PharmaMag 2013

Serving the Profession of Pharmacy
+17,308 fans
ISSN-2309-0286
www.youngpharmacists.com
PharmaMag-2013
Editors and Publishers

Farrukh Mehmood
Tariq Ahmad
(PharmD)
(flywithoutwings_19@hotmail.com)
(PharmD)
(tareeqahmad@hotmail.com)
City of Publication: Lahore

Country code: PAK
Status of Publication: Current serial (c)
Start Date of Publication: 200909
Frequency: Annual (a)
Language: English (eng)
Medium: Online (cr)
ISSN : 2309-0286
Issue: 5th
YoungPharmacists
PharmaMag 2013
pharmamag@hotmail.com
Editorial
Get Involved and Stay Informed. The days of passively pursuing your own career while ignoring the bigger picture are
long gone (if they ever existed). Keep a pulse on the developments that impact the profession of pharmacy any way you can.
Being informed will better prepare you for the next wave of change. Joining organizations, going to board of pharmacy
meetings, or writing letters to politicians are all ways to become more involved.
Farrukh Mehmood
YoungPharmacists
PharmaMag 2013
Contributors
Furqan Munir
(PharmD)
As-Salama Hospital, Khobar
Saudi Arabia
Zia Mehmood
Network Administrator
Spleen Manufacturing (Pvt.) Ltd
Lahore
YoungPharmacists
PharmaMag 2013
Contents
The Issue Of Bioequivalence, Therapeutic Equivalence, And By Khurram Rehman; PharmD, University of
Generic Substitution Of Medicines For Treatment Of Epilep- Lahore; MS Pharmaceutical Analysis, Research
sy And Suggested Ways To Overcome The Problems Assistant/ Ph.D Student, University Kebangsaan
Malaysia
Spread Of Niegleria fowleri In Pakistan With Its Brief By Maliha Bari; PharmD, Dow University of
Information, Diagnosis, And Treatment Health Sciences Karachi; Management Trainee
Officer, Geofman Pharmaceuticals
Pakistan
Management of Respiratory Distress Syndrome in Infants By Eiman Akram; PharmD, Lahore College for
Women University Pakistan
06
08
11
Myths about Thalassemia By Jony Mallik; B.Pharm (Hons.), M.Pharm,

Southern University Bangladesh
15
Microbial Limit Tests By Farrukh Mehmood; PharmD, R.Ph.;

Microbiologist, Highnoon Laboratories Ltd.,
Lahore, Pakistan
21
Syringomyelia By Amna Hafeez; PharmD

Living With Liver Cancer... By Mehrish Memon; PharmD
Mismanagement of Hypertensive Emergency in a Patient By Muhammad Qamar; Lecturer of Clinical

Suffering from Recurrent Stroke Pharmacy, School of Pharmacy, Management
and Science University, Malaysia
The "New" Health Miracles: Probiotics By Iqra Mansha; PharmD, Lahore College for
Women University Pakistan
Indications, Contraindications, Precautions, and Counseling By Azzah Khadim; Mariam Ashraf; PharmD
Parameters of Patients with Coronary Atherosclerosis and (Final Prof) University College of Pharmacy,
Hepatitis Punjab University, Lahore Pakistan
Pregnancy A Crucial Stage for Women That Must Need By Jony Mallik; B.Pharm (Hons.), M.Pharm,
Special Care Southern University Bangladesh
Priyanka Das; B.Pharm (Hons.), BGC Trust University, Bangladesh
24
26
30
32
35
38
The Issue Of Bioequivalence, Therapeutic Equivalence, And

Generic Substitution Of Medicines For Treatment Of Epilepsy
And Suggested Ways To Overcome The Problems
The use of generic drugs to replace brand name drugs is a frequent topic among all types of healthcare professionals. This is
because the generics are very cheap compared to expensive innovators.
The US food and drug administration FDA approves generic
forms of brand-name drugs if they are able to show bioequivalence, as well as standards in drug content (active drug and excipient), and manufacturing. According to FDA for a drug to be
bioequivalent it should be both pharmaceutical equivalent and
therapeutic equivalent.
In contrast to the FDA's position several epilepsy specialists and
societies, including an American Academy of Neurology, have
expressed concern that generic substitution of branded drugs carries a greater potential risk of detrimental patient outcomes in
epilepsy than in many other conditions. This increase in risk is
attributed to the narrow therapeutic range of antiepileptic drugs
(AEDs)
Therefore many physicians and patients answer no to the question; are generic AEDs always equivalent to brand? Several cases
have been reported in various studies, which had seizure frequency increase after they were switched to generic antiepileptic
drugs.
There are several studies performed on antiepileptic drugs like
Phenytoin, Valproic acid, Carbamazepine, Gabapentin and Zonisamide. Many of those studies concluded that changing from a
brand antiepileptic drug to a generic may result in seizures. But
the current FDA therapeutic equivalence testing regulations may
not be adequate for AEDs and suggests that more clinical evidence is needed. Physicians, pharmacists, patients and policy
makers should be aware that for some patients there may be risks
associated with switching from brand to generic AEDS
By Khurram Rehman
PharmD, University of Lahore
MS Pharmaceutical Analysis
Research Assistant/ Ph.D Student
University Kebangsaan Malaysia
Therefore many physicians and patients answer no to the question; are generic AEDs always equivalent to brand? Several cases
have been reported in various studies, which had seizure frequency increase after they were switched to generic antiepileptic
drugs.
There are several studies performed on antiepileptic drugs like
Phenytoin, Valproic acid, Carbamazepine, Gabapentin and Zonisamide. Many of those studies concluded that changing from a
brand antiepileptic drug to a generic may result in seizures. But
the current FDA therapeutic equivalence testing regulations may
not be adequate for AEDs and suggests that more clinical evidence is needed. Physicians, pharmacists, patients and policy
makers should be aware that for some patients there may be risks
associated with switching from brand to generic AEDS.
Another study interprets that most generic AED products provide
total drug delivery (AUC) similar to reference products. The differences in peaks between formulations are more common.
Switches between the generic AED products may cause greater
changes in plasma drug concentrations than generic substitutions
of reference products.
Among the AEDs, phenytoin and carbamazepine have the most
complex factors potentially influencing bioavailability, poor solubility in water. And non linear pharmacokinetics and age related
pharmacokinetics. Meaning studies in adults may not always
translate to the pediatric population.
None of the data published so far are sufficient to provide a firm
evidence base that there is a problem with generic AEDs. The
FDA believes that there are no documented examples of a generic product manufactured to meet approved specifications that
cannot be used interchangeably with the corresponding brand
name drug. However, the majority of physicians and patients
perceive that generic AEDs are not always equivalent to brand
counterparts. This perception influences prescribing practices and
there are many brand-necessary prescriptions for AEDs. It is unknown whether these brand-necessary prescriptions prevent
breakthrough seizures or lessen adverse effects. It is unknown
PharmaMag-2013
Page 06
The Issue Of Bioequivalence, Therapeutic Equivalence, And

Generic Substitution Of Medicines For Treatment Of Epilepsy
And Suggested Ways To Overcome The Problems
how these specified prescriptions affect the cost of healthcare.
Brand-necessary prescriptions increase the medicine costs but
may decrease costs in terms of adverse events and quality of life.
At the current time, a definitive scientifically valid study needs to
be done to answer the question. There are two possible outcomes.
Generics are truly equivalent, that is, the FDA is correct. In that
case we need to educate healthcare providers and our patients.
The other possibility is that one, some, or many of the generic
AEDs are not equivalent. In that case, the FDA needs to reconsider the rules it uses to determine that these products are equivalent.
the small variations in plasma concentration of the magnitude

currently allowed by the FDA. Until such studies are completed,
health-care providers and people with epilepsy would do well to
proceed cautiously when switching to generic formulations, with
health-care providers communicating to patients the potential
risks and benefits of substitution.
The debate over substitution of brand name drugs with generic
formulations is a serious one, especially with regard to AEDs.
Those with epilepsy do not have tried a generic formulation if
there is any risk of a breakthrough seizure or toxicity. Although
some states require substitution with generic formulation if it is
available, the pharmacist can maintain some control over this
situation by alerting the prescriber physician to the mandated
substitution and discussing with them the associated risks. The
pharmacist must also educate the patient on the risk breakthrough
seizures and the implications for the patients life. If generic substitution occurs the same manufacturer of the generic form
should be used throughout treatment to avoid the same bioequivalence issues in changing between generic drugs as between generic and brand name drugs. The FDA stands strongly behind its
requirements for therapeutic equivalence and many generic forms
are used every day, safely and effectively. However, AEDs and
other drugs with narrow therapeutic index may require closer
scrutiny and more stringent criteria. Currently available data on
generic forms of AEDs are very limited.
The ultimate goal is to have truly equivalent generics that are

accepted by all as being interchangeable without concern for
safety and efficacy. This will result in cost savings and better
quality of care. The only remaining issues would be that pills
may be confused when the generic manufacturer changes because the pills look different or because the excipients are different, and rarely a patient may be allergic to one of the inactive
ingredients.
Moreover, people with epilepsy at the extremes of age (children
or older adults) often have decreases in hepatic enzyme activity
and protein binding, potentially making them more susceptible to
bio-in equivalence with generic formulation substitution.
The first step is to assess whether problems occurring after generic AED formulations switches are related to bio-in equivalence between the formulations. Further studies to identify patient subgroups or specific factors that may increase the risk of
bio in equivalence with generic formulation substitution would
also be valuable then other causes of the many complaints by
health-care providers and patients then could be evaluated in a
randomized, controlled trial designed to test therapeutic equivalence with additional outcomes of adverse effects and seizure
frequency. For example, such a study might determine that some
people with epilepsy experience seizures or adverse effects with
PharmaMag-2013
Page 07
Spread Of Niegleria fowleri In Pakistan With Its Brief

Information, Diagnosis, And Treatment
Introduction:
Naegleria fowleri (commonly referred to as the "brain-eating

ameba or brain-eating amoeba"), is a free-living microscopic
ameba_*, (single-celled living organism). It can cause a very
rare, but severe, infection of the brain called primary amebic meningoencephalitis (PAM). The ameba is commonly found in
warm freshwater (e.g. lakes, rivers, and hot springs) and soil.
Naegleria fowleri usually infects people when contaminated water enters the body through the nose. Once the ameba enters the
nose, it travels to the brain where it causes PAM, which is usually fatal. Infection typically occurs when people go swimming or
diving in warm freshwater places, like lakes and rivers. In very
rare instances, Naegleria infections may also occur when contaminated water from other sources (such as inadequately chlorinated
swimming pool water or heated and contaminated tapwater) enters the nose 1, 2, 3.
By Maliha Bari
PharmD
Dow University of Health Sciences,
Karachi
Management Trainee Officer
Geofman Pharmaceuticals
Pakistan
A)Direct visualization12,13: The motile amebae can often be seen

moving rapidly under a microscope when looking at a fresh samWhere Naegleria fowleri is Found
ple of CSF. The amebae can also be stained with a variety of
Naegleria fowleri is a heat-loving (thermophilic) ameba found stains, such as Giemsa-Wright or a modified trichrome stain, for
1, 2
around the world . Naegleria fowleri grows best at higher tem- identification.
peratures up to 115F (46C) and can survive for short periods at
higher temperatures 4, 5. Naegleria fowleri is naturally found in B)Immunohistochemistry (IHC)12,13: A specific antibody to
warm freshwater environments such as lakes and rivers 6-10, natu- Naegleria fowleri can be used in conjunction with another antirally hot (geothermal) water such as hot springs 11, warm water body that deposits a chemical or glows under specific types of
discharge from industrial or power plants 12, 13, geothermal well light (Indirect fluorescent antibody [IFA]) to directly
water 14, 15, poorly maintained or minimally chlorinated swim- stain the amebae in tissue.
ming pools 3, water heaters 16, and soil 6, where it lives by feeding on bacteria and other microbes in the environment. Sampling C)Polymerase Chain Reaction (PCR)14,15,16:
of lakes in the southern tier of the U.S. indicates that Naegleria Specific molecular tools can amplify DNA from the amebae in
fowleri is commonly present in many southern tier lakes in the CSF or tissue to specifically identify if the amebae are present.
U.S. during the summer 6-10. Naegleria is not found in salt water, Looking at strains or subtypes of Naegleria fowleri can be done,
like the ocean.
but little is known about the natural populations in the environment, which makes it difficult to interpret what the findings
When Infections Occur
mean.
Number of case reports of PAM by month of illness onset and
probable water exposure, United States, 1962-2011.
D)Ameba culture 17: The sample is added to a growth plate covInfections linked to freshwater swimming mostly occur during ered in bacteria that can serve as a food source for Naegleria
the heat of summer in July and August when water temperatures fowleri. Incubating at higher temperatures selects for Naegleria
peak and water levels are low. Infections can increase during heat fowleri growth, which can be seen as tracks made by the ameba
wave years as water temperatures increase.
as it moves across the plate eating the bacteria. Growing
Naegleria fowleri in mammalian cell culture and looking for
Diagnosis & Detection
toxic cell effects is also possible.
PAM and Naegleria fowleri infection can be diagnosed in the
laboratory by detecting11:
E)Environmental Detection: Water samples can be collected,
concentrated, and put into culture to grow and select for
1)Naegleria fowleri organisms in cerebrospinal fluid (CSF), bi- Naegleria fowleri. Samples can be tested using the serologic or
opsy, or tissue specimens, or
molecular methods described above.
2)Naegleria fowleri nucleic acid in CSF, biopsy, or tissue speci- Treatment
mens, or
Primary amebic meningoencephalitis (PAM) caused by
Naegleria fowleri infection have been fatal 18, there have been
3)Naegleria fowleri antigen in CSF, biopsy, or
two welldocumented survivors (one from the US in 1979 19,20and
tissue specimens.
one from Mexico in 200321) who received the following treatment courses:
Naegleria fowleri Test Methods
PharmaMag-2013
In these two cases, the following combination of three drugs was

