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nucleotidase or
GGTP indicates that the source is primarily hepatic. With normal 5
nucleotidase or GGTP, it
is nonhepatic cause. ALP is increased in pregnancy due to placental ALP. Non hepatic causes
of elevated ALP include bone disorders (eg: healing fractures, osteomalacia),
hyperthyroidism, hyperparathyroidism, diabetic mellitus, renal failure. ALP concentration
can be lowered by a number of conditions including, hypothyroidism, hypophosphatemia,
pernicious anemia.
2. 5- NUCLEOTIDASE
Normal range: 0-11 units/L
5- nucleotidase is found in many tissue (including liver, brain, heart, blood vessels),
serum 5- nucleotidase is elevated only in hepatic diseases.
3. -GLUTAMYL TRANSPEPTIDASE
Normal range: 1-94 units/ L
Glutamyl transpeptidase (GGTP or GGT), a biliary excretory enzyme, can also help
determine whether an elevated ALP is of hepatic injury. It is found in kidney, pancreas,
spleen, heart, brain, liver and seminal vesicles. GGTP concentration is elevated in alcoholic
liver disease, pancreatic diseases, MI, severe COPD, diabetes, kidney disease.
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4. BILIRUBIN
Total bilirubin: 0.3-1 mg/dl
Indirect (unconjugated, insoluble) bilirubin: 0.2-0.7 mg/dl
Direct (conjugated, water soluble) bilirubin: 0.1-0.3 mg/dl
Pediatrics:-2-6mg/dl (24hr infant), 6-8mg/dl (48hr infant), 0.3-1mg/dl (>1 month old)
Bilirubin metabolism begins with the breakdown of red blood cells in many parts of the
body. Red blood cells contain haemoglobin, which broken down to haeme and globin. Haeme
is converted to bilirubin (insoluble organic compound), which is then carried by albumin in
the blood to the liver. In the liver, most of the bilirubin is chemically attached to glucuronic
acid using enzyme glucuronyl transferase (water soluble) before it is released in the bile. This
conjugated (attached) bilirubin is called direct bilirubin & unconjugated bilirubin is called
indirect bilirubin.
Total serum bilirubin = direct Bilirubin + indirect bilirubin.
Conjugated bilirubin is released into the bile by the liver and stored in the gallbladder, or
transferred directly to the small intestines. Bilirubin is further broken down by bacteria in the
intestines, and those breakdown products contribute the colour of the faeces. A small
percentage of these breakdown compounds are taken again by the body, and eventually
appear in the urine. Jaundice is a yellowing of the skin and the white part of the eye, which
occurs when bilirubin builds up in the blood at a level greater than approximately 2.5 mg/dl.
This might happen due to liver disease or bile duct blockage.
HEPATOCELLULAR INJURY
The aminotransferase & lactate dehydrogenase (LDH) assess hepatocellular inflammation
or injury. These enzymes are located inside the hepatocytes.
Drugs causes hepatocellular injury:-
Acetaminophen
Allopurinol
INH
Ketoconazole
Methotrexate and NSAIDs etc.
Non drug causes: CHF, Liver infection, Wilsons disease.
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1. ASPARTATE AMINOTRANSFERASE (AST)
Normal AST: <35units/L, newborns/infants:- 20-65 IU/L.
Critical value :-> 80IU/L.
AST (aspartate aminotransferase) is an enzyme found in high amounts in liver and less
amount in heart muscle skeletal muscle cells, kidney, brain, lungs, intestine.
An increase in ALT levels may be due to:
Acute pancreatitis
Cirrhosis
Death of liver tissue (liver necrosis)
Hepatitis (viral, autoimmune)
Lack of blood flow to the liver (liver ischemia)
Liver disease
Liver tumour
An increase in AST levels may indicate:
Acute haemolytic anaemia
Acute pancreatitis
Acute renal failure
Cirrhosis
Heart attack
Hepatitis
2. LACTATE DEHYDROGENASE (LDH)
Normal range:-100-225 IU/L
LDH is found in most human tissues but primarily in myocardium, liver, skeletal
muscle, brain, kidney and RBCs. LDH has 5 isoenzymes and type 5(LDH
5
) is corresponds to
liver disease. Although LDH
5
is less sensitive to liver disease than the amino transferase,
elevated concentration occurring patients with hepatitis, biliary obstruction, meta stable liver
disease or exacerbation of cirrhosis.
3. ALPHA-1 ANTITRYPSIN
Alpha-1 antitrypsin is a laboratory test to measure the amount of alpha-1 antitrypsin
(A1AT) in your blood. It helps in identifying emphysema in adults and liver disease
(cirrhosis) in children and adults. If there is no A1AT, certain digestive proteins (enzymes)
released by white blood cells and cause widespread damage in the lungs and liver.
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TEST FOR DETOXIFICATION
HEPATIC ENCEPHALOPATHY
Diffused metabolic dysfunction of brain occurs due to acute or chronic liver failure.
Ammonia is formed by catabolism of protien within the gut lumen by conversion of serum
glutamine into ammonia by enterocyte in intestine and enters the blood from intestine. Liver
removes >90% of ammonia by first pass metabolism. This may effect in liver failure.
1. AMMONIA
Normal range: 10-80mg/Dl or 17-41mol/L (Adults & pediatrics)
New born: 90-150 g/dl
In patients with cirrhosis, ammonia concentration in serum or CSF may increase.
Ammonia levels are used primarily to evaluate patients with hepatic encephalopathy or coma.
Ammonia conc. can be elevated in patients:
With inborn disorders of urea cycle
With Reyes syndrome
On very high protein diet
TESTS FOR HEPATITIS
Test for the Hepatitis A Virus (HAV), measure the HAV antibodies of either IgM or IgG
types. These antibodies are present at the onset of jaundice and usually resolve over 2-3
months. In type B Hepatitis; the hepatitis B virus (HBV) is a DNA virus. This virus is
surrounded by a protein called the surface antigen (HBsAg). Inside this coat, a core (HBcAg)
protein coat surrounds the DNA & DNA polymerase.
Another protein that seems to be in this virus is the e-antigen (HBeAg). In response to
infection with hepatitis B virus, the body produces antibodies to the antigen, antisurface
antigen (anti-HBS), anticore antigen (anti-HBC) and anti-e antigen (anti-HBE). All of these
antibodies can detect in clinical laboratory. In Hepatitis C, there is elevated LFTs for 6
months. ALT and AST values commonly in 60-100 IU/L range. Chronic active Hepatitis C
can be confirmed by a liver biopsy.
