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Clinical Pharmacy Practice Experience

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‘Experience is the best teacher” …

‘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 i

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  • 1. [SHREY HOSPITAL] 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[Parth Dhanani] Page 1
  • 2. [SHREY HOSPITAL] CertificateThis is to certify that Mr.PARTH KUMAR DHANANI(10BPW618) of Semester X of B. Pharm (Hons.), 5-yearIntegrated Programme, Institute of Pharmacy, NirmaUniversity, Ahmedabad, has undergone training at SHREYHospital from 25/05/2010 to 08/09/2010 and has satisfactorilycompleted 400 hours in the Pharmacy Practice Experience.Date: 9/9/2010Shri Dharmanshu ChhayaManagerShrey Hospital Ltd.Near AMCO Bank,Stadium Circle, Navrangpura,Ahmedabad - 380 009Phone: 26468616 to 20, 40017777Mobile No. - 98250-23371.EMail: shreyhospitals@yahoo.co.in Seal of the HospitalProfessor In charge Head of Department Seal of the Institute Director[Parth Dhanani] Page 2
  • 3. [SHREY HOSPITAL] Index Chapter No. Topic Page No. Introduction Clinical Pharmacy Practice 5–6 1. Importance of Clinical Pharmacy Practice Training 2. Objectives 7 – 10 Introduction and Overview of Training Training Site 3. 11 – 16 Training Site Features Training Duration Training Schedule 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[Parth Dhanani] Page 3
  • 4. [SHREY HOSPITAL] ACKNOWLEDGEMENTThis project has been prepared to give brief knowledge to ―Clinical experience inShrey Hospital of 400 hours ‘‘.this project has to be undertaken and completed as perthe direction of the syllabus.I am very thankful to Mr.Dharmanshu Chhaya, for his constant, restless guidancethrough 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 clinicaldoubts and also gave us his personal attention to better understanding of the practicalconnection of clinical aspects to my theoretical knowledge as well as his incites tobetter development of my clinical experience in Shrey.I would also like to convey my gratitude to Mr.Bharathai Mahant, The Director of theShrey Hospital, for allowing us to use the resources of the hospital, which werehelpful in completion of my thesis.At this stage I, specially, thank professors Incharge Mr. Bhavik Shah of Institute ofPharmacy, Nirma University, for the moral support and constant encouragement inthe accomplishment of my project work in semester: X of B.Pharm honors.Thanking you,Mr. PARTHKUMAR DHANANI (10BPW618)[Parth Dhanani] Page 4
  • 5. [Chapter 1] 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 patients 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 patients 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. [Parth Dhanani] Page 5
  • 6. [Chapter 1] 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 drugs 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. [Parth Dhanani] Page 6
  • 7. [Chapter 2]CHAPTER 2: OBJECTIVES: Pharmacy profession has entered doctor‘s clinics and hospitals as the ―clinicalpharmacist‖. Clinical pharmacy is a branch of pharmacy where the pharmacist role isto provide patient care. Clinical pharmacist is an important part of the healthcareteam. The pharmacist works in coordination with the doctors for the better patienthealthcare. 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 drugs potential[Parth Dhanani] Page 7
  • 8. [Chapter 2] 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.[Parth Dhanani] Page 8
  • 9. [Chapter 2] 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[Parth Dhanani] Page 9
  • 10. [Chapter 2] 2. Administering drugs 3. Documenting professional services 4. Reviewing drug use 5. Communication 6. Counseling 7. Consulting 8. Preventing Medication ErrorsScope 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)[Parth Dhanani] Page 10
  • 11. [Chapter 3]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: Figure 1 Layout of shrey hospital1) 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 nurses 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[Parth Dhanani] Page 11
  • 12. [Chapter 3] - 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.[Parth Dhanani] Page 12
  • 13. [Chapter 3]  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[Parth Dhanani] Page 13
  • 14. [Chapter 3] 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[Parth Dhanani] Page 14
  • 15. [Chapter 3]  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 Epilepsy3) 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.[Parth Dhanani] Page 15
  • 16. [Chapter 3]  Renal TransplantHaemodialysis:  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[Parth Dhanani] Page 16
  • 17. [Chapter 4]CHAPTER 4:Overview of Routine Activities at HospitalWeek: 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 Figure 2 ICCU staff  24 hr running air conditioner  Ventilators near all beds  Dialysis Unit  Services - Hemodialysis - Hemofilteration - Plasma Exchanges - Continuous Ambulatory peritoneal Dialysis Figure 3 Dialysis Unit  Charges per sitting  OT: Operation Theater  Live video recorder of all operations.  All measure operations except cardiac surgery performed in Hospital. Figure 4 Operation Theatre[Parth Dhanani] Page 17
  • 18. [Chapter 4]  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 Figure 5 Lithotripsy Centre  Wards  Doctors take round at each ward Figure 6 ICCU ward regularly  Combined Ward all on the first, second and third floor, separated by the facilities provided like, Deluxe, Super Deluxe, Special, Figure 7 General ward and Semi Special  Nurshing staff and consulting offices available at each floor.[Parth Dhanani] Page 18
  • 19. [Chapter 4]  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 Figure 9 Indoor Accommodation medical officer round the clock[Parth Dhanani] Page 19
  • 20. [Chapter 4] 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 & 4Cardiovascular 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[Parth Dhanani] Page 20
