLY
Serum (LT160mg/dl/2h)
Blood (LT140mg/dl/2h)
CHILD(LT 120mg/dl/2h)
PROCEDURE
:
Collect venous blood 2 hours after the client finishes eating breakfast or lunch
Food is restricted for 2 hours after breakfast or lunch before the test, but water is not.
Slide70Factors Affecting
Laboratory Results
SMOKING
SAME WITH GLUCOSE FASTING BLOOD
SUGAR(DRUG INFLUENCE)
Slide71GLUCOCORTICOIDS(CORTISONE
)
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
Slide72CONSEQUENCE:
Hyperglycemia
(false positive result)
MANAGEMENT:
Drugs that affect test results should not be taken prior taking laboratory tests if possible.
Slide73GLUCOSE TOLERANCE TEST(GTT)
Blood glucose is then measured at set intervals for two to three hours following ingestion of glucose
Urine samples may be collected and tested for glucose at the same times blood is taken for the GIT
Glucose 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
Slide74GLUCOSE TOLERANCE TEST(GTT)
The blood glucose concentration above which glucose can be detected in urine is called the renal threshold for glucose(160-180mg/dl)
The presence of glucose in urine may be the indication of DM.
Slide75GLUCOSE TOLERANCE TEST(GTT)
It 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.
PURPOSE
of the test
;
-to confirm diabetes mellitus in selected patients
-to help diagnose
hypoglycemia
and
malabsorption
syndrome.
Slide76GLUCOSE TOLERANCE TEST(GTT)
RESULTS
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
Increased
glcose
tolerance,may
indicate
insulinoma
malabsorption syndrome,addisons disease, hypothyroidism, etc.
Slide77GLUCOSE TOLERANCE TEST(GTT)
PRECAUTIONS:
Exercise or stress may decrease the glucose level.
Specify on the laboratory request when the patient last ate, and when the last
pretest
dose of insulin or oral
antidiabetes
drug was given
If the sample is to be drawn by a technician, tell the patient the exact time the
venipuncture
must be performed.
Slide78GLUCOSE 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
Slide79GLUCOSE 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.
Slide80GLUCOSE 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.
Slide81GLUCOSE TOLERANCE TEST(GTT)
ELEVATED BY:
CORTISONE
ORAL CONTRACEPTIVES
ESTROGENS
DIURETICS
THIAZIDES
SALICYLATES
ASCORBIC ACID
Slide82ORAL
CONTRACEPTIVES(progesterone and
estrogen
)
ORAL
GLUCOSE TOLERANCE TEST
MOA(INTERACTION)
There is a reduction in the rate of absorption of carbohydrates from the GI tract
Slide83CONSEQUENCE(EFFECT)
Hyperglycemia
(false positive result)
MANAGEMENT:
Drugs that affect test results should not be taken prior taking laboratory tests if possible
.
Slide84DRUG LABORATORY TEST INTERACTION
3. CREATININE
Slide85CREATININE 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
Slide86Creatinine
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
Slide87Creatinine
Clerance
CREATININE CLEARANCE MEASURE OF EXTENT OF RENAL FUNCTION
above 80- normal
50- 80- slightly reduced
30-50- mild renal failure
10-30- moderate renal failure
less than 5- 10- severe renal failure
NORMAL CREATININE LEVELS IN URINE (based on a 24hour basis)
male: 14-26 mg/kg
female: 11-20 mg/kg
Slide88Creatinine
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
Slide89Creatinine
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
Slide90Creatinine
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)
Slide91Creatinine
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
Slide92Creatinine
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
Slide93Creatinine
Clerance
INCREASED CREATININE CLEARANCE
High cardiac output
pregnancy
INCREASED URINE CREATININE
Gigantism
hypothyroidism
diabetes mellitus
acromegaly
rhabdomyolosis
Slide94Creatinine
Clerance
DECREASED URINE CREATININE
Hyperthyroidism
anemia
muscular dystrophy
Slide95ASCORBIC ACID- CREATININE TEST INTERACTION
Ascorbic acid (Vitamin C)
a water- soluble vitamin
It is used for the prevention and treatment of scurvy.
Slide96ASCORBIC 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
Slide97ASCORBIC 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
Slide98CEFOXITIN - CREATININE TEST INTERACTION
Cefoxitin
a semi- synthetic, broad spectrum
cepha
antibiotic.
derived from
cephamycin
C, which is produced by
Streptomyces
lactamdurans
.
Slide99CEFOXITIN - 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
Slide100CEFOXITIN - 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
Slide101IBUPROFEN - CREATININE TEST INTERACTION
Ibuprofen
a non-steroidal anti- inflammatory drug (NSAID)
used to relieve pain and reduced fever and inflammation
Slide102IBUPROFEN - 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
Slide103IBUPROFEN - 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.
Slide104DIURETICS - CREATININE TEST INTERACTION
Diuretics
medicines that aid the elimination of sodium ( salt) and water from the body.
Slide105DIURETICS - 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.
Slide106DIURETICS - 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.
Slide107Summary
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.
Slide108DRUG LABORATORY TEST INTERACTION
4. BLOOD UREA NITROGEN (BUN)
Slide109Blood 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*
Slide110Blood 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.
Slide111Blood 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.
Slide112Blood 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.
Slide113Blood Urea Nitrogen (BUN)
CLINICAL IMPLICATIONS
:
Increased BUN levels
Decreased BUN levels
Slide114Blood Urea Nitrogen (BUN)
Clinical Implications:
High values of BUN (
Azotemia
) may indicate:
-
Kidey
disease
-diabetes
-Hypertension
-Dehydration
-high protein levels
-Addison's disease
-GIT bleeding
-tissue damage (severe burns)
-Elders may have increased BUN*(kidneys are unable to concentrate urine adequately)
Slide115Drug that
increase
BUN level:
allopurinol
(
Alloprin
)
aminoglycosides
(
Garamycin
)
furosemide
(
Lasix
)
indomethacin
(Indocin)methotrexate (MTX)aspirin
amphotericinB
carbamazepine
(
Tegretol
)
vancomycin
(
Vancocin
)
propranolol
(
Inderal
)
rifampin
(
Rifadin
)
spironolactone
(
Aldactone
)
tetracyclines
thiazide
diuretics
triamterene
(
Dyrenium
)
Slide116BUN
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)
Slide117BUN
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
Slide118Blood 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*
Slide119Drug that
decrease
BUN level:
Amikacin
Ascorbic acid
Capreomycin
cefotaxime
Chloramphenicol
Levodopa
Phenothiazine
Streptomycin
Slide120BUN
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
Slide121BUN
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
Slide122BUN
Phenothiazin
Analysis
PHENOTHIAZINE
-7-hydroxy compound is further metabolized by conjugation with
glucoronic
acid, and the conjugate is excreted
Slide123BUN
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
Slide124BUN
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.
Slide125Blood Urea Nitrogen (BUN)
INTERVENTION:
Pre Test Patient Care
Post test Patient after Care
Slide126Renal 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
Slide127Laboratory 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
Slide128Laboratory 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.
Slide129Summary
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