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EXERCISE NO: 2 DATE: 12/03/13
INTERPRETATION OF LABORATORY DATA
AIM
To analyze and interpret the lab data of a patient presented with viral hepatitis A.
SUBJECTIVE EVIDENCE
Patient complains of fever and vomiting since one day. Also complains of
discoloration of skin and eye since one day.
OBJECTIVE EVIDENCE
Liver enzymes estimation shows as following:
AST - 4030 iu/l
ALT 4360 iu/l
Albumin - (+++) present
Bilirubin:
Total -8mg/dl
Direct - 5.6mg/dl
HAV IGM antibody -1.68(positive)
INTERPRETATION
The patient has a history of viral fever. Normal direct bilirubin level is 0.1-0.3. Elevated
bilirubin implies hepatic disease that interferes with the excretion of bilirubin from the
hepatocytes or clearance of bile from the liver. It is also found in other conditions like
hemolysis or infective RBC production.
Hepatitis is a term that technically refers to a histologic pattern of inflammation of
hepatocytes. The laboratory reflection of hepatitis is a hepatocellular injury pattern which is
marked primarily by elevated aminotrasferases. Here both the aminotransferases ie, AST and
ALT are elevated. Presence of HAV IgM antibody confirms the viral hepatitis A. The
patients history of viral fever again reinforced the confirmation.
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PLANNING
The liver function test report shows viral hepatitis A in this patient. The tests like AST,
ALT are done. The test for viral hepatitis A ie, HAV IgM antibody test is done which
confirmed the disease as viral hepatitis A. By using this laboratory parameter treatment can
be planned for this patient.
CONCLUSION
Interpretation of liver function test of patient diagnosed as viral hepatitis A.
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III. LABORATORY ASSESSMENT OF RENAL FUNCTION TEST
Kidney plays a vital role in the body homeostasis with their ability to excrete and
reabsorb various exogenous and endogenous substances selectively. The functional unit of
kidney consists of one million nephrons. Glomerulus allows substance with molecular weight
up to 40,000. So this prevents passage of plasma proteins and RBC. Kidney filters about
180L of fluid each day, of this only 1.5L is excreted as urine.
INDICATORS OF RENAL FUNCTION
1. SERUM CREATININE
Normal range: For adults: 0.7-1.5mg/dl
For childrens: 0.2-0.7mg/dl
Creatinine and its precursor creatinine are non-protein nitrogenous of the bloods. After
synthesis in the liver; creatinine diffuses in to the blood stream and taken up by muscle cells.
Some of them convert in to creatinine phosphate. The daily production of creatinine is about
2% total body creatinine, which remains constant of muscle and is not significantly changed.
Causes of changes in serum creatinine include following:
A rise in serum creatinine (S.cr) indicates worsening of renal function
Renal dysfunction, urinary tract obstruction always decrease excretion
In addition drugs such as cimetidine, triametrine, amiloride, spirinolactone, inhibit
tubular secretion of creatinine.
Other factor like muscle mass, gender, period of time that has elapsed after the insult
also influence the renal function
2. CRETININE CLEARENCE
Normal:-90-140ml/min
It represents the rate at which creatinine is removed from the blood by the kidneys,
roughly approximates GFR. Calculation requires the knowledge of urinary creatinine
excretion (usually over 24hr) and concurrent serum creatinine levels.
Cl
CR
Cl
CR
=Creatinine clearance in ml/min
U= Conc. of creatinine in urine,
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V=Urine volume ml/min,
P=Serum creatinine conc.
BSA=Patients body surface area
BSA (m
2
) =
Estimation of creatinine clearance without urine collection
One method of estimation uses the Cockroft & Gault, which is based on body weight, age and
gender.
Cl
CR
=
In females, the result has traditionally been multiplied by 0.85.
3. BLOOD UREA NITROGEN
Normal range: 8-20mg/dl
Blood urea nitrogen (BUN) is less sensitive indicators of renal function. It may be
elevated due to dehydration, blood loss, shock, severe heart failure, high protein diet. But it
elevated in the case of severe hypertension, Glomerular nephritis, tubular necrosis,
pyelonephritis, polycystic kidney etc.
4. SERUM ELECTROLYTES
a. SODIUM
Normal range: 135-145mmol/lit
The principal role of Na is to regulation of serum osmolality, fluid& acid base balance.
Kidneys are `primary organ responsible for the controlling body Na &water. Glomeruli filter
about 180L of water and 600g of sodium per day. Less than 2L of water and 0.1-40gm of
sodium end up in the urine. Aldosterone and ADH are mainly responsible for control of water
and Na acting at distal convoluted tubule and collecting duct.
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b. POTASSIUM
Normal range:3.5-5.0mmol/L
The kidney is the primary organ involved in the control and elimination of potassium.
Potassium is freely filtered at the glomerulus and almost completely absorb in the tubule.
Aldosterone is important factor acting at the distal tubule increase potassium secretion.
Presence of anions in the distal tubules can increase potassium loss.
5. URINALYSIS
Urinalysis are used to search for evaluate renal and non-renal problem.
a. PROTEIN
Normal range: 0-1 150mg/day
Abnormal permeability of the glomerular limiting membrane allows large quantities of
albumin to enter the urine.
Little proteinuria (<0.5g/day): Heamoglobinuria, high BP, fever,Renal tubular
damage, exercise.
Moderate proteinuria (0.5-3g/day): chronic glomerulonephritis, diabetic
nephropathy, pyelonephritis.
Major proteinuria (>3g/day): Lupus nephritis, chronic glomerulonephritis.
b. PH
Normal range: 4.5-8.0
In general acidic urine detects bacterial colonization. Alkaline urine may be seen with
urinary tract infection caused by urea splitting bacteria such as Proteus mirabilis, tubular
defects causing decreased net tubular hydrogen ion secretion.
c. SPECIFIC GRAVITY
Normal range 1.010-1.025
Specific gravity determination helps to determine kidneys concentrating ability.
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d. GLUCOSE
Normal range- none
The normal renal threshold for glucose is a blood glucose level of about 180mg/dl;
glucose does not normally appear in urine. Glycosuria indicates Diabetes mellitus.
e. KETONES
Ketones do not normally appear in urine. Ketonuria indicates uncontrolled DM; but it
may also occur with starvation and with low carbohydrate diets.