Page 08

used successfully (in addition to Steroids to control cerebral
edema):
Amphotericin B (IV +/- intrathecal) (one patient received Am- ing was that this parasite travelled to the brain through the nose
photericin B [AMB] for 14 days and the other patient received it and people normally used water to clean their nose during abulafor 9 days)
tion for prayers.33
AND
Rifampicin (or al) 10 mg/kg/day (one survivor received this
dosage in three divided doses for 9 days; the other received it
every 24 hours for 1 month)
AND EITHER
Fluconazole (IV or or al) 10 mg/kg/day (one survivor initially
received this dosage IV every 24 hours but fluconazole was later
switched to oral administration because the hospital ran out of IV
stock)
OR
Miconazole (IV) 350 mg per square meter of body-surface
area per day in three divided doses (one survivor received this
regimen for 9 days
We also recommend the use of
Azithromycin. Azithr omycin has both in vitro and in vivo
(mouse model) efficacy against Naegleria fowleri and appears to
be synergistic when administered with AMB23,26. Therefore,
azithromycin may be tried as an adjunct to AMB.
Investigational Drugs
Dr Musa Khan, head of WHOs Disease Early Warning System in

Pakistan, confirmed that all the deaths had occurred in the southern city of Karachi. Authorities are planning to launch a local
campaign to ensure the supply of clean water to its 18 million
residents. People who have contracted the amoeba suffer from
very mild symptoms such as fever, nausea, vomiting, stiff neck
and headaches.It usually takes five to seven days to die after infection.34 Authorities are planning a campaign to raise awareness
among health workers and the public, said Dr. Musa Khan, head
of the WHO's Disease Early Warning System in Pakistan. Most
health centers had already been alerted, he said. "People should
avoid getting water too deep into their nostrils and make sure
their water supply is properly treated," he said. Khan noted that
residents should not panic, adding that there is a remote chance
of the parasite expanding its breadth of exposure. "There is no
need to panic over these deaths. There is a remote chance for the
spread of this deadly disease," said Khan. "It is a water-borne
infection and we are thoroughly inquiring about its arrival and
spread here."35 The amoeba is a very effective killer with a death
rate over 98 percent. Dr. Musa Khan, head of the WHO's Disease
Early Warning System in Pakistan, stated : "People should avoid
getting water too deep into their nostrils and make sure their water supply is properly treated 36 Sindh Health Minister Sagheer
Ahmed said that 10 deaths had been confirmed from the brain
eating amoeba since July including three this month and most of
them were young people who used public swimming pools. "The
meeting has decided that the Karachi Water and Sewerage Board
should increase chlorine concentrations in water at its major
treatment and pumping stations," he said. "The health department
has also been told to increase public awareness about the water
borne parasite through various methods. ," he said. 33
Recently, an investigational drug, miltefosine27, a breast cancer

and anti-leishmania drug, has shown some promise against the
free-living amebae in combination with some of these
other drugs. Miltefosine has shown in vitro and mouse model
amebicidal activity against Balamuthia, Naegleria fowleri, and
Acanthamoeba 28,28,29and has been used to successfully treat pa- Khan said authorities were planning a campaign to raise awaretients with Balamuthia infection 30 and disseminated Acan- ness among health workers and the public, and that most health
centers had already been alerted.
thamoeba infection31.
References
Niegleria in Pakistan
Pakistani health officials in the country's biggest city, Karachi,

are said to be "very concerned" about a recent spate of deaths
caused by a rare brain-eating microbe.
It is estimated that 98 percent of infections end up being fatal,
with the patient dying 7-14 days after exposure. 31A rare braineating amoeba is responsible for at least 10 deaths in the Pakistani city of Karachi in recent months, health officials believe.
Musa Khan, in-charge of the World Health Organization's Disease Early Warning System in Pakistan, also confirmed that the
deaths were reported from Karachi. A Sindh health department
official said what was of grave concern to everyone at the meet
PharmaMag-2013
1)Yoder JS, Eddy BA, Visvesvara GS, Capewell L, Beach MJ. The epidemiology of primary amoebic meningoencephalitis in the USA, 19622008. Epidemiol Infect. 2010;138(7):968-75.
2)Visvesvara GS. Free-living amebae as opportunistic agents of human
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4)Griffin JL. Temperature tolerance of pathogenic and nonpathogenic
free-living amoebas. Science. 1972;178(63):869-70.
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identification of Naegleria fowleri from water and soil samples by nested PCR. Parasitol Res 2004;93: 21117.
7)Wellings FM, Amuso PT, Chang SL, Lewis AL. Isolation and identification of pathogenic Naegleria from Florida lakes. Appl Environ Microbiol 1977;34:6617.
8)John DT, Howard MJ. Seasonal distribution of pathogenic free-living
amebae in Oklahoma waters. Parasitol Res 1995;81:193201.
9)Duma RJ. Study of pathogenic free-living amebas in fresh-water lakes
in Virginia. EPA Publication.1980;EPA-PB-126369, Summary, 1981 is
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10)Ettinger MR, Webb SR, Harris SA, McIninch SP, C Garman G,
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11)Council for State and Territorial Epidemiologists (CSTE). Case Definitions for Non-notifiable Infections Caused by Free-living Amebae
(Naegleria fowleri, Balamuthia mandrillaris, and Acanthamoeba
spp.) [PDF - 10 pages]. Infectious Disease Committee. 2012
12)Visvesvara GS. Amebic meningoencephalitides and keratitis: challenges in diagnosis and treatment. Curr Opin Infect Dis. 2010;23(6):5904.
13)da Rocha-Azevedo B, Tanowitz HB, Marciano-Cabral F. Diagnosis
of infections caused by pathogenic freeliving amoebae. Interdiscip Perspect Infect Dis. 2009;2009:251406.
14)Qvarnstrom Y, Visvesvara GS, Sriram R, da Silva AJ. Multiplex real
-time PCR assay for simultaneous detection of Acanthamoeba spp.,
Balamuthia mandrillaris, and Naegleria fowleri. J Clin Microbiol.
2006;44(10):3589-95.
15)Robinson BS, Monis PT, Dobson PJ. Rapid, sensitive, and discriminating identification of Naegleria spp. by real-time PCR and meltingcurve analysis. Appl Environ Microbiol. 2006;72(9):5857-63.
16)Marciano-Cabral F, MacLean R, Mensah A, LaPat-Polasko L. Identification of Naegleria fowleri in domestic water sources by nested PCR.
Appl Environ Microbiol. 2003;69:5864-9.
17)Visvesvara GS. Parasite Culture: Acanthamoeba and Naegleria spp.
In: Garcia LS, editor. Clinical Microbiology Procedures Handbook. 3rd
ed. Washington, DC: ASM Press; 2010.
18)Yoder JS, Eddy BA, Visvesvara GS, Capewell L, Beach MJ. The
epidemiology of primary amoebic meningoencephalitis in the USA,
1962-2008. Epidemiol Infect. 2010;138:968-75.
19)Seidel J, Harmatz P, Visvesvara GS, Cohen A, Edwards J, Turner J.
Successful treatment of primary amebic meningoencephalitis. New Engl
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20)Visvesvara GS, Moura H, Schuster FL. Pathogenic and opportunistic
free-living amoebae: Acanthamoeba spp., Balamuthia mandrillaris,
Naegleria fowleri, and Sappinia diploidea. FEMS Immunol Med Microbiol. 2007;50:1-26.
21)Vargas-Zepeda J, Gomez-Alcala AV, Vasquez-Morales JA, LiceaAmaya L, De Jonckheere JF, Lores-Villa F. Successful treatment of
Naegleria PAM using IV amphotericin B, fluconazole, and rifampin.
Arch Med Res. 2005;36:83-6.
22)Goswick SM, Brenner GM. Activities of therapeutic agents against
Naegleria fowleri in vitro and in a mouse model of primary amebic
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Chemother. 2003;47:524-8.
24)Ferrante A. Comparative sensitivity of Naegleria fowleri to amphotericin B and amphotericin B methyl ester. Trans R Soc Trop Med Hyg.
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PharmaMag-2013
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singly and in combination. Antimicrob Agents Chemother. 1979;16:21720.
26)Soltow SM, Brenner GM. Synergistic activities of azithromycin and
amphotericin B against Naegleria fowleri in vitro and in a mouse model
of primary amebic meningoencephalitis. [PDF - 5 pages] Antimicrob
Agents Chemother. 2007;51:237.
27)Kaminsky R. Miltefosine Zentaris . Curr Opin Investig Drugs.
2002;3:550-4.
28)Schuster FL, Guglielmo BJ, Visvesvara GS. In-vitro activity of
miltefosine and voriconazole on clinical isolates of free-living amebas:
Balamuthia mandrillaris, Acanthamoeba spp., and Naegleria fowleri.
J Eukaryot Microbiol. 2006;53:121-6.
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Shin HJ. Effect of therapeutic chemical agents in vitro and on experimental meningoencephalitis due to Naegleria fowleri. [PDF - 7 pages]
Antimicrob Agents Chemother. 2008;52:4010-16.
30)Walochnik J, Obwaller A, Gruber F, Mildner M, Tschachler E, Suchomel M, Duchene M, Auer H. Anti- Acanthamoeba efficacy and
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32)Brain-Eating Amoeba Behind Karachi Deaths
33)Parasite known as 'brain-eating amoeba' kills 10 people in Pak - Indian Express
34) Health Brain-Eating Amoeba Kills 10 in Karachi [VIDEO] UK
35) Brain-eating amoeba hits Pakistani city | The Bell Jar 36) BrainEating Amoeba Kills 10 Pakistanis; Water Sources Being Tested : Enstarz
Page 010
Management of Respiratory Distress Syndrome in

Infants
Alternative Names
Hyaline membrane disease; infant respiratory distress syndrome
(IRDS); Respiratory distress syndrome in infants; RDS - infants
By Eiman Akram
PharmD
Lahore College for Women
University
Pakistan
Introduction
Respiratory Distress Syndrome (RDS), also known as hyaline

membrane disease, is a condition associated with severe breathing difficulty seen predominantly in premature infants. RDS is
caused by a primary deficiency of surfactant, a substance that
coats the alveoli (air sacs) in healthy lungs and prevents them
from collapsing during exhalation. As a result of this deficiency,
the baby cannot take up enough oxygen.
RDS rarely occurs in full-term infants. In fact, nearly all infants
born before 28 weeks of pregnancy develop RDS.
There are two main types of respiratory distress syndrome

(RDS). The first is seen in premature babies and is the type dealt
with in this article. The second is seen in adults and is known as
acute respiratory distress syndrome (ARDS).
Respiratory distress syndrome remains a major cause of morbidity and mortality in preterm infants, especially in the extremely
low birth weight infants <1000 g. RDS is more common in premature infants because their lungs aren't able to make enough surfactant.
Without enough surfactant, the lungs collapse and the infant has
to work hard to breathe. He or she might not be able to breathe in
enough oxygen to support the body's organs. The lack of oxygen
can damage the baby's brain and other organs if proper treatment
isn't given.
Most babies who develop RDS show signs of breathing problems
and a lack of oxygen at birth or within the first few hours.
Most babies who develop

RDS show signs of breathing
problems and a lack of oxygen at birth or within the first
few hours
Most infants who develop RDS show signs of breathing problems at birth or within the next few hours. If they're not given the
right treatment, their brains and other organs may suffer from the
lack of oxygen.
From the current perspective, RDS is the most common respiratory disorder of premature newborns, and its incidence is directly
proportional to the degree of prematurity.
Etiology:
Neonatal RDS occurs in infants whose lungs have not yet fully
developed.
The disease is mainly caused by a lack of a slippery, protective
substance called surfactant, which helps the lungs inflate with air
and keeps the air sacs from collapsing. This substance normally
appears in fully developed lungs. Neonatal RDS can also be the
result of genetic problems with lung development.
Pulmonary surfactant contains 3 surfactant-specific proteins: SPA, SP-B, and SP-C. These proteins are synthesized primarily by
type II cells.
The lack of surfactant proteins precludes tubular myelin formation, a surfactant conformation with surface tension activity,
PharmaMag-2013
Page 11

