Clinical Pharmacy Final

1 CLINICAL PHARMACY
AL SHIFA COLLEGE OF PHARMACY

DRUG INFORMATION QUERY

INTRODUCTION
The provision of drug information is the most fundamental responsibility of clinical
pharmacist. The information may be specific to an individual patient as an integral part of
pharmaceutical care, or relative to a group of patients, such as in the context of a disease
management programme. The term medicine is used to highlight the services related to
medicinal drugs rather than drug of abuse.
The term drug information was developed in early 1960s. The first drug information
centre was established at the University of Kentucky in 1962. However in India drug
information services and centres are still in their infancy and we have only a few services that
qualify as drug information centre.
Pharmacists have unique range of knowledge and skills which are required for drug
information practice. These include knowledge of pharmaceutics, pharmacology,
pharmacokinetics and pharmacotherapy. All of these are required to optimise the use of drugs
in treatment and prevention of disease.
DEFINITION
Drug information refers to the provision of unbiased, well referenced, and critically
evaluated up to date information on any aspect of drug use.
The drug information service (DIS) refers to activities that are part of the overall pharmacy
service or pharmaceutical care process.
Drug information centre (DIC) refers to the specialized facility that provides drug
information to those who need it.
A drug information specialist refers to a new breed of pharmacist who is expert in drug
information monitoring.
OBJECTIVES
To uplift the profession of pharmacy.
To improve patient compliance and therapeutic outcome.
To advise and educate patients for the proper use of drugs.
To advise and educate patients regarding drug addiction, alcoholism, smoking
hazards and other socio-medical problems.
Advise on self-medication for minor complaints.
2 CLINICAL PHARMACY

Advise on public health issues.
Other activities like publishing newsletters or bulletins, conducting seminars, group
discussions, campaigns etc.

PROVIDERS OF DRUG INFORMATION
Knowledgeable about data storage and retrieval methods
Able to objectively evaluate scientific literature
Able to apply information to the specific patient situation
An effective communicator with patients, health care professionals, administrators
and the media.

MODIFIED METHOD TO ANSWER A DRUG INFORMATION ENQUIRY
There are many types of drug information requests. The most common relate to
therapeutics, adverse drug reactions, dosage and administration, drug interaction and use of
drugs in pregnancy and lactation. Other question may concern aspects of drug
pharmacokinetics, pharmaceutical stability, compatibility, poisoning, toxicity and drug
availability.
There are seven steps to answering an enquiry
STEP 1: Secure demographics of requester
The requesters name, position, training and anticipated knowledge are important to
determine the approach and final response to the question.
For example, an elderly patient and a cardiovascular specialist may each enquire about
the availability of an investigational medication; however each brings a different frame of
reference to the request.
STEP 2: Obtain background information
The ability to obtain background information is essential for systematic approach. This
has been the most difficult step. Sufficient background information must be obtained in a
limited time period. The background questions should be specific for the nature of the
request. Background information includes the patients age, weight and sex. In addition, the
patients diagnosis, other medication such as co-morbidities and hepatic and renal function
are often important to assess. It is also advisable to find out if the requester has checked any
resources previously so as to avoid duplication of work. Finally the urgency of the request
should be ascertained.

3 CLINICAL PHARMACY

STEP 3: Determine and categories the ultimate question.
The ultimate question may differ significantly from the original question if the requester
posed a general question, and the pharmacist has used his expertise to obtain background
information. Adequate background information is needed to determine the ultimate question.
For example: if a doctor is concerned about the safety of prescribing Metronidazole to a
patient taking Simvastatin, the question can be categorized as a drug interaction query.
STEP 4: Develop search and conduct search
The information resources are selected based on the probability of containing the desired
data. For example given in step 3, standard references on drug interactions are first-line
resources as both simvastatin and metronidazole have been in clinical use for many years. If
one of the drugs was a recently introduced drug, a Medline search would be more
appropriate. The resources may be used based on ease of access or the pharmacists
familiarity with particular resources. The resources used in answering the question should be
documented and this will help in understanding the usefulness of various resources at times
of budget allocation.
STEP 5: Perform evaluation, analysis and synthesis
The information retrieved must be critically reviewed. Application of the techniques and
skill for literature evaluation and knowledge of statistical analysis may be used. For the
response to be relevant and useful to the requester, the information must be analysed and
synthesized with consideration of the background information obtained previously. Analysis
involves the critical assessment of the nature and merit of factors which may be relevant to
the question. Synthesis involves the careful integration of critical information about the
patient, disease and medication along with pertinent background information to arrive at a
judgment or conclusion. Analysis and synthesis together assist in forming opinions, arriving
at judgment, and ultimately drawing conclusions.
STEP 6: Formulate and provide response
This involves a series of steps that must be performed completely, objectively and in a
logical sequence. Patient factors, disease factors, medication history and other relevant
background information and special circumferences should be considered. Once this data is
collected and carefully assembled it must be critically analysed and evaluated before
providing the final response. The way in which answers are communicated plays a major role
in determining how drug information is accepted by physician. The response to a question
must include restarting the request and clearly identifying the problems, issues and
circumstances that are relevant to the question. Specify recommendation must be
scientifically sound and clearly justified. In the hospital setting the majority of questions will
be answered verbally and responses should be brief, concise and accurate and provided in a
timely manner.

