DRUG LAB INTERACTION Diploma - PowerPoint Presentation

Slide1

DRUG LAB INTERACTION

Diploma

(Clinical Chemistry)

Dr

.

Basma

Al-

Sudani

Lecture 1

Slide2

Laboratory 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

Slide3

Features 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

Slide4

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

Slide5

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

Slide6

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

Slide7

FALSE POSITIVE

-indicates a given condition is present when it is not

FALSE NEGATIVE

-it appears negative when it should not

Slide8

QUANTIATIVE TEST

Test with normal values reported in ranges

QUALITATIVE TEST

Test with positive or negative outcomes

SEMIQUANTITATIVE TEST

Those with varying degrees of positivity

Slide9

The 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

Slide10

DRUG LABORATORY TEST INTERACTION

SERUM BILIRUBIN

Slide11

Bilirubin

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.

Slide12

Bilirubin

It is extracted and

biotransformed

mainly in the liver, and excreted

in bile and urine.

Slide13

Formation 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.

Slide14

Formation of

Bilirubin

4.Biliverdin is a hydrophilic compound that is reduced by

biliverdin

reductase

into the hydrophobic compound

bilirubin

Slide15

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.

Slide16

Formation of

Bilirubin

Primary site of synthesis:

-SPLEEN

Secondary site of synthesis:

- LIVER & BONE MARROW

Slide17

Two Types of

Bilirubin

Prehepatic

Posthepatic

Slide18

TYPES

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

Slide19

TYPES

SYNONYMS

CHARACTERISTICS

Posthepatic

Conjuganted

Glucoronide

Direct-reacting

Freely

crosses

glomerular

filtrate

Formed by enzymatic activity, in liver

Gives

diazo

rx

in

aqueos

medium

Slide20

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 tissues

Diffuses – yellow colour

Doesn’t diffuse

Van den bergh

Indirect +

Direct +

Slide21

Serum Bilirubin

A break down product of

porphyrin

ring of

heme

– containing proteins , found in blood in 2 fractions – conjugated/

unconjugated

Slide22

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

Slide23

Serum

Bilirubin

(direct and total )

Direct or conjugated

bilirubin

is frequently the result of obstructive jaundice, either from

extrahepatic

or

intrahepatic

origin.

Slide24

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

Slide25

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

Slide26

How 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

Slide27

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

Slide28

Procedure

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

.

Slide29

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

Slide30

Clinical 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

Slide31

Clinical 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

Slide32

Aspirin

Is a weak organic acid that is unique among the NSAIDs in that it irreversibly acetylates (and thus, inactivates)

cyclogenase

.

Slide33

Aspirin

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.

Slide34

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

EFFECT:

-Iron deficiency

anemia

(false negative value)

MANAGEMENT:

-Avoid taking aspirin prior to laboratory test.

Slide35

Hydralazine

-this drug cause direct

vasodilation

, acting primarily on arteries and arterioles.

Slide36

Hydralazine

TYPE OF DRUG INTERACTION:

-

Drug-laboratory interaction with serum

bilirubin

MECHANISM OF INTERACTION:

-

increase the

bilirubin

serum level

Slide37

Hydralazine

EFFECT:

-

Changes in the liver function test (false positive value)

MANAGEMENT:

-Complete chemical and biochemical recovery occurs after discontinuation.

Slide38

Allopurinol

-

purine

analog.

-the primary metabolite is

alloxanthine

, which is also

xanthine

oxidase

inhibitor.

-its active metabolite are excreted in the feces and urine.

Slide39

Allopurinol

TYPE OF DRUG INTERACTION:

-

Drug-laboratory interaction with serum

bilirubin

.

MECHANISM OF INTERACTION:

-

increases the

bilirubin

serum level.

Slide40

Allopurinol

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

Slide41

DRUG LABORATORY TEST INTERACTION

2. GLUCOSE LEVEL

Slide42

What is Glucose?

THE PRINCIPAL FUEL FOR ALL BODY ACTIVITIES.

PRINCIPAL AND ALMOST

EXCLUSIVELYCARBOHYDRATE CIRCULATING IN

BLOOD.

Most important simple sugar in human metabolism.

Slide43

Formation of Glucose

Glycogenesis

(glucose-glycogen)

Glycogenolysis

(glycogen –glucose)

Gluconeogenesis

(

monocarbohydrate

like

glycerol-glucose)

Glycolysis

(glucose –lactate and

pyruvate

)

Slide44

Definition 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

Slide45

Depressed

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.

Slide46

Glucose 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

Slide47

Glycogen

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

Slide48

Glucagon

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

Slide49

2 Types of Disorders of

Glucose Metabolism

Hyperglycemia

Hypoglycemia

Slide50

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)

Slide51

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

Slide52

Critical 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

Slide53

Glucose Test

-used to aid in diagnosing and managing diabetes, or in managing

hypoglycemia

.