  • 21. [Chapter 4]Week: 5 & 6Respiratory 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 AlklosisWeek: 7Renal System  ARF  Pre renal ARF  Intrinsic ARF  Post Renal ARF  CRF  GFR Classification  Causes  Pathology  Intervention  Electrolyte imbalance[Parth Dhanani] Page 21
  • 22. [Chapter 4]  Na/K/Mg/Ca/Hco3 imbalance  Dialysis  Heamodialysis  Peritoneal DialysisWeek: 8 & 9GI Disorder and Liver Dysfunction  Ascities  Cirrhosis  Hepatitis  Hepatic Encephalopathy  IBD, IBS (Inflammatory bowel disease/Syndrome)  Jaundice  Portal Hypertension  Typhoid feverWeek: 10 &11CNS Disorder  Coma  Epilepsy -Types -Drugs -Drug Interaction  EEG/CT scan  GBS  Migraine  MRI  Neuro surgery  Stroke -Hemorrhagic Stroke -Ischemic Stroke[Parth Dhanani] Page 22
  • 23. [Chapter 4]  ShockWeek: 12Endocrine 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 & oxytosinWeek: 13 & 14Infectious Disorder  Dengue  Fever and it several types  Malaria  Tuberculosis  Viral Infections  UTIWeek: 15Poisoning  Alcohol poisoning  Carbon monoxide poisoning  Chemical poisoning  Drug poisoning[Parth Dhanani] Page 23
  • 24. [Chapter 4]  Food Poisoning  Heavy metal poisoning  Organo phosphorous Poison with case presentation  Radon poisoningParticipation 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[Parth Dhanani] Page 24
  • 25. [Chapter 4]  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.[Parth Dhanani] Page 25
  • 26. [Chapter 4] Figure 10. Drugs’ arrangementDispensing:  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.[Parth Dhanani] Page 26
  • 27. [Chapter 4]  Shrey Pharmacy does not have the license for Narcotics so no locked storage is required. Figure 12 Storage of medicinesRecords 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[Parth Dhanani] Page 27
  • 28. [Chapter 5]CHAPTER 5: Case studiesCASE 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[Parth Dhanani] Page 28
  • 29. [Chapter 5] 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 patientINVESTIGATION DAY 1 DAY 2Hb 6.3 8.5TC 26,200 26,000DC 68/17/1/12/2 73/20/2/5/0PC ↓se 82,000 1,66,000PT ↑se Total 24 sec --- Control 13.2 secRBS 120 mg/dL --- (75-115mg/dL)Urea ↑se 193.47 --- (10-20mg/dL)Creatinine ↑se 8.88 (<1.5mg/dL) ---Sodium 135.26 142.37Potassium 4.7 4.1S.Bilirubin ↑se 1.41 (0.3-1mg/dL) ---[Parth Dhanani] Page 29
  • 30. [Chapter 5]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.[Parth Dhanani] Page 30
  • 31. [Chapter 5] • 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 themothers 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 liketyrosine 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[Parth Dhanani] Page 31
  • 32. [Chapter 5]  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 D D NAME 1 2 Inj. Pipzo 4.5 mg in i.v. 12hrly Piperacillin + √ √ 100ccNS tazobactam Inj. Metrogyl 100ml i.v. 8hrly Metronidazole √ √ Inj. Pantodac 40mg i.v. OD Pantoprazole √ √ Inj. Levepil 500mg in i.v. 8hrly Levetiracetam √ √ 100ccNS Inj. Lasix 2amp i.v. BD Furosemide √ √ Inj. FFP 250ml i.v. 8hrly Fresh frozen √ √ plasma[Parth Dhanani] Page 32
  • 33. [Chapter 5] Inj. Dopamine 2@ in i.v. 6hrly Dopamine √ √ 50ccNS Inj. Febrinil 1@ i.v. sos Paracetamol √ √ Inj. Falcigo 60mg i.v. OD Artesunate √ √ Inj. D25% 500ml i.v. 10ml/hr Dextrose √ √ Inj. Sodium (0.6*wt*HC i.v. 13@ straight Bicarbonate √ √ bicarbonate O3 def.) & 0.6*48*9 = 13@ 6hrly 259.2mEq Inj. Duphalac 15ml i.v. 8hrly Lactulose √ √ Inj. Vit K1 1@ in i.v. OD Vit K1 √ √ 100ccNS Inj. Norad 2@ in i.v. 6hrly Nor adrenaline - √ 50ccNS Pipzo Dose Calculation:Table 3 Pipzo dose calculation Creatine Dose Dose interval Clearance 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[Parth Dhanani] Page 33
  • 34. [Chapter 5] DRUG RELATED ISSUE:Table 4 Drug interactions DRUGS INTERACTIONS MANAGEMENT lactulose ↔ Electrolyte loss and increase the The recommended dosage Artesunate risk of torsade de pointes and duration of use should ( moderate) ventricular arrhythmia. not be exceeded. Electrolye Electrolyte disturbances including supplements needed to be hypokalemia and administered. hypomagnesemia. Artesunate The mechanism is decreased Avoid the consumption of ↔ food clearance of Artesunate due to grapefruits and grapefruit (moderate) inhibition of CYP450 3A4- juice. To ensure maximal mediated first-pass metabolism in oral absorption, artemether- the gut wall by certain lumefantrine should be taken compounds present in grapefruits. with food. Furosemide Potentiate the pharmacologic In general, laxatives should ↔ lactulose effects of diuretics. Laxatives can only be used on a short- (Moderate) cause significant losses of fluid term, intermittent basis in and electrolytes 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.[Parth Dhanani] Page 34
  • 35. [Chapter 5]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)[Parth Dhanani] Page 35
  • 36. [Chapter 5]  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 24.8 sec --- --- Control 13.4 sec INR 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 --- ---[Parth Dhanani] Page 36
  • 37. [Chapter 5] Gamma-glutamyl 156.73 (1-94 --- --- transferase 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:[Parth Dhanani] Page 37
  • 38. [Chapter 5] - 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 (Laennecs 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:[Parth Dhanani] Page 38
  • 39. [Chapter 5]Table 6 Mediation of Liver cirrhosis patient DRUG DOSE ROA DURA GENERIC D D D D TION NAME 1 2 3 4 Inj. Magnex 1.5 mg i.v. 8hrly Cefoperazone+ √ √ √ √ Forte in salbectam 100cc NS 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 Oral Sos Diclofenac -- √ -- √ plus Proctodesyl Enema Ethyl -- -- √ √ aminobenzoate/Ec osulide[Parth Dhanani] Page 39