Infants
thus promoting alveolar instability and collapse. Low levels of
SP-A and SP-B are characteristically found in tracheal secretions
and lungs of newborns with RDS.
Exams and Tests
Pathophysiology:
Immature type II alveolar cells produce less surfactant, causing

an increase in alveolar surface tension and a decrease in compliance. The resultant atelectasis causes pulmonary vascular constriction, hypoperfusion, and lung tissue ischemia. Hyaline membranes form through the combination of sloughed epithelium,
protein, and edema.
The most important investigation in an infant with respiratory

distress is a chest X-ray.
The chest radiograph reveals decreased lung inflation
(homogenous opaque infiltrates) indicating contrast in airless
lung tissue seen against air-filled bronchi, with diffuse symmetrical reticulogranular (ground glass appearance) lung fields. Decreased lung volumes also can be detected.
History while stabilizing a baby with severe respiratory distress,
it is important to get a good history. We need to know the gestation and if the baby is premature it is important to know if antenatal steroids have been given or not.
Most infants are less than 34 weeks gestation and the incidence
and severity increase with decreasing gestation age.
Avoiding unnecessary or poorly timed cesarean sections can

also reduce the risk of RDS
Symptoms:
Management
The management of infants is complex and requires a multidisciplinary team approach to obtain best outcomes. The application
of the basic principles of neonatal care, such as thermoregulation,
Grunting sounds, especially when exhaling (breathing out). cardiovascular and nutritional support, treatment of early neonatal infection, is crucial to achieve the therapeutic goals. Clearly,
Retractions. The skin between and around the ribs pulls in surfactant replacement therapy, continuous positive airway preswhen the baby inhales (breathes in). The middle of your baby's sure (CPAP), and mechanical ventilation in its different modalities are the mainstay for the respiratory support of these patients.
chest may also sink deeply in as he breathes.
Very fast breathing, or periods of no breathing (apnea).
Nasal flaring. The two nose openings become larger with

breathing.
Pale or blue colored skin, lips, and nail beds.
Risk Factors:
The condition is more common in boys, and the incidence is

higher in infants whose mothers have diabetes, because of delayed pulmonary maturity.
PharmaMag-2013
Page 12

Infants
120-150ml / (kg.d) and added electrolyte condition for the better
oral feeding, so that part of parenteral nutrition supplemented.

2. Oxygen therapy and mechanical ventilation
1) Oxygen:
The baby needs extra oxygen to help him breathe better. The
oxygen may be warmed and mixed with mist (water vapor).
Caregivers place a clear oxygen hood the baby's head.
The oxygenator does the work of the lungs by oxygenating the
blood and removing carbon dioxide. The continual air pressure
provided by the ventilator prevents the collapse of the air sacs.
As the infants lungs mature and begin to produce surfactant
usually within three to five days after birththe child is weaned
from the ventilator.
2) Continuous positive airway pressure and normal frequency
Prevention:
Reducing premature birth is the most effective preventive method against RDS. Even if preterm birth cannot be prevented, the
administration of a very short course (two doses 24 hours apart)
of antenatal steroids to the mother has been shown to be highly
effective in decreasing the severity and incidence of RDS.
Antenatal steroids also decrease the incidence of other important
complications of prematurity, including intraventricular hemorrhage and bronchopulmonary dysplasia.
mechanical ventilation.
The baby may need CPAP (continuous positive airway pressure)
given through nasal prongs. With CPAP, the baby will have a
long, plastic tube with two tiny tubes sticking up from it (nasal
prongs). The nasal prongs are gently inserted into the baby's nostrils (nose openings) and taped in place. CPAP helps the baby
keep his lungs filled with air.
3) Others: high frequency oscillation or high frequency jet ventiIn some cases, medicines called corticosteroids may be given to
help speed up lung maturity in the developing baby. They are lator can often reduce the frequency of the negative effects ventioften given to pregnant women between 24 and 34 weeks of
pregnancy who seem likely to delivery in the next week.
lator in order to obtain better results.
Antibiotics are often administered if bacterial infection is susAvoiding unnecessary or poorly timed cesarean sections can also
pected clinically or because of leukocytosis, neutropenia, or hyreduce the risk of RDS.
poxemia. Ampicillin and gentamicin are often used together
Treatment
based on their effectiveness and synergy. Extracorporeal membrane oxygenation, similar to an artificial external lung, is used
1. General treatment (Nursing)
as a last resort in critical circumstances. Oral feedings are often
1) Insulation: placed infant in the warm box and maintain skin withheld if the respiratory rate exceeds 80 breaths per minute.
temperature at 36.5 .
3. Surfactant replacement therapy
2) Monitoring: temperature, respiration, heart rate, blood pres-
Introduction of surfactant replacement for the treatment of RDS,

successfully treated with a modified bovine surfactant extract
(Surfactant-TA, Surfacten, Tokyo Tanabe, and Tokyo Japan)
3) to ensure the supply of fluids and nutrition: the 1st day of 5% administered via endotracheal tube. All infants demonstrated
remarkable improvement in oxygenation and decreased ventilatoor 10% glucose solution 65-75ml / (kg.d) gradually increased to ry requirements.
Today, several types of animal based surfactants have been apsure and blood gas.
PharmaMag-2013
Page 13

Infants
proved for clinical use. After endotracheal intubation, surfactant
suspension is administered through the endotracheal (ET) tube
and the infant is supported, until extubation is possible, with positive pressure ventilation and continuous positive airway pressure
(CPAP) therapy as needed. High frequency ventilation has been
shown to improve the short term management of these infants.
Conclusion
Respiratory distress in a newborn is a challenging problem. It
occurs in 4 to 6 percent of infants. Many of the conditions causing respiratory distress are preventable. Early recognition and
prompt management are required.
Despite huge advances in care, RDS remains the most common
single cause of death in the first month of life. The general principles of neonatal care and a team approach should be applied to
maximize the occurrence of good short-term and long-term outcomes.
RDS requires the expenditure of major health financial resources. The need for assisted ventilation comprises one of the
major costs of the care of premature infants.
PharmaMag-2013
Page 14
Myths about Thalassemia

Introduction
BLOOD not just a word, is a sea of chemicals. Blood consists
of about 55% of plasma and 45 % of corpuscles. Among them a
very vital one is RBC (Red Blood Corpuscle)/ Erythrocytes. The
quantities of them may vary in male & female. As we know that
RBC is the warehouse of Hemoglobin so it also be vary in two
sign of human being. Hemoglobin is the iron-containing oxygentransport metalloprotein in the red blood cells of all vertebrates
as well as the tissues of some invertebrates. Each hemoglobin is
consists of heme and globin where heme is the form of iron and
globin is actually protein form with two different chain called
(alpha) & (beta) chain. Each chain has two sub-chain respectively they are 1 & 2, 1 & 2.
By Jony Mallik
B.Pharm (Hons.)
M.Pharm
Southern University
Bangladesh
bin disorder, the most common is anemia.

Anemia is the critical pathological condition of blood when the
total count of hemoglobin in RBCs become lower than that of
normal count. There are different kinds of anemia thus it is occurs via various way. Anemia, one of the more common blood
disorders, occurs when the level of healthy red blood cells
(RBCs) in the body becomes too low. This can lead to health
problems because RBCs contain hemoglobin, which carries oxygen to the body's tissues. Anemia can cause a variety of complications, including fatigue and stress on bodily organs.
Anemia can be caused by many things, but the three main bodily
mechanisms that produce it are:
Hemoglobin in the blood carries oxygen from the respiratory 1. excessive destruction of RBCs
organs (lungs or gills) to the rest of the body where it releases the
oxygen to burn nutrients to provide energy to power the functions of the organism, and collects the resultant carbon dioxide to 2. blood loss
bring it back to the respiratory organs to be dispensed from the
organism.
3. inadequate production of RBCs
Among many other causes, anemia can result from inherited disorders, nutritional problems (such as an iron or vitamin deficiency), infections, some kinds of cancer, or exposure to a drug or
toxin.
Anemia Caused by Destruction of RBCs
Hemolytic anemia occurs when red blood cells are being destroyed prematurely. (The normal lifespan of RBCs is 120 days;
in hemolytic anemia, it's much shorter.) And the bone marrow
(the soft, spongy tissue inside bones that makes new blood cells)
simply can't keep up with the body's demand for new cells. This
can happen for a variety of reasons. Sometimes, infections or
certain medications such as antibiotics or anti-seizure medicines are to blame.
Anemia
Among the different kinds of RBC disorder as well as Hemoglo
PharmaMag-2013
Page 15

A very potent hemolytic anemia is Thalassemia and its a very
crucial cause of death today. Thalassemias are inherited blood
disorders. "Inherited" means that the disorder is passed from parents to children through genes. Thalassemias cause the body to
make fewer healthy red blood cells and less hemoglobin than
normal. Hemoglobin is an iron-rich protein in red blood cells. It
carries oxygen to all parts of the body. Hemoglobin also carries
carbon dioxide (a waste gas) from the body to the lungs, where
it's exhaled. People who have thalassemias can have mild or severe anemia . Anemia is caused by a lower than normal number
of red blood cells or not enough hemoglobin in the red blood
cells.
childhood and are lifelong conditions. Doctors diagnose thalassemias using blood tests. The disorders are treated with blood
transfusions, medicines, and other procedures.
A) Genetic Classification of the Thalassemia
1.
Alpha
Thalassemia
Alpha thalassemia occurs when one or more of the four alpha

chain genes fails to function. Alpha chain protein production, for
practical purposes, is evenly divided among the four genes. With
alpha thalassemia, the "failed" genes are almost invariably lost
from the cell due to a genetic accident.
(i) The loss of one gene diminishes the production of the alpha
protein only slightly. This condition is so close to normal that it
can be detected only by specialized laboratory techniques that,
until recently, were confined to research laboratories. A person
with this condition is called a "silent carrier" because of the difficulty in detection.
(ii) The loss of two genes (two-gene deletion alpha thalassemia)
produces a condition with small red blood cells, and at most a
mild anemia. People with this condition look and feel normal.
The condition can be detected by routine blood testing, however.
Overview
Normal hemoglobin, also called hemoglobin A, has four protein
chainstwo alpha globin and two beta globin. The two major
types of thalassemia, alpha and beta, are named after defects in
these protein chains. Four genes (two from each parent) are needed to make enough alpha globin protein chains. Alpha thalassemia trait occurs if one or two of the four genes are missing. If
more than two genes are missing, moderate to severe anemia
occurs. The most severe form of alpha thalassemia is called alpha
thalassemia major or hydrops fetalis. Babies who have this disorder usually die before or shortly after birth. Two genes (one from
each parent) are needed to make enough beta globin protein
chains. Beta thalassemia occurs if one or both genes are altered.
The severity of beta thalassemia depends on how much one or
both genes are affected. If both genes are affected, the result is
moderate to severe anemia. The severe form of beta thalassemia
is known as thalassemia major or Cooley's anemia. Thalassemias
affect males and females. The disorders occur most often among
people of Italian, Greek, Middle Eastern, Southern Asian, and
African descent. Severe forms usually are diagnosed in early
PharmaMag-2013
(iii) The loss of three alpha genes produces a serious hematological problem (three-gene deletion alpha thalassemia). Patients
with this condition have a severe anemia, and often require blood
transfusions to survive. The severe imbalance between the alpha
chain production (now powered by one gene, instead of four) and
beta chain production (which is normal) causes an accumulation
of beta chains inside the red blood cells. Normally, beta chains
pair only with alpha chains. With three-gene deletion alpha thalassemia, however, beta chains begin to associate in groups of
four, producing an abnormal hemoglobin, called "hemoglobin
H". The condition is called "hemoglobin H disease". Hemoglobin
H has two problems. First it does not carry oxygen properly,
making it functionally useless to the cell. Second, hemoglobin H
protein damages the membrane that surrounds the red cell, accelerating cell destruction. The combination of the very low production of alpha chains and destruction of red cells in hemoglobin H
disease produces a severe, life-threatening anemia. Untreated,
most patients die in childhood or early adolescence.
(iv) The loss of all four alpha genes produces a condition that is
incompatible with life. The gamma chains produced during fetal
life associate in groups of four to form an abnormal hemoglobin
called "hemoglobin Barts". Most people with four-gene deletion
Page 16

alpha thalassemia die in utero or shortly after birth. Rarely, four
gene deletion alpha thalassemia has been detected in utero, usually in a family where the disorder occured in an earlier child. In
utero blood transfusions have saved some of these children.
These patients require life-long transfusions and other medical
potentially life-threatening condition. The severity of the disorder
support.
depends in part on the combination of genes that have been inherited: beta-0-thal/ beta-0-thal; beta-0-thal/ beta-(+)-thal; betaExample of an Inheritance Pattern for Alpha Thalassemia
(+)-thal/ beta-(+)-thal. The beta-(+)-thalassemia genes vary
greatly in their ability to produce normal hemoglobin. Consequently, the clinical picture is more complex than might otherwise be the case for three genetic possibilities outlined.
2.
Beta
Thalassemia
The fact that there are only two genes for the beta chain of hemoglobin makes beta thalassemia a bit simpler to understand than
alpha thalassemia (2). Unlike alpha thalassemia, beta thalassemia
rarely arises from the complete loss of a beta globin gene. The
beta globin gene is present, but produces little beta globin protein. The degree of suppression varies. Many causes of suppressed beta globin gene expression have been found. In some
cases, the affected gene makes essentially no beta globin protein.
In other cases, the production of beta chain protein is lower than
normal, but not zero (beta-(+)-thalassemia). The severity of beta
thalassemia depends in part on the type of beta thalassemic genes
that a person has inherited.
Example of an Inheritance Pattern for Beta Thalassemia