Slide54

MECHANISM 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

Slide55

Laboratory Tests

GLUCOSE FASTING BLOOD SUGAR(FBS)

GLUCOSE POSTPRANDIAL(FEASTING BLOOD

SUGAR)-(Two hour postprandial blood

sugar,PPBS

)

GLUCOSE TOLERANCE TEST-ORAL(GTT)(SERUM)

Slide56

FASTING 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

Slide57

FASTING 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

Slide58

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)

Slide59

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.

Slide60

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)

Slide61

Drug Influence

DECREASED

:

Insulin excess

ELEVATED

:

ACTH

Cortisone

Diuretics

Furosemide

Ethacrynic

acid

Anesthesia

drugs

Levodopa

Slide62

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

Slide63

CONSEQUENCE(EFFECT)

Hyperglycemia

(false positive result)

MANAGEMENT

Potassium

sparing diuretics substitution

Slide64

INSULIN

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

Slide65

CONSEQUENCE(EFFECT)

Hypoglycemia

(false negative result)

MANAGEMENT

Reducing the dose of insulin

Slide66

Glucose 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

Slide67

Glucose 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

Slide68

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

.

Slide69

Glucose 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.

Slide70

Factors Affecting

Laboratory Results

SMOKING

SAME WITH GLUCOSE FASTING BLOOD

SUGAR(DRUG INFLUENCE)

Slide71

GLUCOCORTICOIDS(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

Slide72

CONSEQUENCE:

Hyperglycemia

(false positive result)

MANAGEMENT:

Drugs that affect test results should not be taken prior taking laboratory tests if possible.

Slide73

GLUCOSE 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

Slide74

GLUCOSE 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.

Slide75

GLUCOSE 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.

Slide76

GLUCOSE 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.

Slide77

GLUCOSE 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.

Slide78

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

Slide79

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.

Slide80

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.

Slide81

GLUCOSE TOLERANCE TEST(GTT)

ELEVATED BY:

CORTISONE

ORAL CONTRACEPTIVES

ESTROGENS

DIURETICS

THIAZIDES

SALICYLATES

ASCORBIC ACID

Slide82

ORAL

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

Slide83

CONSEQUENCE(EFFECT)

Hyperglycemia

(false positive result)

MANAGEMENT:

Drugs that affect test results should not be taken prior taking laboratory tests if possible

.

Slide84

DRUG LABORATORY TEST INTERACTION

3. CREATININE

Slide85

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

Slide86

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

Slide87

Creatinine

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

Slide88

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

Slide89

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

Slide90

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)

Slide91

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

Slide92

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

Slide93

Creatinine

Clerance

INCREASED CREATININE CLEARANCE

High cardiac output

pregnancy

INCREASED URINE CREATININE

Gigantism

hypothyroidism

diabetes mellitus

acromegaly

rhabdomyolosis

Slide94

Creatinine

Clerance

DECREASED URINE CREATININE

Hyperthyroidism

anemia

muscular dystrophy

Slide95

ASCORBIC ACID- CREATININE TEST INTERACTION

Ascorbic acid (Vitamin C)

a water- soluble vitamin

It is used for the prevention and treatment of scurvy.

Slide96

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

Slide97

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

Slide98

CEFOXITIN - CREATININE TEST INTERACTION

Cefoxitin

a semi- synthetic, broad spectrum

cepha

antibiotic.

derived from

cephamycin

C, which is produced by

Streptomyces

lactamdurans

.

Slide99

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

Slide100

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

Slide101

IBUPROFEN - CREATININE TEST INTERACTION

Ibuprofen

a non-steroidal anti- inflammatory drug (NSAID)

used to relieve pain and reduced fever and inflammation

Slide102

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

Slide103

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.

Slide104

DIURETICS - CREATININE TEST INTERACTION

Diuretics

medicines that aid the elimination of sodium ( salt) and water from the body.

Slide105

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.

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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.

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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.

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DRUG LABORATORY TEST INTERACTION

4. BLOOD UREA NITROGEN (BUN)

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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*

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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.

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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.

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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.

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Blood Urea Nitrogen (BUN)

CLINICAL IMPLICATIONS

:

Increased BUN levels

Decreased BUN levels

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Blood 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)

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Drug 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

)

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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)

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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

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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*

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Drug that

decrease

BUN level:

Amikacin

Ascorbic acid

Capreomycin

cefotaxime

Chloramphenicol

Levodopa

Phenothiazine

Streptomycin

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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

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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

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BUN

Phenothiazin

Analysis

PHENOTHIAZINE

-7-hydroxy compound is further metabolized by conjugation with

glucoronic

acid, and the conjugate is excreted

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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

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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.

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Blood Urea Nitrogen (BUN)

INTERVENTION:

Pre Test Patient Care

Post test Patient after Care

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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

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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

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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.

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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