  • 40. [Chapter 5] Liq. Looz 2@ i.v. 6hrly Lactulose -- -- √ √ Inj. Dytor 1/2 @ i.v. 6hrly Torasemide -- -- √ √ Drug related issue:Table 7 Drug interactions DRUGS INTERACTIONS MANAGEMENT Gentamicin Coadministration of parenteral Use of aminoglycoside ↔ aminoglycoside antibiotics or antibiotics in combination Torasemide oral neomycin in combination with loop diuretics should with loop diuretics may generally be avoided. (Major) potentiate the risk of oto- and Serial, vestibular, nephrotoxicity due to additive or audiometric, and renal synergistic pharmacologic function tests should be effects of these drugs. performed before and during therapy if coadministration is necessary. Gentamicin Coadministration of The lowest effective ↔ aminoglycoside and dosages of aminoglycosides Cefoperazone cephalosporins may increase the and cephalosporins should risk of nephrotoxicity. be used when they are (Moderate) prescribed in combination. Renal function should be monitored closely. Diclofenac ↔ 1. Concomitant use of Avoiding dehydration and Torasemide nonsteroidal anti-inflammatory carefully monitoring the drugs (NSAIDs) and diuretics patients renal function and (Moderate) may adversely affect renal blood pressure. If renal function due to NSAID insufficiency or inhibition of the renal synthesis hyperkalemia develops, of prostaglandins that help both drugs should be[Parth Dhanani] Page 40
  • 41. [Chapter 5] maintain renal perfusion in discontinued until the dehydrated states. condition is corrected. 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. Penicillamine : Oral administration of Mineral supplements or ↔ Calcium aluminum, copper, iron, zinc, other products containing carbonate magnesium, and possibly other polyvalent cations should minerals such as calcium may be administered at least two (Moderate) decrease the gastrointestinal hours before or two hours absorption of penicillamine, and after the penicillamine dose. vice versa. The proposed mechanism involves chelation of penicillamine to polyvalent cations, which leads to formation of a nonabsorbable complex. 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)[Parth Dhanani] Page 41
  • 42. [Chapter 5]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:[Parth Dhanani] Page 42
  • 43. [Chapter 5]  CVS: S1S2 Normal  CNS: NAD  R.S. : Normal  P/A : Soft  Stool: Not passed Lab investigations:Table 8 Lab investigation of MI patientINVESTIGATION DAY 1 DAY 2Hb 12.1 12.9TC 8350 8010DC 95/6/1/0/0 77/9/3/10/1PC ↓se 2,05,000 1,57,000PT ↑se Total 21.3 sec --- Control 13.2 secRBS 120 mg/dL --- (75-115mg/dL)Creatinine ↑se 9.14 (<1.5mg/dL) ---Sodium 141.76 139.11Potassium 5.6 5.34Magnesium 2.47 (1.8-2) 2.39S.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) ---[Parth Dhanani] Page 43
  • 44. [Chapter 5]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.[Parth Dhanani] Page 44
  • 45. [Chapter 5] 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 patients 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,[Parth Dhanani] Page 45
  • 46. [Chapter 5] 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 GENERIC D D D D TION NAME 1 2 3 4 Inj. NTG + Ns 50mg i.v. 0.5ml/h Nitroglycerine √ √ √ √ r 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 -- √ √ √[Parth Dhanani] Page 46
  • 47. [Chapter 5] Neb. Budamate --- Nasal 8hrly Budesonide -- √ √ √ Tab. Calpol 500mg Oral TID Paracetamol -- √ √ √ Liq. Cremaffin 3Tsf Oral --- Paraffin -- -- √ √ Tab. Ultrazec --- Oral Sos Tramadol + PCM -- -- √ √ Advice: - Smoking cessation - Regular exercise - Sensible - Limitation of alcohol intake. Drug related issue:Table 10 Drug interactions DRUGS INTERACTIONS MANAGEMENT Theophylline The risk of seizures may be Caution is advised. ↔ Tramadol increased during coadministration of tramadol (Major) with theophylline that can reduce the seizure threshold. Clopidogrel Coadministration with proton Use of Pantoprazole should ↔ pump inhibitors (PPIs) may preferably be avoided in Pantoprazole reduce the cardioprotective patients treated with effects of clopidogrel. The clopidogrel. (Major) proposed mechanism is PPI If gastroprotection is inhibition of the CYP450 2C19- necessary, H2-receptor mediated metabolic antagonists or antacids bioactivation of clopidogrel. should be prescribed whenever possible. Diltiazem ↔ Aspirin may reverse the Close observation for Aspirin antihypertensive effect of prolonged bleeding time[Parth Dhanani] Page 47
  • 48. [Chapter 5] (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 increases the rate Theophylline levels in the ↔ of theophylline absorption from upper range of normal. Pantoprazole sustained-release formulations. Patients should be advised (Moderate) Chronic use of proton pump to report any signs of inhibitors produce sustained theophylline toxicity hypochlorhydria, which may including nausea, vomiting, enhance peristalsis in the small diarrhea, headache, intestine and antiperistalsis in restlessness, insomnia, or the proximal colon where irregular heartbeat to their theophylline is absorbed. 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[Parth Dhanani] Page 48
  • 49. [Chapter 5]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:[Parth Dhanani] Page 49
  • 50. [Chapter 5]  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[Parth Dhanani] Page 50
  • 51. [Chapter 5] Diagnosis: - PANCREATITIS - DIABETES MELLITUS  PATHOPHYSIOLOGY:Table 12 Flowchart of Pancreatitis Pathophysiology Acute injury Initial Insult * Zymogen activation * Ischaemias * Duct obstruction Release of Generation of Release of vasoactive cytokines active enzymes substances eg. TNF, IL-1,PAF Vascular damage Inflammation Tissue damage and cell death  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.[Parth Dhanani] Page 51
  • 52. [Chapter 5]  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.[Parth Dhanani] Page 52