B) Clinical Classification of the Thalassemias
1.
Alpha
Thalassemia
Alpha thalassemia has four manifestations, that correlate with

the number of defective genes. Since the gene defect is almost
invariably a loss of the gene, there are no "shades of function" to
(i) one-gene beta thalassemia has one beta globin gene that is obscure the matter as occurs in beta thalassemia.
normal, and a second, affected gene with a variably reduced production of beta globin. The degree of imbalance with the alpha (i) Silent carrier state. This is the one-gene deletion alpha thalasglobin depends on the residual production capacity of the defec- semia condition. People with this condition are hematologically
tive beta globin gene. Even when the affected gene produces no normal. They are detected only by sophisticated laboratory methbeta chain, the condition is mild since one beta gene functions ods.
normally. The red cells are small and a mild anemia may exist.
People with the condition generally have no symptoms. The con- (ii) Mild alpha-thalassemia. These patients have lost two alpha
dition can be detected by a routine laboratory blood evaluation. globin genes.They have small red cells and a mild anemia. These
(Note that in many ways, the one-gene beta thalassemia and the people are usually asymptomatic. Often, physicians mistakenly
two-gene alpha thalassemia are very similar, from a clinical point diagnose people with mild alpha-thalassemia as having iron defiof view. Each results in small red cells and a mild anemia).
ciency anemia. Iron therapy, of course, does not correct the anemia.
(ii) two-gene beta thalassemia produces a severe anemia and a
PharmaMag-2013
Page 17
(ii) Thalassemia intermedia. Thalassemia intermedia is a confusing concept. The most important fact to remember is that thalassemia intermedia is a description, and not a pathological or genetic diagnosis. Patients with thalassemia intermedia have significant anemia, but are able to survive without blood transfusions.
The factors that go into the diagnosis are:
The degree to which the patient tolerates the anemia.
The threshold of the physician to transfuse patients with thalassemia.

(iii) Hemoglobin H disease. These patients have lost three alpha
globin genes. The result is a severe anemia, with small, misshapen red cells and red cell fragments. These patients typically have
enlarged spleens. Bony abnormalities particularly involving the
cheeks and forehead are often striking. The bone marrow works
at an extraordinary pace in an attempt to compensate for the anemia. As a result, the marrow cavity within the bones is stuffed
with red cell precursors. These cells gradually cause the bone to
"mold" and flair out. Patients with hemoglobin H disease also
develop large spleens. The spleen has blood forming cells, the
same as the bone marrow. These cells become hyperactive and
overexpand, just as those of the bone marrow. The result is a
spleen that is often ten-times larger than normal. Patients with
hemoglobin H disease often are small and appear malnourished,
despite good food intake. This feature results from the tremendous amount of energy that goes into the production of new red
cells at an extremely accelerated pace. The constant burning of
energy by these patients mimics intense aerobic exercise; exercise that goes on for every minute of every day.
(iii) Thalassemia major. This is the condition of severe thalassemia in which chronic blood transfusions are needed (3). In some
patients the anemia is so severe, that death occurs without transfusions. Other patients could survive without transfusions, for a
while, but would have terrible deformities. While transfusions
are life-saving in patients with thalassemia major, transfusions
ultimately produce iron overload. Chelation therapy, usually with
the iron-binding agent, desferrioxamine (Desferal), is needed to
prevent death from iron-mediated organ injury.
Relationship of the Genetic and Clinical Classifications of Thalassemia
The advent of modern molecular biology permits the genetic
classification of thalassemias, outlined earlier in this document.
A rough correlation exists between the clinical and genetic classifications. The relationship between genetics and clinical state is
not absolute, however:
(iv) Hydrops fetalis. This condition results from the loss of all thalassemia trait (minor)- normal beta gene/ thalassemia
four alpha globin genes. The affected individual usually suc- gene ( beta zero or +)
cumbs to the severe anemia and complications before birth.
2.
Beta
Thalassemia
thalassemia intermedia- often two beta-(+)-genes
(i) Thalassemia minor, or thalassemia trait. These terms are used thalassemia major- two beta-(+)-genes (where the plus is not
substantial); beta-(+)-gene/ beta-0-gene; beta-0-gene/ beta-0interchangeably for people who have small red cells and mild (or
gene
no) anemia due to thalassemia. These patients are clinically well,
and are usually only detected through routine blood testing. Physicians often mistakenly diagnose iron deficiency in people with Signs and Symptoms of Thalassemias
thalassemia trait. Iron replacement does not correct the condition.
The primary caution for people with beta-thalassemia trait involves the possible problems that their children could inherit if A lack of oxygen in the bloodstream causes the signs and symptheir partner also has beta-thalassemia trait. These more severe toms of thalassemias. The lack of oxygen occurs because the
body doesn't make enough healthy red blood cells and hemogloforms of beta-thalassemia trait are outlined below.
bin. The severity of symptoms depends on the severity of the
disorder.
PharmaMag-2013
Page 18

No Symptoms
Alpha thalassemia silent carriers generally have no signs or

symptoms of the disorder. The lack of alpha globin protein is so
overload). This can damage organs and tissues, especially the
minor that the body's hemoglobin works normally.
heart and liver.
Heart disease caused by iron overload is the main cause of death
Mild Anemia
People who have alpha or beta thalassemia trait can have mild in people who have thalassemias. Heart disease includes heart
anemia. However, many people who have these types of thalasse- failure, arrhythmias (irregular heartbeats), and heart attack.
mia have no signs or symptoms.
Mild anemia can make you feel tired. Mild anemia caused by Infection
alpha thalassemia trait might be mistaken for iron-deficiency Among people who have thalassemias, infections are a key cause
anemia.
of illness and the second most common cause of death. People
who have had their spleens removed are at even higher risk beMild to Moderate Anemia and Other Signs and cause they no longer have this infection-fighting organ.
Symptoms
People who have beta thalassemia intermedia have mild to moderate anemia. They also may have other health problems, such as:
Slowed growth and delayed puberty. Anemia can slow down
a child's growth and development.
Bone problems. Thalassemia may cause bone marrow to
expand. Bone marrow is the spongy substance inside bones that
makes blood cells. When bone marrow expands, the bones become wider than normal. They may become brittle and break
easily.
An enlarged spleen. The spleen is an organ that helps your body
fight infection and remove unwanted material. When a person
has thalassemia, the spleen has to work very hard. As a result, the
spleen becomes larger than normal. This makes anemia worse. If
the spleen becomes too large, it must be removed.
Thalassemias Treatment
Treatments for thalassemias depend on the type and severity of

the disorder. People who are carriers or who have alpha or beta
thalassemia trait have mild or no symptoms. Theyll likely need
little or no treatment.
A) Standard Treatments
i) Blood Transfusions
People who have hemoglobin H disease or beta thalassemia major (also called Cooley's anemia) have severe thalassemia. Signs
and symptoms usually occur within the first 2 years of life. They
may include severe anemia and other health problems, such as:
A pale and listless appearance
Poor appetite
Dark urine (a sign that red blood cells are breaking down)
Slowed growth and delayed puberty
Jaundice (a yellowish color of the skin or whites of the eyes)
An enlarged spleen, liver, or heart
Bone problems (especially with bones in the face)
Transfusions of red blood cells are the main treatment for people
who have moderate or severe thalassemias. This treatment gives
you healthy red blood cells with normal hemoglobin. During a
blood transfusion, a needle is used to insert an intravenous (IV)
line into one of your blood vessels. Through this line, you receive
healthy blood. The procedure usually takes 1 to 4 hours. Red
blood cells live only for about 120 days. So, you may need repeated transfusions to maintain a healthy supply of red blood
cells. If you have hemoglobin H disease or beta thalassemia intermedia, you may need blood transfusions on occasion. For example, you may have transfusions when you have an infection or
other illness, or when your anemia is severe enough to cause
tiredness. If you have beta thalassemia major (Cooley's anemia),
youll likely need regular blood transfusions (often every 2 to 4
weeks). These transfusions will help you maintain normal hemoglobin and red blood cell levels. Blood transfusions allow you to
feel better, enjoy normal activities, and live into adulthood. This
treatment is lifesaving, but it's expensive and carries a risk of
transmitting infections and viruses (for example, hepatitis). However, the risk is very low in the United States because of careful
blood screening.
Complications of Thalassemia
ii) Iron Chelation Therapy
Severe Anemia and Other Signs and Symptoms
The hemoglobin in red blood cells is an iron-rich protein. Thus,

regular blood transfusions can lead to a buildup of iron in the
blood. This condition is called iron overload. It damages the liver, heart, and other parts of the body.
To prevent this damage, doctors use iron chelation therapy to
remove excess iron from the body. Two medicines are used for
Heart and Liver Diseases
iron chelation therapy.
Regular blood transfusions are a standard treatment for thalasse Deferoxamine is a liquid medicine that's given slowly under
mias. Transfusions can cause iron to build up in the blood (iron
Better treatments now allow people who have moderate and severe thalassemias to live much longer. As a result, these people
must cope with complications of these disorders that occur over
time.
PharmaMag-2013
Page 19

the skin, usually with a small portable pump used overnight. This
therapy takes time and can be mildly painful. Side effects include
problems with vision and hearing.
Deferasirox is a pill taken once daily. Side effects include headache, nausea (feeling sick to the stomach), vomiting, diarrhea, B) Possible Future Treatments
joint pain, and tiredness.
Researchers are working to find new treatments for thalassemias.
For example, it might be possible someday to insert a normal
hemoglobin gene into stem cells in bone marrow. This will allow
iii) Folic Acid Supplements
Folic acid is a B vitamin that helps build healthy red blood cells. people who have thalassemias to make their own healthy red
Your doctor may recommend folic acid supplements in addition blood cells and hemoglobin.
to treatment with blood transfusions and/or iron chelation thera- Researchers also are studying ways to trigger a person's ability to
make fetal hemoglobin after birth. This type of hemoglobin is
py.
found in fetuses and newborns. After birth, the body switches to
making adult hemoglobin. Making more fetal hemoglobin might
make up for the lack of healthy adult hemoglobin.
iv) Blood and Marrow Stem Cell Transplant
A blood and marrow stem cell transplant replaces faulty stem
cells with healthy ones from another person (a donor). Stem cells
are the cells inside bone marrow that make red blood cells and
other types of blood cells.
A stem cell transplant is the only treatment that can cure thalassemia. But only a small number of people who have severe thalassemias are able to find a good donor match and have the risky
procedure.
PharmaMag-2013
Thalassemias Prevention?
You cant prevent thalassemias because theyre inherited (passed

from parents to children through genes). However, prenatal tests
can detect these blood disorders before birth.
Family genetic studies may help find out whether people have
missing or altered hemoglobin genes that cause thalassemias. If
you know of family members who have thalassemias and you're
thinking of having children, consider talking with your doctor
and a genetic counselor. They can help determine your risk for
passing the disorder to your children.
Page 20
Microbial Limit Tests