MICROSCOPIC EXAMINATION OF URINE
a. Hematuria: It is the presence of RBCs in urine) may indicate conditions such as
trauma or a systemic bleeding disorder.
b. Crystals: Which is pH dependent may occur normally in acid or alkaline urine. Uric
acid crystals may form in acid urine; phosphate crystals may form in alkaline urine.
c. Bacteria: Bacteria do not normally appear in urine. The finding of 20 or more
bacteria per High Power Field (HPF) may indicate a UTI; smaller values may
indicate urethral contamination.
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EXERCISE NO: 3 DATE: 14/04/13
INTERPRETATION OF LABORATORY DATA
AIM
To analyze and interpret the lab data of a patient presented with chronic renal
failure.
SUBJECTIVE EVIDENCE
The patient complaining of pedal oedema for 10days .Patient is known case of
hypertension and acute glomerular nephritis. He had puffiness of face, anorexia,
dyspepsia and nocturia.
OBJECTIVE EVIDENCE
Blood urea: 85mg/dl
S.creatinine: 5.5mg/dl
S.Ca2+: 7.2 mg/dl
S.K+: 3.4 mEq/L
INTERPRETATION
Normal level of serum creatinine is 0.6-1.6mg/dl.A rise in S.cr almost always indicates
worsening of renal function. Renal dysfunction, urinary tract obstruction always decreases
excretion of drugs such as cimetidine, triametrine, amiloride, spiranolactone, in-habits tubular
secretion of creatinine.
Normal blood urea nitrogen (BUN) is 15-45. BUN is less sensitive indicators of renal
function. It may be elevated due to dehydration, blood loss,shock,severe heart failure, high
protein diet. But it elevated in the case of severe hypertension Glomerular nephritis tubular
necrosis pyelonephritis and polycystic kidney.
Normal serum potassium is 4.5-5.5meq/l.Here it is reduced. Normal serum calcium is 8.5-
10.5mg/dl. Here both of these ions are reduced which also confirms the electrolyte
imbalance.
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PLANNING
The renal function tests report pointing chronic renal failure in this patient. By using this
parameters treatment can be planned for this patient.
CONCLUSION
From subjective evidence and objective evidence from lab parameter was very much
suggestive of chronic renal failure.
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IV. LABORATORY ASSESSMENT OFCARDIAC FUNCTION TEST
LABORATORY TESTS USED IN ACD
Three Criteria for the diagnosis of acute myocardial infarction (AMI) are clinical
presentation, electrocardiography and elevated biochemical markers. Clinical presentation
will not distinguish among unstable angina (UA), NSTEMI, and STEMI. ECG differentiates
between NSTEMI and STEMI. Cardiac-specific biochemical markers are used to
differentiate between UA and MI.
BIOCHEMICAL MARKERS
Criteria of ideal biochemical marker for the diagnosis of acute coronary syndrome include:
High specificity
High sensitivity
Rapidly released into the blood stream after myocardial injury.
Persists for sufficient time.
Measured level of marker is directly proportional to the myocardial injury.
Assay technique should be available, easy to perform, inexpensive, rapid
1. CARIAC SPECIFIC TROPONIN I AND CARDIAC SPECIFIC TROPONIN T
Diagnostic level: Troponin T (Tn T) <0.1 ng/ml
Diagnostic level: Troponin I( Tn I) <1.5 ng/ml
Troponin is a protein complex. 3 subunits: troponin C (TnC), troponin I (TnI), troponin T
(TnT). These are located in filaments of myofibrils. Regulate Ca
2+
mediated interaction of
actin and myosin. TnC expressed by myocardial cells in cardiac and skeletal muscles are
identical. Monoclonal antibody-based immunoassays are used to detect TnI and TnT.
After myocardial injury serum TnT, TnI begin to rise and get elevated within 3-12 hrs,
peak in 24 hrs (TnI), 12hr-2 days (TnT) and return to normal in 5-10 days (TnI), 5-14 days
(TnT). Troponins are most beneficial in identifying AMI 6hrs or more after symptom onset.
Causes of detectable serum levels of troponin:
MI, Cardiac surgery, Coronary angiography, Heart failure, renal failure,
pulmonary embolism, Rejection of heart transplant.
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2. CREATIN KINASE
Normal range: Males-40-200 iu/l
Normal range: Females-35-150 iu/l
CK is found in skeletal muscle, myocardium, and brain. It is an enzyme that stimulates
the transfer of high energy phosphate groups. Circulating CK is directly proportional to the
individuals muscle mass. CK level rise 4-8 hrs after the onset of chest pain associated with
AMI, peak in 24 hrs and return to normal in 3-4 days
Causes of elevated CK levels:
Cardiac causes (myocarditis, pericarditis, AMI), skeletal muscle causes (myxedema
muscular dystrophy seizures trauma vigorous exercise malignant hyperpyrexia), medications
(amphotericin b, clofibrate, ethanol, lithium halothane, barbiturate poisoning intramuscular
injection), other causes (renal failure, hypothyroidism, cerebrovascular accident, severe
hypokalemia).
3. CREATIN KINASE ISOENZYME
Normal range: CK-MB<12 iu/l
Enzyme CK is a dimer of two B monomers (CK-BB), two M monomers (CK-MM), or a
hybrid of two (CK-MB). CK-BB is found in brain, lungs, intestinal tract. CK-MM is found in
skeletal and cardiac muscles.CK-MB found predominantly in myocardium but also in skeletal
muscle and it is specific for myocardial tissue and has been used for the diagnosis of AMI.
Serum CK-MB begin to rise 3-12 hrs after onset of symptoms, peak in 24 hrs and return to
normal in 2-3 days.
Causes of elevated CK-MB:
Myocardial damage (MI, myocardial puncture/trauma, pericarditis and myocarditis), systemic
diseases with cardiac involvement (hyperthermia and hypothermia), others (surgery, tumors,
athletic activity, hypothyroidism, renal failure and subarachnoid hemorrhage)
a. CK-MB Isoforms
Two isoforms of CK-MB are CK-MB
1
and CK-MB
2.
CK-MB
2
is released into the
circulation following an AMI, and it is metabolized into negatively charged CK-MB
1
. In
healthy individuals both are in equilibrium. Normal levels are 0.5-1iu/l for each isoform.
These lack cardiac specificity and also assays are not widely available.
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b. Myoglobin
It is a low molecular weight heme protein found in cardiac and skeletal muscle. Serum
levels rise in 1-4hrs and peak 6-7hrs after onset of symptoms. It will return to normal in 24
hrs.