  • 53. [Chapter 5] Medications:Table 13 Medications for Pancreatitis patient GENERIC D D D DRUG DOSE ROA DURATION NAME 1 2 3 Inj. Magnex 3g i.v. 12hrly Cefoperazo √ √ √ forte in ne+ 100ccNS salbectam Inj. H.Actrapid --- S/C i.v. 12 hrly √ √ √ acc Inj. Pantodac 40mg i.v. OD Pantoprazol √ √ √ e Inj. Emeset 1@ i.v. 8 hrly Ondansetro √ √ √ n Inj. Contramol 1@(50m i.v. 8 hrly Tramadol √ √ √ in 100ccNS g) Inj. RL at 1@ (150 i.v. 200ml/hr Ringer √ √ √ ml) Lactate Inj. KCl 1@ in 2@/day Potassium √ √ √ 1NS@ Inj. Febrinil 1@ i.v. Sos Paracetamol √ √ √ DRUG RELATED ISSUE: DRUGS INTERACTIONS MANAGEMENT Ondansetron Concurrent use of 5-HT3 No particular intervention is ↔ Tramadol receptor antagonists may reduce required. However, the the analgesic efficacy of possibility of a diminished Tramadol. The proposed therapeutic response to mechanism is antagonism of Tramadol should be[Parth Dhanani] Page 53
  • 54. [Chapter 5] serotonin-mediated effects of considered during Tramadol at the spinal level. concomitant therapy with 5- HT3 receptor antagonists. Insulin ↔ The effect of insulin may be If co administered, close lvp solution potentiated, and the risk of monitoring of blood glucose with hypoglycemia increased. level is required. potassium (KCl in NS)  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.[Parth Dhanani] Page 54
  • 55. [Chapter 5]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[Parth Dhanani] Page 55
  • 56. [Chapter 5]  CNS: Altered sensorium  R.S. : Clear  P/A : Soft  Vomiting: Nil Lab investigations:Table 14 Lab investigation of Ulcerative Colitis TEST OBSERVED NORMAL VALUE 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 11.1-13.1 Conrol:13.5 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 92.28IU/L 20 to 140 IU/L. Phosphates 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[Parth Dhanani] Page 56
  • 57. [Chapter 5]  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[Parth Dhanani] Page 57
  • 58. [Chapter 5] 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 ulcersFigure 21 Pyoderma gangrenosum on the leg Figure 22 Endoscopic image Medication:Table 15 Medications for UC patientNAME DOSE ROA GENERIC D D D D NAME 1 2 3 4Inj. Ceftop 0.5g + 0.5g i.v. Cefoperazone & √ √ √ √ sulbactam0Inj. Levoflox 500mg/100ml i.v. Levofloxacin √ √ √ √Inj. Metrogyl 500mg/100ml i.v. Metronidazole √ √ √ √Tab. Texim-O 200mg Oral Cefixime -- -- -- --[Parth Dhanani] Page 58
  • 59. [Chapter 5]Inj. Forcan 2mg/100ml i.v. Fluconazole √ √ √ √Inj. 25% 30mg i.v. 25% dextrose √ -- -- --DextroseInfusionInj. Saline 0.9% 1000 ml i.v. Sodium Chloride √ √ √ √Inj. Calcium 10 %/10 mL i.v. Calcium √ √ √ √Gluconate GluconateInj. 5mg i.v. Magnesium √ √ √ √Magnesium SulphateSulphateInj. Albumin 20% i.v. Human albumin √ √ √ √Infusion PCV i.v. Pack cell volume √ √ √ --Liq. Mesacol 4 mg /60 ml Anal Mesalamine √ √ -- --EnemaTab. Mesacol 400 mg Oral Mesalamine -- -- √ √Inj. Efcorlin 100 mg i.v. Hydrocortisone √ √ √ √ Sodium SuccinateTab. 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 i.v. Phytonadione √ -- -- -- syringeTab. Becosules Oral B-complex -- -- -- √Inj. Emsetron 2ml i.v. Ondansetron √ √ -- --Inj. 100mg/2ml i.v. Tramadol HCL √ √ -- --[Parth Dhanani] Page 59
  • 60. [Chapter 5]TramagesicTab. 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 ↔ 1. The risk of seizures may be Caution is advised if Levofloxacin increased during tramadol is administered coadministration of tramadol with any substance that can (Major) with any substance that can reduce the seizure reduce the seizure threshold. threshold, particularly in 2. Many of these agents also the elderly and in patients exhibit CNS- and/or with epilepsy, a history of respiratory-depressant effects, seizures, or other risk which may be enhanced during factors for seizures. their concomitant use with tramadol. Prednisolone Concomitant administration of Patients should be advised ↔ corticosteroids may potentiate to stop taking the[Parth Dhanani] Page 60
  • 61. [Chapter 5] Levofloxacin the risk of tendinitis and tendon fluoroquinolone, avoid rupture associated with exercise and use of the (Major) fluoroquinolone treatment. The affected area, and promptly mechanism is unknown. 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 Coadministration with Caution is advised. Dosage ↔ fluconazole may increase the adjustments as well as Prednisolone plasma concentrations of drugs clinical and laboratory that are substrates of the monitoring may be (Moderate) CYP450 3A4 isoenzyme. The appropriate for some drugs mechanism is decreased whenever fluconazole is clearance due to inhibition of added to or withdrawn from CYP450 3A4 activity by therapy. fluconazole. Ondansetron Concurrent use of 5-HT3 No particular intervention ↔ Tramadol receptor antagonists may reduce is required. However, the the analgesic efficacy of possibility of a diminished (Moderate) tramadol. The proposed therapeutic response to mechanism is antagonism of tramadol should be serotonin-mediated effects of considered during tramadol at the spinal level. concomitant therapy with 5-HT3 receptor antagonists.[Parth Dhanani] Page 61
  • 62. [Chapter 5]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:[Parth Dhanani] Page 62
  • 63. [Chapter 5]  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 PatientTEST DAY 1 DAY 2Haemoglobin ↓se 12.1 12.9Total count 5900 5568ESR 05 (1–25mm/hr) ---Platelet count 2,67,000 3,12,000RBS ↑se 158.8 (70 – 110) 179.03Creatinine 0.7 0.67Urea 17 14Sodium ↓se 125.3 135.9Potassium 3.31 2.97SGPT 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) 16.6CPK MB ↑se 33.99 (0-7ng/L) 24.03[Parth Dhanani] Page 63
  • 64. [Chapter 5]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 oneof 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 PathophysiologyPATHOPHYSIOLOGY:[Parth Dhanani] Page 64
  • 65. [Chapter 5] UA/NSTEMI can be caused by a reduction in oxygen supply and/or by anincrease 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[Parth Dhanani] Page 65