The Microbial Limit Tests are designed to perform the qualitative
and quantitative estimations of specific viable microorganisms
present in samples. It includes tests for total viable count
(bacteria and fungi) and Escherichia coli. The most care must be
taken in performing the tests, so that microbial contamination
from the outside can be avoided. When test samples have antimicrobial activity or when they include antimicrobial substances,
these antimicrobial properties must be eliminated by dilution,
filtration, neutralization, inactivation, or other appropriate means.
The tests should be conducted for samples prepared by mixing
multiple portions randomly chosen from individual ingredients or
products. When samples are diluted with fluid medium, the tests
must be conducted quickly. Due attention must be paid to the
effective quality control and the prevention of biohazard.
Total Viable Aerobic Count
This test is to determine mesophilic bacteria and fungi which

grow under aerobic conditions. Psychrophilic, thermophilic, basophilic, and anaerobic bacteria and microorganisms which require specific ingredients for growth may give a negative result,
even if they exist in a significant number.
There are four methods for this test:
1) Membrane filtration method
2) Pour plate method
3) Spread plate method
4) Serial dilution method (most probable number method).
An appropriate method should be taken from among these four,
depending on purposes. If automated methods are comparable or
superior in sensitivity and accuracy to the methods given here,
they may be used. Different media and incubation temperature
are required for the growth of bacteria and fungi (molds and
yeasts). The serial dilution method is applicable only to bacteria.
(Image 01)
Preparation of Test Fluids
To dissolve or dilute the sample, use phosphate buffer (pH 7.2),

sodium chloridepeptone buffer solution, or fluid medium used for
the test. Unless otherwise specified, use 10 g or 10 ml of the sample. However, a different weight or volume of the sample should
be used, depending on the nature of the sample. Adjust the test
fluid to pH 6 to 8. Use the test fluid within one hour after preparation.
Fluid Samples or Soluble Solid Samples: Take 10 g or 10 ml of
the sample and mix with the buffer or fluid medium given above
to make 100 ml. Use this mixture as the test fluid. For a fluid
sample including insoluble substances, shake well just before
mixing make a homogeneous suspension. Insoluble solid samples
Take 10 g of the sample, grind to a fine powder, and suspend it in
the buffer or fluid medium given above to make 100 ml. Use this
suspension as the sample fluid. A larger volume of the buffer or
PharmaMag-2013
By Farrukh Mehmood
PharmD, R.Ph.
Microbiologist
Highnoon Laboratories Ltd.
Lahore, Pakistan
fluid medium than specified here may be used to make a suspension, depending on the nature of the sample. If necessary, a
blender may be used to disperse the insoluble particles well in the
suspension. Also, an appropriate surfactant (e.g., 0.1% w/v polysorbate 80) may be added to help dissolve the sample.
Fatty Samples: For semisolid samples and liquids consisting
mainly of lipid, take 10 g or 10 ml of the sample; emulsify the
sample in the buffer or fluid medium given above using a surfactant such as polysorbate 20 or polysorbate 80, and make to 100
ml. Use this emulsified sample as the sample fluid. If necessary,
warm at a temperature not exceeding 45C to emulsify the sample. Avoid warming for not longer than 30 minutes.
Procedure
(1) Membrane Filtration Method
This method is applied to the sample which contains antimicrobial substances. Use membrane filters of an appropriate material
with a pore size of 0.45 m or less. Filters about 50 mm across
are recommended, but other sizes may be used. Sterilize the filters, filtration apparatus, media, and other apparatus used. Usually, measure two test fluids of 10 ml each; pass each sample
through a separate filter. Dilute the pretreated test fluid if the
bacteria concentration is high, so that 10 to 100 colonies can develop per filter. After filtration, wash each filter three times or
more with an appropriate liquid such as phosphate buffer, sodium
chloride-peptone buffer, or fluid medium. The volume of the
washings should be about 100 ml each. If the filter used is not
about 50 mm in diameter, use an appropriate volume of washing,
depending on the size of the filter. If the sample includes lipid,
polysorbate 80 or an appropriate emulsifier may be added to the
washings. After filtration, for bacteria detection, place the two
filters on a plate of soybean-casein digest agar medium, and for
fungi detection, add an antibiotic to the medium and place them
on a plate of one of Sabouraud glucose agar, potato-dextrose
agar, or GP agar media. Incubate the plates at least for 5 days at
30-35C for bacteria detection and at 20-25C for fungi detection, and count the number of colonies. If counts obtained are
Page 21

considered to be reliable in shorter incubation time than 5 days,
these counts may be adopted for calculation of the viable count.
each of another three test tubes and mix to make 100-times dilutions. Third, add 1 ml of each of the 100-times dilutions to each
of the remaining three test tubes and mix to make 1,000-times
dilutions. Incubate all 12 test tubes for at least 5 days at 30 - 35
C. No microbial growth should be observed for the control test
tubes. If the determination of the result is difficult or if the result
is not reliable, take a 0.1ml fluid from each of the 9 test tubes and
place it to an agar medium or fluid medium, incubate all media
for 24 to72 hours at 30 to 35C, and check them for the absence
or presence of microbial growth. Calculate the most probable
number of microorganisms per ml or gram of the sample, using
the table given below.
(2) Pour Plate Method

Use petri dishes 9-10 cm in diameter. Use at least 2 agar media
for each dilution. Take 1 ml of the test fluid or its dilution into
each petri dish aseptically, add to each dish 15 to 20 ml of sterilized agar medium, previously melted and kept below 45C, and
mix. For bacteria detection, use soybean-casein digest agar medium and for fungi detection, use one of Sabouraud glucose agar,
potato-dextrose agar, and GP agar media, to which antibiotic has
previously been added. After the agar solidifies, incubate at least
for 5 days at 30 to 35C for bacteria detection and at 20 to 25C
for fungi detection. If a large number of colonies develop, calculate viable counts based on counts obtained from plates with not
more than 300 colonies per plate for bacteria detection and from
plates with not more than 100 colonies per plate for fungi detection. If counts are considered to be reliable in a shorter incubation time than 5 days, these counts may be adopted.
(Image 02)
(3) Spread Plate Method
Place 0.05-0.2 ml of the test fluid on the solidified and dried surface of the agar medium and spread it uniformly using a spreader. Proceed under the same conditions as for the Pour Plate Method, especially about petri dishes, agar media, incubation temperature and time, and calculation method.
The number of test tubes in which microbial growth is observed,

when the amount of the sample given
below (per test tube) is
added
0.1 g or
0.01 g or
1 mg or 1
0.1 ml
0.01 ml
l
3
3
3
3
3
2
3
3
1
3
3
0
3
2
3
3
2
2
3
2
1
3
2
0
3
1
3
3
1
2
3
1
1
3
1
0
3
0
3
3
0
2
3
0
1
3
0
0
The most probable

number of microorganisms
per gram
or ml
1100
1100
500
200
290
210
150
90
160
120
70
40
95
60
40
23
Note: When the number of test tubes showing microbial growth

is not more than two for test tubes containing 0.1 g or 0.1 ml of a
sample, the most probable number of microorganisms is possibly
100 or less per gram or ml of the sample.
(4) Serial Dilution Method (Most Probable Number Method)

Use 12 test tubes: 9 containing 9 ml of soybean-casein digest
medium each and 3 containing 10 ml of the same medium each
for control. Prepare dilutions using the 9 tubes. First, add 1 ml of
the test fluid to each of three test tubes and mix to make 10-times
dilutions. Second, add 1 ml of each of the 10-times dilutions to
PharmaMag-2013
Page 22
(Image 01)
(Image 02)
PharmaMag-2013
Page 23
Syringomyelia
Syringomyelia is the formation of fluid filled cavity or cyst

(syrinx) within the spinal cord that may enlarge with time causing damage to the spinal cord along with pain, stiffness and
weakness in shoulder, neck, back and legs.
By Amna Hafeez
PharmD
Signs And Symptoms
Other symptoms include loss of the ability feeling to extremes

hot and cold especially in hand, headache, facial pain and numbness, spinal curvature and bowel and bladder function problem.
Signs and symptoms may develop with time with, although sudden onset may occur with coughing and straining followed by
weakness, progressive loss in sensation and weakness in arms
and legs.
Complications
Complications include scoliosis, motor movements, chronic pain removal of tumor is necessary.
and Horner syndrome. If condition not treated in time it may re- Drainage of cavity (drainage just stop progression, have no concern with the elimination of symptoms associated with syringosult in injury to spinal cord.
myelia) using drainage tubes, catheter and valve .This system is
also called shunt.
Causes
Physical therapy management depends upon severity and impact
Chiari formation (congenital abnormality of the brain, in of the disease. Neurological examination clears that at which
which part of brain tissue may protrude into the Spinal cord). level the syrinx occur. Physical therapy techniques include following:
Spinal cord tumor
RoM (range of motion) stretching and mobilization of neck
Spinal cord injuries
and upper limb.
Inflammation surrounding spinal cord
Muscle strength
Meningitis
Neck stability
Arachnoiditis
Balance
Tethered spinal cord syndrome
Copying
Spinal scar tissue
Occupational therapy
Diagnosis
Syringomyelia is diagnosed by number of ways.

Magnetic resonance imaging of spine and spinal cord ( help
in beginning stage diagnosis).
Electromyography that measures the muscle weakness
Cerebrospinal fluid pressure level and analysis of cerebrospinal fluid by performing lumbar puncture
Computed axial tomography that scan patient head to detect
any tumor and hydrocephalus
Myelogarm
Treatment
Surgery is the only treatment for syrigomyelia.The main purpose of surgery is to provide more space for the cerebellum at the
base of skull and cervical spine to treat Chiari formation. Sometimes additional operations are necessary for successful eradication of syringomyelia.
Congenital syringomyelia may require piece of cervical vertebrae
at the site of cavity formation to be removed.
If syringomyelia is due to tumor, that result in obstruction then
PharmaMag-2013
Medication
To alleviate the pain during syringomyelia single or combi
nation of medicines are used; but is not concerned with the

removal of syringomyelia.
Analgesics are the best ever option to treat syringomyelia. In
one pain management plan, an around-the-clock opiate such
as fentanyl patches or Oxycontin are used in conjunction
with a fast-acting opiate.
For classical back pain weak or strong opioids are used such
as Tramdol along with medications that relives neuropathic
pain symptoms shooting and stabbing pain (neurontin).
Cortisteroids, such as prednisolone, or non-steroidal antiinflammatory drugs may relieve the symptoms but not the
deterioration. Long term use of these drugs is not advised.
Anticonvulsants, such as gabapentin have been successful in
some more severe cases, but they may be very expensive. Pregabalin, amitriptyline and oral opioids (pethidine or
methadone) are alternatives.
Methylsulfonylmethane
(MSM) is recommended by some veterinary neurologists as
Page 24
Syringomyelia
a dietary supplement.
Drugs which reduce the production of cerebrospinal fluid,
including proton pump inhibitors such as omeprazole, and
the diuretic, furosemide (Lasix), and spironolactone, may be
useful,but clinical data on their use and effectiveness is lacking. Carbonic anhydrase inhibitors, such as acetazolamide
also serve to decrease the flow of cerebrospinal fluid, but
their adverse side effects of abdominal pain, lethargy, and
weakness limit long term use.
Life Style Changes
Playing high impact sports such as football.

Straining during bowel movement
Excessive coughing
Sky diving
Chinese Art Of Healing
Avoid such activities that may worse the symptoms of syringo- Qigong is a traditional form of Chinese energy excise and healmyelia such as
ing art for the body and mind. Qigong is ideal for reestablishing balance between body and mind and for helping to
heal people who are struggling with chronic degenerative conditions such as paralysis, diabetes, and syringomyelia.
PharmaMag-2013
Page 25
Living With Liver Cancer...

About The Liver
The liver is the largest organ in the digestive system and second
largest organ in the human body. It is a blood-rich, wedge-shaped
gland located in the right side of the abdomen, below the diaphragm and near the colon, right kidney, duodenum, gallbladder
and stomach.
By Mehrish Memon
PharmD
Location And Anatomy Of The Liver
What Is Liver Cancer

Overview
Liver cancer is characterized by the growth or spread of abnormal or malignant cells in the liver tissue.
Liver cancer (hepatocellular carcinoma) is a cancer from the liver. It is also known as primary liver cancer or hepatoma. The
liver is made up of different cell types (for example, bile ducts,
blood vessels, and fat-storing cells). However, liver cells and is
called hepatocellular cancer or carcinoma.
Risk Factor
Important Functions of the Liver
The primary function of liver is to filter what an individual eats,

drinks, breathes and gets on their skins. The liver also carries out
a variety of other important functions including:
PRODUCTION: the liver in involve in building proteins that are important for cell growth.
STORAGE: The liver acts as storage site for carbohydrates, iron and vitamins until the body
needs them. The liver stores and releases blood
sugar or glucose into the bloodstream to provide
energy for the body to function.
BILE SECRETION: the liver produces bile, a substance that helps the digestion and absorption of
food assists in digestion. Ile is a yellowishbrown or green liquid stored in the gall bladder.
ELIMINATION: finally, the liver breaks down substances like alcohol, drug and waste products
PharmaMag-2013
A major risk factor for the development of HCC is cirrhosis/

cirrhosis is an ongoing liver disease that involves the repeated
breakdown and repair of the liver tissue, eventually leading to a
loss of liver functions. Several different factors can lead to a cirrhosis, most common are:
Page 26
Symptoms May Include

HBV)hepatitis B virus(
ore thanm) %05 (
HCV)hepatitis C virus(
Weight loss, lack of appetite, itching of the skin, unususal tiredness, feeling very full after a small meal, a hard lump on the
right side just below the rib cage, jaundice, ascites, nausea.
What Is Staging System, And What Does It Have

To Do With Disease
There are a no of different staging system for liver cancer.
excessive alcohol
consumption
seisead liver yfatt
icoholalcnon
aflatoxicosis
diabetes
Sign & Symptoms:
Staging is important, because

it helps doctors determine
which type of treatment to use
in individual patients.
PharmaMag-2013
Page 27

Doctors often use the categories below to describe a person's
liver cancer.
Localized resectable - The cancer is found only in the liver and
the entire tumor can be removed by surgery.
Localized and locally advanced unresectable - The cancer is
found only in the liver and it has not spread. However, it cannot
be removed (resected) by surgery. This might be because you
have cirrhosis and you would not have enough healthy liver tissue left after surgery. Your cancer might also be localized unresectable if it has spread throughout the liver or it is too close to
where the liver meets the main arteries, and bile duct.
Advanced - The cancer has spread throughout most of the liv-
er or it is has spread to the lymph nodes or other organs. The

tumor cannot be removed by surgery.
Recurrent recurrent disease is cancer that has come backeither to the liver or to another part of the body-after initial treatment or surgery.
Choice Of Therapy For Liver Cancer

Care is frequently co ordinated through a multidisciplinary
group of physician specializing in hepatoma. This team of specialists usually includes surgeons, oncologists, radiologists, gastroenterologist, radiation therapists and pathologlists.
The best treatment for primary liver cancer is to remove surgically, removing the part of liver containing the tumor may result in a
cure and long term survival.
1: Surgical Resection (Removal)

Liver Transplant
At what stage are most people with liver cancer Diagnosed?