It is most effective in ruling out AMI. Other causes that increase myoglobin serum level are
skeletal muscle injury, trauma, and renal failure.
c. Lactate dehydrogenase
Normal range:-100-210 iu/l
It is a low molecular weight heme protein found in cardiac and skeletal muscle. Serum
levels rise in 1-4hrs and peak 6-7hrs after onset of symptoms. It will return to normal in 24
hrs. It is most effective in ruling out AMI.Other causes that increase myoglobin serum level
are skeletal muscle injury, trauma, renal failure.It is found in various organs and tissues like
heart, liver, lungs, kidneys, RBC. Due to lack of specificity it is not used widely. Elevation of
LDH
1
or ratio LDH
1
/LDH
2
greater than 1 was used in the diagnosis of AMI.
d. Aspartate amino transferase
Normal: Males-0-37iu/l
Normal: Females-0-31iu/l
It is an enzyme involved in amino acid synthesis. It is distributed in liver, heart,
skeletal muscle, red blood cells, kidneys, and pancreas. Serum level of AST rises within 12
hrs. of AMI, peak in 24-48hrs, and return to normal in 3-4 days.
MISCELLANEOUS LABORATORY TESTS
1. SERUM GLUCOSE
Normal- 70-110mg/dl
After AMI due to stress serum glucose will be elevated and persists for several week.
2. WHITE BLOOD CELLS
Normal-4.8-10.8*10
3
cells/mm
3
WBC may be increased in patients with AMI.
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3. ESR
Normal: Males-1-15 mm/hr
Normal: Females-1-20mm/hr
It is related to acute phase reactants that increase in patient with AMI. Peak on day
4or5; remain elevated for 3-4wk.
4. LIPID PANEL
Total cholesterol and low-density lipo protein may be decreased in 48-72hrs post MI
and persist for 6-8wks.
LABORATORY TESTS USED IN THE EVALUATION OF HEART FAILURE
1. NATRIURETIC PEPTIDES
These are naturally secreted hormones that are released by various cells in response to
increased volume or pressure.
Various types of natriuretic peptides are: Atrial natriuretic peptide (ANP), B-type
natriuretic peptide (BNP), C-type natriuretic peptide (CNP), Dendroaspis natriuretic peptide
(DNP).BNP and ANP are the cardiac specific peptides. BNP is found in higher concentration
in cardiac ventricles. It is secreted by left ventricular myocytes in response to volume
overload and increased ventricular wall tension. Precursor of BNP is preproBNP which is
enzymatically cleaved into proBNP. This is again cleaved into biologically active C-terminal
32 aa BNP and inactive N-terminal-proBNP (NT-ProBNP).
Plasma levels of both BNP and NT-ProBNP are elevated due to increased volume and
ventricular myocyte stretch in patients with heart failure. These are the markers in patients
with heart failure, IHD. There levels may be varied according to gender, age, renal function;
obesity. Normal levels are higher in women than men.
a. BNP
Diagnostic cutoff: 100PG/ML
b. NT-proBNP
Diagnostic cut off: 125pg/ml for patients <75yrs
Diagnostic Cut off: 450pg/ml for patients>75yrs
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OTHER BIOCHEMICAL MARKERS
CK AND CK-MM isoform will be useful for genetic screening in patients and family
members at increased risk of cardiomyopathy that will progress to heart failure.
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EXERCISE NO: 4 DATE: 14/05/13
INTERPRETATION OF LABORATORY DATA
AIM
To analyze and interpret the lab data of a patient presented with unstable angina.
OBJECTIVE EVIDENCE
CKMB - 70
AST - 73
LDH - 550
ECG shows ST elevation.
SUBJECTIVE EVIDENCE
Patient was complaining of chest pain since morning and it was aggravated after few
times. Pain was sudden in onset which increases on strain and relieving till taking rest.
INTERPRETATION
Based on subjective evidence, the disease was diagnosed as unstable angina.
Objective evidence of cardiac enzymes like CKMB, AST, LDH were found to be elevated.
Elevation of CKMB is indicative of myocardial infection.
PLANNING
The cardiac function tests report pointing myocardial infarction in this patient. By using this
lab parameter treatment can be planned for this patient.
CONCLUSION
From the subjective and objective evidence from lab parameter was very much suggestive of
myocardial infarction.
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REFERENCE
1. Comprehensive Pharmacy Review by Leon Shargel, Alan H.Mutnaick, Paul
F.Souney, Larry N.Swanson:775 789.
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MEDICATION HISTORY INTERVIEW
DEFINITION
It is defined as the process of interviewing the patient about their medications, current or
past, for the purpose of developing and planning ongoing pharmaceutical care.
The most fundamental responsibility of a clinical pharmacist is to ensure each patient
receives effective, safe and cost effective drug therapy. Drug therapy review refers to the
process by which a pharmacist reviews a patients medication regimen to ensure that the drug
therapy meets these objectives. This is a complex process which involves the assessment and
interpretation of clinical information from a diverse range of sources. The review process
draws upon the clinical pharmacists skill in pharmacotherapeutics, clinical
pharmacokinetics, adverse drug reactions, drug interactions, interpretation of laboratory data
and communication skills. For drug therapy review to be effective, these skills must be
combined with sound clinical reasoning and judgment.
Drug therapy review can take place in both hospital and community settings. In hospitals,
drug therapy review can be undertaken at any time during the patients admission, but is most
commonly performed when the patient is admitted to the hospital, during pre-ward round
preparation and during ward rounds. In acute care setting, daily review is desirable to keep up
with changes in the patients condition and drug therapy. Ideally the pharmacist should
follow the patients progress from the day of admission until the day of discharge.
As a first step in drug therapy review, pharmacists need to collect information which will
assist them to determine the appropriateness of drug therapy. This includes the patients age,
sex, body weight, social history, current and recent medication, allergy and sensitivity status,
presenting complaints, past medical history and results of relevant laboratory tests and other
investigations. This enables the pharmacist to understand the patients disease condition, the
reason why certain drugs are being administered and the patients daily clinical progress. This
understanding is the foundation for drug therapy review. Relevant information can be
obtained from a variety of sources including case notes, medication chart, nursing notes,
observational charts, and laboratory results and through discussions with medical and nursing
staff and patient interview.
