clinical pharmacy practice experience
DESCRIPTION
‘Experience is the best teacher”Now, at the end of Hospital Training, I am pleading to say that NIRMA UNIVERSITY has intellectually included Hospital Training as part of B.Pharm. Hons. ‗S academic curriculum (Semester X). This hospital training has given me a chance to get exposed to practical work. What I have studied in semester 9, I have able to implement it in semester X hospital training.I have already completed B.Pharm. And have studied subjects like Pharmaceutics, Pharmacognosy, etc. But in this course, I have been exposed to clinical field, not only theoretical aspect, but practical aspect as well which, according to me, the most exciting experience of my field is. According to my merit rank (calculated on the basis of semester 9 marks); I have got a chance to get trained in Shrey Hospital under the guidance of Dr. Chirag Joshi sir. He is the one who holds and manages the Intensive Coronary Care Unit (I.C.C.U) on one hand alone. It has been great experience to obtaining under such qualified and experienced person.On the first day of my training, I along with fellow members was introduced to medical staff and have been introduced to different departments like ICCU, Operation theatre, dialysis unit, Radiology department, Pathology Lab, Lithotripsy, Pharmacy and various wards and these sessions were included in week one schedule.During second week, I was allocated to pharmacy. I got exposed to the way to handle prescription and reading as well. I came to know the arrangement of medicines. Different medicines of same company were kept in one shelf and were arranged according to their alphabetical order in the same shelf. I also came to know about medication handling & storage, dispensing, ADR and medication order identification while handling prescription. By this pharmacy experience I came to know about extreme use of antibiotics i.e. irrational use we can say. Pharmacists here in pharmacy have overcome the mistakes done by doctor in hurry e.g. dose, freq.etc.Our case studies began third week onwards and were continued till the end of training. Herein I studied different cases pertaining to most of the system of body. Dr. Chirag sir explained us the format of presenting the case like Patient demographics,chief complains, past history, past medication history, vital signs, systemic examination, laboratory investigation, other diagnostic tests (X-ray, USG, and MRI), medications, adverse reactions and then other related discussions. Sir explained us how to take history of patient and assigned me the case along with other fellow members which we have to present before him on the next day by preparing in the format what he had taught to us. Sir fully explains us the case according to format and carries on interaction as well. This include why a particular treatment is preferred (based on patient‘s economic status), how to overcome drug interactions and ADRs. He fully explains the treatment along with the available options of medicines e.g. Cephalosporins. He gives us a brief introduction over different class of the same along with brand names and the spectrum they cover. He explained all the part of case from entering in the hospital to discharge from hospital, every reason for single treatment. And I also saw some cases of particular of my interest like poisoning, alcoholic patient, renal failure.During this practical training I also involved in ward round participation. I used to go with Chirag sir and learn the way treat the patient and maintain patient history notes. I used to check drug dose and dosing frequency. I also used to take patient history which is also critical in understanding patient‘s case. During ward round participation, I came to real practice experience as I was in front of the patient and use knowledge in dealing with patient.All in all, it was the best experience that I have undergone in my field. This would be greater than anything in clearing my future registered pharmacist exam iTRANSCRIPT
[SHREY HOSPITAL]
[Parth Dhanani] Page 1
A PROJECT REPORT OF
CLINICAL PHARMACY PRACTICE EXPERIENCE
Carried out at Shrey Hospital, Ahmedabad,
SUBMITTED TO
NIRMA UNIVERSITY
IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE AWARD OF
DEGREE OF
Bachelor of Pharmacy (Hons.)
By
Mr. PARTHKUMAR.D.DHANANI (10BPW618)
Semester X
UNDER THE GUIDANCE OF
Mr. Bhavik Shah, M.Pharm
INSTITUTE OF PHARMACY
NIRMA UNIVERSITY
SARKHEJ-GANDHINAGAR HIGHWAY
AHMEDABAD-382481,
GUJARAT, INDIA
SEPTEMBER 2010
[SHREY HOSPITAL]
[Parth Dhanani] Page 2
Certificate
This is to certify that Mr.PARTH KUMAR DHANANI
(10BPW618) of Semester X of B. Pharm (Hons.), 5-year
Integrated Programme, Institute of Pharmacy, Nirma
University, Ahmedabad, has undergone training at SHREY
Hospital from 25/05/2010 to 08/09/2010 and has satisfactorily
completed 400 hours in the Pharmacy Practice Experience.
Date: 9/9/2010
Shri Dharmanshu Chhaya
Manager
Shrey Hospital Ltd.
Near AMCO Bank,
Stadium Circle, Navrangpura,
Ahmedabad - 380 009
Phone: 26468616 to 20, 40017777
Mobile No. - 98250-23371.
EMail: [email protected]
Seal of the Hospital
Professor In charge Head of Department Seal of the Institute Director
[SHREY HOSPITAL]
[Parth Dhanani] Page 3
Index
Chapter No. Topic Page No.
1.
Introduction
Clinical Pharmacy Practice
Importance of Clinical Pharmacy
Practice Training
5 – 6
2. Objectives 7 – 10
3.
Introduction and Overview of Training
Training Site
Training Site Features
Training Duration
Training Schedule
11 – 16
4. Overview of Routine Activities at Hospital 17 – 27
5. Case Studies 28 – 99
6. Results and Discussion About Learning Experience 100 – 106
7. Other Activities and Participation 107 – 123
8. Summary 124 – 125
9. References 126 - 127
10. Annexure 128 – 136
[SHREY HOSPITAL]
[Parth Dhanani] Page 4
ACKNOWLEDGEMENT
This project has been prepared to give brief knowledge to ―Clinical experience in
Shrey Hospital of 400 hours ‘‘.this project has to be undertaken and completed as per
the direction of the syllabus.
I am very thankful to Mr.Dharmanshu Chhaya, for his constant, restless guidance
through his busy schedule .and for his warm welcoming to the Shrey Hospital family.
Also I would be thankful to Dr.Chirag Joshi(M.D) who guided me in all the clinical
doubts and also gave us his personal attention to better understanding of the practical
connection of clinical aspects to my theoretical knowledge as well as his incites to
better development of my clinical experience in Shrey.
I would also like to convey my gratitude to Mr.Bharathai Mahant, The Director of the
Shrey Hospital, for allowing us to use the resources of the hospital, which were
helpful in completion of my thesis.
At this stage I, specially, thank professors Incharge Mr. Bhavik Shah of Institute of
Pharmacy, Nirma University, for the moral support and constant encouragement in
the accomplishment of my project work in semester: X of B.Pharm honors.
Thanking you,
Mr. PARTHKUMAR DHANANI (10BPW618)
[Chapter 1]
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CHAPTER 1:
Introduction to Pharmacy Practice Experience:
Pharmaceutical care is defined as ―a patient-centered, outcomes oriented
pharmacy practice that requires the pharmacist to work in concert with the patient
and the patient's other healthcare providers to promote health, to prevent disease,
and to assess, monitor, initiate, and modify medication use to assure that drug
therapy regimens are safe and effective.‖
The potential for medication therapy management services provide an
additional career opportunity for pharmacy graduates. Pharmacists usually rotate
between different pharmacy services offered by shrey hospital. These may include:
clinical pharmacy
medicines information
medicines management
aseptic/technical service
dispensary services
community pharmacy services
primary care
Importance :
Pharmacy student‘s main focus on patient cares and emphasizes the
pharmaceutical care model.
Pharmaceutical care is ―the responsible provision of drug therapy for the
purpose of achieving definite outcomes that improve a patient's quality of life.‖
Pharmacy practice‘s aim is to guide pharmacy educators in pharmacy practice,
to educate pharmacy students and to guide pharmacists in practice to update
their skills.
Role of pharmacist is to ensure that a patient‘s drug therapy is appropriately
indicated, the most effective available, the safest possible, and convenient for
the patient.
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Purpose of training and expectations that a clinical pharmacist looks
forward:
Counseling patients on the effects, dosage and route of administration of their
drug treatments, particularly those who require complex drug therapy.
Communicating effectively with patients' relatives, community pharmacists,
general practitioners etc.
Communicate with physician and discuss the cases which enrolled in shrey
hospital.
Ensuring medicinal products are stored appropriately and securely to ensure
freshness and potency.
Ensuring medication reaches the patient in the correct form and dose - this may
include tablets, capsules, ointments, injections, inhalers and creams.
Liaising with physicians, nurses and other fellow health care professionals to
ensure the delivery of safe, effective and economic drug treatment.
Monitoring every stage of medication therapy to improve all aspects of delivery
and reporting patient side effects.
Provide help to main pharmacist of hospital for writing guidelines of drug use
within the hospital, preparing bulletins and implementing hospital regulations.
Providing information to individual wards on budgets and expenditure on drugs.
Participating in ward rounds, taking patient drug histories and contributing to the
treatment decision-making process - this includes highlighting a drug's potential
side effects, identifying harmful interactions with other drugs and assessing the
suitability of treatments for patients with particular health conditions.
Preparing and quality-checking sterile medications under special conditions.
Provide help to pharmacist and pharmacy assistant for the accurate dispensing
and timely distribution of drugs and medicines for inpatients or outpatients.
Provide help and supervising the work of other staff.
Responding to medication-related queries from within the hospital, other
hospitals and the general public and if needed then communicate with physician
about the queries.
[Chapter 2]
[Parth Dhanani] Page 7
CHAPTER 2:
OBJECTIVES:
Pharmacy profession has entered doctor‘s clinics and hospitals as the ―clinical
pharmacist‖. Clinical pharmacy is a branch of pharmacy where the pharmacist role is
to provide patient care. Clinical pharmacist is an important part of the healthcare
team. The pharmacist works in coordination with the doctors for the better patient
healthcare. They have some very specific roles which aim at assuring patient safety.
Some of the roles are as follows:
Patient medication history interview.
Medication order review.
Patient counseling regarding safe and rational use of drug.
Adverse drug reaction monitoring.
Drug interaction monitoring.
Therapeutic drug monitoring.
Participating in ward rounds.
Providing drug information at the drug information and poison information
centre.
Build upon drug literature evaluation skills and engage in evidence-based
medicine approaches. Drug information is utilized in all pharmacy practice
settings, and research is no exception.
Publish and present results of the research project at a national meeting. One of
the essential tenets of research is being able to conduct research and present the
research results to other healthcare professionals.
Attend grand rounds and other seminars in order to further enhance the
educational experience. Clinicians and other researchers from both inside and
outside the institution present interesting topics on a weekly basis, and there are
many ongoing lectures that present topical cutting-edge material in a variety of
subject areas. These sessions will be used to further enhance the educational
process.
Participating in ward rounds, taking patient drug histories and contributing to the
treatment decision-making process - this includes highlighting a drug's potential
[Chapter 2]
[Parth Dhanani] Page 8
side effects, identifying harmful interactions with other drugs and assessing the
suitability of treatments for patients with particular health conditions.
Counseling patients on the effects, dosage and route of administration of their
drug treatments, particularly those who require complex drug therapy.
Monitoring every stage of medication therapy to improve all aspects of delivery
and reporting patient side effects.
Communicating effectively with patients' relatives, community pharmacists,
general practitioners etc.
Preparing and quality-checking sterile medications under special conditions.
Ensuring medicinal products are stored appropriately and securely to ensure
freshness and potency.
Ensuring medication reaches the patient in the correct form and dose - this may
include tablets, capsules, ointments, injections, inhalers and creams.
Provide help to pharmacist and pharmacy assistant for the accurate dispensing
and timely distribution of drugs and medicines for inpatients or outpatients.
Provide help and supervising the work of other staff.
Responding to medication-related queries from within the hospital, other
hospitals and the general public and if needed then communicate with physician
about the queries.
Provide help to main pharmacist of hospital for writing guidelines of drug use
within the hospital, preparing bulletins and implementing hospital regulations.
Providing information to individual wards on budgets and expenditure on drugs.
Communicate with physician and discuss the cases which enrolled in shrey
hospital.
Collaborate with other research professionals both on and off site to expand
research experience. Current research projects involve co-researchers at
independent sites, and the clinical pharmacist will be interacting with, and
responding to healthcare professionals at these sites. The development of the
ability to work with others both on and off-site will be strengthened and
communications skills will be solidified in this environment. In addition,
networking opportunities for the fellow are possible.
[Chapter 2]
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Integrate the fellow within the research process. Clinical pharmacist will actively
participate in ongoing research that relates to pharmacy practice. These will
include grants that are related to adverse drug events, medication prescribing and
patient safety as it relates to pharmacy issues. He/she will be encouraged to think
critically and input his/her opinion regarding the direction of the research projects.
As the they will be actively engaged in the research process, the insights that the
fellow can provide can become instrumental in the research process and lead to
educational growth for the fellow.
Build upon drug literature evaluation skills and engage in evidence-based
medicine approaches. Drug information is utilized in all pharmacy practice
settings, and research is no exception.
Clinical pharmacist will interact with faculty in both the Department of Pharmacy
Practice and Department of Pharmaceutical Sciences. He/she fellow will be
encouraged to seek opportunities to collaborate with colleagues who share similar
teaching and research interests.
Within the system of health care, clinical pharmacists are experts in the
therapeutic use of medications. They routinely provide
medication therapy evaluations and recommendations to patients and other health
care professionals.
Clinical pharmacists are a primary source of scientifically valid information and
advice regarding the safe, appropriate, and cost-effective use of medications.
Clinical pharmacists are also making themselves more readily available to the
public. In the past, access to a clinical pharmacist was limited to hospitals, clinics,
or educational institutions.
However, clinical pharmacists are making them available through a medication
information hotline, and reviewing medication lists, all in an effort to prevent
medication errors in the foreseeable future.
In some states, clinical pharmacists are given prescriptive authority under protocol
with a medical provider (i.e., MD or DO), and their scope of practice is constantly
evolving. In the United Kingdom clinical pharmacists are given independent
prescriptive authority.
Basic components of clinical pharmacy practice:
1. Prescribing drugs
[Chapter 2]
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2. Administering drugs
3. Documenting professional services
4. Reviewing drug use
5. Communication
6. Counseling
7. Consulting
8. Preventing Medication Errors
Scope of clinical pharmacy:
Drug Information
Drug Utilization
Drug Evaluation and Selection
Medication Therapy Management
Formal Education and Training Program
Disease State Management
Application of Electronic Data Processing (EDP)
[Chapter 3]
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CHAPTER 3:
Introduction and Overview of Training
Introduction and overview
of hospital training include
visit to various departments
of Shrey Hospital that are
as follows:
1) Intensive coronary care unit (ICCU):
An intensive coronary care unit (ICCU) is a hospital ward specialized in the
care of patients with heart attacks, unstable angina and various other cardiac
conditions that require continuous monitoring and treatment.
All rooms have dialysis capabilities, and one is equipped with negative air
flow. The nurse's station is designed for direct observation of the patients and
houses the central monitors.
The Intensive Coronary Care Unit (ICCU) is located on the 4th floor of the
shrey hospital. It is a single hall unit, with no through traffic. All rooms are
private, and equipped with individual monitors, wall oxygen, suction, and an
emergency power system.
There are two emergency code carts maintained in the ICCU with portable
monitoring equipment. Supplies and other equipment are centralized. A
waiting room is adjacent to the unit.
Equipment & Facility:
ICCU is managed by highly trained doctors.
10 Bedded Well Equipped ICCU with Central Station.
All Beds equipped with Multi Para Monitors with
- ECG
- SPO2
Figure 1 Layout of shrey hospital
[Chapter 3]
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- NIBP
- RESP
- Invasive BP
- Temperature
Bed side multi Para monitors with invasive pressure monitoring, Infusion
pumps, pacemakers, defibrillators, ultrasonic nebulizers, bed side oxygen,
vacuum, air lines.
2nd Invasive Line
Availability of Pacemaker.
Bedside Oxygen, Vacuum Line.
Bedside Digital X- Rays.
10 State of art ventilators.
Capnography Monitor Available.
Defibrillator (BPL)
Facility for Bedside Dialysis.
ICCU Managed Round the Clock by Qualified Intensivists.
Intra Aortic Balloon Pump.
Infusion Pumps----Syringe Pumps, Volumetric Pumps.
Latest Crasn Carts.
Muscle Pulsator to Prevent DVT.
Multiple Parameter central Station
Ultrasonic nebulizer.
Activities performed in ICCU:
Counseling to patients
Exercise:
In an exercise program is to determine patient‘s risk of complications from
exercise. This is usually done by performing an exercise test on a treadmill.
Patients can also build exercise into their daily routine by taking a brisk walk
.Over time most people can gradually increase the intensity of exercise in their
workout.
[Chapter 3]
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This program will consider patient‘s fitness level, heart health, any physical
limitations, the amount, intensity and duration of exercise needed to improve
heart health, and the need for supervision.
The exercise should use large muscle groups and include aerobic exercise.
Walking, jogging, swimming, cycling, rowing, and stair climbing are some
examples.
Supportive care:
Manage diabetes — People with diabetes are at an increased risk of
developing complications after a heart attack. Tight control of blood sugar can
help to reduce the risk of these and other types of complications. Tight control
can be achieved by losing weight, managing your diet, exercising, monitoring
blood sugar levels regularly, and taking oral medications (for people with type
2 diabetes) or insulin (for people with type 1 and sometimes type 2 diabetes).
Stop smoking — Cigarette smoking markedly increases your risk of coronary
heart disease and heart attack, and stopping smoking can rapidly reduce these
risks. One year after stopping smoking, the risk of dying from coronary heart
disease is reduced by about one-half, and the risk continues to decline with
time.
Treat high cholesterol — Medicine to lower blood cholesterol levels is also
recommended after a heart attack.