4 CLINICAL PHARMACY

STEP 7: Conduct follow-up and documentation
Follow- up is the process of verifying the appropriateness, correctness, and completeness
of a response after it has been given. When recommendations are made, follow-up should
always be done in a timely manner. This allows pharmacist to know if the recommendations
were accepted and implemented. Patient- specific requests generally provide opportunities for
follow-up. In a hospital setting this may involve visiting the ward and offering additional
advice and information. This type of follow-up provides opportunities for pharmacists to
become involved in direct patient care, independently of ward round participation or routine
patient counselling. Documentation of the DI query is essential for purposes of quality
assurance, budget allocation, and promotions of the DI service and to minimize liability. The
documentation may be as a simple form or an extensive review and summary of all processes
completed.

DRUG INFORMATION RESOURCES
Drug information is stored in a variety of media including textbooks, journals,
newsletters, microfiche, optical disks and computer systems. The information regarding the
drugs can be broadly classified into three categories
1. Primary resources
Primary literature consists of research studies or clinical experience which has not been
previously published. This includes clinical trials, short reports, case reports and letters to the
editor which describe clinical events such as adverse drug reactions or unexpected clinical
outcomes. Examples of journals which publish primary literature include:
Annals of Internal Medicine,
Lancet,
The New England Journal of Medicine,
Journal of American medical Association.
Advantage
Provide the most current information
Share opinion with other health professionals
Keeps abreast of professional news
Keeps up with the new developments in pathophysiology, diagnostic agents
and therapeutic regimen
Disadvantage
No guarantee of accuracy
Inadequacy of articles are common

5 CLINICAL PHARMACY


2. Secondary resources
Secondary resources provide an overview of previously published work, and include
indexing and abstracting services of the primary literature. Examples of secondary resources
include the abstracting services like;
DRUGDEX
International Pharmaceutical Abstracts
The indexing services BIOSIS previews
ClinAlert
Embase
Iowa Drug Information System (IDIS) and Medicine. An indexing system
provides only bibliographic information that is indexed by topic and provides
the original abstract or full text with no interpretation. On the other hand, an
abstracting service provides content by interpreting the original reports and
creating summaries based on the abstracting services editorial guidelines.
PubMed from the National Library of Medicine. It is an examples of
Online resources
Advantage
Valuable tools for quick and selective screening of the primary literature for
specific information, data, citation and articles
Provide sufficient information to serve as references for answering drug
information requests

Disadvantage
Reviews a finite number of journals
Usually describe only articles and clinical studies
Abstracts are generally interpretations

3. Tertiary resources
These consist of general literature including textbooks and full-text computer database.
Examples of tertiary resources include
United States Pharmacopoeia Drugs,
Remingtons Pharmaceutical Sciences
Merck Index,
Red Book,
Martindale:
Tertiary resources are the most commonly used sources of information because they are
easy to use, convenient, concise, and compact.
6 CLINICAL PHARMACY


Advantage
Provide easy and convenient access to a broad spectrum of related topics
Background information on drugs and diseases available

Disadvantage
Gap between recent developments and actual publication of books
Omission of pertinent data
Misinterpretation of literature possible

4. Internet

The Internet expands the ability to search therapies that have been recently published or
discussed in the media. An Internet search maybe required for the following: company
specific information, issues currently in the news, alternative medicine, or U.S. government
information. The most popular Web browsers are Mozilla Firefox and Microsoft Internet
Explorer. A variety of search engines, software tools for searching the Internet, have been
developed. General search engines (AltaVista, Google, Yahoo, Ask, Dogpile) attempt to
index as much of the Internet as possible.

Disadvantage
Information obtained may not be peer reviewed or edited before release.
Information may be only as reliable as the person who posted it and the users
who read and comment on its content.
A web site should be evaluated by its source (author) of information. The
name, location, and sponsorship should be disclosed.
Drug Information Centre can provide information regarding drugs, their toxicity and
treatment round the clock. In the absence of any available treatment, the centers give only
first aid advice and recommend symptomatic treatment. Answering enquiry, or dealing with
request or information forms an integral part of the daily routine for all pharmacists. For this
purpose Drug information request forms are available in the DIC, which is filled up by the
pharmacist who is in charge.

REFERENCE
1. The Text Book Of Clinical Pharmacy Practice by G.Parthasarathi, Karin Nyfort
Hansen, Milap C Nahata, 267 281.
2. Comprehensive Pharmacy by Leon Shargel, Seventh Edition, 694-710
7 CLINICAL PHARMACY

EXERCISE NO: 1 DATE: 03/03/13

QUERY
Available dosage forms of rabeprazole and its adverse drug reactions?
ANSWER
1. Rabeprazole available dosage forms are tablet, injections and vials
2. The adverse drug reactions include
REFERENCE
1. Gastroesophageal Reflux Disease, Barbara G.; DiPiro, Joseph T.;
Schwinghammer, Terry L.; Hamilton, Cindy W. Pharmacotherapy Handbook,
6th Edition, McGraw-Hill Publishers, 203-207.
2. Micromedex, www.medscape.com.