  • 66. [Chapter 5] Figure 25 Endothelial dysfunction influence MEDICATIONS:Table 18 Medications of U.Angina patient GENERIC D D D D D D DRUG DOSE ROA FRE NAME 1 2 3 4 5 6 QUE NCY Tab. Clavix 75mg Oral BD Clopidogrel √ √ √ √ √ √ Tab. 150mg Oral OD Aspirin √ √ √ √ √ √ Ecospin Inj. NTG 50mg i.v. 1ml/h Nitroglycerin √ √ √ √ √ -- in 50ml NS r Tab. Indur 30mg Oral 1-1-0 Isosrbide -- -- -- -- -- √ mononitrate Tab. 50mg Oral BD Metoprolol √ √ √ √ √ √ Betaloc[Parth Dhanani] Page 66
  • 67. [Chapter 5] Tab. 40mg Oral 1HS Atorvastatin √ √ √ √ √ √ Atorva Tab. 2.5mg Oral 1OD Ramipril √ √ √ √ √ √ Ramace Inj. Lasix 2amp. i.v. BD Furosemide √ √ -- -- -- -- Tab. 20+50 Oral 1-1-0 Furosemide + -- -- √ √ √ √ Lasilactone Spironolacto ne Inj. 0.6mg i.v. BD Low Mol.Wt. √ √ √ √ √ -- Clexane Heparin Liq. Looz 10ml Oral HS Lactulose √ √ √ √ √ √ Tab. Alprex 0.5mg Oral 1 HS Alprazolam √ √ √ √ √ √ Inj. KCl in 3amp. i.v. 2ml/h Potassium -- √ √ √ √ √ 50ccNS r supplement Inj. accord i.v. ----- Short acting √ √ √ √ √ √ Actrapid ing to insulin RBS DRUD RELETED ISSUE:Table 19 Drug interactions DRUGS INTERACTIONS MANAGEMENT Furosemide Diuretics and beta-blockers may Monitoring of serum ↔ increase the risk of hyperglycemia potassium levels, blood Metoprolol and hypertriglyceridemia in pressure, and blood glucose is patients with diabetes or latent recommended during diabetes. coadministration.[Parth Dhanani] Page 67
  • 68. [Chapter 5] Metoprolol Inhibition of catecholamine- Regular monitoring of blood ↔ Insulin mediated glycogenolysis and glucose levels and be aware glucose mobilization in that certain symptoms of association with beta-blockade hypoglycemia such as can potentiate insulin-induced tremors and tachycardia may hypoglycemia in diabetics and be masked. delay the recovery of normal blood glucose levels Furosemide Coadministration makes The possibility of first-dose ↔ Ramipril hypotension and hypovolemia hypotensive effects may be more likely than does either drug minimized by initiating alone. Some ACE inhibitors may therapy with small doses of attenuate the increase in the the ACE inhibitor, or either urinary excretion of sodium discontinuing the diuretic caused by some loop diuretics. temporarily or increasing the salt intake approximately one week prior to initiating an ACE inhibitor. Heparin ↔ Concurrent administration of If coadministered, close Nitroglycerin heparin and intravenous evaluation of the coagulation nitroglycerin may lead to a status of the patient is decreased anticoagulant effect. required and heparin dose titrated as needed.[Parth Dhanani] Page 68
  • 69. [Chapter 5]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[Parth Dhanani] Page 69
  • 70. [Chapter 5]  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 2,46,000 2,37,000 2,41,000 (1,30,000—4,00,000) 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- 118.6 --- 120)[Parth Dhanani] Page 70
  • 71. [Chapter 5] 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.[Parth Dhanani] Page 71
  • 72. [Chapter 5] 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.[Parth Dhanani] Page 72
  • 73. [Chapter 5] MEDICATIONS:Table 21 Medications of peritonitis patient GENERIC D D D DRUG DOSE ROA FREQU NAME 1 2 3 ENCY Inj. 1.5g i.v. 8 hrly Cefoperazone+ √ √ √ Magnex salbectam forte Inj. 1@ (40mg) i.v. OD Pantoprazole √ √ √ Pantodac Inj. Emeset 1@ i.v. 8 hrly Ondansetron √ √ √ Inj. 1@(50mg) i.v. sos for Tramadol √ √ √ Contramol pain 100ccNS Inj. DNS 500ml i.v. Dextrose √ --- --- Inj. 1@ i.v. 150ml/hr --- √ √ DNS/RL Inj. NS 120ml i.v. Chloride √ √ √ Inj. 1@ i.v. Sos Paracetamol √ √ √ Febrinil DRUG RELATED ISSUE:Table 22 Drug interactions DRUGS INTERACTIONS MANAGEMENT[Parth Dhanani] Page 73
  • 74. [Chapter 5] Ondansetron Concurrent use of 5-HT3 No particular intervention is ↔ Tramadol receptor antagonists may reduce required. However, the the analgesic efficacy of possibility of a diminished Tramadol. The proposed therapeutic response to mechanism is antagonism of Tramadol should be considered serotonin-mediated effects of during concomitant therapy Tramadol at the spinal level. with 5-HT3 receptor antagonists. Insulin ↔ Potassium repletion may If co administered, close lvp solution partially or completely reverse monitoring of blood glucose with glucose intolerance in some level is required. potassium patients with liver cirrhosis. The (KCl in NS) effect of insulin may be potentiated, and the risk of hypoglycemia increased.[Parth Dhanani] Page 74
  • 75. [Chapter 5]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[Parth Dhanani] Page 75
  • 76. [Chapter 5]  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 92.28IU/L 20 to 140 IU/L. Phosphates 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 :[Parth Dhanani] Page 76
  • 77. [Chapter 5]  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[Parth Dhanani] Page 77
  • 78. [Chapter 5] 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[Parth Dhanani] Page 78
  • 79. [Chapter 5]  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 GENERIC D D D D DRUG DOSE ROA FREQ. NAME 1 2 3 4 Inj. Monocef 1g i.v. BID Ceftriaxone Inj. Pantocid 40mg i.v. BID Pantoprazole Inj. DNS 100ml/ i.v. --- Dextrose hr 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 250/50 Oral BID OD 0 Tab. Tryptomer 10mg Oral ½ HS[Parth Dhanani] Page 79
  • 80. [Chapter 5] Tab. Faldex --- Oral BID Tab. Bizaden- --- Oral BID forte Inj. Actrapid Acco. i.v. ----- Short acting √ √ √ √ to RBS insulinNon 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 therapySuggestion:  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[Parth Dhanani] Page 80