It's not unusual for liver cancer to be diagnosed at more advance
stages, because many people don't have unususal symptoms in
the early stages of the disease. The majority of the patients are
diagnosed at more advanced stages.
Screening And Diagnosis
The goals of Screenig are to diagnose HCC earlier and to improve prognosis. With the incidence of HCC on the
rise ,screening is important for individuals at risk.
Hepatocellular Carcinoma (HCC)
Liver cancer may be discovered in a routine checkup if the doctor

feeks hard lumps in the abdomen or by imaging examinations. To
confirm a diagnosis of liver cancer, doctor may use the following :
BLOOD TEST , including:

complete blood count,
alpha-fetoproteins
tumor marker test.
ULTRASOUND, COMPUTED TOMOGRAPHY, MRI,
BIOPSY.
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Page 28
2. A similar technique, using

microscopic radioactive particles
instead of chemotherapy injected
into the blood vessels, is called
radioembolization or selective internal radiation therapy (SIRT).
This uses radioactive yttrium attached to glass microspheres and
may be as effective as chemoembolization for small and multiple
tumors.
3. Radiation therapy uses highdose energy like X-rays aimed at
a small part of the body and can
frequently destroy cancer cells.
The liver, though, may be more
sensitive to the radiation than the
tumor is, so standard radiation is
seldom used. However, there are
new specially focused techniques
called conformal or stereotactic
radiation that may be useful in
certain cases.
PharmaMag-2013
4. Chemotherapy refers to drugs

that are usually given by pill or
by vein. They are designed to
work throughout the entire body,
not just the liver, so tumors outside the liver will be treated as
well. Recently, agents that directly attack the microscopic blood
vessels in the tumor, called antiangiogenic drugs, have proven to
be very helpful. Sorafenib, the
first drug to be approved specifically for hepatoma, was introduced in 2007. Sorafenib is a pill
that slows the growth of the cancer and helps keep many patients
alive longer.
Page 29
Mismanagement of Hypertensive Emergency in a

Patient Suffering from Recurrent Stroke
Abstract
A 66-year-old man was presented to emergency department of

Hospital Pulau Pinang with complaints of general weakness, pain
in lower limb, history of known cerebrovascular accident and
medication history of Metroprolol, Diltiazem, Hydrochlorothiazide, Ranitidine and Gemfibrozil. Patient blood pressure and
heart rate on admission to the hospital were 180/120 mm Hg and
40 beats per minute respectively. Metoprolol was withheld and
therapy was started with IV Atropine stat. Patient was referred to
medical ward. On the same day blood pressure reached to
200/130 mm Hg. To treat hypertensive emergency immediate
release (IR) sublingual Nifedipine and intravenous Isosorbide
dinitrae were added to the patients past medication of Diltiazem,
Hydrochlorothiazide, Ranitidine and Gemfibrozil, which reduced
BP to 150/90 mm Hg. The main issue in the present case was
inappropriate use of IR Nifedipine and rapid and too much reduction of BP in hypertensive emergency in patient suffering from
recurrent stroke. The discrepancy between evidence-based recommendations and real-time practice in the clinical settings is not
uncommon. The use of IR Nifedipine and too much and too rapid
reduction of BP should be discouraged to avoid uncontrolled BP
reduction and precipitation of ischemic events.
By Muhammad Qamar
Lecturer of Clinical Pharmacy
School of Pharmacy,
Management and Science University
Malaysia
controlled hypertension. Metoprolol was withheld and therapy

began with intra venous (IV) Atropine, along with patients past
medications of Diltiazem, Hydrochlorothiazide, Ranitidine,
Gemfibrozil. The patient was referred to medical ward. On the
same day after ECG report, the attending medical doctor at medical ward concluded that the patient is suspected of bradycardia
secondary to B-blockers and recurrent stroke. At the same time
Key Words
very high blood pressure (200/130 mm Hg) was noted. To treat
Guidelines, Hypertensive emergency, Nifedipine, Stroke.
hypertensive emergency immediate release (IR) sublingual Nifedipine and intravenous Isosorbide dinitrae were added to the paIntroduction
tients past medication, which resulted in too rapid and too much
Hypertensive emergency is a form of severe hypertension charac- decrease in patients BP to a level of 150/90 mm Hg.
terized by a severe elevation in blood pressure (> 180/120 mm
Hg) complicated by evidence of impending or progressive target
organ dysfunction. Examples of target organ dysfunction include
coronary ischemia, disordered cerebral function, cerebrovascular Discussion
events, pulmonary edema, and renal failure. Prompt recognition Despite the availability and wide dissemination of guidelines
and early treatment of hypertensive emergency is crucial in pre- which document the best available practices for management of
venting or halting progressive target organ damage [1]. Accord- hypertension, deviation from guidelines in clinical practice is not
ing to Malaysian Clinical Practice Guidelines on management of uncommon [7]. According to CPG (2008) BP control in hyperhypertension (CPG 2008) BP of the emergency hypertensive tensive emergency is best achieved with parenteral drugs [1].
patient should be reduced rapidly by 25% over a period of 3 to 12 Malaysian guidelines treatment options for hypertensive emerhours but not lower than 160/90 mm Hg, because too rapid re- gency are given in Table 1. In past IR Nifedipine due to its fast
duction of BP (within minutes to hours) may precipitate ischemic acting and ease of administration was the drug of choice for treatevents [1]. Oral or sublingual drugs with rapid onset of action ing hypertensive crises [2]. But later on its use was found to be
like immediate release (IR) Nifedipine can result in an uncon- associated with life-threatening adverse effects such as severe
trolled BP reduction and may precipitate ischemic events; there- hypotension, cerebral ischemia, acute myocardial infarction, refore its use is discouraged in the treatment of hypertensive emer- flex tachycardia, conduction abnormalities, and even death [3-5,
8, 9]. Nifedipine causes BP lowering through peripheral vasodigency [1-6].
lation. The use of IR Nifedipine in hypertensive emergency can
be life threatening particularly in patients suffering from cerebral
Case Description
ischemia and due to this reason its use is discouraged by hyperA 66-year-old man who fell in bathroom was presented to emer- tension management guidelines [1, 6]. In the present case the
gency department of Hospital Pulau Pinang, Malaysia with gen- patient was suffering from recurrent stroke; a condition in which
eral weakness, pain in lower limb, mild shortness of breath cerebral perfusion is directly proportional to the systematic BP.
(SOB), history of known cerebrovascular accident (CVA) and Too rapid and too much BP reduction in such patients as obmedication history of Metroprolol, Diltiazem, Hydrochlorothia- served in the present case can lower cerebral perfusion to the
zide, Ranitidine and Gemfibrozil. On examination patient had BP ischemic area and thus worsen the target organ damage [8].
reading of 180/120 mm Hg, with heart rate of 40 beats per minute. The attending doctor at emergency department made the
impression of sinus bradycardia, electrolyte imbalance and un
PharmaMag-2013
Page 30
Mismanagement of Hypertensive Emergency in a

Patient Suffering from Recurrent Stroke
Conclusion
To avoid life threatening adverse effects such as severe hypotension, cerebral ischemia, acute myocardial infarction, cardiac arrhythmias, and death, the use of IR Nifedipine which causes too
rapid and too much reduction in BP should be discouraged in
hypertensive emergency. The present case report shows doctors
non adherence to guidelines recommendations while managing
hypertensive emergency which can pose a serious threats to patients lives. Remedial measures like continuing medical education and availability of clinical pharmacist to participate in collaborative practices can line up the doctors practices in compliance with guidelines.
Conflict Of Interest
3. Wachter, R.M. Symptomatic hypotension induced by nifedipine in the

acute treatment of severe hypertension. Arch Intern Med 1987; 147(3):
556-558.
4. OMailia, J.J., G.E. Sander, and T.D. Giles. Nifedipine-associated
myocardial ischemia or infarction in the treatment of hypertensive urgencies. Ann Internal Medicine 1987; 107(2): 185-186.
5. Peters, F.P.J., C. Zwaan, and L. Kho. Prolonged QT interval and ventricular fi brillation after treatment with sublingual nifedipine for malignant hypertension. Arch Intern Med 1997; 157(22): 2665-2666
The author declare no conflict of interest, in part or whole. No

6. Chobanian, A.V., et al. Seventh report of the Joint National Commitfunding was received for this study.
tee on prevention, detection, evaluation, and treatment of high blood

pressure. Hypertension, 2003; 42(6): 1206-1252.
Acknowledgement
We thank all the doctors and record keeping staff of Hospital 7. Borzecki, A.M., S.A. Oliveria, and D.R. Berlowitz. Barriers to hypertension control. Am Heart J 2005; 149(5):785-794.
Pulau Pinang, Malaysia for helping us in collecting the data.
8. Jung, S.Y., et al. Short-acting nifedipine and risk of stroke in elderly
hypertensive patients. Neurology 2011; 77(13):1229-1234.
References
1. Malaysian Hypertension Guideline Working Group. Clinical Practice

Guidelines on Management of Hypertension, 3rd ed. 2008. MOH/P/ 9. Schwartz, M., et al. Oral nifedipine in the treatment of hypertensive
PAK/156.08 (GU).
urgency: cerebrovascular accident following
2. Mansoor, A.F. and L. von Hagel Keefer. The dangers of immediaterelease nifedipine for hypertensive crises. P & T 2002; 27(7): 362-365.
PharmaMag-2013
Page 31
The "New" Health Miracles: Probiotics

What are Probiotics?
The Food and Agriculture Organization of the United Nations

(FAO)
defines
probiotics
as
"live microorganisms, which, when administered in adequate
amounts, confer a health benefit on the host."
By Iqra Mansha
PharmD
Lahore College for Women
University
Pakistan
live bacteria in it?
It's all about balance.

Our digestive system normally has what we would call "good"
bacteria and "bad" bacteria. Maintaining the correct balance between the "good" bacteria and the "bad" bacteria is necessary for
optimal health, which is goal of Probiotics.
Gastro-Intestinal Tract
Probiotics are bacteria that help maintain the natural balance of
organisms (micro-flora) in the intestines. The largest group of
probiotic bacteria in the intestine is lactic acid bacteria, of which
Lactobacillus acidophilus, found in yogurt with live cultures, is
the best known. Yeast is also a probiotic substance.
Within your gastrointestinal tract, there is intestinal micro-flora

or micro-biota. The complex ecosystem of GIT contains over
400 bacterial species. Small amounts can be found in your stomach and small intestines, but the majority is found in your colon.
The intestinal micro-flora aid in digestion, synthesize vitamins
and nutrients, metabolize some medications, support the development and functioning of the gut, and enhance the immune system.
Root of the word

comes from Greek
Pro: means
"Promoting"
Biotic: means
"Life."
Probiotics are also available as dietary supplements. They are

actually alive bacteria. Most people think of antibiotics and antibacterial products when you mention bacteria. Both of those kill
bacteria so why would you want to consume anything that has
PharmaMag-2013
Page 32

Probiotics may seem new to the food and supplement industry,
but they have been with us from our first breath.
Help prevent infections in the digestive tract.