8 CLINICAL PHARMACY


QUERY
Indication, content and available dose of Belar Forte tablet?

ANSWER
1. Indications are allergic and inflammatory disorders and congenital adrenal
hyperplasia.
2. Content is Betamethasone
3. Available doses are 0.5mg, 1mg.

REFERENCE
1. Psoriasis, Barbara G.; DiPiro, Joseph T.; Schwinghammer, Terry L.; Hamilton,
Cindy W. Pharmacotherapy A physiological Approach, 7th Edition, McGraw-
Hill Publishers, 1604
2. http://mims.com
3. http://Micromedex.com,

9 CLINICAL PHARMACY


QUERY
What are the adverse effects of the insulin injections?
ANSWER
Possible adverse effects of the insulin injections include hypoglycemia, insulin
resistance, lipoatrophy, hypokalaemia, blurred vision.

REFERENCE
1. Diabetes Mellitus, Barbara G.; DiPiro, Joseph T.; Schwinghammer, Terry L.;
Hamilton, Cindy W. Pharmacotherapy A physiological Approach, 7th Edition,
McGraw-Hill Publishers, 1216
2. http://mims.com
3. http://Micromedex.com

10 CLINICAL PHARMACY

EXERCISE NO: 4 DATE: 18/ 07/ 13

QUERY
How use the Rotahaler ?
ANSWER
1. Hold rotahaler vertically and put capsule into square hole. Make sure top of rotacap
is level with top of hole.
2. Hold rotahaler horizontally, twist barrel sharply forwards and backwards. This
splits capsule into two.
3. Breathe out gently. Keep rotahaler level and put mouthpiece between lips and teeth
and breathe in the powder quickly and deeply
4. Remove rotahaler from mouth and hold breath for about 10 seconds
5. If any powder is left repeat breathe in.
6. Open the Rotahaler and discard the empty capsule.

REFERNCE
1. Asthma, Barbara G.; DiPiro, Joseph T.; Schwinghammer, Terry L.; Hamilton,
Cindy W. Pharmacotherapy A physiological Approach, 7th Edition, McGraw-Hill
Publishers, 472
2. http://nartc.com


PATIENT COUNSELLING

INTRODUCTION
Safe and effective drug therapy depends on patients being well informed about their
medication. In India health care is provided at primary, secondary and tertiary levels. Lack of
information may lead to therapeutic failure, adverse effect, additional expenditure on
investigation and treatment or even hospitalization. Many drugs problem and their
consequences can be addressed by patient education.
DEFINITION
Counseling is a special form of interpersonal communication in which feelings, thoughts
and attitudes are expressed, explored and clarified.
OBJECTIVES OF PATIENT COUNSELING
To provide correct information about drugs to the patient.
It can support and help the patient to regain a sense of competence and skill at
times of crisis.
It can help to educate the patient about vaccination and immunization
procedures on mass sterilization issues, contraception, programme etc.
Patient counseling refers to the process of providing information, advice and
assistance to help patient to use their medication appropriately.
During counseling, the pharmacist should assess their patient understanding
about his or her illness and its treatment and provide advice to information
which will assist the patient to take their medication in the most safe and
effective manner.
It provides realistic action suitable for different clients and circumstances.
It helps to enhance determination, self-confidence and improve family and
community relationship and quality of life.
AIMS OF PATIENT COUNSELING
Effective patient counseling aim to produce the following results
Better patient understanding of their illness and the role of medication in its
treatment
Improved medication in its adherence
More effective drug treatment
Reduced incidence of adverse effect and unnecessary health care costs.
Improved quality of life for patient
Better strategies to deals with medication related adverse effects.
Improved professional support between patient and pharmacist.


STEPS INVOLVED IN PATIENT COUNSELING
Counseling is a two way communication process and interaction between the patient and
the pharmacist and is essential for counseling to be effective.
1. PREPARING FOR THE SESSION
The success of counseling depends upon the knowledge and skill of the counselor. The
pharmacist should know as much as possible about the patient and his/her treatment details.
In hospitals it can be possible by referring the patient case notes. In community pharmacy
setting, source of information includes the patient and their prescription and in some cases a
record of previous dispensing for the patient. If the patient is receiving a medication which is
unfamiliar to the pharmacist then a drug information reference should be consulted before
counseling commences.
In some cases if the patient is in a hurry or in pain, is non-communicative, it is very
difficult to counsel the patient effectively. In this situation, the aims of counseling may need
to be modified or with the patients agreement the session may be postponed to a later date.