Treat high blood pressure — Medicines to control high blood pressure are
often recommended after a heart attack. It is important to take these
medications exactly as prescribed.
Healthy Diet for Heart:
Diet counseling is helpful for people who need to lose weight or reduce
cholesterol levels. A registered dietitian is the best person to consult about
foods that are helpful, appropriate portion sizes, total calorie
recommendations, and realistic ways to change bad eating habits.
Fruits And Vegetables - These foods decrease the risk of cardiovascular
diseases including coronary heart disease (CHD) and stroke. Cruciferous
vegetables (i.e., broccoli, cabbage, cauliflower, brussel sprouts), green leafy
[Chapter 3]
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vegetables, citrus fruits, and vitamin C-rich fruit and vegetables may lower the
risk of cardiovascular disease to the greatest extent.
Fibers - Eating a diet that is high in fiber can decrease the risk of coronary
heart disease and stroke by 40 to 50 percent. Eating fiber also protects against
type 2 diabetes, and eating soluble fiber (such as that found in vegetables,
fruits, and especially legumes) may help control blood sugar in people who
already have diabetes. The recommended amount of dietary fiber is 20 to 35
grams of fiber per day.
Fat - High blood cholesterol levels increase the risk of coronary heart disease.
Eating foods lower in certain types of fat and cutting back on foods that
contain cholesterol can lower cholesterol levels and reduce the risk of
coronary heart disease. Saturated fats and Trans fats should be avoided.
Sodium – Sodium restriction is also very necessary for heart disease patients.
2) Neurology Department:
Description:
The department of Neurology provides Routine outdoor, indoor and dedicated
emergency and neuro-intensive care especially, after surgery and stroke.
Besides management of patients with all neurological disorders, outdoor
speciality clinics are set up for the following neurological conditions:
Movement disorders, headache, epilepsy, neuro-muscle diseases,
neuropsychiatry, pediatric neurology and pain.
Facility and Services:
Emergency neurosurgery services round the clock on all days.
Intensive Care facility for critically ill patients.
Routine out-door and in-door neurosurgery services.
Sophisticated equipment available in the department to carry out the following
electro diagnostic procedures for example, electroencephalography (EEG) and
video telemetry, electromyography (EMG).
Common Neurosurgical Procedures:
Craniofacial surgery
Endoscopic surgery
[Chapter 3]
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Radio surgery and Stereotactic radiotherapy
Surgery for spasticity
Spinal surgery
Surgery for aneurysms/arteriovenious malformations
Surgery for movement disorders
Surgery for complex brain tumors
Skull base surgery
Stereotactic surgery
Surgery for Epilepsy
3) Continuous Ambulatory Peritoneal Dialysis Unit (C.A.P.D):
Automated Peritoneal Dialysis Machines are also available. Patients are
trained in ambulatory peritoneal dialysis in the department.
This form of dialysis for chronic renal failure can be done easily at home and does
not require any machine.
4) Renal Care department:
3 Latest Dialysis Machine available on 3rd
floor of shrey hospital for CRF and
ARF patients.
Round The Clock Availability of Dialysis Technician facility and also Bed
Side Multi-Para Monitors Available in Dialysis Department.
There are Doing SLED in Critically ill Patients and also available Separate
Double RO Filtration Plant of Dialysis Water.
Water used in dialysis is Bacteria Free, Zero TDs, Periodically cultures clone
for removing contamination.
Facilities and services:
The Department takes care of all types of nephrology cases, e.g. acute renal
failure, chronic renal failure, acute and chronic nephritis, nephrotic syndrome,
renovascular hypertension, collagen disorders involving kidneys etc.
Facility for CRRT (continuous renal replacement therapy) for critically ill
patients requiring dialysis and MARS (molecular adsorptive regenerative
system) for liver failure is also available.
[Chapter 3]
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Renal Transplant
Haemodialysis:
Plasmaphoresis for renal as well as non-renal cases
Short term dialysis prior to transplantation
To reduce incidence of hepatitis B and C rigorous precautions are taken and
such patients are dialyzed on separate machines.
Haemodialysis for acute as well as chronic renal failure patients
Haemodalysis is also done in cases of drug over dosage
[Chapter 4]
[Parth Dhanani] Page 17
CHAPTER 4:
Overview of Routine Activities at Hospital
Week: 1 Introduction to Hospital departments
ICCU: Intensive Cardiac Care Unit
10 beds
Computer showing all present
vitals of all patients in ICCU.
Advanced life supporting
instruments
Nursing and Medical officers
staff
24 hr running air conditioner
Ventilators near all beds
Dialysis Unit
Services
- Hemodialysis
- Hemofilteration
- Plasma Exchanges
- Continuous Ambulatory
peritoneal Dialysis
Charges per sitting
OT: Operation Theater
Live video recorder of all
operations.
All measure operations
except cardiac surgery
performed in Hospital.
Figure 2 ICCU
Figure 3 Dialysis Unit
Figure 4 Operation Theatre
[Chapter 4]
[Parth Dhanani] Page 18
Assembly of Operation Theatre
Pathology Department:
ABGA
Blood glucose meters (Wards, departments, GP surgeries and
ambulance services)
Sweat Conductivity meter (Paediatrics)
Blood gas analysers
Bilirubinometer (SCBU)
Nutritional Analysis
HbA1c analyser in Paediatrics
Lithotripsy Centre
Ambulatory Lithotripsy facilities
TMT ( Tread Mill Test ) for
cardiac evaluation of the patients
Wards
Doctors take round at each ward
regularly
Combined Ward all on the first,
second and third floor, separated
by the facilities provided like,
Deluxe, Super Deluxe, Special,
and Semi Special
Nurshing staff and consulting offices available at each floor.
Figure 5 Lithotripsy Centre
Figure 6 ICCU ward
Figure 7 General ward
[Chapter 4]
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OPD (Out Patient Department)
All departmental specialists with interns are available at OPD
site.
It is very affordable to patient compare to other private
hospitals.
Week: 2
Pharmacy:
Figure 8 Shrey Pharmacy Store
Delivery of emergency medicines to the ICCU by Pharmacist.
Pharmacy manager teaches that how to manage the stoke of all
medicines.
Arrangement of medicine by Company name or by disease.
Software like ―VISUAL‖ to dispense medicine
Option of Indoor Accommodations:
Various options are available
for indoor accommodation
suiting to the need & budget of
the patients.
Each floor has a specious
nursing station supervised by
medical officer round the clock
Figure 9 Indoor Accommodation
[Chapter 4]
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and services of physician (MD) are available whenever
required.
Hospital has sitting space for visitors and waiting area have
kiosks of TV, Telephone, Tea, Coffee and mineral water.
Week: 3 & 4
Cardiovascular System
Hypertension
Heart failure
ECG
Arrhythmia and Pacemaker
RHD and Infective Endocarditis
IHD
Stable Angina
Unstable Angina
Prinzmetal Angina
MI
CPR
Basic Life Support (BLS)
-Airways
-Breathing
-Circulation
Advanced Cardiac Life Support (ACLS)
-Defibrillation
-Emergency Medication with Adrenalin, Dopamine, Atropine.
Drugs
[Chapter 4]
[Parth Dhanani] Page 21
Week: 5 & 6
Respiratory System
Pneumonia
COPD
Drugs
Tuberculosis
Asthma
Tracheotomy
We have seen the live Tracheotomy in ICCU.
Ventilation
Catheter
Tracheostomy
Respiratory Failure
Hypoxia
Hypercapnea
ABGA Analysis
Mixed Respiratory Acidosis
Mixed Respiratory Alklosis
Week: 7
Renal System
ARF
Pre renal ARF
Intrinsic ARF
Post Renal ARF
CRF
GFR Classification
Causes
Pathology
Intervention
Electrolyte imbalance
[Chapter 4]
[Parth Dhanani] Page 22
Na/K/Mg/Ca/Hco3 imbalance
Dialysis
Heamodialysis
Peritoneal Dialysis
Week: 8 & 9
GI Disorder and Liver Dysfunction
Ascities
Cirrhosis
Hepatitis
Hepatic Encephalopathy
IBD, IBS (Inflammatory bowel disease/Syndrome)
Jaundice
Portal Hypertension
Typhoid fever
Week: 10 &11
CNS Disorder
Coma
Epilepsy
-Types
-Drugs
-Drug Interaction
EEG/CT scan
GBS
Migraine
MRI
Neuro surgery
Stroke
-Hemorrhagic Stroke
-Ischemic Stroke
[Chapter 4]
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Shock
Week: 12
Endocrine disorder
Diabetes Mellitus
Hormones
-Anterior Pituitary Hormone
• ACTH: Adrenocortico Trophic Hormone
• GH: Growth Hormone
• LH / FSH: Luteinizing hormone/Follicle
Stimulating Hormone
• PRL: Prolactine
• TSH: Thyroid Stimulating Hormone
-Posterior Pituitary Hormone
• Vasopressin & oxytosin
Week: 13 & 14
Infectious Disorder
Dengue
Fever and it several types
Malaria
Tuberculosis
Viral Infections
UTI
Week: 15
Poisoning
Alcohol poisoning
Carbon monoxide poisoning
Chemical poisoning
Drug poisoning
[Chapter 4]
[Parth Dhanani] Page 24
Food Poisoning
Heavy metal poisoning
Organo phosphorous Poison with case presentation
Radon poisoning
Participation in Ward round with Clinician:
Ward round is an integral part for pharmacists during hospital training.
Participation in ward rounds and meetings with the patient is of benefit to the
pharmacist as well as the patients.
A clinical pharmacist as we know is the third pillar of the healthcare team
following the doctor and the nurse.
Goals of ward round participation :
Optimize drug treatment by influencing therapy selection, implementation and
monitoring
Provide information on pharmacology, pharmacokinetics and other aspects of
the patient‘s therapy.
Gain an improved understanding of the patient‘s clinical details, planned
investigations and therapeutic goals.
Activity during ward rounds :
Assimilate additional information about the patient which may be relevant to
their drug therapy
Contribute information regarding the patient‘s drug therapy e.g.; suggestions
for monitoring, information on new drugs
Communicating with physician about changes in drug therapy.
Considering the impact of changes to the care plan, and making necessary
alterations.
Discussing alterations to therapy with the patient where appropriate. Detect
ADRs and interactions
[Chapter 4]
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Follow up outstanding issues afterward round and discuss with physician and
pharmacist
Investigate unusual orders or doses
Participate in discharge planning
Responding to any enquiries generated.
Ward round performance :
Introduction: Introduce our self to patient and their relative and specify the
purpose of ward round.
Keeping notes: Always keep notebook and pen during ward round and sketch
down the important information during the ward round like the vital sign of
patient during ward round.
Making queries: When wanting to make a query, wait till the consultant
makes his assessment regarding the patient and plan out the management as
disturbing at this time might not be a good idea. Following this, indicate your
intension to ask a question and if allowed you can pose a question which is
relevant to that patient.
Recording a discussion: Discuss with physician about our quires and make
record in notebook about that discussion. Refer this note on next ward round.
Making summary: At the end of the ward round, make a summary of what
was discussed and list out the areas needing further reading or practice to
perform better as a clinical pharmacist.
PHARMACY STORE:
Shrey hospital have a Pharmacy department (Medical Store) located on
ground floor.
Arrangement of Medicine:
The medicines in Shrey Pharmacy are arranged in shelves according to
the company they belong. In that particular company shelf, the drugs
are arranged in alphabetical order.
[Chapter 4]
[Parth Dhanani] Page 26
Figure 10. Drugs’ arrangement
Dispensing:
The team provides medicines for many areas both on and off site. They
provide services to in-patients and out-patients from every clinical area.
The Pharmacy ensures that there is a round the clock availability of a
sufficient quantity of drugs.
Figure 11 Dispensing of drugs
Storage of Medicine:
The medicines are stored in the Pharmacy at room temperature.
Special medicine such as insulin and certain injectables which degrade
at room temperature are kept in the refrigerator and the temperature of
the refrigerator is checked every morning by the ATO.
[Chapter 4]
[Parth Dhanani] Page 27
Shrey Pharmacy does not have the license for Narcotics so no locked
storage is required.
Figure 12 Storage of medicines
Records Maintenance:
The inventory list is printed every morning and that is done by the ATO.
The expiratory is done in the starting of every month by computer as well as
manually.
Figure 13 Record maintenance
[Chapter 5]
[Parth Dhanani] Page 28
CHAPTER 5: Case studies
CASE STUDY 1: ECLAMPSIA
Patient details:
Patient name: XYZ
Age: 23 years
Sex: Female
Weight: 48 kg
Height: 5‘3‖
Date Of Admission: 20/07/10
Date of Discharge: 22/03/10
Chief complaints:
Generalized tonic clonic convulsion after delivering first child
Edema on lower limb since 4 days
Low U/O since 2 days
Fever since 1 day
Unconsciousness since 1 day
Past history:
No significant past history
Past medication:
No past medication history
Family History:
Low socio-economic class
No disease running in family
Delivered first child
Social History:
Married
Normal diet & sleep
No tobacco
No alcohol
[Chapter 5]
[Parth Dhanani] Page 29
On admission vital data:
Temperature: 101 oF
Pulse : 140 / MIN (N:60-90 / MIN)
B.P. : 900/50 mmHg (N: 140 / 90mmhg)
R.R. : 16 / MIN (N: 14 – 18 / MIN)
SPO2: 98% Normal
Systemic examination:
CVS: S1S2 Normal
CNS: Unconscious
R.S. : Normal
P/A : Soft
Lab investigations:
Table 1 Lab investigation of Eclampsia patient
INVESTIGATION DAY 1 DAY 2
Hb 6.3 8.5
TC 26,200 26,000
DC 68/17/1/12/2 73/20/2/5/0
PC ↓se 82,000 1,66,000
PT ↑se Total
Control
24 sec
13.2 sec
---
RBS 120 mg/dL
(75-115mg/dL)
---
Urea ↑se 193.47
(10-20mg/dL)
---
Creatinine ↑se 8.88 (<1.5mg/dL) ---
Sodium 135.26 142.37
Potassium 4.7 4.1
S.Bilirubin ↑se 1.41 (0.3-1mg/dL) ---
[Chapter 5]
[Parth Dhanani] Page 30
SOPT ↑se 138.5 (0-35U/L) ---
S.Ammonia 39.59 ---
LDH ↑se 2835 (14-26%)
---
pH ↓se
7.21 (7.38-7.44)
---
pCO2 ↑se
52 (35-45mmhg) ---
PO2 ↑se 67 (80-100mmhg) ---
Bicarbonate ↓se
11 (20-30mE/L) ---
X – Ray : Normal
USG (Abdomen):
- Retain products
- ARF
CT Scan (Brain): Bilateral ischaemia
Diagnosis:
- ECLAMPSIA (leading cause of death)
- POST PARTAL ENCEPHALOPATHY
- SEPTICAEMIA
- ARF
- LIVER INJURY
BACKGROUND:
• Ten percent of all pregnancies are complicated by hypertension
(HTN).Eclampsia and preeclampsia account for about half of these
cases worldwide.
• In 1619, Varandaeus coined the term eclampsia in a treatise on
gynecology.
[Chapter 5]
[Parth Dhanani] Page 31
• DEFINITION: Eclampsia is defined as the clinical presentation
of an unexplained seizure, convulsion, or altered mental status in
the setting of the signs and symptoms of preeclampsia. It is
considered a complication of severe preeclampsia.
• A woman with preeclampsia develops:
--- High blood pressure (>140 mmHg systolic or >90 mmHg diastolic)
--- Protein in the urine
--- Swelling (edema) of the legs, hands, face or entire body.
PATHOGENESIS:
In eclampsia, placenta does not form a normal system of arteries
[Illness (diabetes or high blood pressure), genetic (inherited) factors and the way the
mother's immune system reacts to the growing placenta]
↓
Placenta does not anchor itself as deeply as expected within the wall of the uterus
↓
As the pregnancy progresses, a placenta creates an abnormal balance of enzymes
(proteins) called growth factors (VEGF)
(Placental production and secretion of antiangiogenic factors such as protein like
tyrosine kinase 1 and activin a that antagonizes VEGF)
↓
ANGIOGENESIS IMPEDANCE
↓
Changes the way that arteries in the mother and the placenta function-
Arteries throughout the body can tighten (become narrower), ↑se BP
[Chapter 5]
[Parth Dhanani] Page 32
Become "leaky" allowing protein or fluid to seep through their walls, which
causes tissues to swell →Edema
Also react to the abnormal growth factor balance by forming clots
Abnormal cerebral blood flow in the setting of extreme hypertension. Vessels
become dilated with increased permeability and cerebral edema occurs and
results in ischemia and encephalopathy → Seizures
Many uterovascular changes occur due to the interaction between fetal and
maternal allografts and result in systemic and local vascular changes. These
system changes contribute to the brain pathology in eclampsia by inhibiting
the regulation of cerebral perfusion.