When patients are admitted to a hospital, medical staff document relevant information
regarding the admission in the patients case notes. This usually includes a list of medications
which the patient is currently taking. This list may be inaccurate or incomplete, particularly in
situations where medical staffs are overburdened with patients. By speaking personally to
patients about their medications, pharmacists are able to obtain further information which
may be of importance to the ongoing medical management of the patients. Interviewing a
patient about their medications also enables the pharmacist to establish a rapport with the
patient, explain their role in patients overall care and commence preliminary counseling on
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medication use. The information obtained from the review can be used as a basis for planning
ongoing pharmaceutical care.
Ideally, a medication history should be taken for all patients. If this is not possible, priority
should be given to those patients where maximum benefit is likely to occur. For example,
patients with poly pharmacy and those with multiple and chronic diseases may benefit more
than patients treated with a single drug or for a self-limiting illness. In some situations
medication history interview may not be possible due to the patients illness, some patients
with psychiatric disorders or with dementia. In these situations it is helpful to speak to the
patients family member or care giver.
ASPECTS OF MEDICATION USE WHICH MAY BE OBTAINED FROM
MEDICATION HISTORY INTERVIEW
History of previous allergies/ADRs.
Purpose of drug use.
Dosing regimen
Perceived side effects
Potential Drug-Drug/food interactions
Treatment with other medicine systems
Adherence to drug regimen
Social drug use
General attitude towards drug use and illness
The nature of patients medication history interview will depend upon the individual
patient. Pharmacists should tailor their questions and discussion according the information
that is needed and the patients ability to provide the information. Whenever possible,
discussions regarding medications should be taken up with both the pharmacist and patient
handling the medication in question. This helps the patient to avoid the possibility of
confusion about which medication is under discussion.
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STEPS INVOLVED IN MEDICATION HISTORY INTERVIEW
1. Patient selection- Get the identity of the patient likely to be benefited
from interview.
2. Self-preparation-Understand patients condition and therapy before
starting interview.
3. Introduction- Introduce you and explain the purpose of interview.
4. Conduct interview- Obtain all relevant information by open- and close-
ended questions.
5. Conclusion-Summarize important points and clarify if necessary.
6. Documentation-Document all data for future reference.
When interviewing patients for their medication history, pharmacists should follow the
procedure outlined above. Long exhaustive interviews may be counterproductive, as some
patients may become tired or distressed. Pharmacists should communicate with patients in
language that the patient can understand. It is important to pay close attention to what the
patient is saying and tailor responses to his or her comments. Using open ended questions
rather than asking closed ended questions encourage patient to give more details about their
disease conditions and medications. Asking questions and receiving information in a non-
judgmental way is also useful.
At the end of the interview the completeness of information which has been completed
should be assessed and any areas of uncertainty should be clarified. Patients should be asked
if they have any questions related to their medications, which may encourage patients to
provide more information that may not have been recalled during the interview. Following
the interview, the list of medications should be compared with the medication chart for any
discrepancies, and to help identify any drug related problems.
Details of medication history are also required for some other purposes:
1. If a patient is on treatment with some other drugs, before declaring that the drug is not
effective, one should be sure that the drug has been taken in adequate doses and for
adequate duration.
2. If the drug has been taken adequately (dose and duration) and the patient has not
shown satisfactory response, there is no meaning of continuing the same drug. He
might require a change of drug or addition of some other drugs. So continuation of
certain drugs without knowing how long he is taking that may lead to toxic effects
particularly, the drugs which have low therapeutic window like digoxin and
anticoagulants.
3. There are some drugs which are to be continued for a long time like drugs for
bronchial asthma, anti-epileptic drugs etc. Abrupt withdrawal of these drugs may lead
52 CLINICAL PHARMACY
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to exacerbation of underlying diseases. Hence unless contraindicated, such type of
drugs have to be discontinued irrespective of the type of present illness.
4. While taking the treatment history do not rely on the name of the drugs told by the
patient, because often they do not tell them correctly. So always analyzing the
prescription is better.
5. In case of infants, it may be required to know the medications, the mother received
during pregnancy and lactation.
REFERENCE
1. The Text Book Of Clinical Pharmacy Practice by G.Parthasarathi, Karin Nyfort
Hansen,Milap C Nahata:220 222.
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EXERCISE NO: 1 DATE: 05/02/13
PATIENT MEDICATION HISTORY INTERVIEW
1. PATIENT DETAILS
Name: Mrs. X Age: 5Month Sex: M
Date Of Birth: 12.10.2012 Date Of Admission:
02.02.13
Ip No:
79267
Height: 37 cm Weight: 5.6 Kg Social Status:
Vegetarian
Pregnancy: NA Allergies: None Address & Contact No:
2. PATIENT MEDICATION HISTORY
Sl no Name of drug Strength Direction
for use
Start date Stop date Remarks
1.
Inj.Isyf-P
(Electrolyte
dextrose)
1pin
STAT
February
2013
February
2013
2.
Inj.Amikacin
(Amikacin
sulphate)
50mg BD February
2013
NIL
3.
Syp.Mintonia
(Zinc acetate),
2.5mg BD February
2013
NIL
4. Flora BC
(Lactic acid
bacillus,Niacina
mide, Vit B6)
2.5ml, TID February
2013
54 CLINICAL PHARMACY
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3. USE OF OTC DRUGS
Check the conditions for which you have used a non-prescription medicine :( put a +
symbol where appropriate.)
Disease condition Yes No
Headache
Ear problems
Cold flue
Allergies
Sinus
Cough
Sleeplessness
Drowsiness
Weight loss
Diarrhea
Hemorrhoids
Joint pain
Rashes
Heart burn
Vitamins
Herbal products
Organic products
Others (specify)
55 CLINICAL PHARMACY
AL SHIFA COLLEGE OF PHARMACY
4. HISTORY OF MEDICAL PROBLEMS
Have you noticed or do you have any of these following :( put a + symbol in the
appropriate box)
Disease condition Yes No
Known kidney problems
Frequent urinary infections
Difficulty in urination
Frequent urination at night
Known liver problems or
hepatitis
Trouble in eating certain
foods
Nausea or vomiting
Constipation or diarrhea
+
Bloody or black bowel
movements
Abdominal pain or cramps
Frequent heart burn or
indigestion
Stomach ulcers on the past
Shortness of breath
Coughing up or tightness
Chest pain or tightness
56 CLINICAL PHARMACY
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Fainting spells or passing
out
Sores on legs or feet
Known blood clot problems +
Leg pain or swelling
Unusual bleeding or
bruising
+
Anemia
Known hormone problems
Arthritis or joint pain
Muscle cramps or weakness +
Memory problems
57 CLINICAL PHARMACY
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5. PATIENT MEDICAL HISTORY
Have you or any of your blood relative had any of these following diseases:
Disease
Self Relative
High blood pressure
Asthma
Cancer
Depression
Lung diseases
Diabetic
Heart disease
Stroke
Kidney disease
Mental illness
Drug abuse
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6. SOCIAL HISTORY
Please indicate your tobacco, alcohol, caffeine and dietary habits.