2. OPENING THE SESSION
The first phase of counseling is used for information gathering. The pharmacist should
introduce himself or herself to the patient and greet them by name. It is best to use titles such
as Mr., Ms., and then switch to the first name. The pharmacist should identify the purpose of
the session very clearly.
For example:
Hello Mr. Unni my name is Vikas and I am a pharmacist. I would to tell you about your
medication. Do you have few minutes to spend with me?
3. COUNSELING CONTENT
The counseling content is considered to be the heart of the counseling session. During this
step the pharmacist explain to the patient about his or her medication and treatment regimen.
Topic commonly covered includes,
Name and strength of the medication
Expected duration of treatment
Expected benefits of treatment
Possible adverse effects
Possible medication or dietary interaction
Advice on correct storage
Information which is given should be tailored to the individual patient. It is important not
to jump to conclusion about why a particular medication has been prescribed. Sometimes the

patient family members may visit the pharmacy to collect the medication. They should be
given suitable advice after gathering information such as their relationship with the patient
and their awareness of the patient disease and medication history.
4. CLOSING THE SESSION
Before closing the session pharmacist or counselor should check the patients
understanding. This can be assessed by feedback questioning. We should finish the session
by asking the patient Do you have any question? Before final closure if time permits
summaries the main points in a logical order. Counselor should give their telephone number
to encourage the patient to make contact if they need further advice or information.

BARRIERS
The common Barriers involved in the patient counseling are,
Patient based barriers
System based barriers
Provider based barriers

1. Patient Related Barriers
It includes;
Culture
Language
Hearing
Vision
Mental status
Gender
Limited patient availability

2. System Based Barriers
It includes;
Lack of space
Lack of staff

3. Provider Based Barriers
It includes;
Lack of knowledge
Lack of time
Lack of training
Lack of confidence
Lack of interest


STRATEGIES TO OVERCOME BARRIERS
To conduct an effective patient counseling, the common requirements are
(1) Availability of pharmacist
(2) Creating an atmosphere for patient
(3) Developing an effective approach to patient counseling
(4) Approach to provide optimum information
To overcome the barrier like lack of confidence is prepared prior to counseling. For
effective counseling communication skill is very important. The communicating process was
carried out either by verbal and nonverbal communication method.

REFERENCES
1 The Pharmaceutical Practice by AJ Winfield and Richards: 44 45
2 A Text Book of Clinical Pharmacy Practice by Parthasarathi: 43 49.


EXERCISE NO: 1 DATE: 05.02.13

PATIENT COUNSELING FOR ACUTE GASTROENTERITIS

AIM
To counsel the patient about the disease
COUNSELING ABOUT THE DISEASE
AGE is the inflammatory disorder of the stomach and intestine.
Affect the body through direct invasion and by endotoxin being released by
the organism
Ingestion of fecal contaminated food and water.
Pain or tenderness of the abdomen is then felt by the patient.
Mild diarrhoea - 2-3 stool, bowel sound, fluid and electrolyte imbalance and
hypernatremia.
COUNSELLING ABOUT LIFE STYLE MODIFICATION
Uncontaminated water and food
Breast feeding at hygienic place
Avoid milk and milk products.
Bland, easy-to-digest foods, such as toast, rice, bananas and potatoes.
Give boiled and cooled foods
Avoid giving raw food items
Clean the area and objects were baby playing



PATIENT COUNSELING FOR HYPOTHYROIDISM

AIM
To counsel the patient about the disease.
Main course is thyroid gland failure
Causes include chronic autoimmune thyroiditis (Hashimoto's disease),
iatrogenic hypothyroidism, iodine deficiency, enzyme defects, thyroid
hypoplasia, and goitrogens.
Adult manifestations of hypothyroidism include dry skin, cold intolerance,
weight gain, constipation, weakness, lethargy, fatigue, muscle cramps,
myalgia, stiffness, and loss of ambition or energy. In children, thyroid
hormone deficiency may manifest as growth retardation.
Physical signs include coarse skin and hair, cold or dry skin, periorbital
puffiness, bradycardia, and slowed or hoarse speech. Objective weakness
(with proximal muscles being affected more than distal muscles) and slow
relaxation of deep tendon reflexes are common

Take iodine containing foods
Iodinated salt, sea vegetables, cows milk, strawberries.
Take high fibrous foods to resolve constipation
Reduce sodium intake.



PATIENT COUNSELING FOR ULCERATIVE COLITIS

AIM
To counsel the patient about the disease.
COUNSELING ABOUT DISEASE

Ulcerative colitis is confined to the colon and rectum, the mucosa and the sub
mucosa.
The patient with toxic mega colon usually has a high fever, tachycardia,
distended abdomen, elevated white blood cell count, and a dilated colon.
The risk of colonic carcinoma is much greater in patients with ulcerative colitis
as compared with the general population.
Ocular complications iritis, episcleritis, and conjunctivitis occur, dermatologic or
mucosal complications are erythema nodosum, pyoderma gangrenosum,
aphthous stomatitis).

COUNSELING ABOUT LIFE STYLE MODIFICATION
Eat small amounts of food throughout the day.
Make sure to chew food very well.
Drink plenty of water.
Avoid high-fiber foods (bran, beans, nuts, seeds, and popcorn).
Avoid fatty, greasy or fried foods and sauces (butter, margarine, and
heavy cream).
Avoid all things that would be bowel irritant (coffee, tea, colas, chocolates),
alcohol, all carbonated beverages, vinegar etc.
Avoid stress and highly emotional situations.
Avoid all additives, flavorings, colorings, baking powder.