Medications:
Table 2 Medications of Eclampsia patient
DRUG
DOSE
ROA
DURATION
GENERIC
NAME
D
1
D
2
Inj. Pipzo 4.5 mg in
100ccNS
i.v. 12hrly Piperacillin +
tazobactam
√ √
Inj. Metrogyl 100ml i.v. 8hrly Metronidazole √ √
Inj. Pantodac 40mg i.v. OD Pantoprazole √ √
Inj. Levepil 500mg in
100ccNS
i.v. 8hrly Levetiracetam √ √
Inj. Lasix 2amp i.v. BD Furosemide √ √
Inj. FFP 250ml i.v. 8hrly Fresh frozen
plasma
√ √
[Chapter 5]
[Parth Dhanani] Page 33
Pipzo Dose Calculation:
Table 3 Pipzo dose calculation
Creatine
Clearance
Dose Dose interval
20-80 4/0.5 8
<20 4/0.5 12
Cl cr = (140 – age yr) * Body wt. = (140-23) * 48 = 8.78
72 * S.cr 72 * 8.88
Inj. Dopamine 2@ in
50ccNS
i.v. 6hrly Dopamine √ √
Inj. Febrinil 1@ i.v. sos Paracetamol √ √
Inj. Falcigo 60mg i.v. OD Artesunate √ √
Inj. D25% 500ml i.v. 10ml/hr Dextrose √ √
Inj. Sodium
bicarbonate
(0.6*wt*HC
O3 def.)
0.6*48*9 =
259.2mEq
i.v. 13@ straight
&
13@ 6hrly
Bicarbonate √ √
Inj. Duphalac 15ml
i.v. 8hrly Lactulose
√ √
Inj. Vit K1 1@ in
100ccNS
i.v. OD Vit K1 √ √
Inj. Norad 2@ in
50ccNS
i.v. 6hrly Nor adrenaline
- √
[Chapter 5]
[Parth Dhanani] Page 34
DRUG RELATED ISSUE:
Table 4 Drug interactions
DRUGS INTERACTIONS MANAGEMENT
lactulose ↔
Artesunate
( moderate)
Electrolyte loss and increase the
risk of torsade de pointes
ventricular arrhythmia.
Electrolyte disturbances including
hypokalemia and
hypomagnesemia.
The recommended dosage
and duration of use should
not be exceeded. Electrolye
supplements needed to be
administered.
Artesunate
↔ food
(moderate)
The mechanism is decreased
clearance of Artesunate due to
inhibition of CYP450 3A4-
mediated first-pass metabolism in
the gut wall by certain
compounds present in grapefruits.
Avoid the consumption of
grapefruits and grapefruit
juice. To ensure maximal
oral absorption, artemether-
lumefantrine should be taken
with food.
Furosemide
↔ lactulose
(Moderate)
Potentiate the pharmacologic
effects of diuretics. Laxatives can
cause significant losses of fluid
and electrolytes
In general, laxatives should
only be used on a short-
term, intermittent basis in
recommended dosages.
Contact physician if they
experience signs and
symptoms of fluid and
electrolyte depletion such as
dizziness, lightheadedness,
dry mouth, thirst, fatigue,
weakness, decreased
urination, postural
hypotension, and
tachycardia.
[Chapter 5]
[Parth Dhanani] Page 35
CASE STUDY 2: CIRRHOSIS OF LIVER
Patient details:
Patient name: XYZ
Age: 20 years
Sex: Female
Weight: 35 kg
Height: 5‘1‖
Date Of Admission: 28/07/10
Date of Discharge: 3/08/10
Chief complaints:
Abdominanal pain
Distension of abdomen
Decreased appetite
Fever
Past history:
No history of HTN/DM/CAD/Asthma
Past medication:
No past medication history
Family History:
No significant family history
Social History:
Single
Normal diet & sleep
No tobacco
No alcohol
On admission vital data:
Temperature: N
Pulse : 120 / MIN (N:60-90 / MIN)
B.P. : 124/70 mmHg (N: 140 / 90mmhg)
R.R. : 16 / MIN (N: 14 – 18 / MIN)
[Chapter 5]
[Parth Dhanani] Page 36
SPO2: 99% Normal
Systemic examination:
CVS: NAD (No Abnormality Detected)
CNS: Unconscious
R.S. : Normal
P/A : Soft
Lab investigations:
Table 5 Lab investigation of Liver cirrhosis patient
INVESTIGATION DAY 1 DAY 2 DAY 3
Hb 8.9 7.9 7.6
TC 14,100 3070 3980
DC 83/5/0/11/1 64/18/1/14/3 72/11/1/15/1
PC ↓se 66,900 42,400 45,900
PT ↑se Total
Control
INR
24.8 sec
13.4 sec
2.17
--- ---
Creatinine 0.36
(<1.5mg/dL)
--- ---
Sodium ↓se 107.31 122.02 114.2
Potassium 3.93 4.1 ---
S.Bilirubin ↑se 1.41 (0.3-
1mg/dL)
--- ---
SOPT ↑se 142.7 (0-
35U/L)
--- ---
Alkaline Phosphatase ↑se 173.51 (70-
120)
--- ---
S.Ammonia 39.59 --- ---
[Chapter 5]
[Parth Dhanani] Page 37
Gamma-glutamyl
transferase
156.73 (1-94
U/L)
--- ---
Albumin 2.61 (3.5-5.5
g/dL)
--- ---
Globulins 12.96 (2-4.1
g/dL)
--- ---
Smear MP not seen --- ---
Arterial blood gas analysis (ABGA):
PH -- 7.54
pCO2 -- 27
HCO3 -- 114
BA -- 23
O2 -- 99 %
TO2 -- 24
USG (Abdomen):
- Shrunken right lobe
- Moderate spleenomegaly
- Small and nodular liver with increased echogenicity with
irregular appearing area
Endoscopy:
Gastroscopy: Exclude the possibility of esophageal varices.
Diagnosis:
- Cirrhosis of liver / Wilson‘s disease
- Ascites/SBP recovered
- Marked Icterus
- No GI bleed pro encephalopathy
Pathophysiology:
[Chapter 5]
[Parth Dhanani] Page 38
-
Figure 14 Liver cirrhosis
Macroscopically, the liver is initially enlarged, but with progression of
the disease, it becomes smaller. Its surface is irregular, the consistency
is firm and the color is often yellow (if associates steatosis).
Depending on the size of the nodules there are three macroscopic
types: micronodular, macronodular and mixed cirrhosis. In
micronodular form (Laennec's cirrhosis or portal cirrhosis)
regenerating nodules are less than 3 mm. In macronodular cirrhosis
(post-necrotic cirrhosis), the nodules are larger than 3 mm. The mixed
cirrhosis consists in a variety of nodules with different sizes.
However, cirrhosis is defined by its pathological features on
microscopy:
1. The presence of regenerating nodules of hepatocytes and
2. The presence of fibrosis, or the deposition of connective
tissue between these nodules.
The pattern of fibrosis seen can depend upon the underlying insult that
led to cirrhosis; fibrosis can also proliferate even if the underlying
process that caused it has resolved or ceased.
The fibrosis in cirrhosis can lead to destruction of other normal tissues
in the liver: including the sinusoids, the space of Disse, and other
vascular structures, which leads to altered resistance to blood flow in
the liver and portal hypertension.
Medications:
[Chapter 5]
[Parth Dhanani] Page 39
Table 6 Mediation of Liver cirrhosis patient
DRUG
DOSE
ROA
DURA
TION
GENERIC
NAME
D
1
D
2
D
3
D
4
Inj. Magnex
Forte
1.5 mg
in
100cc
NS
i.v. 8hrly Cefoperazone+
salbectam
√ √ √ √
Inj. Vit K1 1 @ i.v. OD Supplement √ √ √ √
Tab. Cilamin 250mg i.v. TID Penicillamine √ √ √ √
Inj. Famocid 20mg i.v. BID Famotidine √ √ √ √
Inj. Zentax i.v. TID Gentamysin √ √ √ √
Inj. FFP 2 @ i.v. Fresh frozen
plasma
-- √ -- √
Tab. Shelcal 500 mg i.v. OD Calcium
carbonate + Vit
B3
√ √ √ √
Tab. Becosule Oral OD Vit B Complex √ √ √ √
Tab. Udiliv 300 mg Oral BID Ursodeoxycholic
acid
√ √ √ √
Inj. H.Alb 20% 20% i.v. 4hrly Supplement √ √ √ √
Tab. Dynapar
plus
Oral Sos Diclofenac -- √ -- √
Proctodesyl Enema Ethyl
aminobenzoate/Ec
osulide
-- -- √ √
[Chapter 5]
[Parth Dhanani] Page 40
Drug related issue:
Table 7 Drug interactions
DRUGS INTERACTIONS MANAGEMENT
Gentamicin
↔
Torasemide
(Major)
Coadministration of parenteral
aminoglycoside antibiotics or
oral neomycin in combination
with loop diuretics may
potentiate the risk of oto- and
nephrotoxicity due to additive or
synergistic pharmacologic
effects of these drugs.
Use of aminoglycoside
antibiotics in combination
with loop diuretics should
generally be avoided.
Serial, vestibular,
audiometric, and renal
function tests should be
performed before and
during therapy if
coadministration is
necessary.
Gentamicin
↔
Cefoperazone
(Moderate)
Coadministration of
aminoglycoside and
cephalosporins may increase the
risk of nephrotoxicity.
The lowest effective
dosages of aminoglycosides
and cephalosporins should
be used when they are
prescribed in combination.
Renal function should be
monitored closely.
Diclofenac ↔
Torasemide
(Moderate)
1. Concomitant use of
nonsteroidal anti-inflammatory
drugs (NSAIDs) and diuretics
may adversely affect renal
function due to NSAID
inhibition of the renal synthesis
of prostaglandins that help
Avoiding dehydration and
carefully monitoring the
patient's renal function and
blood pressure. If renal
insufficiency or
hyperkalemia develops,
both drugs should be
Liq. Looz 2 @ i.v. 6hrly Lactulose -- -- √ √
Inj. Dytor 1/2 @ i.v. 6hrly Torasemide -- -- √ √
[Chapter 5]
[Parth Dhanani] Page 41
maintain renal perfusion in
dehydrated states.
2. Hypotensive effect of the
diuretics may be reduced
because inhibition of
prostaglandins can lead to
unopposed pressor activity and,
consequently, elevation in blood
pressure.
discontinued until the
condition is corrected.
Penicillamine
↔ Calcium
carbonate
(Moderate)
: Oral administration of
aluminum, copper, iron, zinc,
magnesium, and possibly other
minerals such as calcium may
decrease the gastrointestinal
absorption of penicillamine, and
vice versa. The proposed
mechanism involves chelation
of penicillamine to polyvalent
cations, which leads to
formation of a nonabsorbable
complex.
Mineral supplements or
other products containing
polyvalent cations should
be administered at least two
hours before or two hours
after the penicillamine dose.
Discharge Medications:
- Inj. Tazect [Piperacillin + Tazobactam (2.25)] in 100ml NS
8hrly ---------------------------------------------------------- 2 days
- Tab. Tarivid [Ofloxacin (200)] (0-0-1) ------------------ 15 days
- Tab. Famocid (20) (1-1)
- Tab. Shelcal (500) (0-0-1)
- Tab. Udiliv (300) (1-1)
- Tab. Cilamin (250) (1-1-1)
- Tab. Zintate [Gentamicin] (1-1-1)
- Tab. Dytor plus [Torasemide] (5+50) (0-0-1)
[Chapter 5]
[Parth Dhanani] Page 42
CASE STUDY 3: MYOCARDIAL INFARCTION (MI)
Patient details:
Patient name: XYZ
Age: 62 years
Sex: Male
Weight: 59 kg
Height: 5‘9‖
Date Of Admission: 17/07/10
Date of Discharge: 22/07/10
Chief complaints:
Chest pain
Difficulty in breath
Past history:
No significant past history
Past medication:
No past medication history
Family History:
Low socio-economic class
No disease running in family
Social History:
Normal diet & sleep
Smoking
Alcoholic
No tobacco
On admission vital data:
Temperature: N
Pulse : 92 / MIN (N:60-90 / MIN)
B.P. : 144/94 mmHg (N: 140 / 90mmhg)
R.R. : 16 / MIN (N: 14 – 18 / MIN)
SPO2: 98% Normal
Systemic examination:
[Chapter 5]
[Parth Dhanani] Page 43
CVS: S1S2 Normal
CNS: NAD
R.S. : Normal
P/A : Soft
Stool: Not passed
Lab investigations:
Table 8 Lab investigation of MI patient
INVESTIGATION DAY 1 DAY 2
Hb 12.1 12.9
TC 8350 8010
DC 95/6/1/0/0 77/9/3/10/1
PC ↓se 2,05,000 1,57,000
PT ↑se Total
Control
21.3 sec
13.2 sec
---
RBS 120 mg/dL
(75-115mg/dL)
---
Creatinine ↑se 9.14 (<1.5mg/dL) ---
Sodium 141.76 139.11
Potassium 5.6 5.34
Magnesium 2.47 (1.8-2) 2.39
S.Bilirubin 0.54 (0.3-1mg/dL) ---
SOPT 31.67 (0-35U/L) ---
CPK-MB 46.72 (0-7 ng/L) ---
Troponin I 13.25 (0-0.4) ---
pH 7.41 (7.38-7.44)
---
[Chapter 5]
[Parth Dhanani] Page 44
pCO2
39.48 (35-45mmhg) ---
PO2 91.93 (80-100mmhg) ---
Bicarbonate
27.84 (20-30mE/L) ---
2D ECG: Abnormalities of wall motion
12-lead electrocardiogram:
- Anterior wall myocardial infarction.
- Low ejection fractions (<40%)
Doppler echocardiography:
- Ventricular septal defect
- Mitral regurgitation
Diagnosis: ACUTE MYOCARDIAL INFARCTION
Pathophysiology:
The most common triggering event is the disruption of
an atherosclerotic plaque in an epicardial coronary artery, which leads to a
clotting cascade, sometimes resulting in total occlusion of the artery.
Atherosclerosis is the gradual build up of cholesterol and fibrous tissue in
plaques in the wall of arteries (in this case, the coronary arteries), typically
over decades.
[Chapter 5]
[Parth Dhanani] Page 45
Figure 15 Occluded Coronary artery in MI
Blood stream column irregularities visible on angiography reflect
artery lumen narrowing as a result of decades of advancing atherosclerosis.
Plaques can become unstable, rupture, and additionally promote
a thrombus (blood clot) that occludes the artery; this can occur in minutes.
When a severe enough plaque rupture occurs in the coronary vasculature,
it leads to myocardial infarction (necrosis of downstream myocardium).
If impaired blood flow to the heart lasts long enough, it triggers a process
called the ischemic cascade; the heart cells in the territory of the occluded
coronary artery die (chiefly through necrosis) and do not grow back.
A collagen scar forms in its place. Recent studies indicate that another
form of cell death called apoptosis also plays a role in the process of tissue
damage subsequent to myocardial infarction.
As a result, the patient's heart will be permanently damaged.
This Myocardial scarring also puts the patient at risk for potentially life
threatening arrhythmias, and may result in the formation of a ventricular
aneurysm that can rupture with catastrophic consequences.
Injured heart tissue conducts electrical impulses more slowly than normal
heart tissue. The difference in conduction velocity between injured and
uninjured tissue can trigger re-entry or a feedback loop that is believed to
be the cause of many lethal arrhythmias.
Another life threatening arrhythmia is ventricular tachycardia (V-
Tach/VT), which may or may not cause sudden cardiac death. However,
[Chapter 5]
[Parth Dhanani] Page 46
ventricular tachycardia usually results in rapid heart rates that prevent the
heart from pumping blood effectively.
Cardiac output and blood pressure may fall to dangerous levels, which can
lead to further coronary ischemia and extension of the infarct.
Medications:
Table 9 Medications of MI patient
DRUG
DOSE
ROA
DURA
TION
GENERIC
NAME
D
1
D
2
D
3
D
4
Inj. NTG + Ns 50mg i.v. 0.5ml/h
r
Nitroglycerine √ √ √ √
Inj. Oxprin 0.8mg i.v. Stat Aspirin √ √ √ √
Inj. Pantocid 40mg i.v. Stat Pantoprazole √ √ √ √
Inj. Emeset 40mg i.v. Stat Onadansetron √ √ √ √
Inj. DNS 1@ i.v. --- Dextrose √ √ √ √
Tab. Eldervit 1@ Oral --- Multivitamin √ √ √ √
Tab. Ecosprin 150mg Oral --- Aspirin √ √ √ √
Tab. Clopivas 100mg Oral OD Clopidogrel √ √ √ √
Tab. Dilzem 30mg Oral TID Diltiazem √ √ √ √
Inj. Decil --- Oral Stat Paracetamol √ √ √ √
Inj. Deriphyllin --- Oral 8hrly Theophylline -- √ -- √
Neb. Levolin --- Nasal 6hrly Salbutamol -- √ √ √
[Chapter 5]
[Parth Dhanani] Page 47
Advice:
- Smoking cessation
- Regular exercise
- Sensible
- Limitation of alcohol intake.
Drug related issue:
Table 10 Drug interactions
DRUGS INTERACTIONS MANAGEMENT
Theophylline
↔ Tramadol
(Major)
The risk of seizures may be
increased during
coadministration of tramadol
with theophylline that can
reduce the seizure threshold.
Caution is advised.
Clopidogrel
↔
Pantoprazole
(Major)
Coadministration with proton
pump inhibitors (PPIs) may
reduce the cardioprotective
effects of clopidogrel. The
proposed mechanism is PPI
inhibition of the CYP450 2C19-
mediated metabolic
bioactivation of clopidogrel.
Use of Pantoprazole should
preferably be avoided in
patients treated with
clopidogrel.
If gastroprotection is
necessary, H2-receptor
antagonists or antacids
should be prescribed
whenever possible.
Diltiazem ↔
Aspirin
Aspirin may reverse the
antihypertensive effect of
Close observation for
prolonged bleeding time
Neb. Budamate --- Nasal 8hrly Budesonide -- √ √ √
Tab. Calpol 500mg Oral TID Paracetamol -- √ √ √
Liq. Cremaffin 3Tsf Oral --- Paraffin -- -- √ √
Tab. Ultrazec --- Oral Sos Tramadol + PCM -- -- √ √
[Chapter 5]
[Parth Dhanani] Page 48
(Moderate)
verapamil. and reduced
antihypertensive effect is
recommended. Patients
should be advised to notify
their physician if they
experience unusual
bleeding, bruising, or
petechiae. Aspirin should be
discontinued if an
interaction is suspected.