a. Nicotine
Never smoked Y
Packs per day(if smoked)
Years of use
b. Alcohol consumption
Never consumed Y
Occasionally N
Drinks/ day or week Never consumed
c. Dietary restrictions if any:
Number of meals/day - 3
Food restrictions if any (salt, sugar, fluid etc.) - Normal diet
d. Other information/comments:
Doctor advised to breast feeding in a hygienic place
Avoid contamination of food.
Clean every area of baby playing.
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EXERCISE NO: 2 DATE: 01.03.13
PATIENT MEDICATION HISTORY INTERVIEW
1. PATIENT DETAILS
Name: Mr. X Age: 5Month Sex: M
Date Of Birth: 18.10.12 Date Of Admission:
26.02.13
Ip No:
31070
Height: 33 cm Weight:5 Kg Social Status:
Non-Smoker And Non-
Alcoholic
Pregnancy: NA Allergies: None Address & Contact No :
2. PATIENT MEDICATION HISTORY
Sl no
Name of drug Strength Direction
for use
Start
date
Stop
date
Remarks
1.
Inj. Isyf-P
(Electrolyte
dextrose)
1 pint
STAT
February
2013
February
2013
2.
Inj. Amikacin
(Amikacin
37.5mg
BD
February
2013
February
2013
3.
sulphate) Inj.
Taxim
250mg
BD
February
2013
February
2013
4.
(Cefotaxim)
Otrivin Mini
(Xylometazoline
Hydrochloride
2 Drops
TID
February
2013
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3. USE OF OTC DRUGS
Check the conditions for which you have used a non-prescription medicine :( put a +
symbol where appropriate)
5.
0.05%w/v) Syp.
AmbrodilS
(Ambroxol HCl
15mg+Salbutamol)
1mg / 5ml).
1.2ml
TDS
February
2013
6.
Nebulization
Asthalin in NS
(Salbutamol).
0.3ml
Q8H
February
2013
February
2013
7. Syp. Calpol
(Paracetamol)
120mg5ml STAT February
2013
Disease condition Yes No
Headache
Ear problems
Cold flue
Allergies
Sinus
Cough
Sleeplessness
Drowsiness
Weight loss
Diarrhea
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4. HISTORY OF MEDICAL PROBLEMS
Have you noticed or do you have any of these following :( put a + symbol in the
appropriate box
Hemorrhoids
Joint pain
Rashes
Heart burn
Vitamins
Herbal products
Organic products
Others (specify)
Disease condition Yes No
Known kidney problems
Frequent urinary infections
Difficulty in urination
Frequent urination at night
Known liver problems or
hepatitis
Trouble in eating certain foods
Nausea or vomiting
Constipation or diarrhea
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Bloody or black bowel
movements
Abdominal pain or cramps
Frequent heart burn or
indigestion
Stomach ulcers on the past
Shortness of breath
+
Coughing up or tightness +
Chest pain or tightness
Fainting spells or passing out
Sores on legs or feet
Known blood clot problems
Leg pain or swelling
Unusual bleeding or bruising
Anemia
Known hormone problems
Arthritis or joint pain
Muscle cramps or weakness
Memory problems
63 CLINICAL PHARMACY
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5. PATIENT MEDICAL HISTORY
Have you or any of your blood relative had any of these following diseases:
Disease
Self Relative
High blood pressure
Asthma
Cancer
Depression
Lung diseases
Diabetic
Heart disease
Stroke
Kidney disease
Neurodegenerative illness
Drug abuse
Others : Seizure birth
+
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6. SOCIAL HISTORY
Please indicate your tobacco, alcohol, caffeine and dietary habits.
a. Nicotine:
Never smoked Y
Packs per day(if smoked)
Years of use
b. Alcohol consumption:
Never consumed Y
Occasionally N
Drinks/ day or week Never consumed
c. Dietary restrictions if any:
Number of meals/day - 3
Food restrictions if any(salt, sugar, fluid etc) - Normal Diet
d. Other information/comments:
Doctor advised to avoid walk out side
Clean the area were baby playing
Only give soft foods
65 CLINICAL PHARMACY
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EXERCISE NO: 3 DATE: 25.05.13
PATIENT MEDICATION HISTORY INTERVIEW
1. PATIENT DETAILS
Name: Mr. X Age: 71yrs Sex: F
Date Of Birth: 18.10.1941 Date Of Admission:
26.02.13
Ip No:
2011/ 042296
Height: 172 Weight: 52 Kg Social Status:
Non-Smoker And Non-
Alcoholic
Pregnancy: NA Allergies: None Address & Contact No :
2. PATIENT MEDICATION HISTORY
Sl no
Name of drug Strength Direction
for use
Start
date
Stop
date
Remarks
1
Inj. Human
Actrapid as per
GRBS (Insulin),
As per
GRBS
TID
June
2013
2.
Inj.Graniset
(Granisetron)
25 mg
TID
June
2013
3. Inj.
Razo(Rabeprazole)
20mg
BD June
2013
4.
Inj. Cebanex
(Cefoperozone
500mg+sulbactum
500mg),
2g
IV BD
June
2013
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3 USE OF OTC DRUGS
Check the conditions for which you have used a non-prescription medicine :( put a +
symbol where appropriate)
5.
T. Amcard AT
(Amlodipine
5mg+atenolol 50
mg)
-
OD
June
2013
6.
Cap. Tamflo
(Tamsulosin),
0.4mg, 1-0-0
0.4mg
1-0-0
June
2013
7. T. Qure
(Levofloxacin)
500mg
BD
June
2013
8. Syp. Potklor
(Potassium
chloride)
-
QID
June
2013
9.