Help control immune response (inflammation), as
in inflammatory bowel disease (IBD).
Probiotics are being studied for benefits in colon cancer, skin infections, and irritable bowel syndrome (IBS).
1. The first is the role that they play in our digestive tract.
The idea is not to kill off all of the bad bacteria. Our body does
have a need for the bad ones and the good ones. The problem is
when the balance is shifted to have more bad than good. An imbalance has been associated with diarrhea, urinary tract infections, muscle pain, and fatigue. Probiotics take in GIT, the things
that our body needs (nutrients from food and water) and absorbs
and helps deliver them to the cells where they are needed.
2. The other way that probiotics help is the impact

that they have on our immune system.
Our immune system is our protection against germs. When it

What are probiotics used for?
doesn't function properly, we can suffer from allergic reactions,
Many people use probiotics to prevent diarrhea, gas, and autoimmune disorders (for example, ulcerative colitis, Crohn's
cramping caused by antibiotics. Antibiotics kill

"good" (beneficial) bacteria along with the bacteria that
cause illness. A decrease in beneficial bacteria may lead to
digestive problems. Taking probiotics may help replace the
lost beneficial bacteria. This can help prevent diarrhea.
A decrease in beneficial bacteria may also lead to other infections, such as vaginal yeast and urinary tract infections,
and symptoms such as diarrhea from intestinal illnesses.
Probiotics may also be used to:

Help with other causes of diarrhea.
disease, and rheumatoid arthritis), and infections (for example,

infectious diarrhea, Helicobacter pylori, skin infections, and vaginal infections). By maintaining the correct balance from birth,
the hope would be to prevent these ailments. Our immune system
can benefit anytime that balanced is restored, so it's never too
late.
What are the different types of probiotics?
Up until the 1960s, the gut micro-flora that they were able to
identify was clostridia, lactobacilli, enterococci, and Escherichia
coli. Since then, innovative techniques have discovered many
more bacteria.
1) Lactobacillus
There are more than 50 species of lactobacilli. They are naturally

found in the digestive, urinary, and genital systems. Foods that
are fermented, like yogurt, and dietary supplements also contain
PharmaMag-2013
Page 33

these bacteria. Lacto bacillus has been used for treating and preventing a wide variety of diseases and conditions.
Some of the lactobacilli found in foods and supplements are:
Lactobacillus acidophilus,
Lactobacillus blugaricus,
Lactobacillus rhamnosus GG,
Lactobacillus plantarium,
Lactobacillus reuteri,
Lactobacillus salivarius,
Lactobacillus casei,
Lactobacillus johnsonii, and
Lactobacillus gasseri.
2) Bifidobacteria
There are approximately 30 species of Bifidobacteria. They make

up approximately 90% of the healthy bacteria in the colon. They
appear in the intestinal tract within days of birth, especially
in breastfed infants.Some of the Bifidobacteria used as probiotics
are
Bifodbacterium bifidum,
Bifodbacterium lactis,
Bifodbacterium longum,
Bifodbacterium breve,
Bifodbacterium infantis,
Bifodbacterium thermophilum, and
Bifodbacterium pseudolongum.
3) Streptococcus thermophilus
This produces large quantities of the enzyme lactase, making it

effective, according to some reports, in the prevention of lactose
intolerance.
Supplementation With A Good Probiotic Is Mandatory To Raise Your Baseline Of Health And
Strengthen Your Immune System.
Are probiotics safe?
Most probiotics are like what is already in a person's digestive

system. Some probiotics have been used for a very long time
throughout history, such as in fermented foods and cultured milk
products. These don't appear to cause illness. But when you first
start using a probiotic supplement, there is a chance that you will
precipitate a die-off of bad bacteria in your intestinal tract. This
can lead to gas, stomach rumblings, and cramping for up to three
weeks.
Conclusion:
There can be no true health or recovery from disease unless you

have colonies of over 100 trillion beneficial microorganisms
flourishing in your intestinal tract, from your mouth to your anus,
aiding in digestion, absorption, the production of significant
amounts of vitamins and enzymes, and working to crowd out all
harmful bacteria -- allowing them no place to gain a foothold.
PharmaMag-2013
Page 34
Indications, Contraindications, Precautions, and

Counseling Parameters of Patients with Coronary
Atherosclerosis and Hepatitis
Anti lipid therapy
01. Drug: Statins (Simvastatin, Ator vastatin, Lovastatin)

Introduction:
Statins are inhibitors of HMG-CoA reductase (a liver enzyme) an
enzyme involved in cholesterol synthesis.*(BNF 53)
By Azzah Khadim; Mariam Ashraf
Indication:
PharmD (Final Prof)
It is used in prevention of CV events in patient with atheroscleroUniversity College of Pharmacy
sis, CVD or diabetes mellitus. *(BNF3)
Side Effects:
Punjab University
Long term use of statins may have two main side effects
Lahore
Muscle pain
Pakistan
Hepatotoxicity
Injury from statins is mainly hepatocellular (with elevation in
AST and ALT) hepatotoxicity is dose related, with higher statin
doses associated with a higher rate of liver enzyme abnormalities.* (Roger Walker)
Conclusion:
04. Drug: Fibr ates (Cipr ofibr ate, Benzafibr ate, FenoStatins are absolutely contraindicated in Active/Chronic liver
fibrate )
disease.
Introduction:
(Statins and Liver disease www.cardiolipid.com)*
Bind to peroxisome proliferation activated receptor alpha
(PPAR-alpha) on hepatocytes which leads to changes in expres(See Image 01)
sion of genes in lipoprotein metabolism. In short it decreases
total cholesterol and LDL-C but increases HDL-C.
02. Drug: Bile acid sequestr ants / ion exchange resins /
bile acid binding agents (cholestyramine)
Indication:
Introductions:
May reduce risk of CAD in patients with low HDL-C and inThey bind with bile acids in the intestine and prevent reabsorp- creased triglycerides.*(BNF 53)
tion and produce an insoluble complex that is excreted in feces. Contraindications:
This depletion of bile acids results in an increase in hepatic syn- It is contraindicated in severe hepatic and renal impairment. *
thesis of bile acids from cholesterol. In short it decreases total (BNF 53)
cholesterol and increases triglycerides.*(Roger Walker)
Conclusion:
Indications:
Fibrates are not drug of choice for this patient.
Hyperlipidimias
Fenofibrate is contraindicated in gall-bladder disease.
Contraindication:
Gemfibrozil is contraindicated in severe hepatic impairment.*
It is in biliary obstruction. *(BNF 53)
(BNF 53 )
Conclusion:
Cholestyramine is also excluded from patients therapy
(See Image 03)
(See Image 02)
03. Drug: Cholester ol absor ption inhibitor s (Ezetimibe)
Introduction:
It interacts with putative cholesterol transporter in the intestinal
brush border membrane and thereby blocks cholesterol re absorption from GIT overall it decreases LDL-C (15-20%)
Small increase in HDL-Cand decrease triglycerides.
(Triglycerides).*(Skyscape)
Indication:
Adjunct to dietary measures and statins in primary hypercholesterolemia.*(BNF 53)
Contraindication:
Avoid in moderate and severe hepatic impairment because it may
accumulate.* (BNF)
Conclusion:
Ezetimibe is contraindicated in this patient.
PharmaMag-2013
05. Drug: Nicotinic acid / Niacin

Introduction:
It decreases LDL-C, TC, and VLDL-C and increases HDL-C.*
(Roger Walker)
Indication:
Arterial bleeding active peptic ulcer disease and breast feeding.*
(BNF53)
Precautions:
Hepatic impairment, renal impairment may cause hepatic toxicity
at high dose. Perform LFT before and during treatment.*(BNF
53)
Counseling parameters:
Assess for signs of jaundice, light colour stool and faint feeling.*
Monitor LFT s and vital signs. *
*Advice patient to adhere to prescribed regimen.
*Tell patient to take medication with food.
Exercise.*
*Tell patient to take low fat diet.
Page 35

Conclusion:
Niacin can be given to this patient with clinical monitoring.
06. Drug: Omega 3 fatty acid compounds
Omega -3 ethyl esters
Omega -3 marine triglycerides
Indication:
Use to reduce triglycerides as an alternative to fibrates.
Cautions:
Omega -3 ethyl esters are/ maybe used with caution in hepatic
impairment.*(BNF 53)
Conclusion:
Omega -3 marine triglycerides can be given to this patient and
Omega -3 ethyl esters are given with caution.
Caution:
Monitor signs of bleeding
Contraindications:
Active peptic ulcer and other bleeding disorder, breast feeding.*
(BNF 53)
Conclusion:
These agents can be given to this patient.
09. Drug: ACEI

Indications:
Reduce serious vasculature events in patients with atherosclerosis
07. Drug: Ispaghul Husk (soluble fibr e)
and normal systolic function.
Indication:
Precautions:
Decreases lipid level and converts cholesterol to bile acid.*(BNF It can be given to the patient except Captopril need some caution
53)
in patient with liver disease.
Conclusion:
Drug: Beta adr ener gic r eceptor blocker s
Indication:
It is also given in order to lower cholesterol level.
Decrease progression and cause regression of plaque. It can also
08. Drug: Antiplatelet agents (Aspir in, Clopidogr el)
be given to patient.
Indication:
Clopidogrel approved for secondary prevention of vascular
events in patients with atherosclerosis.
Aspirin clearly reduces risk of atherosclerotic cardiac disorder
(Image 01)
PharmaMag-2013
Page 36

(Image 02)
(Image 03)
PharmaMag-2013
Page 37
Pregnancy A Crucial Stage for Women That Must

Need Special Care
Introduction
Pregnancy is the fertilization and development of one or more

offspring, known as an embryo or fetus, in a woman's uterus. In a
pregnancy, there can be multiple gestations, as in the case of
twins or triplets. Childbirth usually occurs about 38 weeks after
By Jony Mallik
conception; in women who have a menstrual cycle length of four
B.Pharm(Hons.); M.Pharm
weeks, this is approximately 40 weeks from the start of the last
Southern University, Bangladesh
normal menstrual period (LNMP). Human pregnancy is the most
studied of all mammalian pregnancies. Conception can be
Priyanka Das
achieved through sexual intercourse or assisted reproductive
B.Pharm(Hons.)
technology. An embryo is the developing offspring during the
first 8 weeks following conception, and subsequently the term
BGC Trust University, Bangladesh
fetus is used until birth.This document provides an overview of
pregnancy; the reproductive process basically play the vital role
to new baby is conceived, incubated and ultimately born into the
world. Many facets of pregnancy are covered starting with the
preparation and planning stages, and moving through conception, being if all goes well. Ovulation is said to occur at the moment
fetal development, labor and delivery, and post-partum (or post- the egg and sperm combine.
birth) stages. The document describes normal, uncomplicated
pregnancy in some detail, and also contains information concerning more difficult pregnancies, including pregnancies for women
with chronic illnesses and other health complications.
Figure: Male sperm running for ovum
Initiation with Ovulation
A pregnancy occurs when reproductive cells from a man and a

woman's body become combined inside a woman's uterus. The
normal way that this occurs is through sexual intercourse, where
the man's penis enters the woman's vagina and ejaculates sperm
(the male reproductive cells) into the vagina during the process
of orgasm or sexual climax. Microscopic though they are, the
sperm are able to move around within the vagina, and make their
way through the cervix and into the uterus where, if the timing is
just right, a female ovum or egg (the female reproductive cell) is
waiting. Sexually mature adult females ovulate (produce eggs)
once each month as a part of their normal menstrual cycle. The
sperm compete to penetrate the outer membrane or covering of
the egg which seals off permanently once a single sperm makes
its way inside. The new sperm and egg combination next exchange genetic material to form a unique blueprint for a new
human being, producing a fertilized egg that will later attach itself to the wall of the uterus and start growing into a new human
PharmaMag-2013
Pregnancy Symptoms Early Signs of Pregnancy

Pregnancy symptoms differ from woman to woman and pregnancy to pregnancy; however, one of the most significant pregnancy
symptoms is a delayed or missed period. Understanding the signs
and symptoms of pregnancy is important because each symptom
may be related to something other than pregnancy. You may experience signs or symptoms of pregnancy within a week of conception. However, it is possible you may not experience any
symptoms for a few weeks. Symptoms to watch for early on include a missed period, headaches, tender breasts, nausea and
Page 38