PATIENT COUNSELING FOR COPD

AIM
To counsel the patient about the disease

Chronic obstructive pulmonary disease (COPD) is defined as a disease
characterized by progressive airflow limitation that is not fully reversible.
The most common conditions comprising COPD are chronic bronchitis
and emphysema.
Chronic bronchitis is associated with chronic or recurrent excess mucus
secretion into the bronchial tree with cough that occurs on most days for at
least 3 months of the year for at least 2 consecutive years when other
causes of cough have been excluded.
Emphysema is defined as abnormal, permanent enlargement of the
airspaces distal to the terminal bronchioles, accompanied by destruction of
their walls, but without obvious fibrosis.
Initial symptoms of COPD include chronic cough and sputum production;
patients may have these symptoms for several years before dyspnoea
develops.
Smoking cessation is the most effective strategy to reduce the risk of
developing COPD.

Vitamins E and C and -carotene containing foods
Avoid close contact with people who have respiratory infection.
Avoid exposure to environmental irritants.
Avoid excessive heat, cold and high altitudes.
Two 15-minute intervals of pleasurable walking or cycling.


INTERPRETATION OF LABORATORY DATA

INTRODUCTION
Laboratory test results are used to investigate potential problems with a patients
anatomy or physiology. The pharmacists usually monitor laboratory tests to:
Assess the therapeutic and adverse effects of a drug
Determine the proper drug use
Assess the need for additional or alternate drug therapy
Prevent test misinterpretation resulting from drug interference

Normal laboratory test results fall within a predetermined range of values, and abnormal
values fall outside that range. The results of most laboratory tests are reported with a
reference range-a numerical range of results for that investigation when performed for a
healthy subject (in the absence of significant disease). The values outside the normal range
may not necessarily indicate disease or the need for the treatment. Conversely, if a result falls
within the quoted reference range this does not necessarily guarantee the absence of disease
or abnormal organ function. For these reasons it is important that a clinical pharmacist should
interpret results with reference to the clinical status of the patient and other relevant
information. A clinical pharmacist must be able to interpret lab data for a number of reasons:
Laboratory data can provide guidance regarding the appropriateness of the
patients current drug therapy. The results may suggest that a particular drug is not
appropriate for the patient and should therefore to be discontinued or avoided
(e.g.: NSAID for a patient with severe renal impairment.
It can also be used as a guide to determine the adequacy of drug response.
The measurement of blood glucose parameters when assessing the effectiveness of
insulin treatment.
Monitoring for the efficacy of treatment.
Laboratory test can also be used to check for signs of serious drug toxicities that
may be reflected by abnormal biochemical or hematological parameters or
elevated liver function tests.

RATIONALE FOR ORDERING LABORATORY TEST
Laboratory test are performed with the expectation of that result will help practitioner
or patient in the following;
Discovery of occult disease
Confirming the suspected diagnosis after signs and symptoms appears
Differential diagnosis of a disease
Determining the stage or activity level of the disease

Determining the recurrence of disease
Evaluating the effectiveness of therapy
Laboratory test can also be subdivided in to discretionary and screening test.
Screening test is performed without clinical indication either on hospitalized patient or
healthy outpatient for early or preventive diagnostic measure. Screening tests are more
valuable when the disease is common salient and treatable.
Discretionary investigation could include items 2-6 the test above. There is
performed discretion of the prescriber based on the provisional diagnosis or proposal for
treatment. The lab investigation involve the estimation of the following samples
Urine
Sputum
Blood
CSF
Faeces
Peritoneal fluid
Laboratory data can be classified as following based on the organs whose function are
analyzed
Hematological test
Liver function test
Renal function test
Cardiac function test Stool microscopy
Culture sensitivity
Pulmonary function test
Thyroid function test

HAEMATOLOGICAL TEST
Haematology provides information about cellular components and non-cellular
component. The routine test include
RBC count , WBC count, Hemoglobin level, Hematocrit
RBC indices :- MCV, MCH, MCHC
Reticulocyte count
ESR
Platelet count
Bleeding time
Clotting time
Prothrombin time


LIVER FUNCTION TEST
It helps in measuring hepatic or biliary inflammation and also helps to assist liver
synthetic and functional capabilities include albumin, globulin, and prothrombin time. Liver
function tests help to find out cholestatic disease through measurement of alkaline phosphate
ALP and gammaglutaryl transpeptidase (GGT). Hepatocellular injury can also rule out by
measuring aspartate aminotransferase (AST) and alanine amino transferase (ALT).

RENAL FUNCTION TESTS
Renal function test are used to measure the functioning capacity of kidney and also for
measuring GFR. The tests include BUN, Serum creatinine. By using creatinine clearance we
can adjust dose, assessment of acute and chronic renal failure, glomerular nephritis, nephritic
syndrome etc.

CARDIAC ENZYMES
These tests are specific to evaluate unstable angina, Myocardial infarction and ischemic
heart disease. To assess the cardiac function test such as biochemical tests ECG and non-
invasive imaging technique can be done. The cardiac enzymes are CKMB and LDH (lactate
dehydrogenase). C-reactive protein and amyloid A protein are also use to detect cardiac
problems.