Inj. Razo
(Rabiprazole),
20mg, STAT
20mg
BD
June
2013
10
Inj. Graniset
(Granisetron),
25mg 1 amp,
STAT
June
2013
Disease condition Yes No
Headache
Ear problems
Cold flue
Allergies
Sinus
67 CLINICAL PHARMACY
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Cough
Sleeplessness
Drowsiness
Weight loss
Diarrhea
Hemorrhoids
Joint pain
Rashes
Heart burn
Vitamins
Herbal products
Organic products
Others (specify)
68 CLINICAL PHARMACY
AL SHIFA COLLEGE OF PHARMACY
4 HISTORY OF MEDICAL PROBLEMS
Have you noticed or do you have any of these following :( put a + symbol in the
appropriate box
Disease condition Yes No
Known kidney problems
Frequent urinary infections
Difficulty in urination
Frequent urination at night
Known liver problems or
hepatitis
Trouble in eating certain foods
Nausea or vomiting
Constipation or diarrhea
Bloody or black bowel
movements
Abdominal pain or cramps
Frequent heart burn or
indigestion
Stomach ulcers on the past
Shortness of breath
Coughing up or tightness
Chest pain or tightness
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Fainting spells or passing out
Sores on legs or feet
Known blood clot problems
Leg pain or swelling
Unusual bleeding or bruising
Anemia
Known hormone problems
Arthritis or joint pain
Muscle cramps or weakness
Memory problems
70 CLINICAL PHARMACY
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5. PATIENT MEDICAL HISTORY
Have you or any of your blood relative had any of these following diseases:
Disease
Self Relative
High blood pressure
Asthma
Cancer
Depression
Lung diseases
Diabetic
Heart disease
Stroke
Kidney disease
Neurodegenerative illness
Drug abuse
Others : Seizure birth
71 CLINICAL PHARMACY
AL SHIFA COLLEGE OF PHARMACY
6. SOCIAL HISTORY
Please indicate your tobacco, alcohol, caffeine and dietary habits.
1. Nicotine:
Never smoked Y
Packs per day(if smoked)
Years of use
2. Alcohol consumption:
Never consumed Y
Occasionally N
Drinks/ day or week Never consumed
3. Dietary restrictions if any:
Number of meals/day - 3
Food restrictions if any(salt, sugar, fluid etc) - Normal Diet
4. Other information/comments:
Doctor advised to take plenty of water
Avoid caffeine, citrus fruit juices
Warm pad apply to abdomen to reduce bladder pressure
Wipe front to back after urination.
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EXERCISE NO: 4 DATE: 25.05.13
PATIENT MEDICATION HISTORY INTERVIEW
1 PATIENT DETAILS
Name: Mr. X Age: 28yrs Sex: M
Date Of Birth: 16.02.1985 Date Of Admission:
16.07.13
Ip No:
112572
Height: 159 Weight: 67 Kg Social Status:
Smoker And Non-
Alcoholic
Pregnancy: NA Allergies: None Address & Contact No :
2. PATIENT MEDICATION HISTORY
Sl no
Name of drug Strength Direction
for use
Start
date
Stop
date
Remarks
1
Inj. H.Actrapid
(Insulin)
As per
GRBS
SC
July
2013
2.
IVF NS
1 pint
IV
July
2013
3.
T.Complete TD
(Multi vitamin
tablet)
-
BD July
2013
73 CLINICAL PHARMACY
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3. USE OF OTC DRUGS
Check the conditions for which you have used a non-prescription medicine :( put a +
symbol where appropriate)
Disease condition Yes No
Headache
Ear problems
Cold flue
Allergies
Sinus
Cough
Sleeplessness
Drowsiness
Weight loss
Diarrhea
Hemorrhoids
Joint pain
Rashes
Heart burn
Vitamins
Herbal products
Organic products
Others (specify)
74 CLINICAL PHARMACY
AL SHIFA COLLEGE OF PHARMACY
4. HISTORY OF MEDICAL PROBLEMS
Have you noticed or do you have any of these following :( put a + symbol in the
appropriate box
Disease condition Yes No
Known kidney problems
Frequent urinary infections
Difficulty in urination
Frequent urination at night
Known liver problems or
hepatitis
Trouble in eating certain foods
Nausea or vomiting
Constipation or diarrhea
Bloody or black bowel
movements
Abdominal pain or cramps
Frequent heart burn or
indigestion
Stomach ulcers on the past
Shortness of breath
Coughing up or tightness
Chest pain or tightness
75 CLINICAL PHARMACY
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Fainting spells or passing out
Sores on legs or feet
Known blood clot problems
Leg pain or swelling
Unusual bleeding or bruising
Anemia
Known hormone problems
Arthritis or joint pain
Muscle cramps or weakness
Memory problems
76 CLINICAL PHARMACY
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5. PATIENT MEDICAL HISTORY
Have you or any of your blood relative had any of these following diseases:
Disease
Self Relative
High blood pressure
Asthma
Cancer
Depression
Lung diseases
Diabetic
Heart disease
Stroke
Kidney disease
Neurodegenerative illness
Drug abuse
Others : Seizure birth
77 CLINICAL PHARMACY
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6. SOCIAL HISTORY
Please indicate your tobacco, alcohol, caffeine and dietary habits.
1. Nicotine:
Never smoked N
Packs per day(if smoked) Occasionally
Years of use
2. Alcohol consumption:
Never consumed Y
Occasionally N
Drinks/ day or week Never consumed
3. Dietary restrictions if any:
Number of meals/day - 3
Food restrictions if any(salt, sugar, fluid etc) - Normal Diet
4. Other information/comments:
Doctor advised to reduce the sugar intake
Reduce heavy and fat containing food
Exercise or regular walking.
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ADVERSE DRUG REACTIONS
DEFINITION
The World Health Organization defines an adverse drug reaction as any
response to a drug which occurs at doses normally used in man for prophylaxis,
diagnosis and therapy of disease or for the modification of physiological function.
Adverse reactions are recognized
hazards of drug therapy. Adverse drug reactions (ADRS) are important causes of
mortality and morbidity in both hospitalized and ambulatory patients. ADR study and
its preventions is todays demand because ADR is the fourth leading cause of death
ahead of pulmonary disease, diabetes, AIDS, pneumonia, accidents, and automobile
deaths. In many countries ADRs rank among the top 10 leading causes of mortality.