Theophylline
↔
Pantoprazole
(Moderate)
Pantoprazole increases the rate
of theophylline absorption from
sustained-release formulations.
Chronic use of proton pump
inhibitors produce sustained
hypochlorhydria, which may
enhance peristalsis in the small
intestine and antiperistalsis in
the proximal colon where
theophylline is absorbed.
Theophylline levels in the
upper range of normal.
Patients should be advised
to report any signs of
theophylline toxicity
including nausea, vomiting,
diarrhea, headache,
restlessness, insomnia, or
irregular heartbeat to their
physicians.
Discharge medication:
- Tab. Diltiazem (30mg) (1-1-1)
- Tab. Ecosprin (75mg) 1OD after meal
- Tab. Clopivas (2.5mg) (1-1)
- Tab. Dytar Plus (10mg) (1-0-1)
- Tab. Deriphylline R (300mg) 1 OD
- Neb. Levolin 6hrly
- Neb. Budamate 8hrly
- Liq. Cremaffin 3 TSF TID
- Oint. Dicloran (Diclofenac)
- Tab. Ultrazec sos for pain
[Chapter 5]
[Parth Dhanani] Page 49
CASE STUDY 4: PANCREATITIS
Patient details:
Patient name: XYZ
Age: 46 years
Sex: Female
Weight: 69 kg
Height: 5‘6‖
Date Of Admission: 12/07/10
Date of Discharge: 15/07/10
Chief complaints:
Abdominal pain since 2 days
NV since 2 days
Fever since 1 day
Past history:
Diabetes Mellitus from last 10 years
No past history of HTN/IHD/Drug Allergy/Chest pain
Past medication:
Glynase MF (Glipizide 5mg & Metformin 500mg)
1 tab OD before break fast
Family History:
No significant family history
Social History:
No tobacco
No alcohol
On admission vital data:
Temperature: 103 oF
Pulse : 92 / MIN (N:60-90 / MIN)
B.P. : 110/70 mmHg (N: 140 / 90mmhg)
R.R. : 16 / MIN (N: 14 – 18 / MIN)
SPO2: 99% Normal
Systemic examination:
[Chapter 5]
[Parth Dhanani] Page 50
CVS: NAD
CNS: NAD
R.S. : Clear
P/A : Soft
Vomiting: Yes
Stool: Not passed (Peristalsis movement absent)
Lab investigations:
Table 11 Lab investigation of pancreatitis patient
DRUG NAME DAY 1 DAY 2 DAY 3
Haemoglobin 14.7 12.6 ---
Total count 14,900 11,400 ---
Platelet count 2,33,000 2,46,000 2,37,000
RBS ↑se 425 (70-110) --- ---
Creatinine 0.8 (0.6-1.2) 0.52 ---
Urea 13.5 14.2 ---
Sodium 137 139.33 ---
Potassium ↓se 3.0 2.8 3.1
Calcium --- 8.3 ---
SGPT ↑se 125 (0 - 35) --- 80.76
Serum Amylase ↑se 2415(35-120) --- ---
Serum lipase ↑se 5580 (0-160) 1520 ---
Serum AlkPo4ase --- 71 (70-120) 124.99
X-Ray: Normal
USG: Prevalence of minimal fluid anterior to pancreas
[Chapter 5]
[Parth Dhanani] Page 51
Diagnosis:
- PANCREATITIS
- DIABETES MELLITUS
PATHOPHYSIOLOGY:
Table 12 Flowchart of Pancreatitis Pathophysiology
The premature activation of pancreatic zymogens within the acinar cells,
pancreatic ischemia, or pancreatic duct obstruction initiates AP and leads to a
series of secondary events that determine the duration and severity of the
injury.
Trypsinogen autoactivation and Trypsinogen activation by the lysosomal
enzyme cathepsin B account for the intracellular activation of Trypsinogen
and the zymogen cascade.
Acute injury
Release of active enzymes
Release of vasoactive substances
Vascular damage
Tissue damage and cell death
Generation of cytokines
eg. TNF, IL-1,PAF
Inflammation
Initial Insult
* Zymogen activation
* Ischaemias
* Duct obstruction
[Chapter 5]
[Parth Dhanani] Page 52
The release of active pancreatic enzymes directly causes local or distant tissue
damage, or may enhance inflammation by activating the alternate complement
pathway.
Trypsin digests cell membranes and leads to the activation of other enzymes
within the pancreas.
Figure 16 Pancreatitis
Figure 17 Pancreatitis
Lipase damages the fat cells, producing noxious substances that cause further
pancreatic and peripancreatic injury.
The release of cytokines by the acinar cell or the inflammatory cells directly
injures the acinar cell and enhances the inflammatory response.
Injured acinar cells liberate chemoattractants that attract neutrophils,
macrophages, and other cells to the area of inflammation.
Vascular damage and ischemia causes the release of kinins, which makes
capillary walls permeable and promotes tissue edema.
The release of damaging oxygen-free radicals appears to correlate with the
severity of pancreatic injury.
[Chapter 5]
[Parth Dhanani] Page 53
Medications:
Table 13 Medications for Pancreatitis patient
DRUG
DOSE
ROA
DURATION
GENERIC
NAME
D
1
D
2
D
3
Inj. Magnex
forte in
100ccNS
3g i.v. 12hrly Cefoperazo
ne+
salbectam
√ √ √
Inj. H.Actrapid
acc
--- S/C i.v. 12 hrly √ √ √
Inj. Pantodac 40mg i.v. OD Pantoprazol
e
√ √ √
Inj. Emeset 1 @ i.v. 8 hrly Ondansetro
n
√ √ √
Inj. Contramol
in 100ccNS
1@(50m
g)
i.v. 8 hrly Tramadol √ √ √
Inj. RL at 1@ (150
ml)
i.v. 200ml/hr Ringer
Lactate
√ √ √
Inj. KCl 1@ in
1NS@
2@/day Potassium √ √ √
Inj. Febrinil 1@ i.v. Sos Paracetamol √ √ √
DRUG RELATED ISSUE:
DRUGS INTERACTIONS MANAGEMENT
Ondansetron
↔ Tramadol
Concurrent use of 5-HT3
receptor antagonists may reduce
the analgesic efficacy of
Tramadol. The proposed
mechanism is antagonism of
No particular intervention is
required. However, the
possibility of a diminished
therapeutic response to
Tramadol should be
[Chapter 5]
[Parth Dhanani] Page 54
serotonin-mediated effects of
Tramadol at the spinal level.
considered during
concomitant therapy with 5-
HT3 receptor antagonists.
Insulin ↔
lvp solution
with
potassium
(KCl in NS)
The effect of insulin may be
potentiated, and the risk of
hypoglycemia increased.
If co administered, close
monitoring of blood glucose
level is required.
Diclofenac is widely used analgesic. But in this case, tramadol is used as
diclofenac being belonging to NSAIDs class, is nephrotoxic, which will
further worsen the condition.
Food has to be administered by naso-jejunum route.
When patient begin to recover, he is first given clear water. If tolerated, then
switched on to soft diet and finally, when patient begin to consume full diet,
he is discharged from hospital.
Right now this patient is on soft diet.
[Chapter 5]
[Parth Dhanani] Page 55
CASE STUDY 5: ULCERATIVE COLITIS
Patient details:
Patient name: XYZ
Age: 39 years
Sex: Female
Weight: 71 kg
Height: 5‘8‖
Date Of Admission: 23/08/10
Date of Discharge: 27/08/10
Chief complaints:
- Altered sensorium since 4 days
- Abdominal pain since 4 days
- Low grade Fever since 3days
- Loose motion since 2 days
- Uneasiness since 2 days
Past history:
No past history of HTN/IHD/Drug Allergy/Chest pain
Past medication:
No past medication history
Family History:
No significant family history
Social History:
No tobacco
No alcohol drinking
No smoking
On admissiently on vital data:
Temperature: 99.6 oF
Pulse : 136 / MIN (N:60-90 / MIN)
B.P. : 110/70 mmHg (N: 140 / 90mmhg)
R.R. : 29 / MIN (N: 14 – 18 / MIN)
SPO2: 99% Normal
Systemic examination:
CVS: S1S2 normal
[Chapter 5]
[Parth Dhanani] Page 56
CNS: Altered sensorium
R.S. : Clear
P/A : Soft
Vomiting: Nil
Lab investigations:
Table 14 Lab investigation of Ulcerative Colitis
TEST
OBSERVED
VALUE
NORMAL VALUE
Hemoglobin 6.0 gm/dl 13.5-17.5 gm/dl
DC 60/3/0/0/0 65/35/3/3/6
Total Blood Count 4,940/cmm 4,000-11,000/cmm
Platelet Count 1,11,000/mm 1,50,000-
4,00,000/mm
INR 1.73 0.8-1.2
PT
Test: 20.5
Conrol:13.5
11.1-13.1
Sodium 113 mEq/L 135 – 145 mEq/L
Potassium 3.87mEq/L 3.5 - 5.0 mEq/L
Magnesium 1.1 mEq/L 1.5-2.5mEq/L
Calcium 2.8mEq/L 4.5-5.5mEq/L
Serum Alkaline
Phosphates
92.28IU/L 20 to 140 IU/L.
Serum Protein 2.84 gm/dl 5.5- 9.0 gm/dl
S.G.O.T 17.39 0 – 42 IU/L
Albumin 1.10 gm/dl .4 – 5.4 gm/dl
[Chapter 5]
[Parth Dhanani] Page 57
Blood culture: Negative
USG: Right colon is mildly inflamed and moderately large
DIAGNOSIS: Ulcerative colitis
Pathophysiology:
Ulcerative colitis (UC) usually begins in the rectum. It may remain
localized to the rectum (ulcerative proctitis) or extend proximally,
sometimes involving the entire colon. Rarely, it involves most of the large
bowel at once.
The inflammation caused by UC affects the mucosa and submucosa, and
there is a sharp border between normal and affected tissue. Only in severe
disease is the muscularis involved. In early cases, the mucous membrane is
erythematous, finely granular, and friable, with loss of the normal vascular
pattern and often with scattered hemorrhagic areas. Large mucosal ulcers
with copious purulent exudate characterize severe disease. Islands of
relatively normal or hyperplastic inflammatory mucosa (pseudopolyps)
project above areas of ulcerated mucosa. Fistulas and abscesses do not
occur.
Toxic or fulminant colitis occurs when transmural extension of ulceration
results in localized ileus and peritonitis. Within hours to days, the colon
loses muscular tone and begins to dilate.
Pseudopolyps
Figure 18 Pseudolyps
The terms toxic megacolon or toxic dilation are discouraged because the
toxic inflammatory state and its complications can occur without frank
megacolon (defined as transverse colon > 6 cm diameter during an
[Chapter 5]
[Parth Dhanani] Page 58
exacerbation). Toxic colitis is a medical emergency that usually occurs
spontaneously in the course of very severe colitis but is sometimes
precipitated by opioid or anticholinergic antidiarrheal drugs. Colonic
perforation may occur, which increases mortality significantly.
Figure 19 Colectomy specimen Figure 20 Tongue, lips, palate and pharynx
ulcers
Figure 21 Pyoderma gangrenosum on the leg Figure 22 Endoscopic image
Medication:
Table 15 Medications for UC patient
NAME DOSE ROA GENERIC
NAME
D
1
D
2
D
3
D
4
Inj. Ceftop 0.5g + 0.5g
i.v. Cefoperazone &
sulbactam0
√ √ √ √
Inj. Levoflox 500mg/100ml i.v. Levofloxacin √ √ √ √
Inj. Metrogyl 500mg/100ml i.v. Metronidazole √ √ √ √
Tab. Texim-O 200mg Oral Cefixime -- -- -- --
[Chapter 5]
[Parth Dhanani] Page 59
Inj. Forcan 2mg/100ml
i.v. Fluconazole √ √ √ √
Inj. 25%
Dextrose
Infusion
30mg i.v. 25% dextrose √ -- -- --
Inj. Saline 0.9% 1000 ml i.v. Sodium Chloride √ √ √ √
Inj. Calcium
Gluconate
10 %/10 mL i.v. Calcium
Gluconate
√ √ √ √
Inj.
Magnesium
Sulphate
5mg i.v. Magnesium
Sulphate
√ √ √ √
Inj. Albumin 20% i.v. Human albumin √ √ √ √
Infusion PCV i.v. Pack cell volume √ √ √ --
Liq. Mesacol
Enema
4 mg /60 ml Anal Mesalamine √ √ -- --
Tab. Mesacol 400 mg
Oral Mesalamine -- -- √ √
Inj. Efcorlin 100 mg
i.v. Hydrocortisone
Sodium Succinate
√ √ √ √
Tab. Delsone 40mg
Oral Prednisolone -- -- -- √
Inj. Nexpro 40mg i.v. Esomeprazole √ √ -- --
Tab. Nexpro 20 mg Oral Esomeprazole -- -- √ √
Inj. MVI Amp. i.v. B-Complex √ √ -- --
Inj. Vitamin K 0.5ml in 1
syringe
i.v. Phytonadione √ -- -- --
Tab. Becosules Oral B-complex -- -- -- √
Inj. Emsetron 2ml i.v. Ondansetron √ √ -- --
Inj. 100mg/2ml i.v. Tramadol HCL √ √ -- --
[Chapter 5]
[Parth Dhanani] Page 60
Tramagesic
Tab. Folvite 5mg Oral Folic Acid √ √ √ √
Tab. Calpol 500 mg Oral Paracetamol √ √ √ --
ADVICE:
- Dietary modification may reduce the symptoms of the disease.
- Lactose intolerance is noted in many ulcerative colitis patients. Those with
suspicious symptoms should get a lactose breath hydrogen test.
- Patients with abdominal cramping or diarrhea may find relief or a
reduction in symptoms by avoiding fresh fruits and vegetables, caffeine,
carbonated drinks and sorbitol-containing foods.
- The use of elemental and semi-elemental formula has been successful in
pediatric patients
DRUG RELATED ISSUE:
Table 16 Drug interactions
DRUGS INTERACTIONS MANAGEMENT
Tramadol ↔
Levofloxacin
(Major)
1. The risk of seizures may be
increased during
coadministration of tramadol
with any substance that can
reduce the seizure threshold.
2. Many of these agents also
exhibit CNS- and/or
respiratory-depressant effects,
which may be enhanced during
their concomitant use with
tramadol.
Caution is advised if
tramadol is administered
with any substance that can
reduce the seizure
threshold, particularly in
the elderly and in patients
with epilepsy, a history of
seizures, or other risk
factors for seizures.
Prednisolone
↔
Concomitant administration of
corticosteroids may potentiate
Patients should be advised
to stop taking the
[Chapter 5]
[Parth Dhanani] Page 61
Levofloxacin
(Major)
the risk of tendinitis and tendon
rupture associated with
fluoroquinolone treatment. The
mechanism is unknown.
fluoroquinolone, avoid
exercise and use of the
affected area, and promptly
contact their physician if
they experience pain,
swelling, or inflammation
of a tendon. In general,
fluoroquinolones should
only be used to treat
conditions that are proven
or strongly suspected to be
caused by bacteria and only
if the benefits outweigh the
risks.
Fluconazole
↔
Prednisolone
(Moderate)
Coadministration with
fluconazole may increase the
plasma concentrations of drugs
that are substrates of the
CYP450 3A4 isoenzyme. The
mechanism is decreased
clearance due to inhibition of
CYP450 3A4 activity by
fluconazole.
Caution is advised. Dosage
adjustments as well as
clinical and laboratory
monitoring may be
appropriate for some drugs
whenever fluconazole is
added to or withdrawn from
therapy.
Ondansetron
↔ Tramadol
(Moderate)
Concurrent use of 5-HT3
receptor antagonists may reduce
the analgesic efficacy of
tramadol. The proposed
mechanism is antagonism of
serotonin-mediated effects of
tramadol at the spinal level.
No particular intervention
is required. However, the
possibility of a diminished
therapeutic response to
tramadol should be
considered during
concomitant therapy with
5-HT3 receptor antagonists.
[Chapter 5]
[Parth Dhanani] Page 62
CASE STUDY 6: UNSTABLE ANGINA (IHD)
Patient details:
Patient name: XYZ
Age: 66 years
Sex: Male
Weight: 64 kg
Height: 5‘10‖
Date Of Admission: 11/07/10
Date of Discharge: 17/07/10
Chief complaints:
Pain in chest since 2 days.
Breathlessness since 1day.