  • 81. [Chapter 5] Clopidogrel Coadministration with proton Use of Pantoprazole should ↔ pump inhibitors (PPIs) may preferably be avoided in Pantoprazole reduce the cardioprotective patients treated with effects of clopidogrel. The clopidogrel. (Major) proposed mechanism is PPI If gastroprotection is inhibition of the CYP450 2C19- necessary, H2-receptor mediated metabolic antagonists or antacids bioactivation of clopidogrel. should be prescribed whenever possible. Aspirin ↔ Combined use of low-dose or During concomitant Piroxicam high-dose aspirin with other therapy, patients should be nonsteroidal anti-inflammatory advised to take the (Moderate) drugs (NSAIDs) may increase medications with food and the potential for serious to immediately report signs gastrointestinal (GI) toxicity, and symptoms of GI including inflammation, ulceration and bleeding bleeding, ulceration, and such as abdominal pain, perforation. bloating, sudden dizziness or lightheadedness, nausea, vomiting, hematemesis, anorexia, and melena. Aspirin ↔ Aspirin may displace valproate Patients should be advised Divalproex from protein binding sites and to notify their physician if sodium inhibit its clearance. Four-fold they experience possible increases in the free fraction of symptoms of toxicity (e.g., (Moderate) valproate have been reported in malaise, weakness, children. Increased therapeutic lethargy, drowsiness, and toxic effects may be nausea, vomiting, or expected to occur. abdominal pain). Amitriptyline Concomitant administration of It may be advisable to ↔ Divalproex valproic acid may increase monitor patients for altered serum concentrations of efficacy and safety. Dose[Parth Dhanani] Page 81
  • 82. [Chapter 5] sodium tricyclic antidepressants. The adjustments or alternate proposed mechanism of action therapy may be necessary if (Moderate) is inhibition of CYP450 hepatic an interaction is suspected. metabolism.[Parth Dhanani] Page 82
  • 83. [Chapter 5]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)[Parth Dhanani] Page 83
  • 84. [Chapter 5]  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 62 % 50-65 % - Eentosinophils 8% 0–3% - Basophils 1% 1–3% - Lymphocytes 9% 25 – 35 % - Monocytes - 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[Parth Dhanani] Page 84
  • 85. [Chapter 5] Sodium 126.62 mEq/L 135 – 145 mEq/L Potassium 3.32 mEq/L 3.5 - 5.0 mEq/L Total Bilirubin : 1.17 mg/dl 0.1 – 1.2 mg/dl - Direct 0.68 mg/dl 0.1 – 0.3 mg/dl - Indirect 0.50 mg/dl 0.1 – 1.0 mg/dl Creatinine 603.34 IU/L 30 – 180 IU/L Phosphokinase ABGA : - - pH 7.37 7.35 – 7.45 30 mmHg 35 – 45 mmHg - pCO2 65 mmHg 80 – 100 mmHg - pO2 17 mmHg 22 – 26 mg Hg - HCO3 92 % ≥ 95 % - SaO2 SGPT 41.07 0 – 42 IU/L Serum Protein Total 7.28 gm/dl 6.3 – 8.2 gm/dl -Albumin 4.34 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[Parth Dhanani] Page 85
  • 86. [Chapter 5]  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 4 include primary sclerosing cholangitis, ulcerative colitis, 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[Parth Dhanani] Page 86
  • 87. [Chapter 5] 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) :[Parth Dhanani] Page 87
  • 88. [Chapter 5]  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 Start Stop NAME Date Date Inj. Magnex 1.5gm Iv 8 hrly Cefoperazone 22/7 26/7 Forte +Sulbactam Inj. DNS 1 lit. i.v. 140ml/ Dextrose 22/7 2/8 hr Inj. Contramol 80 mg i.v. Sos Tramadol 22/7 2/8 in 100cc 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 Iv 8 hrly Ondasetron 24/7 2/8 in 100cc NS Inj. Febrinil 150mg Iv 8hrly Paracetamol 22/7 2/8 in 10cc Inj. Lasix 80mg Iv 6 hrly Furosemide 24/7 25/7 in 10cc Neb. Duolin 2 Neb. Qid Levosalbuta 22/7 24/7 Inhalati mol Sulphate[Parth Dhanani] Page 88
  • 89. [Chapter 5] on and Ipratropium Bromide Inj. Deriphyllin 16 units Iv Bid Hydroxyethyl 24/7 25/7 sc b bf, Theophylline 12 units b dinner Inj. Vit K1 1 amp Iv Qd Vit k 22/7 22/7 Neb. Levolin 2 Neb. Bid Levosalbuta 25/7 2/8 Inhalati mol on 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 Iv 8hrly Aztreonam 31/7 2/8 in 100ml NS Inj. Eldervit 1 amp Iv Qid Multivitamin 31/7 2/8 in 100cc Syp. Sparacid 2 TSF Oral Qid Sucralfate 31/7 2/8 Inj. KCl 20/5ml Iv 4ml/hr Potasium 22/7 30/7 NS Inj. 1 amp Iv 4 hrly NaCl 24/7 29/7 Sodabicarbona iv[Parth Dhanani] Page 89
  • 90. [Chapter 5] 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 1.5gm iv 8 hrs Antibiotic (Cefoperazone+Sulbactam) Inj. DNS 1 lit. (140ml/hr) Dehydration Inj. Contramal ( Tramadol ) 80 mg in 100cc iv 8 Analgesic sos 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[Parth Dhanani] Page 90
  • 91. [Chapter 5] Inj. Febrinil ( Paracetamol) 150mg in 10cc iv Analgesic & Antipyretic Inj. Syscan (Fluconazole) 10ml i.v. Antimicrobial DRUG RELTED ISSUE: DRUG INTERACTIONS MANAGEMENT Ondansetron ↔ Concurrent use of 5-HT3 No particular intervention Tramadol receptor antagonists may is required. However, the (Moderate) reduce the analgesic possibility of a efficacy of tramadol. The diminished therapeutic proposed mechanism is response to tramadol antagonism of serotonin- should be considered mediated effects of during concomitant tramadol at the spinal level. therapy with 5-HT3 receptor antagonists. Fluconazole ↔ Concurrent use of two or Caution and clinical Ondansetron more drugs that can cause monitoring are (Moderate) QT interval prolongation recommended if multiple may increase the risk of agents associated with QT ventricular arrhythmias, interval prolongation are including ventricular prescribed together. tachycardia and torsades de Patients should be advised pointes, due to additive to seek medical attention arrhythmogenic potential if they experience related to their effects on symptoms that could cardiac conduction. indicate the occurrence of torsades de pointes such as dizziness, palpitations, or syncope.[Parth Dhanani] Page 91
  • 92. [Chapter 5]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)[Parth Dhanani] Page 92
  • 93. [Chapter 5]  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 15 mL/min 90 - 120 mL/min FILTERATION RATE 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 109.88 IU/L 44-147 IU/L PHOSPHATASE SERUM PROTEINS Total 5.3 g/dL Total 60-85 g/ dL SERUM ELECTROLYTES 120 mEq/L 137-149 mEq/L • SODIUM 4.95 mEq/L 3.5-5 mEq/L • POTASSIUM[Parth Dhanani] Page 93
  • 94. [Chapter 5] 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 91% 44-74% • Lymphocytes 6% 24-44% • Eosinophils 1% Upton 3% • Monocytes 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[Parth Dhanani] Page 94
  • 95. [Chapter 5]  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.[Parth Dhanani] Page 95
  • 96. [Chapter 5] MEDICATIONS:Table 30 Medications of UTI patient DRUG DOSE ROA DURATION GENERIC NAME DAY 1–7 Inj. Sodium 120 I.V 6 amp as bolus Sodium bicarbonate √ bicarbonate mEq 6 amp hourly Inj. Actrapid 4-6-4 S.C Q 6 hr Insulin √ units Inj. Zostum 1g I.V For the first 12 cefoperazone + √ hrs 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 I.V QD Reduced folinic √ in 100cc acid NS Inj. Optineuron 1 amp in I.V QD Vitamin √ 100 mL[Parth Dhanani] Page 96
  • 97. [Chapter 5] 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 interactionsDRUGS INTERACTION MANAGEMENTFurosemide ↔ Loop diuretics enhance the It is advisable to obtain aCefoperazone nephrotoxicity of some serum creatinine level within cephalosporins by an 48 hours and periodically(Moderate) unknown mechanism. during therapy.[Parth Dhanani] Page 97
  • 98. [Chapter 5]Ofloxacin and Both drugs prolong the QT Patients should be advised toOndansetron interval of heart. seek medical attention if they experience symptoms as(Moderate) dizziness, palpitations, or syncope.Ofloxacin and Insulin Quinolone antibiotics may Blood glucose should be interfere with the therapeutic monitored closely whenever(Moderate) effects of insulin Quinolone are prescribed to patients.[Parth Dhanani] Page 98
  • 99. [Chapter 6]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 No of ME No of ADRs case ME +DI per ADRs per case 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 5 7 1.4 0 0 disease 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[Parth Dhanani] Page 99
  • 100. [Chapter 6] 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 0Table 33 Bar graph of disease wise classification 14 12 10 9 8 7 6 6 5 Total cases 4 4 3 3 3 No.of Mes 2 ME/Case 2 1 1 1 1 1 1 1 0 Gender-wise Classification of Cases:Table 34 Gender wise classification Gender Cases ME ME/Case Male 34 50 1.47 Female 16 27 1.68[Parth Dhanani] Page 100
  • 101. [Chapter 6]Table 35 Bar graph of gender wise classification 50 45 40 34 35 30 Cases 25 ME 20 16 ME/Case 15 10 5 0 Male Female Age-Wise classification:Table 36 Age wise classifications Class Cases ME ME/Case Paediatrics 4 1 0.25 Adult 25 40 1.60 Geriatrics 21 36 1.71[Parth Dhanani] Page 101
  • 102. [Chapter 6]Table 37 Pie chart of age wise classification Cases 4 21 Pediatrics Adults 25 Geriatrics 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.[Parth Dhanani] Page 102
  • 103. [Chapter 6]  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.[Parth Dhanani] Page 103
  • 104. [Chapter 6]  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[Parth Dhanani] Page 104
  • 105. [Chapter 6]  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.[Parth Dhanani] Page 105
  • 106. [Chapter 7]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)[Parth Dhanani] Page 106
  • 107. [Chapter 7] 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[Parth Dhanani] Page 107
  • 108. [Chapter 7]  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. Figure 33 Airway assessment Figure 31 Tilt head and lift Figure 32 Place the hands on the chest 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. Figure 34 Ambu’s Bag  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. Figure 35 Rebreathing mask 2. Rebreathing mask:[Parth Dhanani] Page 108
  • 109. [Chapter 7]  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. Figure 36 Venture masks  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 Figure 37 Endotracheal  The breathing tube is passed through into the Intubation 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. Figure 38 Laryngoscope  Vocal cords, upper airway can be injured. Blades  Curved and straight blades are used for adults[Parth Dhanani] Page 109
  • 110. [Chapter 7] 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 Figure 39 Tracheostomy 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. Figure 40 IV cannula 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 Figure 41 Nasal cannula 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 42 Central venous catheter[Parth Dhanani] Page 110
  • 111. [Chapter 7] 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 Figure 43 Feeding tubes 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 44 Insulin device[Parth Dhanani] Page 111
  • 112. [Chapter 7]  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 Figure 45 How to pacemaker kept in ventricle Insulin Devices: Insulin Types: - Rapid acting- Humalog, Novo log[Parth Dhanani] Page 112
  • 113. [Chapter 7] - 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 Figure 46 Sharp container Glargine (Lantos) Cloudy or milk look: NPH, Lente, and Ultralente. Insulin syringes: Choosing a syringe: which insulin concentration its 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[Parth Dhanani] Page 113
  • 114. [Chapter 7]  Get Supplies: Insulin (Verify), Syringe, Alcohol wipe, Disposable gloves, Sharps container  Wash hands and apply gloves  Clean the insulin vial  Select injection site Figure 47 Injecting air into bottle  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 Figure 48 Push the plunger in  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[Parth Dhanani] Page 114
  • 115. [Chapter 7] (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[Parth Dhanani] Page 115
  • 116. [Chapter 7] 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.[Parth Dhanani] Page 116
  • 117. [Chapter 7] 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.[Parth Dhanani] Page 117
  • 118. [Chapter 7]  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 Figure 52 Normal ECG pattern - 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[Parth Dhanani] Page 118
  • 119. [Chapter 7]  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:[Parth Dhanani] Page 119
  • 120. [Chapter 7]  Tissues in the body dont 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.[Parth Dhanani] Page 120