So there is a need to study ADRs seriously to create awareness about ADRs among
patients to motivate health care professionals in the hospital to report ADRs to
minimize the risk. It is important in detection of lack of efficacy, detection and
prevention of counterfeit and sub stranded products in clinical practice. Early
detection, evaluation and monitoring of ADR are essential to reduce harm to patients
and thus improve public health
FEATURES OF ADR
The important features of adverse drug reactions are:-
1. There is some evidence that a drug is responsible for the reaction
2. It is unintended and occurred at normal doses used clinically
3. The effects of the reaction is either harmful to the patient
4. ADRs are preventable and many healthcare professionals are in a position to
identify them at an early stage.
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CLASSIFICATION OF ADR
1. Traditional Classification
As proposed by Rawlins and Thompson (1977)
a. Type A (Augmented): These include the common, pharmacologically
predictable, dose related reactions, which improve when the medicine is
withdrawn. Eg: Insulin induced hypoglycemia
b. Type B (Bugs): These are pharmacologically predictable and they also
improve when the medicine is withdrawn but they involve interaction with a
microorganism. Eg: Sugar containing medicine promoting dental caries
2. Newer Classification
As proposed by Simon Wills and David Brown (1999)
a. Type A (Augmented)
b. Type B (Bugs)
c. Type C (Chemical)
d. Type D (Delivery)
e. Type E (Exit)
f. Type F (Familial)
g. Type G (Genetotoxicity)
h. Type H (Hypersensitivity)
i. Type U (Unclassified)
DETECTION AND MONITORING OF ADRS
Detection of an ADR is crucial in the management of any patient. Always
suspect a drug as cause of symptoms in a patient .all drugs have potential to
cause ADRs although most produce no ill effects in most of the patients. ADRs
contribute to overall healthcare costs by increasing morbidity and mortality.
80 CLINICAL PHARMACY
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Adverse event detection systems have included manual methods and
combination of both electronic and manual review process.
METHODS OF MONITORING ADVERSE DRUG REACTIONS
Although all new drugs undergo clinical trials to demonstrate efficacy and
detect adverse effects, only the most common ADRs, will probably have been
detected by the time the drug is marketed. In addition, clinical trials are unlikely to
have been carried out on some groups of patients, such as the elderly or pregnant
women. Pharmaceutical products must therefore be monitored after marketing to
identify any more unusual, serious or delayed adverse effects. Adverse event
detection systems have included manual methods and combination of both electronic
and manual review process.
1. Manual Methods
Manual adverse event detection systems offer the ability to detect a wide array
of adverse events, and with some methods, a substantial proportion of events. The
systems described below are limited by either physician reluctance to use them or the
resource requirements to maintain the system
a. Provider voluntary reporting methods
Incident reporting
Prompted spontaneous reporting
b. Provider involuntary reporting methods
Chart Review
Observers
Patient interviews
2. Combined Modalities
3. The UK Yellow Card System
4. Anecdotal reports (Case reports)
5. Cohort studies (Prospective studies)
6. Case control studies (Retrospective studies)
7. Record linkage studies
8. Hospital-based population studies
9. International ADR reporting
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10. Patient-cantered studies.
BASIC PRINCIPLES OF EFFICIENT REPORTING
1. Report the adverse reaction immediately after it occurs.
2. If possible, take the decision to report whilst the patient is still with you, so
that the details can be filled in at once on the reporting form.
3. Think about any other factors which may contribute in causing the event such
as other prescribed drugs, self-medication, herbal products, food, chemicals,
ask the patient particularly about other medicines taken.
4. If you get any supplementary data later, e.g. if the same patient develops the
effect again or if something happens which increases your suspicion or seem
to exclude the reaction, please send in a supplementary note immediately
using ADRs reporting form with the patient identifiers.
5. All reports must have the following four data elements
a. An identifiable patient
b. A suspected adverse effect
c. A named suspected drugs
d. An identifiable reporter
6. Always write legibly.
MANAGEMENT OF THE ADVERSE REACTION
1. Confirmation of the ADRs indicates what assisted in confirming the
suspected adverse reactions.
For example:
a. Drug reactions confirmed by disappearance of the reaction after stopping
administration of the drug or reducing the doses.
b. Recovery on withdrawal of suspected drug(s) if no other drug is
withdrawn and no therapy given.
c. Recovery follows treatment of the reaction in addition to withdrawal of
drug.
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2. Mention the criteria for regarding the reaction as serious.
3. Mention any treatment given to the patient after experiencing the ADRs.
4. Outcome: indicate the outcome of the adverse reaction by marking X in the
appropriate box with dates in case of fatal outcome.
PREVENTIVE MEASURES FOR ADVERSE DRUG REACTION
Comprehensive and ongoing ADR monitoring, evaluating and reporting
programs need to be initiated that should focus on the assessment of incidence,
prevalence, category, severity, preventability, costs and burdens of adverse drug
reactions. This will help ensure that patients receive safe medicines and mortality
or morbidity due to ADRs is considerably reduced. The most ideal way to
manage ADRs is to prevent its occurrence in predictable cases. However, if it has
occurred, therapeutic measures become necessary. Preventive measures are:
1. Never use any drug unless there is good indication. If the woman is
pregnant do not use a drug unless the need is imperative.
2. Choose an alternative therapy of relative efficacy and safety. Eg: if patient
is allergic to penicillin, choose other alternative like amoxicillin.
3. Using a prophylaxis to other drugs to prevent future ADRs. Eg: penicillin
should be injected subcutaneously for skin test to prevent the occurrence of
anaphylaxis.
4. Allergy and idiosyncrasy are important causes of adverse drug reactions.
Ask if the person had previous reactions. There may also be family history
of adverse reactions to drugs that share a common characteristic indicative
of inherited disorder. (Eg: Glucose-6- phosphate dehydrogenase
deficiency).
5. Ask if the person is already taking other drugs including self-medication
drugs interactions may occur.
6. Age and hepatic or renal impairment may alter the metabolism or excretion
of drugs so that much smaller doses may be needed. Genetic factors may
also be responsible for variations in metabolism.
7. Prescribe a few drugs as possible and give clear instructions to elderly
patients or any patient likely to misunderstand complicated instructions.
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8. Whenever possible use a familiar drug. With a new drug are particularly
alert for or unexpected events.
9. If serious adverse events are liable to occur, warn the patient.
10. Implementation of program designed to educate patient about their
medication and potential for ADRs.
11. Documentation of ADRs is necessary to avoid re exposure
REFERENCES
1. Remingtons The science and Practice of Pharmacy, 21
st
edition, volume 2
by Lippincott Williams and Wilkins; 2007:1961
2. A Text Book of Pharmacy Practice by K.G.Revikumar: 233 257.