Past history:
Diabetes mellitus from last 10 years
Hypertension from last 10 years
No past history of Drug Allergy/TB/Asthma
Past medication:
Tab. Glycomate GP [Glimipride, metformin hydrochloride]
Tab Ramace (ramipril 25mg) OD
Family History:
No significant family history
Social History:
Chewing tobacco
Smoking
No alcohol drinking
On admission vital data:
Temperature: 98.8 oF
Pulse : 84 / MIN (N:60-90 / MIN)
B.P. : 140/90 mmHg (N: 140 / 90mmhg)
R.R. : 16 / MIN (N: 14 – 18 / MIN)
SPO2: 98% Normal
Systemic examination:
[Chapter 5]
[Parth Dhanani] Page 63
CVS: S1S2 normal
CNS: NAD
R.S. : Clear
P/A : Soft
Vomiting: Nil
Stool: Not passed
Lab investigations:
Table 17 Lab investigation of Unstable Angina Patient
TEST DAY 1 DAY 2
Haemoglobin ↓se 12.1 12.9
Total count 5900 5568
ESR 05 (1–25mm/hr) ---
Platelet count 2,67,000 3,12,000
RBS ↑se 158.8 (70 – 110) 179.03
Creatinine 0.7 0.67
Urea 17 14
Sodium ↓se 125.3 135.9
Potassium 3.31 2.97
SGPT 16 (0 – 35 U/L) ---
pH ↓se 7.19 (7.38) ---
pCO2 38 (35-45) ---
pO2 ↓se 67 (80-100) ---
Bicarbonate ↓se 14 (21-30 MEq/L) 16.6
CPK MB ↑se 33.99 (0-7ng/L) 24.03
[Chapter 5]
[Parth Dhanani] Page 64
Troponon I ↑se 10.5 (0-0.4) 6.1
ECG:
- Cardiomegally
- Lateral wall ischaemia
- Pulmonary edema
DIAGNOSIS: UNSTABLE ANGINA (IHD)
BACKGROUND:
UA is defined as angina pectoris or equivalent ischemic discomfort with at least one
of three features:
Occurs at rest (or with minimal exertion) usually lasting _ 10 min,
It is severe and of new onset (i.e., within the prior 4 to 6 weeks), and/or
Occurs with a crescendo pattern (i.e., distinctly more severe, prolonged, or
frequent than previously).
Figure 23 Unstable angina Pathophysiology
PATHOPHYSIOLOGY:
[Chapter 5]
[Parth Dhanani] Page 65
UA/NSTEMI can be caused by a reduction in oxygen supply and/or by an
increase in myocardial oxygen demand (e.g., by tachycardia or severe anemia)
superimposed on a coronary obstruction.
Four pathophysiologic processes that may contribute to the development of
UA have been identified:
Plaque rupture or erosion with superimposed nonocclusive
thrombus, believed to be the most common cause;
Dynamic obstruction [e.g., coronary spasm, as in Prinzmetal variant
angina (p. 1448)];
Progressive mechanical obstruction [e.g., rapidly advancing
coronary atherosclerosis or rest enosis following percutaneous
coronary intervention (PCI)];
Secondary UA related to increased myocardial oxygen demand
and/or decreased supply (e.g., anemia). More than one of these
processes may be involved in many patients.
Figure 24 Process of Atherosclerosis
[Chapter 5]
[Parth Dhanani] Page 66
Figure 25 Endothelial dysfunction influence
MEDICATIONS:
Table 18 Medications of U.Angina patient
DRUG
DOSE
ROA
FRE
QUE
NCY
GENERIC
NAME
D
1
D
2
D
3
D
4
D
5
D
6
Tab. Clavix 75mg Oral BD Clopidogrel √ √ √ √ √ √
Tab.
Ecospin
150mg Oral OD Aspirin √ √ √ √ √ √
Inj. NTG
in 50ml NS
50mg i.v. 1ml/h
r
Nitroglycerin √ √ √ √ √ --
Tab. Indur 30mg Oral 1-1-0 Isosrbide
mononitrate
-- -- -- -- -- √
Tab.
Betaloc
50mg Oral BD Metoprolol √ √ √ √ √ √
[Chapter 5]
[Parth Dhanani] Page 67
Tab.
Atorva
40mg Oral 1HS Atorvastatin √ √ √ √ √ √
Tab.
Ramace
2.5mg Oral 1OD Ramipril √ √ √ √ √ √
Inj. Lasix 2amp. i.v. BD Furosemide √ √ -- -- -- --
Tab.
Lasilactone
20+50 Oral 1-1-0 Furosemide +
Spironolacto
ne
-- -- √ √ √ √
Inj.
Clexane
0.6mg i.v. BD Low Mol.Wt.
Heparin
√ √ √ √ √ --
Liq. Looz 10ml Oral HS Lactulose √ √ √ √ √ √
Tab. Alprex 0.5mg Oral 1 HS Alprazolam √ √ √ √ √ √
Inj. KCl in
50ccNS
3amp. i.v. 2ml/h
r
Potassium
supplement
-- √ √ √ √ √
Inj.
Actrapid
accord
ing to
RBS
i.v. ----- Short acting
insulin
√ √ √ √ √ √
DRUD RELETED ISSUE:
Table 19 Drug interactions
DRUGS INTERACTIONS MANAGEMENT
Furosemide
↔
Metoprolol
Diuretics and beta-blockers may
increase the risk of hyperglycemia
and hypertriglyceridemia in
patients with diabetes or latent
diabetes.
Monitoring of serum
potassium levels, blood
pressure, and blood glucose is
recommended during
coadministration.
[Chapter 5]
[Parth Dhanani] Page 68
Metoprolol
↔ Insulin
Inhibition of catecholamine-
mediated glycogenolysis and
glucose mobilization in
association with beta-blockade
can potentiate insulin-induced
hypoglycemia in diabetics and
delay the recovery of normal
blood glucose levels
Regular monitoring of blood
glucose levels and be aware
that certain symptoms of
hypoglycemia such as
tremors and tachycardia may
be masked.
Furosemide
↔ Ramipril
Coadministration makes
hypotension and hypovolemia
more likely than does either drug
alone. Some ACE inhibitors may
attenuate the increase in the
urinary excretion of sodium
caused by some loop diuretics.
The possibility of first-dose
hypotensive effects may be
minimized by initiating
therapy with small doses of
the ACE inhibitor, or either
discontinuing the diuretic
temporarily or increasing the
salt intake approximately one
week prior to initiating an
ACE inhibitor.
Heparin ↔
Nitroglycerin
Concurrent administration of
heparin and intravenous
nitroglycerin may lead to a
decreased anticoagulant effect.
If coadministered, close
evaluation of the coagulation
status of the patient is
required and heparin dose
titrated as needed.
[Chapter 5]
[Parth Dhanani] Page 69
CASE STUDY 7: PERITONITIS
Patient details:
Patient name: XYZ
Age: 5O years
Sex: Male
Weight: 77 kg
Height: 5‘7‖
Date Of Admission: 3/08/10
Date of Discharge: 7/08/10
Chief complaints:
Fever since 5 days
Abdominal pain since 4 days
Past history:
No past history of DM/HTN/IHD/Asthma
Past medication:
No significant past medical history
Family History:
No significant family history
Social History:
Smoking (20-25 cigarettes per day)
Non alcoholic
On admission vital data:
Temperature103 oF
Pulse : 120/min (N:60-90 / MIN)
B.P. : 90/60 mmHg (N: 140 / 90mmhg)
R.R. : 16 / MIN (N: 14 – 18 / MIN)
SPO2: 98% Normal
Systemic examination:
CVS: S1S2 normal
CNS: Conscious
R.S. : Clear
P/A : Soft
[Chapter 5]
[Parth Dhanani] Page 70
Vomiting: Yes
Stool: Not passed
Lab investigations:
Table 20Lab investigation of Peritonitis patient
TEST DAY 1 DAY 2 DAY 3 DAY 4
Haemoglobin 11.8 10.1 8 9
Total count 3360 7900 6100 5130
Platelet count 2,33,000
(1,30,000—4,00,000)
2,46,000 2,37,000 2,41,000
Creatinine 0.89 1.20 --- ---
Urea 13.5 14.2 --- ---
Sodium 137 139.33 --- ---
Potassium 4.7 3.68 3.75 ---
Calcium --- 8 --- ---
Chloride ↓se 4.37 (95-105) 4.89 --- ---
SGPT ↑se 118.9 113 63.65 ---
Serum Amylase ↑se 2415 --- --- ---
Serum lipase ↑se 5580 1520 --- ---
Serum AlkPo4ase --- 78 (30-
120)
118.6 ---
[Chapter 5]
[Parth Dhanani] Page 71
X-RAY:
- Soft tissue opacity in both lower zones of peritoneal cavity.
- Minimal right pleural effusion
USG:
- Mildly enlarged liver, spleen & kidney
- Bowel: minimal dilation, excessive fluid filled
DIAGNOSIS: PERITONITIS
BACKGROUND:
Peritonitis is an inflammation of the peritoneum; it may be localized or
diffuse in location, acute or chronic in natural history, infectious or aseptic in
pathogenesis.
Acute peritonitis is most often infectious and is usually related to a
perforated viscus (and called secondary peritonitis). When no bacterial
source is identified, infectious peritonitis is called primary or
spontaneous.
Acute peritonitis is associated with decreased intestinal motor activity
resulting in distension of the intestinal lumen with gas and fluid.
Figure 26 Acute Peritonitis Figure 27 Peritonitis dialysis associated
The accumulation of fluid in the bowel together with the lack of oral
intake leads to rapid intravascular volume depletion with effects on
cardiac, renal, and other systems.
[Chapter 5]
[Parth Dhanani] Page 72
PATHOGENESIS:
Infectious agents gain access to the peritoneal cavity through a
perforated viscus, a penetrating wound of the abdominal wall, or
external introduction of a foreign object that is or becomes infected
(for example, a chronic peritoneal dialysis catheter).
In the absence of immune compromise, host defenses are capable of
eradicating small contaminations. Large numbers of mixed aerobic and
anaerobic bacteria, particularly when persistently infused, can lead to
peritonitis.
The conditions that most commonly result in the introduction of
bacteria into the peritoneum are ruptured appendix, ruptured
diverticulum, perforated peptic ulcer, incarcerated hernia, gangrenous
gall bladder, volvulus, bowel infarction, cancer, inflammatory bowel
disease, or intestinal obstruction.
Bacterial peritonitis can also occur in the apparent absence of an
intraperitoneal source of bacteria (primary or spontaneous bacterial
peritonitis). This condition occurs in the setting of ascites and liver
cirrhosis in 90% of the cases, usually in patients with ascites with low
protein concentration (_1 g/L).
Aseptic peritonitis may be due to peritoneal irritation by abnormal
presence of physiologic fluids (e.g., gastric juice, bile, pancreatic
enzymes, blood, or urine) or sterile foreign bodies (e.g., surgical
sponges or instruments, starch from surgical gloves) in the peritoneal
cavity or as a complication of rare systemic diseases such as lupus
erythematosus, porphyria, or familial Mediterranean fever.
Chemical irritation of the peritoneum is greatest for acidic gastric juice
and pancreatic enzymes. In chemical peritonitis, a major risk of
secondary bacterial infection exists.
[Chapter 5]
[Parth Dhanani] Page 73
MEDICATIONS:
Table 21 Medications of peritonitis patient
DRUG
DOSE
ROA
FREQU
ENCY
GENERIC
NAME
D
1
D
2
D
3
Inj.
Magnex
forte
1.5g i.v. 8 hrly Cefoperazone+
salbectam
√ √ √
Inj.
Pantodac
1@ (40mg) i.v. OD Pantoprazole √ √ √
Inj. Emeset 1 @ i.v. 8 hrly Ondansetron √ √ √
Inj.
Contramol
100ccNS
1@(50mg) i.v. sos for
pain
Tramadol √ √ √
Inj. DNS 500ml i.v. Dextrose √ --- ---
Inj.
DNS/RL
1@ i.v. 150ml/hr --- √ √
Inj. NS 120ml i.v. Chloride √ √ √
Inj.
Febrinil
1@ i.v. Sos Paracetamol √ √ √
DRUG RELATED ISSUE:
Table 22 Drug interactions
DRUGS
INTERACTIONS
MANAGEMENT
[Chapter 5]
[Parth Dhanani] Page 74
Ondansetron
↔ Tramadol
Concurrent use of 5-HT3
receptor antagonists may reduce
the analgesic efficacy of
Tramadol. The proposed
mechanism is antagonism of
serotonin-mediated effects of
Tramadol at the spinal level.
No particular intervention is
required. However, the
possibility of a diminished
therapeutic response to
Tramadol should be considered
during concomitant therapy
with 5-HT3 receptor
antagonists.
Insulin ↔
lvp solution
with
potassium
(KCl in NS)
Potassium repletion may
partially or completely reverse
glucose intolerance in some
patients with liver cirrhosis. The
effect of insulin may be
potentiated, and the risk of
hypoglycemia increased.
If co administered, close
monitoring of blood glucose
level is required.
[Chapter 5]
[Parth Dhanani] Page 75
CASE STUDY 8: STROKE
Patient details:
Patient name: XYZ
Age: 63 years
Sex: Male
Weight: 73 kg
Height: 5‘9‖
Date Of Admission: 28/08/10
Date of Discharge: 31/08/10
Chief complaints:
Right sided paralysis from 1.5 month
Inability to stand and speak since few weeks
Fracture on right lower limb few days ago
Past history:
Diabetes mellitus from last 10 years
No past history of Drug Allergy/TB/Asthma
Past medication:
Tab. Glycomate GP [Glimipride, metformin hydrochloride]
Family History:
No significant family history
Social History:
Non smoker
Non alcoholic
On admission vital data:
Temperature103 oF
Pulse : 97/min (N:60-90 / MIN)
B.P. : 160/120 mmHg (N: 140 / 90mmhg)
R.R. : 16 / MIN (N: 14 – 18 / MIN)
SPO2: 99% Normal
Systemic examination:
CVS: S1S2 normal
CNS: Conscious & NAD
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R.S. : Clear
P/A : Soft
Stool: Not passed
Lab investigations:
Table 23 Lab investigation of Stroke patient
TEST RESULTS NORMAL VALUE
Hemoglobin 11.5 gm/dl 13.5-17.5 gm/dl
Platelet Count 4,92,000 1,50,000-4,00,000/mm
Bleeding Time 7.43 2-9.5 min
Creatinine 0.91 0.6-1.3 mg/dL
Urea 73 60-100 ml/min
RBS 200.8mg/dl 74-115mg/dL
BUN 16.97 10-20 mg/dL
Sodium 142.28 mEq/L 135 – 145 mEq/L
Potassium 3.87mEq/L 3.5 - 5.0 mEq/L
Magnesium 1.69 mEq/L 1.5-2.5mEq/L
Calcium 4.8 mEq/L 4.5-5.5mEq/L
Serum Alkaline
Phosphates
92.28IU/L 20 to 140 IU/L.
Serum Protein 8.84 gm/dl 5.5- 9.0 gm/dl
S.G.O.T 17.39 0 – 42 IU/L
CT scan of brain :
Infarct in left external capsule and periventricular location.
Presence of archanoid cyst on left side in the frontal region.
MRI :
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Small area of gliosis in left cerebral region
Acute Infarct in left external capsuloganglionic and left temporal parietal
region.
Arachnoid cyst along with left frontal convexity.
MR-Venogram: Appears unremarkable except hypoplastic left transverse
sinus
Carotid Doppler study :
Shallow non obstructive plaque is seen in carotid bulb on right side.
Long segment soft plaque is seen in common carotid artery on left side
with max.
DIAGNOSIS: STROKE
PATHOPHYSIOLOGY:
ISCHEMIC STROKE:
In carotid atherosclerosis, progressive accumulation of lipids and
inflammatory cells in the intima of the affected arteries, combined with
hypertrophy of arterial smooth muscle cells, results in plaque formation.
Eventually, sheer stress may result in plaque rupture, collagen exposure,
platelet aggregation, and clot formation.
The clot may remain in the vessel, causing local occlusion, or travel
distally as an embolism, eventually lodging downstream in a cerebral
vessel. In the case of cardiogenic embolism, stasis of blood in the atria or
ventricles of the heart leads to the formation of local clots that can become
dislodged and travel directly through the aorta to the cerebral circulation.
The final result of both thrombus formation and embolism is an arterial
occlusion, decreasing cerebral blood flow and causing ischemia distal to
the occlusion.
Reduction in the provision of nutrients to the ischemic cell eventually
leads to depletion of the high-energy phosphates (e.g., ATP) necessary for
the maintenance of membrane integrity.
Subsequently, extracellular potassium accumulates at the same time that
sodium and water is sequestered intracellularly, leading to cell swelling
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and eventual lysis. Electrolyte imbalance also leads to depolarization of
the cell and influx of calcium into the cell.
The increase in intracellular calcium results in the activation of lipases,
proteases, and endonucleases and the release of free fatty acids from
membrane phospholipids. The depolarization of the neuron leads to the
release of excitatory amino acids, such as glutamate and aspartate that
perpetuate the neuronal damage when released in excess.
The accumulation of free fatty acids, including arachidonic acid, results in
the formation of prostaglandins, leukotrienes, and free radicals. In
ischemia, the magnitude of free radical production overwhelms normal
scavenging systems, leaving these reactive molecules to attack cell
membranes and contribute to the mounting intracellular acidosis. All these
events occur within 2 to 3 hours of the onset of ischemia and contribute to
the ultimate cell death.
Later targets for intervention in the pathophysiologic process involved
after cerebral ischemia include the influx of activated inflammatory cells,
starting from 2 hours after the onset of ischemia and lasting for several
days.
Figure 28 Ischaemic Shock Figure 29 Haemorrhagic Shock
HEMORRHAGIC STROKE
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[Parth Dhanani] Page 79
Presence of blood in the brain parenchyma causes damage to the surrounding
tissue through the mechanical effect it produces (mass effect) and the
neurotoxicity of the blood components and their degradation products.
Compression of the tissue surrounding the hematoma also may lead to
secondary ischemia in some cases.
Approximately 30% of intracerebral hemorrhages continue to enlarge over the
first 24 hours, and clot volume is the most important predictor of outcome,
regardless of location.
Much of the early mortality of hemorrhagic stroke (up to 50% at 30 days) is
due to the abrupt increase in intracranial pressure that can lead to herniation
and death.