CEREBROSPINAL FLUID
CSF analysis is done to find any infections. In CSF analysis protein, glucose, chlorides
are measuring. Viral infections also affect CSF.

STOOL EXAMINATION
Stool microscopy can be done in case of any blood tinch in stool or faeces occult.

CULTURE SENSITIVITY
The samples are cultured and the sensitivity and resistants pattern of microorganism can
be done. It will help to appropriate therapy.


PULMONARY FUNCTION TEST
This test useful in case of respiratory diseases it will helps in the diagnosis, evaluation
and monitoring of disease. By performing PFT lung damage, obstruction and restrictive
disease can be detected. PFT include lung volume and lung flow tests. Lung volume tests are
tidal volume, vital capacity, total lung capacity, residual volume etc. The later include FEV,
FEV1, FVC, and PEFR.

THYROID FUNCTION TESTS
This test is used to find out hypothyroidism and hyperthyroidism. Hypothyroidism may
be due to defect in thyroid, in pituitary or hypothalamus. By measuring the amount of T3, T4,
TSH can differentially diagnoses the severity.
Thyroid function tests include: - measurement of T
3
AND T
4
. Evaluate the integrity of
hypothalamus, pituitary, Thyroid axis. Assess inherent thyroid gland function detect
antibodies.



I. LABORATORY ASSESSMENT OF ANEMIA

Anemia can be defined as a decrease in either the RBC count or Hb count. Patient with
mild anemia are often asymptomatic but severely symptomatic patients manifest shortness of
breath, tachycardia, and palpitation even at rest.
Patient with anemia (RBCHb)
Review RBC indices, especially MCV

MCV> 100fl MCV:81-99 fl MCV 80 fl
Macrocytic anemia Normocytic anemia Microcytic anemia
Possible causes:
Vit B12 deficiency
Folic acid deficiency
Drug induced bone
marrow toxicity
Possible causes:
Acute blood loss anemia
Hemolytic anemia
Anemia of chronic disease
Possible causes:
Iron-deficiency
anemia

MACROCYTIC ANEMIA
It is associated with abnormally enlarged erythrocytes. The two most common causes
are vit-B12 and folic acid deficiency. Drugs that cause macrocytic anemia mainly interfere
with proper utilization, absorption, and metabolism of other vitamins.

MICROCYTIC ANEMIA
It is associated with abnormally small erythrocytes. Iron deficiency is the primary cause
of microcytic anemia. Iron is necessary for the hemoglobin synthesis. Serum ferritin
concentration reflects total body iron stores and can be used for evaluating patients with
microcytic anemia.
Iron deficiency is usually due to:
In adequate dietary intake
Increased iron requirement
In pregnancy

NORMOCYTIC ANEMIA
Both the MCU and MCHC are within the reference range
Three causes are;
Acute blood loss anemia: patients with acute hemorrhage can have a
dramatic drop in the RBC count
Hemolytic anemia: if hemolysis is rapid and extensive, severe anemia can
develop RBC indices remain unchanged. A specialized test called anti
globulin test (coombs test) is used.

Test Vit-B12
deficiency
anemia
Folic acid
deficiency
anemia
Iron
deficiency
anemia
Hemolytic
anemia
RBC
Hgb
Hct
MCV
MCH
MCHC

Reticulocytes
or or or
Serum vit
B12

Serum-folic
acid

Serum-iron
&ferritin

Antiglobulin
test
Positive




AIM
To analyze and interpret the lab data of a male patient presented with Anemia

SUBJECTIVE EVIDENCE
Patient was complaining about generalized weakness

OBJECTIVE EVIDENCE
The hematology report shows the following;
Hb: 5.0 gm/dl
TRBC: 3.37 mil/cumm
MCV: 56 fl
MCH: 15 pg
MCHC: 26 %
PCV: 19%
RDW: 18.3%

INTERPRETATION
Based on subjective evidence like generalized weakness; physician suspect that the patient
is aneamic. Also physical examination shows pallor was present.
Based on the objective evidence such as decreased Hb, MCV, MCH, and MCHC;
indicating the patient suffering from iron deficiency aneamia. The haemoglobin level was
decreased (5.0 gm/dl), it also confirm IDA.
From the subjective and objective evidence it was confirmed that patient was suffering
from iron deficiency anaemia. Objective evidence is more support to confirm the diagnosis.
In this patient MCV is decreased. It is a strong supportive evidence for IDA. Decreased
MCH shows the pigmentation of RBC. It is hypochromic (less pigmented) than the normal
RBC.


HAEMOGLOBIN
The normal level of hemoglobin in male is 14-18 g/dl. The patient hemoglobin level is
5.0 gm. /dl; the decreased hemoglobin level shows the decreased oxygen carrying capacity of
cell. This decreased capacity will lead to hypoxia. The drastic decrease in oxygen carrying
capacity will cause further complication. It was found that increase in hemoglobin level seen
in patients who are living in high altitude.

HEMATOCRIT (Hct) OR PACKED CELL VOLUME (PCV)
Normal range: 42-52% for males and 37-47% for females.
Hct is the percentage volume of blood that is composed of erythrocytes.