  • 121. [Chapter 7]  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 bodys 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.[Parth Dhanani] Page 121
  • 122. [Chapter 7]  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.[Parth Dhanani] Page 122
  • 123. [Chapter 8]CHAPTER 8: SUMMARY‘Experience is the best teacher”Now, at the end of Hospital Training, I am pleading to say that NIRMAUNIVERSITY has intellectually included Hospital Training as part of B.Pharm.Hons. ‗S academic curriculum (Semester X). This hospital training has given me achance to get exposed to practical work. What I have studied in semester 9, I haveable 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 onlytheoretical aspect, but practical aspect as well which, according to me, the mostexciting experience of my field is. According to my merit rank (calculated on thebasis of semester 9 marks); I have got a chance to get trained in Shrey Hospital underthe guidance of Dr. Chirag Joshi sir. He is the one who holds and manages theIntensive Coronary Care Unit (I.C.C.U) on one hand alone. It has been greatexperience to obtaining under such qualified and experienced person.On the first day of my training, I along with fellow members was introduced tomedical staff and have been introduced to different departments like ICCU, Operationtheatre, dialysis unit, Radiology department, Pathology Lab, Lithotripsy, Pharmacyand 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 handleprescription and reading as well. I came to know the arrangement of medicines.Different medicines of same company were kept in one shelf and were arrangedaccording to their alphabetical order in the same shelf. I also came to know aboutmedication handling & storage, dispensing, ADR and medication order identificationwhile handling prescription. By this pharmacy experience I came to know aboutextreme use of antibiotics i.e. irrational use we can say. Pharmacists here in pharmacyhave 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 oftraining. 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,[Parth Dhanani] Page 123
  • 124. [Chapter 8]chief complains, past history, past medication history, vital signs, systemicexamination, laboratory investigation, other diagnostic tests (X-ray, USG, and MRI),medications, adverse reactions and then other related discussions. Sir explained ushow to take history of patient and assigned me the case along with other fellowmembers which we have to present before him on the next day by preparing in theformat what he had taught to us. Sir fully explains us the case according to format andcarries 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 alongwith brand names and the spectrum they cover. He explained all the part of case fromentering 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, alcoholicpatient, renal failure.During this practical training I also involved in ward round participation. I used to gowith Chirag sir and learn the way treat the patient and maintain patient history notes. Iused to check drug dose and dosing frequency. I also used to take patient historywhich 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 knowledgein dealing with patient.All in all, it was the best experience that I have undergone in my field. This would begreater than anything in clearing my future registered pharmacist exam in US. Havingthis experience, I came to know that this place where I should be.[Parth Dhanani] Page 124
  • 125. [Chapter 9]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 & Dales 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[Parth Dhanani] Page 125
  • 126. [Chapter 9] 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[Parth Dhanani] Page 126
  • 127. [Chapter 10]CHAPTER: 10ANNEXURE. 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[Parth Dhanani] Page 127
  • 128. [Chapter 10] 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 SHEETConsultant:Pt‘s Name:CHIEF COMPLAIN: Room No. Reg. No.KNOWN CASE OF: Date:GEN. EXAMINATION:SYSTEMIC EXAMINATION:[Parth Dhanani] Page 128
  • 129. [Chapter 10] 2. Investigations: INVESTIGATIONS An ISO 9001:2000 Certified HospitalConsultant: Room No:Pt.‘s Name: Reg. No:DateHbTCDCESRPCRCBTCTP.T.SmearUrineStoolRBSPPBSFBSUreaCreatinineNa+K+CL-Ca++S.Bill : TotalDirectIndirectS.G.P.T.S.G.O.T.S.Alk.Po4aseS.AmylaseS.LipaseS.Protein :TotalAlb.Glb.TT[Parth Dhanani] Page 129
  • 130. [Chapter 10] X – Rays : USG: MRI/C.T. SCAN : Sputum : R Ascitic Fluid M Plural fluid Stain C.S.F. : C S Other :[Parth Dhanani] Page 130
  • 131. [Chapter 10] 3. Examination sheet SHREY HOSPITALS PVT. LTD. An ISO 9001:2000 Certified HospitalPlot No. 270/5/B, Near AMCO Bank, Stadium circle, Navrangpura, Ahmedabad- 380009. PHONE: 079-26468620, 40017777 EXAMINATION SHEET Consultant: Room No: Pt.’s Name: Reg. No. : Date-Time Findings Reg. No.:[Parth Dhanani] Page 131
  • 132. [Chapter 10] 4. T.P.R., & Input/output Chart SHREY HOSPITAL PVT. LTD. Room No. Reg. No. Date T.P.R. & INPUT/OUTPUT CHATConsultant: Pt.’s Name:TIME T P CVP IN PUT IVF OUT PUT RBS INSULIN A/G Stool Total ACC Oral I Urine Asp Vomit I/V TO V CVP Fluid OR U/OA.M.89101112P.M.1235678Total DAY CHAT NIGHT CHART TOTALOralIVUrineStoolVomit[Parth Dhanani] Page 132
  • 133. [Chapter 10] 5. Admission and discharge record: 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 OUT PUT RBS INSULI A/ Stool Total ACC N G Vomi I/V Oral IV. Urin Asp TO t Fluid e m Liq m Liq CVP l l OR U/O8 P.M.9 P.M.10 P.M.11 P.M.12 MidNight1 A.M.2 A.M.3 A.M.4 A.M.5 A.M.6 A.M.7 A.M.8 A.M.TOTAL[Parth Dhanani] Page 133
  • 134. [Chapter 10] 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 Reg. No.: Room no.: Date: Time: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 Date: Time: Hospitalization Days: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[Parth Dhanani] Page 134
  • 135. [Chapter 10] 7. Case study format:[Parth Dhanani] Page 135