MEDICATIONS:
Table 24 Medications of Stroke patient
DRUG
DOSE
ROA
FREQ.
GENERIC
NAME
D
1
D
2
D
3
D
4
Inj. Monocef 1 g i.v. BID Ceftriaxone
Inj. Pantocid 40mg i.v. BID Pantoprazole
Inj. DNS 100ml/
hr
i.v. --- Dextrose
Tab. Folvite 5mg Oral TID Folic Acid
Tab. Ecosprin 150mg Oral OD Aspirin
Inj. Clopivas 75mg i.v. OD Clopidogrel
Tab. Unicobal 1@ Oral OD
Tab. Atorvas 10mg Oral HS
Tab. Valance
OD
250/50
0
Oral BID
Tab. Tryptomer 10mg Oral ½ HS
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[Parth Dhanani] Page 80
Tab. Faldex --- Oral BID
Tab. Bizaden-
forte
--- Oral BID
Inj. Actrapid Acco.
to RBS
i.v. ----- Short acting
insulin
√ √ √ √
Non Pharmacological Therapy:
Do not make patient stand up
Water bed till patient recover to stand and walk
Patient may sit up in the bed
Change the patient‘s position at least every 2 hr in order to increase
blood circulation
Exercise patient‘s limbs carefully according to therapists' instructions
Keep the patient‘s mind active
Physical touch and relaxed conversation to promote emotional health
Rehabilitation by speech therapy, occupational therapy and physical
therapy
Suggestion:
Restrict salt intake in diet
Avoid alcohol and smoking
Avoid fat containing food.
Avoid sugar intake to control blood sugar level
Eat more fruits, vegetables, whole grains, nuts ,etc
DRUG RELATED ISSUE:
Table 25 Drug interactions
DRUGS INTERACTIONS MANAGEMENT
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Clopidogrel
↔
Pantoprazole
(Major)
Coadministration with proton
pump inhibitors (PPIs) may
reduce the cardioprotective
effects of clopidogrel. The
proposed mechanism is PPI
inhibition of the CYP450 2C19-
mediated metabolic
bioactivation of clopidogrel.
Use of Pantoprazole should
preferably be avoided in
patients treated with
clopidogrel.
If gastroprotection is
necessary, H2-receptor
antagonists or antacids
should be prescribed
whenever possible.
Aspirin ↔
Piroxicam
(Moderate)
Combined use of low-dose or
high-dose aspirin with other
nonsteroidal anti-inflammatory
drugs (NSAIDs) may increase
the potential for serious
gastrointestinal (GI) toxicity,
including inflammation,
bleeding, ulceration, and
perforation.
During concomitant
therapy, patients should be
advised to take the
medications with food and
to immediately report signs
and symptoms of GI
ulceration and bleeding
such as abdominal pain,
bloating, sudden dizziness
or lightheadedness, nausea,
vomiting, hematemesis,
anorexia, and melena.
Aspirin ↔
Divalproex
sodium
(Moderate)
Aspirin may displace valproate
from protein binding sites and
inhibit its clearance. Four-fold
increases in the free fraction of
valproate have been reported in
children. Increased therapeutic
and toxic effects may be
expected to occur.
Patients should be advised
to notify their physician if
they experience possible
symptoms of toxicity (e.g.,
malaise, weakness,
lethargy, drowsiness,
nausea, vomiting, or
abdominal pain).
Amitriptyline
↔ Divalproex
Concomitant administration of
valproic acid may increase
serum concentrations of
It may be advisable to
monitor patients for altered
efficacy and safety. Dose
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sodium
(Moderate)
tricyclic antidepressants. The
proposed mechanism of action
is inhibition of CYP450 hepatic
metabolism.
adjustments or alternate
therapy may be necessary if
an interaction is suspected.
[Chapter 5]
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CASE STUDY 9: CANCER OF GALL BLADDER
Patient details:
Patient name: XYZ
Age: 59 years
Sex: Male
Weight: 71 kg
Height: 5‘8‖
Date Of Admission: 22/07/10
Date of Discharge: 02/07/10
Chief complaints:
Abdominal Pain
Nausea / Vomiting
Low grade fever
Past history:
No significant past history
Past medication:
No past medication history
Family History:
Low socio-economic class
No disease running in family
Social History:
Married
Normal diet & sleep
Chewing tobacco
Non alcoholic
On admission vital data:
Temperature: Normal
Pulse : 100 / MIN (N:60-90 / MIN)
B.P. : 104/60 mmHg (N: 140 / 90mmhg)
R.R. : 16 / MIN (N: 14 – 18 / MIN)
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SPO2: 92% Normal
Systemic examination:
CVS: S1S2 Normal
CNS: Conscious
R.S. : Normal
P/A : Soft
Lab investigations:
Table 26 Lab investigation of CA gall bladder pat
TEST RESULTS NORMAL VALUE
Hemoglobin 13.6 gm/dl 13.5-17.5 gm/dl
Total Blood Count 10,000 /cmm 4,000-11,000/cmm
Differential Count :
- Neutrophils
- Eentosinophils
- Basophils
- Lymphocytes
- Monocytes
62 %
8 %
1 %
9 %
-
50-65 %
0 – 3 %
1 – 3 %
25 – 35 %
2 – 6 %
Platelet Count 1,85,000 /mm 1,50,000-4,00,000/mm
Prothrombin Time 18.1 sec 10-12 sec
Creatinine 1.1 gm/dl 0.5-1.5 gm/dl
C- reactive protein 216.41 mg/L < 8 mg/L
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Sodium 126.62 mEq/L 135 – 145 mEq/L
Potassium 3.32 mEq/L 3.5 - 5.0 mEq/L
Total Bilirubin :
- Direct
- Indirect
1.17 mg/dl
0.68 mg/dl
0.50 mg/dl
0.1 – 1.2 mg/dl
0.1 – 0.3 mg/dl
0.1 – 1.0 mg/dl
Creatinine
Phosphokinase
603.34 IU/L 30 – 180 IU/L
ABGA : -
- pH
- pCO2
- pO2
- HCO3
- SaO2
7.37
30 mmHg
65 mmHg
17 mmHg
92 %
7.35 – 7.45
35 – 45 mmHg
80 – 100 mmHg
22 – 26 mg Hg
≥ 95 %
SGPT 41.07 0 – 42 IU/L
Serum Protein Total
-Albumin
7.28 gm/dl
4.34 gm/dl
6.3 – 8.2 gm/dl
3.4 – 5.4 gm/dl
Transabdominal Ultrasonography :
Thickened gallbladder
A mass in the gallbladder
MRCP (Magnetic Resonance Cholangiopancreatography) :
Medical imaging technique that uses magnetic resonance imaging to
visualise the biliary and pancreatic ducts in a non-invasive manner
[Chapter 5]
[Parth Dhanani] Page 86
Chronic Gall Stones present
Chest X – Ray : Normal
CT Scan (Brain): Tumor is present
Diagnosis:
- CA Gallbladder
- Obstructive Jaundice
- ARF
- Hyponatremia
- Hypokalemia
Pathophysiology:
Gallbladder cancer arises in the setting of chronic inflammation. In the
vast majority of patients (>75%), the source of this chronic inflammation
is cholesterol gallstones. The presence of gallstones increases the risk of
gallbladder cancer 4- to 5-fold.3 Other more unusual causes of chronic
inflammation are also associated with gallbladder cancer. These causes
include primary sclerosing cholangitis, ulcerative colitis, 4
liver flukes,
chronic Salmonella typhi and paratyphi
infections, and Helicobacter infection.
Figure 28 Cancer of gall bladder
However, chronic gallbladder inflammation is likely only part of the cause
of the malignant transformation seen in gallbladder cancer. Many other
factors have been identified. Ingestion of certain medications (e.g., oral
contraceptives, INH, methyldopa) can increase the risk of gallbladder
cancer. Likewise, certain chemical exposures (e.g., pesticides, rubber, and
[Chapter 5]
[Parth Dhanani] Page 87
vinyl chloride) and occupational exposures associated with working in the
textile, petroleum, paper mill, and shoemaking industries increase the risk
of gallbladder cancer.
In addition, exposures through water pollution (organ pesticides, e.g.,
dichlorodiphenyltrichloroethane and benzene hexachloride); heavy metals
(e.g., cadmium, chromium, lead); and radiation exposure (e.g., radon in
miners) are associated with gallbladder cancer.
Obesity7
may contribute to gallbladder cancer through its association with
gallstones, its association with increased endogenous estrogens, or through
the ability of fat cells to secrete a large number of inflammatory mediators.
Hereditary nonpolyposis colon cancer.
Abnormal anatomy such as congenital defects with anomalous
pancreaticobiliary duct junctions and choledochal cysts increase the risk of
gallbladder cancer. The tumor is usually located in the fundus of the
gallbladder.
Local spread through the gallbladder wall can lead to direct liver invasion,
or, if in the opposite direction, leads to transperitoneal spread (20% of
patients at presentation), with implants on the liver, on the bowel, and in
the pelvis.
Tumor may also directly invade other adjacent organs such as the stomach,
duodenum, colon, pancreas, and extrahepatic bile duct. At diagnosis, the
gallbladder is often replaced or destroyed by the cancer, and
approximately 50% of patients have regional lymph node metastases.
MEDICATIONS:
External Beam Radiation :
EBRT works by directing an external "beam" of radiation onto areas of
the body that are affected by gallbladder cancer
High-energy X-ray machine
Percutaneous Transhepatic Biliary Drainage (PTBD) :
[Chapter 5]
[Parth Dhanani] Page 88
PTBD is an invasive and effective therapeutic method of relieving
benign or malignant biliary obstruction and may be life saving if the
patient is septic.
The drainage is achieved by inserting a plastic tube, called a catheter,
through a tiny incision of the skin into the obstructed bile duct.
Table 27 Medications of CA gall bladder patient
NAME DOSE ROA FREQ. GENERIC
NAME
Start
Date
Stop
Date
Inj. Magnex
Forte
1.5gm Iv 8 hrly Cefoperazone
+Sulbactam
22/7 26/7
Inj. DNS 1 lit. i.v. 140ml/
hr
Dextrose 22/7 2/8
Inj. Contramol 80 mg
in
100cc
i.v. Sos Tramadol 22/7 2/8
Inj. Pantocid 40mg i.v. Bid Pantoprazole 22/7 25/7
Tab. Pantodac 40mg Oral Bid Pantoprazole 26/7 2/8
Inj. Emeset 32 mg
in
100cc
NS
Iv 8 hrly Ondasetron 24/7 2/8
Inj. Febrinil 150mg
in 10cc
Iv 8hrly Paracetamol 22/7 2/8
Inj. Lasix 80mg
in 10cc
Iv 6 hrly Furosemide 24/7 25/7
Neb. Duolin 2
Inhalati
Neb. Qid Levosalbuta
mol Sulphate
22/7 24/7
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[Parth Dhanani] Page 89
on and
Ipratropium
Bromide
Inj. Deriphyllin 16 units
sc b bf,
12 units
b
dinner
Iv Bid Hydroxyethyl
Theophylline
24/7 25/7
Inj. Vit K1 1 amp Iv Qd Vit k 22/7 22/7
Neb. Levolin 2
Inhalati
on
Neb. Bid Levosalbuta
mol
25/7 2/8
Liq. LOOZ 20 ml Oral Bid Lactulose 25/7 2/8
Tab. Dolo 650 mg Oral OD Paracetamol 26/7 30/7
Inj. Zienam 500mg
in
100ml
NS
Iv 8hrly Aztreonam 31/7 2/8
Inj. Eldervit 1 amp
in
100cc
Iv Qid Multivitamin 31/7 2/8
Syp. Sparacid 2 TSF Oral Qid Sucralfate 31/7 2/8
Inj. KCl 20/5ml
NS
Iv 4ml/hr Potasium 22/7 30/7
Inj.
Sodabicarbona
1 amp
iv
Iv 4 hrly NaCl 24/7 29/7
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[Parth Dhanani] Page 90
te
Tab. Folvite 10 mg Oral Qid Folic Acid 31/7 2/8
Inj. Syscan 10ml Iv Bid Fluconazole 31/7 2/8
DIETARY MODIFICATIONS:
No milk and milk products
Soft/ Liquid diet
No fatty and oily food
Avoid Spicy food
DISCHARGE MEDICATIONS:
Table 28 Discharge medications
Name of Medicine Dose Use
Inj. Magnex Forte
(Cefoperazone+Sulbactam)
1.5gm iv 8 hrs Antibiotic
Inj. DNS 1 lit. (140ml/hr) Dehydration
Inj. Contramal ( Tramadol ) 80 mg in 100cc iv 8
sos
Analgesic
Tab. Folvite (Folic Acid) 10 mg qd Folic acid
supplement
Tab. Pantodac (Pantoprazole) 40mg bid Antacid
Inj. Emeset (Ondasetron) 32 mg in 100cc NS iv Anti emetic
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Inj. Febrinil ( Paracetamol) 150mg in 10cc iv Analgesic &
Antipyretic
Inj. Syscan (Fluconazole) 10ml i.v. Antimicrobial
DRUG RELTED ISSUE:
DRUG INTERACTIONS MANAGEMENT
Ondansetron ↔
Tramadol
(Moderate)
Concurrent use of 5-HT3
receptor antagonists may
reduce the analgesic
efficacy of tramadol. The
proposed mechanism is
antagonism of serotonin-
mediated effects of
tramadol at the spinal level.
No particular intervention
is required. However, the
possibility of a
diminished therapeutic
response to tramadol
should be considered
during concomitant
therapy with 5-HT3
receptor antagonists.
Fluconazole ↔
Ondansetron
(Moderate)
Concurrent use of two or
more drugs that can cause
QT interval prolongation
may increase the risk of
ventricular arrhythmias,
including ventricular
tachycardia and torsades de
pointes, due to additive
arrhythmogenic potential
related to their effects on
cardiac conduction.
Caution and clinical
monitoring are
recommended if multiple
agents associated with QT
interval prolongation are
prescribed together.
Patients should be advised
to seek medical attention
if they experience
symptoms that could
indicate the occurrence of
torsades de pointes such
as dizziness, palpitations,
or syncope.
[Chapter 5]
[Parth Dhanani] Page 92
CASE STUDY 10: URINARY TRACT INFECTION
Patient details:
Patient name: XYZ
Age: 68 years
Sex: Female
Weight: 73 kg
Height: 5‘3‖
Date Of Admission: 15/07/10
Date of Discharge: 22/07/10
Chief complaints:
Abdominal pain & distention from 1 day
Pedal edema & Decreased urine output from 3 days
Breathlessness from 1 day
Past history:
Diabetes Mellitus (10 years)
Hypothyroidism (3 years)
Mastectomy for (L) breast
Past medication:
Chemotherapy CMF (cyclophosphamide, methotrexate, and
fluorouracil)
Eltroxin (levothyroxin sodium) 100 mcg
Actrapid (human soluble insulin)
Family History:
Father suffered from Diabetes.
No other significant disease in family.
Social History:
Non-smoker
No alcohol consumption
On admission vital data:
Temperature: 100 oF
Pulse : 140 / MIN (N:60-90 / MIN)
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B.P. : Q120/90 mmHg (N: 140 / 90mmhg)
R.R. : 16 / MIN (N: 14 – 18 / MIN)
SPO2: 99% Normal
Systemic examination:
CVS: S1S2 Normal
CNS: Unconscious
R.S. : Normal
P/A : Soft
Lab investigations:
Table 29 Lab investigation of UTI patient
TEST PATIENT’S VALUE NORMAL
VALUE
SERUM CREATININE 4.64 mg/dL 0.8-1.4
GLOMERULAR
FILTERATION RATE
15 mL/min 90 - 120 mL/min
UREA 45 mg/dL 7–21 mg/dL
SERUM BILIRUBIN 0.8 mg/dL 0.2-1.2
SGPT 29.92 U/L 0-45 U/L
ALKALINE
PHOSPHATASE
109.88 IU/L 44-147 IU/L
SERUM PROTEINS Total 5.3 g/dL Total 60-85 g/ dL
SERUM
ELECTROLYTES
• SODIUM
• POTASSIUM
120 mEq/L
4.95 mEq/L
137-149 mEq/L
3.5-5 mEq/L
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TSH 0.01 U/L 0.5-5.0 U/L
Pus cells(Urine) 70-80 -
RBC(Urine) 40-50 -
Epithelial cells(Urine) +1 -
Hb 15.8 g/dL 13.8-18.2 g/Dl
Differential count
• Neutrophils
• Lymphocytes
• Eosinophils
• Monocytes
91%
6%
1%
3%
44-74%
24-44%
Upton 3%
Upto 4%
Platelet 172,600/ µL 150,000-450,000/
µL
pH 7.34 7.35-7.45
pCO2 26 mmHg 35-45 mmHg
pO2 73 mmHg 80-100 mmHg
HCO3 14 mmHg 22-26 mmHg
USG of Abdomen:
Both kidneys are swollen
As both cortex and medulla are distinguishable it suggest ARF
DIAGNOSIS:
Urinary Tract Infection
Acute Renal Failure
Metabolic Acidocis
Hypertension
[Chapter 5]
[Parth Dhanani] Page 95
Sepsis
Hypothyroidism
PATHOPHYSIOLOGY:
The bladder wall is coated with various mannosylated proteins, which
interfere with the binding of bacteria to the uroepithelium. As binding
is an important factor in establishing pathogenicity for these
organisms, its disruption results in reduced capacity for invasion of the
tissues.
Moreover, the unbound bacteria are more easily removed when
voiding.