The Hct value is
usually 3 times than Hb value. Lowered Hct may be due to significant hemorrhage, anemia,
over hydration.
High Hct values may indicate polycythemia vera or dehydration. PCV value is
decreased in iron deficiency anemia.

RBC INDICES
Mean cell volume (MCV) : - (82-98 fl)
MCV is the average volume of RBC. MCV can be finding out from RBC. Abnormally
small cells (with decreased MCV) are called microcytic. The most common cause of
decreased MCV and microcytisis is iron deficiency. Decreased MCV indicate abnormality in
the Hb synthesis. MCV also falsely increased in hyperglycemia. Both folate deficiency and
vitamin B12 causes increase in MCV.
Mean cell hemoglobin (MCH) : - (27-33pg/cell)

MCH is the percent volume of Hb per RBC
MCH= Hg b/ RBC
The MCH is decreased in iron deficiency anemia and also decreased in MCH will cause
the diminishing in the cell color result in hypochromic cell.
MCH is increased in both vit B12 and folate deficiency anemia. It is not affecting MCH
in hemolytic anemia.


Mean cell hemoglobin concentration (MCHC): (31-35 gm/dl)
MCHC can be estimated by Hgb / Hct
MCHC is routinely low in iron deficiency anaemia. MCHC also decreased in
decrease Hb synthesis.
MCHC is increased in anaemia of chronic disease. MCHC is normal in vit B12
deficiency and folic acid deficiency.

DIAGNOSIS
The patient diagnosed as iron deficiency anemia.

PLANNING
The test done in this patient is suggestive of iron deficiency anemia. The treatment option
based to the type of anemia. The best option in this patient is oral iron preparation ferrous
sulphate 200 mg TID and packed cell.

CONCLUSION
From the subjective and objective evidence pointing out the patient suffering from iron
deficiency anemia (microcytic hypochromic anemia)


II. LABORATORY ASSESSMENT OF LIVER FUNCTION TEST

Investigation of liver disease often begins with obtaining a panel of liver tests generally
referred to as the liver function test panel or liver functions tests (LFTs). This level may vary
slightly between hospitals and labs but generally includes the Aminotransferase (aspartate
aminotransferase (AST) and Alanine aminotransferase (ALT)), Bilirubin, Alkaline
phosphatase, and Albumin).

TEST FOR SYNTHETIC LIVER FUNCTION
The function of the liver is to synthesize proteins that circulate in the blood, including
albumin and clotting proteins. Measurement of the levels of these proteins in the blood
provides a direct reflection of the ability of the liver to synthesize them. Tests of synthetic
function are not sensitive to low levels of liver damage or dysfunction. Inadequate protein
synthetic function is mainly limited to hepatic cirrhosis, scarring of the liver that can result
from years of alcohol abuse, inflammation, or massive liver damage. (E.g. due to alcoholic
liver disease, severe viral hepatitis or potentially lethal toxin ingestion). In these situations,
measuring synthetic function may be useful in determining prognosis by reflecting the degree
of hepatic failure. The most commonly used tests of protein synthetic function are serum
albumin levels and prothrombin time.
1. ALBUMINS

Normal range: 3.5-5.5 grams/dl
Albumin is a major plasma protein that is involved in maintaining plasma oncotic
pressure and the binding and transport of numerous hormones, anions, drugs, fatty acid. The
normal serum half-life of albumin is about 20 days. Because of albumins long half life,
serum albumin measurements are slow to fall after the onset of hepatic dysfunction (e.g.:
complete cessation of albumin production results in only 20% decrease in serum
concentration after 8 days). For this reason, levels are often normal in acute viral hepatitis or
drug related hepatotoxicity. Alternatively albumin is commonly reduced in patients with
chronic synthetic dysfunction due to cirrhosis.
Hypoalbuminemia (< 2- 2.5 g/dl)
At very low concentrations, patients can develop peripheral edema, ascites, or pulmonary
edema. Low albumin concentrations affect the interpretation of total serum calcium and
concentrations of drugs that are highly protein bound (eg: phenytoin and salicylates).


Hyper albuminemia (> 3 g/dl)
It is seen in patient with marked dehydration, where it is associated with concurrent
elevations in blood urea nitrogen and hematocit. Patients taking anabolic steroids may
demonstrate truly increased albumin concentrations, but those on heparin or ampicillin may
have falsely elevated results with some assays. Hyperalbuminemia is asymptomatic.

2. PREALBUMIN

Normal range: 19.5 35.8 mg/ml
Prealbumin is similar to albumin in several respects: it is synthesized primarily by the
liver and is involved in the binding and transport of various solutes (thyroxin and retinol) and
it is affected by similar factors that affect albumin levels. The primary difference between the
two proteins is that prealbumin has a short half-life (2 day than albumin, compared to 20 days
for albumin) and a smaller body pool than albumin.

3. INTERNATIONAL NORMALIZED RATIO (INR) AND PROTHROMBIN
TIME

: INR: 0.9-1.1

PT: 11.1-13.1 sec
PT Normal range: 11.1-13.1 sec
These two tests measure the speed of a set of reaction in the extrinsic pathway of the
coagulation cascade. A coagulation deficit correlates with prothrombin time. Either hepatic
impairment or vitamin K deficiency may lead to a deficiency in activated coagulation factor
with subsequent prolongation of PT/INR. Both synthetic failure and vitamin K deficiency
may also cause prolongation of activated partial thromboplastin time but to a lesser degree
than PT/INR. The PT/INR is prolonged due to malabsorption, warfarin administration, or the
absence of vitamin K in diet.


TESTS ASSOCIATED WITH EXCRETORY LIVER FUNCTION AND
CHOLESTASIS
Laboratory tests do not distinguish between intra- and extrahepatic cholestasis. This
distinction is usually made radiographically. Laboratory abnormalities primarily associated
with cholestasis include elevation of alkaline phosphatase (ALP, 5-nucleotidase, -glutamyl
transpeptidase (GGTP), and bilirubin.
1. ALKALINE PHOSPHATASE (ALP)

Normal range: 30-120 units/ml
Alkaline phosphatase refers to a group of enzymes whose exact function remains
unknown. These enzymes are found in many body tissues including the liver, bone, small
intestine, kidney, placenta, and leukocyte. Normal ALP concentration may vary with age. In
children and adolescents, elevated ALP concentrations result from bone growth, which may
be associated with elevations as high as 3 times the adult normal range. Clinically ALP
elevation is associated with cholestatic disorder. ALP concentrations more than 4 times
normal suggest a cholestatic disorder. If ALP is elevated with elevated 5
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.


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.


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.


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.





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.


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.


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,

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.

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.


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.




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.


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.


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.


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.


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.


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


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.




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.



REFERENCE
1. Comprehensive Pharmacy Review by Leon Shargel, Alan H.Mutnaick, Paul
F.Souney, Larry N.Swanson:775 789.


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

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.


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

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.



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


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)


4. HISTORY OF MEDICAL PROBLEMS
Have you noticed or do you have any of these following :( put a + symbol in the
appropriate box)
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

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


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


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.




1. PATIENT DETAILS

Name: Mr. X Age: 5Month Sex: M
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 :

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



3. USE OF OTC DRUGS
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

Headache
Ear problems
Cold flue
Allergies
Sinus
Cough
Sleeplessness
Drowsiness
Weight loss
Diarrhea


appropriate box
Hemorrhoids
Joint pain
Rashes
Heart burn
Vitamins
Herbal products
Organic products
Others (specify)


hepatitis

Trouble in eating certain foods
Nausea or vomiting




movements

indigestion

Shortness of breath

+

Coughing up or tightness +
Fainting spells or passing out
Known blood clot problems
Unusual bleeding or bruising
Anemia
Muscle cramps or weakness
Memory problems


Disease

Self Relative
High blood pressure

Asthma

Cancer

Depression

Lung diseases

Diabetic

Heart disease

Stroke

Kidney disease

Neurodegenerative illness

Drug abuse

Others : Seizure birth

+



6. SOCIAL HISTORY
a. Nicotine:
Never smoked Y
Years of use

b. Alcohol consumption:
Never consumed Y
Occasionally N

c. Dietary restrictions if any:
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




1. PATIENT DETAILS

Name: Mr. X Age: 71yrs Sex: F
26.02.13
Ip No:
2011/ 042296
Height: 172 Weight: 52 Kg Social Status:
Non-Smoker And Non-
Alcoholic

Sl no

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



3 USE OF OTC DRUGS
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

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)

4 HISTORY OF MEDICAL PROBLEMS
appropriate box


hepatitis

Nausea or vomiting


movements

indigestion

Shortness of breath



Anemia
Memory problems

Disease

Self Relative
High blood pressure

Asthma

Cancer

Depression

Lung diseases

Diabetic

Heart disease

Stroke

Kidney disease


Drug abuse



6. SOCIAL HISTORY
1. Nicotine:
Never smoked Y
Years of use

2. Alcohol consumption:
Never consumed Y
Occasionally N

3. Dietary restrictions if any:

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.




1 PATIENT DETAILS

Name: Mr. X Age: 28yrs Sex: M
16.07.13
Ip No:
112572
Height: 159 Weight: 67 Kg Social Status:
Smoker And Non-
Alcoholic


Sl no

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


3. USE OF OTC DRUGS

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)

appropriate box


hepatitis

Nausea or vomiting


movements

indigestion

Shortness of breath



Anemia
Memory problems

Disease

Self Relative
High blood pressure

Asthma

Cancer

Depression

Lung diseases

Diabetic

Heart disease

Stroke

Kidney disease


Drug abuse



6. SOCIAL HISTORY
1. Nicotine:
Never smoked N
Packs per day(if smoked) Occasionally
Years of use

2. Alcohol consumption:
Never consumed Y
Occasionally N

3. Dietary restrictions if any:

4. Other information/comments:
Doctor advised to reduce the sugar intake
Reduce heavy and fat containing food
Exercise or regular walking.



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.



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.

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

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.


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.

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.

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1 CLINICAL PHARMACY

AL SHIFA COLLEGE OF PHARMACY

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