Need Special Care
lower backaches. If you have been sexually active and are experiencing any of these symptoms, it is important to take a pregnancy
test
Spotting or Light Bleeding:
Stages of Pregnancy
Implantation bleeding can be one of the earliest pregnancy symptoms. About 6-12 days after conception, the embryo implants The First Trimester (Weeks 112)
itself into the uterine wall. Some women will experience spotting The first trimester of pregnancy lasts from conception until 12
as well as some cramping.
weeks gestation (pregnancy length). Women usually dont realize
they are pregnant until at least two weeks into the first trimester,
Delay/Difference in Menstruation:
when they miss their period. During the first trimester, your
A delayed or missed period is the most common pregnancy growing baby is developing at an amazing rate.
symptom leading a woman to test for pregnancy. When you become pregnant, your next period should be missed. Many women Some important developments that occur during
can bleed while they are pregnant, but typically the bleeding will this stage include:
be shorter or lighter than a normal period.
The development of the placenta and umbilical cord. These
structures are important for bringing nutrients from the
Swollen/Tender Breasts:
mother to the fetus, and for removing waste products from
the fetus back to the mother's body.
A swollen or tender breast is a pregnancy symptom which may
begin as early as 1-2 weeks after conception. Women may notice The development of the amniotic sac, a fluid-filled membrane that cushions the developing fetus.
changes in their breasts; they may be tender to the touch, sore, or
swollen.
The development of all major organs. The heart begins to
beat on or around the 25th day after conception.
Fatigue/Tiredness:
The development of the neural tube, which goes on to form
Feeling fatigued or more tired is a pregnancy symptom which
the brain and spinal cord.
can also start as early as the first week after conception.
The development of limb buds, which are the beginnings of
arms and legs.
Nausea/Morning Sickness:
This well known pregnancy symptom will often show up be- The development of fingers, toes, ears, ankles, wrists, and
eyelids. By the end of the first trimester the fetus will have
tween 2-8 weeks after conception. Some women are fortunate to
finger and toenails and will have buds in its mouth area
not deal with morning sickness at all, while others will feel nauthat will go on to become baby teeth.
seous throughout most of their pregnancy.
Backaches:
The Second Trimester (Weeks 1328)
Lower backaches may be a symptom that occurs early in preg- For many women, the middle part of pregnancy (the second trinancy; however, it is common to experience a dull backache mester) is the most comfortable pregnant period. The second
trimester is a good time to prepare yourself and your home for
throughout pregnancy.
the arrival of the new baby. This is the time to begin preparing a
nursery or other space for the baby, to learn about breast feeding,
Headaches:
and to study books about early childcare.
The sudden rise of hormones in your body can cause you to have Development: The second trimester marks a period during
headaches early in pregnancy.
which the developing fetus becomes active, and begins to move,
kick and swallow. Around the fifth month of pregnancy, the fetus
Frequent Urination:
gains the ability to turn from side to side or head over heels. It is
Around 6-8 weeks after conception, you may find yourself mak- usually around this point in the pregnancy (between the 18th and
ing a few extra trips to the bathroom.
22nd weeks) that most women experience "quickening", or the
ability to feel fetal movement. It is also during this stage that the
Food Cravings or Food Aversions:
fetus begins to sleep at regular intervals. By the end of the second
While you may not have a strong desire to eat pickles and ice trimester the fetus is around 8 to 12 inches long and weighs up to
cream, many women will feel cravings for certain foods when 1 pound.
they are pregnant. This can last throughout your entire pregnancy. Some women develop adversions to certain types of food The Third Trimester (Weeks 2940)
early in pregnancy and this too can last for the next 9 months.
The final stage of pregnancy, weeks 29 through 40, is often
PharmaMag-2013
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Need Special Care
Prenatal Care
Prenatal care (medical care delivered before you give birth) is

important for the health of both mother and baby. This medical
care can begin before you are actually pregnant. However, it really must begin as soon as you know you are pregnant in order to
help insure that you have a healthy pregnancy. During your first
prenatal care visit, your doctor will gather information about
your disease history, personal habits (alcohol and drug use, exercise habits, the type of work that you do, etc.), family history (of
multiple births, diseases, complicated pregnancy in close relatives, etc.), and any previous pregnancies, miscarriages, and/or
abortions you may have had. It is also important that you share
any complications that you may have experienced during previous pregnancies. As part of the initial exam, your doctor may
perform an ultrasound test, and or blood tests. A pelvic exam is
also sometimes performed.
Universal Precautions for Every Pregnancy
Caffeine. Studies have shown that large amounts of caf-
feine can cause birth defects or premature birth. It is recommended that pregnant women limit their intake of caffeinated beverages to 1 or 2 per day, or that they avoid caffeine
altogether.
Cigarettes, Drugs, and Alcohol. Use of Tobacco
products decreases blood flow to the developing baby, decreasing the amount of oxygen the baby receives. The toxic
effects of tobacco smoke can lead to low birth weight, miscarriage or stillbirth, and increased risk of cerebral palsy,
mental retardation, and other serious problems summarized
here.
Use of Alcohol and many illegal drugs including Marijuana,
Cocaine, Heroin, PCP, LSD, Ketamine, Esctasy, Various
glues and solvents, and Methamphetamine can cause serious
issues for the developing baby including Fetal Alcohol Syndrome (FAS), brain damage, mental retardation and other
growth and development problems which are summarized
here.
Certain medications. Certain medications, both prescription and over-the-counter, can be harmful to your developing fetus. For instance, Ibuprofen may harm your fetus.
Propranolol may cause premature labor due to uterine contraction. You should alert your doctor/pharmacist of all the
medications you are taking (or plan to take) so that he or she
can advise you as to whether or not use of those medicines
during pregnancy will be safe.
Cat Feces. The disease Toxoplasmosis is carried in cat
feces (poop), and may very likely kill your developing fetus
should you contract it. For this reason, pregnant women
should not directly handle cat feces. If you cannot avoid
changing your cats litter box even though you are pregnant,
be sure to wear rubber gloves while scooping and handling
material. Carefully wash your hands immediately afterward.
Hot Tubs. The use of hot tubs during pregnancy has been
linked to increased risk of miscarriage.
Everything you eat, smoke, drink or otherwise ingest while pregnant affects not only your body but also the developing body of
your baby. Do not assume that because you feel fine eating,
drinking or smoking something that this something is also
healthy for your baby. Your baby's developing body is far more
fragile than yours. Your baby's dividing and growing cells contain fragile genetic material that can be poisoned by various sub-
stances that you wouldn't think twice about eating. Should such
poisoning occur, your baby may develop abnormally and be born
with birth defects, mental retardation, poor growth or other substantial undesirable complications.
Pregnant women should avoid certain foods and substances because of the way those foods and substances can negatively affect developing babies. The following list provides an overview
of the types of things that can be dangerous during pregnancy.
Depending on your particular pregnancy and history of complications or health concerns, however, there may be additional things
that you need to avoid. Be sure to talk to your doctor about what
you should avoid so as to best keep yourself and your baby
healthy.
Certain Foods. Pregnant women should not eat:
raw shellfish
raw fish
raw meat
The above restrictions on what a pregnant woman can eat, ingest
or do can feel overwhelming, particularly if you haven't already
unprocessed, unpasteurized (raw) or aged cheese
been living a healthy lifestyle. You may need to give up some
unprocessed or unpasteurized (raw) dairy products
unhealthy habits. The most important thing you can do to ensure
that you will have a healthy baby is to make smart decisions that
These foods can be contaminated with infection-causing bacteria will keep you healthy.
that can cause miscarriage.
Pregnant women should also avoid consuming some ocean fish
(such as tuna, salmon, shark, swordfish, tilefish and mackerel)
whether or not such fish are cooked, because those fish are likely
to contain dangerously high levels of mercury, a heavy metal that
is associated with neurological and brain defects.
PharmaMag-2013
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Need Special Care
marked by excited expectation of the babys arrival. At this
stage, it is a good idea to have your hospital overnight bag
packed and ready to go.
Development: The growing fetus begins to be aware of its
surroundings as the third trimester gets underway. Early in the
third trimester, the fetus begins to open and close its eyes and
suck its thumb. He or she also begins to respond to light and
sound. As the fetus continues to grow, it has less and less room to
move around. Some women report being able to identify the
shape of an elbow or a heel poking into their abdomen. At the
end of this trimester, (and the end of the pregnancy), the fetus
moves into the position for birth, which usually means he or she
moves into a "head down" position lower in the mother's abdomen, nearer to her pelvis.
Figure: Stages of Pregnancy
Preparing your Body for Pregnancy
Your lifestyle can affect the health of your future baby, even prior to conception. Because your developing baby will entirely
depend on your body for nourishment and protection, it is wise to
alter your lifestyle prior to conception so that you eliminate any
bad habits or risk factors that might compromise your health.
Avoid Toxins. Many parts of your daily routine that you en-
gage in without a second thought can be quite harmful to your

developing baby. You will endanger your developing fetus, for
instance, if you smoke, or drink alcohol, or use certain drugs,
including certain prescription medications your doctor may have
recommended! Although you may take it for granted that these
are safe in moderation, they have a much more powerful and
negative effect on a developing fetus than they do on a fullgrown adult. In addition to stopping smoking drinking alcohol,
and using any recreational drugs prior to getting pregnant, you
should also meet with your doctor to review all the prescription
medications you are currently taking to determine whether they
PharmaMag-2013
are safe for you to continue to use during pregnancy. The topic of
what to avoid while pregnant is covered in greater detail below in
the section titled "Universal Precautions".
Prenatal Vitamins. Your baby requires vitamins and minerals in order to develop properly. Various serious birth defects can
occur if you allow yourself to develop a vitamin deficiency while
pregnant. For this reason doctors recommend that pregnant women take a prenatal vitamin supplement. You may want to consider
taking prenatal vitamins even before you become pregnant so as
to prepare your body for the demands of pregnancy.
One important advantage to taking prenatal supplements before
you become pregnant is the inclusion of folic acid in these supplements. It is particularly important that your body have enough
folic acid on board during the early part of your pregnancy because folic acid prevents a very serious developmental complication called a neural tube defect from occurring. Pregnant women
and those women hoping to become pregnant soon should take
between 800 and 1,000 micrograms of folic acid each day.
Look for the following vitamins and minerals at roughly the following dosages when selecting prenatal vitamins at the store:
Vitamins and Minerals
Amounts
Folic acid
800-1,000 mcg
Vitamin D
400 IU
Calcium
200-300 mg
Vitamin C
70 mg
Thiamine
1.5 mg
Riboflavin
1.6 mg
Pyridoxima
2.6 mg
Vitamin B12
2.2 mcg
Niacinamide
17 mg
Vitamin E
10 mg
Zinc
15 mg
Iron
30 mg
Prenatal multi-vitamins are available either with a prescription or

over-the-counter like regular vitamins. As both types of vitamins
provide the same benefit, the only advantage to obtaining your
vitamins through a prescription is that your insurance company
may pay for their cost that way.
Page 41

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Serving the Profession of Pharmacy

Editors and Publishers

City of Publication: Lahore

Myths about Thalassemia By Jony Mallik; B.Pharm (Hons.), M.Pharm,

Microbial Limit Tests By Farrukh Mehmood; PharmD, R.Ph.;

Syringomyelia By Amna Hafeez; PharmD

Mismanagement of Hypertensive Emergency in a Patient By Muhammad Qamar; Lecturer of Clinical

The Issue Of Bioequivalence, Therapeutic Equivalence, And

The Issue Of Bioequivalence, Therapeutic Equivalence, And

the small variations in plasma concentration of the magnitude

The ultimate goal is to have truly equivalent generics that are

Spread Of Niegleria fowleri In Pakistan With Its Brief

Naegleria fowleri (commonly referred to as the "brain-eating

A)Direct visualization12,13: The motile amebae can often be seen

Naegleria fowleri Test Methods

In these two cases, the following combination of three drugs was

Spread Of Niegleria fowleri In Pakistan With Its Brief

Dr Musa Khan, head of WHOs Disease Early Warning System in

Recently, an investigational drug, miltefosine27, a breast cancer

Pakistani health officials in the country's biggest city, Karachi,

Spread Of Niegleria fowleri In Pakistan With Its Brief

ties of Naegleria fowleri strain HB- to selected antimicrobial agents,

Management of Respiratory Distress Syndrome in

Respiratory Distress Syndrome (RDS), also known as hyaline

There are two main types of respiratory distress syndrome

Most babies who develop

Management of Respiratory Distress Syndrome in

Exams and Tests

Immature type II alveolar cells produce less surfactant, causing

The most important investigation in an infant with respiratory

Avoiding unnecessary or poorly timed cesarean sections can

Nasal flaring. The two nose openings become larger with

The condition is more common in boys, and the incidence is

Management of Respiratory Distress Syndrome in

120-150ml / (kg.d) and added electrolyte condition for the better

oral feeding, so that part of parenteral nutrition supplemented.

3. Surfactant replacement therapy

2) Monitoring: temperature, respiration, heart rate, blood pres-

Introduction of surfactant replacement for the treatment of RDS,

Management of Respiratory Distress Syndrome in

Myths about Thalassemia

bin disorder, the most common is anemia.

Myths about Thalassemia

Alpha thalassemia occurs when one or more of the four alpha

Myths about Thalassemia

Example of an Inheritance Pattern for Beta Thalassemia

Alpha thalassemia has four manifestations, that correlate with

Myths about Thalassemia

The degree to which the patient tolerates the anemia.

The threshold of the physician to transfuse patients with thalassemia.

thalassemia intermedia- often two beta-(+)-genes

Myths about Thalassemia

Alpha thalassemia silent carriers generally have no signs or

Treatments for thalassemias depend on the type and severity of

ii) Iron Chelation Therapy

Severe Anemia and Other Signs and Symptoms

The hemoglobin in red blood cells is an iron-rich protein. Thus,

Myths about Thalassemia

You cant prevent thalassemias because theyre inherited (passed

Microbial Limit Tests

Total Viable Aerobic Count

This test is to determine mesophilic bacteria and fungi which

Preparation of Test Fluids