Figure 29 UTI
The use of urinary catheters (or other physical trauma) may physically
disturb this protective lining, thereby allowing bacteria to invade the
exposed epithelium.
During cystitis, E. Coli overcomes the defenses by invading superficial
umbrella cells and rapidly increasing in numbers to form intracellular
bacterial communities. By working together, bacteria build themselves
into structures that are more firmly anchored in infected cells and are
more resistant to immune system assaults and antibiotic treatments.
This is often the cause of chronic urinary tract infections.
[Chapter 5]
[Parth Dhanani] Page 96
MEDICATIONS:
Table 30 Medications of UTI patient
DRUG DOSE ROA DURATION GENERIC NAME DAY
1 – 7
Inj. Sodium
bicarbonate
120
mEq
I.V 6 amp as bolus
6 amp hourly
Sodium bicarbonate √
Inj. Actrapid 4-6-4
units
S.C Q 6 hr Insulin √
Inj. Zostum 1 g I.V For the first 12
hrs
cefoperazone +
salbectam
√
Inj. Magnex forte 1.5 g I.V q 8 hr cefoperazone +
salbectam
√
Inj. Metrogyl 100 mL I.V q 8 hr Metronidazole √
Inj. Tarivid 200 mg I.V q 12 hrs Ofloxacin √
Inj. Lasix 2 amp I.V q 12 hrs Furosemide √
Tab. Thyronorm 50 mcg Oral OD Thyroxin sodium √
Inj. Leucovorin 15 mg
in 100cc
NS
I.V QD Reduced folinic
acid
√
Inj. Optineuron 1 amp in
100 mL
I.V QD Vitamin √
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NS Supplement
Emeset 4 mg Oral q 8 hr Ondansetron √
Vibact D 500 mg Oral q 8 hr Lactobacilli √
Tab. Dolo 500 mg Oral Q 8 hr Paracetamol √
DISCHARGE MEDICATION:
Tab Tarivid(ofloxacin) 200mg 1-0-1 for 5 days
Tab folvite(folic acid) 5mg 0-1-0 for 5 days
Tab Thyronorm (thyroxin) 50mcg 1-0-0 continue
Tab Optineuron (vitamins) 0-1-0 for 5 days
Inj. Actrapid (human soluble insulin)
PATIENT Counseling:
Wipe carefully the front and back area of the genitalia.
Empty the bladder frequently.
Drink enough liquids since the bacteria are flushed out when it gets in
the urinary tract through this process.
DRUG RELATED ISSUE:
Table 31 Drug interactions
DRUGS INTERACTION MANAGEMENT
Furosemide ↔
Cefoperazone
(Moderate)
Loop diuretics enhance the
nephrotoxicity of some
cephalosporins by an
unknown mechanism.
It is advisable to obtain a
serum creatinine level within
48 hours and periodically
during therapy.
[Chapter 5]
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Ofloxacin and
Ondansetron
(Moderate)
Both drugs prolong the QT
interval of heart.
Patients should be advised to
seek medical attention if they
experience symptoms as
dizziness, palpitations, or
syncope.
Ofloxacin and Insulin
(Moderate)
Quinolone antibiotics may
interfere with the therapeutic
effects of insulin
Blood glucose should be
monitored closely whenever
Quinolone are prescribed to
patients.
[Chapter 6]
[Parth Dhanani] Page 99
CHAPTER: 6 Results and Discussion of Learning Experience
Result:
MEDICATION ERRORS AND ADR REPORTING MONITORING:
Total No. of Case Studied: 50
Total No. of Medication Error found: 77 (1 ME +76 DI)
Total No. of Medication Error per case: 1.54
Total No. of Adverse Events/ Reaction found: 1
Total No. of Adverse Events/ Reaction per case: 0.02
Disease-wise Classification of Medication Errors:
Table 32 Disease wise classification
Diseases Total
case
No of
ME +DI
ME
per
Case
No of
ADRs
ADRs
per case
Rheumatoid arthritis 3 6 2.0 0 0
Diabetes 3 5 1.66 1 0.2
Renal Disease 6 12 2 O 0
Liver disease 9 10 1.11 0 0
Cardiovascular
disease
5 7 1.4 0 0
Fever cases 7 5 O.7 0 0
Cancer 4 3 O.75 0 0
Gastric Disorder 3 5 1.66 0 0
HIV 1 0 0 0 0
Hernia 1 0 0 0 0
[Chapter 6]
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Table 33 Bar graph of disease wise classification
Gender-wise Classification of Cases:
Table 34 Gender wise classification
3 3
6
9
5
7
43
1 12
1 1 1 1 1
0
2
4
6
8
10
12
14
Total cases
No.of Mes
ME/Case
CNS 2 5 2.5 0 0
Hyperthyroidism 1 1 1 0 0
Appendicitis 1 0 0 0 0
Dog Bite 1 2 2 0 0
Gall Stones 1 3 3 0 0
Pancreatitis 1 2 2 0 0
Gender Cases ME ME/Case
Male 34 50 1.47
Female 16 27 1.68
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Table 35 Bar graph of gender wise classification
Age-Wise classification:
Table 36 Age wise classifications
0
5
10
15
20
25
30
35
40
45
50
Male Female
34
16
Cases
ME
ME/Case
Class Cases ME ME/Case
Paediatrics 4 1 0.25
Adult 25 40 1.60
Geriatrics 21 36 1.71
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Table 37 Pie chart of age wise classification
Discussion:
The learning experience at Shrey Hospital was absolutely unique and
taught us about the practical aspects of the pharmacy and the health
care profession. We had learnt all the theoretical part till now, and now
it was the time to get the practical knowledge.
First, we learned about the Pharmacy Store. The Pharmacy deal with
the maintenance of drugs and consumables in the hospital. The
functions of this department include inventory management of drugs,
consumables and sutures. It also handles the billing of drugs,
consumables and sutures, if required. The Pharmacy ensures that there
is a round the clock availability of a sufficient quantity of drugs and
consumable material for the patients in a mode that neither hinders
efficient clinical work, nor it becomes a threat to the survival of the
Pharmacy.
4
25
21
Cases
Pediatrics
Adults
Geriatrics
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Shrey pharmacy works following similar operating procedures and
guidelines. The team provides medicines for many areas both on and
off site. They provide services to in-patients and out-patients from
every clinical area. Shrey have dedicated and motivated team of
pharmacist and support staff who aim to deliver a seamless service to
all our patients and other clients.
The medicines in Shrey Pharmacy are arranged in shelves according to
the company they belong. In that particular company shelf the drugs
are arranged in alphabetical order.
The staff is well trained so that they know the location of each
medicine or the company to which it belongs to.
Storage of Medicine :
The medicines are stored in the Pharmacy at room temperature.
Special medicine such as insulin and certain injectables which
degrade at room temperature are kept in the refrigerator and the
temperature of the refrigerator is checked every morning by the
ATO.
Shrey Pharmacy does not have the license for Narcotics so no
locked storage is required.
Records Maintenance :
The inventory list is printed every morning and that is done by
the ATO.
The expiratory is done in the starting of every month by
computer as well as manually.
The computer stores the record of the expiry date of each batch
they have in stock.
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The record of the dispensing of drugs and the patient record is
stored in the computer.
Ordering of Drugs :
The ordering of drugs is done by phone in Shrey Hospital.
The names of the medicines are listed down during the day in a
sheet of paper when they are out of some medicine or only few
are left.
At the end of the day the ordering is done by pharmacist on
phone.
Inpatient treatment program:
As the name implies, those who receive help through an
inpatient treatment program remain at treatment facility 24
hours per day. After the intensive inpatient treatment is
complete, it is generally suggested that the patient receive
extensive outpatient treatment.
Clinical services provided to patients are essential components
of the Department of Pharmacy Services role at the Medical
Center. These services include:
Receipt and evaluation of all doctor orders, not just
medication orders, to ensure the best medication management.
Orders are reviewed to ensure the absence of allergies and drug
interactions, appropriateness of medication selection, dosage,
route and duration of therapy.
Therapeutic drug monitoring for medications with a narrow therapeutic
index. e.g.: aminoglycosides, vancomycin and anticoagulation
therapies.
Rounds with the multidisciplinary care team
Drug information
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Education of nurses, doctors and patients
Participation in medical and pharmacy teaching programs
Outpatient treatment program :
An outpatient treatment program, on the other hand, allows the
patient to remain at home while undergoing treatment
This makes it possible for patient to continue working and to be
with his family while undergoing care. In an outpatient
program, the patient attends treatment during the day.
When it comes to choosing the right recovery program, there
are many factors to consider. For example, an outpatient
treatment program may be best for a person that:
1. Needs to continue working every day while undergoing
treatment.
2. Cannot afford to pay for inpatient treatment, which tends to
be quite costly.
Has a supportive household that will ensure he attends
treatment programs and carries through with program goals
while at home
A partial hospitalization program has many of the same
advantages of an outpatient treatment program.
[Chapter 7]
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CHAPTER: 7
SEMINARS AND PRESENTATIONS
1. Seminar on ACLS and CPR:
Key Issues in ACLS (Advanced Cardiac Life Support):
Cardiac Functioning
Respiration
Circulation
Quick BLS Review:
Give 2 rescue breaths. Each breath over 1 second, enough to make the
chest rise.
Check the pulse for minimum of 5 seconds but no longer than 10
seconds. If no pulse or unsure, start CPR!
Compression to ventilation ratio 30:2; after advanced airway no need
to interrupt compressions (Rate 100/m)
BLS Key Concepts
Avoid Hyperventilation (Do not ventilate too fast or too much volume)
Push hard and fast, allow complete chest recoil, minimal interruptions
Compress chest depth of 1.5 to 2 inches at a rate of 100 compressions
per minute.
Chest compression should not be interrupted except for: (coronary
perfusion pressure)
Shock delivery
Rhythm check
Ventilation (until an advanced airway is inserted)
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Resume CPR immediately after shock. Interruption in CPR for rhythm check
should not exceed 10 seconds. Do not interrupt CPR:
To insert cannula or to give drugs
To listen to the heart or to take BP???
Waiting for charging the Defibrillator
Figure 30 Algorithm for basic life support for adults
Priorities
Primary importance:
Prompt CPR
Early Defibrillation for VF/VT
Secondary importance:
Insertion of advanced airway
IV Access and Drug administration
ACLS always starts with BLS
―Are you OK?‖ Is the patient conscious?
Call for help.
Do primary survey: ABCD
Airway- Is it opens?
Breathing- moving air? Look, Listen, and Feel
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Circulation- checks pulse, start CPR!
Defibrillation- if VF or pulseless VT
Introduction to CPR:
Rescuers should be taught to place the hands on the centre of the chest
instead of wasting time by using the ―rib margin‖ method.
Rescue breathing by tilting head and lifting a chin
Airway assessment by listen at the victim‘s mouth for sound breaths
and feel the air on the cheek.
2. Seminar on maintaining Respiratory Function, Nutrition and Fluid:
1. Ambu‘s Bag:
A bag valve mask is a hand-held device used to
provide ventilation to a patient who is not
breathing or who is breathing inadequately. The
device is a normal part of a resuscitation kit.
The device is used extensively in the operating
room to ventilate an anaesthetized patient in the minutes before a
mechanical ventilator is attached. The
device is self-filling with air, although
additional oxygen can be added.
2. Rebreathing mask:
Figure 32 Place the hands on the chest
Figure 31 Tilt head and lift Figure 33 Airway assessment
Figure 34 Ambu’s Bag
Figure 35 Rebreathing mask
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Deliver oxygen from storage to lungs
3. Ventury mask:
The Ventury mask is used to deliver a known oxygen
concentration to patients on controlled oxygen therapy.
Are considered high-flow oxygen therapy devices.
The kits usually include multiple jets in order to set the
desired FIO2, which are usually color coded,
Blue = 24%; Yellow = 28%; White =
31%; Green = 35%; Pink = 40%; Orange
= 50%.
The color varies with different brands and the user must check the
instructions
4. Endotracheal Intubation:
Placing a breathing tube into the patient‘s
body. It is needed when patient can no longer
cough and clear secretions or difficulty in
breathing.
Inserted through mouth or nose
The breathing tube is passed through into the
nose passage and slips into the patient‘s
airway
Require sedation when inserting a tube
through the mouth
The person uses the Laryngoscope to move
the patient‘s tongue out of the way to see the
airway clearly.
Vocal cords, upper airway can be injured.
Curved and straight blades are used for adults
Figure 36 Venture masks
Figure 37 Endotracheal Intubation
Figure 38 Laryngoscope Blades
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and children
5. Tracheostomy:
A Tracheostomy is a surgical procedure to create
an opening through the neck into the trachea. A
tube is usually placed through this opening to
provide an airway and to remove secretions from
the lungs.
It is done when large object blocking the airway, cancer of neck,
paralysis of the muscles of the neck, severe neck and mouth injuries.
Risks of the procedure are bleeding, infection, nerve damage and scar
tissue in the trachea
It takes time for patient to learn how to communicate with others
Cannulation: is a tube that can be inserted into the body, for the
delivery or removal of fluid.
1. Intravenous cannula: It is inserted into a vein,
for the administration of intravenous fluids,
obtaining blood samples or administering
medicines.
2. Nasal Cannulation: inserted into the mouth or
nostril and used to deliver a gas, gas mixture and to
measure airflow into and out of the nostrils.
Central venous catheter: It is a catheter placed into
a large vein in the neck (internal jugular vein), chest
(subclavian vein OR femoral vein).
It is used to administer medication or fluids,
obtain blood tests, and directly obtain the
central venous pressure.
Medications, such as inotropes and
Figure 39 Tracheostomy
Figure 40 IV cannula
Figure 41 Nasal cannula
Figure 42 Central venous catheter
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amiodarone, by central line.
3. FEEDING TUBES:
It is temporary and to provide nutrition in chronic conditions. Different
types of feeding tubes are:
1. Nasogastric tube (NG tube) - is passed through the nostrils, down the
esophagus and into the stomach.
2. Gastric (G) feeding tube- is a tube inserted
through a small incision in the abdomen into
the stomach. It is usually used to avoid the
risk of aspiration pneumonia. It is suitable for
long term feeding about 6 months.
3. J tube (jejunostomy tube): is a tube inserted
through the abdomen and into the jejunum
4. Tube position is checked by, testing pH of the aspirate and taking X-
rays
4. Seminar on Pacemaker and Insulin Devices:
Pacemakers:
What is a pacemaker?
A pacemaker is a sophisticated electronic device that
does two things:
Figure 43 Feeding tubes
Figure 44 Insulin device
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Analyzes the function of the heart‘s own electrical system.
When necessary, it sends tiny, precisely-timed electrical signals to the
heart, to correct certain abnormalities in the heart‘s electrical system.
How do pacemakers work? Consist of two major parts:
The generator is a tiny, hermetically sealed computer along with a
battery to run it in a titanium container. Size is of a 50-cent piece, and
approximately three times as thick. The battery life today is 5 – 8
years.
The lead is a flexible insulated electrical wire. One end is attached to
the generator and the other end is passed through a vein into the heart.
Most pacemakers today use two leads – one placed in the right atrium
and the other in the right ventricle.
Two types of Pacemakers:
Single-Chamber Pacemakers:
In a single-chamber pacemaker,
only one wire (pacing lead) is
placed into a chamber of the
heart. Sometimes it is the upper
chamber, or atrium. Other times
it is the lower chamber, or
ventricle.
Dual chamber pacemaker: one
wire kept in arterial and one
kept in ventricle
Insulin Devices:
Insulin Types:
- Rapid acting- Humalog, Novo log
Figure 45 How to pacemaker
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- Short acting- Regular
- Intermediate acting- Lente, NPH
- Long acting- Ultralente, Glargine
Storage: Refrigeration or store at temperature less than 86 °F. Refrigerate
unopened vials and insulin pens.
Insulin devices:
Insulin syringes
Insulin Pens
Insulin jet injectors
Insulin infusion pumps
Inhaled insulin
Delivery devices under development
Insulin appearances:
Clear (like Water):
i. Rapid-acting insulins : lispro (Humalog)
and aspart (Novo log
ii. Short-acting insulin (Regular) insulin
iii. Longer-acting insulin: Insulin
Glargine (Lantos)
Cloudy or milk look: NPH, Lente, and Ultralente.
Insulin syringes:
Choosing a syringe: which insulin concentration it's designed for
its capacity, the needle gauge (or thickness)
the needle length, Size: 30, 50, 100 units
U 40- Orange color syringe, U 100- Yellow color syringe
Syringe & Vial: Preparation
Figure 46 Sharp container
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Get Supplies: Insulin (Verify), Syringe, Alcohol
wipe, Disposable gloves, Sharps container
Wash hands and apply gloves
Clean the insulin vial
Select injection site
Clean the injection site
Check the insulin dose
Remove the cap from syringe
Pull the plunger down to number of units
to be administered
Inject air into bottle
Draw out prescribed number of units of
insulin
Pinch up the skin.
Push needle into skin at 90.
Release pinch.
Push the plunger in, Count to ―5‖...
Remove needle and dispose of syringe.
Document time, dosage, site, and blood glucose value.
Important Note: If fast acting insulin contaminated with short acting
insulin during mixing, then insulin will not work as quickly it does. So inject
air into the slower/longer-acting insulin first - but do NOT draw up any insulin
and remove the syringe. Inject air into the faster-acting insulin, draw up
insulin, remove bubbles, then remove the syringe and then draw up the slower
acting insulin to make mixed insulin.
Insulin jet injectors: Uses pressure to penetrate and send a fine spray of
insulin through the skin.
5. SEMINAR ON ECG
The 12-lead electrocardiogram
Figure 47 Injecting air into bottle
Figure 48 Push the plunger in
[Chapter 7]
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(ECG) remains one of the most useful clinical tools in the evaluation of the
cardiac patient. Its use is widespread
And can be of use as part of the assessment process in many presentations
such as:
Chest pain
Shortness of breath
Blackouts
Palpitations
Syncope
And many others…
However, the 12-lead ECG must be looked at carefully and in a systematic
way and this often takes many years to master. The ECG should always be
used along with the patient‘s history. Each month an ECG will be presented
with a short patient history for the reader to analyze. In this first edition, a
systematic approach to analyzing ECGs is presented along with a normal 12-
lead ECG (Figure 1) so that the reader can practice applying the framework to
the ECG. The framework uses ten rules that can be applied to any ECG.
Figure 49 the normal echocardiogram
[Chapter 7]
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THE TEN RULES
1. A starting framework for the systematic approach to the 12-lead ECG.
For positioning
2. Of the leads see Figure 2 and for the view of the limb leads see Figure
3.
3. All waves are negative in aVR. This has to be so: aVR represents
electrical activity as seen from the right shoulder. The sinus node is
placed top right in the heart nearest the right shoulder and the electrical
activity is moving downwards and leftwards towards the left ventricle.
4. The ST segment starts on the isoelectric line, except in V1 and V2
where it may be elevated (not >1 mm). The normal ST then curves
gently in the direction of the T wave and should not remain exactly
horizontal The PR interval should be 0.12–0.2 seconds. A longer PR
implies AV block, a shorter PR may indicate a vulnerability to
supraventricular arrhythmias
5. The QRS complex should not exceed 0.11–0.12 seconds. A wider QRS
is sometimes seen in healthy people but may represent an abnormality
of intraventricular conduction
6. The QRS and T waves tend to have the same general direction in the
standard (limb) leads. For example, if the QRS in aVL is dominantly
positive than the T wave in that lead should also be positive. Slight
disparities are likely to be normal
7. The R wave in the precordial (chest) leads grows from V1 to at least
V4 where it may or may not decline again.
8. A spurious abnormality frequently occurs in R wave size or growth
because of faulty placement of precordial leads
9. The QRS is mainly upright in I and II. Otherwise there is axis
deviation
10. The P wave is upright in I II and V2 to V6. By implication they may be
flat or negative in other leads
11. There is no Q wave or only a small q (< 0.04second in width) in me, II
and V2 to V6. A narrow q is expected in V6 and represents the early
septal activation.
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12. The T wave is upright in I, II and V2 tom V6. The end of the T wave
should not dip below the baseline. This is sometimes seen in unstable
angina
Figure 50 Definitions of ECG leads
Figure 51 Positioning of chest leads
The diagnosis of the normal electrocardiogram is made by excluding any
recognized abnormality. Its description is therefore quite lengthy.
[Chapter 7]
[Parth Dhanani] Page 118
normal sinus rhythm
each P wave is followed by a QRS
P waves normal for the subject
P wave rate 60 - 100 bpm with <10%
variation
- rate <60 = sinus bradycardia
- rate >100 = sinus tachycardia
- variation >10% = sinus arrhythmia
normal QRS axis
normal P waves
height < 2.5 mm in lead II
width < 0.11 s in lead II
for abnormal P waves see right atrial hypertrophy, left atrial hypertrophy,
atrial premature beat, hyperkalaemia
normal PR interval
0.12 to 0.20 s (3 - 5 small squares)
for short PR segment consider Wolff-Parkinson-White syndrome or
Lown-Ganong-Levine syndrome.
for long PR interval see first degree heart block and 'trifasicular' block
normal QRS complex
< 0.12 s duration (3 small squares)
For abnormally wide QRS consider right or left bundle branch block,
ventricular rhythm, hyperkalaemia, etc.
no pathological Q waves
no evidence of left or right ventricular hypertrophy
normal QT interval
Figure 52 Normal ECG pattern
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Calculate the corrected QT interval (QTc) by dividing the QT interval
by the square root of the preceding R - R interval. Normal = 0.42 s.
Causes of long QT interval
myocardial infarction, myocarditis, diffuse myocardial
disease
hypocalcaemia, hypothyroidism
subarachnoid hemorrhage, intracerebral hemorrhage
drugs (e.g. sotalol, amiodarone)
hereditary
normal ST segment
No elevation or depression
causes of elevation include acute MI (e.g. anterior, inferior), left
bundle branch block, normal variants (e.g. athletic heart, Edeiken
pattern, high-take off), acute pericarditis
causes of depression include myocardial ischaemia, digoxin effect,
ventricular hypertrophy, acute posterior MI, pulmonary embolus, left
bundle branch block
normal T wave
causes of tall T waves include hyperkalaemia, hyperacute myocardial
infarction and left bundle branch block
causes of small, flattened or inverted T waves are numerous and
include ischaemia, age, race, hyperventilation, anxiety, drinking iced
water, LVH, drugs (e.g. digoxin), pericarditis, PE, intraventricular
conduction delay (e.g. RBBB)and electrolyte disturbance
6. Seminar on Shock, CT scan, MRI and Coma:
Shock:
[Chapter 7]
[Parth Dhanani] Page 120
Tissues in the body don't receive enough oxygen and nutrients to allow
the cells to function. Cellular death, heart attack (cardiac arrest) progressing
to organ failure and finally, to whole body failure and death.
Types of shock:
Septic shock: Results from bacteria multiplying in the blood and
releasing toxins.
Treated with antibiotics depending on the source and type of
underlying infection.
Require large amount of fluids to maintain BP.
Cardiogenic shock: happens when heart is damaged and unable to
supply sufficient blood to the body.
May require cardiac catheterization to unblock an artery or in
some cases heart transplantation.
Hypovolemic shock: caused by severe blood and fluid loss, this makes
heart unable to pump enough blood to the body.
Treated with fluids, may require multiple blood transfusions in
severe cases.
Neurogenic shock: caused by spinal cord injury as a result of a
traumatic accident or injury.
Difficult to treat and often irreversible and causes problems with the
natural regulatory functions of the body.
Anti-inflammatory medicine such as steroids
In some cases surgery is needed.
Anaphylactic shock: is a type of hypersensitivity or allergic reaction.
Treated with antihistamines like, diphenhydramine, epinephrine
Steroids like methylprednisolone and sometimes H2 blocker
medicines.
CT scan:
This is a noninvasive medical test that helps physicians to diagnose
and treat medical conditions.
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Contrast agents are iodine based and are absorbed by abnormal
tissues. They make it easier for the doctor to see tumors within the
brain tissue.
One of the fastest tools for diagnosis of chest, abdomen, and pelvis.
Identify injuries to the lungs, heart and vessels, liver, spleen, kidneys,
bowel or other internal organs.
Measure bone mineral density for the detection of osteoporosis.
MRI:
It is more useful in neurologic, musculoskeletal, cardiovascular, and
oncological imaging as it provides much greater contrast between the
different soft tissues of the body than CT scan.
Radio waves 10,000 to 30,000 times stronger than the magnetic field
of the earth are sent through the body. This affects the body's atoms,
forcing the nuclei into a different position.
As they move back into place they send out radio waves of their own.
The scanner picks up these signals and a computer turns them into a
picture.
The tissue that has the least hydrogen atoms (such as bones) turns out
dark, while the tissue that has many hydrogen atoms (such as, fatty
tissue) looks much brighter.
Coma:
It is a state in which a patient is totally unaware of both self and
external surroundings, and unable to respond to external stimuli.
Causes of coma: (AEIOU-TIPS)
A: Alcohol.
E: Epilepsy or Exposure to heat and cold
I: Insulin (Diabetic emergencies)
O: Overdose or Oxygen deficiency
U: Uremia (kidney failure)
T: Trauma (Shock or head injury)
I: Infection or Iatrogenic.
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P: Psychosis or poisoning.
S: Strokes.
Management of Coma:
ABC: Airway, Breathing, Circulation
COMA COCKTAIL: 50 ml of 50%Dextrose + Thiamine 100 mg +
Naloxone 0.4 mg (adults)
Treat metabolic disturbances
Stop seizures with anti-epileptics
Lower intracranial pressure
Treat infections
Ventilation and Ryle‘s tube.
[Chapter 8]
[Parth Dhanani] Page 123
CHAPTER 8: SUMMARY
‘Experience is the best teacher”
Now, at the end of Hospital Training, I am pleading to say that NIRMA
UNIVERSITY has intellectually included Hospital Training as part of B.Pharm.
Hons. ‗S academic curriculum (Semester X). This hospital training has given me a
chance to get exposed to practical work. What I have studied in semester 9, I have
able to implement it in semester X hospital training.
I have already completed B.Pharm. And have studied subjects like Pharmaceutics,
Pharmacognosy, etc. But in this course, I have been exposed to clinical field, not only
theoretical aspect, but practical aspect as well which, according to me, the most
exciting experience of my field is. According to my merit rank (calculated on the
basis of semester 9 marks); I have got a chance to get trained in Shrey Hospital under
the guidance of Dr. Chirag Joshi sir. He is the one who holds and manages the
Intensive Coronary Care Unit (I.C.C.U) on one hand alone. It has been great
experience to obtaining under such qualified and experienced person.
On the first day of my training, I along with fellow members was introduced to
medical staff and have been introduced to different departments like ICCU, Operation
theatre, dialysis unit, Radiology department, Pathology Lab, Lithotripsy, Pharmacy
and various wards and these sessions were included in week one schedule.
During second week, I was allocated to pharmacy. I got exposed to the way to handle
prescription and reading as well. I came to know the arrangement of medicines.
Different medicines of same company were kept in one shelf and were arranged
according to their alphabetical order in the same shelf. I also came to know about
medication handling & storage, dispensing, ADR and medication order identification
while handling prescription. By this pharmacy experience I came to know about
extreme use of antibiotics i.e. irrational use we can say. Pharmacists here in pharmacy
have overcome the mistakes done by doctor in hurry e.g. dose, freq.etc.
Our case studies began third week onwards and were continued till the end of
training. Herein I studied different cases pertaining to most of the system of body. Dr.
Chirag sir explained us the format of presenting the case like Patient demographics,
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[Parth Dhanani] Page 124
chief complains, past history, past medication history, vital signs, systemic
examination, laboratory investigation, other diagnostic tests (X-ray, USG, and MRI),
medications, adverse reactions and then other related discussions. Sir explained us
how to take history of patient and assigned me the case along with other fellow
members which we have to present before him on the next day by preparing in the
format what he had taught to us. Sir fully explains us the case according to format and
carries on interaction as well. This include why a particular treatment is preferred
(based on patient‘s economic status), how to overcome drug interactions and ADRs.
He fully explains the treatment along with the available options of medicines e.g.
Cephalosporins. He gives us a brief introduction over different class of the same along
with brand names and the spectrum they cover. He explained all the part of case from
entering in the hospital to discharge from hospital, every reason for single treatment.
And I also saw some cases of particular of my interest like poisoning, alcoholic
patient, renal failure.
During this practical training I also involved in ward round participation. I used to go
with Chirag sir and learn the way treat the patient and maintain patient history notes. I
used to check drug dose and dosing frequency. I also used to take patient history
which is also critical in understanding patient‘s case. During ward round participation,
I came to real practice experience as I was in front of the patient and use knowledge
in dealing with patient.
All in all, it was the best experience that I have undergone in my field. This would be
greater than anything in clearing my future registered pharmacist exam in US. Having
this experience, I came to know that this place where I should be.
[Chapter 9]
[Parth Dhanani] Page 125
CHAPTER 9:
References
BOOKS:
1. Clinical Pharmacology and Therapeutics
2. Clinical Simulations in Pharmacology Vol – 1/ by Lippincott
Williams and Wilkins
3. Clinical Simulations in Pharmacology Vol - 2 / by Lippincott
Williams and Wilkins
4. Clinical Physiology and Pharmacology: The Essentials / by
Farideh Javid and Janice McCurrie
5. Clinical Pharmacy and Therapeutics / Ed by Roger Walker and
Clive Edwards
6. Applied Therapeutics: The Clinical Use of Drugs / by Mary
Anne Koda-Kimble and Lloyd Yee Yong
7. Handbook of Clinical Pharmacy / by A. V. Yadav, B. V. Yadav
and T. I. Shaikh
8. Applied Therapeutics: The Clinical Use of Drugs / by Mary
Anne Koda-Kimble, Lloyd Yee Young, Brian K. Alldredge,
Robin L. Corelli, B. Joseph Guglielmo, Wayne A. Kradjan and
Bradley R. Williams
9. Applied therapeutics clinical use (2005)
10. Mechanistic toxicology (2007)
11. Rang & Dale's Pharmacology
12. Medical Pharmacology at a Glance by Michael J. Neal
13. Principles of Pharmacology / by H. L. Sharma and K. K.
Sharma
Websites:
1. www.wikipedia.com
2. http://emedicine.medscape.com/article/150215-overview
3. http://www.emedicinehealth.com/gout/article_em.htm
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4. http://www.medicinenet.com/kidney_failure/article.htm
5. http://www.asthma.net.in/app/default.asp
6. Comprehensive Pharmacy Review by Leon Shagel
7. DiPiro – Pharmacotherapy
8. http://emedicine.medscape.com/article/278641-overview
9. http://www.medicinenet.com/jaundice/article.htm
[Chapter 10]
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CHAPTER: 10
ANNEXURE.
1. Patient‘s history record sheet
2. Investigations
3. Examination sheet
4. T.P.R., & Input/output Chart
5. Admission and discharge record
6. Prehospitalization form
7. Case study format
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1. Patient’s history record sheet:
SHREY HOSPITALS PVT. LTD.
An ISO 9001:2000 Certified Hospital
Plot No. 270/5/B, Near AMCO Bank, Stadium Circle, Navrangpura, AHMEDABAD-9.
PHONE: 26468620, 40017777
PATIENT’S HISTORY RECORD SHEET
Consultant:
Pt‘s Name:
CHIEF COMPLAIN:
KNOWN CASE OF:
GEN. EXAMINATION:
SYSTEMIC EXAMINATION:
Room No.
Reg. No.
Date:
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2. Investigations:
INVESTIGATIONS
An ISO 9001:2000 Certified Hospital
Consultant:
Pt.‘s Name:
Date
Hb
TC
DC
ESR
PC
RC
BT
CT
P.T.
Smear
Urine
Stool
RBS
PPBS
FBS
Urea
Creatinine
Na+
K+
CL-
Ca++
S.Bill : Total
Direct
Indirect
S.G.P.T.
S.G.O.T.
S.Alk.Po4ase
S.Amylase
S.Lipase
S.Protein :
Total
Alb.
Glb.
TT
Room No:
Reg. No:
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X – Rays :
USG:
MRI/C.T. SCAN :
Sputum : R
Ascitic Fluid M
Plural fluid Stain
C.S.F. : C
S
Other :
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3. Examination sheet
SHREY HOSPITALS PVT. LTD.
An ISO 9001:2000 Certified Hospital
Plot No. 270/5/B, Near AMCO Bank, Stadium circle, Navrangpura, Ahmedabad-
380009. PHONE: 079-26468620, 40017777
EXAMINATION SHEET
Consultant:
Pt.’s Name:
Room No:
Reg. No. :
Reg. No.: Date-Time Findings
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4. T.P.R., & Input/output Chart
SHREY HOSPITAL PVT. LTD.
Room No. Reg. No. Date
T.P.R. & INPUT/OUTPUT CHAT
Consultant: Pt.’s Name:
TIME T P CVP IN PUT IVF
ACC
TO
CVP
OR
U/O
OUT PUT RBS INSULIN A/G Stool
Vomit
Total
I/V
Fluid
Oral I
V
Urine Asp
A.M.
8
9
10
11
12
P.M.
1
2
3
5
6
7
8
Total
DAY CHAT NIGHT CHART TOTAL
Oral
IV
Urine
Stool
Vomit
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5. Admission and discharge record:
SHREY HOSPITAL PVT. LTD.
T.P.R. & INPUT/OUTPUT CHAT
Consultant: Pt.’s Name:
TIME T P CVP IN PUT IVF
ACC
TO
CVP
OR
U/O
OUT PUT RBS INSULI
N
A/
G
Stool
Vomi
t
Total
I/V
Fluid Oral IV. Urin
e
Asp
m
l
Liq m
l
Liq
8 P.M.
9 P.M.
10 P.M.
11 P.M.
12 Mid
Night
1 A.M.
2 A.M.
3 A.M.
4 A.M.
5 A.M.
6 A.M.
7 A.M.
8 A.M.
TOTAL
Room No. Reg. No. Date
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6. Prehospitalization form:
SHREY Hospitals PVT. LTd.
An ISO 9001:2000 Certified Hospital
Plot No. 270/5/B, Near AMCO Bank, Stadium Circle, Navrangpura, Ahmedabad-380009. PH.: 079
26468620, 40017777
ADMISSION RECORD
Name:
Address:
City/ Town: Pin:
Occupation: Age: Sex: Ph. :( O) (R)
Consultant:
Phone: (O) (R) (Mobile)
“I/We agree to abide by the schedule charges and Regulation of the Nursing Home”
*Any legal matters are Subject to Ahmedabad jurisdiction only.
Sign. With Name:
DISCHARGE RECORD
Diagnosis:
OUTCOME:
Better when discharged.
There was no improvement on discharge
Patient was discharged on request.
Patient/Relatives took discharge against medical advice.
Patient was transferred to another hospital. Doctor’s Signature
Please see reverse for subsequent treatment, if any
Reg. No.: Room no.: Date: Time:
Date: Time: Hospitalization Days:
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7. Case study format: